ADivP 02 (A) Med

ADivP-2(A)/MDivP-2(A)
MULTINATIONAL GUIDE TO
DIVING MEDICAL DISORDERS
0410LP1003216
2000
i ORIGINAL
INTENTIONALLY BLANK
ii ORIGINAL
March 2001
PUBLICATION NOTICE ROUTING
1. ADivP-2(A)/MDivP-2(A), MULTINATIONAL GUIDE TO DIVING _________________

MEDICAL DISORDERS, is available in the Navy Warfare Publications _________________
Library. ADivP-2(A)/MDivP-2(A) is effective on receipt.
_________________
2. Document is written primarily for NATO medical officers but it should also _________________
be of use to other NATO personnel who may be involved in the supervision _________________
of diving or the emergency care of divers. As well as containing information _________________
about the pathogenesis, signs, symptoms and treatment of diving disorders,
_________________
the text contains details of diving procedures in order to give insight into the
way diving problems arise underwater and the actions divers take to avoid _________________
them. _________________
_________________
_________________
Navy Warfare Library Custodian
Navy warfare library publications must be made readily

available to all users and other interested personnel within the
U.S. Navy.
Note to Navy Warfare Library Custodian
This notice will assist you in providing information to cognizant personnel. It is not accountable.
IIa (Reverse Blank) ORIGINAL

NORTH ATLANTIC TREATY ORGANIZATION
MILITARY AGENCY FOR STANDARDIZATION (MAS)
NATO LETTER OF PROMULGATION
September 2000
1. ADivP-2(A)/MDivP-2(A), MULTINATIONAL GUIDE TO DIVING OPERATIONS is

a dual titled UNCLASSIFIED Allied Publication / Multinational Manual. The agreement of
nations to use this publication is recorded in STANAG 1372.
2. ADivP-2(A)/MDivP-2(A) is effective on receipt. It supercedes ADivP-2, which shall

be destroyed in accordance with the local procedure for the destruction of documents.
3. This MM may be released to a non-NATO nation by a NATO nation or command, on a

need to know basis, without further authorisation from MAS or NATO Headquarters. This
MM shall not be released by a non-NATO nation. The releasing nation is responsible for:
a. Providing updates of the publication to receiving nations as required.
b. Informing MAS when distributing this MM to other nations.
4. This MM shall not be posted on any freely accessible information or media facility.
5. Change proposals may be submitted by any nation either through a sponsoring NATO
nation or directly to UK as the NATO custodian.
iii ORIGINAL
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iv ORIGINAL
CHAPTER RECORD OF RESERVATIONS BY NATIONS

1 NONE
2 NONE
3 NONE
4 NONE
5 CA
6 CA
7 NONE
8 NONE
ANNEX CA, DA.
v ORIGINAL
NATION SPECIFIC RESERVATIONS

CA a. Para 0509: Canadian procedures may differ.
b. Para 0605 Subpara (4): Canadian procedures may differ.
c. Para 0610 and figure 6-1: Canadian procedures may differ.
d. Para 0612 Subpara (5): Canadian procedures may differ.
e. Para 0614: Canadian procedures may differ.
f. Annex C: (NATO Diving Incident Medical Record Form)-
Canada will use a national form.
DA Annex C: Denmark will not use the Diving Incident Medical
Record Form.
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viii ORIGINAL
RECORD OF CHANGES
Change date Date Entered Effective Date By Whom Entered
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x ORIGINAL
TABLE OF CONTENTS
CHAPTER 1 FITNESS TO DIVE
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0101
Medical Standards . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0102
Medications and Diving . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0104
CHAPTER 2 BREATHING GAS DISORDERS
SECTION 1 - RESPIRATORY GASES
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0201
Hypoxia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0202
Oxygen Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0203
Hypocapnia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0204
Hypercapnia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0205
SECTION 2 - INERT GASES
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0206
Nitrogen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0207
Helium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
0208
Hydrogen and Other Inert Gases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0209
SECTION 3 - CARBON MONOXIDE
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0210
Causes and Prevention of Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . 0211
Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0212
Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0213
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0214
CHAPTER 3 BAROTRAUMA
SECTION 1 - INTRODUCTION
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0301
SECTION 2 - EAR, NOSE AND THROAT BAROTRAUMA
ENT Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0302

Sinus Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0303
External Ear Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0304
Middle Ear Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0305
xi ORIGINAL
Alternobaric Vertigo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0306

Caloric Vertigo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0307
Middle Ear Oxygen Absorption Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0308
Inner Ear Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0309
Dental Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0310
SECTION 3 - PULMONARY BAROTRAUMA
Pulmonary Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0311

Pulmonary Barotrauma of Descent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0312
Pulmonary Barotrauma of Ascent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0313
Interstitial Emphysema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0314
Arterial Gas Embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0315
Pneumothorax . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0316
SECTION 4 - BAROTRAUMA OF OTHER TISSUES
Face Mask Barotrauma of Descent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0317

Drysuit Barotrauma of Descent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0318
Whole Body Barotrauma of Descent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0319
Gastrointestinal Barotrauma of Ascent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0320
CHAPTER 4 ACUTE DECOMPRESSION ILLNESS
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0401
Inert Gas Exchange in Body Tissues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0402
Decompression Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0403
Decompression Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0404
Mixed Gas Diving . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0405
SECTION 2 - PATHOGENESIS
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0406
Sources of Gas Bubbles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0407
Distribution of Gas Bubbles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0408
Bubble Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0409
Predisposing Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0410
SECTION 3 - PRESENTATION
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0411
Descriptive Terminology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0412
Additional Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0413
Summary Table . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0414
xii ORIGINAL
CHAPTER 5 MANAGEMENT OF DIVING ACCIDENTS
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0501
SECTION 2 - MEDICAL SUPPORT OF DIVING OPERATIONS
Provision of Medical Support . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0502

Diving Medical Officer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0503
Occasions for Consulting a Diving Medical Officer . . . . . . . . . . . . . . . . . . . . . . . . . 0504
SECTION 3 - FIRST AID MEASURES
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0506
Rescue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0507
Clinical Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0508
First Aid Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0508
First Aid Treatment of Acute Decompression Illness - Flow Chart . . . . . . . . . . . . . 0509
SECTION 4 - EVACUATION
Command and Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0510

Evacuation Considerations and Requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0511
Portable Recompression Chambers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0512
SECTION 5 - INVESTIGATION OF DIVING ACCIDENTS
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0513
CHAPTER 6 THERAPEUTIC RECOMPRESSION
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0601
Principles of Therapeutic Recompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0602
Therapeutic Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0603
Adjunctive Treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0604
SECTION 2 - GUIDELINES FOR HYPERBARIC THERAPY
Hyperbaric Treatment Facilities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0605

Preparations for Hyperbaric Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0606
General Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0607
xiii ORIGINAL
SECTION 3 - TREATMENT SCHEDULES
Omitted Decompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0608

Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0609
Decompression Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0610
NATO Therapeutic Recompression Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0611
National Therapeutic Recompression Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0612
Non-Standard Treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0613
Recompression Therapy Abort Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0614
SECTION 4 - CARE IN THE RECOMPRESSION CHAMBER
Chamber Attendants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0615

Recompression Chamber Practice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0616
Chamber Treatment of Oxygen Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0617
SECTION 5 - MANAGEMENT AFTER INITIAL RECOMPRESSION
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0618
Treatment of Refractory Decompression Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0619
National Protocols for the Treatment of Refractory Decompression Illness . . . . . . . 0620
Flying After Therapeutic Recompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0621
Return to Diving After Decompression Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0622
CHAPTER 7 THE LONG TERM HEALTH EFFECTS OF DIVING
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0701
Dysbaric Osteonecrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0702
Chronic Hearing Loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0703
Chronic Neurological Damage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0704
Pulmonary Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0705
Other Chronic Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0706
CHAPTER 8 OPERATIONAL HAZARDS
SECTION 1 - THERMAL PROBLEMS
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0801
Hypothermia and Hazards of Cold Water Diving . . . . . . . . . . . . . . . . . . . . . . . . . . . 0802
Local Hypothermia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0803
Heat Stress and Hazards of Warm Water Diving . . . . . . . . . . . . . . . . . . . . . . . . . . . 0804
xiv ORIGINAL
SECTION 2 - DIVING IN POLLUTED WATER
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0805
Hazard Identification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0806
Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0807
Support System and Body Protection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0808
Operating and Handling Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0809
Use of Atmospheric Diving Suits or Small Manned Submersibles . . . . . . . . . . . . . . 0810
SECTION 3 - HAZARDOUS MARINE LIFE
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0811
Predatory Marine Life . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0812
Venomous Marine Life . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0813
SECTION 4 - OTHER HAZARDS
Near Drowning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0814

Underwater Blast Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0815
Underwater Noise and Sonar Transmissions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0816
Otitis Externa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0817
Caustic Cocktail . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0818
Disorientation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0819
Disinfection of Diving Equipment in Contact with Saliva . . . . . . . . . . . . . . . . . . . . 0820
xv ORIGINAL
ANNEXES
ANNEX A National Authorities Responsible for Initiating Treatment of Diving

Casualties and Emergency Contact Numbers.
ANNEX B Diving Casualty Signal Status Report Code.
ANNEX C NATO Diving Incident Medical Record Form.
ANNEX D Neurological Examination.
ANNEX E National Authorities for Guidance on the Hazards of Pollution.
ANNEX F Glossary of Medical Terminology.
ANNEX G Belgian Navy Therapeutic Recompression Tables.
ANNEX H Canadian Navy Therapeutic Recompression Tables.
ANNEX I Danish Navy Therapeutic Recompression Tables.
ANNEX J French Navy (Gers) Therapeutic Recompression Tables.
ANNEX K German Navy Therapeutic Recompression Tables.
ANNEX L Greek Navy Therapeutic Recompression Tables.
ANNEX M Italian Navy Therapeutic Recompression Tables.
ANNEX N Royal Netherlands Navy Therapeutic Recompression Tables.
ANNEX O Norwegian Navy Therapeutic Recompression Tables.
ANNEX P Portugese Navy Therapeutic Recompression Tables.
ANNEX Q Spanish Navy Therapeutic Recompression Tables.
ANNEX R Turkish Navy Therapeutic Recompression Tables.
ANNEX S Royal Navy Therapeutic Recompression Tables.
ANNEX T United States Navy Therapeutic Recompression Tables.
ANNEX U Medical Equipment for Recompression Therapy.
xvi ORIGINAL
ANNEX V National Specialists for Diving Accident Autopsies.
ANNEX W National Depth - Time Limits for Cerebral O2 Toxicity.
ANNEX X Bibliography
xvii ORIGINAL
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xviii ORIGINAL
PREFACE
ADivP-2(A)/MDivP-2(A), the Allied Guide to Diving Medical Disorders, is written primarily

for NATO medical officers but it should also be of use to other NATO personnel who may be
involved in the supervision of diving or the emergency care of divers. As well as containing
information about the pathogenesis, signs, symptoms and treatment of diving disorders, the text
contains details of diving procedures in order to give insight into the way diving problems arise
underwater and the actions divers take to avoid them. A glossary of medical terms is included
for non-medical personnel.
The key function of a NATO manual is to provide a common base of terminology and procedures
so that NATO nations may operate together with the minimum of difficulty. The most important
information presented within this manual is therefore not that which describes the causes and
mechanisms of individual diving medical conditions, but that which describes the common
terminology that can be used to transfer information about cases between doctors of different
nations. This is particularly true for decompression illness and the new descriptive terminology
which is described in Chapter 4. Another major advance facilitating the interoperability of
NATO Nations is the agreement on a common treatment schedule for therapeutic recompression
of decompression illness which is described in Chapter 6. At the annexes, this manual also
contains emergency contact information for obtaining specialist diving medical assistance from
each NATO Nation, and details are given of individual Nation’s therapeutic recompression tables.
Many of the recommendations about diving procedures put forward in manuals of diving
medicine are based simply on empirical observations or theoretical knowledge about diving
disease. To further the understanding of the origins of these recommendations, interested parties
are referred to the general reference texts and key individual references that are quoted at the
completion of each section and at Annex F.
xix ORIGINAL
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xx ORIGINAL
CHAPTER 1
FITNESS TO DIVE
ORIGINAL
CHAPTER 1
FITNESS TO DIVE
CONTENTS
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0101
Medical Standards . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0102
Medications And Diving . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0103
1-1 ORIGINAL
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1-2 ORIGINAL
CHAPTER 1
FITNESS TO DIVE
0101. Introduction
a. Medical standards for diving differ considerably from those of other military
activities because of the unique environmental and physical conditions encountered
underwater. Medical conditions can affect fitness to dive either because they present an
unacceptable risk of death or injury during a dive, or risk the mission, or because the
severity of the condition is worsened by diving. Fitness to dive is also affected by those
medical conditions which may result in the onset of symptoms which could be confused
with decompression illness and therefore make diagnosis and treatment difficult.
b. An individual’s fitness to dive rests on a number of factors including the extent of

abnormalities or the severity of disease present, the individual’s response to treatment
and the type of diving in which he is to participate. A completely comprehensive list of
conditions which permanently exclude a person from diving can not be provided
therefore, but this chapter aims to outline those conditions that are generally accepted
internationally to alter a person's fitness to dive. Assistance should always be sought
from national advisers in operational diving medicine in all cases of doubt. To assist in
decisions on fitness to dive, the conditions listed below in italic print are generally
considered to be disqualifying conditions for diving applicants. Those conditions in
normal print may be permitted in individual cases.
c. Below are medical fitness criteria for entry into diving. Should injury or illness
afflict a trained diver, the determination of his or her fitness to return to diving should
be made by a specialist in diving medicine.
d. Medical criteria for fitness to return to diving after acute decompression illness is
given in Article 0622.
0102. Medical Standards

The following conditions listed by system may affect an individuals fitness to dive:
a. Skin. Any untreated chronic or acute skin disorder, including the cutaneous
manifestations of systemic disease, other than mild, localised conditions will disqualify
a candidate. Particular care should be paid to the condition of the skin of career divers.
The presence of an acute skin infection renders a candidate unfit for saturation diving
until this is effectively treated. Chronic skin infections are incompatible with saturation
diving.
1-3 ORIGINAL
b. Ears, Nose and Throat
(1) Chronic or recurrent sinusitis; chronic or recurrent outer or middle ear

discharge; severe allergic conditions of the upper respiratory tract; Meniere’s
disease or previous stapedectomy render a candidate unfit to dive. Cases of viral
labyrinthitis and nasal polyps are temporarily unfit to dive and should be referred
to an ENT specialist. Perforation of the tympanic membrane, unless adequately
healed or surgically corrected, is also a disqualifying condition.
Note. Any history of ENT surgery should be referred for specialist assessment
before diving.
(2) Hearing should be assessed by audiometry and be of an acceptable standard on

entry into diving. Subsequently, reduced categories of hearing may be acceptable
on the advice of an ENT specialist. The tympanic membrane must be clearly seen
on examination and evidence of adequate ear clearing obtained at initial
examination by observing the ear drum while a Valsalva manoeuvre is performed.
(3) Exostoses are acceptable providing they do not occlude the external auditory
canal.
c. Respiratory System
(1) Symptomatic asthma is an excluding criterion. Where there is a history of

reversible, obstructive airways disease, cases should be judged individually and
considered fit to dive only when pulmonary function testing, performed at a
specialist laboratory, shows no evidence of abnormal bronchial ability in response
to a challenge or bronchodilatation.
(2) Chronic obstructive airways disease or areas of potential air trapping such
as lung cysts, bullae and blebs; pleural effusion; lung fistula; bronchiectasis;
pulmonary fibrosis; neoplasm and unresolved pneumothorax are conditions which
are incompatible with diving.
(3) A history of perforating chest injury or open chest surgery may disqualify if
there is evidence of residual pulmonary or pleural scarring. The reason for the
surgery should be established.
(4) Pulmonary tuberculosis, unless limited to a calcified primary focus is

incompatible with diving. Equally, active sarcoidosis or other restrictive
pulmonary conditions preclude diving.
(5) A history of spontaneous pneumothorax precludes diving. Pneumothorax

other than spontaneous pneumothorax may be acceptable providing at least three
months have elapsed since resolution and it has been determined by detailed
pulmonary assessment that no residual impairment remains.
1-4 ORIGINAL
d. Cardiovascular System
(1) Any organic heart disease; coarctation of the aorta; any history or evidence
of coronary insufficiency or myocardial ischaemia, even if treated by coronary
artery bypass grafting are normally disqualifying conditions. Cardiomegaly should
disqualify unless it is established by specialist investigation to be the consequence
of athletic training. Ventricular septal defects, or significant right-to-left shunts are
incompatible with diving unless surgically corrected.
(2) Cases of valvular stenosis or regurgitation should be referred for specialist

opinion and, if necessary, surgical correction before a decision on fitness to dive can
be made.
(3) All arrhythmias except sinus arrhythmias and ventricular extrasystoles which
disappear with increasing heart rate are normally disqualifying, and should be
referred for specialist opinion. They are normally cause for rejection.
(4) Conduction defects are normally cause for rejection. However, first degree
and right bundle branch block may be acceptable providing it is determined by
specialist opinion that it is an isolated finding.
(5) Peripheral vascular insufficiency is cause for rejection.
(6) Blood pressure should be recorded with the candidate in the supine position
and using the fifth Korotkov sound. It should not exceed 140/90 at entry to diving.
A reading of up to 150/95 may be permissible in trained divers in the absence of
stigmata of hypertension.
(7) Symptomatic haemorrhoids and severe varicose veins are relative

contraindications to diving.
e. Alimentary System. Chronic inflammatory bowel disease; acute or chronic active

hepatic disease; symptomatic gall bladder disease are incompatible with diving.
Abdominal wall herniation is a contraindication to diving unless adequately repaired.
Peptic ulceration also disqualifies unless there is endoscopic evidence of healing and the
candidate has been asymptomatic without medication for at least six months.
f. Musculo-skeletal System
(1) The presence of juxta-articular (‘A’) lesions of dysbaric osteonecrosis

diagnosed by x-ray precludes further diving. A shaft (‘B’ lesion) excludes
participation in experimental diving.
1-5 ORIGINAL
(2) Divers must have unimpeded mobility and dexterity. Any limitation should
be assessed on the basis of the diver's ability to perform his work and, particularly,
its possible impact on his safety. It is important to take into account work which the
diver may be required to undertake on the surface, such as operating from small
boats in adverse weather conditions.
(3) Successful surgery for prolapsed intervertebral disc is usually unacceptable

unless the neurological examination is normal and there is no functional
impairment.
(4) Fractures of the skeletal axis or long bones, with or without internal fixation,
are not normally an impediment to diving provided that there is adequate union and
function.
g. Nervous System
(1) The initial neurological examination must be particularly rigorous with

attention paid to documenting variations from normal. Similar care should be taken
at periodic examinations to confirm that no hitherto unrecognised neurological
change has taken place. This is particularly important if there has been an episode
of dysbaric illness since the preceding diving medical examination.
(2) When first detected significant neurological abnormalities may merit specialist
referral. To avoid possible confusion over a subsequent diagnosis of a dysbaric
disorder, it is important that any abnormal findings are reported to the diver and
clearly recorded in the diver’s Log Book.
(3) Conditions with the potential to preclude diving are as follows:
(a) Epileptic fits including petit mal and idiopathic partial seizures. Febrile
convulsions up to the age of five should not be considered a bar to diving.
(b) A history of depressed skull fracture, penetrating head injury or

intracranial surgical procedure.
(c) Severe speech impediment preventing clear communication.
(d) Migraine unless mild and unaccompanied by visual, speech, motor or

sensory disturbance and not requiring frequent suppressive medication.
(e) Divers with a history of head injury need to be assessed individually and,
where appropriate, referred for specialist neurological opinion. Severe head
injuries (resulting in loss of consciousness for more than 30 minutes or
resulting in post-traumatic amnesia of more than one hour) will disqualify a
candidate for entry into diving unless he or she is neurologically intact and has
been symptom-free, requiring no medication, for at least twelve months
following the injury. Lesser injuries similarly may constitute a bar to diving
if there are residual neurological signs.
1-6 ORIGINAL
(f) A history of bacterial or viral meningitis or encephalitis is compatible

with diving providing that the candidate has been asymptomatic for at least 12
months and there is no evidence of neurological sequelae.
h. Mental Health. A history of past or present psychiatric or psychological disorder,

including abuse of alcohol or drugs, should be considered a contraindication to diving
unless the examining physician having taken specialist advice as required, that it is of
a minor nature and unlikely to recur.
i. Visual Standards. Visual standards vary between Nations and National standards
should apply. In determining visual fitness to dive, it is important to consider that it is
frequently the tasks that a diver may be required to undertake on the surface rather than
underwater which may limit an applicant’s fitness to be a diver.
(1) Visual field should be normal using the confrontation test.
(2) Fundi should be normal.
(3) A history of detached retina generally precludes diving.
(4) National standards with respect to the use of soft contact lenses should apply.
(5) Radial keratotomy renders a diver unfit to dive for at least 12 months
following the operation. Following specialist review, diving may be permitted by
some Nations.
j. Fitness and Fatness
(1) Divers should be aerobically fit. This may be assessed using a variety of
maximal or sub-maximal tests.
(2) Divers should not weigh more than 20% above the relevant figure from
national standard service height/weight tables unless it is considered that, in view
of the person's morphology and muscular development, the excess is not due to fat.
Candidates who are found to be unfit to dive on the basis of obesity should be
referred for dietary advice.
k. Dental Standards. Candidates require a high standard of dental fitness. Teeth

should be sound or adequately restored and the gum and supporting bones should be
healthy. Malformations or missing dentition should be assessed in the light of the
candidate's ability to retain a mouthpiece and effect an adequate seal, bearing in mind
that dentures should be removed when diving. Crowns and fixed bridgework must be
scrutinised annually. If in doubt as to a candidate’s dental fitness, the examining
physician should seek the opinion of a dental officer.
1-7 ORIGINAL
l. Genito-urinary System
(1) Symptomatic renal calculi and malformations of the urinary system will be
cause for rejection unless adequately treated.
(2) Sexually transmitted diseases preclude diving until successfully treated. HIV
testing does not form part of a routine diving medical examination. The
employment of those known to be HIV positive will be in accordance with national
policy.
m. Endocrine System. Detailed specialist investigation of endocrine conditions is not

normally required. However, where abnormalities are detected clinically, these should
be investigated and referred to a specialist for a decision of fitness to dive. Diabetes
mellitus is a contraindication to diving.
n. Haematological Conditions. Requirements for blood screening vary between

Nations. Abnormalities revealed should be referred for specialist assessment. Sickle cell
anaemia is a contraindication to diving.
o. Female Divers. Standards for males apply equally to females, however, pregnancy
is a disqualifying condition.
0103. Medications and Diving
a. A diver’s continued fitness to dive when suffering from an illness that requires drug
medication demands careful consideration as either the illness itself or the drugs
involved may compromise diving safety. Drug side effects such as hypotension may
directly affect fitness to dive, but medications also have a variable and in some cases
unpredictable effect under pressure.
b. The information available about the safety of most drugs for use in the hyperbaric
environment is very sparse and physicians are therefore advised to take a very cautious
approach. If necessary, a diving medicine specialist should be consulted before ruling
on the suitability of a drug for use in diving. Some examples of drugs prescribed for
common conditions and their suitability are given in the following list:
(1) Analgesics stronger than paracetamol may exert CNS effects that potentiate
nitrogen narcosis. Antihistamines, sedatives and all other drugs affecting the CNS
are incompatible with safe diving.
(2) Antibiotics are believed to be safe if the condition for which they are used is
not a bar to diving.
(3) Antimalarials may be prescribed with cautions about possible side effects.
1-8 ORIGINAL
(4) NSAIDs, The use of Non Steroidal Anti Inflammatory Drugs for the
prevention of DCI is controversial.
(5) Beta-adrenergic blockers, frequently prescribed for hypertension, may reduce

exercise tolerance which could be critical in an emergency situation.
(6) Diuretics may cause electrolyte imbalance or dehydration which would

potentiate decompression illness.
(7) Oral contraceptives were postulated to cause an increased risk of

decompression sickness due to their effects on coagulation. This effect is probably
not significant with low dose agents.
(8) Pseudoephedrine, a frequently used component of anticongestant preparations,

has numerous potentially dangerous side effects which include tachycardia, anxiety,
tremor, vertigo and drowsiness. Rebound congestion after the effects of topical
decongestants have worn off can also become a problem during the ascent from a
dive.
(9) Alcohol, any diver exhibiting the acute effects of alcohol intoxication is unfit
to dive.
1-9 ORIGINAL
Bibliography:
MILLER K W, PATON W D M, SMITH D A and SMITH E B (1973). The Pressure Reversal

of General Anaesthesia and the Critical Volume Hypothesis. Molecular Pharmacology 9,131-
143.
1-10 ORIGINAL
CHAPTER 2
BREATHING GAS DISORDERS
ORIGINAL
CHAPTER 2
CONTENTS
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0201
Hypoxia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0202
Oxygen Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0203
Hypocapnia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0204
Hypercapnia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0205
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0206
Nitrogen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0207
Helium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0208
Hydrogen and Other Inert Gases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0209
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0210
Causes and Prevention of Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . 0211
Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0212
Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0213
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0214
2-1 ORIGINAL
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2-2 ORIGINAL
CHAPTER 2
0201. Introduction
a. This section deals with the gases of respiration, oxygen and carbon dioxide, and
examines the causes and effects of divers suffering from too much or too little of each
of these gases. Physiological problems often occur underwater because divers are
exposed to the pressures of depth. However, some of the difficulties related to
respiratory processes can occur at any time because of an inadequate supply of oxygen
or inadequate removal of carbon dioxide from the tissue cells. Depth may modify these
problems for the diver, but the basic difficulties remain the same. Fortunately, the diver
has normal physiological reserves to adapt to environmental changes and he is only
marginally aware of small changes. The extra work of breathing underwater reduces the
overall ability to do heavy work at depth, but moderate work can be done with adequate
equipment at the maximum depths currently achieved in diving.
b. An understanding of normal respiratory physiology, the control of respiration and

the physical restrictions of underwater breathing equipment is required, and a basic
review of these topics follows in this introduction.
c. Respiration
(1) Cellular energy is obtained by the process of respiration. Respiration is the

process of transforming oxygen and fuel into carbon dioxide during oxidation,
releasing energy and water. The lungs provide the necessary diffusing surface for
oxygen uptake and carbon dioxide release, with deep tissue exchange of these gases
by the circulating blood.
(2) The complete process of respiration includes six important phases:
(a) Ventilation of the lungs with fresh air (Breathing)
(b) Exchange of gases between blood and air in lungs (Diffusion)
(c) Transport of gases by blood (Circulation)
(d) Exchange of gases between blood and tissue fluids (Diffusion)
(e) Exchange of gases between the tissue fluids and cells (Diffusion)
(f) Use and production of gases by cells (Metabolism)
2-3 ORIGINAL
(3) If the process of respiration stops or is seriously reduced, tissue cells will
either die or cease to function normally. Nervous system tissue is extremely
susceptible to interruption of oxygen or fuel, making the brain a sensitive target
organ.
d. Alveolar/Capillary Gas Exchange. Oxygen and carbon dioxide are exchanged in

the alveolar air spaces via extensive thin-walled pulmonary alveolar capillary beds. The
gas partial pressures in the blood leaving the lung is approximately equal to that of
aveolar air. Alveolar ventilation and perfusion are critical determinants of adequate gas
exchange.
e. Respiratory Tract Ventilation (Breathing). Ventilation of the respiratory system

is important in establishing the proper composition of gases in the alveoli for exchange
with the blood. The following definitions help in understanding respiration (Figure 2-1).
(1) Respiratory Cycle. One complete breath consisting of an inspiration and

exhalation, including any pause that may occur between the movements.
(2) Respiratory Rate. The number of complete respiratory cycles that take place
in one minute. At rest, a normal adult will have a respiratory rate of approximately
12 to 16 breaths per minute.
(3) Total Lung Capacity (TLC). The total volume of air that the lungs can hold
when filled to capacity. It is normally between five and six litres.
(4) Vital Capacity. The volume of air that can be expelled from the lungs after a
full inspiration. The average vital capacity is between four and five litres.
(5) Tidal Volume. The volume of air moved in or out during a single normal
respiratory cycle. At rest, the tidal volume generally averages about one-half litre.
Tidal volume increases considerably during physical exertion. Inspiratory and
expiratory reserve volumes make up the difference between a tidal volume and the
vital capacity.
(6) Ventilatory Dead Space. That portion of the respiratory system that contains
no alveoli and in which little or no gas exchange of gas between air and blood takes
place. In an adult, ventilatory dead space normally amounts to less than 0.2 litre.
The end-expiratory dead space is rebreathed in the following inspiration. It is
essential to minimise volume of dead space in diving equipment in order to allow
the diver maximum effective tidal volume.
2-4 ORIGINAL
Fig. 2-1. Lung Volumes
f. Lung Volumes. In Fig 2-1 the heavy line is a tracing derived from a subject
breathing to and from a sealed recording bellows. Following several normal tidal
breaths, he inhales maximally, then exhales maximally. The volume of air moved
during this maximal effort is called the vital capacity. During exercise, the tidal volume
increases, using part of the inspiratory and expiratory reserve volumes. The tidal volume,
however, can never exceed the vital capacity. The residual volume is the amount of air
remaining in the lung after the most forceful expiration. The sum of the vital capacity
and the residual volume is the total lung capacity.
g. Control of Breathing. The alveolar ventilatory minute volume increases with

exercise to control blood levels of carbon dioxide, pH and oxygen.
(1) Carbon dioxide receptors in the brainstem respiratory area control the rate and
depth of breathing to maintain circulating carbon dioxide levels within the normal
range.
(2) Oxygen receptors in the carotid arteries and aorta stimulate the respiratory
centre to increase breathing rate and depth if oxygen falls to a very low level. These
receptors, however, are not as sensitive as those for carbon dioxide.
(3) In addition to the mechanisms above, the respiratory centre may be stimulated
by emotions such as excitement and fear and also by voluntary control.
(4) The regulation of ventilation is sufficiently effective in healthy adults at sea

level that the partial pressures of oxygen and carbon dioxide in arterial blood are
maintained at approximately the same levels during work as at rest.
2-5 ORIGINAL
h. Breathing Resistance and Dyspnoea
(1) The ability to perform useful work underwater depends on the diver’s ability
to move enough gas in and out of his lungs to provide sufficient oxygen to the
muscles and to eliminate metabolically produced carbon dioxide. There are two
main physical factors which impede this ability: increased gas density and
resistance of the breathing apparatus. Even in a dry hyperbaric chamber without a
breathing apparatus, the increased gas density may cause divers to experience
shortness of breath (dyspnoea). If breathing air, this dyspnoea usually becomes
apparent at very heavy workloads at depths below 35m. If breathing helium-oxygen,
dyspnoea usually becomes a problem at heavy workloads in the 280-300m range.
At great depths (450-500m), dyspnoea may occur even at rest.
(2) The breathing limitations imposed by the underwater breathing apparatus

result from two main sources: flow resistance and static lung load.
(a) Flow resistance is due to the obstruction of flow of gas through tubes,
hoses, and orifices in the diving equipment. With increased density, a higher
gas supply pressure must be maintained to keep gas flowing at the same rate.
Increased pulmonary work by the diver is required at higher gas densities to
maintain the required alveolar minute ventilation. When flow resistance
increases to the extent that maximum pulmonary work is required to maintain
alveolar ventilation, further increases in resistance will result in hypercapnia.
(b) Static lung load is the result of breathing gas being supplied at a different
pressure than the hydrostatic pressure surrounding the lungs. Variations in
static lung loading can occur with changes in the relative position of the lungs
and the breathing regulator. With the regulator below the lungs, gas will be
supplied at a pressure above that of the lungs, whereas with the regulator
above the lungs, it will be supplied at a lower pressure. With closed-circuit
breathing apparatus, the static lung loading varies with the position of the
counterlung compared to that of the lungs. Excessively high static loads
(either positive or negative) may cause dyspnoea without any increase in the
partial pressure of carbon dioxide in blood.
(3) Although efforts are made to ensure that all UBA used by NATO nations meet
adequate breathing standards so that flow resistance and static lung loading
problems are minimized, all UBA have their limitations and divers must have
sufficient experience to recognize them. If the UBA does not impede ventilation,
the diver’s own pulmonary system may limit his ability to ventilate. Whether due
to limitations of the equipment or limitations imposed by the diver's own respiratory
system, the end result may be symptoms of hypercapnia or dyspnoea without
increased carbon dioxide blood levels. This is commonly referred to as ‘beating the
lung’ or ‘overbreathing the rig’. Most divers will decrease their level of exertion
when they begin to experience dyspnoea, but in some cases, depending on the depth
and type of UBA, the dyspnoea may continue to increase for a period of time after
stopping exercise. When this occurs, the inexperienced diver may panic and begin
to hyperventilate which increases the dyspnoea. The situation rapidly develops into
2-6 ORIGINAL
one of severe dyspnoea and uncontrollable hyperventilation. In this situation, if

even a small amount of water is inhaled, it can cause spasm of the muscles in the
larynx called laryngospasm, followed by asphyxia and possible drowning. The
proper reaction to the dyspnoea is to stop exercising, ventilate the UBA if possible,
take even, controlled breaths until the dyspnoea subsides, evaluate the situation, and
then proceed carefully.
0202. Hypoxia
Hypoxia is defined as a deficiency of oxygen which is required for tissue cells to
maintain normal function.
a. Causes of Hypoxia. There are many causes of oxygen deficiency which mostly
involve interference with the normal oxygen supply to the tissues:
(1) Lower partial pressure of oxygen in the breathing gas supply. It is the partial
pressure rather than the proportion of oxygen in the inspired gas which is important.
Air contains about 21% oxygen and thus provides an oxygen partial pressure of
about 0.21 bar at the surface. A PO2 of 0.14 bar will cause the onset of hypoxic
symptoms and if the PO2 is reduced to 0.11 bar, most individuals will become
hypoxic to the point of being nearly helpless. Consciousness is usually lost at about
0.10 bar, and at much below this level, permanent brain damage and death will
probably result. In diving, lower proportions of oxygen in the breathing gas can be
used as long as the ambient pressure is sufficient to maintain an adequate PO2. For
example, 5% oxygen would result in a PO2 of 0.20 bar at 30m. On ascent, however,
the diver would rapidly experience hypoxia if the oxygen percentage was not
increased.
(2) Dilution Hypoxia can occur with closed or semi-closed underwater breathing
apparatus. A diver using these types of equipment continually removes oxygen
from the gas held inside the counterlung by the process of respiration. Carbon
dioxide and nitrogen are exhaled but the former is removed by an absorbent. If
oxygen is the only gas being used, the diver will commence the dive breathing it at
100% concentration but this will be gradually reduced as nitrogen is washed out of
the body. Normally, insufficient nitrogen is washed out to result in a hypoxic gas
mixture. If mixed gas is being breathed, it is occasionally possible for exhaled
nitrogen to render the mixture in the counterlung hypoxic near the surface.
However, operating drills are designed to ensure that this does not occur.
(3) Blockage of all or part of the pulmonary system air passages. This may be
caused by vomit, secretions, water, foreign objects or, very rarely, as a result of
mediastinal emphysema. Interference with ventilation of the lungs may also result
from pneumothorax or paralysis of the respiratory muscles from spinal cord injury.
These inhibit breathing and cause both hypoxia and hypercapnia. This condition
is correctly called asphyxiation. Drowning is the commonest cause of asphyxiation
and the ultimate cause of death in the majority of diving fatalities.
2-7 ORIGINAL
(4) Decreased oxygen exchange at the alveolar/capillary membrane. This may

be caused by the accumulation of fluid in the tissues (oedema), a mismatch of blood
flow and alveolar ventilation, lung damage from near-drowning or smoke
inhalation, bronchospasm or obstruction of the pulmonary vascular tree caused by
overwhelming showers of bubbles in the venous circulation - pulmonary
decompression illness or ‘chokes’.
(5) Interference with blood transportation of oxygen may be caused by anaemia,

carbon monoxide poisoning, or inadequate blood flow.
(6) Interference with oxygen utilization at the cellular level. In the diving setting
this may be caused by carbon monoxide poisoning.
(7) Failure of Respiratory Control. This is caused by suppression of the

respiratory centres as may occur in severe narcosis, decompression illness and
hypocapnia associated with breath-hold diving.
(8) Hypoxia in Breath Hold Diving. The brainstem respiratory center triggers
inspiratory effort primarily as a result of increased arterial partial pressure of carbon
dioxide (PaCO2) and is much less sensitive to decreased partial pressure of oxygen
(PaO2). Hyperventilation causes a reduction in PaCO2 and extends the time
required for it to increase to a level sufficient to stimulate inspiration, but does not
correspondingly increase the PaO2. During descent, air in the lungs is compressed
and the partial pressure of all constituent gases increases, temporarily increasing
PaCO2. As the breath-hold dive progresses, the oxygen partial pressure falls as
oxygen is metabolised but continues at an adequate level during descent and bottom
phases. The lowered PaCO2 delays the stimulus to breathe during these phases.
Upon ascent however, both the PaO2 and PaCO2 fall rapidly, in accordance with
Boyle’s and Dalton’s laws, and the PaO2 may fall below that required to maintain
conciousness. If the PaCO2 was initially driven sufficiently low by
hyperventilation, the chemoreceptors may not provide an adequate stimulus to
breathe. Loss of conciousness in these circumstances may lead to drowning.
(9) Paradoxical Blackout of the Combat Swimmer. Loss of consciousness may

occur when combat swimmers switch from oxygen to air on completing a dive.
This loss of consciousness is thought to be due to cerebral hypoxia resulting from
two factors:
(a) An intense vasoconstriction of the cerebral blood vessels due to prolonged

hyperoxia. (See Paragraph 0203.c.- Cerebral Oxygen Toxicity).
(b) Depression of the respiratory centres due to a reduction of PaCO2

associated with hyperventilation during exercise. The resulting loss of
consciousness is generally short-lived and has no after-effects. However, if
the diver is in the water, there is a risk of drowning.
2-8 ORIGINAL
b. Clinical Features
(1) Severe hypoxia will stop the normal function of all cells in the body and will
eventually kill them. However, the cells of brain tissue are by far the most
susceptible to its effects and unconsciousness and death can occur from brain
hypoxia before the effects of hypoxia on other tissues become apparent.
(2) There is no reliable warning of the onset of hypoxia. It can occur

unexpectedly, making it a particularly serious hazard. A diver who loses his gas
supply is in obvious danger of hypoxia, but the diver will be aware of this hazard
and usually has time to do something about it. A diver who gradually uses up the
oxygen in a closed-circuit rebreathing rig, on the other hand, may have little
warning of impending loss of consciousness.
(3) When hypoxia develops, the pulse rate and blood pressure are commonly
increased. A small increase in ventilation may occur, which may be marked if the
hypoxia is complicated by a simultaneous rise in inspired carbon dioxide. The diver
may feel slightly euphoric. Other symptoms and signs of hypoxia which may be
noticed either by the diver or a colleague include:
(a) Lack of concentration.
(b) Lack of muscle control.
(c) Inability to perform delicate or skilled tasks.
(d) Drowsiness.
(e) Weakness.
(f) Loss of consciousness.
c. Prevention. Because of its insidious nature and potentially fatal outcome,

prevention of hypoxia is essential. In open-circuit SCUBA and helmet diving, hypoxia
is unlikely unless the gas supply has too low an oxygen content. On mixed-gas
operations, strict attention must be paid to gas analysis, cylinder line-ups, and predive
checkout procedures. In closed- and semi-closed-circuit UBA, the counterlung should
be purged in accordance with Operating Procedures, and oxygen sensors, if fitted, should
be monitored closely throughout the dive.
2-9 ORIGINAL
d. Treatment
(1) A diver suffering from severe hypoxia must be rescued promptly. Hypoxia’s
interference with brain functions will produce not only unconsciousness but also
failure of the respiratory control centres. If a victim of hypoxia is given gas to
breathe with an adequate oxygen content before his breathing stops, he will usually
regain consciousness shortly and recover completely. For SCUBA divers, this
usually involves bringing the diver to the surface and administering oxygen. For
surface-supplied mixed-gas divers, it involves switching to an alternative gas supply
or employing a ‘bail out’ bottle.
(2) Divers who have suffered prolonged hypoxia are likely to require full
cardiorespiratory resuscitation.
0203. Oxygen Toxicity
a. If O2 is breathed at a high partial pressure (greater than 0.5 bar) for long periods it
becomes toxic to the lungs causing pulmonary oxygen toxicity. If a very high partial
pressure of O2 is breathed (greater than about 1.7 bar), even for short periods of time, it
may rapidly become toxic to the central nervous system causing cerebral oxygen
toxicity.
b. Pulmonary Oxygen Toxicity
(1) For practical purposes, pulmonary oxygen toxicity will not arise from normal
air ‘bounce’ diving to less than 50 metres. However, there are circumstances where
pulmonary O2 toxicity may occur. Although the time and depth limitations imposed
on O2 breathing sets are designed to avoid this, tolerance to O2 may vary
considerably both within and between individuals. Diving near the time/depth
limits, particularly when such dives are performed repetitively, may provoke
pulmonary O2 toxicity in sensitive individuals. Patients being treated with fully
extended oxygen treatment tables may also experience pulmonary O2 toxicity,
particularly where repeated treatments are applied.
(2) Clinical Features. These often start with a tickling sensation in the throat
which is worse on inspiration and which may provoke coughing. After a few hours
of continued O2 exposure, the tickle is gradually replaced by a sensation of
substernal burning and coughing becomes uncontrollable. Shortness of breath
eventually prevents even mild exertion. In sensitive individuals, the first symptoms
of toxicity may be provoked by breathing 100% O2 bar for as little as three hours.
Pulmonary oxygen toxicity results in a progressive reduction of vital capacity.
(3) Unit Pulmonary Toxic Dose. Where prolonged exposure to hyperbaric oxygen
is necessary, such as during recompression therapy, an estimate of the reduction in
vital capacity can be calculated. A UPTD calculation table is provided below.
2-10 ORIGINAL
PO2 − 0.5
A formula for calculation of k value is provided k =
0.5
Table 2-1. UPTD Calculation
PO2 k PO2 k PO2 k

