Diving and
fifth edition

Diving and
fifth edition

Carl Edmonds was the OIC of the Royal Australian Navy Diving Medical Unit,
Foundation President of the South Pacific Underwater Medical Society and Director
of the Australian Diving Medical Centre, Sydney, Australia
Michael Bennett is Academic Head, Wales Anaesthesia and Senior Staff Specialist,
Diving and Hyperbaric Medicine, Prince of Wales Hospital and University of New
South Wales, Sydney, Australia
John Lippmann is Founder and Chairman of Divers Alert Network Asia-Pacific,
Ashburton, Australia
Simon J. Mitchell is a Consultant Anaesthesiologist and Diving Physician, and Head,
Department of Anaesthesiology, University of Auckland, Auckland, New Zealand

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Carl Edmonds, OAM, MB, BS (Sydney), MRCP Simon Mitchell, MB ChB, PhD, Dip DHM, Dip
(Lond.) FRACP, FAFOM, DPM, MRC Psych, Occ Med, Cert DHM (ANZCA), FUHM,
Director, Diving Medical Centre, Sydney, Head of Department, Department of
Australia (1970–2000) Anaesthesiology, University of Auckland,
Formerly, Officer in Charge Royal Australian Navy Auckland, New Zealand (2011–present)
School of Underwater Medicine (1967–1975) Consultant in Diving and Hyperbaric Medicine,
Formerly, President, South Pacific Underwater Slark Hyperbaric Unit, North Shore Hospital,
Medicine Society (1970–1975) Auckland, New Zealand (2012–present)
Consultant in Underwater Medicine to the Royal Formerly, Medical Director, Wesley Centre for
Australian Navy (1975–1991) Hyperbaric Medicine, Brisbane, Australia
Consultant in Diving Medicine (1967 until retired (1998–2002)
in 2015) Formerly, Director, Slark Hyperbaric Unit, Royal
New Zealand Navy Hospital, Auckland,
Michael Bennett, MB, BS (UNSW), DA (Lond.), New Zealand (1995–1998)
FFARCSI, FANZCA, MM (Clin Epi) (Syd.),
MD (UNSW), Dip DHM, FUHM John Lippmann, OAM, BSc, Dip Ed, MAppSc
Director, Department of Diving and Hyperbaric Founder, Chairman and Director of Research,
Medicine, Prince of Wales Hospital, Sydney, DAN (Divers Alert Network) Asia-Pacific
Australia (1993–2008) (1994–present)
Academic Head, Wales Anaesthesia, Sydney, Author or co-author of: The DAN Emergency
Australia (2012–present) Handbook, Deeper Into Diving, The Essentials
Formerly, President, South Pacific Underwater of Deeper Sport Diving, Scuba Safety in
Medicine Society (2008–2014) Australia, Oxygen First Aid, First Aid and
Formerly, Vice-President, Undersea and Hyperbaric Emergency Care, Automated External
Medical Society (2006–2007 and 2011–2012) Defibrillators, Advanced Oxygen First
Conjoint Associate Professor in Anaesthesia and Aid, Basic Life Support, Cardiopulmonary
Diving and Hyperbaric Medicine, University Resuscitation, Decompression Illness, Am I
of New South Wales, Sydney, Australia Fit to Dive? and various incarnations of these
(2010–present) books.



Authors v
List of abbreviations xi
Preface and excerpts from earlier editions xiii
Dedication xv
Acknowledgements xvii

Part 1 DIVING 1

1 History of diving 3
2 Physics and physiology 15
3 Free diving 27
4 Diving equipment 37
5 Undersea environments 53

Part 2  DYSBARIC DISEASES: Barotraumas 63

6 Pulmonary barotrauma 65
7 Ear barotrauma 81
8 Sinus barotrauma 103
9 Other barotraumas 115


10 Decompression sickness: pathophysiology 125
11 Decompression sickness: manifestations 141
12 Decompression sickness: prevention 153
13 Decompression sickness: treatment 167
14 Dysbaric osteonecrosis 185


15 Inert gas narcosis 205
16 Hypoxia 217
17 Oxygen toxicity 229


viii Contents

18 Carbon dioxide toxicity 245
19 Breathing gas preparation and contamination 255
20 High-pressure neurological syndrome 267

Part 5  AQUATIC DISORDERS: The drowning syndromes 273

21 Drowning 275
22 Pathophysiological and clinical features of drowning 285
23 The management of drowning 291
24 Salt water aspiration syndrome 303
25 Why divers drown 309


26 Seasickness (motion sickness) 321
27 Thermal problems and solutions 325
28 Cold and hypothermia 329
29 Infections 339
30 Scuba divers’ pulmonary oedema 357
31 Trauma from marine creatures 367
32 Venomous marine animals 377
33 Fish poisoning 397
34 Underwater explosions 405


35 The ear and diving: anatomy and physiology 413
36 The ear and diving: investigations 421
37 The ear and diving: hearing loss 429
38 The ear and diving: vertigo and disorientation 435
39 Cardiac problems and sudden death 449
40 Neurological disorders of diving 459
41 Psychological and neuropsychological disorders 467
42 Miscellaneous disorders 487
Carotid sinus syndrome 487
Caustic cocktail 488
Cold urticaria 488
Dental disorders 488
Hyperthermia 489
Musculoskeletal problems 489
Compression (hyperbaric) arthralgia 489
Cramp 489
Decompression 490
Lumbosacral lesions 490
Temporo-mandibular joint dysfunction 490
Tank carrier’s elbow 491
Ocular disorders 492
‘Bubble eyes’ 492

Contents ix

Ocular problems from corneal lenses 492
Ocular fundus lesions 492
‘Swimmer’s eyes’ (blurred vision) 493
Trauma 493
Other disorders 493
Pulmonary oedema and dyspnoea 493
Diving diseases 493
Asthma provocation 493
Cold urticaria 494
Deep diving dyspnoea 494
Skin reactions to equipment 494
Contact dermatitis (mask, mouthpiece and fin burn) 494
Angioneurotic oedema (dermatographia) 494
Allergic reactions 495
Burns 495
Diaper Rash (nappy rash) 495
Fin ulcers 495
Trauma 495
43 Drugs and diving 497
44 Long-term effects of diving 509


45 Stress responses, panic and fatigue 519
46 Why divers die: the facts and figures 527
47 Unconsciousness 551
48 First aid and emergency treatment 557
49 Oxygen therapy 567
50 Investigation of diving accidents 575
51 Investigation of diving fatalities 583


52 Medical standards for snorkel divers 603
53 Medical standards for recreational divers 607
54 Medical standards for commercial divers 623
55 Asthma 629
56 Cardiac and peripheral vascular disease 649
57 Insulin-dependent diabetes mellitus 657
58 Age and diving 673
59 Diver selection 681


60 Female divers 687
61 Breath-hold diving 697
62 Technical diving 703
63 Divers with disabilities 719

x Contents

64 Submarine medicine 725
65 Occupational groups 731
66 Diving in contaminated water 737
67 Deep and saturation diving 739


68 Hyperbaric equipment 747
69 Hyperbaric medicine 755

Appendix A: Decompression tables 767

Appendix B: US Navy recompression therapy tables 785

Appendix C: Recompression therapy options 793

Appendix D: Diving medical library 797

Appendix E: Diving medical training 801

Appendix F: Diving medical organizations and contacts 803

List of abbreviations

ADS atmospheric diving suit FEV1 forced expiratory volume in 1 second
ADV automatic diluent valve FIO2 fraction of inspired oxygen
AGE arterial gas embolism FVC forced vital capacity
ALS advanced life support HBOT hyperbaric oxygen therapy
ARDS acute respiratory distress syndrome HPNA high-pressure neurological syndrome
ATA atmosphere absolute IBCD isobaric counterdiffusion
ATG atmosphere gauge ICP intracranial pressure
BCD buoyancy compensator device IDDM insulin-dependent diabetes mellitus
BLS basic life support ILCOR International Liaison Committee on
BOV bail-out valve Resuscitation
BSAC British Sub-Aqua Club IPE immersion pulmonary oedema
CAD coronary artery disease IPPV intermittent positive pressure
CAGE cerebral arterial gas embolism ventilation
CCR closed-circuit rebreather ISO International Organization for
CMF constant mass flow Standardization
CPAP continuous positive airway pressure lpm litres per minute
CPR cardiopulmonary resuscitation MOD maximum operating depth
CSF cerebrospinal fluid msw metres of sea water
CSL Commonwealth Serum Laboratories NEDU Navy Experimental Diving Unit
DAN Divers Alert Network NOAA National Oceanic and Atmospheric
dB decibel Administration
DCI decompression illness NUADC National Underwater Accident Data
DCIEM (Canadian) Defence and Civil Centre
Institute of Environmental Medicine OPV over-pressure valve
DCS decompression sickness PaCO2 alveolar pressure of carbon dioxide
DDC deck decompression chamber PaCO2 arterial pressure of carbon dioxide
DPV diver propulsion vehicle PADI Professional Association of Diving
EAD equivalent air depth Instructors
ECC external cardiac compression PaO2 alveolar partial pressure of oxygen
ECG electrocardiogram PaO2 arterial partial pressure of oxygen
ECMO extracorporeal membrane oxygenation PCO2 partial pressure of carbon dioxide
ECoG electrocochleography PEEP positive end-expiratory pressure
EEG electroencephalogram PEF peak expiratory flow
ENG electronystagmography PFO patent foramen ovale
EPIRB electronic position-indicating radio PICO2 inspired partial pressure of carbon
beacon dioxide


xii  List of abbreviations

PIO2 inspired partial pressure of oxygen SDPE scuba divers’ pulmonary oedema
PMCT post-mortem computed tomography SMB surface marker buoy
PMDA post-mortem decompression artefact SPUM South Pacific Underwater Medicine
PMV pressure maintaining valve Society
PN2 partial pressure of nitrogen SSBA surface-supply breathing apparatus
PO2 partial pressure of oxygen SWAS salt water aspiration syndrome
PPV positive pressure ventilation UHMS Undersea and Hyperbaric Medical
RAN Royal Australian Navy Society
RCC recompression chamber UPTD unit of pulmonary toxic dose
RGBM reduced gradient bubble model USN United States Navy
RMV residual minute volume (also VC vital capacity
respiratory minute volume) VER visual evoked response
SCR semi-closed-circuit rebreather VGE venous gas emboli
scuba self-contained underwater breathing VPM varying permeability model
apparatus V/Q ventilation-perfusion

Preface and excerpts from
earlier editions

This book is written for doctors and paramedics a comprehensive clinical text. We tried to remedy
who are called on to minister to the medical needs this. Our primary focus remains on the diving cli-
of those divers who venture on or under the sea. nician, the physician responsible for scuba divers,
It was based on our experience in dealing with a the diving paramedic and the exceptional diving
vast number of diving accidents and with trouble- instructor who needs some guidance from a prac-
shooting many diving problems, and it is also an tical reference text.
attempt to integrate the experience and more eru- Diving accidents are much better defined,
dite research of others. investigated and treated than when we com-
The very generous praise bestowed by review- menced writing on this subject, many years ago.
ers on the first edition of Diving and Subaquatic It  was our intent to present, as completely as
Medicine, and its surprising acceptance outside the ­possible, an advanced and informative book on
Australasian region, inspired us to prepare further clinical diving medicine. We have avoided the
editions of this text. ­temptation to write either a simplistic text or a
In the later editions, we attempted to be less research-­oriented tome.
insular. Instead of an Australian book about This text encompasses the range of diving dis-
Australian experiences, we sought the advice and orders experienced by divers. It presents all aspects
guidance of respected friends and colleagues from of diving medicine from ancient history to the
other countries, and from other disciplines, espe- latest trends, in a concise and informative man-
cially in the United Kingdom, the United States, ner. Each disorder is dealt with from a historical,
Canada, Japan and mainland Europe. This has not aetiological, clinical, pathological, preventive and
prevented us from being judgemental and selective ­t herapeutic perspective. Summaries, case histories
when we deemed it fit. This is still a very special- and revision aids are interspersed throughout. For
ized field where evidence-based medicine is in its the doctor who is not familiar with the world of
infancy. Truth is not always achieved by voting, diving, introductory chapters on physics and phys-
and consensus is often a transitory state. We have iology, equipment and the diving environments
documented what we believe to be current best have been included.
practice. The future will judge this. The inclusion of anecdotes and occasional
The extension of diving as a recreational and humour may lessen the load on the reader, as
commercial activity has led to the bewildered it does on the authors. As in previous editions,
medical practitioner’s being confronted with div- each chapter is edited by one of the authors, with
ing problems about which he or she has received overview and peer review available from the oth-
little or no formal training. Doctors interested in ers. This means that not always will there be exact
diving had previously found themselves without agreement among authors, and there may be some


xiv  Preface and excerpts from earlier editions

variation among chapters. This is inevitable when will experience as much excitement, fascination,
evidence and consensus are not always complete. achievement, ­camaraderie and fun from diving as
It is also healthy for the future. we have.
Three of the four previous authors have
departed from this scene, and the fourth is about Carl Edmonds, 2015
to leave. The baton needs to be passed. Our leg- on behalf of all previous
acy and intent are that our younger colleagues and new authors of this text.

lating about an appropriate dedicatee for their text. Pluto solved our dilemma. He was We could not decide between Paul Bert.Dedication This book is dedicated to the memory of Pluto. Al Behnke.. even though he never left dry land.B.S. and J. xv . Haldane. who study when the original three authors were postu- died. a much loved basset hound who strolled into our Jr. I have often been asked who Pluto was.


John Lippmann.Acknowledgements Carl Edmonds. previous editions. but they are not to blame for the final text. John Hayman and our clinical tutors – the divers. They include the following: xvii . Richard Chole John Pearn We wish to acknowledge the assistance given David Dennison Peter Sullivan by the Royal Australian Navy. Michael Bennett Peter Bennett Eric Kindwall and Simon Mitchell would like to thank Chris­ Ralph Brauer Clarrie Lawler topher Lowry. Glen Egstrom John Tonkin duce excerpts from their diving manuals. the Royal Navy and Chris Edge Ed Thalmann the United States Navy for permission to repro. our families who have suffered unfairly. John Pennefather and Robyn Walker Greg Briggs Christopher Lawrence for their invaluable contributions to previous edi. upon which material in this latest fifth edition Jim Caruso Owen O’Neill is based. Our gratitude is extended to these valued colleagues. and to David Elliott John Williamson the many pioneers on whose work we have so heav. Des Gorman David Yount ily drawn. Numerous experts have been consulted to Originally published in 1976 by the Diving Medical review and advise on specific chapters of this or Centre (Australia) ISBN 09597191-0-5. Ian Calder Dale Mole tions.


1 Part     Diving 1 History of diving 3 2 Physics and physiology 15 3 Free diving 27 4 Diving equipment 37 5 Undersea environments 53 .


which. advanced from the first timid dive to an indus. to this The origins of breath-hold diving are lost in time. were used by soldiers as water canteens and water. Some attribute the change in fishers have dived for sponges. and the women collected shells and plants. in earlier pattern to better endurance of the women in cold days. Greek divers still search the waters to 1184  BC. industries involving breath-hold diving persist. with depth. as well as for washing. dived for the Tuamoto Archipelago. underwater exploration had men. By 4500 BC. and special 3 . 1 History of diving Breath-hold diving 3 Modern military diving 8 Early equipment 4 Deep diving 9 Modern diving equipment 6 Recreational diving 12 Self-contained equipment 7 Further reading 12 BREATH-HOLD DIVING In other parts of the world. until the nineteenth century when helmet diving There is a long history of the use of divers equipment was introduced. Africa for sponges. allowing the intrepid for strategic purposes. precautions were being taken ment to that offered by modern ­governments and against divers. By Roman times. They sabotaged enemy ships by bor- of the Mediterranean Sea as far afield as northern ing holes in the hull or cutting the anchor ropes. likely in the first instance gathering shell. a point many divers Breath-hold diving for sponges continued seem keen to disprove. Divers were involved in to gamble their lives in order to reach the deeper operations during the Trojan Wars from 1194 sponge beds. In more recent times. Others pay homage to the folklore that div- wound dressings. The attackers in their turn used divers to goods. to some extent. The shells and seaweed are a prized part of Korean try that supplied the community with shells. has been restricted to the women. Anchor cables were made of iron diving companies. serving as tenders. ing reduces the virility of men. or diving time. an extinct primitive human. diving and pearls. Archaeologists claim that the Neanderthal women of Japan and Korea. Many divers would prefer this arrange. chain to make them difficult to cut. and the pearl divers of human. Originally the male divers were fisher- canoes. Notable examples include the Ama. food and Japanese cuisine. with the men From the ancient Greek civilization until today. food. The diver’s share of the cargo was increased remove the obstructions. Divers were also used to construct underwater The ancient Greeks laid down the first rules defences designed to protect ports from the attack- on the legal rights of divers in relation to salvaged ing fleets. The Ama has existed as a group for more than fish by wading at low tide before diving from 2000 years.

Officially recorded Snorkels. when the goods past customs. as long as the line is used to tions of the ‘event’. Jonah was at best a reluctant pioneer native divers for pearling. Some claim that Alexander the Great descended Free diving appears to have evolved as a modern in a diving bell during the third century BC. salvage and smuggling diver. mask or weights) Sri Lanka observed pearl diving on the Coromandel who pulls himself or herself down and then up a Coast. descent. breathing tubes made from reeds and depths in excess of 210 metres have been achieved bamboo (now plastic. is discussed in indicated by their value on the slave market. sport in the mid-1940s. These include the following: is most unlikely that the artisans of the time could In ‘no limits’. No weights can be removed during the dive. pleasure by having one of her divers fasten a salted ‘Free immersion’. the fleet against underwater attackers. but that the divers could ‘Static apnoea’ involves resting breath-holding reach 27 metres by using a weight on a rope to assist (usually lying in a pool) with the face submerged. Because his descent was ies to repel sharks. Mono- An interesting early report indicated that some fins or bi-fins can be used. The exploits of Jonah are described with for 15 minutes. submariner than a diver. supporting evidence. The history of submarine escape. The Spaniards exploited these involuntary. The demand for divers was submariner may become a diver. The most skilled of the American native div. on the technicality that he was more a secret chemical that they rubbed over their bod. depths of 10 to 15 metres. but there is a shortage of sunset. seventeenth The history of diving with equipment is long and and eighteenth centuries reported that these divers complex. or both. Mark constant weight apnoea but without the use of fins. a diver can use any means to travel make glass as depicted in most of the illustra- down and up the line. but this weight is standing by having his divers ensure a constant sup. when they wished to surface. descent. encompasses was said to have taken 3 days to swim past him! It a variety of disciplines. ing prices up to 150 gold pieces. They could dive from sunrise to conviction in one text. Antony participated in a fishing contest held in With ‘variable weights’. developed in many parts of the world. Columbus . the cable. aided by an inflatable balloon. They reported that the most diving was to weighted line. involves Marco Polo and other travellers to India  and a finless diver (with optional suit. They allow a ‘Constant weight apnoea’ diving is where descent diver to breathe with the head underwater. limited. were assisted by have been achieved using this method. an attendant who hauled on a rope attached to the ‘Dynamic apnoea’ measures the distance cov- net. Currently the sport. The divers were noted to hold their nose during ered in a pool during a single breath-hold. the diver again descends Cleopatra’s presence and attempted to improve his with the aid of a weighted sled. Further reference is made to ance to tobacco! They also claimed to possess a him later. Ascent is achieved by finning or pulling up ply of fish on his line. This may have been a product measure the distance. One fish which is steadily gaining popularity. 7 days a week and attributed their endur. stories attributed to him were spectacular. and some of the fish among Italian spearfishers. Chapter 64. Travellers who observed them during the sixteenth. although the diver is inferred that the Greeks used them. and in the early stages it is mixed with could descend to 30 metres and remain submerged legend. Aristotle and ascent occur along a line. fetch. which emerged in places fish to his hook.4  History of diving guards with diving experience were used to protect not permitted to pull on this line to assist movement. initially as a competition Details of the event are vague. rubber or silicone). were using this method. Roman divers were also involved in Mark Anthony’s ‘Constant weight without fins’ is the same as attempt to capture the heart of Cleopatra. They carried a net to put the oysters in Officially recorded times in excess of 11 minutes and. EARLY EQUIPMENT ers came from Margarita Island. Most divers descend down a of artistic licence or evidence that the incident is line using a weighted sled and return to the surface based more in fable than in fact. where equipment was difficult to obtain. The Queen showed her dis.

It could also be claimed that he had the basis of the experi- mental cryogenic diving set in which gas is carried in liquid form and purified by freezing out carbon dioxide. open at the bottom. In 1691. occu- more likely a float or life jacket. were salvaged Leonardo da Vinci sketched diving sets and fins. each weighing more than 1000 kg.1  Edmond Halley’s diving bell. These consist of a weighted chamber. tage of a large dead space. Another Italian. 50 bronze cannons. the diver to the area close to the bell. the English astrono. connected to the bell.1). The one to 1 1/2 hours were recorded. Another of his ideas was for the diver to have a ‘wine skin to contain the breath’. 1691. Figure 1. Early equipment  5 reported that the North American Indians would with air in barrels (Figure  1. Edmond Halley. The first fully documented use of diving bells dates from the sixteenth century. is connected to some sort of bladder or bag. realized that Leonardo was in error and that the diver’s air would have to be purified before he breathed it again. blocked the ­diver’s a method of supplying air to a diver from a hose vision and imposed impossible loads on the breath. The Australian aborigines plied with air from weighted barrels. The mer who predicted the orbit of the comet that bears weighted barrels of air that were used to replen- his name. he had the basic idea of a rebreathing set. in 30  metres of water in Stockholm harbour. The length of hose restricted ing muscles. The tube barotrauma. through. The drawing one of the earliest recorded sufferers of middle ear shows a man with a tube in his mouth. spears or general construction work. Dives to 20 metres for up people have ‘invented’ long hose snorkels. dated 1511. Halley was dated 900 BC as an early diving set. Borelli. a method of supplying fresh air was devel- oped. The tube length pied by one person and with no air supply to was a metre or more and so impossible to breathe it. which were used a similar approach to hunt wild duck. so it is probably safe to assume that there was no practical diving equip- ment in Europe at that time. treasure recovery and were able to capture the birds with nets. Halley’s bell was sup- even their bare hands. Later. It is not Some have interpreted an Assyrian drawing known whether this was successful. It is Swedish divers had devised a small bell. Between 1659 and 1665. apart from snorkels. This was probably the first recorded design of a self-contained breathing apparatus. His drawings appear tentative. a reed and keeping their bodies submerged. Halley also devised designed by Vegetius. in 1680. The early use of bells was limited to short periods in shallow water. Borelli suggested that the air could be puri- fied and breathed again by passing it through a copper tube cooled by sea water. from the Vasa. Various hauled from the surface. With this devel­ swim toward wild fowl while breathing through opment  diving bells became more widespread. Diving bells were the first successful method of increasing endurance underwater. With this concept. in which one or more people could be lowered under water. They They were used for salvage. This Swedish warship had sunk One set was really a snorkel that had the disadvan. . patented a diving bell that was supplied ish the air can be clearly seen.

The origins diving school on HMS Excellent later that year. with borrowing and stealing of at least they were until the diver bent over or fell. The Royal Engineers were taught to dive by Siebe’s firm came to be the major manufac. The and John Deane continued to use it up to the Siebe suit was found to be greatly superior to the time of the Crimean War. During the second half of the nineteenth cen- tury. reliable air pumps were developed. This task would not be easy for divers. and evolution from open helmet and standard Decompression sickness was noted. which set up their first acceptable equipment of this type. which cover the head and shoulders. and among the major users of this equipment. Divers were given fresh dry . the diver could control his immigrant engineer who later became a natural. possibly for the marketing advan. This type of being in service for 75 years. These were able to supply air against the pressures experienced by divers. The diver could control buoyancy opments from the Siebe closed helmet was the US by adjusting the flow through the outlet valve and Navy Mark 5 helmet. which obstructed the anchorage at Spithead. assisted by ropes from the surface. or if the hose or pump leaked. Also. from the bottom of the helmet. MODERN DIVING EQUIPMENT The first people to be exposed to a pressure change in a vessel on the surface were patients exposed to higher or lower pressure as a therapy for vari- ous conditions – the start of hyperbaric medicine. with communications to allow the diver to confer face into the helmet.2). If this happened. The Deane brothers were the inventors Engineers on dives on the wreck of the Royal George. following the development discussed several designs that were developed at of these diving suits. They then established a training facility overstated. This equipment consisted of a ladder or rely on his tenders to do this. the helmet is fitted (Figure 1. is still in use. equipment. depth easily. with a few refinements. other designs. Siebe’s apparatus allowed the diver Standard rig. One of the devel- an outlet valve. a rigid helmet sealed to a flexible waterproof suit In more modern versions. which marketed the first ­diving to the Royal Navy. civilian divers in 1939–40 while on the Royal turer. Several people had the idea of using these pumps for diving and devel- oped what are now called open helmets.6  History of diving The  guns were recovered by divers working from a bell. The diver could breathe because the head and neck were in air. albeit not dress were the subject of a study by Bevan. Air was pumped down to the diver. A diver in an open helmet had to climb ized British citizen). at Gillingham in 1844 where they reintroduced tages gained by his firm. several types the helmet flooded and the diver was likely to of diving suits and a bell were used by the Royal drown. or standard diving dress.2  Augustus Siebe’s first helmet. and the excess air escaped Figure 1. The origins of diving medical research can also be traced to these experiments. but his role in the design may have been George. or the same time. Air was pumped down from the sur. was to bend over or even lie down without the risk of first produced in 1840 by Augustus Siebe (a Russian flooding the helmet. It probably set a record by thus the volume of air in the suit. even with the best of modern equipment. and excess air bled off through with another diver or the surface. By the mid-nineteenth century. ideas from each other. who recognized in divers.

Haldane are the fathers of tus (scuba) is used to describe any diving set that diving medicine. but it seems likely that this was done on in 1904. who made a scuba in tion of gas bubbles in the body and suggested that which the compressed air was stored in a copper it could be prevented by gradual ascent. There is a brief report of an American decompression sickness was caused by the forma. This theory was tested on goats and then on men 1918 by Ohgushi. set was supplied with air from the surface that was Haldane concluded from Paul Bert’s results that breathed on demand via a mouthpiece. a Scottish scientist. Haldane. they were exposed to a dangerous degree of nitro- Decompression sickness was also observed in gen narcosis. the working area is SELF-CONTAINED EQUIPMENT pressurized to keep the water out. equipment in the East River in New York in 1831. Most of these The next year they raised a submarine near Hawaii men would have been suffering from decompres. However. The gas was released showed that pain could be relieved by a return to into a hood that covered the upper half of his body. Self-contained underwater breathing appara- Paul Bert and J. and Alexander Lambert had recovered behalf of Guillaumet. The first work- book is still used as a reference text even though able form probably dates from the early nineteenth it was first published in 1878. The divers used air. He also pipe worn around his body. Accumulation of carbon dioxide was controlled by aged by the diver’s returning to the pressure of the allowing the respired gas to escape through a small caisson. but deeper dives had been recorded.S. It was fitted a diver could be hauled safely to the surface from with a compressed air reservoir so that the diver 10 metres with no evidence of decompression sick. workers employed in pressurized caissons and tunnels. Self-contained equipment  7 undergarments because the ‘rheumatic’ pains they Haldane also developed ­several improvements to the suffered were attributed to damp and cold. gold bullion from a wreck in 50 metres of water in Another early development was the Rouquayrol 1885. specially designed recompres. Such cases were initially man. Condert died while diving with his some job sites within a few years. Bert showed that century. provided limited by the amount of air in the reservoir. carried on the back. S. J. higher pressures. was appointed In 1838. Paul Bert published a text book allows the diver to carry the breathing gas sup- La pression barométrique based on his studies of ply with him or her. who was Japanese. as a scuba. based on old drawings. A patent for a similar device was 30 metres. divers suffered paralysis that was attributed to In 1914. This was a remarkable sion sickness because they were diving for up to feat considering that the salvage techniques had to three times the accepted limits for dives without be evolved by trial and error. The endurance. Haldane’s work culminated in an open could be operated with a supply of air from the water dive to 64 metres in 1906 and the publication surface or as a scuba with an air supply cylinder of the first acceptable set of decompression tables. In these operations. His invention. could detach himself or herself from the air hose ness. His system in chambers. There are several claims to its the physiological effect of changes in pressure. in France for a back-mounted. The history of decompression sickness is discussed in Chapter 10. twin-hose demand lem of decompression sickness in divers. Dr Manuel Guillaumet filed a patent to a Royal Navy committee to investigate the prob. engineer. It was then replaced by fresh gas from the sion chambers were introduced and utilized at storage pipe. US Navy divers reached 84 metres. but he had developed partial paralysis from and Denayrouze device of 1865 (Figure  1. for a few minutes. also filed in England earlier that year by William Greek and Swedish divers had reached 58 metres Newton. Charles Condert. that time was spent at each stage to allow absorbed The first successful scuba with an air supply nitrogen to pass out of the body in a controlled man. as well as decompression sickness. The diver controlled the air . He deduced from this that a diver could be sur. hole. from a depth of 93 metres. Other diving equipment used. At that regulator that was supplied with air from hoses time the Royal Navy had a diving depth limit of to the surface. This decompression sickness. appears to have been developed and patented in ner. was faced from greater than 10 metres in stages. so decompression stops. fatigue from zeal and overexertion.3).

A. although Rouquayrol and Denayrouze. devised by significance as an intelligence operation. it Le  Prieur in 1933. was needed. unfortunately. who was French. This was an oxygen set in which carbon dioxide was absorbed by rope soaked in caustic potash. evaluated for use in gas-powered cars and was far it is interesting to note that the idea of the chariot smaller than the Rouquayrol-Denayrouze device. but. but they may be considered separately because of the difference in principles involved. The attack was a success the diver’s teeth. was widely used and was an important milestone During the First World War.P. designed by J. 1865. clearing of channels blocked by wrecks. the diver carried a coincided with the fall of the Austro-Hungarian compressed air bottle on the chest and released air Empire. Closed-circuit oxygen sets were developed dur. until 1918. and the ship was already in friendly into the face mask by opening a tap. Italy developed a in the development of the modern scuba. hands! The potential of this method of attack was In 1943. Another scuba was devised by in that the ship was sunk. human torpedo or chariot that was used in 1918 to attack an Austrian battleship in Pola Harbour supply by triggering air flow into the mask with in what is now Croatia. The first known successful rebreathing set was designed by English engineer H. In this set. and Davis took out patents on a small submarine ing the same period as the modern scuba. . largely restricted to the salvage of damaged ships. in 1849. One significant clandestine operation conducted during the First World War was the recovery of code books and minefield charts from a sunken German submarine. com- pared with the standard rig. It was an Second World War with divers wearing oxygen adaptation of a reducing valve that Gagnan had rebreathing sets as underwater pilots. the set was used in flooded mines and tunnels where the extra mobility. and assorted ships’ husbandry duties. They put it to use in the first popular scuba as we know it today. rebreathing sets. The patent for the first known prototype of an oxygen rebreather was given to Pierre Sicard. This equipment was the precursor of oxygen sets used in clandestine operations in both world wars and of other sets used in submarine escape. In these and human torpedo controlled by divers in 1914. fire- fighting and mine rescue.8  History of diving These sets are often called scuba. In passing. was suggested to the British Admiralty in 1909. This was of more Figure 1. the diver is supplied with oxygen This was pre-dated by a one-person submarine and the carbon dioxide is removed by absorbent. MODERN MILITARY DIVING The military use of divers in warfare was. Fleuss in 1878. Because of the absence of lines and hoses from the diver to the surface. Cousteau and Gagnan developed the noted by the Italian Navy. This device the diving activity was also kept secret.3  The aerophore. Great risks were taken with this set and its successors when used underwater because the work of Paul Bert on oxygen toxicity was not widely known. Holland in 1875.

This both unrewarding and dangerous. eliminate decompression requirements. only 10 kilometres away. ­toxicity in attempts to understand the condition. divers clearing mines. one can reduce or Gibraltar and Alexandria. and a tanker. mines and was silent during operation for work on They first surveyed the approaches to several poten. standard diving rig. It is nor- cessful attempts with loss of life. Professor Elihu Thompson. new decompression schedules were developed that icity (Chapter 17). they cleared the obstructions that could impede the DEEP DIVING landing craft. This work was important because used periods of oxygen breathing to reduce decom- most of these offensive operations were conducted pression time. to remove the Italian mines before they exploded. ­conducted by the British Admiralty Experimental In Gibraltar. deep diving research had enabled British Clearance Divers and the US Navy Sea. but their most of survival if something went wrong. a special type of underwater war Diving Unit in conjunction with Siebe Gorman evolved. and launched several needed to reduce the number of people at risk from attacks that were opposed by British divers who tried accidental explosions in mine-clearing operations. The change to a self-contained set was Spain. The reduction. In 1919. The twentieth century. of decompression Divers from the allied nations made s­everal time was desirable in increasing the diver’s chances successful attacks on enemy ships. is breathed again after the carbon d­ ioxide has been 1941. The equip- important offensive roles were in the field of recon. this idea was did not often praise his enemies. The nitrogen narcosis at these depths made such dives subjects were the unsung heroes of the work. research tried to extend its depth capability beyond The research back-up to these exploits was largely 60 metres. the submers- devoted to improvement of equipment and the ible decompression chamber was introduced and investigation of the nature and onset of oxygen tox. Dives were made to 107 metres. Helium diving resulted from a series of tors deliberately and repeatedly suffered oxygen American developments. Churchill ing apparatus that was first used extensively by had previously been responsible for rejecting sug. In most operations. They used equipment is that. a scientist. Exploits of by Siebe Gorman and Co. the idea was not practical because . By the early Marines. at Land Teams (SEALs) evolved from these groups. acoustically triggered mines. Air. ment was constructed from non-magnetic materi- naissance and beach clearance. three teams managed to enter removed. or elimination. suggested that nitro- Oxygen-nitrogen mixtures were first used for gen narcosis could be avoided by replacing the diving by the Royal Navy in conjunction with a nitrogen in the diver’s gas supply with helium. by increasing the ratio of oxygen divers riding modified torpedoes to attack ships in to nitrogen in the breathing gas. Equipment was improved. sailors and conscientious objec. group of scientists. a role they After the First World War. said they showed adapted to a self-contained semi-closed rebreath- ‘extraordinary courage and ingenuity’. This development was gestions that the Royal Navy use similar weapons. they succeeded in mally used with equipment in which most of the gas sinking several ships in Gibraltar harbour in mid. Ltd. Ltd. tial landing sites. The Italians had a secret base in neutral and Co. Deep diving  9 Diving played a greater part in offensive opera. This approach was based on an At that stage. als to reduce the likelihood of activating magnetic the divers worked from submarines or small boats. Later that year. One of the more famous exploits of an American diving group was to land unofficially and The search for means to allow humans to descend leave a ‘Welcome’ sign on the beach to greet the US deeper has been a continuing process. Even Sir Winston Churchill. spearheading the invasion of Guam. but by divers wearing oxygen breathing apparatus. the Royal Navy d­ iving repeated during and after the Gulf War. The which depth the narcosis induced by nitrogen inca- Clearance Divers get their name from their work in pacitated most humans. idea proposed by Sir Leonard Hill and developed tions during the Second World War. who During the Second World War. The advantage of this note include those of the Italian Navy. clearing mines and other obstructions. This allows reduction of the total gas vol- Alexandria harbour and damage two battleships ume required by the diver. After a series of unsuc. After a choice had been made. divers to reach depths in excess of 90  metres.

Other European workers followed Zetterstrom Modern air or gas mixture helmets have sev- with radical approaches to deep diving. whose decompression algorithm has been adapted The primary gas supply normally comes to the and used in many of the early and current genera. In 1945. By the end of the 1930s. omitting his planned gas transition and decompression stops. Between the two world wars. used for both compressed air and . divers in a compression chamber had reached a ­pressure equal to a depth of 150 metres. and a dive to 128 metres was made in Lake Michigan. who developed and ­gas-tight sealing system reduces the chance of a tested several sets of decompression tables and diver’s drowning by preventing water inhalation. Americans Bob Kirby and Bev has become a significant cost. Later. The most complex of these Hydrogen has been used successfully both for have separate cylinders of oxygen and diluting decreasing the density of the breathing gas mixture gas. He died of hypoxia and decompression sickness shortly after encouraged the development of more sophisti- reaching the surface. Research into the use of helium was conducted during the 1920s and 1930s. For hydrogen diving. A model. Modern gas mixture sets have evolved as A  second gas supply is available from a cylinder the result of several forces.4). a Swedish engineer.10  History of diving helium cost more than US $2000 per cubic foot. and the probabil. The price of helium on the diver’s back. Unfortunately. A demand system reduces the amount of dive in the open sea in December 1962 (Figure 1. following the ­exploitation of natural gas supplies that contained helium. The Swiss eral advantages compared with the older equip- worker Keller performed an incredible 305-metre ment. the diver received adequate ­oxygen. the use of hydrogen in gas mixtures for deep diving was first tried by Arne Zetterstrom. the price dropped to about 3 cents per cubic foot. the United States had a vir- tual monopoly on the supply of helium and thus ­dominated research into deep diving. but they have been continually refined hydrogen will be more widely used in deep dives. cated mixed gas sets. and improved. combined Morgan led the way with a series of helmet sys- with a desire to increase the diver’s mobility. The first of these sets was developed in ity of a helium shortage in the future. and the formation of an explosive mixture of oxygen and hydrogen was prevented. may mean that the 1950s. Zetterstrom dived to 160 metres in Figure 1. has tems. In this manner. diver from the surface or a diving bell and may tions of diving computers. cylinder. compared with the standard rig.4  Prof Bühlmann (rear) and Hannes open water. The cheapness of systems that regulate the release of gas from each hydrogen compared with helium. changed to 4 per cent oxygen in nitrogen and then changed to 4 per cent or less oxygen in hydro- gen. be combined with heating and communications. This. an error was made Keller prepare for the first simulated dive to by the operators controlling his ascent. He demonstrated that hypoxia and risks of explosion could be avoided if the diver used air from the surface to 30 metres. hauled him up too fast. The He was assisted by Bühlmann. The composition of the diver’s inspired gas and ameliorating the signs and symptoms of high. and they 3000 m (1000 ft) on 25 April 1961. gas used. is maintained by the action of electronic control pressure neurological syndrome.

5  A Kirby-Morgan 97 helmet. articulated submersibles resembling ­ among others. and these long periods in an elevated pressure environment suits were not widely used. people paid for this progress. Behnke. Deep diving  11 equivalent to almost 200 metres. one-person. sion units and were replaced by the Canadian Progress in saturation diving was rapid. . depths and durations of exposure. They can either transfer to a separate chamber on the submarine’s surface support vessel or remain in the submarine for their period of decompression. Atmospheric diving suits (ADSs) are small. The use of this equip- ment offers several advantages. Lives were lost. become routine for work in deep water. The stimu- tant development in commercial diving since lus for this work is partly military and partly com- the Second World War. In 1965. In saturation diving systems. have been used to depths of around 400 metres. The could be kept under pressure for long periods and needs of the oil companies have resulted in strenu- decompressed slowly at the end of their job.5. A US Navy Medical Officer. rather ous efforts to extend the depth and efficiency of the than undertake a series of compressions and risk associated diving activities. and two divers spent 2 days at a depth Newtsuit was designed to meet the Navy’s needs. enabled div- Between 1921 and 1934 an American. Divers work on the rigs and pipelines ­diving researcher. Figure 1. Operations can also be conducted from small submarines or submersibles with the divers operating from a compartment that can be opened to the sea. Unfortunately. The well-known were patients treated in a hyperbaric chamber. another cham- ber is used to transfer the divers under pressure to and from their work sites. Despite the credit given to Behnke and Bond. the for. suggested that caisson workers needed to exploit oil and natural gas fields. decompression sickness after each. which have propellers the French-inspired Conshelf experiments and to aid movement and can be fitted with claws for the American Sealab experiments seeking greater manipulating equipment. a technical expert who is not a diver can observe and control the operation from gas mixtures. the diver becomes a small submarine. so avoiding 24 hours at 60 metres in the Mediterranean Sea off the hazards of increased and changing pressures. is shown in Figure 1.6). In the second case. Dr Orval ers to spend long  periods at substantial depths. pressurized people to 3 ATA for up However. Robert Stenuit spent maintain an internal pressure of 1 ATA. Additionally. In 1997. This evolution of the 60 metres. The submarine speeds the diver’s movement around the work site. an American mercial. and there has been a significant incidence of bone necrosis induced by these experiments. In the coast of France. George Bond. the divers live either in an underwater habitat or in a chamber on the surface. These helmets within the submarine. provides better lighting and carries extra equip- ment. with ‘Newtsuit’ and the WASP. In 1962. these were never fitted with propul- to 5 days and decompressed them in 2 days. effect. British ‘JIM’ suit. The mobility and dexterity of divers wear- it could be noted that the first people to spend ing early armoured suits were limited. the ADS 2000 was developed in con- mer astronaut Scott Carpenter spent a month at junction with the US Navy. Cunningham. first used in 1972. and they men in chambers. adopted this idea for diving. The a suit of armour (Figure  1. Operations involving saturation dives have Saturation diving is probably the most impor. These suits are fitted first of these dives involved tests on animals and with pressure joints to enable articulation.

Hitchcock FA. RECREATIONAL DIVING Ohio: College Book Co. are the elimination of decompression sickness as a problem. spread to Britain and the United States and the thruster system to allow the pilot to navigate rest of the world. diving has become a operational and certified by the US Navy in recreational activity that is often combined with 2006 when it was used successfully on a dive to tourism and photography. Columbus. Bevan J. London: ing. Another Whitstable Trade. The potential advantages of breathing liquids ­discussed in greater detail in later chapters. This Davis RH. pathfinders. Bevan J.6  Armoured diving suits. Ltd. mainly by enthusiasts in Italy and the south Submex. coast of France who were keen spearfishers. past and present (JIM). Translated by Hitchcock MA. in which the lungs are and further penetrations provide.. 1943. easily underwater. 1996. and wrecks and seek the excitement that deeper Liquid breathing trials. 1955. Others explore caves 610 metres. 2009. Bert P. was also the area where compressed air scuba 6th ed. The Infernal Diver. As a sport. have developed and in some areas are the modern been reported to have been conducted in laborato. diving rapidly 610 metres (2000 ft) and had an integrated dual. . Gorman & Co. It was designed to enable a diver to descend to Cousteau and others. diving developed as a result of the work of Hass. These groups and their problems are ries. London: Siebe. Special inter- flooded with a perfluorocarbon emulsion and the est groups such as cave and technical divers have body is supplied with oxygen in solution. freedom to descend to virtually any depth and the possibility of the diver’s extracting FURTHER READING the oxygen dissolved in the water. The ADS 2000 became fully From this beginning. Barometric Pressure (1878). Amateur diving started with breath-hold div.12  History of diving Figure 1. London: Submex. Deep Diving and Submarine Operations..

Diver 1972. Further reading  13 Dugan J. Translated by This chapter was reviewed for this fifth edition by Michael M. London: Hamish Shelford WO. Reinhold. Dugan J. Ohrelius B. 1962. Into the Deep. Washington. 2008. National Academy of Sciences. Breathhold Diving and the Ama of Japan. the King’s Ship. John Lippmann. Vasa. New York: Van Nostrand Systems Command. Ohgushi’s Peerless Respirator. PRO-010 (2008). Washington. Washington. 1978. World Beneath the Sea. 1341. US Navy Diving Manual Revision 6 SS521-AG- DC: National Geographic Society. DC: Naval Sea Marx RF. Pub. Man Explores the Sea.(Nov):32–34. DC: National Academy Press. 1967. Rahn H. 1965. London: Cassell. . 1956. Skin Hamilton.


move down into a mine or into the sea. At sea level. These of air above. people regard this pressure as caused by the mass This  reading is called an absolute pressure. the pressure ­relevant chapters on specific diving disorders. gases and diving 15 Inert gas exchange 22 Pressure units 16 Buoyancy 22 Pressure and the diver’s body 16 Energy expenditure 23 Water pressure and lung inflation 17 Altitude and saturation diving 23 Pressure and volume changes 17 Physical aspects of the marine environment 24 Respiration in water and under pressure 19 Heat 24 Temperature and volume changes 19 Light 24 Partial pressures in gas mixtures 20 Sound 25 Solution of gases in liquids 20 Diving gases 25 Gas movement in body tissues 21 Further reading 26 INTRODUCTION is that atmospheric pressure is generated by ­collisions of  the molecules of gas in accordance A basic knowledge of the physics and physiology with the kinetic theory of gases. These readings are called gauge pres- ­bottle after it is sealed. This is called either of two reference points. Most with respect to a vacuum. i. but most aspects of diving physi. The of the atmosphere pressing down on them. Aspects of physics The pressure decreases as we move upward and physiology that have a wide application to div. 2 Physics and physiology Introduction 15 Metabolic gas exchange 21 Pressure. through the atmosphere and increases as we ing are discussed in this chapter. Because ology and pathophysiology are relegated to the water is much heavier than air. about 40  per cent of that at sea level. changes e­xperienced by divers over a particu- lar depth  change are much  greater than those PRESSURE. medical problems encountered. we are exposed to the Pressure is measured in a variety of units from pressure exerted by the atmosphere. At the top Some of the basic physiological implications are of Mount Everest the atmospheric pressure is also mentioned. It can be expressed the atmospheric or barometric pressure. 15 . On the surface of the Earth. although its contents are sures. The physically correct ­explanation units are commonly abbreviated to ATA and ATG. Either explanation of  diving is essential to understand most of the is acceptable for the following discussion. the absolute pressure is 1 atmo- contained and are no longer exposed to the column sphere (1 ATA) and the gauge pressure is 0. GASES AND DIVING encountered by climbers or a­viators as they change altitude. zero pressure.e. A flaw second method measures pressures above or below in this argument is that the pressure remains in a local pressure.

90 (34) feet fresh water and is transmitted through them.06 0. = 1.95 0.0075 0.9806 x 0.06895 68.9869 x 1 10−5 0. Therefore. the pressure is 2 ATA and 1 ATG. the increased pressure pushes on the skin.36 1 0.6 1 1000 736 14.3 0. the pressure is 10 ATA and Pressure and the diver’s body 9 ATG. and the blood pressure.00102 1. = 0.70 1 Newton 0.333 0.736 0.001333 1.0703 70.02 0.001 1 0. starting from 1 ATA or or feet of sea water. pressure increases. Table 2.16  Physics and physiology Common examples are the barometric pressure Pressure units used by weather forecasters. Many people have difficulty in understanding why the pressure of the water does not crush the diver. With descent in water. at 10 metres.013 1013 1.1 98.001316 133. science.9681 0. it is plagued with many units of pressure.9806 0.02 x 0.033 1033 760 14.9806 x 105 0. Table  2.01451 (mb) 10−3 1 kg/cm2 0.51 1 millibar 0.08 (10) metres sea water virtually incompressible. the = 760 millimetres mercury (mm Hg) system remains in balance.1 lists 1 atmosphere less than the absolute pressure.1  Pressure conversion factors (commonly The answer to this problem may be considered in used approximations shown in brackets) two parts: The solid and liquid parts of the body are 1 atmosphere = 10. which is an absolute pressure.0102 0.02 1020 750.013 bars back against the water pressure.987 105 1 1000 1.01422 (1 cm H2O) 10−3 1 mmHg 0.9806 980. Table 2. example.07 (33) feet sea water to them does not cause any change in volume = 33.001 1 0.01 1. bars. 0 ATG at the surface.1013 megapascals (MPa) which in turn pushes on the tissues underneath.70 1 .22 1 gm/cm2 968.013 x 105 1. The gauge pressure remains torr and several other rarer units.2  Pressure conversions gm/cm2 mm lb/in2 atm n/m2 or Pa bars mb kg/cm2 (cm H2O) Hg (psi) 1 atmosphere 1 1.033 kg/cm2 and so the pressure is transferred through the = 14.9869 x 100 0.3 kilopascals (kPa) sion.1451 (N)/m2 or 10−5 10−5 x 10−3 Pascal (Pa) 1 bar 0.7) lbs/in2 body until  the  skin on the other side is pushed = 1.2 14.2. so a pressure applied = 33. For conversions for the more commonly used units. remains the same’. A complete throughout the fluid such that the pressure ratio conversion matrix is provided in Table 2. pounds per square inch. metres increases by 1 atmosphere. This is in accordance = 760 torr with Pascal’s Principle.3 51.696 (14. which states: ‘A pres- = 1 ATA sure exerted anywhere in a confined incompress- Note: Actual conversions from sea water depth to ATA ible fluid is transmitted equally in all directions depend on salinity and temperature. the pressure ­pascals and multiples such as the kilopascal. each 10 metres of depth in sea water.01934 1 lb/in2 (psi) 0. For These include absolute and gauge atmospheres. After immer- = 101.00136 1. which is a gauge Because diving involves facets of engineering and pressure reading. At 90 metres.06804 6895 0.7502 0.

tidal volume. ERV. surrounding water acting on the walls of the lung This reduces the amount of air the diver can inhale to balance any tendency of the lungs to expand. A snorkel diver is inhaling air from the surface. diver’s lungs if the air space was exposed to an inter. the effect of pressure on the gas spaces When a diver is using breathing equipment. There is. for example. In both these cases. This is caused in part by the hydro- static pressure of the water compressing the thorax. expiratory reserve volume. ficiently more than the surrounding atmospheric Conversely.. inspiratory reserve volume. capacity by about 10 per cent (Figure  2. 1993. face-down. On the right. residual volume. provided that and this is at surface pressure. This is because in this orientation. gases and diving  17 However. the water pres- Immersion up to the neck in water reduces vital sure is helping to inflate the lungs. This change in turn reduces the compliance the lungs. diver whose air is released at mouth pressure can inhale to greater than normal vital capacity but Water pressure and lung inflation could not exhale to the normal residual volume. in the gas space is close to that of the surrounding If upright in the water. The various components of lung volumes are labelled on the left. Curve 1 is the volume change during quiet breathing. This reduces the volume of blood in lower. middle ears. Respiration and exertion. they would overexpand and burst. insp. there is also a loss of gravitational When a diver descends. Pressure and volume changes With immersion. The applied pressure at the point from which the gas is inhaled pressure does not cause any problems if the pressure can be different from the pressure at the chest. In: Bennett PB. the increased pressure of effects. VC. 4th edn. when descending. (Redrawn from Lamphier EH. Max expiratory 1 pressure pressure 3 TV 40 Relaxation volume 2 20 ERV 1 0 –100 –50 0 50 100 150 200 RV Pressure (cmH2O) 0 Figure 2.1  Lung volumes and intrapulmonary pressure. Pressure. IRV. veins and increases thoracic blood vol- spaces within the diver’s body. TV. sinuses and  intestines. nal pressure of 100 metres of water. of the lungs.1 shows lung volumes). . this pressure is balanced by the pressure exerted by the air is at a lower pressure than the diver’s lungs. no physical damage to a released at the pressure at the level of the mouth. a tissue. The phyisology & medicine of diving. Camporesi EM. in the diver’s body is more complex. a scuba diver is inhaling air water. inspiratory. If because part of the inhalation force is used in over- the lungs were exposed to an internal pressure suf. vital capacity. the surrounding water compresses gas in the gas mainly leg. with permission). 6 100 5 2 80 IRV Relaxation Lung volume (litres) pressure 4 60 % Vital capacity VC Max insp. RV. coming this pressure difference. airway pressure and the maxi- mum effort that can be made for inhalation and exhalation of air are plotted. London:WB Saunders Co Ltd. Elliott DH. the relationships among lung volume. These spaces include ume. and curve 2 is the volume change during a maximum inhalation starting at the residual volume.

0m 10 m 20 m 30 m 40 m 2 litres at 5 ATA (40 metres). The effects of this law are important in age it. the diver’s respiratory volume is about During ascent into the atmosphere. the increasing pressure in the The same volume changes with pressure occur water is transmitted through the body fluids to the in bubbles in tissue or blood. with the pressure in The volume of a mass of gas in a flexible con. as the pressure decreases. the expanding gas will exert pressure gas space is to remain constant as the pressure is on the surrounding tissue and will eventually dam- increased. For example. This means that the absolute pressure multiplied by volume has 4 a constant value. To a mathematician. the diver must move a greater mass of and to 40 litres at 0. Figure 2. The relationship between changes in volume of a gas 8 and the pressure applied to it is described by Boyle’s Law. during descent on breath. Unless gas is vented gas has to be added if the volume of a container or from the space. where 2 P and V are pressure and volume.5 ATA in density of this breathing gas under increased (an altitude of about 5000 metres or 18 000 feet) pressure. gas changes are greatest near the surface. cal effect can limit the diver’s capacity to do work. this means that P × V = K or P1 × V1 = P2 × V2. tion (Figure  2. Again. Barotrauma is the general name for an injury hold dives. If air  entry Gas volumes expand when pressure decreases does not take place to equalize pressures. It should be noted that volume During ascent. such as the sinuses or the middle ear.2  Effect of Boyle’s Law: While breathing underwater. the volume tissue surrounding the gas spaces and to the gas changes are greatest close to the surface. . within body spaces will expand. An injury spaces themselves. this physi- 10 300 metres or 33 400 feet). the body should increase to equal the surrounding pressure. Because of the increase 10 litres of air would expand to 20 litres at 0. this is accompanied by a decrease in lung caused by pressure change. Air should enter cavities with rigid walls. result in rupture of the tympanic membrane. Pressure changes in the middle ear can also many aspects of diving medicine. This means that the same rate on the surface. During descent. and this constant changes with the mass of gas considered. This states: ‘if the temperature remains con- Volume (litres) stant. In some situations.18  Physics and physiology This is one of the many aspects of diving medicine 10 that is concerned with the relationship between pressure change and change of gas volume. such as congestion. oedema or haemorrhage. the reverse the same as it would be if he or she worked at the happens and the gas expands. then a and contract when pressure increases. volume. The pressure in any gas space in caused by pressure change is called barotrauma. pressure difference between the space and the sur- rounding tissue will develop. the volume of a given mass of gas is inversely 6 proportional to the absolute pressure’. and expands during ascent or pressure reduc. 10 litres of gas  at sea level pressure (1 ATA) will be compressed to: 0 1 ATA 2 3 4 5 ATA 5 litres at 2 ATA (10 metres). In the lungs. Conversely. Pressure depth 1 litre at 10 ATA (90 metres).2). the gas space being less than in the surrounding tainer decreases with pressure or depth increase tissue. The results are ­tissue ­distortion and ­damage.25 ATA (an altitude of about gas with each breath.

7°C = 280°A. A more tains enough air for 100 minutes at 1 ATA would useful expression of the law is as follows: last about 50 minutes at 2 ATA (10 metres) or 20  minutes at 5 ATA (40 metres) for dives with V1 V2 V = or = K the same energy expenditure. gas for a given workload. this can limit the capacity to do T1 T2 work. Continued exposure So the reduced pressure is a result of tempera- to dense gas. not a leaking valve or fraud by the air cause an adaptive response. more than the centigrade temperature. supplier. A cylin- perature has changed to T2°A. . there is an der is rigid and the pressure falls as the gas cools. However. the 1 per cent oxygen and helium mixture is 6. at depth. it should be gas if it is released at 5 ATA. V1 = V2 used in breathing. The absolute temperature (A°) is always 273° A consequence of this is that a cylinder that con. This is because the T1 T2 T gas in the cylinder expands to a smaller volume Where V1 is the volume of a mass of gas at tem- when it is released against the ambient pressure at peratures T1°A and V2 is its volume after the tem- depth than it would if used at the surface. These factors can lead to fatigue of the inspiratory muscles and reduce maximum 200 × V1 P2 × V2 = breathing capacity and the work output. 320 280 mize this load. At 10 ATA.3 kg/cubic metre. at 40 ATA. A temperature-pressure problem that often The density of the breathing gas can be causes discord can be used to illustrate the use of reduced by replacing nitrogen with a lighter gas this equation. A div- remembered when considering gas volumes and ing physician needs to keep this in mind when how they may change. the density of a 47°C. the body responds by using less P2 = 175 ATA. the cylinder. as is encountered in deep dives. or 40 metres. The combined laws can be expressed more molecules in a given space. The use of lighter gas helps to reduce den- the gas so the cylinder may be charged with gas at sity. increased tendency for the flow to become turbu- lent. he or she worked at the same rate on the surface. at 1 ATA is about 1. This requires greater effort and P1 × V1 P2 × V2 involves an increase in the work of breathing. To mini. estimating the amount of gas needed for any task Boyle’s and Charles’ Laws may be combined and or therapy. volume of a mass of gas is proportional to the abso- ratory volume is about the same as it would be if lute temperature’. gas is compressed and there is an from P1 and T1 to P2 and T2 with a volume change increase in density of the gas because there are from V1 to V2. This can result in the development of hypercapnia. gases and diving  19 Respiration in water and under Temperature and volume changes pressure Charles’ Law states: ‘If the pressure is constant. This is the effect of temperature on such as helium. used if temperature and pressure both change  – With depth. In = some situations. the diver’s respi.7 kg/ diver may find that he or she has only 175 ATA in cubic metre. der that contains 5000 litres of gas if it is released This law has much less relevance to diving at the sea surface would yield only 1000 litres of medicine than Boyle’s Law. may ture change. This causes a further increase in the energy 47°C = 320°A. Pressure. The gas compressor heats metre. For example. So. For  example. In this case V1 = V2 because the cylin- As the density of a gas increases. A diver may ask to have the compressed air cyl- the density of air would be about 13 kg/cubic inder filled to 200 ATA. the While breathing air underwater. the density of air the pressure in a gas cylinder. as the universal gas equation: a diver must move a greater mass of gas with each  breath. When the diver gets in the water at 7°C.

If incorporated in compressed breathing be conducted with allowance for this or by putting gas and delivered at high partial pressures. (b) total pressure 1 ATA.4  Henry’s Law. This law implies that an equilib- + – – + + + – – – rium is established with each gas passing into and + + + – – – out of any solution in contact with it (Figure 2. Figure 2. the right gas mixture. which is approximately The mixture will need to be 40 per cent oxygen 80  per cent nitrogen and 20 per cent oxygen. it will be necessary to put 150  ATA of manipulated to the diver’s advantage. it should contain 120 ATA of nitrogen (60 per cent 0. 1 ATA of each component of the mixture. 0. partial pressures of nitrogen. The pressure of each calculate how to prepare a cylinder charged with constituent in a mixture is called the partial pres. For example. both a calculated weight of each gas in the cylinder.3  Dalton’s Law: (a) two spaces each at 1 ATA. the and 60 per cent nitrogen (Dalton’s Law). it may Henry’s Law states: ‘at a constant temperature. . air (assumed to be 80 per cent nitrogen in  this The partial pressures of breathing gases can be exercise). At high pres- Undesirable effects can also occur.6 and 0. Air from an sures. In air. of 200). an individual’s body tissues contain about 1 litre of gaseous nitrogen in solu- (b) tion.002 per cent carbon mon.3 per cent Boyle’s Law accurately.8 ATA. At 2 ATA (10 metres) these partial pres. For example. helium does not follow the predictions of industrial area may contain more than 0. ness (DCS) by decreasing the percentage of inert This simple mixing process cannot be used as gas in the mixture. and oxygen. Mixing can oxide. sure (Figure  2. If this is to be obtained from compressed sures will rise to 1. 0.2 ATA. Solution of gases in liquids It may be necessary to combine Boyle’s and Dalton’s Laws in calculations. compressed air into the cylinder (30 ATA of oxy- the composition of the gas breathed may be modi.20  Physics and physiology Partial pressures in gas mixtures be decided that a diver should be given a mixture with a partial pressure of 0. the gas laws can be used to occupied the total volume’. successfully with helium mixtures.2  ATA nitrogen in a recompression chamber a mixture of gases is the sum of the pressures that pressurized to 2 ATA.4). (c) total pressure 2 ATA.8 ATA oxygen and Dalton’s Law states: ‘the total pressure exerted by 1. It is less compressible than carbon dioxide and 0. the ideal gas described by Boyle’s Law. the amount of a gas that will dissolve in a liquid (a) is proportional to the partial pressure of the gas + + + – – over the liquid’. gen and 120 ATA of nitrogen) with 50 ATA of fied to reduce the chance of decompression sick. oxygen. If the diver dived to 10 metres and breathed – + + – + + + – – – – – – + + – + + – + Gas Gas (c) – + – +– + + + – + + – – + – + + – Gas in solution Gas in solution Figure 2. constituents could be toxic unless measures were taken to remove these contaminants before use.3). respectively. At sea level (1 ATA).4 ATA. If oxygen and air are the would be exerted by each of the gases if it alone only gases available.5 ATA each component of the mixture. If the gas total pressure at sea level (1 ATA) is the sum of the is to be prepared in a cylinder charged to 200 ATA.

depends on several factors. this happens. Nitrogen is more soluble in fats the same as at normal pressure. When the Gas transfer from the lungs to the tissues is depen. The time taken for any inert gas to reach a another. is reduced. and second. gradient. If a rapid total pressure drop occurs. If fusion. from the solubility coefficients of the gas in the When the total pressure. gas must pass out The rate of gas movement between two points of solution. This can take hours. In a permeable substance such oxygen at a partial pressure above 3 ATA. This causes higher alveolar pressures and the  lungs. For example. That is. or the partial pressure components of the tissue. gas molecules dissolve in the tis. gas molecules can migrate by dif. by the depression of respiration induced by high arterial Gas movement in body tissues oxygen tensions. the nitrogen comes out of solution Elevated pressures of oxygen facilitate oxygen in the blood or tissues. but they may interfere with the elimi- may lead to DCS. Pressure. there will not be any complications. The carbon dioxide gradient is nor- time for gases to enter and leave solution or form mally in the opposite direction. champagne would go of inert gases becomes important and there are flat as soon as the cork was popped. solve in a liquid depends on the liquid. down a concentration gradient from the lungs to Henry’s Law is also time dependent. gas exchange mechanisms are basically far fewer bubbles. of gas transfer. If it is eliminated from solution through Law. gases and diving  21 air at 2 ATA. points that are close together (a steep gradient) It should be noted that each gas has a different and a greater permeability both increase the rate solubility and the amount of any gas that will dis. inspired oxygen partial pressure is elevated. thus forming bubbles that transport. in accord with Henry’s Law. then twice as many molecules will be in new equilibrium depends on the solubility of the the first tissue to produce the same partial pressure gas in the tissues and the rate of gas supplied to in the tissue. and the is an increase in oxygen transport in solution in gas supplied to a portion of tissue depends on the the plasma (Henry’s Law). The other major factor is the permeabil- The physiological effects of the solubility of ity of the tissue. A large partial pressure between two oxygen toxicity. and this low partial pressure until the partial pressure of can prevent the transport of carbon dioxide in the the dissolved gas is uniform. the excess nitrogen must pass from the breathing mixture in accordance with Dalton’s body. carbon dioxide is very soluble in water compared Metabolic gas exchange with other common gases. The amount depends With increasing depth. form of carbaminohaemoglobin. by direct interference with the transport of carbon dioxide. This information can be estimated each tissue. If a gas have twice as much nitrogen in solution in the is twice as soluble in one tissue compared with body. In this situation. the total as body tissues. The exchange bubbles. there dent on the cardiovascular circulation. The difference in par- a tissue may contain more gas than it can hold in tial pressure and the distance between the two solution. When the diver the partial pressures of the constituents of the surfaces. not the number of gas molecules. a diver breathing air absorbs nitrogen exchange. oxygen requirement may be carried in solution. It takes the tissues. there is an increase in on depth and time of exposure. changes in the finer details of metabolic gas At depth. In some cases. more gas would dissolve and he or It is the dissolved gas pressures that tend to equil- she would eventually reach equilibrium again and ibrate. If this was not so. . the haemoglobin may be still satu- sue fluids and tend to move from areas of high to rated with oxygen in the venous blood. bubbles may form and points may be combined into a concentration may cause DCS. When one is inhaling blood perfusing it. Beer aerated with com- pressed air instead of carbon dioxide would have In divers. Oxygen diffuses and oils than in aqueous solutions. an expression of the ease of gas gases are also relevant in nitrogen narcosis and movement. nation of carbon dioxide in two ways: first. of a particular gas. arterial pressures of the inhaled gases.

g. consequently. It determines the effort the diver haemoconcentration and decreased plasma volume. An interesting combination of the effects of Boyle’s Law and Archimedes’ Principle is shown Diving is associated with a tendency to retain by the changes in buoyancy experienced by a diver carbon dioxide. est at the feet and least at the head. In addition. If the diver displaces more water. must make to dive. the tively buoyant. This can be achieved tial pressures. the diver has negative buoyancy. a little more water and. he or be less sensitive to elevated carbon dioxide par. there may also be an displaces. ­peripheral partially immersed in liquid. Causes include contamination of the breathing gas A diver can change buoyancy in several ways. A diver is an stress. the diver will experience some difficulty in descending. When pressure is reduced at the in buoyancy. the external dead space of the equipment. ­circulation where the hydrostatic pressure is great- centration gradients of gases. If there is an less than a full one. it is desirable to ­ inflate or deflate to make him positively. as needed. which makes descent difficult. depending on the initial pressure excess of gas. to avoid duplication. the transfer is reversed. This causes gas transfer consumed from it. laws. These changes result in an increase in central object immersed in water and is therefore affected blood volume. steel. pensator device (BCD) – a device used to control tibility to oxygen toxicity. then it can come out of solution as bub. wearing BCD or a compressible suit. If a diver weighs less than the The effect of haemoconcentration on normal weight of water he or she displaces. An empty cylinder can weigh 1 to 2 kg end of the dive. DCS and inert gas buoyancy. If the diver wears a weight belt. he or she will become nega- chapters on DCS. is buoyed up by a force vasoconstriction will occur in response to any cold equal to the weight of liquid displaced’. For these reasons. This reduces the total ventilation by retaining more air in the lungs.e. supply. displaced and. increased total pressure is usually accompa. In some situations. Their size decreases if the pressure is increased. leading to diuresis and subsequent by this principle. he or she increases inadequate ventilation or failure of the absorbent weight by a significant amount and displaces only system. It has an air space that the diver can narcosis. as a result. they are also subject to the same physical gravity-free state experienced by astronauts. negatively control the f­actors that cause carbon dioxide or neutrally buoyant.22  Physics and physiology The result is an increased tissue carbon diox. the diver’s buoyancy. the hydrostatic gradients in the circulatory BUOYANCY system are almost exactly counterbalanced by the ambient water pressure. the diver will dives is not major except that it gives divers a tend to float to the surface – i. It can also be requirement during working dives. will assist descent and make ascent more difficult. In air. physiological excuse for well-developed thirst and tive buoyancy. For an immersed diver. Elevated achieved by inflating the diver’s buoyancy com- ­arterial carbon dioxide levels increase suscep. If bubbles Immersion creates a condition resembling the do occur. the volume of fluid earlier. The increased pressure reduces the topic is not considered in detail here. nied by an increase in nitrogen (and/or other inert The weight of a scuba cylinder decreases as gas is gas) pressure (Dalton’s Law). she will increase buoyancy. These bubbles are the cause of DCS. As indicated volume of gas in the BCD or suit. which increase in the inspired carbon dioxide pressure. Inert gas exchange As the diver descends he or she will pass through a zone where he or she is neutrally buoyant and. and the size and type of the ­cylinder (e. diver weighs more than the weight of water he or she ide level. bles. This reduces the volume of Archimedes’ Principle states: ‘any object. he or she has posi. if the The topic if inert gas exchange is considered in the diver descends further. Urine production . retention. will decrease There is a tendency for experienced divers to buoyancy. If the sometimes the need to urinate. Therefore. alloy). and this will lead to an increase to the body tissues. a standing person has a pressure gradient in the and gas enters or leaves them depending on the con. wholly or pooled blood in the leg veins. If slightly posi- tively buoyant at the surface with air in the BCD.

. Fresh water is less dense an oxygen consumption of 1. However. realistic for practical purposes. through the diver’s airways and breathing appara. This increases the resistance to gas flow and exhale at an adequate rate during ascent. These results show that when a diver starts from an environment where oxygen consumption underwater of more than the pressure is greater than 1 ATA. tion with various other factors associated with the diving environment.2 knots would cause an oxygen consump. presumably because the absence of ing of the physics involved. at sea level. while swim. gravitational effects reduces the energy required to A diver operating in a high mountain lake is maintain posture underwater. this diver will have to exhale 60  lpm (air consumption measured at the depth faster during ascent. The diver’s energy ment or underwater habitat. or in combina. There is an breathing oxygen at 3 ATA. increases the work of breathing and reduces doubling in gas volume occurs during the last ventilatory capacity. A swim of 0. chamber The other effect of increased central blood experiments. A diver who ascends from the diver was swimming and oxygen consumption 10 metres (2 ATA) to the surface (1 ATA) with- at 1 ATA). This is DIVING discussed in Chapter 39. ing at higher altitudes. unless it tial pressures in hyperbaric environments could is fitted with a relief outlet.5 lpm and an air consumption of In addition. thus limiting div. These conditions expenditure when inactive may be lower than introduce complexities that require understand- found on land. High-altitude diving may require that the depth ing to around 400 to 500 metres for useful work. Another minor correction will be required cause an air consumption of almost 40 lpm and if it is a fresh water lake. There is a series of variations Measurements of energy expenditure. returning to a lower surface pressure than a diver Typical gas consumption and energy expendi. Tables are available for div- ­factor for deep diving. have been a mountain lake where the pressure on the sur- made using indirect calorimetry and by predic. tion of about 2. an air consumption of 20 lpm and an oxygen con.5 ATA. if the pressure density (helium) of around 8 g/litre appears to be at the surface was 0. 0. and values greater when divers operate from a pressurized compart- than 2 lpm are quite common.8 lpm. Our normal idea of diving is that a diver descends ENERGY EXPENDITURE from sea level. so the diver is exposed to a slightly of 1. can precipitate cardiovascu. and returns when the dive has finished. Another variation occurs tion from heart rate. Therefore. showed that the maxi- increase in cardiac output as a result of increased mum aerobic work performance was not signifi- stroke volume. improve physical performance.4 lpm. However. A diver may have to dive in ming on the surface and underwater. and many dive computers are programmed to compensate for this. ALTITUDE AND SATURATION lar dysfunction in susceptible individuals. the diver may need to modify the decompression sumption of 0. the diver would have increases the tendency to form bubbles. This decreases the pressure at which the ture levels are as follows: diver is while releasing inert gas after a dive and so For a slow swim. Immersion alone. they may not realize that a similar tus. in which the subjects exercised while volume is on cardiac performance. or duration of dive and the rate of ascent be reduced to allow for the lower than normal surface pressure Gas density may prove to be the limiting at the end of the dive. Altitude and saturation diving  23 rates of more than 300 mL/hour cause problems It may be expected that the higher oxygen par- for divers trying to keep their dry suit dry. A fast swim than salt water. Most divers realize this breathing. cantly increased. A maximum breathing gas 5 metres of ascent to the surface.5 knots. This happens 3 litres/minute (lpm) is possible. lower pressure change per unit depth. out exhaling would find that the volume of gas Increased gas density increases the work of in the lungs has doubled. face is less than 1 ATA. from this situation.8 knots would plan. 1 ATA.

The eventual return to the surface can take many the diver was in an air environment. or gas. The use of such environments has proved to In warm environments. are illuminated with a torch. can cool or heat up at a temperature that would be comfortable in an air environment. The net light. boundary layer. The result is that a than normal depths. Because of quickly than he or she would in air of the same the greater absorption of reds by water. light is absorbed most. divers can continue to lose heat who needs to pass over hills or mountains when over several days of repetitive diving. it is possible for a diver be invaluable where deep or long dives are required to suffer heat stress. However. cern in most circumstances. PHYSICAL ASPECTS OF THE MARINE ENVIRONMENT Light Heat Even in the cleanest ocean water. even Heat loss is also increased in warming the at shallow depths. avoid DCS. even by a relatively small A diver in water or a helium-rich environment amount. A diver who is wearing a pro- (see Chapter 67). Some dives and ascents will require and evaporative cooling is prevented. in a helium dive is more significant. the deep ocean appears black. when a diver dives and then flies or ascends into the atmosphere can become saturated with water. Part of the appeal of diving at cooler inhaled air or gas.24  Physics and physiology A diver living in a human-made environment The heat transfer by conduction is also increased where the pressure is high can operate to deeper in a helium environment. only about Diving and exposure to high pressures change 20 per cent of the incident light reaches a depth of the heat transfer from a diver’s body. vision and can tend to even out illumination. and causes distortion of colours and is responsible for causes a convection current that tends to remove the blue-green hues seen at depth. and lights are result is that a diver cools or heats up much more needed for observation or photography. mountains. either by the clothes or the hair and the with a wave length of 480 millimicrometres (blue). the heat lost Coastal water. with more suspended material. days. Red and orange the layer of warmed water. is some insulation from the air trapped near the Clean water has a maximum transparency to light body. The water This variation of absorption with wave length adjacent to the skin is heated. it is necessary to transport a diver with DCS. some illu- temperature. tective suit cannot lose heat by sweating because Another pressure-related problem can occur the sweat cannot evaporate. night is that objects that have a blue-green colour most of this heat is used to humidify the dry air in natural light have a new brightness when they used for diving and is not sufficient to cause con. Absorption and is compounded because at depth. This problem is encountered by a diver Despite wearing thermal insulation in warm tourist who wants to fly home after diving or one tropical waters. For a diver breathing air. there 10 metres and only 1 per cent reaches 85 metres. Because of the absorption of ated by movement of the diver or the water. about 530 millimicrometres. expands slightly. There may be an increase in manifestations of DCS when the pressure is decreased. where the diver operates from a base at tain body warmth at a water. In a pressure chamber. helium diver may need external heating to main- tion diving. Helium has has a maximum transparency in the yellow-green a greater specific heat than nitrogen. This system is used in satura. temperature increased pressure and becomes equilibrated with where external warming would not be required if it. . to there is helium in the mixture. somewhat insidiously. It is also encountered when hypothermia can develop. This process is acceler. The problem band. and ‘silent’ returning from a dive. mination is needed to see the true colours. The heat the diver to ensure that adequate time is spent at stress for a given temperature is also increased if the surface before ascending to high altitude. In water this is lost. In air. the mass of gas scattering of light by suspended particles restrict inhaled is increased.

from the surface. when breathing helium mixtures and can render mal. Helmet divers can communicate eas- for this distortion. Some scuba divers have Masks also restrict vision by narrowing the mastered the art of talking by taking their demand peripheral fields.1 ATA in their inspired air. For this reason. mental diving may involve the use of other gas mixtures. this refractive power is from water to air. for diving. military. speech unintelligible. technical and experi- but can also impose their own problems. Commercial. molecular weight 32) gitudinal mode of vibration. Practice and adaption of the hand–eye co-­ water. In water. This  can make the light intensity the same in all sounds travel farther than higher-pitched sounds. valve from their mouth and speaking into an air tend large visual angles. lost and the eye is incapable of focussing. so sounds ­oxygen should be present at a partial p ­ ressure of at travel greater distances under water. This is not so if the diver has an air space to ordination system allow the diver to compensate speak into. Diving gases  25 Air Water Light rays Eyes Glass of Apparent Actual face mask position position or helmet Figure 2. the air-metal-air pathway. Sound in water is transmitted as waves with a lon. At high altitude people survive with less than 1470 metres/second in fresh water at 15°C. except when describing the size ily by touching their helmets together and using of fish (Figure 2. Oxygen (atomic weight 16. Attempts have been made to improve the diver’s vision by modification of the face mask. which mixtures cause speech distortion. A face Both high-pressure air and helium-oxygen mask provides an air-cornea boundary. This is greater restores refraction at the cornea surface to nor. However. by water. most transmission of sound in air over water but reduces of the refraction of light rays occurs at the air– the transmission of sounds from air to water and cornea interface. and scattering by suspended particles reduce visual DIVING GASES acuity. These can be relatively successful gas. At higher partial . ground mask lenses and and other oxygen–nitrogen mixtures as a breathing contact lenses. Refraction also occurs at the face mask sur. a better transmitter of sound than air.2 ATA to avoid hypoxia. Both absorption of light space created by cupping their hands. The speed of sound is  the essential constituent of all breathing mix- is about 1530 metres/second in sea water and tures. and they distort objects that sub. This reflection also enhances the When the eye focusses on an object in air. mainly at the glass–air boundary. and this makes objects appear closer than they It is often thought that divers cannot talk under- are. Low-pitched least 0. the Most diving is based on the use of compressed air use of coloured filters. Distortion in air causes the face. which reduces apparent contrast. This results voice to become more nasal and crisp as the pres- in an apparent size increase of about 30 per cent sure increases. directions and is an important factor in causing Transmission of sound is enhanced by reflection loss of orientation. Water is 0. it is desirable to give the Sound reader some salient points on the gases mentioned in this text and related literature.5  Displacement of image in water.5).

FURTHER READING sures. The two major advantages of helium and 3 deal with these topics in a manner that are that it does not cause narcosis and. fears of explosion. nitrogen is of Doolette DJ. Explosions can be prevented if Nitrogen is often considered to be physiologically the oxygen level does not exceed 4  per  cent. increases the work of breathing. In to another gas near the surface. Hyperbaric condi- major importance in diving.) its lightness. New York: Wiley. (Vol. 2011. Hydrogen causes solution. Chapters 2 be used alone. cost.2 to 2. Helium-oxygen (eds). Schandelmeier NR to breathe than most alternatives. Neuman TS (eds). Comprehensive 50 metres and as a part of more complex mixtures Physiology. molecular weight 28) ment for helium. at depths less than tions. (HPNS) (see Chapter 20). the effect is likely to cause the diver to make mistakes. called the high-pressure neurological syndrome Oxygen toxicity is discussed in Chapter 17. The speech of a diver at depth may need electronic . 2008. where nitrogen should not Systems Command.comprehensivephysiology. Despite these disadvantages. molecular weight 2) effect on the respiratory centre and minute volume has the advantage of being readily available at low will remain close to normal. and inert.com/ Helium (atomic weight 4) is a light. Hypoxia can be p ­ revented by c­ hanging an oxygen–nitrogen mixture ascends too rapidly.8 ATA. The other problem with the able in a recompression chamber. These factors may lead to its use as a replace- Nitrogen (atomic weight 14. breathe. It WileyCDA/ is found in natural gas wells in several countries. inert gas.26  Physics and physiology pressures oxygen causes oxygen toxicity. time (albeit often with a different profile) than an New York: Plenum Press. to and from the diver. http://www. Vol 1.55 ATA causes pulmonary the distortion. composed mainly of nitrogen.8 ATA. equivalent saturation dive with the diver breath- ing air because helium diffuses more rapidly than This chapter was reviewed for this fifth edition by nitrogen. DC: Naval Sea greater than 50 metres. At higher partial pres. US Navy Diving Manual Revision 6 SS521-AG- Helium is used to dilute oxygen for dives to depths PRO-010 (2008). The Underwater Handbook: A Guide to mixtures can allow a shorter decompression Physiology and Performance for the Engineer. where oxygen use of helium is that it is associated with a disorder may be used at partial pressures of up to 2. helium-oxygen mixtures are easier Schilling CW. Werts MF. can such a mixture is breathable at depths in excess of cause DCS if a diver who has been breathing air or 30 metres. and shorter exposure to more than more susceptible to heat and cold because the high about 1. Prolonged processing to make it understandable because of exposure to more than 0. The use of helium can cause several problems. Oxygen is vasoactive. than about 3 ATA. The other problem that restricts the use Brubakk AO. it may cause nitrogen narcosis at depth (see thermal and speech distortion problems similar to Chapter 15). John Lippmann. Philadelphia: Saunders. oxygen has little Hydrogen (atomic weight 1. The risk of these problems may be accept. In the range 0. 1976. 1. because of assumes no previous knowledge. Bubbles.5 ATA results in central nervous system thermal conductivity speeds the transfer of heat effects. Washington. 2004. 5th ed. In: Pollock DM (ed). Because of its lightness it is the easiest gas to high oxygen tensions cause vasoconstriction. A diver in a helium atmosphere is oxygen toxicity. there is a demonstrable decrement in the diver’s performance. at greater depths. At partial pressures of nitrogen greater those encountered with helium. Mitchell SJ. Bennett and of nitrogen is that its density at increased pressure Elliot’s Physiology and Medicine of Diving. The reluctance to use stems from is the major component of air – about 79 per cent.