(Bar) (Bar) (Bar)
0.5 0.00 1.3 1.48 2.1 2.64
0.6 0.26 1.4 1.63 2.2 2.77
0.7 0.47 1.5 1.78 2.3 2.91
0.8 0.65 1.5 1.93 2.4 3.04
0.9 0.83 1.7 2.07 2.5 3.17
1.0 1.00 1.8 2.22 2.6 3.31
1.1 1.16 1.9 2.36 2.7 3.44
1.2 1.32 2.0 2.50 2.8 3.57
(a) The calculated k value is multiplied by the period of time, in minutes,

spent at each oxygen partial pressure. These values are them summed to
generate the total UPTD value for the exposure. A standard NATO Table VI
for a single exposure without extension is equivalent to 625 UPTD’s.
Generally, a dose of 1425 UPTD is considered to be the upper limit of
acceptable exposure resulting in approximately a 10% reduction in vital
capacity. This limit is advisory and may be exceeded under the instructions
of a Diving Medical Specialist.
(b) Normally, a complete recovery from the effects of pulmonary O2 toxicity

can be expected. The time taken for recovery depends largely on the extent
of the exposure and where there is a substantial decrement of vital capacity,
this may take days or weeks.
(4) Treatment. Reduce the concentration of O2 in the breathing mixture,

preferably to 0.2 Bar. Depending on their severity, symptoms will gradually
diminish over a few hours and complete resolution can be expected within a few
days.
2-11 ORIGINAL
c. Cerebral Oxygen Toxicity
(1) Pathogenesis
(a) Cerebral oxygen toxicity can occur when divers are continuously exposed
to more than about 1.7 atmospheres of oxygen for a period of minutes to hours
but the actual mechanism remains unknown in spite of many theories and
much research. Susceptibility to central nervous system oxygen toxicity
varies from person to person. Individual susceptibility will vary from time to
time, and for this reason divers may experience cerebral oxygen toxicity at
exposure times and pressures previously tolerated. Because it is the partial
pressure of oxygen itself that causes toxicity, the problem can occur when
mixtures of oxygen with nitrogen or helium are breathed at depth. Oxygen
toxicity is influenced by the density of the breathing gas and the characteristics
of the diving system used. Thus, allowable limits for oxygen partial pressures
differ to some degree for specific diving systems. Closed system oxygen
rebreathing systems require the lowest partial pressure limits, whereas surface-
supplied helium-oxygen systems permit slightly higher limits. Other external
factors contributing to the development of oxygen toxicity are:
i. Carbon dioxide retention
ii. Immersion in water. Divers can tolerate a higher partial pressure of

oxygen during dry, chamber dives.
iii. High work rates during oxygen exposure.
iv. Hyper- or hypothermia.
(b) The symptoms of cerebral O2 toxicity may, paradoxically, be made

transiently worse when the PiO2 is reduced. If an early symptom of oxygen
toxicity occurs and the diver’s inspired PO2 is lowered, he or she may still
convulse up to two or three minutes later. This is the so-called ‘Off
Phenomenon’. It should be noted that this is different to paradoxical cerebral
ischaemia. (See Paragraph 0202.a and d.).
(c) There is no evidence that a diver's susceptibility to oxygen toxicity is

increased after an episode of cerebral O2 toxicity although divers may be more
inclined to notice warning symptoms during subsequent exposures to oxygen.
(2) Clinical Features
(a) The symptoms and signs are highly variable and, as there is no fixed O2
exposure at which toxicity becomes apparent and susceptibility varies both
between individuals and within the same person from day to day, there is no
cerebral equivalent of the UPTD. It is not unusual for the first sign of cerebral
O2 toxicity to be a grand mal convulsion. At the height of the seizure the body
2-12 ORIGINAL
becomes rigid, known as the ‘Tonic’ phase of the convulsion. This is

followed by the ‘Clonic’ phase during which random impulses to various
muscle groups may cause uncontrolled jerking movements and occasionally
violent thrashing, which lasts for a minute or so. As with other grand mal
convulsions, there may be a loss of continence and the patient may be injured
by a fall, violent movement or tongue biting. If the diver is in the water
(rather than a chamber), there is a risk of drowning if the mouthpiece is
expelled. During the tonic phase of the convulsion, there is a risk of
pulmonary barotrauma if the diver loses control of buoyancy and ascends or
if a buddy attempts to assist the diver to the surface. After the convulsion,
brain activity is depressed and a post-convulsive (postictal) depression
follows. The patient is usually unconscious and quiet for a while, then
semiconscious and restless. He will then usually sleep on and off, waking up
occasionally though still not fully rational. The depression phase may last for
as little as 10 minutes, or as long as an hour or more. At the end of this period,
the patient will often become suddenly alert and complain of no more than
fatigue, muscular soreness, and possibly a headache. After an oxygen toxicity
convulsion, the diver will usually remember clearly events up to the moment
when consciousness was lost, but will remember nothing of the convulsion
itself, and little of the postictal phase.
(b) Sometimes, recognition of early symptoms may provide sufficient

warning to permit a reduction in oxygen partial pressure and prevent the onset
of more serious symptoms. These early symptoms may not always appear
however and most are not exclusively symptoms of oxygen toxicity.
Twitching of facial muscles, particularly around the mouth, is perhaps the
clearest warning of oxygen toxicity. Other warning symptoms are shown
below:
i. Nausea - May be intermittent.
ii. Vomiting.
iii. Dizziness.
iv. Abnormalities of vision or hearing - Tunnel vision (loss of ability to

see things to the sides) is one of the more frequent visual symptoms.
v. Difficulty in breathing - the diver may have air huger, may sense an
increase in breathing resistance for no apparent reason, or may have
trouble taking a full breath into his lungs.
vi. Anxiety, confusion, irritability.
vii. Unusual fatigue.
2-13 ORIGINAL
viii. Incoordination, clumsiness.
ix. A ‘cold sweat’.
(3) Treatment
(a) If a tethered diver thinks he has symptoms of oxygen toxicity, the diver
should inform the Diving Supervisor who should take action to lower the
oxygen partial pressure by decreasing the diver's depth or venting the UBA
with a gas of lower oxygen content. If the diver convulses, the UBA should
be ventilated immediately with a gas of lower oxygen content.
(b) If a convulsion occurs underwater, the diver’s depth should be kept as

constant as possible until at least the tonic phase of the convulsion subsides.
He should then be returned to the surface where the breathing apparatus
should be removed and he should be placed in fresh air to recover. If further
convulsions occur, which is rare, sufficient restraint should be used to prevent
self-injury. Do not force the mouth open but ensure that an airway is
maintained once the convulsion has subsided. The casualty should be kept
under observation by his fellow divers or in a sick bay for at least 12 hours
following a convulsion.
(c) Because of the risk of pulmonary barotrauma if a diver surfaces during an

oxygen convulsion, the possibility of decompression illness should be
considered in the event of subsequent neurological abnormalities. The period
of confusion and disorientation which follow a seizure may complicate the
diagnosis but recompression is indicated in cases of doubt.
(d) If a convulsion occurs in a compression chamber, one attendant should be

able to keep the patient from thrashing against hard objects and being injured.
Complete restraint of the patient’s movements is neither necessary nor
desirable. The oxygen mask shall be removed immediately. It is not
necessary to force the mouth open to insert a bite block while a convulsion is
taking place. After the convulsion subsides and the mouth relaxes, a clear
airway should be maintained until the diver regains consciousness. Breathing
almost invariably resumes spontaneously. (See also paragraph 0617).
(4) Prevention. The prevention of acute toxic accidents caused by oxygen consists
in keeping within the pressure safety limit which varies according to the type of
apparatus. When the use of a high partial pressure of oxygen is advantageous or
necessary, divers should take sensible precautions, such as being sure the breathing
apparatus is in good order, avoiding excessive exertion, and heeding abnormal
symptoms that may appear.
0204. Hypocapnia
a. Hypocapnia is defined as a reduction in the partial pressure of carbon dioxide in the

blood and tissues.
2-14 ORIGINAL
b. Carbon dioxide is continuously formed by tissues as a waste product of metabolism

which requires elimination by exhalation in expired air. Hypocapnia, a reduction in
PaCO2, only occurs when the rate of elimination of CO2 exceeds its rate of production
in the tissues - hyperventilation. This may occur voluntarily (such as prior to a breath
hold dive) or as a consequence of stress or anxiety.
c. The symptoms of hypocapnia are rarely more than lightheadedness and vague
tingling sensations but additional symptoms such as weakness, headaches, numbness,
faintness, and blurring of vision may appear later with prolonged hyperventilation. The
anxiety which can occur with the development of these symptoms may lead to a further
increase in ventilation and severe hypocapnia which results in muscular spasms, loss of
consciousness, and eventually, shock. Severe cases are extremely rare in diving. The
symptoms of hypocapnia can be confused with those of neurological decompression
illness and may present a diagnostic challenge particularly in anxious trainee divers.
0205. Hypercapnia
a. Hypercapnia is defined as the presence of a raised level of carbon dioxide in the

blood and tissues.
b. Causes. In diving operations, an excess of carbon dioxide in the blood is generally

the result of a raised concentration in the breathing gas or in the body as a result of:
(1) Insufficient ventilation of a diver in surface-supplied equipment which results

in a build-up of CO2 in the mask or helmet. This is the most common cause of
hypercapnia and commonly occurs when the diver turns down an air control valve
to reduce background noise and enhance communications with the surface.
(2) Inadequate CO2 scrubbing when using closed-circuit equipment.
(3) Inadequate ventilation. This can be caused by several factors:
(a) Improper breathing techniques eg ‘skip breathing’: repetitive short breath

holds between each breath used by some SCUBA divers trying to conserve gas
supplies. The raised PO2 generally encountered in diving can reduce the
uncomfortable shortness of breath that accompanies inadequate ventilation
thus allowing hypercapnia to develop.
(b) Excessive dead space in the equipment caused by malfunction of non

return valves or poor design.
(c) Excessive breathing resistance caused by increased gas density, the

malfunction or poor design of breathing equipment, or wearing a constricting
suit which inhibits the diver taking a full breath.
2-15 ORIGINAL
(4) Asphyxia. This condition is caused by complete ventilatory failure leading to

hypercapnia and hypoxia. (See also paragraph 0202.)
(5) Carbon Dioxide Retention. In a small proportion of the normal population the
ventilatory response to a raised PaCO2 is blunted. This generally causes no
difficulty until the individual is required to exercise hard using breathing apparatus.
In such circumstances, the PaCO2 may rise to a point where the toxic effects of CO2
become pronounced and this may be in the absence of usual warning sign of
hyperventilation.
c. Prevention
(1) Ensure that the CO2 absorbent is fresh, dry, dust free and correctly packed.
(2) Do not exceed the endurance of the canister.
(3) Ensure that the breathing technique is correct. Rapid, shallow breathing can
result in CO2 retention.
d. Clinical Features
(1) An increase PaCO2 stimulates the respiratory centre to increase the breathing
rate and volume, and the heart rate is also often increased. Ordinarily, the increased
respiratory drive is sufficiently uncomfortable to warn a diver before the CO2
becomes toxic. However, variables such as work rate, depth, and the composition
of the breathing mixture may produce changes which mask the effects of excess
carbon dioxide. This is especially true in closed-circuit equipment when failure or
expenditure of the carbon dioxide absorbent material allows a carbon dioxide build
up in the presence of a high PO2. Above a Pi02 of 0.5 bar, the shortness of breath
usually associated with excess carbon dioxide may not be excessive and may go
unnoticed by the diver, especially if he is breathing hard because of exertion.
Additionally, nitrogen narcosis can mask the condition because a diver under the
effects of narcosis may not notice differences in his breathing rate. For these
reasons, a diver must be particularly alert for any marked change in his breathing
comfort or cycle (such as shortness of breath or hyperventilation) as a warning of
hypercapnia.
(2) The symptoms of severe hypercapnia are similar to those of hypoxia:

confusion, inability to concentrate, drowsiness, loss of consciousness, and
convulsions. Such effects become more severe as the degree of hypercapnia
increases. A diver breathing a gas containing 0.1 bar of CO2 will generally lose
consciousness after a few minutes. Breathing 0.15 bar of CO2 for any length of time
will cause muscular spasms and rigidity.
2-16 ORIGINAL
(3) High partial pressures of CO2 cause cerebral vasodilation. This may partially
explain the headaches often associated with carbon dioxide intoxication, although
these headaches are more likely to occur following the exposure than during it. The
increase in cerebral blood flow which results from vasodilatation is thought to
explain why CO2 toxicity is associated with cerebral oxygen toxicity. CO2 toxicity
is also believed to be associated with an increases risk of decompression illness, but
the reasons for this are less clear.
(4) The following list summarises some of the warning symptoms of hypercapnia
which an alert diver may recognise before become unconscious:
(a) Breathlessness.
(b) Nausea, headaches, anxiety.
(c) Sweating, flushing of the skin and palpitations.
(d) Light headedness, collapse.
d. Treatment
(1) Treatment of hypercapnia consists entirely on reducing the burden of CO2.

This can be achieved by a combination of two methods: firstly be encouraging the
diver to stop all activity and relax to minimise the production of CO2 and secondly
ensuring that the inspired gas has as low a concentration of CO2 as possible.
(2) If the diver is using a counterlung, he or she should flush through and breathe
deeply. If surface supplied equipment is being used, signal for more air and
increase mask or helmet ventilation - if this brings no relief the diver should abort
the dive. Simply ascending should bring some improvement as the PCO2 will fall
with decreasing hydrostatic pressure.
(3) A diver who loses consciousness because of excess carbon dioxide in his
breathing medium, and does not aspirate water, generally revives rapidly when
given fresh air. If not, medical attention should be obtained as soon as possible.
Because the first sign of hypercapnia may be unconsciousness and it may not be
readily apparent whether the cause is hypoxia or hypercapnia, oxygen should be
provided. This will also serve to reduce the hypercapnia. Divers surfacing
unconscious and who do not rapidly recover, should be treated as if they have acute
decompression illness. Hypercapnia alone does not normally result in permanent
brain injury.
2-17 ORIGINAL
0206. Introduction
a. Inert gases combine with other elements only with difficulty. However, when a
breathing gas mixture is inhaled, the inert gas component diffuses into the blood in the
same way as oxygen and, via pulmonary venous blood, is distributed to the tissues.
When breathed under pressure, these gases may be toxic, particularly to the nervous
system, resulting in narcosis.
b. The physical properties of inert gases influence both their diffusibility and solubility
in tissues. The rate at which a gas diffuses is inversely proportional to the square root
of its molecular weight (Graham’s Law) and therefore gases with a low molecular
weight diffuse rapidly. The narcotic effect of the inert gases correlates with their
molecular weight and solubility in lipids. The advantages and disadvantages of the
diluent gases commonly used in breathing mixtures are discussed below.
0207. Nitrogen
a. Nature. Atomic weight 14

Molecular weight 28
Colourless, odourless, tasteless, chemically inert gas
78.03% of the atmosphere by weight
4.7 times more soluble in olive oil than water.
b. Advantages. Fresh air is readily and cheaply compressed to provide a suitable

breathing mixture for dives of up to 50m depth.
c. Disadvantages. Nitrogen has several disadvantages.
(1) Toxicity
(a) Nitrogen narcosis or ‘raptures of the deep’ was first described by Junod
in 1835 although the effect was only attributed to nitrogen by Behnke 100
years later.
(b) Clinical Features. The clinical features of nitrogen narcosis can be

summarised as impaired intellectual and neuromuscular performance, changed
mood and behaviour, similar to alcohol intoxication, hypoxia and early
anaesthesia. Individuals vary in their susceptibility to nitrogen narcosis and
some habituation to the effects can be achieved by frequency of exposure.
There is no danger from the narcotic effect itself and the effect wears off
rapidly on reducing depth. The hazard is that a narcosed diver may act
inappropriately, sustain an injury or drown while his concentration is
impaired.
As a rough guide, the table below shows the effects of nitrogen narcosis
breathing air at various pressures:
2-18 ORIGINAL
ppN2 EAD
1.6-3-2 bar 2-4 bar Mild impairment of performance on unpractised tasks.

Mild euphoria.
3.2 bar 4 bar Reasoning and immediate memory affected more than motor co-
ordination and choice reactions.
Delayed response to visual and auditory stimuli.
3.2-4.8 bar 4-6 bar Laughter and loquacity may be overcome by self control.
Idea fixation and over-confidence. Calculation errors.
4.8 bar 6 bar Sleepiness, hallucinations, impaired judgement.
4.8-6.4 bar 6-8 bar Convivial group atmosphere. Talkative.

Dizziness occasionally reported. Terror reaction in some.
Uncontrolled laughter approaching hysteria in some.
6.4 bar 8 bar Severe impairment of intellectual performance.

Manual dexterity less affected.
6.4-8.0 bar 8-10 bar Cross delay in response to stimuli.

Diminished concentration. Mental confusion.
8.0 bar 10 bar Stupefaction, euphoria, hyperexcitability.

Severe impairment of practical activity and judgement.
Mental abnormalities and memory defects.
Deterioration in handwriting.
Almost total loss of intellectual and perceptive faculties.
>8.0 bar >10 bar Severe hallucinations.

Unconsciousness. Death.
(c) Potentiating Factors. The narcotic effect of nitrogen is potentiated by the

following factors:
i. Alcohol.
ii. Sedatives.
iii. Cold.
iv. Fatigue.
v. Hard work.
2-19 ORIGINAL
vi. Apprehension and anxiety.
vii. Hypercapnea.
(d) Prevention
i. Depth limitation according to the experience of the diver.
ii. Work-up dives. These do not necessarily prevent narcosis but they
enable the diver to become habituated to the effect.
iii. Deep dives should be conducted using an alternative inert gas in the
breathing mixture. Helium is the usual choice.
(e) Treatment
i. Decrease the depth of the dive.
ii. In serious cases, which are very rare, the diver should surface. The
effects of narcosis resolve rapidly once the inspired partial pressure of
nitrogen is reduced.
(2) Decompression Illness. As a gas with a slower rate of diffusion and a higher
solubility than helium, nitrox mixtures are more likely to cause DCI for any dive
requiring decompression stops according to diffusion based models of DCI.
(3) Density. Although not generally a problem in the air diving range, this
property makes the gas more difficult to breathe with increasing pressure. This
leads to a reduced work capacity and CO2 retention.
0208. Helium
a. Nature. Atomic Weight 4.003

Colourless, odourless, non-toxic inert gas.
Found in natural gas wells of some countries.
1.7 times more soluble in olive oil than water.
b. Advantages. Helium has several advantages for use as a component of a breathing

mixture. It is non-toxic and is therefore used as a replacement for nitrogen at depths
when nitrogen becomes toxic. It is seven times less dense than nitrogen which lowers
the work of breathing at high pressures.
2-20 ORIGINAL
c. Disadvantages
(1) Thermal Conductivity. The thermal conductivity of helium is 5.7 times that
of nitrogen. Respiratory heat loss becomes increasingly significant with increasing
depth and endurance of dives. Heating of the breathing mixture as well as the diver
may be required for deep dives.
(2) Communications. Helium causes a significant distortion to human speech

(similar to Donald Duck). An electronic process is often required to make it
intelligible.
(3) Expense. Helium is considerably more expensive than other commonly used
diluent gases. Recovery systems are commonly fitted to saturation dive complexes
to permit the gas to be recycled.
(4) Availability. Not every hyperbaric chamber has Helium available as a

treatment option.
0209. Hydrogen and Other Inert Gases
a. Hydrogen. Hydrogen (atomic weight 1, molecular weight 2) is the lightest gas and
is half the density of helium. It is non-toxic and it is readily available at low cost from
natural gas supplies or the electrolysis of water. These factors have lead to experiments
to assess its use as a replacement for helium in very deep dives. The major disadvantage
of hydrogen is its combustibility. If the concentration of oxygen in a hydrox mixture
exceeds 4% there is a risk of explosion. Consequently, it can only be employed in
saturation diving. Hydrogen also causes similar speech and thermal problems as helium.
Finally, in deep dives, hydrogen has been shown to be highly narcotic and has induced
a psychotic state in divers at pressures in excess of 25 ATA.
b. Other inert gases have properties which prohibit their use in diving. Neon (atomic
weight 20) is less narcotic than nitrogen but its production by the fractional distillation
of liquid air is very costly. Argon (atomic weight 40), Krypton (atomic weight 84) and
Xenon (atomic weight 131) are all denser and more narcotic than nitrogen.
2-21 ORIGINAL
INTENTIONALLY BLANK
2-22 ORIGINAL
0210. Introduction
Carbon Monoxide (CO) is a colourless, odourless, non-irritant gas produced as a product
of the partial combustion of hydrocarbons with oxygen. It is an extremely toxic gas which
renders cells hypoxic by displacing oxygen from haemoglobin and other haem-containing
molecules and thereby interfering with cellular metabolism. If it is allowed to contaminate a
diver’s breathing gas, a partial pressure of as little as 0.002 bar can prove fatal. Thankfully
accidental CO poisoning of divers is rare, but chamber operators may be called upon to treat
cases that have been caused by self-poisoning with car exhaust fumes or accidental poisoning due
to faulty central heating systems.
0211. Causes and Prevention of Carbon Monoxide Poisoning
a. CO poisoning from the contamination of breathing gas is avoidable. The most

common cause of contamination is due to the intake of an air compressor drawing in
exhaust fumes from its own internal combustion engine. For this reason air intakes must
be sited upwind and well away from the compressor's engine or other exhaust fumes.
b. CO contamination can occur from within a compressor itself through use of an

incorrect lubricating oil which forms CO as a breakdown product. A defective
compressor may generate local ‘hot spots’ which cause otherwise safe oils to break
down and liberate CO. Compressors must therefore be serviced and maintained to the
highest standards.
c. For these reasons, breathing gas must be obtained from authorised, reputable
sources to ensure that the gas supplied is free of contamination.
0212. Pathogenesis
CO binds with haemoglobin approximately 200 times more readily than oxygen. It also
binds with other haem-containing molecules, such as myoglobin and cytochrome a3. These
effects serve to render metabolically active tissues hypoxic. Additionally, there is evidence that
CO injures endothelium, particularly in the cerebral vasculature, and may have an action on cells
similar to nitric oxide. Because of the multifocal action of CO, measurement of COHb alone
may be misleading as an indicator of the severity of poisoning which is more fully assessed by
the clinical status of the patient.
0213. Clinical Features
a. The clinical features of CO poisoning are similar to those of hypoxia but also
include: pallor (the classical ‘cherry red’ lips are rare), severe headache, dizziness,
nausea and vomiting, reduced visual acuity and, eventually, loss of consciousness. In
a diving setting, unconsciousness can occur without reliable warning signs when the
PiCO is sufficiently high to cause rapid poisoning or where the toxic effects of CO have
a rapid onset. These effects may be masked by a high PiO2. This is because more
oxygen is carried in plasma and CO may be displaced from haemoglobin by competition
from increased numbers of oxygen molecules. Consequently, the onset of symptoms
may be delayed until the diver begins to ascend at which point the diver may lose
consciousness with little warning.
2-23 ORIGINAL
b. When toxicity develops more gradually, symptoms such as tightness across the
forehead, bitemporal headache, nausea or vomiting may be warning symptoms.
c. A further feature of CO poisoning is the development of late neuropsychiatric

deficits. These long term sequelae usually take the form of personality changes or
memory difficulties and may develop within days or weeks of exposure. Treatment of
acute poisoning with hyperbaric oxygen has been shown to reduce the incidence of these
sequelae.
0214. Management
a. The immediate treatment of carbon monoxide poisoning consists of removing the

diver from exposure and providing as close to 100% oxygen as possible. This can be
achieved by use of a tight-fitting mask and demand regulator.
b. Hyperbaric oxygen should be provided as early as possible. Short oxygen tables

such as NATO Tables V or VI are appropriate for this purpose. Deeply unconscious
patients needing ventilatory assistance should be intubated and stabilised prior to
recompression.
c. The source of breathing gas for a diver suspected of suffering carbon monoxide
poisoning should be identified, isolated and analysed. Only if it is shown to be free from
contamination should it be used by other divers.
d. If after the first treatment, symptoms and signs remain, a second treatment with
HBO is indicated. Further treatments may be required until either the patient is
asymptomatic or treatment results in no further sustained improvement.
2-24 ORIGINAL
CHAPTER 3
BAROTRAUMA
ORIGINAL
CHAPTER 3
BAROTRAUMA
CONTENTS
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0301
ENT Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0302

Sinus Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0303
External Ear Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0304
Middle Ear Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0305
Alternobaric Vertigo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0306
Caloric Vertigo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0307
Middle Ear Oxygen Absorption Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0308
Inner Ear Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0309
Dental Barotrauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0310
Pulmonary Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0311

Pulmonary Barotrauma of Descent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0312
Pulmonary Barotrauma of Ascent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0313
Interstitial Emphysema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0314
Arterial Gas Embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0315
Pneumothorax . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0316
Face Mask Barotrauma of Descent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0317

Drysuit Barotrauma of Descent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0318
Whole Body Barotrauma of Descent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0319
Gastrointestinal Barotrauma of Ascent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0320
3-1 ORIGINAL
INTENTIONALLY BLANK
3-2 ORIGINAL
CHAPTER 3
BAROTRAUMA
0301. General
a. The tissues of the body can withstand tremendous pressure. Divers have made open-
water, working dives to deeper than 300 msw and, in experimental situations, have been
exposed to a depth of 701 msw. Despite the pressure experienced at such depths, the
great majority of medical complaints arising from the effects of pressure changes occur
in the shallow phases of dives. The cause is barotrauma, which is tissue injury arising
from changes in the volume of a gas phase in, or adjacent to, tissues which occurs with
changes in pressure in accordance with Boyle’s Law.
b. The injury which arises from a reduction in volume of gas in a diver's equipment
or body cavity as pressure is increased is called barotrauma of descent or squeeze. The
opposite effect, caused by the expansion of gas is called barotrauma of ascent. It is
recognised that changes in volume caused by changes in pressure are greatest near the
surface. During descent from the surface to 10 msw, the pressure doubles, and the
volume of gas in a sealed, soft-walled container halves. In contrast, during a 10 msw
descent from 30 msw to 40 msw the pressure increases by 25% and the volume of gas
in a sealed, soft-walled container is reduced by 20%. Therefore, the effects of
barotrauma are more likely to occur near the surface. A sustained pressure difference
across delicate tissues of as little as 5 kPa may be injurious. However, it is important
to recognise that barotrauma rarely occurs in divers who have normal anatomy and
physiology, are using properly functioning equipment and correct diving procedures.
c. There are four conditions that must be present for barotrauma to occur:
(1) There must be a gas-filled space. Most of the body is fluid and not
compressible. However, gas naturally present within the body (e.g. sinus) or next
to the body (e.g. face mask) can cause injury to body tissues when its volume
changes in accordance with Boyle’s Law.
(2) The space must have mainly rigid walls. Where the walls are elastic, such as
in the bowel, the compression or expansion of gas will not cause tissue injury
because there will be little or no pressure difference generated between the gas and
surrounding tissue.
(3) The space must be enclosed. In situations where the gas volume can be
restored to the predive volume (e.g. by inflating a dry suit or clearing the ears),
squeeze can be avoided.
(4) There must be a change in ambient pressure.
3-3 ORIGINAL
d. The predominant symptom of barotrauma is pain. As the gas volume within the
space is reduced on descent, pain may be accompanied by bleeding as overfilled blood
vessels rupture due to the increased transmural pressure. This may serve to reduce the
relative negative pressure. On ascent, the reverse can occur resulting in a decreased
blood flow to the vascularised lining of the gas space. Other symptoms may be
produced as the function of specific target organs is compromised as discussed below.
3-4 ORIGINAL
0302. ENT Anatomy
a. Sinus Anatomy.
(1) The sinuses are cavities, usually six or seven in number, in the bony structure
of the skull. Their main function is to lighten the skull, but they also give resonance
to the voice, as can be noticed by the change in voice in a person with a severe cold
or catarrh.
(2) The sinus cavities are lined with a mucous membrane similar to that in the
nose and, to provide means of equalisation of pressure between the cavities and the
atmosphere, they are connected to the nasal cavity by narrow canals known as ostia.
(3) Figure 3-1 below shows the positions of the sinuses in a human skull.
Figure 3-1. The Sinus Cavities
b. Anatomy of the Ear
(1) The anatomy of the ear is illustrated in Fig 3-2. The ear is divided by
anatomical boundaries into three sections: the external, middle and inner ear. The
external ear is separated from the middle ear by the tympanic membrane and both
these cavities are gas-filled. The inner ear contains no gas but the thin membranes
of the round and oval windows can be subject to barotrauma due to pressure
differences between the middle and inner ear. There are three bones in the middle
ear: the malleus, the incus, and the stapes. The malleus is connected to the
tympanic membrane and transmits sound vibrations to the incus, which in turn
transmits these vibrations to the stapes, which relays them to the inner ear fluid
3-5 ORIGINAL
(enolymph) via the oval window. The round window connects the outer fluid-
containing (perilymph) compartment inner ear with the middle ear and thereby
permits the vibration generated by sound waves to leave the inner ear.
Figure 3-2. Diagrammatic Representation of the Outer, Middle and Inner Ear
(2) The Eustachian tube connects the middle ear to the back of the throat and its
function is to equalise the pressure in the middle ear with ambient pressure so that
the tympanic membrane can vibrate freely without a pressure differential across it.
In the healthy individual it is only lightly closed and usually opens during the act
of swallowing or yawning. Under the substantial and rapid pressure change
experienced during descent, the tube sometimes does not open freely and discomfort
is felt as the tympanic membranes are stretched inwards. This discomfort can be
overcome by two methods: swallowing or yawning to use the muscles in the back
of the throat to stretch the Eustachian tube open; or performing a Valsalva
manoeuvre to forcibly blow air up the tube. The act of clearing and pressure
equalisation is evident either as a feeling of relief or as an audible click in the ear.
During ascent the air escapes on its own and active clearing is not usually
necessary.
3-6 ORIGINAL
(3) The inner ear contains two important organs, the cochlea and the vestibular
apparatus. The cochlea is the hearing sense organ and damage to it can result in
symptoms of hearing loss and tinnitus (ringing in the ears). The vestibular
apparatus senses balance and acceleration. Damage to this may cause vertigo,
which is the false sensation of a spinning type of motion. This distinct sensation of
spinning needs to be differentiated from the more vague complaints of dizziness or
light headedness caused by other conditions. Vertigo is usually specific to injury
to the inner ear or its related nervous pathways.
0303. Sinus barotrauma
a. Sinus Barotrauma of Descent. (Sinus Squeeze)
(1) Sinus squeeze may occur when the ostia which vent the sinuses into the nasal
cavity are obstructed by mucus, tissue swelling or nasal polyps. The frontal and
maxillary sinuses are most commonly affected. If a sinus is not ‘cleared’ during
descent, the air pressure within it becomes less than the pressure within their
mucosal lining. As a result, the mucosal blood vessels dilate and if the relative
pressure is reduced sufficiently they may rupture and haemorrhage into the sinus
space. This process is painful and may be sufficiently intense to halt the diver's
descent. Unless substantial tissue injury has occurred, a return to atmospheric
pressure will bring about immediate relief. A dull ache may persist for several
hours after an acute sinus squeeze, often with a small amount of bloody nasal
discharge.
(2) The best means of managing sinus squeeze is to avoid it. Divers should not
dive if any signs of nasal congestion, allergy or a head cold are evident. The effects
of squeeze can be limited during a dive by halting the descent and ascending a few
meters to restore the pressure balance. If the space cannot be equalized (by
swallowing or blowing against a pinched-off nose), the dive should be aborted. The
treatment of sinus squeeze consists of administration of nasal decongestants and
symptomatic pain relief. Systemic antibiotics may be required if there is evidence
of infection and, very rarely, antrostomy may be needed for persistent sinus pain
which is unresponsive to decongestants.
b. Sinus Barotrauma of Ascent. (Reverse Sinus Squeeze) If an ostium becomes

blocked during a dive, which can occur from mucosal swelling or blood clots from
barotrauma of descent, sinus barotrauma may occur during the ascent phase of a dive.
In such cases, the sinus pain is caused by a relatively increased pressure within the sinus
and this may persist for some hours after the dive. Quite commonly, relief is
accompanied by a squeaking sound as gas, often accompanied by a bloody nasal
discharge, escapes from the sinus. Individuals with redundant nasal mucosa, polyps, or
cysts are also at risk of this type of barotrauma.
3-7 ORIGINAL
0304. External Ear Barotrauma
a. External Ear Barotrauma of Descent
(1) Cause. If the external auditory meatus is blocked by an obstruction such as

wax, a tight-fitting hood or otitis externa (Paragraph 0618), the pressure in the
outer ear can not equilibrate with the ambient pressure. During descent therefore,
a relative vacuum develops in both the outer and middle ear. When the ears are
cleared, the tympanic membrane balloons outwards, in the opposite direction to that
which occurs in more conventional middle ear barotrauma. (NB. Because of this
movement, the term reversed ear is sometimes used to describe this condition). If
this persists for more than a few minutes, injury to the epithelial lining of the
external auditory meatus and the tympanum may occur, consisting of oedema and
petechial haemorrhages which occasionally progress to more substantial
haemorrhages into the ear canal in the form of large ecchymoses or frank
haemorrhage.
(2) Prevention. Divers should not dive:
(a) wearing a tight-fitting hood.
(b) using ear plugs.
(c) with an external ear infection.
(3) Symptoms and Signs
(a) The onset of pain, similar to that which occurs in the more classic middle
ear barotrauma but which is made worse by clearing the ears.
(b) There may be a mild conductive deafness, vertigo and nausea until the
pressure is relieved. A more marked conductive hearing loss occasionally
occurs in severe reversed ears if the ossicular chain becomes disarticulated.
(c) The lining of the external ear canal is often swollen and haemorrhagic.
There may be bleeding from the ear.
(d) There may be a perforation of the tympanic membrane, but this is

unusual.
(4) Treatment. Patients with reversed ears should be seen by an ENT Specialist,
particularly if a perforation of the tympanic membrane is suspected or observed.
Perforations of the eardrum usually heal fairly rapidly, but a diver is unfit for diving
until healing has taken place. In order to prevent infection, do not interfere with the
external ear canal and do not instil ear drops which may be ototoxic. Most cases
resolve spontaneously, although occasionally a surgical repair may be required.
3-8 ORIGINAL
0305. Middle Ear Barotrauma
a. Middle Ear Barotrauma of Descent. (‘Ears’) This is the most common diving-
related medical problem.
(1) Pathogenesis
(a) Middle Ear Squeeze is caused by the failure or inability of a diver during
descent to equalise pressure in the middle ear cavity. During descent, the
volume of gas in the middle ear decreases in accordance with Boyle’s Law.
To restore its volume, the diver encourages air to pass down the Eustachian
tube (ET) by ‘clearing the ears’. In a few divers, the ET is open all the time
so no conscious effort is necessary to achieve this. For most, however, the ET
is naturally closed and some action must be taken to allow this passage of air.
Many can accomplish this by yawning, or moving the jaw around. Some may
need to perform a modified Vasvalva manoeuvre (divers valsalva) which is
against a closed nose and mouth (rather than a closed glottis).
(b) If the eustachian tube is blocked, the ear can not be cleared. During the
initial phase of descent, the decreasing volume of the middle ear is
compensated for by the ear drum bulging inwards. Soon, however, the ear
drum reaches its limits of inward distensibility and the air pressure in the
middle ear falls below the external water pressure. This relatively negative
pressure causes the blood vessels of the ear drum and the lining of the middle
ear to dilate, leak and finally rupture. If the descent is continued, either the ear
drum will rupture allowing the immediate equalisation of the middle ear, or
bleeding into the middle ear resolves the dysequilibrium by replacing air with
non-compressible fluid.
(2) Clinical Features
(a) The initial symptom is a sense of pressure and fullness in the ear. With
further descent, sharp pain is experienced in the affected ear(s). The initial
presentation of symptoms occur most commonly within the first 2-3 metres of
descent. If the pain is not relieved by successful equalisation manoeuvres, this
should prevent further descent. If the tympanic membrane ruptures, relief of
the pain will be almost immediate. If this results in the ingress of water to the
middle ear, caloric vertigo due to a thermal imbalance between the two ears
may result. Occasionally, a diver may experience no pain during descent, but
be found to have clinical evidence of middle ear barotrauma after the dive is
over.
(b) Following the dive, residual symptoms may include pain and a sensation
of fullness in the ear. In a small proportion of cases, blood may be visible in
the mouth or nose.
(c) The ears should be examined with an otoscope by suitably trained

personnel. Six grades of middle ear barotrauma have been described.
3-9 ORIGINAL
Table 3-1. Examination Guide
Grade Symptom
Grade 0 Symptoms with a normal otoscopic appearance.
Grade 1 Diffuse redness and retraction of the tympanic membrane.
Grade 2 Grade 1 changes plus slight haemorrhage within the tympanic membrane.
Grade 3 Grade 1 changes plus gross haemorrhage within the tympanic membrane.
Grade 4 Dark and slightly bulging tympanic membrane from free blood in the middle
ear; an air fluid level may be present.
Grade 5 Perforation of the tympanic membrane. Blood may be seen within or issuing
from the ear canal.
(d) A conductive hearing loss may be present in more severe forms of

barotrauma, but this is rarely more than 20 dbA. Hearing loss is generally
temporary and normal function returns within 4-5 days. If the hearing loss is
greater than 20 dbA, the possibility of ossicular chain disruption should be
considered. This is particularly likely if perforation of the TM has occurred
in the superior, posterior aspect of the drum.
(3) Prevention
(a) A number of physical conditions predispose the diver to middle ear

squeeze; upper respiratory infection (URI), allergic or vasomotor rhinitis,
pharyngitis, dental malocclusion, hypertrophic adenoid tissue, and the inability
to perform a divers valsalva manoeuver.
(b) Ear clearing should be accomplished by yawning, moving the jaw or

performing gentle divers valsalva. Another effect of the Valsalva manoeuvre
is to increase intracranial pressure and if a powerful Valsalva manoeuvre
against a closed glottis is performed the combination of raised intracranial
pressure and reduced pressure in the middle ear, may be sufficient to cause the
round (and occasionally the oval) window membranes to rupture. (See
Paragraph 0308) Eustachian tube opening is usually accomplished most
easily if the descent is made feet first and the diver clears his ears frequently.
If too large a pressure difference is allowed to develop, the Eustachian tube
will collapse making further attempts to clear the ears fruitless. If difficulty
clearing the ears is encountered on descent, the diver should ascend and try to
equalise the middle ear pressure before attempting to descend again. Any
diver with chronic ear clearing problems should be referred to an ENT
Specialist for further examination.
3-10 ORIGINAL
(4) Treatment
(a) The treatment required depends on the degree of barotrauma but no diver
with middle ear barotrauma should return to diving until healing is complete.
As a general principle, nothing should be instilled into the ear. Some general
guidelines for time to recovery are given in Table 3-2.
Table 3-2 Recovery Time
Grade Symptom Period

Grade 1-2 (mild) 8-72 hours
Grade 3 (moderate) 2-8 days
Grade 4-5 (severe) 2-6 weeks
(b) Moderate cases may require topical or systemic nasal decongestants and
symptomatic pain relief. If perforation of the membrane has occurred, a
systemic antibiotic such as ampicillin may be given and the ear should be kept
dry. If the perforation of the membrane is located in a superior and posterior
position, the possibility of disruption of the ossicular chain should be
considered.
(c) If there is vertigo or any suggestion of inner ear barotrauma, the patient
should be referred to an ENT Specialist.
b. Middle Ear Barotrauma of Ascent. If the Eustachian tube becomes blocked

during a dive as may occur in sensitive individuals breathing cold, dry gas, this limits
the rate at which gas may leave the middle ear during ascent. As a consequence
overpressure in the middle ear may cause the ear drum could bulge outwards. Degrees
of blockage significant enough to cause pain are rare, but lesser degrees of blockage with
asymmetry between right and left sides are thought to be a mechanism for Alternobaric
Vertigo of Ascent. (Paragraph 0306).
c. Barotraumatic Facial Palsy. In a small number of individuals, the facial nerve is

exposed to middle ear pressure as it traverses the temporal bone. If the middle ear is
pressurised during ascent due to failure of the Eustachian tube to vent, the vascular
supply of the facial nerve may be compromised, resulting in an ischemic neuropraxia.
Generally 10-30 min of overpressure are necessary for symptoms to appear. During this
period, nausea and vertigo may be present. The syndrome is characterised by a
unilateral facial palsy of the lower motor neurone type. When the syndrome presents
shortly after surfacing, it may be difficult to distinguish the condition from
decompression illness. Once the middle ear vents, full facial function generally returns
in 10 minutes to 2 hours.
3-11 ORIGINAL
0306. Alternobaric Vertigo.

Alternobaric vertigo (sometimes known as Lündgren Syndrome) is defined as a
condition of transient dizziness arising during descent or ascent which is related to asymmetry
of changes in middle ear pressures. It is a common problem which occurs particularly during
ascent and when travelling in the upright position. The transient sensations of vertigo,
disorientation and nausea do not usually last for more than a few minutes but can be hazardous
if they occur at depth. The condition can largely be avoided by ensuring that the ears are cleared
properly. When it occurs, the diver should stop and hold on to a shot line or buddy until the
sensation wears off.
a. Alternobaric Vertigo of Ascent
(1) Alternobaric vertigo of ascent commonly has a sudden onset when the diver
reaches the surface. It is invariably transient, and may be accompanied by a feeling
of fullness or pain in the affected ear. Relief of vertigo is usually rapid and may be
accompanied by a hissing sound in one or both ears. The vertigo is also relieved if
the diver descends a few meters. If alternobaric vertigo of ascent continues after
completion of the dive, the afflicted diver may demonstrate Rombergism,
nystagmus, and a bulging tympanic membrane may be seen via otoscope.
(2) During ascent, gas in the middle ear expands in accordance with Boyle's Law.
If this gas is prevented from escaping through a sticky or partially blocked
Eustachian tube, pressure in the middle ear will increase. This causes pressurisation
of the fluid in the inner ear leading to a reduced perfusion pressure and reduced
inner ear circulation. Symptoms are most likely to occur when there is asymmetry
of pressure between the right and left sides.
(3) There appears to be a relationship between the inability to clear the ears
successfully and the occurrence of alternobaric vertigo of ascent and the condition
is frequently associated with upper respiratory tract infection or atopy.
(4) Usually, no treatment is required for alternobaric vertigo of ascent, which

resolves spontaneously.
(5) It may, occasionally, be confused with audiovestibular decompression illness.

However, the latter condition can be differentiated from alternobaric vertigo
because it is persistent and commonly accompanied by deafness and roaring
tinnitus.
b. Alternobaric vertigo of descent.
(1) Alternobaric vertigo of descent occurs much less frequently. It may present
before equalisation, but most often occurs immediately after an equalisation in
which one ear has been cleared more completely than the other. Symptoms and
signs include transient vertigo, which often follows a Valsalva manoeuvre, a
sensation of fullness in the affected ear, and tinnitus. Its likelihood of occurrence
is reduced by slow descent rate and avoidance of forceful ear-clearing procedures.
3-12 ORIGINAL
(2) There is no specific treatment for alternobaric vertigo of descent, which

resolves spontaneously over a few minutes.
0307. Caloric Vertigo

Normally, immersion results in water entering both ears more or less simultaneously.
Consequently, the vestibular apparatus in the inner ear is cooled at a similar rate on each side.
However, if one ear is partially or completely blocked by a tight-fitting hood or with ear wax,
there may be a difference in the rate of cooling of the two sides. Unequal stimulation can also
occur with perforation of a tympanic membrane. Under such circumstances a powerful sensation
of vertigo may result. As with alternobaric vertigo, this tends to be a transient sensation. The
vertigo lasts until the water warms to body temperature. The symptoms will be most intense
when the diver is in a head down orientation. By assuming an upright posture, the symptoms
will be ameliorated.
0308. Middle Ear Oxygen Absorption Syndrome
a. Cause. Middle ear oxygen absorption syndrome refers to the negative pressure
which may develop in the middle ear following a long oxygen dive in which gas with
a very high percentage of oxygen enters the middle ear cavity. Following the dive, the
oxygen is slowly absorbed and metabolised by the tissues of the middle ear. If the
eustachian tube does not open spontaneously, a negative pressure relative to ambient
may develop. Symptoms may become apparent some hours after a long oxygen dive.
A fluid level in the middle ear may be seen on otoscopy (serious otitis media). Middle
ear oxygen absorption syndrome is difficult to avoid but usually does not pose a
significant problem because symptoms are generally minor.
b. Symptoms. The diver may notice mild discomfort and hearing loss in one or both
ears. There may also be a sense of pressure and a moist, crackling sensation. Attempts
at equalizing the pressure in the middle ear using a Valsalva manoeuvre are usually
successful, although occasionally a decongestant may be required.
0309. Inner Ear Barotrauma
a. Pathogenesis
(1) Inner ear barotrauma is caused by a pressure differential between the middle
and results in rupture of the oval or round window. It is more usual for the round
window than the oval window to rupture, because the latter is protected somewhat
by the fibrous attachment of the foot of the stapes. Rupture of the round window
causes perilymph to leak into the middle ear space and the condition is also known
as perilymph fistula.
(2) There are two main mechanisms by which a pressure differential may act
across these membranes to cause inner ear barotrauma. Either may be sufficient to
cause rupture, but more usually it is a combination of the two mechanisms acting
together. The mechanisms are:
3-13 ORIGINAL
(a) Middle Ear Barotrauma of Descent.
(b) Increased Intracranial Pressure, Most usually caused by forceful Valsalva

manoeuvres to relieve middle ear squeeze.
b. Clinical Features. Classically, inner ear barotrauma is characterised by marked

vertigo, roaring tinnitus, a sensation of fullness in the affected ear, a neurosensory
hearing loss, nystagmus, nausea, vomiting and Rombergism. The patient may also
report a sensation of bubbling in the involved ear. However, the number and extent of
these symptoms may vary. Symptoms can be of sudden onset although, if the rupture
in the round window is small, it may take some time for sufficient fluid to leak out to
provoke these symptoms and consequently, presentation may be delayed for hours or,
very occasionally, days. Quite commonly the diver may not notice symptoms until after
surfacing. Unlike alternobaric or caloric vertigo, the symptoms are persistent.
(1) Hearing Loss. There may be a conductive hearing loss associated with middle
ear barotrauma or a neurosensory hearing loss, the density of which may fluctuate.
It should be remembered that the most common cause of a neurosensory hearing
deficit in divers is noise.
(2) Vertigo. It is important to differentiate true vertigo from other more vague
symptoms such as dizziness, lightheadedness, fainting and weakness. True vertigo
is characterised by a false sense of motion that is whirling or rotational in nature
and results from abnormal vestibular function either in the inner ear or the eighth
nerve pathways. Dizziness without a sense of rotation is unlikely to be due to
vestibular dysfunction. The presence of nystagmus is diagnostic in discerning
vertigo from dizziness.
d. Diagnosis and Treatment
(1) The diagnosis of inner ear barotrauma should be considered whenever any
inner ear symptoms occur following a dive. However, it is not an easy diagnosis
to make with confidence as a similar syndrome may be caused by bubble formation
in the inner ear following a deep dive or, occasionally, involvement of the eighth
nerve pathways in cerebral decompression illness. For this reason, the term Acute
Audiovestibular Decompression Illness may be used in cases where a firm
diagnosis can not be made. Diving-related differential diagnoses include
alternobaric or caloric vertigo, underwater blast injury and acute noise exposure.
Recompression of a diver with acute audiovestibular decompression illness will not
be harmful, even if it is caused by inner ear barotrauma, provided that the simple
precautions outlined in Chapter Eight are followed. Should the symptoms fail to
improve after three 20 minute oxygen periods at 18 msw or an equivalent dose of
oxygen, the diagnosis of inner ear barotrauma is likely to be correct and little is to
be gained by prolonging the hyperbaric oxygen treatment.
3-14 ORIGINAL
(2) Where a diagnosis of inner ear barotrauma is made with confidence (e.g.
following a short, shallow dive with a clear history of difficulty with ear clearing)
the patient should be managed with bed rest with the head elevated. Anti-emetic
medication may be of benefit. Investigations should include an
electronystagmogram and audiogram. Symptoms usually resolve spontaneously
within 2-3 days after which surgical exploration and repair of the fistula may be
indicated.
0310. Dental Barotrauma

Dental barotrauma results from changes in volume of a small pocket of gas which may
be generated by decay or remain lodged under a poorly prepared or cracked filling. If this pocket
of gas communicates with the pulp cavity, small changes in volume of the pocket of gas can
cause severe pain. In some circumstances, such as saturation dives, further gas may diffuse into
the pocket during the descent or bottom phases of the dive and if this does not vent during ascent
the tooth may explode. Treatment consists of proper dental repair. local analgesics may be
required for persistent pain.
3-15 ORIGINAL
Bibliography:
Alfandre, H.J. Aerotitis media in submarine recruits. USN Submarine Medical Center Research
Report No. 450, May 1965.
Bayliss, G.J.A. Aural barotrauma in naval divers. Arch. Otolaryngol. 88:49-55, 1968.
Molvaer, O.I. Alternobaric facial palsy. Medecine Aeronautique et Spatiale, Medecine

Subaquatique et Hyperbare. 18:249-250, 1979.
Neuman, T.H. Seattle, G. Beaver, and P G Linaweaver. Maxillary sinus barotrauma with cranial
nerve involvement. Case Report. Aviat. Space Environ. Med. 46:314-315, 1975.
Beasley, J .W. Inner ear damage due to barotrauma. Wisconsin Med. J. 73:5143-5145, 1974.
Farmer, J.C. Diving injuries to the inner ear. Ann. Otol. Rhinol. Laryngol. 86 (Suppl. 36): 1-20,
1977.
Farmer, J.C. Inner ear injuries in diving-dinnerential diagnosis of inner ear decompression
sickness and inner ear barotrauma. In: Underwater Physiology VII. Proceedings of the Seventh
Symposium on Underwater Physiology, edited by A. J. Bachrach and M.M. Matzen. Bethesda
Md: Undersea Medical Society, Inc., 1981.
Ingelstedt, S., A. Invarsson, and O. Tjernstrom. Vertigo due to relative over-pressure in the
middle ear. Acta Otolaryngol. 78:1-74, 1974.
Lundgren, C.E.G. On alternobaric vertigo -- epidemiologic aspects. In: Proceedings of the First
Annual Scientific Meeting of the European Undersea Biomedical Society, edited by C.M. Hesser
and D. Linnarsson. Forsvarsmedicin 9:406-409, 1974.
Miller, J.M., A.Axelsson, D. McPherson, and W. Potter. Mechanisms of Aural Barotrauma. In:
Underwater Physiology VII. Proceedings of the Seventh Symposium on Underwater Physiology,
edited by A.J. Bachrach and M.M. Matzen. Bethesda Md: Undersea Medical Society, Inc.,
1981.
Pang, L.A. Sudden sensori-neural hearing loss following diving and treatment by recompression:
A report of two cases. Trans. Am. Acad. Opthamol. Otolaryngol. 78:436-443, 1974.
Tjernstrom, O. Middle ear mechanics and alternobaric vertigo. Acta Otolaryngol. 78:376-384,
1974a.
Tjernstrom, O. Further studies on alternobaric vertigo. Acta Otolaryngol. 78:221-231, 1974b.
Vorosmarti, J., and M.E. Bradley. Alternobaric vertigo in military divers. Mil. Med. 135:182-
185, 1970.
3-16 ORIGINAL
0311. Pulmonary Anatomy
a. The lungs are a pair of light, spongy organs which form the functional end of the
respiratory tract where the exchange of oxygen and carbon dioxide between the blood
and atmosphere takes place. During the respiratory cycle, air enters the lungs through
the right and left main bronchi which arise from the trachea. Like the branches of a tree,
these bronchi divide into smaller and smaller bronchioles, which then divide into
alveolar ducts, alveolar sacs, and eventually alveoli. In total there are 22 generations of
airways from the trachea which lead to about 150 million alveoli in each lung. Each
alveolus is lined with a thin membrane and is surrounded by a network of capillaries at
which gas transfer occurs. The total area of the alveolar walls in contact with capillaries
in both lungs is about 70 square meters.
b. The lungs are elastic organs which collapse like balloons if removed from the body.
The mechanics of taking fresh air into the lungs (inspiration or inhalation) and expelling
used air from the lungs (expiration or exhalation) are shown Fig 3-3. By elevating the
ribs and lowering the diaphragm, air is sucked into the lungs as they expand within the
enlarging chest cavity. When the ribs are lowered again and the diaphragm rises to its
original position, air escapes as the lungs return to their resting dimensions.
Figure 3.3. The Process of Inspiration
c. The external surfaces of the lungs are covered by a pleural membrane which reflects
over on itself to line the internal surface of the chest wall and the mediastinum thereby
separating the chest cavity into two halves. The pleural space, which separates the two
surfaces (visceral and parietal) of the pleura, is maintained at a slightly negative pressure
and contains a small amount of fluid which acts as a lubricant to allow the lungs to
expand and contract freely during respiration. If for any reason air is allowed to enter
this space the lung will collapse, generating a condition known as a pneumothorax.
3-17 ORIGINAL
d. It is not possible, even with a maximal exhalation, to completely empty the lungs.
A residual volume of gas, which in a normal adult is about a litre, remains in the lung.
0312. Pulmonary Barotrauma of Descent
a. Pulmonary barotrauma of descent (lung squeeze) may occur the following

situations:
(1) During deep breath-hold diving.
(2) When a diver’s air supply can not be maintained during a rapid descent. (eg.
when a heavily weighted diver wearing standard diving dress makes an accidental,
uncontrolled descent)
(3) The loss of surface supply pressure to a diver in standard dress with
failure/absence of a non return valve.
b. Three physiological factors determine the depth at which pulmonary barotrauma of

descent may occur:
(1) The ratio of the volume of gas in the lung at the start of the dive to the residual
volume.
(2) The compressibility of the chest.
(3) The distensibility of the pulmonary vascular bed.
c. During descent on a breath-hold dive, the gas within the lungs is compressed in
accordance with Boyle’s Law. The ratio of the lung volume at the surface to residual
volume determines the depth to which a breath-hold diver can dive before his lungs are
compressed to a volume which is less than the residual volume. For example, a diver
with a lung volume of 6 litres at the start of a dive and a residual volume of 1 litre, could
dive to a depth of 6 ATA (50 msw) before the volume of gas in the lung was compressed
to less than 1 litre. Below that depth, and depending on the compressibility of the chest
wall, the intra-pulmonary pressure becomes negative compared to ambient pressure. If
descent continues, this negative intra-pulmonary pressure will cause a shift of blood into
the thorax. Once the thoracic blood volume has reached its maximum, further descent
will result in pulmonary oedema and, eventually, frank pulmonary haemorrhage. It is
recognised that, in most circumstances, the capacity of the thoracic vasculature is
sufficient to compensate for any loss of lung volume in breath-hold diving. As a
consequence, pulmonary barotrauma of descent is very rare.
d. Symptoms and signs of lung squeeze (assuming that the diver is returned to the
surface) include chest pain, dyspnea, cyanosis, haemoptysis, and clinical evidence of
pulmonary oedema. Treatment of severe lung squeeze may include tracheal intubation,
positive pressure ventilation, suction and the administration of supplemental oxygen.
3-18 ORIGINAL
e. It is not clear whether or not cases of thoracic squeeze have occurred as the
condition is poorly documented. Possible casualties of lung squeeze usually drown and
the presence of pulmonary oedema in a drowned subject does not necessarily indicate
thoracic squeeze.
0313. Pulmonary Barotrauma of Ascent

Pulmonary barotrauma of ascent occurs when gas, which is normally retained within the
alveoli, leaves its natural confines to enter the interstitial space within the lung, the pleural cavity
or the blood stream. Gas may enter one or all of these sites and the collection of symptoms
produced is sometimes called the pulmonary overinflation syndrome.
a. Pathogenesis. The mechanisms of lung rupture are incompletely understood. At

the simplest level, if gas which has been breathed while at depth is trapped within the
lung during ascent, then the resulting expansion in volume of that gas, in accordance
with Boyle’s Law, may be sufficient to cause the architecturally delicate pulmonary
tissue to rupture. Experimental evidence indicates that an over-pressure of as little as
80 mmHg (0.1 bar) is sufficient to cause lung rupture. Consequently, if gas is trapped
in the lung, an ascent from 1 m to the surface could theoretically result in pulmonary
barotrauma and at least one carefully documented case is known in which this has
occurred. Practically, therefore, pulmonary barotrauma can arise from dives to any
depth. There are five principal ways in which gas may become trapped in the lung:
(1) Involuntary breath-holding. This may be due to spasm of the glottis, as

occurs: during convulsions (e.g. as a result of cerebral oxygen toxicity); or as a
reflex, such as following the aspiration of water into the nose or throat. This may
also occur in association with loss of consciousness in association with near
drowning. Sudden exposure to cold, such as may occur if a dry suit is punctured
may provoke a gasping reflex and breath-holding.
(2) Voluntary breath-holding. Classically, this occurs in trainees who make a

panic ascent. It may be provoked by running out of air or a caustic cocktail. Very
occasionally, this may occur in divers who inappropriately perform a valsalva
manoeuvre during ascent.
(3) Phrenic spasm. This can occur if an instructor delivers a blow to the abdomen
of a trainee to encourage exhalation during ascent. It is an extremely dangerous
practice and should not be permitted.
(4) Pulmonary pathology. Both acute (e.g. reversible airways obstruction) and
chronic (e.g. tuberculosis, emphysema) pulmonary pathology may cause airways
obstruction. However, because such conditions have traditionally rendered
personnel unfit to dive, their association with pulmonary barotrauma are frequently
poorly documented.
3-19 ORIGINAL
(5) Idiopathic. Numerous cases of pulmonary barotrauma have occurred in which

no evidence of pulmonary pathology has been found and exhalation during ascent
has been witnessed by independent observers. Consequently, there almost certainly
remain other causes of the condition, which have yet to be identified.
b. Prevention. A number of preventive measures are taken:
(1) Divers and those undergoing training for escape from submarines are trained
not to hold their breath during ascent.
(2) Both divers and submariners are carefully screened for evidence of obstructive
lung disease which may result in the trapping of gas. This applies both at entry into
the branch and during employment. Those suffering from short-term respiratory
illness should not dive or undertake submarine escape training until they are
asymptomatic.
(3) Other preventative measures which help to promote safe ascents include the
careful planning of dives, adherence to the plan and the avoidance of emergencies,
such as running out of air.
(4) Divers must maintain a safe breathing pattern underwater. The normal pattern
of respiration involves inspiration, expiration and then a pause. Some divers
develop a pattern of breathing, called skip breathing, which involves inspiration,
a pause and then expiration. The pause in this case is effectively a breath-hold
which may result in barotrauma if the diver ascends.
c. Clinical Features. The symptoms and signs of pulmonary barotrauma of ascent

depend on the sites to which free gas escapes. Each site may be affected in isolation or
in combination with the others. The features produced by gas entering each site are
discussed under their own headings in the rest of this chapter.
(1) Gas entering the interstitial space of the lung, which is the most common site
affected, will cause interstitial emphysema.
(2) Gas entering the bloodstream will cause arterial gas embolism.
(3) Gas entering a pleural space, the least common site affected, will cause a
pneumothorax.
0314. Interstitial Emphysema
a. The term interstititial emphysema defines the presence of free gas bubbles between
tissue cells. This generally occurs in connective tissue planes. The condition can be
described further by the anatomical site of the bubbles:
3-20 ORIGINAL
(1) Mediastinal Emphysema If sufficient gas escapes into the interstitial tissue
space of the lung, it will track along the outside of the airways and blood vessels
into the mediastinum. The presence of a little gas in the mediastinum is often
symptomless. However, if tissues are stretched by a substantial amount of gas, mild
to moderate retrosternal pain may be felt. Other possible symptoms include
shortness of breath, a sensation of fullness in the chest or throat, a change in the
tone of the voice or hoarseness, and a cough which may produce slightly blood-
stained sputum.
(2) Subcutaneous Emphysema Gas in the mediastinum may migrate up into the
subcutaneous tissues of the neck and, occasionally, the head. It is not usually
painful and may only be detected by noticing swelling or crepitation (the skin
‘crackles’) in the neck.
(3) As well as migrating upwards into the subcutaneous tissues of the neck, gas
may also track caudally in the retroperitoneal plane to appear as sub-diagphramatic
gas on radiography. Gas may also be found outlining the liver, spleen, kidneys and
great vessels of the abdomen extending, very occasionally, into the pelvis.
b. Treatment
(1) Asymptomatic mediastinal emphysema and subcutaneous emphysema usually

resolve gradually without specific treatment. If there are troublesome symptoms,
resolution will be accelerated by breathing 100% O2 on the surface. In the very rare
instances where there are serious symptoms, recompression may be necessary.
Compression to 10m for an hour breathing 100% O2 should be sufficient.
(2) All cases of interstitial emphysema need to be thoroughly examined for other
manifestations of pulmonary barotrauma of ascent: pneumothorax and arterial gas
embolism/decompression illness.
0315. Arterial Gas Embolism

If gas from a ruptured lung enters the pulmonary microcirculation, it will be transported
to the left side of the heart and from there be distributed to the body as arterial gas emboli. Two
organs which are particularly susceptible to functional disturbance as a result of such emboli are
the brain and heart. Consequently, divers or submarine escape trainees who have sustained
decompression pulmonary barotrauma should be carefully examined for evidence of cardiac or
neurological disorders. In the past, it was considered possible to make a diagnosis of arterial gas
embolism in patients who experienced the onset of neurological symptoms during decompression
or shortly after surfacing from a dive. This diagnosis was made even in the absence of any other
evidence of decompression pulmonary barotrauma. It is now recognised that such a diagnosis
may be inaccurate, since other conditions may present in a similar manner. Consequently, except
in isolated and specific circumstances where the mechanism is known (such as iatrogenic gas
embolism, or symptoms arising from very shallow dives), neurological symptoms or signs
presenting after a hyperbaric exposure should be termed acute neurological decompression
illness. (see Chapter 4 Acute Decompression Illness).
3-21 ORIGINAL
0316. Pneumothorax
a. A pneumothorax occurs when alveolar gas escapes into a pleural cavity. Two
forms of pneumothorax may occur:
(1) Simple Pneumothorax. This is the more common type and occurs when a
leakage of gas into a pleural cavity partially collapses the lung, causing varying
degrees of, but normally minimal, respiratory distress. The onset of a
pneumothorax is commonly accompanied by a sudden, sharp chest pain and may
be followed by difficult, rapid breathing and a reduction of normal chest movements
on the affected side if the pneumothorax is large. Tachycardia, a weak pulse and
anxiety may accompany these symptoms. This is not a life-threatening condition
because it is possible to survive with one intact lung. In the context of pulmonary
barotrauma, pneumothoraces are normally small and unilateral.
(2) Tension Pneumothorax. In certain instances, the damaged lung may allow air
to enter but not exit the pleural space. Successive breaths gradually enlarge the
pneumothorax and progressively increase the pressure exerted on the lung. If
uncorrected, this force will cause it to collapse completely. With increasing
pressure in the pneumothorax, the mediastinum is shifted to the opposite side of the
chest compressing the heart and the ‘good’ lung. The symptoms commonly become
progressively more serious, beginning with tachypnoea and progressing to cyanosis,
hypotension, shock and, unless corrected, death. Tension pneumothorax is a rare
condition under normal conditions at the surface. However, a simple pneumothorax
which occurs at depth may increase in size during decompression and effectively
become a tension pneumothorax. If a diver’s condition deteriorates during ascent,
especially if the symptoms are respiratory, a tension pneumothorax should always
be suspected and the ascent halted.
b. Treatment
(1) A simple pneumothorax normally improves with time as air is naturally

reabsorbed. A small simple pneumothorax can be treated by breathing 100% O2 on
the surface which serves as a nitrogen pump, causing reabsorption of the nitrogen
component of the pneumothorax. A larger simple pneumothorax and all tension
pneumothoraces should be treated with 100% O2 on the surface and a chest drain
connected to a non-return valve or an underwater seal. Non-return valves, such as
the Heimlich valve, are preferable for casualties who may require evacuation or
recompression treatment.
(2) A diver believed to be suffering from pneumothorax needs to be thoroughly

examined for the other manifestations of pulmonary barotrauma of ascent,
particularly for neurological decompression illness.
(3) A pneumothorax is not a contra-indication to recompression therapy if oxygen

tables are used, but care must be taken to observe the patient for deterioration
during the ascent phases. Should this occur, recompression to relieve the symptoms
and aspiration of the pneumothorax via a large-bore cannula will be required in the
chamber. Formal drainage may be required after the completion of the chamber
therapy.
3-22 ORIGINAL
Bibliography:
Broome JR. Smith DJ. Pneumothorax as a complication of recompression therapy for cerebral
arterial gas embolism. Undersea Biomedical Research. 19(6):447-55, 1992 Nov.
Leitch, D.R. Unusual case of emphysema. Brit. Med. J., 8 Feb 1969, p. 383.
3-23 ORIGINAL
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3-24 ORIGINAL
0317. Face Mask Barotrauma of Descent
a. Face mask barotrauma of descent is caused by a relatively negative pressure

developing within the mask compared with ambient pressure. This situation can occur
during descent if a diver fails to equalise the pressure in his mask by nasal exhalation or,
when an oro-nasal mask is being used, by a malfunction of the air supply to the face-
mask. Because the rigid walls of the mask are unable to collapse, the pressure
differential causes facial tissues to be forced into the mask.
b. Mild degrees of face mask squeeze can go unnoticed during the dive, but
subconjunctival haemorrhages may be apparent on surfacing. More severe degrees of
squeeze also cause facial swelling, bruising and nosebleeds. Treatment is not usually
required in mild cases but cold compresses may be useful in the more severe.
Prevention of face mask squeeze can be accomplished by having the diver exhale into
his mask during descent. Goggles should never be worn while diving, because pressure
inside the goggles cannot be equalised.
0318. Drysuit Barotrauma of Descent

Dry suit barotrauma of descent results from the failure to add air to a membrane type
drysuit during descent. Compression of the existing air in the suit causes it to collapse around
the body. Skin caught in the folds of the suit is pinched and cutaneous haemorrhage occurs
causing multiple red striae. These striae are most commonly seen around the axillae and groin
since most drysuits are designed with excess material in these areas to allow ease of movement.
The striae are generally not painful. Commonly, the skin discolouration disappears in a few
hours without treatment of any kind. In more severe cases, the red striae turn to the familiar
colours of bruising in 12 to 24 hours and they usually disappear within 3 or 4 days. No treatment
is necessary, and the condition can be prevented entirely if the drysuit pressure is equalised by
the addition of air during descent. It is, however, important to recognise this condition to ensure
that it is not confused with acute cutaneous decompression illness.
0319. Whole Body Barotrauma of Descent

Whole body barotrauma of descent may occur when the air supply to a diver in surface
supply diving equipment is inadequate to balance the water pressure. This could be precipitated
by a fall into water of greater depth with absence or failure of the safety non-return valve or by
malfunction or maladjustment of the gas supply or exhaust valves. All body organs that are
affected by barotrauma of descent could then be damaged and there may be significant
barotrauma to the head and neck which may be squeezed into a rigid, surface-supplied diving
helmet.
0320. Gastrointestinal Barotrauma of Ascent

Normally, any gas within the intestine expands during decompression to its original
volume before the dive. Consequently, gastrointestinal barotrauma is rare. However,
swallowing gas (aerophagia) when under pressure is dangerous because serious gastrointestinal
barotrauma, resulting in colicky abdominal pain, abdominal distension and ‘tinkling’ bowel
sounds, resembling bowel obstruction, may occur and very occasionally, rupture of the bowel
may result.
3-25 ORIGINAL
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3-26 ORIGINAL
CHAPTER 4
ACUTE DECOMPRESSION ILLNESS
ORIGINAL
CHAPTER 4

CONTENTS
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0401
Inert Gas Exchange in Body Tissues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0402
Decompression Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0403
Decompression Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0404
Mixed Gas Diving . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0405
SECTION 2 - PATHOGENISIS
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0406
Sources of Gas Bubbles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0407
Distribution of Gas Bubbles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0408
Bubble Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0409
Predisposing Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0410
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0411
Descriptive Terminology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0412
Additional Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0413
Summary Table of Common Diving Complaints by Time Onset . . . . . . . . . . . . . . . 0414
4-1 ORIGINAL
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4-2 ORIGINAL
CHAPTER 4
0401. General
a. Bubbles of inert gas which form within tissues as a result of decompression, or

which are released into the blood stream from pulmonary barotrauma, can result in the
condition known as acute decompression illness (DCI). These bubbles act both directly
and indirectly to induce tissue injury. Direct, physical effects of bubbles include the
obstruction of blood vessels and the disruption and deformation of tissues at their site
of generation or growth. The indirect effects result largely from the tissue reaction to the
presence of bubbles and include inflammation and activation of blood clotting
mechanisms.
b. The resulting symptoms depend on the location and size of the bubble or bubbles
and these may be protean as most systems in the body can be rendered dysfunctional by
the presence of bubbles within them (see Paragraph 0409). Common symptoms
include: pain in, or around, joints; skin rashes; dysfunction of special senses such as
visual, vestibular and auditory pathways; other sensory deficits, motor weakness, loss
of consciousness, convulsions and, more rarely, death. Constitutional manifestations are
common and DCI may present as a ‘flu’-like illness.
c. The definitive treatment of DCI is recompression and hyperoxygenation (see also

Paragraph 0602). This involves returning the victim to pressure in a chamber,
breathing a high partial pressure of oxygen, which serves to:
(1) Reduce the size of bubbles, to force them back into solution, and
(2) Enhance the elimination of inert gas
0402. Inert Gas Exchange in Body Tissues
a. Gases in a breathing mixture enter the lungs and dissolve in the blood in accordance
with HENRY’S LAW which states that: ‘At a constant temperature the mass of gas that
dissolves in a given mass of liquid with which it is in contact is almost directly
proportional to the partial pressure of that gas’. The solution of gases in tissues is a more
complex problem, which remains incompletely understood. Additional factors which
influence the rate at which tissues take up inert gas include: the molecular weight of the
gas, tissue perfusion and the partition coefficient of the gas between the tissue and blood.
b. Nitrogen, representing approximately 80% of air, is the most common inert gas
breathed by divers. When another inert gas, such as helium, is used in the breathing
mixture, the tissues will take up become saturated with that gas in the same process as
for nitrogen. However, the time required to reach saturation will be different for each
gas.
4-3 ORIGINAL
c. Oxygen is also subject to the same physical laws regarding solution in the body. It
is not considered in any further detail, however, because its role in the development of
decompression illness is considered to be very minor, or it is readily metabolised.
d. At atmospheric pressure, breathing air, about 1 - 1½ litres of nitrogen are dissolved

in the blood and tissues. Although individual molecules will enter and leave the body,
the amount of nitrogen will remain constant because the gas tensions in the atmosphere
and body are in equilibrium. In such a state, the body is said to be saturated with inert
gas. When a diver is exposed to a raised pressure, this equilibrium is disturbed and there
is a net flow of gas molecules into the body, in an approximately exponential function,
until a new equilibrium is reached. The precise time taken for the whole body to saturate
at a new depth varies between individuals and is dependent on numerous factors. It is,
however, independent of the pressure change and takes of the order of 24 hours.
e. Individual tissues can be classified according to the rate at which they take up and
eliminate gas. Tissues which equilibrate rapidly are called ‘fast tissues’ and those which
equilibrate slowly, ‘slow tissues’. Arterial blood is the fastest since it absorbs nitrogen
directly from the lungs and equilibrates within seconds. The brain is also a fast tissue
because of its extensive blood supply. Slow tissues such as fat, tendon and cartilage take
many hours to equilibrate.
0403. Decompression Tables
a. If the rate of ascent from a dive is too rapid, tissues will become supersaturated with
inert gas and bubbles may form. Although body tissues are capable of tolerating both
a degree of supersaturation and some, such as adipose tissue, a bubble burden, it is
recognised that it is the presence of bubbles which underlies the onset of decompression
illness. Decompression tables have therefore been developed to regulate the rate of
decompression and thereby largely avoid divers developing DCI. The most commonly
used technique is for the diver to stop at various depths and for various periods of time
to allow the inert gas to leave body tissues. This is known as ‘stage decompression’.
b. The process whereby gas is absorbed into and eliminated from tissues is
incompletely understood and for this reason, no mathematical formula precisely defines
the process. The many algorithms which have been developed, and from which most
decompression tables have been derived, are generally based upon perfusion-limited or
diffusion-limited models of inert gas exchange and include constants which have usually
been determined by experimental observation.
c. Because there are a number of factors which are thought to influence tissue inert gas
exchange in individual circumstances ( see Paragraph 0410) adherence to even well-
tested tables does not guarantee that a diver will avoid decompression illness if several
of these factors combine to produce a particularly stressful dive. Unfortunately, it is
unlikely that all of these risk factors are known and the influence of none of them on the
risk of DCI has been quantified. Consequently, decompression tables and dive
computers cannot be relied upon to define zero-risk dive profiles. Diving supervisors
should recognise conditions which are likely to impose a higher than average risk of DCI
and consider decompressing the diver in accordance with the next longer or next deeper
profile of the decompression tables being used.
4-4 ORIGINAL
0404. Decompression Procedures
a. No-Decompression Diving. Not all decompression is carried out by staged ascent

to the surface. The depth-bottom time coordinates of some dives are such that no
decompression stops are required. These are the so called ‘no stop dives’.
b. Surface Decompression Diving. Because there is commonly a delay between

surfacing and the onset of DCI, it is possible to surface the diver before decompression
has been completed and then return the diver to depth in a compression chamber for
subsequent completion of the decompression. This procedure is preferred in
circumstances when:
(1) The surface support unit must leave the dive site quickly,
(2) The in-water conditions are hazardous. This could be because of the water
temperature, the sea state or imminent in-water explosions.
(3) The in-water decompression time for deep dives is protracted.
c. Diving at Altitude. Ambient pressure decreases with altitude. Decompression

conducted above sea level using a profile for the same dive at sea level, will generate a
higher inert gas overpressure in the body tissues. Therefore when diving at altitude, the
decompression should be adjusted to account for this.
d. Oxygen Decompression Diving. By employing oxygen-breathing during

decompression, a greater gradient for inert gas elimination from tissues is generated
which can be used to shorten decompression time substantially. The use of oxygen
decompression, however, is possible only at depths whereby cerebral oxygen toxicity,
particularly, is avoided. Depending on the design of the breathing apparatus, it may not
be practical to supply oxygen to a diver during in-water stops. Nonetheless, oxygen
decompression is an integral part of helium-oxygen, surface-supplied diving techniques,
and is used routinely with surface decompression.
0405. Mixed Gas Diving

Oxygen mixtures that contain a higher concentration of oxygen than that of air can be
used as the breathing medium to reduce the required decompression time. As has been discussed,
the need for decompression stops on ascent is determined by the amount of inert gas which has
been absorbed. If oxygen is used to dilute inert gas, within the bounds of safety with respect to
oxygen toxicity, less inert gas is absorbed during the dive and, consequently, decompression time
can be reduced. For example, a diver breathing air at 30m inhales nitrogen at a partial pressure
(PiN2) of 3.2 bar. If the diver breathed a mixture of 60-percent nitrogen, 40-percent oxygen
instead of air, the PiN2 would be 2.4 bar, which is the PiN2 of air at 20m. This is known as the
equivalent air depth (EAD) which is used for planning the decompression.
4-5 ORIGINAL
SECTION 2 - PATHOGENESIS
0406. Introduction
The pathogenesis of decompression illness is still an area which is incompletely
understood due to the complexity of the disease process and the number of organ systems that
can be affected. The information presented in this section aims to give a clear outline of the
possible origin and distribution of gas bubbles in DCI and to provide an introduction into the
means by which these bubbles may exert their deleterious effects.
0407. Sources of Gas Bubbles
a. The prime initiating factor for decompression illness is the formation or release of
bubbles into the blood and/or tissues as outlined in Section 1 to this Chapter. These
bubbles may originate from two sources:
(1) Dissolved Gas. During decompression, inert gas moves from the tissues into
the blood where it is carried to the lungs and exhaled. If this process occurs in a
controlled manner, so that the inert gas tension does not reach a sufficient level of
supersaturation for bubbles to form, the decompression will progress uneventfully.
However, if the rate of decompression is such that the capacity of the tissues,
cardiovascular system and lungs to remove inert gas is exceeded, the degree of
supersaturation may reach the point at which the gas no longer remains in solution
and bubbles start to form. These bubbles may form anywhere in the body in tissues
or blood.
(2) Pulmonary Barotrauma of Ascent. Bubbles may enter the bloodstream in the
form of arterial gas emboli as the result of pulmonary barotrauma of ascent, as
discussed in Chapter 3 Section 3. Bubbles arising from this mechanism are
normally confined to the blood stream.
b. Although bubbles may arise from these two fundamentally different processes, it is
often difficult, in individual cases, to be certain of the origin of disease-provoking gas.
Indeed, with respect to some organ systems, such as the ear and lungs, it may even be
difficult to distinguish between a condition caused by dissolved gas coming out of
solution and the results of barotrauma. Consequently, it is now recognised that, for
practical purposes, the distinction between the conditions that used to be known as
decompression sickness and arterial gas embolism was artificial. As a result, the term
Decompression Illness, which is descriptive rather than pathogenetic, is now being used
to reflect this.
0408. Distribution of Gas Bubbles

As the symptoms of decompression illness are a consequence of the site of bubbles rather
than their origin it is appropriate to discuss the distribution of gas bubbles formed by either of
the mechanisms mentioned above.
4-6 ORIGINAL
a. Bubbles of Dissolved Gas. These bubbles may form within the tissues or blood.
(1) Tissues. Bubbles forming directly within the tissues are known as
autochthonous bubbles. These may form within any body tissue although the
evidence is that they occur most commonly in fatty tissues. Some tissues, such as
adipose tissue can tolerate a significant bubble burden without serious
consequences. Other tissues, such as the spinal cord, appear to tolerate very few
autochthonous bubbles before dysfunction is apparent.
(2) Blood
(a) Arterial Blood. It is unlikely that many bubbles form within arterial blood
which, as the fastest tissue, is equilibrated with ambient inert gas tensions
having recently passed through the lungs. In addition, arterial blood pressure
will oppose bubble formation and growth. Theoretical calculations indicate,
however, that bubble formation may be possible if the rate of ascent is very
rapid.
(b) Venous Blood. Numerous studies using techniques such as doppler

ultrasound have demonstrated the presence of venous bubbles in divers during
decompression from apparently innocuous dive profiles and in asymptomatic
divers. These are known as ‘silent bubbles’. The body is capable of tolerating
these bubbles because the lungs are excellent bubble filters, removing the
bubbles from the circulation by allowing their contents to diffuse into the
alveoli. This capacity to act as a filter is finite and if the bubble burden is such
that it is exceeded, they will transit the lungs and reach the arterial side of the
circulation. Large numbers of bubbles within the pulmonary circulation cause
the symptoms of pulmonary DCI.
(c) The transit of venous bubbles to arterial blood may occur before the
pulmonary filter is overwhelmed. In approximately 25-30% of the normal,
adult population, the septum which separates the upper chambers of the heart
contains a potential or actual defect which is known as a Patent Foramen
Ovale or PFO. This is a relic of the foetal circulation and normally results in
no ill-effects. However, it does offer a possible route for bubbles to bypass the
pulmonary filter and consequently, along with other right-to-left shunts, has
the potential to promote the arterialisation of otherwise relatively harmless
venous bubbles.
b. Arterial Gas Emboli from Pulmonary Barotrauma of Ascent. These bubbles

will be distributed to all body tissues in accordance with their blood flow.
0409. Bubble Effects
a. Autochthonous Bubbles. How these bubbles provoke decompression illness has

yet to be completely clarified. Hypotheses for the means whereby they exert their
deleterious effects on tissue function include:
(1) Physical disruption of tissue architecture. It is inevitable that bubbles forming

de novo will result in some disruption of tissue architecture. In some tissues, such
as adipose tissue, this may not matter. However, in others, such as nervous tissues,
the presence of bubbles may severely disrupt tissue function.
4-7 ORIGINAL
(2) Interruption of tissue microcirculation. Bubbles which form in close

proximity to small blood vessels are liable to interrupt blood flow through the vessel
either by causing it to stretch and rupture or by compression. In some instances,
tissues which reside in rigid compartments, such as the bone marrow, may be
vulnerable to a ‘compartment syndrome’ as the evolution of gas bubbles raises the
compartment pressure.
(3) Derangement of tissue biochemical activity at the tissue-bubble interface. eg.

histamine release and resultant oedema.
b. Arterial Bubbles. How bubbles in arterial blood interfere with tissue function is
also incompletely understood. One obvious mechanism is that they physically obstruct
small blood vessels and thereby cause tissue ischaemia. The behaviour of bubbles in the
cerebral circulation has been studied extensively. Embolic bubbles move along cerebral
arteries until they reach a vessel of smaller diameter. They then elongate into a
cylindrical form and arrest in the circulation when the frictional resistance due to contact
with endothelium exceeds the perfusion pressure. The presence of a bubble causes an
immediate and maximal vasodilatation such that the bubble once again proceeds down
the vascular tree. The evidence from animal studies is that the residence time of gas
bubbles in the cerebral circulation is short, of the order of 10 minutes. It is now thought
that much of the injury which results from bubble embolism of the brain is due to the
consequences of traumatic injury to the delicate endothelial lining of cerebral blood
vessels, which, in places may be stripped away from the vessel wall. This results not
only in a breakdown of the blood-brain-barrier and the resultant leaking of potentially
harmful blood constituents into the brain, but also, by exposing blood components,
particularly leucocytes, to the damaged blood vessel wall, a tissue reaction to injury is
promoted. Ironically, it is the physical and biochemical consequences of this reaction
which may actually result in a further deterioration of cerebral blood flow and function.
c. Bubble Effects are sometimes described as Direct or Indirect. The direct effects
would include the physical disruption of tissues caused by autochthonous bubbles and
hypoxia caused by direct blockage of blood vessels from gas emboli. These effects are
thought to be responsible for the majority of symptoms which arise rapidly after the
onset of disease. Many of these effects may be temporary and occasionally casualties
make an apparently complete and spontaneous recovery. It is common for some
improvement to occur spontaneously. However, secondary deterioration or relapse also
occurs are this is thought to be caused by the indirect and largely inflammatory effects
of bubbles. Recompression therapy for the primary bubble effects has the actions of
physically reducing bubble size, forcing them back into solution and increasing tissue
oxygenation. In the brain, it is thought that cerebral oedema is reduced by the
vasoconstrictive effects of oxygen. Recompression therapy for the indirect effects of
bubbles almost certainly operates via alternative mechanisms including a powerful anti-
inflammatory action.
0410. Predisposing Factors

There are a number of individual and environmental factors that may influence
development of DCI. In general the risk factors include any condition that may contribute to poor
physical fitness or poor circulatory efficiency. In addition to the factors outlined in the list below,
there are almost certainly risk factors which have yet to be recognised as DCI may occur in
healthy, fit divers who have no apparent predisposing conditions.
4-8 ORIGINAL
a. Factors for which there is evidence for an increased risk of DCI:
(1) Heavy exercise before, during or after the dive. There is evidence that mild
exercise during decompression may reduce the risk of DCI.
(2) Cold water.
(3) Reduced aerobic capacity.
(4) Age.
(5) Repetitive dives.
(6) Flying or going to altitude after diving.
b. Factors which may increase the risk of DCI:
(1) Dehydration. This may be due to alcohol/caffeine consumption preceding the

dive, high ambient temperature, sweating or voluntary avoidance of fluids before
a dive.
(2) Obesity (increased percentage body fat).
(3) Extreme fatigue before the dive.
(4) Previous injuries or history of decompression illness.
(5) Infections.
(6) Hot shower or bath immediately after the dive.
(7) Infrequent hyperbaric exposure.
(8) Yo-Yo diving.
(9) Smoking.
4-9 ORIGINAL
0411. Introduction
a. Acute decompression illness (DCI) is a syndrome of numerous possible

manifestations which may develop following decompression. It is thought to be initiated
by the presence of bubbles of gas in body tissues - including the blood stream. Although
the means whereby these bubbles cause tissue dysfunction have yet to be fully
elucidated, the manifestations have been recognised for many years.
b. In the past, the symptoms and signs of DCI were grouped together into syndromes
according to the anatomical site and presumed mechanism of disease. A distinction was
made between decompression sickness (DCS) and effects of barotrauma, such as arterial
gas embolism (AGE). DCS was sub-classified into types according to its perceived
severity: Mild (Type 1) and Serious (Type 2) decompression sickness. It is increasingly
recognised, however, that these terms were of very limited value because it may be
difficult or impossible to be certain of the disease mechanism in many instances.
Consequently, a descriptive terminology has been developed which can be used where
the mechanism is not known for certain. This system is based upon a unified syndrome
of Acute Decompression Illness in which the evolution of the condition and the
manifestations are described. In addition it is recognised that, in fully describing a case,
it is necessary to note:
(1) The time to onset of each of the manifestations,
(2) An estimate of the inert gas burden in the diver,
(3) Whether there is any evidence of barotrauma,
(4) The response to recompression and the results of any investigations.
0412. Descriptive Terminology

In the following paragraphs the evolution and manifestation terms that form the basis of
the terminology are described. By using terms from each section in the phrase ‘decompression
illness’, a highly flexible diagnostic label can be applied to any case. This label imparts a great
deal of information and does not require the observer to guess at either a mechanism of the
disease or location of the lesion. Consequently it should be possible for the terminology to be
applied consistently. The term Acute is used to distinguish these conditions from possible
chronic consequences of diving such as dysbaric osteonecrosis. The general format of the
terminology is therefore:
a. Acute [Evolution Term], [Manifestation Term(s)], Decompression Illness.
b. Examples of how the terminology is used include:
(1) Acute, relapsing neurological, decompression illness, or
(2) Acute, progressive, limb pain and cutaneous decompression illness.
4-10 ORIGINAL
c. Evolution Terms. The evolution term is used to describe the development of the
condition PRIOR TO RECOMPRESSION. Because DCI is frequently a highly dynamic
condition, the term used may change from one observation to the next, eg a condition
may probably present initially as being ‘progressive’ as the patient becomes increasingly
aware that something is wrong. It may then stabilise for a period and be described as
‘static’. The patient may then undergo a substantial improvement, occasionally to
complete resolution of the symptoms, and at that stage the condition would be described
as ‘spontaneously improving’. Occasionally, after a period of improvement, the
symptoms return or new symptoms appear, in which case the condition would be
described as ‘relapsing’. Below there are more detailed descriptions of the evolution
terms:
(1) Progressive. A condition may be described as progressive if the number or

severity of symptoms or signs is increasing. Examples would include an increasing
severity of limb pain or the involvement of additional joints or a neurological
presentation in which the loss of motor or sensory function is becoming more
profound or where the extent of any loss of function is increasing, such as the
cephalad extension of a deficit with a predominantly spinal distribution. The
development of a new manifestation, such as a neurological symptom or sign in
addition to another manifestation, such as limb pain, also represents progression of
the condition. Terms such as ‘rapidly’ or ‘slowly’ may be used to enhance the
description of this evolution where this is appropriate. ‘Rapidly’ and ‘slowly’
would refer to the progression of symptoms over a period of minutes or hours
respectively.
(2) Static. This is self explanatory. Neither the severity or number of

manifestations is changing substantially.
(3) Spontaneously Improving. It is common for a number of presentations of

decompression illness to improve, albeit transiently in certain instances, without
recompression. Substantial improvement must occur for this term to be applied.
As with other evolution terms, ‘improving’ should only be used to describe events
prior to recompression.
(4) Relapsing. Occasionally, cases which have improved spontaneously undergo

a secondary deterioration. This is particularly true of some neurological
manifestations. This term is used to describe such cases. When a condition gets
worse in the absence of any spontaneous improvement it should be described as
‘progressive’. ‘Relapsing’ should be reserved for cases which have, at some stage
in their evolution, undergone substantial, spontaneous improvement.
d. Manifestation Terms. There are a number of manifestations of decompression

illness which occur commonly and these are outlined below. They may occur alone or
in combination. Occasionally, unusual cases occur and in such instances, the use of
additional descriptive terms may be required.
4-11 ORIGINAL
(1) Pain
(a) Limb Pain. In military diving, this is probably the most frequent
manifestation of decompression illness. It is used to describe the deep aching
pain in or around one or more joints which may begin during decompression
or after completion of a dive. Following ‘bounce’ dives, the upper limbs tend
to be involved more often than the lower limbs and the shoulder is involved
particularly frequently. Conversely, in saturation divers, aviators and
compressed-air (caisson) workers, it is the lower limbs and particularly the
knees which are involved most commonly. The pain usually begins gradually
and is poorly localised; it may resolve spontaneously and is then known as a
‘niggle’. Niggles may flit from joint to joint. If the pain gets worse, it
becomes more readily localised and is described as a dull, boring ache, similar
in character to tooth ache. Sometimes the joint is held in a particular position
that is least painful, but pain is seldom made worse by movement. If the pain
is in a lower limb, weight bearing may be poorly tolerated on that limb. On
examination, there are often no objective signs. Occasionally, there is a skin
rash over or adjacent to the affected joint. Notably, the ‘classical’ signs of
inflammation: redness, swelling, warmth to the touch and tenderness are
missing. Even cases of apparently straight-forward limb pain must be FULLY
EXAMINED. A patient in pain may not notice mild paraesthesia or a small
area of numbness. Ensure that no neurological symptoms can be detected
before the choice of a therapeutic table is made. Limb pain decompression
illness usually resolves completely, even without treatment over a period of
12-72 hours. However, deliberate withholding of recompression is difficult
to justify. Not only is rapid relief of pain usually obtained but, particularly in
cases where there has been a rapid onset of pain after surfacing, the onset of
subsequent neurological symptoms may be prevented.
(b) Girdle Pain. This is a poorly localised, aching or ‘constricting’ sensation

which is generally in the abdomen, pelvis, or occasionally, in the chest. Girdle
pain in the context of DCI is generally considered ominous since it frequently
portends neurological deterioration.
(2) Neurological
(a) Involvement of the nervous system may be subtle, multifocal and

consequently of bewildering variety and difficult to localize. Both the central
and peripheral nervous systems may be involved and the manifestations can
be broken down into the loss of certain functions: higher functions, which
would include aberration of thought processes or affect, loss of memory,
dysphasia etc; alteration to the level of consciousness, including seizures; loss
of co-ordination; loss of strength or sensation with almost any distribution;
dysfunction of special senses and loss of sphincter control, especially of the
bladder. It is likely that many of these disorders involve the brain. In these
cases, some loss of consciousness to the point of disorientation is a frequent
finding and coma may occasionally ensue. Visual symptoms are common, as
are motor and other sensory deficits. Because this disease may be subtle, it is
most important that a diving supervisor knows his divers. Otherwise signs
such as a change of mood, dulling of intellect and loss of short-term memory
may go unrecognised.
4-12 ORIGINAL
(b) It is apparent that the spinal cord is also involved in neurological

decompression illness with some frequency. It may appear to be involved
alone or with other parts of the nervous system.
(c) Dives which readily appear to provoke disease with a predominantly

spinal cord distribution are short, deep dives with a rapid ascent to the surface.
The onset of symptoms commonly occurs shortly after reaching the surface,
with about half of serious cases becoming symptomatic within 10 minutes.
Less than 10% of serious cases present more than 4 hours after completing the
dive. In severe cases, the condition is often heralded by the onset of girdle
pain. Shortly afterwards, the patient may notice pins and needles, numbness
and muscular weakness in the legs which rapidly progresses to paraplegia. It
is possible for all four limbs to be involved and, in severe cases, shock may
complicate the clinical picture. In less severe cases, the onset is not so
dramatic and the progression to paraplegia may be delayed and incomplete.
There may be little in the way of girdle pain in such cases. On examination,
it is often possible to determine a ‘level’ above which spinal cord function is
apparently normal. This level is often in the lower thoracic or upper lumbar
segments. However, it is recognised that different levels may be determined
for motor innervation and the various sensory modalities. The bladder is
frequently involved. The patient may report difficulty initiating urination, but
more often, this will be detected by the absence of urinary output and the
presence of a distended bladder on examination of the abdomen.
(d) Unless the fulminant condition is rapidly treated with recompression,

complete recovery is unlikely. The prognosis for cases with a less dramatic
onset is better. Even without recompression some spontaneous improvement
generally occurs. Nonetheless, improvement will be more rapid and complete
with recompression.
(3) Audio-Vestibular. This is a unique subclass of neurological decompression

illness. It is thought that there are two mechanisms whereby the audio-vestibular
system may be involved: Barotrauma and tissue injury caused by bubble formation.
Possible targets of this second mechanism include the cochlea, the eighth nerve
nuclei and cerebellar or cortical pathways. In individual cases it may be very
difficult to distinguish between these mechanisms or sites of injury by clinical
examination alone. As a consequence this term may be used to describe the
syndrome which includes: vertigo (a sense of rotation), tinnitus, nystagmus and loss
of hearing after a dive. Nausea and vomiting may accompany these symptoms, but
of themselves are not sufficient to imply audio-vestibular involvement in
decompression illness. Experimental and anecdotal evidence now exists to show
that recompression does not appear to have an adverse affect on pathology due to
round or oval window rupture. Therefore, if the mechanism of disease is uncertain,
appropriate recompression therapy should be undertaken at the earliest opportunity.
All such cases should then be referred for specialist investigation to establish the
need for further treatment of a perilymph fistula.
4-13 ORIGINAL
(4) Pulmonary. As has been mentioned before, involvement of the lungs in

decompression illness may be due to two quite distinct processes: decompression
pulmonary barotrauma and the cardiopulmonary consequences of massive venous
gas embolism. Although the mechanisms involved are distinctly different, it may
be difficult to distinguish between them immediately in a clinical setting, because
many of the symptoms and some of the signs are shared: chest pain, cough,
haemoptysis, shortness of breath, cyanosis and, rarely, shock. Progressive disease
may be due to either a tension pneumothorax or massive gas embolism of the lungs.
Where there has been a dive which has induced a low gas burden, it is most likely
that a pneumothorax is the cause of the problem. This may be diagnosed clinically
from the classic signs: cyanosis and respiratory distress; evidence of mediastinal
shift away from the affected side; hyperresonance and reduced respiratory
movements and breath sounds on the affected side. An x-ray, if available, will
confirm the diagnosis. The presentation of patients with massive, overwhelming
venous gas embolism of the pulmonary circulation has been described, although it
is very rare and generally associated with deep dives and missed decompression.
These patients usually become symptomatic within about half an hour of reaching
the surface. The condition commences with central chest pain and a cough, which
may be aggravated by taking deep breaths or inhaling cigarette smoke.
Breathlessness and central cyanosis follow and, shortly thereafter, signs of shock.
The condition is commonly progressive and the patient may deteriorate rapidly:
cardiovascular collapse, loss of consciousness and death may follow, unless the
patient is recompressed. Apart from cyanosis and respiratory distress, there are no
signs of a pneumothorax and progression to neurological manifestations.
(5) Cutaneous. The skin may be affected by diving in a number of ways. Two
very common manifestations of decompression, which are not generally regarded
as illnesses, are suit ‘squeeze’ and itching in the absence of a rash. The term
‘cutaneous’ decompression illness should be used to describe the condition which
generally presents with a red rash and severe itching which is usually on the trunk.
After a time, the rash commonly progresses to cyanotic mottling or marbling of the
skin. When further describing the condition, it is desirable to identify the location
of the disorder.
(6) Lymphatic. Occasionally, lymph nodes may become enlarged and tender and
this may be associated with oedema. The skin feels thickened and may have the
‘pitted’ appearance of orange peel. If pressure is applied to the skin, for example,
by the thumb and released after about a minute or so, a visible indentation remains.
(7) Constitutional. There are a number of non-specific symptoms which occur

after diving and which, if severe or if accompanied by other manifestations, may be
considered part of the decompression illness syndrome. These include headache,
excessive fatigue, malaise (which may include nausea and, possibly, vomiting) and
anorexia.
(8) Although it is desirable for the observer to describe each of the manifestations,
in rare, highly complex cases, rather than enumerate a long list of manifestations,
it may be appropriate to use the term ‘multisystem’.
4-14 ORIGINAL
0413. Additional Information
a. The Time of Onset. Decompression illness usually presents within a short period
of time following a dive, although occasionally this may be delayed by as much as 48
hours. Symptoms may become apparent before surfacing in saturation and occasionally
in bounce dives, particularly where decompression has been omitted. Most symptoms
occur after surfacing, however, and the majority of serious neurological or pulmonary
symptoms are usually manifest within about 30 minutes. The onset of limb pain also
occurs in this time period but this may be delayed for many hours after a dive. It should
be remembered that decompression illness may be provoked or made worse many hours
after a dive if the diver takes a flight. If a diver has been asymptomatic for 48 or more
hours after a dive and has not flown, then symptoms which develop subsequently are
probably not dive-related. The time of onset should be recorded as the time in minutes
or hours from surfacing from the last dive to the onset of each manifestation of
decompression illness. If a flight was taken after the last dive, this should also be
recorded.
b. Gas Burden. When considering possible mechanisms for decompression illness,

it is desirable to have an idea of the amount of gas that is likely to be present in the
various tissues. At present there is no convenient means of summarising this.
Consequently it is important that the dive profile is recorded as accurately as possible.
Where a dive computer or depth-time recorder was worn, the information should be
retrieved from this source.
c. Evidence of Barotrauma. This is particularly important in the case of pulmonary

and audio-vestibular decompression illness as discussed above. However, any evidence
of barotrauma, such as involving the middle ear or lungs should be recorded. It is
important that only hard physical signs are treated as evidence of barotrauma.
d. Response to Recompression. Quite often, the only means of confirming a

diagnosis of decompression illness is if there is some measure of improvement following
recompression. Consequently, it is important to record the response to recompression.
There are an increasing number of investigations which are performed on cases of
decompression illness, such as tests for a patent foramen ovale, electrophysiological tests
and perfusion scans of the brain. The results of all investigations form an important part
of any case notes.
0414. Summary Table of Common Diving Complaints by Time of Onset

Table 04-1 shows the common illnesses associated with diving. The table gives an
index of how likely various diving conditions are to present at different phases of a dive. The
most likely diagnosis for each phase is shown with +++, diagnoses which are not possible are
shown as such. The table is divided into two parts. Those conditions above the double line are
possible in most forms of diving whereas those below the double line are only likely to be
associated with closed or semi-closed breathing circuits. Nitrogen narcosis will not occur when
the breathing gas is oxy-helium.
4-15 ORIGINAL
Table 4-1. Diagnosis of Common Diving Complaints by Time of Onset (Phase of Dive)
DESCENT BOTTOM PHASE ASCENT ON SURFACE ON SURFACE

< 10 MINUTES > 10 MINUTES
DECOMPRESSION Not Possible Not Possible + +++ +++

ILLNESS (Profile dependent & more likely (Profile dependent) (Profile dependent)
near the surface)
AURAL AND +++ +/- +++ ++ +/-

SINUS Barotrauma usually associated with Reverse squeezes Delayed onset of symptoms Delayed onset of
BAROTRAUMA travel; possible delayed onset from (eg perilymph fistula) symptoms
descent
ALTERNOBARIC/ + +/- ++ + Not Possible

CALORIC Delayed onset from descent Possible, most likely time Only possible in the first few
VERTIGO minutes
NITROGEN +/- +++ +/- Not Possible Not Possible

NARCOSIS Only 30m or deeper Deep diving on air or nitrox Symptoms should improve with
4-16
ascent
CO2 POISONING- +/- ++ + +/- Not Possible

HYPERCAPNIA With too low flow, or accumulation in With too low flow, inadequate CO2 With too low flow or exhaustion of Unlikely unless continuing to Recovery should
diving dress on surface scrubbing or improper breathing CO2 canister breath from rig on the surface be rapid
OXYGEN ++ + ++ +/- Not Possible

DEFICIENCY - Possible: if mix improper, inadequate Less likely due to increased partial Only possible if breathing
HYPOXIA/ flow, reducer obstruction pressure improper mix on surface
ANOXIA
CNS OXYGEN +/- + +/- +/- Not Possible
TOXICITY Possible if improper mix With long bottom time and high Less likely since PO2 is decreasing `Off-phenomenon'
PO2
ORIGINAL
CHAPTER 5
MANAGEMENT OF DIVING ACCIDENTS
ORIGINAL
CHAPTER 5
CONTENTS
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0501
Provision of Medical Support . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0502