Practised HUMANS AS FREE DIVERS in some societies for thousands of years. human diving capabili- ing’ or ‘snorkel diving’) is regarded as the purest ties are paltry in comparison with those of marine and most natural form of diving. recreational attendant risk of exhaustion of oxygen (O2) free divers and spearfishers often wear a mask. Near the surface. Free to achieve remarkable depths. fins. For example. ern specialized equipment. knife and bag. wetsuit and weights and carry a spear gun. 3 Free diving Introduction 27 Oxygen stores 33 Humans as free divers 27 Oxygen consumption and the diving The challenge of increasing depth 28 response 34 The challenge of increasing duration 29 Anaerobic metabolism 35 The challenge of avoiding gas toxicities Diving technique 35 and decompression sickness 32 Pressure changes 35 Record diving 32 Hypothermia 35 Diving marine mammals 33 Further reading 35 INTRODUCTION snorkel. The challenge of increasing depth. Competitive free divers may Free diving refers to dives made from surface to also employ specialized devices such as weighted ­surface during voluntary apnoea on a single breath. bulky equipment.1). with its compressed during descent. sleds for descent and inflatable lift bags for ascent No underwater breathing apparatus is used. free diving in its simplest form requires no equipment at all. fins. this will render the diver negatively buoyant as he 2. the addition of goggles or face masks allows for clear vision but There are two principal (and somewhat inter- introduces a gas space that must be ‘equalized’ to related) challenges in free diving: prevent barotrauma. the diver is free to move weight- lessly and silently in the underwater world. The challenge of increasing duration. wetsuits gen- erate positive buoyancy that decreases as they are 1. Even with such mod- diving (also often referred to as ‘breath-hold div. buoyancy vests and thermal protection suits may Record-holding free diver present new problems. If a weight belt is used attendant risk of pressure-related injury to gas- to offset the initial positive buoyancy of the wetsuit. stores. Unencumbered by mammals and other sea animals (Table 3. Nevertheless. The You’re running on reserve tank and introduction of various p ­erformance-enhancing there’s no warning before you hit empty! apparatus such as face masks. containing spaces. weight belts. with its or she begins the ascent. 27 .

a simple application of Boyle’s Law. compressed as depth increases. result in trauma to the chest wall or sure (because of the surrounding water pressure) lung itself. missing from these early attempts to predict maxi- The lung is of particular relevance to free divers mum depth were the distensibility of the pulmo- because. would be capable of greater depths before injury occurred. effectively allowing gas. The factors that were Chapter 7). and their volumes spheres absolute [ATA]) without suffering obvi- may need to be compensated if barotrauma is to be ous lung barotrauma and that free divers regularly avoided. A greater engorgement of the pulmonary should t­ heoretically be able to breath-hold dive to circulation is likely if the transthoracic pressure 30  metres (4 ATA) where the total lung volume increases further. the lung volume of a free diver is progressively for compressions below predicted residual volume. unlike divers using underwater breathing nary vasculature and the concomitant potential for apparatus who compensate intrapulmonary pres. Thus. intrapulmonary blood pooling to compensate for sure and volume with each breath of compressed compression of lung volume. include the middle ear (see mum calculated in this way.4 atmo- to compression during descent.28  Free diving Table 3.5  litres thorax.7 litre of blood into the of 6  litres and a residual volume of 1. The negative transthoracic pressure gen- lung volume was compressed to residual volume erated by having the airway open to a pressure of because compression to smaller volumes could.1  Depth penetrations of human divers and marine animals Comparative depth penetrations Depth (m) Human free (breath-hold) diver • ‘Constant ballast no fins’ 101 • ‘No limits’ 214 Human diver using underwater breathing apparatus • Bounce dive (surface to surface) 318 • Saturation diving lockout from bell >400 Sperm whale 1150 Northern elephant seal 1500 Wreck of Titanic 3810 Octopus species 5639 Deepest known fish 7703 Amphipod crab 9789 Deepest manned submersible dive 10 911 Deepest part of ocean ~11 000 A third challenge that is most relevant to the would be compressed to the residual volume more extreme exponents of free diving is the (1.5  litres). a diver with a total lung ­capacity results in a shift of about 0. related exposure to markedly elevated gas partial A  corollary was that divers with a larger total pressures with related risks such gas toxicities and lung capacity and/or a smaller residual volume decompression sickness. The beginnings of such compensation can be seen It was long believed that the limiting factor on with simple head-out immersion in an upright depth in free diving would be the point at which subject. sinuses (see Chapter 8) and mask. Obvious examples. The challenge of increasing depth The fallacy of the ‘residual volume limit’ is immediately clear when it is considered that a Any anatomical or equipment gas spaces are ­subject human has descended to 214 metres (22. which are discussed descend to depths greater than a theoretical maxi- elsewhere in this text. . 1 ATA while the thorax is exposed to greater pres- logically.

5 litres. If this Competitive breath-hold divers have had end-tidal becomes excessive. Because of the high alveolar . There is also some evidence that well-practised free divers can induce a decrease in sensitivity of the The challenge of increasing duration medullary respiratory control centre to CO2. change) aggressively employ hyperventilation and tional residual capacity) have been calculated to are highly motivated not to breathe for as long as be approximately 1. then both fluid extravasation CO2 pressures as low as 20 mm Hg measured at the from capillaries to the alveolar space and frank end of their typical pre-apnoea routine. However. Interestingly.1 (b) and through the effects of changing ambient p­ressure 3. a human’s competitors in static apnoea events (effectively stores are relatively small. This before the onset of a strong urge to breathe. one could predict that a resting man an added and significant risk factor for critical who has an O2 consumption of 300 mL per minute hypoxia. the volume of O2 involved is effec- will cause the lung’s remaining gas volume to tively inconsequential. If nearly all this O2 can be changing ambient pressure during a free dive as extracted. This brings the discussion to able among individuals. There is little doubt that hyperventilation has been parison with the challenges of increasing duration a contributory factor in many free diving deaths. or they can learn to resist the uncomfortable urges to It is self-evident that oxygenation is maintained breathe that CO2 generates as its arterial pressure from steadily dwindling O2 stores during a free rises. problem is referred to as pulmonary barotrauma The obvious danger associated with hyperven- of descent or ‘lung squeeze’. When the breath-hold diver descends. symptomatic hypoxia is not frequent as increased at total lung capacity whose value is vari. (b) a breath-hold dive to it can be confounded in two important ways: by the 10 metres and (c) a breath-hold dive to 10 metres use of hyperventilation before breath-holding and with prior hyperventilation. This has haemorrhage are possible. tilation is that it will extend the breath-hold dura- esting and potentially of increasing importance as tion closer to the point where the arterial Po2 falls free diving depths are extended. pressure of O2 [Po2] above approximately 25 mm Figure 3. pressed. this is currently a below that required to maintain consciousness. however. This store would be possible. The total O2 stores in breath-holding competitions without pressure a 70-kilogram man at resting lung volume (func. cantly enhances O2 stores. most untrained humans can only change with the partial pressure of the gases in the breath-hold for approximately 1 minute because lungs. ambient pressure change. although dive. and there is evidence the effect of prolonging the breath-hold duration from competitive free diving that both occur. In contrast to marine mammals. The reverse takes place during ascent back This inherent inability to breath-hold voluntarily toward the surface. Although hyperven- ertheless come a point where pulmonary vascular tilation does increase the alveolar O2 content to a capacitance is maximized and further descent small extent.1 (c). Humans as free divers  29 Notwithstanding this remarkable and fortu. bolic gases during (a) a breath-hold period without ness) is clearly protective in free diving. minor contributor to free diving accidents in com.1 shows alveolar pressures of the meta- Hg must be maintained to avoid loss of conscious. as their volume is decreased and gas inside is com- ing levels of O2 (although the two are synergistic). the the drive to breathe is dependent largely on rising partial pressures of the gases in the lungs increase pressures of carbon dioxide (CO2) rather than fall. sures rise during descent according to Boyle’s Law. there will nev. or both. Arterial gas tensions during breath-hold dives utes. would completely deplete his O2 stores in 5 min. This is tinued consumption. In reality. Although it is inter. often done in the mistaken belief that it signifi- nate mechanism for compensation. In Figure 3. ambient and thus alveolar gas partial pres- during descent and ascent from a free dive. would be expected. This leads to concomitant rises to the point of critical hypoxia (an arterial partial and falls in alveolar and arterial Po2. What hyperventilation can develop an increasingly negative pressure relative achieve is a marked lowering of arterial CO2 levels. Hyperventilation refers to taking a series of The rise in O2 is somewhat reduced because of con- rapid deep breaths before breath-holding. to the environment and surrounding tissue. underwater.

than expected from gas laws alone.1  Alveolar pressures of the metabolic gases during (a) a breath-hold period without ambient pressure change. ongoing oxygen metabolism. The dive with prior In contrast. there is a sufficient alveolar-arterial volume of the alveolar gas increases.1 (c) had a in alveolar Po2 as the lung re-expands and the longer bottom time as would be expected when . during ascent there is a rapid fall hyperventilation depicted in Figure 3. This is greater gradient to allow continuing O2 uptake for a con. 2 ATA Ascent (c) Figure 3.30  Free diving 200 60 Alveolar carbon dioxide tension CO 2 Alveolar oxygen tension 150 40 (mmHg) (mmHg) Oxy 100 ge n 20 50 Hypoxic zone Time (s) 0 20 40 60 80 (a) 200 60 CO Alveolar carbon dioxide tension 2 Alveolar oxygen tension Oxy 150 gen 40 (mmHg) (mmHg) 100 20 50 Hypoxic zone Time (s) 0 20 40 60 80 Descent On bottom Ascent 2 ATA (b) 200 60 Alveolar carbon dioxide tension CO2 Alveolar oxygen tension 150 40 (mmHg) (mmHg) Oxy 100 g en 20 50 Hypoxic zone Time (s) 0 20 40 60 80 Descent On bottom. (b) a breath-hold dive to 10 metres and (c) a breath-hold dive to 10 metres with prior hyperventilation. Po2 at depth. thus reflecting siderable time.

relaxation techniques and practice. The dangers of breath-hold that conserves the oxygen for the heart diving and hyperventilation are discussed further and the brain. when I begin my pre-­immersion prepa- A concurrent and unwanted side effect of these rations my resting heart rate is 75 bpm. The first of these is an attempt to expedite the 4 January 2014 so-called diving reflex that can be observed in all air breathing vertebrates but that is highly devel.. The obvious risk is that the diver as much as possible. output is a result of the body’s decreas- tion induces splenic contraction. Once I have reached a ditioning. On several immersions when ‘open’ to manipulation by skilled  ­divers. to 55 bpm. a previous world record holder. ballast no fins world depth record of 101 metres. diovascular performance is ­ influenced Although these are autonomically mediated phe. Indeed. Physiology for freediving in Chapter 16. ing needs for oxygen and energy con- lating red blood cells. slowdown. deep relaxation it drops. onds it has slowed to 30 bpm. on his website Francesco “Pippin” oped in marine mammals (see later). by other factors. and such falls in alveolar and arterial The training I do is targeted at creat- Po2 during ascent would be even more dramatic ing a physiology that conserves oxygen on deeper dives. New Zealand Listener Magazine. ventricu. At the same time. it does seem plausible that it is 14  bpm. I institute one last com- that there is considerable inter-subject v­ariability mand to my heart to slow down. At this in the potency of the diving reflex. articulated it thus: sure of O2 develops by the time the diver reaches the surface. there is a strong belief among free divers physical conditioning. increasing circu. As I duction combined with sympathetic sensitization begin my descent. is such a different set of effects to what In addition to hyperventilation. under direct control of the that increases blood pressure and in turn elicits a Central Nervous System. both controversial. Its his approach in more detail: principal effector arm is a marked sympathetically mediated increase in peripheral vascular resistance My heart. their muscles very quickly. This 10 minutes after entering a stare of probably arises from vagal inhibition of nodal con. and that it tends point my heart is down to a mere 10 to to wane with age.. that elite free discovering exactly what they consist of. loss of conscious. there are two is found in any other sport that we’re still other strategies. Humans as free divers  31 prior lowering of the arterial CO2 makes the diver interview William Trubridge. and the bradycardia reduces O2 survival in the undersea environment consumption by the heart. divers use or manipulate in order to extend their duration underwater. holder of the constant more comfortable remaining at depth for longer. in a matter of sec- of ectopic pacemakers. begins a rapid vagally mediated bradycardia. Not surprisingly.. In a 2014 all of the above mentioned factors are . Peripheral vasoconstriction sumption. This efficiency in energy has the effect of reducing the circulation of blood conservation is of vital importance for to the peripheries. Central redistribution while in a state of apnea. As an example. and mental that they can manipulate the process through con. preparation.. processes is a predisposition to arrhythmias. described initiated by apnoea and also by facial cooling. foremost being my nomena. It can be seen that a lower alveolar partial pres. This diminution of my cardiac there is some evidence that the sympathetic activa. My car- lar ectopic beats are common. of blood makes more O2 available to vital organs. Given depth of 110 m. This reflex is Ferreras. Similarly. I need to shut ness during either the final phase of ascent or on down that oxygen flow to the muscles arrival at the surface is a recurring event at free so that they can work anaerobically and diving competitions. Whereas some- could experience critical arterial hypoxaemia one who is extremely fit would be able as the alveolar Po2 is rapidly falling in the latter to supply a high amount of oxygen to stages of the ascent.

This technique involves using the glossopha.32  Free diving ideal I  have obtained readings of an The challenge of avoiding gas incredible 7 bpm! Obviously these find. Despite the extreme depths reached by free div- ume of air carried by several litres. high-pressure neurologi- mended. There are sporadic reports of excessive pack. and in certain soci- water! eties these divers are accorded celebrity status. although there may be a strong report- volume because the gas is held in the lungs under ing bias operant here. overt effects of nitrogen narcosis are only rarely does not translate directly into an increase in lung reported. and it is therefore impossible to further. there are some extreme free divers who fact that O2 is being consumed from the moment have developed the technique of glossopharyngeal apnoea begins. of the high positive transpulmonary pressures and the short duration of the dives therefore lim- that can reach 60 mm Hg or even more. There its any effect. are pushing deeper. unlikely explanation given the very short exposures. although this ers. exponents of lung packing can increase the vol. narcosis (see Chapter 15). is to let the sinuses Trained free divers have been able to achieve (and to some extent the middle ears) flood with remarkable underwater feats. complications usually associated with com- tion underwater is so-called ‘lung packing’. exsufflation. Nevertheless. In view of these cause. . there are increasing numbers of ness resulting from profound reduction in venous stories of strange sensations and ‘funny turns’ dur- return associated with high intrathoracic pres. enabling an increase in the total lung capacity by predictions of inert gas tensions following up to 20 per cent. generate a Valsalva manoeuvre to clear the ears or sinuses. tion (particularly the former) during free diving opens up the possibility that extreme exponents The second controversial strategy used by will suffer gas toxicities and decompression sick- elite free divers to extend both depth and dura. more pressed gas diving. packing in the opposite direc. An alternative approach to avoiding Record diving barotrauma under these conditions. the starting fraction of inspired O2 of 0. some reported events (e. It is impossible to know their exact sure during the act of packing.21 and the est value). alone simply because the partial pressure of nitro- egy. as extreme free divers are also reports of hypotensive loss of conscious. These sorts of problems are likely to depth when the lungs are compressed at or below become more common as record depths are pushed residual volume. and one that has been proven radiologically.g. Cerebral O2 toxicity seems an for any possible edge. tion. Neurological decompression correctly referred to as glossopharyngeal insuffla. Nevertheless. facial or diaphragmatic twitching) are very typical tion. It may also be that narcosis positive pressure and is therefore compressed. that is. Largely for completeness (and for curious inter. it is unlikely that packing cal syndrome (see Chapter 20) and cerebral O2 tox- will be abandoned by extreme free divers looking icity (see Chapter 17). sickness in breath-hold divers has been reported. Although some cases may be caused by arterial ryngeal muscles to pump air into the lungs. but potential explanations include nitrogen potential hazards the technique cannot be recom. ness. toxicities and decompression ings are augmented by the power of sickness mind over body that I have developed over the years. through the study and The combination of increasing depth and dura- practice of Yoga. is not as likely as predicted on the basis of depth Therein lies the potential problem with this strat. gen in the relevant tissues takes time to equilibrate ing leading to pulmonary barotrauma because with the partial pressure of nitrogen in the lungs. Adept (see Chapter 10). However. ing these dives. thus gas embolism following pulmonary barotrauma. This extra volume potentially repeated and closely spaced deep breath-hold increases the depth at which lung compression dives do suggest that pathological bubble forma- becomes hazardous (as described earlier) and tion from dissolved inert gas is certainly possible also represents an increase in the O2 stores. This is used in those situations near terminal of O2 toxicity.

­ survive extended breath-holding. Dolphins can reach speeds of 20 knots with invariable development during the latter stages of remarkably low energy consumption. barotrauma. tion exposures that appear to defy conventional rent record depths are 214 metres for male divers wisdom with respect to limits of hypoxia? How and 160 metres for female divers. rope-guided tice. no use can dive to 1500 metres. The record is currently 101 metres for male seal can stay submerged for 2 hours.org/competitive/worlds-records. nitrogen The absolute limit of these hazardous ‘experi. pulmonary oedema (skin or fur) and the development of flippers or or cardiac dysrhythmias. energy-conserving head achieve long periods underwater are both physi- immersion exposure. Records are also held for static apnoea. hypoxic blackouts.  A  ­dorsal ascent. The At the opposite end of the spectrum is so-called Weddell seal regularly dives for food to greater no limits free diving. narcosis. with swimmers using fins for propulsion. . mind-boggling 11 minutes 35 seconds for male participants and 9 minutes 2 seconds for female Oxygen stores participants. The relative contribution of the lungs. set by Tanya Streeter in 2002. decompression sickness. Underwater breath-hold horizontal distances All diving mammals have an increased total body (dynamic apnoea with fins) of 281 metres (male O2 store. low-friction body surface by pulmonary haemorrhage. dedicated competitions sanctioned by an umbrella society are run according to strict protocols. The records cited The study of diving animals offers the scientist an here are valid for January 2015 but may have been ideal opportunity to study the physiological con- superseded at the time of reading. as the name implies. The cur. time. duration and underwater have been achieved in 50-metre swimming pools distance. interest to diving physicians to see how diving ani- The purest form of depth record is referred to as mals avoid the perils induced by exposure to pres- constant weight apnoea without fins and involves sure and hypothermia. Of more interest to as a result of rapidly developing hypoxia as they the diving physician and physiologist are the approach the surface. usual dives are 20 to 30 minutes in duration. can breath-hold underwater for 1 to 2 minutes sled for descent. O2 toxicity or high-pressure neurologi- ments’ remains unknown. which tows them back to the surface. although divers and 69 metres for female divers. On reaching the target depth. Death may be precipitated at depth streamlined shape. Quite often these divers require rescue by blowhole in whales and dolphins also aids standby divers because they become unconscious energy efficient respiration. mechanisms to cope with prolonged apnoea. return to the surface with the same weights car. Diving marine mammals  33 Records are attempted for various categories of swimmers) and 234 metres (female swimmers) diving involving depth. DIVING MARINE MAMMALS Physiologists and physicians need to be aware of these remarkable achievements. they and descend to 10 to 15 metres. The current records are a ological and biochemical. detach themselves from the sled and pull a pin that How are marine mammals able to achieve releases compressed air from a cylinder into a lift these remarkable underwater depth and/or dura- bag. A complete sequences and defence mechanisms required to list of current records is available at: http://www. The  adaptations that allow diving animals to which is a motionless. with some prac- at all. Divers hold onto a weighted. The northern elephant seal and the sperm whale ried down (if any) and. Because of the potential risks involved. The latter is the also do they achieve these feats without develop- longest-standing free diving record at the present ing some of the disorders (e. Cerebral hypoxia is an fins.g. This is the most extreme cate. but it seems likely that cal syndrome) that are the subjects of subsequent depth record increments will become smaller and chapters in this book? smaller as immutable physiological barriers are Obvious anatomical adaptations include a approached. The southern elephant of fins. It is also of great aidainternational. than 100 metres and can remain submerged for up gory in respect of depth and requires no swimming to 60 minutes. Typical humans.

This function is augmented in many species of marine mammals by a bulbous enlarge- Oxygen consumption and ment of the root of the aorta. Such animals are under the control of multiple reflexes. adrenal (versus ~25 per cent in humans). Other tissues that are most critical for a tiny proportion (~5 per cent) is found in the lungs survival (e. Indeed. retina. and the relatively hypoxic conditions associated with this myoglobin increase is proportional to the diving and that these adaptations are more pro- diving capacity of the animal. The increase in left not be sufficient during long dives. Deep diving mammals do not dive at full lung The term diving response refers to a sequence capacity and may exhibit reduced lung perfusion of physiological events. It is possible and this is important to maintain perfusion of that this adaptation is more important for keeping vital organs. but its role in marine mammal diving adaptation is Because stroke volume falls by only about 30 per uncertain. brain. but O2 still needs to be arterial tree during the long diastolic intervals conserved. especially in the swim muscles. They also have a markedly increased niped skeletal muscles have an enhanced oxidative myoglobin concentration (5 to 12 times that found capacity to maintain aerobic metabolism under in a human). it can be readily calculated that characteristic of diving. in pregnant seals. The seal essentially shuts augmenting O2 storage and delivery during a dive off the flow of blood to non-essential tissues and is the pre-dive sequestration of oxygenated red organs. the predominant effector of this reduction is after release on one dive typically takes far longer the bradycardia. O2 con- have increased blood volume (~15 per cent of body servation is thus partly accomplished by selective mass versus ~5 to 7 per cent for humans). This reduces cardiac work be further regulated by a valve-like sphincter in the and O2 consumption. Maintenance of arterial pressure is blood haematocrit (and viscosity) at optimal levels facilitated by the stretching of the elastic walls of when the animal is not diving than for improving large arteries during systole and their recoil dur- oxygenation during dives. such as the kidneys. preferentially distributed to swimming rather than About 70 per cent of the total O2 store is found in non-swimming muscles. The fact that this occurs is not disputed. Blood may be blood has a higher haemoglobin concentration. until it resurfaces. cells in the spleen followed by the release of these Rapid onset of bradycardia (to as low as 10 per cells by splenic contracture during a dive. the placenta) are An intriguing and controversial mechanism for also selectively perfused. thus providing an elastic capacitance for myoglobin described earlier all contribute to the maintaining pressure and flow into the constricted seal’s impressive O2 supply. than the typical surface interval between subse. The entire human aorta if the submerged seal continued to metabolize at contains less volume than the aortic bulb alone in the same rate as before diving. any benefit served despite this reduction in cardiac output. A substantial reduction in vena cava. cardiac output has been shown in Weddell seals. and the redistribution of circulating blood. its O2 stores would seals of a similar body weight. spinal cord. The time cent of baseline rate) at the start of a dive may be course of release into the systemic circulation may seen in diving species. including apnoea. may be restricted to the initial dive. ventricular afterload that would be expected as a ingly. haemoglobin and seals. Arterial blood pressure is reasonably well pre- quent dives during a dive series. glands and. brady- during dives for reasons discussed later. the aortic bulb. period of a dive. Only muscles. which of O2 is stored in blood and muscle. The the diving response aortic bulb approximately doubles the diameter of the ascending aorta in harbour and Weddell The increases in blood volume. It has been noted that re-sequestration cent. Thus.34  Free diving blood and muscles storage areas depends on the supplied preferentially to vital organs during the diving pattern of the animal. Studies indicate that pin- the blood. these animals exhibit multiple strategies consequence of elevated peripheral resistance and aimed at conserving O2 and ensuring that it is decreased large artery compliance is reduced by . Myoglobin carries nounced in swimming than in non-swimming approximately 25 per cent of the total O2 sore. ing diastole. so the bulk cardia and redistribution of cardiac output. Not surpris.g.

106:284–292. With prolonged dives certain tissues switch to anaerobic metabolism. which may occur The electrocardiogram of the diving animal in repetitive diving. Undersea and Hyperbaric compression during deep dives include a flexible Medicine 2004. A reduction of blood flow to the skin increases lower the pH of the blood and can lead to acido. Hochoachka PW. Examples can be found in the fins and acid into the blood for metabolism by the liver. when not diving. perfusing blood minimizes accumulation of nitro- taining stroke volume. Acidosis is avoided by confining anaero. Deep diving mammals do not dive on a full these changes may include the gradual diminution lung volume. How the elephant seal and sperm whale avoid the high-pressure neurological syndrome during Anaerobic metabolism their impressive diving feats is not yet understood. Oxygen and Structural adaptations to accommodate thoracic the diving seal. Also. which produces lactic acid Hypothermia as a by-product. Working muscles are close to the surface and have little fat insula- Diving technique tion. Journal of Applied Physiology Pressure changes 2009. Quarantining of pulmonary gas from and O2 consumption while at the same time main. The physiology 75 per cent of the descent. The physiological result in up to a 60 per cent reduction in energy basis of diving to depth: birds and mammals. toxicity because the partial pressures never reach atrial node by a ventricular pacemaker site. these tissues release the lactic to the core. It likely also reduces nitrogen shows some progressive changes during pro. have a raised metabolic rate to produce heat.31:81–95. insulation of the fat layer and allows surface cool- sis. ering capacity. causing a weakening of the heart’s ability to ing. costs. As well as limiting nitrogen uptake. Thornton SJ. Other dangerous levels. In addition to bradycardia. Further reading  35 this unique anatomy. Gliding is used during dives exceeding Annual Review of Physiology 1998. or even abolition of the P wave. There is an increased tolerance to A thick layer of blubber and a relatively low ­surface lactic acid in the muscles through increased buff. gen (decompression sickness). When the rial blood and heating venous blood as it returns animals resurface. Cardiac rhythm this means that the animal is not exposed to O2 is then apparently set independently of the sino. contract. longed apnoeic dives. Modified diving behaviour to limit muscle activity and thus O2 consumption has been demonstrated in Weddell seals. many animals. Lundgren CEG. however. which reduces cardiac work descent. The net result is a diminished help the animal avoid pulmonary barotrauma of peak ­systolic pressure. narcosis. which is not transmitted to the internal core. Prolonged downward gliding. flippers of whales and seals. as a result of reduc- ing buoyancy with lung compression at depth can Kooyman GL.60:19–32. rib cage. . 18  metres in depth and occupies approximately Lindholm P. High levels of lactic acid. FURTHER READING with minimal muscular effort. and pathophysiology of human breath hold diving. stiffened alveolar ducts and attachments of the diaphragm such as to permit some shifting of This chapter was reviewed for this fifth edition by abdominal contents into the thorax. Ponganis PJ. area to reduce heat loss maintain core temperature. These changes Simon Mitchell. cardiac dysrhythmias occasionally appear. Well-developed countercurrent heat exchange sys- bic metabolism to the skeletal muscles and other tems also aid in conserving heat by cooling arte- tissues isolated from the blood supply.


habitats and underwater vehicles 51 Surface-supply breathing apparatus 41 Further reading 52 INTRODUCTION comfort but also some protection from box jelly- fish and other stings. choose from a selection of corrective lenses that sate for the buoyancy of the suit. forehead and dent or novice. A diver with visual problems can thermal insulation and a weight belt to compen. or hel- equipment mets that cover the entire head. Alternatively. 37 . It should be possible to block the nostrils with- DIVING out disturbing the mask seal to enable the wearer to perform a Valsalva manoeuvre. are not suitable for diving. It may also help the reader to cover the nose. The nose understand the stresses experienced by the novice must be enclosed in the mask so that the diver can diver. exhale into it to allow equalization of the pressure between the face and mask with the water environ- EQUIPMENT FOR RECREATIONAL ment. Traditionally. The mask usually covers the eyes and diving operations are dealt with in the second part nose. This is of importance in under. which do not diving equipment. masks were made from rubber. Full-face masks that Snorkeling/breath-hold diving cover the mouth as well as the eyes and nose. The the equipment can cause. The first part of this chapter deals with the equip- ment used by most recreational divers. The more MASK complex and unusual types of diving equipment A mask is needed to give the diver adequate vision that are used by technical. a wetsuit may be added for hardened glass. used by snorkelers – a mask. particularly for the stu. In colder climates. 4 Diving equipment Introduction 37 Safety and protective equipment 42 Equipment for recreational diving 37 Dive boats 45 Snorkeling/breath-hold diving equipment 37 Professional or technical diving equipment 46 Self-contained underwater breathing Breathing systems 46 apparatus – scuba 39 Chambers. mask seals by pressing on the cheeks. snorkel and a pair of The faceplate of the mask should be made from fins. Swimming goggles. commercial or military underwater. are more commonly used by professional divers and are considered in the The simplest assembly of diving equipment is that section on professional ­diving equipment. In tropical waters. of the chapter. Attention is paid to the problems although now most are made from silicone. These are designed a ‘stinger suit’ provides not only a little thermal to attach directly to certain masks. are commercially available. under the nose with a soft silicone edge to prevent standing the medical problems that are related to entry of water.

Fins allow the diver to swim faster and his or her normal visual field. underwater or buoyancy on the surface. Unfortunately. a quick-release buckle may not be fitted (or may be ing its shape and some other means. the surface. and most are moulded to allow the diver to grip the tube with the teeth to thread onto a belt. However. Ocular damage can occur if hard cope with waves breaking over him or her (and corneal lenses are used for diving (see Chapter 42). and they free the diver’s arms most marked when the diver tries to look down for other tasks. Because of this. The tube is positioned to pass upward near fit into pouches. if the diver has poor tech- which mask gives a good seal. springs and materials. A typical snorkel restricts the maximum breath. the diver becomes entangled. Some people with allergy prob. Such situations include anatomical dead space. The situations in which snorkel by lengthening it. sometimes leading to panic. Others have little effect. modify. if the diver is out of is not a viable option. This restriction can be a danger if the feet by straps or are moulded to fit the feet. especially if he or she has to a swim against mastered. although this is rarely an issue with silicone. SNORKEL WEIGHTS The typical snorkel is a tube. but the wearer needs to become there is a lurking predator just outside the field accustomed to them. The U-bend near the mouth end. space above the water. If it is not learned and a diver. a  leaking mask can become a major a current. The restriction is more efficiently. with a pre-moulded or creatable ers require extra weights to submerge easily. there are Various attempts have been made to develop fins some masks available with a tilted lens to provide a that give greater thrust with special shapes. FINS All masks cause a restriction in vision. it is necessary for a diver ing capacity to about 70 per cent of normal. The fins are normally secured to toward the feet. for example. through the tube while floating on the surface and Whatever weighting mechanism is used needs to looking down. These problems add to the breathing gas. adding valves. A mouthpiece is fitted weights are made from lead. the ­volume of the snorkel also increases the diver’s surface in an emergency. into the snorkel) and a current that may force the Certain contact lenses may be lost if the mask diver to swim hard. such as in caves where there is no air All snorkels impose a restriction to breathing. or remain on. Some of these fins can restriction worrying and may possibly fear that improve the thrust. about 40 cm long and Even without the buoyancy of a wetsuit. the wearer’s ear to enable him or her to breathe attached to a buoyancy compensator device (BCD). or enable the diver Many attempts have been made to ‘improve’ the to remain on. valves. With Fins (or flippers) are mechanical extensions of most masks. The to ditch the weight belt to reach. increasing an emergency in which the scuba diver cannot the diameter substantially to reduce the resistance inflate the BCD. some div- 2 cm in diameter. or is unable to. There is little de-activated) are those where it would be danger- evidence of the success of most of these attempts. The loss of a fin may also cause problems for expel water from the mask. for scuba divers. of vision. previously lodged in the snorkel. lems react to the rubber of the mask. mask. Any water in the snorkel should be be fitted with a quick-release buckle or other mech- expelled by forceful exhalation before the diver anism to allow a diver to drop the weights quickly inhales through the snorkel. take reports of divers inhaling foreign bodies that have preventive action. controlled flex. to minimize water nique or if the diver has not used fins for an extended entry. Experimentation is also needed to find if fins are the wrong size. There have also been anecdotal floods and the diver fails to. The visual field varies with the style of Divers often get cramps. In some circumstances. The diver needs to master a technique to period. either on a belt or. all compet- The more nervous beginner may find the visual ing for the diver’s dollar. either in the foot or calf. ous to ascend. the diver can see about one third of the feet. divers often fail to .38  Diving equipment prescription lenses can be ground and glued to a difficulties of a diver who may be struggling to variety of masks. and so aid his or her return to. Some weights are designed to and lips. or fails to attain appropriate orientation problem. better downward field of vision.

This sys. is 160 to diver is likely to become unconscious and inflating 300 bar (2300 to 4350 psi). It allows a more realistic self-­assessment of the desire to scuba dive and the subsequent rewards. With the confidence gained in snorkeling and breath-hold diving and the associated aquatic skills. The valve is held open by ment with the diver if it is dropped. reduces the pressure from cylinder pressure to the the belt will hopefully fall away. In the most common breath. Experience with this gear is excellent training for a potential scuba diver. The first-stage In many fatal diving accidents the diver did not release his or her weights. the diver is also less likely to become as dependent on the breath- ing apparatus. demand valve system. of gas to the diver is triggered by the diver’s inspi- ing and practice help to reinforce the skill so that it ratory effort and is closed by expiration or cessa- will become more automatic when required.1  First stage reducer valve: the gas The simplest form of breathing apparatus con. the tap for this omission is not clear. relatively warm water. In the event of unconsciousness. Unfortunately. Adequate initial train. let pressure at this value. pushing the first stage valve seat down and shut- tem was in use until the 1930s. causing the diver equivalent of about 10 ATA greater than the pres- to rise to the surface. but much of the ting the gas flow off.1 and Figure 4. a snorkel diver needs a suit to keep warm. to the second stage valve) falls. the BCD is not an option or may not be sufficient The first stage of the valve system (see Figure 4. Equipment for recreational diving  39 release the belt if they are in difficulty. Holding the belt away from sure surrounding the diver. The reason underwater breathing apparatus (scuba). turned on to obtain each breath of air. It also tion of inspiration. Unbalanced piston (open) high-pressure seat Spring This basic free diving equipment is adequate Piston Water entry for diving in shallow. called the working pressure. the force of a spring until the pressure above the first stage piston builds up and forces the valve seal down on the seat. The flow the result of stress or panic. operating principles of a simple regulator and quately on this important emergency drill. when deep). but it is likely often is replaced by a two-stage valve system. thus shutting off the gas. valve (at about pressure) 10 atmospheres above water Self-contained underwater breathing pressure) apparatus – scuba Figure 4. needs to be reinforced periodically. escapes from the cylinder until the pressure above the piston increases to a level where the sisted of a gas source and a tap that the diver force on the piston can compress the spring.2 (a) and (b) show the much of the current training fails to focus ade. Figure 4. The air is stored in a cyl- An alternative drill of taking the belt off and inder at a maximum pressure that is determined holding it in one hand (preferably away from the by the design of the cylinder. . Suits are discussed in High pressure air ‘O’ ring To demand (at cylinder Chapter 27. For most cylinders body) is useful in some situations in which the this pressure. In cold climates. This is normally ing apparatus.1) (e. The valve opens again when diver’s time and concentration were taken up in the pressure above the piston (and in the hose operating the tap.g. the Aqualung or self-contained because the diver has taken another breath. and it regulates its out- the body should reduce the chance of entangle. The diver can gain the basic skills without the extra complications caused by scuba gear.

The purge button is used to trigger a flow of gas from the supply without the need to inhale from the regulator. In others. The arrows indicate air flow. valve opens and closes as gas is drawn from the Expired gas passes out of the second stage ­system  by  the diver. can enter the water chamber and helps the spring gas flow increases with respiratory effort because to hold the valve open. the ambient water the valve opens more. This pressure difference forces the exhaust valve open and allows exhaled air to escape. The second-stage valve is usually Most divers have little difficulty using scuba. This adjust. the water through an exhaust valve. pressure in the mouthpiece chamber. This causes the diaphragm to curve in and tilt the air supply valve open.2(b). the dia- phragm moves back into the position shown in Figure  4.2 (b). allowing the diver to breathe pressure is transmitted indirectly. takes the regulator from the mouth while under- When the diver inhales. In some regulators. and the air supply valve shuts. At this stage. the diaphragm The scuba regulator is designed to provide curves inward and depresses the lever (see the diver with a gas supply matched to his or Figure 4. As the diver does so. normally.2  SCUBA demand valve (a) during inspiration and (b) exhalation. when they first don it. open until inhalation ceases. At the end of inspiration air continues to flow until the pres- sure in the mouthpiece equals the pressure in the water chamber. In the demand valve. The inlet valve opens and remains her respiratory needs. However. During exhalation the pressure in the mouthpiece is greater than that in the surrounding water. The purge button allows the diver to ment of  the s­upply pressure with water pressure is open the inlet valve to force any water out of the designed to prevent the flow decreasing as the diver regulator. or second- stage valve. During inspiration the diver decreases the pressure in the mouthpiece. called the demand valve.2 (a)). at this stage the diaphragm will return to the position shown in 4. the weight and . he or she reduces the water or if the seal around the mouthpiece is poor. The diver may need to do this if he or she descends.40  Diving equipment Purge button Diaphragm Water chamber High-pressure air valve (open) Exhaust valve (closed) High-pressure air supply Valve lever Mouthpiece (a) High-pressure air valve (closed) Exhaust valve (open) (b) Figure 4.

A major problem is that user has no indication of when the gas supply will a diver who is entranced by the scenery. a small motor and air Some modern systems transmit the cylinder pres. such as pul- systems and is valuable. An advantage of these systems is of the cylinder are proportional to the pressure. The aerosol pulling a lever that opens the reserve valve. the divers tow a float that supports measure of the remaining air supply. A diver needs to ensure monary barotrauma. the inspiratory effort required for mobility. Therefore. Also. as it passes through the first stage and can ice up restricts the diver’s range and depth to the length of with the piston frozen in the open position. some because he or she forgets to check the gauge. Two modified forms of SSBA have found sup- sure gauge connected to the cylinder by a hose. problem with this is that the valve lever may be times cause a syndrome called salt water aspira. air supply can be as large as needed. The air for SSBA may be stored in large to cause a flow does not vary until the cylinder is tanks or compressed as required. The pressure gauge provides the diver with a In the other. often called a ‘hookah’ system. port in some circles. Water prevent divers from running out of air is a reserve can enter through a hole in the mouthpiece if the valve. However. valve. additional reserve. and may aggravate that he or she has a cylinder or cylinders with back problems. The div. causing tion ­syndrome. Most divers have a console that includes a pres. One can cause distress to the diver and may some. Then the pressure in the hose to the pressor. . that. sure via radiofrequency signals rather than via a This apparatus supplies air to one or two divers. This condition is considered in Chapter 42. the divers are unable to so the gauge is often called the ‘contents gauge’. In operation it resembles a boiler safety mouthpiece is poorly attached or through the dia. This occurs because the air cools ment. Its advantages are that the diver problem can be reduced by using a first stage that is freed from the cumbersome air cylinders and the is designed for operation in cold water. Equipment for recreational diving  41 bulk will make them awkward. The contents an air cylinder. the compressor needs to be reliable and this warning may be minimal or absent with mod. inadvertently put into the ‘on’ position. is increased resistance on inhalation. is economi- second stage falls and the flow decreases. Another common problem is valve dysrhythmia. This equip- may ‘freeze up’. In one. Another problem associated with demand valves is that they may cause pain in the temporo. A significant problem is that the the volume this represents. hose. it is prudent for the diver to carry a trating on a task or distracted may run out of air small bail-out cylinder and regulator. the air escapes to the diver until the cylinder phragm or exhaust valve if either is faulty. In the water. A leak pressure falls to the level at which the reserve valve can generate an aerosol if the water reaches the seats. the buoyancy of the adequate gas supply for the planned dive. if the hoses are short. fail. The use of a com- almost empty. rather than sickness (DCS). The remainder of the air can be released by inlet valve of the second-stage valve. or it may trigger other medical the diver to use the reserve of gas without being conditions such as asthma or possibly a cardiac aware of this. failure. the first stage of the regulator ­supplied by a hose from the surface. cally attractive because the air is compressed to a er’s first warning that the cylinder is almost empty lower pressure than that required for storage tanks. and an set offsets its weight. The diver’s lips should be sealed around the A traditional and almost obsolete system to mouthpiece to prevent the entry of water. reach the depth needed to develop decompression Divers tend to say they have 50 bar left. An novice users may forget that they are still exposed audible low-air warning is incorporated into some to the other hazards of scuba diving. instead of being Because the first stage regulates the pressure to restricted by the diver’s carrying capacity and need the second stage. Surface-supply breathing apparatus mandibular joint. The the air supply hose. surface-supply breathing apparatus (SSBA). A diver can also use a demand valve with air In very cold water. concen. pressor during operation. However. there needs to be an observer to monitor the com- ern regulators. compressor are supported on a float on the surface.

Its effectiveness is reduced by loss of heat with forms. helped to avoid many serious diving accidents. Many accidents involve human. This can the air supply is very small. this has potential hazards. There is an opening with a waterproof seal to allow tially be a second scuba set. the insula- an air supply failure. If the fare. often pre. Pressure buddy-breathing. The  most accidents are considered. into spaces between the suit and the diver soon warms to skin temperature. which reduces heat loss. It is trolled and monitored in a similar manner to nor. enabling only a few lead to an uncontrolled ascent. Another other common form of thermal pro- a second source of air (redundant supply) that is tection is the drysuit. feet and hand openings. Foamed Neoprene has EMERGENCY AIR SUPPLIES insulation properties similar to those of woollen Emergency air supplies can take a variety of felt. known as Spare Air (Submersible drysuit or he or she may lose control of buoyancy Systems. is now favoured. At 30 metres of depth. One commercially The diver needs training in the operation of a available device. For cave divers this may essen. lation of a wetsuit decrease with repeated use. The use of gas in the foam also means that the diver’s buoy- a second regulator attached to the scuba set. a procedure in which two divers decreases insulation by reducing the size of the air shared an air supply in the event one of them had cells in the foam. This point mia. proper training. but this will mean that the diver is too buoyant However. a smaller cylinder with an indepen. quate gas for a relatively safe ascent. surface (see Figure  27. The water that leaks with coping with them. able or is unwilling to cooperate. dent air supply is available but not commonly used. Inc. The buoyancy and insu- rig will be of use if the diver with gas is not avail. It is also sometimes possible for a diver to Safety and protective equipment breathe air from the BCD for a short period of ascent. This protection is normally provided by insu- is developed in Chapter 46. However. who have relatively ready access changes on the gas in the suit. plied from the scuba cylinder or a separate supply. infection and buoy- adequate health and fitness. ancy control problems. mon sense. mistakes. sometimes inverted. or assist ­air-foamed Neoprene rubber. The compression of the dure often did not work in an emergency. This is watertight and has available to each diver without external assistance seals round the head. The drysuit allows the with substantial mandatory decompression obliga. tions. prolonged dives to minimize the risk of hypother- dictable and thus correctable. For this reason. often ancy decreases as he or she goes deeper. The diver called an octopus rig. in which deaths and lated clothing. are discussed here. In the early days it was common to rely on water movement and increasing depth. made from ment that reduce the hazards of diving. Almost all accidents are preventable. .42  Diving equipment In some resort areas. important that a redundant supply provides ade- mal scuba instruction and equipment hires. For this reason.). The gas can be sup- to the surface. and the authors do not ascribe the popularly held THERMAL PROTECTION belief that these accidents are attributable to an ‘act Thermal protection is needed in cold water or on of God’. For technical divers the diver to get into the suit. However. and its introduction and widespread use have diver does not. deep dives or dives requiring decompression. dent regulator can be used. by excessive addition of air into the suit. The best safety measures available to a diver are including aspiration of water. Several items of equip. he or she needs to limit the weights. is carried by some divers. common protection is a wetsuit. A BCD with an indepen- appropriate and functional equipment and com. a redundant gas supply is also essential.1). has now become standard can compensate for this by wearing a BCD. and A gas supply and exhaust valve are needed to allow they often carry what is known as a stage cylinder. diver to wear an insulating layer of warm clothes. these devices are hired by breaths for ascent. neither buddy-breathing nor an octopus when closer to the surface. Such use should be con. these devices novices who have had no training and who may be are not commonly used and are not sufficient for medically unfit to dive. the diver to compensate for the effect of pressure For most divers. Both anecdote and analysis of tion of a wetsuit is about one third of that on the diving accident statistics showed that this proce.

picking up a heavy object on the bottom). The diver can find himself or A depth gauge. as well as reducing the amount of weight carried. a most undignified and potentially diver is operating in a depth or time zone where dangerous posture. DIVE COMPUTERS BUOYANCY COMPENSATOR DEVICES Dive computers use a depth (pressure) sensor. tionized diving because of their flexibility and . measure pressure by the reduc- through hoses. depth gauges by divers. ing medical problems including pulmonary baro. Electronic. and DCS release gas are fitted so the diver can reduce buoy. are more often used by commercial divers. these computers diver to hover in the water and adjust for any factor enable dive times well beyond those permitted by that causes density to increase (e. although tems include hot water pumped down to the diver now rarely used. Capillary gauges. the need to check the accuracy of gauges is often tion similar to that of a significantly thicker wetsuit overlooked. Users are well expanding gas in the BCD increases its lift and advised to use more conservative limits than the in turn increases the rate of ascent. Heat can also be supplied to a diver to help mechanical and capillary gauges have been used as him or her keep warm. Faulty gauges have caused divers to and so increase the level of comfort for the wearer. most people diagnosed with DCS these Divers can lose control of their buoyancy days have been diving within the limits indicated while ascending. ancy by venting gas from the compensator. s­ peeding the ascent. but they can provide thermal protec. timer. pers. heart rate (Figure 4. especially on multi-level and pression. for tracking decompression status if using tables. In fact. bags [wings]) worn by the diver and attached to a They are encoded with a decompression algo- gas supply from the regulator. dive computers have revolu- trauma and DCS. with the current designs this useful ben- accumulate around the legs.g. from where it cannot efit has been largely foregone. The excess gas can also expand the feet of the suit and cause the DEPTH GAUGES diver’s fins to pop off. develop DCS. display and various other features. These seals help to reduce the amount of water Although the modern digital gauges are relatively entering and leaving the suit and so reduce heat loss. Some have a small separate air bottle and/or gas consumption. decompression stops may be needed. an important feature enhanced seals at the neck. the as theoretically safe by their devices. although these are now rare. repetitive dives. Most gauges record the maximum depth reached Semi-drysuits are essentially wetsuits with by the diver during the dive. The ability to change buoyancy allows the recalculating every few seconds. becomes inverted in the water. wetsuit com. ‘factory settings’. The BCD allows the rithm  – a set of mathematical equations designed diver to adjust buoyancy underwater or helps bring to simulate the uptake and elimination of inert gas the diver to the surface and/or support him or her within a diver’s body. Equipment for recreational diving  43 when the excess of gas expands. and diver warm. Various chemical and electrical tion in volume of a gas bubble in a graduated capil- heaters are also available. Several valves to ‘guesstimate’ a diver’s actual saturation. the excess gas may However. As the diver starts to ascend. Some of the more sophisticated Most BCDs can be inflated via a hose from the models take into account ambient temperature regulator. remains a significant concern with computer users. Despite this. In the past. By sampling the depth and there. and some even measure that can also be used as an emergency air sup. or otherwise an unconscious diver face-up on the surface. accurate. feet and zip. be vented through the exhaust valve. adjust the computer to more conservative modes. The commonly used sys. tables on most dives. BCDs consist of an inflatable vest (or back-mounted microprocessor. there can occasionally be problems (as They are not as effective as drysuits in keeping the there often were with mechanical gauges). Some models enable the user to uncontrolled ascent can lead to a variety of div. hands. However.3). timer and a means of calculat- herself floating on the surface with the suit grossly ing decompression are needed if an unsupervised overinflated. BCDs were also designed to float If the diver tries to swim downward. External heat supplies lary tube and were useful only at shallower depths. Such a rapid. they can still only ply.

with some lost cylinder. There summoning assistance. Each diver has the duty to aid transmitters are issued to divers. swept away by current. and/or divers surfacing distant from the boat. Some consist of a receiver and line. commonly on the boat (or can be elsewhere). safety sausages sidered foolhardy to dive without some method of and other surface marker buoys (SMBs). whistles. Most commercial divers are also commercially available electronic diver do this with an underwater telephone or signal location devices. This can lead to stranding lation. series with the BCD inflator. which is usu. the amount of gas remaining in the supply of divers at sea for extended periods.3  Two of the more sophisticated current model recreational dive computers (a) Galileo Sol (Scubapro. Divers who do not want the encumbrance of a number of transmitters. and (b) Vytec (Suunto. Various devices are available to try to prevent COMMUNICATION this problem. These are generally driven by breathing ings to caution the wearer when he or she ascends gas and are attached to the low-pressure hose in faster than the recommended rate. often tents gauge indicates the pressure and. stances. The common enables a charter operator to track its divers con- problem in the use of the buddy system is attract. This system the other if one gets into difficulty. and individual called a ‘buddy pair’. The con. the vastly increased underwater times enabled. forever.44  Diving equipment   Figure 4. USA). Commonly used location devices Because of the risks in diving. One such device is . include horns. mirrors. ing more frequently used. whether adapted for use by divers. tinuously. Finland). ally substantially slower than traditional rates used with most decompression tables. and these are becom- intentional or otherwise. by extrapo. The receiver is located a link to the surface can dive in pairs. DIVER LOCATION DEVICES Sometimes divers can be difficult to sight on the CONTENTS GAUGE surface after a dive because of the sea conditions The role of this gauge is discussed earlier. Suitable electronic position-indicating ing the attention of the buddy if he or she is looking radio beacons (EPIRBs) have been developed or elsewhere or if separation has occurred. it is generally con. Underwater audible signalling devices are com- Possibly their greatest contribution to diving mercially available and are useful in such circum- safety is the incorporation of ascent rate warn.

It allows the diver. authorities to perform a search and rescue. A lazy shot line is a weighted the flag is not recognized or is ignored. It aids recovery of div. It leads from the stern of the boat to the anchor chain. These are designed to warn boat operators to tern search. Unfortunately. It is often used Diving flags.e. to reach the anchor when the current is too strong to swim to it. This A diving platform or ladder is needed on most can be a problem in some developing countries. When diving in caves or some wrecks. . lights or other signals as required to mark the dive site and as a descent and ascent by the local maritime regulations should be avail- line. able. shown in Figure 4.4. Also. This is a continuous line to the entrance is needed so that it can be followed if the divers become disorientated or when visibility is lost because of torch failure or formation of an opaque cloud by disturbed silt. Dive boats Boats used for diving range from kayaks and canoes to large. BC.4  Nautilus Lifeline. They can be especially helpful Propellor guards. The diver can hold onto the line at antics of other craft. may need to be picked up after drifting away from the main vessel. In some conditions. is desirable if there is any depends on adequate monitoring of distress sig. a second safety boat or tender may be needed. boats to facilitate the diver’s return from the water. or if the current is insignificant. from the dive boat or from a buoy. slow down or keep clear. Consideration should be given to the recovery of LINES an unconscious or incapacitated diver. rescue tem such as a water jet. in many places the  depth mark. boat is being used. rather than lifted. divers who lished and practised. Equipment for recreational diving  45 A lead line is often used to assist the diver on the surface. and in most line that does not reach the bottom and is used for areas ‘boat propeller attacks’ cause more deaths decompression stops. Canada. and an appropriate system should be estab- the ‘Jesus line’ as it saves sinners – i. as well as the willingness and ability of local ing operations. which is A ‘mermaid’ line is attached to the stern of the boat ideally done with the diver positioned horizontally. However. than shark attacks. In some places they can ers that can be used to show the decompression offer legal. Each diver should be within arms reach of the main line. and extends down-current. a ‘guide line’ should be use. protection from the stop depths. the softer air-filled hull is less likely than a A shot line is a weighted line that hangs down rigid hull to injure a diver. Divers Figure 4. It can also be the centre for a circular pat. chance that the engine will be engaged during div- nals. (Some call this boats. specialized vessels that support deep and saturation diving. The facilities required depend on the nature of the diving. but there are minimum requirements. or a safe propulsion sys- when diving in remote locations. who has entered the water at the stern of the boat. This can be very difficult with both large and small ers when they surface downstream. if not physical. It can be marked with depth mark. into the boat. Recovery into an inflatable have erred and surfaced down-current from the craft is often an easier alternative because the diver dive boat!) This is not needed if a lifeline or pickup can be dragged.

For these tasks. squeeze the diver’s soft tissues up into the helmet. If the hose breaks. systems and the high gas flow is the noise this ing system that can be operated with no telltale generates. The gas flow round the circuit is reprocessing. For example. confer with the surface support. involve comparatively shallow common system. this is well in excess of that More specialized equipment is used for some needed with a demand system. military diving where an element of stealth is The other problem associated with free-flow required. Such tasks could be conducted with scuba head is in a rigid helmet. The diver was sup- This section deals with the more specialized equip. plied with a continuous flow of air that was pumped ment used by professional and military divers. One type uses a full-face mask that compressed as needed by a motor-driven compres. called standard rig. an oxygen rebreath. the professional diver is working in Demand systems were developed to gain a a small area for long periods. ing system with an oxygen-nitrogen mixture may This is prevented by fitting a one-way valve that be used. Several types of equipment are in in a hose. the military diver’s tasks. stealth is again required to avoid activating form of barotrauma. joined onto a flexible suit gear of the type described earlier. measured demand. and some of those of the but the same principle is still in use. for which oxygen-helium oxygen-helium mixtures are used. The hand-operated pumps have long gone. For most tasks. In the most professional diver. Because of this. The rig is Breathing systems converted into a rebreathing system. This can consumed may be fitted. generated by a Venturi system that does away with the need for valves to control gas flow. native supply of breathing gas in a cylinder on his or her back. the diver was also bubbles may be used. so they are commonly of fresh breathing gas must be sufficient to flush fitted into a helmet or full-face mask. In the early days. the pressure of the water tends to mine may be too deep for an oxygen set. a rebreath. Equipment fitted that covers the body. A method of reducing the gas gas loss gives cost and logistical savings. The flow required devices. For deep dives. Communication The main problem with the system is that the flow devices operate better in air. some method of reducing the becomes excessive. . Many of pump. free-flow systems. It is normal for the diver to have an alter- on local hazards and the distance from assistance. the cost of gas mixtures are used. some units be achieved by the diver’s using a rebreathing sys. cheeks and under the sor. the diver’s depths. The cable for the communication system and chin. If the pump or air supply the noise. The diver can control buoy- with communication devices allows the diver to ancy by controlling the amount of air in the suit. seals round the forehead. where For even deeper tasks. with a flow of hot water may also be used to warm ment (see Chapter 48) should be chosen depending the diver. he or reduction in gas consumption compared with she does not need the mobility of the scuba diver. They also enable the diver to The breathing gas normally comes from the surface talk underwater. the airflow may either be continuous or on to do this is about 50 litres/minute (lpm). at the operating depth. Another hose joined onto the face mask.or magnetically triggered circuits. This supplies the diver with breathing PROFESSIONAL OR TECHNICAL gas if the main supply should fail. as down a hose by assistants turning a hand-operated well as some recreational technical divers. which has a separate set of problems that are considered in a OPEN-CIRCUIT BREATHING SYSTEMS later section. either supplied from storage cylinders or common use. The back of the diver’s head may be exposed a hose connected to a depth measuring system are to the water or covered with a wetsuit hood that is often bound to the gas supply hose. stops flow back up the hose.46  Diving equipment The first aid kit and emergency medical equip. In dealing with explosive exposed to the risk of a particularly unpleasant mines. incorporate a canister of carbon dioxide absorbent tem or returning the exhaled gas to the surface for to purify the gas. In these carbon dioxide from the helmet. DIVING EQUIPMENT Free-flow systems were used in the first com- mercial air diving apparatus.

the amount features peculiar to each type are then highlighted of gas we inhale with each breath must also increase separately. lowing is a summary of some advantages and These helmets may also be used at greater disadvantages of rebreather systems. Advantages When compared with a demand valve held in ●● Vastly reduced gas consumption. gas flow pattern.5. the we consume about 25 per cent of the oxygen that main difference lies in the way that the oxygen level we inhale with each breath. Although both types by metabolism. the situation becomes substantially worse when we Because of the similarity between SCR and CCR descend on open-circuit scuba equipment. ●● Excellent duration in relatively small unit. The helmets are often less comfortable apparatus can offer substantial reductions in gas than the face masks. nasal mask in the helmet reduces rebreathing of This  is  called a ‘rebreather’. their common features are discussed first. and As the depth and pressure increase. especially the mouth. of which 19 litres are being exhaled into circuit. When we breathe on the surface. vigilance and maintenance. humidified gas. Although this may not seem very efficient. CCRs are the most complex but also would be exhaled back into the surrounding atmo. reduce the risk of drowning and can allow the ●● Greater complexity and vastly increased need diver to converse with people on the surface. removing the an anticlockwise pattern. For largely historical reasons. SCRs are less complex but less effi- would breathe in 4 litres of oxygen each minute. rebreathers the ocean unused! of UK or European origin usually have a clockwise One solution to this inefficiency of gas con. sets. of the breathing gas. The increased safety and the advantages of a ●● Improved decompression efficiency because of clear verbal communication system have led to the maintenance of ‘optimal PO2’. REBREATHING SYSTEMS Rebreathers fall into one of two main types – Respiration is designed to provide our tissues with closed-circuit rebreathers (CCRs) and semi-closed- oxygen and to eliminate carbon dioxide produced circuit rebreathers (SCRs). . the most efficient and most capable with regard to sphere. but they give better thermal consumption over open-circuit systems. However. we In general. cient and have depth limitations dependent on the of which 1 litre would be consumed and 3 litres gas selection. covert while breathing high partial pressures of oxygen operations. and such breathing exhaled air. to compensate. we The usual gas flow pattern found in a rebreath- would need to breathe 100 lpm from our cylin. higher overall risk. A return expanded upon in the following paragraphs: hose may be used to allow collection of the exhaled gas at the surface for reprocessing. ●● Different hazards to diver. Thus. which are depths. This is important if the diver the breathing of warm. if our respira. tory minute volume (RMV) were to be 20 lpm. all the systems mentioned earlier have during deep diving. fragile environments such as caves. ing set is shown in Figure  4. at 40 metres (5  ATA). Disadvantages Sets that use a helmet and a full-face mask ●● Significant initial cost. for training. (PO2). recirculate all. The fol- and impact protection. is consumed by the diver back into the circuit. The movement of der to achieve the same 20 lpm surface RMV. adoption of helmets by most diving firms. whereas those of US origin have sumption is to recirculate the gas. is controlled and added into the circuit. depth and duration. where helium mixtures are used. Thus. this is not uni- carbon dioxide and adding only the oxygen that versally so. the major advantage of reducing the chance of the ●● Reduction of cold stress and dehydration by diver’s drowning. or part. Professional or technical diving equipment  47 Another type is fitted in a full helmet. This inhaled and exhaled gas is controlled by one-way 100  litres of air would contain about 20 litres of valves at the mouthpiece as the gas flows round the oxygen. An oro. becomes unconscious and/or has a convulsion ●● Lack of bubbles good for photography.

ATA. In most units. . there is a mechanism that releases and to provide an adequate volume of the mixture. This the use of these units to limit the PO2 to 1. Venting Closed oxygen rebreathing apparatus has the of excess gas is needed in CCR sets when the diver particular advantage that a small unit may give a ascends and the gas in the counterlung expands.48  Diving equipment Mouthpiece with one-way check valves a continuous flow of oxygen into the circuit. These operations.  dilu- As the diver descends. A unit weighing less than 15 kg In SCR sets. CO2 scrubber The unit can be operated as a closed system because. the gas in the breathing bag will contain a high concentra- Gas inflow tion of oxygen. gas must be added from tion hypoxia if the oxygen is impure or the diver a high-pressure cylinder into the breathing loop neglects to flush nitrogen from the lungs and so that a constant volume is maintained within the c­ ounterlung and oxygen toxicity if the diver the system. Figure 4. oxygen units. As oxygen is con- sumed. and prevents excess pressure building up. a depth valve [ADV]). diluted with nitrogen that was in the lungs and body of the diver when he or she put the unit on. when he or she goes deeper and the gas in the breath- Counterlung ing bag is compressed. bubbles and quietness of this unit are also impor- The carbon dioxide absorbent is usually a mix. The counterlung is filled with oxygen from the cylinder. a trigger mechanism that operates like a and a diluting gas are fed into the breathing loop demand valve releases more gas into the bag.8 addition of gas will affect buoyancy. In at rates required to keep the PO2 within safe limits other units.6 to 1. tant in some specialized roles such as clandestine ture of calcium and sodium hydroxides. In some In closed-circuit mixed gas systems.5  A stylised rebreather layout. chemicals react with carbon dioxide to form car- bonates and water. although too high for recreational expands and contracts as the diver breathes. excess gas vents regularly through the can allow dives of more than 2 hours. the volume of the bag decreases. It is standard practice to flush the counter- Breathing hoses lung with oxygen at set intervals to ‘denitrogenate’ = Direction of gas flow before starting the dive to prevent a build-up of diluting gases. added via a regulator-type valve (automatic diluent To reduce the risk of oxygen toxicity. A manually operated method of adding oxygen to the breathing bag is also usually fitted.6 ATA is usually maintained. where a lower risk is appropriate It ­normally incorporates a relief valve (over-­pressure and consequently a PO2 significantly lower than valve [OPV]) that releases surplus gas into the water 1. Possible problems with these units include car- bon dioxide toxicity if the absorbent fails. a range generally deemed acceptable for mili- The counterlung acts as a gas storage bag that tary operations. long endurance. A manually controlled valve allows limit of about 6 to 8 metres is often imposed on the diver to add extra gas if it is required. technical diving. This will be needed when the diver puts the unit on. as shown: Rebreathing units are quieter and have a greater endurance than scuba units. The M(OH)2 + CO2 → MCO3 + H2O extra hazards and costs involved restrict their use and demand significant extra Closed-circuit oxygen systems are the sim- ­training. The lack of relief valve. maintenance and vigilance. unless something goes wrong. or when the diver needs to increase buoyancy. the gas is automatically de­scends too deep. plest CCR sets.

6  Electronic closed-circuit mixed gas rebreather layout. the manufacturer’s recommendation and maintains diver inhales breathing gas from the counterlung the work of breathing within the specifications of and exhales through the carbon dioxide absorber the unit. The basic system is three redundant oxygen sensors (galvanic fuel cells) shown in Figure 4. and should the controlling cost of an SCR diving apparatus. However. such that it does not exceed the As with the closed-circuit oxygen unit. lead to fatal malfunctions. This system would appear to be the most effi- Although all rebreather divers should know cient breathing system. is continually bled into the unit). It is more economical in their PO2 at all times. trimix (helium.5 per cent of the the PO2 at all times. and this oxygen concentration are often fitted to allow the fall is detected by oxygen sensors. to date. the diluent gas should not have a PO2 greater Diluent Oxygen than a predetermined set-point at depth (prefera- bly a little lower so that an ‘oxygen spike’ does not Figure 4. as well as having a limited life (usually ~18 months). divers also either raise Both mechanically and electronically controlled the ‘set-point’ or flush the unit with oxygen during units are commonly seen in recreational diving. As the diver consumes Manual controls and displays indicating the oxygen. These advantages computer fail. Microprocessor If the volume of gas in the bag falls. It enables a diver tem to be forced to know his or her PO2 at all times to go deeper for longer and with fewer encum- (although in most systems a basal flow of oxygen brances than other equipment. At a certain diver to override the controls if the automatic level. Air. To manage the latter. tions of the oxygen sets and the greater complexity Most modern mixed gas CCRs use a series of of the closed mixed gas sets. ­control fails. the PO2 in the counterlung falls. For the for- mer. the diver should Figure 4. this trig- Solenoid gers a second valve that adds diluting gas (dilu- valve ent) from a separate cylinder. the As an example of the efficiency of this type of requirement to manage the PO2 in this system can equipment.7. the cost of helium the diver using an electronic rebreather to know for a CCR apparatus was about 2. although must be balanced against the greater initial cost the chances that the computer will fail in an elec. it has been estimated that in a helium create problems during times of high task loading. The selec- tion of the gas is determined largely by oxygen toxicity and work of breathing issues. happen during descent when diluent is added to the loop). the final decompression stop at 6 metres to shorten and there has been much controversy as to which decompression time. a valve injects more oxygen into the circuit. This allows for the ­comparison of the outputs of the sensors because PO2 display they are relatively fragile and prone to failure. Professional or technical diving equipment  49 to track the PO2 in the loop. neither system has been shown to offer a SCRs offer some of the saving in gas obtained in survival advantage and all rebreather divers should the closed systems while avoiding the depth limita- make a habit of knowing their PO2 at all times. This complexity can tronic rebreather are very low. The reality is that. there is less obvious compulsion for series of dives to 180 metres. . maximum depth. In many cases.6 shows the fundamental features of this calculate the density of the gas at the proposed system. saturation dive program involving a prolonged In contrast. the diver would be at risk. back into the counterlung. arrangement is safer. and complexity of the system. nitrogen and oxygen) or heliox (helium and oxy- gen) may be used as the diluent depending on the planned depth and profile of the dive. the oxygen-breathing apparatus. the above argument hinges terms of gas usage than any other gear apart from on the requirement for the diver in the manual sys.

Hypoxia may result if the gas flow decreases. a fixed volume of gas supply before descending. Two major structed from non-magnetic materials. The high oxygen concentrations in both SCR Constant mass flow and CCR systems mean that the diver may not injector absorb as much nitrogen as he or she would if Demand breathing air. On occasion. such duration of exposure. If they are con- as the breathing mix instead of oxygen. almost ficient oxygen to the loop. 20 per cent when the diver is working at the maxi. with supply. descends too quickly when The oxygen concentration in the diver’s inspired diving at a particular PO2 (set-point) or uses a mix- gas is determined by the flow into the system. that the diver will receive sufficient oxygen while Oxygen toxicity can occur if the diver exceeds working on the surface. keyed respiratory minute volume (RMV keyed) type has some advocates. Both CCR and SCR systems introduce a variety of In a typical CMF SCR system. the gas flow and potential hazards (see Chapter 62): composition are chosen for maximum efficiency Carbon dioxide accumulation can occur if for the proposed dive. This level may be changed depending on the exceeded because of a diver’s high demand. The most com. although CCRs are now mon is the constant mass flow (CMF) type. an SCR system with a flow of 12 lpm related deaths that occurred between 1998 and gives an eightfold saving of gas compared with 2010 estimated that the fatality rate for CCR users . The flow is then chosen so as with exertion.50  Diving equipment a demand system when the diver is consuming 1 lpm of oxygen. used for dives near mines. with as high an oxygen concentra.7  Semi-closed rebreathing system. The reduced gas flow with these sets means that they SCRs typically use oxygen-enriched air (nitrox) can be designed to make little noise. his or her depth limit. First. solenoid or electronics failure. ber material is used for too long. This can occur if the scrub- gas is chosen. but unless the PO2 in the Nitrox loop is actually measured. the ture with too much oxygen in it. thus mak. if the scrubber tion as possible without creating an unacceptable is incorrectly attached or if the scrubber’s instan- risk of oxygen toxicity at the planned maximum taneous capacity to remove carbon dioxide is depth. this has resulted in problems. ing too rapidly to enable the solenoid to add suf- As a safety precaution with an SCR. especially with US cave Problems with rebreathers divers. This can be caused by omitting to turn on the gas In the RMV keyed sets. Hypoxia can also occur invariably an excess of gas is added to the loop if the diver works harder than expected or if a mix and is vented through the relief valve. It ranges from close to that in the supply diluent cylinder or if the solenoid or manual oxy- ­bottle when the diver is resting down to about gen injection valves jam open. and ascend- ‘new’ gas added via a demand valve. although they have become Figure 4. increasingly popular in recreational diving. A review of the 181 reported recreational CCR- However. This can give a decrease in the valve decompression needed. the diver must ‘guess- timate’ the PO2 for decompression purposes. This saving would increase if the scuba diver was working harder and consuming more air. Military divers have traditionally been the main users of SCR sets. with too little oxygen is used. the composition of the the scrubber fails. they can be types of SCR are in common use. but the more often used for mine countermeasures. This can occur if diver’s consumption and loss through the relief an excessively oxygen-rich mix was added to the valve. exhausting the oxygen is dumped from the circuit with each breath. mum expected rate. ing these devices less efficient on gas than CCRs.

Larger found on large submersibles. The author also suggested that CCRs have a ­pressurized environment. for habitats and SDCs the gas is generally supplied Habitats are underwater houses that accom. a canister with a manually operated system for add- procedure that allows a diver to be decompressed ing oxygen. Life support systems are required to provide The most complex SDC may carry the diver at con. habitats and stant pressure from a deck decompression cham. and chambers used for deep saturation dives. called a recompression chamber. ing systems can involve a hand-powered pump Deck decompression chambers (DDCs) can to force gas through a carbon dioxide absorption be small and used for surface decompression. ered include underwater houses and pressurized The diver had no control in mid-water and had to houses at the surface. types of suit had legs that gave the diver the ability ter equipment. such as and from deep dive sites. pression illness and other diseases that respond to These have automatic closed systems with provi- compression. These include vehicles that enter underwater. It was suggested that this risk could be spheric pressure. The most complex systems are those in a dry chamber instead of in the water. often called personnel transfer capsules. are hoisted and lowered to transport divers to One atmosphere diving equipment. The accommodations to be consid.or gas-filled environments. In other Submersible decompression chambers (SDCs). be lowered and hoisted from the surface. Professional or technical diving equipment  51 was about 10 times that of recreational open-­circuit or a small submarine that keeps the diver in a divers. pressure and DDCs are also used to house divers for pro.e. longed periods under elevated pressure. seals the diver in a pressure-resistant increase the diver’s range and endurance (i. mal atmospheric pressure. 25-fold increased risk of component failure com. Simple gas purify- weeks at a time. A small motor vehicles and propeller that pulls the diver along gives increased speed with reduced effort. compartment. They help to lower costs . exposed to the same pressure as the must be self-contained for transport vehicles. at ambient pressure in a dry environment or in a wet environment. modate divers in air. as a relay station and store for gas and equipment. chambers with a respirable atmosphere. to walk on firm surfaces if there was little current. nuclear submarines chambers can be used to treat divers with decom. and they also regulate temperature. These ber (DDC) to the work site and back. divers are carried to their work by an SDC helium to be used again. Gas from the surface can be supplied in a free They are used by divers to rest between excursions. often used by ‘hands’ for the diver to work underwater. In this Gas reclaimers are mainly used to recover case. Some subma- Divers may use several special types of vehicles rines have a lock system to allow divers to leave and and living facilities. flow and escape out the bottom or be recirculated Divers have lived in some of these habitats for through a purifying system. possibly after several weeks. It has flexible arms with tools on the diver propulsion vehicles [DPVs]. the pressure in the pared with manifolded twin-cylinder open-­circuit DDC is lowered slowly to return the diver to atmo- systems. designs. from the surface. such as the Newtsuit and WASP system. The system environment. humidity. partly offset by carrying a redundant bail-out Transport vehicles can carry the divers at nor- system. The simplest work on the same principles as a diver’s breath- SDC consists of a bell chamber that is open at the ing apparatus. and in some vehicles the diver may bottom and allows the diver to decompress in a dry even be wearing a breathing apparatus. the occupants of all these vehicles. These Chambers. propelled vehicles to the JIM suit. At the end of the job. but surrounding water. and they may also be used submarine. habitats and underwater include vehicles towed by a boat. The early technical divers) and machines to carry underwa. in which case the chamber may be sion for removing trace contaminants and odours. are used the diver controls a set of propellers that make him to transport divers and any attendants from the or her a cross between a diver and a one-person surface to the work site.

43(2):78–85. Britz HC. Diving and John Lippmann. Other types use a chromatographic technique to Aviation. Fock A. DC: Naval Sea Bozanic JE.org/ presentation/ FURTHER READING US Navy Diving Manual Revision 6 SS521-AG- PRO-010 (2008). Cronjé FJ. Space and Environmental Medicine separate the gases. Rebreather Forum 3. Fatal respiratory failure during a ­technical leaving pure helium to be stored and used again. Washington. Flagstaff. 2007. Mastering Rebreathers. http://www. Systems Command. Hyperbaric Medicine 2010. Arizona: Best Publishing Company.78(2):81–86. Meintjes J. cools the gas until the other gases are liquefied. One type Mitchell SJ. .rf30. rebreather dive at extreme pressure. Analysis of recreational closed-circuit This chapter was reviewed for this fifth edition by rebreather deaths 1998–2010. 2008. 2002.52  Diving equipment by reducing the amount of gas used.

water flows and so forth. a buddy. A variety ments. Nevertheless. sives (see Chapter 34). in the inexperienced diver and of physical stress in If the diver does not have a compromised air sup- the more skilled diver is appreciated only when one ply. Other environmental topics ments of different environmental diving conditions. ice. 15. These a communication facility. ALTITUDE DIVING nations for diving fitness and the assessments of diving accidents will be less than adequate. ­a ltitude and fresh water diving (see Chapter  2). such as the have specific chapters devoted to them. lines to other diving environments. The term altitude diving refers to diving at an alti- Some aspects of the environments have physi. ited air supply will result in drowning. tude of 300 metres or more above sea level. The induction of fear (even ‘safety’ lines). Non- ological and pathological sequelae and therefore diving disorders should be considered. They cannot be automatically extrapolated of materials can trap the diver. 46  and 68) and marine animal injuries (see ­equipment and who appreciates the specific require. including kelp.  explo- For the diver who is adequately trained and physi. This is a Diver training is specific to the environment in situation common to many of the hazardous envi- which the diver is trained. depth (see Chapters 2. medical text is that unless the physician compre- hends the problems and dangers. that are covered more comprehensively in diving the sea is rarely dangerous. who is aware of the limitations of the 20. the medical exami. They include dyspnoea and hypoxia induced by high altitude 53 . Specialized techniques ronments. cally fit. a calm state of mind and environmental stresses are mentioned in this and a diving knife or scissors will cope with most of other chapters. overhangs. The reason for including them in a these circumstances. hazardous and unforgiving if attention is not paid Being kept underwater and exceeding the lim- to all these factors. it can be texts are summarized in this chapter. 5 Undersea environments Introduction 53 Night diving 59 Altitude diving 53 Water movements 59 Cave and wreck diving 55 White water 59 Cave diving 55 Surge 59 Wreck diving 56 Inlets and outlets 59 Cold/ice diving 56 Tidal currents 59 Deep diving 57 Surf 61 Fresh water diving 58 Further reading 62 Kelp diving 58 INTRODUCTION the effects of cold (see Chapters 27 and 28). including caves and wrecks and under are recommended to cope with different environ. examines each specific environmental threat. fishing nets and fishing lines. then knowledge of the environment. Chapters 31 and 32).

It influences the decom. in a mountain the volume of gas in the lungs has doubled. Another pressure problem occurs when a diver. Equivalent effects rect. as regards logue and mechanical types) may try to indicate a decompression requirements. pression obligations. if the dive was carried out at tion is based on the useful. sea level if the diver is to avoid decompression sick. in a motor vehicle or an according to this ‘gauge’ depth. indicates the depth by an air-water boundary. It automatically adjusts to the extent that it always who dives at sea level. The diver’s equipment can also be affected or If this ratio is less than 2:1. compared with identical dives and questionable. the diver could plan the dive and decompression ness. then flies or ascends into the reads zero depth on the surface. the depths and durations of as in high mountain lakes. the nitrogen load in tissues above 3000 metres. the safe durations before flying or repet- this is strongly discouraged. For example. of ascent to the surface. Other decompression meters are sickness. Theoretically. A diver who ascends from 10 metres returns there when he or she has finished the dive. as in aircraft Thus. Thus. Problems stem from the physics during ascent. but not strictly cor. or div. but it would 0. Diving at altitudes higher than afterward. if the dive had sion. If the diver ascends. itive diving. the dive of 0. which can more pressure reached during the dive and the final rapidly get out of control at altitude. the reduced pressure will expand ‘silent’ was very courageous. (2 ATA) to the ocean surface (1 ATA) would find that A diver may have to dive at altitude. where the pressure on the surface is divers realize this and exhale at a controlled rate less than 1 ATA. damaged by exposure to altitude (e.5 ATA) from sea level could be followed (Boyle’s Law).5 ATA. and the applicability of other dive comput- ing at altitude. required with fresh water. Formulae are available to con- resent actual diving conditions and are used to vert the equivalent altitude decompressions to sea explain the problems as simply as possible. could dive only to 5 metres (1 ATA) depth would have to reach more than 5 metres before he or she had to worry about decompres. Another problem of diving in a high-altitude tional idea of diving is that a diver descends with lake is the rate at which a diver may have to exhale the sea surface (1 ATA) as the reference point and during ascent. tube. They may not realize that an equiva- at this altitude. travel). The conven. a capillary than salt water. ers to altitude diving or saturation excursions is sion sickness.5 ATA. Deeper dives show that the diver had reached 10 metres when or greater ascents may require the diver to pause at he or she was only at 5 metres depth. thereby aggravating the diseases rection for altitude. exposures at sea level. Divers who fly from sea level to dive at altitude. before it even started measuring. the ascent rates recommended during The following numerical examples do not rep. thus level decompressions. may commence the dive . perhaps bending the needle. This means sure gauges start to register only when the pressure that a diver from the sea surface (1 ATA) can dive is greater than 1 ATA. and some need to be ‘re-zoned’ of pulmonary barotrauma and decompression at the dive site.5 ATA. ana- to 10 metres (2 ATA) and ascend safely. exposure to altitude after diving. increases the danger of decompres. an altitude (pressure) of 0. the following descrip. avoiding complicated mathematics. Fresh water is less dense The other common depth gauge. then a diver can ascend damaged by high-altitude exposure. with little theoretical risk. bubbles or increase the gas gradient to produce Many electronic dive computers do permit cor- larger bubbles.5 ATA by an immediate ascent to a pressure (altitude) of altitude. This statement ignores the minor correction commenced at an altitude of 0. These gauges (oil-filled. Most lake or dam.54  Undersea environments and the altitude sickness that frequently develops decompression stops. diving and so forth. with a surface pressure the diver reaches 1 ATA pressure. until in a high mountain lake. lent doubling in gas volume occurs in only 5 metres For simplicity’s sake. pressure determines the decompression required. The volume of mountains after the dive. Some pres- safely without pausing during ascent. For a diver starting from 0.75 ATA. traditional theory that the ratio between the are encountered with buoyancy. this gauge would read zero. A diver operating negative depth. but only if he or she airplane. a 5-metre gas trapped in the capillary decreases with depth dive (1.g.