Diving Medical Officer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0503
Occasions for Consulting a Diving Medical Officer . . . . . . . . . . . . . . . . . . . . . . . . . 0504
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0505
Rescue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0506
Clinical Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0507
First Aid Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0508
First Aid Treatment of Acute Decompression Illness - Flow Chart . . . . . . . . . . . . . 0509
Command and Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0510

Evacuation Considerations and Requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0511
Portable Recompression Chambers.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0512
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0513
5-1 ORIGINAL
INTENTIONALLY BLANK
5-2 ORIGINAL
CHAPTER 5
0501. General
a. Divers suffer illnesses and injuries for preventable reasons. These include: failure
to observe regulations and instructions; the failure of others to carry out correct drills;
or the inadequate maintenance, repair or testing of breathing apparatus or other
equipment. Some incidents, however, occur due to other factors. For example,
decompression illness may arise from dives within accepted decompression profiles and
non-diving medical problems may present for the first time underwater. Furthermore,
divers, like others who work at sea, are vulnerable to unpredictable changes in the
elements.
b. When accidents and incidents do occur, there are very few that can not be managed
successfully if the right facilities and skills are available. The emergency handling of
a casualty may be divided into four phases: rescue, assessment, treatment and
evacuation.
c. Section 2 of this chapter describes the medical support of NATO diving operations,
Section 3 describes the first three of these phases and evacuation is dealt with in
Section 4.
d. Factors to be considered in the investigation of diving accidents are dealt with in

Section 5.
5-3 ORIGINAL
INTENTIONALLY BLANK
5-4 ORIGINAL
0502. Provision of Medical Support
a. National Regulations. National regulations for the provision of on site medical

support of diving operations are given at Table 5-1.
b. Availability of Recompression Facilities
(1) A list of the signal addresses of National Authorities responsible for initiating
treatment of NATO diving casualties is given at Annex A.
(2) A message is to be sent to the Local Area Commander before commencing

diving operations in waters controlled by him, using the format:
Precedence: Priority
Classification: Unclassified
Action: National Area Commander
Information: In accordance with national rules
SIC: LOA (Diving matters - General)
1. Nationality and name of vessel or unit involved in the diving

operations in local waters in position (latitude and longitude) at (zone)
time.
2. Type and duration of diving operation to be conducted.
3. Request information on location and availability of nearest

therapeutic recompression facility.
4. Request information on what type of diving medical assistance is

available and at what notice.
c. In the event of a recompression facility being required for an emergency treatment,

signal action should be taken in accordance with Paragraph 0510.
5-5 ORIGINAL
0503. Diving Medical Officer
Definitions:
a. General Duties Naval Medical Officer (GDNMO). A qualified physician who

has undergone general military training in order to provide medical support to a naval
base or surface naval vessel.
b. Diving Medical Officer (DMO). A qualified physician who has received

additional training in Diving Hyperbaric medicine and who has achieved a high level
of competence in the diagnosis and management of diving related illness.
c. Diving Medicine Specialist (DMS). A qualified physician and DMO who through
additional training and experience has attained a sufficiently high level of
clinical/academic competence to advise national staff in all matters concerning diving
and hyperbaric medicine.
d. Specialist Status. Some nations issue a Diploma of Hyperbaric Medicine, or other

national credit, so enabling the DMO or DMS to be formally recognised on that nations
specialist register.
5-6 ORIGINAL
Table 5-1. Diving Medicine Training of General Duty Naval Medical Officers and
Diving Medical Officers
NATO NATIONS
NATION GDNMO DMO Specialist Status
BE No formal theoretical training. 1 year formal training in France, program No
constructed of a number of 14 day
modules.
CA 6 hour basic training in Medical officers serving the diving No
environmental medicine which community:
includes some diving medicine. 2 week basic diving medicine course.
DMO: additional 3 weeks of theoretical
training plus 1 week of practical training
at diving unit.
DA 1 week theoretical course. 1 + 2 weeks advanced course at DCIEM, No
Canada.
FR From 1998: 2 years formal training (university & No
2 weeks basic theoretical training. hospital).
Year 1: clinical training.
Year 2: research and practical training.
GE 1 week theoretical training. 5 weeks theoretical training, 3 weeks No
practical dive training.
IT 20 hours theoretical training. DMO: 6 months internal training. Yes
DMS: 3 years university based training.
NL 2 weeks theoretical training. DMS: 1 year formal internal/hospital No
training. Year 2 for selected candidates
primarily research.
NO 1 week theoretical training No further in house training. No
Further competency achieved through
participation and attendance on
international courses.
PL - - -
PO 4 weeks theoretical training. Training in FR or SP according to No
programmes indicated for those nations.
SP None 2 years formal training, mixed military ?
and civilian. Year 2 primary research and
practical training.
UK 1 week formal theoretical training. DMO: Minimum 6 internal training at No
Compulsory 2 day refresher course INM. Includes practical diving,
at maximum 5 year interval. submarine escape and hyperbaric
medicine.
DMS: As above plus accredited Yes
specialist in Occupational Medicine. (occupational
medicine)
US None DMO: 24 weeks including 3 weeks Yes

theoretical training in diving medicine
and 6 weeks practical dive training.
5-7 ORIGINAL
PARTNERSHIP FOR PEACE NATIONS
NATION GDNMO DMO Specialist status

Bulgaria - - -
Finland No formal programme (on the 2 year fully credited academic Yes
job training and supervision) training
Estonia No programme No programme No
Latvia No programme No programme No
Lithuania No programme No programme No
Romania - - -
Slovenia - - -
Sweden 2 weeks training: Additional 3 courses each lasting 3 No
1 week diving medicine, days and covering aspects of diving
1 week clinical hyperbaric medicine and submarine escape.
medicine
5-8 ORIGINAL
Table 5-2. Medical and Paramedical Personnel for On Site Support

of Diving Operations
NATION Medical Personnel

Diving Non-specialist Diving/Medical Attendant Paramedic
Medical Officer Medical Officer in Corpsman Technician Personnel
Support of Diving
Operations
BE There is currently no There is currently no A diving medical All divers are
requirement for medical requirement for medical technician is assigned to all trained in first aid
support of diving support of diving operations vessels which have a and emergency
operations hyperbaric chamber. A procedures. All
hyperbaric chamber is divers are trained
stood by in support of in the diagnosis
diving operations deeper and first aid of
than 45 msw. diving medical
problems.
CA Experimental diving for Do not support diving Assigned to all diving All divers are
decompression operations units, usually for surface trained in first aid
methodology, experimental supplied diving and for and emergency
trials of new diving initial diving training procedures. All
apparatus and saturation clearance diving
diving. supervisors are
trained in the
diagnosis and
treatment of diving
medical problems.
DA Experimental diving, tests All initial diving training. Assigned to all diving Assigned to all
of new breathing apparatus educating units. diving commands.
or diving procedures. Exit
and re-entry exercises.
Diving training beyond 50
msw.
FR All diving operations with Do not support diving All diving operations with
Trimix. operations. mixed gas.
Experimental Diving Tests
of new breathing apparatus
or diving procedures.
GE Test of new breathing Test of new breathing All diving operations. CDO- Clearance
apparatus or diving apparatus or diving Diving Officer
procedures. All Diving procedures. All Diving CODO - Combat
operations beyond 50 msw. operations beyond 50 msw. Diving Officer
All exercises of combat All exercises of combat SWDO - Ship’s
swimmers during initial swimmers during initial Diving Officer
training. Submarine training. CDC - Clearance
Escape Training Diving CPO
CODO - Combat
Diving CPO
SUDC - Ship’s
Diving CPO
SDC - Salvage
Diving CPO
GR - - - -
5-9 ORIGINAL
Table 5-2 Medical and Paramedical Personnel for On Site Support of Diving
Operations (Continued)
NATION Medical Personnel

Diving Medical Officer Non-Specialist Medical Diving Medical Paramedic
Officer in Support of Attendant Corpsman Personnel
Diving Operations Technician
IT Experimental diving, heliox All diving beyond 40 Assign to all diving All divers and
diving and saturation diving. msw. Night time diving. commands which supervisors are
Diving from 0-40 msw, have/have not a hyperbaric trained in first aid
that by the opinion of the chamber. and emergency
diving officer/ supervisor, medical procedures
may be particularly
dangerous, hard of
difficult. Escape
operations from
submerged submarines.
NL Experimental diving, tests of All initial diving training. Assigned to all diving Diving Officer DO
new breathing apparatus or commands which Frogman Officer
diving station procedures. have/have not a hyperbaric FO
Exit and re-entry exercises. chamber. Diving Master DM
Diving training beyond 50 (CPO)
msw. Signal Master SM
(PO)
Frogman Instructor
FI (CPO)
NO Submarine Escape Training All basic diving training Submarine Escape training -
PO Large scale sabotage diving - All diving operations -
operations
SP Experimental and Saturation Diving deeper than 75m. All diving operations All divers and
diving Submarine escape training which requires a supervisors are
and escape exercises from hyperbaric chamber. trained in first aid
submerged submarines. and emergency
medical procedures
TU All diving operations beyond - All diving and Hyperbaric All divers and
190 fsw and diving casualty Chamber Operations supervisors are
treatments trained in first aid
and emergency
medical procedures
UK 1. Ship’s Diving
Currently there is no requirement for medical or paramedical support of ship’s diving operations.
2. Clearance Diving
Currently there is no requirement for medical or paramedical support of clearance diving operations.
3. Experimental Diving
There are no requirements laid down for medical support of experimental diving operations but Ethical Committee
scrutiny of all protocols ensures adequate provision
US All diving operations beyond - Assigned to all diving All divers and
57 msw. commands which have a supervisors are
hyperbaric chamber. trained in first aid
and emergency
medical procedures.
5-10 ORIGINAL
0504. Occasions for Consulting a Diving Medical Officer
a. A Diving Medical Officer should be consulted in the following circumstances:
(1) All diving accidents which occur when no Medical Officer is on site.
(2) When there is uncertainty about the diagnosis, or where the clinical condition
is complicated by trauma.
(3) All cases of decompression illness.
(4) Unusual diving incidents.
(5) If a patient fails to respond to recompression or if a patient’s condition

deteriorates during treatment.
(6) If unforseen events occur during hyperbaric treatment (eg loss of chamber
pressure, loss of O2 supply etc).
b. If for any reason difficulty is encountered contacting a Diving Medical Officer, the
attending non-specialist Medical Officer or diving supervisor should not delay treatment
but proceed with first aid measures and therapeutic recompression.
5-11 ORIGINAL
INTENTIONALLY BLANK
5-12 ORIGINAL
0505. Introduction
a. Objectives. There are three basic objectives to first aid which are common to
accidents and incidents of any cause, including those related to diving. They are:
(1) To sustain life.
(2) To prevent the worsening of any condition.
(3) To promote recovery.
b. General Principles
(1) The general principles of standard first aid practice are also common to diving-
related incidents. The casualty may need to be rescued and removed from danger,
he will need to be assessed to determine his injuries and appropriate first aid
treatment will need to be initiated. Evacuation to a definite treatment facility, the
final phase of first aid, is discussed in Section 4.
(2) Patients will often show some improvement with first aid treatment,
occasionally to the point of apparent recovery. The first aider should not be
persuaded that there is no longer a need to refer a casualty for specialist medical
attention because many diving related conditions are associated with a risk of
relapse or secondary deterioration. This is particularly the case with victims of
decompression illness or near drowning.
0506. Rescue
The circumstances surrounding individual diving accidents or incidents can be extremely
varied but the rescue phase can always be considered in the same way. To be effective, the
management of a rescue must begin without delay. There is a need to swiftly assess the situation,
plan a course of action and then act accordingly.
a. Assessment. This is a continuous process of evaluating all the relevant factors

throughout a rescue situation. Experienced divers will often recognise the factors that
could lead to an incident before the incident even occurs.
b. Plan. The first consideration in any plan should be the safety of the rescuers, but
speed of action and the likely effectiveness of the rescue operation are also important
considerations.
0507. Clinical Assessment
a. The extent to which a clinical assessment is performed is entirely dependent on the

urgency of treatment. In the majority of occasions encountered in diving, effective, safe,
first aid treatments can be initiated before a final diagnosis has been formed.
5-13 ORIGINAL
b. Once a casualty has been removed from danger, clinical assessment should always
begin with Airway, Breathing, Circulation and Gross Neurological Function. Standard
cardio-respiratory resuscitation should be started as required and if gross neurological
abnormalities such as a reduced level of consciousness, confusion or weakness are
obviously apparent, immediate action should be taken to arrange for recompression
therapy. Decompression illness is not the only cause of neurological injury in military
divers, but it must always be regarded as a possible cause requiring urgent
recompression therapy until proven otherwise. Practically the only exception to this rule
arises in the immediate management of casualties using equipment and gas mixtures
which make acute cerebral oxygen toxicity the most likely diagnosis. First aid and
treatment of oxygen toxicity is discussed at Paragraph 0203.
c. A more detailed history and examination can take place after this assessment of
basic cardiorespiratory and gross neurological function. This history and examination
will also be appropriate for divers who have not required rescue but have nevertheless
experienced difficulties during a dive or developed a medical complaint following a
dive. The NATO Diving Incident Medical Record at Annex C should be used as a
standardised form for recording the details of the history and examination. Detailed
instructions for the completion of this form are given at Annex C and an outline of what
is required is given below:
(1) The examiner must compile a History of the case which should include facts
ranging from the dive profile to the progression of the medical problem. The
following questions will help to determine the diagnosis and hence, the necessary
treatment. The results of these questions should be used to complete the first page
and history sections of the report form.
(a) What type of dive did you make? With what depth and time profile? With
what equipment and gas mix? Did anything unusual occur?
(b) What other dives have you made in the last 72 hours?
(c) When did you first notice that something was wrong? Before, during or
after which dive - and how many minutes after surfacing? If during the dive,
did the symptoms occur while descending, on the bottom or during ascent?
(d) Describe what is wrong with you.
(e) Has the problem got worse or improved since you first noticed it?
(f) Have any additional symptoms developed?
(g) Have you ever had a similar problem before?
(h) Have you ever had diving related problems before?
5-14 ORIGINAL
(2) Once the history is complete, the casualty must be examined. A General
Systems Examination should be performed in accordance with examiner’s level of
medical expertise. Particular care should be taken to examine the chest and neck
for signs of pulmonary barotrauma of ascent and to examine the skin for rashes of
acute skin decompression illness.
(3) A full Neurological Assessment should then be undertaken. Details of how to

perform a neurological examination are provided for non-medical personnel at
Annex D.
d. If a neurological deficit becomes apparent at any stage of this detailed history and
examination, first aid treatment measures for acute decompression illness should begin
at once and arrangements for urgent recompression therapy must be made. The history
and examination can then be continued at a suitable point during evacuation or when the
patient is stabilised in a recompression chamber.
0508. First Aid Treatment
a. Resuscitation. Standard techniques of cardio-respiratory resuscitation should be

used.
b. Oxygen Administration. Except in cases of cerebral oxygen toxicity, ventilation

with 100% O2 is the most effective form of first aid for all diving related medical
problems. It should be administered by a tight-fitting mask with a demand valve
regulator or other apparatus designed to deliver as close to 100% O2 as possible. Most
forms of hospital mask and nasal cannulae, which employ a continuous flow of oxygen,
deliver much less than 100% O2 and rapidly empty oxygen cylinders. Consequently,
such equipment should only be used when there is no better alternative. 100% surface
oxygen breathing is no substitute for hyperbaric oxygen treatment of decompression
illness. Even after complete relief on normobaric oxygen treatment, a recurrence of
severe symptoms may occur. All cases of DCI should be transferred to a hyperbaric
facility for evaluation and treatment.
c. Fluids. Dehydration invariably complicates diving related medical problems,

especially decompression illness. Rehydration should therefore commence at the earliest
opportunity.
(1) Conscious Patients who can protect their airway are to be given oral fluids.
At least one litre of still water or appropriately diluted fruit squash should be drunk
initially. Additional fluid should be consumed until a substantial urine output is
provoked. In the absence of a urine output the abdomen should be examined for the
presence of an enlarged bladder. If the bladder is enlarged and the patient has
difficulty initiating urination, catheterisation should be undertaken by appropriately
trained personnel. Establishment of an intravenous administration route should be
considered for individuals with symptoms of serious DCI where equipment and
sufficiently experienced personnel are available. (See Section 0508c.(2).)
5-15 ORIGINAL
(2) Semiconscious and comatose patients should be given intravenous fluids by

appropriately trained personnel. Start rehydration by infusing one litre of normal
saline, Ringer’s Lactate or Hartmann’s solution over 30 minutes and then a further
litre over the next hour. Alternatively, fluids can be titrated against urine output
which should be maintained above 0.5 ml/kg/h. The use of Dextran is controversial
since it may provoke idiosyncratic adverse reactions and an increased tendency to
bleed. Equally, solutions containing glucose should be avoided since these appear
to compromise the recovery of ischaemic nervous tissue. Bladder catheterisation
may be required if the level of consciousness does not improve or if the spinal cord
is involved and the bladder becomes palpable.
d. Analgesics. Symptoms of pain may be masked by the administration of analgesics

and this may complicate monitoring of the progress of the patient. These should only be
given where there is little likelihood of recompression within 2 hours and, where
possible, after consultation with a diving medicine specialist. The drug of choice is
Paracetamol. Nitrous oxide (ENTONOX) should NOT be used. Being a gas, it is
highly soluble in other gases and consequently it tends to make inert gas bubbles grow
which aggravates decompression illness. The use of aspirin or other non-steroidal anti-
inflammatory agents as an analgesic or adjunctive treatment is controversial. (See
Section 0604c.)
e. Nursing
(1) Diving casualties should be nursed and transported in a horizontal, rather than
head down posture. This is because exercise is thought to predispose to and
possibly aggravate decompression illness. If a diver is unconscious or vomiting, or
if patency of the upper airway is suspect, the recovery or coma position should be
used. Divers with respiratory distress (such as following a blast injury) may be
more comfortable in a sitting position.
(2) Attention must be taken to remove all wet clothing and keep the casualty
warm.
f. Recompression. This is regarded as a definitive treatment rather than a first aid

measure and is therefore discussed under its own heading in Chapter 8. There is no
place for in-water therapeutic recompression even for cases of decompression illness that
arise a very long way from a recompression facility. These casualties should be
managed on land in a safe, warm environment where they can rest, breathe 100% O2 and
be adequately rehydrated.
g. Other First Aid Treatments. Some diving-related disorders such as hyperthermia

require specific first aid treatments that are documented in the individual sections
relating to that disorder. (See Sections 0802 and 0804.)
5-16 ORIGINAL
0509. First Aid Treatment of Diving Related Injury
5-17 ORIGINAL
INTENTIONALLY BLANK
5-18 ORIGINAL
0510. Command and Co-ordination
a. Command. The National Authority responsible for treatment of diving casualties

in the area will advise the NATO Area/Sub-area Commander immediately about the
specific action to be taken and should activate the multi-place hyperbaric facility which
is situated nearest to the diving accident.
b. Communications
(1) In the event of a diving accident requiring immediate medical assistance

and/or evacuation of a casualty, a message is to be sent using the following format:
(see also ADivP-1/MDivP-1 paragraph 0211).
Precedence: Immediate
Classification: Unclassified
Action 1. NATO Area/Sub-area Commander

Action 2. National Area Commander
Action 3. Authority responsible for initiating treatment of diving
casualties in the area.
Information: In accordance with national rules.
SIC: LOL (Diving Matters - Accidents/Incidents)
Subject: Diving Accident
1. Nationality and name of vessel or unit involved in the diving

accident in position: (latitude and longitude) at (zone) time.
2. Details of accident and symptoms of the casualty (using the Diving

Casualty Signal Status Report Code detailed at Annex B)
3. Assistance required.
4. Any other facts or requirements.
5-19 ORIGINAL
(2) Whenever possible, direct telephone communications should also back up the
signal action. Emergency contact numbers are given at Annex A and diving units
should also have received information in reply to their pre-dive signal given at
Paragraph 0502.
0511. Evacuation Considerations and Requirements
a. Choice of Facility. Injured divers must first be resuscitated, stabilized and finally
retrieved to a definitive treatment facility under controlled conditions as early as
possible. The choice of treatment facility to which the casualty is taken depends on the
casualties clinical state, the diagnosis, the medical support available at each facility and
whether there is a need for recompression therapy.
(1) All cases of trauma and diving-related conditions which do not require
recompression therapy should be evacuated to the nearest medical facility with an
accident and emergency, or equivalent, unit.
(2) Cases of decompression illness who do not have life threatening cardio-
respiratory involvement should be evacuated to the nearest multi-place, multi-
compartment recompression chamber.
(3) Cases of decompression illness who do have life threatening cardio-respiratory

involvement present a tremendous challenge to those in charge of their immediate
care. Advice must be taken from a Diving Medical Officer on the relative merits
of immediate recompression based against the need to stabilise the casualties
cardiorespiratory function. Individual recompression facilities also need to be
consulted on whether they have the necessary medical expertise to manage such
casualties on site. A casualty with a pneumothorax and decompression illness may
be managed at a recompression facility, but an unconscious casualty with a
compromised airway may benefit from initial evacuation to an accident and
emergency unit followed by evacuation to a recompression chamber after
stabilisation.
(4) Casualties of pulmonary barotrauma of ascent without neurological

involvement should be evacuated to a medical facility with access to a
recompression chamber in case neurological features become apparent, although the
delayed onset of such symptoms or signs are very rare.
b. First Aid Measures. The first aid measures detailed in Section 3, including the
administration of oxygen and fluids for decompression illness should continue during
evacuation. The casualties vital signs should be continuously monitored before and
during emergency evacuation and he should be accompanied by an attendant who knows
the history of his condition and is capable of continuing First Aid should he deteriorate.
The NATO Diving Incident Medical Record at Annex C should be completed and
accompany the patient during transportation.
5-20 ORIGINAL
c. Mode of Transfer
(1) Casualties with life threatening conditions and those with decompression
illness must be transferred as swiftly as possible since delay in transportation may
mean the difference between total recovery, permanent neurological injury or even
death. The decision between air, sea and ground transport should be based on
minimizing the delay prior to recompression, although the sea state may preclude
transit by boat and the road surface, traffic conditions or altitude of a land route may
make even a short ambulance journey unacceptable.
(2) If the casualty has to be transported by an aircraft or helicopter without a

pressurised cabin, the pilot should fly as low as is compatible with safety, preferably
not above 300 m (1000 ft), to prevent a further reduction in ambient pressure which
may provoke or exacerbate decompression illness. If aircraft with pressurised
cabins are used, the cabin pressure should be maintained at the equivalent of 300
m altitude where possible.
0512. Portable Recompression Chambers

These chambers can be used to evacuate a casualty to a multiplace, multicompartment
recompression chamber that is fitted with a transfer under pressure (TUP) facility. These
portable recompression chambers have significant drawbacks: they can only be used safely to
transport fully conscious, clinically stable casualties (Paragraph 0605), and their use is illegal
in some NATO Nations.
5-21 ORIGINAL
INTENTIONALLY BLANK
5-22 ORIGINAL
0513. General
a. The principle of accident investigation is to evaluate the cause or causes of an

accident on the basis of three possibilities:
(1) Human biological failure
(2) Equipment failure
(3) Faulty procedures
b. The Diver. It is important to get as much information as possible from the diver
and his colleagues or any other eye witnesses. Some of the important aspects are:
(1) Experience. This includes both general diving experience and also his
experience in performing the particular task in the particular conditions with the
particular equipment.
(2) Past Medical History. Illness or recent treatment incompatible with diving
(eg. trauma, peptic ulceration). Diving history, including any previous accidents or
incidents.
(3) Personal History. The diver’s motivation should be considered including the
possible effect of any emotional problems.
(4) Pre-Dive Activities. Consideration should be given to the diver’s food and
drink in relation to the dive. The real risk of a hangover is that it can lead to
underwater vomiting. It is also associated with an increased risk of decompression
illness and N2 narcosis. Another consideration is that the diver’s pre-dive activities
may have tired him excessively.
(5) Medical Examination. This should be carried out as soon as possible after the
incident and both the examination and the record of it should be meticulous.
(6) In all cases of diving accidents a full toxicological/drug analysis on blood and
urine is recommended.
(7) Post Mortem. If the diver is dead it is most important to get photographic
evidence of any lesions at the earliest opportunity and take x-rays of the skull, chest
and abdomen. A post-mortem examination and inquest must be carried out in
accordance with the laws of the appropriate country.
Specialised autopsy techniques are necessary for a valid post-mortem

examination after underwater accidents, and it should be understood that the
discovery and location of gas bubbles are at best of doubtful significance and
are of no significance at all if the diver died while under pressure.
5-23 ORIGINAL
c. The Dive. This part of the investigation should cover the dive itself and the
climatic conditions at the time under the following headings:
(1) The diver’s narrative
(2) Witnesses narratives
(3) Object of the dive
(4) Depth and duration of the dive
(5) Frequency of dives
(6) Tides and sea state
(7) Water temperature
(8) Underwater visibility
d. The Equipment. The general condition of the apparatus should be noted. The gas
valves should be shut off and the number of turns needed must be noted. Any relief
valve must be sealed. Once the set has been sealed it should be sent if possible to have
the breathing gases analysed, including that in the counterlung (if fitted). If appropriate
it is important to warn the analyst that the gas may be pure oxygen because analysis by
chemical absorption (Scholander or Lloyd-Haldane apparatus) would be harmful to the
apparatus.
e. Records. It is vital that all diving accidents are reported to a central authority so
that the causes may be analysed.
5-24 ORIGINAL
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GORMAN, D. F. (1987) The Redistribution of Cerebral Arterial Gas Embolism. Ph.D. thesis,
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5-26 ORIGINAL
CHAPTER 6
THERAPEUTIC RECOMPRESSION
ORIGINAL
CHAPTER 6
CONTENTS
General . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0601
Principles of Therapeutic Recompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0602
Therapeutic Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0603
Adjunctive Treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0604
Hyperbaric Treatment Facilities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0605

Preparations for Hyperbaric Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0606
General Principles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0607
Omitted Decompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0608

Carbon Monoxide Poisoning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0609
Decompression Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0610
NATO Therapeutic Recompression Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0611
National Therapeutic Recompression Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0612
Non-Standard Treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0613
Recompression Therapy Abort Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0614
SECTION 4 - CARE IN THE RECOMPRESSION CHAMBER
Chamber Attendants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0615

Recompression Chamber Practice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0616
Chamber Treatment of Oxygen Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0617
General. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0618
Treatment of Refractory Decompression Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0619
National Protocols for the Treatment of Refractory Decompression Illness . . . . . . . 0620
Flying After Therapeutic Recompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0621
Return to Diving After Decompression Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0622
6-1 ORIGINAL
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6-2 ORIGINAL
CHAPTER 6
0601. General
a. This chapter covers therapeutic recompression used for the treatment of

decompression illness, omitted decompression and carbon monoxide poisoning.
b. The treatment regimens apply to conditions which range in severity from pain in a
limb to life-threatening cardiopulmonary collapse. In consequence, the degree of
medical expertise necessary to complete the treatment will vary depending on the illness
involved. Certain procedures, such as introducing intravenous lines and inserting a chest
drain or urinary catheter, require special training and should not be attempted by
untrained individuals.
c. Recompression treatment can be conducted satisfactorily only in a compression

chamber capable of holding at least two people and which is fitted with two
compartments to allow personnel to be locked in or out. Unless stated to the contrary,
this section deals with such treatment.
0602. Principles of Therapeutic Recompression

While first aid measures of oxygen administration and rehydration will assist the
casualty, the definitive treatment for the dysbaric disorders is recompression. This is thought to
have three principle effects:
a. Reduction of the volume of gas bubbles in accordance with Boyle’s law. This effect
will have a particularly important role in cases of DCI treated shortly after surfacing
when the bubbles which are thought to initiate tissue injury are still present.
b. To promote the reabsorption of inert gas bubbles in accordance with Henry’s Law.
By increasing the partial pressure of inert gas in bubbles, the gas will return to solution
in the tissues.
c. Increased tissue PO2. This is will reverse any ischaemia caused by the presence of
bubbles. Under hyperbaric conditions, the extra oxygen is carried in solution in plasma
which may perfuse vessels with partially obstructed lumens more readily than oxygen
which is bound to haemoglobin. In addition, hyperbaric oxygen has a number of other
effects which may be beneficial to the casualty:
(1) Vasoconstriction, which may serve to reduce tissue oedema.
(2) Anti-inflammatory actions.
6-3 ORIGINAL
(3) Inhibition of leucocyte binding to injured endothelium.
(4) Improves microvascular perfusion
0603. Therapeutic Tables

Therapeutic tables for the treatment of decompression illness have been developed,
adapted and used by NATO Nations so that a large number of different therapeutic tables now
exist. Similarities do, however, exist between many of these tables as they have usually been
developed for a specific purpose. For example most Nations would have a short oxygen table
for a ‘mild’ case of DCI (eg. limb pain DCI) or carbon monoxide poisoning, a long, shallow
oxygen table for more severe cases of DCI (eg. neurological DCI), a long, deep air/oxygen table
and saturation, or near-saturation tables for the management of the most severe cases of DCI.
There are no randomised trials to show that differences between individual Nations' tables of the
same type result in a significantly different clinical response, so all the tables may be successfully
used to treat DCI. In the interests of NATO standardisation and interoperability, tables of the
same type have been grouped together and given a NATO name for identification. This may
allow a common approach to the treatment DCI to be adopted by Nations. Details of this
schedule are given at Paragraph 0610, details of NATO Tables are given at Paragraph 0611
and details of individual Nations tables are given at the Annexes.
0604. Adjunctive Treatments
a. Steroids have been used for the treatment of serious decompression illness.
Although there is no statistical evidence that they improve the outcome, they may reduce
the incidence of secondary deterioration. 12-20 mg dexamethasone may be given by
SLOW intravenous or intramuscular injection as an initial loading dose and repeated 6
hourly for up to 48 hours thereafter. High dose parenteral methylprednisolone
(30mg/kg) has been reported to be beneficial in the treatment of traumatic cervical cord
injury but no effect on spinal cord evoked response has been noted in animal studies of
decompression illness. Steroids should only be administered by appropriately trained
chamber attendants and only when authorised by a Diving Medical Officer.
b. Lignocaine has been shown to reduce brain dysfunction and accelerate recovery of
brain function after air embolism in experimental animals when administered both
prophylactically and therapeutically. There are limited case reports of similar beneficial
effects in human subjects treated for decompression illness, suggesting a role for use if
lignocaine in selected patients. Further multicentre human studies are required to
determine relative efficacy and safety of this possible adjunct before it can be endorsed
as an acceptable standard treatment.
c. Aspirin and other anti-platelet agents have been shown to have mixed effects in
human and animal studies of the treatment of decompression illness. Despite their
positive early effects on platelet accumulation, some risk of post-reperfusion rebleed into
nervous system tissues has been demonstrated and this may adversely affect the
outcome. Their use as an adjunct is therefore controversial.
6-4 ORIGINAL
d. Diazepam has been shown to be effective in controlling the vestibular symptoms

of neurological decompression illness. Successful use of this drug does however
obscure the symptomatic end point for recompression treatment, limiting its usefulness
in practice.
e. Some other treatments may be considered, in accordance with national regulations.

Some examples of this include Pentoxyphillin, which has an action on blood red cells,
and Nicergolin, an alpha blocker used as a vasodilator of cerebral vessels in cases of
inner ear damage.
6-5 ORIGINAL
0605. Hyperbaric Treatment Facilities
a. Monoplace Recompression Chambers
(1) Three types of monoplace recompression chamber exist. Those designed for
surface decompression procedures, those designed as portable recompression
chambers for casualty transfer and those designed for hospital treatment of non-
diving conditions that respond to hyperbaric oxygen therapy. None of these
chambers were designed for the treatment of acute decompression illness and their
use is inappropriate for several reasons:
(a) Clinical examination of the casualty in order to monitor the effects of

treatment and adjust the treatment schedule as necessary is impossible.
(b) No attendant is available to provide basic life support if the patient

deteriorates.
(c) Deep or prolonged treatment tables are rarely possible because of the
physical limitations of the chamber.
(2) Despite this, successful treatments have been carried out in monoplace
chambers but the circumstances of each case have to be very carefully considered
before treatment begins. If it is possible to transport the patient to a multiplace
chamber within a short period (minutes rather than hours) this is likely to be
preferable to commencing treatment in a monoplace chamber. The casualties
clinical condition is also important. Under no circumstances should an unconscious
patient be recompressed in a monoplace chamber. The risks of life threatening
complications such as vomiting and aspiration occurring inside the chamber are
higher than the risks from a delay before recompression in an appropriate facility
when first aid measures can still be effectively administered during the delay. The
decision whether to carry out therapy in a monoplace chamber or to transport the
patient to a multiplace chamber rests with the Diving Supervisor, although the
advice of a Diving Medical Officer should be obtained as soon as possible.
(3) If a monoplace chamber is to be used, consideration must be given to the need

to keep the patient adequately hydrated during treatment, consistent with the
restrictions imposed by a monoplace chamber. In particular, the need for urinary
catheterisation should be addressed prior to commencing recompression.
6-6 ORIGINAL
(4) Only oxygen tables should be used. The patient should initially be compressed
R
on NATO Table VI unless this schedule is extended or modified on the advice of
a Diving Medical Officer. Every effort must be made to transport the portable
chamber to the nearest available multiplace chamber with a TUP facility by the
quickest and safest means, recognising that in some Nations, the use of
transportable chambers is illegal. The advice of a Diving Medical Officer should
be sought before committing a casualty to recompression in a monoplace chamber,
even for apparently trivial incidents, since the treatment will be conducted under
less than ideal conditions.
(5) Removal from a Monoplace Chamber in an Emergency. In the event of a

casualty undergoing recompression in a monoplace chamber becoming
unconscious, having a seizure, or requiring some form of urgent medical attention,
the chamber may be decompressed in one minute to allow access to the patient.
However, a patient should NEVER be decompressed during the tonic phase of a
convulsion when breath-holding is common.
b. Multiplace, Multicompartment Recompression Chambers. These are the

hyperbaric treatment facilities of choice as they allow constant monitoring and attending
of a patient. Medical personnel with specialist skills may be locked into the chamber if
required and prolonged treatments may be performed in these chambers.
0606. Preparations for Hyperbaric Therapy
a. Military divers who have been passed fit to dive are unlikely to have
contraindications to hyperbaric therapy. The effects of hyperbaric pressure on some
items of medical equipment and the difficulty of performing some medical procedures
inside the relatively cramped conditions of the chamber mean that some preparatory and
precautionary measures may need to be taken prior to commencing treatment.
(1) Divers unable to maintain an adequate airway and adequate respiratory effort
should undergo endotracheal intubation prior to recompression. Water should be
used rather than air in the cuff.
(2) Unconscious divers should be catheterised. Water should be used rather than
air in the balloon.
(3) IV access may be required for administration of fluids or drugs.
(4) Divers with a large pneumothorax may require a chest drain to be inserted.
Problems may otherwise occur during the ascent phase of recompression therapy.
(see Paragraph 0316)
(5) Divers with evidence of bronchospasm may need to be treated with

bronchodilators, but caution is necessary as there is a theoretical possibility that
some bronchodilator agents may also dilate the pulmonary arterioles and increase
the ‘arterialisation’ of trapped venous bubbles.
6-7 ORIGINAL
b. Within the need to provide rapid recompression, where required by national

regulations divers should be consented for recompression therapy and advised of
the benefits of treatment and possible side effects such as oxygen toxicity and
barotrauma.
0607. General Principles

There are some useful general principles to bear in mind while treating a patient:
a. ALWAYS
(1) Treat promptly and adequately. Do not delay treatment while awaiting the
attendance of, or consultation with, medical personnel. The initial examination,
prior to recompression, should establish the presence of gross abnormalities but
should not delay the treatment of seriously ill patients. As soon as signs of
decompression illness (particularly neurological) are elicited, the patient should be
placed in the chamber and recompressed. The remainder of the examination can
then be completed under pressure. Patients should be examined again at depth of
relief or treatment depth and on the completion of treatment. Areas of altered
sensation should be outlined with a pen so that the extent of sensory abnormalities
can be can be monitored.
(2) Treat an unconscious casualty for acute neurological decompression illness

unless this can be excluded with certainty.
(3) Have a qualified attendant in the chamber at all times during recompression
and ensure the attendant’s safety. In particular, attention should be paid to his or her
decompression.
(4) Check and record the patient’s condition and vital signs periodically. Check
frequently if his or her condition is changing rapidly or the vital signs are unstable.
Maintain an accurate fluid balance chart. Complete the relevant sections of the
NATO Diving Incident Medical Record. (see ANNEX C)
(5) Follow the Treatment Tables accurately and maintain the normal descent and
ascent rates unless a Diving Medical Officer recommends change.
(6) Maintain oxygen usage within the time and depth limitations prescribed by the
Treatment Table and be alert for warning signs of oxygen toxicity.
(7) Observe the patient after treatment for any recurrence of symptoms. Observe
for at least one hour after limb pain or cutaneous decompression illness, and for at
least six hours following treatment for more serious manifestations.
6-8 ORIGINAL
b. NEVER
(1) Permit any shortening or other alteration to the tables except under the
direction of a Diving Medical Officer.
(2) Permit the use of 100% oxygen deeper than 18 m (60 ft).
(3) Fail to treat doubtful cases.
6-9 ORIGINAL
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6-10 ORIGINAL
0608. Omitted Decompression
a. When a diver has surfaced without completing the necessary in-water stops, action
must be taken to prevent the onset of decompression illness. The actions required
depend on National regulations and the decompression table being used, the time it will
take to achieve recompression and the recompression facilities available. General
principles are as follows:
(1) If the diver can be safely be returned to the water and reach his deepest
omitted, or partly omitted stop within a very short period from surfacing, some
Nations using particular decompression tables allow the diver to return to the stop
and complete stop times as appropriate for the depth and time of the original dive.
(2) If the requirements of paragraph (1) above cannot be met but facilities are
available for recompression within a recompression chamber on site within a
specified minimum time, the diver should undergo surface decompression in
accordance with a recognised surface decompression table.
(3) If neither paragraph (1) or (2) are possible, the first aid measures of oxygen
and fluids should be administered and arrangements should be made for urgent
recompression at an available facility. NATO Tables V or VI may be used
depending on the amount of decompression missed.
b. It must be stressed that these actions are only for asymptomatic divers who have
missed decompression stops. Any diver who develops symptoms must be treated with
a therapeutic table in accordance with Paragraph 0610.
0609. Carbon Monoxide Poisoning

Any diver who surfaces unconscious or with a neurological deficit should be treated for
acute DCI in accordance with Paragraph 0605. NATO Table V is a short oxygen table which
is available for cases of carbon monoxide poisoning where decompression illness can be
excluded.
0610. Decompression Illness
a. The treatment schedule for decompression illness is most easily portrayed as a flow
chart and it is shown in Fig. 6-1. It will be seen that all patients begin therapy by
compression to 18m on 100% O2 and that the treatment table to be used may then be
determined at various points by the patient’s response to treatment. The flow chart also
allows extension of some tables and movement between tables which may be necessary
with changes in a patient’s clinical state.
b. The NATO tables referred to in the flowchart are described at Paragraph 0611.
Individual Nations treatment tables are at the Annexes.
6-11 ORIGINAL
c. Decompression illness should always be treated using the appropriate oxygen or

air/oxygen recompression table. Air only tables are included in the list of NATO tables
for use only when oxygen is unavailable. A Diving Medical Officer should always be
consulted in this case.
6-12 ORIGINAL
THE PRINCIPLES OF MANAGING THE THERAPEUTIC RECOMPRESSION OF

Fig 6-1.
6-13 ORIGINAL
0611. NATO Therapeutic Recompression Tables

NATO Therapeutic Recompression Tables are groups of National tables that can be used
for a similar purpose (See also Paragraph 0603).
a. Short Oxygen Tables
TABLE V Equivalent tables: US 5

Goodman 1 (BE)
OHB (FR)
HBO (GE)
9SH (NL)
60 & 61 (UK)
b. Long, Shallow Oxygen Tables
TABLE VI Equivalent tables: US 6

62 (UK)
Goodman 2 (BE)
c. Long, Deep Table With Oxygen
TABLE VII Equivalent tables: US 6A

6A (mod) (GE, CA)
TABLES A and B (FR)
SND (GE)
63 (UK)
d. Saturation or Near-Saturation Tables
TABLE VIII Equivalent Tables: US 4

US 7
US 8
TABLE C (FR)
64 & 65 (UK)
e. Air Tables. Wherever possible, oxygen tables should be used. Some of the
air/oxygen tables detailed above may also be used with air only for treatment of DCI
when no oxygen is available and on the advice of a Diving Medical Officer.
TABLE I Equivalent tables: US 1A
TABLE II Equivalent tables: US 2A

TABLE D (FR)
52 (UK).
6-14 ORIGINAL
0612. National Therapeutic Recompression Tables

The treatment algorithm shown at Figure 6-1 represents the philosophy of NATO
nations, however, the timings, treatment depths and gas mixtures will vary depending upon
National Protocols.
a. National therapeutic tables are described at the Annexes.
b. Additional instructions common to all tables are outlined below:
(1) Descent Time. This varies between tables and is not included in the elapsed
time.
(2) Elapsed Time. The timing of each table starts when maximum pressure is
reached, and is given in hours and minutes opposite each step of the table.
(3) Stops. The duration of stops is given, and the periods where oxygen should
be breathed are indicated.
(4) Ascent
(a) The rate of ascent varies between tables, but with all the tables this
becomes most critical near the surface, where the rate of change of pressure
is greatest. If, as the compression chamber nears the surface, air begins to
escape round the door seal, compensation by admitting more compressed air
may be needed.
(b) The rate of bleed must be kept constant. If the rate is slower than that
required by the table it is not to be compensated for by subsequent
acceleration. The ascent should be halted if the rate is exceeded, or if the
ascent cannot be controlled accurately during flushing of the chamber.
(5) Chamber Ventilation. Chamber ventilation will ensure that the partial pressure R
of O2 remains adequate and carbon dioxide does not accumulate. Ventilation is
accomplished by flushing the chamber with air for 2 minutes in every 15 minutes,
unless oxygen breathing is in use without an overboard dump. In this case
ventilation should be increased by flushing for 3 minutes in every 15 minutes. It is
important that as much movement of air as possible should be achieved during this
period. If a life support system is installed ensure the CO2 canister is changed when
the CO2 level exceeds .5kPa. The oxygen level should be controlled at between 20-
25% to limit fire risk.
0613. Non-Standard Treatments

Only a Diving Medical Officer may prescribe changes to treatment protocols or use
treatment techniques other than those described. The standard treatment procedures should be
considered minimum treatments; treatment procedures should never be shortened unless
emergencies arise which require the chamber occupants to leave early.
6-15 ORIGINAL
0614. Recompression Therapy Abort Procedures
a. Once recompression therapy is started, it should be completed unless the patient

R
dies or it is considered that continuing the treatment would place the surviving chamber
occupants in mortal danger.
b. If it appears that the patient has died, a Medical Officer should confirm this before
the treatment is aborted. Once this is done, the attendant(s) may be decompressed either
by completing the treatment table, or by following a modified air decompression table
as described in paragraph c below.
c. A standard air decompression table can be applied, using the maximum depth and
bottom time of the exposure in the chamber, but modified by having all the chamber
occupants breathe O2 as soon as a depth of 9 metres or shallower is reached. Oxygen
breathing periods of 25 min on O2 followed by 5 min on air, are continued until the total
time on O2 is one-half or more of the total decompression time. This procedure may be
used even if gases other than air (ie. oxy-nitrogen or oxy-helium mixtures) were breathed
during the treatment. Upon surfacing, chamber occupants are treated as if they had
surfaced from a normal dive.
d. Very occasionally, conditions outside the chamber may require treatments to be

aborted. For instance, the ship on which the chamber is located may be in imminent
danger of sinking, or a fire or explosion may have severely damaged the chamber system
to such an extent that completing the treatment is impossible. In these cases, the abort
procedure described above could be used for all chamber occupants (including the
patient(s)) if time is available. If insufficient time is available, the following may be
done:
(1) If deeper than 18 metres ascend immediately to 18 metres at the rate of 1 metre
per minute.
(2) Once the chamber is at 18 metres or shallower, put all the chamber occupants
at 100% O2 continuously.
(3) Follow as much of a standard air decompression table as possible, breathing

O2 all the time. If the bottom time is so great that it is outside the table calculations,
then use the stop times in NATO Table VIII divided by 3 from 18 metres to the
surface. If the chamber is at 18 metres or shallower when the decision to abort is
made, start breathing 100% O2, remain at the initial depth for D of the remaining
decompression time, then follow Table VIII to the surface using D of the stop
times.
(4) When no more time is available, bring all chamber occupants to the surface
(try not to exceed 3 metres per minute) and keep them on 100% O2 during
evacuation for as long as possible.
(5) Immediately evacuate all chamber occupants to the nearest alternative

recompression facility. If no symptoms occurred after the treatment was aborted,
use NATO Table VI.
6-16 ORIGINAL
SECTION 4 - CARE IN A RECOMPRESSION CHAMBER
0615. Chamber Attendants
a. Attending the Patient
(1) An attendant who is familiar with the symptoms and signs of diving-related
disorders and their treatment should be inside the chamber during recompression.
However, immediate recompression of seriously ill patients should not be delayed
by waiting for a suitably experienced attendant.
(2) If the patient requires skilled medical procedures a Diving Medical Officer
should accompany the patient into the chamber. He should remain only as long as
needed. However, recompression should not be delayed by waiting for him to
arrive. If the chamber is sufficiently large, a second attendant may accompany him.
(3) If only one Diving Medical Officer is present, his time in the chamber should
be kept to a minimum because his effectiveness is greatly diminished when there.
If periods in the chamber are necessary, these should be timed, as far as possible,
to avoid a decompression obligation.
(4) Inside the chamber, the attendant is to ensure that the patient is lying down and
is positioned to permit the free circulation of blood to all his extremities. Particular
care should be taken to ensure care of pressure points in paralysed patients.
(5) The attendant must watch the patient constantly and report any alteration to
symptoms or signs. The timing of any changes will be important factors to consider
in the choice of treatment table. Other responsibilities of the attendant are:
(a) Operation of the internal chamber and air-lock doors.
(b) Communication with outside personnel.
(c) Providing first aid as required by the patient.
(d) Administering O2 and fluids to the patient.
(e) Providing assistance to the patient as required.
(f) Ensuring that ear defenders are worn during compression, decompression
and venting of the chambers.
6-17 ORIGINAL
b. Attending Frequency. Normally, attendants must allow a surface interval of at

least 24 hours between consecutive treatments on the short oxygen tables. If a
retreatment has to be undertaken sooner than this, the attendant will require additional
O2 breathing periods at 9 metres as described in individual treatment tables. A surface
interval of at least 48 hours is required between consecutive long air tables.
c. Attendants Return to Diving. Attendants for short oxygen tables must allow a
surface interval of 12 hours from completing the table and undertaking no-stop diving.
A surface interval of 24 hours must elapse before conducting dives which require
decompression stops. Attendants for NATO Tables I, II or VIII must allow a surface
interval of at least 24 hours before returning to diving.
d. Oxygen Breathing. When the chamber attendant is required to breath O2 at 9 m

or during the ascent from 9 m a second attendant is not required inside the chamber
provided that the original attendant remains fully functional. However, at the Diving
Supervisors discretion a second attendant may be locked in at any time.
e. Flying. Attendants for short oxygen tables must allow a 12 hour surface interval
before flying. Attendants for NATO Tables I or II must not fly for 24 hours after
treatment, and attendants for a NATO Table VIII must not fly for at least 36 hours.
0616. Recompression Chamber Practice

The following practices are recommended during treatment in a chamber.
a. On reaching maximum depth, the patient, if conscious, is to be questioned and

examined as completely as possible to assess the extent of relief or the presence of
previously unnoticed symptoms and signs.
b. The patient should be checked periodically, particularly during the ascent phases of
a table, when symptoms are most likely to recur. Air breaks provide good opportunities
to perform thorough examinations.
c. Patients must be woken for periodic examinations, but they may be allowed to sleep
at other times during treatment.
d. Conscious patients may eat and drink in the chamber during air breaks.
0617. Chamber Treatment of Oxygen Toxicity

Pulmonary and cerebral oxygen toxicity may occasionally occur during chamber
treatments. Recognition of these conditions is described in Chapter 2.
6-18 ORIGINAL
a. Pulmonary Oxygen Toxicity. Pulmonary oxygen toxicity is unlikely to develop

on short oxygen tables even if they are fully extended. On long air/oxygen tables the
large amounts of oxygen that may have to be administered may result in end-inspiratory
discomfort, progressing to substernal burning and severe pain on inspiration. Substernal
burning should normally be cause for discontinuing oxygen breathing in patients who
are responding well to treatment. However, if significant neurological deficit remains
and improvement is continuing (or if deterioration occurs when oxygen breathing is
interrupted), oxygen breathing should be continued as long as considered beneficial or
until pain limits inspiration. If oxygen breathing must be continued beyond the period
of substernal burning, or if the 4 hour air breaks on long air tables cannot be used
because of deterioration upon the discontinuance of oxygen, the oxygen breathing
periods should be changed to 20 min on oxygen, followed by 10 min breathing chamber
air. The Diving Medical Officer (DMO) may tailor the above guidelines to suit
individual patient response to treatment.
b. Cerebral Oxygen Toxicity
(1) At the first sign of cerebral oxygen toxicity, the patient should be taken off
oxygen and be allowed to breathe chamber air. All time breathing air is ‘dead
time’. Fifteen minutes after all symptoms have subsided, oxygen breathing may be
restarted and the interrupted O2 period completed. If symptoms of cerebral toxicity
develop again, interrupt oxygen breathing for another 15 mins and contact a DMO.
If a DMO cannot be contacted resume Table after 15 minutes. If cerebral oxygen
toxicity develops a third time, discontinue oxygen for one hour (dead time) and then
resume the treatment table. If symptoms of decompression illness are still present
and the patient continues to show symptoms of oxygen toxicity, the DMO will have
to decide whether oxygen should be continued and whether or not decompression
should be attempted or continued, or whether deeper recompression is needed.
(2) The onset of cerebral oxygen toxicity is unlikely in resting individuals at

depths of 15 msw or shallower, and very unlikely at 10 msw or shallower no matter
what the level of activity. However, patients with severe cerebral decompression
illness may be abnormally sensitive to oxygen. Convulsions unrelated to oxygen
may also occur. If an oxygen convulsion occurs, the only thing that need be done
is to remove the patient from oxygen and prevent him from hurting himself. The
patient's head should be kept gently back and his jaw prevented from falling
backward and obstructing the airway. It is not necessary to force the patient's
mouth open to insert any airway or bite block while the patient is convulsing.
(3) Administration of Diazepam 10mg slow i.v. or Clonazepam 1mg slow i.v. or
i.m. may be considered as a prophylactic measure against further convulsion where
continued administration of hyperbaric oxygen is considered to be important.
6-19 ORIGINAL
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6-20 ORIGINAL
0618. General
a. Recovery from decompression illness may be incomplete, even after therapeutic

recompression. The following guidance on the management of cases should be followed
after recompression.
b. All cases in which there are residual symptoms or signs must be transferred to an
appropriate hospital for observation and any necessary investigation. In cases where
there has been an apparently full recovery, less serious cases may be allowed home, if
accompanied, one hour after the completion of treatment. Where there have been
serious manifestations, such as involvement of the nervous or cardiopulmonary systems,
patients should be admitted to a hospital for observation for at least 12 hours. Before
departure, all patients should be briefed on what action to take in the event of a
recurrence of symptoms.
0619. Treatment of Refractory Decompression Illness
a. Following standard hyperbaric treatment, which may have included a saturation

therapy, patients with refractory residual symptoms and signs should be evacuated to a
specialist hyperbaric treatment centre where they should undergo a full clinical
assessment to establish a baseline on which progress of subsequent therapy may be
judged. At the same time the requirement for additional supportive treatment, such as
physiotherapy, can be assessed.
b. As preceding therapy will have involved considerable exposure to oxygen the

possibility of pulmonary oxygen toxicity should be considered. Baseline pulmonary
function testing (e.g. FVC) should be performed initially and periodically during the
course of treatment.
c. Current medical opinion suggests that repeated daily hyperbaric oxygen therapy is
of benefit to divers suffering from refractory decompression illnesses. As a minimum
standard of treatment, patients should be recompressed once daily to a depth of 9 metres
(30 feet) of seawater, breathing 100% oxygen (1.9 ATA). A period of not less than 1
hour should be spent at depth. Rates of descent and ascent should be determined by
national practice. The use of air breaks should also be determined by national practice.
d. The patient should be examined daily to determine the response to therapy. As a

minimum standard, therapy should be continued for as long as sustained improvement
occurs.
e. The above regimen may be enhanced by other therapeutic measures such as

physiotherapy and medications at the discretion of the physician responsible who should
ideally be a Diving Medical Officer.
f. A full evaluation should be performed by a Diving Medical Officer to determine

fitness to resume diving.
g. A summary of national protocol is provided at Paragraph 0620.
6-21 ORIGINAL
0620. National Protocols for the Treatment of Refractory Decompression Illness
REGIMEN
BE: USN Table 5 or twice daily 3 x 30 minutes 2.5 ATA HBO.
CA: No formal protocol - patients treatment on an individual basis.
DA: USN Table 5 daily until patient static.
FR: HBO (2.5 ATA) twice daily for up to 21 days.
GE: Depth 14msw (2.4 ATA) 3x30 mins. HBO; 2x10 min air breaks; 1-2 until
clinical improvement ceases.
GR: Depth 15 msw, 30 min O2, Decompression to 10 msw, 60 min O2,

Decompression to 5 msw, 60 min O2, EXIT HBC. Above scheme twice daily
for 7 days, after that until patient static.
IT: As for CA
NL: As US/UK
NO: The National implementation document is an open civil publication authorised

for use in the Royal Norwegian Navy and is summarised as follows:
Treatment with USN Table 5 once or twice daily until no further improvement
occurs. Alternatively, the patient may be treated at 14 msw (2.4 ATA) for
three periods of 30 min O2 - breathing with 5 min air breaks. Five cases of
non- or poor response to traditional treatment have been treated with heliox
saturation at 18 msw (PO2 = 0.5 bar) with cycles of 100% O2 - breathing until
no further improvement occurred. Its high cost and unknown efficacy
compared with traditional treatment makes this an exceptional treatment
choice.
PO: USN Table 5 once daily, for up to 5 days. 3 x 30 minutes HBO (1.2 ATA)
with 100% O2 once daily until improvement ceases.
SP: USN Table 5 once or twice daily for 5 days followed by HBO at 2.5 ATA for
one hour, or 1.9 ATA for one hour until patient static. Physiotherapy
commencing on the first day.
TU: USN Table 6 once daily for 10-15 days, IV Fluids, aspirin and Vitamin B
complex vitamins
6-22 ORIGINAL
UK: RN Table 61 (USN Table 5) or RN Table 62 (USN Table 6) daily until static.
US: USN Table 5 twice daily; USN Table 6 once daily (Neurological symptoms);
Daily treatments at 30 feet as prescribed by a Diving Medical Officer may be
performed if pulmonary oxygen toxicity from previous treatments is known
or suspected.
0621. Flying After Therapeutic Recompression

Patients with limb pain, lymphatic or cutaneous decompression illness who have had
complete resolution of all symptoms may fly 24 hours after completing the therapeutic table.
Patients with neurological, pulmonary or multisystem decompression illness, who have had a
complete resolution may not fly for at least 48 hours. Patients surfacing asymptomatic from
NATO Table VIII, or other tables of similar long duration may not fly for 72 hours. Patients with
residual symptoms should not fly for at least 72 hours after completion of their final
recompression table and only after consultation with a Diving Medical Officer.
0622. Return to Diving After Decompression Illness
a. Divers who were treated using NATO Table V with complete relief, may return to
normal diving at least 24 hours after surfacing from the treatment. If there is any doubt
about the presence of serious symptoms, the diver should be examined by a Diving
Medicine Specialist before returning to diving.
b. Divers who have required treatment with NATO Table VI and who have had
complete resolution of limb pain, skin or lymphatic symptoms, may resume normal
diving on the seventh day following treatment, following consultation with a Diving
Medicine Specialist.
c. Divers who had neurological symptoms limited to patchy, altered peripheral

sensation (tingling or numbness), which resolved completely during treatment with
NATO Table VI, may resume diving after at least 14 days and following a review by a
Diving Medical Officer.
d. Divers who have experienced incomplete recovery, or suffered more serious

symptoms and signs, should be carefully assessed for return to diving by a Diving
Medical Officer.
e. Divers who have suffered from pulmonary barotrauma must be referred to a Diving
Medical Officer for a decision on fitness to resume diving. A minimum period of 28
days lay off is usually required in those that are fit to return to diving.
6-23 ORIGINAL
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6-24 ORIGINAL
CHAPTER 7
THE LONG TERM EFFECTS OF DIVING
ORIGINAL
CHAPTER 7
THE LONG TERM HEALTH EFFECTS OF DIVING
CONTENTS
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0701
Dysbaric Osteonecrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0702
Chronic Hearing Loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0703
Chronic Neurological Damage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0704
Pulmonary Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0705
Other Chronic Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0706
7-1 ORIGINAL
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7-2 ORIGINAL
CHAPTER 7
THE LONG TERM HEALTH EFFECTS OF DIVING
0701. Introduction
a. The most well known long term occupational health hazard of diving results from
the incomplete resolution of acute neurological decompression illness. In recent years
however, attention has been drawn to the possibility that a number of medical
conditions can arise directly from the long term effects of diving, rather than from the
incomplete resolution of acute DCI.
b. Dysbaric Osteonecrosis (DON) is the most well recognised chronic form of

decompression illness that is a long-term hazard to divers and other compressed-air
workers. It is a rare condition amongst military divers and occurs more commonly in
groups who ignore good diving practice.
c. Various epidemiological studies have investigated other possible long term effects
of diving. Some studies have shown that divers may suffer a greater degree of hearing
loss than the general population and claims have been made that they may also suffer
from other long term effects of diving such as chronic neurological damage, retinal
damage and subfertility. Unfortunately many of these studies lack adequate controls or
report purely incidental findings which have no known clinical relevance, so it is not
possible to draw many significant conclusions from this work at present.
0702. Dysbaric Osteonecrosis

Dysbaric Osteonecrosis (DON) is a chronic form of decompression illness that is a
long-term hazard to divers and other compressed-air workers. In military divers the incidence
of necrosis is very low, and progression to the symptomatic stage is almost unknown.
a. Epidemiology
(1) Dysbaric Osteonecrosis (DON) describes lesions found in the medulla or

cortex of long bones. The lesions are histologically similar to those related to a
large group of conditions including connective tissue disorders, alcoholism and
steroid use. The relationship of crippling bone disease and exposure to pressure was
noted long before the development of radiography and theories of limits on-time and
depth of exposure.
(2) Caisson workers work as labourers and miners while exposed to higher than
sea level pressure of air. In the past work schedules were based on the work
required rather than on the physiological consequences to the worker. The severe
morbidity seen in these populations caused the institution of decompression
schedules. There are two types of morbidity associated with these exposures. The
most common effect is the relatively rapid onset (always within 24 hours, usually
within hours of surfacing) of decompression
7-3 ORIGINAL
sickness that included pain, weakness or paralysis. This frequently led to permanent
loss of function, particularly before the concept of treatment with pressure was
instituted. Even in the relatively unscathed population that continued to work in the
profession there was a gradual increase in long term morbidity, which manifested
mostly as ‘diver’s bone rot’. This has been investigated over hundreds of years, and
it is still unclear whether these lesions are solely the result of decompression illness
events, or whether there is a separate pathogenesis entirely.
(3) It is fairly clear that uncontrolled hyperbaric exposures (as experienced by

abalone fishermen, Chinese commercial divers and caisson workers prior to modern
controls) can lead to very significant rates of DON. Most of these occupations
include long repetitive working dives with little or no attempt at decompression.
Most of these individuals have had decompression illness at least once, and
treatment probably was not available, timely or adequate. Age, length of time in
higher pressure environments and total number of dives all increase the risk of bone
lesions as does a positive history of decompression illness. Treatment-resistant pain
in the affected joint is a strong risk factor for ensuing osteonecrosis of the area.
There are, however, cases of DON in which no history of decompression illness can
be elicited. It is possible that the modern concept of indications for treatment (far
more aggressive than in the past) is part of the reason for a decreasing incidence of
the disease. That is, what would have previously been called ‘decompression stress’
may now be called decompression illness, and treated with recompression. It is
therefore difficult to attribute a cause and effect relationship between decompression
illness and DON when the precise definition of decompression illness has varied
over decades.
(4) The institution and revision of diving tables to limit time at depth appears to
have decreased the incidence of DON in military and commercial diving
populations throughout the world in the last 50 years. There are guidelines that
suggest that the risk of developing lesions is practically non-existent diving
shallower than 30 metres, but there are case reports from submarine accidents and
other unplanned saturation profiles shallower than this that have produced DON.
Similarly, although risk increases with the number of dives, there are case reports
after single exposures. Most of these unusual case reports involve inadvertent
saturation at depth from submarine accidents, and do not provide evidence that the
shallow water non-decompression diver is at any significant risk.
(5) There are a few documented cases of bone lesions caused by hypobaric
exposure, usually with a past history (sometimes of multiple incidents) of
decompression sickness not resolving at ground level, and usually not treated or
inadequately treated.
7-4 ORIGINAL
(6) DON bone lesions are usually categorised as shaft lesions or juxta-articular
lesions. Shaft lesions are considered clinically insignificant as they do not progress
to disease (except in one case report of a massive medullary lesion, and in the very
remote but reported possibility of progression to neoplasm). There are many shaft
lesions for every juxta-articular lesion, and there are many juxta-articular lesions for
every case of clinical subchondral bone collapse. The reported incidence in
different studies may be based on the number of lesions detected on long bone
survey, the number of juxta-articular lesions, or the number of divers who go on to
have clinical bone disease. The following estimates of incidence should therefore
be considered with caution in light of the above disclaimers.
(7) Unrestricted diving (common in populations of commercial fishermen in

Japan, China and Australia) can lead to bone lesions in 50% to 80% of the
population. The usual range of incidence for bone lesions in caisson workers (prior
to changes in the shift length limits) was 20%. Military divers vary from 2.5% to
1.7%. The ratio of juxta-articular lesions to total lesions is reported from ½
(Japanese Fishermen) to less than 1/10. The chance of a juxta-articular lesion
progressing to disabling symptoms has been observed from c to 1/10. Higher
incidences have been documented within the military and industrial diving
populations for diving deeper than 100 feet on air, and for diving from 300 to 600
fsw on helium mixes. Saturation diving exposure is likewise a higher risk category
within the documented 2.5% to 1.7% prevalence of total lesions.
(8) The advent of the use of Doppler monitoring to validate dive tables has made
possible the creation of new dive tables for air diving, heliox diving (both 84/16 and
constant mass flow), and surface decompression. Each alteration of the dive tables
in use by the military should change the risk of DON according to the correlation
with decompression sickness, and there is good evidence to suggest that the risk will
decrease with the doppler-monitor validated tables.
(9) The recent adoption of dive computers and oxygen-enriched mixes by the
civilian diving population has been postulated to increase their risk of DON. In the
past the civilian (or sport diver) who did not make decompression dives had
essentially no risk since diving medicine experts have failed to find any evidence
of the disease in this population.
b. Pathogenesis
(1) DON causes lesions which are virtually identical to those associated with many
other metabolic and drug related conditions. The distribution of the lesions is
unique, with the head, neck and shaft of the femur and humerus (and rarely the
distal femur) carrying essentially all of the ‘hits’. The common mechanism of
emboli (fat or gas or other) leading to the obstruction of end arteries in a rigid
compartment is physiologically appealing but it does not explain the distribution of
3/1 humerus to femur. This is the exact opposite seen with alcoholism related
lesions.
7-5 ORIGINAL
(2) The theory of vasospasm related to raised oxygen partial pressures could
explain the areas of damage as an ischemic phenomenon, but the distribution of the
lesions is difficult to account for.
(3) An explanation that could encompass the embolic or the vasospasm theory is
the damage mechanism of raised intramedullary pressure. This could be caused
initially be venous back-pressure due to blocked outflow through the bone, leading
to increased vascular permeability and edema. In a closed rigid system the physical
size of a bubble might significantly increase core pressure. Severely provocative
profiles in experimental animals have led to lesions when recompression treatment
was delayed longer than four hours. This has supported the clinical intervention of
core decompression of the affected joint on an acute basis.
(4) The pathogenesis of DON is under active investigation. While an exact

understanding of the mechanism may not be necessary to evaluate investigation
methods and treatment plans, it certainly provides ample room for argument on both
topics.
(5) Observation of lesions affecting the femoral head has shown that the likelihood
of lesions becoming symptomatic varies with the amount of the articular surface
which is involved. The involvement of more than 50% of the articular surface has
been postulated to go on to symptomatic subchondral bone collapse in 85% of
cases, regardless of whether appropriate conservative treatment is received. The
prognosis of lesions which involve less than 25% of articular area is 100% recovery.
c. Investigation
(1) Plain film radiography has been used to identify and follow progression of
lesions for more than 60 years. Correct identification and classification of lesions
is problematic. Variations in the positioning of the joint alter the estimation of the
area of articular bone involved. Interpretation of films has been shown to vary with
the readers information on the diving history.
(2) DON lesions may take form 3 to 12 months to show up on X-ray. The visual
evidence of a lesion on X-ray can take the form of a lucency (surrounding bone
becomes less dense) crescent sign (lucency underlying the articular cortex due to
failure of the trabeculae) and collapse of the articular surface. These lesions
probably present a progression, but DON is frequently undetected until the articular
surface has collapsed. Although sclerosis is a sign of bone repair, it does not
necessarily represent a clinically sound joint.
(3) Bone Scintigraphy Scanning may be positive within 14 days and provides a
much more dynamic impression of healing or progression. However the radiation
dose from repeated scans limits its use.
7-6 ORIGINAL
(4) Magnetic Resonance Imaging is an extremely sensitive test for bone marrow
changes and can provide information within days of the insult. It can provide a
measure of the area involved, but is not highly specific.
(5) The cost, availability, sensitivity and specificity and timing of the study to be
selected must be considered in the employment of these techniques to diagnose,
investigate and treat DON. There are obvious drawbacks to the use of scintigraphy
scans and MRI as population screening tools.
(6) The current rate of DON in military divers is extremely low. Our current
understanding of pathogenesis and risk factors suggests that the use of doppler-
monitor validated tables should decrease the risk over time. The population
screening method that will be safe, affordable and the least disruptive depends on
the incidence of DON expected in the population.
d. Treatment
(1) Active research suggests that permanent damage may ensue within 4 hours of
a severe insult. The definitive treatment is recompression on a therapeutic profile
such as a Treatment Table 6, as though treating a pain symptom of acute
decompression sickness. Repeated treatment profiles may be indicated depending
on the response.
(2) Core decompression may improve the short and long term condition of the
bone if undertaken within the first two to three days.
(3) Rest of a joint will improve the prognosis of a lesion prior to the finding of
lucency beneath the articular surface or collapse of the articular cortex. Once these
radiographic changes are present conservative treatment does not seem to have any
effect on the rate of progress to joint dysfunction, although it may improve short
term symptoms.
(4) The long term consequence of collapse of a certain percentage of articular

surface (particularly in a weight-bearing joint) is joint dysfunction possibly
requiring total joint replacement.
(5) Shaft lesions do not tend to be clinically significant, although there are two
case reports of painful lesions and a very remote possibility of malignant change in
the lesion over time.
e. Prevention
(1) Diving according to decompression tables has been shown to be extremely

effective in preventing the majority of cases of DON, however the expected rate of
decompression illness (depending on the table) suggests that there will continue to
be some risk also of DON.
7-7 ORIGINAL
(2) The incidence of DON in CF members exposed to decompression diving,

including saturation, mixed gas and experimental profiles is much less than the
reported 1.7% prevalence of lesions in the USN study reported from 1977. The
trend in this condition seems to be a clear decrease in prevalence over time, and
repeat long-bone surveys every five years will be adequate to measure any further
changes in the incidence of the disease.
0703. Chronic Hearing Loss

At present there is no strong evidence to indicate that hearing loss in divers is due to a
chronic form of inner ear DCI, but some studies have shown that divers are subject to an
increased incidence of hearing loss compared to the general population. Several reasons may
explain this increased incidence. Divers are at risk of both aural barotrauma and acute
audiovestibular DCI and either one of these conditions could leave a diver with residual hearing
damage after recovery from the acute event. Excessive noise level exposure may also explain
the sensorineural hearing loss as divers have been shown to be subject to particular noise hazards
in the conduct of their profession. Examples of the noise hazard include the venting of
recompression chambers and the use of helmets with excessively noisy gas flow. Further studies
are required in this area to exclude these known causes of deafness and determine if there is any
chronic effect from hyperbaric exposure itself.
0704. Chronic Neurological Damage

A great deal of work has been done to investigate the possibility of long term
neurological or psychological damage in divers, much of it based on the theory that silent
symptomatic bubbles in the bloodstream may cause minor injuries which may eventually
summate to cause neuro/psychological problems or dementia. So far little of clinical relevance
has been proven however. Most of the evidence from psychometric tests and studies suggesting
a neurological syndrome has been circumstantial without adequate controls and the positive
findings in some studies such as those investigating EEG changes or the cerebral changes visible
by neuroimaging techniques have no clinical relevance. If a neurological syndrome does exist
it is likely that both its prevalence and significance are low but further studies may resolve this
issue in the future.
0705. Pulmonary Function

There is evidence from literature which suggest two long-term effects of diving on the
lung.
a. Changes in static lung volumes due to increased work of breathing dense gas
mixtures, and development of small airways dysfunction. The reduction in expiratory
flow rates seems to correlate with diving exposure.
b. A reduction in pulmonary diffusion capacity has been demonstrated after saturation

dives. Possible contributions to this effect are: hyperoxia and venous gas microemboli.
based on risk assessment, regular pulmonary function tests must be done for selected
categories of divers.
7-8 ORIGINAL
0706. Other Chronic Effects

Two studies of divers’ retinae by fluorescein angiography have found a significant
number of changes compared with and non-divers. The changes seen could be explained by
vascular obstruction for which there are a number of possible mechanisms in diving but the
clinical relevance of the changes is unknown as the divers were all asymptomatic and without
detectable visual deficits. A longitudinal study of many divers may reveal their significance. As
the entire body is exposed to hyperbaric pressure during diving, there is the distinct possibility
that some systems may be chronically affected by these exposures. Often the clues to such
possible effects arise from incidental findings but it is possible that further research into these
findings may expose significant new information on the long term health effects of diving.
7-9 ORIGINAL
Bibliography:
MOLVAER O I and ALBREKTSEN G (1990). Hearing deterioration in Professional Divers:

An Epidemiologic Study. Undersea Biomedical Research 17, 231-246.
EVANS S A and SHIELDS T G (1992) A Critical Review of the Literature on the Potential Long
Term Consequences of Diving. Aberdeen RGIT.
Long-term Health Effects of Diving. International Concensus Conference. Godoysund, Norway,

6-10 June 1993.
7-10 ORIGINAL
CHAPTER 8
OPERATIONAL HAZARDS
ORIGINAL
CHAPTER 8
OPERATIONAL HAZARDS
CONTENTS
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0801
Hypothermia and Hazards of Cold Water Diving . . . . . . . . . . . . . . . . . . . . . . . . . . 0802
Local Hypothermia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0803
Heat Stress and Hazards of Warm Water Diving . . . . . . . . . . . . . . . . . . . . . . . . . . 0804
SECTION 2 - DIVING IN POLLUTED WATER
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0805
Hazard Identification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0806
Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0807
Support System and Body Protection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0808
Operating and Handling Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0809
Use of Atmospheric Diving Suits or Small Manned Submersibles . . . . . . . . . . . . . . 0810
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0811
Predatory Marine Life . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0812
Venomous Marine Life . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0813
Near Drowning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0814

Underwater Blast Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0815
Underwater Noise and Sonar Transmissions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0816
Otitis Externa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0817
Caustic Cocktail . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0818
Disorientation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0819
Disinfection of Diving Equipment in Contact with Saliva . . . . . . . . . . . . . . . . . . . . 0820
8-1 ORIGINAL
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8-2 ORIGINAL
CHAPTER 8
OPERATIONAL HAZARDS
0801. Introduction
a. In addition to decompression, thermal problems arising from environmental exposure

pose the major consideration when planning operational dives and selecting equipment.
The human body functions effectively within a relatively narrow range of internal
temperature and the average, or normal, core temperature of 37°C is maintained by
natural mechanisms of the body, aided by artificial measures such as the use of protective
clothing when external conditions tend toward cold or hot extremes. The body’s
thermoregulatory control mechanisms are, however, only capable of generating or losing
certain amounts of heat. If the environmental conditions are such that heat is lost or
gained faster than the rate at which these mechanisms can cope, thermal stress will occur,
resulting in either too high a temperature (hyperthermia) or low a temperature
(hypothermia). It both conditions mild exposures will lead mainly to discomfort, but it
is important to be aware of the signs and symptoms of more severe thermal stress.
b. The principal temperature control problem encountered by divers is keeping the body
sufficiently warm. The high thermal conductivity of water, coupled with the normally
cool-to-cold waters in which divers operate, can result in rapid and excessive heat loss.
The working diver commonly experiences heat loss during immersion and often expects
to be uncomfortably chilled at the end of a dive. Bottom time limits may be determined
by the diver's tolerance to cold rather than by decompression considerations. Rewarming
before a repeat dive may then be as important as calculating residual nitrogen levels.
c. Divers use protective suits which afford very good insulation against heat loss.
Insulation may be so good that divers may suffer hyperthermia whilst performing physical
exercise or if an inappropriately well insulated suit is worn in warm conditions. Even
unsuited divers can also suffer heat stress when operating in some of the warmest waters
of the world.
0802. Hypothermia and Hazards of Cold Water Diving
a. Two different physiological responses to immersion in cold water are possible

depending on the degree of thermal protection worn and the water temperature: an acute
cold shock response seen in relatively unprotected individuals who are suddenly
immersed in very cold water, and a sub-acute hypothermic response seen in cases of
longer term heat loss.
8-3 ORIGINAL
(1) Acute Cold Immersion. A sudden drop in skin temperature such as on entry
into the water or the rapid influx of cold water into a diving suit can result in a
profound physiological response known as the ‘cold shock response’. This consists
of an immediate increase in pulse rate and blood pressure and a period of rapid,
gasping breathing. Even competent swimmers may be unable to co-ordinate
breathing and swimming movements and inhale water. This lack of control makes
survival in rough, cold water very unlikely. The rapid pulse and high blood pressure
response may also result in circulatory failure in unfit people. Fortunately, because
divers intentionally entering cold water wear protective clothing, such experiences
in diving are very rare.
(2) Sub-acute Cold Immersion. If some form of protective clothing is worn, the
initial responses to immersion may be blunted and the diver will gradually develop
symptoms and signs of hypothermia as cooling continues. Discomfort is followed
by shivering, an involuntary muscular contraction to produce heat, and a diver's
ability to perform useful work becomes seriously impaired. Manual dexterity is
reduced and the sense of touch is dulled. With further cooling the ability to
concentrate and think clearly is soon lost. At this stage, a diver is more prone to
make mistakes which could be fatal.
b. Pathogenesis
(1) A diver may lose body heat by conduction, convection or, more rarely,
radiation.
(a) Conduction. This is the direct transmission of heat through a substance

or through materials in contact with each other. An unprotected diver will lose
heat to the surrounding water by direct conduction through the skin, the rate
at which he loses the heat depending upon the difference in temperature
between the body and the water. Immersion in water at 33oC will result in no
net heat loss or gain from the body - so called thermoneutral immersion. If the
water temperature is less than 32° to 33°C, the temperature difference between
the diver’s body and the water is such that if unprotected he will lose heat
faster than his body can produce it and he will chill at rest. Immersion in water
below about 23oC will soon result in the unprotected diver becoming chilled.
(b) Convection. This is the transmission of heat by the movement of air or

liquids. The unprotected diver standing more or less still underwater will lose
heat, not only by conduction but also by the fact that the water in contact with
his skin, warmed by conduction, will expand and, becoming slightly lighter than
the surrounding water, will rise to the surface to be replaced by cold water.
Thus convection currents are set up that take away the water warmed by
conduction through the skin and the diver is continuously bathed in cold water
taking its place. Provided the water temperature is not less than 15°C, a
good-fitting wool undersuit may suffice to prevent the diver from being chilled.
In colder water, insulation with a ‘dead’ air space must be provided by wearing
a wool undersuit under a watertight suit or by wearing a ‘wet’ suit of cellular
foam material that does not lose its insulating value when wet and which
reduces convection effects on the diver's skin by trapping a film of water.
8-4 ORIGINAL
(c) Radiation. This is the transfer of heat by infra red electromagnetic

radiation as experienced when standing in sun light or in front of an electric
radiator. The amount of body heat the diver loses by radiation is negligible
compared with the losses by conduction and convection. However, significant
heat gain may be experienced via radiation in surface layers under bright sun
light and radiant heat gain can be particularly problematic for the occupants of
compression chambers located on the upper deck in bright sunlight.
(2) The body’s ability to tolerate cold environments is due to insulation,

thermoregulation and protective behavioural responses to cold. Temperature is not
uniform throughout the body. It is appropriate to consider the body in terms of an
inner core where a constant or uniform temperature prevails, and a superficial region
through which a temperature gradient exists from the core to the body surface. Over
the trunk of the body, the thickness of the superficial layer may be one inch (2.5 cm).
The extremities become a superficial insulating layer when their blood flow is
reduced to protect the core. Once in the water, heat loss through the superficial
layer is lessened by the reduction of blood flow to the skin. The automatic,
cold-induced vasoconstriction (narrowing of the blood vessels) lowers the heat
conductance of the superficial layer and acts to maintain the heat of the body core.
When the extremities are initially put into very cold water, vasoconstriction occurs
and the blood flow is reduced to preserve body heat. In the presence of a normal
core temperature, the vasoconstriction is not prolonged and periodic bursts of
vasodilatation occur - the hunting reaction of Lewis. This response is substantially
blunted in the presence of a lowered core temperature and the vasoconstrictive
response serves to preserve core temperature.
(3) Much of the heat lost from the trunk is transferred over the short distance from
the deep organs to the body surface by physical conduction, which is not under any
physiological control. Most of the heat lost from the body in moderately cold water
is from the head and trunk and not the limbs.
(4) In dry conditions, exercise increases heat production and body temperature.
Paradoxically, exercise in cold water may cause the body temperature to fall. Any
movement which stirs the water in contact with the skin creates turbulence that
encourages convective heat loss. Experimental evidence indicates that if the legs
alone are exercised, there may be a net gain in heat. However, whole body
movement, particularly if the arms are exercised, results in an increased rate of heat
loss.
(5) Increased heat production (for example by shivering) requires an increase in

oxygen consumption and, consequently, respiratory minute volume. Inhaled gases
are heated in the upper respiratory tract. More energy is required to heat the denser
gases encountered at depth than at the surface. Thus a diver who is cold will loose
increasing amounts of heat through the respiratory tract as a function of
thermogenesis and depth. Breathing mixtures containing gases with a high heat
capacity, such as helium, exacerbate this process.
8-5 ORIGINAL
c. Causes and Prevention of Hypothermia
(1) Hypothermia is prevented by selecting an appropriate diving suit (wet suit, dry
suit, hot water suit) after considering both the water temperature and the planned
duration of the dive. Less insulation will improve the diver’s dexterity and ability to
swim, but will also contribute to a greater loss of heat and increase the risk of
hypothermia. Adequate thermal support for divers is a necessity if operations are to
proceed safely. An appropriately dressed diver can work in very cold water for
prolonged periods of time but hypothermia in divers is still occasionally seen,
usually a result of errors such as:
(a) Inappropriate choice of diving suit.
(b) A leaking dry suit.
(c) Long periods of inactivity.
(d) Exposure to wind-chill after leaving the water.
(e) An inadequate supply of hot water (volume or temperature) when wearing

a hot water suit.
(2) Hypothermia can therefore be readily avoided through careful dive planning
and by following the following recommendations:
(a) Wear a diving suit and, where necessary, thermal undergarments

appropriate to the water temperature.
(b) Check for leaks before leaving the surface.
(c) If the use of inadequate thermal protection is unavoidable, the use of

surface decompression procedures will help reduce cold exposure.
(d) Wear a windproof cover if exposure to the elements continues after

surfacing.
(e) Ensure that the hot water supply to a hot water suit is of sufficient volume
and at an adequate temperature. It should be remembered that if the loss of
body heat is gradual, the diver may not recognise that he is becoming
hypothermic.
(f) Do not re-expose a diver to cold water until he is thoroughly re-warmed.

A diver will subjectively feel warm long before the warming process is
complete. A diver is not completely re-warmed until sweating is induced.
8-6 ORIGINAL
d. Clinical Features
(1) Responses to falling core temperature are individual. Eventually, however,

mental confusion and irrational actions or responses will occur resulting in a diver
who is incoherent and unable to himself out of the water or handle gear. No matter
what the core temperature, individuals in this state are in serious danger and require
immediate assistance and rewarming.
(2) Beside a falling core temperature, local hypothermia especially of the hands,
may render a diver useless for underwater work.
(3) Hypothermia is defined as a central body temperature below 35oC. Three

phases of hypothermia are recognised based upon the patient’s symptoms and signs
(Table 8-1). Both cold water and immersion induce a diuresis which provoked
dehydration. This in turn will reduce performance and may increase the diver’s
susceptibility to decompression illness more than that caused by cold alone.
Table 8-1. Phases of Hypothermia

Core Temperature (°C) Symptoms and Signs
35-36 Shivering
Imminent Hypothermia Feels Cold
Normal Mental State
33-35 Raised Metabolic Rate
Mild Hypothermia Raised Respiratory Rate
(Excitation Phase) Raised Heart Rate
Maximal, Uncontrollable Shivering (at 35oC)
White/Bluish Skin
Confusion/Disorientation
30-33 Reduced Metabolic Rate
Deep Hypothermia Reduced Respiratory Rate
(Adynamic Phase) Reduced Heart Rate, Supra ventricular Extra
Systoles/Reduced Shivering - may be Absent
Atrial Fibrillation
Metabolic & Respiratory Acidosis
Hypovolaemia
Apathy/Hallucinations
Limb Stiffness
<30 Unconsciousness - Unresponsive to Pain
Very Deep Hypothermia Absent Tendon Reflexes
(Paralytic Phase) Fixed, Dilated Pupils
Ventricular Fibrillation may Occur <28oC
Cardiac Arrest Likely <25oC
Pulmonary Oedema <24oC
Cerebral Oedema <20oC
8-7 ORIGINAL
e. Management
(1) The treatment of hypothermia consists of rewarming the victim. In mild cases,
when the diver is only chilled, treatment is still important if diving operations are to
continue. Hypothermia severe enough to cause confusion or unconsciousness is a
medical emergency and rewarming must be started immediately. First aid measures
consist of the prevention of further heat loss and evacuation. The casualty must be
handled with care and maintained, as far as possible, in a horizontal position during
and following removal from the water to prevent cardiovascular collapse. Wrapping
the casualty in a plastic bag or polythene sheet provides a very effective way of
reducing evaporative heat loss and further cooling.
(2) Basic cardiopulmonary resuscitation should be started if necessary. However,

caution should be exercised in making the decision to commence cardiac massage,
since this will have to be continued until the patient is fully re-warmed. If a
significant delay is expected before rewarming can commence, then cardiac massage
should not be started. It should be remembered that cardiac resuscitation in the
severely hypothermic diver may precipitate ventricular fibrillation - which may prove
fatal.
(3) Passive and active re-warming methods can be used to manage cases of
hypothermia. Many of the suggested methods of active re-warming require
significant support equipment and monitoring and very few have been tested in
controlled trials with large numbers of patients. Active external methods of re-
warming (e.g. in a warm water bath) requires attentive monitoring of vital signs.
Active internal warming methods (e.g. by peritoneal dialysis) requires hospital level
facilities. The most common method of re-warming the hypothermic diver is by
immersion in warm water, either in a bath or instilled under the diver’s suit. Rapid
re-warming if necessary, is best accomplished using water 38-44oC. Using hotter
water than 45oC may burn the diver’s skin. If no hot water is available, dry the diver
and provide warm clothes, a sleeping bag or blankets and a warm room. Caution
should be used with chemical hot packs or electric pads or blankets which can scald
or burn the skin. A diver in a stable condition who is shivering under dry insulation
(blankets, sleeping bag) will rewarm safely. Hot showers are useful in rewarming
chilled divers who are conscious, able to stand without assistance and who have
adequate hydration. Wet suits do not have to be removed for a hot shower to be
effective. However, a tight fitting wet suit may constrict the peripheral circulation
and should be removed. Since warm water will cause peripheral vasodilation,
individuals who are dehydrated may faint in a shower. Consequently, if a shower is
to be used, the casualty should be seated and attended.
8-8 ORIGINAL
(4) If the diver is dehydrated, fluids should be administered. For conscious

casualties, this can be achieved by the oral route using warm beverages which are
free of caffeine or alcohol (may cause additional diuresis and further dehydration).
In unconscious divers, the intravenous route must be used employing warmed fluids
(normal saline). In profound hypothermia, the victim may appear dead, with
undetectable pulse and respirations, dilated pupils and an ashen-grey colour of the
skin. In such a case, resuscitation and rewarming must be started immediately, even
if the diver has not been breathing for some time. Resuscitation of a hypothermic
diver must not be abandoned until rewarming has been completed as hypothermia
is protective to the ischaemic brain and the recovery of function can occur despite
prolonged apnoea. Such measures should be continued until the casualty’s body
temperature is within the normal range and he continues to be unresponsive to
resuscitation. For this reason, a victim of hypothermia should not be pronounced
dead until he is warm and dead.
0803. Local Hypothermia
a. In addition to general hypothermia, cooling of the hands, in particular, may cause

marked decrements in the performance of divers. In unacclimatized divers, immersion
of the hands in water below about 12°C results in a progressive loss of sensation, manual
dexterity and grip strength. This effect is directly due to the cooling of the tissues of the
hand. In acclimatized individuals, who have a normal core temperature, intermittent
bursts of vasodilatation (Cold-Induced Vasodilatation - CIVD) may maintain the skin
temperature above water temperature and hence delay the onset of, or abolish, the
decrement in function.
b. In unacclimatized divers, passive thermal protection (gloves or mitts) will be required

to maintain function in water at, or below this temperature. Below about 5oC and for
prolonged dives active thermal protection (heating) will be required.
0804. Heat Stress and Hazards of Warm Water Diving
a. An individual is considered to have developed hyperthermia when the core

temperature rises 1oC above normal (37oC). The maximum core temperature considered
safe is 39oC. Diving in very hot weather or in high water temperatures requires
precautions be taken to safeguard both the surface team and divers from heat stress.
Specific guidelines based on temperature/time exposures are not available at this time but
as a general rule, personnel should be alert for possible signs of hyperthermia when
conducting diving operations in water warmer than 30oC and/or air temperatures above
32oC. Unless actively prevented, pre-dive heat exposure may lead to significant
dehydration with subsequent detriment to underwater performance and, possibly, an
increased decompression risk. Hyperthermia is also associated with a reduced tolerance
to cerebral oxygen toxicity and consequently of particular importance to oxygen
swimmers. The magnitude of the heat stress to which a diver will be exposed will depend
on:
(1) The water temperature
8-9 ORIGINAL
(2) The duration of the dive
(3) The insulative qualities of the diver’s dress
(4) The work rate of the diver
The onset of hyperthermia will vary between individuals. Those with a high level of
physical fitness and low levels of body fat are less likely to develop hyperthermia.
Adequate hydration reduces the risk regardless of morphology.
b. Pathogenesis
(1) The metabolism of the body generates enough heat to warm 2 litres of ice-cold
water up to body temperature every hour. During short periods of heavy work up
to 10 times as much heat can be generated. Unless this heat is lost, the body
temperature will increase. Small increases may occur without ill effect. However,
once the temperature of tissues reaches about 41oC, cells become injured and serious
illness can result.
(2) The body loses excess heat in several ways. A small amount is lost with the
exhaled breath. Heat is also transferred by the circulation to the surface of the skin,
where it is dissipated through a combination of conduction, convection, and
radiation. The evaporation of moisture released by the sweat glands results in a
substantial heat loss and is the most effective cooling technique in hot conditions.
If the body is working hard and generating greater than normal quantities of heat,
skin blood vessels dilate and the sweat glands increase their activity to permit a
greater heat loss.
(3) On the surface, a hot and humid atmosphere reduces the effectiveness of most
of these mechanisms and so limits the safe maximum workload which can be
undertaken. In warm tropical waters (temperature greater than about 32oC) these
cooling systems become sufficiently ineffective that a working diver may readily
develop signs of heat stress. Protective suits also render most of these cooling
mechanisms ineffective.
c. Causes and Prevention of Heat Stress. The following paragraphs detail some of
the avoidable factors involved in the production of heat stress.
(1) Over-exertion in tropical waters when wearing a ‘dry’ suit, or a ‘wet’ suit
which is too thick for the water temperature. Experience has shown that a
lightweight ‘wet’ suit or overalls are suitable where the water temperature is over
about 25°C. If overalls are worn, which have no inherent positive buoyancy, divers
should, where possible, wear a flotation device. If the water temperature is above
about 30oC the amount of work which can be undertaken underwater will be limited.
8-10 ORIGINAL
(2) Wearing a diving suit at the surface while unprotected from the sun. All
personnel involved in diving operations should be sheltered from direct sunlight as
far as is practical. Divers and standby divers deployed in inflatable boats should be
draped in light coloured towels which should be kept wet to allow evaporative
cooling. Diving apparatus should be treated similarly.
(3) Excessive heating of a hot water diving suit.
(4) Dehydration. Dehydration is both a cause and an effect of heat stress. It is

defined as an excessive loss of water from the body tissues and is accompanied by
a disturbance in the balance of essential electrolytes, particularly sodium, potassium,
and chloride. It is caused by inadequate fluid intake compared to the amount of fluid
lost through routes such as perspiration, respiration and the urinary tract (immersion
diuresis) which is a consequence of the central pooling of venous blood and release
of atrial naturietic factor. It has frequently been shown that the thirst drive alone
may not provoke an adequate fluid intake. This therefore requires active
management and sufficient fluid should be consumed to provoke the frequent
production of large quantities of clear urine. Drinks containing alcohol or caffeine
should be avoided since they exacerbate dehydration.
(5) Lack of Experience. In most circumstances, experienced divers pace

themselves to avoid heat stress. However, even with proper preparation, heat stress
may occur and divers should be familiar with the early signs and symptoms so that
a dive may be aborted before an incident occurs.
(6) Poor Acclimatisation. Continuous exposure to heat results in an adaptive

process whereby the efficiency of heat loss mechanisms, particularly sweating, and
electrolyte retention is enhanced. At least five consecutive days of acclimatisation
to heat are needed for this to occur. Exercise enhances the rate of acclimatisation.
Where possible, sufficient time for acclimatisation should be permitted before
attempting long, working dives. It is important that both divers and support
personnel are allowed to acclimatise.
(7) Hyperthermia is a potential problem for the occupants of compression

chambers or bells which are exposed to direct sunlight or which are sited in areas of
high ambient temperature. Where possible, chambers should be shielded from the
elements and the internal atmosphere air conditioned. Where this is not possible, the
temperature within the chamber should be monitored and the chamber surface
cooled as required to maintain a habitable environment.
d. Clinical Features Signs and symptoms of hyperthermia can vary between

individuals. Since there are a number of factors which may combine to provoke
hyperthermia in a diver which may occur when surface support personnel may not
consider it particularly hot, the diagnosis should always be considered and the diagnosis
should not be based solely on the classical signs and symptoms of heat stress for land
exposures.
8-11 ORIGINAL
(1) Breathing rates higher than normally expected for the rate of work are an early
warning sign. Excessive breathing rates, maintained for more than 1-2 minutes, can
produce light-headedness, muscle twitching, cramps, headache or unconsciousness.
(2) Mental abilities begin to deteriorate with core temperatures greater than
38.5oC. The ability to learn and retain new information will be impaired. Swimming
patterns or work behaviour may become progressively more erratic. By the time the
diver’s core temperature approaches 39oC noticeable mental confusion may be
present.
(3) The likelihood of hyperthermia increases with dive time. Dehydration may
occur mainly through sweating; urination may be absent. A weight loss of 1kg after
a dive indicates a loss of one litre of body water. Losses greater than two litres
indicate marked dehydration and may provoke muscle cramps in the absence of
hyperventilation.
(4) A rapid and rising pulse rate can indicate severe hyperthermia. Divers may
experience sensation of being hot, fatigued, disorientated or nauseated before they
collapse. Collapse may occur suddenly and without prior warning signs. As with
hypothermia, hyperthermia may be insidious in onset.
(5) The following are the more common symptoms and signs of heat stress in
diving:
(a) Dizziness, restlessness and headache. Feeling of being hot and

uncomfortable.
(b) Rapid pulse and usually, but not always, excessive sweating. Low urine
output.
(c) Initially, the skin will be clammy and cool to the touch. As heat
exhaustion progresses the skin becomes dry and flushed in appearance.
(d) Raised temperature.
(e) Twitching and cramp.
(f) Exhaustion, confusion, reduced level of consciousness, coma and

eventually death.
e. Management
(1) All cases of hyperthermia must be cooled to reduce core temperature. In mild
cases, removing the diver to a shaded or cool area may be sufficient. In more severe
cases, cooling can be achieved by lying the diver down and applying a fine mist of
25-30oC water to his skin and using a fan to enhance evaporation. Cold water or ice
should never be used on the whole body since this will cause vasoconstriction which
decreases blood flow to the skin, which may slow the process of lowering core
temperature.
8-12 ORIGINAL
(2) Conscious patients should be given non-alcoholic beverages to drink, one litre
every hour for each kilogram of weight loss. Adequate rehydration is achieved when
the patient produces urine that is pale to clear. It may take 2-4 hours for a severely
dehydrated diver to produce urine. Failure to urinate after four hours of fluid
replacement, may indicate renal failure.
(3) A prolonged core temperature of greater than 39oC can produce muscle
weakness or tremors, muscle cramps, nausea, vomiting or cardiovascular collapse.
Appearance of any of these signs or symptoms must be treated as a medical
emergency; cooling and hydration treatments must be started immediately.
(4) Unconscious patients should be rehydrated via intravenous fluid replacement.