This water may contain at depth. however. powerful lights and a safety reel and its (depths. but also the complication of diving in fresh. by immediate surfacing. water. ment must be duplicated for a long return swim. Sometimes the roof of the cave is supported by the water. there are added specific problems. It is a diving axiom that entry into a cave is follows: based on the presumption that the return will have to be carried out in zero visibility. and it may remain that way for weeks. to be accompanied by a diver who has consider- able modifications for altitude exposure include able cave experience – in that cave – and whose the Buhlmann and Canadian Defence and Civil judgement is trustworthy. involves not only the setting of goal-oriented The minimum extra safety equipment includes objectives. and the greater passageways. clay silts can be The techniques of cave diving are very rigidly delin. Cave and wreck diving  55 with an already existing nitrogen load in excess of The diver descends. but the delineation of maximum lim. a compass. and possibly while rescuing a disabled debris that has not decomposed as it would in the companion. who have equilibrated at access. neutrally buoyant and should swim more than a cols. and ‘residual nitro. the ‘sea level’ divers are bends and is faced with multiple passages. It is for this reason eated. breathing should be continued from the scuba CAVE AND WRECK DIVING equipment. Planning was there. Completion of was so unlucky for the roof to collapse while the open water scuba training course is inadequate he was there’ is incorrect. Safety in cave diving is not usually achievable It  includes not only the problems already men. It collapsed because he preparation for cave and wreck diving. so when entering this pocket. all necessary equip- tioned. lights. and when this water is These enclosed environments are hazardous to replaced by air from the diver’s tanks. limestone caves). Cave diving and wreck diving are can collapse. Under these conditions. it is necessary Decompression tables that supply accept. Thus. the silt that can be stirred up if the diver swims along the lower part of the cave or in a head-up Cave diving position (as when negatively buoyant). cause multiple fatalities. Undertaking a specialized course in altitude gen and high carbon dioxide levels (especially in diving is a basic prerequisite. this particular type of diving safe. very fine and easily stirred up. passes down a shaft. sometimes non-respirable because of low oxy- ties. the more applicable is this statement. Sometimes it is inevitable. ●● No direct ascent to the surface (i. as exhaled bubbles . goes around a few the lower pressures. the function of these lights. For visibility. distances). ficulties inherent in diving through a labyrinth of They are not as well researched. often through a small that of the local divers. each diver takes at least two ●● Disorientation and entrapment. A great danger is ●● Enclosed spaces and panic. and totally replaceable with spares during the Altitude exposure and altitude diving are more dive. ocean and may therefore threaten entrapment. Most people who have difficulties with cave metre above the bottom of the cave. and the diver should be the use of reels and lines and the lost diver proto. be totally lost in a few seconds as the silt curtain and unfortunately cave diving problems tend to ascends. safety). and to make gen’ tables must be employed. It is equally important Institute of Environmental Medicine (DCIEM) that the equipment is both suited to cave diving tables (see Appendix A).e. other factors can interfere with ●● Loss of visibility. in total in effect doing a repetitive dive. the roof open water divers. darkness. Apart from the obvious environmental dif- hazardous extensions of conventional diving. Visibility can diving have not followed the recommended rules. The common claim that ‘the diver more complex than they first appear. The main problems are as line. that fins should be small. If there is little natural water movement. the altitude. The Air pockets found in the top of caves are sites are often distant from diving medical facili. Specialized training includes dive planning. Thus. often very cold.

dive profile display. the sudden loss of visibility that dive computer (this can include a contents gauge. A principle of 30 minutes of exposure to very cold water (less cave diving is that safety lies in retracing the entry than 5°C).g. The diver should ascend as far as is safe and pass) attached to the harness under the left arm. pressed air and if there is a rapid expansion of air. e. There is the effects of a cold environment on physiological no requirement for excess buoyancy because safety performance. as in the water vapour (potential ice crystals) in the com- normal open ocean diving. The gauges and decompression must be modified for fresh water and altitude. lines especially cause entanglement if they are ifolded together. Preferably no more than three divers should which produces further cooling in both first and undertake a single dive. Thin. With the failure of Specialized cave diving training is a ­prerequisite one regulator. Layering of salt penetrations. tent. Otherwise. sharp objects. may cause air pockets and disrupt the wreck’s All the instruments should be standardized. and the penetration is with the flow. The freezing from increased air moored or buoyed at the surface and weighted or flow follows exertion. entangle- and fresh waters also causes visual distortion and ment is likely with rapid ascents. See Chapters 27 and 28 for to be vertical with the head out of water). this pressure to the lower pressure demand valve and reserve air supply may not be adequate because the then to environmental pressures (adiabatic expan- air consumption is greater when returning against sion) results in a drop in temperature. Exhausted gas from scuba face supply. the dangers of unexploded ordnance. in cave diving is not usually equated with a direct A major difficulty with cold and ice diving is the ascent. to prevent entanglement on any safety lines. They are so obvious that most people will down at the top. offering two regulator outlets. The reel is used for horizontal Octopus rigs become more problematic to use . the watch goes on the left wrist. wait until the silt cloud settles down. making a common air supply. Thus. divers precede the lead diver. given that often divers cannot Wreck diving swim alongside each other. fixed at the bottom. hyperventilation or panic. the compass on the right wrist and the water caves.56  Undersea environments dislodge silt from the ceiling. The obvious problems are those of cold and hypo- The buoyancy compensator is often bound thermia. buddy breathing is often impractical under Wreck diving has potentially similar problems cave conditions. supply – or as an octopus rig. stability. the hazards of instability of the structure and the For recreational divers to explore caves. com. The second regulator must have a long hose. ideal equipment is a reliable compressed air sur. after about 20 to prevent accidental inflation of vests. thus. especially if blurring. be removed and replaced with exhausted ones to usually in the free-flow position. Because of space limita- tions. it has is advisable. COLD/ICE DIVING The knife is strapped to the inside of the left leg. any carbon dioxide cylinders should tendency of many single hose regulators to freeze. the second one may be used for the air for this diving environment. In addition. non-floating The usual equipment includes double tanks man. If there is water flow within Expansion of air as it passes from the high tank the cave. to move the buoyancy centre more avoid them by the use of heating systems. The first stage or the second stage dive each should have a minimum of one third of may then freeze internally. the depth gauge Silt in wrecks is usually heavier than that in still above it. drysuits toward the centre of gravity (cave divers do not need or efficient wetsuits. It is therefore the current. not vertical. This situation is aggravated if there is path by the use of lines and not by ascent. can occur when silt is stirred up may be less persis- decompression meter. the initial air supply. not advisable to purge regulators if exposed to very Vertical penetrations need a heavy shot line cold temperatures. toxic cargo and fuel. with a complete scuba back-up rig. and on completion of the second stages. if these are applicable. An extra air supply (‘pony’ bottle) to some cave and ice diving. but allowed to slacken.

diver. is probably safer. two divers wide. compression. as well as on the diver. Despite all this. is also of value in identifying the regulator will freeze and induce an out-of-air situ. freeze and may also allow water and heat exchange. oils or alcohols and so forth. or heat pads can be used. diminished manual dexterity containing areas with silicone. Beyond the 30-metre limit the effect of narco- siderable thickness. They then <5°C – 9-mm-thick wetsuit move into a dark. in an emergency common in polar and ice diving. or at great depth. Rubber suits can become sharp a back-up scuba system is a requirement. and divers become enraptured. Surface supply two divers may need to exit simultaneously. first (depth compensated) stage of the regulator. Heat sis becomes obvious. A  bright light. as with cave diving. There with an emergency scuba. they should be given right of way. An emergency air source wetsuits. It is essential that direct contact must always spring. the competitive element sometimes temperatures. Hood. As a general rule. This should in the exhalation chamber of the second stage may be by a heavy-duty line attached to the diver via a also freeze the demand mechanism. at least to observers. regulator freezing is close over by freezing. with the desire to dive deeper. resulting from wetsuit Unheated wetsuits do not give sufficient insula. such as becomes too compressed and loses much of its the buoyancy compensator. where small difficulties expand. opening. and this must be planned for. If large diving mammals contest the open- ation. because insulating ability. The line must also be securely fas- flow of gas or ‘internal’ freezing with no flow. we had to employ a wetsuit or other thick cloth- ‘External’ ice is formed in and around the ing under a drysuit. Allowing room for only one diver non-metallic second stages are less susceptible to enter ignores two facts. (which require lower temperatures to freeze) or The entry hole through the ice should be at least with an air flow from the regulator. the minimum thickness of the ego trippers and a challenge to adventure seekers. literally. First. causing free bowline knot. Buoyancy. tened at the surface. Zippers are best avoided because they cave diving. is less efficient. The Modifications designed to reduce freezing of dive should be terminated as soon as there is a the water in the first stage include the use of very reduced gas supply or any suggestion of cold expo- dry air and the replacement of first-stage water-­ sure with shivering. and If the penetration under the ice is in excess of so these should be removed to reduce the likeli. The gas pads must not be in contact with high-oxygen supply is more rapidly exhausted and the regulator gases because overheating can result. with an inevi- tion at depth (beyond 18 metres) when the Neoprene table reliance on problematic equipment. In Antarctic diving. and if well-fitting drysuits ‘Divers do it deeper’ represents a problem with are unavailable. eerie world where colours do not <10°C – 7-mm-thick wetsuit penetrate. Moisture from the diver’s breath or water be maintained with the entry-exit area. ing in the ice. as with and brittle. In that case. should be a surface tender with at least one standby lator diving. The reserve air ­supply . where <20°C – 5-mm-thick wetsuit safety is farther away and where the leisure of rec- <30°C – 3-mm-thick wetsuit reational diving is replaced with an intense time urgency. non-­ compressible of this increased air flow. to gain greater dura- octopus rigs. Buoyancy compensators should be small and with DEEP DIVING an independent air supply. as in the following examples: overrides logic. The newer. Under ice there is little use for snorkels. a distance equated with a breath-hold swim. Second. then hood of snagging. hanging below the surface at It must be presumed in under-ice diving that the the entry-exit hole. tion. Neoprene should increase with decreased water Unfortunately. Deep diving  57 under these conditions. Ice diving is in many ways similar to cave div- thus blocking the orifice and interfering with the ing. the hole tends to to freezing. gloves and booties should be of a con. inflatable drysuits or heated suits are (pony bottle) has replaced buddy breathing and required. or twin tank–twin regu. has become negative.

Many of the older. ‘go deep’ before they have adequately mastered the Twisting and turning produce entanglement. The growth is less in turbid or unclear consequences. is related to panic actions and/or increased speed cialty courses may be devised to entice divers to and activity of the diver while in the kelp bed. but it does seem the area and the adjacent beach. have snug medium in which most divers were trained. are useful as thickening.e. Kelp can be used overly dramatic. Heliox (helium-oxygen mixtures) water. speci- ascents. of thermal stress.e. The danger of entanglement ways of separating divers from their dollars. Thus. diver’s glass of beer (après dive. Acceptable descend vertically feet first to where the stems are weights in sea water may be excessive in fresh water. ulator hose. are fatal. e. they tend to wear knives on the inside of the The main problem with fresh water is that it is not the leg. If they do become snagged. It is of interest commercially decompression obligations. The epitome of bad practice in kelp diving they need to be corrected for diving in dams. Because these waters are often it tends to result in a ‘kelp sandwich with a diver stationary. i.g. they produce a clear area There are also many organisms that are destroyed within the kelp. It is It allows a good estimate of clarity of the water by unwise to cut kelp from the regulator with a knife assessing the length of plant seen from the surface. lakes. as well as to attach other Emergency procedures. such as Naegleria. In kelp beds there is usually an strands with one’s teeth. more difficult to achieve while wearing gloves). but at the expense rocky bottom. and ascent rates become Giant members of this large brown algae or more critical. into which they then move. are equalizing their ears. communication and altered a Spanish galleon. and the buoyancy compen. as one descends. thicker and there is less foliage to cause entangle- Depth gauges are calibrated for sea water. for more romantic divers. a reduces the narcosis of nitrogen. situation will produce more rapid activity. independent instructors Kelp has caused many diving accidents. are more difficult. is to perform a head first roll or back roll because quarries and so forth. tape the buckles on the fin straps. They by sea water but that thrive in warm fresh water. as an anchor chain for people to use when they sator inflation takes longer and uses more air. a reef or. This may be excellent as abundance of marine life. diver’s flags. as well as in stabilizing the froth on the adverse sequelae (see Chapter 62). filling’. there may be dramatic thermoclines. often would qualify recreational divers only to 30 metres. spe.58  Undersea environments does not last as long. ensure that they do not run out of air because this Some of these. it to 180 degrees. suspending and emulsify- or even by rebreathing equipment. i. when it will often snap (this is ests. with the diver totally bound up into a ‘kelp ball’ Now. Some divers have suggested biting the vailing current. Divers their buoyancy appreciation is distorted. divers should avoid unneces- KELP DIVING sary hand and fin movements. Kelp can be sepa- rated either by the use of a knife or by bending Kelp beds are the equivalent of underwater for. of course). seaweed may grow in clear water to depths of Overcoming some problems leads to unintended 30 metres. Kelp can be useful in many ways to the diver. Kelp usually grows on hard surfaces. without first clearly differentiating it from the reg- The kelp blades indicate the direction of the pre. and the kelp offers other regards dietary supplementation. tables are less reliable. especially free and ­buoyant objects such as floats. which can be compensated by larger and heavier cylinders. requiring adjustments for thermal protection and The kelp is pushed away by divers as they slowly buoyancy. The decompression men bags and so forth. and so ment. but with many ing agents. with instructor organizations seeking other that becomes a coffin. Inadequate gas supplies because it is harvested to produce alginates. descend and ascend. shallows. kelp being high benefits such as dampening wave action both in in both B vitamins and iodine. Divers who are accustomed to kelp diving usually take precautions to ensure that there is FRESH WATER DIVING no equipment that can snag the strands of kelp. quick-release buckles and not use lines. . surf mats.

Emergency procedures Surge are not as easy to perform without vision. Any navigational aid needs to be independently because of a pressure gradient through a restricted lighted. on the surface. There is a greater fear at night. Free swim.g. and at least two reliable torches ‘blow hole’). Signals include a circular torch motion (‘I am These currents are very important to the diver. in which one actually crawls along Because of the force of water movement. used correctly. lines). stick (Cyalume light) should be attached firmly blue holes or rock areas near surf (an underwater to the tank valve. extra care is needed for night diving. there is a continuous water flow. If OK. and it can also be very physically demanding. rents. The lat- him or her momentarily. A whis. anchor. This can be can become a hostage to the sea. often try to swim against it. at least direction. It is encountered in some caves. Otherwise. who tom or some object (e. the recommendation is usually to dive deeper. On entry the diver Inlets and outlets sometimes encounters surface debris that was not obvious from the surface. and water cocks (taps). is a sign Frequently. A compass is usually required. Water movements  59 Kelp does float. divers are lost at sea because of cur- requesting pickup. Sometimes these currents can be vertical and . The snorkel should have a fluo. Any kicking that is performed must be air bubbles. Occasionally. Other divers use the ming mid-water and without objects to focus on surge by swimming with it. given by shining the light onto the signaling hand. Protection is by not has not the same capabilities of detecting divers at occluding these inlets and by avoiding the area or night. Waving a light in an arc. A chemoluminescent glow extrude) the diver. covering it with a large grating. the exit. how about you?’) or rapid up and down move. as well as implying strong currents or turbulent surface conditions. Traditional signals can be ter event can be both embarrassing and terrifying. without excessive currents or water ­ecology. visibility and buoyancy. Under these condi- tions. who him or her in. done only if the body and legs are kept flat on the surface. buoys. like a bath plug. they are likely to take the never be shone at a diver’s face because it blinds diver where he or she does not want to go. which can siphon and hold (or even buddies and so forth. thus using the buoyancy of both the body White water and the kelp. and it can often be traversed on WATER MOVEMENTS the surface by a very slow form of dog paddling or ‘kelp crawl’. Accidents involving submerged stingrays Tidal currents and needle spine sea urchins are more likely. water inlets in ships’ hulls and in outlets in dams rescent tip. This dramatically interferes with both very shallow and slow. orientation and panic in inexperienced divers. over the kelp. and by using the palms of the hands to push the kelp below and behind as one proceeds This water is white because of the foaming effect of forward. For inexperienced divers it The to-and-fro movement of water produces dis- is advisable to remain close to the surface. movements and with easy beach access – diving between the boat and the shore. in human-made structures such as the should be carried. they take the diver where he or she ments (‘something is wrong’). The light should wants to go. or corals when the surge moves in the opposite Preferably the site should be familiar. This approach may be detrimental to the in daylight. Marine creatures are sometimes more difficult to see. the bot. a diver the surface of the water. opening. A diver in NIGHT DIVING white water is a diver in trouble. Because of the impaired visibility. then hold onto rocks causes apprehension to many divers. This includes the boat. The pressure gradient may tle and a day-night distress flare are sometimes of slowly draw the diver into its source and then seal great value in summoning the boat operator. but good for survival.

incorrectly. and ready to save the sinner – irrespective of reli- after they have used most of their air. the surface than they are on the sea bed because of diver ensures that he or she does not let go the line.to 5-knot currents. of the boat – while using the other hand to keep the Tidal currents are usually much faster on the face mask and demand valve in place. The Jesus ATA is used on the outward trip. subtract the the others are entering the water. it may be possible to reach up to 1. 80 is now floating away with the current. More than one diver has lost an progress or none at all against a 1-knot current. they can descend and cult situation and far more hazardous. being transported by the current. navigational error). The against 4. rescue a companion. For brief to the anchor because this may occasionally move periods. This is a very diffi. but who also had enough air to descend rescued. in the direc- of the usable air and allow the current to bring the tion of the current. when divers have. say 40 ATA. When they consider terminating the dive. such as at Palau (espe. but most div. is a float line or ‘Jesus’ line. and then the line is also of immense value at the end of the dive return is made with ample air to allow for misad.e. This would not have happened had a dive plan been While they are having their look around they are constructed and followed correctly. and this is the recommended way Divers sometimes relate their successful swims to reach the sea bed upstream from the boat. they have a gious persuasion. This line drags safer to swim against the current for the first half 100 metres or more behind the boat. The ‘half-tank rule’ is worked out by tak. very hard return swim against the current. with the other end to the so it is. They tend to exaggerate the speed of the stern of the boat. say 200 ATA. and the top of the anchor line.g. it does happen to the best divers. line. It should have enough play in it current as the hours go by. They submerge and ‘just have a look around’. and it has some floats to ensure diver back to the boat for the second half of the that it is always visible to divers on the surface. exhausted their air venture (e. at a rate of 30 metres every minute in a 1-knot of great solace to realize that the Jesus line is there current. attract who surfaced upstream from the boat and floated the attention of the boat lookout and hope to be back to it. the anchor line. Ras Muhammad.60  Undersea environments cannot be combated by swimming or buoyancy. The average swimmer can make very slow adjacent divers. Thus. because of their diminished air supply. First. In fact. the aver. for this example. If this is not available. line or inflate the buoyancy compensator. It is dive. and it can cause damage to the knots. A helpful observation is that the The diver then pulls himself or herself forward to boat will usually face the current with its anchor the anchor line and descends. if there is a Any diver worth his or her salt knows that it is current. often of value to have one diver on this line while ing the initial pressure. and it is boat. cially Pelalu). the Great Barrier The lines attached to the boat are of extreme Reef and Cozumel. Perhaps the most important line. and divide stray diver who has not followed instructions and this by 2. friction effects. the boat in a strong surface current may find that well downstream from the boat and have to cope it is impossible to make headway without a Jesus with a faster. eye from this ‘freak accident’. than that of use their compass to navigate back to the anchor the experienced diver who used the half-tank rule. Occasionally. are famous for their currents. 160 ATA. reach the anchor line? A line may be attached to ers experience this as a significant problem. i. . surface current. underwater and return with ease if desired or to Certain popular diving areas. The diver on the ‘reserve’ pressure (the pressure needed to charge line virtually acts as a backstop to catch the odd the regulator). supply or when they come to the surface for some Untrained divers tend to make unplanned other reason and find themselves behind the boat.2 knots. i.e. upstream and the stern of the boat downstream. anchor chain should not be followed right down age fast swim approximates 1.5 if the boat moves. On entry. away from the however. there is and multiple fatalities are not uncommon. dives. and especially during to allow divers to sit on the side of the boat and to the après-dive euphoria (1  knot = approximately hold it with one hand – the hand nearest the bow 2 km/hour). They Even divers who surface only a short way behind surface. How may the diver A half-knot current is tolerable. importance when there are currents. 80 ATA.

This requires extreme have to be held on during the exposure to breaking care in boat handling. it is the oppo- site. reefs or other (in preference to walking) through the wave area. before entry and not re-adjust face masks and fins tected and are of value only once on the surface. . is a far more ●● An inflatable 2-metre-long bag. jacket. The regulator must be attached firmly to the carry a float to inform the safety boat of their posi. that Surf serves as a safe haven. typical of divers swim. usually safer and more pleasant because the sedi- ing large volumes of air. to attract attention. with all his or her equipment.e. Water movements  61 Buddy breathing while swimming against a off Florida and the Torres Strait. The safety boat Entry of a diver through the surf is loads of fun is a second craft – not anchored – and this. referring to water ●● Personal floatation devices. has little to commend it. the standing diver The concept of ‘hanging’ an anchor. is soon as possible. e. and he or she crouches The raising of the diver’s flag under such ­conditions. needs a guard on a tumultuous moving experience and is a salutary its propeller. The ●● A towed buoy. the mercy of the elements. As although it may appease some local authorities. Even the octo. the recommen- con (EPIRB). When the surf is unavoidable. the diver submerges and swims often not recognized by the elements. Some currents are continuous. For the diver. The diver may use the apparently calmer water Divers can now carry a personal location bea. con or emergency position-indicating radio bea. navigational hazards. are likely to give an hour or more of slack water pus (spare) regulator is problematic at depth or with the change of tide. the standing It should never be placed between the diver and currents of the Gulf of Mexico. the Gulf Stream the wave. tion behind the divers as they drift. diver. of the current can be predicted by the tidal height. a float or also toward a buddy. it can be boat that is driven among divers. When a wave does break. ment settles and enhances visibility. and ensuring that there is a stable anchorage. Otherwise. surf and avoids rips. colour. all times. especially of value if diving in fast dation is that the diver should be fully equipped currents. The face mask and snorkel drift dive may be planned. An alternative air supply the correct time for slack water. This ensures that the surfer enters the devices. At these times diving is when two people are simultaneously demand. reference has to be (a reserve or pony bottle) is of value. into the wave. This may be an anchored boat. with divers presents the smallest possible surface area to it. The diver walks backward into the surf while look- When the current is too strong or the depth or ing over his or her shoulder at the breakers and sea bed is not suited to an anchored boat. there should be at least one accessible fixed diving exit. The cue options include the following: major problem is that people tend to delay their entry at about the line of the breaking surf. with feet well separated. various res. The fins There are other problems with currents. ●● Pressure tested distress flare (smoke/light). To attract the safety boat. but tidal currents strong current is often impossible. It allows the surface craft to maintain its posi. easily identifiable. if it has an made to the tidal charts for that area. To ascertain ming against a current. so that it is easily recoverable at tion. The speed adequate capacity. including moored boats. until he or she is well through the surf line. and and face mask must be firmly attached beforehand these are especially related to general boat safety because it is very easy to lose equipment in the surf. in areas with tidal currents. is that ‘White is right but green is mean and ●● Personal electronic. Divers remain together and waves. shoulder forward. called the vulnerable target for the wave’s momentum than is ‘safety sausage’. sonic or luminous location blue is too’. any swimmer. to ride the rip into the ocean.  he or she braces against the wave. The warning given to surfers. and leans. then this is towed behind. like any to an experienced surf diver. drifting in the water near it and the boat being at i. In dive planning. reminder of the adage ‘he who hesitates is lost’. sideways.g. with a clip. These devices need to be pressure pro. If the diver has a float.

Australian Antarctic (ANARE) Diving Manual. Jacksonville. 2013. Carl Edmonds. except then the surf is of value. Dept of Defence. NOAA Diving Manual. 2nd ed. Australia Current edition. . be used to speed the exit by swimming immediately National Oceanographic and Atmospheric behind it or after it has broken.K. DC: Naval Sea British Sub-Aqua Club Diving Manual. Current edition. 2008. Australian Antarctic Division. U. Washington. This chapter was reviewed for this fifth edition by Lippmann J. Current edition. in front of the diver and is carried by the wave. DC: US Government Printing Office. US Navy Diving Manual Revision 6 SS521-AG- Tasmania. ABR 155. Florida: entry. ISBN: 9781905492220.62  Undersea environments Exit should be based on the same principle as Exley S. Melbourne: Submariner Publications. 1981. PRO-010 (2008). The float then goes Administration. Mitchell S. Hutchinson. The wave may National Speleological Society. Systems Command. Washington. ACT. Royal Australian Navy. 5th ed. Deeper Into Diving. FURTHER READING Royal Australian Navy Diving Manual. 2005. Canberra. Basic Cave Diving. Kingston.

2 Part     Dysbaric Diseases: Barotraumas 6 Pulmonary barotrauma 65 7 Ear barotrauma 81 8 Sinus barotrauma 103 9 Other barotraumas 115 .


and if gas breathed at depth is not trapping disease in the lung). Pulmonary barotrauma (PBT) of ascent is the the incident range was 1 to 19 per 1000 escapes. 6 Pulmonary barotrauma Introduction 65 Mediastinal emphysema 74 Pathophysiology 65 Pneumothorax 74 Predisposing factors 69 Cerebral arterial gas embolism 75 Clinical features 69 Diving after pulmonary barotrauma 78 Pulmonary tissue damage 69 Prevention 78 Mediastinal emphysema 69 Dive training 78 Pneumothorax 71 Medical selection 78 Arterial gas embolism 71 Syncope of ascent 78 Treatment 74 References 79 Aggravation of pulmonary barotrauma 74 Further reading 79 Pulmonary tissue damage 74 INTRODUCTION In non-hooded ascents (in which the trainee must breathe out continually during the ascent).1 and 0. the contraction and ing decompression and airline passengers during expansion of gases with descent and ascent are ascent to altitude (though the last two situations accommodated with ease. most serious of the barotraumas. For highly compliant organs such as escape ascent training. It can occur in tially subject to volume change as ambient p­ ressure compressed air divers. those of gastrointestinal tract. The lungs are less com- are rare and invariably associated with gas-­ pliant. Injury appears dependent to (in which the trainees head is enclosed by a hood some extent on both volume distension of lung providing a breathable air space) had an incident tissue and development of a harmful transmural rate for PBT between 0.6 per 1000 escapes pressure gradient. adequately vented during ascent. and it causes The incidence in recreational diving is unknown. however. not surprisingly. Thus. This disorder is known as PBT of ascent. evidence that the degree of overpressure required 65 . submariners undertaking changes. It is a clinical manifestation of Boyle’s Law because PATHOPHYSIOLOGY it affects the lungs and results from overdisten- sion and rupture of the pulmonary tissue by All gas-filled spaces within the body are poten- expanding gases during ascent. hooded buoyant ascent poorly understood. there is and a fatality rate 10 to 50 times lower than that. concern in all types of diving operations. transmural pres- A 1988 review1 of submarine escape training sure gradients sufficient to cause injury may result. hyperbaric patients dur. from 11 nations showed that despite careful selec. tion procedures and extremely high standards of The pathophysiology of PBT is complex and training and supervision.

shown to gas can track upward along the trachea to lie sub- be harmful in cadaver studies. There is also some evidence expand in both sites. creating a shear stress sels.g. stitium allows gas to track along the outside of the It seems that a distended lung is damaged by a pulmonary airways and blood vessels toward the lower transmural pressure. Because these vessels are with lung volumes close to TLC. Although this damage may remain asymptom. sneezing or coughing ers with arterial gas emboli also had mediastinal generates enough pressure to exceed the elastic emphysema. can also be influ- between the two zones. is rupture of alveoli adjacent to the visceral pleura. It is notable gives rise to mediastinal emphysema. Experimentally. and the diver will die instantly.66  Pulmonary barotrauma to cause lung tissue injury depends on the extent to When alveoli rupture. This  find. disorder in the majority of the cases was cerebral quent event.1). into the arterial circulation. in an upright diver in an injury to the adjacent healthy tissue. is introduced to the pulmonary veins and carried mal lung volumes. Gas from ruptured alveoli rate. Its subsequent escape into the mediastinum the lung is prevented from distending2. surface may be unmasked and clinically relevant These events may occur singly or in combina- in diving. commonly referred expanding (e. The bubbles tend to Calder4 reported that the site of injury was incon. either enter any blood vessels that are injured tures2. particularly larger bubbles. of PBT submarine escape training accidents. during ascent. cadaver lungs have been simultaneously or escape into the lung intersti- shown to rupture with a positive inflation pressure tium. 7 with arterial gas embolism also had limits of the lung. The former process will cause alveolar gas to of 70 mm Hg. because of inexperience with their and small vessels are stretched and may tear. 15 div- the lungs are close to TLC. the gested that this may be an asymptomatic yet fre. par- ing may be explained by differing compliance in ticularly the brain. when PBT is most likely to . The most feared (and probably the most ity and its subsequent expansion with ascent in a ­common) of these events is arterial gas embolism. by thoracic binding). thus. 4 had only age. from the lung into the mediastinum or chest cav. However. During overdistension of the lung. that a transmural pressure of 70 mm Hg. pressures up to as ‘arterial gas embolism’. can be generated by cutaneously at the base of the neck. pneumothorax (3 bilateral. the leakage of gas sema. whereas a higher trans. the escaping gas can which the lung is splinted by its surrounding struc. but it is usually associated with close to maxi. a significant proportion of the cardiac output. may predispose the great that the left ventricle can become air-locked individual to PBT. However. Both these situations. mediastinal and cervical subcutaneous emphy- atic and go unreported at 1 ATA. It is also possible that lung ‘injuries’ that are then gas may enter the pleural cavity and produce benign. and 1 had only unilateral pneumothorax. small and often compressed by distended air sacs. the more compliant healthy that the distribution of bubbles in large blood ves- tissue will expand more. the capillaries Novice divers. Scarring within the lung parenchyma has long smaller and variable amounts of gas are entrained been considered to increase risk of PBT. More commonly. Denison3 reported cases of pulmonary tion. In addition. if there total lung capacity (TLC) before ascent. (e.g. Therefore. tend to swim with other lung tissue. Escape into the inter- to 110 mm Hg are tolerated before rupture occurs. hilum of the lung where the pleura is discontinu- mural pressure is required to cause injury when ous. unnoticed and possibly frequent at the a pneumothorax (Figure 6. are likely to suffer the ­greatest the scar and surrounding tissue. Finally. If gas begins to exposure to bubbles. he postulated that when arterial gas embolus (CAGE). thus giving an ascent from only 1 metre if the lungs are near rise to ‘subcutaneous emphysema’. in which back to the heart. distribute with flow. a procedure used by many divers in an attempt to air embolism may not result until overdistension is conserve air. Skip breathing. From there. In a Royal Navy series5 of 109 non-fatal cases rupture occurring with deep inspiration and sug. thus possibly resulting in dam. Rarely. diver may be symptomatic or even life-threatening. but if the thorax is prevented from enter the arterial circulation. 4 unilateral). is a voluntary reduction in breathing relieved by exhalation. This shear stress may result enced by buoyancy. along equipment and the environment. those organs receiving sistently related to the site of the scar. the volumes of gas are so the lungs are held close to TLC.

Smaller bubbles can leak of sodium is followed by cellular oedema redistribute through the microcirculation and thus and depolarization. Bubbles that are ­supply impairs neuronal ability to regulate intra- large enough that their leading end occupies sev. transient obstruction to flow in a tissue sensitive tion is interrupted by the systemic capillary beds. even Passage of these bubbles through the circula.g. the latter resulting in release . Clearly. Even larger bubbles of the aortic arch and are more likely to enter the redistribute in this way as the gas inside them is vessels supplying the upper body and brain.1  Pulmonary barotrauma of ascent. absorbed and they shrink. however. cellular ionic homeostasis because of breakdown in eral generations of branching arterioles may stick the sodium-potassium pump. occur). the brain) may result in damage Bubble behaviour and effects at this point are before bubble redistribution occurs. Pathophysiology 67 Gas in supraclavicular region Surgical emphysema Rupture of alveoli Pleural cavity Pneumothorax Ruptured alveoli showing gas in pulmonary veins Air embolism Figure 6. to hypoxia (e. larger bubbles tend to track around the roof cause minimal obstruction. Uncorrected inward and cause obstruction to flow. Loss of oxygen largely ­influenced by their size.

The resulting cerebral tory events). evidence from animal studies that shows a second. New York: Plenum Press. 1984. trapped in the pulmonary veins and heart cham- Even the redistribution of bubbles is not a benign bers. quots of gas. In: Schilling CW. glutamate) and a cascade of may reflect bubble redistribution) followed by a injurious events that may lead to early neuronal ­secondary deterioration (caused by the inflamma- death or delayed apoptosis.68  Pulmonary barotrauma Table 6. Although there is little proof that this pro- event. Carlston CB. This ing the heart. Secondary deterioration may also be caused by onset unconsciousness and/or multifocal stroke. The understandable focus on cerebral effects ary decline in blood flow and neuronal function in of arterial gas embolism should not be allowed to cerebral tissue following redistribution of small ali. until the diver is seen at a hyperbaric and other forms of secondary damage. the coronary arteries and cause myocardial isch- lism is thought to explain the frequent observation aemia and arrhythmias. Note: Data were compiled from case histories and records of initial post-accident examinations. Mathias RA. It is also possible for bubbles to enter sort of inflammatory sequel to arterial gas embo. Diagnosis and treatment of gas embolism. supine position. the examina- tions were always carried out within 5 minutes of onset of symptoms. of excitotoxins (e. Bubbles may cause endothelial disruption as cess is materially affected by postural changes. There is clear chamber. The Physician’s Guide to Diving Medicine. this decline is caused by these processes It has already been suggested that large amounts and does not take place if the animal is depleted of of gas can cause early cardiac arrest by air lock- white blood cells before the bubble exposure. obscure the potential for effects on other organs. even in the presence of apparent tory cytokines which can also cause tissue oedema recovery. possibility underpins the frequent advice to keep and white blood cells adhere to the damaged vessel an apparent victim of arterial gas embolism in a walls. re-embolization by further bubbles that have been like events (see later).g. this they pass through small arterioles and capillaries. The heart may also be of initial improvement in early symptoms (which affected indirectly by disturbance in function of . eds. dysfunction m ­ anifests most commonly as sudden. In the case of submarine escape training accidents. Their activation leads to release of inflamma.1  Presenting signs and symptoms in 114 Royal Navy submarine escape training accidents and 74 scuba diving accidents involving arterial gas embolism Percentage incidence Submarine Signs and symptoms escape training Scuba diving Coma with convulsions 7 18 Coma without convulsions 29 22 Stupor and convulsion 14 24 Collapse 8 4 Vertigo 14 8 Visual disturbance 6 9 Headache 2 1 Unilateral motor changes 17 14 Unilateral sensory changes 10 8 Unilateral motor and sensory changes 6 1 Bilateral motor changes 1 8 Bilateral sensory changes 1 1 Source: From Pearson RR.

yet this spiromet. i. liver enzymes are commonly elevated after arterial an explosive exhalation of expanded gases may be gas embolism. when distended. Nevertheless. a feeling of fullness in the throat. result in local compliance changes. i. Clinical features  69 the brainstem cardiovascular centres by cerebral CLINICAL FEATURES arterial emboli. features afterward. high- injury has occurred in these organs. The  voice predisposing factor. pulmonary fibrosis. after alveolar rupture gas Although many cases of PBT may be caused by may escape into the interstitial pulmonary tissues voluntary breath-holding during ascent or by the and track along the loose tissue planes surround- pathological lesions mentioned earlier. A frequent finding with some Symptoms may appear rapidly in severe cases. dyspnoea. pulmonary tissue damage are not invariably pres- lae. the lungs are cases (Case Report 6. but the symptoms of pneumothorax. gas trapping cough and haemoptysis.e. a pneumoprecordium may be misdiagnosed exhibited none of the contributory pathological as a pneumopericardium (Figure 6.2). a finding suggesting that subclinical accompanied by a characteristic sudden. sarcoidosis. out any of the following diagnoses.e. it takes time for gas to migrate to the sites where it Brooks and colleagues6 demonstrated that a lower provokes symptoms. to the nerve in a relatively compliant tissue space ric parameter has not been shown to be causally would achieve nerve damage.2). faulty breathing apparatus or water inhalation.1 and Case Report 6. gia and retrosternal discomfort. rapid ascent. asthma. ent. For example. dyspha- ees. many medical changes are described as ‘tinny’ and have been standards refer to the requirement for the ratio attributed to ‘submucosal emphysema’ of the upper of forced expiratory volume in 1 second (FEV1) airways and/or recurrent laryngeal nerve damage. tumors. and this finding further supports the sug. As previously described. this seems rare in practice. These divers were the pleura is stripped off the heart and mediasti- also passed as medically fit before the dive and num. and their absence should never be used to rule infection and inflammation. In very rare severe gestion that reduced pulmonary compliance is a cases syncope and shock are ­possible. these symptoms or airway obstruction. Clearly. pleural adhesions. pitched cry. it is clear ing the airways and blood vessels into the hilar that these risk factors are not present in all cases. cysts and bul. related to PBT in trainees who have no evidence Clinical signs include subcutaneous emphy- of lung disease. Symptoms may include a voice than predicted forced vital capacity (FVC) was change including hoarseness or a brassy monotone. Although lung damage resulting from barotrauma can produce respiratory symptoms in the absence of any of the other associated compli- PREDISPOSING FACTORS cations. creatinine kinase levels (skeletal muscle fraction) and some At the point of surfacing in a panic ascent situation. regions and thence into the mediastinum and neck About half the submarine escape ascent trainees (subcutaneous emphysema). When correct exhalation techniques. Precipitating factors include inadequate exha- lation or outright breath-holding during ascent Mediastinal emphysema (often in association with panic). Predisposing disorders include lesions that may symptoms that may be seen include dyspnoea. It is likely that many other tissues are affected by arterial bubbles without necessar. Interestingly. to FVC (FEV1/FVC ratio) to be greater than 75 to although it is difficult to see how bubbles external 80 per cent of predicted levels. of these subjects is a reduction of compliance at or  they may be delayed for several hours in lesser maximum inspiratory pressures. sema  of neck and upper chest wall. Delay less distensible (stiffer) and are exposed to more may reflect that the symptoms are often ‘mild’ or that stress than normal diver’s lungs. Pulmonary tissue damage ily producing symptoms. It may also extend who develop PBT have been observed to carry out into the abdomen as a pneumoperitoneum. associated with PBT in submarine escape train. These include sub-pleural may occur in association with any of the complica- blebs of the type associated with spontaneous tions of PBT discussed later. crepitus .

He then noted a restriction in his air supply and thought he had exhausted his gas. An hour and a half after the dive. from air stripping the pleura from the edge of the cardiac shadow. but later. he decided to see the doctor because he was not feeling well. CASE REPORT 6. Subsequent lung function stud- ies showed that pulmonary compliance was reduced below predicted values. bilateral generalized crepitus over the chest and positive Hamman’s sign. was having his second dive in scuba equipment at a depth of 5 metres when he noted a slight pain in his chest. It was then noted that his voice was altered in quality and that he had subcutaneous emphysema in both supraclavicular fossae.1 RJN. Diagnosis: Pulmonary barotrauma with mediastinal emphysema and coronary artery embolism. he noted that he was breathing heavily and felt weak. he developed a fullness in his neck (a ‘tightness’) and dysphagia. He was treated with 100 per cent oxygen and improved rapidly.70  Pulmonary barotrauma Figure 6. III and aVF. He was asymptomatic after the dive. He opened his reserve valve and ascended to the surface. An electrocardiogram showed ischaemic changes in leads II. . a 19-year-old. During lunch. Chest x-ray study and electrocardiogram were normal 6 days later. A few minutes later he noted slight retrosternal chest pain.2  Pulmonary barotrauma of ascent: chest x-ray film showing mediastinal emphysema causing the ‘tram track’ sign. during physical training. Chest x-ray study showed gas in the upper mediastinum and neck.

He was treated with 100 per cent oxygen and bed rest. coughing and movement. tachycardia and hypotension. developed epigastric discomfort toward the end of a 90-minute. Pneumothorax Arterial gas embolism If the visceral pleura ruptures. rather include diminished chest wall movements. the latter being more common ­obstruction. which increased in intensity over the next few hours. forming monary veins and thence into the systemic cir- a haemopneumothorax. He had no clinical evidence of pneumothorax.3). Diagnosis: Pulmonary barotrauma with mediastinal emphysema. He was considered permanently medically unfit to dive. The pneumothorax may be culation. No pneumothorax was seen and the lung fields were clear. The pain extended from the epigastrium to the base of the throat. signs enlarged mediastinum with air tracking along the of shock and x-ray evidence of pneumothorax cardiac border or in the neck. Approximately 15 minutes after leaving the water. has occasionally ished breath sounds and hyper-resonance on the produced cardiac tamponade with its classic clini. The dive was otherwise unremarkable.2 TC. Clinical signs may be absent. and he made four controlled ascents during the dive to change his tools. 11-metre scuba work dive. . hypoxia. he developed retrosternal chest pain. affected side. air enters the pleural This dangerous condition is the result of gas cavity and expands during any subsequent ascent. faint heart sounds. an experienced Navy clearance diver. an inflammatory cascade (see earlier). passing from the ruptured alveoli into the pul- It may be accompanied by haemorrhage. decreased cardiac dull. It also extends along the major branches of the aortic arch adjacent to the trachea and oesophagus superiorly into the base of the neck on both sides. with complete resolution of his symptoms. The spread of air appears to be mainly along the major vessels of the aortic arch into the base of the neck’. in particular there were no palpable subcutaneous emphysema and no positive neurological signs. it is seen surrounding the descending aorta at the level of the carina. although he had at times worked hard. The pain was pleuritic in nature and aggravated by inspiration. Pneumothorax from diving has the same ness to percussion. Examination was unremarkable. left recurrent clinical features and management as pneu- laryngeal nerve paresis and in severe cases cyanosis. under the skin (described as the sensation of egg- shell crackling. A computed tomography (CT) scan of the chest was reported as showing ‘air in the mediastinum. (Figure 6. There may be radiological evidence of an fected side with a tension pneumothorax. this is seen around the oesophagus in the retrocardiac recess. Clinical features  71 CASE REPORT 6. dimin- than gas in the pericardial sac. Precordial emphy- sema may be palpable and produce Hamman’s Symptoms usually have a rapid onset and sign  – crepitus related to heart sounds that can include sudden retrosternal or unilateral (some- sometimes be heard at a distance from the patient. or they may between the pleura and the pericardium. He was not dyspnoeic. Chest x-ray study revealed the presence of surgical emphysema in the neck and superior medi- astinum. Inferiorly. mothorax from other causes. times pleuritic) pain. infarction and activation of following dramatic emergency ascents. where it can cause vascular damage or unilateral or bilateral. tracheal deviation toward the unaf- cal signs. by divers). and there was no associated cough or haemoptysis. Superiorly. with dyspnoea and tachy- An extension of the mediastinal gas into the tissues pnoea.

3). ascent practices. the abnormalities. which develop dysrhythmias).72  Pulmonary barotrauma Figure 6. which is usually was 8 minutes in a single case. disoriented or MANIFESTATIONS uncoordinated after emerging from the water. immediately after ascent. . typically occurs immediately on surfacing or very visual disturbances. paraesthesiae or sensory soon afterward. convulsions and longest interval to onset of symptoms and signs varying degrees of paresis. and The manifestations of CAGE may include the 17 per cent had presented with paresis (6 cases with following: upper monoparesis and 6 with hemiparesis). ●● Cardiac-type chest pain and/or abnormal Serious neurological symptoms consistent electrocardiograms (ischaemic myocardium. aphasia. Most of the clinical series refer to the brain ●● Loss of consciousness and other neurologi- (CAGE) as the dominant site of disease. 23 per cent had become confused. with cerebral involvement. right-sided pneumothorax with a slight hemothorax. vertigo. 34 per cent of the divers suffered loss of consciousness within seconds of surfacing. Onset cal abnormalities such as confusion. In one large series5 of CAGE. (see Chapter 10) than by CAGE. by spinal decompression sickness (DCS) ring in excess of 10 minutes. must be regarded as air embolism and treated accordingly until In a series of 88 cases of CAGE7. There were no cases occur. mainly from free a definitive diagnosis has been made.3  Pulmonary barotrauma of ascent causing a large. with all other div. lateralized (Case Report 6. Paraplegia with ers showing evidence of CAGE within 5 minutes a sensory level is more likely to be caused of completing the dive.

First. he gave a gasp. arterial bubbles from PBT may enter tis- sidered most likely caused by PBT and CAGE. and distinguishing between them is 53 per cent had some spontaneous improvement unimportant from a management point of view. He was noted to be groaning at this time but soon after appeared dead. It seems clear pression and ‘arterialized’ across a right-to-left that divers who exhibit symptoms of CAGE shunt (see Chapter 10) are large enough to cause may show partial or even complete recovery the stroke-like syndromes seen after PBT and within minutes or hours of the incident. before therapy. As dis. haemoptysis) is with CAGE is a haemorrhagic or thromboembolic surprisingly common and should not influence cerebrovascular accident (CVA) occurring coinci- the diagnosis. dentally with ascent from diving. and it is far more rological symptoms after a dive that could be likely that cerebral symptoms occurring after a . Confusingly. quadriplegia. izing signs. occur but are extremely rare. 77 per cent with coma improved The management is virtually identical (see later). Thirty min- utes after the dive he was compressed to 50 metres but with no response. Resuscitation was commenced imme- diately. sue micro-vessels and grow as a result of inward especially where the time and depth exposure diffusion of supersaturated tissue inert gas (see would normally be considered ‘unprovocative’ for Chapter 10). In addition. lateral- able. such recovery is unreli. Third. Chapter 10). CAGE. but there are several relevant points. and mani- festations best explained by spinal involvement DIFFERENTIAL DIAGNOSIS (paraplegia. Diagnosis: air embolism resulting from PBT of ascent. Manifestations best explained by episode. bubbles are unlikely to form cussed earlier. 19 years old and in good health. Unfortunately. In another series presented by Pearson5 that considered provocative for DCS is more problem- included scuba divers without access to imme. it remains uncertain whether the venous neous improvements were not always sustained.g. from a compressed gas dive should always be con. Clinical features  73 CASE REPORT 6. cerebral involvement (unconsciousness. Thus. referred to as type III DCS.3 AI was a relatively inexperienced diver. diate recompression. and and DCS. loss of anal or bladder Focal cerebral symptoms and signs (including tone) are most likely caused by DCS. aphasia) are most likely Recurrence of symptoms has an ominous prog. his eyes rolled upward and then he floated motionless. While he was being rescued from the water it was noted that blood and mucus were coming from his mouth and that he was unconscious. Second. this may reflect redistribution of from dissolved gas in the brain tissue itself (see the embolus through the cerebral vasculature. an absence of signs of the presumed baro. 15 per cent had complete the principal competing diagnoses are CAGE spontaneous remission within 4 hours. loss of vision. bubbles formed from dissolved gas after decom- and 15 per cent of the divers died. Autopsy verified the pres- ence of pulmonary barotrauma (PBT). This mechanism has sometimes been DCS (see Chapters 10 and 11). are concomitant symptoms of PBT). As previously men. These sponta. Such events do The differential diagnosis for rapid-onset neu. unconsciousness) arising immediately after ascent the two diagnoses may coexist and even interact. using oxygen. to some degree before treatment. tioned. He was performing a free ascent from 10 metres. On reaching the surface. for the purposes of diagnosis. It may not occur or it may not be sustained. to result from PBT and CAGE (especially if there nostic significance. Resuscitation was continued while he was rushed to the nearest recompression chamber. Another diagnosis that may cause confusion traumatic injury to the lung (e. Even those divers who become comatose may emphasis should be placed on the putative organ improve to a variable degree after the initial involvement. atic.

cardiovascular support a tension pneumothorax during a reduction in and therapeutic recompression using oxygen may ambient pressure. if necessary (see earlier). the patient is asymptomatic. With mild symptoms. if a diver with PBT it should be remembered that in doubt. Similarly. Several ani- mal studies were not able to show an advantage in Pulmonary tissue damage the initial deep excursion. although care must cases of DCS. Higher rates may peripheral hospitals staffed by doctors unfamiliar be appropriate to allow lower tidal volumes and with diving medicine. It is still considered ing or the acute respiratory distress syndrome. peeping’ with excessively high rates. be taken not to cause ‘breath stacking’ or ‘auto- Previously it was considered important to dif. observation and rest In particular. whereas CAGE to minimize both inflation pressures and the pos- was treated using USN Table  6A (which includes sibility of coughing on the endotracheal tube. from any other cause. oxygenation by administration of sufficient oxy- pression has become the priority rather than estab. This may take 4 to 6 hours. However.g. exclusion of air As a general principle.74  Pulmonary barotrauma dive are the result of a diving disorder. Failure to do this risks development of If symptoms are severe. the If a victim of PBT requires mechanical ventilation. unless clinically indicated to treat hypoxia. Pneumothorax coughing. e. Management of mediastinal emphy- during air evacuation or decompression from sema varies according to the clinical severity. be useful. or before recompression if there is out positive pressure will increase the gradient another problem such as CAGE or DCS that justi. gen. US Navy (USN) Table 6. relevant subsequently to assess the likelihood of Positive-pressure respiration could increase the whether PBT occurred because this diagnosis has extent of lung damage and should be used only implications for future risk in diving. . and. The same problem arises in minimal inflation pressures. TREATMENT Mediastinal emphysema Aggravation of pulmonary barotrauma The need for therapy may not be urgent in medi- astinal emphysema. and ferent. areas. treatment for these disorders should take further decompression (e. Positive end- ferentiate between CAGE and DCS because the expiratory pressure should probably be avoided recommended recompression regimen was dif. The treatment is similar to that of near drown- lishing the ‘correct’ diagnosis. recom. ascent to altitude precedence.8-ATA oxygen the diver should be kept well sedated and relaxed table. an initial deep excursion to 6 ATA). for removal of nitrogen from the emphysematous fies recompression in the presence of a pneumo. Cardiovascular support may be required. principal reason for mentioning this differential a pressure-control mode should be used. DCS was treated with a 2. employ- diagnosis is the frequent inappropriate attribu. always have a chest drain inserted before any air 100 per cent oxygen administered by mask with- evacuation. a diver with pneumothorax should may be all that is necessary. increased respi- ratory activity. If hyperbaric treatment) can aggravate the problem. breathing against a resistance. physical exertion. Indeed. thorax. at all stages of managing embolism or pneumothorax is necessary. ing the lowest inflation pressures required to tion of CAGE to a CVA when divers are taken to achieve adequate tidal volumes. Valsalva’s maneuver and mechanical ventilation may also result in further pulmonary The treatment of a pneumothorax follows the stan- damage or in more extra-alveolar gas passing dard principles used in treating a pneumothorax into the mediastinum or into the pulmonary veins.g. Consequently. and most centres now manage patients with CAGE and those with DCS Treatment involves the maintenance of adequate identically (see Chapter 13).

a large intravenous angiocatheter) in the second OXYGEN interspace. mid-clavicular line. via a close-fitting mask. or if there is a is mandatory before recompression. on his or her back if conscious PBT such as CAGE are present. dard intercostal drain. (rarely) follow the resumption of an erect position. Most treatment facilities use a conventional tion. If this is not emboli. compressed and for an uncertain period of time Pneumothorax must always be considered (usually one to two oxygen periods) while breath- if a diver develops respiratory symptoms such ing oxygen. A sudden deterioration in the clinical state may sion. Compression reduces bubble size. The presence of a pneumothorax is not a con. Treatment of CAGE is urgent. this is no longer this may assist redistribution through the arterial . The current advice is that the patient should be traindication to recompression if other sequelae of nursed horizontally. could be used as a Oxygen (100 per cent). Larger pneumothoraces reducing cerebral perfusion pressure and promot- justify the insertion of an intercostal catheter. let alone a seriously ill victim requiring resuscita. the placement of an intercostal catheter from causing airway obstruction. possibility of aspiration of stomach contents or sea ing a chest drain in a hyperbaric chamber must water). This position was recommended to discour. However. then insertion of a smaller catheter (e. be experienced in this procedure. Ideally. This will the possibility of compounding the embolic brain often appreciably reduce the size of the pneumo. heart chambers and pulmonary veins and that The decompression should be halted and careful this gas could be released from those locations by clinical examination undertaken. The effect of delay ●● To ensure that any subsequent bubbles intro- on treatment outcome is to increase mortality and duced through injured lungs are composed of morbidity. POSITIONING RECOMPRESSION The ‘modified Trendelenburg’ position or the Recompression should be instituted as soon as head-down left lateral position was recommended possible. The patient is initially allowed to difficult in the noisy confines of a recompression sit or stand once recompressed to the initial treat- chamber. which is virtually impossible to ing in the recompression chamber before being maintain even in a conscious cooperative patient. Some authorities even recommended the first 30 minutes of 100 per cent oxygen breath- a 45-degree angle. ing cerebral oedema. must be vented before resumption of decompres. However. which could be connected This would suggest the continued existence of gas to a Heimlich valve for expediency. this would be achieved with a stan.g. side in the ‘coma’ position (preventing the tongue pression. and the cerebral vessels. 2. The patient is kept horizontal for at least in the past. allowed to move and possibly redistribute emboli. Treatment 75 Small pneumothoraces may resolve with the recommended because of its impracticality and administration of 100 per cent oxygen. injury by increasing central venous pressure. because and/or the airway is not threatened. should be administered in transit to the chamber: ●● To improve oxygenation of hypoxic tissues. while the chamber is being hyperbaric environment. Staff manag. then it ment depth and after a period of oxygen breathing. temporizing measure. If a pneumothorax is found.8-ATA oxygen table such as the USN Table 6 (see age bubbles passing into the aorta from entering Chapter 13). possible. thorax within a few hours. instead of nitrogen. oxygen. particularly in A similar position should be maintained in the management of underwater seal drains in the transit to the chamber. Cerebral arterial gas embolism ●● To help dissolve bubbles. This advice recognizes the potential as chest pain or dyspnea during decompression for further gas to be trapped in places such as the from a hyperbaric treatment (Case Report 6. which is often postural change.4). or lying on the the pneumothorax may re-expand during decom.

and arrangements were made to go to the rig in the morning of day 4. Recompression to 135 feet relieved all symptoms. where he had complete relief and felt normal. The diver was recompressed to 185 feet and a treatment schedule was implemented. at 105 feet. The diving superintendent at this point informed Mr A (a senior diving supervisor). where. At this point a special treatment was instituted at Mr A’s instructions. with the diver feeling fine until day 2 at 02:53 hours. the diver had recurrence of symptoms. It was decided to attempt decompression once more to see whether the diver could be decompressed all the way or whether there would be a further recurrence of symptoms. The doctor was informed of the treatment to date and of the diagnosis and was asked to bring the necessary needles with him to vent a pneumothorax. and. and his condition had steadily deteriorated. The dive job was carried out successfully and was completed without incident in 13 minutes. The diver was recompressed according to the treat- ment schedules and then decompressed. the rig medic administered an injection of painkiller at 22:45 hours of day 4. the diver had been decompressed to a depth of 60 feet. and the doctor arrived at the rig. The chamber atmosphere was at this point changed over to a saturation atmosphere. During decom- pression upon reaching 90 feet. however. Mr A. The doctor left the rig by evening of day 4. The diver was recompressed to 100 feet. At 23:25 hours while reaching 83 feet in the decompression. where he obtained com- plete relief.4 This case was described by a diver/doctor. whereupon he was recompressed to 125 feet. decided that the problem could not be an ordinary decompression problem and was reasonably certain that the symptoms were the result of a pneumothorax. carried out a bounce dive to 492 feet. On day 4 at 10:49 hours Mr A. He stated that it was a routine case and that he would be available ashore for consultation. using a helium-oxygen system. upon reaching 75 feet during his decompression. because of severe pain. At this point Mr A. the doctor made a cursory examination of the diver without taking his temperature and diagnosed the diver’s condition as ‘full blown pneumonia and pleurisy of the left lung’ and ruled out the possibility of a pneumothorax. He experienced a second recurrence of the symptoms at 85 feet during decompression. the diver reported tightness in his chest. He had now diagnosed the case as a burst lung problem and discounted any kind of bend. the doctor stated that this would be the case with pneumonia and that he had previously treated a very similar case. on shore that a treatment procedure was being carried out. Decompression was uneventful. the diver again complained of breathing difficul- ties. At this point the doctor took over the treatment and instructed the diver to be decompressed at the rate of 3 feet per hour and emphasized the fact that the diver would experience severe chest pains during decompression as a result of the pneumonia. On day 3 at 13:00 hours. and the diver was decompressed at a saturation decompression rate. The doctor was challenged on the fact that the diver obtained relief by recompression. At 13:49 hours while the diver was at 80 feet. at this point requested the opin- ion of a second doctor regarding the diver’s treatment and condition. the diver complained of restriction to his breathing. Attempts were unsuccessfully made to obtain another doctor to go to the rig. A doctor was called. some shortness of breath and discomfort while breathing. . When the diver reached 85 feet. On day 1 the diver. By the morning of day 5. By the afternoon of day 4 the diver was treated with penicillin injections.76  Pulmonary barotrauma CASE REPORT 6. the symptoms redeveloped and other treatment proce- dures were instituted. in his incident report. and he was once more recompressed to 185 feet for therapeutic decompression at 14:33 hours.

ADJUVANT AND SUPPORTIVE THERAPY Radiological investigations such as CT. with little apparent effect. Rehydration may be crucial if there is hypo- genated state of the blood assists in rapid bubble tension or haemoconcentration. signs of vascular filling. and by 09:15 he was pronounced dead by the doctor. Chapter 13). Intravenous fluid resolution. and ued until there is full recovery or no sustained 60 mg/hour administered thereafter for the dura- improvement over two consecutive treatments (see tion of the infusion (usually 24 to 48 hours). and cardiopulmonary resuscitation may be may assist in the diagnosis and management of DCS necessary. CAUSE OF DEATH 1. Treatment 77 The attending doctor was notified of these attempts and of the worsening of the diver’s condition. These investigations are most helpful . this would usually be achieved with a treatment may be of value in those neurologically 1  mg/kg loading dose given over 5 minutes.g. considered a stan- dard of care in this setting. however. The cause of the pneumothorax was unknown. During the early hours of day 6. exposes chamber atten. Death resulted from a tension pneumothorax of the left lung (postmortem finding). and micro-circulation into the veins. This is In  an environment conducive to its safe admin- becoming progressively less popular because it is istration. activation and some of the related inflammatory There are no drugs with proven efficacy in consequences. These treatments are contin. anced electrolyte crystalloid should be titrated to tory to benefit. and the diver’s condition was worsening. it was learned that the diver had a slight chest cough on the day before the incident and complained to the rig medic of some pain on the left side of his chest and over the central area. protective agent in this acute setting. urine output. lignocaine could still be considered in logistically challenging. that the pneumonia was disappearing and that the decompression rate was to be increased so that the diver could be transferred to a hos- pital as soon as possible. In a healthy adult male opposing concepts. cases strongly suggestive of CAGE. 2. however. A loading dants to increased risk and seems unnecessary. and CAGE. Repetitive hyperbaric oxygen patient. USN Table 6A). Lignocaine is not. During day 5 the diver received injections of penicillin and painkiller. the treatment of CAGE. magnetic Coronary artery gas embolism may cause cardiac resonance imaging and single photon emission CT arrest. further drugs were administered. before continuation with an oxygen table. 120  mg administered over the second hour. hyper. fol- impaired patients who do not recover fully on the lowed by 240 mg administered over 1 hour. to enhance are some supportive data from animal models of the redistribution of obstructing arterial emboli CAGE and human studies in cardiac surgery 8. The dose in combination with an infusion regimen 4-ATA 50 per cent oxygen-nitrogen Comex tables designed to produce a therapeutic antiarrhyth- may be an acceptable compromise between these mic level is appropriate. haemody- baric oxygen helps to suppress white blood cell namics and haematocrit. The  doctor had been summoned and examined the patient at 03:40 hours while the diver was at 39 feet. first compression. There has been interest A variation in this technique is to expose the in the  use of lignocaine (lidocaine) as a neuro- patient to an initial short 6-ATA compression dur. Oxygenation of damaged tissues and resuscitation with a non–glucose-containing bal- a reduction of cerebral oedema may be contribu. and there ing air breathing (e. As discussed elsewhere. At 09:00 hours the diver’s pulse had stopped. The denitro. The doctor stated that the diver’s condition had improved.

have centered on standards of fitness for for gas trapping. If there is a high index of suspicion dence. thus predisposing to further problems by automatic exclusion from diving. High-resolution or spiral techniques. diving chest x-ray study. disorientation or lightheadedness and associated ing at depth and during ascent. but they should take second place to recom. does not mitigate the risk of other barotraumatic ing must be acknowledged. intrapulmonary fibro- a contraindication for further scuba diving. a single full-plate chest x-ray film is acceptable. major dive training agencies have abandoned tion and oedema. that led to the pneumothorax. the diver may have and inflammation.78  Pulmonary barotrauma in post-recompression diagnosis and evaluation of full recompression facilities on site. The so-called syncope of ascent is a cause of a tran- tra. often described as either avoided include skip breathing. ditch and recov. It is widely considered that an incident of PBT is tumors. In the recreational diving set. Considerable effort goes into instilling this man. and some degree of its own merits. (e. Some (spontaneous pneumothorax and been sustained and may produce local scarring on known gas trapping lesions in particular) merit healing. and determina- ations are largely based on first principles rather tions about diving are made for each case based on than hard outcome data. In most cases. instead simulate it in a horizontal orientation. and occasionally gas in acute free ascent training from bottom to surface. ‘asthma’) imply an increase in the magnitude It must be acknowledged that these consider. previous penetrating chest wounds reasons are two-fold: first. buddy breath. and 54 and involve the exclusion of candidates ting this is often resolved by fully informing the with significant pulmonary disorders as described diver of all the relevant issues and leaving the diver earlier. pression therapy in the acute phases. and the diver is highly motivated Medical standards are dealt with in Chapters 53 to continue diving. dangerous diving practices to be sitory state of confusion. and emergency free ascent training ness. However. more sophisticated lung func- divers and modification of training and diving tion tests are indicated. infection. These studies may show areas of infarc. and cases. with resultant . This becomes most injuries arising from the same predisposing lesions problematic when there is doubt over the diagno. asthma. with a sensation of imminent loss of conscious- ery t­raining. These disorders may result demonstrated a pulmonary abnormality or pre. in local compliance changes or airway obstruc- disposition. pleural adhesions. The sis. In addition. whereas others alteration of lung compliance. Medical selection DIVING AFTER PULMONARY BAROTRAUMA Predisposing disease includes previous spontane- ous pneumothorax. CT scans of the lungs are useful in demonstrating emphysematous cyst and pleural thickening but Dive training also frequently reveal lung changes whose signifi- cance is uncertain. of risk that is very context sensitive. and. Pleurodesis for spontaneous pneu- uncertainty over the validity of considering prior mothorax may protect from pneumothorax but PBT an automatic contraindication to further div. cysts. sis of PBT itself. pulmonary damage has tions. sarcoidosis. Diver evaluation may involve the perfor- to make a decision about continued diving as an mance of respiratory function tests and a pre- informed risk acceptor. or reduce its inci. PREVENTION some groups insist upon inspiratory and expira- tory x-ray studies to demonstrate air trapping in Attempts to prevent PBT. In recent years treatment. It is caused by inadequate exhalation of the when there are no experienced medical staff and expanding lung gases during ascent. the latter view. Entry level recreational divers are taught that the most important rule in scuba diving is to breathe SYNCOPE OF ASCENT normally at all times and never hold your breath.g. second.

Aberdeen: European the past. Undersea 3. was carried out by divers and submariners.57:931–938. Cerebral protection by lidocaine during cardiac REFERENCES operations. In: Proceedings of XIV Annual retain the air in the lungs instead of exhaling it. Pearson RR. tivity and arterial gas embolism. Leitch DR.26:55–64. Medicine 1944.25(suppl):39. Long Term Health Effects of Diving. differential diagnosis. Lung racic pressure causing an impairment of venous function reference values for FEV(1). Annals of Thoracic Surgery 1999. Technology Centre. Pulmonary function: long term Biomedical Research 1986. 1984. Carlston CB. the results of screening 3788 Royal Navy ing rapid ascents. Pulmonary barotrauma Lund T. Francis TJR. . Elliott DH. arterial gas embolism. In: Lundgren CEG. Elliott DH. 1. Autopsy and experimental emphysema of the lungs and mediastinum. Stepke BK. Weathersby PK. 1999. Miller JN. Macklin CC. Respiratory barotrauma. In: Hope A. free ascent training from 18 to 30 metres Underwater and Baromedical Society. 1978.67:1117–1124. but Federation of American Societies for it could sometimes be a step in the progression to Experimental Biology. eds. Mathias RA. Harrison JAB. Increased elastic recoil as a determinant of 2. Proceedings of the Sixth Underwater Because there is no actual lung disease.13(3):317–335. Pulmonary pulmonary barotrauma in divers. Malignant interstitial 4. It is analogous to cough syncope. it is Physiology Symposium.23:281–358. The Lung at Depth. Wiig H. Mitchell SJ. 6. Ng CKY. Pellett O. Undersea and Hyperbaric Medicine Colebach HJH. Green RD. Physiology 1976. New York: Marcel Gorman DF. 1988. in divers and the treatment of cerebral eds. In: Schilling CW. Assessment of medical risk FURTHER READING in pressurized submarine escape train- ing. Calder IM. eds. In Meeting of EUBS. Undersea Biomedical Research 1985. Cerebral vasoreac- Dekker. (1976). effects of diving on the lung. Further reading  79 distension of the lungs and an increase in intratho. Norway: Norwegian Underwater Environmental Medicine 1986. Pearson RR. return. Aviation. Ryder SJ. when the pressure gradients are submariners and submariner candidates by magnified. Space and Bergen. trauma in man. The Physician’s Guide to Diving Medicine. This chapter was reviewed for this fifth edition by 5. Denison DM. Barnard EEP. this was a typical situation in which this disorder Clinical and radiological features of 88 occurred – it caused considerable problems with cases of decompression barotrauma. Macklin MT. Pethybridge RJ. observations on factors leading to baro. New York: Plenum Press. Halsey MJ. Bethesda MD: technically incorrect to describe this as PBT. and 7. 8. Gorman DF. Brooks GJ. FEV(1)/FVC ratio and FEF(75-85) derived from Syncope of ascent most commonly occurs dur. FVC. Browning DM. Diagnosis and treatment of gas Simon Mitchell. Smith MM. embolism.12(2):165–182. this disease. Denison DM. 1988. Francis TJR. 1994. and also when the diver attempts to spirometry.


1). divers’ disorders. Barotrauma problems may contribute to panic Barotrauma is defined as the tissue damage caused and diving deaths in novice divers or to permanent by expansion or contraction of enclosed gas spaces. ●● External ear (when a sealed gas space exists). alternobaric vertigo) 93 Pneumocephalus/intracranial haemorrhage 101 Treatment 94 Reference 101 Inner ear barotrauma 94 Further reading 101 INTRODUCTION Middle ear barotrauma is the most common form. It is probably the most com- mon occupational disease of divers. which in turn are caused by the may affect any of the following: changes in e­ nvironmental pressure with descent and ascent (Boyle’s Law). reversed ear) 82 Symptoms 96 Middle ear barotrauma of descent (middle Investigations 97 ear squeeze) 83 Treatment 98 Pathophysiology 83 Prognosis 99 Symptoms 85 Middle ear barotrauma complications 100 Treatment 87 Seventh nerve palsy 100 Prevention 88 Otitis media 100 Middle ear autoinflation techniques 90 Mastoiditis 100 Middle ear barotrauma of ascent (reverse Meningitis 101 squeeze. Barotrauma of descent is a result of a failure or ●● Inner ear (which adjoins a gas space) (Figure 7. This confusion still exists in it is in this zone that ear barotrauma is more fre. balance and hearing loss. experienced to Barotrauma refers to damage to tissues some degree by most. many clinical reports today. quently experienced. resulting from changes in volume of gas Ear (also called otological or aural) barotrauma spaces. and so sickness symptoms. according to Boyle’s Law and its pressure-volume In the earlier literature on caisson workers’ and changes. an inability to equalize pressures within the ear 81 . ●● Middle ear (which incorporates an enclosed gas space). 7 Ear barotrauma Introduction 81 Overview 94 External ear barotrauma of descent Pathophysiology 95 (external ear squeeze. otological barotrauma symptoms The volume change in gas spaces with depth is were hopelessly confused with decompression proportionally greatest near the surface. disability – tinnitus.

middle ear and sinus cavities easier. and so baro- i. and the chambers and by caisson workers (who work under contracting space may be taken up by engorgement increased pressure). This. . water entry is Round ear window prevented. oedema and haemor. in hypobaric or hyperbaric lage and bone. and space exposure. Breathing helium-oxygen gases when diving sion of tissues around the expanding gas within the makes equalization of pressures (‘autoinflation’) in ear. local congestion and Eardrum Eustachian haemorrhage.1  Basic anatomy of the ear. Barotrauma is classified according to its ana- rhage. when the diver descends from the surface (1 ATA pressure) to 10-metre depth (2 ATA pressure) with an occluded external ear. outward bulging of the tympanic membrane. middle. Barotrauma of ascent is the result of the disten. includ- ing many references to barotrauma.e. squeeze’ to describe it. It may occur in any combination in the It is commonly called a ‘squeeze’ by divers. when environmental pressures are reduced. or inner ear. Similar problems are encountered with aviation Because enclosed cavities are surrounded by carti. i. descent.e.2). General information on the ear in diving. together with the enclosed compressed tomical sites and whether it is caused by ascent or gas. water enters and replaces the Cochlea air in the canal during descent. Contraction of the contained gas is then Middle ear compensated by tissue collapse. of the mucous membrane. common disorder encountered by divers. on ascent. Divers use the misnomer ‘reverse trauma is less. This is observed when a pressure tube gradient between the environment and the blocked external auditory canal is +150 mm Hg or more. tissue distortion is limited. External If the external ear is occluded. REVERSED EAR) Nerve Because the external auditory canal is usually open to the environment. Bleeding and tissue Ear plug or wax swelling into canal 2 ATA 1 ATA Ear plug or Air at 1 ATA wax pushed Eardrum inwards bulges outwards Figure 7.2  External ear barotrauma. external. equalizing the pressures. EXTERNAL EAR BAROTRAUMA OF DESCENT (EXTERNAL EAR Ossicles Vestibular system SQUEEZE. Figure 7. 2 metres descent in water (Figure 7. is included in Middle ear barotrauma of descent is the most Chapters 35 to 38.82  Ear barotrauma cavities as the volume of contained gas decreases. assists in equalizing the pressure imbalance.

moving the jaw or swallowing MIDDLE EAR BAROTRAUMA OF or by voluntarily inflating the middle ear cav- DESCENT (MIDDLE EAR SQUEEZE) ity by the Valsalva manoeuvre. appear normal. A diver moving from the surface (1 ATA) to 10-metre depth (2 ATA) with a blocked Eustachian tube. . It fills d ­ uring tic solution warmed to body temperature and descent and empties on ascent. inflation) via the Eustachian tubes during descent.3  Middle ear barotrauma of descent. Pathophysiology ics and local treatment (see Chapter 29). large exos. Occasionally. Eustachian tubes open. Perforation of this m ­ embrane is uncommon. foreign bodies such as mask straps. More commonly.3). This condition is easily prevented by ensuring The Eustachian tubes may open when the pressure patency of external auditory canals and avoiding gradient between the pharynx and middle ear ear plugs or tight-fitting hoods that do not have cavity reaches 10 to 30 mm Hg. toses. Diving marine animals avoid this disorder by tenance of a dry canal. Equalization of pressure occurs when the cally possible. tight-­ An abnormal pressure difference (gradient) causes fitting hoods and mechanical ear plugs. It follows the failure to equilibrate develop when the environmental pressure (­external Drum Ear canal bulges Middle inward Tissue swelling ear cavity and bleeding 1 ATA 2 ATA Ear drum Blockage of Eustachian tube Figure 7. having an arterio-venous plexus in the middle ear possibly cleansing of the canal with an antisep. barotrauma. ­accommodating ­prohibition of diving until all epithelial surfaces the volume changes. This can be achieved nor- mally by yawning. Middle ear barotrauma of descent (middle ear squeeze)  83 The common causes of blockage of the external middle ear and environmental pressures (auto­ auditory canal include wax or cerumen. it is caused by Examination of the external auditory canal may faulty technique during attempted voluntary reveal petechial haemorrhages and blood-filled cuta- middle ear autoinflation. descent. 25 cm. Clinical symptoms are usually mild. removal of any occlusion. a subjective sensation of pressure will cal treatment. These figures the- apertures over the ear to permit water entry. a slight difficulty in equalizing the middle ear is Any condition that blocks the Eustachian experienced. which causes failure to equalize the middle ear cavity and consequent middle ear barotrauma of descent. oretically equate to an underwater depth of about External ear barotrauma of ascent is theoreti. Treatment for this condition includes main. that responds to the pressure changes. neous blebs that may extend onto the tympanic mem- brane. The procedure is termed ‘equalizing’ or ‘clearing the ears’ by divers Middle ear barotrauma of descent is by far the most and ‘middle ear autoinflation’ by otologists. Following ascent there may be an ache tube predisposes the diver to middle ear in the affected ear and/or a bloody discharge. Secondary infection may result in a recurrence of the pain and may require antibiot. common organic medical disorder experienced by If the Eustachian tubes are closed d ­uring divers and patients undergoing hyperbaric medi. the tissue damage (Figure 7.

showing greater anatomical detail. It is likely then to 10. or after about Eustachian tube. a 150 mm Hg ultimate damage from not equalizing the pressure pressure change and causing a volume reduction in the middle ear cavity.8 metres.4 metres. the fewer autoinflation manoeuvres sion and haemorrhage as a pressure-equalizing are required per unit depth to prevent symptoms. a locking effect may likely with rapid descents or from old perfora- develop on the Eustachian tube and prevent suc. mucosal congestion.3 metres. vascular capillary fragility. matic tympanum’ of older texts). middle ear congestion and haemorrhage. for in gradings of middle ear barotrauma of descent. with .84  Ear barotrauma Heamorrhage Retracted and effusion tympanic developing in membrane middle ear Figure 7. Eventually it may rupture. The ­tympanic panic membrane is partly moveable and can membrane will become haemorrhagic (the  ‘trau- offset some pressure change. Discomfort or pain may be noted with a It is commonly inferred that perforation is the descent from the surface to 2 metres. 25 to 30 cm descent in water (Figure 7. the extreme degrees of haemorrhage described If the middle ear pressure is then equalized. rhages in the tympanic membrane. If a diver continues descent without equaliz- ing. another 20 per cent middle ear volume reduction Many tympanic membrane perforations caused (and its associated ear pain to occur) the diver by diving are not associated with gross haemor- must descend to 4. pressure gradients to sea water depths are This partly compensates for the contraction of air not strictly appropriate because the tym- within the otherwise rigid cavity.4  Middle ear barotrauma of descent.4). oedema and haemor- rhage within the middle ear cavity are associated Note: Extrapolations from physiological with inward bulging of the tympanic membrane. and so forth. cessful autoinflation. then to 7. to the tympanic membrane) exceeds that in the thereby becoming congested and obstructing the middle ear cavity by 20 mm Hg. tions and scarring. Perforation is more If equalization is delayed. and perforation follows of less than 20 per cent in the middle ear cavity. process – the former demonstrating tympanic For this reason. the deeper that perforation competes with middle ear effu- the diver goes. Thus. barotrauma is more evident near membrane fragility and the latter demonstrating the surface than at greater depths. This effect results when There is a time factor in the development of the tubal mucosa is drawn into the middle ear.

when air flows more readily upward into within the first 10 metres because of the greater the vertical tubes. This causes ●● Upper respiratory infections and allergies. This occurs flier in the correct ‘equalizing ahead of the descent’ in some divers who seem particularly insensitive technique (see later). volume changes occurring down to this depth. with very patent Eustachian pressure gradient is allowed to act over a prolonged tubes. middle ear barotrauma of ascent or inner ear baro- trauma (see later). For others. mucosal polyps and so forth. e. respiratory irritants. respec- ●● Inadequate autoinflation techniques. pain is automatically relieved. mechanical obstructions such Symptoms consist initially of a sensation of pres- as mucosal polyps or individual variations in size. instant equalization of pressures by allowing water ●● Premenstrual mucosal congestion. there is a sensation of vertigo dur- ●● Drugs – cocaine. when the diver swims repeated short ascents after they notice discomfort downward. both of which can follow and . followed by increas- shape and patency of the tube. attention to autoinflation is not of much time. by mucosal congestion as a manifestation of upper respiratory tract infections. descent  varies with the foregoing factors as well Middle ear barotrauma of descent has two as with the speed of descent and the adequacy of major causes: autoinflation techniques. sure or discomfort in the ear.g. shock. Eventually. barotrauma of descent. Occasionally. warms to that of the body. Unless asso- ●● Descent to the point of ‘locking’. entry into the middle ear cavity. venous pressure. Higher numbers are reported in patients receiving hyperbaric medical treatment and in Blockage of the Eustachian tubes may be caused aviation exposures. This pain may be Aviation exposure may also cause middle ear sufficiently severe to prevent further descent. tory irritants. beta blockers. otitis media. early and positive following the final metre or so of descent. Middle ear barotrauma of descent (middle ear squeeze)  85 greater degrees resulting from longer exposure to The incidence of middle ear barotrauma of unequalized middle ear pressures. middle ear autoinflation techniques are needed. per 1000 dives for male and female divers. especially novice divers and those when not autoinflating the ears at maximum depth with less patent Eustachian tubes. to the barotrauma effects and also when a small For some divers. It is easier if the diver descends Difficulties are more frequently encountered feet first. ciated with vomiting or panic. and it is similar to diving Occasionally. Risk factors have been proposed. effects of some drugs. however. tively. Factors leading to blockage of the usually after a descent of 1. Symptoms venous congestion. septal deviation. Some divers reduce the symptoms (but not the Opening of the Eustachian tubes is more diffi- disorder) by slowing the descent or engaging in cult in the inverted position. position of the head – see Chapter 38).5 to 10 metres (100 to Eustachian tube include the following: 760 mm Hg pressure) from the surface. allergies. respira. when using scuba in a swimming pool or import. but this is not as common as in parasympathomimetics.3 and 11. indicating ear problems in 4. a diver may have few or no symp- exposure. based on surveys of dive masters and ●● Pathological processes of the upper respiratory instructors. the water temperature within the middle ear cavity ●● Cigarette or marijuana smoking. nausea and vertigo may follow the caloric stimula- ●● Delay in autoinflation during descent tion by the cold water (depending on the spacial (­flying or diving). After an initial ●● Gross nasal disorders. this condition is ●● Horizontal or head-down position.9 tract obstructing the Eustachian tube. This has been attributed to increased (the ‘yo-yo’ descent). ing pain if descent continues. seldom dangerous because it quickly settles when ●● Alcohol ingestion. rupture of the ear drum may occur. ing the descent. It also may be countered by training the toms despite significant barotrauma.

below and behind the handle of the malleus or Damage and disease involve the whole of the adjacent to previous scarring. This hearing loss disappeared after 2 weeks when the perforation had almost healed over. A full or blocked sensation may and complex pathologies may be observed.1 JQ performed three scuba dives. W. nal ear. haemorrhage over the handle of the malleus and the membrana flaccida and a small haem- orrhage anterior to the handle of the malleus. He then went down to 3 metres ‘to see if I could clear them’ for his second dive. This is sometimes associated with a mild illustrated on the front of Plate 1. if it occurs. Following this first dive his ears felt ‘full’ or ‘blocked’. before it resolves. Nevertheless. It is especially appropriate for hyperbaric usually only temporary (hours or days). but in the first dive he did manage to achieve this after he had reached 5 metres. It is Plate 1. more variable in the affected ear. Blood is occasionally seen in the exter. In severe units where specialist otologists are available and cases. conductive deafness involving low frequencies and A specialized otological classification was pre- is the result of haemotympanum. Teed’s observa- Blood or blood-stained fluid may be expelled tions on submariners. is raphy must precede diving. there may be a mild residual pain by diving paramedics.1. to a depth of 5 metres. and it gave way with a ‘hissing out’. as are be felt. grades (1 to 5) is simple enough to be identifiable trauma of descent. middle ear spaces and subsequent Eustachian . be caused by middle ear barotrauma of descent. The foregoing classification was based on It may also result from the Valsalva manoeuvre. with the same result. On the third dive he felt pressure in his ears during descent and again could equalize them only after he had reached the bottom. possibly with crackling or bubbling sounds tions (Table 7. an impractical situa- usually either an oval or crescent-shaped opening tion in the recreational setting at this stage. The reason for the disorder in the middle ears was that they had ‘equalized’ by haemorrhaging and perforation. The grades are shown in trauma of descent results in congestion of the Table 7. near a haemorrhagic tympanic membrane. this time using c­ onsiderable pressure. Daily audiograms revealed a 15-dB loss in this ear throughout the 150. classification is that tympanic membrane photog- Tympanic membrane perforation. After ascent he again noted that his ears felt blocked and he again attempted to equalize them. The right ear had similar features. Lieutenant Commander R. The tympanic membrane appearance of the higher Following a dive that caused middle ear baro. modified by Macfie and from the middle ear during ascent and run into subsequently including a symptomatic grade 0 by the nasopharynx (to be spat out or swallowed) Edmonds – where there is no obvious tympanic or  appear from the nostril on the affected side membrane disorder but a clear description of mid- (­epistaxis). considerable pressure was used in attempted autoinflation.86  Ear barotrauma CASE REPORT 7. fluid in the middle sented by O’Neill and is shown on the back of ear or some dampening effect on the ossicles. grades based on the otoscopic appearance of the Recent overt or sub-clinical middle ear baro- tympanic membrane. He was not able to equalize the p ­ ressure in his middle ears during descent. middle ear cleft (middle ear space and mastoid) Middle ear barotrauma is classified into six and not just the tympanic membrane. Suddenly pain developed in the right ear. On o ­ toscopic examination of the left ear there was a grade III aural barotrauma with a very dark tympanic mem- brane. dle ear discomfort on descent and relief on ascent. fluid may be felt in the middle ear for longer may eventually supersede traditional classifica- periods. but with a large perforation (which caused the hissing sound as air escaped) posterior to the tip of the handle of the malleus.2). Diagnosis: middle ear barotrauma of descent.to 4000-Hz range. The main difficulty with O’Neill’s as it becomes aerated.

tube  blocking. Source: Compiled from Teed. gross haemorrhage or perforation. if the Clinical management consists of the following: middle ear is almost totally full of fluid. ●● Systemic or local decongestants occasionally inflation. Dept. is evidence of a pre-existing or developing A patulous Eustachian tube can also follow infection. of the Eustachian tube opening or the t­ympanic ●● Systemic antibiotics. Macfie and Edmonds. cost of middle or inner ear disease. tests. either descent barotrauma or forceful attempts at and possibly with culture and sensitivity Valsalva techniques (see Chapter 37). of Hyperbaric Medicine. Grade II – Injection plus slight haemorrhage within the substance of the tympanic membrane. Sometimes the Eustachian tube may be nar. but at the ●● Avoiding all pressure changes such as diving. New York Medical College. possi- bly preventing further attempts. Autoinflation becomes progres. rowed and produce a ‘hissing’ sound during auto. Clinical Assistant Professor of Medicine. Medical Director. especially along the handle of the malleus. Grade IV – Free blood in the middle ear as evidenced by blueness and bulging.2  O’Neill’s classification of middle ear barotrauma O’Neill grade Potential intervention/treatment Grade 0 Eustachian tube dysfunction Grade 0 Baseline photograph depicting anatomical Encourage frequest equalization maneuvers on descent appearance of the tympanic membrane Slow/non-linear/controlled descent Symptoms despite no change (injury) from Consider medical therapy on 2 or more failed attempts baseline photo at equalization Grade 1 Barotrauma Grade 1 Erythema increase from baseline Encourage frequest equalization/ Increased fluid or air trapping noted in the Slow/non-linear/controlled descent middle ear space Consider medical therapy Grade 2 Barotrauma Grade 2 Any bleeding noted in the tympanic ENT referral membrane-middle ear space Restrict diving until tympanic membrane returns to Perforation baseline Source: Supplied by Owen J. then there is little problem with further descents. but only where there membrane movement. until resolution.1  Middle ear barotrauma of descent – tympanic membrane grading Grade 0 – Symptoms without signs. Middle ear barotrauma of descent (middle ear squeeze)  87 Table 7. Grade III – Gross haemorrhage within the substance of the tympanic membrane. Grade V – Perforation of the tympanic membrane. O’Neill. Treatment sively more difficult with repeated descents. Grade I – Injection of the tympanic membrane. Phelps Memorial Hospital Center. as opposed to the normal ‘popping’ sound (very rarely). flying and forceful autoinflation techniques. . Alternately. Table 7.

which may be affected indication for such surgical procedures as tym. thus permitting a slow It is important to clearly identify and correct descent and some descent barotrauma with resul- the contributing factors (pathological processes tant congestion of the middle ear orifices of the and autoinflation technique) in each case before tube – which then block on ascent and cause middle diving or flying is resumed. more so than nasopharyngeal sprays. agents and the increased incidence of middle ear With perforation (grade 5). then and management if such a hearing loss is present. when the tympanic tube patency and middle ear pressure changes can . There is rarely an mucosa or middle ear orifice. The reason for this may be that deconges- and managed conservatively. this investigation them to facilitate middle ear autoinflation tech- can aggravate it. difficulties with descent Prevention are less dangerous than with ascent. by otologists as a reason for avoidance of decon- dle ear has been demonstrated during otoscopy. Eustachian ing a Valsalva manoeuvre. a prospective comparison of topical decongestants. if the condition is uncomplicated cations. Diving can be resumed when resolution is The rebound congestion of the mucosa is cited c­ omplete and voluntary autoinflation of the mid. tants are more effective in improving nasal airflow panic membrane may appear normal much ear. the authors of this text rarely b degree of force needed to autoinflate. The ­ arotrauma cases. Autoinflation is best checked by otoscopic It is possible to measure the force or pressure examination of the tympanic membrane dur. by the same pathological process. ear distension and ascent barotrauma (see later). decongestant nasal drops or sprays may margin- Impedance audiometry (tympanometry) may ally improve the patency of the Eustachian tubes. In barotrauma. vide an estimation of the probable ease of pressure Serial audiometric examination should be equalization when diving. If there is a perforation. to verify a tympanic membrane perforation that is Pseudoephedrine may reduce aviation-induced difficult to visualize. will pro- of value (see Chapter 36). unless healing is incomplete or if the both local and general. gestants.88  Ear barotrauma In treating many thousands of middle ear membrane will be seen to move outward. are effective only in the lesion recurs with minimal provocation. be used to follow the middle ear pathological These agents are of value to trainees who can use changes. Prevention of this disorder consists of ensuring practice and instruction in middle ear autoinflation patency of the Eustachian tubes before diving and and the use of correct diving techniques are much appropriate training in autoinflation techniques to more effective than drugs in ensuring Eustachian be used while diving. these drugs did not seem to be of value in prevent- ing middle ear barotrauma. Although the tym. panoplasty. recovery may take barotrauma of ascent encountered with these medi- 1  to 2 months. barotrauma problems to some degree. recovery with the systemic problems of sympathomimetic may take from 1 day up to 2 weeks. Serial audiograms should be performed on The use of decongestants to improve Eustachian all but the most minor cases of middle ear tube patency while diving is to be discouraged. this test is needed niques and improve this skill on land before diving. In most cases. Decongestants. but the diving clinician is also concerned If there is no perforation (grades 0 to 4). necessary to open the Eustachian tubes. recurrent perforation frequently results from the Eustachian tube than in influencing the tubal premature return to diving. Occasionally. From the safety aspect. and thereby affecting the pharyngeal cushions of lier. and the use decongestants or antibiotics. tube patency and reducing barotrauma. marginally obstructed tube. and especially in the novice diver. undertaken to exclude any hearing loss and to assist If either tympanic membrane appears to move in other diagnoses (especially inner ear barotrauma) sluggishly or if much force is necessary. Investigations are degree of movement of the ear drum.

proteolytic or allegedly mucus-softening enzymes the diver may employ autoinflation after each to be of value. stretches the pharyngeal muscles and puts This allows for air to move more slowly into the the offending tube in a more vertical position. See Chapter 36 for more Correct middle ear autoinflation for divers: information. use of these ear plugs does not the allergens (e. they would breath during descent. immediately before descent. 1. plastic.g. external ear space during pressurization (descent) thus capitalizing on the pressure gradient of in a chamber.e. the clinic – the following errors are commonly ●● Autoinflate the middle ear on the surface encountered. ‘equalizing ahead of the dive’ When dealing with divers who have not ade. because of the external ear obstruc- After an upper respiratory tract infection tion. Thus. other than the effect on the tym- be advised of the dangers of delaying middle panic membrane. will concentrate on his or her s­ truggle waiting at depth. Divers barotrauma may be slower in developing. The use of these ‘hyperbaric plugs’ will delay 3. Diving with problems that cause Eustachian the inward distortion of the tympanic membrane tube obstruction. and the sary before diving is resumed safely. to equalize. This indicates a negative middle ear p ­ ressure.e. ears. ●● Do not descend if pressure is felt on Commonly the novice diver. ●● Practice and ensure reliable middle ear quately autoinflated their middle ears during autoinflation on land. instead of the ears. There are repeated promotions of ear plugs to 2 . both divers and aviators. Not autoinflating early enough. consider descent – despite the ability to perform this in diving. Alternately. Abort the dive. the discomfort and pain of the ‘nega- has cleared. Only then. reduce the symptoms of middle ear barotrauma in zontal or. even worse. until the sensation of pressure is felt. avoid dairy products for change the pathological features of middle ear 12 to 24 hours before diving). these ear plugs are employed is as follows: A small able to tilt that ear toward the surface while malleable. Open water diving. to descend and will often be 2 to 3 metres ●● Do not dive if you have upper respiratory underwater before remembering to clear the disorders. Middle ear barotrauma of descent (middle ear squeeze)  89 be measured if specialized impedance audiometers are employed clinically. This manoeuvre is fitted with an airtight seal into the external ear. Divers should barotrauma. drugs or allergies. such as cigarette smoke. it is advis. Attempting to autoinflate while in the hori. another week or two is neces. Thus. tive’ pressure in the middle ear are less. ­waiting Use a descent line. compressible and porous plug attempting autoinflation. such as mucosal conges. outward. disrupts control of the descent and thus con. (being pulled into the middle ear) given that the tion from such factors as infections. who have an allergic diathesis should avoid Nevertheless. HYPERBARIC EAR PLUGS tributes to this barotrauma. irritants membrane tends to move in the opposite direction. head-down position. i. the water. This situation is referred to as ‘equalizing behind the dive (­ exposure)’ and is overcome by autoinflating on the surface before descent Some physicians have claimed the use of local and with each metre of descent. ­performing a Valsalva manoeuvre before ●● Do not use multiple ascents (yo-yo) or descent. i. and the inner ear all remain (being dependent . The principle on which If only one ear causes difficulty. have the same complications as decongestants. the oval and round windows in achieving it. ●● Autoinflate with the head upright. the damage to the mid- ear a­ utoinflation and of using excessive force dle ear mucosa. ●● Autoinflate every 1 metre of descent. Even if they did work. without use of a descent line or anchor line.