Caution should be exercised in fluid administration early in the treatment, when
peripheral vasodilation is present. Subsequent vasoconstriction may result in fluid
overload and pulmonary oedema .
(5) All but the mildest cases must be evacuated to hospital, because heat illnesses
readily, and occasionally rapidly, deteriorate to life-threatening severity.
Complications include muscle, liver or kidney damage. Furthermore,
thermoregulation may take some time to return to normal and core temperature
should be carefully monitored for at least 48 hours. Divers who have suffered a
severe case of hyperthermia may be more sensitive to subsequent heat stress and
caution should be exercised before allowing these persons to resume warm water
diving.
8-13 ORIGINAL
INTENTIONALLY BLANK
8-14 ORIGINAL
SECTION 2 - DIVING IN POLLUTED WATERS
0805. Introduction
Some degree of contamination and/or pollution is evident in practically every harbour in
the world. Divers will be required to operate in polluted waters and handle toxic substances.
Little detailed information is available and the following is provided for guidance purposes only.
The effects of exposure may become evident immediately or may be delayed for many years,
especially in the case of exposure to carcinogenic substances. Depending on the type of toxic
substance encountered it may be advisable to introduce short or long term biological and medical
surveillance of exposed personnel.
0806. Hazard Identification

The particular hazard may need detailed identification before a decision to dive and what
equipment to use can be made.
a. Definition of Polluted/Contaminated Water/Environments. A workplace that

contains a chemical, biological or radiological material in sufficient concentration that
should any quantity of it be ingested, absorbed or inhaled is liable to endanger the health
and safety of a diver.
b. Hazard Analysis. The following types of hazard should be determined by available

means:
(1) Location of spills

Recreational contact
Drinking water supplies
Bioaccumulation of toxins in fish and shellfish harvested from rivers
Occupational exposure of divers and support personnel
(2) Depth: an assumption of 0 to 30 metres would be appropriate for typical spills

areas.
(3) Environmental factors: currents, sea state and wind would be factors in
migration and dispersal of a contamination. Currents will have greatest significance
for the diver and support personnel.
(4) Existence of debris or wreckage: bottom conditions, Diver/ROV entanglement

or tearing of a diving suit is a serious potential problem in the case of debris on the
bottom. Some chemicals sink and collect in pockets on the bottom providing small
areas of potentially pure contamination.
(5) Shore facilities available: the locations are significant in terms of being able
to respond rapidly with equipment and personnel.
(6) Pressure: changes to the physical properties of substances under pressure may
alter their potential hazard to divers.
8-15 ORIGINAL
c. Known Contaminants/Pollutants. The following main categories of contaminants

or pollutants are known to be potentially hazardous to divers.
(1) Biological contaminants: There are three types of biological hazards: Bacteria,
Protozoans and Viruses.
(2) Petroleum products: They are grouped into eight different types of products:
(a) Crude petroleum
(b) Residual fuel oil
(c) Gasoline
(d) Distilled fuel oil
(e) Asphalt, creosote, coal tar
(f) Solvents
(g) Diesel oil
(h) Waste or other oil
d. Hazardous Materials: The UN Identification Numbers include nine categories of

hazardous materials:
(Class 1) Explosives: nitroglycerine, picric acid
(Class 2) Gases: compressed, liquified, or dissolved under pressure
(Class 3) Flammable liquids: hydrocarbons, alcohols
(Class 4) Flammable solids or substances
(Class 5) Oxidising agents: halogens
(Class 6) Poisonous substances:
(1) Irritants: bromine
(2) Simple asphyxiants: carbon dioxide, nitrogen
(3) Blood asphyxiants: aniline, nitrobenzene
(4) Tissue asphyxiants: hydrogen cyanide
8-16 ORIGINAL
(5) Respiratory paralysers: hydrogen sulphide, carbon disulphide, acetylene,

ethylene, dyethil ether, ethyl alcohol
(6) Substances that disrupt liver and kidney function: arsenic, lead, cadmium,
mercury
(7) Substances that attack muscle: strychnine
(8) Substances that attack bone marrow: toluene, xylene, naphthalene
(9) Substances that interfere with vital nerve impulses: organic phosphates,
methyl alcohol
(Class 7) Radioactive substances
(Class 8) Corrosives:
(1) Acids: hydrochloric acid, sulphuric acid, acetic acid, chromic acid and
acrylic acid
(2) Bases: sodium hydroxide, potassium hydroxide
(Class 9) Miscellaneous dangerous substances:
(1) Water reactive materials: lithium, sodium, potassium, hydrides,

phosphides, chlorides.
e. Radiological contamination: Divers may be responding to an emergency when the

diving area is contaminated with a radiation source, or when they may be required to
perform inspection, repair or maintenance in the fuel pools of nuclear reactors.
0807. Monitoring
The type, frequency and duration of biological or medical monitoring of divers exposed
to hazardous or toxic substances will be determined by the substance involved and by national
standard of practice. The recognition and identification of substances is of paramount importance
if adequate and appropriate monitoring of exposed personnel is to be conducted by medical
authorities.
a. Clarification of Exposure Levels. Following definitions are used:
(1) Lethal Dose (LD 50): the amount of material that will kill half of a biological
sample in a controlled experiment during a given period. The lethal dose is
expressed in milligrams of toxin per kilogram of body weight of the biological
sample exposed.
(2) Lethal Concentration (LC50): the poisonous substance is introduced into a

closed container in a specified ratio of parts per millions by volume of air for a
specific time killing half the biological sample during the best period.
8-17 ORIGINAL
(3) Threshold Limit Value (TLV): specifies the maximum amount of a toxic
substance that an average person in reasonable health may be exposed to repeatedly
on a daily basis with no ill effect.
(4) Maximum Allowable Concentration (MAC): absolute maximum tolerable

exposure to a particular chemical at one time.
(5) Short Term Exposure Limit (STEL): the maximum level of exposure to a
chemical permissible for a 15 minute period.
(6) Immediately dangerous to life and health (IDLH): environments that pose an
immediate threat to life or health, or exposure to contaminants that are likely to have
an adverse cumulative or delayed consequence on health.
b. Treatment After Exposure. The medical treatment after exposure will be

conducted in accordance with the specific medical emergency procedures directed by a
competent medical team.
0808. Support System and Body Protection

The diving support system should include surface support protection both respiratory and
physical as well as the divers respiratory equipment and physical equipment.
a. Protection for Surface Personnel. The surface tenders and support personnel may
experience as great a hazard as the diver in support of contaminated/polluted diving.
Respiratory and physical protection must be available for surface support personnel.
(1) Breathing apparatus: the one for military NBC/CBR activities may be used.
(2) Physical protection: the military NBC/CBR protecting cloth gives sufficient
protection for surface personnel except for stand-by divers. (They must dress in the
same diving dress as the divers).
b. Protection for the Diver: The type of protection identified for the diver will be
determined partly by the expected hazard, the type of work required and the urgency of
the work to be completed:
(1) Breathing apparatus: A surface supplied diving system with a positive

pressure (free flow) helmet is preferred for polluted water diving. Should a demand
diving helmet be the equipment available, it should be modified with two exhaust
valves in series to avoid splashback.
(2) Body protection: A dry suit connected to a positive pressure (free flow)
helmet, with attached dry gloves is the best protection for the diver. It will normally
preclude any contact between the human body and the contaminant.
8-18 ORIGINAL
c. Contaminant Resistant Equipment. There is no material that protects the diver

under all conditions or from all contaminants. For a wide range of diving operations in
contaminated water, the use or dry suits composed of vulcanised rubber and a diving
helmet, or overpressure breathing system, is acceptable. However there will be situations
when additional protection will be required. Coated exterior fabric dry suits may be
difficult to decontaminate.
0809. Operating and Handling Procedures

There are several decisions that must be made prior to committing a diver to a
contaminated dive or exposure to hazardous substances. The urgency of the required operations,
the natural environmental effects (i.e. weather, current, type of body of water), the diving
equipment available, and the protective equipment available for surface support personnel must
all be considered, the nature and extent of this, will be determined by the specific hazard
encountered. It is imperative that potential hazards are identified, accurately labelled or marked
and that adequate data is available to divers to take reasonable precautions to minimise exposure.
Diving in contaminated and polluted water, must consider two problems: the diving itself and the
surface contamination hazard. The diving supervisor for such tasks, should be qualified in all
NBC/CBR aspects, if he is not, he should be advised by a separate NBC/CBR specialist
nominated by the tasking authority. (See Annex E).
a. Threat Analysis. Before diving in contaminated water an analysis of the situation

is required:
(1) The following information should be determined for the duration of the
operations:
(a) Geographic location
(b) Contaminant and its concentration
(c) Depth and location of work site
(d) Wind, weather and sea conditions
(e) Currents
(f) Water and air temperature
(g) Visibility
(2) To ensure an adequate threat evaluation the tasking authority should complete
the form at Table A.
b. If possible, a photographic/video survey of the underwater situation should be

undertaken. After making a thorough threat analysis it will be possible to identify
required diving equipment or decide that it would be better to use a ROV for the
operation. The ROV can be used for investigation, in tandem with the diver (for
observation/direction, for light, for equipment transport), it should be considered for solo
use when the risk of pollution or contamination is unacceptable.
8-19 ORIGINAL
c. Pre-Dive Safety Precautions. The following pre-drive safety precautions should

be adhered to during polluted/contaminated water diving:
(1) Diver actions: Before diving, the diver must ensure that all the material he
needs for the operation in particular is available and properly set up. He should
check his dry suit for leaks. He should test the communication equipment.
(2) Surface support personnel actions: The surface support personnel must ensure
that the following equipment work and are set up correctly:
(a) Diving equipment
(b) Individual protection suits and breathing equipment
(c) Communications
(d) Decontamination station
(e) First Aid Equipment
(f) Emergency facilities and personnel
d. Handling Contaminated Materials. All material removed from the polluted water
should be treated as contaminated. Before their disposal they should decontaminated and
packed in a suitable container.
e. Decontamination Procedures. After every dive into contaminated or potentially

contaminated water, the divers must be decontaminated to avoid danger to themselves
or supporting personnel. It is appropriate to use military NBC/CBR procedures. Areas
that need special attention during decontamination procedures include zippers, seams in
the suit, helmet seals and the soles of the diver’s boots.
0810. Use of Atmospheric Diving Suits or Small Manned Submersibles

The use of atmospheric diving suits (ADS) and small manned submersibles may offer a
solution to the problems associated with diving in polluted waters. As well as the time and depth
advantages of these systems, they afford superior protection for the operator. Nonetheless, their
use should be carefully planned. Personal protective equipment should be worn by the operator
inside an ADS/submersible to guard against the possible effects of contamination breaching the
system. A high concentration of certain contaminants may severely damage the ADS/submersible.
System decontamination may also require special consideration.
8-20 ORIGINAL
TABLE A
Tasking Authority DTG of Incident Date of compilation Geographic Location
1. CONTAMINANT SITUATION
Contaminant Concentrations - Units Depth Sample Location
2. LOCAL CONDITIONS
a. Present conditions
Wind Current Surface Surface Underwater Air

Sea Visibility Visibility Temperature
Condition
Dir. ST. Dir. ST
b. Forecast conditions in 6 hours
Wind Current Surface Surface Underwater Air

Sea Visibility Visibility Temperature
Condition
Dir. ST. Dir. ST INC/DEC. INC/DEC. INC/DEC.
3. LOCAL BATHYTHERMOGRAPHIC READINGS
o
Depth C/oF Depth o
C/oF
4. POSSIBLE HAZARDS IN THE OPERATION AREA
5. AVAILABLE DOCUMENTATION/INFORMATION
8-21 ORIGINAL
INTENTIONALLY BLANK
8-22 ORIGINAL
0811. Introduction
Dangerous marine animals can be categorised into three groups; those that are predatory
and produce trauma; those that are venomous; and those that are poisonous if ingested. The latter
do not pose a specific hazard to divers.
0812. Predatory Marine Life
a. Sharks
(1) There are approximately 350 known species of shark. Most inhabit the
temperate or tropical zones, and live in relatively shallow waters off the continents
and islands. Those believed to be of greatest concern are the great white shark, mako
shark, tiger shark, oceanic whitetip and the hammerhead. All sharks have such a
characteristic physical appearance that recognition is not a problem. Any shark
should be considered potentially dangerous. Shark bites are usually concentric
slashes, and the bite may contain bits of teeth around its edges. The shark’s multiple
rows of teeth and strong jaws inflict severe bites; amputations and extensive wounds
are common. Death is caused by massive haemorrhage and shock.
(2) Prevention:
(a) Do not urinate in the water or swim with abrasions or bleeding wounds.
(b) Avoid splashing on the surface.
(c) Avoid swimming/diving in the late afternoon or night when sharks tend to
feed.
(d) Stay with a buddy/partner or group.
(e) Avoid swimming/diving in water with low visibility where possible.
(f) Avoid playing with or killing sharks.
(g) Avoid carrying or tethering fish near the body.
(h) If sharks are encountered, calmly leave the water at the first opportunity.
It may be necessary to descend to the seabed or to the protection of rocks if
leaving the water is not possible.
(i) Making loud noises, blowing bubbles, splashing, or creating a commotion

is of no value in deterring sharks and may attract them.
(j) Avoid dark-coloured garments which contrast with light skin.
(k) Avoid carrying or wearing shiny objects.
8-23 ORIGINAL
(l) If an attack is inevitable face the shark and be prepared to fend it off with
anything at your disposal.
(m) Shark repellants are of questionable value.
(3) First Aid Treatment:
(a) Remove the victim from the water.
(b) Commence first aid treatment immediately, do not delay first aid by
rushing the casualty to hospital.
(c) Control the haemorrhage: Apply direct pressure to wounds, elevate limbs,
occasionally, it may be necessary to apply a tourniquet, but this should be
avoided if possible.
(d) Reassure the patient.
(e) Call for medical assistance.
(f) Give nothing by mouth.
(4) Medical Management:
(a) Ensure the airway is patent and breathing is adequate.
(b) Control haemorrhage and resuscitate with intravenous fluids.
(c) Administer analgesia.
(d) Administer tetanus prophylaxis and broad spectrum antibiotics.
(e) Refer for definitive surgical management.
(b) Killer Whales. Killer whales are one of the most dangerous animals in the sea,
however, they are believed to be a relatively minor hazard to humans. A diver should
leave the water as quickly as possible if one is sighted.
(c) Barracuda. Barracuda are encountered throughout tropical and subtropical waters.
The great barracuda is found in the Caribbean around the West Indies, from Brazil to
Florida, and in the Indo-Pacific from the Red Sea to Hawaii. These fish are attracted by
anything that enters the water, particularly bright-coloured or reflective objects. The
wounds are usually smooth slashes, produced by long canine teeth. Treatment of
barracuda wounds is identical to that for shark bites.
8-24 ORIGINAL
(d) Moray Eels. Moray eels are seldom found except in tropical and subtropical waters.
They are bottom dwellers and are frequently found lurking among rocks and corals.
They seldom attack unless provoked. The wound of a moray eel consists of severe
lacerations inflicted by strong knife-like or crushing teeth. Bleeding may be profuse.
Treatment is identical to that for shark bites.
(e) Octopuses. Octopuses introduce their venom by biting; they may be killed by
stabbing them between the eyes and manoeuvring the knife from side to side. The
symptoms of an octopus bite are seldom severe although it may cause pain very quickly.
There may be signs of inflammation, and local burning or stinging sensations. Recovery
from these bites is usually uneventful, although it may take several days. Octopus bites
should be treated in the same way as venomous fish stings.
(f) Groupers. Groupers are found in temperate and tropical waters. They may attain
a length of over 4 metres and a weight of over 450 kg. They are curious and bold. Their
feeding characteristics and size make them hazardous to divers. Their mouth can engulf
a diver. Several fatal attacks have been reported. Treatment of grouper wounds is
identical to that for shark bites.
(g) Crocodiles & Alligators
(1) These animals are found in fresh and salt water in the tropical and sub-tropical
regions. They are highly dangerous. Treatment of wounds is identical to that for
shark bites.
(2) Prevention:
(a) Do not wade, swim, stand, canoe or dive in tropical waterways where
these animals.
(b) Take notice of local advice.
(c) An attack may be thwarted by throwing objects at the animal, hitting its
snout or gouging its eyes.
(h) Seals & Sealions. These are curious, friendly and intelligent animals, found in cool
waters. During the mating season, the males may snap at swimmers, but they are usually
not ferocious. Divers should stay away from these animals, however, especially during
the breeding season or when young are in the water.
(i) Giant Clams. Giant clams do not actually bite, but an unwary diver might be
trapped if the clam's valves closed on the diver’s foot or hand. This rarely happens
because it normally takes several seconds for the clam to close. It is possible for a victim
to release himself by severing the clam’s adductor muscles with a knife.
8-25 ORIGINAL
0813. Venomous Marine Life
a. Venomous fish
(1) There are many different species of venomous fish, such as Stingrays,
Stonefish, Weeverfish, Scorpionfish, Rabbitfish, Ratfish, Stinging sharks,
Surgeonfish and Toadfish. They are found in all the oceans and seas of the world.
(2) The symptoms of venomous fish sting are similar among species. Immediate
local pain occurs and gradually increases in severity, only abating after a few hours.
Pain may extend to the regional lymph nodes and paralysis of the surrounding muscle
may occur. Systemic symptoms, such as muscular spasms in the affected limb,
nausea, hypotension, and cardiovascular shock, are occasionally present although
death is rare.
(3) First Aid:
(a) Lie the casualty down.
(b) Gently extract the stinger.
(c) Encourage a little bleeding.
(d) Irrigate the area with water or saline.
(e) Rest and elevate the affected limb.
(f) Immerse the limb in water at 35oC, raise the temperature to 45-50oC.
(g) Keep the limb immersed for 30-90 minutes or until the pain no longer
recurs after the limb is removed.
(a) Inject 1% lignocaine solution, without adrenaline, if the pain is severe and
does not respond to hot water.
(b) If pain and distress do not respond to local measures systemic analgesics
and narcotics may be necessary.
(c) Monitor cardiovascular status and treat systemic manifestations

symptomatically.
(d) Clean, debride and dress the wound.
(e) Administer tetanus prophylaxis.
(f) Administer broad spectrum antibiotics if infection occurs.
8-26 ORIGINAL
(5) Stingrays. There are many species of ray, many of which are venomous. They
are found throughout the temperate and tropical regions. Their stinger is located on
the upper side of the tail at variable distances from the base of the tail. Sting rays
generally lie on the bottom of the ocean in shallow water. They are usually well
camouflaged and partly covered with sand. When stepped on, the ray strikes upward
with its tail, driving the spine deeply into the foot or leg. The wound is jagged and
dirty, and the venom produces severe pain; large quantities of venom can cause
generalized effects. The treatment of stingray injury is identical to that of other
venomous fishes.
(6) Stone Fish. Probably the most venomous of all fishes, stonefishes are found
in the tropics. Their dorsal spines are capable of piercing footwear and skin. Local
and systemic symptoms may be severe. The treatment of stonefish injury is identical
to that of other venomous fishes. Injection of hyoscine butylbromide into the site has
shown good results if given early. An antivenom is available.
b. Venomous Coelenterates
(1) COELENTERATA include over 9000 species. They can be simply divided
into free-swimming jellyfish and attached or stationary coelenterates. Jellyfish are
found in all oceans, but are most prevalent in the equatorial band. Attached
coelenterates are also found most commonly in warmer waters. All coelenterates
sting by releasing venom from the cells on the tentacles, which are equipped with
thread-like tubules, nematocysts.
(2) The local and systemic manifestations vary according to species; the extent of
the area involved; the age and weight of the casualty; and the thickness of the skin
at the injury site. Local skin irritation ranges from mild pricking to a stinging
sensation, to burning, throbbing or shooting pain. A linear erythematous papular
eruption is most common. However, urticarial vesicles, oedema, or cutaneous
haemorrhages may also occur. Systemic effects may include fever, shock, muscular
cramps, paraesthesia, hypaesthesia, nausea and vomiting, severe headache,
lacrimation, hypersalivation, laryngeal oedema, paralysis, delirium, convulsions, or
death.
(3) First Aid/Medical Management:
(a) Lay the casualty down and provide reassurance.
(b) Wash the affected area in vinegar to remove tentacles (fresh water will fire
any remaining nematocysts).
(c) Gently remove tentacles using gloves, or an instrument, taking care not to
burst further nematocysts.
(d) Rewash in sea water once all tentacles are removed.
(e) Local application of ice packs may help to relieve discomfort.
(f) Apply a lignocaine based local anaesthetic ointment.
(g) Treat systemic manifestations supportively.
8-27 ORIGINAL
(4) Wear protective clothing in the water (eg. overalls and wetsuits, gloves, face
mask and footwear).
(5) Portuguese Man O’War. The Portuguese Man O’War is found in temperate
and tropical waters. It has a gas filled sac, usually blue coloured. It floats on the
surface and drifts in the wind. It has one or more long tentacles which may be up to
10 metres in length. The symptoms, signs and medical care are identical to other
coelenterates.
(6) Box Jellyfish/Sea Wasps
(a) Box-jellyfish are usually only found in the warm waters of the Indo-Pacific
region. They may weigh as much as 3 kg with tentacles as long as 3 metres.
Since there are up to 15 of these long almost invisible strands a swimmer can
be injured without knowing the cause. Pain is immediate and excruciating on
contact with the tentacles. Confusion, loss of consciousness and drowning are
relatively common. In severe cases there is little that can be done and death
from cardiorespiratory arrest can occur in minutes. Skin necrosis and ulceration
commonly develop 7-10 days after the sting has occurred.
(b) The treatment of box-jellyfish stings is identical to other coelenterates,

however, the following additional measures may be required:
i. Continuous intensive monitoring is indicated.
ii. Box-jellyfish antivenom has been developed by the Commonwealth

Serum Laboratories in Melbourne.
iii. Systemic and topical steroids have been recommended.
iv. Sedation may be required.
(7) Fire Coral
(a) Fire coral is found in tropical waters. This coral is often not easy to
recognise but has a missive exoskeleton covered with numerous minute pores.
The nematocysts ate non-mobile, activated only when touched by the diver.
(b) Symptoms are usually limited to painful skin welts, barring an allergic
reaction to the toxins of the neomatocysts.
(c) Treatment is identical to that for ceolenterates.
8-28 ORIGINAL
c. Blue Ringed Octopuses
(1) These creatures are the most dangerous of the octopods and are common
around Indo-Pacific Ocean islands and countries. They are yellowish brown but
develop bright blue rings on their tentacles when excited. The bite is small and
initially painless. After a few minutes a progressive painless paralysis becomes the
dominant feature. This lasts between 4 and 12 hours. These bites have a mortality
of 25%. Respiratory paralysis is the cause of death.
(2) First Aid:
(a) Wash out the toxin with any fluid available.
(b) Apply a pressure bandage and immobilise the limb.
(c) Rest the casualty in the recovery position.
(d) Do not leave the casualty unattended.
(e) Send for medical assistance.
(f) Reassure the casualty.
(g) If necessary commence cardiorespiratory resuscitation.
(a) Provide first aid.
(b) Avoid the use of respiratory depressants.
(c) Intubate and ventilate the patient where appropriate.
(d) Do not give oral fluids/food to paralysed casualties.
(e) Provide eye protection and care.
(f) Treat other symptoms and signs supportively.
d. Sea Snakes
(1) Sea snakes are mainly found in the tropical Indian and Pacific Oceans, and most
of the species prefer sheltered coastal waters and river mouths. They are not found
in the Atlantic ocean. They can be recognised by the paddle-like flattening of their
tails. Sea snakes have poorly developed fangs and the teeth marks vary in number
from 4 to 10. They are able to float on the surface for long periods; although they
are air breathers they can remain submerged for long periods of time.
8-29 ORIGINAL
(2) Unprovoked attacks are very rare, but the species vary in disposition. Since the
venom is extremely potent, it pays to treat all sea snakes with respect and distance.
There may be a latent period of 20 minutes to several hours after biting before the
onset of symptoms and this has led some victims to fail to associate the bite with
subsequent illness.
(3) Early Symptoms Include:
(a) A general malaise and anxiety; some may experience mild euphoria.
(b) A sensation of thickening of the tongue.
(c) A generalized feeling of muscular stiffness.
(d) Aching or pain on movement.
(4) Later Symptoms Include:
(a) Weakness that progresses to actual inability to move and includes the
whole body within an hour or two; it begins with the legs and moves upward.
(This paralysis is usually of the flaccid or flexible type, but the spastic or rigid
type is sometimes seen.)
(b) Ptosis.
(c) Trismus.
(d) Bulbar, facial and ocular paralysis.
(e) Hypotension, cardiac failure.
(f) Muscular spasms; myonecrosis leading to myoglobinuria and acute renal

failure.
(g) Respiratory distress leading to paralysis.
(h) Convulsions.
(i) Unconsciousness.
(j) Death occurs in about 25% of cases.
(5) The following points may be helpful in distinguishing snake bite from other
types of marine-life injury:
(a) The victim has usually been in the water or working with nets in a coastal
area or near a river mouth.
8-30 ORIGINAL
(b) Pain was absent immediately after the initial wound.
(c) Fang marks (two circular dots or two, pairs of dots half an inch or so
apart) should be visible at the site of pain.
(d) Symptoms generally develop in the manner described above.
(6) First aid is identical to that for the blue-ringed octopus, but in addition, if
possible, capture and kill the snake and have it identified (it may prove to be a
harmless type).
(a) Provide first aid.
(b) Admit to hospital for intensive care.
(c) Give anti-venom treatment at the earliest possible moment in severe cases.
Be prepared to treat anaphylaxis.
(d) Force fluids to increase renal excretion of venom and to prevent renal
damage from myoglobin. If acute renal failure supervenes, haemodialysis may
be necessary.
(e) Intubate and ventilate if respiratory paralysis is a feature.
(f) Provide sedation and anticonvulsant therapy if needed, but avoid morphine
because of its respiratory depressive effects.
e. Cone Shells
(1) Cone shells are found in tropical and sub-tropical waters. They are
characterised by their conical shape. Many have attractively coloured shells which
encourage people to pick them up. The danger is that these have a well developed
harpoon-like venom apparatus situated at the narrow end of the shell. If they have
to be handled it is safest to pick them up by the blunt end but even then the hand is
within reach of the ‘sting’. The harpoon can penetrate clothing and they should not
be put in the pocket.
(2) The initial puncture may or may not be painful. Within 10-30 minutes numbness
and tingling arise and may involve the whole body. A progressive paralysis ensues
and deterioration continues for up to six hours. Recovery usually occurs within 24
hours. Treatment is identical to that for the blue-ringed octopus.
8-31 ORIGINAL
f. Sea Urchins
(1) Sea urchins are found in all oceans. They have spines which can penetrate the
skin and discharge toxin into the wounds. The spines are brittle and usually break off
into the wound. The casualty generally recalls contact with the urchin. Penetration
gives rise to intense burning pain and swelling. The pain and swelling subside in
about 12 hours but secondary infection may make the condition last longer. Systemic
symptoms may occur with a bulbar paralysis and respiratory difficulty.
(a) Immobilise the limb.
(b) Carefully pull out any visible spines.
(c) Immersion of the limb in hot water may relieve the pain.
(d) If necessary commence cardiopulmonary resuscitation.
(e) Local anaesthesia will relieve the pain.
(f) Examine, debride, X-ray and dress the wound.
(g) Magnesium sulphate paste is useful as a poultice.
(h) Treat systemic manifestations symptomatically.
g. Sponges. Sponges are found from the tropics to the polar regions. They can
produce contact dermatitis with localised burning, itching and swelling. In severe cases
there may be systemic symptoms such as malaise, nausea and muscular weakness.
Treatment is symptomatic as for contact dermatitis and care should be taken to avoid
enlarging the area of contact by rubbing affected hands across the face or eyes.
h. Worms
(1) Most dangerous species of worms are tropical. Annelid worms are segmented
and carry bristles, which can penetrate the skin. Other worms bite. Annelid injury
causes local burning, itching, stinging, paraesthesia, a papular eruption and oedema.
(a) Remove the bristles with adhesive tape.
(b) Apply alcohol, vinegar or calamine lotion.
(c) Bed rest may be necessary.
(d) Treat systemic symptoms with steroids and anti-histamines.
(e) Administer resuscitation where necessary.
8-32 ORIGINAL
0814. Near Drowning
a. Introduction. Drowning, defined as death by immersion in fluid, is the ultimate

cause of death in the majority of diving fatalities. The usual sequence of events involves
aspiration of fluid following the breath-hold break-point or panic followed by progressive
hypoxemia leading to loss of consciousness, cardiac arrhythmias and eventual cardiac
arrest. Near drowning is the term used to describe those who survive or are rescued.
b. Cause. Divers, despite being properly equipped, trained and supervised may still
succumb to drowning as the result of difficulties brought on by any of the following
factors:
Trauma
Hypothermia
Exhaustion
Acute medical events eg. seizures
Acute DCI
Nitrogen Narcosis
Oxygen or other gas toxicity
Entrapment/Exhaustion of air supply
Panic
Hyperventilation prior to breath-hold diving
c. Clinical Features. The clinical features depend on the severity of the incident. The
most severe cases may be recovered from the water cyanised and comatose with absent
vital signs and subsequently make a remarkable recovery. Less severe cases may have
no change in conscious level but suffer from dyspnoea, retrosternal chest pain and a
cough productive of pink frothy sputum. Water frequently enters the stomach during the
drowning process and there may be vomiting. Occasionally, the process of water
entering the nose or pharynx provokes laryngeal spasm, which may prevent water
entering the lungs. It may still prove fatal, is known as ‘dry drowning’ and occurs in
about 10% of drowning victims.
d. Management
(1) Initial management consists of simple, prompt, effective, life support measures.
The unconscious diver should be returned to the surface as rapidly as possible, his
airway cleared and Exhaled Air Resuscitation (EAR) started immediately. On
recovery into a boat or on land, cardiac massage should begin if required and oxygen
should be administered if available. There may be justification for withholding
cardiac massage in hypothermia cases where an undetectable or weak pulse may be
present and there is a risk that the physical effects of massage may induce a cardiac
arrhythmia.
(2) There is no need to attempt to drain the lungs of fluid. The benefits from this
action are unproven, there may be little water in the lungs in cases of dry drowning
and attempts to drain the lungs may induce vomiting with the subsequent risk of
aspiration of gastric contents. Consequently, priority should be given to
administering effective cardiopulmonary resuscitation.
8-33 ORIGINAL
(3) Further care depends upon the severity of the case. Mild cases may only
require the administration of oxygen by mask and 12-24 hours in hospital for
observation for the onset of a delayed respiratory distress syndrome or ‘secondary
drowning’. Unconscious casualties may require intubation and positive pressure
ventilation, despite the presence of spontaneous ventilation, in order to correct
hypoxia and respiratory acidosis.
(4) Care should be taken in the secondary survey to establish the cause of
drowning and determine if there are any associated problems such as trauma or
hypothermia. If there is evidence to suggest that the diver has DCI, near drowning
is not a contraindication to recompression.
0815. Underwater Blast Injury
a. Introduction. Divers frequently work with explosives or are involved in combat

0swimming and therefore may be subject to the hazards of underwater explosions. The
blast injuries caused by underwater explosions may also be seen in shipwreck survivors
who are immersed as explosions occur. The majority of information about these injuries
was obtained from experimental and clinical data collected during the two World Wars.
b. Underwater Blasts
(1) An explosion is the violent expansion of a substance caused by the gases

released during rapid combustion. Shock waves generated by an underwater
explosion travel at the speed of sound and are transmitted further and with much
more intensity in water than in air because of the incompressibility of liquids. When
they reach a submerged human, these shock waves are transmitted directly through
the skin and soft tissues, which have a similar density to water, until they reach a
tissue/gas interface where the tissues are subjected to violent disturbance which may
cause ‘shredding’.
(2) The amount of damage to the body is influenced by a number of factors.

Injuries are caused by a pressure wave (pulse) which starts with a maximum (peak
pressure) that rapidly decays over time. It is the area under the pressure/time curve
referred to as the impulse that determines the extent of the injuries caused. To
complicate the issue it is not only the primary impulse that must be considered, but
also its reflection from the bottom, solid objects in the water and, to a lesser extent,
the surface. The strength of the impulse reflected from the bottom is dependent on
its nature. Mud and sand attenuate the impulse to a greater extent than more solid
surfaces such as rock. Because of its reflection, the impulse near the bottom will
be greater than near the surface. Determining a safe horizontal distance from the
underwater explosion is very complicated and must include consideration of the
following factors:
(a) Size of the explosive charge.
(b) Depth of the charge.
(c) Depth of the diver.
(d) Depth of water in the area.
8-34 ORIGINAL
(e) Whether the area is in enclosed waters (e.g. harbour) or in open water.
(f) The extent of injury that is considered acceptable.
(2) For a diver near an explosion, shallower means safer. A diver expecting an
imminent explosion should seek to surface rather than increase the horizontal
distance between himself and the explosive charge. He should only try to increase
his horizontal separation from the charge after reaching the surface.
(3) In accordance with the theory of the effect of underwater explosions (see ATP
6(B) Volume I - Mine Warfare Principles) the distance at which an underwater
explosion will have no appreciable effect on divers and underwater swimmers is
given by the formula:
R = 2703 w
where R is the distance in metres and W the weight of the charge in Kg TNT
equivalent.
Note. For charges smaller than 2Kg the figure obtained from this formula may be
reduced by a factor of 3.
(4) In addition to this formula, several nations have developed their own tables of
acceptable horizontal distances from underwater explosive charges. During joint
NATO operations the most conservative criteria should be used.
b. Prevention of Injury
(1) If at all possible, the diver should avoid being in the water if underwater
explosions are expected.
(2) If this is not possible, the diver should endeavour to remove as much of his
chest and abdomen from the water by lying on the surface and swimming on his
back. To assist this process, it may be appropriate to over-inflate the dry suit.
(3) If unable to reach the surface, the smallest area of the body should be presented
towards the charge.
(4) A drysuit with thick undergarments offers the best protection from an
underwater explosion.
c. Symptoms and Signs of Injury. If an underwater explosion occurs when divers

are in the water, severe injury or death may result. The lungs are particularly vulnerable
and most early deaths are caused by pulmonary injury. Some of these deaths may also
be caused by central nervous system injury caused by the shock waves rapidly
compressing the chest and abdomen to increase cerebral venous pressure and provoking
haemorrhage. The intestines are also vulnerable where they contain gas, and small
haemorrhages in the intestinal walls occur at the furthest ranges at which injuries are
observed. The following symptoms or signs may be apparent:
8-35 ORIGINAL
(1) Unconsciousness, headaches or neurological signs.
(2) Shortness of breath, coughing, haemoptysis.
(3) Haematemesis, melaena or rectal bleeding.
(4) Chest and abdominal pains.
(5) Hearing loss and signs of aural barotrauma.
d. Management
(1) Triage of casualties and basic resuscitation as appropriate. Treatment for

circulatory shock.
(2) Evacuation must take into consideration the risks of worsening circulatory
shock by early transport before stabilisation of the casualty and of respiratory
difficulties worsened by air transport.
(3) All casualties must be admitted to hospital for observation as in the early stages
there may be no external signs of injury despite severe internal injuries. Casualties
should be maintained on intravenous fluids with nasogastric suction until the full
extent of their injuries is ascertained.
(4) Subsequent management will depend on the site and extent of the injuries, but
may include positive pressure ventilation, blood transfusion, laparotomy and
abdominal surgery.
0816. Underwater Noise and Sonar Transmissions
a. In air, sound travels at about 335 metres per second, but the speed of sound varies
greatly in other substances. In water, sound travels more than four times as fast as in air.
Both air and water transmit sound well, but it is greatly attenuated at an air/water
interface. All but one ten-thousandth part of the sound energy is lost when being
transmitted from air to water; therefore, for divers to hear each other or to hear sounds
from the air above them, the sounds must originally be very loud. The fact that sound
travels much faster in water than in air also makes it almost impossible for a diver to
pinpoint a source of sound underwater.
b. Breathing an oxy-helium gas mixture or air at raised pressure changes the voice to
a higher pitch. The higher the pressure the greater this effect becomes until at great
depths the voice becomes so distorted that telephone communication is almost
impossible. This effect is due to the different speed of sound in gases of different
densities. Unscramblers have been developed to correct the change of frequency under
these conditions and allow intelligible speech to be transmitted when using oxy-helium
mixtures.
8-36 ORIGINAL
c. There are two main effects of exposure to intense noise underwater; an acute effect
on the vestibular system which may result in disorientation, and longer term damage to
the hearing mechanism which may result in noise-induced deafness. Divers must
therefore be protected from exposure to underwater noise and sonar transmissions and
be screened for long term hearing loss at routine medicals.
d. Stand Off Distance Calculations. National stand off distances for divers exposed
to underwater noise and sonar transmissions are usually calculated by the following
mechanisms. Tables of actual distances can be found in national publications.
(a) Exercises. Stand off distances are usually based on current in-air criteria with
corrections for the difference in hearing threshold in air and underwater and the
difference between the effects of pure tone and broad band noise. In practice, the
calculated distances are normally so large that sonars can not normally transmit when
divers are in the water.
(b) Operations. The threshold of oculo-gyral sensitivity is used as the basis for
calculating stand off distances from sonar in the exceptional circumstances when it
is operationally essential to continue sonar transmissions when divers are in the
water. The threshold of oculo-gyral sensitivity for hooded divers is about 175 dB
re 20 µPa and for non-hooded divers is about 165 dB re 20 µPa. Experiments have
shown that disorientation effects do occur at exposures slightly above these
threshold levels.
0817. Otitis Externa
a. Cause. Repeated wetting can cause breakdown of the skin which lines the external
ear canal and this then allows the bacteria and fungi which are normally present to
multiply and produce symptoms of infection. The water in which the dive is being
performed does not have to be contaminated for otitis externa to occur. It is a condition
which most commonly occurs during saturation diving, although frequent immersion of
the ears such as when participating in intensive diving courses, can promote the
condition.
b. Prevention
(1) This is a completely preventable condition.
(2) 7% Aluminium acetate solution or Otic Domeboro® ear drops will prevent
infection if applied after each wet dive. These solutions are bacteriostatic and
astringent. Three or four drops of the solution should be poured into each ear in
turn and left for a minimum of 5 minutes.
(3) During intensive diving operations the drops should be applied at least every
morning and night, and after each wet dive or shower.
(4) Ear wax should not be allowed to build up within the external ear canal as it
prevents the successful application of prophylactic drops.
8-37 ORIGINAL
c. Symptoms and Signs
(1) Itching and/or a wet feeling in the affected ear are usually the first symptoms.
These may progress to severe local pain as the external ear becomes swollen and
inflamed. There may either be a watery or creamy, foul-smelling discharge from the
ear.
(2) Swelling of lymph nodes in the neck which may make jaw movement painful.
(3) Fever and other constitutional symptoms in severe cases.
d. Treatment
(1) A temporary cessation of diving so that the ear can be kept dry.
(2) Continued use of aluminium acetate drops plus appropriate antibiotic ear-
drops. An absorbent wick may be used if necessary.
(3) In serious cases, systemic antibiotics may be necessary.
0818. Caustic Cocktail
a. Cause. If water enters a closed-circuit breathing apparatus, it will eventually mix

with the CO2 absorbent (usually a mixture of calcium hydroxide with a small amount of
sodium hydroxide) to form a strong alkaline solution, which may cause chemical burns
to the face, mouth, epiglottis, lungs and stomach.
b. Prevention
(1) Ensure that the equipment has no leaks before diving.
(2) If leaks become apparent during the dive - surface as soon as possible.
c. Treatment
(1) Remove the diver from the water. Remove the set as quickly as possible.
(2) If the diver is suspected of having swallowed a cocktail give copious drinks of
fresh water. Salt water may be used to rinse out the mouth but should not be
swallowed, since it may induce vomiting and cause further burning.
(3) Wash all contaminated external surfaces liberally with fresh or salt water.
(4) Caustic burns to the eye should be treated by washing the eye with large
volumes of water for at least 20 minutes. If necessary, the eyelids should be held
open while this is done. Refer to an eye unit, casualty department or Medical Officer
immediately.
8-38 ORIGINAL
(5) A caustic cocktail readily provokes panic, especially in inexperienced divers.

This may result in a rapid ascent and breath-holding (to avoid inhaling further alkali).
Consequently, divers who as the result of a caustic cocktail, make a rapid ascent to
the surface should be observed carefully for 12 hours following the dive for evidence
of pulmonary barotrauma or neurological decompression illness and should be seen
by a Medical Officer before diving is resumed.
0819. Disorientation
a. In the three dimensional underwater environment, accurate orientation is essential

to allow a diver to complete tasks safely and make a safe return to the surface. On the
surface, a man’s orientation depends on sensory information provided by his visual,
proprioceptive and vestibular systems but the intensity of these stimuli is often reduced
underwater and disorientation can become a significant problem.
b. On land, visual cues usually play the most important role in orientation but divers
may frequently be exposed to underwater conditions so dark or murky that vision is
reduced to such a level that they have no visual reference points. In these situations he
depends on proprioceptive and vestibular information alone. Proprioceptive and
vestibular cues derived by gravitational effects on the body are also much reduced
underwater and the inexperienced diver may become disorientated due to sensory
deprivation. These circumstances readily lead to panic, uncontrolled ascent, near-
drowning and other incidents. Alert, experienced and composed divers learn to rely on
practical clues such as those given in the following list to assist in orientation:
(1) Ease of breathing is affected by the relative depths of SCUBA demand valve
first and second stages.
(2) Exhaust bubbles rise.
(3) Heavy objects such as weight belts still exert downward pressure.
(4) Gas volume changes in the sinuses or ears can be felt with changes in depth.
(5) Mild suit squeeze can often be felt in the most dependant parts of a drysuit.
c. Disorientation can still arise in experienced divers as in conditions of reduced

visibility an extraordinary reliance can be made on input from the vestibular system
which is itself exposed to many causes of dysfunction in the underwater environment.
These include barotraumas to the external, middle and inner ears, alternobaric vertigo,
caloric vertigo and decompression illness.
0820. Disinfection of Diving Equipment in Contact with Saliva
a. Introduction. When diving breathing apparatus is used by successive divers, there

is a risk that disease may be transferred from diver to diver via any saliva that remains in
or on the apparatus. A wide variety of pathogenic agents (viruses, bacteria, fungi and
protozoa) can be found in saliva. These include:
8-39 ORIGINAL
(1) Viruses: Hepatitis (A, B and C), Cytomegalovirus, Epstein-Bar virus, Herpes,
HIV, Haemorrhagic fever viruses.
(2) Bacteria: Styphylococci, Streptococci, Meningococcal, Mycobacteriae.
(3) Fungi: Candida.
(4) Parasites: Protozoa.
The risk of cross infection between divers is increased because of mictotrauma of the
gums caused by the divers mouthpiece which permits the possibility for saliva and blood
to mix.
b. Prevention. Prevention of cross infection involves a variety of measures which

include vaccination (eg. Hepatitis A & B), identification and exclusion from diving of
individuals with certain infectious diseases (eg, tuberculosis) and restricting shared use
of breathing apparatus. However, the most effective and commonly used method of
preventing cross-infection remains disinfection.
c. Disinfectants. Disinfection of open circuit regulators and mouthpieces can be

achieved by dipping in a suitable disinfectant solution for an appropriate period of time
prior to each use. The disinfection of closed and semi-closed circuit apparatus is
complicated as saliva can be found in all parts of the breathing loop (mouthpiece, hoses.
valves, counterlung and rubber assembly). To ensure that semi-closed and closed circuit
apparatus is effectively disinfected it is essential that the breathing loop is disassembled
and all parts cleaned with an appropriate disinfectant. During operational use disinfection
of the mouthpiece, hoses and valves alone is sufficient to minimise, but not completely
eliminate the possibility of cross infection. Disinfection of Built in Breathing Systems
(BIBS) masks within a hyperbaric chamber can be achieved by dipping in an appropriate
disinfectant or, as the BIBS mask has no direct contact with the mouth, by wiping or
spraying with an appropriate disinfectant spray or wipe. To be effective a disinfectant
needs to have the following qualities:
(1) To be active against all pathogens likely to be encountered.
(2) To be safe to use with diving apparatus.
(3) To have no toxic or irritant effect on the diver or maintainer.
Disinfectant agents used by NATO nations with a brief description of the cleaning
process used are listed at Table 8-2.
8-40 ORIGINAL
Table 8-2. Disinfection of Diving Equipment
NATION DISINFECTANT COMPOSITION CLEANING PROCESS

PRODUCT CONTACT TIME AND
RINSE
BE DETTOL Chloroxylenol 4.9% 10 min/rinse in fresh
water.
CA SAVLON 1% Chlorexidine 0.3% Used for disinfection of
Centrimide 3% diving equipment and
chamber BIBS
DA TEGO 103 Halogenated tertiary Used for disinfection of
amine diving equipment and
(amphotenisides) chamber BIBS
FR ENDOSPORINE Gluteraldehyde 2% 10 mins/rinse
STERANIOS SEKUCID meticulously in fresh
water
GE TEGO PUR 2% Halogenated tertiary No standard procedure.
amine (Project investigating 15
(amphotenisides) min. soak)
IT TEGO 103 Halogenated tertiary Used for disinfection of
NL DETTOL Chloroxylenol 4.9% 5 min/rinse in fresh water
NO TEGO 103 Halogenated tertiary Used for disinfection of
PO GLUTERALDEHYDE+ Solution of 60 min/rinse with fresh
ACETALES Glutaraldeido 5.5% water
+ Acetales 8.6%
SP Alcohol No standard procedure
for diving equipment.
Alcohol used for diving
equipment and chamber
BIBS
UK TRIGENE Halogenated tertiary Minimum 2 mins
amine (preferably 5 mins).
(amphotenisides) Shake to remove excess
fluid and then allow to
dry naturally
US TRIGENE 2% Halogenated tertiary Used for recompression
TEGO 2000 amine chambers. 10 mins/rinse
(amphotenisides) in fresh water
Poloxamer-iodine
0.5%
8-41 ORIGINAL
Bibliography:
NEAL. J.M. (1985). Near Drowning.Journal of Emergency Medicine 3, 41-52.
HULLER, T and BANZINI, Y. (1970). Blast Injuries of the Chest and Abdomen. Archives
of Surgery 100, 24-30.
WOLF, N. M. (1970). Underwater Blast Injury :A Review of the Literature. US Navy

Submarine Research Laboratory Report Number 646.
8-42 ORIGINAL
ANNEXES
A TO X
ORIGINAL
ANNEX A
NATIONAL AUTHORITIES RESPONSIBLE FOR INITIATING TREATMENT

OF DIVING CASUALTIES AND EMERGENCY CONTACT NUMBERS
BE: COMOPSNAV
Graaf Jansdijk 1
B 8380 Zeebrugge
Belgium
Tel: 050/55.87.13
+32/50.55.87.13
Signal Message Address: COMOPSNAV
CA : Director Diving Safety

National Defence Headquarters
MGEN George R Pearkes Bldg.
101 Colonel By Drive
Ottawa,
Canada KIA 0K2
Tel: Working Hours (613) 995 6193

Emergencies (613) 996 7811
Signal Message Address: NDHQ OTTAWA// DDIVES//
Emergencies 24 Hrs NDOC OTTAWA// DUTY DDIVES STAFF//
Other CA Emergency Signal Addressees:
East: FDU SHEARWATER

West: FDU ESQUIMALT
Central: DCIEM TORONTO//OC EDU//
Medical: DCIEM TORONTO//CDM
Emergency Medical Contact: DCIEM Consultant in Diving Medicine

Tel: (416) 635-2079
24 Hour Pager (416) 246-3155
DA: Admiral Danish Fleet

PO Box 483
DK 8100 Aarhus C
Tel: (+45) 89 43 30 99 (The Duty Officer)
Signal Message Address: ADMIRALDANFLEET
e-mail: sok@sok.dk
A-1 ORIGINAL
FR: COMISMER
B.P. 84
83800 Toulon-Naval
Tel: Code + 33 - 494020622 or 494020341
Fax: 33-494021795
Signal Message Address: COMISMER
GE: SAR - Leitstelle

24960 Gluecksburg
Uferstrasse
Germany
Tel: + 49 - 04631, Ext 6013
Fax: + 49 - 04631 666 554
Telex No: 022560
Callsign for wireless communications: Morse - DHM 42
Voice callsign: Glueckburg Rescue
Callsign for wireless communication: Morse - DHM 42
Voice - Gluecksburg Rescue
GR: Hellenic Navy General Staff

Medical Directorate (DYG)
Section I
Stratopedon Papagou - Holargos
Athens, Greece
Tel: 6520468
Signal Message Address: COMMEDEAST
IT: MOD ITALY - Navy General Staff

00100 - ROMA
Attn: Chief of Staff/COMSUBIN
Tel: (06) 3601600
Signal Message Address: MARISTAT - ROMA
NL: Commandant Mijnendienst

Diving Medical Centre
Postbus 10.000
1700 CA Den Helder
The Netherlands
Tel: (0) 223-653076 or + 31-223-653076/658220
E-Mail: dmc.post@dpkm.navy.disp.mindef.nl
Signal Message Address: DNLDMC
A-2 ORIGINAL
NO: Norwegian Naval Diving School

PO Box 26 Haakonsvern
N-5886 Bergen, Norway
Message Address: COMTRAINSUB
Tel: +47-55 50 33 42 / Fax: +47-55 50 22 22.
Civilian emergency communication centre: +47-55 32 30 03
Diving Medical Office

P.O. Box 26 Haakonsvern
5886 Bergen, Norway
Message Address: NAVDISVEST
Tel: +47-55 50 21 60. Fax: +47 55 50 37 92
Out of working hours: 47 55 50 22 22
Civilian emergency communication centre +47 55 32 30 03
PO: POL - Estado-Maior da Armada

1188 Lisboa Codex
Portugal
Signal Message Address: MOD PORTUGAL NAVY
Servico De Medicina
Hyperbarica DO
Campo De Santa Clara
1200 Lisboa
PORTUGAL
Tel: Hospital Da Marinha

In working hours: 01-8863141, 01-8879971
Out of working hours: 01-8863145
Telex: 01-12587
Fax: 01-8881531
Signal MessageAddress: To: HOSPITALMAR

Info: ESQLAMERGMAR
Esqla De Mergulhadores
Base Naval De Lisboa
Alfeite
2800 Almada
PORTUGAL
Tel: Esqla De Mergulhadores 01-27682(33)/28
Fax: 01-2766822
Signal Message Address: To: ESQLAMERGMAR
Info: HOSPITALMAR
A-3 ORIGINAL
SP: AJEMA
Seccion de Operaciones
Calle MONTALBAN numero 2
Madrid 28014
Espana
Tel: 91/379 5960/5118/5120/5367 +34-91-3795960
E-Mail: opemon@teleline.es
Signal Address: AJEMA// SIC: LAA
SW: Naval Centre

Naval Medicine
S-130 61 Harsfjarden
Sweden
Tele: 08-502 630 00 +46-8-502 630 00
Fax: +46-8-502 638 40. Naval Medicine 46-8-502 636 87
Emergency non working hours:

Armed Forces HQ
S-107 85 Stockholm, Sweden
Tele: 08-788 81 14. +46-8-788 81 14
Fax: +48-8-664 28 17
E-Mail: vbhkv@hkv.mil.se
TU: Deniz Kuvvetleri Komutanligi

Harekat Baskanligi
Bakanliklar - Ankara
Turkey
Signal Message Address: CINCTURNAV/ANKARA
Tele: ++90-(312)-417-3065
Fax: ++90-(312)-417-6250
UK: RN Superintendent of Diving

Reclaim Building
Horsea Island
Cosham
Hampshire
PO6 4TT
Tel: +44 2392 224143 or 224145
Fax: +44 2392 224150
Signal Message Address: RNSUPDIV PORTSMOUTH
A-4 ORIGINAL
Emergency Numbers for Diving Accidents or Incidents:

Offfice hours: +44 2392 768026
Fax: + 44 2392 504823
24hrs:+ 44 07831 151 523
Signal Message Address: INM ALVERSTOKE
US: US Navy Supervisor of Diving (Administrative Only)

COMNAVSEASYSCOM (NAVSEA OOC-3)
Navy Department
Washington DC 20362
Tel: +01-703-607-2766
Signal Message Address: COMNAVSEASYSCOM, Washington DC
Other US Emergency Signal Addressees:
NORTH EAST : SUBASE, NEW LONDON, CT

MID ATLANTIC : COMNAVBASE, NORFOLK, VA
SOUTH : COMNAVBASE, CHARLESTON, SC
GULF COAST : NAVXIDIVINGU, PANAMA CITY, FL
CARRIBEAN : COMNAVACTSCARIB, ROOSEVELT ROADS, PR
EUROPE : CINCUS NAVEUR, LONDON, UK
SOUTH WEST : COMNAVBASE, SAN DIEGO, CA
NORTH WEST : COMNAVBASE, SEATTLE, WA
HAWAII : COMNAVBASE, PEARL HARBOR, HI
A-5 ORIGINAL
INTENTIONALLY BLANK
A-6 ORIGINAL
ANNEX B
DIVING CASUALTY SIGNAL STATUS REPORT CODE
1. The following codes should be used to present casualty information on signals requesting
immediate medical assistance and /or evacuation of a casualty in accordance with Chapter 5
Section 4, Paragraph 0510.
a. Details of Dive Leading to Accident:
A0 Time of Descent
A1 Maximum depth of diving
A2 Total diving time
A3 Stops done
A4 Which stops done
A5 Type of breathing gas (compressed air/mixed gas; state proportions)
A6 Diving equipment
A7 Kind of effort (heavy, medium, light)
A8 Condition of diver on arrival at surface
A9 Time of first symptoms after dive
A10 Has the diver used any medication
A11 Enough oxygen available for treatment
A12 Kind of treatment started (tables + numbers)
A13 Time treatment started (local time)
A14 Short description of accident
b. Previous Dives:
B1 Date
B2 Time of Descent (hours)
B3 Maximum depth of diving (metres)
B4 Total diving time (min)
B5 Any stops done Yes/No
B6 Which stops done
c. Items to be Checked:
C1 Regular pulseYes/No
C2 Breathing rate /min
C3 Pulse rate / min
C4 Orientation OK? (in time and person)Yes/No
C5 Amnesia (for recent or previous happening)Yes/No
C6 Muscle strength (normal)Yes/No
C7 Normal speech Yes/No
B-1 ORIGINAL
d. Symptoms:
D1 Joint Pains Yes/No

D2 Headache Yes/No
D3 Nose Bleeding Yes/No
D4 Chest pain Yes/No
D5 Tightness of the chest Yes/No
D6 Muscle spasm Yes/No
D7 Weakness of muscles Yes/No
D8 Paralysis Yes/No
D9 Problems with breathing Yes/No
D10 Skin problems (change of colour) Yes/No
D11 Numbness Yes/No
D12 Itching Yes/No
D13 Hearing problems Yes/No
D14 Dizziness Yes/No
D15 Equilibrium Problems Yes/No
D16 Impression of falling Yes/No
D17 If falling, which direction
D18 Problems of vision Yes/No
D19 Anxiety Yes/No
D20 Nausea vomiting Yes/No
D21 Convulsions (if unconscious) Yes/No
D22 Unconscious Yes/No
If any answer in Section D is ‘Yes’ give specific localisation
e. Other Specific Symptoms:
E1 Short description as required
B-2 ORIGINAL
ANNEX C
NATO DIVING INCIDENT MEDICAL RECORD FORM
1. The NATO Diving Incident Medical Record Form presented at this annex should be
reproduced and then completed when a diver is referred for illness following a dive since it R
provides a template for a thorough evaluation by medical personnel. Dates should be recorded:
day- month - year. Times should be written in the 24-hour clock, in local time. Names should be
recorded in full, first names first, then the family name which should be underlined. This form
is designed to serve both as a means of gathering information and as a medicolegal record for the
evaluation. Therefore, it is important that the form is completed as thoroughly as possible.
2. Page 1 - Personal Details of Diver and Recent Dives
a. Diver’s Personal Details. Record the diver’s nationality, unit, name, rank, service
number date of birth, diving qualification and the date it was awarded.
b. Details of Dives in the Last 72 hours. All dives undertaken in the previous 72
hours should be recorded using one line for each dive. Note the maximum depth reached
even if the time at that depth was brief. The duration of the dive is from surface to
surface and should be given in minutes as shown. The dive profile describes the depth
and the time spent at each depth. The icons are a graphical representation of possible
dive profiles. The first box represents a standard square profile dive where a decent is
made to a certain depth, the diver stays at that depth for a period of time and then
ascends to the surface in a controlled manner making decompression stops as necessary.
The second box from the left represents a dive where the ascent is slow. The third box
represents a multilevel dive. The fourth is a dive with an emergency or precipitate
ascent. The question mark should be used to represent a dive where the profile is
unknown. A check should be placed in the box which best represents the dive profile
undertaken. This section also provides space to record any decompression stops made
and the surface interval between one dive and the next. This interval should be recorded
in hours and minutes as shown.
c. Brief Summary of the Incident. The date, time and location of the incident
should be recorded. Extra space is provided to record any other relevant information
about the incident. Any unusual features not recorded in the details of last dive section
should be included.
3. Page 2 - History of the Principal Manifestations
a. This page has a number of boxes one for each type of manifestation. The most
important piece of information about each manifestations is the date and time that is
started. The patient should be specifically questioned about each of the manifestations
and negative responses recorded by circling ‘NONE’ in the appropriate box.
b. Manifestations. These are separated into groups: pain; skin; lymphatic;

neurological etc. Each symptom should be recorded in the most appropriate box with the
date and time of onset. Any additional symptoms, which do not fit in the first five
categories, should be recorded in the constitutional section.
C-1 ORIGINAL
4. Page 3 - History and Past Medical History
a. Narrative. This large space is for the medical attendant to make notes on the
history of the presenting complaint as in any other medical history. The symptoms
should be described and other diagnostic information recorded. Non-diving illnesses
may present during or following diving and such a diagnosis should not be overlooked.
Date and time of the most recent alcohol consumption should be recorded if within the
last 24 hours.
b. Evolution. This box provides a summary of the main symptoms, the time after the
dive that they started and shows whether the symptom is: spontaneously improving (SI);
staying the same, static (ST); getting worse, progressive (PR); getting worse again after
a period of substantial improvement, relapsing (RE); or if it has disappeared completely,
resolved (RS). On the left under manifestation you should write a description of the
symptom, SKIN is the example printed on the form. Then the time and date during
which the symptomatology is described should be written in and finally the evolution of
the symptom during that time. Thus from the example on the form: we know that from
20:00 on 19 Aug the patient had skin symptoms which were getting worse but by 22:00
the symptoms had peaked and remained the same until midnight, when they began to
improve. The symptoms continued to improve until 02:00 when we assume the
symptoms are better. If more boxes are needed, for instance if there was a relapse of
symptoms, then write ‘CONTINUED’ under ‘MANIFESTATION’ and use the boxes
on the new line in the same way as before. This section should be filled in for each
manifestation.
c. Past Medical History. Any medical problems, diving related or otherwise, should
be recorded in this space. Previous decompression illness, lung disease, cardiovascular
disease, neuro-logical disorders, ear nose and throat problems, metabolic disease such
as diabetes mellitus and any other medical or surgical conditions should be noted, even
if they do not seem relevant. Any drugs taken by the diver should be recorded, with
doses. The date of the last diving medical should be recorded as should details of the
diver’s social habits such as smoking and alcohol intake.
5. Pages 4 and 5 - Clinical Examination

It will be assumed that the examination is conducted on the surface, prior to
recompression unless otherwise stated. Any examination findings at depth should be recorded
in the ‘Additional Examination Notes’ section.
a. Examining Doctor. The name of the doctor conduction the clinical examination
should be recorded along with his position for example general medical officer,
Emergency room attending, Diving Medical Officer, etc.
b. General Examination. In this box the results of a general examination should be

recorded next to the appropriate system headings on the left. Abnormalities present
should be recorded in detail next to the appropriate heading. If a field is left blank this
will be taken to mean that the test was not done, if the test was done and was normal this
should be recorded by writing ‘NORMAL’ or ‘N’. Of particular importance is
examination of tympanic membranes, the neck for subcutaneous emphysema, skin for
rash or swelling (lymphoedema) and lymph nodes for tenderness and swelling.
C-2 ORIGINAL
c. Neurological Examination. Annex D details a method of performing a

neurological examination for non medical personnel.
(1) Higher Function. The assessment of higher cerebral function should be

recorded here. Next to ‘Mental status’ there are some examples of information
required, but any abnormality of higher function must be recorded. The patient’s
personality can be affected by decompression illness and asking a friend of the
patient whether the patient's behaviour is normal is desirable. The level of
consciousness should be recorded using the Glasgow Coma Scale.
(2) Coordination. In this, section abnormalities of coordination should be

recorded. The tests indicated should be carried out and the results recorded in the
space provided. If normal, record this and if not, the abnormality should be
described avoiding ambiguous terms.
(3) Reflexes. The reflexes should be tested and the results recorded here in the
following way: if normal write ‘N’, if brisk write ‘B’, if sluggish write ‘S’ and if
absent despite reinforcement, write ‘A.’ The status of the reflex should be written
in this way in the space provided to the right of the ‘R’ or ‘L’ in the box. For the
plantar reflex write ‘up’ or ‘own’ or as an alternative draw an arrow pointing to the
top of the page for upgoing plantar reflex or at the bottom of the page for
downgoing reflex.
(4) Cranial Nerves. This box shows the cranial nerves, which may be examined.
If normal this should be recorded next to the nerve number which is written in
Roman numerals. If normal is written it will be taken to mean normal both sides.
Any abnormality should be described taking care to record which side it is on.
(5) Power. On the right side of this box is a key which shows first how to record
movements for example flexion is written ‘FL’. Below is a power scale where the
muscle power is described by a number between 0 and 5. Each muscle group should
be tested and its movement recorded. If movement at a joint is normal write
‘NORMAL’ under movement and if the power of all muscle groups around the joint
is normal writing ‘5’. If there are abnormalities they must be individually recorded.
(6) Sensation. The location of any abnormality of sensation should be indicated

by shading areas on the diagram. If different modalities of sensation are affected in
different distributions a variety of shading styles may be used to represent different
modalities.
d. Additional Examination Notes. Any information gathered during the examination

which has not been recorded elsewhere or the results of examination at depth should be
recorded in this section.
e. Diagnosis. The diagnosis reached, based on history and examination should be

recorded in this box. If a decompression illness is diagnosed, it should be written down
using the classification with which the doctor is familiar.
C-3 ORIGINAL
6. Pages 6 and 7 - Treatment
a. Treatment Prior to Recompression. Fluid therapy is important in any diving

illness. It should be recorded by circling the route of administration, writing in the
volume given and indicating the type of fluid given. Breathing high concentrations of
oxygen (ideally 100%) is important first aid. The duration, concentration, flow rate and
mode of delivery should be recorded. Concentrations of oxygen approaching 100% will
only be achieved by a reservoir system or by demand valve attached to a supply of pure
oxygen. Any drugs administered, dose and route of administration should be recorded.
If the diver is recompressed the mode of transport, date and time of arrival and the name
and location of the chamber should be recorded.
b. Recompression. The date and time the treatment table commenced should be
recorded in the appropriate column on the left. Each line represents one treatment table,
as some patients require more than one treatment extra lines are available. The table
number should be circled if a NATO table V or VI, or the name or number written in if
it is not. Table VI may be extended at either 18 or 9 meters and if this is necessary it
should be recorded by circling ‘x1’ or ‘x2’ as shown next to the relevant depth for one
or two extensions respectively. If the table is not extended ‘x0’ should be circled for both
depths. In the column on the right are options to describe the state of the patient at the
end of the treatment. The most appropriate should be circled. Other information about
the treatment can be recorded in the large space for ‘treatment narrative’.
c. Fluid Balance Chart. This should be completed in the conventional way for fluid
balance during recompression treatment. Urinary catheterization may be necessary,
particularly in cases of spinal cord decompression illness where bladder problems may
occur. Most injured divers will be dehydrated and should be given appropriate fluids
either orally or intravenously depending on the clinical condition.
d. Medication. All drugs given during treatment at the chamber should be recorded
in this section, using generic names.
e. Treatment Narrative. This large space is for the doctor to record important
clinical information not recorded elsewhere. The point at which the diver gets relief of
symptoms and signs, problems during treatment and any other information of relevance
may be recorded.
f. Disposition. The outcome of treatment should be recorded.
g. Final Diagnosis. The full clinical diagnosis reached by the attending doctor should
be written. The attending doctor should sign and date the form.
8. Page 8
a. Continuation Notes. This page and extra copies of it can be used to record
additional notes or expand on areas where there has insufficient space elsewhere on the
form. It is desirable to review patients about a month after the incident. At this
consultation the date and any residual symptoms or signs should be recorded. Any
further treatment or specialist referral should then be noted.
C-4 ORIGINAL
NATO DIVING INCIDENT MEDICAL RECORD
RESTRICTED - MEDICAL (When Completed)
NATIONALITY UNIT
Name of person involved
Rank Service No Date of Birth
Diving Qualification Date of Qualification
Details of Last Dive
Dive Dress MEMBRANE DRY SUIT/NEOPRENE DRY SUIT/WET SUIT/HOT WATER SUIT/OVERALLS/NONE/FINS/BOOTS/OTHER
(Circle) Details:
Diving Set SCUBA AIR, SURFACE SUPPLIED AIR, SURFACE SUPPLIED MIXED GAS, O2 CC, MIXED GAS CC, OTHER (Specify)
(Circle) Details: CC = CLOSED CIRCUIT
Breathing AIR / NITROX / HELIOX / OTHER %O2 Entry into Water SMALL CRAFT / SHIP / JETTY /
Gas (Circle) (Specify) From: (Circle) OTHER
Details: Details:
Type of Dive ATTENDED / MARKED /FREE SWIM / SEARCH GROUP / SURFACE SWIMMER / SOLO / PAIRS / OTHER
Details:
Task SEABED SEARCH / SHIP’S BOTTOM SEARCH - SHIP’S HUSBANDRY / U/W ENGINEERING /OTHER/ (Specify)
(Circle)
Estimated LIGHT / MEDIUM / Current Water Wind Air Temp

Work Rate HEAVY Temp 0
Force (Dry Bulb) 0
Knots C C
Details of Dives Within Last 72 hours
Start Max. Bottom Dive Profile Decompression Stops Table
Date Dive Depth Time (Tick) Depth (m), Time (min) Used
(D/M/Y) (Time) (m) (min) ? D T D T D T D T D T
Incident date: Time: Location:

Brief summary of the incident:
C-5 ORIGINAL
HISTORY - PRINCIPAL MANIFESTATIONS

Circle the appropriate manifestations and note the time (24hr clock) and where necessary, the DATE of ONSET
Where there is no evidence of a manifestation circle NONE.
PAIN NONE Date and Time of ONSET SKIN NONE Date and Time of ONSET
Girdle
Elbow R L Itching
Wrist R L
Hip R L Redness
Knee R L
Ankle R L Marbling
Other
(specify) Other
(specify)
LYMPHATIC NONE Date and Time of ONSET
Lymph node enlarged/painful
NEUROLOGICAL NONE Date and Time of ONSET
Level of
Consciousness
Higher Function Abberation of thought / Loss of Memory / Personality change / Dysphasia / Seizure
Special Hearing loss / Vertigo / Tinnitus / Nystagmus / Visual impairment

Senses
Strength
Sensation Numbness / Paraesthesiae
Sphincter Bladder / Bowel

Function
PULMONARY NONE Date and Time of ONSET
Cough/ SOB / Chest Pain / Haemoptysis / Subcutaneous Emphysema / Voice Change / Pneumothorax
CONSTITUTIONAL NONE Date and Time of ONSET
Anorexia / Excessive Fatigue / Malaise / Headache / Vomiting
C-6 ORIGINAL
NARRATIVE
EVOLUTION: From the history above, summarise the significant changes in each principal manifestation PRIOR TO
RECOMPRESSION. These changes may be expressed as : unchanged in intensity (STATIC); getting worse
(PROGRESSIVE); SPONTANEOUSLY IMPROVING, getting worse again after a period of substantial improvement
(RELAPSING); or it may have disappeared completely (RESOLVED); If no time interval is specified, it will be assumed that
the evolution term used applies to the entire period prior to recompression.
Note the TIME INTERVAL (including dates where necessary) of any change.
MANIFESTATION Time Interval Evolution Time Interval Evolution Time Interval Evolution
Example: SKIN 19 Aug 2000-2200 PR 19 Aug 2200-2359 ST 20 Aug 0001-0200 SI
RELEVANT PAST MEDICAL HISTORY

State details of any recent medical condition
Medication:
Date of last Diving Medical Examination
oz/gm
Smoker YES/NO Average Smoked Cigarettes/Day Cigars/Day Tobacco/Week
Date and Time of Average weekly 1 unit = ½ pint of beer

Last Alcohol Alcohol consumption Units/week 1 glass of wine
1 tot of spirits
C-7 ORIGINAL
Patient Examined By
GENERAL SYSTEMS EXAMINATION
ENT
Cardiovascular System
Pulmonary System
Skin
Lymphatic System
GI System
NEUROLOGICAL ASSESSMENT
Orientation in time / space / memory / mood / cognitive function
Mental Status
COORDINATION REFLEXES (Normal, Brisk, Sluggish, Absent)

Biceps R L Knee R L
Gait Finger/nose
Triceps R L Ankle R L
Heel-to-toe Walk Rapid movement
Supinator R L Plantar R L
Heel shin slide Romberg
Abdominal R L Cremaster R L
CRANIAL NERVES
Vision Mouth/Throat
II IX
Visual Fields Sensation
Pupils/Eye Gag, Palate

X
Movements III, IV, VI Movement
Nystagmus
Shoulder/Neck XI
Facial Sensation
V Tongue XII
Corneal Reflex
Facial
VII
Expression
Hearing VIII
POWER
JOINT R/L MOVEMENTS (see key) POWER (see scale) MOVEMENT KEY
Record Tone as appropriate FLEXION
Shoulder EXTENSION
Elbow ABDUCTION
Wrist ROTATION
Fingers POWER SCALE

Hip 0 No movement possible
Knee 1 A flicker of movement
Ankle 2 Muscle contracts but can’t overcome
Toes gravity
3. Can overcome gravity but not the
examiner
4. Slight weakness
5. Normal
C-8 ORIGINAL
Use the diagram to report locations of sensory abnormalities - light touch, pin prick, temperature sensation, vibration, proprioception,
joint position sense, etc
ADDITIONAL EXAMINATION NOTES
DIAGNOSIS
C-9 ORIGINAL
TREATMENT PRIOR TO RECOMPRESSION

Fluids None IV Oral Volume ml Type
Oxygen None Duration Min Inspired PO2 % Flow l/min
Means of Delivery Oronasal mask / Nasal cannulae / Demand system / ET tube / Other
Drugs: Name, Dose, Route

Transport to Chamber Air Road Sea Date/Time of arrival at Chamber
Name of Chamber
RECOMPRESSION (Record ALL Recompression Treatments for this incident)
Date Start Table Description / Profile Max Depth Duration
NATO Table V / Table VI / Other (specify) Extensions: 18m x0 x1 x2 9m x0 x1 x2
NATO Table V / Table VI / Other (specify) Extensions: 18m x0 x1 x2 9m x0 x1 x2
FLUID BALANCE
Fluid Given Route Date/ Volume Running Fluid Out Date/Time Volume Running
Time (ml) Total (ml) Total
TOTAL IN TOTAL OUT

MEDICATION
Drug Name Dose Route Date / Time Signed
C-10 ORIGINAL
TREATMENT NARRATIVE
Include time to relief of symptoms/signs and whether complete or partial; any problems during treatment, including details of any transfer to
alternative tables; the patient’s condition at the end of initial treatment and progress during any re-treatment.
Fit to dive / Temporarily unfit to dive (number of weeks) Permanently unfit / Hospital / Duty / Deceased
Disposition
Final Diagnosis
Name of Doctor Rank Signature Date
C-11 ORIGINAL
CONTINUATION SHEET Page No

Use this page for additional notes for History, Narrative, Additional Examination Notes, Treatment Narrative, or
any other areas where insufficient space is available to record all necessary details.
Rank Service No Date of birth Age
Name of Doctor Rank Signature Date
C-12 ORIGINAL
ANNEX D
NEUROLOGICAL EXAMINATION
1. This Annex provides a systematic approach to the neurological examination of divers.

It is not as thorough as the examination carried out by a Diving Medical Officer or other Medical
Officer in cases of decompression illness but provides a basic guide for the assessment of diving
casualties for non-medical personnel. The examination is detailed using the headings presented
in the NATO Diving Incident Medical Record Form.
2. Mental Status. This is characterised by their alertness, orientation and thought

processes. Obtain a good history, including the dive profile, present symptoms and how these
symptoms have changed since onset. The patient’s response to this questioning and that during
the neurological examination will give you a great deal of information about his mental status.
a. Orientation in time place and person: Does the patient know who and where he is
and the current date and time?
b. Memory:
(1) Short Term: The patient should be asked to repeat back the names of three
simple objects which he is asked to remember. Five minutes later his short term
memory score is recorded as the number of correctly recalled objects out of three.
(2) Long Term: The questions asked should be reasonable and you must know the
answer to the questions you ask. Examples could include asking the name of the
National Leader or recent events.
c. Mood: It must be recorded whether the patient’s mood is appropriate to the

circumstances or whether his mood is flat or excited.
d. Cognitive Function: This is the intellectual process by which one becomes aware
of, perceives or comprehends ideas and involves all aspects of perception, thinking,
reasoning and remembering. Some suggested methods of assessing this function are:
(1) The patient should be asked to spell a word, such as ‘world’, backwards. The
patient should be asked to count backwards from 100 by sevens. The number of
incorrect responses are recorded.
3. Level of Consciousness
This is recorded using the Glasgow Coma Scale. The following scores are added together
to give the Glasgow Coma score in the range 3 to 15.
D-1 ORIGINAL
a. Eyes Open: Spontaneously-4

to verbal command-3
to pain-2
remain closed despite these stimuli-1.
b. Best Motor Response:
Obeys verbal commands-6

On giving a painful stimulus:
localises pain-5,
flexion withdrawal-4,
abnormal flexion (like decorticate rigidity)-3
extension response-2
no response at all-1.
c. Best Verbal Response:
Orientated and converses-5

disorientated but converses-4
inappropriate words-3
incomprehensible sounds-2
no verbal response at all-1.
4. Coordination. (Cerebellar/Inner Ear Function).
a. Gait. A good indicator of muscle strength and general coordination is to observe

how the patient walks. A normal gait indicates that many muscle groups and general
brain functions are normal. More thorough examination involves testing that
concentrates on the brain and inner ear. In conducting these tests, both sides of the body
must be tested and the results must be compared. These tests include the following
b. Heel-to-Toe Walk. The tandem walk is the standard ‘drunk driver’ test. While
looking straight ahead, the patient must walk a straight line, placing the heel of one foot
directly in front of the toes of the opposite foot. Signs to look for and consider deficits
include:
(1) Does the patient limp?
(2) Does the patient stagger or fall to one side?
c. Heel/Shin Slide. While standing, the patient touches the heel of one foot to the
knee of the opposite leg, foot pointing forward. While maintaining this contact, he runs
his heel down the shin to the ankle. Each leg should be tested.
D-2 ORIGINAL
d. Finger/Nose. The patient stands with eyes closed and head back, arms extended to
the side. Bending the arm at the elbow, the patient touches his nose with an extended
forefinger, alternating arms. An extension of this test is to have the patient, with eyes
open, alternately touch his nose with his fingertip and then touch the fingertip of the
examiner. The examiner will change the position of his fingertip each time the patient
touches his nose. In this version, speed is not important, but accuracy is.
e. Rapid Movement. The patient slaps one hand on the palm of the other, alternating
palm up and then palm down. Any exercise requiring rapidly changing movement,
however, will suffice. Again, both sides should be tested.
f. Romberg. With eyes closed, the patient stands with feet together and arms
extended to the front, palms up. Note whether the patient can maintain his balance or if
he immediately falls to one side. Some examiners recommend giving the patient a small
shove from either side with the fingertips.
5. Reflexes
The biceps, triceps, knee and ankle tendon jerk reflexes should be tested. An adequate
examination requires relaxation on the part of the patient. Grade as normal, no response,
hypoactive or hyperactive (compared to normals that you have tested). Note especially if the
upper and lower reflexes are similar. Be sure to strike with an equal, light force and use sharp,
quick taps in order to get the best response. Generally, if a deep tendon reflex is abnormal due
to dysbaric disease, other abnormal signs will also be found.
a. Biceps. Hold the elbow with your thumb on the biceps tendon - elbow should be
slightly bent and the arm relaxed. Tap your thumb and feel the biceps contract.
b. Triceps. Tap just above the elbow with the elbow bent. Note contraction of the
muscle.
c. Knee. Tap below the knee cap on the tendon and note the contraction of the
quadriceps and movement of the lower leg.
d. Ankle. Place slight pressure on the toes to stretch the achilles tendon and tap this
tendon. Feel the toes contract as the achilles tendon shortens.
e. Babinski Reflex. Firmly stroke a thumb up the inside of the sole of the foot and
note whether the big toe moves up or down. Most normal subjects move their toes
down. If there is no reaction use something like a car key to apply the pressure - it might
tickle but it should not hurt.
6. Cranial Nerves
The cranial nerves are the 12 pairs of nerves emerging from the cranial cavity through
various openings in the skull. Beginning with the most anterior (front) on the brainstem, they are
appointed Roman numerals. An isolated cranial nerve lesion is an unusual finding in
decompression sickness or gas embolism, but deficits occasionally occur and you should test for
abnormalities. The cranial nerves must be quickly assessed as follows:
D-3 ORIGINAL
a. (I) Olfactory. The olfactory nerve, which provides our sense of smell, is usually
not tested.
b. (II) Optic. The optic nerve is for vision. It functions in the recognition of light and
shade and in the perception of objects. This test should be completed one eye at a time
to determine whether the patient can read. The patient should be asked if he has any
blurring of vision, loss of vision, spots in the visual field or peripheral vision loss (tunnel
vision). More detailed testing can be done by standing in front of the patient and asking
him to cover one eye and look straight at you. In a plane midway between yourself and
the casualty slowly bring your fingertip in turn from above, below, to the right and then
to the left of the direction of gaze until the patient can see it. Compare this with the
earliest that you can see it with the equivalent eye. If a deficit is present, roughly map
out the positions of the blind spots by passing the finger tip across the visual field.
c. (III) Oculomotor, (IV) Trochlear, (VI) Abducens. These three nerves control eye
movements. All three nerves can be tested by having the patient’s eyes follow the
examiner’s finger in all four directions (quadrants) an then in towards the tip of the nose
(giving a ‘crossed-eyed’ look). Inability to move either eye in a particular direction
indicates a loss of function of the specific cranial nerve responsible for ocular muscle
function. The oculomotor nerve can be further tested by shining a light into one eye at
a time. In a normal response, the pupils of both eyes will constrict.
d. (V) The Trigeminal Nerve governs sensation of the forehead and face and the
clenching of the jaw. It also supplies the muscle of the ear (tensor tympani) necessary
for normal hearing. Sensation is tested by lightly stroking the forehead, face and jaw on
each side with a finger or wisp of cotton wool.
e. (VII) The Facial Nerve controls the face muscles. It stimulates the scalp, forehead,
eyelids, muscles of facial expression, cheeks and jaw. It is tested by having the patient
smile, show his teeth, whistle, wrinkle his forehead and close his eyes tightly. The two
sides should perform symmetrically. Symmetry of the nasolabial folds (lines from nose
to outside corners of the mouth) should be observed.
f. (VIII) The Acoustic Nerve controls hearing and balance. Test this nerve by
whispering to the patient, rubbing your fingers together next to the patient’s ears or
putting a tuning fork near the patient’s ears.
g. (IX) The Glossopharyngeal Nerves transmit sensation from the upper mouth and
throat area. It supplies the sensory component of the gag reflex and constriction of the
pharyngeal wall when saying ‘aah’. This nerve is tested by touching the back of the
patient’s throat with a tongue depressor. This should cause a gagging response. This
nerve is normally not tested.
D-4 ORIGINAL
NATO UNCLASSIFIED ADivP-2(A)/MDivP-2(A)
h. (X) The Vagus Nerve has many functions, including control of the roof of the
mouth and vocal cords. The examiner can test this nerve by having the patient say ‘aah’
while watching for the palate to rise. Note the tone of the voice, hoarseness may also
indicate vagus nerve involvement.
i (XI) The Spinal Accessory Nerve controls the turning of the head from side to side
and shoulder shrug against resistance. This nerve is tested by having the patient turn his
head from side to side. Resistance is provided by placing one hand against the side of
the patient’s head. The examiner should note that an injury to the nerve on one side will
cause an inability to turn the head to the opposite side or weakness/absence of the
shoulder shrug on the affected side.
j. (XII) The Hypoglossal Nerve governs the muscle activity of the tongue. An injury
to one of the hypoglossal nerves causes the tongue to twist to that side when stuck out
of the mouth.
7. Power
It is common for a diver with decompression illness to experience muscle weakness. All
muscle groups should be tested and compared with the corresponding group on the other side,
as well as with the examiner. The arms and legs are tested separately. Each muscle group should
be compared to the same group in the opposite limb. Muscle strength is graded (0-5) as follows:
a. (0) Paralysis. No motion possible.
b. (1) Profound Weakness. Flicker or trace of muscle contraction.
c. (2) Severe Weakness. Able to contract muscle but cannot move joint against
gravity.
d. (3) Moderate Weakness. Able to overcome the force of gravity but not the
resistance of the examiner.
e. (4) Mild Weakness. Able to resist slight force of examiner.
f. (5) Normal. Equal strength bilaterally (both sides) and able to resist examiner.
g. Upper Limbs. Six muscle groups may be tested in the arm as follows. The
deltoids are tested by having the patient raise his arm sideways against resistance. The
latissimus dorsi are tested by lowering the arm at the shoulder joint. The biceps are
tested by bending the arm at the elbow and the triceps by straightening the arm at the
elbow. The forearm muscles are tested by bending the wrist against resistance, opening
and closing the hand, and by gripping with the hands. Finally the hand muscles are
tested by observing grip strength and spreading the fingers against resistance.
D-5 ORIGINAL
NATO UNCLASSIFIED ADivP-2(A)/MDivP-2(A)
h. Lower Limbs. The strength of the legs can be quickly assessed by having the
patient walk on his toes and on his heels. Following this have the patient squat down
and walk while squatting (duck walk). These tests should adequately assess lower
extremity strength. For a more detailed examination, muscle strength should be tested
at each joint as in the upper limb. Hip strength is tested by raising and lowering the
thigh against resistance and moving the thigh away from and towards the midline against
resistance. Knees can be tested by straightening and bending the knee against resistance.
8. Sensation
The patient may complain of pain, numbness, or tingling in one or more areas. These
are common presentations of decompression illness and the area of abnormal sensation should
be outlined on the skin and a diagram drawn in the medical record. Pin prick, soft touch,
vibration, and proprioception are senses usually tested by a doctor but the tests of sharp/dull
discrimination and light touch normally suffice when a doctor is not present.
a. Sharp/Dull Discrimination. Test whether the patient can discriminate between the
gentle application of a sharp point or the blunt clasp of a safety pin. Complete a test of
the head, trunk, arms and legs. Be sure to check both sides.
b. Light Touch. This can be tested in the same way using a finger or wisp of cotton
wool.
D-6 ORIGINAL
ANNEX E
NATIONAL AUTHORITIES FOR GUIDANCE ON THE HAZARDS OF

POLLUTION
NATION ADDRESS TELEPHONE/FAX

BE AMINAL - KONING ALBERTLAAND 20 BOX Tel: 02/553.80.02
8 1000 BRUSSELS BELGIUM +32/2.553.80.02
CA DIRECTOR OF DIVING SAFETY Tel: (01) 613.995.6193
NATIONAL DEFENCE HEADQUARTERS Fax: (01) 613.996.7807
MGEN GEORGE R. PEARKES BUILDING
101 COLONEL BY DRIVE
OTTAWA
CANADA
K1A OK2
DA 1. AGENCY OF ENVIRONMENTAL
PROTECTION
STANDGADE 29
DK 1401 COPENHAGEN K Tel: 32 66 01 00
2. POISON INFORMATION CENTRE

RIGSHOSPITALET
TAGENSVEJ 18
DK 2200 COPENAGHEN N Tel: 35 35 71 22
E-1 ORIGINAL
FR Military Authorities
1. PREFET MARITIME/COMMANDANT Tel: 494 02 04 43

EN CHEF POUR LA MEDITERRANNEE Fax: 494 02 07 70
ENVIRONMENT OFFICER
2. PREFET MARITIME/COMMANDANT Tel: 298 22 14 62

EN CHEF POUR L’ATLANTIQUE Fax: 298 22 07 32
ENVIRONMENT OFFICER
3. PREFET MARITIME POUR LA Tel: 233 92 65 90

MANCHE ET LA MER DU NORD Fax: 233 94 24 00
ENVIRONMENT OFFICER
Civilian Agencies
Chemical Contaminants
CENTRE ANTI-POISONS Hôpital Fernand Tel: (01) 40 37 04 04
WIDAL 200, Fauborg St Denis 75 010
PARIS
Biological Contaminants
INSTITUTE FRANCAIS DE Tel: (01) 47 23 55 28
RECHERCHE POUR L’EXPLOITATION Fax: (01) 47 23 55 28
DE LA MER (FREMER) Telex: 610775
66 Avenue d’Iéna
75 116 PARIS
Radioactive Contaminants
1. SERVICE CENTRAL DE PROTECTION Tel: (01) 39 76 04 32

CONTRE LES RAYONNEMENTS
IONISANTS (SCPRI)
2. INSTITUTE DE PROTECTION ET DE Tel: (01) 46 54 49 29

SECURITE NUCLEAIRE (IPNS or (01) 46 54 49 30
E-2 ORIGINAL
GE 1. WEHRWISSENSCHAFTLICHES Tel: 08122-57220

INSTITUT FUER Fax: 08122-57312
MATERIALUNTERSUCHUNGEN (WIM)
85435 ERDING,
LANDSHUTER STRASSE 70
2. WEHRWISSENSCHAFTLICHES Tel: 01592-1360

INSTITUT FUER ABC-SCHUTZ Fax: 01592-136355
29633 MUNSTER
HUMBOLDSTRASSE
GR
IT CENTRO ITALIANO ANTIVELENI Tel: (02) 66101029 or
OSPEDALE MAGGIORE (02) 64442523
MILANO
NL RIJKSINSTITUT VOOR VOLLISGEZONDHEID Tel: (0)30-2749111
EN MILIEU-HYGIENE (24 hours emergency
back up only)
Tel: (0)30-2748888
(Doctors only)
NO Military:
NORWEGIAN DEFENCE INSTITUTE

PO BOX 25
N 2007 KLELLER, NORWAY
MESSAGE ADDRESS: NDRE Tel: +47-63 80 78 00
Civilian:
NORWEGIAN POISON CENTRAL REGISTRY

PO BOX 8189
0034 OSLO NORWAY Tel: +47-2260 84 60
NORWEGIAN ENVIRONMENTAL CONTROL

AGENCY,
DEPARTMENT OF OIL SPILLING
MOLOVEIEN 7
N 3191 HORTEN, NORWAY Tel: +47-33 04 41 61
PO
E-3 ORIGINAL

SP Identification and Procedures for Toxic Substances:
DIRECCION GENERAL DE LA MARINA
MERCANTE
Calle RUIZE DE ALARCON NO1
MADRID 28014 Tel: 91/ 5979000
SPAIN +34/ 91/ 5979000
Analysis and Information on specific hazards

associated with toxic substances:
INSTITUTO TOXICOLOGIO NACIONAL
Calle LUIS CABRERA NO9 Tel: 91/ 5620420
MADRID 28002 +34/ 91/ 5620420
ESPANA E-Mail:
sit@mad.inaltox.es
SW ARMED FORCES HQ Tele: 08-788 81 14
S-107 85 +46-8-788 81
STOCKHOLM Fax: +48-8-664 28 17
SWEDEN E-Mail:
vbhkv@hkv.mil.se
TU KURTARMA VE SUALTIE KOMUTANLIGI Tel: 90(216)3222580
CUBUKLU ISTANBUL 90(216)3310090
Fax: 90(216) 3310525
UK 1. MOD NAVY OCCUPATIONAL Tel: +44 2392 768075
HYGIENE SERVICE (Working hours only)
THE INSTITUTE OF NAVAL MEDICINE or +44 2392 768020
ALVERSTOKE (Duty Officer)
GOSPORT Fax: +44 2392 504823
HAMPSHIRE PO12 2DL
2. THE POISONS REFERENCE CENTRE

(FOR ADVICE TO DOCTORS ONLY) +44 1816 359191
NEW CROSS HOSPITAL
AVONLEY ROAD
LONDON SE14 5ER
US 1. HEADQUARTERS: Unites States Coast Tel: (919) 331-6000
Guard Nationa Strike Force Co-ordination - Fax: (919) 331 -6012
ELIZABETH CITY NC
2. Atlantic Area: Strike Force Atlantic FORT Tel: (609) 724-0008

DIX NY Fax: (609) 724-0232
3. Pacific Area: Strike Force Pacific Hamilton Tel: (415) 883-3311

Field - NAVATO CA Fax: (415) 883-7814
4. Gulf of Mexico: Strike Force Gulf of Tel: (205) 639-6601

Mexico MOBILE AL Fax: (205) 639-6610
E-4 ORIGINAL
Notes:
CA: Information on hazardous materials can be found in the ‘Workplace Hazardous Materials
Information System (WHMIS)’ which is available at all major Canadian government and civilian
agencies.
GE: If chemical or bacteriological pollution occurs when diving, hygienist of the area
(Wehrbereich/Territorialkommando) will identify the toxic substances by assistance of special
laboratories in town. If the pollution occurs in Northern Germany along the shoreline of Baltic -
or North Sea (Navy), identification will be carried out by Territorialkommando Kiel and
Wehrbereichsverwaltung I. Abt. II A3/Afnorth Feldstrabe 70.
US: By contacting one of the listed locations and providing basic identification information of
objects suspected of containing toxic substances the Strike Force will access its Marine Safety
Information System (MSIS). The MSIS is a computer based system capable of performing a
database search for toxic substances and providing information on specific hazards associated
with toxic substance and disposal/handling guidance.
UK: The UK has no single authority with responsibility for providing guidance on the
identification of, and protection from, pollutents in water. HM Coastguard, Harbour Masters,
Local Authorities, the National Rivers Authority and the Health and Safety Executive are useful
sources of information in addition to the contacts listed above.
E-5 ORIGINAL
INTENTIONALLY BLANK
E-6 ORIGINAL
ANNEX F
GLOSSARY OF MEDICAL TERMINOLOGY
Adipose tissue: Fatty tissue
Analgesia: Pain relief
Anorexia: Loss of appetite for food
Anoxia: The absence of oxygen supply to the body
Asphyxia: The cessation of life due to a lack of oxygen
Astringent: Causing contraction
Bacteriostatic: Agent which inhibits the growth of bacteria
Blow-up A rapid uncontrolled ascent missing all planned

stops
Cardiac arrest: The cessation of heart function
Cardiopulmonary resuscitation: The re-establishment of heart and lung action, by

artificial ventilation and external cardiac
compression
Cardiovascular: To do with the heart and blood vessels
Coma: Complete lack of consciousness
Crepitation: Crackling sound
Cutaneous: To do with the skin
Cyanosis: A bluish tinge seen in tissues which are low in

oxygen
Dysphasia: Difficulty with speech
Embolism: The blocking of a blood vessel by a clot or foreign

material
Eructation: Belching
Erythema: Redness of the skin
F-1 ORIGINAL
Eustachian tube: The tube connecting the middle ear and the throat
Grand mal convulsion: An epileptic fit
Haemoptysis: The coughing up of blood
Haemorrhage: Bleeding
Hyperbaric oxygen: High pressure oxygen
Hypercapnia: An excess of carbon dioxide
Hyperresonance: Drum like sound on tapping of the chest
Hypotension: Low blood pressure
Hypothermia: Below normal body temperature
Hypoxia: Reduced oxygen supply
Intracranial pressure: The pressure within the skull
Ischaemia: Deficient blood supply
Mediastinal shift: Movement of the space between the lungs to one

side
Mucous membranes: The thin layer of skin lining some parts of the
body
Narcosis: State of sleepiness produced by a drug
Nystagmus: Involuntary and jerky repetitive movement of the

eyeballs
Oedema: Fluid in the tissues
Omitted Decompression An ascent in which one or more planned stops are

missed in whole or part
Ostium: The opening of any tubular passage
Otitis externa: Inflammation of the external auditory canal of the

outer ear
Otoscope: An instrument for inspecting the ear
F-2 ORIGINAL
Ototoxic: Having a toxic effect on the ear
Palpitations: The sensation of a rapid of irregular heartbeat
Paraesthesia: The sensation of tingling
Paraplegia: Paralysis of the legs and lower part of the body
Petechial haemorrhages: Small spots of bleeding within the tissues
Pneumothorax: The collapse of a lung through introduction of air

between the lining of the lung and the rib cage
Pulmonary oedema: Fluid in the lungs
Pulmonary resuscitation: The re-establishment of lung action by artificial

ventilation
Residual volume: The amount of air remaining in the lungs after

forced expiration
Retrosternal: Behind the sternum (breast bone)
Septum: A partition between two cavities
Sternum: The breast bone
Subconjunctival haemorrhage: Bleeding which occurs under the membrane lining

the outside of the eyeball
Subcutaneous emphysema: The presence of air or gas beneath the skin
Therapeutic: Describes a treatment which improves or cures a

condition
Thermoregulation: Temperature regulation
Tinnitus: Ringing in the ears
Tympanic membrane: The eardrum
Vasoconstriction: Narrowing of the blood vessels
Ventricular fibrillation: An uncoordinated activity of the main chambers of

the heart which stop it pumping blood effectively
F-3 ORIGINAL
Vertigo: Dizziness
Vestibular: Describes the parts of the ear which detect

acceleration (movement) of the body and
contributes to maintaining balance
Vital capacity: The amount of air expelled from the lungs after a
deep inspiration
F-4 ORIGINAL
ANNEX G
BELGIAN NAVY THERAPEUTIC RECOMPRESSION TABLES
1. Belgian Navy Therapeutic Recompression Tables

These are identical in all respects to those used in the United States Navy.
G-1 ORIGINAL
INTENTIONALLY BLANK
G-2 ORIGINAL
ANNEX H
CANADIAN NAVY THERAPEUTIC RECOMPRESSION TABLES
1. Canadian Navy Treatment Tables 5, 6, 6A, 7 and 8

These tables are identical to US Navy tables of equivalent numbers.
2. Canadian Navy Treatment Table 6 Modified

This table is used where symptoms have not been completely relieved after two
oxygen periods at 60 fsw.
3. Canadian Navy Treatment Table 6A Modified

This is a 165 fsw HeO2 and O2 table used for cases of arterial gas embolism where
the symptoms have not completely resolved after the second O2 period of 60 fsw on Table
6A.
4. Canada does not use USN Table 5 except in cases of symptom free omitted
decompression.
H-1 ORIGINAL
Standard Oxygen Treatment Tables.
Table - 5
Depth Time Breathing Total Elapsed Time