Most amateur divers need the production of mild external ear barotrauma to use an active technique. and myringotomy is often required. 100 cm H2O. the same effect on the flate the middle ear actively. As the candidate autoinflates the external ear have been used in the false belief that middle ear. the middle ear and the nasopharynx. ber). move. closing the mouth and exhaling so that the chambers. reflects light (either the membrane flaccida or the Gadgets that connect the oral cavity with the circumference). The only TECHNIQUES thing that has really changed is that the symp- tom of pain with middle ear barotrauma has been Passive opening of the Eustachian tubes is the lessened. although it toms of middle ear barotrauma are as follows: is not always possible. in which case ably reliable in predicting which candidates will the diver should not be diving. . This is achieved by using middle ear without inducing external ear baro. possible aggravation of during descent. the persistence of pathological fea. tympanostomy The Valsalva manoeuvre is probably the most tubes can be inserted. In each case.e. diving. If repeated that interfere with the application of this new skill. and vertigo from unequal middle ear Sometimes reluctant trainees use the failure to pressures when the plugs are not inserted equally autoinflate ears as an acceptable excuse to avoid into both sides. practice of the are required for hyperbaric exposure in patients ­technique is recommended on land. under their voluntary of descent. easily understood. It involves occluding the nos- As an alternative for divers in recompression trils. slow the barotrauma ter is employed either by focusing on the light reflex disorder as described earlier and increase the pos. recommended. ideal and natural way to equalize pressure between The potential costs of reducing the symp. before subject- who are comatose or who have a tracheostomy ing the novice to hyperbaric and aquatic conditions or orotracheal or nasotracheal tubes. Different candidates perform them Professor Joe Farmer stated that myringotomies with varied ease. while the examiner is observing the tympanic mem- ‘Diving’ ear plugs. passive equaliza- ascent barotraumas affecting the ear because of tion of ear pressures is more common. in which a restricted opening brane and its movement with an otoscope. This could happen only if there is diving tympanometry (see Chapter 36) are reason- a tympanic membrane perforation. an alternative to myringotomy in conscious separates the cushions of the Eustachian tube and patients is to have repeated pauses or a very slow forces air up this tube into the middle ear. The lat- replaces the ceramic filter. middle ear barotrauma is particularly fre. However. It is part of the routine diving medical examina- An alternative to the hyperbaric ear plugs is to tion to ensure that the diving candidate can autoin- pressurize more slowly (i. who should need only one such treat. equate autoinflation and diving technique. accepting slower barotrauma and giving pressure required to achieve this is usually 20 to more opportunity for autoinflation. During ascent. and active the disorder induced in the middle ear during techniques are rarely needed. descent. many divers fail because of an inad- hyperbaric treatment (in a recompression cham. or on another part of the tympanic membrane that sibility of ascent barotrauma. a positive pressure manoeuvre described to the diver trauma to achieve it).90  Ear barotrauma on the pressure gradient between the middle ear MIDDLE EAR AUTOINFLATION space and its surrounding body tissues). treatments are considered likely. pressure in the nasopharynx is increased. have trouble resulting from Eustachian tube disor- In patients who are unconscious and need ders. This ment. Other times they are scared to use suffi- It is doubtful that the masking of middle cient nasopharyngeal pressure for fear of causing ear  disease by reducing the symptoms is a wise damage. the tympanic membrane moves outward. which will inflate the middle ears and tures of ear barotrauma affecting the middle ear prevent the pain and discomfort of barotrauma mucosa and inner ear. they overcome the effect of impaired middle ear Investigations using otoscopy and modified autoinflation. The following techniques for autoinflation  are quent. The descent. control.

In the performed on divers indicate that they do not . it is more likely from the middle ear on that side. This is not a sensible way to equalize the middle ear. You may wish to assist the slow ear by pointing it toward the surface as you equalize the middle ear. drawn-out sound. correct middle ear equaliza- tion (‘ahead of the dive’) may well fix both. 3. I descend a bit slower than my buddies. Client: One ear equalizes before the other. Answer: If you have any difficulty with middle ear equalization. Answer: Why? If you are not equalizing the middle ear promptly or sufficiently. then employing techniques that result in relatively negative middle ear pressures. Or. It is not a long. Answer: Although the blood may be from your sinus. In the horizontal Valsalva to increase intrathoracic pressure. following expansion of air with ascent. Remember bubbles? They rise. By the second dive. See earlier. Answer: This suggests a narrowed Eustachian tube. Eustachian tube obstruction and other disorders that may be temporary or permanent. Answer: You have probably produced some middle ear congestion (barotrauma) in the first dive but continued the dive. possibly from inadequate middle ear equaliza- tion and barotrauma. Valsalva technique. Air travels more easily up than down in the water. cause middle ear congestion and Eustachian tube blockage. and so middle ear equalization is more difficult. Answer: Not a problem. Client: When I dive and equalize the middle ear. I hear a squeaking sound in my ear. In either case. Answer: It is likely that the ‘water’ is really fluid in your middle ear from barotrauma. Client: I sometimes have a bit of blood from my nostril (or in my throat). you start off with significant middle ear con- gestion. Middle ear autoinflation techniques  91 Middle ear equalization answers to clients’ problems Client: 1. Descend feet first and you can blow air up the Eustachian tube. I may ascend until the ear clears (yo-yo technique). without problems. 2. vertical position and in the ified from that employed originally by Antonio horizontal ‘ear-up’ position. I halt my descent and wait a bit. then these proce- dures merely allow the middle ear to fill with blood or tissue fluids and thus allow further descent with less pain or discomfort. I use alcohol ear drops to dry them out. novice divers average 40  cm The Valsalva manoeuvre used by divers is mod- H2O in the head-up. Client: I have middle ear equalization problems when I swim down the shot line. It results in middle ear congestion. Trials ‘­ear-down’ position they need 50 cm H2O. Client: I can often dive once. crackling) after the dive. If there is any pressure. The sound you should hear when you equalize the middle ear and the ear drum moves outward is a click or pop. Client: I am trying to use swallowing to equalize the middle ear. The force necessary for successful autoinflation vertical. but cannot equalize the middle ear on other dives. Use the positive pressure Valsalva technique (or Lowry or Edmonds techniques) before and during descents. Or. Using the about 60 cm H2O. See earlier. Answer: This requires greater force to autoinflate the middle ear because you are trying to force air down the Eustachian tube. Client: If there is any water in my ears (fullness. It takes a split second to achieve. It is normal. swimming-down position they average will vary with the diver’s body position.

It is also of value during descent when BTV are not usually successful. then the sure in the middle ear with the Toynbee manoeuvre candidate is advised to repeat the most effective may be negative (less than environmental). If there is any pharynx and the middle ear. usual with divers. pulmonary and otological The Edmonds number 2 technique is to barotrauma. the Valsalva manoeuvre nasopharyngeal opening of the Eustachian tube. sometimes called the béance tubaire voluntaire or mouth and glottis are closed. Lowry. Pressure of less than 10 cm H2O cular skill. com. Here the diver is asked As divers become more experienced. Thus. with the mouth and nose closed. (similar to the start of a yawn) so that the lower With the latter. the nostrils. foramen ovale) thus increasing the possibility of Soft palate contraction is a technique whereby paradoxical gas embolism with diving.92  Ear barotrauma produce the prolonged high thoracic pressures by rocking the lower jaw forward and downward often encouraged by cardio-thoracic physiologists. followed by the Toynbee. hypertension and hypotension. Despite the rather con. of the Toynbee and Valsalva techniques. lifting the soft palate she moves the back of the tongue downward. This involves occlusion of the best technique. and the diver can ver- middle ear without pressurizing the nasopharynx. venous haemorrhages. occlud- mouth and nose. they tend to identify the uvula hanging down from the pos- to use such techniques as jaw movements. is tried first. A combination of techniques has also been pro. An interesting variation of the BTV is may accompany this manoeuvre. difficulty remaining with equalization. determined by hearing both ears click. swallowing. the nose. swallow Some techniques (Valsalva. but this is not technique is extremely valuable in resistant cases. procedure a few times a day and achieve success. and the elevated BTV. arterial and time. The autoinflation. It is upward (‘lifting the Adam’s apple’). have developed this mus- Eustachian tube. the problems induced by prolonged teeth project well in advance of the upper teeth and high Valsalva pressures include cardiac arrhyth. during otoscopy. mouth then suck your cheeks in. then raising it as he or mencing a yawn. then a swallowing movement that is The major problem is not the danger of middle ear made continuous with a Valsalva manoeuvre. and it is of value When examining potential divers. have the disadvantage of a transitory pressure fusing (and impossible to achieve) instruction. This and so forth. over the years. advantage of distending the middle ear and thus The Edmonds technique is rather similar and allow further descent without the problems of involves the opening of the Eustachian cushions a negative middle ear pressure developing and . In the author’s movement of the Eustachian cushions produces a practice. demonstrate either the Frenzel technique or the ing ascent. Thus. The Frenzel manoeuvre involves closing the thereby moving the Eustachian cushions. performing the Valsalva manoeuvre at the same mias. and then tion of the pressure within this space. Edmonds) and blow at the same time’. before com- posed. diver is thus advised to ‘hold your nose. the final pres. the Lowry with an equalization of pressures between the naso. gastric reflux. opening the contracting the muscles of the mouth and pharynx Eustachian tube and forcing air up the tube. but the dangers of not autoinflating. known Academic arguments abound as to which is as the Lowry technique. A very successful one is the combination mencing diving. stress incontinence and advise the diver to ‘block your nose. close your the possible shunting of blood through right-to. both externally and internally ing the nasopharynx and causing minimal eleva- (this is achieved by closing of the glottis). the diver contracts and raises the soft palate. ify it by hearing his or her own humming sounds The Toynbee manoeuvre involves swallowing reverberate in the ears. the Roydhouse technique. then puff them left vascular shunts (atrial septal defects and patent out – quickly’. which allow for equalization of the opens the Eustachian tubes. and then the Edmonds techniques. Whichever works is the best. the that may extend into the thorax. on land. and it is usually employed by experienced tongue can be used as a piston to compress the air divers who have relatively patent Eustachian tubes trapped in the nasopharynx and force it up the and who. These techniques have the It is easily learned with practice. terior of the hard palate. attempts to in relieving the overpressure in the middle ear dur.

and so experience vertigo following the be more effective in reducing descent than ascent ascent. but sometimes mild. During ascent. middle ear their middle ears who have been referred to the barotrauma of descent and/or the use of nasal authors of this text have suffered more from inad. symptoms may aggravate this condition. subse- one or both ears. but it is inadequate for diving assessment ing ascent and/or perforation of the tympanic because it fails to demonstrate the procedure membrane. the middle ear opens passively. To ascertain the extent of this the Eustachian tube. Also. can ing from increased middle ear pressure difference often descend to great depths before they need (alternobaric vertigo). When the pressures in both Toynbee. nasopharyngoscope. . Eustachian tube. may reach the surface while still having an asym- sal membranes and do improve nasal air flow. their effect on the Eustachian tube is greater at the or residual damage from excessive middle ear nasopharyngeal orifice. Most cases of vertigo from middle ear baro- Some otologists have recommended the use of trauma of ascent are mild. ally more serious than middle ear barotrauma of tion. Wave safety. ear damage. i. Occasionally. who have mobile tympanic affected ear (reverse squeeze) or vertigo result- membranes. it is usu- if there is easy and frequent middle ear autoinfla. Because it may prevent ascent. the stimulus to vertigo ceases. They also tions coexist. Middle ear barotrauma of ascent (reverse squeeze. They either equalize the pressures passively descent. severe pain dur- ease. Eustachian tube obstruction. It tends tympanogram (see Chapter 36) and examina. that is required. expanding with Other techniques (Toynbee. alternobaric vertigo)  93 producing middle ear congestion and Eustachian MIDDLE EAR BAROTRAUMA OF tube obstruction. autoinflate their ears by using less pressure. may include sensations of pressure or pain in the Experienced divers. These techniques are therefore ASCENT (REVERSE SQUEEZE. This instrument been instances of temporary or permanent inner is certainly of value in assessing middle ear dis. nounced in the horizontal position. In each case the common factor equate diver instruction than from Eustachian is probably congestion and therefore blockage of tube obstruction. voluntary autoinflation of the The vertigo is most pronounced when the diver middle ear. and there have tympanic membrane movement. which may force open the less patent Autoinflation was successful using the Valsalva. Middle ear barotrauma of ascent usually fol- Most patients with an inability to autoinflate lows recent. The spinning ing middle ear autoinflation include the modified is toward the ear with the higher pressure. Other divers Decongestants probably do work on the muco. these drugs may pressure. BTV) are effective ascent. quent opening of the tube is easier. which allows an uncomplicated return to or produce negative middle ear pressures. gases within the middle ear. better for novice divers and for those who have ALTERNOBARIC VERTIGO) trouble with middle ear autoinflation. but metry of pressure within the middle ear cavities. with 4 per cent unsuccessful in sure. This is not always so. however. and these techniques If the Eustachian tube restricts release. Lowry or Edmonds technique in 96 per middle ears are equalized with the ambient pres- cent of subjects. resembling small spinnakers. seventh nerve palsy. middle ear barotrauma. problem.e. action or descent can also cause a negative mid. dle ear pressure with resultant congestion and with a pressure gradient of less than 50 cm H2O. decongestants. Thus. these condi- to equalize their middle ear pressures. lasting seconds or min- the pneumatic otoscope to demonstrate passive utes. to develop when the middle ear pressures differ by tion of the Eustachian cushions with a fibre optic 60 cm H2O or more. 200 consecutive otoscopic examinations The mild vertigo is often rectified by further were recorded on potential diving candidates. ascent. assumes the vertical position and is least pro- Other investigations of more value in assess. They also assist in equalizing sinus pressures and avoiding This disorder is caused by distension of enclosed sinus barotraumas.

immediately follow the dive. and decongestants are sometimes rec.94  Ear barotrauma Otoscopic examination often reveals evidence they have other disadvantages. nounced around the circumference of the tympanic Prevention is best achieved by avoiding nasal membrane than along the handle of the malleus. Occasionally. jaw movements or per. the use of oxygen inhalation or mini. flation of middle ear. use the tech- nerve palsy is another possible complication. if present. middle ear equalization techniques during descent Hearing loss in the affected ear. exercise. Vertigo is often increased with Usually. This testing is not generally required. the diver may be able to take reme. A short descent may relieve symptoms comfort or danger if the diver’s ascent is restricted and allow middle ear equalization. diver to descend with marginal improvement in Congestion of blood vessels is common but is less Eustachian tube patency and inadequate autoin- than with descent barotrauma. particular care should be taken to ear barotrauma with sensorineural hearing loss is ensure that if it does recur the diver will always a possible complication (see Chapter 37). Usually. . Equalization INNER EAR BAROTRAUMA may be easier if the affected ear is facing the sea bed. Seventh have adequate air to descend briefly. permitting the of tympanic membrane injection or haemorrhage. ●● Structural abnormalities that make the divers and if the middle ear is still distended. ing on it and thus exerting external pressure on the water column in the external ear). Inner experienced. especially topical ones. descent. the Valsalva technique. The tym. neither type of drugs is needed. Vestibular function has been tested experimen- forming a Toynbee manoeuvre (see earlier) will tally during pressure changes in a recompression relieve the discomfort. ●● Subsequent application of excessive force to vention of future episodes is addressed. most effects are short-lived. Only cochlear injury occurs in 40 per cent. Unless descent barotrauma is pre- be conductive and follow damage to the tympanic vented. ommended to improve Eustachian tube patency. Otherwise. membrane or the middle ear structures. nausea and vomiting. Rarely the diver is seen soon after the event. It is more pro. by symptoms. may (see earlier). ment should consist of prohibition of diving until ●● Previous difficulty in equalizing middle ear clinical resolution has occurred. niques described earlier and then gradually ascend. procedures described earlier may be satisfactory. Tinnitus is a common infection. as may sudden pressure chamber. they have the opposite effect. the first aid susceptible to this damage. unless Combined cochlear and vestibular injury is they prevent a causal middle ear barotrauma of ­experienced in 50 per cent. thereby using the pressure gradient along the Overview now vertical Eustachian tube. are rarely of use in preventing this disorder. and treat. nal ear with the tragus or middle lobe. but Only vestibular injury occurs in 10 per cent. Once middle ear barotrauma of ascent has been panic membrane may rupture occasionally. then push. Decongestants. sensorineural hearing loss may mal recompression is effective. to replicate the sequence of events and applied to the external ear (by occluding the exter. altitude changes and head movements. There is always the possibility of inner ear damage Treatment in divers who have any of the following: Fortunately. or it may develop over Antibiotics are used if there is evidence of the next few hours or days. Some patients may complain of vertigo. In these cases. verify the aetiology and diagnosis (see Chapter 38). normal hearing pressures. For first aid. ascent barotrauma is likely to recur. ●● A history of ear barotrauma of any type. Systemic decongestants are more effective. achieve this equalization. and vestibular function are demonstrated and pre. A low-on-air situation could cause extreme dis- dial action. decongestants and by training the diver in ­correct The tympanic membrane may appear to be bulging. association.

10 per cent.5  Diagrammatic representation of the ear anatomy. An dive. 10 per spontaneously or may be caused by trauma. espe- cent ascent). cially with head injury. Inner ear damage is also reported in aviators and flight In the event of otological barotrauma. see Chapter 35 (Figure 7. brane rupture within the labyrinth. cent and inner ear barotrauma occurred in 12 per cholesteatoma or any sudden increase in intra- cent. It can develop middle ear barotrauma (88 per cent descent. In the eventful dive. 98 per cent experienced cranial or labyrinthine pressure. 10 per cent Perilymph fistulae from the labyrinthine win- were in free divers. hearing loss. most occurred in experienced divers. treated conservatively. 80 per cent. For anatomi- cal background. the disorder may aviation middle ear barotrauma occurred in 24 per be related to congenital syphilis. The perilymph leak is inner ear barotrauma. The incidence of symptoms was as fol. This disorder Pathophysiology has been reported from dives as shallow as 2 metres and has been observed in a surfer who dived under a Middle ear barotrauma is the most common cause wave. but most divers were der in some patients. straining. ear. nose and throat disease was dows are now well recognized and result in a leak- present beforehand in 48 per cent. a sen- attendants. variable in volume and may come from the round window (most often). In general medical practice. Animal experiments reproduce the pathologi. Both conservative and surgical treatments spinal fluid (CSF) is sufficient to induce this disor- had a two thirds success rate. 38 per cent. Various inner ear cal features with equivalent depths of 1 to 6 metres. and dysacusis. . space. 86 per cent. tinnitus A perilymph fistula is a common pathological or demonstrable vestibular damage implies entity of inner ear disease. of the ossicular chain can cause an oval window Incus Fluid in External Oval window inner ear ear Stapes Malleus Ear drum Air in middle ear Round window Cochlear duct Eustachian tube Figure 7.5). Inner ear barotrauma  95 There may be no otoscopic signs. other infections. weight lifting and physical lows: tinnitus. disorders have been demonstrated. previous diving age of perilymph into the mastoid or middle ear middle ear barotrauma occurred in 62 per cent. and 38 per cent had symptoms within some increased pressure of 120 mm H2O in the cerebro- hours. Tinnitus and vertigo often Any procedure that involves manipulation responded to early treatment. sorineural or combined hearing loss. duced can be transmitted into the inner ear by the Sixty two per cent noted symptoms during the cochlea and possibly the vestibular aqueducts. of inner ear damage in diving. the oval window or a mem- In a series of 50 cases of inner ear barotrauma. The intracranial pressure wave so pro- vertigo.

This can cochlear aqueduct during the Valsalva manoeu. the inner ear. be very rapidly returned to its normal position. neural hearing loss in 83 per cent. If the middle ear pressure is poral bones after inner ear barotrauma. vre and ‘blowing out’ the round window into the middle ear. develop at any stage of the dive or afterward. mainly ­perilymph. the less likely it is to sustain perma. The aque- duct constricts with age. develop in water as shallow as 1. experimental or clinical support. thereby rupturing the round win- The initial presentations with verified peri. The loss trauma. The more quickly the ear replenishes its logical processes for the inner ear damage. and End artery spasm. thrombosis and gas or lipid this includes ear barotrauma of diving or aviation embolism are aetiological proposals that have little exposure. If at this stage a Other anomalies or malformations are sometimes forceful Valsalva manoeuvre is performed. These anomalies may be detected on through the helicotrema. may not be sufficiently rapid to avoid damage to A progressive sensorineural loss or vertigo that the inner ear structures that results in haemor. but they are not so amenable Exposure to environmental pressure change to treatment. as a result.96  Ear barotrauma perilymphatic fistula. labyrinthine window ruptures. haemorrhage and acoustic the low or middle frequencies are affected. autopsy. tures are common. These anomalies may be detected dle ear cleft that causes the tympanic membrane to by high-resolution CT scans. may indicate an occasional association brane moves inward because of the pressure gradi. and this may explain why Many of these divers develop the first symptoms children are more susceptible. tinnitus in 63 per cent and aural fullness in orrhages and internal inner ear membrane rup- 25 per cent. has been demonstrated. dow membrane bulges outward. the mitting the entry of air into the cochlea and causing relative endolymph hydrops (similar to Ménière’s sensorineural hearing loss. scious patients and guinea pigs. there is detected that may indicate a predilection for inner a sudden increase in the pressure within the mid.3 metres. after the completion of the dive while performing . develops hours or days after a barotrauma incident rhages or rupture of the round window membrane. thus indicating The hearing may fluctuate. high-resolution computed tomography (CT) scans. The prognosis is better when only membrane ruptures. This causes a displacement of perilymph munication. disease) and the possible electrolyte imbalances Increasing the CSF pressures by 120 to 300 mm Hg affect the dynamics of the hearing and vestibular can also transmit pressure through the cochlear systems. with enlarged vestibular and/or cochlear aque- ent. vertigo in 77 per It is likely that cochlear and vestibular haem- cent. and this disorder occurs in Inner ear barotrauma has occurred in uncon- up to 7 per cent of patients after stapedectomy. is most likely the result of a fistula of the round The other explanation involves a pressure window with leakage of the perilymph into the wave transmitted from the CSF through a patent middle ear and/or air into the perilymph. the A tear of Reissner’s membrane results in an stapes to move outward and the round window to isolated loss in one or two frequencies (tested In be pushed inward. Stretching of the round window. depending on the that a forceful Valsalva manoeuvre is not a neces- replacement of perilymph. so that the round win. and the damage may become permanent aqueduct and increase the perilymph pressure in if it is not corrected. or at not equalized during descent. the tympanic mem. ear barotrauma. thus per- of pressure within the perilymphatic system. This has been demonstrated in animal Symptoms experiments. or hearing loss may sary prerequisite. progress slowly or suddenly as the perilymph Animal experiments suggest multiple patho- leaks out. Rupture of the round window membrane can lymph fistulae are sudden or fluctuating sensori. The reversed flow of perilymph 100-Hz increments between 400 and 1300 Hz). the foot plate of the stapes is pushed ducts that allows for a greater CSF-perilymph com- inward. intralabyrinthine nent  damage. dow. with a rise of CSF pressure. is possibly one of the most common causes. There are two postulated mechanisms for this Post-mortem histological examination of tem- disorder in diving.

This fistula is more Investigations likely in divers who have had surgical treatment of otosclerosis.g. ●● Tinnitus of variable duration. incidents. Unfortunately. Inner ear barotrauma  97 energetic tasks. the symptoms up to 8000 Hz (with bone conduction if the loss may progressively diminish as adaptation occurs. Caloric testing is indicated only order may progress to destruction of the vestibular if the tympanic membrane is intact or if the tech- system. ●● Clinical features of an associated middle toms may indicate perilymph fistula. serial The symptoms of inner ear barotrauma may investigations may be necessary. often with a severe vestibular lesion that may persist until surgical repair. the perilymph. immediately and fully investigated by serial mea- In the cases that initially. as a result of exertion. lymph fistulae. e. vertigo may persist or recur nique guards against pressure or fluid transmis- while the fistula persists or recurs. Meningitis is a possible complication of peri- frequency hearing loss that resolves over the subse. over hours or days. based on the foregoing c­ riteria. Aural fullness and hyper. tinnitus and hearing loss should be vary from almost unnoticeable to incapacitating. Cochlear injury is permanent in more than half cede or overshadow the delayed and progressive the cases. of cochlear or vestibular trauma. Persistence of vestibular symp. is in the <4000 Hz range) and positional electro- Even though the symptoms may diminish. frequent in patients with inner ear haemorrhages. Impairment of speech discrimination may pre. In other cases. quent 1 to 3 weeks and may be mistakenly interpreted as a therapeutic success. temporary. Progressive deterioration of sensorineural ●● Vestibular disturbances such as nausea. Bone conduction audio- Inner ear barotrauma is suspected in the pres- grams are indicated to identify this condition. To demonstrate inner ear barotrauma. tinnitus. vomiting and ataxia. ear barotrauma (with or without conduc- Deafness is of the sensorineural type. haemorrhage and lymph or increased leakage into the middle ear. vertigo. sion into the middle ear. perilymph fistula. probably caused by dam- age from the stapes foot plate. tus and the hearing loss. predominantly or surements of clinical function. . Any combina- include those of vestibular origin such as vertigo. hyperacusis. The subsequent fistula follows a rise ●● Sensation of blockage or fluid in of pressure in the CSF. vertigo. which further aggravate both the tinni- acusis are described. is frequent. pulling up the anchor. It also may be variable and altered by changing head positions. If  left untreated. the sensorineural hearing loss is by no means certain. This may be because the middle ear (including the Symptoms associated with inner ear baro- round window) has been damaged by the earlier trauma may include the following: barotrauma. have been observed. either tive hearing loss). perilymph fistula. the dis. the diver is more predisposed to similar water sound. nau- nausea. There is often an associated conductive or lower. Vestibular symptoms sea. with a roaring. Sudden tinnitus and hearing loss may be more ●● High-frequency or total hearing loss. whereas vestibular symptoms are usually hearing loss. popping or running enced. daily audiometry solely involve vestibular function. hearing. disorientation and loss and position-induced hearing loss indicate a ataxia. Once inner ear barotrauma has been experi- Tinnitus. nystagmography. ence of hearing loss. the clinical differential diagnosis possibly because of the buoyancy of air in the peri. vertigo or ataxia. Oval window fistulae. tion of middle ear barotrauma symptoms. fluctuating hearing vomiting. a total loss (all frequencies) or a selectively high- frequency loss (4000 to 8000 Hz). may become total and/or permanent. the cochlear aqueduct and the affected ear.

with severe hear- tory of antecedent trauma is vague or remote. blowing. required before vestibular symptoms are attributed 4. loud sounds 30 degrees and careful monitoring of otologi- of low frequency. is positional pure tone audiom. In diagnosing ­perilymph fistulas. Tullio attempted. given irrespective of which of the other treat- Other investigations are sometimes thought ment procedures are followed. there is progressive deterioration in hearing. coughing. to be even more sensitive than the basic electro. some clinicians recommend ear cies when the patient lies supine. acuity. fast move- ear uppermost. to allow the associated middle Investigations that may be of value include tem. This is a judgement call without have not been particularly helpful in diagnosis or a great deal of experimental evidence to assist. is the haemorrhages to resolve. 48 hours in cases of severe hearing loss. to Kohut suggested that the presence of Hennebert’s allow the inner ear membranes to heal and sign. improvement with bed rest. In patients A  perilymphatic fistula test or elevated SP/AP with developing hearing loss. or its equivalent the Tullio phenomenon. sexual etry. This instruction is pressure. for 30 minutes. but 5. Loud noises should improves more than 10 dB in at least two frequen. sneezing. nose inner ear damage. Otherwise. but this may be at the poral bone polytomography and high-resolution expense of more permanent sensorineural and contrast imaging techniques. 40 per cent had improvement. Avoid any increase in CSF pressure. Treatment should be initiated promptly. such as perilymphatic fistula. round window may not withstand the pres- In patients with perilymph fistula. straining with defecation. treatment of diving induced perilymph fistulae. vestibulo-spinal response (body sway) operative intervention should be considered. ment has ceased and for a week or more. It may stop vertigo and may reduce There is no agreed upon diagnostic test with tinnitus. both of which may be disabling. With hearing loss. pneumatic otoscopy or tympanometry). almost as a Hennebert showed that an increase in pressure in matter of habit. In a enough sensitivity and specificity to identify the survey of 197 cases of presumed perilymphatic presence or absence of perilymph fistula reliably. ear pressure changes. fistula (not necessarily related to diving). and the hearing ment or physical exertion. It may be delayed for 1 to 2 weeks in less nomenon) and electrocochleography. lifting weights. as opposed to other causes of from the Valsalva manoeuvre. perform middle ear autoinflation. Objective test. reactions to stress (Hennebert’s or the Tullio phe. induced by any activity that increases the pressure 2. turography. Divers very commonly placed from the perilymph-leaking windows. Bed rest should continue until all improve- nystagmogram. the vertigo is sure wave.98  Ear barotrauma A test proposed to support the diagnosis of 1. The theoretical plugs or other devices to reduce the external explanation for this improvement is that air is dis. ear disorder to heal. or if gated to verify this disorder include dynamic pos. Fitzgerald reported that 87 per cent of patients Treatment with vestibular symptoms had complete or nearly complete relief. Other tests being investi. 3. severe cases. the already damaged described a similar response with loud sounds. The patient lies horizontal with the affected activity. If a fistula is . Until now they hearing loss. tragus cal changes are indicated. If there is no improvement within 24 to to a perilymph fistula. ing loss or incapacitating vertigo. repair to the ratio (cochlear summating potential and auditory round or oval window will prevent the further nerve action potential) on electrocochleography leakage of perilymph and has proved curative significantly raises the likelihood of perilymphatic in some cases. Almost total bed rest with the head elevated to in the ear canal (ascent and/or descent. Reconstructive micro-aural surgery is their discrimination is improving. Advise the patient that under the ear canal could produce nystagmus in patients no ­circumstances should autoinflation be who were known to have perilymph leakage. sometimes restoring hearing fistula. indicated when there is deterioration or no ing becomes especially important when the  his. the Valsalva manoeuvre. be avoided.

Vasodilators (e. subsequently. Vertigo is usually suppressed by cerebral inhibition within a few weeks. the disorder. The other vestibular stimulation (caloric or alter. possibly the effect of repair or death of to show any favourable effect. For most cases. Treatment of vertigo is based on routine med. Smart. be of value in other forms of sudden hearing which was employed in most cases in earlier loss. because of alternobaric vertigo. Others employ tech. if the middle ear is autoinflated with but especially those precipitated by minimal descent. is of value. Inner ear barotrauma  99 not visualized during middle ear exploration. ing to the conservative treatment regimen for The authors of this text would advise against 4 to 6 hours a day for 3 days. as a cause of He or she may continue to have occasional vertigo. Prognosis ical principles. but After inner ear barotrauma there may be an may be precipitated by sudden movement or apparent complete cure or persisting residue. has yet to be quantified. with or without steroids. tinnitus or vestibular asymmetry persists. leakage more obvious. and so it warrants fur- a graft should still be applied to the window ther consideration and investigation. If medical evacuation by air is required. the authors then a hazard in all occupations that involve bal- sometimes add 100 per cent oxygen breath. Middle ear surgical exploration is not has the potential to aggravate the fistula and indicated in cases of inner ear haemorrhage increase the perilymph flow into the middle because it is not a harmless procedure.g. is rarely needed now if conservative this text have tried it in patients with inner treatment is given conscientiously. the patient will never be able to this type of hearing loss. Aspirin is to be damaged sensory endings. In these ground level is necessary. which is relatively harmless procedure. to this disorder in divers is given by Elliott and The same applies if permanent hearing loss. It may persist if the fistula remains ing) may improve for a few weeks. the gas expansion removes middle provocation and in patients who have poor ear fluid on ascent. . Hyperbaric oxygen therapy has been used baric vertigo. for the Valsalva manoeuvre. it is prudent to advise against any further An excellent review of the various approaches hyperbaric (scuba or free diving) exposure. ance. Hyperbaric oxygen therapy ing. 7. generalized hearing loss. It has been 6. it will rarely improve hear. remaining high-frequency loss is usually perma- 8. dive or fly safely. and in ear during descent – both from the relatively rare cases it can induce further or complete negative middle ear pressures and the need hearing loss. but little evidence exists 12 months. of middle ear barotrauma with conductive tula. If the vestibular system is damaged and asym- Steroids have no verified place in treatment of metry persists. Hyperbaric oxygen therapy may niques to increase the CSF pressure. Prohibition of diving and flying is essential for responsible for apparent ‘cures’ in some cases the first few weeks following a perilymph fis. After ear barotrauma. nicotinic nent. and then the patent. The authors of years. exposure to heights or driving. Other regimens. cases. cochlear acuity (especially lower-frequency hear- nobaric). but had to proceed to surgery 2 weeks’ delay. acid. As a aggravated by sudden head movement. misdiagnosed and an aircraft with the cabin pressurized to reported as inner ear barotrauma. no reason to believe that recompression ther- Some surgeons use colour dyes to make the apy per se. employing air or normoxic gases. avoided because of its anticoagulant effects. which has followed some cases of and recommended by some experienced unilateral inner ear damage. to be aggravated by the influence of ageing. 9. Surgery. hyperbaric therapists. carbogen) have been recommended by Tinnitus often improves over the next 6 to some investigators. There is because sometimes the fistula is intermittent. piloting aircraft because of the danger of alterno- 10. Eustachian tube function or nasal disease. Air entry into the perilymph.

. with a sensorineural pattern in both ears. Diagnosis: inner ear barotrauma (with perilymph fistula of the round window) caused by middle ear barotrauma of descent and forceful autoinflation. Seventh nerve palsy Both physicians and otologists frequently omit to interrogate patients with Bell’s palsy regarding The seventh or facial cranial nerve may be affected. resulting in sensorineural hearing loss. It manifests as a unilat- eral facial weakness similar to Bell’s palsy. and it Although not frequent.2 This diver. impossible. of fluid and blood in the mastoid. He continued to dive despite the pain and performed forceful autoinflations. over the next few days. paralysis of the stapedius muscle. otitis media is an occa- tends to recur in the same patient if the cause is sional complication of middle ear barotrauma. especially during CASE REPORT 7. anatomy of the facial canal. Also. Thus. This not only is a during ascent and could force its way into this serious illness in its own right. who had been exposed to gunfire in the past. diving and aviation exposure. being part of the middle ear cleft. The diver became progressively more deaf. as may impaired taste in the anterior part tion of diving – either free or with equipment  – of the tongue on the same side. based on the COMPLICATIONS theoretical pathophysiology involved. This is open to the Thus. to remove air from the seventh nerve canal. and the mouth is pulled to responds in the same way as the middle ear to a the normal side. but is also a possible ­seventh nerve canal. The cheek is smooth. The round window was packed. with the same result. cause of narrowing of the Eustachian tube and fur- Paralysis of the facial nerve makes frowning ther middle ear barotraumas. together with a frequent drip of peri- lymph fluid into the middle ear. the production and food collects between the cheek and gum. with the middle ear collecting fluid that forms a The reason for this disorder is explained by the medium for growth of organisms (see Chapter 29). Exploratory surgery was performed. this disorder sometimes follows Otitis media middle ear barotrauma. Recorded in both avia- tors and divers. A fistula of the round window was observed. not corrected. Transient episodes of vertigo were noted. prevents the eye from closing on that side and causes drooping of the lower eyelid (which Mastoiditis may result in tears running down the face because they do not drain into the nasolacrimal duct). their swimming. He noted tinnitus. illness. and he also experienced ear pain and vertigo during ascent. The mastoid. Subsequent audiograms over the following month revealed a considerable improvement in hearing. Otoscopic examination of the tympanic membrane revealed the effects of barotrauma. A similar procedure was performed 5 days later in the other ear. middle ear air expands indicate a middle ear infection. from chorda tym- once permanent inner ear damage has been pani involvement. middle ear barotrauma should be considered to traumatic pathology.100  Ear barotrauma Too many cases of inner ear barotrauma have A metallic taste may be noticed at the start of the recurred for these authors to propose a resump. ear pain developing hours or days after middle ear in some people and so shares its baro. experienced considerable pain and dif- ficulty in equalizing both middle ears during a dive to 10 metres. Whistling becomes impossible. Early treatment could include inhalation of MIDDLE EAR BAROTRAUMA 100 per cent oxygen for some hours. causing ‘facial baroparesis’. Hyperacusis may result from ­demonstrated. negative pressure situation.

Diving Medicine for SCUBA Divers. haemorrhage Edmonds C. South Pacific Underwater Medicine Another rare complication from the middle ear cleft Society Journal 1991. Pneumocephalus/intracranial Forsvarsmedicin 1973. Miller J. Annals of Otology and Laryngology changes. Otolaryngologic aspects of conducive to bacterial growth. Paparella MM. and the Carlson S. Anatomical Perilymphatic fistula: Washington DC experi- effects of sudden middle ear pressure ence. the patient usually Neck Surgery 1979. Parell GJ. has pain and tenderness over the mastoid. Smart DR. Temporal bone pathology in scuba d ­ iving Archives of Otolaryngology 1972. Edmonds C. deaths. Otolaryngology and Head and Neck Goldmann RW. Getson P. Brasseux CO. Otological Aspects of Diving. JAMA 1986. result. Fitzgerald DC. mastoiditis. 1993. Lowry C. Otolaryngology and Head and Under these circumstances.87(5):569–572. blood) to rupture into the middle cranial fossa. A literature review of the assessment and management of inner ear 1. In: Bennett P. Edmonds C. Thomas R. www. Annals of Otology 1979:88:368–376. (air. Edmonds C. 1973. is frequently very thin Subaquatic Medicine. Forsvarsmedicin 1973. quence of diving. eds. Alexsson A. the tegmen tympani of Edmonds C. scuba diving. Inner ear b ­ arotrauma. Brown M. Pacific Underwater Medicine Society Journal trauma. Jones J. Pneumocephalus as a conse- Surgery 1993. Les accidents labyrinthiques aigus and a complication of both labyrinthine fistula au cours de la plongée sous-marine. with air 44(4):243–245. Tonkin J. meningitis is a possible extension 1970. Hess C. A literature review of barotrauma in divers and recommendations the assessment and management of inner for returning to diving. Meningitis Conde JF. middle ear–mastoid space. Otological and paranasal sinus prob- Hyperbaric Medicine Journal 2014 (in press).9(3):404–405. Prevention pathological features can be demonstrated by CT of hyperbaric associated middle ear baro- scans of the temporal bone. imaging (see Chapter 8). London: Saunders.. The bony roof over the 1973. 5th ed.95:556–563. Annals of Emergency Medicine 1992. Round window rupture in diving. Thomas R. Dysbaric peripheral nerve involve- ment. sinusitis and so forth Demard F. . South occupied by blood and fluid from descent baro. Parell GJ.9(3):416–422. strated by CT brain scans and magnetic resonance Sydney: Australian Medical Publishing Co.21(4):190–197. FURTHER READING 4th ed. Blackwood FA. trauma. Auricular and sinus barotrauma. Becker GD.255:3154–3156. Silverman M. McKenzie B. Sydney: Diving Medical or incomplete. Edmonds C. Freeman P. headache. Pennefather into the epidural or sub-dural areas. Further reading  101 descent. Medicine Journal 2014. of otitis media. allowing for the contents of this space Centre. 1997. J. Pennefather J. lems in diving. with the pathological features demon. Antonellip J.divingmedicine. Elliott E.109:514–521. Elliott H.21(12):1468–1471. and pneumocephalus. 2013.106:830–837. Inner ear barotrauma: a retro- ing from the expansion of gas in a space that is now spective clinical series of 50 cases.info.44(4):243–245 tions for returning to diving. and mastoid air cells is pneumocephalus. can develop and produce the conditions Becker GD. Diving and Hyperbaric ear barotrauma in divers and recommenda. A  rupture into the cranial cavity. REFERENCE Elliott E.21(3):309–315. The Physiology and Medicine of Diving. Diving and Farmer JC. Smart DR. produces a sudden and excruciating Edmonds C. and/or fluids. Diving and the petrous temporal bone. Freeman P. Acta oto-rino-laringológica ibero-americana Although rare.

Bennett Symposium. Ear and sinus problems scuba divers. Medical review. Theory of membrane breaks Medicine Society Journal 2003. Bradley ME. Sudden deafness and Money KE. Alternobaric vertigo. Vorosmarti J.119:455–457. The abnormally patulous Saunders. Miyake H. in s­ udden hearing loss. 4th ed.102  Ear barotrauma Hagberg M. 1944. Jansen EC. Parell GJ. Acta US Naval Medical Bulletin. Archives of Lundgren GEC. Research 1985. Vesterhauge S.20:845–861. Incidence and risk O’Neill OJ. Rhinology. Eustachian tube. South Pacific Underwater Medicine Services Journal Canada 1964. Medscape Reference. Space. Canadian Journal ear barotrauma associated with hyperbaric of Applied Sport Sciences 1985. South Pacific Underwater Simmons FB. Klokker M. eds. ­fistula. 5th ed. In: Fifth International in underwater divers. Hyperbaric Medicine 2003. Ornhagen H. Vancouver. Inner ear barotrauma in Hunter ES.­ trauma on descent from 8000 ft cabin medscape. Albrektsen G. Eustachian tube function in SCUBA divers Pullen FW.115:1–12.135:182–185. 35(5):850–856. Otol Neurotol.26(1):8–13. Neurochirurgica 1967. perilymph equalizing earplugs do not prevent baro. Research 1988.42:293–306. Neuman TS. ENT problems of diving. Sakakibara K. American Journal of Otology 2014. Predictors of middle and sinuses in scuba divers. Markham JW. Annals This chapter was reviewed for this fifth edition by of Otology. Supplement 1985. IHC publication.33:127–133.3(1):131–140. barotrauma. in professional divers. Meyers AD. Military Medicine Molvaer OI. Otological Clinics of North Kitajima N. Inner ear.12(1):77–84.88:41–48. in press. and Laryngology Carl Edmonds. in Undersea and Hyperbaric Medicine a retrospective cohort study. Takahashi H. The O’Neill grading system for factors for symptoms of ear and sinus among the evaluation of the tympanic membrane. Buckingham IP. Undersea Biomedical Yanagit N. Aviation. Philadelphia: Pulec JG. The clinical features of pneumo. Sakakibara B.30(2):93–102. Altered America 1970. 2004. Forsvarsmedicin and Elliott’s Physiology and Medicine of 1973. emedicine. Tjernstrom O. Farmer JC. Bennett MH. Otolaryngology and sport scuba diving: update and guidelines.13(3):270–272. eds. 1992. Undersea Biomedical Hyperbaric Conference. In: Bove A. and Environmental April 26. Philadelphia: Saunders.1:511. oxygen therapy. ­vertigo in military divers. Hahn FW. The Valsalva manoeuvre: a critical Macfie DD.15(4):271–282. Alternobaric 2003. British Medical Journal 1965. hazard. Undersea and journal. 1001 disorders of the ear. ­hyperbaric oxygen therapy: clinical reports Damage to the middle ear and the inner ear of 25 patients. Alternobaric vertigo: a diving Otolaryngology 1968. Sugita-Kitajima A. Calder IM.16(1–2):1–78. Alternobaric vertigo 1970. Diving. Teed RW. Factors producing obstruction of cephalus based on a survey of 284 cases the auditory tube in submarine personnel. Kitajima S. Proceedings Molvaer OI. nose Lehm JP.10(2):99–103.com/article/856806 updated altitude. Neblett LM. Archives of Otolaryngology in diving. Roydhouse N. Davis’ Diving Medicine. .76(11):1079–1082. male and female dive masters and instructors: 2015. 2010. Medicine 2005. Pressure Roland PS. Taylor D.9(3):410–415. with a report of 11 additional cases. et al. Canada 973:389–401. Bove and 1993. of the First European Undersea Biomedical In: Brubakk AO. Otorhinological aspects of diving. Society Journal 1996. Davis J. Becker GD. Stockholm. Perilymphatic fistula induced by with alternobaric vertigo.

‘being shot’ sensation. These investiga. It is the clinical ●● Grade III – a severe pain or a ‘bee sting’ or manifestation of Boyle’s Law as it affects the para. symptoms. Although ●● Grade II – characterized by pain over the sinus barotrauma is the second most common dis. The pathological changes found within the the pilot had to descend rapidly to relieve sinuses included: Mucosal detachment. affected sinus for up to 24 hours. and symptoms Weissman and associates3 described a series of usually cleared spontaneously.2. As the tors used the following grading system: sinus mucous membrane was pulled away from 103 . submuco. sal haematoma. Grade III cases 15 cases of frontal sinus barotrauma in aviators. If such a sinus was opened. If the pain was not nasal sinuses (Figure 8. blood clots in membranous sacs. Usually. and swell. the sinus and the nasopharynx. amounts of blood-tinged fluid were found. aviators with grade I and II baro- ing of the mucous membrane. mucosa with submucosal haemorrhages. resulted in oedema and congestion of the sinus Most of these cases were grade III. apart from individual case studies.1). sure was well described by Campbell1. small reports. ume of the gas spaces within the paranasal sinuses Serosanguineous fluid sometimes drained during ascent or descent – when those changes could from the sinus. but no x-ray changes. sinus barotrauma from aviation expo. there has been very little thickening of the mucosa seen on x-ray detailed documentation. In the 1940s. small haemorrhages within the mucosa. The injury results from the changes in vol. quickly relieved by the Valsalva manoeuvre. with or without the use of not be compensated for by the passage of air between decongestants. trauma did not seek medical aid. 8 Sinus barotrauma Aviation experience 103 Acute sinusitis 110 Diving experience 104 Chronic sinusitis 110 The first Australian series 104 Pneumocephalus/haemorrhage/ The second Australian series 105 neurological involvement 111 Sinus barotrauma of descent (sinus squeeze) 107 Surgical emphysema 111 Investigations 108 Differential diagnosis 111 Sinus barotrauma of ascent 108 Treatment 111 Other manifestations 108 Prevention 113 General symptoms 108 References 113 Maxillary nerve involvement 109 AVIATION EXPERIENCE ●● Grade I – a transient discomfort that cleared promptly and had only slight mucosal oedema. There was ease in diving medicine.

DIVING EXPERIENCE The first Australian series Comprehensive reviews of diving-related sinus barotraumas were not easy to find. Flottes4. A rea. Sinus x-ray studies Fagan. where all such cases were referred for medical sonably large clinical series of divers with sinus opinion i­rrespective of severity6. quoted widely thereafter. This Sinus barotrauma has been described in ­various series included 50 consecutive cases of sinus baro- texts on diving medicine5.1  Accessory para-nasal sinuses. This series described Incising this mass brought forth a spurt of old minor and acute cases and was complemented by blood. It included many .104  Sinus barotrauma Frontal sinus Ethmoidal sinus Orbit Nasal septum Nasal cavity Maxillary sinus Frontal sinus Ethmoidal sinus Maxillary sinus Sphenoidal sinus Figure 8. aviation sinus barotrauma grades 1  and 2. ment. in The cases in this series were equivalent to Campbell’s 1965. with clots. barotrauma was first described in Australia by sure. but initially without trauma as they were observed in a Navy environ- specific clinical series being documented. described sinus barotrauma in divers. a haematoma formed. the periosteum by the negative intrasinus pres. McKenzie and Edmonds in 19766 and was showed an air-fluid level or a polypoidal mass. another series of 50 more serious cases in patients who were referred for definitive treatment7.

trauma. Pain disease was not easily detected. 32 per cent had a history of previous sinus baro. otoscopy showed evi. more than an incidental observation. The importance has been stressed by Epistaxis was the second most common symp. by default. by its design. produced by scuba diving. nasal and sinus disorders. but the initial devel- This prospective Australian series. ing. dive instructors or profes- 12 per cent of the maxillary sinus cases. It was rarely Thomas and colleagues8. The dis- the maxillary sinus in 74 per cent of the cases. in tribution was skewed strongly to the extremely the frontal sinus in 24 per cent and in the ethmoid experienced. the presenting This series has inappropriately been used to imply headache developed and progressed while at that such intervention is never applicable in the depth. the affected sinuses did not rep.g. remain common medical problems of div- tal area. this study was done more their first open water diver training course. In 12 per cent of the patients. The second Australian series Even though these were inexperienced divers. Diving experience  105 cases that might otherwise have not attended for It has. and others referred for medical treatment of sinus baro- gave a history of intermittent or long-term symp.e. licate the clinical sites and manifestations. Either These cases were in more experienced d ­ ivers – mucosal thickening or a fluid level was observed in 88  per cent had in excess of 50 dives. Campbell’s aviation sinus barotrauma grade 3. in emergency wards or ear. sure or free diving. These patients were toms referable to the upper respiratory tract. i. 68 per cent of the presenting in patients with recurrent or delayed symptoms. The investi- dence of middle ear barotrauma on the tympanic gations frequently involved computed tomography membrane. or symptoms developed during or on descent. sequent ascents or descents. more likely to present for treatment. throat consulting rooms. occurring in 58 per cent of cases. Becker and Parell9. even those that manifest In this series. tom. exploration nor surgery was required in any case. (CT) scans of the sinuses. Antibiotics were prescribed if there was and narrowed from the repeated insults they pre-existing or subsequent sinusitis. Freeman. been used as being typical of all treatment. Neither sinus sustained. the divers were undergoing necessarily valid. These findings contrast with the ing more than 5 years of experience. It could usually be made worse with sub- treatment of sinus barotrauma. e. Also. in patients upper respiratory tract inflammation. sional divers. with 70 per cent of the divers hav- in 15 per cent. with repetitive or more significant problems were In 48 per cent of cases. opment of the headache during a time in which included relatively minor cases of sinus barotrauma. The cases in this series were equivalent to trauma. there was no substantial change in depth did . In one case it was referred to the upper den. Pain than 4 decades ago. seen within 1 month of the latest incident. before computer imaging tech- was the predominant symptom in all the cases on niques became commonplace and when sphenoidal descent and in 75 per cent of those on ascent. aviation expo. many workers including Edmonds. concern to the diver but not usually of great sever- ity. the ethmoid in 16 per cent and the maxillary in 6 per Sinus barotrauma and its complications cent. It was the sole symptom in 25 per cent of the cases of ascent barotrauma. A fluid level was present in being dive masters. the sinus ostia or ducts may have become scarred tants. perhaps of Neblett10 and Roydhouse11. nose and they developed in 32 per cent during or after ascent. That extrapolation is not In the majority. occasionally magnetic resonance imaging (MRI). Because of the extreme amount of Most of these divers required no treatment or diving exposure in this group. and many clinical manifestations. recurrent infections or The cases were self-selecting because the divers hay fever. sinus barotrauma cases. was referred to the frontal area in 68 per cent. sinus endoscopy and Radiologically. was reported in 19947. it is presumed that responded to short-term use of nasal deconges. Half had a history of recent A series of 50 more severe cases. and complications.

mucosal congestion) pressure with descent. The substitution of the feet first descent CT scans showed more identifiable and definitive (preferably down a shot line). In 8 per cent of the patients there was a very clear-cut and dramatic sensation of a bursting or popping during depth changes. The series there would frequently be a head first descent. as a measure to replace a contracting air space A similar sudden sensation can also occur from in the sinus during descent. see Chapter 7). the sinus were on descent and half on ascent. and the full or heavy sensation within the sinus may take some time to develop. various radiological descriptions.2 and of Mann and Beck12. produced by the negative intrasinus order (e. that the sensation results if disease is to be avoided. These are now described in medical texts used by Sphenoidal involvement was common. the Valsalva One of the cases involved the ethmoidal area. blood or effusion. In these cases monly. with sudden excruciating described in aviation medicine as the ‘popping of pain. from the obser. a ‘gunshot’. over the eye’ and ‘like being struck on the head with a club or bat’. most com- diving and equalization techniques. The current use of MRI and CT scans of the A similar problem developed if descents were sinuses made diagnosis and treatment more defini- slow. at a depth of 0. tive in most of these cases. This may have an effect the patient had a subsequent small. and manoeuvre. divers from a haemorrhage stripping up the mucosa of inappropriately used this development of the dis- the sinus. repetitive incidents of sinus baro. MRI using T1- quent positive-pressure middle ear equalization and T2-weighted imaging was more diagnostic in manoeuvres. differentiating blood from mucosal thickening14. (Figure 8.2). the ization. opacification and. pathological features (Figure 8. divers13. sinus The blood or effusion gradually accumulating in surgery or nasal surgery was needed in 12 per cent. to allow the dive to the rupture of an air sac or release of pressure continue. together with fre.2  Ethmoidal haemorrhage. i. it is believed that a small degree of negative pressure is sustainable within the sinuses. half Figure 8. Exceeding this pressure may be sufficient to cause a gradual effusion to develop. This may Divers in these categories were advised of the be followed by a ‘hissing’ sensation of air move. On the contrary. It has been burst during ascent. from a distended sinus during ascent. without symptoms12. however. polyps trauma appeared to be provoked by inappropriate or polypoid masses. because of discomfort noted in the sinus.e.g. Of these. oval haema. of aerating the sinuses before major disease and toma noted over the ethmoid region within hours haemorrhage develop. It is presumed.106  Sinus barotrauma cause some confusion in the initial physician’s assessment.g. This may be appro- vations of Campbell1. which may then relieve discomfort and pain. but it is not prudent well as from this series. Previous radiological descriptions included In 10 per cent.5 to 1 metre below the surface. mucous cysts. ‘like a bee sting adjoining skin. Extrapolation would suggest that diving-related barotrauma could occur with a reduction in sinus air volume of 5 to 10 per cent. appeared to rectify the situation. . degree of pain and discomfort. Following ethmoidal sinus barotrauma of descent.3). the sinus equalizes the pressure and reduces the often with excellent results. and/ reported by the authors was no different in the or swallowing as a method of middle ear equal. then bruising and haemorrhage into the a  ­champagne cork’. Sinus endoscopy. correct methods of descent and to use positive ment. mucocoeles. From the aviation literature. haematomas. as priate for an emergency dive. between the eyes. a thickening of the mucosa. pressure middle ear equalization (e.

The pain is usually over the frontal sinus. the sedative Ostia blockage may be the result of sinusitis with effects of narcosis may distort the clinical features. Also. over the maxillary division of the fifth nerve is pos- ness or pressure. blood or mucus may be extruded into the nose or pharynx. diver neither ascending nor descending. they are not painful on movement. . When expels blood and mucus from the sinus ostium. Sinus barotrauma of descent (sinus squeeze)  107 Figure 8. expansion of the enclosed air exclude the diagnosis of sinus barotrauma. and so forth. sal congestion and haemorrhage compensate for Headache developing during the dive. Computed tomography scan and magnetic resonance imaging have replaced x-ray studies in identifying sinus disorders. however. It may be preceded by a sensation of tight. During ascent. less As described with ear barotraumas. sneezing or holding the head down may Symptoms include pain over the sinus during aggravate the pain and make it throb.3  Sinus barotrauma affecting mastoid and sphenoidal sinuses. with the the contraction of the air within the sinus cav. chronic sinus problems be referred to the upper teeth on the same side. frequently it is retro-orbital and probably  sphe- traumas are more frequently noted in female divers noidal. abnor- diving frequency (more in dive instructors than in mal or loose. SINUS BAROTRAUMA OF DESCENT ascent but may continue as a persistent dull ache (SINUS SQUEEZE) for several hours. should not ity. sinus baro. rhinitis. mucosal hypertrophy and congestion. Numbness descent. are an increasing problem with age and excessive Although the teeth may feel hypersensitive. muco. Left fluid level in petrous bone and loss of pneumatization of mastoid air cells. Maxillary pain is not common but may and in the young. dive masters15). The pain usually subsides with sible (see later). nasal polyps noticeable but produce a misleading history. On ascent. small changes of depth may not be particularly redundant mucosal folds in the nose. Coughing. this develops at considerable depth. on the same If a sinus ostium is blocked during descent. side as the sinus disease.

operative intervention was not indicated. This disease is aggravated by rapid ascent. as from fluid within the sinus (continuous from the in free ascent training. emergency ascents. Examination revealed a deviated nasal septum to both right and left. The newer imaging tech- niques can clearly demonstrate these features General symptoms (Case Report 8. with hyperaemic nasal mucosa. The ethmoid and sphenoidal sinuses OTHER MANIFESTATIONS may also be affected. but he was unable to proceed beyond 6 metres because of a severe tearing headache in the frontal region. it may fracture the walls and track along the soft tissues and cause surgical Investigations emphysema. If the expanding air cannot escape through the sinuses. He had often complained of nasal blockage and had various treatments for this. occasionally noticed a trace of blood from his face mask following ascent. on ascent. He equalized his face mask. a sensation of openings by mucosal congestion. opacity or fluid lev- the air may rupture into the cranial cavity and els. disclose thickened mucosa. CT or MRI scan may or mastoid sinuses. with or with- of the nose occasionally rupture and cause a small out pain. On reaching the bottom. haematoma or discolouration of the skin between Bleeding from the nostril on the same side as the the eyes (see Figure 8. serous or mucous cysts. Because the airways were patent on both sides of the nasal septum. In a small number of the cases (8 per cent). His first dive to 12 metres for 10 minutes was uneventful. the  dive) or the development of chronic sinusitis Uncommonly. often affecting the ethmoidal Sinus x-ray examination. some SINUS BAROTRAUMA OF ASCENT additional symptoms did not appear to be eas- ily explicable on the basis of local sinus disease. the severe sharp pain recurred. and this provided some relief. preventing escape of expanding gases of injury.2). The ostium or its mucosa will then cases of sinus barotrauma. The patient’s nasal mucosa returned to normal after he abstained from cigarette smoking. Occasionally. X-ray studies showed gross mucosal thickening in both maxillary sinuses. This disorder may follow the occlusion of sinus These included nausea or vomiting. folds or sinus impending syncope and disorientation at the time polyps. subma- dive). These occurred in the more dramatic (Figure  8. He then continued the descent feet first but still had some slight pain. . including cautery. haemorrhage. Rupture of air cells may cause severe and sudden pain. There was also some slight shadowing on the right frontal sinus. develop. but on reaching the surface he noted mucus and blood in his face mask.1 DN. a 22-year-old sports diver. and haemorrhage commonly follows. The radiological signs cleared over the next 2 weeks. other manifestations may or mucocoeles. CASE REPORT 8. A dull frontal headache persisted for 3 hours after the dive. During ascent it lessened in severity. infection (usually starts a few hours after rine escape and so forth. Diagnosis: sinus barotrauma of descent.108  Sinus barotrauma The superficial ethmoidal sinuses near the root blow out into the nasal cavity. sinus disorder is sometimes the only manifesta- Discomfort persisting after the dive may result tion. The maxillary and frontal sinuses are commonly involved.4). the right being completely opaque. After a brief surface interval he again descended. The opacities produced by the barotrauma cause a pneumocephalus or a small intracranial may be  haemorrhagic.1).

traverse the maxillary sinus16. Other manifestations  109 Bone Mucous membrane Air Nasal cavity Mucous plug or polyp Surface at 1 ATA. on the same side as the affected Two separate branches of the maxillary division maxillary sinus.4  Diagrammatic changes of sinus barotrauma from obstruction of sinus ostia on the surface (top). with numbness over the In 4 per cent of the cases the pain was referred to skin of the cheek on the same side. air volume 1 Mucous membrane congestion Blood Air Blood vessel Rupture of mucous membrane Descent to 2 ATA. air volume 2/3 Figure 8. the upper teeth. then descent to 10 metres (2 ATA). halving the sinus air volume and replacing this with fluid and mucosal swelling (middle). effusion). of trigeminal nerve can thus be affected as they ment of the posterior superior alveolar nerve.5 ATA. air volume 1/2 Air Blood Ascent to 1. This is presumably an involve. Maxillary nerve involvement In  another 4 per cent there was involvement of the  infraorbital nerve.17: the infraorbital . the gas expands and discharges fluid (blood. During ascent.

sinusitis. Problems with neurapraxia are more for this reason that the authors of this text now common with ascent than descent. Journal of Laryngology and Otology 1987. The next day he had swollen right eyelids. One same side. vigorously treat with antibiotics any persistence of gesting that impaired circulation is more frequent symptoms following sinus barotrauma. then the infection ing over it.101:386–389. a professional career. Thus. If. complications are more frequent. Three days later he complained of persistent right facial pain. especially if the diver has experienced the dive and extended into subsequent days. the scarred and narrowed ostia may be of great temic symptoms. one considers the second Australian survey. Acute sinusitis In 18 per cent of the severe cases there was a continuation of the initial barotrauma episode Campbell1 stated that infection occurs only rarely. The criteria for this diagnosis included a continu- ation of sinus symptoms in excess of 1 month.) . com- than congestion or haemorrhage of the nerve as a mencing hours after the dive or continuing into basis of the presentation. the following day. Chronic sinusitis lary division. and acute sinusitis into a syndrome of chronic and his series may be equitable. tion. value in both prolonging their diving career The patients with sinus barotrauma who sub. with recurrent barotraumas develop- with its more serious cases. There is a possibility of involvement of any divi- sion of the trigeminal nerve. with the initial Australian survey6. pre-existent. it often 28  per  cent of the severe cases. This condition becomes a culture medium it runs along the lateral or inferior wall of the max. cellulitis may extend from the ethmoidal or max- ness over the upper teeth. in terms of selec. but re-developed a sudden severe pain over his right cheek on ascent. An occasional case of orbital paraesthesia over the cheek and the latter a numb. Chronic sinusitis is a long-term effect of div- Acute sinusitis developed some hours after ing. Blindness in a diver following sinus barotrauma. usually with an affects ­commercial divers near the end of their ­exacerbation of pain over the affected area. in repeated barotrauma episodes.2 A 24-year-old professional trainee diver descended to 40 msw for 30 minutes despite an upper respiratory tract infection and descent-induced pain over his right maxilla and orbit. a finding sug. blocked nose and epistaxis. Then micro-surgery to open purulent nasal discharge and generalized sys. for organisms introduced by the flow of air into the illary sinus. mucopurulent nasal discharge and mild pyrexia.e. X-ray studies confirmed right maxillary and eth- moidal sinusitis. i. (From Bellini MJ. He slowed his descent to reduce these symptoms. with involvement of the sphenoidal sinus18. In another 14 per cent the chronic sinusitis was ever. how. The former produces a numbness or sinus during descent.2). and it is a medical emergency. CASE REPORT 8. gums and mucosa on the illary sinusitis. Bleeding was evident after ascent. and improving their  life style from detrimental sequently developed a sinus infection possibly did chronic sinusitis. In some cases pain and hypersensitivity case proceeded to blindness (Case Report 8. in his face mask. It is are observed. Antral washout and antibiotics were administered but did not prevent an extension of the orbital cellulitis and retinal artery thrombosis with permanent and total right-sided blind- ness.110  Sinus barotrauma nerve as it runs along the wall of the maxillary so because of the haemorrhage and effusion in the sinus and the posterior superior alveolar nerve as sinus. including its maxil.

The only other case of incorrect diagnosis was This condition is not infrequently observed at one subsequently attributed to a dental aetiol- autopsy when the diver has descended while alive ogy (barotrauma associated with pneumatization but unconscious. produces an excruciating and mistakes. These were understandable air and/or fluids. meningitis and other neurologi. where the gas space has expanded. has been well recorded by Markham19. and it is one of the dangers In 6 per cent of the ‘serious’ cases. with and treated as such. cases. ­ethmoidal tion. an initial diag- associated with sinus barotrauma5. At the time of presentation. in association DIFFERENTIAL DIAGNOSIS with sinus injury in general medicine. and there should be no hesitation in sudden headache. Patients with a sinus This disorder has been seen on a number of occa. Attention is best ­surgical emphysema (usually from the ethmoidal paid to prevention. if diving is has passed from other sinuses. In other instances. Sinus mucocoeles. It  has been well nosis of decompression sickness was made. Sphenoidal sinus trauma and subsequent sinusitis may result in involvement occurred in 6 per cent of the ‘serious’ orbital cellulitis. confused with cerebral decompression sickness trauma. lesions with neurological sequelae. even though Lew and his colleagues18 referred not only to the the diver may have died. inducing para-nasal sinus baro. and then being brought to the surface. with potential vision-threatening Sphenoidal sinusitis is not easy to demonstrate ocular complications. but also to its Extension of infections following sinus baro. CT brain scans or doubt regarding the diagnosis. or upper respiratory tract infection may require sions and was described previously5. Most of the effects of sinus barotrauma are minor and rapidly regress if diving is suspended and the Surgical emphysema underlying or consequential inflammatory dis- order of the sinus is treated. allowing for than miss and mistreat a case of cerebral decom- the contents of this (air. Surgical drainage of air expanding in the sinuses and erupting into of acute lesions is rarely indicated. produced with plain x-ray films. often with complicating sinus infec- during ascent of gas in a space (mastoid. some hours after the dive. A rupture into the cranial cavity. The tracking antibiotics and decongestants. which could be and sphenoidal sinus) that has been partly occu. blood) to rupture into pression sickness. It would be prefera- MRI. into the epidural areas21. can also cause space-­occupying MRI or CT scans. cians to recognize it and to not appreciate its poten- Orbital haemorrhage may also result from the tially serious complications (Case Report 8.3). see Plate 2). unless there are the surrounding tissues can manifest as orbital neurological or other sequelae. Demonstrable on MRI. Treatment 111 Pneumocephalus/haemorrhage/ first occur as a localized manifestation in the facial neurological involvement tissues. association with ‘deep sea diving’. and this case was there- trauma. symptoms of sphenoidal sinusitis. It is important because of the failure of clini- cal problems21–25. but it is often obvious on during barotrauma. . sinus though a fracture of the egg-shell–thin ­lamina Even mucoceles and chronic sinus disease papyracea. The presence of pneumocephalus. the middle cranial fossa. around a carious tooth). including optic neuropathy and blindness. with the pathological features administering hyperbaric therapy if there is any demonstrated by radiology. and the d­ isorder can suspended. pressure gradient. TREATMENT these disorders require referral of the patient to an ophthalmic surgeon21–25. the case subsequently demonstrated to be sinus Pneumocephalus results from the expansion barotrauma. with demonstrated by Goldmann20 (see Figure 9. fore not included in the series. the air usually resolve without intervention.3). the clinical pattern was pied by blood and fluid from the descent baro. The temporal bony roof over the sinuses is ble to miss and mistreat a case of sinus barotrauma frequently very thin or incomplete.

following sinus barotrauma. who required As with the original series. Nevertheless. These patients usually responded to dure. but he sustained clinically obvious sphenoidal sinus baro- trauma of descent. cromoglycate. 5.g.13. Patients with infective sinusitis. usually with endoscopy and equal numbers fell into each ‘treatment’ group. who required sinus Our general impression was that approximately exploration. 3. more than 50 per cent treatment of the infections. endoscopic sinus surgery appropriate regimens of: is advancing rapidly and may offer value to a. has been made to the value of surgery in and who were advised to not dive until this had aviators with sinus barotrauma. usually by decon. The frontal sinus c. the lesion (a mucocele or haematoma) cleared up within 2 weeks. cedures22.112  Sinus barotrauma CASE REPORT 8. i. Other times it was needed of patients: to improve nasal air flow. The intractable group. Feet-first descent. ethmoid and sphe- face (immediately before descent) and then noid sinuses can be treated to widen the sinus at regular intervals of half to 1 metre or so ostia. use of steroid nasal sprays. by Bolger. Reference in the literature. the maxillary.e. on the sur. Parsons and Matson26 in 1. The sixth group continued to have difficulties the nasal disorders. This is equalization ahead considered the treatment of choice in military of the dive (see Chapter 7). Positive pressure manoeuvres to autoinflate cases. Those who were using inappropriate diving tional endoscopic sinus surgery was tempered techniques. enthusiasm of these investigators for func- 2. mucocoeles diving medical texts6. It is during descent. Those who responded to medical treatment of 6.3 ID was not part of the ‘serious’ case series. allergic or vasomotor ­rhinitis). In the ‘serious’ cases (the second Australian or redundant mucosa that caused obstruc- series). Although operative intervention was contemplated in this case. by the possible complications of this proce- ously. These have been described previ. is less amenable to this treatment but may be ratory tract inflammations. infections. thus preventing sinus barotrauma. aviators in the United States. topi- cal or generalized decongestants. . vent problems completely. In some cases Various attitudes to the current treatments are surgery was required to produce patency of ­discussed in the previously cited references and the ostia and to remove polyps. of the divers in the second series had a history gestants and antibiotics. Avoidance of diving exposure during respi. This caused some concern because of the proximity to other important structures around this sinus and the possibility that the computed tomographically verified space-occupying lesion was neoplastic. patients with the more serious and chronic b. the treatment could be divided into groups tion to the ostia. reconstruction.26. 4.7. or nasal surgery. tion (e. avoidance of All patients were strongly advised to not dive nasal irritants and allergens and cessation of during times of upper respiratory tract inflamma- smoking (tobacco or marihuana). symptoms Some clients were moved between treatments commencing hours after the dive or persisting because various measures failed to resolve or pre- into the following day. explored in some cases. This included the topical and usually ceased diving.24. following abstinence from diving. With current endoscopic surgical pro- both middle ears and sinuses. The guarded happened. The authors of this of diving with such conditions at the time of the text so treat any persistence of symptoms barotrauma. Those whose disorder cleared up spontaneously 1990.

Rhinology. Roydhouse N. Annals of Otology 1945. dle ear equalization (‘equalizing ahead of the dive’. Feet-first descents are preferable Canadian Journal of Applied Sport Sciences (i. evaluation with MR imaging. McKenzie B. Pennefather J. nose and sinuses in scuba divers. be of value. head upright). Tonkin J. South Pacific Underwater Medicine Prevention of sinus barotrauma is achieved by Society Journal 1994. Edmonds C. manoeuvre.115:1–12. Campbell PA. assist in persons so predisposed. Slow descents and ascents will Otorhinolaryngology 1976. Roberts PT. among male and female dive masters course and treatment. (Sudafed) are often used. Hackney are required to demonstrate any efficacy of these DB. 2003. Avoidance of allergens may 1974. teolytic or allegedly mucus-softening enzymes to 2013. Edmonds C. Thomas R. Sphenoid sinus- 5. case report and review. Radiology 1987. Otolaryngology nasal abnormalities may be needed. Diving itis. Markham JW. Pennefather J. infections. Campbell PA. Mann W. Edmonds C. Correction of aspects of scuba diving. of Otology. Hagberg M. and Laryngology sure techniques during descent.85:61–64. study. 10. Aviation. Otolaryngologic with local steroid nasal preparations.divingmedicine.54:69–83. Cessation of smok. and sinus barotrauma. and Laryngology 1976. Green RS. Flottes L. Divers. ization methods). Paranasal sinus haemorrhages: drugs. ear.53:291–301. Ornhagen H. Bilaniuk LT. Annals of Otology and instructors: a retrospective cohort 1944.21(4):190–197. Sydney. Annals of Otology. 19. Beck C.309:1149–1154. Dysbaric peripheral nerve 4. Acta Rhinology. Weissman D.e. Neither drug type is as effective as using scuba diving: update and guidelines. 1971. and the techniques used for mid. with a report of 11 additional cases. Maxillary sinus barotrauma: 3. Diving 1983. The clinical features of pneu- 6. References 113 PREVENTION 7. Medical Centre. Zimmerman RA. Positive pres. oto-rino-laringológica ibero-americana 18. refraining from diving with upper respiratory tract 8. McKenzie B. assist in aeration of the sinuses as well 11. see 12. Garges LM.24(1):13–19. . Aerosinusitis. Edmonds C. Baker AS. patency of the sinus ostia. Parell GJ. Incidence and risk factors for symptoms of ear and sinus 1. Becker GD. REFERENCES 15. Thomas R. Southwick FS. Neurochirurgica 1967. Otological Aspects of Diving. 17.16(1–2):1–78. www. Undersea and Hyperbaric Medicine 2. sinusitis or rhinitis. Freeman P. Acta Medicine Society Journal 1991. Aerosinusitis: a resume. et al. 1001 disorders of the as the middle ears (as opposed to the passive equal. Blackwood F.. reduce the sinus damage where there is only marginal 13. Neblett LM. Edmonds C. Diving Medicine for Scuba Some physicians have found the use of pro. as may treatment 9. 5th ed. New England Journal of Medicine and Subaquatic Medicine. ing will reduce the likelihood of mucosal irritation Sydney: Australian Medical Publishing Co. South Pacific Underwater caused by underwater immersion. Sinus mocephalus based on a survey of 284 cases barotrauma in divers. Aerosinusitis: its causes.30(2):93–102. Barotrauma of the ear and sinuses involvement. as are topical nasal decon. Webber AL.16(4):453–483.162(2):499–503. Montgomery WW. Space and Frontal sinus barotrauma.82(2):160–162. Fagan P. Sinus barotrauma: a bigger picture. Lowry C. 1985. Well-controlled experimental trials 14. Laryngoscope Environmental Medicine 1985. Edmonds C. Annals the correct equalizing techniques. Archives of Chapter 7) are advised.10(2):99–103. such as the Valsalva Supplement 1985. 1972. Lew D.214(2):167–173.56(8):796–802. Otolaryngology and sport gestants.info.87(5):569–572. 1965. and Head and Neck Surgery Systemic decongestants such as pseudoephedrine 1979. 16.

AJNR loss in a scuba diver. Bolger WE. Parsons DS. Hunter ES. Foster T. 4th ed. Carl Edmonds. Aviation. 2004. Cortes MDP. Davis J. Farmer JC.Aug 20. eds. Bove and Davis’ Diving Medicine.1136/bcr-2013-010309.28(1):31–34. Becker GD. BMJ Case Reports American Journal of Neuroradiology 2013. Parell GJ. Goldmann RW.110:1358–1360. . Pneumocephalus 24. Lepawsky M.61(2):148–156. Matson RE. 2000. JAMA lems in diving. Ear and sinus prob- as a consequence of diving.26:1218–1219. Medicine 1990.114  Sinus barotrauma 20. Space and Environmental 23. Orbital hemor. doi: 2005. 21. pii: bcr2013010309. Longridge MS. Nugent RA. Butler FK.255:3154–3156. Sphenoidal sinus as ­temporal lobe injury ­secondary mucocoele presenting with acute visual to ­temporal bone rupture. 1986. Philadelphia: Saunders. Gurney N. In: Bove A. Undersea and Hyperbaric Medicine This chapter was reviewed for this fifth edition by 2001. consequences of scuba diving with Functional endoscopic sinus surgery in chronic ­sinusitis. 22. Mowatt L. rhage following face-mask barotrauma. 10. Laryngoscope aviators with recurrent sinus barotrauma. Barotrauma p ­ resenting 25. Neurological 26.

barotrauma is often encountered in older divers. then gas expansion on ascent may Dental barotrauma has been called a­ erodontalgia be restricted by the blood in these spaces. jaw. the Teeth with full cast crowns may be susceptible tooth may cave in (implode) on descent or explode to air being forced into the cemented material on ascent. thus or barodontalgia when it is applied to altitude resulting in distension and pain. intensity light may reveal the micro-fractures. Sensitivity to cold may ­evident with resin cement.g. because of slowed descent. to a lesser extent. Fast rates between the crown and the tooth – especially with of ascent or descent will precipitate this. but often with- In the first presentation. 9 Other barotraumas Dental barotrauma 115 Miscellaneous barotrauma 119 Equipment barotrauma 116 Localized surgical emphysema 119 Facial barotrauma of descent (mask squeeze) 116 Pneumoperitoneum 119 Skin barotrauma of descent (suit squeeze) 116 Pneumocephalus 119 Genito-urinary barotrauma 116 Bone cyst barotrauma 120 Head and body barotrauma of descent Cranial nerve palsies 120 (diver’s squeeze) 117 Other disorders 121 Suit barotrauma of ascent (‘blow up’) 117 Further reading 121 Gastrointestinal barotrauma 118 Stomach rupture 118 DENTAL BAROTRAUMA descent. also localize the tooth. The gas may enter around the edge of trauma occurs in cases involving a carious tooth the filling. Pain may prevent further through interruptions of the mucosa. along. impacted teeth or other oral maxillofa. As pres- fractures of the enamel and dentine (Figure 9. bone cysts. side or associated with fillings that were poorly Because of the aetiologies described earlier. During descent. There are three common presentations Divers sometimes experience dental baro- of dental barotrauma. gas spaces may exist in out the gas space able to be readily visualized on the roots of infected teeth. in dental x-ray films. the inserted or have undergone secondary erosion. trauma reliably at a certain depth. If. symptoms are not noticed. sure differences across the cementum develop. A second type of presentation of dental baro- cial disease. Micro-leakage of gas is not as identify the affected tooth. blood and effusion. Pressure a zinc phosphate cement or. Transillumination with a high- necrotic or inflammatory areas of the pulp. glass applied to individual teeth may cause pain and ionomer cement. along dying nerves. the contracting gas space is A third form of dental barotrauma involves the replaced with the soft tissue of the gum or with tracking of gas into tissues (surgical emphysema). adjacent to the tooth or through micro. causing considerable pain. with a cavity and very thin cementum. e. diving 115 . exposure.1).

other dental disorders (see Chapter 42). c­onjunctival avoidance of all diving after dental extractions haemorrhages. The skin tends to be sucked into these folds. The condition is usually painless and clears within nal to. Skin barotrauma of descent lary nerve (see Chapter 8). dental extractions or manipu. haemorrhage may be. leaving linear weal marks or bruises. facial tissues will be forced into this space during Genito-urinary barotrauma descent. used to assist male divers to uri- sures during descent. the face. purpuric haemorrhages. This may also manifest (suit squeeze) as a burning sensation along the mucobuccal fold.116  Other barotraumas Figure 9. In some diving masks. as well as referred pain from the maxillary sinus or the maxil. This condition is encountered mainly with dry- EQUIPMENT BAROTRAUMA suits (especially if the air inlet hose is not func- tional) or poorly fitting wetsuits. Facial haemorrhage and gross swelling Figure 9. sure is equalized by exhaling gas into the mask. showing collapse of delineate the mask area. Clinical features of mask barotrauma include Preventive measures include biannual dental puffy oedematous facial tissues especially around checks (including x-ray examinations if indicated). Prevention involves exhal- The differential diagnosis of sporadic or constant ing into the face mask during descent. Treatment pain in the upper bicuspids or the first and second involves avoidance of diving until all tissue dam- molars. ible masks or adding flexible gas containers to the lations.2  Facial barotrauma of descent (central figure). so that facial barotrauma nate out of the drysuit during long-duration dive is almost inevitable with descent (limited to the exposures. a few days.1  Dental barotrauma. with goggles). Dental treatment had converted an open cavity into one covered by a silver amalgam filling. During descent Facial barotrauma of descent the air spaces are reduced in volume and trapped (mask squeeze) in folds in the suit. This severe ‘mask squeeze’ developed with a failure of surface supply of compressed air to a full-face mask. pressure. from the P-valve. forcing gas into tissues. Scuba regulators produce a positive oral eye space. must include age is healed. although orbital Treatment consists of analgesia and dental repair. the eyes. there is no way of equalizing the pres. Unless pres. but in contact with. A face mask creates an additional gas space exter. orbital haemorrhages and hae­ and surgery until complete tissue resolution has matoma and generalized bruising of the skin occurred (i. intact mucosal surface) and slow underlying the mask (Figure 9.2 and Plate 2). This condition is rarely serious. The condom catheter is exposed to the . eyes and surrounds. It did not have a non-return valve. Barotrauma is avoided in these situations by employing very flex- after oral surgery.e. descent and ascent. the first right bicuspid during a dive to 20 metres. such as with swim A variant of suit barotrauma is the genital ‘squeeze’ goggles. but not localized in one tooth.

3). similar result when the diver loses compressed air pressure. a bulg- ing sensation in the head and eyes. as a result of a compressor or supply line failure. Suit barotrauma of ascent (‘blow up’) Head and body barotrauma of During ascent in a standard diving (‘hard hat’) descent (diver’s squeeze) suit.3  Barotrauma of descent. A squeeze (a descent barotrauma equivalent) of the face. Similarly induced drysuit pressure during descent may also assist.g. haemorrhages occur in the brain. Total body squeeze. conjunctiva. The sequence physical trauma. imprisonment of the diver and clavicles. by from the abdomen and lower extremities into the use of a balanced P-valve.g. The clinical features include the following: ­dyspnoea and a heavy sensation in the chest. heart. There is a suits. as used in standard diving. the expanding gas must be able to escape.4). e. the suit and occupant may This may result in barotrauma of ascent. trauma equivalent) are possible. Diagrammatic representation. thus causing fractured pression sickness. head and neck because of the negative pres- valve into the system. of events may occur dramatically if the heavily With the decreasing use of standard diving weighted diver falls off his or her stage.  the helmet. as is a subsequent ears and sinuses. These pathological changes are urinary infection from organisms incubated in the caused by the effects of barotrauma on the enclosed drysuit tubing.4  ‘Blow up’. and and a pneumatization of the urine (an ascent baro. of the drysuit from tubing disconnection. e. usually Pseudomonas species. as may be areas associated with rigid walls. These gas spaces and by a pressure gradient forcing blood problems may be reduced. bleeding from the lungs. Figure 9. this emergency is now not often encountered. bizarre injuries and death. gastrointestinal tract. If extra gas is balloon and cause increased buoyancy and a rapid not added during descent to compensate for the and uncontrolled ascent to the surface (Figure 9. which adds a one-way thorax. may If it does not. but not eliminated. decom- be forced into the helmet. the female equivalent (the ‘she-P collecting sys. a non-return valve is inserted in the air supply line. To prevent this. A rigid helmet. Equipment barotrauma  117 same pressure gradients as the drysuit. nose. respiratory Another problem with this equipment is flooding mucosa and other soft tissues. swelling in the Figure 9. Suit barotrauma of ascent. neck and shoulders. Adequate equalization of the sure differential in the  helmet. and then oedema and haemorrhages within the skin tem’). then the whole suit will expand like a permit this trauma (Figure  9. . effects of Boyle’s Law.

It is monary barotrauma. These radiological abnor- ascent and may result in eructation. Guarding of the abdomen and the eyes. thus making the oesophageal-gastric Kingdom experienced a similar embarrassing fate. however. rarely  severe.S. and the treatment must then be on such as belts. The ­simple tric contents are likely to be present in the peri- procedure of releasing tight-fitting restrictions toneal cavity. of course. an amount of approxi- Although not common. and it usu- Norwegian divers were badly affected during ally required a pressure of 96 to 155 mm Hg. Treatment involves slowing the rate of ascent. general medical and surgical grounds. pneumoperitoneum GASTROINTESTINAL BAROTRAUMA was present in all cases. If there has been a full-thickness tear. malities can. ages and heavy meals can contribute and are best As a general rule. abdominal discomfort and colicky pains. techniques. showed these to be full thickness. positioned tension were constant. with a large and rapid expansion of gas in excessively or from failure to deflate during ascent. stomach rupture and even ization of the lesions. erable symptomatic relief. notable examples of mately 4 litres or more of gas was necessary before gastrointestinal barotrauma are recorded. more than 30 metres. haematemesis (33 per cent) and dys- sation of head and neck distension and bulging of pnoea (50 per cent). vomiting. Performing the Valsalva manoeuvre 100 per cent oxygen as a first aid measure and while in the head-down position may also cause even hyperbaric oxygen as an initial treatment air to pass into the stomach. the stomach. junction act like a one-way valve. In the patients reviewed. Carbonated bever. phagia. reason given for the localization to the lesser cur- Reclaim in 1961. The pressure gradient toms including vomiting (25 per cent). The 122-metre dives using helium-oxygen. but sometimes this extended to include a pneumomediastinum and Gas expansion occurs within the intestines on even pneumothorax. lesser curvature of the stomach. on H. decompression of the pneu- avoided before and during exposure to hyperbaric moperitoneum is best achieved using surgical conditions. Two rupture of the stomach would develop. 2. also be produced by pul- tus. . eructation. responding vature is that there the gastric wall is composed of very well to hyperbaric oxygen therapy for gas only one muscular layer. compared with the three gangrene. or breathing bag. but can occasionally cause syncopal Gastroscopy allowed identification and local- and shock-like states. then gas- stopping ascent or even recompression. and laparoscopy usually death. Swallowing Treatment of rupture of the stomach is essen- to equalize middle ear pressures is one cause of tially a surgical procedure. (16 per cent).118  Other barotraumas but a variant is likely with divers who use a drysuit. The abdominal pain and dis- has a counterlung. obstructing from imbibing flat champagne. shock occasionally developed. this organ may rupture with ascent.M.5 ATA and deteriorated into a shock state with It is postulated that rapid distension of the abdominal distension and pains before ascent was stomach will increase the angle of His and com- terminated. A group of officials celebrating the press the cardia against the right diaphragmatic successful construction of a caisson in the United pillar. An Australian lad. position who are using rebreathing equipment that with rapid ascents. may have some value under some circumstances. usually on the Inexperienced divers are more prone to aero. On x-ray examination. belching from the bag to the diver’s head results in a sen. such as a buoyancy vest or salvage/lift bag if inflated Rarely.  fla. girdles and so forth may give consid. A clinically dissimilar and relatively minor A review was conducted of 12 cases associated manifestation is noticed by divers in an upright with relatively deep dives. predisposing to this condition. drank a ‘flat’ celebratory lemonade at layers elsewhere. breathing aerophagia. with various other symp- below the head and neck. Stomach rupture It also can occur with other inflatable objects.

and com. in the erect position). and follow-up radiology or scans to verify a lung to the subdiaphragmatic area. The and the thinned petrous temporal bone into the surgical emphysema. especially with barotrauma of ascent or sion or craniotomy could be considered in dire underwater explosions. plete resolution occurs within hours. be verified by positional skull x-ray study or com- nary barotrauma. The most common cause is a fracture of the Occasionally. If untreated. The sudden air into the orbit (see Chapter 8 and Plate 3). sit- mediastinum to the retroperitoneal area. naso-ethmoid bones. but diving should be avoided occupying lesion may supervene. although the effects of a space-­ is rarely indicated. The lamina papyracea. when the expanding gas ruptures into shell thickness. When these bones are fractured. a rupture of a gastrointesti. which para-nasal sinuses) are affected by ascent baro- separates the nasal cavity and the orbit. The clinical presentation may have all the Treatment is by administration of 100 per cent clinical features of a catastrophic intracerebral oxygen with a non-pressurized technique. sneezing. is possible.5). Otherwise. Treatment is by administration of 100 per This disorder may result from the entry of gas into cent oxygen with a non-pressurized technique. can be verified radiologically as it damage. the cranial gas spaces (mastoid. pressures. any area where the integument. and then ting upright. event. ruptured pulmonary bulla dissecting along the Treatment includes the following: bed rest. Orbital surgical emphysema. . This may follow descent increase in pressure in the nasal cavity or ethmoidal barotrauma. when haemorrhage occupies the ­ sinus from ascent or a Valsalva manoeuvre may force gas space and its orifice is blocked. recompres- nal viscus. circumstances. tracks into loose subcutaneous tissue. skin or mucosa is Usually. On theoretical grounds. such as a subarachnoid haemorrhage. may be needed. producing adhesions. to track under the vre. may result Pneumocephalus from diving with facial skin. any the cranial cavity. and surgical man- association with tracking mediastinal emphysema agement of a ruptured gastrointestinal viscus from pulmonary barotrauma. 100 per cent oxygen inhalation for many could permit the direct passage of air from the hours. reduction of the air volume. is of egg. Diagnosis can This disorder has been observed with pulmo. could cause significant brain sign of crepitus. with movement of air from a puted tomography scan (Figure 9. nose blowing. Although hours. severe enough to occlude the palpebral fissure completely. usually through the tegmen tympani is common with buccal and dental lesions. as described earlier. intranasal or sinus injuries. bursting of gas and/or blood into the cranial Surgical emphysema over the mandibular area cavity. It is also possible that previous injury other manoeuvres that increase nasopharyngeal to the lung or diaphragm. Miscellaneous barotrauma  119 MISCELLANEOUS BAROTRAUMA The condition may be detected by chest x-ray study or positional abdominal x-ray study (gas Localized surgical emphysema under the diaphragm. Excruciating headache immediately on ascent resolution may take many days. Neurological until this resolution is complete and the damaged signs may follow brain injury or cranial nerve integument has completely healed. the disor- Another possible cause of pneumoperitoneum der may last a week or so. complete resolution occurs within broken and in contact with a gas space. with its associated physical epidural  space. altitude exposure. other sites are possible. lesions. trauma. and subsequent infection is. avoidance of the Valsalva manoeu- released into the peritoneum. Management of the cause (pulmonary or the classical site involves the supraclavicular areas in gastrointestinal) is required. It is likely that the condition could be aggravated Pneumoperitoneum by excessive Valsalva manoeuvres (‘­equalizing the ears’) or ascent to altitude (air travel). or diaphragm. Recompression is probable.

It is possible that sacroiliac joints.6  Bone cysts causing pain during ascent and or descent. and may sive tissue-damaging barotraumatic effects last for hours after the dive. (Courtesy of Dr B. These lesions can be caused by the implo- into the area. W. air could be forced into the nerve canals as the raphy or ­magnetic resonance imaging scan may gas expands with ascent. showing gas at the vertex. next to the sacro-iliac joint. L. but it does not respond to recompression tomography section showing gas anteriorly. (a) An x-ray study showing a translucent cyst in the right ilium. lesions (fifth or seventh) attributed to neura- seous bone cyst.) Cranial nerve palsies Bone cyst barotrauma Patients occasionally present with cranial nerve Occasionally. An x-ray study. (b) A computed sickness. The pelvic bones are during descent. (b) A computed tomography scan showing two air cysts in the right ilium.5  Pneumocephalus from sinus baro- trauma of ascent. The nerve damage var- demonstrate the lesions (Figure 9.120  Other barotraumas Figure 9. Goldman. in the ileum and near the spaces during ascent or both. (Courtesy of Dr R.) Figure 9. pain may develop from an intraos. the distension in enclosed gas most  often involved. probably with haemorrhage praxia. often transitory but occasionally has been confused clinically with decompression long-lasting. These presentations are usually . (a) The x-ray lateral view. Hart. This disorder ies greatly. during descent or ascent. computed tomog.6). therapy and is sometimes aggravated by it.

1985. Molvaer OI. Drucker S. . Etiologia de paralisia facial Stein L. and the diver may be aware of the feel. Lubbers PR.22(1):87–96. nerve involvement. (MSCT) and MRI in a fatal scuba div- ment. Space and Environmental Medicine 1974. Undersea Biomedical ascent. but these have not yet been PG. 1974. Philadelphia: Saunders. JAMA 1986. Acta excess of the mean capillary perfusion pressure. Diving dentistry: a review Goldmann RW. 2003. of the dental implications of scuba diving. The relief as gas Military Medicine 1999. Boussuges AH. South Pacific Underwater Medicine ing incident. Brantly PN. Rodda JC. Pneumocephalus as a con. Settle H. This infers that the cause may be cephalus based on a survey of 284 cases ischaemic. Diving and Hyperbaric Medicine 2009. Barodontalgia. et al. Dental distress.21(4):190–197. Otorhinological aspects of diving. escapes may coincide with improvement in the Markham JW. Fortes-Rego J.39(4):210–212. as described earlier (see Chapters 7 and 8).56(3):265–271. Genito-urinary infection and barotrauma This chapter was reviewed for this fifth edition by as complications of “P-valve” use in drysuit Carl Edmonds. 2003.13(4):465–468. JAMA 1978. Neurochirurgica 1967. Other gas spaces have been observed in the body 5th ed.239(3):223. sequence of diving. Zell BK.g. Oxygen inhalation may assist.16(1-2):1–78. Thali MJ. the dive. Jarczyk PA. Hood JA.46:314–315. Neuman TS. Lyons KM. 3154–3156. Further reading  121 associated with barotrauma symptoms and signs. Hart B. eds. Other disorders In: Brubakk AO. Zadik Y. Arquivos de neuro-psiquiatria 2008. Yen K. Virtopsy: post- mortem multislice computed t­ omography Edmonds C. Flynn ET. ing of distension of the gas space. Rose DM. Eidsvik S.164(3):221–227. Journal of Forensic Science Society Journal 1991. Dysbaric peripheral nerve involve.48(6):1–9. Rupture of the stom- sion may be indicated. Molvaer OI.32:131–139. in the kidneys. there may be a delay of many minutes after Research 1986. or even recompres. Undersea and Hyperbaric Medicine 1995. Linaweaver nucleus pulposus). FURTHER READING Plattner T. Bennett and Elliott’s Physiology and Medicine of Diving. Facial b ­ aroparesis. ach complicating diving accidents. Maxillary sinus barotrauma with cranial identified as having dysbaric manifestations. with a middle ear or sinus pressure in with a report of 11 additional cases.12(4):495–463. Harris R. (e. the intervertebral disc and Neuman T. Alert Diver SEAP periferica. divers. Beaver G. Molenat FA. Compression pain in a diver with intraosse- With the cranial nerve palsies produced by ous pneumatocysts. Aviation.July:8–12.255:​ Australian Dental Journal 2011. The clinical features of pneumo- neurapraxia. Spontaneous Undersea Biomedical Research ­pneumoperitoneum after scuba diving.


3 Part     Decompression Sickness 10 Decompression sickness: pathophysiology 125 11 Decompression sickness: manifestations 141 12 Decompression sickness: prevention 153 13 Decompression sickness: treatment 167 14 Dysbaric osteonecrosis 185 .


a HISTORICAL PERSPECTIVE pressurized vertical shaft sunk into sites that would otherwise be flooded such as pylon sites in bridge Von Guericke developed the first effective air construction or mine shafts extending below the pump in 1650. At one extreme Pasley noted rheumatism and excessive fatigue in it may be rapidly fatal. in 1670. variable and There was a long hiatus before related effects to some extent unpredictable disorder with a wide were recognized in humans. but it may also occur in aviators humour of the eye of a viper. DCS is a puzzling. albeit 125 . juices and soft parts of the body’. presumed pathological vector of DCS. and men could work at the bottom. the ‘blood. 10 Decompression sickness: pathophysiology Introduction 125 Fate of bubbles after formation 134 Historical perspective 125 Pathological effects of bubbles 136 Uptake and elimination of inert gas 127 Presence of bubbles in blood 136 Bubble formation 129 Distribution of bubbles in blood 136 Gas micronuclei 129 Tissue bubbles 138 Venous bubbles 130 Multiple disorders in single organ systems 139 Arterial bubbles 132 Alternative hypotheses and future directions 140 Tissue bubbles 133 Further reading 140 INTRODUCTION Shortly afterward. Perhaps not surprisingly. ing for space walks. He designed and constructed what came to be known as a ‘caisson’. This permitted pressurization of water table. the shaft. non-specific symptoms. may manifest with mild. Robert Boyle exposed experimental animals to the effects of increased Decompression sickness (DCS) is a disease caused and decreased pressures. The divers were presumably suffering from DCS. The air pressure excluded water from gas for respiration at elevated ambient pressure. In the 1840s Colonel range of potential presentations. subject of much interest among divers and diving A French mining engineer. whereas at the other it divers employed on the wreck of the Royal George. cases of DCS in humans in 1841. it is the most widely rec. described physicians alike. not surprising because their bottom times exceeded ognized medical complication of diving and the the accepted limits by a factor of three. The snake was ‘tor- ascending to altitude in unpressurized or semi. tured furiously’ by the formation of bubbles in pressurized aircraft or in astronauts decompress. It is most commonly seen in divers in this case moving to and fro in the aqueous after surfacing. a bubble. ent pressure. His reports of these primarily by bubbles formed from dissolved gas in experiments included the first description of the blood and/or tissue following a reduction in ambi. Jean Triger.

a surgeon from the Manhattan ers were the result of this intravascular liberation Eye and Ear Hospital in New York. . noted in the of gas. Not surprisingly. There were almost certainly Paul Bert. the cases of sudden death in compressed air work. ache. Triger himself suffered knee pain half of the body. into the gas phase during or following decom- Hoppe-Seyler repeated the almost 200-year-old pression. convulsions and loss of conscious- sons. He believed River caisson tunnel in New York. aware of the value of recompression. but this was In 1872. versy regarding the speed and manner in which div- there may be elements of paralysis that. Sufferers among the that was attributed to the breathing of compressed workers on the Brooklyn Bridge caissons in New air and equated this with the caisson workers’ dis. interfered with circulation in the heart and lungs. others failed. hot baths. Andrew Smith. such as head- on several occasions after pressure exposure in cais. are most frequently confined to the lower dry environment. atropine.126  Decompression sickness: pathophysiology under whatever pressure was required to maintain a appear. in the early 1890s. Two physicians. in 1854. It was lem with mortality and morbidity. published a report indicating the inert gas (nitrogen in the case of compressed air nature of the disease. He constructed the first specialized pared the clinical course of severe and fatal cases treatment chamber. may be present. problems were not eliminated. working on the Hudson sionally seen in obstetrics and surgery. and in 1857 he described the to hasten decompression. ergot. Instead he of compressed air work and collected descriptions used hot poultices. aggravated by an erect position. the victims often described an occupational illness of sponge divers assumed a stooping posture. in the hips and lower extremities was generally Le Roy de Mericourt. He com. during the early part of the times in the trunk as well. ice packs. a host of other tures to a fashionable stoop in walking. in 1869. Moir. he noted. Because pain remedy this. There may or may not twentieth century there was considerable contro- be epigastric pain and vomiting. He suggested careful decompression from ­caisson ­exposures and that the blood was filled with gas bubbles that by recompression therapy for symptomatic cases. of symptoms of workers given insufficient decom. whiskey and ginger – or morphine if the pression after exposure to high pressure. Cerebral symptoms. when they ers and caisson workers should be decompressed. in 1878. which was practiced by sophis- nineteenth century to explain the aetiology of this ticated metropolitan women at the time. as reported by characterized. and in proj- Smith described ‘caisson disease’ or ‘com. Although some informed physicians were by their comrades. reduced the DCS that rapid decompression would be responsible for death rate from 25 per cent of the work force per a rapid release of the gas that had been taken up by annum to less than 2 per cent by the use of more the tissues under increased pressure. He also recommended recompression to 1870s the origin of the term ‘bends’. ects requiring exposure to relatively high pressures pressed air illness’ in 1873 as a disease dependent to construct tunnels under New York’s East River in on increased atmospheric pressure. and as their use expanded there were fatalities ness. by moderate or severe Keays in 1909. He suggested that some of gen recompression therapy. and Gal. In some cases. Pol and clusive manner that DCS is primarily the result of Watelle. who likened their angular pos- postulating a role for bubbles. pain in one or more of the extremities and some. vertigo. demonstrated in a most con- manifestations of DCS. of DCS with that of the venous air embolism occa. York were the objects of good-natured ridicule ease. but always the early 1900s there remained a significant prob- developing after reduction of the pressure. He was disorder. in 1872. termed the imaginative theories were proposed during the ‘Grecian bend’. Freidburg reviewed the development unacceptable to some of his patients. He used various oxygen concentrations Boyle experiments. together with case histories to divers and caisson workers) dissolved in blood and demonstrate the relationship between decompression tissues during pressure exposure and then released and onset of symptoms. demonstrated the value obstruction of pulmonary vessels by bubbles and of oxygen inhalation once experimental animals the inability of the heart to function adequately developed DCS and proposed the concept of oxy- under those conditions. However. and episodes of paralysis.

proposed  equations to describe tissue inert gas ­ kinetics and proposed that limiting inert gas super- saturation (see later) during decompression was the key to preventing DCS. Unlike highly soluble of nitrogen (PaN2) ‘immediately’ equilibrates.2  Nitrogen uptake in a hypothetical Underwater breathing apparatus supplies the perfusion-limited tissue compartment during a diver with air at ambient pressure. UPTAKE AND ELIMINATION OF INERT GAS Pamb Because it is believed that DCS is primarily caused 4 by bubble formation from dissolved gas taken up PaN2 into tissues during a dive. but also by the blood-tissue partition and most common approach in decompression coefficient for nitrogen. the pressure of nitrogen in the tissue and arterial PN2 occurs very quickly.1).1  A tissue depicted as a single well- stirred perfusion-limited ‘compartment’. Dives to depths beyond the recre. Thus. the arterial-tissue PN2 dif.1 atm (not the arterial blood. it is appropriate to exam- 3 ine process of gas uptake and elimination in some Pressure (atm) detail. inspired pressure of nitrogen and the alveo- olar pressure of nitrogen will result in its uptake into lar pressure of nitrogen rise to ~3. whereas tissues . John Scott Haldane. as predicted by Henry’s Law. poorly perfused tissues will take up gas slowly. In contrast. anaesthetic vapours. and the arterial pressure its distribution to the tissues. Figure 10. (Adapted with permission from a figure by gas kinetics. There are multiple ways in which blood-tissue at a rate determined substantially by tissue per- gas exchange can be conceived. Ptiss ational diving range are performed using mixed gases that contain helium (see Chapter 62). Tissues with luxurious modelling is to consider a tissue to be a well-stirred perfusion will take up inert gas quickly. where oxygen rebreath- ers may be used. the exchange of dissolved Dr David Doolette. the inspired dive to 30 metres (4 ATA) using air. the assumption is that the breathing 0 10 20 30 40 50 gas is air and therefore that the relevant inert gas Minutes is nitrogen. than blood will equilibrate quickly. The arterial-tissue difference decays in a mono-exponential fash- cess can largely be ignored in consideration of inert ion. whereas perfusion-limited compartment (Figure 10. His decompression tables. and depicted in the figure). These issues are discussed in Chapter 12.2). Exposure to an elevated alve. Figure 10. and variants of Haldane’s meth- odology are still in use for planning decompression today.) nitrogen between blood and tissues is influenced by several factors. For the general purpose of this 0 discussion. The key 1 point is that one or more inert gases are breathed in all but very shallow dives. Pamb is the (and alveolar) pressure of nitrogen (PN2) is directly ambient pressure in atmospheres (atm). Uptake and elimination of inert gas  127 An English physiologist. the equilibration of alveolar In contrast. Similarly. but the simplest fusion. and this pro. Within such a model. (Ptiss) is slower to equilibrate. Most diving is performed using air as the 2 respired gas. first published in 1908. The proportional to depth. tissues in which nitrogen is less soluble ference declines mono-exponentially (Figure 10. resulted in a remarkable reduction in the incidence of DCS in both diving and caisson work.

128  Decompression sickness: pathophysiology

with high solubility for nitrogen will equilibrate the tissue comes into equilibrium with the arterial
slowly. Thus, for the purposes of conceptualizing tension. Similarly, the longer the diver remains at
nitrogen kinetics (and for decompression model- depth, the further toward saturation the various
ling), the body is often regarded as a set of parallel tissues will progress.
compartments with differing kinetic properties for The principles discussed earlier in relation
nitrogen exchange (Figure 10.3). to nitrogen uptake remain relevant to nitrogen
A notional depiction of differing nitrogen elimination during and after ascent from a dive.
kinetics for each of the five hypothetical tissues Ambient pressure decreases as the diver ascends.
in Figure 10.3 is illustrated in Figure 10.4. It can As ascent begins, the alveolar and arterial pres-
be seen that by the end of the period at depth the sures of nitrogen will decline, and this will imme-
inert gas tension in the ‘faster’ tissues has equili- diately create a diffusion gradient for nitrogen
brated with arterial blood, whereas tensions in elimination from those tissues that equilibrated
the slower tissues have not. Those tissues in which with arterial PN2 at the bottom. As the ascent pro-
equilibration occurs are said to be ‘saturated’ with ceeds, similar outward diffusion gradients will be
inert gas for that depth. If sufficient time were established in increasing numbers of slower tissues
spent at depth, then all tissues would eventually that had absorbed less nitrogen during the bot-
saturate, a principle used in so-called saturation tom time. Because the kinetics of nitrogen elimi-
diving in which divers live under pressure for nation in these tissues is slower and the ascent is
extended periods in the knowledge that no fur- relatively fast, the tissues will tend to develop
ther inert gas uptake can occur (unless they ven- a state of ‘supersaturation’ in which the sum of
ture deeper), and after becoming ‘saturated’ there
is no increment in their decompression obligation
if they remain under pressure longer. In contrast, 4
the pattern of tissue equilibration with inert gas
at the end of the period at depth on a typical rec- PaN2
reational dive will look more like that depicted in 3
Pressure (atm)

Figure 10.4. Some of the faster tissues may be satu- P1 P2
rated and the slower tissues will not be. It should P3
be self-apparent that the deeper the dive, the 2 P4
higher the tissue nitrogen pressures will be when

1 P5

0 10 20 30 40 50

1 2 3 4 5 Figure 10.4  Nitrogen uptake in five hypothetical
perfusion-limited tissue compartments during
a dive to 30 metres (4 ATA) using air. Pamb is the
ambient pressure in atmospheres (atm). The
inspired pressure of nitrogen and the alveo-
lar pressure of nitrogen rise to ~3.1 atm (not
Figure 10.3  Conceptual depiction of body tis- depicted in the figure), and the arterial pressure
sues as parallel compartments with differing of nitrogen (PaN2) immediately equilibrates.
kinetic properties (1 ‘fastest’ to 5 ‘slowest’ – see The tissue pressures of nitrogen are slower to
Figure 10.4) determined largely by perfusion and equilibrate, with only tissues 1 and 2 approaching
tissue composition. Pa, arterial pressure of inert saturation within the duration of the exposure
gas. (Adapted with permission from a Figure by depicted. (Adapted with permission from a figure
Dr David Doolette.) by Dr David Doolette.)

Bubble formation  129



Pressure (atm)
Ptiss Pss

0 10 20 30 40 50 60 70 80 90 100 110 120

Figure 10.5  Nitrogen uptake and elimination in a hypothetical tissue compartment during and after a
dive to 30 metres (4 ATA) using air. The tissue does not equilibrate with the arterial nitrogen pressure
(PaN2) (become saturated) during the bottom time, but because nitrogen elimination does not match
the rapidly declining ambient pressure (Pamb) early in the ascent, the tissue becomes supersaturated; that
is, the sum of dissolved gas in the tissue (of which most is nitrogen under these circumstances) exceeds
the ambient pressure. The supersaturation pressure (Pss) is represented by the vertical distance between
the tissue pressure (Ptiss) and ambient pressure. (Adapted with permission from a figure by Dr David

dissolved gas pressures in the tissue exceeds the BUBBLE FORMATION
ambient pressure. This is depicted for a single tis-
sue in Figure 10.5. Depending on the rate of ascent, Gas micronuclei
the very fastest tissues may avoid this condition
because they eliminate nitrogen extremely quickly, It is noteworthy that relatively small gas supersat-
but tissues with slower kinetics are likely to become urations seem capable of provoking bubble forma-
supersaturated at some point in the ascent. tion in vivo yet huge supersaturations are required
Supersaturation of a tissue establishes a diffu- to provoke bubble formation in pure solutions.
sion gradient for gas to pass from tissue to blood This is almost certainly because of massive pres-
to alveolus, thus facilitating inert gas elimination. sures caused by surface tension forces at the
However, it is also the pivotal condition required fluid-gas interface of an evolving bubble. These
for dissolved gas to separate into the gas phase, that are inversely proportional to bubble radius, and a
is, to form bubbles. small bubble nucleating de novo from supersatu-
These bubbles are generally accepted to be the rated dissolved gas would need to overcome them.
pathological vectors in DCS, and the means by The most popular and widely accepted explana-
which they cause harm are discussed in detail in tion for in vivo bubble formation from relatively
the following section. In general terms, a greater small supersaturations is the postulated presence
degree of supersaturation will drive more bubble of tiny gas micronuclei in blood and possibly tis-
formation with a correspondingly higher risk of sues. These micronuclei are hypothesized to act as
developing DCS symptoms. Not surprisingly, most seeds for the inward diffusion of supersaturated
dive planning algorithms, used by divers to control gas after ascent from a dive, thus causing them to
their time/depth exposures and decompression grow into bubbles.
procedures, invoke some means of calculating and Both the source and nature of these micronuclei
controlling supersaturation during decompression are uncertain, but one suggestion is that they are cre-
as a core function. This is also discussed in more ated by tribonucleation in tissues where movement
detail later. creates momentary areas of depressurization within

130  Decompression sickness: pathophysiology

Liquid Bubble

Unsaturated Super Super
Gas nucleus
solid saturated saturated

(a) (b) (c)

Figure 10.6  Depiction of a gas micronucleus resident in a crevice on a blood vessel wall. In the unsatu-
rated state (a), the nucleus is quiescent. When the underlying tissue becomes supersaturated (b), gas
diffuses into the nucleus and causes it to grow until such time that a bubble breaks off (c), after which
the cycle will be repeated.

the tissue fluid or blood. Bubbles created under such diffuse into the micronucleus, thus causing it to
circumstances are usually tiny and rapidly involute grow and bud off bubbles in an analogous man-
in response to the high pressures caused by surface ner to the steady stream of bubbles that can be
tension mentioned earlier that force the gas back seen issuing from specific points on the wall of
into solution. However, micronuclei theory holds a glass containing a carbonated beverage. The
that some of these bubbles acquire a stabilizing essential features of this notion are illustrated in
outer layer of surface active molecules (these being Figure 10.6.
extremely common in vivo) that reduce surface ten- Another theory invoked to explain bubble for-
sion and increase the life span of the bubble, which mation within tissues themselves is that if tribo-
now becomes a micronucleus. nucleation on movement or impact creates tiny
Evidence supporting the existence of micronuclei bubbles in a tissue that is supersaturated at the
is largely circumstantial, beginning (as described time, the supersaturated gas will diffuse into the
earlier) with the mere fact that bubbles can form in bubbles and not only prevent their early involu-
vivo following relatively small supersaturations. In tion, but also cause them to grow. This is analogous
addition, in vivo experiments in which a short ‘spike’ the act of shaking an open soda bottle and could
to particularly high pressure was imposed before a explain bubble formation even in the absence of
decompression demonstrated less bubble formation persistent gas nuclei.
than expected; a finding implying that at least some
micronuclei had been crushed out of existence during Venous bubbles
the high-pressure spike. Consistent with the notion
(mentioned earlier) that tissue movement may result Of all the sites where bubbles form from super-
in regeneration of micronuclei, one famous experi- saturated dissolved gas, most is known about
ment using shrimps showed that ‘exercise’ following bubbles in the veins. This reason in no small part
the ­high-pressure spike partially reversed the spike’s is that Doppler technology has made it relatively
prevention of subsequent bubble formation. simple to detect bubbles moving in the venous
Variations and parallel theories exist. For system. Doppler ultrasound systems can detect
­example, it has been proposed that micronuclei flow in blood vessels and generate an audible flow
could reside in imperfections or crevices in cap- signal. The passage of a bubble through the ultra-
illary walls and that when the underlying tissue sound beam causes a characteristic ‘chirp’ over
becomes supersaturated, nitrogen molecules will and above the background ‘whooshing’ sound of

Bubble formation  131

the flowing blood. More recently, high-quality Spencer’s grading system monitors the precor-
echocardiography has become feasible with the dium for bubbles with the subject sitting quietly:
use of small portable devices. This allows direct
visualization of bubbles as they arrive in the right Grade 0 – No bubble signals on Doppler.
side of the heart. Much research about the qual- Grade I – An occasional bubble but with most
ity of decompression has been conducted using cardiac periods free.
quantitative estimates of venous bubble ‘grades’ Grade 2 – With many, but less than half, of the
as the outcome measure. cardiac periods containing Doppler signals.
It has become clear that when bubbles form Grade 3 – Most of the cardiac periods contain-
from supersaturated dissolved gas in blood they ing showers or single bubble signals, but not
first appear in the veins (as opposed to the arter- dominating or overriding the cardiac motion
ies, which are discussed later). This is logical signals.
because these bubbles almost certainly develop Grade 4 – The maximal detectable bubble signals
in the capillary beds of supersaturated tissues, sounding continuously throughout the heart
and they can be expected to distribute with the cycle and overriding the amplitude of the nor-
flow of blood into the venous system. Bubbles mal cardiac signal.
may be present minutes after a dive, but their
detection typically peaks around 30 minutes The Kisman-Masurel classification system was
after surfacing and then may be sustained for designed with the aim of easily incorporating the
several hours. Studies in animals suggest that bubble signal into a computer program. The bubble
these bubbles vary in size between 19 and 700 signal is divided into three separate c­ategories  –
micrometres. This variability is difficult to inter- ­frequency, percentage of cardiac cycles with ­bubbles/
pret because once formed, bubbles may coalesce duration of bubbles and amplitude. Each component
to create larger bubbles. Nevertheless, when it is is graded separately and then a single-digit bubble
considered that capillary diameter is somewhere grade is awarded. The primary site for monitoring
around 5 to 10 micrometres, it is clear that even is the precordium over the right side of the heart.
the smallest of these bubbles are likely to interact Monitoring is conducted at rest and after a specified
physically with any tissue bed that they enter. movement, typically a deep knee bend (squatting up
Bubbles forming in the veins, often referred and down in a continuous fashion). Although this
to as ‘venous gas emboli’ (VGE), pass to the right system appears more complicated than the Spencer
side of the heart and thence to the lungs, where system, it is the preference of many researchers and
they encounter a capillary network for the first is easily learned.
time. Given that the pulmonary circulation is a Both systems suffer from interobserver error
low-pressure system, it is perhaps not surpris- with some difficulties in subjectivity. Although
ing that the lungs are an efficient filter for VGE. computer-based counting programs are being
Removal of most incoming VGE by the lungs has developed, human observers are still more accu-
been documented in numerous experiments in rate than the automated models.
both animals and humans. In most cases this does Most studies of VGE formation have had one or
not appear to be associated with obvious harm, both of two interrelated goals in mind – first, to
although harm can occur (see later) and this is establish the relationship between appearance of
probably d­ ependent on the number of bubbles and VGE and DCS; and second, refining decompres-
their rate of arrival. sion strategies. In regard to the first goal, it has
The formation of VGE after diving has been become abundantly clear that VGE are commonly
extensively studied. These studies have required a detectable after recreational dives that do not result
standardized means of quantifying the detected in DCS. Indeed, even the presence of high-grade
bubbles. There are two bubble classification and bubbles is often not associated with the appearance
scoring systems commonly in use: the meth- of symptoms, and the positive predictive value of
ods described by Spencer, and by Kisman and VGE grades for DCS is thus poor. Large studies do
Masurel. report a correlation between VGE grade and risk

132  Decompression sickness: pathophysiology

Table 10.1  The incidence of decompression sickness associated with venous gas
emboli grades (Kisman-Masurel system) following human dive trials at the
Canadian Defence and Civil Institute of Environmental Medicine

Bubble grade All grades 0 I II III IV
Subjects 1726 819 287 183 365 72
DCS 35 0 3 2 23 7
Incidence (%) 2.03 0 1.1 1.1 6.3 9.7
DCS, decompression sickness.
Source: Data reported by Nishi R, Brubakk AO, Eftedal OS. Bubble detection. In: Brubakk AO,
Neuman TS, eds. Bennett and Elliott’s Physiology and Medicine of Diving. 5th ed.
London: Harcourt Publishers; 2003:501–529.

(Table 10.1), but this is not precise enough for VGE (venous-to-arterial) transfer of VGE. This can
grades to be used in diagnosis of DCS. occur via several ­recognized ‘shunt’ pathways.
The lack of a ‘diagnostic correlation’ between The lesser known and least researched of these
VGE and DCS symptoms is perhaps not surpris- pathways are pulmonary ‘shunts’. The existence of
ing when it is considered that some manifesta- such shunts has been known for some time. They
tions of DCS are almost certainly not directly can be detected in some subjects at rest and in
caused by VGE (see later). However, even the many subjects during exercise. Indeed, their physi-
weak correlation demonstrated in Table 10.1 sug- ological role may be to unload the right side of the
gests that numbers of VGE are at least indicative heart to some extent during heavy exercise. The
of the probability of significant bubble disorders increasing use of echocardiography in the obser-
in other sites, and this has encouraged the use vation of bubble behaviour after diving, and also
of VGE grading as an admittedly imperfect tool in saline contrast tests for patent foramen ovale
for assessing and refining decompression strat- (PFO; see later), has revealed that VGE can some-
egies. The ongoing use of VGE grading in this times be seen emerging from the pulmonary veins
regard is also influenced by the lack of readily into the left side of the heart. Thus, these bubbles
acceptable alternative outcome  measures. For have crossed the pulmonary circulation rather
example, performing manned dive trials using than an intracardiac shunt. It is notable that one
DCS as the outcome requires extremely large small study failed to detect pulmonary shunting of
studies  and  may encounter ethical objections. VGE in divers exercising after a dive. Nevertheless,
It should be obvious from this discussion that pulmonary shunts may contribute to the develop-
although VGE counts are a useful tool in decom- ment of the DCS syndromes known to be associ-
pression research, great care must be taken over ated with right-to-left shunting of VGE (see later),
the conclusions that are drawn in relation to the especially where there is no PFO to explain the
risk of DCS. mechanism.
The better known and most widely researched
Arterial bubbles pathway is an intracardiac shunt, usually a PFO.
The foramen ovale is a communication through
Bubbles almost certainly do not form from the atrial septum that during fetal life allows blood
d issolved nitrogen in the arterial circulation
­ arriving at the right side of the heart in the inferior
because once the venous blood passes through vena cava to be directed straight across the septum
the lungs, the dissolved PN2 in the blood and into the left atrium, thereby by-passing the right
alveoli should have equilibrated, and the arte- ventricle and pulmonary circulation. With the
rial blood leaving the lungs will no longer be haemodynamic changes that occur at birth, the
supersaturated. Bubbles can be introduced into foramen ovale closes in a valve-like manner, with
the arterial circulation by pulmonary baro- the higher left atrial pressures tending to keep it
trauma (see Chapter  6) and also by left-to-right shut. In the majority of people, the tissue pads that

Bubble formation  133

close the foramen ovale become ‘healed’ in the atrial pressure rises. The results are often crudely
shut position, but in a minority (some 25 to 30 per graded as follows: 0 = no bubble shunting; 1 = few
cent), the foramen ovale remains open, or at least bubbles shunted even during a Valsalva manoeu-
able to open should pressures in the right atrium vre; 2 = moderate numbers of bubbles shunted
exceed those on the left for any reason. This is during a Valsalva manoeuvre; 3 = spontaneous
referred to as a ‘patent’ foramen ovale (PFO). shunting of bubbles without a Valsalva manoeuvre.
As implied earlier, a PFO can be found in 25 to There has been debate about whether echocar-
30 per cent of adults who are unaware they have diography should be transthoracic (less expensive
one, and most go through life suffering no ill effects. and less invasive) or transoesophageal (better-
However, there are now multiple case-control quality imaging) for these tests. In general, it is
studies that collectively demonstrate associations agreed that in expert hands and provided good
between the presence of a PFO and DCS involving views can be obtained, transthoracic echocardiog-
the brain, spinal cord, inner ear and skin. In the var- raphy is ideal for this purpose. In fact, it is more
ious relevant studies, these associations are estab- likely to result in accurate studies because patients
lished by a substantially higher prevalence of PFO are typically better able to cooperate with provoca-
among cases of DCS than found among control tive manoeuvres such as Valsalva manoeuvres than
divers who have not suffered DCS. If we ­cautiously during transoesophageal echocardiography, when
accept that causation can be inferred from this patients may be uncomfortable or sedated. If trans-
association, the clear implication is that VGE that thoracic views are poor, then a transoesophageal
become ‘arterialized’ across a PFO are important in investigation should be considered. Another vari-
the pathophysiology of these forms of DCS. The way ant of the ‘PFO test’ is the use of carotid or tran-
these small arterial bubbles may cause harm is dis- scranial Doppler imaging to detect bubbles in the
cussed in more detail later. Another unsurprising respective arteries after injection of saline contrast
and consistent finding among the relevant studies is and a Valsalva manoeuvre. These tests detect a
that the size, or more correctly the shunting behav- right-to-left shunt, but they do not definitively
iour, of the PFO seems important. Thus, a grade 1 distinguish among the lesions that are potentially
(see later) or ‘small’ PFO is likely to represent little if permitting it (e.g. PFO, pulmonary shunt, atrial
any risk, whereas a grade 3 or spontaneously shunt- septal defect).
ing PFO almost certainly imparts extra risk for the
relevant forms of DCS. Tissue bubbles
Not surprisingly, divers may request testing for
the presence of a PFO. The issues of which div- Bubble formation from dissolved nitrogen in tissues
ers should be tested for a PFO and what should is plausible wherever the supersaturation conditions
be done when a PFO is found are discussed later are favourable. However, this is the least understood
in Chapter  12; however, the testing process is and documented of the processes likely to contrib-
described briefly here because some of the ter- ute to DCS mainly because, unlike bubbles moving
minology that arises is relevant to discussion of in blood, tiny bubbles in tissue are difficult to detect
the pathogenicity of arterial bubbles. The pro- with current technology, and studying small patho-
cess involves performing echocardiography while logical bubbles in tissue post mortem is notoriously
introducing agitated saline (which somewhat difficult.
paradoxically contains many small bubbles) into a The spinal cord is the most scrutinized organ
peripheral vein. The arrival of the bubbles in the in this regard. The 1990s saw a number of studies
right side of the heart often causes its virtual opaci- published that demonstrated ‘non-staining space-
fication on echocardiography, and the left side of occupying lesions’ 20 to 200 micrometres in diam-
the heart is then monitored to see whether bubbles eter and presumed to be bubbles in the spinal cord
cross the interatrial septum. Release of a Valsalva white matter after provocative decompressions.
manoeuvre causes a temporary rise in right atrial These experiments determined that the supersatu-
pressure and is used to unmask a PFO that remains ration threshold was moderately high for forma-
closed most of the time but that can open if right tion of these bubbles and that significant bubbling

134  Decompression sickness: pathophysiology

in the spinal cord white matter was unlikely unless periosteum and marrow. Similar reasoning has
dives were deeper than 25 metres. They also deter- led to the hypothesis that bubbles may form in
mined that tissue bubbles tend to form in the spi- peripheral nerve tissues. Patchy paraesthesiae in a
nal cord early, because as supersaturation declines non-dermatomal distribution are common symp-
quickly after surfacing the probability of bubble toms that have not been linked to the presence of a
formation also rapidly declines. right-to-left shunt, and it follows that tissue bubble
The brain tissue is not considered a likely site formation is the likely cause. It is plausible that
for bubble formation because of its luxurious per- bubbles could form in the myelin of a peripheral
fusion, which prevents significant or prolonged nerve, or elsewhere within the perineurium, and
supersaturation after most plausible decompres- cause neurapraxia through a mass effect. However,
sions. However, nitrogen is eliminated more slowly this mechanism is not substantively proven.
from the inner ear than the brain, and there is Finally, one presumed location for bubble for-
some experimental evidence for bubble forma- mation most appropriately categorized as ‘tissue’ is
tion in inner ear tissue itself. The inner ear is also the lymphatic system. The infrequent occurrence
uniquely vulnerable to enhancement of local tissue of discrete regional areas of oedematous soft tissue
supersaturation by a process frequently referred swelling, often accompanied by other symptoms of
to as ‘isobaric counterdiffusion’ (IBCD). This can DCS, has led to the assumption that bubbles may
arise during decompression from deep dives in form in lymphatic drainage channels and cause
which the diver makes a switch from a breathing stasis.
mix containing helium to one containing nitrogen
(see Chapter 62). Such switches are undertaken Fate of bubbles after formation
in the belief that they accelerate decompression
because helium in the tissues will diffuse into The pathogenicity of bubbles is described later,
blood faster than the nitrogen in the blood will but it is interesting to reflect on what happens to
diffuse into the tissue. The inner ear has a unique a notional bubble in tissue over time if only to
and relevant anatomy. There are relatively large discuss the concept of the so-called oxygen win-
unperfused reservoirs of helium (in the perilymph dow because this will arise again in several subject
and endolymph) that can eliminate accumulated areas.
helium only via the vascularized labyrinthine tis- We must begin by assuming that when a diver
sue. This maintains an elevated partial pressure of surfaces from a dive, a bubble forms from dissolved
helium in the vascular labyrinth after the switch to supersaturated nitrogen in a tissue. While the tis-
a nitrogen-based mix, while at the same time this sue remains supersaturated with nitrogen the bub-
tissue is also exposed to high pressures of nitro- ble will grow, but eventually the PN2 in the tissue
gen diffusing inward from the blood stream. This will come to equilibrium with that in the blood
‘counterdiffusion’ process may transiently enhance and alveoli for an air breathing subject at 1 atm.
any pre-existing supersaturation of helium and The bubble will not grow any more, and one may
result in bubble formation. then ask ‘What is to stop the bubble, once formed,
In addition to clinically relevant and largely from simply sitting in the tissue unresolved for
proven tissue bubble formation in the spinal cord long periods?’ There are two reasons.
and inner ear, there is strong circumstantial evi- First, the pressure inside a spherical bubble is
dence that tissue bubble formation is the cause of always likely to be greater than 1 atm, creating a
musculoskeletal pain in DCS. Specifically, the lack driving force for the inert gas contained therein to
of any association between the presence of PFO diffuse into tissue, thence to blood and alveolus.
and musculoskeletal pain in DCS suggests that This is because some pressure will be generated
in situ bubble formation is the most likely cause, by surface tension at the bubble–tissue fluid inter-
rather than bubbles arriving in the arterial blood. face and because some pressure will be generated
The exact location of tissue bubbles responsible for by surrounding tissue that has been displaced by
musculoskeletal pain is unknown, but there are the bubble. These factors are summarized by the
multiple possibilities including tendons, ligaments, following equation, whose middle term describes

Bubble formation  135

pressure resulting from surface tension and whose PO2, but this is difficult to measure, so we have to
final term describes pressure resulting from tissue speculate a little. Relevant data are summarized in
displacement: Table 10.2.
Note from Table  10.2 that for the purposes of
2σ 4 πr 3B this discussion it is assumed that a tissue bubble
Pbub = Pamb + +
r 3Vtis has an internal pressure equivalent to ambient
(760  mm  Hg). As discussed earlier, the typical
where Pbub is the pressure inside the bubble, Pamb internal pressure of a bubble in tissue is probably
is the ambient pressure, σ is the surface tension of higher, which would actually enhance the effect
the fluid, r is the bubble radius, Vtis is the volume described here, but for the purposes of illustrating
of tissue affected by bubble displacement, and B is the oxygen window, we will assume that the inter-
a term describing the bulk modulus of elasticity of nal pressure is same as ambient. The gas contained
the tissue. within the bubble will be composed of water
Second, even during air breathing, there is a vapour at a pressure equivalent to the saturated
small partial pressure gradient for nitrogen diffu- vapour pressure for water at 37°C (47 mm  Hg),
sion from bubble to tissue created by the oxygen and oxygen and CO2 in equilibrium with the tis-
window. This arises primarily because of the solu- sue pressures of those gases. The balance of the
bility difference between the oxygen consumed and bubble gas must be nitrogen, and by Dalton’s Law
the carbon dioxide (CO2) produced by metabolism. of partial pressures, the PbubN2 must be given by
The partial pressure of oxygen (PO2) in alveolar gas this equation:
during air breathing is approximately 100 mm Hg,
and after exchange with the blood, the PO2 in arte- PbubN2 = Pbub – (PbubO2 + PbubCO2 + PH2O)
rial blood is about 95 mm Hg. Oxygen is carried to
the tissues, where a given number of molecules are where PbubN2 is the pressure of nitrogen inside the
consumed through metabolism and replaced with bubble, Pbub is the pressure inside the bubble that in
a similar number of molecules of CO2. Removal of this example we are considering to be the same as
these oxygen molecules drops the PO2 from 95 mm ambient pressure (760 mm Hg), PbubO2 is the par-
Hg in arterial blood to 40 mm Hg in venous blood. tial pressure of oxygen in the bubble, PbubCO2 is the
However, because CO2 is much more soluble, the partial pressure of CO2 in the bubble, and PH2O
addition of the same number of molecules of CO2 is the saturated vapour pressure for water at 37°C.
to the venous blood only raises its partial pressure Table  10.2 shows that this resolves to a PN2 of
to 46 mm Hg (from 40 mm Hg in arterial blood). approximately 637 mm Hg which is about 64 mm
The PO2 in the tissues where the oxygen is actually Hg greater than the PN2 in the tissue, venous blood
being consumed is slightly lower than the venous and alveoli (573 mm Hg). This difference, which

Table 10.2  Approximate gas partial pressures in millimetres of mercury at various sites during air
breathing at a surface pressure of 1 ATA

Gas partial pressure
Sample O2 (mm Hg) CO2 (mm Hg) N2 (mm Hg) H2O (mm Hg) Total (mm Hg)
Alveolar gas 100 40 573 47 760
Arterial blood 95 40 573 47 755
Venous blood 40 46 573 47 706
Tissues ~30 ~46 573 47 696
Tissue bubble ~30 ~46 637 47 760
Note: The data for nitrogen assume that sufficient time has passed since a dive for nitrogen partial pressures
(PN2) in blood and tissues to have equilibrated with alveolar pressures. The different PN2 in the bubble is
explained in the text.

136  Decompression sickness: pathophysiology

creates a gradient for diffusion of nitrogen from of bubbles forming in blood into those effects a­ rising
the bubble to the tissue, is referred to as the ‘oxy- ­primarily because of the presence of ­bubbles in blood
gen window’. We reiterate that it is created by the and those arising from their distribution in blood via
dissolved gas partial pressure difference that arises the circulatory system.
from removing relatively insoluble oxygen from
solution and replacing it with very soluble CO2. Presence of bubbles in blood
As discussed again later, the oxygen window
could be further enhanced by breathing oxygen. The presence of bubbles in blood appears capable
Although this markedly elevates the alveolar and of activating reactive formed elements such as
arterial PO2, it has a much smaller effect on venous platelets and white blood cells, as well as inflam-
and tissue PO2 because the small amount of extra matory cascades such as the kinin, complement
oxygen dissolved in the arterial blood will be pref- and coagulation systems. The means by which
erentially removed and metabolized, thereby dra- this occurs are not clearly established, but there
matically dropping the PO2 back down to near are several possibilities for interactive activa-
normal levels. The venous PO2 (and therefore the tions involving known mechanisms. For exam-
venous oxygen saturation) may be marginally ele- ple, platelet and coagulation activation can occur
vated. Because the same amount of oxygen is con- through exposure to foreign surfaces such as
sumed and the same number of molecules of CO2 is glass or to collagen beneath damaged endothe-
produced, there will be virtually no effect on tissue lium. Bubbles may act in a similar way by acting
or venous PCO2. Thus, the PbubN2 as calculated ear- as a foreign surface or by damaging endothelium,
lier will change very little, while at the same time the latter having been demonstrated experimen-
the alveolar, arterial and tissue PN2 will fall mark- tally. Similarly, white blood cells can be activated
edly; potentially to zero if 100 per cent oxygen is by damage to endothelium.
breathed for long enough. The difference in PN2 There is rarely any obvious evidence of a role
between bubble and surrounding tissue will be cor- for these inflammatory activations in the patho-
respondingly exaggerated, and nitrogen will diffuse genesis of milder forms of DCS, although it has
out of the bubble more quickly. The same is true if been suggested that constitutional symptoms
the bubble is compressed. In this case, the Pbub in such as fatigue and malaise may occur as a result.
the foregoing equation is elevated, whereas bubble These processes may be important in producing
oxygen, CO2 and water vapour are little affected, specific serious manifestations. For example, one
even if oxygen is breathed during the compression. hypothesis for spinal cord injury that has been
The existence of the oxygen window, even dur- substantially demonstrated in an animal model
ing air breathing at 1 atm, at least partly explains holds that bubbles initiate coagulation in the
why bubbles of nitrogen cannot exist in a stable epidural veins, thereby leading to venous sta-
condition in tissues. It also explains why bubbles sis and a venous infarction in the spinal cord.
involute even more quickly during oxygen breath- Inflammatory responses may also be important
ing, especially when combined with recompression. contributors in severe or fulminant DCS. For
example, disseminated intravascular coagulation
PATHOLOGICAL EFFECTS can lead to a coagulopathy, and such patients
OF BUBBLES may also develop severe haemoconcentration
and shock secondary to the endothelial ‘leaki-
Having reviewed the processes that give rise to bubble ness’ that can follow inflammatory activations.
formation after decompression, the discussion now
turns to consideration of the potential pathological Distribution of bubbles in blood
effects of those bubbles. As discussed earlier, bubbles
may form from dissolved gas in blood and/or tissue, It has been previously noted that bubbles form-
and this section considers their potential pathologi- ing from supersaturated dissolved gas first appear
cal effects within those broad ‘anatomical’ categories. in the veins. In addition to any inflammatory
The ­discussion further subdivides the consequences responses and resulting harm that this may elicit

Pathological effects of bubbles  137

(described earlier), these bubbles can be trans- dynamic and cannot be investigated easily, our
ported in the circulatory system to sites distant knowledge of their role in DCS is poor, although
from their point of origin. they are potentially very significant.
The most obvious target organ in the distribu- The behaviour of PFOs is better characterized.
tion of VGE is the lungs. As previously discussed, it As described earlier, some PFOs shunt sponta-
seems that for the most part the lungs can tolerate neously, and there are data suggesting that such
and efficiently remove even grade IV VGE without lesions are the most significant in causation of
obvious harm. However, on relatively rare occa- DCS. Other PFOs require provocation to raise
sions divers may develop symptoms caused by the right atrial pressure sufficiently to open the com-
arrival of VGE in large numbers over a sufficiently munication. This can be provided by something
short space of time to exceed a poorly under- as simple as bending and straightening, strain-
stood clinical threshold. The trapping of copious ing to lift something or possibly even coughing.
bubbles in the pulmonary vasculature can cause Along with the Valsalva manoeuvre, all these
a significant rise in pulmonary artery pressure, a provocations have in common the tendency
ventilation-perfusion mismatch and the various transiently to impede venous return to the right
inflammatory changes described earlier. These side of the heart, thereby causing a brief exag-
events manifest as dyspnea, retrosternal chest pain gerated ‘rush’ of blood into the right atrium on
and cough, a constellation of symptoms sometimes termination of the impediment. This transiently
referred to as the ‘chokes’, but more correctly called increases the right atrial pressure and may open a
cardiopulmonary DCS. Symptoms typically occur PFO that is normally kept closed by the prevalent
within the first 30 minutes after surfacing, but the positive left-to-right pressure gradient.
natural history is variable. There may be rapid pro- The previously mentioned association between
gression to hypotension, collapse and occasion- the presence of a PFO and cerebral, spinal, inner
ally death, probably as a result of acute right-sided ear, and cutaneous DCS implies that the passage
heart failure. There are also many stories of these of small VGE into the arteries can injure these
symptoms resolving spontaneously, especially if organs. How these small bubbles cause injury is
oxygen is breathed, because this would markedly uncertain, although there are several possibilities.
enhance the rate at which bubbles are eliminated
from the pulmonary circulation. Not surprisingly, BRAIN
because the substantial numbers of VGE required It is known that a large bubble or bubbles emboliz-
to produce cardiopulmonary symptoms are pre- ing the arterial supply to the brain can interrupt
dictive of a potential for distribution of VGE in to flow sufficiently to cause ischaemic injury. Patients
the arterial system (see later) and also of a strong embolized by large aliquots of gas in iatrogenic
provocation for bubble formation in tissues, it is accidents and pulmonary barotrauma events can
not surprising that cardiopulmonary DCS is often develop stroke-like syndromes that are often mul-
followed by symptoms of other organ involvement. tifocal (see Chapter 6). However, it is uncertain
VGE may also distribute into the arterial that bubbles in the size range that typically arise
circulation via pulmonary shunts or a PFO as in the veins after decompression would cause such
previously described. Little is known about the injuries. Unlike solid emboli, bubbles are known
factors that promote pulmonary shunting of to redistribute through the microcirculation, and
VGE, although formation of large numbers of small bubbles are likely to do so very quickly.
VGE appears important, and experiments in Therefore, it seems implausible that small VGE
non-diving situations suggest that exercise is passing to the arterial system would cause large
a likely risk factor. One small study in animals cerebral infarctions. When such lesions are seen
also suggested that use of theophylline (a bron- after diving, there should be a high index of sus-
chodilator) reduced the efficacy of the lungs as a picion for arterial gas embolism secondary to pul-
filter for VGE; however, whether this effect was monary barotrauma.
via recruitment of shunts or another mechanism Nevertheless, it is plausible that sufficient num-
is unknown. Because these shunts appear to be bers of these small bubbles entering the cerebral

138  Decompression sickness: pathophysiology

circulation may result in dysexecutive symptoms (implying that arterialized VGE play a role) and
such as cognitive impairment, memory impair- the finding that these patients often present with
ment and confusion, which are often labelled only inner ear symptoms even though a much
‘cerebral DCS’. Exactly how small bubbles do this, larger number of VGE must have distributed to the
however, is not certain. One possibility that has brain. Although less well studied, it is likely that
some experimental providence is that the passage similar mechanisms can be responsible for spinal
of small bubbles through the microcirculation DCS, which probably has inert gas kinetics similar
causes endothelial disruption with consequent to those of the inner ear. Moreover, irrespective of
inflammatory changes such as the activation and whether the bubbles grow from inward diffusion of
accumulation of white blood cells (see Chapter 6). supersaturated nitrogen, the spinal cord and inner
This can cause a secondary decline in blood flow ear circulations are almost certainly vulnerable to
with a consequent degree of hypoxia, perivascular the same pro-inflammatory effects of bubble pas-
infiltration by the formed elements of blood, the sage as described earlier for the brain.
release of inflammatory mediators and the devel-
opment of tissue oedema; all of which may inhibit SKIN
or injure nearby neurons. The widespread occur- Other than the finding that arterialized VGE are
rence of this sort of event in the cerebral circula- implicated, exactly how the arrival of small bub-
tion could explain the ‘global’ cerebral impairment bles in the arterial supply to the skin precipitates
typically seen in cerebral DCS. rash and itch is uncertain, although it could con-
ceivably involve all the mechanisms (ischaemic
OTHER VULNERABLE NEUROLOGICAL and inflammatory) mentioned earlier in rela-
ORGANS tion to the brain and other neurological organs.
Neurological organs other than the brain, such Indeed, one histopathological study of the cutis
as the inner ear and spinal cord, are almost cer- marmorata form of skin DCS reported endothe-
tainly exposed to fewer arterial bubbles than the lial disruption and perivascular inflammatory
brain because of their markedly poorer perfusion, infiltrates entirely consistent with bubble-induced
meaning that fewer bubbles will be carried to these vasculitis. Questions remain, however, such as
organs. Paradoxically, these organs may be more the reason for the typical finding of a localized
vulnerable to ischaemic injury caused by small lesion (often on the trunk) when arterialized VGE
bubbles for the same reason. must distribute widely to cutaneous vascular ter-
Modelling studies have demonstrated that after ritories. As with the selective vulnerability of the
a dive the inner ear, for example, remains super- inner ear to vascular bubbles, the answer may lie
saturated with nitrogen for much longer than the in differing levels of post-dive inert gas supersat-
brain, which washes out excess nitrogen within uration making some areas of skin more vulner-
minutes. Thus, if VGE cross a PFO 15 minutes after able than others.
a dive and enter the basilar artery, most of them
will distribute to the brain, and perhaps a few will Tissue bubbles
find their way into the tiny labyrinthine artery.
However, whereas those VGE distributing to the As discussed earlier, bubbles may form in tissues
brain will distribute through tissues that are not where the supersaturation conditions are favour-
supersaturated, those entering the inner ear micro- able. Once formed these bubbles could cause
circulation will be exposed to supersaturated nitro- harm through the following mechanisms: direct
gen and will likely grow as this gas diffuses into damage to immediately adjacent tissue; indirect
the bubble. Thus, despite being exposed to smaller trauma within any tissue displaced by the bub-
numbers of bubbles, the inner ear may be selectively ble (e.g. stretching or compression of axons in
vulnerable to ischaemic injury because enlarging the spinal cord or a peripheral nerve); ischaemia
bubbles will be more likely to cause flow stasis. This caused by pressing externally on blood ves-
mechanism may help explain the repeated reports sels; haemorrhage through disruption of nearby
of an association between PFO and inner ear DCS blood vessels; stimulation of pain receptors; and

Pathological effects of bubbles  139

Bubbles formed from
supersaturated dissolved gas

In organ In venous
tissues blood

Shunted eg PFO Not shunted

Organs via
& inflammatory Filtered
effects rs by lungs
± growth by tissue be
m /
inert gas diffusion e nu ngs
r g l u rt
a o a
If l yt e
Ischaemia j ur ht h No obvious harm
in rig
Organ injury

Figure 10.7  Summary of key pathophysiological processes in decompression sickness. PFO, patent
­foramen ovale.

incitement of inflammatory reactions initiated to resolve during recompression even if the incit-
by tissue injury. ing bubbles were removed. In contrast, a brisk
The pathophysiological paradigm for DCS improvement soon after recompression could sug-
described earlier is summarized in Figure 10.7. gest that tissue bubbles pressing on surrounding
structures were the main culprit because in this
Multiple disorders in single case bubble resolution could be expected to elicit
organ systems some benefit.
The other important example is the inner ear,
It will not have escaped the astute reader’s atten- which, as previously described, may be injured
tion that in the case of some organs this discussion either by bubbles forming within the tissues
has proposed more than one way in which they can or by bubbles that have shunted from the veins
be injured by bubbles in DCS. and arrive in the arterial system. As explained,
The most conspicuous example is the spinal if these arterial bubbles arrive while the inner
cord, in which injury may be caused by: bubbles ear remains supersaturated with nitrogen, then
forming in the spinal tissue itself, by bubbles incit- they may expand as tissue nitrogen diffuses into
ing coagulation in the epidural vertebral venous the bubble. It is generally presumed that cases
plexus and by bubbles formed in the veins distrib- of inner ear injury arising during decompres-
uting to the cord via a right-to-left shunt and the sion from deep dives are most likely to be caused
arterial circulation. It is emphasized that this is not by bubbles forming within the inner ear tissue
self-contradictory and that in fact the spinal cord itself, particularly if symptom onset is tempo-
may be injured by all these mechanisms under rally related to a switch from a helium-based
various circumstances. The existence of these vari- breathing mix to air or nitrox. It is impossible
ous forms of bubble pathology may help explain to distinguish among disorders in cases aris-
inconsistent results when divers with spinal DCS ing after surfacing, but the strong association
are recompressed. For example, failure to elicit any between such cases and the presence of a large
improvement may be explained by coagulation PFO ­ suggests that a s­ignificant proportion of
in the epidural veins that would not be expected them are caused by arterial bubbles.

140  Decompression sickness: pathophysiology

ALTERNATIVE HYPOTHESES complex it seems to become. For example, it seems
AND FUTURE DIRECTIONS clear that microparticles are not homogeneous;
they have different origins, some appear to have
One newer avenue of research in relation to DCS mixed origins and they seem to have variable
pathophysiology that is very active but not con- inflammatory potential. Some larger micropar-
cluded as this book goes to press relates to the ticles even appear to have characteristics of gas
role of so-called intravascular ‘microparticles’. micronuclei and may contain a core of gas.
Microparticles are small fragments of membrane This is an exciting line of research that is in its
material that are shed from the surface of some infancy but that has the potential to modify our
formed elements of blood and also endothelium. pathophysiological paradigm for DCS significantly.
Their presence in the circulation appears to acti- Alternatively, it may transpire that microparticles
vate or amplify inflammatory processes and are little more than an interesting epiphenomenon.
coagulation, and as a result they appear capable It is a subject for those interested in the detail of
of initiating or at least exacerbating vascular this matter to watch closely.
injury. Microparticles are increased in a variety
of disease states including sepsis, myocardial FURTHER READING
infarction and vasculitis.
Microparticle numbers also appear to be Carraway MS, Key NS. The microbubble or the
increased by decompression stress, that is, in microparticle? Journal of Applied Physiology
the presence of tissue supersaturation with inert 2011;110:307–308.
gas. This raises the possibility that some of the Doolette DJ, Mitchell SJ. Hyperbaric conditions.
pathophysiological events in DCS that are cur- Comprehensive Physiology 2011;1:163–201.
rently attributed to circulating bubbles may in Francis TJR, Mitchell SJ. The pathophysiology
fact be caused or exacerbated by microparticles. of decompression sickness. In: Brubakk AO,
However, many questions remain unanswered. Neuman TS, eds. Bennett and Elliott’s
For example, is microparticle generation in Physiology and Medicine of Diving. 5th ed.
decompression stress secondary to bubble for- London: Harcourt Publishers; 2003:530–556.
mation, or is there some other unknown con- Mitchell SJ, Doolette DJ. Selective vulnerability
sequence of inert gas supersaturation that is of the inner ear to decompression sickness
responsible? How can the invariably wide dis- in divers with right to left shunt: the role of
tribution of harmful microparticles be recon- tissue gas supersaturation. Journal of Applied
ciled against the selective vulnerability of certain Physiology 2009;106:298–301.
organs such as the spinal cord and inner ear in Nishi R, Brubakk AO, Eftedal OS. Bubble
DCS? Similarly, why does the brain seem rela- detection. In: Brubakk AO, Neuman TS,
tively resistant to harm when in fact its luxurious eds. Bennett and Elliott’s Physiology and
perfusion would render it at highest risk of expo- Medicine of Diving. 5th ed. London: Harcourt
sure to microparticles? Publishers; 2003:501–529.
The answers to such questions are unlikely to
be simple. The more effort that goes into research- This chapter was reviewed for this fifth edition by
ing the microparticle phenomenon, the more Simon Mitchell.

Decompression sickness: manifestations

Introduction 141 Inner ear decompression sickness 147
Terminology and classification 141 Cerebral decompression sickness 148
Clinical manifestations: general Lymphatic decompression sickness 148
considerations 143 Combined presentations 148
Specific clinical manifestatIons 144 Fulminant decompression sickness 148
Mild decompression sickness 144 Differential diagnosis 149
Pulmonary decompression sickness 147 References 151
Cutaneous decompression sickness 147 Further reading 151
Spinal decompression sickness 147

INTRODUCTION in ­relation to terminology and classification of
the dysbaric diseases.
Decompression sickness (DCS) is an extremely
variable disease with multiple possible symptoms, TERMINOLOGY AND
many of which are non-specific. There are no labo- CLASSIFICATION
ratory tests or other investigations that confirm the
diagnosis, and diving physicians frequently have The pathophysiology of cerebral arterial gas embo-
to integrate knowledge of diving, diver behaviour, lism (CAGE) and decompression ­sickness (DCS)
DCS pathophysiology, DCS presentation and other is described in Chapters 6 and 10, respectively.
competing diagnoses in formulating an appropri- Although both CAGE and DCS are bubble-induced
ate response to reports of symptoms after diving. disorders and they share some commonality in
Not surprisingly, there are frequent diagnostic pathophysiology and manifestations, the tradi-
conundrums. This often occurs in the context of tional approach to terminology (and the one largely
situations where the implications of the diagnosis used in this book) was to treat them as separate
are profound, such as when the victim is aboard a entities. Thus, symptoms presumed to be caused
charter boat in a remote location and evacuation by formation of bubbles from supersaturated inert
will cause a major disruption to multiple high-­ gas after diving were labelled DCS. Symptoms
paying customers. These situations can be very considered likely the result of the introduction
challenging for the diving physician. of gas into the pulmonary veins after pulmonary
This chapter outlines the known patterns of barotrauma were most commonly labelled arterial
presentation and manifestations of DCS based gas embolism (AGE), or CAGE, given that cerebral
largely around effects by organ system. Before involvement usually dominated the clinical pic-
proceeding to that discussion, however, the dis- ture. DCS was further subdivided into type 1 and
cussion attempts to clarify some confusing issues type II categories. Type I was initially a designation


142  Decompression sickness: manifestations

for cases with musculoskeletal pain as the only ‘CAGE’ and presumed secondary to pulmonary
symptom, and it is still sometimes referred to as ­barotrauma. Although (as mentioned in Chapter
‘pain only DCS’. However the definition has sub- 10) there is some doubt about whether ‘arterial-
sequently been inconsistently modified and may ized’ VGE are large enough to produce the gross
variously include rash, lymphatic symptoms and focal cerebral lesions that can occur when air enters
some mild neurological symptoms. Type II indi- the circulation after pulmonary barotrauma, these
cated the presence of neurological symptoms, but concerns resonated in the diving medicine com-
the unintended consequence of this was to give munity. In particular, uncertainty developed about
equal weight to symptoms with disparate prog- using diagnostic labels such as DCS and CAGE
nostic significance such as patchy paraesthesiae that implied the underlying pathophysiology.
and gross motor dysfunction, hence the shifting of This matter came to a head in 1991 with the host-
the former into the type I definition. The authors ing of a consensus meeting to debate the matter in
of this text consider the type I and type II classifi- the United Kingdom1. The meeting generated a sys-
cation to be ambiguous and largely without value tem for characterizing dysbaric disease in descrip-
and do not recommend its use. tive terms as an alternative to diagnostic labels
The separation of CAGE and DCS as clinical implying a particular underlying pathophysiology.
diagnoses was predicated on the perceived con- Thus, the clinical syndromes previously labelled as
trast between the stereotypical ultra-short latency either DCS or CAGE were amalgamated under the
of focal cerebral symptoms in CAGE and the typi- ‘umbrella term’ ‘decompression i­llness’ (DCI), with
cally longer latency, broader symptom range and a descriptive paradigm in which an evolutionary
tendency to spinal rather than cerebral involve- term and an organ system term would be applied to
ment in DCS. This diagnostic paradigm was chal- each symptom. A simplified interpretation appears
lenged after publication (in 1989) of two studies in Table 11.1.
associating patent foramen ovale (PFO) with Thus, a diver presenting with worsening muscu-
neurological DCS. As discussed in Chapter  10, loskeletal pain after a dive is said to have ‘progres-
the only plausible explanation for an association sive musculoskeletal DCI’. A diver presenting with
between PFO and neurological DCS was that the sudden loss of consciousness immediately after a
PFO allowed venous gas emboli (VGE) to enter rapid ascent and who is subsequently recovering is
the arterial circulation and to thence be carried said to have ‘remitting neurological (cerebral) DCI’.
to vulnerable organs. Although diving physicians Under the more traditional pathophysiology-based
had been aware of the possibility for right-to-left nomenclature, these divers would likely be diag-
shunting of VGE before this, these studies brought nosed with ‘type I DCS’ and ‘CAGE’, respectively.
the issue into sharper focus and fuelled speculation Although this system conveys useful infor-
on whether right-to-left shunting of VGE could, mation and avoids implying p ­ athophysiological
in at least some cases, be responsible for short- i nterpretations that may be wrong, there are
latency focal cerebral symptoms typically labelled problems with it. First, it is imprecise when the

Table 11.1  Descriptive classification system for decompression disorders

Evolutionary term Organ system term
Static Musculoskeletal
Remitting Cutaneous
Progressive Neurological (appended with cerebral, spinal, peripheral)
Relapsing Vestibulocochlear
Note: Each symptom is given an evolutionary term, an organ system term and the diagnosis of DCI
­(decompression illness).

Clinical manifestations: general considerations  143

nature of the pathophysiological insult is known onset and the victim’s reporting the problem,
and inadequate when there is intent to imply particularly when mild symptoms are involved.
a  specific underlying mechanism. Clearly, the Sometimes there are obvious reasons why this
authors of this text encounter this situation in may be so, such as an asymptomatic diver retir-
the pathophysiology chapters of this book where ing for the night several hours after the last
the DCS/CAGE terminology is used (while avoid- dive and waking with symptoms in the morn-
ing the terms type I and type II in relation to ing. However, ‘denial’ and seeking alternative
DCS). Second, the umbrella term ‘decompression explanations for symptoms on the part of the
illness’ is too similar to ‘decompression sickness’, diver are often contributory. This stems in part
and the two are often used interchangeably by from a long-standing stigma about the diagnosis
commentators who do not appreciate the differ- that has its roots in the entrenched notion that
ent meanings described here. Finally, the descrip- if someone has DCS then he or she must have
tive terminology has become a significant source done something incompetent or wrong. The way
of conflict in the field, with frequently polarized in which this belief can affect the behaviour of
views on its utility. A compromise proposed in divers needs to be understood by any physician
the last edition of another major diving medicine assessing a possible DCS case. Thus, not only
text published in 2003 was to retain the DCS/ do divers have a tendency to denial of symp-
CAGE terms in discussion of pathophysiological toms and consequent late presentation, they
mechanisms, but to use the descriptive terminol- may also then misrepresent timing of onset to
ogy in clinical discussions. Albeit sensible, this avoid criticism for late reporting. This needs
policy has not been consistently applied. It is fair to be borne in mind when applying the typical
to say that the classification of decompression symptom latencies described earlier to a diag-
disorders remains ‘messy’ and inconsistent in the nostic paradigm. Another reason for symptom
modern literature. denial among divers is the understanding that
early reporting of symptoms may result in ter-
CLINICAL MANIFESTATIONS: mination of a dive trip and/or a logistically dif-
GENERAL CONSIDERATIONS ficult (and ­potentially expensive) evacuation for
­recompression treatment. Given such motiva-
DCS is precipitated by a decrease in environmen- tion to downplay problems, it is hardly surpris-
tal pressure. Although seemingly obvious, this ing that physicians who eventually see evacuated
means that any symptoms arising during descent divers at receiving units frequently find more
or during the period at depth (before ascent) will serious symptoms than were reported in initial
not be caused by DCS (unless the symptoms have discussions by telephone.
been ‘carried over’ from a previous decompres- Divers learn that for any depth, a period of
sion). Most cases arise after arrival of the diver at ‘bottom time’ can be spent there that, when not
the surface, although there may rarely be onset exceeded and when followed by direct ascent to
of symptoms during the ascent; particularly on a the surface at the correct rate, is associated with
dive with long decompression stops. This should an acceptably small level of tissue nitrogen super-
be considered an ominous sign that more seri- saturation (see Chapter 10) and a correspondingly
ous symptoms are likely after surfacing. If cases small risk of DCS. These acceptable bottom times
across the entire range of severity are considered, are often referred to as ‘no decompression limits’.
more than 50 per cent of patients develop symp- More advanced exponents (see Chapter 62) learn
toms within 1 hour of surfacing, and 90 per cent how to stage their ascent appropriately using
have symptoms within 6 hours. If severe mani- ‘decompression stops’ to maintain a small level
festations such as motor weakness are considered of risk if the no decompression limit is exceeded.
alone, most will begin to manifest within the Some divers inappropriately come to see adher-
first hour. ence (or not) to no decompression limits or to
Notwithstanding these estimates, there is fre- decompression stop prescriptions as the thresh-
quently a significant latency between symptom old for a binary outcome. Thus, they may believe

1  A schema for classification of the clinical manifestations of DCS. toms are the most common. Such events are often characterized as DCS’ by a consensus workshop hosted by Divers representing a ‘provocation’ for DCS. A  schema for classifying the pression limit was slightly exceeded.1. New Zealand interprets mild non-specific symptoms arising between 1995 and 2012. in turn. and this could influence the way a physician with cases treated at Auckland. only 36 per cent had objec- after the dive. This. and ment for divers in remote locations. of 520 patients tive’. for completeness. Indeed. Dive planning algorithms are dis. Such system. significant because if the diver meets the agreed criteria for the mild designation. Similarly. also puts how they are calculated or monitored by divers is DCS into the broader context of ‘decompression important for the diving physician evaluating a illness’ as described earlier. an issue that is ‘fulminant’. notwithstanding the previous comments. clinical manifestations in this way is shown in An appreciation of no decompression limits and Figure  11.144  Decompression sickness: manifestations ‘exceed the limits and you will get DCS’ and ‘stay manifestations of DCS categorized by organ within the limits and you can’t get DCS’. omitting It is logical first to discuss the constellation of recommended decompression stops or ascending ­symptoms that were defined as constituting ‘mild too rapidly. but Alert Network (DAN) and the Undersea and at the opposite end of the risk spectrum. potential DCS case because. but they can contribute to clinical terminology in which reference is often strange c­ onduct such as symptom denial if a dive made to ‘spinal DCS’. a dive well Hyperbaric Medical Society (UHMS) in 20042. high forth in preference to the older type 1 and type anxiety and illness behaviour because a no decom. II designations. Clinical syndromes of DCI Bubble formation Pulmonary from dissolved gas barotrauma DCS CAGE 'Mild' Pulmonary Cutaneous Spinal Inner ear Cerebral Lymphatic Commonly Rarely Combinations Fulminant DCS Figure 11. inside the no decompression limit with a perfect Presentations with one or more of the mild symp- controlled ascent would be considered ‘unprovoca. ‘combined’. which. This corresponds to commonly used ­ beliefs are clearly false. has important implications With the exception of the constellations of for decision making about evacuation and treat- symptoms designated ‘mild’. This is clinically cussed further in Chapter 12. at the other extreme. ‘cerebral DCS’ and so was within the limits or. this section considers the  clinical discussed further later. then the work- SPECIFIC CLINICAL shop consensus holds that he or she would not be MANIFESTATIONS disadvantaged in the long term if not recom- pressed. tive signs found on examination3. it remains true that a dive is Mild decompression sickness likely to carry a higher risk if there are events such as exceeding a no decompression limit. .

a high index of 4. S. Specific clinical manifestatIons  145 The symptoms in the mild category are as bubbles and provides relief) is not a valid ­strategy.g. often with poorly defined boundaries. and it may be described as ‘patchy tingling’. Various references characterize the typi. LOC = loss of consciousness.  adopting different positions and rubbing) to most unusual to base a diagnosis of DCS solely on effect relief. Similarly. fatigue is an almost invariable circumstances. and it is surpris- severe.O su T Pa a Le oth Co us ar W tig in in a o em g e Symptoms Figure 11. Note fatigue and lethargy appeared as separate entries in the database and so are shown separately here even though they likely represent the same phenomenon. multiple non-dermatomal distributions and may monly reported in hips. and it may a general sense of unwellness (malaise) are also migrate. ment that is yet to declare itself in a more obvious 3. shoulders and migrate. 70 60 50 Percentage of cases 40 30 20 10 0 . symptom in DCS (Figure 11. Itch and rash of the superficial erythematous suspicion must be maintained for spinal involve- type. distribution are likely related to spinal involve- and extra-articular pain (e. Subjective sensory changes in a non-­dermatomal symptoms may be indicative of spinal involve- distribution. and other spinal manifestations (e. Constitutional symptoms such as fatigue and way. Affected divers often remark that unlike common but very non-specific and difficult to musculoskeletal pain they have suffered in other interpret.g. there seems little they can do consequence of a long day of diving. manometer cuff as a diagnostic aid (inflating the Itches and light erythematous or ‘scarlatini- cuff over the affected area allegedly compresses form’ rashes. the presence of constitutional symptoms. assumed to be musculoskeletal in origin. it is com.C L. the whole ‘upper ment and do not meet the definition of mild. the use of a sphygmo. ment. if a diver presents with bilateral and malaise. In that regard. Sensory changes that lie in a dermatomal elbows. boring ache’. Musculoskeletal pain.2).g. the localization is often poor. ingly common (see Figure  11.O B nn a Vi gy He C itus M arin ugh He ingl in ad ing Fa che Nu akn ue Di bne s zz ss Na ess gn ea e th er Ra l sh Ur Itch At ry s yl s a m es os or los Ti axi Sx itiv . SOB = shortness of breath. However. motor and sensory change) must be diligently excluded Musculoskeletal pain is the most frequent by competent examination.2). It is often described Subjective sensory change is most commonly by patients as a ‘deep. symmetrical shoulder or hip pain. and indeed. . follows: It is notable that new back pain or abdominal pain following diving must never be automatically 1. It would be (e. It may occur in cal location as ‘joint pain’. arm’) is also well recorded. knees.2  Percentage of 520 DCS and CAGE cases complaining of various symptoms. It is common for pain Constitutional symptoms such as fatigue and to exist in more than one location. These 2. Indeed.

However. because this could herald the imminent appear- tribution. they can effectively occur the mild designation could not be applied unless anywhere. if recompression of other conditions to designate a case as ‘mild’. advocating withholding of recompression for all shop also required compliance with a number patients with mild cases. In addition to fitting the qualitative symptom It must be emphasized that the workshop was not definitions described previously. but variable Back and abdominal pain is not mild Fatigue/malaise Usually early onset.3. Despite this potential for acceler- workshop2. the mild designation should not be many physicians have retrospectively suggested ‘signed off’ for 24 hours. At the present time headache sits and hyperbaric oxygen are likely to accelerate reso- outside the mild categorization laid down by the lution markedly. However. the 2004 work. the workshop did ‘Deep boring ache’ Musculoskeletal pain Proximal joints Usually early onset. with the trunk being the most common ance of new (and non-mild) symptoms. This why there is a separate ‘box’ for cutaneous DCS in stipulation recognized the potential for undetected Figure 11. They are usually proximal in dis. may migrate Subjective sensory change Usually noticed after other sx Objective numbness is not mild Erythematous rash Often on trunk but ‘anywhere’ Rash/itch Usually early onset Cutis marmorata is not mild Figure 11. recompression headache alone.3  Symptoms of DCS that were designated “mild” by the 2004 remote DCS workshop2. is readily available. Second. .146  Decompression sickness: manifestations are less common than pain but still relatively fre. Headache is a very non-specific symptom The natural history of mild DCS symptoms (as and has many potential causes in diving. and that is neuros’ by divers with no medical training). Although defined earlier) is for spontaneous resolution even in it is often reported by divers presenting with other the absence of therapy. it would be extremely unusual face oxygen therapy will often accelerate r­ ecovery. involved site. disadvantage if the patient was not recompressed. the obvious symptoms appeared mild. Indeed. then 2004 consensus workshop2 concluded that provided it would be reasonable to continue to designate the the presentation met the criteria for mild DCS. but if a diver presented with mild symp. Another symptom that deterioration. then the best course of action First.1 even though most skin manifestations objective neurological manifestations even when fit within the mild category. while any of the symptoms were clearly worsening quent (Plate 3). to make the diagnosis of DCS based on a post-dive and in respect of pain in particular. the mild designation could not be applied is to treat the diver. The cutis marmorata form of cutaneous the patient had undergone a competent neurologi- DCS (see later) is not considered mild because it is cal examination (which does not include ‘5-minute often associated with neurological DCS. ated symptom resolution by recompression. case as mild provided the other criteria outlined there was little or no evidence for any long-term later are met. in The symptoms of the mild DCS syndrome are recognition of the potential for (rare) delayed summarized in Figure 11. but fatigue Constitutional symptoms common after diving May be noticed the next day Cognitive dysfunction is not mild ‘Patchy tingling’ Non-dermatomal. Third. the toms (strictly as defined here) and a headache. There is little doubt that sur- symptoms of DCS. headache. and the patient should be should have been included in the mild category is periodically reviewed during this time.

Often referred to as cardiopulmonary DCS. even if pulmonary symptoms begin to resolve. the symptoms may spontaneously under any circumstances. This disorder typically produces symp- onset is usually early after diving and is more likely toms within the first 30 minutes after diving. nal cord. and the first symptom is usually bilateral sen- pression stops have been omitted for some reason). and it quite quickly and can even change appearance may be aggravated by a switch from a helium- over a short period of observation. in a very serious manifestations such as spinal DCS.g. Examination findings are typically consis- Cardiac arrest and death may rapidly follow. treatment is the priority. the latter most duce sensory change and weakness in the upper likely reflecting rapidly progressive hypotension. following a provocative profile (e. Cutis marmorata has a marbled. location and extent of lesions is usually not nec- Because large numbers of VGE are required to essary or helpful. it is not surpris. Inner ear DCS manifests with vestibular symp- quent association with more serious manifesta. However. There may also be retrosternal chest with a loss of bladder sensation and tone and a loss pain and a progression from confusion to loss of anal tone. limb. but as it progresses it becomes less ing gas. The skin Inner ear decompression sickness manifestation known as cutis marmorata sits outside the mild definition because of its fre. the rash almost invariably still has hours of decompression to complete. and detailed examination to delineate the erates the resolution of VGE affecting the lungs. tent with loss of upper motor neuron function Alternatively. appearance in which areas of deep erythema and Two distinct patterns of evolution are recognized. Despite its often can incapacitate the diver at a time when he or she dramatic appearance. Specific clinical manifestatIons  147 identify s­urface o ­ xygen and other adjuvants (see resolves with no obvious injury to the cutaneous Chapter 13) as acceptable alternatives to recom. but in DCS there may be resolve. Once the approximate extent of spinal involvement ing that symptoms of involvement of other organs is understood. permanent sequelae are Cutaneous decompression sickness common even after treatment with recompression and hyperbaric oxygen. nausea. timely instigation of recompression often accompany or follow pulmonary DCS. remote location). The rash can evolve dives while the diver is still submerged. produce pulmonary symptoms. which give rise to the colloquial name ascending paraplegia. The rash can based breathing gas to a nitrogen-based breath- be itchy at first. especially with surface oxygen administration. where decom. Cervical involvement may also pro- of consciousness and collapse. This is particularly dangerous because it irritating or sometimes painful. The significance of cutis marmorata is its pression in mild cases where recompression would moderately frequent association with other more be difficult or hazardous to access (e. especially at first presentation. blotchy cochlear symptoms (tinnitus. This is usually associated ‘the chokes’. and itch as part of the mild constellation of DCS symptoms has already been discussed. especially if oxygen breathing is quickly patchy involvement of different regions of the spi- commenced because this almost certainly accel. which often ascends from distal to The diver may complain of cough and shortness ­proximal. recovery is possible. sory change. shortly followed by weakness producing of breath.g. The natural history of spinal DCS is variable. ataxia) or tions. The common. this although a thoracolumbar distribution is most manifestation is rare and potentially fatal. there should be a high index of suspicion for other In cases that progress to weakness. This makes spinal DCS the The designation of superficial erythematous rash most feared and debilitating of the dysbaric diseases. deafness) or both. vomiting. thus . Spinal decompression sickness Pulmonary decompression sickness All levels of the spinal cord may be involved. toms (vertigo. tissues. Thus. spontaneous manifestations. sometimes cyanotic change are interrupted and The first occurs during decompression from deep bounded by areas of pallor.

whereas an isolated monoarthropathy after diving always raises suspicion of an alterna- Cerebral decompression sickness tive diagnosis such as a muscular strain. The second occurs after arrival ­ shoulder area appear selectively vulnerable. but it can create a conspicuously utes of the dive. The at the surface from more typical recreational air disorder usually develops over a period of hours dives. although the authors thy. It may lie over sites where there is in place. this does not appear in isolation. there is clear evidence The latter type of presentation is described in of widespread systemic effects of bubbles such Chapter  6. permanent loss of hearing may occur. but plete resolution.148  Decompression sickness: manifestations forcing an early ascent with substantial missed or at other locations. As described in Chapter 10. baric oxygen. the foregoing symptoms. Although the vestibular appa. Other concentration. These different presentations prob. a mono- arthropathy combined with patchy paraesthesiae DCS can manifest with dysexecutive syndromes and an erythematous rash would be a much more in which the diver complains of difficulties with convincing basis for the diagnosis of DCS. Lymphatic DCS appears as per se. . If patients with fulminant DCS are recom- subcutaneous swelling that is often s­ urprisingly pressed without appropriate supportive therapy localized. lation of symptoms described as constituting the date asymmetrical vestibular function that takes mild DCS syndrome. This form of the disease is frequently fatal are aware of cases in which permanent cognitive unless there is expert and comprehensive inter- sequelae have been reported. Such combinations can be place over weeks to months and usually results in useful in helping to formulate the diagnosis. In this regard. fluid resuscitation. likely that such symptoms arise from exposure of the brain to VGE that have arterialized across a Fulminant decompression sickness right-to-left shunt such as a PFO. shock and coagulopa- is poorly characterized. it is certainly possible that long-term injury can follow Combined presentations inner ear DCS. the outcome is likely to be poor (Case ­musculoskeletal pain (which may be coincidental) Report 11.g. memory. in addition to combinations of arterial circulation after pulmonary barotrauma.1). it seems most spinal DCS. and there do not appear to be they are responsive to recompression and hyper. For spontaneous resolution of vertigo and ataxia. Both may resolve spontaneously. The previously described manifestations can all ratus may be permanently damaged. It seems unlikely that these small VGE can cause the focal stroke. In particular. be a more pressing priority than recompression ous manifestations. In this setting the diver is recompressed or not. but like manifestations typically associated with larger the term is sometimes used to describe those bubbles that may be introduced to the cerebral cases in which. but combinations of symp- usually result in long-term symptoms. These manifestations are frequently and any of the other forms of DCS. The natural history of cerebral DCS as haemoconcentration. It is not usu- the onset is typically seen within the first 30 min. common combinations include mild symptoms tive functions. any long-term sequelae. particularly the constel- well-recognized ability for the brain to accommo. The upper thorax and decompression. it is notable that access to supportive therapy such as sedation. enlarging the breast area ably have a ­different pathophysiological basis (see in a male patient). mood and other cogni. odd appearance (e. There is a toms are very common. and pharmacologic support of haemodynamics may Lymphatic symptoms are among the more curi. pulmonary noticed ‘late’ when the diver returns home or to DCS and spinal DCS. example. Whether treated or untreated. The natural history is to com- Chapter 10). although usually involving moderate depth after diving and will eventually resolve whether exposure (greater than 25 metres). vention. ally painful. appropri- Lymphatic decompression sickness ate airway management. Fulminant DCS is a poorly defined entity. and cutis marmorata and work.

an evaluation of the ‘provo. base excess. 5.24. arterial and central venous lines placed and was aggressively fluid resuscitated and supported with vasopressors as the chamber was prepared for recompression. DCS has many non-specific symptoms. Muscular and soft tissue Chapter 12) would be considered more provoca. Other disorders that may mimic on the presence of fatigue alone. for example. Malaise can DCS are briefly considered here. having been treated with oxygen by a non-rebreather mask. 2. and it may also be caused involved rapid ascent or involved risk factors (see by many other problems. migratory monoarthropathy with a history consis- with DCS becoming less likely with greater symp. He had marked widespread cutis marmorata and quadriplegia. especially where the diver has a non- in this chapter) is also contributory to diagnosis. and he arrived at a major tertiary hospital with a hyperbaric unit less than 1 hour after surfacing. there is such as bruising may help. He was diagnosed with fulminant DCS and catheterized. interna- tional normalized ratio. Examination findings tom latencies after diving. Such illnesses are common on diving trips. 254g/l). Diagnostic uncertainty and the diving with left shoulder and arm pain and being non-specific nature of many DCS symptoms will diagnosed as musculoskeletal DCS. The initial blood tests revealed marked haemocon- centration (haemoglobin. Although the occur in many systemic illnesses. Differential diagnosis  149 CASE REPORT 11. where there is heavy lifting and ample no decompression limits with no untoward events. The pulse was 152. viral illness can induce significant mal- poral relationship between diving and symptom aise. so care is needed integrated to give a definitive answer on diagnosis. Some of the more described. ticular. There have been a few There is no substitute for knowledge and experi. a dive that breached no decompression limits Musculoskeletal pain is the most common sin- without adequate decompression (see Chapter 12). especially in respect qualitatively consistent with one or more of those of some of the mild symptoms. The attribution of symptoms following diving and there are often several differential diagnoses to DCS is contingent on the symptoms being that should be considered. common or important differential diagnoses for cation’ of the dive is useful but not definitive.1 A rebreather diver suffered an equipment malfunction after 9 minutes at 110-metre depth and made an uncontrolled ascent to the surface. When sedation was withdrawn after 24 hours. inevitably result in recompression of divers with Fatigue is extremely common after diving. Thus. A helicopter evacuation was extremely expeditious. . lactate. was well inside the ronment. and in par- authors of this text emphasize the fact that a tem. coagulopathy (activated partial ­thromboplastin time. and peripheral pulses were unpalpable. After two further recompressions he. made an essentially complete recovery. −12). he had recovered almost all motor function. He quickly resumed breathing and regained con- sciousness when cardiopulmonary resuscitation was initiated. although cutis marmo- no formula in which these various factors can be rata can look a little like bruising. This should be The timing of symptom onset (discussed previously considered. tent with a non-DCS cause. opportunity for minor trauma. Unfortunately. He was sighted arriving at the surface and retrieved onto the boat. DIFFERENTIAL DIAGNOSIS onset is compelling evidence of a diving-related problem. cases of myocardial ischaemia manifesting after ence in this regard. gle symptom of DCS. consistent symptoms caused by another disorder and the diagnosis of DCS would never be made from time to time. He was complaining of dys- pnoea and severe back pain. DCS symptoms are outlined in this section. in interpreting skin change. where he was found to be unconscious and apnoeic. injuries are common events in the diving envi- tive than one that. After sedation and intubation he was recompressed on a maximally extended US Navy Table  6.0) and metabolic evidence of shock (pH. had large-bore intravenous access estab- lished. 105. somewhat remarkably. 7. In addition.

but the diagnoses have significantly differ- monary oedema (rare) (see Chapter 30). oxygen ent implications for subsequent management. spinal (e. The main clue of the most difficult and troublesome d ­ ifferential to DCS as a cause would be early onset (usually diagnoses in diving medicine – the separation ­ within minutes) after diving. Nevertheless. although the increases suspicion of IEBT. if the dive involved a gas switch from a high-helium sibility of pulmonary oedema. degenerative spinal disease (e. Near drowning would almost the rates at which the middle ears vent expand- certainly be indicated by a clear history of some ing gas through the Eustachian tubes. manifest for the first time early after diving. or subcutaneous emphysema in the supracla. This is sort of distress event and inhalation of water. Both disorders may manifest with pulmonary irritation such as pulmonary baro. known as ‘alternobaric vertigo’. Nevertheless. near drown. Pulmonary oedema has not DCS emerged. Moreover. diving. the symptoms explanation for persistent vestibular symptoms would be limited to pulmonary involvement.g. Oxygen toxicity symptoms decisions about treatment have to be made. and frequently in association with barotrauma such as haemoptysis. ciguatera fish poisoning) (see Chapter 33) can symptoms arising early after diving should never cause marked widespread paraesthesiae. such as chest pain and The diagnosis of inner ear DCS involves one cough. Immersion pulmonary oedema can and a clear history of difficulty with ear ‘clearing’ be a difficult differential diagnosis. mandates recompression therapy. A dive that is very non- symptoms often first appear at depth and force provocative for DCS would also tip the diagnostic termination of the dive. longer latency than pulmonary DCS. Symptoms that appear at suspicion toward IEBT. The presence of other viral Spinal symptoms following diving are almost illness symptoms such as fever and coryza. after a dive. This phenomenon Salt water aspiration syndrome usually has a is relatively common. as well as be rationalized to an alternative diagnosis without myalgias and malaise. an extremely good reason. and of spinal DCS can also occur in the Irukandji some toxic ingestions that may occur on dive trips syndrome (see Chapter 32). but Patchy paraesthesiae and rash can occur as a the symptoms would be unilateral and frequently result of contact exposures with irritants such as preceded by a history of previous problems. particularly descriptions of pulmonary DCS refer to the pos.150  Decompression sickness: manifestations especially where participants have travelled long The  appearance of other DCS manifestations distances on airplanes and have been exposed to would point strongly to DCS as the diagnosis. would be expected only at the end of very long Transient vertigo (usually lasting seconds) can periods of oxygen exposure in technical diving also occur during ascent if there is a difference in (see Chapter  62).g. ‘sciatica’) could rate diagnosis. DCS toxicity (very rare) (see Chapter 17). which invariably the result of DCS. Other allergies can cause rash. whereas recom- ing (see Chapter 22) or salt water aspiration syn. not infrequently there been a feature of definite pulmonary DCS seen is ambiguity around the diagnosis. Pulmonary barotrauma these patients may warrant referral for round win- could be suspected if there was a history of rapid dow surgery. A key point that frequently resolves or panicked ascent. although some dive would tip suspicion the other way. vestibular and/or cochlear symptoms early after trauma (rare) (see Chapter 6). immersion pul. and difficult by these authors. many other travellers. whereas a more provocative depth are not DCS. these may repre. Nevertheless. Alternobaric vertigo should never be used as an in all these differential diagnoses. pression is relatively contraindicated in IEBT and drome (see Chapter 24). can occur in many settings. transitory and self-limiting. to a high-nitrogen mix. pneumothorax difficulty equalizing pressures in the middle ears. . this between DCS and inner ear barotrauma (IEBT) does not rule out other causes of diving-induced (see Chapter 7). Manifestation before decompression rules out DCS. In addition. if the dive was unprovocative the problem is that IEBT often manifests first dur- for DCS or if there were clear signs of pulmonary ing descent. Pulmonary symptoms. or if other manifestations of sent misdiagnoses. It is possible that are not usually seen in DCS. The marine stingers (see Chapter 32) and soaps used to abdominal and back pain that may be a feature clean wetsuits. vicular area. can help with accu.

either DCS or CAGE. Doolette DJ. eds. Medical Society. et al. although it will delay Francis TJR. 2. Francis TJR. Bennett and Elliott’s toms appearing early after diving are caused by Physiology and Medicine of Diving. The related symptoms are appearance cerebral symptoms after diving where often initially noticed at depth. The circumstances of the gas from a common source. Smith DH. Mitchell SJ. divers suffering ­cerebrovascular and Hyperbaric Medicine 2014. pulmonary barotrauma or cerebral DCS caused There may also be a history of foul-tasting breath- by the left-to-right shunting of VGE across a PFO ing gas or multiple divers affected if they breathed or pulmonary shunts. Neuman TS. may also be caused by a gas toxicity such as car- there is often diagnostic ambiguity around the bon monoxide exposure. . Auckland. eds. Manifestations of access to therapies such as thrombolysis or clot decompression disorders. Maryland: Undersea patible with a CAGE event. Further reading  151 As previously discussed in relation to classifi. Simon Mitchell. 1991. 5th ed. it is Undersea and Hyperbaric Medical Society likely that gross focal symptoms are more com. and this provides a the competing diagnoses are CAGE secondary to clue that something other than DCS is responsible. dive may provide definitive clues. Bethesda. Equally. eds. London: Harcourt Publishers. New Zealand 1996–2013. This is FURTHER READING unlikely to be harmful. Marginal Decompression Illness in Remote pression according to the same regimen is now Locations – Workshop Proceedings. accidents have been recompressed before the misdiagnosis has been discovered. Haas RM. Another possible cause of gross focal symp. Decompression Illness: The Forty Second irrespective of the circumstances of the dive. Workshop. CAGE would be plausible and cerebral DCS highly REFERENCES implausible as an explanation for the rapid onset of focal cerebral symptoms after a panic ascent 1. Vann RD. Diving and on occasion. the prevalent response to either diagnosis (see Washington. because most cerebral symp. retrieval. toms is a cerebrovascular event coincident with Decompression illness in divers treated in completion of a dive. 3. In: Brubakk AO. the prioritization of recom.44:20–25. pression as first-line therapy without detailed investigation to exclude cerebrovascular accident This chapter was reviewed for this fifth edition by is appropriate for most cases. Describing during training in a swimming pool. in respect of cerebral DCS versus CAGE. symptoms are more likely to be caused by DCS. Dysexecutive symptoms arising after diving cation of the bubble-induced dysbaric disorders. Hannam JA. 2003:578–599. In addition. 2005. For example. Wachholz C. However. whereas dysexecutive and Hyperbaric Medical Society. Mitchell SJ. DC: Undersea and Hyperbaric Chapter 13). Such events have occurred. Management of Mild or the diagnosis is almost irrelevant because recom. Sames C.


cal m ­ odels that allow such calculations include ning approaches have.2. it is not surprising ambient pressure to establish the degree of super- that divers pay great heed to means of preventing saturation. thereby tracked throughout a dive. supersaturation of inert gas during decompression causes bubbles to form in sufficient numbers or size Basic principles (and in the right location) such that some poorly defined clinical threshold is exceeded and symp. gas tensions within tissues can be calculated and pression’) to reduce the probability of DCS. and adjustments to the dive profile can it. the mathemati- it is not surprising that all decompression plan. at their core. These dis- Given the potentially serious consequences of solved gas pressures can then be compared with decompression sickness (DCS). Decompression planning is the process decompression planning assumes that the inert of controlling depth. virtually any approach to toms occur. it is the express intent of this account computers and the amelioration of putative risk to discuss the broad principles of adapting tis- factors for DCS. 12 Decompression sickness: prevention Introduction 153 Exercise 163 Decompression planning 153 Hydration 164 Basic principles 153 Temperature 164 Gas content versus bubble models 156 Obesity 165 Dive tables. sue supersaturation calculations into decom- pression planning tools. As could be Because tissue gas supersaturation is the fun. time and the ascent (‘decom. As mentioned earlier. rather than the related DECOMPRESSION PLANNING ­mathematics. DCS occurs when accounts elsewhere1. and elimination in Chapter 10. These preventive measures can be broadly clas. anticipated from the discussion of gas uptake damental condition required for bubbles to form. Those wishing to study the math- ematical principles and methods can find relevant As discussed in Chapter 10. a means of tissue perfusion and the blood-tissue partition 153 . be made to prevent supersaturation from exceed- sified into two categories: the appropriate control ing safe thresholds. Both are discussed in this chapter. With the intended audience of depth and time exposures using dive tables or in mind. planning software and dive Age 165 computers 160 Dive sequences 165 Amelioration of risk factors 161 References 166 Patent foramen ovale 161 INTRODUCTION calculating the pressure of dissolved inert gasses in a range of tissues throughout a dive.

ent pressure and is often referred to as the ‘ambient sues behave in a manner analogous to one of the pressure line’. This able tissues per se. for all depths. the format introduced in Figure 12. tissue gas pressure may have not purport to be scaled correctly or to –represent equilibrated with ambient pressure in some ‘fast’ any particular tissue accurately. ing at any particular depth. as will be described. During time spent at the bottom depth. whereas in other ‘slower tissues’ it may not In Figure 12. Other  tissues  with slower (see later). Time is not illustrated that could prevail at the end of a period at depth in in the diagram but requires assumptions to be respect of tissue gas pressures in a range of tissues made about its passage. and tissue gas pressure is Figure  12. labelled ‘Tissue pressure = ambient pressure’. Depending on the kinetics of individual tissues tant to appreciate that this and subsequent figures and the time spent at depth. ambient pressure (depth) is shown (Figure 12. there is no further and these tissues can be described as ‘saturated’ with change in ambient pressure until the ascent begins inert gas for  that  depth. tissues. The bottom depth is reached at sure (thus having reached the ambient pressure line). It should be clear that while remain- hypothetical compartments used in decompres. It is impor. e e ur ur ss ss re re Tissue gas pressure Tissue gas pressure tp tp This tissue is now en en bi ‘saturated’ with inert bi am am gas at this depth = = re re su Depending on their su es es kinetics. See text early part of a dive.1 is the line sidered in these models are not real or identifi. there can be no supersaturation data into decompression p ­ lanning. as depicted by line B.2  Gas pressures in a range of hypotheti- tension in a hypothetical single tissue during the cal tissues at the end of a period at depth. The models merely consider a represents the point. where the pres- range of hypothetical tissues with different inert sure of dissolved gas in tissue is equal to the ambi- gas kinetics and assume that the relevant real tis. other ‘slower’ pr pr ue ue tissues will have lower ss ss Ti Ti pressures B Depth of dive A Ambient pressure (∼depth) Ambient pressure (∼depth) Figure 12. at the end of a period in this chapter are illustrating principles and do at the bottom depth. and so there is time. kinetics will have absorbed less inert gas and will inert gas will dissolve into the t­ issue and the tissue have lower tissue gas pressures. for further explanation.2 illustrates a hypothetical situation shown on the vertical axis. on the horizontal axis. The descent properties. the tissue gas pressure sion calculations. See text for explanation. also pertinent to reiterate that the ‘tissues’ con.1. therefore. the tissue gas pressure in one or more tissues little time for inert gas uptake and little increase in may have reached equilibrium with ambient pres- tissue gas pressure. Depending on the duration of the bottom occurs over a short space of time.154  Decompression sickness: prevention coefficient for the relevant gas(es) as inputs. The other notable feature in Figure 12. cannot rise above this line because once tissue gas To illustrate the incorporation of tissue gas pressure equals ambient pressure.2). further pressure gradient to drive diffusion of gas the relevant events during a dive are depicted using into the tissue unless the diver descends deeper.1  Depiction of changes in inert gas Figure 12. the point indicated.1. It is inert gas tension will increase. Line A (represented by the grey dots) with differing kinetic represents descent at the start of a dive. .

for further explanation. evolved over time.3  Development of supersaturation in a especially for tissues with fast kinetics. Figure 12. See text allows greater supersaturation at deeper depths. twice the ambient pressure. A. and the fixed ratio concept was ics. The principles by which these work are illus- trated for a single tissue in Figure 12. science between the so-called ‘gas content models’ In Figure 12. The supersaturation pressure is decompression. For the moment. and line B repre- Tissue gas pressure 4 3 sents the increase in tissue gas pressure as inert Super- gas is absorbed during the time spent at that depth saturation ­(bottom time).3. For the tion when modelling decompression in this way sake of simplicity. not washed out at a rate that matches the fall in This approach was moderately successful. this discussion temporarily ignores indicted by the double-ended arrow in Figure 12. the rule hypothetical single tissue during ascent. In Figure 12.4. it is assumed that this tissue has is ‘How much supersaturation is acceptable?’ The reached the ambient pressure line (and is thus satu.3.3. stop was imposed to allow the tissue gas pressure to whereas in this tissue the accumulated inert gas is fall while the ambient pressure remained constant. and this approach is contrasted with in tissue gas pressure as inert gas is absorbed dur. line C in Figure 12. line A in Figure  12. Buhlmann and based on physiological predictions with subsequent empirical modifica- tions. the fall in tissue gas pressure could more closely eventually dropped in favour of ascent rules that match the falling ambient pressure.3. By the end of the bottom time the illustrated tissue has reached the ambient pressure B line (grey dot at point 2) and is thus saturated with inert gas. This was Haldane’s sure during the early part of the ascent. and line B represents the increase tent models. As is typical. but in this tis. The most famous ambient pressure (point 5) and the tissue is thus of these sets of rules were the Zurich Limits for 16 hypothetical tissues (the ZH-L16 limits) prescribed by A. In a tissue with very fast kinet. At this point a decompression pressure decreases quickly as depth changes. As in Figure 12. the ascent rule is shown as 5 1 a series of values for maximum allowable tissue Ambient pressure (∼depth) gas pressures plotted against depth and is labelled ‘supersaturation limit’ for simplicity. Ambient often-cited 2:1 ratio.1). This tissue has reached the The original gas content model proposed by ambient pressure line (grey dot at point 2) and is Haldane held that ascent could proceed until such thus saturated with inert gas.4 represents the changes in tissue gas pressure and ambient pressure during the early part of the A ascent.4 rep- 2 resents descent to the bottom depth indicted at C point 1 at the start of the dive. Line C represents the time as the tissue gas pressure in any tissue reached changes in tissue gas pressure and ambient pres. and ‘bubble models’. but it ambient pressure.4. the focus of sents descent to the depth indicated at point 1 at the this discussion is on the more traditional gas con- start of the dive. bubble models later. means of deriving an answer to this question intro- rated with inert gas) at the end of a long bottom time.3 (as in Figure 12. As in Figure  12. at a rate not exceeding . Direct ascent (line C). the fact that multiple tissues are involved and It should be clear at this point that the key ques- focusses on the behaviour of a single tissue. prescribed maximum allowable supersaturations sue it can be seen that by point 3 on the ascent. line A repre. the (sometimes referred to as ‘M-values’) for different tissue gas pressure (point 4) markedly exceeds the tissues across a range of depths. Decompression planning  155 For the purposes of illustrating the principles of ‘supersaturated’. duces a controversial dichotomy in decompression This is illustrated in Figure 12. ing the time at depth.

press according to the model. tive approaches that may (potentially) be more Whichever tissue is closest to its maximum super. the permitted duration for a Figure 12. saturation limit at any stage of the ascent becomes it has long been known that even decompressions the ‘controlling tissue’. . Dives requir- until the tissue gas pressure equals the maximum ing decompression stops are routinely undertaken allowed (point 3). Such models have been very useful for illustrating some of the basic concepts successful.4  Representation of a decompression no decompression dive (referred to as a ‘no decom- protocol determined by a gas content model pression limit’) becomes progressively shorter as ascent rule for a hypothetical single tissue. the to control decompression was almost  ubiquitous. Moreover. The involvement of multi- it lim 2 ple tissues and the effect of tissue gas kinetics on n C tio Tissue gas pressure ra decompression stop durations are not captured in tu diagrams such as Figure 12. we are usually not considering such events always results in interest in alterna- only one tissue but multiple tissues simultaneously.4. proceeds 60. the depth increases. Eventually. 30. at which time the first ‘decom. the process can certainly still occur even when divers decom- is much more complex in reality. to point 4. In ‘real’ decom. whose numbers can be correlated higher levels of inert gas during the bottom time).156  Decompression sickness: prevention tissues with slower kinetics tend to be controlling later in the ascent for the shallower stops. ­successful. After the tissue has ‘off-gassed’ suffi- ciently. the ascent is resumed with stops imposed Gas content versus bubble models each time the supersaturation limit is approached as depicted in Figure  12. These stops tend to be longer because the slower tissues take longer to outgas. DCS underlying decompression planning. This B means that dives are planned to be of modest depth and duration so that a direct ascent to the surface (at the correct rate) can be made at any point in the A dive without the gas pressure in any tissues cross- ing the supersaturation limit. this will be one of performed in accordance with established guide- the tissues with faster kinetics early in the ascent lines frequently result in the formation of venous (because these tissues are likely to have accumulated gas emboli (VGE). For example.and 40-metre dives as a  maximum prescribed by the model. the US Navy air diving table prescribed no decom- pression limits for 18-. respectively. Similarly. there is As described earlier. enon took place when the use of gas content models ling at that point will outgas quickly. that is. Because tissue inert 4 1 gas pressures will reach higher levels more quickly Ambient pressure (∼depth) at greater depths (where the inspired inert gas pressures are higher). as discussed in Chapter  10. Typically. (albeit imprecisely) with the risk of DCS.4 are ent kinetic behaviour.4. but are not invariably so. thresholds across the range of tissues with differ- Although diagrams such as Figure  12. rsa 3 pe It is appropriate to acknowledge at this point Su that recreational divers undertaking entry level courses are taught ‘no decompression diving’. 25 and 5 minutes. The occurrence of pression modelling. for many years See text for further explanation. Much of This means that the early ­decompression stops are the early research that revealed this VGE phenom- shorter because the faster tissues that are control. gas content models regulate sufficient outgassing in the tissue to allow direct ascent and impose decompression stops to maintain ascent to the surface while remaining just under tissue supersaturation below empirically derived the supersaturation limit. by recreational divers who refer to themselves as pression stop’ is imposed at a depth corresponding ‘technical divers’ (see Chapter 62).

3 and 12. It was even suggested that by imposing with stops imposed each time the maximum deeper initial decompression stops a diver could supersaturation is approached. ­factors. between decompression of a hypothetical single tion from micronuclei (see Chapter 10) of a given tissue prescribed by a gas content model (black line) and a bubble model (grey line). calculations suggested that shorter initial ascents (and therefore smaller initial supersaturations) than allowed by gas content models would result decompression stop would be imposed at a depth in ‘excitation’ of smaller populations of micronu.5. Using advanced physics. then direct ascent (line C) would proceed less fatigued after dives. it lim A school of thought that had been around for D n C Tissue gas pressure tio some time. combined with the burgeoning influence mum allowed (point  3). Decompression planning  157 Thus. rsa 3 pe Bubble model advocates had taken note of the Su ­frequently high VGE counts after decompression conducted according to gas content models and advanced the notion that. bubble modellers Figure 12. became an article of . reduce the requirement for the shallow decom. approaches to decompression using the same for. In contrast. the ascent would be resumed formation. After the tissue has off- clei and therefore help prevent initiation of bubble gassed sufficiently. A stylized comparison between these two sion stops and smaller initial s­upersaturations. was the so-called ‘bubble-model’ approach. the supersaturation limit or widely discussed anecdotal observations from M-value line as prescribed by a gas content model several prominent divers that insertion of deep is depicted.4. the emerging recreational technical diving world of the late 1990s and early 2000s was fertile ground for well-meaning advocates of alternative approaches to decompression.5  Stylized depiction of differences purported to be able to quantify bubble forma. but came to prominence during this 2 ra tu period. line A in Figure 12.5 than the maximum allowed by the gas content represents descent to the bottom depth indicted model. Moreover. the end of the  bottom time the illustrated tissue There was a compelling theoretical attraction to has reached the ambient pressure line (grey  dot the concept of using ‘deep stops’ to ‘control bubble at point 2) and is thus saturated with inert gas. the ascent prescribed by a ­typical pression stops later in the ascent because initiation bubble model (depicted by the grey arrows) involves of bubble formation would have been controlled shorter initial ascents. deeper initial decompres- earlier. By later in the ascent. they pro- A posed that initiation of bubble formation probably occurred during exposure to the relatively large 4 5 1 supersaturations allowed by gas content models Ambient pressure (∼depth) during the long ascent to the first decompression stop. There were also some As in Figure  12. and if the diver was following such a stops into their ascents seemed to result in feeling model. formation early in the ascent’. corresponding to point 4. See text for size for a given level of supersaturation. at which time the first of Internet communication. based on the belief that the process of bub- at point 1. the failure B of these models to control bubble formation effec- tively could increase the risk of DCS even when the diver did everything right. and line B represents the increase in ble initiation had been controlled earlier and that ­tissue gas pressure as inert gas is absorbed ­during this allowed exposure to greater supersaturation the  time  spent at that depth (bottom time). surfacing with a tissue gas supersaturation greater As in Figures 12. In the early 2000s these until the tissue gas pressure equalled the maxi. A  bubble model could also (as depicted) allow mat as previous figures is shown in Figure 12. at least in part.4. and their further explanation.

in Figure 12. GF-High (black dot labelled 90 per cent).158  Decompression sickness: prevention faith among deep recreational technical ­divers that GF-Low and a higher GF-High produces a decom- bubble model approaches to decompression were pression profile that resembles a bubble model superior even though no formal testing of the decompression.6 for algorithms had been undertaken. At the ration of fast tissues early in the ascent and then start of decompression. but even users further stops imposed when the tissue supersatu- of these algorithms began to manipulate them to ration approaches the modified supersaturation make them behave more like bubble models. See text for further tissues at the point of surfacing. It largely went unnoticed when represents descent to the bottom depth indicted at VPM was revised into VPM-B to increase shallow point 1. lowering the first gradient factor lim- its supersaturation in the fast tissues early in the Figure 12. One limit defined by a line joining the chosen GF-Low technique for such a manipulation that became (black dot labelled 20 per cent) and the chosen and remains popular is the use of so-called ‘gradi. ity model [VPM] and the reduced gradient bubble As in previous figures. gradient factors GF 20/90 on the d ­ ecompression and lowering the second will produce longer shal. There was wide. 20 per cent of the supersaturation limit. These fractions have come to be known as gradient fac- tors. By the ascents and longer shallow stops were derided as end of the bottom time the illustrated tissue has being a recipe for ‘bending and mending’ (an allu. a GF-Low of 20 per cent and a GF-High of 90 per spread adoption of the two most readily available cent (in common use this terminology would be bubble model algorithms (the varying permeabil.5. abbreviated to ‘GF 20/90’). The ascent then continues with to program for use in computers. if a diver elects to limit supersaturation it lim to 80 per cent of the usual difference between ambi. this is ra tu it rsa referred to as ‘gradient factor 80’ or ‘GF 80’.6 model [RGBM]). Not sur- Ambient pressure (∼depth) prisingly. it is clear that it is now very different saturation limit by redefining maximal permis- sible supersaturation as a fraction of the difference between ambient pressure and the limit. If this ent factors’. . and line B represents the increase in tis- stop time after reports of DCS began to emerge. This is illustrated in Figure 12. Thus. point 2) and is thus saturated with inert gas. line A in Figure  12. and the second (often referred to as GF-High) controls supersaturation in the slower 90% tissues at the point of surfacing. This involves limiting supersaturation approach is compared with the two profiles shown to less than permitted by the conventional super. reached the ambient pressure line (grey dot at sion to causing bubble formation with supersatu. sue gas pressure as inert gas is absorbed during Gas content models with their relatively rapid early the time spent at that depth (bottom time).6  The stylized effect of imposing ascent by imposing deeper decompression stops. per. prescribed by a gas content model for a ­single lower stops to reduce supersaturation in the slower hypothetical tissue. Typical nl im pe atio implementations of the gradient factor method ur Su t rsa pe require the diver to select two gradient factors: d su ifie the first (often referred to as GF-Low) notionally M od B controls supersaturation in the fast tissues early in the ascent. point a stop is imposed at the depth correspond- haps because they were easier to understand or ing to point 3. Choosing a low explanation. at which The use of gas content models did persist. the initial ascent (line  C) fixing the problem with long shallow stops late in is allowed to proceed until the tissue reaches the ascent). C n 20% Tissue gas pressure tio 2 ent pressure and the supersaturation limit. The algorithm A then interpolates a series of modified M-values in 3 1 between these two user-specified points.

and temperature effects were standardized across ble model decompressions are collectively referred the groups by having all divers wear no thermal to as ‘deep stop’ approaches to decompression. and line B clearly work in the majority of dives. It explain it have focussed on the likelihood that is acknowledged that the preceding discussion of protection of fast tissues from supersaturation bubble model theory represents a gross oversim. The trial was ceased at this point because ational divers was subjected to some human test. However. . As in previous ­figures. but the fact tive as thought. B comes after air dives to 170 feet for 30 minutes with same-­duration decompression on air prescribed by A either a gas content model or a bubble model. the difference became significant on sequential ing. the gas content model allows model decompression (solid black arrows) and greater supersaturation in faster tissues early in the a bubble model decompression (grey arrows) on ascent and distributes decompression time shal. it has increased supersaturation in the slow tissues never been tested in a practical sense. The bubble This result was not the outcome expected or models and gradient factor manipulations of gas hypothesized by the investigators. protection in water at a temperature of 30°C. but this is an invalid argument in the absence line A in Figure  12. The divers performed model decompression. and it comes at the expense of remains. There The ZH-L Buhlmann gas content model that were 11 cases of DCS in 198 dives in the deep stops forms the basis for most tables and computers group and 3 cases in 192 dives in the shallow stops designed to guide decompression diving by recre. Both 4 5 1 decompression protocols are US Navy models that are not used by recreational divers. Decompression planning  159 from the unmodified gas content model decom. albeit minimal for the trimix diving and depth analysis. D n Tissue gas pressure tio C 2 suring VGE after diving and suggest that deep ra tu stops may not reduce the appearance of VGE as rsa pe previously widely assumed.7  The stylized effect of a gas content tive approaches. range for which it is now implemented. illustrated in Figure 12. by far the Su most significant development has been the 2011 F publication of a study performed by the US Navy E 3 Experimental Diving Unit (NEDU) at Panama City in Florida3. and the bubble model imposes deeper stops (arrows originating at point 2) and a hypotheti- early in the ascent and thereby distributes decom. mal. group. These approaches bottom depth (indicted at point 1). Advocates later in the ascent because they are continuing frequently cite the ubiquitous nature of deep stop to absorb gas during deep stops. Attempts to content models have had essentially no testing.7 represents descent to the of comparative outcome data. This principle is approaches as some sort of proof that they are opti. no matter how attractive the theory. early in the ascent does not seem to be as effec- plification of a complicated matter. cal slower tissue (arrows originating at point 3). but they never. For obvious reasons. use of gradient factors with a low GF-Low and bub. but whether represents the increase in tissue gas pressure as they are optimal is an unresolved question.7. this study was that the primary outcome measure pression and substantially similar to the bubble was DCS in human subjects. Ambient pressure (∼depth) theless have characteristics that reflect the respec- Figure 12. Debate over this issue has been rekindled with the publication of several studies that have sug- gested that the emphasis on deep stop approaches to decompression may need to be reconsidered. The investigators compared out. pression time deeper. tissue gas pressure in a hypothetical fast tissue lower. it lim Several of these studies have focussed on mea. The remarkable feature of See text for further explanation. the a standardized workload during the bottom time.

The dive tables also provided a series of steps evant because the experiments involved air diving (with minimal calculation) for divers to account and used a deep stop profile that is not exactly the for the effect of inert gas accumulated but not yet same as that prescribed by VPM-B. decompression limits. it is and is thus saturated with inert gas. The most frequently used ­content model decompression gives the  tissue items of information were the no decompres- ­little more time to absorb inert gas as illustrated sion limits (see earlier) provided by these tables. the gas scuba diving courses. tection of fast tissues early in the ascent) is worth as an added precaution. pression limit for subsequent dives. and readily available. it seems plausible to suggest that we have this was not true of computers. advocates have tried to portray the study as irrel. Dive tables. In contrast. and dive computers ceed until the faster controlling tissue reaches the maximum supersaturation limit. later). whereas increasingly common to see combinations such as the slower tissue represented by the grey dot at 40/70 or 50/70 now. Bubble model tine no decompression dives. and its presence. Tables were inexpensive by recreational technical divers is not established. divers could look up the allowable bottom sing begins once the tissue reaches then crosses time they could spend at any particular depth and the ambient pressure line. In the slower scuba air divers wanting to plan simple dives. by line E because absorption ceases and outgas. Such stops are probably the disadvantage of the increased gas loading that useful in reducing the incidence of DCS on rou- occurs in slower tissues as a result. whose tissue gas pressure at the begin. These were model allows a shorter ascent (line D) to the first most popular before the 1990s among recreational stop at a depth indicated by point 5. the bubble that divers can use to plan their dives. planning software sion allows an the initial ascent (line C) to pro. entry level dive computers have become deep stops. whereas gradi- tom time the tissue represented by the grey dot ent factor combinations such as 10/90 were popu- at point 2 has reached the ambient pressure line lar during the height of belief in deep stops. More recently. this is referred for dives using accelerated decompression on oxy. thus ensur- reduce the emphasis on deep stops (by increasing ing that the diver who carries one is receiving . to as ‘residual nitrogen’.to 5-minute ‘safety stop’ the proposed benefit of using a bubble model (pro. has the effect of reducing the no decom- divers) suggest that the same disadvantageous pat. eliminated after previous dives when planning fur- analyses of ‘real-world’ VPM-B profiles prescribed ther ‘repetitive’ dives. and some entry level diving courses no lon- It is clear that the optimal approach to decom. At the start of decompression. whereas in the early days however. their use was taught as part of all recreational ning  of  ascent is indicated by point  3. where the Dive tables are pre-calculated and pre-printed first decompression stop is imposed at a depth implementations of a decompression algorithm indicated by point 4. not sur- gen (such as are typically undertaken by technical prisingly. (by decreasing the GF-High). ger teach their use. By the end of the bot. Whether this is a good or bad pression from the deep bounce dives undertaken thing is impossible to say. at 3 to 5 metres during the final part of the ascent. One trend that is emerging as this much more reasonably priced and have the advan- book goes to press is the use of gradient factors to tages of avoiding calculation errors. the deep still make a direct ascent to the surface without stops prescribed by the bubble model will result decompression stops. Thus. In contrast. and tissue. Nevertheless. evolved an approach that risks ­overemphasizing however. gas content model decompres. Even though no decom- in further inert gas absorption by this tissue pression was prescribed for dives ‘inside’ the no (line F). most training agencies The NEDU study forces us to question whether advocated the use of a 3. tern of protecting fast tissue from supersaturation The use of dive tables has declined dramati- early in the ascent at the expense of slower tissue cally with the rise in use of dive computers (see supersaturation later still occurs.160  Decompression sickness: prevention inert gas is absorbed during the time spent at the GF-Low) and re-emphasizing shallow stops that depth (bottom time). Thus. point 3 is still absorbing inert gas. In air diving.

ear or cutaneous DCS and. spinal diver are now available. all with little or no effort on the part Many divers have enthusiastically embraced such of the diver. possibly. The degree of shunt facili- Dive computers that the diver carries under. as previously described. yet cerebral. Amelioration of risk factors  161 accurate time and depth information. Such Patent foramen ovale software is effectively an electronic dive table and is often used to generate tables that are transcribed The role of the patent foramen ovale (PFO) in the onto underwater slates for specific missions. even if the event involved a form of DCS that has erences such as gradient factors. decompression ceiling and expected time PFOs in divers who wish to continue diving. The crucial question is this: ‘How pression algorithms programmed into them and should this knowledge be applied to reducing risk with various levels of adaptability for decom. musculo- can connect to the oxygen cells in a rebreather skeletal DCS). to surfacing. some Planning software that runs a decompression of which have already been mentioned. cussion forums report an episode of DCS. equipment.g. to replicate on pre-printed tables. These parameters are continuously Another more radical strategy would be to screen updated as the depth varies and the dive duration all prospective divers before entry to the sport. gas mixes and decompression prefer. open. to repair large tion. Advanced computers allow the diver ideas. lengthens. in which it was pointed out that PFO appears asso- sion plan can be tailored specifically to the diver’s ciated with an increased risk of cerebral.g. In addition. tated by the PFO has consistently been found to water have become increasingly popular since the be significant. However. sible. There are clearly factors beyond merely having a PFO and AMELIORATION OF RISK FACTORS producing venous bubbles that are involved in the chain of events leading to the relevant forms Appropriate manipulation of the depth-time of DCS. When participants on Internet diving dis- to choose the equipment being used (e. inner display of parameters such as depth. if not impos.g. laptop and tablet computers. manipulated or managed to reduce risk further. Some computers never been associated with a PFO (e. a cho- circuit or rebreather systems) and the gas mixes rus of advice to check for a PFO inevitably follows. didates can be expected to have one) and so is the tion in a head-up display constantly visible to the formation of VGE after diving. dive dura. can be algorithm (and often multiple decompression algo. rithms) can be purchased for use on desktop. . The multitude of combinations and that a right-to-left shunt allows VGE to enter the permutations of circumstances that can be ‘run’ by arterial circulation. as well as telephones. unimportant. then distribute widely in the body and cause harm. Advanced computers that perform mon (around 30 per cent of divers or diving can- these functions and provide all relevant informa. spinal. The pathophysiology of DCS is discussed in Chapter 10. gas content model. and at this time we are not certain what profile as discussed in the preceding section on they are. and most of in managing the risk of DCS. certain these computers provide ascent rate alarms. plausible explanation for this increase in risk is dient factors). PFO is very com- decompression. They track time and depth One obvious strategy would be to screen div- exposures in real time and provide a constant ers for PFO after an episode of neurological. decisions to screen divers (see Chapter 62) so that they ‘know’ the inspired for PFO or to repair any lesion that is discovered partial pressure of oxygen used by the diver and are not straightforward. advantage of such software is that the decompres. of DCS?’ pression planning. and inner ear DCS cases remain rare. The most ences (e. Screening all prospective divers by decompression planning is obviously important using an expensive invasive test (see Chapter 10). and these small bubbles can such software would be very difficult. can incorporate this information in calculating As pointed out in Chapter 10. bubble model. vestibulocochlear and cutaneous DCS. known or suspected risk factors for DCS. These being important and very small shunts seemingly computers run software with one or more decom. gra. with large and spontaneous shunts early 1990s and are now almost ubiquitous. being breathed and to adjust decompression pref.

it nevertheless has sig- having the test. with the aim of preventing To mitigate the risk implied by a large PFO. shunt. incomplete in up to 10 per cent of cases. it may be appropriate to test divers option to cease diving is self-explanatory  and who have had one of the relevant forms of DCS. but anecdotally the numbers are There are data suggesting that a grade 1 PFO (see growing. position. The test result is likely to be positive in at least transvenous catheter technique that leaves an 30 per cent of cases (or more depending on the occluder device across the atrial septum. antiplatelet agent for 6 months after placement. Despite these concerns. lowering the GF-High to force longer shal- should always be explained to the diver before test. of PFO in diving. but the  following points factors. over the typical 2-hour with strongly positive results for right-to-left period of maximum VGE formation after a dive. Breathing oxygen during those stops would also help. 3.g. It is context). a pulmonary shunt. The In contrast. or manoeuvres that could Transient symptoms of cerebral arterial gas encourage right-to-left shunting across a PFO embolism have been reported following tests (e. as many seem to explantation of devices that are causing compli- believe. low decompression stops at the end of the dive. It is not known how many result is positive. A positive test result after an episode of DCS These risks include formation of blood clots on does not guarantee that the PFO was the cause the device. open heart surgery is required for diver is ‘resistant’ to DCS. them from diving). As a corollary to point 3. Having a PFO repaired involves the use of a 2. some of which are life-­t hreatening. but there are some risks.  lifting or s­training). VGE production or have the PFO repaired. a spontaneously shunting about the repair option is that data demonstrating . but the general aim is to reduce the in terms of decompression stress. although repair may be difficult options to choose from (see later). It is also inevita. Other than the potential for harm dur- Chapter 10) is of little or no consequence and can ing and after the procedure.162  Decompression sickness: prevention which  would detect the target lesion in about (grade 3) PFO is likely to confer increased risk and 30  per cent of subjects (and potentially exclude merits a response. one of the concerns be ignored. Modification of diving particularly if there have been multiple events or if practice to reduce VGE production is an impre- the event(s) followed dives that seem unprovocative cise business. ing is undertaken. Options for achieving this include diving enthusiasts who have never had DCS but who are well within no decompression limits. repairing a PFO disturbances and new mild aortic regurgitation. 5. provocation for bubble formation on arrival at the ble that the diving physician will be approached by surface. and the diver may then have some an effective treatment. modify diving practice in an attempt to reduce sible nor justified. most procedures have satisfactory results. the an event that occurs perhaps once in 10 000 dives diver effectively has three options: cease diving. The bubble contrast echocardiographic test avoidance of any heavy exercise that could open is relatively safe. if decompression diving using gradient these circumstances. In contrast. discovered after an episode of DCS does not Patients are routinely required to take a potent guarantee that another event will not occur. the response should take account divers have taken this option to mitigate the risk of the size or shunting behaviour of the lesion. ensuring aware of the association of serious DCS with PFO that safety stops are completed. and like many medical pro- options. cations. It is also If the diver does not intend to take one of those an invasive procedure. Chapter 62) but planning the dive as though using Referring for testing may be appropriate under air and. using nitrox (see and who wish to be tested for this heart condition. loosening of the occluder from its of the DCS. then there is little practical point in cedures considered ‘safe’. In a related vein. and the PFO is closed If screening for a PFO is undertaken and the without complications. (even in an unscreened population). unpalatable to many. nificant risks. the appearance of new heart rhythm 4. A negative test result does not mean that the Occasionally. is neither sen. advice could also include 1.

Things changed with the publica- randomized. Amelioration of risk factors  163 that repair reduces subsequent risk of DCS are Exercise incomplete. The mecha- nism for this protective effect is unclear. ing reduces VGE counts after diving. effect seemed to wear off. specifically marized in Figure 12. and then ascent and decompression . Restoration of micro- nuclei numbers by whatever process is responsible Figure 12. There are no widely recommended practical strat- ing serious neurological decompression sickness egies designed to take advantage of this phenome- (DCS). et al. The final results are based on very small non. repair of patent foramen ovale (PFO) in prevent.97:1932–1937. heavy exercise between 2 and 20 hours before div- tism of their dives. Many diving enthusiasts may reduced  mortality in a rodent model of severe well be prepared to take this risk for the apparent DCS. Patent foramen ovale closure in recreational divers: The effect of exercise during diving may depend effect on decompression illness and ischaemic on its timing. but caution is given to the issue of exercise before diving and its required in interpreting these data because the relationship with risk of DCS. Mordasini R. The typical pattern is that activity brain lesions during long-term follow-up. (Data from of DCS. Tested for PFO although as a sidebar to this line of research it was discovered that exogenously administered nitric 39 no PFO 65 positive for PFO oxide also appeared to reduce post-dive VGE. to be considered in multiple contexts. There is one comparative study that followed divers with large PFOs discovered after The relationship between DCS risk and exercise is DCS who self-selected into groups undergoing a complex and evolving issue. By 48 hours after exercise.5/10. exercise may disturb stable micronuclei so that they subsequently involute. divers who continued diving exercise after diving. Zbinden R.000 Neuro DCI 35/10. and exercise needs repair or not4. and the divers were not a good thing.) moderately. It has been suggested that exercise produces some 26 underwent closure 39 no closure sort of endothelial conditioning effect that results in fewer suitable sites for micronuclei to grow when 5-year follow-up the surrounding tissue becomes supersaturated. Perhaps the best that can be said is that going numbers of cases (1 case of DCS in the closure for a run (or something similar) between 2 and group and 4 cases of DCS in the no closure 24  hours before diving may help reduce the risk group). the tion of a remarkable series of experiments dem- study does provide some reassurance that there is onstrating that a single bout of heavy exercise a positive return on the risk exposure associated approximately 20 hours before diving markedly with ­having a repair. This may be particularly true of those ing into human research is incomplete. exercise during diving and In this study.000 the population transiently. exercise before diving. DCI.8  Key features and results of the study for producing them would explain the decay in by Billinger and associates on the efficacy of benefit over time following the exercise episode. decompression illness. Translation of this find- left shunt.8. without repair had a markedly higher rate of Until the early 2000s. The study and its results are sum. thus reducing Neuro DCI 0. Mean 295 dives Mean 175 dives Similarly. Early speculation that it was mediated by nitric oxide 104 divers with neurological DCI seemed disproved when protection persisted in the presence of a nitric oxide synthase inhibitor. Heart during the bottom time sees the diver exercising 2011. Notwithstanding this concern. little attention had been DCS than those who had a repair. Billinger M. but there conducting deep technical dives who may see little have been several studies demonstrating that practical potential for improving the conserva. the protective benefit of eliminating their anatomical right-to. other than general numbers of DCS cases arising after the repair speculation that being physically fit was probably decision were so small.

There is one study in which pigs deprived of tional diving. who appear prone to VGE formation. to than normally hydrated pigs after decompression. dehydration) is one in risk may therefore be achieved by reducing work of the most widely recognized of the alleged risk at depth and maintaining gentle levels of exercise factors for DCS among divers. the supplementation of normal fluid intake more harmful. a causative role in such cases. exercise may contribute to their excitation into seems higher when diving is conducted in cold growth. diuresis. landmark study performed by the US NEDU5. of course. This finding the use of a longer safety stop (for a no decompres. There is evidence that appropriate precaution. This is probably a after diving.164  Decompression sickness: prevention (if any) are largely done at rest. not the least of which during exercise. gas elimination during the decompression. ration pressure exposure had more severe DCS Similarly. may be coincidental. In diving VGE numbers after diving. As a somewhat arbitrary shunts into the arterial system. is encouraging but falls short of proving that good sion dive) or lengthening of the p ­ rescribed shal. It is widely accepted that this explains the perception Hydration that dives involving hard work at the bottom are associated with greater risk of DCS. Nevertheless. dehydration could impair this process. mitigation of this risk involves It is a complicated study with multiple arms and refraining from exercise or lifting for a period profiles. although the timing is unclear. but the most important observation was . and because perfusion is impor- is that there are many reports of symptoms of DCS tant for inert gas washout. it is speculated that where there are micronuclei in tissues supersaturated with inert It has long been observed that the risk of DCS gas. There is also evidence that realistic levels sidered unwise. for example. Although a reduction that dehydration actually imputes increased risk. sea sickness and immersion Exercise after diving has generally been con. limited human data have shown that usually possible to fin gently against the resistance supplemental hydration just before diving reduces of the down line or decompression stage. This ‘period’ should definitely extend disadvantageous pattern of exercise because it will for at least several hours because this corresponds result in increased perfusion and inert gas uptake to the peak and duration of VGE formation after (in some tissues at least) during the bottom phase typical dives. It is cer- This. in recreational diving it is afforded water and administered a diuretic during a satu- by. A reduction Hydration (or more correctly. At a practical level. thus producing bubbles. There is some evidence in given to the matter. but the validity of this concern is unknown. There are no universally divers are prone to dehydration through factors accepted guidelines for ‘padding’ decompression such as exposure to hot conditions. would make sense. ity of water on boats. low stops in a decompression dive would be an the proposition makes sense. exercise (particularly that involv. where they may be guide. Second with a litre of water over the hour before diving (and similarly). in work at depth can be impractical in occupa. but there are tainly true to say that no one has ever demon- plausible reasons to believe that exercise may have strated dehydration to be beneficial. in a decompression diving situation. there is remarkably little proof support of these notions. hydration is protective in humans. For all the attention during decompression. use of diver propulsion vehicles. ing lifting or straining) may promote right-to- left shunting of VGE across a PFO with the same Temperature result. of ‘dehydration’ reduce regional tissue perfusion Several concerns are noted. as described in Chapter 10. maintain gentle exercise during decompression it is In addition. but how long of the dive and then decreased perfusion and inert is unknown. it seems plausible that arising during periods of work soon after diving. First. especially in subjects where hard work at the bottom cannot be avoided. This would be conditions. Longer would be better. exercise may It follows that maintenance of hydration can promote the passage of VGE across pulmonary probably only be good. poor availabil- in this way. The potentially dramatic effect of tem- analogous to shaking an open bottle of carbonated perature on risk of DCS was demonstrated in a drink. Finally.

many divers take showers early in the phases. and the risk the cold/warm series. In post-diving period with no problems. warm/cold conditions is highly relevant. If there is a lesson to be learned from whereas others have not. thus giving an are likely to have a lower functional capacity and a opportunity to reduce conductive heat loss into the higher risk of cardiac events is probably of greater water and to take hot fluids orally. This single report has achieved considerable set of dives (referred to as cold/warm). Some data suggest that remaining warm after As alluded to earlier. for the bottom phase of the dive and 36°C for the It is plausible that sudden warming of supersatu- decompression. but the dramatic belief that because nitrogen is highly soluble in change in DCS risk between the cold/warm and fat. Extreme risk of an incomplete recovery if they suffer serious divers in cold water caves have even established event. there is a report of took a 120-foot for 30-minute dive with decom. The ideal time to turn these heating sys. differs according to which table or decompression . divers tend to start a that have addressed this issue) purporting to show dive warm and become progressively colder dur. whereas in the warm/ cold series. It dives conducted while dissolved inert gas in tis- is therefore probably sensible to avoid becom. which are now widely There are some data suggesting that older divers available. an obese person can absorb more nitrogen. The divers wore no thermal protection. once again. there were no cases of DCS of such events seems very low. It has long been believed that obesity is a risk fac- sure protection make the conditions difficult to tor for DCS. obesity is a condition that is often asso- cold during a dive should be avoided as much as ciated with reduced functional capacity and other possible. losing weight for multiple reasons. Amelioration of risk factors  165 the comparison of outcomes when divers under. In the second set of dives (referred rated superficial tissue could decrease gas solubil- to as warm/cold). two cases of DCS arising in temporal relation to pression as prescribed by a US Navy dive table exposure to hot water in a shower early after div- under two different thermal conditions. are at higher risk of DCS and perhaps at higher tems on would be during decompression. reversed between the bottom and decompression However. especially one that was ‘repetitive dives’. health problems. There is conflict in the literature diving would be the markedly more hazardous with some studies (probably the majority of those warm/cold situation. importance than concern about the risk of DCS. The fact that older divers under pressure. Almost paradoxically. However. As previously. which would include the use of drysuits Age with state of the art undergarments and possibly even active heating systems. there is always the option of ‘padding’ or extending decompression for decompression dives conducted Dive sequences in cold water. It can be Whether this is a practically relevant consideration argued that the condition most analogous to real is controversial. there is conflict in the underwater habitats where the diver can remain literature on this subject. Sequential production of VGE and the incidence of DCS. but not immersed. however. In one ing. sue remains after a previous dive are referred to as ing cold early after a dive. Thus. there were 7 cases of DCS in 32 dives Obesity (22 per cent). in 80 dives (0 per cent). multiple dives in a single day diving (despite a cold environment) may reduce are common in recreational diving. based largely on the ‘first principle’ interpret in real-world terms. Obese divers would benefit from Practical strategies to mitigate the risk of div. ing the dive. Whatever the truth of the NEDU temperature study it is that becoming this matter. ing in cold water include optimizing exposure pro- tection. the temperature conditions were ity and precipitate symptomatic bubble formation. the divers penetration into the diving community and is the were immersed in water at a temperature of 26°C cause of much anxiety about showers after diving. an association between risk of DCS and obesity. The water temperatures and the lack of expo. The definition of repetitive diving provocative from a decompression point of view.

but as in repetitive diving second dive takes place in the presence of residual itself. considers that complete outgas. provided residual inert gas is adequately accounted for in calcula. in being once daily) from the TR 11-06. That alone could be reason enough Irrespective of the definition. follow-up. 5th ed. One particular form  of  repetitive  diving  that  is Panama City. This is the perfor- mance of a repetitive dive deeper than the previous This chapter was reviewed for this fifth edition by dive (or than another dive in the ­repetitive sequence). phenomenon reported from occupational envi. Hyperbaric repetitive dives per se as being associated with conditions. Inc. Doolette DJ. 2007: NEDU TR 06-07. Gerth WA. typical repetitive dives undertaken by recreational 4. Diving Unit. Simon Mitchell. Mitchell SJ. the Professional Association of Diving depth diving. . 2007: NEDU frequently differ (e. the term ‘reverse profile’ is a misnomer assumptions about total outgassing time. Gerth WA. Heart 2011. There are no convincing data that clearly identify 2. One argument 1. ing undertaken by recreational divers is repetitive. eds. Incidence of Decompression Sickness in Air pressed air work is reliably noted to fall over a Decompression Dives. be considered more hazardous provided residual then tissue gas loading during the second will com. or those bubbles Medicine of Diving. 2003:419–454. London: may undergo further growth after the second dive. Doolette DJ. Gerth WA. the sequence. Comprehensive Physiology increased risk. For because what is really being d ­ iscussed is reverse example. Harcourt Publishers. the truth relat. it is not clear why reverse profile diving should dissolved inert gas remaining after a previous one. whereas the Canadian manipulation of the repetitive function of com- Defence and Civil Institute of Environmental mon dive tables reveals that avoidance of reverse Medicine (DCIEM) table works on a much longer profiles results in more allowable bottom time over total outgassing time of 18 hours. In: Brubakk AO. Nevertheless. Florida: multiday sequence of exposures. Panama City. 5. Decompression that is sometimes advanced in this regard is that theory. The origins of the edict that reverse Instructors. the situation is made even 2011. Mordasini R. although subsequent deeper excursion. Cursory sing occurs after 6 hours. it is clear that if a to avoid reverse profiles. Florida: Navy Experimental associated with considerable controversy is so. profile diving is hazardous are unclear. REFERENCES tion of no decompression limits or decompres- sion protocols for subsequent dives. Ruterbusch VL. it is not clear why it should be. called  ‘reverse profile’ diving. inert gas from the previous shallower dive(s) is ade- pound on that remaining from the first. Perhaps quately accounted for in calculation of no decom- for this reason it has frequently been taught that pression limits or decompression protocols for the repetitive diving is a risk factor for DCS. Long ET. divers: effect on decompression illness and ing to risk in these situations is unclear. divers that may involve up to four or more short Patent foramen ovale closure in recreational exposures per day. Redistribution of Decompression Stop Time ronments in which the incidence of DCS among From Shallow to Deep Stops Increases a cohort of workers undertaking diving or com. Zbinden R. bubble formation after the first dive alters inert Bennett and Elliott’s Physiology and gas kinetics on the second dive. Billinger M. Indeed. et al.166  Decompression sickness: prevention algorithm is used because there is variability in In this sense.g. less clear by the existence of an acclimatization 3. so it is not surprising that many of the DCS cases The Influence of Thermal Exposure on Diver arise in repetitive diving. Neuman TS. These exposures Navy Experimental Diving Unit.97:1932–1937. Tikuisis P. Susceptibility to Decompression Sickness.1:163–201. Gault KA. Part of the ischaemic brain lesions during long-term problem relates to the fact that so much of the div.

of air pressure. yet the approach to their manage- the following cases: ment is similar. ●● Inner ear DCS after helium breathing. ●● A joint bend developing hours after a long shal- low dive. 1935 ●● A dramatic crisis involving pulmonary. quent case of illness. DCS ­established tables. scious. see Chapter 48. ●● Respiratory symptoms followed by the rapid This chapter deals with the definitive manage. nary efficiency of recompression. ●● Saturation DCS as the diver very slowly pressed air illness. Robert Davis. put back into a chamber and ●● The same diver subjected to an extreme brought back to life by the application ­excursion from saturation. 167 . ment of decompression sickness (DCS). or will ●● A cerebrovascular incident after a short bounce be backward in applying it to a subse. development of paraplegia. takes many forms. Consider single regimen. hae- matological and neurological systems after explosive decompression from saturation or INTRODUCTION from gross omitted decompression. gravely ill or uncon. 13 Decompression sickness: treatment Introduction 167 Surface oxygen administration 176 Recompression 168 Drug therapy 176 Depth of recompression 168 Underwater treatment 178 Standard recompression tables 170 In-water air treatments 178 Gas mixture 171 Underwater oxygen therapy 179 Delay to recompression 172 Medical attendants 180 Recurrence of symptoms 173 Return to diving and flying 181 Cerebral arterial gas embolism 175 Safe diving practices 182 Adjunctive therapy 175 References 183 Position 175 Further reading 183 General care 176 No-one who has seen the victim of com. approaches the surface. will forget the extraordi. the optimal These cases cannot be managed optimally by a treatment varies  with circumstance. to 50 metres. and although recompres- sion is often the treatment of choice. For ●● Mild joint pain DCS after a shallow dive in information on the first aid management of the a diver who has remained well within the diving accident victim.

usually within days or weeks.3). There is also evidence that once a . The gas mixture to be used. seasickness and bubble-induced fluid shifts out There are three factors to consider after decid- of the intravascular compartment. tity of gas dissolved in the body during the original ●● Reduce the length of any intravascular gas dive. nitrous oxide anesthesia). Oxygen ●● An increase in the diffusion gradient of gas out breathing is used to increase the washout of inert of the bubble (see Figure 10. 1. ●● Increase the surface area of the bubble This is not a particularly satisfactory technique relative to its volume. with the patient reactions that follow.168  Decompression sickness: treatment The guiding principle of treatment for DCS is ●● Reduce the bubble-tissue and bubble-blood recompression followed by a slow decompression interfaces and the secondary inflammatory back to atmospheric pressure. is the clinical manifestation of a gas bubble lodged sure to push bubbles out of the tissues into in a vulnerable area. roids. This approach was best bubble to increase and perhaps collapse typified by the now defunct concept of treating avia- the bubble. it is necessary to recompress the venous circulation. It is the depth and duration of the original dive. If left untreated. then recompression to 4 ATA ●● Cause the surface tension acting on the should relieve the symptoms. hopefully devoid of symptoms and signs. according to standard tables of recompres- include excessive movement of the patient.e. Care should be taken to avoid circumstances 3. irrespective of its distribution. whereas non-steroidal 2. The pressure (depth) required for therapy. three dif- lution of cases of neurological DCS without ferent approaches are possible: recompression therapy. dehydrated as a consequence of cold water diure- sis. Many adjuvant ing a diver needs recompression therapy: therapies have been tried. thus enhancing gas because it is designed to cope with the total quan- diffusion out of the bubble. Recompress to a predetermined fixed depth. in the body. including antiplatelet agents. the pain of joint DCS resolves Depth of recompression spontaneously. to reduce the size of that particular bubble. most with little evidence of effect. anti-inflammatory drugs (NSAIDs) and lidocaine 3. corticoste. Recompress to a depth that produces ­clinical likelihood of dysbaric osteonecrosis or subclini. Fluid replace. Recompress to a pressure (depth) dependent on require treatment or remain symptomatic. have shown some promise. expo. ment is recommended because divers are often ●● Restore normal tissue function. The rate of decompression. Because DCS column and hence allow perfusion pres. tor DCS merely by descent to ground level. most patients 1. The aim of recompression treatment is to produce RECOMPRESS TO A PRESSURE (DEPTH) the following1: DEPENDENT ON THE DEPTH AND DURATION OF THE ORIGINAL DIVE ●● An immediate reduction in bubble size. There have been reports of spontaneous reso.g. Only the third is in common practice these days. but each has some logic to it under certain RECOMPRESSION circumstances. however. relief of symptoms and then tailor the gas cal neurological injury. that will aggravate the ‘bubbling’ of DCS. which will gas and promote bubble resolution. irre- ●● Reduce the compressive effect of bubbles spective of the total quantity of inert gas dissolved on adjacent tissues. which This technique uses the principle that if a dive to will 4 ATA produces DCS. These i. In deciding the depth of recompression. ­mixtures for decompression from that depth. sure to altitude and the breathing of certain gases (e. sion therapy. not known whether untreated DCS increases the 2. ●● Relieve ischaemia and hypoxia. heparin and dextrans.

an appropriate breathing gas is invaluable in seri. RECOMPRESSION USING STANDARD RECOMPRESS TO A DEPTH OF RELIEF RECOMPRESSION SCHEDULES This empirical approach was used first in underwa. This approach uses standard recompression tables ter recompressions to reduce the depth exposure as roughly divided into the following groups: far as possible. ble. oxygen tables start at 9 to 18 metres. at a lesser depth. ●● Helium-oxygen (heliox) tables. based on the assump. it requires a sound knowledge of saturation decom- The one advantage of this approach. It is still applicable. even compression to very high reduction bubble size and allow increased surface pressures may not completely e­ liminate that bub. is evident when a diver develops DCS ferent gas mixtures. Recompression 169 bubble is formed. The freedom to be able to choose any depth to ●● Oxygen tables. ●● Air tables. This is rarely required but available in many modern facilities. Figure 13.1). the patient is recompressed to the Many such tables have been published by both depth at which all major symptoms disappear. A recompres- depth will ensure that there is no tissue-to-bubble sion chamber (RCC) should have a mixed gas capa- pressure gradient that could cause bubble growth bility to support such operations. ●● Saturation decompression. Bennett. apart from pression and the ability to mix and administer dif- its simplicity. both underwa- ter and in chambers. Note the provision of both physiological monitoring and mechanical ventilation while under pressure. ous cases (Figure 13. thus leaving bubble nuclei to re-expand on This approach is not without difficulty because decompression. (Photograph by M. As traditionally used for deep and s­aturation exposures.) . the world. tension to promote bubble resolution. Under nervous system and pulmonary oxygen toxicity these conditions. Both air and heliox tables start at 30 and tion that the additional pressure would result in a 50  metres. a prompt return to the original become important considerations.1  A severely injured diver with decompression sickness who is treated in a ­recompression ­chamb er at 18 metres. plus commercial and military organizations around one additional atmosphere. Nitrogen narcosis and central very soon after surfacing from a deep dive. achieve an acceptable clinical result and then select ●● Oxygen tables with deep excursions.

air tables may be considered. . and these were the stan. The flexibility to treat patients who did not respond or physiological advantages are in the speed of ­ in facilities that may not be appropriate to apply bubble resolution and increased oxygenation of the guidelines. recent and not the result of gross or disability. The US to a mask. 3 AND 4 AND tables). The treatment tables were deemed oxygen tables has received worldwide acceptance satisfactory if the subjects did not surface with as the starting point for all standard recompression DCS after one of the treatment tables! therapy. but they are often reported air tables include logistical problems with pro. require compression only to 18 metres (2. acceptable. exceeding these parameters may be omitted decompression. to-extravascular bubble during the early phase of jects made normal dives. In cases of potential death toms are mild. gen in the intravascular bubble-to-blood interface sion Tables 1 to 4 in 1945. 55. recompression. to 40 hours.8 ATA) and A prudent diving physician will advise non. if oxygen is unavailable and the RCC saturation treatments depend on the depth of can logistically support a treatment table lasting up symptom relief. the oxygen parameters should not exceed those larly if pulmonary involvement is already present). Although the pressure gradient of nitro- Navy (USN) first published their air recompres. 2A. These tables Standard recompression tables are shorter. oxygen and gas mixture tables for The introduction of standard oxygen tables using recompression are presented in Appendix B and 100 per cent oxygen interspersed with short air Appendix C. which required decom. What has previously dived in excess of 18 metres. there is remarkable about these tables is that they were could well be a gas pressure gradient from tissue- never tested on subjects with DCS. to less than half the volume reduction achieved with the 50-metre standard air AIR TABLES (US NAVY 1A.170  Decompression sickness: treatment deep excursions are commonly to 30 metres and However. ROYAL spent at each depth and the rate of decompression. Although some authors have reported sig- During the 1960s. the periods to be OXYGEN TABLES (US NAVY 5 AND 6. Divers Alert experts to adhere to strict treatment guidelines. breathing ‘oxygen breaks’ gives more flexibility and improved results (Figure 13. increased fire hazard. pression. the success rate 50 per cent on the air tables resulted in the devel. reported failure rates of up to nificant failures with these tables. 72 AND 73) the occasional intolerance of a distressed patient These tables are used increasingly rarely. are therefore logistically achievable. is increased with oxygen breathing. tion in bubble size (i. is higher than with the air tables that preceded opment of the shallow oxygen tables. oxygen toxicity and ROYAL NAVY 52. icity (see  Chapter 17). at 80 to 90 per cent. it is suggested that increased density of air under pressure (particu. but were then subjected to a treatment With the foregoing qualifications. but retain his or her own of  all DCS is treated with these tables. These tables clearly state the gas mixture to be used (usually oxygen or heliox). Success rates for complete resolu- to use air tables because of the problems they bring tion of symptoms vary with both severity and the and their variable benefits. 54. The test sub. NAVY 61 AND 62 AND COMEX 12) Standard air. For this reason. this text covers tissues.e. aggravation of symptoms Whenever oxygen is used. them. longed decompression. the use of table instead. 53. Unless one is f­ollowing attendants and respiratory distress caused by the established safe protocols. nitrogen narcosis and DCS in the paid to oxygen toxicity.2). needing only 2 to 5 hours. more than one set of treatment techniques. and no better-performing alternative has Many experienced clinicians today are reluctant been identified. as Network (DAN) reports that about 80  per cent depicted in the manuals. likely to result in neurological or pulmonary tox- The results are often not adequate unless the symp. if the diver dard treatment tables for more than 20 years. The difficulties with time to recompression. The Disadvantages include the less immediate reduc- standard tables are as follows. attention must be during ascent. 71.

a breath- 50 metres using a modified USN Table 6A. but it may also be associated with a further tory cases. In general. These tables may also be used the option exists to go on to a deeper table using after recompression to depth of relief in severe a mixed gas such as a Comex 30 (Figure  13. Plate  3). The customary deep excursion over the shallow 18-metre oxygen treatment tables are inappropriate because of the tables in divers. This table was initially SATURATION TABLES (US NAVY 7) introduced as a treatment of cerebral a­rterial gas  embolism (CAGE) in submarine escape Saturation treatments are used when divers have trainees (with a low nitrogen load). Recompression 171 Descent rate = 7. cases and when other tables have failed. and the oxygen per- in severe cases of DCS or cases not responding. Recompression results in a reduction of bubble gen at depths greater than 18 metres. although developed DCS during or just after decompres- later studies have not shown any benefit from this sion from saturation exposures. a standard USN Table  6 at 18 metres. however.3 m/sec Oxygen breathing 18 Air breathing Total elapsed time (excluding descent) = 285 min 9 Pressure (msw) 2. In refrac. Although based on little evidence. increased pressure is applied. Ideally. An initial period at 18 msw (60 feet) breathing 100 per cent oxygen with air breaks is followed by a slow ascent to 9 msw (30 feet). Heliox mixtures (50/50) are substituted for oxy. centages are less. Depths are expressed here as metres of sea water (msw).4 20 5 20 5 20 5 30 15 60 15 60 30 Time (minutes) Figure 13. OXYGEN TABLES WITH DEEP EXCURSIONS A 2011 workshop reviewed the evidence for the (US NAVY 6A) AND HELIOX TABLES use of 30-metre heliox recompression and made (COMEX 30) some recommendations concerning the appro- USN Table  6A involves the addition of an ini. some centres advocate initial use of the Comex Gas mixture 30-metre table for severe neurological DCS. by a standard Table  6. there is then the opportunity to go to uptake of gas into the bubble. This is . size.3. fuses out. priate use of these more challenging treatment tial period of breathing air at 50 metres followed schedules2.5 m/sec Ascent rate = 0. Royal ing mixture would be selected that diffuses into Navy (RN) Table  64 or Comex 50 breathing the bubble at a slower rate than the inert gas dif- heliox mixtures.2  The US Navy Treatment Table 6 (or Royal Navy Table 62). resulting in bubble shrinkage. extreme gas loads in ‘slow’ tissues and the often Most centres now recommend starting with excessive oxygen exposures required.

3  The Comex 30 treatment table. present. ●● The depth effect of recompression is less The initial increase in bubble size with oxygen important the longer the symptoms have been may be explained by the fact that at equal par. breathing oxygen. treatment table selected. one r­eason that the oxygen tables are preferred In determining which therapeutic table should to the air tables because no further inert gas can be selected. The red areas on the Comex 30 table represent the patient breathing a 50/50 mix of oxygen and helium. ●● The natural history of the disease: sion using heliox has been beneficial in treating ●● The longer the surface interval before DCS after air dives. there was an initial increase ●● The value of pressure: and then decrease in bubble size. The final version of the Comex 30 heliox table appeared in the 1986 Comex medical book. The green areas on the graph represent the time spent by the patient breathing pure oxygen.172  Decompression sickness: treatment Modified Comex treatment table TT30 30 Depth (metres of seawater) 28 24 20 16 12 8 4 0 0 30 60 90 120 150 180 210 240 270 300 330 360 390 420 450 Time (minutes) Figure 13. bubble size. When compression occurred while many others do not. especially relevant to patients with respiratory Even using air tables. Breaks in oxygen therapy are scheduled and are shown as the blue areas on the tables. There is anecdotal evidence that recompres. Hyldegaard and associates3 symptoms. whereas with ●● Recompression will prevent bubble growth heliox there was a progressive shrinkage in bub. as are the effects of ischaemia and the Heliox is also easier to breathe at depth than air – chemical and cytological reactions to the bubble. tial pressure differences the flux of oxygen in fat is twice that of nitrogen and four times that of Delay to recompression helium3. the less likely they are to demonstrated in a model of spinal DCS that. while breathing air. subsequent progress may be related more to the time There is little available evidence to suggest heliox elapsed before recompression than to the specific tables are more effective than the oxygen tables. so that multiple similar versions are in use around the world. are lessened. the DCS are recompressed on oxygen. there is a steady increase in ●● Neurological symptoms have sequelae. worsen over time. and hasten resolution. Rivera4 demonstrated ‘chokes’. With prompt treatment although many centres will move to a heliox table for the destructive tissue distension effects of bubbles the difficult or non-resolving acute case (Table 13. This may explain the initial worsening of symptoms seen occasionally when patients with Once a manifestation of DCS has developed.1). Since then it has been modi- fied by many users. remember: be absorbed. This table is an adaptation by Dr Xavier Fructus of an older nitrox table developed by Dr Barthelemy at the French Navy diving facility (GERS) in the late 1950s. The maximum excursion is to 30 msw breathing 50 per cent oxygen in helium (heliox 50). that if initial treatment was administered less than . ble size.

breathing gases and oxygen not safe at maximum pressure. and so forth. most More complex. the approach to the As a good general rule. patients with DCS do sometimes after injury. as should the efficiency of the mask seal. Many these. Gas switching Air and oxygen only. ●● Non-diving general medical diseases. The fact that some authority has promulgated a The delay among the dive. particularly neurological. staff-intensive and recompression facilities can do requiring heliox supply. there was RECURRENCE OF SYMPTOMS a 95 per cent probability of relief. full recovery is not evident. caused DCS in attendants who did not even have . with oxygen Requires great care. Patients who delay seeking medical assistance may benefit from recompression even up to 14 days Nevertheless. if symptoms recur dur- patient who presents 30 minutes after a dive with ing treatment. Comex 30) Maximum depth (pressure) 18 msw (2. ●● Pulmonary barotrauma and each of its clinical consideration should be given to the options of manifestations (see Chapter 6).2). both the recompression schedule an ascending paralysis is different from the patient and the clinical management should be ques- who presents 48 hours after a dive with shoulder tioned. most diving physicians deteriorate during recompression therapy. The diagnosis should be reassessed.1 One air table (USN 4. considering the following: commencing with an 18-metre oxygen table or even a 30-metre heliox table. DCS. Cases not responsive to oxygen tables. This rate falls to 77 per cent if the delay exceeds 6 hours. Mixed rates. The would not consider deep or saturation tables for composition of the breathing mixture should be patients with these late presentations. results. the development therapeutic table does not make it effective. The first patient’s neurological injury is likely has been adequate recompression and supportive to progress with time.0 ATA) Duration (not extended) 4 hr 45 min 7 hr 30 min (some versions vary) Resources required Relatively easily acquired. RN 54) frequently and Case Report 13.1  Comparison of the features of standard 18-metre oxygen tables and 30-metre heliox tables Oxygen tables (e.g. rapidly progressive forms of DCS. USN. Severe cases. Features RN 62) Heliox table (e. affecting target organs. Three safe at maximum pressure. facilities not equipped for this. rehydration will not and may undergo spontaneous resolution.8 ATA) 30 msw (4. including correct positioning. of these authors. If using the former. The first patient should be treated aggressively.g. Consider confirmed. To illustrate these principles. however. Recurrence of symptoms  173 Table 13. 30  minutes after symptoms developed. made to these tables during the professional lives tance and propose the most rational therapy. Evidence base Hundreds of thousands of Some non-random comparisons applications with high success with oxygen tables. and of symptoms and the presentation for treatment there have been many modifications and deletions allows the clinician to assess the clinical impor. whereas the shoulder pain therapy. US Navy. two illustrative case histories (Case Report 13. The physician should ensure that there pain. Common indications All DCS. decompression sickness. going deeper and changing gas mixtures if early or ●● Complications of DCS. USN TT6.

1 The patient made a dive to 18 metres for 60 minutes on scuba. Comex 30).174  Decompression sickness: treatment CASE REPORT 13. and thus there will be no significant pressure gradient pushing nitrogen into the bubble. the tissues will have equilibrated fully with the atmo- spheric pressure. Third. The bubble. must be presumed to represent a re-expansion of . it is not going to get significantly worse as long as the patient avoids further exposure to hypobaric or hyperbaric conditions. will have a nitrogen pressure of approximately 1 ATA. then surface oxygen would be appropriate. the likelihood of progres- sion from the theoretical ‘minor symptom’ to a major case of DCS is much higher. First. but this time the left shoulder symptoms followed 10 minutes after a 30-metre dive for 30 minutes with a rapid ascent and omitted decompression. if other more serious symptoms develop. has been removed from at the shallow stops. The therapeutic approach to this diver is to recompress him to the maximum depth at which 100 per cent oxygen can be used therapeutically. and if a satisfactory response is obtained and maintained. Even assuming that the left shoulder pain is musculoskeletal and not referred neurological or cardiac. The diver has presented for assistance immediately after the symptom developed.e. Comment: This is not only a mild case of DCS. as the bubble is at the same ambient pressure as the body. Second. to decompress him from that depth. The isolated symptom of left shoulder pain developed 5 hours after the dive and had been present for 24 hours before the diver presented for medical treatment.1. CASE REPORT 13. At this depth there would be no tissue-to-bubble nitrogen gradient. The authors of this text would select a 30-metre 50 per cent heliox treatment schedule (e. The administration of 100 per cent oxygen will enhance this gradient further. Comment: This is a very different situation from Case Report 13. patient and attendant from 18 metres to prevent If similar and significant symptoms recur.g. the tissues surrounding the bubbles may well have nitrogen supersat- uration pressures of almost 4 ATA. they this problem. Recompression treat- ment at 18 metres will not rapidly reverse the tissue-to-bubble nitrogen gradient and. Oxygen is now used by both the US Navy Manual. Under these conditions. The short air embolism Table  5A. There had been no dives for a month before this. existing on the surface. On the contrary. there will be a mild gradient in the opposite direction. If recompression was not feasible. By the time the medical assessment was made (29 hours after the dive).2 This patient has symptoms identical to those of the patient in Case Report 13. it may be necessary to recompress him deeper on heliox (or an oxygen and nitrogen mixture). USN Table 6 at 18 metres. It is difficult to which many of us believed to be a contributor to understand how it could then improve patients deaths during treatment. more symptoms are likely to develop (remembering that DCS manifestations may continue to arise over the next 24 hours). increasing the size of the latter until the tissue gas tension becomes equated with the bubble gas tension. The authors’ approach to such a mild case would be to relieve the patient’s symptoms and perhaps to reduce the possibility of subsequent bone damage (although there is no clear evidence that this latter is really possible) by recompression on an oxygen treatment table – probably at 18 metres. it is likely to become worse. there will be a gradient between the tissues and the bubbles.1. i. a nitrogen load to start with. because the symptom developed soon after the dive.

which was not completely removed. affecting marginal ischaemia or nerve irritability from myelin sheath damage. This will oxygen table for 1 to 2 hours) on the ­following day. Both recompression and altitude exposure alter ●● Lipid. may affect these minor symptoms. because the increased venous pressure may cause . These authors the brain. given that the bubbles would preferen- use standard oxygen tables. it would be a sisting for weeks to months after DCS – are not great coincidence if it were to reproduce the same uncommon and do not require intervention. It is probable that most of these symptoms Position are transient and more anxiety provoking than functionally important. baric ‘air breaks’. vary according to the manifestations. unless these type treatments inappropriate and brief deep symptoms have some ominous clinical signifi. Patients should be Although redistribution could be expected to reassured that such minor symptoms – often per- respond to recompression therapy. carbon dioxide and pH) and ●● Re-perfusion injury. Other regimens may be applied. Adjunctive therapy  175 a bubble. hyperbaric oxygenation or a conventional sicians now use a standard 18-metre oxygen table therapy table. Minor residual musculoskeletal or periph. and  chasing ●● The possibility of pneumothorax. is illogical and has increased Occasionally. It is such as: very unusual for even a patient with serious case to receive more than five or six treatment tables. symptoms as the original lesion. cance.to 14-metre General medical treatment is required. it is was recommended for patients suspected of having common practice to continue with intermittent CAGE to prevent re-embolization. these symptoms to obtain a complete ‘cure’ ●● Fitness for further diving and its investigations. blood gases (oxygen. complications to both attendant and patient. platelet or fibrin deposits or emboli. such as USN Table 6. This practice is no longer recommended but the use of repeated diving therapeutic tables. and such as extended Table  6 (USN) with its hyper- treated accordingly. ●● The presence of pulmonary tissue damage. Previously a head-down or Trendelenburg position With spinal cord or cerebral damage. to reduce the incidence of minor persistent symp- toms. ●● The possibility of little or no inert gas loading It is not necessary to recompress repeatedly for in the tissues (thus making long saturation minor and fluctuating symptoms. as described earlier. presumably by ●● Redistribution of gas emboli. Recurrences of the original symptoms or the CEREBRAL ARTERIAL development of other serious symptoms should GAS EMBOLISM be seen as resulting from inadequate ­treatment or caused by aggravation of the problem by Although recompression treatment of CAGE tra- ­re-exposure to nitrogen at depth or on the surface. eral nerve disease is very common. It has become common ADJUNCTIVE THERAPY practice to follow a formal r­ecompression table with an ‘oxygen soak’ (typically a 9. diving phy- (if mild). ●● The inflammatory tissue reaction to the bubble. there may be other explanations. Paraesthesia and other symptoms developing If the CAGE is not caused by DCS and is a man- while undergoing recompression therapy may ifestation of pulmonary barotrauma. excursions more valuable). on tially rise to the higher vessels through the effect of a daily schedule. becomes demoralizing and exhausting for both patient and attendants. buoyancy. ditionally involved a deep excursion to 50 metres Recurrence of symptoms requires surface oxygen followed by a standard USN Table  6. The head-down hyperbaric oxygen therapy until all subjective and position was originally used to divert emboli from objective improvement has ceased. then the fol- reflect the development of oxygen toxicity (see lowing other factors should be considered: Chapter 17) and therefore are not necessarily an indication to extend the therapy.

In one series6. surface oxygen was shown to be Hartman’s solution. Most available masks do not read- bated by hyperglycemia. strate the value of surface oxygen. including an electrocardiogram (ECG). Other risks involve most patients with spinal DCS. Surface oxygen administration and current practice tends toward repeated treat- ments for residual symptoms. a highly selected population. For the same reasons. This increases blood viscosity and reduces ●● Treat developed DCS. The haematological effects of DCS may aggravate ●● Reduce the size of inert gas bubbles. Behnke both symptoms and outcome from DCS. report suggests up to 50 per cent symptom resolu- men ovale. with a target of ●● Possibly improve oxygenation of damaged urinary output of 1 to 2 ml/kg per hour. serious cases should be intravenously hydrated with non–sugar-containing electrolyte fluids. and low-molecular-weight dextran in saline sion facilities are not readily available. Rehydration is impor. the coma position and advised not to strain or per. tribution to oxygen toxicity. mask is used. the series did demon- trolytes and plasma osmolarity can be determined. renal failure and bleeding – to date no cent oxygen with intermittent air breaks is advantage over crystalloids has been reported. Many classes of drugs have been tried to improve Albert R. ●● Prevent recurrences of DCS. Although the value of administering 100  per anaphylaxis. vital signs should be moni. ily p ­ roduce 40 per cent oxygen in the inspiratory Urinary catheterization will be required for gas even at very high flows. and it may reduce the likelihood that other from the lower limbs may increase the ­possibility symptoms will develop (a Divers Alert Network of paradoxical gas embolism through a patent fora. During treatment. When it is has been used in the past to prevent rouleaux for. given early and Intravenous colloids are rarely used but may be of for some hours. One area that has been relatively over- looked recently is the administration of Drug therapy oxygen at normobaric pressure. as will careful skin the inflammable nature of oxygen and the con- and body maintenance. unquestioned. In addition. dehydration from immersion and cold-induced ●● Prevent development of DCS. in remote areas where recompres- value. blood flow to the major organs. increased venous return rarily. Although this was ological saline is preferable until the serum elec. This approach is particularly of value before not be raised. if sometimes only tempo- cal disorder. the legs should tion)5. as detected by Doppler. ●● Enhance inert gas elimination. often relieve symptoms. diuresis. General care ●● Prevent venous gas emboli. Commonly. and oxygen after recompression therapy to prevent the this should not cause difficulties in most chambers. whether orally or intravenously. reduction of DCS sequelae after recompression5. Oxygen has been demonstrated to: form Valsalva manoeuvres. an inadequate avoided because cerebral injury may be exacer. Ringer’s lactate or physi. the DAN report of 1996 suggested mation. Drug use has often been . Few have July 1990 stood the test of time. recurrence of DCS symptoms and avoid repeated treatments. tant. used in transit. Problems with using colloids include fluid overload. an effective treatment for DCS. however this practice is  now unusual.176  Decompression sickness: treatment increasing intracranial pressure and decreasing The administration of 100 per cent oxygen will cerebral perfusion. Some diving physicians prefer to use 100 per cent tored. The patient should be supine or in subjecting the patient to altitude. Patients with tissues. expand the blood volume rapidly and that oxygen will result in some DCS cures and a reduce the likelihood of intravascular coagulation. thus aggravating the neurologi. problems do arise with inexpe- Glucose and other carbohydrate fluids must be rienced personnel.

if ever. The clinical value of most drugs is less than tive influences on susceptible individuals. platelet aggregation. On the one hand. from treating DCS but from treating cerebral but on average one less recompression session was oedema associated with traumatic and vascular required10. in the AMINOPHYLLINE same dosage as used for cardiac dysrrhythmias. and many advocated because of their effect on the coagu- practitioners have abandoned this approach after lation pathway. this benefit seemed confirmed when the drug was associated with a cerebral protective effect when it ANTICOAGULANTS was used prophylactically in patients undergoing left-sided heart valve surgery 9. Correction of specific coagulation their  inhibitory effect on platelet aggregation defects seems a more logical approach to the and their wider anti-inflammatory and analgesic rare complication of disseminated intravascular actions. however. This experience came not similar with or without the NSAID tenoxicam. for example. Lidocaine (formerly lignocaine in the United Kingdom) is recommended with caution. It results in the dilatation of the mental evidence to support this recommendation. Currently. after diving. sion. in cases of disseminated intravascular coagula- tion that had no evidence of systemic infarction ANTI-INFLAMMATORY AGENTS and bleeding. many diving physicians rec. NSAIDS will tem- porarily relieve many of the symptoms of DCS CORTICOSTEROIDS and may hasten the resolution of those symptoms The use of corticosteroids has previously been following recompression. and there are reports in animal studies linking aspirin with an increased risk of LIDOCAINE dysbaric osteonecrosis. There is evidence that antiplatelet agents such as pressions. rhagic disease. Aspirin has a variety of other nega- tion. bronchospasm. However. and on the other. There have been metic drugs. related brain injury. no definitive studies to support its use in DCS- pression table. such as remarkable. Adjunctive therapy  177 based on the results of animal experimentation ANTIPLATELET DRUGS using extreme exposures and/or very rapid decom. It can be harmful following activation may modify the activation of the coag. . when given prophylacti- Some agents may be of value if they are adminis. with the increased likelihood drugs proposed include those that increase tis. the haemorrhagic disorders of the spinal cord ulation pathway by bubbles if given early enough and inner ear and other DCS manifestations. cally. NSAIDS have been advocated because of both used in DCS. and the systemic circulation. and probably other sympathomi- severe cerebral and spinal DCS. The one double-blind ­justified on the belief that this class of drugs randomized controlled study of these agents may reduce cerebral oedema and modify the suggested that the results of recompression were ­i nflammatory process. aspirin or dipyridamole. the effect on platelet coagulation in DCS. They were said to be indicated unsuccessful use in their own practice. may be contraindicated in dysbaric a couple of hopeful case reports and some experi- diving accidents. DCS. there are no controlled studies to There is some logic in the use of pharmacological support the use of these drugs in the treatment of agents to reduce.8. brain injury. There are more arguments against the use of microthrombi and neurological oedema. pulmonary vasculature and a profuse release of A beneficial effect of lidocaine has been demon- bubbles trapped in the pulmonary circulation into strated in animal models of air embolism7. for Aminophylline. Later studies did Heparin and coumarin derivatives have been not confirm these findings. modify platelet action following decompres- tered before the actual decompression accident. Just as the use of corticosteroids ommend the adjunctive use of an NSAID for 5 to has been discredited in brain injury. and therefore of limited applicability. These drugs are now rarely. there are 7 days. of aggravating inner ear or spinal cord haemor- sue perfusion and/or expedite inert gas elimina. beginning during or after the first recom. Other aspirin than for it.

within minutes of symptoms developing. reported use in diving humans. In this situation the water. Some of the breathing techniques (see the famous sequence in disadvantages of include severe sepsis. and this practice has the administration of modest amounts of increased been abandoned because of serious side effects in oxygen administration. the movie The Abyss). respiratory The failure of DCS to respond to recompres- depression or interference with the clinical picture. in tiated within 8 hours of traumatic spinal injury which the intravenous administration of a modest resulted in a significantly greater neurological volume of perfluorocarbon may rapidly denitro- recovery in a large randomized trial (the sec. exerts the pressure. out causing any significant drowsiness. there was no clinically significant increase the blood oxygen-carrying capacity with improvement in function. compressors that will not reliably supply divers ested in further investigation. most of which have handle in the RCC. however. exciting possibilities for use in diving medicine. This is likely to Most have only scuba cylinders or simple portable change. such in treatment. the prevention of DCS by some cases. Also of interest are the potential to [NASCIS  2]11). In DCS there are no published trials administration before diving and the extension supporting methylprednisolone use. underwater air recom- pression was effectively used in Hawaii. hyperglycemia. where long periods were spent the patient. and cortico. Sometimes chambers are not readily as diazepam. These com. of deep diving limits by the utilization of liquid steroids are no longer recommended. Although this with a toxic-confusional state as a result of involve. The dosage remote localities such as Northern Australia. (the patient and the attendant) for the depths and . to help control vertigo. but otherwise a 10-mg initial dose may under water and standard diving equipment was be supplemented by 5 mg every few hours. carry the compressed air supplies or compressor and the authors of this text are not aware of any facilities necessary for the extra decompression. and they may not tolerate the never been reported. hemorrhage. treatment is frequently disparaged. These fascinating compounds have been developed This was also the experience of professional shell in the efforts to produce an artificial blood sub. with good PERFLUOROCARBONS results. RCC. Potential uses include the treatment of DCS. anaphylaxis and an increased sus- ceptibility to oxygen toxicity. For this reason. It may also be useful in the occasional patient compressors sited on the diving boat. pounds have the ability to absorb enormous vol. These patients can be very difficult to and it has had many successes. these agents are experimental only. It may be of considerable value in By far the most traditional of the non-chamber reducing the incidence and degree of oxygen tox. because several groups are inter. This was certainly so in those oronasal mask without an anxiolytic. it has often been ment of the neurological system from either DCS the only therapy available to severely injured divers. divers of Australia. and this treatment should not be entered into with- umes of oxygen and nitrogen and present several out appropriate planning and resources. especially in patients with serious cases who therapy. instead of an require extensive exposure to oxygen under pres. available. Most amateurs or semi-professionals do not At this time. UNDERWATER TREATMENT BENZODIAZEPINES In-water air treatments Diazepam (Valium) has been recommended for use in DCS. in the must be regulated according to the clinical state of pearl fishing areas.178  Decompression sickness: treatment Although high-dose methylprednisolone ini. with. many problems may be encountered. sion therapy. used. treatments of DCS is underwater recompression icity. Air supply is ­usually from sure. with very poor lung function when they are acutely Despite the value of underwater air recompres- unwell in an intensive care setting. or CAGE. at least until underwater oxy- stitute and to enable liquid respiration in patients gen therapy became available. sion therapy is often related directly to the delay Vestibular DCS may require suppressants. genate the tissues and eliminate any intravascu- ond National Acute Spinal Cord Injury Study lar bubbles.

urgent need for management of cases in remote ing DCS in the attendants and aggravating it in ­localities  – remote in both time and distance the diver.g. Seasickness in the zation. ment is based are well known and not contentious. Protected site with calm water. 2. Underwater treatment  179 durations required. The advent of night. rising seas. Table 13. The same caveats about organi- hypothermia becomes likely. Hookah air supply for attendant diver. it should never is now practised even when experts are not avail- be undertaken without careful consideration of able to supervise it. Suitably trained attendant(s) to ensure appropriate decompression rate and gas supply. Ability of the patient diver to be safely immersed for the duration of the table (e. Although in the absence of an RCC from hyperbaric facilities. the resources available and the environmental The physiological principles on which this treat- conditions. Suitable diving platform (boat or wharf) above column of water to >9-metre depth. Nitrogen narco. 8. Full-face mask. Human resources 1. tiredness and ing extra nitrogen loads. As a result of the suc- it may be the only treatment available to pre. A suitable communication system with divers.2  Minimum requirements for the safe conduct of in-water oxygen tables Equipment 1. decreasing the depths required for the the return to the open ocean a very serious deci. 3. apeutic efficiency. 7. reduced exposure time and improving overall ther- sion. 4. applied to the underwater treatment of DCS. avoid- inclement weather. increasing oxygenation exhaustion and boat safety requirements make to tissues. thereby produc. The treatment often has to be aborted because The procedures were developed in response to an of these difficult circumstances. oxygen treatment (Table 13. Attendant diver (breathing air). Regulator and hoses (minimum 12 metres – marked in 1-metre intervals) rated as ‘oxygen-safe’ and maintained appropriately. Appropriately trained individuals to oversee the procedures. 2. Environmental factors 1. Freedom from unacceptable tidal fluctuation and current. resources and sea conditions are applicable injured diver. increasing nitrogen elimination gradients. cess of this treatment. 2. Appropriate thermal protection for prolonged immersion. . Water temperature compatible with thermal protection available. it vent death or severe disability.2). Environmental conditions are Underwater oxygen therapy not usually conducive to underwater treatment. Suitable method for weighting diver and attendant to avoid unwanted changes in depth. sis produces added difficulties in the diver and the Beginning in 1970. not having seizures or unconscious). and its ready availability. this option has been attendant. Because of the considerable depth required. 3. 5. At least one G-sized (7000 litres) oxygen cylinder – medical grade. 4. 6. the diving attendants and the boat when comparing underwater air and underwater tenders is a significant problem. Often the depths required can be achieved only by The advantages of oxygen over air tables include returning to the open ocean. 3.

be present. Hawaiians have included a deep air ‘dip’ before USE OF UNDERWATER OXYGEN underwater oxygen treatment.4). be used. dirty or lubricated with oil. oxygen therapy are designed to make for safety. an addi- are problematic.3 Oxygen is supplied at maximum depth of 9 metres and Case Report 13. as are accurate clinical assessments – and tables is 2 hours 6 minutes. and is designed to reduce the Standard devoted to ensuring that facilities are many hazards associated with conventional aware of appropriate safety and training for these underwater air treatments. parts of Australia. but some- The techniques and equipment for underwater times surprisingly effective and rarely. Many divers so treated oxygen breathing. system. with respiratory volume measurements and chest x-ray MEDICAL ATTENDANTS examination if possible. No equipment should be used with oxygen General medical treatment is required during the unless it is assessed ‘oxygen safe’ or if it is contami. After duration of treatment and complete resolution surfacing. The relative value of proposed first aid regimens phisticated countries. based hyperbaric facilities require their hyper- The underwater oxygen treatment table is not baric workers to have undergone a formal training meant to replace formal recompression therapy program. interspersed with air breath. The prompt re-immersion of the diver allowed shorter ascent is at the rate of 12 minutes/metre. The duration of the three required. if available. recompression sessions. 1 hour off basis. from a surface supply. even in medically unso. underwater oxygen was first applied rienced personnel and comprehensive hyperbaric mainly for minor cases of DCS. men. ease and ready availability. and the superiority of expe- apy tables. It is embarrassing to produce DCS in ­supportive and pharmacological adjuncts to the attendants during recompression therapy. Because this treatment is applied in remote bles  trapped in arteries to transfer to the venous localities. not superior to portable RCCs. facilities is not being challenged. if needed. and the ascent should be controlled First aid and resuscitation techniques are often by the surface tenders. resumed diving within days. underwater heliox. These times may be extended for another of complications. usually on a 1 hour on. Apart from the relative paucity occurred. Underwater quently found to be of considerable value in serious oxygen treatment is considered as a first aid regi- cases. Ascent is ­ commenced There have now been many hundreds of cases after 30 minutes in mild cases. unattended in RCCs. It is necessary to consider the possibil- in chambers. . the major lesson learned was that 30 ­minutes if there has been no improvement. Twenty-five cases were well supervised before this technique increased suddenly in popularity. 2 hours 36 minutes and for these reasons it is desirable to have a trained 3 hours 6 minutes. and to be applied with equipment usually found in hyperbaric attendants have an entire Australian remote localities. or 60 minutes of underwater air and underwater oxygen treat- in severe  cases. It is an emergency procedure. in an attempt to TREATMENT force bubbles back into solution or to allow bub. but it was subse. many cases are not well documented. Patients should not be left nated. particularly while they are An air breathing diver attendant should always breathing increased oxygen concentrations. As for conventional oxygen ther. if ever. TECHNIQUE Two such cases are described (Case Report 13. if significant improvement has ments recorded12.180  Decompression sickness: treatment although the indications for treatment have caused treatment of recompression sickness should still some confusion. able ity that DCS may occur in the attendants. detrimental. Most hospital- twice daily. it is likely this approach is now in tional deep descent and surface oxygen treatment) widespread use in the Pacific Islands and remote needs to be clarified. The customary workers13. the patient should be given periods of of DCS manifestations. Although accurate estimates (underwater oxygen. ing. The treatment can be repeated medical attendant in the chamber.

with a surface interval of 1. and very primitive airstrip facilities. while searching for the wreck of HMS Pandora about 100 miles from Thursday Island in the Torres Strait. Two hours were allowed at that lesser depth. The involuntary extensor spasms recurred every 10 minutes or so.5 hours. but because of very hazardous air and sea conditions. muscular pains and weakness. the patient was unable to walk. another 12 hours would be required before the patient could have reached an established recompression centre (distance. The patient was transferred to the hospital. CASE REPORT 13. It was about 36 hours after the dive before the patient was flown to the regional hospital on Thursday Island. severe back pain. The National Marine Operations Centre was contacted for assistance. A few minutes after surfacing. During that time an underwater oxy- gen unit was prepared. Two attempts at underwater air recompression were unsuccessful when the diving boat returned to its base moorings. and the patient was then decompressed. Within 15 minutes of surfacing. and the patient was immersed to 8 metres of depth (the maximum depth off the wharf). clouding of consciousness. involuntary extensor spasms.4 A 23-year-old female sports diver was diving with a 2000-litre (72 cubic feet) scuba cylinder in the Solomon Islands (nearest recompression chamber was 3500 km away and prompt air transport was not available). Return to diving and flying  181 CASE REPORT 13. slow and slurred speech. increased tendon reflexes and equivocal plantar responses. with 8 minutes of decompression. back pain. intention tremor. with evidence of both cerebral and spinal involvement. pains in both knees and abdominal cramps. and she was given oxygen via a facemask for 3 hours without significant change. Decompression at 12 minutes/meter was uneventful. progressively increasing incoordination and paresis of the lower limbs. Within 15 minutes she was much improved. No decompression staging was possible. and the patient was accompanied to a depth of 9 metres (30 feet) off the wharf. then numbness and paraesthesiae. An underwater oxygen unit was available on Thursday Island for use by the pearl divers. Both the Air Force and the Navy had been involved in the organization. generalized weakness. where neurological DCS was diagnosed. the diver developed paraesthesiae. it is important to consider the ●● Was the development of DCS consistent with following: the diving exposure? . and after 1 hour she was asymptomatic. except for small areas of hypoaesthesia on both legs. the dive depth was 34 metres and the duration approximately 20 minutes. 3000 km [2000 miles]). severe weakness of lower limbs with impaired sensation.3 A 68-year-old male salvage diver performed two dives to 30 metres for 20 minutes each. and a commercial aircraft subsequently flew the patient to Australia. He had marked ataxia. difficulty in micturition. very severe headaches. RETURN TO DIVING AND FLYING ●● Has there been a good response to treatment? ●● Are there any residual symptoms and signs When considering a return to diving after an attributable to DCS? episode of DCS. There was total remission of all symptoms and signs. she developed respiratory distress. On examination at Thursday Island. allegedly because of the increasing attentions of a tiger shark.

Canadian Defence and Civil Institute diving. with a resultant renders the individual permanently unfit to dive. A further insult may result in this exposure. that DCS may involve greater areas of the brain ●● Incorporate a ‘safety stop’ of 3 to 5 minutes at and spinal cord than are detected clinically – a 3 to 5 metres on every dive. These times should PADI tables) is now exceedingly rare. tiday repetitive diving are commonly reported. the patient with DCS ommend to these divers that they delay flying or should be counseled on safe diving practices. the second episode of enriched air) for air. quite the reverse. If there has been a less than complete recovery ●● Restrict diving to two dives a day. with a long following neurological DCS. . Rapid and frequent ascents and mul. a cause for this increased suscep. It is the policy of the authors of this text to rec- Before a return to diving. ●● Consider substituting nitrox (oxygen cally evident. safe to fly or ascend to altitude following an episode tibility should be actively sought (e. stay well scans and neuropsychological testing as indicated within the no decompression limit rather than by the clinical condition. computer. If the episode of DCS occurs after a relatively There is a lack of good scientific data on when it is trivial exposure. their limits. so this is a very real practical problem. ●● Add a depth/time penalty for future diving. with a Diving according to published dive tables (e. these computers do not seem to ●● Was there any evidence of associated pulmo. and almost all be extended for divers with continuing symptoms diving is controlled by a personal diving computer. pulmonary of DCS. dive to that limit. have been associated with a higher incidence of nary barotrauma? DCS – if anything.g. pression should be followed up clinically with i. divers with DCS disregard for decompression schedules or from are usually very reluctant and financially inconve- simply stretching accepted computer algorithms to nienced if they cannot return home for 4 to 6 weeks. Patients with incomplete recovery after recom. with DCS numbers falling across most jurisdictions. For ●● Use a decompression schedule that has been this reason. ●● Have a rest day after each 3 days of diving. Although greeted with some initial skepticism by tibility to DCS? dive physicians. see Appendix A) or a reputable personal diving sure to an inert gas load. subclinical damage extending to become clini. the authors of this text recommend tested and has a known and acceptable risk of a minimum period of 4 weeks before a return to DCS (e. brain imaging the decompression limits for a 40-minute. characteristic of some degree of neurological ●● Ensure conservative flying after any diving redundancy. vidual not dive again. but dive according to neurological DCS may result in a significantly the air tables. within the tissues only to re-expand with an expo. With a computer. patent foramen ovale). the preferred minimum of 1 week. Recommendations vary from 24  hours to barotrauma.g. after recompression. especially in the presence of bubbles.182  Decompression sickness: treatment ●● Does the individual have an increased suscep. return of symptoms.e.g. Autopsy evidence suggests ●● Perform slow ascent rates. for a dive to 16 metres for 35 minutes use appropriate investigations. tion of the authors of this text is that the indi. techniques.g. The bubble micronuclei discussed earlier pulmonary barotrauma (see Chapter  6) usually may expand with altitude exposure. electroencephalography (EEG). Evidence of 42 days. the recommenda. Evidence supports the existence of bubbles for some days or weeks after DCS and recompression Safe diving practices therapy – a function of the slower rate of gas elimi- nation. surface interval. Because many diving destina- Many episodes of DCS result from a complete tions are in remote tropical areas. Therefore. e. Bubble micronuclei may exist indefinitely of Environmental Medicine [DCIEM] tables. ascending to altitude for 2 weeks if possible. bone 18-metre dive. worse outcome.

A randomized. Adjuvant drug Journal 1976. Catron PW. Rivera JC. Mitchell SJ. Bennett MH. 9. 5th ed.322:1405–1411. Sickness Among Divers: Hyperbaric oxygen facilities.70:97–102. Undersea Biomedical Research Kensington. Flynn ET. UHMS workshop no.18(5–6):361–371.17(2):92–97. embolism. Medicine 1990. .23(10):1515–1521. West D. reduces compression requirement. Treatment 10. Australian Standard (AS) 2299. Undersea and Hyperbaric Medicine 2. Moon R. Flynn ET Jr. An Analysis of 935 Cases. Data. Medical Society. Decompression Research 1982. Treatment of Serious Decompression cerebral ischaemia induced by air Sickness and Arterial Gas Embolism. 1979. in the treatment of decompression et al. Spencer MP. Annals of Thoracic Surgery 1999. Neuman TS. Journal of Neurosurgery UHMS workshop no.30(3):195–206. United States Navy Experimental Diving FURTHER READING Unit research report 1-63. eds.2. Undersea Biomedical 6. eds. Effect of ing the symptom-free diver to a few 2-hour ses. 1982. asymptomatic bubbles and micronuclei by expos. lidocaine on somatosensory evoked sions of breathing 100 per cent oxygen. Mcdermott review. and a further possibility is to charter an air. 20. Evans DE. 2003:600–650. DAN Report on Diving Accidents and Durham. Thomas LB. 12. 1989. New England Journal of 3. 4. eds. Management. Durham. of the decompression disorders. Mitchell S. The adjunctive treatment of decom- In: Brubakk AO. Moon RE. North Carolina: Divers Alert Bove AA. Hyldegaard O. Effect of lidocaine after ­experimental Davis J. sickness in diving. treatment of acute ­spinal cord injury: Diving and Hyperbaric Medicine results of the second National Acute Spinal 2012. Bennett pression illness with a non-steroidal and Elliott’s Physiology and Medicine ­anti-inflammatory drug (tenoxicam) of Diving. Diving Accident Unit. Pellett O. 1996. The basis for drug therapy in decom- Network. Bennett MH. Edinburgh: Saunders. O2. Mitchell SJ. Kobrine AI. Cerebral protection by lidocaine during cardiac REFERENCES operations. Navy Experimental Diving Bennett PB. Collins WF. 1. Maryland: Undersea Hyperbaric 1991. Panama City. UHMS workshop no. Moller M. controlled trial of ­illness: the Hyperbaric Technicians and methylprednisolone or naloxone in the Nurses Association 2011 w ­ orkshop. Stroke craft whose cabin pressures are kept at 1 ATA (not 1992. (2012) The use of deep tables 11. 2003. Dutka AJ.32(3):171–180. North Carolina: Duke University. Decompression 13. 1990. canine cerebral air embolism. Edmonds C. North Carolina: Undersea Fatalities: 1996 Edition Based on 1994 Hyperbaric Medical Society. Part 2. Cord Injury Study. pression sickness. Kay E. matter. Undersea Biomedical Research JJ.9(2):91–111. and N2O-O2 breath. Clark JB. Effect of He-O2. Bracken MB. 5. How J. therapy for decompression sickness: a 7. before response and ­cerebral blood flow after flying. Hallenbeck JM. Shepherd MJ. ed. 41. In-Water ing on injected bubbles in spinal white Recompression. 48. 1963. Gorman DF. Gorman DF.9(2):161–174. King D. Mcdermott J. Dominguez A. Florida. 1999.67:1117–1124. Further reading  183 In rare situations one may attempt to remove 8. Young D. Mink R. Singapore Medical Catron PW. Durham. within many people’s capability!). Madsen J.

Elliott DH. London: Medical Research Council. 1996. Moon RE. Society Journal 1998. The Physiology and Medicine of Diving. Flagstaff. Treatment of 137 Cases of illness. Treatment of the decom. US Navy Diving Manual. 1993. Treatment of This chapter was reviewed for this fifth edition by Decompression Illness. Volume 1: Air Diving. Adjuvant therapy for decompression Slark AG.184  Decompression sickness: treatment Moon RE. 1996. RNPL report 8/62. eds.28(3):144–149. eds. London: Balliere Tindall. In: Bennett PB. Kensington. Maryland: Undersea Hyperbaric Medical Society. Gorman DF. UHMS workshop no 45. South Pacific Underwater Medicine Decompression Sickness. Sheffield P. . Arizona: Best Publishing Company. 1962. pression disorders. Michael Bennett. Moon RE.

as 7 hours. and that shaft lesions are usually asymptomatic. at 242 kPa. 3 months of the presumed causative diving expo- In 1912. in 1943. sub- between initial joint ‘bends’ and subsequent x-ray sequently developed osteonecrosis. Sydney. noted that several months elapsed between Aseptic necrosis of bone has been described in the hyperbaric exposure and the joint symptoms ­diving lizards (mosasaurs) of the cretaceous period. in 1931 in the China sea after changes. but when there is most recently in 20141. Taylor. neck and shaft lesions 191 Invasive investigations 198 Symptoms 191 Prevention 198 Neoplasia 191 Treatment 199 Radiology and differential diagnosis 191 Surgical treatment 199 Juxta-articular lesions (A lesions) 196 Radiological technique 199 Head. divided into two shifts. infarction of work at a pressure of 117 kPa (less than 12 metres areas of bone associated with exposure to pressure of sea water equivalent).1). neck and shaft lesions (B lesions) 196 References 200 Further reading 200 INTRODUCTION evidence of bone atrophy and sclerosis. although in retrospect the man appeared DON has been known to develop within to have ‘septic’ necrosis. Twynam first suggested a clear relationship between pressure exposure and a causal relationship between bone necrosis and the subsequent development of aseptic necrosis. 185 . Three of five men who escaped from the ers on the Elbe tunnel at Hamburg. in 1913. The condition has been reviewed disease has gone by many names. exposures. This tieth century. 14 Dysbaric osteonecrosis Introduction 185 Other investigations 196 Incidence 186 Bone scintigraphy (bone scans) 196 Aetiology and pathogenesis 187 Single position emission computed Pathology 190 tomography 197 Clinical features 190 Computed tomography 197 Juxta-articular lesions 191 Magnetic resonance imaging 198 Head. and also for as short a time has been recognized since the turn of the twen. suggested a relationship being at a depth of 38 metres for 2 to 3 hours. there were 500 cases of decompression sure and has occasionally resulted from ‘once only’ sickness (DCS) reported among the caisson work. now use the term ‘dysbaric osteonecrosis’ (DON) son worker constructing the Iron Cove Bridge in (Table 14. In humans. Bassoe. and 9 had bone submarine Poseidon. although the association with human diving may Osteonecrosis has been observed following caisson not be entirely germane. we pressure exposure in 1888 in a case report of a cais.

lesions. joint replacement had been conservatively esti- sion practices. i. Osteonecrosis affecting hips and shoulders among divers more than 30 years old. In 1989. and commercial diving operations where strict a To be distinguished from other causes of bone decompression schedules are adhered to. Diver’s bone rot. Barotraumatic osteoarthropathy. about 0.6 per cent if they had been deeper. All prospective workers had osteonecrosis pre-­employment x-ray studies. experience and also who had exposures to greater For example. ranging from 2. and those workers Caisson arthrosis. It is rare in recreational sport scuba divers.5 per cent in the US Navy to Ischaemic necrosis of bonea. Most cases in most series involve shaft dates from the 1970s and 1980s.1  Some synonyms for dysbaric evidence of necrosis. Another UK study of caisson workers. and in 1989. The pressure ranged from 9 to 36 lb/square inch (62 to 248 kPa) gauge. with only one decompression per day. Some representative surveys are listed in Table 14.2 per cent2. Earlier UK studies on professional divers indi- Other factors influencing the results include the cated that lesions occurred significantly more com- difficulty in obtaining adequate follow-up and the monly among the older men who had longer diving different decompression regimens used. which may has frequently been reported in commercial diving reflect increased exposure rather than age itself. The reported incidence in divers is exceedingly Avascular necrosis of bonea. exceed 150 metres had an incidence of 2. Figures should be lesions. at the Clyde Tunnel in Glasgow depths. most of the clinical and epidemio. per cent. Caisson disease of bone. closely associated with joints. the incidence is much higher in the self-employed diving fishers of Japan. which have no long-term significance to considered cautiously because the radiologists or health and well-being. articular (next to a joint surface).186  Dysbaric osteonecrosis Table 14. 19 per cent of the workers sur. the follow-up period was relatively short.2. workers. The disease affected the shoulder decompression.e. Only 0. dives with long bottom times and often inadequate erature in 1941. a doubtful 80 per cent in Chinese commercial divers.7 per cent had positive Approximately one fourth of the lesions were poten- lesions. ity of malignant change. Lowry reported that the preva- sumably following the advent of strict workplace lence of crippling osteoarthritis leading to total health and safety rules based on sound decompres. Aseptic necrosis of bonea. Hawaii and Australia. mated at more than 2 per cent in Australian aba- logical work that informs the following discussion lone divers1. The lower incidences are reported in military series Diver’s crumbling bone disease. ent radiological techniques and diagnostic criteria. showed an incidence of DON of . whereas necrosis. UK Medical  Research Council Decompression There was a  definite increase in incidence among Sickness Council Panel had x-ray studies of 1674 saturation divers and those with a history of DCS. fishers.7 per cent. The Medical Research Council Decompression Sickness Central Registry has x-ray studies for INCIDENCE nearly 7000 professional divers.4 per cent of the compressed air only 241 compressed air workers were surveyed ­divers who had never exceeded 50 metres had these of a total of 1362. on the Bay Area Rapid Transit tunnelling proj. a study by Jones and Behnke tially serious. By 1972. pre. the which rose to 7. Also in 1972. The helium-breathing divers who did not veyed had lesions. of whom 19. However. There is also a higher incidence joint. with ect in San Francisco revealed no clinical or x-ray 2200 subjects. undertaken until the 1960s. variable. Because the incidence Asymptomatic shaft lesions appeared in about 4 of DON has fallen dramatically since that time. except for the rare possibil- physicians in each survey may have used differ. with lesions were excluded. half of which were juxta. Davidson reported there were only 12 cases of Detailed studies of the incidence of DON were not subchondral bone collapse. Hyperbaric osteonecrosis. The The first report of DON in a diver appears to Australian diving fishers undertake relatively deep have been by Grutsmacher in the German lit.

The most com- Although rare. and they have divers in common. e. (nearly all shoulder disease) have been reported. is fracture of the neck of the femur. virtually scuba divers who breathe compressed air never seen with DON. DON is simply one to 60 per cent for workers who had worked for in a long list of causes of aseptic necrosis.4 Tamura (1983)a. haps one of the most fascinating. unreported sufferers. ent. some disturbance of fat metabolism.g. may be associated with specific systemic or ana- although it is likely that there are many other tomical abnormalities (Table 14. even though multiple and bilateral. associations. A few cases sis disorders. This variation in distribu- at depths of less than 50 metres and who tion suggests that the pathogenesis may be differ- ­follow the customary decompression tables. Osteonecrosis is also frequently reported in asso- Whether the incidence of bone lesions is ciation with those diseases in which there is related more to the cumulative effects of hyper.5 (1976) Wade et al. Aetiology and pathogenesis  187 Table 14. such as Legg-Calvé-Perthes disease. (1978) Hawaiian fishing 20 65 Davidson (1981) North Sea commercial 4422 4. often involve the articu- Dysbaric osteonecrosis is rare in recreational lar surface of the knee and ankle joints. The incidence rose In terms of clinical pathology. but per- 15 years in compressed air. is also not clearly defined. several cases have been reported mon cause of aseptic necrosis of the femoral head in aviators not exposed to hyperbaric conditions.1 a The Kawashima and Tamura survey is an extension of the Ohta and Matsunaga survey. The necrotic lesions of high-dose steroid therapy.3).4 Lowry et al. and these emboli obstruct end arteries in rigid . Certain specific isolated-site bone necro- The disease is rare in sport divers.2  Reported incidence of dysbaric osteonecrosis in divers Total Percentage Investigators (year) Type of diver number positive (%) Ohta and Matsunaga Japanese shellfish 301 50.5 (1974)a Fagan and Beckman Gulf coast commercial 330 27 (1976) Elliot and Harrison Royal Navy 350 4 (1976) Harvey and Sphar US Navy 611 2. Aseptic osteonecrosis may occur within the general population not exposed to hyper. pancreatitis. and steroid administration are the most common The incidence of avascular necrosis of bone. necrosis). The lesions were more often in older AETIOLOGY AND PATHOGENESIS men with more exposure to pressure and also cor- related significantly with DCS. without any known risk factors (idiopathic aseptic baric environments.(1986) Australian abalone 108 25 Kawashima and Japanese shellfish 747 56. alcoholism and cirrhosis. 17  per cent. even if the pathological features are identical. Gorman and Sandow3 and It has been postulated that many of these Wilmhurst and Ross4 published two typical case conditions may be associated with fat emboli reports. a single event increasing with multiple exposures Gaucher’s disease and hyperlipidaemia. Trauma is unknown. diabetes baric exposures than to the statistical chance of mellitus.

and they may well have obstructed venous ing decompression. which pathological changes become irreversible. tion of  DCS (see Chapter 12). There are. Others propose that the fat in bone marrow disruption of bone marrow or other fat tissue takes up large amounts of nitrogen during longer or a combination of the foregoing mechanisms. Bubble formation within bony lacunae and cally apparently safe decompression schedules. • Specific bone necrosis disorders (Legg-Calvé-Perthes. • Occlusive vascular disease. a fatty liver. • Sarcoidosis. • Alcoholism. polyarteritis nodosa). • Trauma (e. • Diabetes mellitus. • Gout. dislocated hip and unrelated fractures). These fat emboli may arise from intra-arterial bubbles. Some affected areas may spontaneously equate decompression. Prompt recompres- been fully elucidated. • Liver disease (fatty liver. • Hyperlipidaemia. gas is liberated from the fat. specifically neurological or serious DCS. leading to areas of infarc- be detected by Doppler techniques during clini. • Polycythaemia/marrow hyperplasia.3  Some causes of aseptic necrosis • Decompression sickness or dysbaric exposure. • Radiotherapy. numerous variations on Bubbles have been found post mortem in the this basic concept. The most widely held belief sion may prevent later deterioration because there is that it results from the decompression phase is probably a critical period of bone ischaemia after and represents a delayed or long-term manifesta. leading to avascular the latter that are more likely to be associated with osteonecrosis. • Haemoglobinopathies (especially sickle cell). carbon tetrachloride poisoning). One theory is that the infarc. • Gaucher’s disease. rheumatoid arthritis. • Haemophilia. During or after decompres- Enhanced coagulability may add to blood vessel sion. and expansion obstruction. musculoskeletal DCS or total DCS. necrotic lesions. There is a definite Osteocytes are known to die after about 4 hours relationship between DON and exposure to inad.g. of anoxia. tion. pressure exposures. Freiberg’s and Kohler’s diseases). • Steroids (Cushing’s syndrome and steroid therapy). ‘silent’ bubbles can outflow from marrow. coalescence of plasma lipoproteins. such as platelet . • Charcot joint.g. with decompression increases intramedullary The exact mechanism leading to bone necrosis pressure. and it is whether arterial or venous. however. whereas others progress to the typical clinical DCS. rather than Changes secondary to intravascular bubbles. lupus erythematosus. Certainly. hepatitis. haversian canals of bone. experimental diving and recover. large venous sinusoids in animal experiments with tion is caused by arterial gas emboli produced dur. • Collagen diseases (e. DCS. several series indicate a relationship with sible following decompression. fractured neck of femur. Kienbock’s. thus compromising blood flow within in association with hyperbaric exposure has not non-compliant bone cavities5. • Pancreatitis. subsequent destruction of osteocytes are also pos- However.188  Dysbaric osteonecrosis Table 14.

Pathogenesis and prevention of dysbaric osteonecrosis. In: Proceedings of the 12th Meeting of the United States-Japan Cooperative Program in Natural Resources (UJNR) Panel on Diving Physiology. Several mechanisms have been postulated. fat or other) do not intravascular space within the rigid bone struc- adequately explain why other tissues do not appear ture may to lead to local bone ischaemia. July 13–14. within the medulla of bone may be transiently Oxygen toxicity is another possible cause of lower than that outside the cortex during a rapid DON. Noro Y. It has to be embolized and why the femur and upper end even been suggested that the absolute pressure of the humerus are particularly affected. and water would then move into ardous diving practices. swelling of fat cells. Release of fat. Given the low rates intravascular bubble counts on Doppler imaging6. of DON in those who practice oxygen decom- It is possible that a number of factors may com. Experimental evidence is available to suggest that incriminating the movement of water into or out both intravascular and extravascular aetiologies of the bone. but a direct pression are associated with large gas gradients cause-and-effect relationship has not been proven. because the intravascular partial pressure of all Asymptomatic or ‘silent’ bubbles during or after inspired gases is transiently much higher than decompression are incriminated in those divers in the tissues. (From Kawashima M. compression. of increased platelet adhesiveness and decreased could inhibit the clearance of gas from the mar- platelet count in volunteers who display higher row during decompression. This intramedullary pressure and ischaemia or.) aggregation and intravascular coagulation. Maryland: National Undersea Research Program. pression techniques. which may produce increased vascular coagulation and exacerbate DON2 . An osmotic aetiology has also been suggested. Thus.1). Expansion of the All embolism theories (gas. that the aetiology is complex and multifactorial. if model is supported by the post-dive observation insufficient to obstruct blood flow completely. may One suggests that the local vasospastic reaction cause further vascular obstruction (Figure 14. Silver Spring. capillary wall. et al. a gradient exists across the who have had neither DCS nor exposure to haz. thromboplastin and vaso-active High oxygen pressures have been shown to cause substances could also trigger disseminated intra. Aetiology and pathogenesis  189 Long hyperbaric exposure & rapid decompression Nitrogen bubbles Bone compartment Syndrome Platelet Fat embolism activation Propagation Intravascular microthrombi coagulation Endothelial damage: Free fatty acids Ischaemia/hemostasis Osteonecrosis Figure 14. Washington DC. and that this alone could promote . the vascular compartment. this seems an unlikely cause bine to produce necrosis in a given situation and of DON.1  Suggested pathogenesis of dysbaric osteonecrosis. Rapid pressure changes during com- are consistent with the bone pathology. to high oxygen pressures leads to ischaemia. Tamura H. 1993.

patients have pain in the area of subsequent necrosis cally. This probably may be indicative of a bone ­compartment syndrome. of increased bone bulk is usually the first detect- able radiological sign. However. These bed. decompression leading to investigation for possible disease. in some cases quite severe. Early lesions are elucidating the precise pathophysiological mecha. may develop insidiously over months or . but it is dif. starts within a few hours of infarction. With in animals such as guinea pigs and mice. observations: Cases of malignant fibrous histiocytoma. with no clear explanation. be arrested before all areas of necrosis have been invaded. Necrosis is first recognized by the absence dating from the DCS incident. ing fractures of the neck of the femur. the area of necrosis is usually before the development of x-ray changes. may develop in conjunction ●● Dysbaric osteonecrosis may follow a single with the prolonged reparative process set in train exposure to pressure. joint. This process resembles that of late segmen- studies in sheep and human post-mortem studies tal collapse. magnetic resonance imaging (MRI) or PATHOLOGY radiological examination. Much research thus cal symptoms. there is some flat- ficult to be convinced that these lesions are strictly tening of the articular surface. Continuing formation of new bone forms a zone of thickened trabeculae separated from Dysbaric osteonecrosis is thought to be a long- necrotic bone by a line of dead collagen. There may be a history of DCS or repeated inadequate ●● Not all divers at high risk develop DON. The revascularization may have been reported. by the necrosis. Secondary bined with hypercoagulability mechanisms. there are reports of persistent limb pain. usually completely asymptomatic and may currently nisms involved. However. Occasional much more widespread than is evident radiologi.190  Dysbaric osteonecrosis venous stasis and bone necrosis. not necessarily temporally related involves the experimental induction of bone necrosis to recent hyperbaric exposure. usually affecting the hip or shoulder lation tissue that extends into the infarcted area. are noted. This area term effect of inadequate decompression. and some occur. It is unclear how Necrotic trabeculae are effectively thickened this apparent violation of Pascal’s Principle could and strengthened by this new growth. not all divers with CLINICAL FEATURES DON have a history of DCS. Histologically. stress fractures appear in the subchondral Studies in larger animals such as sheep that have bone. a definite connection between The development of effective strategies for pre. but such transient differences in pressure lesions even disappear. lesions near articular cartilage. super- imposed on DON. Persistent limb pain of o­ steocytes in the bone lacunae. It is at this stage that clini- a capricious and chronic disease. Various animal models have been developed to The necrotic trabeculae not strengthened by study the aetiology of DON because of the obvious the revascularization process may eventually difficulties in early detection and monitoring of such collapse under a load. which may progress to typical DON. ●● Although there appears to be a relationship between DCS and DON. and with further comparable to those of divers and caisson workers. ment. The underlying necrosis causes progres- a large fatty marrow compartment in long bones sive detachment of the articular surface from its similar to humans have been more successful. ●● Not all divers who have DCS develop DON. as seen in ischaemic necrosis follow- tend to support raised intramedullary pressure com. the site of DCS and the site of bone lesions has been vention and treatment depends on further research notoriously difficult to establish. load. Revascularization then commences from areas Symptoms of pain and restricted joint move- of viable bone to form an area of vascular granu. degenerative osteoarthritis often develops in Any theory must account for the following affected joints. be detected only by bone scintigraphy (radioactive isotope scan).

Symptoms referable to juxta-articular lesions depend on the position and severity of the bone damage. The lesions predominate in caisson workers and divers working in undisciplined or Neoplasia experimental conditions. They are lesions: Is the radiological lesion under examina- usually asymptomatic and are seldom of ortho. neck and shaft (B) lesions. The in five of these will be treated by arthroplasty or risk appears greatest with large medullary lesions. They may and further reduces joint movement. e. Secondary degenerative osteoar- These are also referred to as joint lesions or thritis follows collapse of the articular cartilage A lesions and are potentially disabling. to a lesser extent. other surgical procedures.g. although a useful range of flexion tion and are classified as juxta-articular lesions may remain. of these lesions is approximately in the ratio of face. the  ankle. it is important to realize that the scintigraphy have emerging roles in earlier diagno. These lesions osteonecrosis have a cause other than the dysbaric do not extend beyond the metaphysis or involve environment? the cortex of the bone. Usually there is pain over the joint. Early diagnosis is based on minor alterations and pathological fracture is a rare complication. and reports have even suggested that causative and that some bone necrosis areas revealed by bubbles may be visualized in the fatty marrow7. Symptoms These may be subdivided into juxta-articular (A) or head. classified by their prognostic i­ mplications.e. these lesions. neck and shaft lesions DIAGNOSIS Lesions away from the articular surface are Two main questions may arise in early or a­ typical referred to as medullary or B lesions. In the shoulder. i. and these changes may take 3 to 6 months from In assessing the radiological diagnosis of the time of initial insult. X-ray lesions are usually found in the large long bones of the upper and lower limbs. The shaft is not weakened. The most common sites are the hips and femur to the humerus. tion either a variant of normal bone ­ structure paedic significance. RADIOLOGY AND DIFFERENTIAL Head. Rare cases have been reported in other joints. scintigraphy never become apparent on the x-ray studies. of movement. Malignant tumours of bone (usually fibrous his- mated that about one in five articular lesions will tiocytoma) have been reported in cases of aseptic progress to articular surface collapse and up to one necrosis. shoulders. Their importance lies in that they may An increase of 50 per cent in the total m ­ ineral demonstrate that people with the lesions are at content of the bone is necessary before it can be rec. lesions. X-ray will show only a fraction of the total lesion. MRI and. There is often some restriction These lesions may be present alone or in combina. arc from 60 to 180 degrees of abduction with dif- ficulty in maintaining abduction against resis- Juxta-articular lesions tance. This There are two major sites for the r­adiological may be aggravated by movement and may radi- lesions. film. Radiology and differential diagnosis  191 years and are caused by secondary degenerative New bone replacement has been observed in these ­osteoarthritic changes. the signs are simi- (A  lesions) and head. a painful (B lesions). 1:2 to 1:3. Lifting heavy weights may precipitate the onset of pain. It is esti. greater risk of further DON. in the trabecular pattern of bone that result in . The most common sites are or p­ erhaps  a  minor dysplasia of bone? Does the the shafts of the femur and humerus. neck and shaft lesions lar to those of a rotator cuff lesion. ate down the limb. sis. although this has not ognized as an area of increased density on the x-ray been proven statistically. The site eventually result in collapse of the articular sur. many of which were asymptomatic.

Members compare their independent written reports before coming to a consensus position. A4 Structural failures. a Translucent subcortical band. . b Collapse of articular cortex. this may remain symptomless. The edge of the cortex looks cancellous bone structure but that are sharply ‘woolly’. showing the promotion of malignancy being the most obvi- the progression of the lesion. At the top of the humerus bone island is essential. Early detection In our enthusiasm to monitor divers at risk. Spherical segmental opac- ity (arrows). Figure 14. This clas- sification is useful to compare results among dif- ferent studies. A2 Spherical opacities. and this work became the province of highly specialized pan- els of independent observers. A3 Linear opacities. a is required in these assessments.9). defined. we of asymptomatic lesions may be verified only must also be aware of the dangers of irradiation – by serial radiological examinations.2 through 14. Considerable skill ous. they have a normal trabec- ular pattern around them and have no clinical significance. Dense areas with intact he eliminated.192  Dysbaric osteonecrosis abnormal densities or lucencies.3  A2 lesion. For a good review of this area see Williams and associates8. A5 Secondary degenerative osteoarthritis. Lesions are classified as in Table 14. Chance cortical bone defects must Figure 14.4  The United Kingdom Medical Research Council radiological classification of dysbaric osteonecrosis A lesions (juxta-articular) A1 Dense areas with intact articular cortex. Originally called a ‘snowcap lesion’.2  A1 lesions. Cysts and areas of sclerosis occur spo- radically in otherwise normal persons but also in other diseases. and the recognition of the normal articular cortex. B lesions (head. are two areas where the trabecular pattern is These are dense areas of bone within the blurred (arrows). In the United Kingdom a central registry for cases and x-ray studies was sponsored by a government body (the Medical Research Council). B3 Translucent and cystic areas. with the long axis run- ning parallel to the long bone. B2 Irregular calcified areas. Thought to develop early in life. Table 14.4 (Figures 14. c Sequestration of cortex. The first decision to make is whether the bone is normal9. neck and shaft) B1 Dense areas. round or oval. Even with good equipment and technique.

the shadow of the linea aspera and its long bone series. to detach. Currently. employment. (a) Translucent subcortical band: this lesion (between arrows) is sometimes Figure 14. avoided.4  A3 lesion. Unnecessary irradiation is to be endosteal crest. and medical history are important in establishing duce confusion in diagnosis include the following: 1.5  A4 lesion. Situated just under the line marked with arrows represents the lesion. (Continued) . Radiology and differential diagnosis  193 diver receives one third of the annual maximum 3. whorled and in closer apposition than the foci of calcifi- cation of DON. Osteoarthritis: Osteoarthritis. the translucent line indi- The extremities of such linear opacities charac.3). articular cortical surface. Linear opacity. Bone islands (see earlier). This practice protects both the diver and the employer from misinterpretation of bony Other causes of osteonecrosis must be excluded changes. and readers are advised to seek up-to-date 4. Both the radiological features Causes of radiological anomaly that may pro. Enchondroma and other innocent tumours: These may calcify. cates that a sliver of the cortical surface is about teristically extend to the cortical margin. not associated recommendations on the frequency of long bone with juxta-articular DON. a common reduction of the joint space. Medullary osteochondroma may show foci of calcification. usually causes a series in occupational divers. (a) 2. The dense called a ‘crescent sign’. (see Table  14. In DON. Normal variants: These include sesamoid recommended dose of body irradiation for one bones. the cartilage space is not have elapsed – with the former only required if ­narrowed unless secondary osteoarthritis has the latter was not done on leaving the most recent occurred. causing an osteoclastic appearance in the shaft of the long bone. which are more circular. Figure 14. with s­ clerosis recommendation is a series at employment and of the underlying bone on both sides of the then on leaving employment if more than 5 years joint.

194  Dysbaric osteonecrosis (b) Figure 14.5 (Continued)  A4 lesion. This condition can supervene on any lesion in which disruption of the articular surface has occurred. (b) Collapse of the articular cortex or subchondral depres- sion: this tomogram shows a fracture line (arrows) developing between the sclerotic part of the bone above (which is being depressed into the femoral head) and the surrounding bone cortex. the cartilage often remains viable so that a joint space of reasonable size ­continues to be radiologically visible despite severe osteoarthritis. Osteoarthritis. Dense areas.7  B1 lesion. (c) Sequestration of the cortex: a loose piece of dead articular cortex has been pushed into the body of the femoral head. and it is unlikely that they will ever cause disability. (c) Figure 14. thus causing the latter Figure 14. . They are typical of the osteonecrotic lesions seen in such sites. can be seen just at and below the junction of the humeral head and shaft (arrows). In osteonecrosis. These areas to appear flattened (arrows).6  A5 lesion.

Irregular calcified areas. Calvé-Perthe’s disease (hip) and Kohler’s disease (tarsal scaphoid). Sometimes the appearance is that of rather 5. whereas multiple being 10 mg prednisone or its equivalent per lesions make the diagnosis easier. Some experts believe these multiple lesions are not osteone- crotic. both with and 1. Haemoglobinopathies: Sickle-cell anaemia. the site of multiple fractures. but rather relate to past damage at the point of a capsule’s insertion into the neck of a bone. fit. scal. Endosteal chondroses of epiphyseal heads. Trauma: DON has been reported remote from ­w ithout ­steroid therapy. disease (second metatarsal head): The osteo- loped edge around a translucent area. A single cyst (arrow) is usually seen in the femoral neck. active diving population who have undergone 6. Translucent areas and cysts. investigations and by demonstrating lesions in This condition is commonly seen in divers. 2.9  B3 lesions. Collagen diseases: Systemic lupus medical assessment (see Chapters 53 and 54). such as Legg- thickening frequently accompanies these lesions. Solitary lesions espe- increases with increased dose. ­erythematosus and rheumatoid arthritis Among the more important are the following: are associated with a very high incidence of osteonecrosis of the hip. These irregularities may also be found at the junction of the shoulder joint capsule and humeral neck. Diagnosis is made by haematological Figure 14. 4. Specific bone necrosis syndromes such as foamy areas in the medulla at the lower end Kienbock’s disease (spontaneous avascular of the femur. necrosis of the carpal lunate) and Freiberg’s Sometimes femoral lesions have a hard. . Sometimes a line of small cysts appears at the point where the hip joint capsule attaches to the femoral neck. Short courses of high-dose ‘pulse’ therapy have also been incriminated. day for 30 days. These causes should be rare in a parameters. often with a calcified margin. the minimum cially require careful assessment. Steroid therapy: The likelihood of osteonecrosis for the professional diver. Alcohol: A history of heavy consumption or The initial diagnosis of DON must be reason- other organ damage may be obtained. have specific age and clinical the  diagnosis. ably certain because it has serious implications 3. the spine and skull. Radiology and differential diagnosis  195 Figure 14.8  B2 lesion. thalassaemia and other variants may also be causative.

Dense areas. studies. head). tion. Use has declined with the greater availabil- ity and lower cost of MRI (see later). but several newer diphosphonate com- Head. Diagnostic radiological parameters include the following: Imaging techniques: Juxta-articular lesions (A lesions) ●● Plain radiography. early detection of the bony reaction to osteone- 5.196  Dysbaric osteonecrosis Symptoms and plain x-ray lesions are both proximal tibia and the proximal humerus. ●● Scintigraphy. The pathological lesion may never produce radio. Structural failure showing as translucent Bone scintigraphy (bone scans) subcortical bands (especially in heads of femur and humerus) and often collapse of articular This investigation had an established role in the cortex with sequestration. osteogenesis at autopsy at 3 months. 15 caisson workers revealed lesions in previously normal areas and worsening of known lesions OTHER INVESTIGATIONS despite cessation of further hyperbaric exposure10. and have been shown to involve necrotic bone and 2. The value of the plain x-ray examination in early Autopsy often reveals the pathological areas are diagnosis is being questioned. A 10-year radiological ­follow-up of may clarify a questionable area. with MRI and They may be bilateral. 1. 1. with new bone laid combined with skilled interpretation are required. These lesions appear to be quite by the radioactive bone-seeking tracer. photon emission computed tomography). best seen in tomo- capable of identifying earlier lesions if sought grams of the head and neck of the humerus (see later). Spherical opacities (often segmental in humeral ●● Magnetic resonance imaging. 3. and other imaging far more extensive than the radiological demarca- techniques are being increasingly used. neck and shaft lesions pounds have been introduced that appear to have (B lesions) relatively higher skeletal affinity and may be more sensitive. and special radiographic techniques the presence of dead tissue. Computed tomography (CT) or bone scintigraphy logical changes. even though These are commonly seen in the distal femur. ­scintigraphy (the latter now seldom used) both 3. noted within 3 to 6 months of MRI changes. r­elatively late manifestations. x-ray changes still had not developed in most cases.10). Linear opacities (usually humeral head). These must be animals as early as 2 to 3 weeks after decompression distinguished from normal ‘bone islands’. methylene diphosphonate (MDP) is the most widely used tracer. Cortical thickening. Secondary degenerative arthritis with crosis. 4. down on the s­ urface of the dead bone. . commonly in the neck and proximal Scintigraphy-positive ‘lesions’ can be produced in shaft of the femur and humerus. The  first radiological signs may be and femur. Cylinder cone and tomography may be used. The experienced r­ adiologist looks for an increase in Emphasis is on minor variations of trabecular bone density as a result of the reactive changes to structure. usually multiple and often and images taken over time with a gamma camera. they may take much longer – even years. Translucent areas and cysts. Dense areas with intact cortex ●● Computed tomography (including single (­usually humeral head). Irregular calcified areas in the medulla. These agents are injected intravenously. but 4. 2. Technetium-99m–labelled necrosis. bilateral. on the scin- different from those of other causes of avascular tigram (Figure  14. Any lesion that There is usually no narrowing of the joint spaces stimulates bone formation is shown as a ‘hot spot’ until later stages. before there are any changes on plain x-ray ­osteophyte formation.

in the right shoulder of a 38-year-old diver who had performed many deep bounce dives on heliox. However. increased concentration of technetium with increased uptake of MDP. are being Single photon emission CT (SPECT) is said to contemplated. (b) X-ray study of the right shoulder 4 months after the first scan. such as rotational osteotomy. and ‘cold’ areas occurring . tural collapse and areas of new growth. improve specificity. i. and are therefore insufficient to establish a firm ­diagnosis. Most of these were experimental dives. these ‘hot spots’ DON. Despite its promise. Other investigations  197   Figure 14. This imaging tech- tomography nique is essential if some of the surgical tech- niques. no matter what the cause is. probably because of the high cost and poor may resolve with no apparent longer-term changes availability of this technology. scintigraphy in early lesions is much more sensitive than radiology but has low Computed tomography specificity because any bone r­ eparative reaction will CT gives greater definition revealing both struc- be detected. Overall. although he never had treatment for decompression sickness and would admit only to the odd minor discomfort in a variety of joints after dives.) Similar findings in humans with biopsy or immediately after occlusion of blood supply may radiological follow-up indicate that the ‘hot spots’ also be detected.10  (a) Qualitative scintigram using technetium-99m–labelled methylene diphosphonate (MDP) that shows a ‘hot spot’. CT scans may help in the diagnosis of early or doubtful Single position emission computed changes on plain x-ray films.e. SPECT occur far earlier and are more numerous than the has not found a routine place in the diagnosis of radiological changes. then. (Photographs courtesy of Dr Ramsay Pearson. Routine screening x-ray studies at the time showed a normal shoulder.

Under these conditions. traditional marked distortion of the marrow signal with areas of necrosis indicated by the dark signal. no evidence that involves the articular surface of the glenohu. T1-weighted images there is evidence of If a juxta-articular lesion is present. fessional divers exposed to frequent hyperbaric MRI of the shoulder joint has been suggested as conditions at depths greater than 15 metres. than conventional plain radiography and can Early recognition is imperative. If the B lesion is thought to be provoked by non- adherence to established diving tables. It is generally accepted that the need for formal decompression staging should be avoided. Doubtful cases should be treated as if Figure 14. There is. unless there is a specific cause for described by Ficat in 198511 as functional explora. MRI is not routinely 2. The problem of what to do when confronted with an asymptomatic B lesion is not yet clear. The disease is rare in recreational scuba ­divers intraosseous phlebography. At present. examination. and the follow- also reveal bone lesions at other sites when a ing investigations are recommended for all pro- lesion has been detected on plain x-ray films. concern. and this offers the best opportunity for early diagnosis. then it is presumed that he or she is par- ticularly predisposed to DON. meral joint. (Figure  14. teaching suggests that all exposure to compression There is also cortical irregularity. it is assumed that the B lesion is induced because of excessive provocation. The latter three compressed air to depths less than 50 metres.11  Magnetic resonance imag. as should experimental or helium diving. these should clearly be followed in the future. serial radiological investigation is cer- tion of bone.198  Dysbaric osteonecrosis Magnetic resonance imaging PREVENTION MRI can detect necrosis of marrow fat within Early recompression of experimental limb bends 2 to 4 days of the ischaemic episode and thus in sheep prevents progression to DON.11). Today. For investigations are often combined in a technique these groups. who follow decompression tables and use only sure measurement and core biopsy. intramedullary pres. irradiation hazards and expense. 3. The process should cease. MRI 3 months after an episode of DCS involv- ing the hips or shoulders. tion. however. Baseline long bone x-ray studies. Invasive investigations Image-guided biopsy of suspicious lesions Invasive investigations have been undertaken to (or  even surgical biopsy) may be appropriate in aid in earlier diagnosis and therapeutic interven. but this approach has not been widely tainly not warranted because of the unnecessary adopted. . and consideration is given to restricting diving to reduce the risk of further lesions. validates the clinical practice of recompression of MRI studies may indicate far greater necrosis all cases of DCS to reduce long-term damage. positive until further radiological assessment ing of the right shoulder. If the diver has adhered to normal decompression tables. MRI examination in doubtful plain x-ray find- used as a screening tool because of the cost of ings or to define extent of lesions. special circumstances. These techniques include arteriography. On these slightly clarifies the issue. the best surveillance technique for professional divers who are exposed deeper than 15 metres 1. a pragmatic approach is more common. this modifies the subsequent course of the ­problem.

2. ers who cease hyperbaric exposure after diagnosis reconstructive techniques offer the best chance of suggests a high likelihood of further progression rehabilitation. shield. The gonads must be protected from ionizing (as described by Ficat11). ­section). but it is not clear whether DON is likely to 3. pre-radiological. Conversely. is recommended. about this form of surgery is that the life of sis must be based on the aetiology and may there. Nevertheless. of the individual diver along with counselling about 4 – Destruction of joint. Total joint replacement Surgical treatment has proved useful in replacing severely affected hip and shoulder joints. avoiding further provocative diving if possible. One comparative study suggests that occasional reports in the literature. A 30 × 25 cm film medullary pressure or positive scan). life expectancy. of lesions. rience is with idiopathic osteonecrosis of the femo- ral head – the site at which osteonecrosis produces RADIOLOGICAL TECHNIQUE the most devastating disability. Core decompression has its advocates. The following projections are required: 0 – Asymptomatic. results are better with this procedure than with the treatment of juxta-articular (A) lesions should core decompression12. angle of approximately 45 degrees to bring . although there are the hip. Radiological technique  199 with close attention given to the functional capacity 3 – Collapse of articular surface. The results are. lar necrosis (Ficat stages 1 and 2 – see the next with destruction of one hip only. ­successfully to treat the early stages of avascu. One interesting RECONSTRUCTIVE TREATMENT study of the long-term outcome in affected div. the prosthesis is unknown because it is used fore have a rational basis in DON that is absent in in a relatively young population with a long idiopathic disease. pre-radiological (i. is determined by the staging of the disease process 2. mainly that a­ ffecting tomatic lesions is less clear. either rotation asymptomatic head. The concern Surgical treatment of disabling aseptic osteonecro. as expected. joints especially if the patient is old or the disease is bilateral. supine position with the trunk rotated at an 2 – Symptomatic. Although healing is seen histologically. better for the earliest stages. Good definition of the trabecular structure of successful following DON. the possi. The type of treatment the bone is important. endeavours to move the weight-­ no active therapy. high (a) Shoulder: An anteroposterior projection index of suspicion confirmed by raised intra. STAGING (FROM FICAT11) 3. the age of the patient and radiation in young divers by the use of a lead the joints involved. It is not yet clear whether the same approach will be more or less 1. and it has been suggested that progress may be unrelated to further diving exposure10. bearing axis away from a localized necrotic Hyperbaric oxygen therapy has been used area. be based on the finding that DON often progresses through the stages outlined later. but the value of the procedure is still questionable. The 1. TREATMENT it is indicated for stage 0 to 2. If accepted. When gross damage to the articular surfaces exists. Annual assessment of these divers will pay close CURATIVE TREATMENT attention to their continued functional capacity. The patient is placed in a 1 – Symptomatic. Osteotomy of the femoral neck. most surgical expe. neck and shaft lesions require or wedge.e. although this may hinder radiographi- cal interpretation. used for stage 0 to 2 disease. radiological pre-destruction. Arthroplasty is indicated for ‘end-stage’ respond in the same way. Vascularized fibular graft procedure has been bility of resolution of radiologically positive asymp. of each shoulder joint. Arthrodesis is possible for a young patient.

Clinical Radiology midpoint of a line joining the anterior. This view should a dive to 30 msw for 30 min. Wenzel MS. Ficat TP. but not in any way obscuring it. Uguen A. The pathophysi- crosis of the shoulder in a sport scuba ologic role of fat in dysbaric osteonecrosis. Gorman DF. Davidson JK. Journal of Bone and Joint Surgery professional divers: a literature review. Dysbaric disorders: a ­ septic core decompression or vascular- bone necrosis in tunnel workers and ized fibular grafting because of ­divers.41(6):579–587. Dysbaric osteonecro- and the elbow is flexed. of MRI in the detection of marrow bubbles mended. Dubielzig RR. islands. King JD. 2014. A 30 × 25 cm film is recom. Blatteau JE.200  Dysbaric osteonecrosis the shoulder to be radiographed in contact 5. EH. Khreisat S. The ­radiologist sis in divers and caisson workers: an animal should centre 2. diver. Role hip joint. The patient is placed in a supine after musculoskeletal decompression position with the feet at 90 degrees to the sickness predictive of subsequent dys- tabletop. Ross K. Undersea & Hyperbaric Medicine Society 12. Lehner CE.19:457–461. Czarnecki DJ. Aaron RK. bringing in 6. Aviation. Posterior ­shoulder 1998. Williams ES. femoral head: early diagnosis and treat- Dewitte JD. Jones JP. . Scully SP. Pontier JD. Bailliere’s Clinical Rheumatology avascular necrosis Journal of Bone 1989. Fueredi. i. show a clear joint space.32:344–345. Joint Surgery American Volume 3.3:1–23. Clinical Radiology ­projection of each knee.28:381–393. 11.80(9):1270–1275.5 cm below the coracoid model. Clinical Radiology should be as near the femoral head as 2008.e.155(1):95–97. The significance of bone the pubic symphysis. Survival analysis of hips treated with 2. Idiopathic bone necrosis of the 1. 2. (b) Hip: An anteroposterior projection of each 7. The field should ­osteonecrosis progress in the absence include the lower third of the femur and of further hyperbaric exposure? A 10-year the upper third of the tibia and fibula. dislocation and humeral head necrosis in a recreational scuba diver. Dysbaric osteone. Doty SB. as much humerus as possible.79(12):1096–1099. film is recommended. Sandow MJ. Uguen M. Wilmhurst P. British Journal of Sports Medicine Clinical Orthopedics and Related Research 1998. An 18 × 43 cm 1997.63:1380–1383. Gempp E.296:256–264. Lanphier. Pougnet R. The radiologist 10. This arm is partially abducted Palta M. radiologic follow-up of 15 patients. Undersea FURTHER READING Biomedical Research 1992. The edge of the gonad ­protector baric osteonecrosis. 1987.67(1):3–9.344:320–322. Ramirez S. Urbaniak JR.5 cm below the dysbaric osteonecrosis. AJR American Journal of Radiology REFERENCES 1990. Does dysbaric ­border of the patella. Jiminez C. superior iliac spine and the upper border of 9. Blood the lateral diaphragms to show only the head platelet count and bubble formation after and shaft of the humerus. with the table. Blatteau J-E. 2008. Ell PJ. 1993. Hendry WT. Adams WM. The radiologist should centre the cone over Bone imaging and skeletal radiology in the head of the femur. Van Blarcom ST. 8. possible. should centre at the level of the upper GA.38:589–592. Dysbaric osteonecrosis among ment. cystic areas and sclerotic areas in (c) Knee: An anteroposterior and lateral dysbaric osteonecrosis. 4. British Volume 1985. Loddé B. and the acromion Space and Environmental Medicine should not overlap the head of the humerus. Clinical Orthopedics and Related process of the scapula and then cone to show Research 1997. Stephant E.

University osteonecrosis – a survey of abalone ­divers. (III UOEH Symposium). In: Proceedings of the This chapter was reviewed for this fifth edition by 12th Meeting of the United States-Japan Michael Bennett. In: Shiraki K. Tamura H. July 13–14. Tamura H. ed. Dysbaric Physiology. Proceedings of the Maryland: National Undersea Research Third International Symposium of UOEH Program. Further reading  201 Kawashima M. Noro Y. . Fukuoka. Pathogenesis and prevention of dysbaric osteonecrosis. of Occupational and Environmental Health: In: Edmonds C. et al. Silver Spring. 1983. Underwater Physiology. 1986:50–62. Hyperbaric Medicine and Washington DC. Osteonecrosis in ­divers Cooperative Program in Natural Resources – prevention and treatment. on Hyperbaric Medicine and Underwater Lowry CJ. Melbourne Diving Medical Centre/National Kawashima M. Safety Council of Australia. Matsuoka S. The Abalone Diver. Jones MW. 1993. (UJNR) Panel on Diving Physiology. eds. Traugott FM.


4 Part     Abnormal Gas Pressures 15 Inert gas narcosis 205 16 Hypoxia 217 17 Oxygen toxicity 229 18 Carbon dioxide toxicity 245 19 Breathing gas preparation and contamination 255 20 High-pressure neurological syndrome 267 .


although at different partial have a peculiar charm and in some persons. that divers became intoxicated at great depth. at 5. The word ‘inert’ indicates that these gases exert their effect without undergoing metabolic Inert gas narcosis (IGN) was comprehensively change in the body. nitrogen. referred to that work for more detail1. rather than inert gas in the reviewed in 2003. B. It is produced by an increased par. tution of a less narcotic respiratory diluent such as tial pressure of some inert gasses. although some narcotic properties have hallucinations in divers breathing compressed air been postulated. in 1878. although highly vari- Inert gas narcosis refers to a clinical syndrome able. neuromuscular performance and changes in mood Effective work at greater depth requires the substi- and behaviour. ‘narks’ and rapture of the deep In  1903. Hill and McLeod described impairment 205 . these changes. Green in directly demonstrated at currently attainable pres. hydrogen and the by Junod. impaired judgement and sures. He was con- is used in some parts of the world as an anaes. krypton. and interested readers are biophysical sense. In compressed helium or hydrogen. argon. air exposure. symp- pressures. also noted and its effects are also called nitrogen narcosis. The first Similar effects have been described with other recorded description of symptoms suggestive of metabolically inactive gases such as the rare gases air intoxication related to hyperbaric exposure was (neon. ducting research into the physiological effects of thetic agent.8 ATA. reported that ‘thoughts anaesthetic gases. depth intoxication. Paul Bert. are caused by been associated with nitrogen narcosis. which have been Many ‘unexplained’ scuba deaths may have observed for more than 100 years. the term coined by Cousteau. sufficient to warrant an immediate The ‘inert’ gas in compressed air is nitrogen. places a depth limit to safe diving with characterized by impairment of intellectual and compressed air at approximately 40 to 50 metres. The effects are progressive with increas- ing depth but not with increasing time at the same HISTORY depth. 1861 observed sleepiness. in 1835. J. The narcosis. who. xenon). return to the surface. Xenon is ‘anaesthetic’ at sea level and toms of intoxication are present’. 15 Inert gas narcosis Introduction 205 Neurophysiological changes 211 History 205 Aetiology 212 Clinical manifestations 207 Prevention 214 Measurement of central nervous system effects 209 References 214 Behavioural approach 209 INTRODUCTION (I’ivresse des grandes profondeurs). No narcotic effect of helium has been ­compression and rarefaction of air.

what shall I do next? – Of course. he says. I get comfort from seeing the fish. tion entitled ‘semi-loss of consciousness’. thinking of course that in a couple of minutes I would be able to resume work. Damant. go mad at things’. You notice things more if there is nothing to do. because I had never experienced a real dose of CO2. say half-a-crown.1:  DESCRIPTIONS OF DIVERS ABOUT THEIR EXPERIENCES AT BETWEEN 250 AND 300 FEET AS REPORTED BY HILL AND PHILLIPS ‘You notice the dark more although it may not be darker. I lost the use of my limbs and let go everything. This was new and strange to me. I stood up. I slid 10 feet and felt I was going unconscious. When asked for a description.1). as if someone in the suit was saying it’. what I thought. I didn’t know. “What is that. . He described how he was aware of every action: ‘If my hand goes out I think of my hand going out’. the light is a comfort and company. I decided to rest a couple of minutes and then go on. and thinking it was a touch of CO2. I began to breathe deep and hearty. in the street. I would pick it up. and their report in 1933 contained a sec- tulated that it was caused by the high partial pres. The impression was of sitting in the stalls and watching the acting of Grand Guignol. He gave the following as an analogy: ‘if I saw a thing of value. it was outside the glass and looked all greenish.206  Inert gas narcosis of intellectual functioning in caisson workers at the  air from the compressors (Case report 15. a feeling of “no life or energy”. ‘I have finished my job. Description of interview of above diver after an aborted deep dive: Practically no hypnoidal effort was required to produce the horrors of that morning’s dive. after stopping and doing the drill for CO2. ‘I left the ladder determined to get to the bottom. After return to effects could be psychological as a result of claus. To such a pitch did he arouse his emotions that he clawed his face to remove the imaginary face-glass and tore his clothes which he mistook for his diving suit (Hill I. an old hand at diving gave the following account: ‘You have to be more careful in deep water. surface.left an impression which is very difficult to describe.5 ATA. It was noted that all divers regained CASE REPORT 15. Deep-sea diving. I made signals to be pulled up and kept repeating them. it takes your mind off everything else’. whether it was a part of CO2. divers answered hand signals but Hill and Phillips suggested in 1932 that the in many cases failed to obey them. At 250 feet I got a recurrence of the tingling and a feeling of lying on my back. While hanging on to the rope I saw my own face in the front glass. Down below I would look at it and think. again and again. escape. likened the mental The Royal Navy appointed a committee to inves- abnormalities and memory defects observed in ­ tigate the problems of deep diving and submarine men at 10 ATA to alcoholic intoxication and pos. “Pull the diver up”. the tank wire in my right hand. Then I seemed to go quite limp. Between sure of oxygen. I have finished and now I must go up’. I thought I would be alright. I will pick it up” and then I feel my hand go out’. Journal of the Royal Navy Medical Service 1932. mad terror…. I heard the order. and the picture of stark. 5. 7 and 11. anyhow. but suddenly something definitely seemed to say – snap inside my head and I started to. it was a distinct “different” feeling. it will become the main thing and you will forget everything else’. in 1930. ‘Suddenly I came over rather “funny”. I was dressed in my shore-going suit. Phillips AE. in deep water you know that you are concentrating… You think of each heave as you turn a spanner… If you go down with a set purpose it becomes an obsession.18:157–173). shall I pick it up? Yes. He described how he thinks very deliber- ately.6 ATA. the divers could not remember the events trophobia or perhaps caused by impurities in of the dive.

30 meters . cent concentrations at 1 ATA had little mental effect.. The 1933 Deep Diving to the overconfidence of mild alcoholic i­ ntoxication. Clinical manifestations  207 full consciousness during the return to 1 ATA. some ­divers are affected subjectively at less than It was not long after this major breakthrough that 30 metres. judge- tion of helium for the nitrogen in compressed air ment.. reported that the addi- tion of carbon dioxide to compressed air wors- ened the mental symptoms.. carbon dioxide retention was implicated. The report also noted great individual variation Normal ­arterial carbon dioxide and oxygen levels.. on air at 60 metres is a dangerous challenge... Committee Report had raised the possibility that Occasionally... Rashbass in 1955 and Cabarrou in 1959 had already refuted the carbon dioxide theory... At a depth of 30 metres (4 ATA)... He postulated that carbon dioxide was an alterna.. demonstrate the key  role of It was not until 1935 that Behnke. concentration and eliminated narcosis. Case and Haldane... the cause of this compressed air intoxication. Buhlmann believed that increased 60 meters . They stated that the narcosis was the result of the raised CLINICAL MANIFESTATIONS partial pressure of the metabolically inactive gas.1). ide concentrations. attention are affected first. nitrogen. Also in 1961... com- pressed air produced a state of ‘euphoria. all divers breathing com- between 10 and 15 ATA. Later work (by Hesser. develops. This effect was pro- gressive with increasing pressure so that at 10 ATA. terror.. by observing signs of narcosis despite methods to Figure 15. Thomson and ­nitrogen in the production of this disorder and the Motley proposed the now generally held theory of relative insignificance of carbon dioxide.. They also invoked the pressed air are significantly affected at a depth Meyer-Overton hypothesis (see the later section of 60 to 70 metres (Figure  15.. retarda. in 1947. at v­arious depths. Adolfson and Fagraeus) (Illustration courtesy of http://p3respiratory6..1  Martini’s law illustrated. neuromuscular co-ordination’... learning.. He explained these changes as being caused by reduced diffusion of carbon dioxide in the increased density of the air. Bean. dioxide are additive in impairing performance. Unconsciousness developed susceptibility to IGN. but high ratio of solubility of nitrogen in oil to water.. such as reasoning. Although there is marked individual variation in stupefaction resulted. airway resistance led to hypoventilation and hypercapnia.. showed that the effects of nitrogen and carbon wikispaces. Diving ensure normal alveolar carbon dioxide levels. in 1941.. The minimum on aetiology) to relate the narcotic effect to the pressure producing signs is difficult to define. the opposite reaction. 45 meters . Behnke and Yarbrough reported that the substitu- The higher functions.com/) . Martini’s law: Each 15-metre (50-foot) depth is tion of the higher mental processes and impaired equivalent to the intoxication of one martini. recent memory. The diver may experi- The nitrogen partial pressure theory was not ence a feeling of well-being and stimulation similar universally accepted. in divers’ reactions but was unable to elucidate the while the diver is breathing air and helium-­oxygen problem. tive cause of depth narcosis. although up to 6 per 15 meters . Seusing and Drube later supported Bean’s views as recently as 1961. demonstrated a reduction in arterial pH during compression and later also showed increased alveolar carbon diox..

208  Inert gas narcosis

This is more probable in the novice who is appre- ­roblems through a ‘practice effect’. Conversely,
hensive in this new environment. Further eleva- anxiety, cold, fatigue, sedatives, alcohol and other
tion of the partial pressure of the inert gas results central nervous system depressant drugs aggravate
in impairment of manual dexterity and progressive narcosis.
deterioration in mental performance, automatisms, Nitrogen narcosis has often been likened to
idea fixation, hallucinations and, finally, stupor alcoholic intoxication, especially the euphoria,
and coma. Some divers complain of a restriction of lightheadedness and motor incoordination. There
peripheral visual field at depth (tunnel vision). They is some evidence that correlates subjective feelings
are less aware of potentially significant dangers of alcohol consumption and IGN, especially the
outside their prescribed tasks (perceptual narrow- variation in intensity experienced among individ-
ing). More recently, abnormal emotional process- uals. In one elegant experiment reported in 2008,
ing has been described, with a suggestion that the Hobbs2 found evidence that heavier drinkers did
emotional  responses to threat are muted with not show a reduction in the effects of nitrogen nar-
increasing IGN. cosis at depth, but they did show tolerance for the
From a practical point of view, the diver may combined effects of narcosis and alcohol. At much
be able to focus attention on a particular task, but greater depths the parallel with general anaesthetic
the memory of what was observed or performed agents is probably closer.
while at depth may be lost when reporting at the Some of the reported observations at various
surface. Alternatively, the diver may have to abort depths breathing compressed air are shown in
the  dive because of failure to remember instruc- Table 15.1.
tions. Repetition and drills can help overcome these

Table 15.1  Some observations on the effects of exposure to compressed air at increasing pressure/depth

Pressure (ATA) Effects
2–4 Mild impairment of performance on unpractised tasks.
Mild euphoria.
4 Reasoning and immediate memory affected more than motor coordination and
choice reactions.
Delayed response to visual and auditory stimuli.
4–6 Laughter and loquacity, which may be overcome by self-control.
Idea fixation, perceptual narrowing and overconfidence.
Calculation errors; memory impairment.
6 Sleepiness; illusions; impaired judgement.
6-8 Convivial group atmosphere: may be terror reaction in some; talkative; dizziness
reported occasionally.
Uncontrolled laughter approaching hysteria in some.
8 Severe impairment of intellectual performance.
Manual dexterity less affected.
8–10 Gross delay in response to stimuli.
Diminished concentration; mental confusion.
10 Stupefaction.
Severe impairment of practical activity and judgement.
Mental abnormalities and memory defects.
Deterioration in handwriting; uncontrollable euphoria, hyperexcitability; almost total
loss of intellectual and perceptive faculties.
>10 Hallucinogenic experiences.

Measurement of central nervous system effects  209

The narcosis is rapidly evident on reaching the than inert gas in producing depth i­ntoxication
given depth (partial pressure) and is not progres- and monitoring the degree of impairment during
sive with time. It is said to be more pronounced ini- practical tasks.
tially with rapid compression (descent). The effect Attempts to quantify the effects of IGN can be
is rapidly reversible on reduction of the ambient roughly divided into two methods. The first is a
pressure (ascent). psychological behavioural approach measuring
Other factors have been observed to affect the performance on tasks such as mental arithmetic,
degree of narcosis. Cold, reduced sensory input, memory, reaction time and manual dexterity. The
and both oxygen and carbon dioxide disturbances second relies on observing a change in some neu-
are interrelated in impairing the diver’s underwa- rophysiological parameter. Some representative
ter ability. In experimental conditions, with an studies are discussed to illustrate points.
attempt to control variables, alcohol and hard work
have been shown to enhance narcosis. Moderate Behavioural approach
exercise and amphetamines may, in certain situ-
ations, reduce narcosis, but some studies have The aspects of behaviour usually studied may be
conversely suggested unpredictable or increased divided into three categories: cognitive ability,
narcotic effects with amphetamines. Increased reaction time and dexterity. The cognitive func-
carbon dioxide and nitrogen tensions appear to be tions are the most affected and dexterity the least.
additive in reducing performance. Task learning One early study measured the performances of
and positive motivation can improve performance. 46 men on simple arithmetic tests; reaction time
Frequent or prolonged exposure produces some and letter cancellation were measured at pres-
acclimatization, but this may reflect a reduction in sures from 3.7 to 10 ATA. This study demonstrated
psychological stress rather than representing true quantitatively the previously observed qualitative
adaptation. For example, Hamilton and associates3 progressive deterioration with increasing pressure
have experimental evidence to suggest that the of compressed air. It also showed that individuals
reported experience of adaption is more subjective of high intelligence were less affected. The impair-
than behavioural. ment noted on arrival at the target pressure was
Direct pathological injury to the diver as a exacerbated by rapid compression.
result of the high pressure of inert gas is unlikely. Another study using simple arithmetic tests of
The danger is rather a result of how the diver may manual skill showed that narcosis was maximal
react in the environment while under the narcotic within 2 minutes of reaching depth, and continued
influence of nitrogen. Impaired judgement can exposure did not result in further deterioration,
lead to an ‘out-of-air’ drowning sequence, with but rather there was a suggestion of acclimatiza-
no other apparent cause of death found. The diver tion. Muscular skill was much less affected than
affected by IGN may also be at increased risk of intellectual performance. Other studies involving
insidious hypothermia (see Chapter 28) because of reaction time, conceptual reasoning, memory and
decreased perception of cold and decreased shiver- psychometric tests all showed progressive deterio-
ing thermogenesis4,5. Jacques Cousteau6 shared his ration with increasing pressure. Narcosis has also
experience of nitrogen narcosis (Case Report 15.2). been measured by tests of intelligence and practi-
cal neuromuscular performance.
MEASUREMENT OF CENTRAL Some work on open water divers suggested a
NERVOUS SYSTEM EFFECTS greater impairment of performance on manual tasks
at depth when anxiety was present. Plasma cortisol
Although suitable and reliable indices of IGN are and urinary adrenaline/noradrenaline (epineph-
not yet available, the search continues. Such tests rine/norepinephrine) excretion ratios were used to
would be useful in predicting individual suscep- confirm the presence of anxiety noted subjectively.
tibility (diver selection), comparing the relative Divers were tested at 3 and 30 metres at a shore
narcotic potencies of different respiratory diluents base and in the open sea. Intellectual functions, as
for oxygen, delineating the role of factors other assessed by memory test, sentence comprehension

210  Inert gas narcosis


We continue to be puzzled with the rapture of the depths, and felt that we were challenged to go
deeper. Didi’s deep dive in 1943 of 210 feet had made us aware of the problem, and the Group had
assembled detailed reports on its deep dives. But we had only a literary knowledge of the full effects
of I’ivresse des grandes profondeurs, as it must strike lower down. In the summer of 1947 we set out to
make a series of deeper penetrations.
…I was in good physical condition for the trial, trained fine by an active spring in the set, and
responsive ears. I entered the water holding the scrap iron in my left hand. I went down with great
rapidity, with my right arm crooked around the shotline. I was oppressively conscious of the diesel
generator rumble of the idle Elie Monnier as I wedged my head into mounting pressure. It was high
noon in July, but the light soon faded. I dropped through the twilight, alone with the white rope, which
stretched before me in a monotonous perspective of blank white signposts.
At 200 feet I tasted the metallic flavour of compressed nitrogen, and was instantaneously and severely
struck with rapture. I closed my hand on the rope and stopped. My mind was jammed with conceited
thoughts and antic joy. I struggled to fix my brain on reality, to attempt to name the colour of the sea
around me. A contest took place between navy blue, aquamarine and Prussian blue. The debate would
not resolve. The sole fact I could grasp was that there was no roof and no floor in the blue room. The
distant purr of the diesel invaded my mind – it swelled to a giant beat, the rhythm of the world’s heart.
I took the pencil and wrote on a board, ‘Nitrogen has a dirty taste’. I had little impression of hold-
ing the pencil, childhood nightmares overruled my mind. I was ill in bed, terrorised with the realisation
that everything in the world was thick. My fingers were sausages. My tongue was a tennis ball. My lips
swelled grotesquely on the mouth grip. The air was syrup. The water congealed around me as though
I were smothered in aspic.
I hung stupidly on the rope. Standing aside was a smiling, jaunty man, my second self, perfectly self-
contained, grinning sardonically at the wretched diver. As the seconds passed the jaunty man installed
himself in my command and ordered that I unloose the rope and go on down.
I sank slowly through a period of intense visions.
Around the 264 foot board the water was suffused with an unearthly glow. I was passing from night
to an imitation of dawn. What I saw as sunrise was light reflected from the floor, which had passed
unimpeded through the dark transport strata above. I saw below me the weight at the end of the sho-
tline, hanging twenty feet from the floor. I stopped at the penultimate board and looked down at the
last board, five metres away, and marshalled all my resources to evaluate the situation without delud-
ing myself. Then I went to the last board, 297 feet down.*
The floor was gloomy and barren, save for morbid shells and sea urchins. I was sufficiently in control to
remember that in this pressure, ten times that of the surface, any untoward physical effort was extremely
dangerous. I filled my lungs slowly and signed the board. I could not write what it felt like fifty fathoms down.
I was the deepest independent diver. In my bisected brain the satisfaction was balanced by satirical
I dropped the scrap iron and bounded like a coiled spring, clearing two boards in the first flight.
There, at 264 feet, the rapture vanished suddenly, inexplicably and entirely. I was light and sharp, one
man again, enjoying the lighter air expanding in my lungs. I rose through the twilight zone at high
speed and saw the surface pattern in a blaze of platinum bubbles and dancing prisms. It was impos-
sible not to think of flying to heaven (Cousteau JY. The Silent World. London: Reprint Society; 1954).

* 297 feet is 90.5 metres (don’t try repeating this experiment!).

Measurement of central nervous system effects  211

and simple arithmetic, showed evidence of nar- Other descriptive symptoms such as ‘fuzzy’, ‘hazy’
cosis in both 30-metre dives, but the decrement (state of consciousness) and ‘less efficient’ (work
was greater in the ocean dives, possibly because capability) and ‘less cautious or self-controlled’
of the greater psychological stress in the open sea. (inhibitory state) may be more reliable indicators
Unsurprisingly perhaps, these effects have not been of effect on performance.
reproduced in the laboratory. Behavioural studies have cast doubt on some
Many experimental protocols have been criti- traditional concepts of narcosis. True adaptation to
cized because the effects of motivation, experience narcosis has not been found in many performance
and learning, for example, are difficult to control. tests. Where adaptation has been found, it is diffi-
Caisson workers participating in a card-sorting test cult to distinguish learned responses or an adapta-
showed some impairment at 2 to 3 ATA, especially tion to the subjective symptoms from physiological
those who had relatively little exposure to pres- tolerance. Carbon dioxide probably has additive
sure. However, with repeated testing, i.e. practice, and not synergistic effects in combination with
this difference disappeared, and no loss of perfor- nitrogen and probably acts by a different mecha-
mance was noted even deeper than 3 ATA. These nism. Behavioural studies have not been able, so
experiments were repeated using 80 naval subjects far, to demonstrate clearly the potentiating effects
at 2  and 4 ATA while breathing air and helium- on IGN of anxiety, cold, fatigue, anti–motion sick-
oxygen mixtures. The only significant impairment ness drugs and other sedatives (except alcohol).
was found at 4 ATA breathing air.
The effects of IGN on behaviour, as measured Neurophysiological changes
by the psychologist, were well reviewed by Fowler,
Ackles and Porlier7, and there has been relatively Attempts have been made to confirm the subjec-
little work in this area since that time. More atten- tive experiences and obtain objective evidence of
tion has been paid to the molecular mechanisms performance decrement, with some neurophysio-
involved. Psychological studies suggest that the logical parameter. The investigations included elec-
behavioural effects of all inert gases that pro- troencephalographic records of subjects exposed
duce narcosis are identical. Human performance to compressed air in chambers. Contrary to the
under narcosis is explained using the ‘slowed expected findings of depression, features suggest-
processing’ model. Slowing is said to result from ing cortical neuronal hyperexcitability were noted
decreased activation or arousal in the central ner- at first. These included an increase in the voltage of
vous system, manifested by an increase in reaction the basal rhythm and the frequent appearance of
time, perhaps with a fall in accuracy. Increases low-voltage ‘spikes’ elicited by stimuli that do not
in arousal, such as by exercise or amphetamines, have this effect at 1 ATA. Experiments in which the
may explain improved performance. Manual dex- partial pressures of oxygen and nitrogen were con-
terity is less affected than cognitive functioning trolled showed that in compressed air these changes
because dexterity requires fewer mental operations are caused by the high oxygen partial pressure.
and there is less room for cumulative slowing of If  nitrogen-oxygen mixtures containing 0.2  ATA
mental operations (processes). Although memory oxygen are breathed, these changes are absent. The
loss and impaired hearing are features of narcosis, depressant effects of nitrogen are then revealed.
these effects are more difficult to explain using the These consist of a decrease in the voltages of the
slowed processing model. A similar alteration in basal rhythm and the appearance of low-voltage
the processing of emotional experience has more theta waves.
recently been proposed by Löftdal and colleagues8. Blocking of electroencephalographic alpha
Studies of the subjective symptoms of narcosis rhythm by mental activity can be observed in
have indicated that the diver can identify these half of the population. The observation that there
symptoms and that they could relate the effect is an abolition of this blocking on exposure to
to the ‘dose’. Euphoria, as described by terms pressure introduced the concept of ‘nitrogen
such as ‘carefree’ and ‘cheerful’, is only one of threshold’. It was found that the time to aboli-
these symptoms and may not always be present. tion of blocking was inversely proportional

212  Inert gas narcosis

to the  square of the absolute pressure (T is value of current methods of measurement of
­proportional to 1/P2) for an individual, although IGN, by the use of neurophysiological changes, is
there was marked variation among subjects. In questionable.
some persons abolition of blocking was noted at
depths as shallow as 2.5  ATA, where no subjec- AETIOLOGY
tive narcosis was evident.
Flicker fusion frequency was investigated in IGN is thought to be produced by the same
an attempt to obtain a measurement that could mechanism as general anaesthesia with gases or
be applied to the whole population. Subjects were volatile liquids. The inert gases and most vola-
asked to indicate when the flickering of a neon tile anaesthetic agents are simple molecules with
light, at a steadily increasing rate, appeared contin- no common structural feature, and they do not
uous. This is termed a ‘critical frequency’ of flicker. undergo chemical change in the body to exert
After a certain time at pressure, the critical fre- their effect. This property suggests that a physical
quency dropped. The same relationship, T is pro- rather than chemical effect must be involved, and
portional to 1/P2, resulted. Critical flicker fusion most research is based on the hypothesis that the
tests have been adapted for the in-water environ- mechanism is the same for all agents (the unitary
ment and continue to be used in the context of IGN hypothesis of narcosis). For this reason, the con-
assessment8. siderable efforts to understand the mechanism of
A more direct measure of central nervous sys- action for anaesthetic agents are thought to have
tem functioning may be obtained by observing direct relevance for IGN.
the effect of inert gas exposure on cortical evoked At the turn of the twentieth century, Meyer
potentials. Evoked potentials are the electro- and Overton noted a strong correlation between
encephalographic response to sensory stimuli. the lipid solubility of an anaesthetic agent and its
A  depression of auditory evoked responses on narcotic potency, and this relationship has become
exposure to hyperbaric air has been shown to cor- known as the Meyer-Overton Hypothesis. Later,
relate with the decrement in mental arithmetic in 1923, Meyer and Hopf stated ‘all gaseous and
performance under the same conditions. The con- volatile substances induce narcosis if they pen-
clusion was that auditory evoked response depres- etrate cell lipids in a definite molar concentration
sion was an experimental measure of nitrogen which is characteristic for each type of cell and
narcosis. However, other work was unable to sup- is approximately the same for all narcotics’. This
port this hypothesis and concluded that there is means that the higher the oil-water partition coef-
a complex relationship among hyperbaric oxygen, ficient (relative solubility) the more potent the inert
nitrogen narcosis and evoked responses. gas. The hypothesis is that inert gas molecules are
Auditory evoked responses as a measure of dissolved in the lipid membranes of neurons and
narcosis are problematic because of sound altera- somehow interfere with cell membrane func-
tion with pressure and the ambient noise during tion so that the higher the proportion of an agent
hyperbaric exposure. Visual evoked responses dissolved in lipid, the more potent the agent as a
(VERs) have been used in an attempt to produce narcotic (anaesthetic). In truth, it has long been
more reliable information. VERs were studied in realized there is more to anaesthetic action than
US Navy divers, and reliable and significant differ- this because there are some discrepancies in this
ences were reported while the divers were breath- relationship (Figure  15.2). For example, although
ing compressed air versus helium-oxygen mixtures both neon and hydrogen have been shown to be
at pressure. A further study using VERs during a narcotic, neon appears to be more so despite a
shallow 2-week saturation exposure with excur- similar oil-water partition coefficient, and argon is
sion dives suggested that some adaptation to nar- about twice as narcotic as nitrogen but again has
cosis occurred, but it was not complete. Reduction a similar oil-water solubility ratio. There are also
of frequency and amplitude of alpha activity when anomalies among the volatile anaesthetics agents,
compared with pre-exposure and post-exposure but, in general, the relationship is much closer than
surface levels were also noted. Nevertheless, the with other physical properties. Intravenous general

Aetiology 213

The Meyer-Overton correlation for anesthetics
Carbon Perfluoroethane
10 tetrafluoride
Sulfur hexafluoride Krypton
Potency of anesthetic drug Nitrous oxide Ethylene
1 Xenon

Fluroxane Enflurane
Diethyl ether
Isoflurane Halothane

0.01 0.1 1 10 100 1000
Olive oil: gas partition coefficient

Figure 15.2  Graphical representation of the Meyer Overton hypothesis. Note the position of nitrogen as
the least potent of the charted narcotic agents.

anaesthetic agents (e.g. thiopentone and propofol) The physical theories, in general, support the
do not fit this relationship and almost certainly concept that the site of action is a hydrophobic
produce narcosis through a different mechanism. portion of the cell, the traditional view being that
The lipid solubility hypothesis has been extended this is the cell membrane. Many studies show that
by the critical volume concept10. Here, the conse- membranes are resistant to the effects of anaes-
quence of the narcotic agent dissolved in the lipid thetics, and other sites have been sought, such as
membrane is proposed to cause swelling of the the hydrophobic regions of proteins or lipopro-
membrane. At a critical volume, the swollen mem- teins. More recent studies have suggested that the
brane somehow produces the clinical features of site of action is a protein, rather than a lipid, and
anaesthesia. Thus, there is a lipid volume change that narcotics act by competitive binding to spe-
that differentiates the anaesthetized from the cific receptors, thus affecting synaptic transmis-
unanaesthetized state. Other factors, in particular sion. It has even been postulated that although
pressure compressibility of the lipid, also affect vol- impairment of cognitive function is a result of
ume. That some narcotic effects can be reversed by the inert gas narcotic effect, impaired motor abil-
application of increased hydrostatic pressure lends ity is a consequence of raised hydrostatic pressure
weight to this hypothesis. (See also Chapter 20, on per se12. Not all experimental observations are eas-
the high pressure neurological syndrome [HPNS]). ily reconciled, and the definitive description of the
Exceptions in both animal and human stud- mechanism of action for volatile anaesthetic agents
ies have led to a further refinement – the multi- at the molecular level remains to be elucidated. For
site expansion model11. This model postulates those interested in delving deeper into this area,
that expansion occurs variably at more than one see Pleuvry13.
molecular site and that pressure does not act The site of action is most likely at a synaptic
equally at the same sites. Thus, hydrostatic pres- level, and many studies have looked at inhibitory
sure effects (see Chapter 20) or narcotic effects may and excitatory neurotransmitters and receptors
predominate. in the central nervous system. Neurotransmitters

214  Inert gas narcosis

studied include noradrenaline (norepinephrine), narcosis, with a progressive improvement of job
serotonin, dopamine, gamma-aminobutyric acid ­performance, approaching ‘surface’ efficiency.
(GABA) and glycine. GABA is the most important For most contemporary deep diving, the effect
inhibitory transmitter in the brain. Potentiation of IGN is avoided by substituting helium, or
of inhibitory pathway synapse receptors (GABA helium-nitrogen, as the diluent gases for oxygen.
receptors) is suspected to be a major component of Oxygen cannot, of course, be used alone because
IGN/anaesthesia, although action at a wide variety of its toxicity at high pressure (see Chapter 17), but
of neuronal sites is likely. it can partially replace nitrogen in various nitrox
Exposure to narcosis raises extracellular dopa- mixtures. Hydrogen is also being used as a substi-
mine in the area of the brain controlling the extra- tute for nitrogen and would be ideal except for the
pyramidal system, at least in rats. This action may formation of an explosive mixture with oxygen.
account for some of the neuromuscular distur- Evidence that helium also has some narcotic
bances of IGN. In contrast, dopamine is increased effect arises from the observation that HPNS is not
when HPNS is exhibited (see Chapter 20). the same under hydrostatic pressure as it is under
helium pressure. It has been postulated that both
PREVENTION helium and oxygen need to be considered when
calculating the narcotic effects of respired gases
In its simplest terms, prevention comes by avoid- under great pressure14.
ing exposure to partial pressures of inert gas Although amphetamines ameliorate narcotic
known to produce intoxication. In practice, safe slowing of reaction time, the use of drugs to reduce
diving on compressed air requires an awareness of narcosis has, as yet, no place in diving. Conversely,
the condition and its effect on performance and divers should be warned of the risks of taking
judgement at depths greater than 30 metres. The central nervous system depressant drugs, which,
maximum depth limit for an air dive should be in the diver, may include alcohol, sedating anti-
between 30 and 50 metres, depending on the div- histamines (in cold and sinus preparations) and
er’s experience and the task to be performed. Safe anti–motion sickness drugs. These drugs may act
diving at a greater depth requires the substitution synergistically with nitrogen in impairing per-
of a less narcotic agent to dilute the oxygen, such formance and judgment, although this has been
as helium, neon or hydrogen (one form of ‘techni- clearly shown only with alcohol15.
cal’ diving).
There is a firm belief among divers that adapta- REFERENCES
tion to IGN can develop over repeated daily expo-
sures and that one can therefore ‘work up’ to deep 1. Bennett PB, Rostain JC. Inert gas narcosis.
dives. Several studies have shown that, although In: Brubakk AO, Neuman TS, eds. Bennett
subjective adaptation can occur, measurement of and Elliott’s Physiology and Medicine of
standing steadiness or reaction time showed no Diving. 5th ed. London: Saunders; 2003.
improvement with repeated exposure3. As with 2. Hobbs M. Subjective and behavioural
alcohol, confidence is not matched by perfor- responses to nitrogen narcosis and ­alcohol.
mance, thus possibly compromising safety. Undersea and Hyperbaric Medicine
Saturation at depths between 30 and 40 metres 2008;35(3):175–184.
is said to allow the development of adaptation. 3. Hamilton K, Laliberté MF, Fowler B.
Excursion dives to greater depths can then be Dissociation of the behavioral and subjec-
made with more safety and improved work perfor- tive components of nitrogen narcosis and
mance. A conventional working dive to 100 metres diver adaptation. Undersea and Hyperbaric
would be inconceivable using air as the breath- Medicine 1995;22(1):41–49.
ing medium. However, operational dives may be 4. Mekjavic IB, Passias T, Sundberg CJ,
performed to 100 metres if the excursion is from Ceiken O. Perception of thermal comfort
a saturated depth of 40 metres. At that depth, during narcosis. Undersea and Hyperbaric
the diver becomes acclimatized to the nitrogen Medicine 1994;21(1):9–19.

References 215

5. Mekjavic IB, Savic SA, Eiken O. Nitrogen 11. Halsey MJ, Wardley-Smith B, Green CJ.
narcosis attenuates shivering thermo- Pressure reversal of general anaesthesia:
genesis. Journal of Applied Physiology a multi-site expansion model. British Journal
1995;78(6):2241–2244. of Anaesthesia 1978;50:1091–1097.
6. Cousteau JY. The Silent World. London: 12. Abraini JH. Inert gas and raised p
­ ressure:
Reprint Society; 1954. evidence that motor decrements are due to
7. Fowler B, Ackles KN, Porlier G. Effects pressure per se and cognitive decrements
of inert gas narcosis on behavior: a criti- due to narcotic action. European Journal of
cal review. Undersea Biomedical Research Physiology 1997;433:788–791.
1985;12:369–402. 13. Pleuvry BJ. Mechanism of action of ­general
8. Löftdahl P, Andersson D, Bennett M. anaesthetic drugs. Anaesthesia and
Nitrogen narcosis and emotional process- Intensive Care Medicine 2008;5(4):152–153.
ing during compressed air breathing. 14. Abraini JH. Some considerations regarding
Aviation Space and Environmental Medicine the narcotic potency of helium and oxygen
2012;83:1–5. in humans. In: Rostain JC, Marquis RE, eds.
9. Balestra C, Lafère P, Germonpré P. Basic and Applied High Pressure Biology IV.
Persistence of critical flicker fusion fre- Medsubhyp Int 1995;5:77–82.
quency impairment after a 33 msw SCUBA 15. Fowler B, Hamilton K, Porlier G. Effects
dive: evidence of prolonged nitrogen narco- of ethanol and amphetamine on inert gas
sis? European Journal of Applied Physiology narcosis in humans. Undersea Biomedical
2012;112(12):4063–4068. Research 1986;13:345–354.
10. Miller KW, Paton WDM, Smith DA, Smith,
EB. The pressure reversal of general anaes- This chapter was reviewed for this fifth edition by
thesia and the critical volume hypothesis. Michael Bennett.
Molecular Pharmacology 1973;9:131–143.


Introduction 217 Hypoxia of ascent 224
Clinical features 219 Hypoxia and breath-hold diving 225
Classification 220 Hyperventilation 225
Hypoxic hypoxia 220 Ascent 225
Stagnant (ischaemic) hypoxia 221 Hypoxia and deep diving 226
Anaemic hypoxia 222 Management 226
Histotoxic hypoxia 222 Hypoxic hypoxia 227
Hypoxia and diving equipment 222 Stagnant hypoxia 227
Exhaustion of gas supply 222 Anaemic hypoxia 227
Low oxygen concentration in the gas supply 222 Histotoxic hypoxia 227
Inadequate flow rates 222 Methods of oxygen delivery 227
Increased oxygen consumption 222 References 228
Dilution hypoxia 223 Further reading 228

INTRODUCTION adenosine triphosphate (ATP), whereas in the
absence of O2, 1 molecule of glucose produces only
Hypoxia in the context of human physiology means 2 molecules of ATP (via the production of lactic
an oxygen (O2) deficiency, or a lower than nor- acid). Thus, anaerobic conditions (hypoxia) drasti-
mal partial pressure of O2 (PO2; also called the O2 cally reduce the available energy.
­tension), in the tissue in question. The term strongly Dry air, at a barometric pressure of 760 mm
implies inadequate O2 availability to bodily tissues. Hg, has a PO2 of 159 mm Hg. When inspired, dry
The brain, liver and kidney, which extract the great- air becomes saturated with water vapour at body
est amount of O2 from the blood to supply their temperature. By this dilution the PO2 drops to
energy requirements, are the first affected by falling 149  mm  Hg. Alveolar gas has a lower PO2 than
O2 levels in the body. Skin, muscle and bone are less inspired air because it is further diluted by carbon
vulnerable because of their lower energy require- dioxide (CO2) and contact with de-oxygenated
ments. O2 does not directly supply the energy but is blood, to around 105 mm Hg. O2 freely diffuses
necessary to liberate the energy required for cellular into the capillaries in the lung so that normal arte-
metabolism from sugar (glucose). rial blood levels are in the region of 100 mm Hg.
Aerobic (‘with O2’) metabolism is much more As the blood moves through the tissue capillaries,
efficient in the production of biological energy O2 moves by diffusion down partial pressure gradi-
than anaerobic metabolism (‘without O2’) and ents to the cells, where it is consumed (Figure 16.1).
is the key to complex life on Earth. For example, in After passage through the tissues the PO2 falls to
the presence of O2, 1 molecule of glucose can pro- approximately 40 mm Hg in mixed venous blood
duce 38 molecules of the energy storage compound coming back into the lungs.


218 Hypoxia

Inspired Barometric
oxygen pressure
concentration PB

Alveolar Oxygen
ventilation consumption
VA Alveolar

Scatter of Venous
V/Q ratios Arterial admixture
blood QS/Qt ratios

Blood Haemoglobin
kPa mmHg flow concentration
I Q Hb
20 150 PO2
Air humidified at 37°C
Dry atmospheric air

15 A
End-expiratory gas

Ideal’ alveolar gas

Arterial blood




0 0
0 15 30 45
Time (mins)

Figure 16.1  The oxygen cascade. On the left is shown the cascade with partial pressure of oxygen (PO2)
falling from the level in the ambient air down to the level in mitochondria, the site of utilization. On the
right is shown a summary of factors influencing oxygenation at different levels in the cascade. (Redrawn
from Nunn JF. Applied Respiratory Physiology. 3rd ed. London: Butterworth; 1987.)

The amount of O2 stored in the body is limited, The result is that, unlike diving mammals, we
as are the high-energy phosphate bonds used to do not have much reserve capacity and cannot stop
store energy. A person breathing air at sea level breathing for long before severe hypoxia intervenes
would hold approximately the following amounts (Table 16.1). During a breath-hold, we are protected
of O2, not all of which is available for use in vital from hypoxia because our breakpoint is usually
organs such as the brain or heart: determined by the rising carbon dioxide tension.
Hyperventilation prior to breath-holding reduces
In the lungs 450 ml arterial carbon dioxide tension and extends our
In the blood 850 ml breakpoint, but at the risk of unconsciousness
Dissolved in body fluids 50 ml from hypoxia.
Bound to myoglobin in muscle 200 ml Basal O2 consumption is of the order of 200 ml/
Total = 1550 ml minute, but in swimming and diving much higher

Clinical features  219

Table 16.1  Effects of hyperventilation on the breath-holding time and alveolar gas
pressure at the breaking point in resting and exercising man

Without With
Effect hyperventilation hyperventilation

Measurements while resting
BH time (sec) 87 146
End-tidal PCO2 (mm Hg)
Before BH 40 21
Breaking point 51 46
End-tidal PO2 (mm Hg)
Before BH 103 131
Breaking point 73 58

Measurements while exercising
BH time (sec) 62 85
End-tidal PCO2 (mm Hg)
Before BH 38 22
Breaking point 54 49
End-tidal PO2 (mm Hg)
Before BH 102 130
Breaking point 54 43
BH, breath-holding; PCO2, partial pressure of carbon dioxide; PO2, partial pressure of oxygen.
Source: From Craig AB. Causes of loss of consciousness during underwater swimming. Journal
of Applied Physiology 1961;16:583–586.

consumption is possible (up to 3 litres/­ minute CLINICAL FEATURES
[lpm]). This explains why hypoxia develops so
rapidly if respiration has stopped while exercise The physiological consequences of hypoxia in general
continues. medicine are well known and are not discussed here.
The delivery of O2 at the cellular level requires The symptoms and signs of hypoxia become obvi-
an adequate inspired PO2 (PIO2), adequate lung ous when the PaO2 drops below about 50 mm Hg.
function and adequate cardiac output. Further, This corresponds to an inspired concentration at sea
because most O2 in the blood is carried bound to level of 8 to 10 per cent. If the fall in PO2 is rapid,
haemoglobin, it also requires adequate functional then loss of consciousness may be unheralded. With
haemoglobin levels. At arterial PO2 (PaO2) below slower falls, an observer may note lack of coordina-
60 mm Hg, the amount of O2 given up to the tissue tion or poor job performance. Euphoria, overconfi-
is greatly reduced. dence and apathy are also been reported. Memory is
Although impairment of aerobic metabo- defective and judgement impaired, leading to inap-
lism is probably the ultimate mechanism of propriate or dangerous reactions to the emergency
death in most fatal diving accidents, hypoxia as that may also endanger others. The diver may com-
a primary event is uncommon in conventional plain of fatigue, headache or blurred vision.
scuba diving (breathing air or nitrox). It is much
more  likely  with mixed gas and rebreathing There are rarely any symptoms to warn the
equipment. diver of impending unconsciousness from
The diving disorders mentioned here are dis- hypoxia.
cussed more fully in their specific chapters.

220 Hypoxia

Hyperventilation may develop in some cases, INADEQUATE OXYGEN SUPPLY
but it is usually minimal if the arterial CO2 tension This condition results from a decrease in O2 pres-
(PaCO2) is normal or low. sure in the inspired gas, which may in turn be
There are marked individual differences in sus- caused by an incorrect gas mixture or equipment
ceptibility to hypoxia. When combined with hypo- failure. CO2 retention is not a feature of this type
capnia or hypercapnia, hypoxia will impair mental of hypoxaemia.
performance earlier than if the diver is normo-
capnic; mental performance may not be severely ALVEOLAR HYPOVENTILATION
impaired until the alveolar-arterial PO2 falls below This condition occurs when the amount of gas flow-
40 mm Hg. Hypoxia may precipitate or exacerbate ing in and out of functioning alveoli per unit time
other pathological conditions, such as coronary or is reduced. It may result from increased density of
cerebral ischaemia. gases with depth or decreased compliance with the
Cyanosis of the lips and nail beds may be drowning syndromes, among other causes. The
difficult to determine in the peripherally vaso- extreme example is breath-holding diving. There is
constricted ‘cold and blue’ diver. Generalized associated CO2 retention.
convulsions or other neurological manifestations
may be the first signs. Masseter spasm is common VENTILATION-PERFUSION INEQUALITY
and may interfere with resuscitation. Eventually, AND SHUNT
respiratory failure, cardiac arrest and death Perfusion of blood past alveoli that are not being
supervene. ventilated causes non-oxygenated blood to move
Diagnostic errors may arise because some of into the systemic circulation. This blood is referred
the foregoing manifestations are common to nitro- to as a ‘right-to-left shunt’ because blood is shunted
gen narcosis, O2 toxicity and CO2 retention. The from the right side of the heart through the lungs
attending physician should also consider cerebral but without picking up O2 or releasing CO2. The
arterial gas embolism and decompression sickness degree of arterial desaturation depends on the pro-
(DCS), should the previously described features portion of the cardiac output that is shunted (the
develop during or after ascent by a diver breathing shunt fraction). Lesser degrees of mismatching
compressed gases. of perfusion and ventilation may be seen in near
drowning, salt water aspiration syndrome, pulmo-
nary O2 toxicity and pneumothorax. Inequality of
CLASSIFICATION ventilation and perfusion may also occur in pul-
Hypoxia (‘anoxia’) has been classified into four monary DCS sickness and pulmonary barotrauma,
types: as well as in deep divers using helium, in whom it is
a consequence of lung cooling.
The arterial CO2 response is variable with
1. Hypoxic. ­ventilation-perfusion disorders, with high levels in
2. Stagnant. severe cases, but mild hypocapnia (low partial pres-
3. Anaemic. sure of CO2 [PCO2]) is more usual if ventilation in
4. Histotoxic. the perfused lung is increased by hypoxic drive.

Hypoxic hypoxia
This defect results from slowed diffusion of O2
This designation covers all conditions ­leading to through a thickened alveolar-capillary barrier.
a reduction in arterial O2 (Figure  16.2). A better This may occur after near drowning and as a result
term would be ‘hypoxaemic hypoxia’. This is the of pulmonary O2 toxicity. CO2 retention is not
common form of hypoxia seen in diving. Causes of characteristic of this type of hypoxaemia because
hypoxaemia, with examples related to diving, are CO2 diffuses through the barrier much more rap-
discussed in the following paragraphs. idly than O2.

Classification 221

Air PIO2 150 mmHg
PIO2 Reduced Reduced ambient
Normal ventilation
Low oxygen
Normal perfusion concentration

O2 CO2 O2 CO2
PaO2 100 mmHg PaO2 reduced
PaCO2 40 mmHg PaCO2 normal
Normal situation

Reduced flow
of gas through
Normal perfusion alveoli

Normal PaO2
PaO2 Venous
reduced admixture
Low PaO2
(b) PaCO2 elevated (c) PaO2 reduced

O2 CO2
PaO2 reduced
PaO2 reduced
PaCO2 normal
PaCO2 normal
(d) or reduced (e)

Figure 16.2  Mechanisms of hypoxaemia (hypoxic hypoxia). (a) Inadequate oxygen supply. (b) Alveolar
hypoventilation. (c) Perfusion of non-ventilated alveoli causing venous admixture. (d) Ventilation-
perfusion inequality. (e) Diffusion defect. PaCO2, arterial partial pressure of carbon dioxide; PaO2,
­arterial partial pressure of oxygen; PIO2, inspired oxygen tension.

There is obviously great overlap among the dif- manifestation resulting from inadequate cardiac
ferent mechanisms by which the various condi- output (see Chapters 6 and 47).
tions produce hypoxaemia. Reduced cardiac output may also be present in
serious DCS when local ischaemia results from
Stagnant (ischaemic) hypoxia gas bubbles obstructing venous return. In addi-
tion, reduced cardiac output may be caused by
Reduced tissue blood perfusion leads to hypoxia gas emboli arising in both DCS and pulmonary
as a result of the continued metabolism of O2 in barotrauma.
the presence of a reduced supply, and it may be Many marine venoms induce stagnant hypoxia,
either regional or general. The extreme form is cir- and localized ischaemia is the cause of many of the
culatory arrest. Syncope of ascent is a transitory symptoms and signs of these envenomations.

222 Hypoxia

Anaemic hypoxia Exhaustion of gas supply
This designation refers to any condition charac- The ‘out of air’ situation remains a major cause of
terized by a reduction in haemoglobin concentra- diving accidents, despite contents gauges, reserve
tion in the blood or alterations in the O2-carrying supplies and training (Case Report 16.1).
capacity of haemoglobin. One cause is traumatic
haemorrhage, with restoration of the blood volume
with fluids. Low oxygen concentration in the
Carbon monoxide poisoning (see Chapter 19), gas supply
in which the formation of carboxyhaemoglobin
Accidental filling of an air cylinder with another
reduces the O2-carrying capacity of the blood,
gas, such as nitrogen, may result in unconscious-
is most often a consequence of contamination of
ness. Low-percentage O2 mixtures (10 per cent O2 or
compressed air.
less), designed for use in deep or saturation diving,
The capacity of haemoglobin to carry O2 is also
would lead to hypoxia if breathed near the surface.
reduced in the presence of alkalaemia, e.g. low
Rusting (oxidization) of scuba cylinders can
PaCO2, and hypothermia.
reduce the O2 content, and It has led to at least one
fatality and several ‘near misses’ (Case Report 16.2).
Histotoxic hypoxia
This term refers to the situation in which adequate
Inadequate flow rates
O2 is delivered to the tissues, but there is a failure Many rebreathing diving sets have a constant flow
of utilization within the cell. Carbon monoxide of gas into the counterlung (see Chapters 4 and
poisons the enzyme cytochrome oxidase, which 62 for an explanation of this equipment). A set
is a vital link in the use of O2 to provide energy designed to use various gas mixtures has a means
for n
­ ormal cell function. Histotoxic hypoxia has of adjusting these flow rates. The flow rate should
also been postulated as a mechanism for inert be set to supply enough O2 for the diver’s maximum
gas narcosis (see Chapter 15) and O2 toxicity (see requirements, in addition to that lost through the
Chapter 17). exhaust valve. The higher the O2 concentration of
the gas, the lower the required flow rate will be,
and vice versa.
If an inadequate flow rate is set for the O2 mix-
EQUIPMENT ture used, then the inert gas (e.g. nitrogen) will
Hypoxia secondary to inadequate inspired O2 accumulate in the counterlung. Low concentra-
results from the failure or improper use of the div- tions of O2 will then be inspired by the diver (Case
ing equipment. Apart from running out of air on Report 16.3). Other causes include blockage of the
open-circuit scuba, this disorder occurs mainly reducer by ice, particles among others.
with the use of closed-circuit or semi-closed-­
circuit rebreathing apparatus. Increased oxygen consumption
Of the following six causes only the first
two mechanisms are possible with open-circuit Most rebreathing sets are designed for maximum
scuba: O2 consumption between 1 and 2.5 lpm depending
on the anticipated exertion. Commonly, the maxi-
1. Exhaustion of gas supply. mum O2 uptake is assumed to be 1.5 lpm. Several
2. Low O2 concentration. studies have shown that divers can consume O2 at
3. Inadequate flow rates. higher rates than these. Values of more than 2.5
4. Increased O2 consumption. lpm for 30 minutes and more than 3 lpm for 10 to
5. Dilution hypoxia. 15 minutes have been recorded without excessive
6. Hypoxia of ascent. fatigue underwater.

Hypoxia and diving equipment  223


Two commercial divers were engaged in making a 110-metre mixed gas dive from a diving bell. The
purpose of the dive was to tie in a 6-inch riser. While one diver was in the water at depth working on
the riser, the diving bell operator excitedly informed topside that the bell was losing pressure and
flooding. The surface operator, who was disconcerted by this information, opened valves to send gas
to the bell. Communication with the bell operator was lost.
The diver who was in the water working on the riser was instructed to return to the bell, which he
did. When the diver arrived at the bell, he found the bell operator unconscious and lying on the deck
of the bell. The diver climbed out of the water into the bell, took off his Kirby-Morgan mask, and
promptly collapsed. When topside personnel realized that they had completely lost communications
with the bell, they made ready the standby divers. The first standby diver was dressed, put on his div-
ing helmet and promptly collapsed unconscious on deck. At this point the bell with the diver and the
bell operator was brought to the surface with the hatch open and without any decompression stops.
The divers were extricated from the bell and recompressed in a deck decompression chamber. Both
the diver and the bell operator died in the deck decompression chamber at 50 metres, of fulminating
decompression sickness.
Examination of the rack (the collection of gas cylinders to be used during the dive) showed that the
rack operator had mistakenly opened a cross-connect valve that should have been ‘tagged out’ (labeled
to indicate that it should not be used). This valve permitted 100 per cent helium to be delivered to the
diving bell and the standby divers, instead of the appropriate helium-oxygen breathing mixture.
Diagnosis: acute hypoxia and fulminant decompression sickness.


MB, a civilian diver, was asked to cut free a rope that was wrapped around the propeller of a diver’s
charter boat. Because of the very shallow nature of the dive (3 metres maximum), he used a small
steel cylinder not often used by divers. After he entered the water, his diving partner noticed that he
was acting in a strange manner and swam to him. At this point the diver was lying on the bottom and
was unconscious but still breathing through his single hose regulator. The diving partner rescued the
unconscious diver and got him on deck. His fellow divers prised the mouthpiece from him and gave
him cardiopulmonary resuscitation, and the diver promptly regained consciousness.
On analysis, the gas in the cylinder was found to be 98 per cent nitrogen and 2 per cent oxygen.
There was sea water present in the interior of the cylinder, together with a considerable amount of rust.
Diagnosis: acute hypoxia resulting from low inspired oxygen(see Chapters 6 and 47) concentration.

This increased exertion may be tolerated the counterlung in response to accumulation of
because of the cooling effect of the environment nitrogen (i.e. dilution hypoxia).
and/or greater tissue utilization with increased
amount of O2 physically dissolved in the plasma. Dilution hypoxia
This indicates that it is possible for a diver to
consume O2 at a greater than the often quoted This term applies mainly to O2 rebreathing sets.
rate under certain conditions. In rebreathing Dilution hypoxia is caused by dilution of the O2
sets, a hypoxic mixture could then develop in in the counterlung by inert gas, usually nitrogen.

and his teeth were firmly clenched on the mouthpiece. but the amount that would diffuse out into before use. The second diver flushed the unconscious diver’s counterlung with gas and took him to the surface. when the counterlung Hypoxia develops when the diver ascends suf- is empty). rather than having a constant flow of ficiently to reduce this PO2 to a critical level (Case gas into the bag. plied only ‘on demand’ (i. Examination of his diving equipment revealed that both main cylinders were empty and the emergency supply had not been used. Equipment investigation revealed that carbon dioxide absorbent activity was normal. 3. CASE REPORT 16. per cent can be breathed quite safely at 10 metres because the partial pressure would still be adequate Dilution hypoxia is more likely if O2 is sup. There 1. be a small contribution. At approximately 3 to 4 metres he noted some difficulty in breathing but continued to ascend and then started to climb on board. he or she may add up to 3 litres of nitrogen to the counterlung. From the gas supply.224 Hypoxia CASE REPORT 16. He was cyanosed around the lips. As the diver continues to use up Report 16. after which the set was turned to atmosphere. the nitrogen remains in the counterlung. After 15 minutes he noted difficulty in obtaining enough gas. (approximately 140 mm Hg). to report 20 per cent.4 RAB was diving to 22 metres while using a semi-closed-circuit rebreathing set with a 40/60 oxygen- nitrogen mixture. The diver started to regain consciousness but was initially still cyanosed. is approximately 1 litre of nitrogen dissolved in the 2.3 AS was diving to 20 metres using a 60/40 oxygen-nitrogen mixture in a semi-closed-circuit rebreath- ing system. Thus. The disorder is therefore most likely the O2. He became aware of his sur- roundings and did not require further resuscitation. Diagnosis: hypoxia of ascent. This would supply inadequate oxygen for the diver’s expected rate of utilization. An inspired O2 concentration of 10 ­activities or for some other reason. the percent- This may also occur if the diver surfaces age of O2 being inspired may drop to well below and breathes from the atmosphere.g. .4). The unwanted nitrogen may enter the system by CO2 will continue to be removed by the absorbent. but reducer flow was set at 2 lpm instead of the required 6 lpm. He stopped to try and adjust his relief valve and then suddenly lost consciousness. Diagnosis: hypoxia resulting from inadequate gas flow rate. Another diver noticed him lying face down on the bottom. On removal of his set and administration of oxygen. to develop at or near the surface. thus leaving a litre or more nitrogen the counterlung to cause dilution hypoxia would in it.e. he recovered rapidly but remained totally amnesic for 10 min- utes. From failure to clear the counterlung of air body. After 36 minutes he was instructed to ascend slowly. if a diver breathes into the Hypoxia of ascent set after a full inhalation. e. Failure to clear the lungs before using the equipment. three methods: thereby avoiding dyspnoea. but he appeared to have some difficulty with this. the percentage of O2 in the inspired gas falls as it is consumed. When asked whether he was well he did not answer. so that the diver was breathing air. By one of the foregoing mechanisms.

After hyperventilating it takes much longer for this level In a simple breath-hold. training (adaptation). with loss of consciousness and subsequent drowning. therefore would decrease rapidly. The alveolar PO2 and PCO2 were often competing. ventilation. Ascent hypoxia was first described in military div- rience the breath-hold diver can delay the need to ers losing consciousness as they surfaced with low inhale by various techniques. against others or them. Under these preceding hyperventilation. the time to reach the irresistible urge Breath-hold divers who train to extend their to breathe (the breaking point) is prolonged. thus increasing the available O2. feet-first descent. The hyperventilation values were both back to ‘normal’ levels. hyperventilation effect is independent of depth and The dangers of hyperventilation and breath- may be encountered in 1-meter-deep swimming hold diving are diagrammatically illustrated in pools. and some nitrogen One way of avoiding this hypoxia is to inhale absorbed and deposited in tissues. he or she is more ‘Hypoxic blackout’ is a reasonable alternative. the O2 to be used and lose consciousness with little or no warning1. for example. and to a lesser extent by a fall to sustain consciousness. gen. The point. to spear a fish or retrieve a catch. often by children trying to swim greater dis.3. the breaking point ­ conditions. the O2 would be 200 mm Hg. until he or she ascended. CO2 and nitro- ing. ascent. and the CO2 80 mm Hg. with descent the pres- (but not with increased safety) by. By the time these selves. appear to be in a satisfactory respiratory status – often to half the normal levels.g. likely to ignore the physiological warning symp- There are two causes of this disorder – hyper. the O2 status. One can water blackout. They the CO2 to be buffered. they are often confused. with earlier hyper- tances underwater. free div. if a diver having 100 mm Hg O2 and 40  mm Hg CO2 in the alveolar gases was imme- Hyperventilation diately transported to 2 ATA. erbates this effect by increasing O2 consumption. inhaling against a closed glottis and diaphrag. spear fishing) risk hypoxia of levels (hypoxic danger zone). with O2 at extended their breath-holding time because it 100 mm Hg and CO2 at 40 mm Hg. toms of an urge to breathe (resulting from the rise ventilation and ascent – and because they may in CO2 level in the blood) and delay the breaking occur concurrently. It illustrates that. Craig observed that swimmers who hyper. centrating on some purposeful goal. Figure  16. CO2 absorbed and buffered. With increased expe. Both would pass into the ventilated could stay longer underwater but then pulmonary capillary blood. some matic contractions. Hypoxia and breath-hold diving  225 HYPOXIA AND BREATH-HOLD The build-up of CO2 is the main stimulus forc- DIVING ing the swimmer to surface and breathe. In breath-hold diving. following experiment: When the swimmer is con- ness from the use of closed-circuit diving suits. Breath-hold time can be extended In breath-hold divers. the diver would washed out a large amount of CO2 from the lungs. the diver may extend the breath-hold (the irresistible urge to breathe) is initiated mainly to the point that PaO2 drops to a level inadequate by a rise in CO2 level. swallow. such as trying it is best avoided in the breath-holding context. Increased exercise exac- in arterial O2. without improving O2 levels in their rebreathing equipment. Because ‘shallow water blackout’ demonstrate this dangerous combination in the was first used in 1944 to describe loss of conscious. with no immersion or (the ‘breaking point’) to be reached. hypoxic blackout is The combination of these two effects (hyper- sometimes called breath-hold syncope or shallow ventilation and exercise) can be deadly. With an expansion of the . In 1961. extra time may allow the PaO2 to fall to dangerous ing competitors. Some O2 can be absorbed and used. This breath-hold and also dive deep (e. Ascent With hypoxia there is little or no warning of impending unconsciousness. and often exercising. the lungs would halve their volume. 100 per cent O2 before the breath-hold. Thus. sure rises proportionately in the alveolar gases.

there is a block in the Other causes of hypoxia in breath-hold diving utilization or transport of O2. Point A. without preceding hyperventilation. lungs to twice their size at depth. more O2 will be mixing of fresh inspired gases and alveolar gases consumed. 22 and 24). the O2 would drop to caused by the cooling effects on the lungs. suggesting that at greater than 50 ATA there an explanation for the ‘7-metre syncope’ described is decreased O2 uptake. the ‘syncope’ or ‘blackout’. and the CO2 will increase toward normal pulmonary ventilation).3  A diagrammatic representation of changes in arterial oxygen and carbon dioxide levels with breath-holding. PaO2. MANAGEMENT HYPOXIA AND DEEP DIVING First aid management involves the basic principles of resuscitation. i. 50 mm Hg (approaching a potentially dangerous Hypoxia may be expected. Saltzman2 has an alternative explana- way to the surface in the top 10 metres (probably tion. com. 100 per cent exposure and thus ocean penetration. capacity is limited by restricted gas flow or increased Further management depends on the aetiology of work of breathing. is rectified by a of consciousness. In deeper dives alveolar-arterial diffusion abnormality and a non- it becomes more likely. the pressures in increased gas density or from pulmonary damage both gases would halve.e. with decreased pH and by French workers). as a result of the gradient between the pulmonary The Chouteau effect (a disputed concept) is blood and alveoli. . nor- monly noted among spear fishers. as a result of such fac- hypoxia level) and the CO2 to 20 mm Hg – if the tors as an increased ‘diffusion dead space’ (caused ascent was immediate. the loss of consciousness may occur on the pressures. apparent clinical hypoxia despite normal inspired The drop in O2 is then able to produce the loss O2 tension that. It has been explained by both an is referred to as hypoxia of ascent.e. at least in goats. This condition moxic hypoxia). extracted from the lungs during the despite adequate inspired O2 pressure and overall ascent. Ventilatory O2 should be administered as soon as possible. include salt water aspiration and the drowning syndromes (see Chapters 21. both resulting from the effects of the hypoxia. establishing an airway and ensur- Animal experiments at great pressures are regu. point B. and with some very deep homogenous mixing of alveolar gas at very high dives. arterial partial pressure of oxygen. with preceding hyperventilation. PaCO2. increasing acidosis. Thus.226 Hypoxia Partial pressure of gases in blood 100 PaO2 80 PaCO 2 Breath-hold PaCO 2 breaking 60 point (CO2) A 40 Hypoxic 20 B danger zone 205 405 605 805 Breaking point Breaking point with without hyperventilation hyperventilation Figure 16. by slowed diffusion of alveolar gases or incomplete Because ascents do take time. arterial partial pressure of carbon dioxide. slight increase in the inspired O2 tension (i. ing that there is ventilation of the lungs and that larly undertaken to determine the limits of human the oxygenated blood is circulating.

foregoing regimens time to have an effect (see Chapters 6. achieved. 13 and 19). Circulation – If pulse absent.g. Histotoxic hypoxia ent causes of tissue hypoxia. Available O2 (i. Need to avoid CO2 accumulation.g. 60 Soft plastic masks (e. progressively reduced while arterial gases or tissue 3. O2 is monitored by transcutaneous oximetry. 50. Ventimask. Desired inspired O2 concentration. mouth-to-mouth or colloid resuscitation. as well as vasodilator drugs. Synthetic blood substitutes or mouth-to-nose respiration followed by show promise but have yet to be introduced to clini- intermittent positive pressure resuscitation cal practice.e. 100 per cent oxygen fusion with packed red blood cells after crystalloid by mask. 4. MC. Anaemic hypoxia jaw forward. First aid and hyperoxygenation as a temporary measure. 40. secretions removed. Blood loss from trauma may require blood trans- Breathing – If breathing.2 (see Chapter 49). and all patients should receive a high inspired O2 concentration. 5. In many cases there may be an overlap of differ. This may require restoration of total plastic masks deliver less than 60 per cent of the Table 16. 35. In the case of carbon monoxide poisoning. Need to assist or control ventilation. efficiency and economy). Harris) Venturi-type masks 4–8 24. Methods of oxygen delivery  227 circulatory volume. cardiac hyperbaric oxygenation may be lifesaving during massage. if not breathing. Most affected areas. with 100 per cent oxygen when available. METHODS OF OXYGEN DELIVERY Hypoxic hypoxia There are various devices or apparatus for the thera- peutic administration of O2 (see also Chapter 49). Airway – Head extended. These patients should be given supplemental Selection of the appropriate mode of administration inspired O2 or ventilated with 100 per cent O2 at depends on a number of factors: whatever pressure is needed to ensure adequate arterial O2 levels.2  Modes of oxygen therapy Apparatus Oxygen (lpm) Concentration (%) Nasal catheters 2–6 22–50 Semi-rigid masks (e. Acceptance of the method by the patient. lower neck flexed. the early critical period. Once these goals have been 1. This form of hypoxia can be treated only by remov- Recompression or hyperbaric oxygenation may ing the toxic substance and using hyperoxygen- be indicated as a temporary measure to allow the ation as a temporary measure. Polymask) 4–8 40–80 Ventilators Varying 21–100 Anaesthetic circuits Varying 21–100 Demand valves Varying 21–100 Hyperbaric oxygen Varying Varying . Edinburgh. the pressure and percentage of O2 can be 2. 28. Stagnant hypoxia Various methods for the administration of O2 The aim of therapy is to increase perfusion to the are shown in Table  16. foreign material. 4–12 35–65 Hudson.

Volume Andersson JPA. Hyperbaric Medical Society Workshop. 31st Undersea and 2. Journal of Lundgren CEG. Shagatay 3. London: 1. Journal of Applied Physiology 2009. Dickinson P. Salzano JV. Craig AB. Undersea and Hyperbaric Medical Society: tion and gas exchange in man. during underwater swimming. Springer Berlin. breath-hold diving. Causes of loss of consciousness Churchill Livingstone.64(3):142–7. Schaefer KE. Journal of Applied Gronning M. Michael Bennett. Prevalence and causes of loss Physiology 2002.6:86–99. Diving response and arterial oxygen Society. Drowning. Troland K. Physiology of Applied Physiology 1961. of consciousness in former North Sea occu- Caine D. . The physiology incorporated. Journal of Kensington. Oxygen. Circulatory adaptation to the requirements of life under more than one FURTHER READING atmosphere of pressure. Section 2.106(1):284–292. Ferrigno (eds). saturation during apnoea and exercise Sundal E.16:583–586.228 Hypoxia fraction of inspired O2 unless a reservoir bag is Lindholm P. Shallow water blackout. in breath-hold divers. Thorsen E. Neuropsychological pational divers. Circulation. Blenkam GD. Applied Physiology 1971. Irgens A. 1985. Effects of pressure on ventila. In: Handbook of Physiology.30(4).93(3):882–886. bral anoxia: a critical review. Kylstra JA. hold diving. Saltzman HA. In: Nunn’s Applied Resipratory Physiology. Journal of the International Neuropsychological Society This chapter was reviewed for this fifth edition by 2000. 7th edition. Heidelberg 2014:571–575. Chapter 11. 1965:1843–1873. Watson DG. DC: American Physiology EKA. International Maritime Health and neuropathological sequelae of cere. 2010. and this increases the risk of CO2 and pathophysiology of human breath- retention. Liner MH. Runow E. 2013. Washington. REFERENCES Lumb A. Lundgren CEG.

2 ATA. manifested by convulsions. there is a decrease in alveolar ing ourselves from oxygen toxicity are a testament and arterial carbon dioxide (CO2) buffering tension to the evolutionary pressure to use this highly caused by the reduction in CO2-carrying capacity reactive molecule. Increased oxygen concentration and increased ambient pressure lead to higher partial pressures of oxygen. A rise in the inspired oxygen of haemoglobin. Oxygen also has a major role in therapy of many diving disorders. oxygen may become toxic at an elevated the body. 17 Oxygen toxicity Introduction 229 Pathology 241 History 230 Prevention 242 Aetiology 232 Other manifestations of toxicity 243 Central nervous system toxicity (the Haematopoietic system 243 ‘Paul Bert effect’) 234 Eye 243 Clinical manifestations 234 Vasoconstriction 243 Pathology 238 Ear 243 Prevention 239 Cancer 244 Treatment 239 References 244 Pulmonary toxicity (the ‘Lorrain Smith effect’) 240 Further reading 244 Clinical manifestations 240 Oxygen toxicity is not encountered in routine scuba diving using compressed air. Although increased PIO2 has no direct PO2. Central nervous system toxicity. is potentially lethal in the diver. It can be delayed by intermittent exposure. Other physiological responses to 229 . Although essential for High PIO2 has several physiological effects on survival. reduce decompression obligations or prolong underwater time. Toxicity can be avoided by controlling the inspired partial pressure of oxygen and/or the dura- tion of exposure. is approximately 0. and the complex systems we have for defend. effect on ventilation. It is a ­consideration when higher partial pressures of oxygen are used in the inspired gas. Pulmonary toxicity is more likely in the longer exposures of saturation chamber diving or hyper- baric oxygen therapy. an increase in the environmental pressure or a combination of both will elevate the The normal partial pressure of oxygen (PO2) in air inspired PO2 (PIO2). Divers may use high-oxygen gas compositions to reduce inert gas narcosis. INTRODUCTION fraction (FIO2).

nopathy of prematurity in pre-term infants and ●● Therapeutic recompression. in 1775 Priestley was among threshold is 0. but did note a damaging effect on the lungs. Lavoisier and Sequin demonstrated that oxy- rebreathing equipment. oxygen toxicity of a substance he called ‘fire air’ that supported is possible in the following situations: combustion (later to be called ‘oxygen’ by Anton Lavoisier) following a similar experiment. whereas at higher pressures was free from ‘phlogiston’.230  Oxygen toxicity high oxygen include vagally mediated bradycardia ●● Saturation diving. near drowning). In diving.6 ATA oxygen.5 0 1 5 10 15 20 25 30 Time (hrs) Figure 17. lung damage.5 ATA.0 Inspired oxygen partial pressure (ATA) 4. . gen at 1 ATA does not alter oxidative metabolism ●● Use of high FIO2 mixtures. There is a small rate-dependent fall in decompression times. air that duration of exposure. and the pulmonary series of experiments. and with prolonged use). The CNS est in its possible therapeutic effects.1  Predicted human pulmonary and central nervous system (CNS) tolerance to high-pressure oxygen. sion. nary only. convulsions. eighteenth century and immediately excited inter- and only these are discussed in detail. to be released from a burning object1.0 it s CNS limits 1. toxic effects on cells of many other organs HISTORY have also been demonstrated. ●● Situations in which oxygen is used to shorten eral vessels. This speculated that ‘the animal powers be too soon delay enables high PO2 to be used for increasingly exhausted in this pure kind of air’.0 ary li m 2. In vitro. cardiac output. Following a threshold is above 1. in ●● Closed-circuit and semi-closed-circuit 1789. in 1772 short periods as the PIO2 rises (Figure 17. visual defects.55 ATA.0 Pu lm on 3.g. ●● Respiratory failure (e. pul. the first to suggest that there may be adverse monary toxicity is the limiting factor regarding effects of ‘dephlogisticated air’ – that is. red blood cell suppres. toxic effects on the central nervous Oxygen was ‘discovered’ in the latter half of the system (CNS) and lungs are of prime importance. 5. Carl Scheele had already postulated the existence In diving and diving medicine. a substance thought neurological toxicity is of prime concern.0 0. ●● Oxygen therapy for diving disorders (pulmo- High PIO2 is known to be associated with reti. Later.1). At 1. myopia and cataracts in adults. Priestley In both the CNS and lungs there is a latent had observed the rapid burning of a candle and period before the onset of detectable toxicity. and vasoconstriction of intracranial and periph. In fact.

in which he presented plained episodes of unconsciousness were noted the results of years of study of the physiological in divers using closed-circuit rebreathing oxygen effects of exposure to high and low pressures. Damant and Philips. Meanwhile. History 231 In 1878. but at 4 hours some subjects noted nausea and a sen- sation of impending collapse. Journal 1947. at lower pressures. This has become Smith effect. The His observations in more than 2000 exposures same effect could be produced by oxygen at 5 ATA. spheric pressure produced paraesthesiae.2)3. ther efforts to delineate the pulmonary limits of Pulmonary changes are also called the Lorrain exposure have been undertaken. Larks exposed to of experiments on oxygen poisoning (Figure 17.7 bar. changes in toxicity could place on the clinical use of oxygen. in 1939 Becker.1:667–672. inhibition of enzyme system He also noted that early changes are reversible and and the role of the endocrine system. II. in 1942. without CO2 the CNS. fur- that higher pressures shortened the time of onset. Workers have looked at such factors as the (approximately 1 ATA) for prolonged periods of role of inert gas and CO2. Lorrain Smith noted the aggravating effects of exercise and underwa- fatal pneumonia in a rat after exposure to 73 per ter exposure. many of his experiments were per- and clearly established the toxicity of oxygen on formed using rebreathing equipment. Freyseng and Clamann found that 65 hours  of The subject in the centre is breathing 100 per exposure to 730 mm Hg oxygen at normal atmo. form the basis of current oxygen diving limits. This showed that although oxygen is essential to sustain prompted Donald. changes in lung surfactant. air at 15 to 20 ATA developed convulsions. ­nausea Oxygen poisoning in man: I. (From Donald KW. the pathologist J. Donald carried out than 5 minutes at 7 ATA oxygen. ings were the marked variation of tolerance and In 1899. it is lethal at high pressures. He sets at what were considered safe depths. blockage of airways and time. two Royal Naval Officers. The chamber is pressurized with air to 3. increasingly important with saturation diving Although numerous animal studies were per- formed. some unex- La pression barometrique. In 1933. also known as the Paul Bert effect. Convulsive symptoms were reported at 16 and 13 minutes. At  3  ATA no effects were seen after 3 hours. 712–717. Smith was aware of the limitations that this atelectasis. Exposure at 4 ATA ­terminated in acute syncope after 43 minutes in one sub- ject and convulsions at 44 minutes in the other. That the dose was important was confirmed in 1941 when Haldane reported a convulsion in less Figure 17. cellular metabolism. Donald suggested a maximum safe cent oxygen at atmospheric pressure. Behnke then reported a series of exposures to hyperbaric oxygen. Bert recorded similar convulsions in other species Unfortunately. depth for oxygen diving of 8 metres. cent oxygen from a mask. to commence a series life.) . He con.2  In 1942 and 1943. evidence of the effect of high-pressure oxygen on humans was sparse until the 1930s. ducted further experiments on mice and gave the Research since the 1980s has been primarily first detailed description of pulmonary changes directed at elucidation of the mechanism of the resulting from moderately high oxygen tensions toxicity. At that time it was believed that 30 minutes of exposure at 4 ATA and 3 hours of exposure at 3 ATA were safe for men at rest. Also.2. He did measurement. British Medical and a decrease in vital capacity (VC). breathed oxygen at 4 ATA. Paul Bert published his pioneer work At the beginning of World War II. extensive testing for oxygen toxicity in divers. Among the more important find- not report respiratory damage1.

are highly oxidative. CO2 may play a role in chemical enzyme catalyzed reactions and are the lowering seizure threshold at the cellular level. In inactivating the enzyme (this may be important in animal studies. paraquat. These -SH groups. It is postulated that adjacent -SH groups are The characteristic feature of chronic pulmonary oxidized to form disulphide bridges (-S-S-). whereas hyperventi- are intermediates formed in many cellular bio. All these species of oxygen. There are a and the excess free radicals may then produce cell great many sites at which oxygen acts on metabolic damage. leading to the formation of excess precedes the convulsions. supplies of reduced glutathione (containing sul- tissue oxygenation and energy metabolism in the phydryl groups) to deal with the free radicals.232  Oxygen toxicity involving prolonged stays under increased ambient is the acceptance by oxygen of four ­electrons to pressure and the use of oxygen mixtures to shorten form water or a stable hydroxyl anion. brain. bleomycin and ozone have the development of cataracts). oxyhaemoglo- peroxide (H2O2) two electrons. hyperoxia has manganese) superoxide dismutase preserves pul- been demonstrated to depress cellular metabolism. dose-dependent effects in catalase. monary gas exchange during hyperoxic lung injury Many enzymes are inactivated by high PO2. Lithium (useful in the treatment selves) have developed antioxidant mechanisms of bipolar disorder) has proved to be effective in to cope with molecular oxygen exposure. changes induced by hyperoxia is a reduction in The oxygen free radical theory of toxicity is the endogenous output of GABA that results widely accepted as an explanation at the molecu. lation may be protective. One the respiratory chain and the enzymes involved in of the demonstrated consequences of enzymatic oxidative phosphorylation. our. inhibits the development of oedema. It was also shown to presence of hyperoxia these mechanisms may be prevent the decrease in brain GABA that normally overwhelmed. oxygen accepts a single electron and hydrogen At greater than 3 ATA PIO2. synaptic transmission. include agents are known to produce oxygen free radicals. Oxygen is a highly reactive element Two of these enzymes. superoxide dismutase and and has wide-ranging. These tions are peroxidation of lipid in cell membranes sites may involve cell membranes. aerobic organisms (e. referred to as AETIOLOGY oxygen radicals. These radicals predispose to convulsions. In the rat lung lithium reactive oxygen forms and direct cellular toxic. including the regulation of blood flow. Both have been demonstrated in rat brain nuclei. These effects are pressure dependent and are Hyperoxia may cause this system to be swamped. glyceraldehyde phosphate dehydrogenase (a key Gamma-aminobutyric acid (GABA) is a trans- enzyme in glycolysis). In the inhibiting convulsions in rats.g. thus oxygen toxicity is pulmonary fibrosis (see later). Examples of unwanted oxidation reac- pathways or on specific cellular functions. and protein oxidation in cell membrane and cyto- port’. as suggested by early workers. in baboons5. The  final reaction bin is not reduced on passing through capillaries . hypoventilation and CO2 inhalation damage (e. in the uncontrolled firing of excitatory nerves and lar level.g. the flavoprotein enzymes of mitter at CNS inhibitory nerve synapses. mitochondria or cell plasm. but result of the reduction of the oxygen molecule by more likely by influencing cerebral blood flow and electrons. Superoxide decompression time. brain levels of GABA appear to protect against and for this reason. Rather than causing an increase in metabo. and known to be susceptible. are involved in maintaining adequate the body. after hyperoxia4. Superoxide anion (O2−) is formed when hence the ‘dose’ of oxygen delivered to the brain. The production of a range of free radicals the development of convulsions. Agents that raise is a normal consequence of aerobic metabolism. unknown. Antioxidants such as glutathione have particularly those containing sulphydryl groups also been shown to offer some protection. (-SH). ‘active trans. convulsions. involved in the development of toxicity. ity through enzyme inactivation and structural Exercise. lipid peroxidation). Enzymes containing all been noted to produce pulmonary fibrosis. and peroxide can react to form the hydroxyl radi- cal OH-. Aerosolized (recombinant human lism. Cells have a system of enzymes to scavenge The precise mechanism of oxygen toxicity is these radicals called the tissue antioxidant system.

Thus. noradrenaline • Amphetamine • GABA • Acetazolamide Chemicals • Aspirin • Paraquat • Atropine • Ammonium chloride • Disulfiram Trace metals • Guanethidine • Iron • Copper ACTH. magnesium and superoxide dis- changes in acid-base balance may modify the syn. cortico- however. given in normal animals. In contrast. noise and other stressful situations also Atelectasis (collapse of alveoli so they are no affect CNS tolerance. aspirin. Light. tribute to pulmonary toxicity. Endocrine studies show that hypophysectomy ing 6 per cent FICO2 and does not cause convul. the general stress reac- longer ventilated) results from absorption of oxy.5 to amounts of inert gas in the inspired mixture. sympatho-adrenal system during convulsions. studies. atro- drome via neurogenic and endocrine mechanisms. This may be related to an activation of the ally enhance the onset of toxicity. it may actu. It does. sions in the presence of a normal PIO2. and more specifically adrenal hormones.1  Factors increasing oxygen toxicity Physiological states Gases • Physical exercise • Carbon dioxide • Hyperthermia • Nitrous oxide • Immersion • ? Inert gases • Stress response Hormones and neurotransmitters Pathological states • Insulin • Fever • Thyroxin • Congenital spherocytosis • ACTH • Vitamin E deficiency • Cortisol Drugs • Adrenaline. some anaesthetics. may gen during 100 per cent oxygen breathing and has have a role in enhancing CNS (and pulmonary) tox- been suggested as a contributory mechanism to icity. 6 mm Hg). and adrenalectomy protect against hyperoxia. among a host of agents that augment toxicity. lithium. If the inert gas is at narcotic levels. Convulsions have been shown to hasten the and toxicity also develops in the presence of inert onset of pulmonary oxygen toxicity in some animal gas. appear that the slight rise in PCO2 reduces tropin) and cortisone reverse this effect and. toxicity. adrenocorticotropic hormone. tect against pulmonary damage. gamma-aminobutyric acid. GABA. when the cerebral vasoconstrictive effects of hyperoxia. Table 17. Adrenergic-blocking drugs.1 contains a list of factors that increase gression of pulmonary oxygen toxicity when oxygen toxicity. Rat studies indicate that the risk of CNS not eliminate CO2. it is not an initiating factor. amphetamine and pentobarbital are Very high levels of inspired CO2 may actually pro. although related GABA. this route can- ­ same PO2. . Therefore. pine. Several observations suggest a role of the auto- oxygen toxicity in divers. Although atelectasis has nomic nervous system in modifying the degree of been demonstrated. Adrenaline. An equivalent rise is caused by breath. CO2 retention is unlikely to con. mutase have a protective effect. Table 17. Aetiology 233 and so is not available for the carriage of CO2 as comparing pure oxygen and diluted oxygen at the carboxyhaemoglobin. Human studies show no difference in the pro. enhance toxicity. Adrenocorticotropic hormone (ACTH. tion. The resultant increase in brain toxicity is enhanced by the presence of even small CO2 tension (PCO2) has proved to be small (2.

and it is the factor limiting depth impending convulsions (but see Lambertsen’s when oxygen supplementation is used.16). or 2. the PIO2 would have been 5. CASE REPORT 17. the diver from reaching a depth and duration at and any unusual symptom should be suspect. hiccups. Report 17. The cause of death. the other a 50 per cent mixture of oxygen and nitrogen (nitrox). Consciousness is main- TOXICITY (THE ‘PAUL BERT EFFECT’) tained up to the time of convulsion and there are apparently no changes in the electroencephalo- In diving. while the circuit from the yellow (nitrox) tank was unmarked.165:262–263. with his mouthpiece out of his mouth and ‘his fins [flippers] moving as if he was shiver- ing’ (as reported by another diver to the Coroner). This allowed the diver to switch from one tank to another rapidly. The two tanks were different colours. reproduced with permission. The diver wore a face mask and separate mouthpiece rather than a full-face mask. disturbance of special Clinical manifestations senses. sensations air is commonly used. A diving fatality due to oxygen toxicity during a ‘technical’ dive. the most dramatic of which is a grand 2  ATA. the circuit from the black (compressed-air) tank was marked with yellow tape. The regulator had a small tear and a bite mark in the mouthpiece. The body was carried up to 15-metre depth and then allowed to ascend freely as the other divers decompressed.7 ATA × 0. tinnitus. and only about half of persons pressed air. bradycardia. ©Copyright 1996. sure of nitrogen (see Chapter 15) usually prevents However.234  Oxygen toxicity CENTRAL NERVOUS SYSTEM mal–type convulsion. dazzle.5. Examination of the subject’s diving equipment revealed that he had been breathing the 50 per cent oxygen/nitrogen mixture for most of the dive (at 47 metres. Facial twitching is a common objective sign A wide range of symptoms and signs has been in chamber exposures to oxygen greater than described. muscular and 13). there is no reliable warning of sets are used.The Medical Journal of Australia. nose and mouth. twitching elsewhere. closed-circuit or semi-closed-circuit rebreathing In practice. Each tank had a separate first stage connected in an unusual fashion by a two-way switch. sickness (DCS) and air embolism (see Chapters 6 dilatation of pupils. (From Lawrence CH.85 ATA). High oxygen pressures are used in facial pallor. which the diver had had made by a local engineering shop. light-headedness. the effect of increased partial pres. Cardiopulmonary resuscitation was attempted. affected describe any premonitory symptoms. as determined by the Coroner. he was seen floating head down.) . hallucinations and confusion. which covers eyes. Towards the end of the 47-metre. dizzi- ing (see Chapter 62). and it signifies an imminent convulsion. incoordination. The which oxygen will become a problem (although most commonly reported signs and symptoms occasional reports can be found). lip twitching. unre- sponsive. are nausea. as there was no response. twitching of hand. 19-minute dive. paraesthesiae (espe- cially fingers). Medical Journal of Australia 1996. ‘Technical’ div. With com. description later). but abandoned after 43 minutes. the list of such manifestations is long. was drowning after oxygen toxicity. This switch supplied a single second-stage mouthpiece. dyspnoea. vertigo. sweating.1 A 47-year-old experienced underwater cave diver with no significant medical history was diving with two tanks – one containing compressed air. permits CNS toxicity (Case of impending collapse or uneasiness (dysphoria). vomiting. CNS oxygen toxicity is more likely when gram before convulsion. in which a higher FIO2 than ness. constriction of therapeutic recompression for decompression visual fields (tunnel vision).

Short dives may be safe at greater tion of hyperoxia and is not necessarily a sign of depths and prolonged ones at shallower depths cerebral toxicity. of the previously listed clinical features are much ●● Dysphoria. ●● Immersion in water rather than in air (e. retching and vomiting are particu. A convulsion is much more dangerous under water because of the added complications of drowning and pulmonary Many of these manifestations are associated barotrauma. Facial pallor is thought a maximum safe depth for pure oxygen diving at to result from the intense peripheral vasoconstric. a chamber). where convulsions are ●● Convulsions. Therefore. Exposure in a compression chamber fingers and toes do not necessarily indicate an is considered to be less hazardous for an equivalent impending convulsion. ●● Dizziness.g.8 ATA). ●● Nausea. Hypothermia is to develop. the greater the PO2 and the longer the on a stage – not battling swell. Many ●● Tunnel vision. about 10 metres. ●● Severe exercise. current and buoy- time of exposure. most authorities have set with other potential causes. the time of importance when oxygen is used to shorten to onset of symptoms cannot be related to a pre. decompression times in the water.g. the paraesthesiae in (Table  17. Shallower maximum safe range of tolerance among individuals.6 75 .2  US Navy oxygen depth time limits in water Normal operations Exceptional operations Depth (ft) Depth (m) Time (min) Depth (ft) Depth (m) Time (min) 10 3 240 30 9 45 15 4. Exposure in water rather than in dry chambers ●● Tinnitus. Factors lowering threshold to larly noted after prolonged exposures between 1 and central nervous system toxicity 2 ATA. prescribe oxygen vasoconstriction on peripheral nerves or simply a exposures at 18 metres (2. Central nervous system toxicity (the ‘Paul Bert effect’)  235 Lip ­twitching may be seen if a mouthpiece is being used. As well as the wide onset of symptoms. likely to hasten the onset of symptoms.2). rare. toxicity ●● Increased arterial carbon dioxide from any cause. Current decompression proce- after exposure and may represent an effect of local dures. Therefore. markedly decreases the tolerance to oxygen. if performed in chambers. Similarly. This observation is also day to day 7.6 150 35 10. An important aspect of toxicity is the great Exercise has also been shown to hasten the variation in susceptibility. the more likely is the toxicity ancy to maintain constant depth. e. more often the first manifestation. Nausea. Despite this ing decompression should be at rest. supported variation. Divers undergo- dictable depth or time of exposure. Table 17. They may persist for hours depth-time profile. there is depths have been set for ‘working’ as opposed to marked variation in one person’s tolerance from ‘resting’ dives on oxygen. and seizure is tight-fitting wetsuit. less apparent in the water. Central nervous system oxygen ●● Hypothermia. in any one diver. ●● Twitching (especially lips).7 25 20 6 110 40 12 10 25 7.

0 Acoustic hallucinations 0.0 Vertigo 8. and incoordi- nation of diaphragm activity in respiration may occur. divers.236  Oxygen toxicity CO2 build-up during exercise has been sug. especially about The danger of convulsions prevents divers the eyes. with inadequate absorbent systems and in poorly The following description of a typical convul- ventilated helmets and chambers.3  Incidence of symptoms resulting from exposure of divers to ‘end-point’ in water Symptoms 388 resting divers (%) 120 working divers (%) Convulsions 9. these phenomena increase The role of inert gas in the exacerbation of oxy.8 Nausea