(FSW) (Minutes) Medium (Minutes)
0-60 1 Oxygen 1
60 20 Oxygen 21
60 5 Air 26
60 20 Oxygen 46
60 5 Air 51
60-30 30 Oxygen 81
30 5 Air 86
30 20 Oxygen 106
30-0 30 Oxygen 136
H-2 ORIGINAL
Table 5
Use: Treatment of Omitted Decompression of less than 30 minutes. Treatment

of DCS where the symptoms were completely resolved during transport to
the chamber and treatment of recurrence of very mild symptoms after initial
treatment of DCS. The patient breathes oxygen from the surface.
Descent Rate: 60 ft/min.
Ascent Rate: 1 ft/min. Do not compensate for slower ascent rates. Compensate for
faster ascent rates by halting the ascent for the appropriate time period.
Time: O2 time begins upon arrival at 60 fsw. If oxygen breathing must be

interrupted due to toxic reactions, discontinue oxygen breathing for 15 min
after the reaction has completely subsided, then resume the table breathing
oxygen from the point of interruption. If a second toxic reaction occurs
deeper than 30 fsw, wait until the reaction has completely subsided. Travel
to 30 fsw at 60 ft/min, wait 15 minutes then resume the table breathing
oxygen from the point of interruption. Add all missed 60 fsw and travel
time to the time at 30 fsw.
Attendant: The attendant breathes air throughout the treatment and must remain inside
for the duration of the treatment. (See Delays).
Delays: Delays result in the attendant being exposed to a longer bottom time and
therefore decompression on O2 may be required. The most common cause
of delays during treatments are to allow the patient to eat or be examined
and the delays associated with O2 toxicity.
Delays deeper than 30 fsw up to a total of 10 minutes and/or delays at 30

fsw or shallower up to a total of 60 minutes do not require the attendant to
go on O2.
Delays longer than the above limits require that the attendant breathe O2 for
the last 30 minutes while travelling from 30 fsw to the surface.
H-3 ORIGINAL
Table - 6
Depth Time Breathing Total Elapsed

FSW) (Minutes Medium Time
(Minutes)
0-60 1 Oxygen 1
60 20 Oxygen 21
60 5 Air 26
60 20 Oxygen 46
60 5 Air 51
60 20 Oxygen 71
60 5 Air 76
60-30 30 Oxygen 106
30 5 Air 111
30 20 Oxygen 131
30 5 Air 136
30 20 Oxygen 156
30 5 Air 161
30 20 Oxygen 181
30 5 Air 186
30 20 Oxygen 206
30 5 Air 211
30 20 Oxygen 231
30 5 Air 236
30 20 Oxygen 256
30-0 30 Oxygen 286
H-4 ORIGINAL
Table 6
Use: Treatment of more than 30 minutes of omitted decompression and all cases
of decompression sickness. The patient breathes oxygen from the surface.
Treatment of Arterial Gas Embolism (AGE) symptoms responding to an
initial 60 fsw recompression. The patient breathes oxygen from the surface.
Treatment of Symptomatic blowup from 60 fsw or less.
Ascent Rate: 1 ft/min. Do not compensate for slower ascent rates. Compensate for
faster ascent rates by halting the scent for the appropriate time period.
Time: O2 time begins upon arrive at 60 fsw. If oxygen breathing must be

interrupted due to toxic reactions, discontinue oxygen breathing for 15
minutes after the reaction has completely subsided, then resume the table
breathing oxygen from the point of interruption. If a second toxic reaction
occurs deeper than 30 fsw, wait until the reaction has completely subsided.
Travel to 30 fsw at 60 ft/min., wait 15 minutes, then resume the table
breathing oxygen from the point of interruption. Add all missed 60 fsw and
travel time to the time at 30 fsw. (Article 3206).
Attendant: The attendant breathes oxygen for the last 30 minutes while travelling from
30 fsw to the surface. (See Delays).
Delays deeper than 30 fsw up to a total of 20 minutes do not require the

attendant to breathe more than the standard 30 minutes of O2. There is no
limit to the length of delays allowed at 30 fsw and shallower on this table.
Delays longer than the above limits require that the attendant breathe a total
of 50 minutes of O2 which includes the 30 minutes while travelling from 30
fsw to the surface.
H-5 ORIGINAL
Table - 6 Modified

(FSW) (Minutes) Medium (Minutes
0-60 1 Oxygen 1
60 20 Oxygen 21
60 5 Air 26
60 20 Oxygen 46
60 5 Air 51
60 20 Oxygen 71
60 5 Air 76
60 20 Oxygen 96
60 5 Air 101
60-45 30 Oxygen 131
45 5 Air 136
45-30 30 Oxygen 166
30 5 Air 171
30 20 Oxygen 191
30 5 Air 196
30 20 Oxygen 216
30 5 Air 221
30 20 Oxygen 241
30 5 Air 246
30 20 Oxygen 266
30 5 Air 271
30 20 Oxygen 291
30 5 Air 296
30 20 Oxygen 316
30 5 Air 321
30 20 Oxygen 341
30 5 Air 346
30 20 Oxygen 366
30 5 Air 371
30 20 Oxygen 391
30-0 30 Oxygen 421
H-6 ORIGINAL
Table 6 Modified
Use: Treatment of DCS where symptoms have not been completely relieved for
two O2 periods at 60 fsw. The patient breathes oxygen from the surface.
Ascent Rate: From 60-30 fsw at a rate of ½ ft/min with one 5 minute stop at 45 fsw.
From 30 fsw to the surface at a rate of 1 ft/min. Do not compensate for
slower ascent rates. Compensate for faster ascent rates by halting the
ascent for the appropriate time period.

breathing oxygen from the point of interruption. If a second toxic reactions
Travel to 30 fsw at 60 ft/min, wait 15 minutes, then resume the table
travel time to the time at 30 fsw.
Attendant: The attendant breathes oxygen for the last 20 minute O2 period at 30 fsw
and during the 30 minutes while travelling from 30 fsw to the surface. (See
Delays).
Delays deeper than 30 fsw up to a total of 20 minutes do not require the

attendant to breathe more than the standard 50 minutes of O2. There is no
limit to the length of delays allowed at 30 fsw and shallower on this table.
Delays longer than the above limits require that the attendant breathe a total
of 70 minutes of O2 which includes the 30 minutes while travelling from 30
fsw to the surface.
H-7 ORIGINAL
Table - 6A

165 60 ft/min 50/50 HEO2 or Air N/A

165 30 50/50 HeO2 or Air 30
165-60 Less than 4 50/50 HeO2 or Air 34
60 20 Oxygen 54
60 5 Air 59
60 20 Oxygen 79
60 5 Air 84
60 20 Oxygen 104
60 5 Air 109
60-45 30 Oxygen 139
45 5 Air 144
45-30 30 Oxygen 174
30 5 Air 179
30 20 Oxygen 199
30 5 Air 204
30 20 Oxygen 224
30 5 Air 229
30 20 Oxygen 249
30 5 Air 254
30 20 Oxygen 274
30 5 Air 279
30 20 Oxygen 299
30 5 Air 304
30 20 Oxygen 324
30-0 30 Oxygen 354
H-8 ORIGINAL
Table 6A
Use: Treatment of Arterial Gas Embolism (AGE) not responding at 60 fsw but
resolving within 30 min at 165 fsw where initially 20 min or less is spent at
60 fsw. Patient should breathe 50/50 HeO2 from the surface to 165 fsw, at
165 fsw and during the ascent to 60 fsw. If 50/50 HeO2 is unavailable, the
patient and/or attendant may breathe air or HeO2 with less than 50% O2
without change to the table.
Treatment of Symptomatic blowup from greater than 60 fsw.
Ascent Rate: From 165 fsw to 60 fsw at a rate of 30 ft/min. From 60 fsw to 30 fsw at a
rate of ½ ft/min with one 5 minute stop at 45 fsw. From 30 fsw to the
surface at a rate of 1 ft/min. Do not compensate for slower ascent rates.
Compensate for faster ascent rates by slowing/halting the ascent for the
appropriate time period.

and during the 30 minutes while travelling from 30 fsw to the surface (See
Delays).
of delays during treatment are to allow the patient to eat or be examined
Delays at 165 fsw or until reaching 30 fsw require the attendant to be

decompressed on the appropriate decompression table until the 60 fsw stop
is reached. Treatment Table 6A can be resumed at this point, but the
attendant should decompress on O2 for a toal of 70 minutes of O2 which
includes the 30 minutes while travelling from 30 fsw to the surface.
Delays at 30 fsw or shallower do not require the attendant to breathe more

than the standard 50 minutes of O2.
H-9 ORIGINAL
Alternate Oxygen Treatment Tables, Table - 6A Modified

0-165 60 ft/min 50/50 HeO2 or Air N/A

165 30 50/50 HeO2 or Air 30
165-60 Less than 4 50/50 HeO2 or Air 34
60 20 Oxygen 54
60 5 Air 59
60 20 Oxygen 79
60 5 Air 84
60 20 Oxygen 104
60 5 Air 109
60 20 Oxygen 129
60 5 Air 134
60-45 30 Oxygen 164
45 5 Air 169
45-30 30 Oxygen 199
30 5 Air 204
30 20 Oxygen 224
30 5 Air 229
30 20 Oxygen 249
30 5 Air 254
30 20 Oxygen 274
30 5 Air 279
30 20 Oxygen 299
30 5 Air 304
30 20 Oxygen 324
30 5 Air 329
30 20 Oxygen 349
30 5 Air 354
30 20 Oxygen 374
30 5 Air 379
30 20 Oxygen 399
30 5 Air 404
30 20 Oxygen 424
30-0 30 Oxygen 454
H-10 ORIGINAL
Table 6A Modified
Use: Treatment of Arterial Gas Embolism (AGE) where the symptoms have not
completely resolved after the second O2 period at 60 fsw on Table 6A.
Patient should breathe 50/50 HeO2 from the surface to 165 fsw, at 165 fsw
and during the ascent to 60 fsw. If 50/50 HeO2 is unavailable, the patient
and/or attendant may breathe air or HeO2 with less the 50% O2 without
change to the table.
Ascent Rate: From 165 fsw to 60 fsw at a rate of 30 ft/min. From 60 fsw to 30 fsw at a
rate of ½ ft/min with one 5 minute stop at 45 fsw. From 30 fsw to the
surface at a rate of 1 ft/min. Do not compensate for slower ascent rates.
Compensate for faster ascent rates by slowing/halting the ascent for the
appropriate time period.

and during the 30 minutes while travelling from 30 fsw to the surface (See
Delays).
of delays during treatment are to allow the patient to eat or be examined
Delays at 165 fsw or until reaching 30 fsw require the attendant to be

decompressed on the appropriate decompression table until the 60 fsw stop
is reached. Treatment Table 6A can be resumed at this point, but the
attendant should decompress on O2 for a toal of 70 minutes of O2 which
includes the 30 minutes while travelling from 30 fsw to the surface.
Delays at 30 fsw or shallower do not require the attendant to breathe more

than the standard 50 minutes of O2.
H-11 ORIGINAL
Table - 7
H-12 ORIGINAL
Table 7
Use: Used for treatment of unresolved and lift-threatening symptoms of

Decompression sickness or Arterial Gas Embolism (AGE) after initial
treatment on Table 6. Use only upon the direction of a Advanced Diving
Medical Officer.
Time: Table begins upon arrival at 60 feet. Arrival at 60 feet is accomplished by

initial treatment on Table 6 or 6A. If initial treatment has progressed to a
depth shallower than 60 feet, compress to 60 feet at 25 ft/min to begin
Table 7.
Maximum duration at 60 feet is unlimited. Remain at 60 feet a minimum

of 12 hours unless overriding circumstances dictate earlier decompression.
Patient begins oxygen breathing periods at 60 feet. Attendant need breathe

only chamber atmosphere throughout. If oxygen breathing is interrupted,
no lengthening of the table is required.
Minimum chamber O2 concentration is 19%. Maximum CO2 concentration

is 1.5% SEV (11.4 mmHg). Maximum chamber internal temperature is
85ºF (para 3).
Decompression starts with a 2 foot upward excursion from 60 to 58 feet.

Decompress with stops every 2 feet for times shown in profile below.
Ascent time between stops is approximately 30 seconds. Stop time begins
with ascent from deeper to next shallower step. Stop at 4 feet for 4 hours
and then ascend to the surface at 1 ft/min.
Note. Ensure chamber lift support requirements can be met before committing to a Table 7.
H-13 ORIGINAL
Table - 8
H-14 ORIGINAL
TABLE 8
Use: Treatment of deep Blowup from surface supplied helium-oxygen dives.
1. Enter the table at the depth which is exactly equal to or next greater than the
deepest depth attained in the recompression. The descent rate is as fast as
possible.
2. The maximum time that can be spent at the deepest depth is shown on the
table. The maximum time for 225 fsw is 30 minutes; for 165 fsw, three
hours. for an asymptomatic diver, the minimum time at depth is 30 minutes
for depths exceeding 165 fsw and two hours for depths equal to or
shallower than 165 fsw.
3. Decompression is started with a 2 fsw reduction in pressure if the depth is

an even number, or with a 3 fsw reduction in pressure if the depth is an odd
number. Subsequent stops are carried out every 2 fsw. Stop times are
shown on the table. The stop time begins when leaving the previous depth.
Ascend to the next stop in approximately 30 seconds.
4. Stop times apply to all stops within the band up to the next quoted depth.
For example, for ascent from 165 fsw, stops of 12 minutes are made at 162
fsw, and at every two foot interval to 140 fsw. At 140 fsw, the stop time
becomes 15 minutes. When travelling from 225 fsw, the 166 foot stop is
five minutes; the 164 foot stop is 12 minutes. Once begun decompression
is continuous. For example, when decompressing from 225 fsw, ascent is
not halted at 165 fsw for three hours. However, ascent may be halted at 60
fsw and shallower for any desired period of time.
5. While deeper than 165 fsw, a helium-oxygen mixture with 16 to 21 percent

oxygen may breathed by mask to reduce narcosis. At 165 fsw or shallower
a 60 percent helium/40 percent oxygen mixture or a 60 percent nitrogen/40
percent oxygen mixture may be given to the diver as treatment gas. At 60
fsw and shallower, pure oxygen may be given to the diver as treatment gas.
For all treatment gases (HeO2, N2O2 and O2 ) a schedule of 25 minutes on
gas and five minutes on chamber air should be followed for a total of four
cycles. Additional oxygen may be given at 60 fsw after a two hour interval
of chamber air. (See USN Treatment Table 7 at Annex T) for guidance.
6. To avoid loss of the chamber seal, ascent may be halted at four fsw and the
total remaining stop time of 240 minutes taken at this depth. Ascend
directly to the surface upon completion of the required time.
7. Total ascent time form 225 fsw is 56 hours, 29 minutes. For a 165 fsw
recompression, total ascent time is 53 hours, 52 minutes and for a 60 fsw
recompression 36 hours.
H-15 ORIGINAL
USC Cataline Hyperbaric Chamber - Consolidated Treatment Tables
H-16 ORIGINAL
ANNEX I
DANISH NAVY THERAPEUTIC RECOMPRESSION TABLES
1. Danish Navy Therapeutic Tables are identical to US Navy Therapeutic Tables of

equivalent numbers.
2. On some occasions DA uses the Royal Navy Therapeutic Table 65.
I-1 ORIGINAL
INTENTIONALLY BLANK
I-2 ORIGINAL
ANNEX J
FRENCH NAVY (GERS) THERAPEUTIC RECOMPRESSION TABLES
1. Presentation of Oxygen Tables
a. There are three oxygen tables designated A, B and C which are of increasing
duration: 5 hours 30 minutes for A, 8 hours for B, and 16 hours 30 minutes for C. The
12 and 9 metre stages may be extended when required by development of the treatment.
b. The maximum recompression pressure is 4 bar (30m).
c. The casualty uses a BIBs mask to breathe mixtures with 40% and 60% oxygen
between 30m and 12m. The neutral diluent gas is nitrogen, except in the case of
respiratory problems, making it possible to re-establish normal ventilation. However,
haemodynamic problems in relation to the arterial circulation when using therapeutic
He/O2 mixtures mean that air use must be reserved for land-based hyperbaric centres
possessing qualified medical personnel.
d. The treatment may be adapted depending on how the patient responds, but the stages
must never be shortened and recompression must never be carried out in the course of
treatment. It is possible to switch from a short table to a longer table, but never from a
long one to a shorter one. In serious cases, and depending on the response, it is possible
to extend the 12 to 9 metre stage for as long as no improvement is apparent.
2. Presentation of Air Tables

The GERS Table D is only used in cases where super-oxygenated mixtures and oxygen
are unavailable, or in place of GERS Table C in cases of irreducible intolerance of oxygen.
3. GERS Therapeutic Tables with Oxygen

The information tabulated below shows depth, pressure, time and mixtures required for
each oxygen table.
a. Rate of Descent: 30 m/min maximum, 10 m/min average
b. Decompression: Ascent between stages is affected at 2min/m or more. When an

oxygen enriched mixture or pure oxygen has been administered at any stage, stay with
this breathing mixture during the change of stage. If a different mixture has to be taken
at the next stage, it must be taken immediately on arrival at the stage.
c. Breathing Mixtures: When the diver is being given the 60% O2 mixture or pure
oxygen to breathe, administer air for 10 minutes every 50 minutes, except during
changes in stage. in this case, delay the breathing of air until arrival at the next stage.
This period is not added to the stage time.
J-1 ORIGINAL
d. To help prevent oxygen toxicity, it is preferable to use 60% O2 or 40% O2 oxygen

enriched mixtures for a while until pure oxygen can be tolerated. He/ O2 mixtures may
be used on the advice of a Diving Medical Specialist, if the breathing mixture for the
dive contained helium or, by way of exception as a last resort, in the event of acute
respiratory insufficiency of obstructive origin.
e. Attendant(s): Insofar as possible, care must be taken to ensure that attendant(s) are
relieved in the compression chamber so that each attendant undertakes a no-
decompression dive. this necessitates seven different attendants for Table C without
extension at 12 or 9 m, for of whom are required in the first two hours
Depth Relative Table A Table B Table C

Metres Pressure
(bar) Time Mixture Time Mixture Time Mixture
30 3 30 min 40% O2 30 min 40% O2 30 min to 2h 40% O2
24 2.4 30 min 60% O2 30 min 60% O2 1 hour 60% O2

Note 1
21 2.1 30 min 60% O2 30 min 60% O2 1 hour 60% O2
18 1.8 30 min 60% O2 30 min 60% O2 1h to 2h 60% or

100% O2
15 1.5 30 min 60% O2 1 hour 60% O2 2 hours 60% or

100% O2
12 1.2 30 min 100% O2 1 hour 100% O2 2h to 12h 100% O2

Note 2
9 0.9 30 min 100% O2 1 hour 100% O2 6h to 12h 100% O2

Note 2
6 0.6 30 min 100% O2 1 hour 100% O2 1h to 2h 100% O2
3 0.3 30 min 100% O2 1 hour 100% O2 1h to 2h 100% O2
Notes:
1. An optional stop of 30 minutes at 27 metres (mixture 40% or 60% O2 may be introduced

if prescribed by a qualified doctor.
2. These periods may be extended if required.
J-2 ORIGINAL
4. GERS Table A - Therapeutic Recompression with Oxygen-enriched Mixtures and

Pure Oxygen
a. Casualty on BIBS with 40% mixture of O2 during recompression.
b. Maximum recompression rate: 30 m/min, average: 10 m/min.
c. Maximum decompression rate between stages: 0.5 m/min.
d. Remain on BIBS during changes in stage.
e. Pure oxygen is administered according to the following sequence: 50 minutes of O2

10 minutes of air, 50 minutes of O2, etc.
f. Check the pulse of the patient for 1 minute every 15 minutes. If it accelerates,
monitor it for 15 seconds every minute and watch out for alarm signs of acute hyperoxia
(muscular contractions in the face, respiratory trouble, distress etc,) in order to suspend
BIBS breathing if necessary.
Cumulative Time on Depth(Metres) Duration of Stage Mixture Breathed

Arrival at Stage Minutes
Hours:Minutes
0 30 30 40 O2
42 24 30 60 O2
1 : 18 21 30 60 O2
1 : 54 18 30 60 O2
2 : 30 15 30 100 O2
3 : 06 12 30 100 O2
3 : 42 9 30 100 O2
4 : 18 6 30 100 O2
4 : 54 3 30 100 O2
5 : 30 0
Notes: On the instruction of a qualified doctor:
1. A 30 minute stop at 27 metres (40% O2 mixture) may be included.
2. Pure oxygen may be breathed from the 18 metre stage (using the sequence 50 minutes
on O2 then 10 minutes on air).
J-3 ORIGINAL
5. GERS Table B - Therapeutic Recompression with Oxygen-enriched Mixtures and

Pure Oxygen.

Cumulative Time on Depth(Metres) Duration of Stage Mixture Breathed

Arrival at Stage Minutes
Hours:Minutes
0 30 30 40 O2
42 24 30 60 O2
1 : 18 21 30 60 O2
1 : 54 18 30 60 O2
2 : 30 15 1 : 00 60 O2
3 : 36 12 1 : 00 100 O2
4 : 42 9 1 : 00 100 O2
5 : 48 6 1 : 00 100 O2
6 : 54 3 1 : 00 100 O2
8 : 00 0
Total Duration 8 Hours
J-4 ORIGINAL
6. GERS Table C - Therapeutic Recompression with Oxygen-enriched Mixtures and

Pure Oxygen

Cumulative Time on Arrival at Depth Duration of Mixture

Stage (Metres) Stage in Breathed
Hours (h) and
Table C Short Table C Long Minutes (m)
Hours : Minutes Hours : Minutes
0 30 30 min to 2h 40% O2
42 2 : 12 24 1h 60% O2
1 : 48 3 : 18 21 1h 60% O2
2 : 54 4 : 24 18 1h to 2h 60% O2
4 : 00 6 : 30 15 2h 60% O2
6 : 06 8 : 36 12 2 or 12h 100% O2
8 : 12 20 : 42 9 6 or 12h 100% O2
14 : 18 32 : 48 6 1h or 12h 100% O2
15 : 24 34 : 54 3 1h or 2h 100% O2
16 : 30 37 0 100% O2
Total Duration 16 hours and 30 minutes (Short). 37 hours (Long)
J-5 ORIGINAL
7. GERS Table D - Therapeutic Recompression using Air
WARNING
TO BE USED IN PLACE OF GERS TABLE C IN CASES WHERE SUPER-

OXYGENATED MIXTURES AND OXYGEN ARE UNAVAILABLE OR IN CASES
OF IRREDUCIBLE INTOLERANCE OF OXYGEN.
a. Maximum recompression rate: 30 m/min, average: 10 m/min.
b. Maximum decompression rate between stops: 0.5 m/min.
c. The time to recompress to 50m is not included in the duration of the first stop.
d. Attendant(s): From 1 to n...... According to available resources.
Cumulative Time on Arrival at Depth Duration of Stage Mixture

Stage (Metres) Breathed
Hours Minutes Hours Minutes
0 0 50 Air
3 16 42 3 Air
3 58 36 30 Air
4 34 33 30 Air
6 40 30 2 Air
10 46 27 4 Air
14 52 24 4 Air
20 58 21 6 Air
27 4 18 6 Air
33 10 15 6 Air
45 16 12 12 Air
51 to 53 22 9 6 to 8 Air
57 to 61 28 6 6 to 8 Air
63 to 69 34 3 6 to 8 Air
69 to 77 40 0 6 to 8
Total Duration 2 days 21 hours and 40 minutes (Short). 3 days 5 hours 40 minutes
(Long)
J-6 ORIGINAL
ANNEX K
GERMAN NAVY THERAPEUTIC RECOMPRESSION TABLES
1. German Navy Treatment Tables 1A and 2A

These treatment tables are to be used for pain only decompression illness where oxygen
breathing is impossible. Treatment table 1a is to be used where improvement is noted at 20
msw, and Treatment Table 2a is to be used where no improvement is noted at 20 msw, or where
symptoms worsen while being treated on Table 1a.
2. German Navy Treatment Tables 3 and 4

These treatment tables are to used for definite or suspected neurological decompression
illness including that caused by air embolism. Treatment Table 3 is to be used if improvement
is noted after 30 minutes at 50 msw, and Treatment Table 4 is to be used when no improvement
is noted after 30 minutes at 50 msw.
3. German Navy Treatment Table 5

This shallow oxygen treatment table is to used for skin symptoms or pain only, or for
missed decompression without symptoms.
4. German Navy Treatment Table 6 mod

This oxygen treatment table is to be used for decompression illness with neurologic or
pulmonary symptoms. A maximum of two 20-minute extensions on oxygen may be added at 18
metres, and a maximum of three 20-minute extensions on oxygen may be added at 9 metres.
5. German Navy Treatment Table 6a mod

This deep oxygen treatment table is to used for cases of severe decompression illness,
neurological deficits, and shock, including that caused by air embolism. It may be extended by
adding up to two 20-minute oxygen breathing periods at 18 metres, and up to three 20-minute
oxygen breathing periods at 9 metres.
6. SND Table
This table for the ‘severest neurological deficits’ is an extension of Table 6A. It allows
a maximum period of 90 minutes at 50m followed by slow staged decompression.
7. German Navy HBO-Table

This treatment table is to be used as a retreatment table for residual symptoms.
K-1 ORIGINAL
K-2 ORIGINAL
Treatment Table 5
Decompression illness -> "pain only" - symptoms
skin symptoms, missed decompression
K-3
ORIGINAL
Treatment Table 6 mod.
Decompression illness with
neurological symptoms, lung symptoms
K-4
ORIGINAL
Treatment Table 6a mod.
Air embolism/serveree decompression illness,
severest neurological deficits, shock
K-5
ORIGINAL
SND-Table (Severest Neurological Deficits)
Non-Responding patient at 50 msw,
air embolism/DCI with life -threatens symptoms
K-6
ORIGINAL
K-7 ORIGINAL
INTENTIONALLY BLANK
K-8 ORIGINAL
ANNEX L
GREEK NAVY THERAPEUTIC RECOMPRESSION TABLES
1. To be added.
L-1 ORIGINAL
INTENTIONALLY BLANK
L-2 ORIGINAL
ANNEX M
ITALIAN NAVY THERAPEUTIC RECOMPRESSION TABLES
1. Italian Navy Therapeutic Treatment Tables 1 to 6, 6A and 7-8

These are identical in all respects and requirements to the US Navy Tables of equivalent
value, but see below for personnel.
2. GERS Table C
This is used in cases if DCI with worsening symptoms, potential seriousness or in cases
of incomplete recovery using Table 6. Identical in all respects to French requirements, but see
below for personnel.
3. Personnel Support Requirements
These are as follows:
Table 1A, 2A and 3. Diving Officer, Medical Officer, Panel Operator, Chamber
Attendant and Corpsman.
Table 4. Diving Officer, Medical Officer, 2 x Panel Operators, 2 x Chamber Attendants

and 2 x Corpsmen. Additional personnel may be required due to length of the treatment.
Table 5. Diving Supervisor, Medical Officer, Panel Operator, Chamber Attendant and
Corpsman.
Table 6. Diving Supervisor, Medical Officer, Panel Operator, Chamber Attendant and
Corpsman.
Table 6A. Diving Supervisor, Medical Officer, Panel Operator, Chamber Attendant and
Corpsman.
GERS Table C. Diving Officer, Medical Officer, 2 x Panel Operators, 2 x Chamber

Attendants and 2 x Corpsmen.
Table 7. Diving Officer, Medical Officer, 2 x Panel Operators, 2 x Chamber Attendants

and 2 x Corpsmen. Additional personnel may be required due to length of the treatment.
Table 8. Diving Officer, Medical Officer, 2 x Panel Operators, 2 x Chamber Attendants.

Additional personnel may be required due to length of the treatment.
M-1 ORIGINAL
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M-2 ORIGINAL
ANNEX N
ROYAL NETHERLANDS NAVY THERAPEUTIC RECOMPRESSION TABLES
1. Royal Netherlands Navy Treatment Tables 5, 6, 6A and 7

2. Table 5
This table is used for omitted decompression.
3. Table 9 SH
Treatment using this table is for refractory DCI after initial treatment. Depth and
times as follows:
a. 1.9 ATA for 180 minutes
b. 6 cycles of 25 minutes O2 with 5 minutes air break in between.
c. Travel to the surface in 30 minutes.
N-1 ORIGINAL
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N-2 ORIGINAL
ANNEX O
NORWEGIAN NAVY THERAPEUTIC RECOMPRESSION TABLES
1. Norwegian Navy Treatment Tables 5, 6 and 6a

2. Norwegian Navy Treatment Table 5A

This table is basically a Table 5 entered from a flowchart after 15 minutes at 50m when
pulmonary barotrauma has not been verified.
3. Norwegian Navy Treatment Table 6He

This table for the most severe cases of DCI uses a 50/50 heliox mixture from 30 to 18
meters and then 100% O2.
O-1 ORIGINAL
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O-2 ORIGINAL
ANNEX P
PORTUGESE NAVY THERAPEUTIC RECOMPRESSION TABLES
1. Portugese Navy Therapeutic Recompression Tables

These are identical to those used by the Royal Navy.
P-1 ORIGINAL
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P-2 ORIGINAL
ANNEX Q
SPANISH NAVY THERAPEUTIC RECOMPRESSION TABLES
1. Spanish Navy Treatment Tables 1A, 2A, 3, 4, 5, 6, 6A, 7

These tables are identical in all aspects to the US Navy Therapeutic Tables of the same
number.
2. Spanish Navy Treatment Tables 1A
a. This table is used when oxygen is not available.
b. For the treatment of Type I symptoms relieved at 66 feet (20 metres).
3. Spanish Navy Treatment Table 2A
b. For the treatment of Type I symptoms relieved deeper than 66 feet (20 metres).
4. Spanish Navy Treatment Table 3
b. For the treatment of Type II and Arterial gas Embolism symptoms that are not
relieved within 30 minutes at 165 feet (50 metres).
a. This table is used when oxygen is available, for the treatment of Arterial Gas
Embolism and Type II Symptoms at 165 feet (50 metres) when no improvement is noted
after 30 minutes.
b. Also when no improvement is noted after 20 minutes at 60 feet (18 metres) (when
using table 6).
c. At 60 feet (18 metres) the breathing periods will be 25 minutes on oxygen and 5
minutes on air.

This table is used to treat Type I (Pain only) symptoms when all symptoms are relieved
within 10 minutes at 60 feet (20 metres) and no other abnormalities are present.
Q-1 ORIGINAL

This table is used to treat Type 1 Symptoms not showing relief within 10 minutes after
arriving at 60 feet (18 metres) and Type II symptoms.
8. Spanish Navy Treatment Table 6A

This table is used to treat Arterial Gas Embolism when complete relief of symptoms is
reached within 30 minutes at 165 feet (50 metres)
9 Spanish Navy Treatment Table 7
a. This table is used for treatment of non-responding Arterial Gas Embolism and
Decompression Illness.
b. Treatment table 7 is an extension at 60 feet (20 metres) of tables 6, 6A and 4.
Q-2 ORIGINAL
ANNEX R
TURKISH NAVY THERAPEUTIC RECOMPRESSION TABLES
1. To be added.
R-1 ORIGINAL
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R-2 ORIGINAL
ANNEX S
ROYAL NAVY THERAPEUTIC RECOMPRESSION TABLES
1. RN Treatment Table 60 - Hyperbaric Oxygen Therapy
a. This table, originally developed by the Royal Adelaide Hospital and modified by the
Royal Navy may be used for the treatment of carbon monoxide poisoning. As an
alternative Table 61 may be used.
b. Proceed as follows:
(1) The patient starts breathing oxygen on the surface.
(2) Descend to 18m over one to two minutes stopping if the patient or attendant
has difficulty clearing his or her ears.
(3) The timing of the treatment begins on reaching 18 metres.
(4) The patient breathes 100% oxygen for two periods of 25 minutes, each
followed by a 5 minute air break.
(5) Ascent from 18 metres to the surface should be at a continuous bleed rate of
3 metres every 5 minutes.
(6) The attendant must breath oxygen during ascent from 9 metres to the surface.
(7) Severe cases may require repeat treatments over a period of days as frequent
as every 12 hours. RN Tables 60 and 61 are suitable for this purpose.
c. Personnel requirements are as follows:
1 x Diving Supervisor
1 x Outside Tenders / Chamber Operators
1 x Qualified Chamber Attendant
1 x Medical Officer (if patient is intubated and artificially ventilated)
d. Other support requirements for this table are:
(1) Chamber medical equipment
(2) Fluids for the duration of the Treatment Table
S-1 ORIGINAL
(3) Built-in Breathing System (BIBS) gas usage for the patient:
(4) Built-in Breathing System (BIBS) gas usage for the chamber attendant:
RN Treatment Table 60 - Hyperbaric Oxygen Therapy
Gauge Depth Stops/Ascent Elapsed time Rate of Ascent

(metres) (minutes) (hours and mins) (metres/minute)
18 25 (O2) 00:00 - 00:25
18 5 (Air) 00:25 - 00:30
18 25 (O2) 00:30 - 00:55
18 5 (Air) 00:55 - 01:00
18 - 0 30 (O2) 01:00 - 01:30 3 m in 5 min
Surface 01:30
2. RN Treatment Table 61 - Short Oxygen Recompression Therapy
a. This may be used for the management of missed decompression and considered for
the treatment of Acute Decompression Illness with limb pain, cutaneous or lymphatic
manifestations ONLY or for cases of carbon monoxide poisoning. In cases of
decompression illness, the patient should be given a careful Neurological Examination
so that involvement of the nervous system, in particular, can be excluded. Table 61 may
also be used for re-treating cases of decompression illness or carbon monoxide poisoning
in which there has been incomplete recovery or a recurrence of symptoms.
(1) The patient starts breathing O2 on the surface.
(2) Descend to 18m over one or two minutes stopping only if the patient or
attendant have difficulty in clearing their ears.
(3) The time of the treatment starts on reaching 18m.
c. If the symptoms of decompression illness are completely relieved within 10

minutes, decompression may proceed in accordance with Table 61. Otherwise use Table
62. Practically, this will mean that only a minority of cases will complete Table 61.
d. The attendant should breathe oxygen during the O2 period at 9 metres and during the
ascent to the surface.
S-2 ORIGINAL
e. Personnel requirements for this Treatment Table are as follows:
1 x Outside Tender / Chamber Operator
f. Other support requirements for this Treatment Table are:
(1) Chamber medical equipment.
(2) Meals and fluids for the duration of the Treatment Table.
(3) Built-in Breathing System (BIBS) gas usage for the patient.
(4) Built-in Breathing System (BIBS) gas usage for the chamber attendant.
RN Treatment Table 61 - Short Oxygen Recompression Therapy
Gauge Depth Stops/Ascent Elapsed Time Rate of Ascent

(metres) (minutes) (hours and mins) (metres/minutes)
18 20 (O2) 00:00 - 00:20
18 5 (Air) 00:20 - 00:25
18 20 (O2) 00:25 - 00:45
18 - 9 30 (O2) 00:45 - 01:15 3 m in 10 min
9 5 (Air) 01:15 - 01:20
9 20 (O2) 01:20 - 01:40
9 5 (Air) 01:40 - 01:45
9-0 30 (O2) 01:45 - 02:15 3 m in 10 min
Surface 02:15
3. RN Treatment Table 62 - Standard Oxygen Recompression Therapy
a. This table is used for the great majority of cases of decompression illness which do
not meet the criteria for Table 61.
(1) The patient starts breathing O2 on the surface.
(2) Descend to 18m over one or two minutes stopping only if the patient or
attendant have difficulty in clearing their ears.
S-3 ORIGINAL
(3) The timing of the treatment starts on reaching 18 metres.
c. Very occasionally, patients who are recompressed shortly after the onset of
symptoms may continue to deteriorate at 18m. If the patient’s condition has not
stabilised within 20 minutes of reaching 18m, compress to 50 m on air or breathing
32½/67½, O2/N2 by BIBS, decompression will then normally be completed using Table
63 or Table 64. In such cases CONTACT A DIVING MEDICINE SPECIALIST. In
very rare instances, continued deterioration may require a transfer to Table 65.
d. If the symptoms have remained static or improved incompletely after three 20

minute periods on 100% O2 at 18m, Table 62 may be extended. One or two further O2
breathing periods, separated by a 5 minute air break may be added on the advice of a
diving medicine specialist. If the symptoms or signs have not resolved after two
extensions at 18m further advice from the diving medicine specialist should be sought.
Depending upon the nature and severity of the symptoms or signs, transfer to Table 64
may be necessary.
e. Symptoms may recur during decompression to 9m. In such circumstance STOP

THE ASCENT and return to 18m. Consult a Diving Medicine Specialist.
f. Symptoms may recur at 9m. Again, consult a diving medicine specialist.

Depending on the nature and severity of the symptoms, a return to 18m or extending the
table at 9m may be necessary. Table 62 may be extended for one or two 1 hour O2
breathing periods at 9m, separated by 15 min air breaks.
g. For an unmodified Table 62 or a Table 62 with one extension, the attendant must
breathe O2 for the last 30 minutes at 9 metres and during the ascent from 9 metres. If
Table 62 is extended more than once, then the attendant should breathe O2 for the whole
of the final O2 period at 9 metres and the ascent to the surface (90 minutes). If the
attendant has undergone a hyperbaric exposure in the preceding 24 hours, an additional
oxygen breathing period at 9 metres should be undertaken.
h. Personnel requirements for this Treatment Table are as follows:
2 x Outside Tenders/Chamber Operators
1 x Qualified Chamber Attendant (Diving Medical Technician or Diving Medical

Officer if possible)
i. Other support requirements:
(2) Meals and fluids for the duration of this Treatment Table
S-4 ORIGINAL
Treatment Table 62 without extensions:
Treatment Table 62 with 2 extensions at 60 feet/18 metres and 30 feet/9

metres:

metres:
RN Treatment Table 62 - Standard Oxygen Recompression Therapy
Gauge Depth Stop/Ascent Elapsed Time Rate of Ascent

18 20 (O2) 00:00 - 00:20
18 5 (Air) 00:20 - 00:25
18 20 (O2) 00:25 - 00:45
18 5 (Air) 00:45 - 00-50
18 20 (O2) 00:50 - 01:10
18 5 (Air) 01:10 - 01:15
18 - 9 30 (O2) 01:15 - 01:45 3 m in 10 min
9 15 (Air) 01:45 - 02:00
9 60 (O2) 02:00 - 03:00
9 15 (Air) 03:00 - 03:15
9 60 (O2) 03:15 - 04:15
9-0 30 (O2) 04:15 - 04:45 3 m in 10 min
Surface 04:45
4. RN Treatment Table 63 - Deep Air - Oxygen Recompression Therapy
a. This table was developed specifically for the treatment of arterial gas embolism.
Given the difficulties in making such a diagnosis and the potential disadvantages
associated with the initial compression to 50 metres, it is considered that the option of
compression to 50 metres should be reserved for patients who continue to deteriorate 20
minutes after an initial recompression to 18 metres breathing oxygen.
b. Proceed as follows: pressurise the chamber, without delay with air to 50 m at the
fastest rate that can be tolerated by the patient and attendant up to 30 metres per minute.
If a gas mixture of 32½/67½ O2/N2 is available, this should be breathed by the patient
via BIBS.
S-5 ORIGINAL
c. If the patient is free of symptoms and signs after 25 minutes, and O2 is available,
then decompression may be commenced using Table 63. If O2 is not available Table 64
should be used, omitting the oxygen.
d. If there are persisting symptoms and signs after 30 minutes at 50 m, no matter how
minor, Table 64 should be used.
e. If the patient is deteriorating at 50 m, contact a Diving Medicine Specialist as a

matter of urgency. It may be necessary to compress the patient further and continue
treatment using Table 65. This should not be contemplated however, unless:
(1) A Diving Medicine Specialist is consulted.
(2) The chamber is capable of supporting a prolonged treatment.
f. Decompression from 50 metres to 18 metres should take 4 min after which Table
63 proceeds as for Table 62, except that the attendant must always breathe O2 during the
final 60 minutes at 9 metres and subsequent ascent. If the attendant has had a previous
hyperbaric exposure within 24 hours, add one additional oxygen breathing period at 9
metres.
g. Personnel requirements for this Treatment Table are as follows:

h. Other support requirements for this Treatment Table are:
(2) Meals and fluids for the duration of the Treatment Table

metres:

metres:
S-6 ORIGINAL
Table 63 - Deep Air - Oxygen Recompression Therapy

50 30 00:00 - 00:30
50 - 18 4 (Air) 00:30 - 00:34 8 m in 1 min
18 20 (O2) 00:34 - 00:54
18 5 (Air) 00:54 - 00:59
18 20 (O2) 00:59 - 01:19
18 5 (Air) 01:19 - 01:24
18 20 (O2) 01:24 - 01:44
18 5 (Air) 01:44 - 01:49
18 - 9 30 (O2) 01:49 - 02:19 3 m in 10 min
9 15 (Air) 0219: - 02:34
9 60 (O2) 02:34 - 03:34
9 15 (Air) 03:34 - 03:49
9 60 (O2) 03-49 - 04:49
9-0 30 (O2) 04:49 - 05:19 3 m in 10 min
Surface 05:19
5. RN Treatment Table 64 - Deep Air - Oxygen Recompression Therapy

This Table is applied as follows:
a. Rate of Descent should be as fast as can be tolerated by the patient and attendant.
This is normally of the order of 30 metres per minute.
b. Ascent between stoppages is to take 5 minutes. This is not included in the stoppage
times, but has been allowed for in the elapsed times.
c. Table 64 may be used breathing air if O2 is not available. If 32½/67½ oxy-nitrogen

mixture is available, this may be given at 50m at the discretion of the Diving Medicine
Specialist (evidence of pulmonary oxygen toxicity must be monitored closely). If O 2 is
available the patient should always start breathing 100% O2 upon arrival at 18m. O2
breathing periods should be of 25 minutes duration followed by 5 minutes breathing
chamber air. The patient should be given a minimum of four O2 breathing periods (for
a total time of two hours) and thereafter to suit the patient’s needs as advised by a Diving
Medicine Specialist. The attendant should begin breathing 100% O2 two hours before
leaving 9m, and both the patient and the attendant should breathe 100% O2 at 6 and 3
metres as shown in the table.
d. Table 64 may be entered at 18m if advised by the Diving Medical Specialist who
will also give instructions on oxygen breathing periods required. This guidance will take
into account oxygen breathing before Table 64 was prescribed.
S-7 ORIGINAL
Note. Prior to committing to Table 64, the Diving Supervisor must ensure that all life
support considerations can be met.
e. Personnel requirements for Treatment Table 64 are as follows:
2 x Qualified Chamber Attendants
Provision should be made for additional personnel because of the length of the
Treatment Table.
f. Other support requirements for this Treatment Table are:
RN Treatment Table 64 - Deep Air - Oxygen Recompression Therapy
Gauge Depth Stops Elapsed Time Rate of Ascent

(metres) (Hours Mins) (hours and mins)
50 2 00:00 - 02:00
42 30 02:05 - 02:35
36 30 02:40 - 03:10
30 30 03:15 - 03:45
24 30 03:50 - 04:20
18 6 ) 04:25 - 10:25 5 minutes between
15 6 ) Note 1 10:30 - 16:30 stops throughout
12 6 ) 16:35 - 22:35
9 12 Notes 1 and 2 22:40 - 34:40
6 1 34:45 - 35:45
1 (O2) 35:45 - 36:45
3 1 36:50 - 37:50
1 (O2) 37:50 - 38:50
Surface 38:55
Notes:
1. Oxygen breathing in accordance with the instructions in paragraph c.
2. The attendant should breathe O2 for two hours before leaving 9m.
S-8 ORIGINAL
6. RN Treatment Table 65 - Long Air Recompression Therapy
a. Table 65 is provided for use when the patient has not responded to treatment on
Table 62, 63 or 64. IT IS ONLY TO BE USED WHEN A DIVING MEDICINE
SPECIALIST HAS BEEN CONSULTED and facilities exist for a prolonged treatment.
b. Table 65 is applied as follows:
(1) Rate of descent should be as fast as tolerable.
(2) Rate of ascent is 1 metre per minute between stops.
(3) Stops are carried out at EVERY METRE for the duration given in Column 3
of the table. The stop time begins when leaving the previous depth.
(4) If 32½/67½ oxy-nitrogen mixture is available this may be given at 50m. Pure
oxygen breathing may be introduced at 18m. Oxygen breathing periods should be
of 25 minutes duration, alternated with 5 minute breaks breathing chamber air.
Caution should be exercised in the repeated use of oxygen due to the risk of toxicity.
(5) The table may be entered at any depth up to 70 m.
Note. The attendant and patient need not breathe O2 during decompression which
can be completed on air.
S-9 ORIGINAL
RN Treatment Table 65 - Long Air Recompression Therapy
Gauge Depth Maximum Time at Depth Stops at Each Metre Maximum Elapsed Time (hours and mins)
(m) (Hours) (mins)
See Note From 70 m From 50 m From 18 m
(1) (2) (3) (4) (5) (6)

70 0.5 0:30
69-51 8 3:02
50 3 6:02 3:00
49-43 20 8:22 5:20
42 5 13:22 10:20
41-37 25 15:27 12:25
S-10
36 8 23:27 20:25
35-31 30 25:57 22:55
30 11 36:57 33:55
29-25 40 40:17 37:15
24 15 55:17 52:15
23-19 50 59:27 56:25
18 No Limit (a) a+59:27 a+56:25 a
17-13 75 a+65:42 a+62:40 a+6:15
12 No Limit (b) a+b+65:42 a+b+62:40 a+b+6:15
11-7 100 a+b+74:02 a+b+71:00 a+b+14:35
6 No Limit (c) a+b+c+74:02 a+b+c+71:00 a+b+c+14:35
5-1 200 a+b+c+90:42 a+b+c+85:40 a+b+c+31:15
ORIGINAL
Surface a+b+c+90:43 a+b+c+87:41 a+b+c+31:16
Note. The time at depth in column 2 need not be completed in full, but must be at least equal to the time in column 3 in the row below.
7. Additional Royal Navy Tables
a. Experience over the past 20 years has shown that O2 tables are superior in most
respects to air tables with the occasional exception of Table 64. The Tables given below
should therefore rarely be needed or used. However they are provided for use if O2 is
unavailable and on the advice of a Diving Medicine Specialist.
b. RN Treatment Tables 52, 53 and 55 - Air Recompression Therapy. These

Tables are applied with the following modifications:
(1) Rate of Descent. This varies between tables and is not included in the elapsed
time.
(2) Ascent. Ascent between stops is to take five minutes. This is not included in
the stoppage times, but has been allowed for in the elapsed times.
RN Treatment Table 52 - Air Recompression Therapy

(metres) Hours Mins (hours and mins)
50 30 00:00 - 00:30
42 12 00:35 - 00:47
36 12 00:52 - 01:04
30 12 01:09 - 01:21
24 12 01:26 - 01:38 5 minutes
18 30 01:43 - 01:23 between stops
15 30 02:18 - 02:48 throughout
12 30 02:53 - 03:23
9 2 03:28 - 05:28
6 2 05:33 - 07:33
3 2 07:38 - 09:38
Surface 09:43
S-11 ORIGINAL

50 30 00:00 - 00:30
42 12 00:35 - 00:47
36 12 00:52 - 01:04
30 12 01:09 - 01:21 5 minutes
24 12 00:26 - 01:38 between stops
18 30 01:43 - 02:13 throughout
15 30 02:18 - 02:48
12 30 02:53 - 03:23
9 12 03:28 - 15:28
6 2 15:33 - 17:33
3 2 17:38 - 19:38
Surface 19:43

50 2 00:00 - 02:00
42 30 02:05 - 02:35
36 30 02:40 - 03:10
30 30 03:15 - 03:45
24 30 03:50 - 04:20 5 minutes
18 6 04:25 - 10:25 between stops
15 6 10:30 - 16:30 throughout
12 6 16:35 - 22:35
9 12 22:40 - 34:40
6 4 34:45 - 38:45
3 4 38:50 - 42:50
Surface 42:55
S-12 ORIGINAL
c. RN Treatment Tables 71 to 73 - Modified Air-Recompression Therapy
(1) Tables 71 and 72 can be used instead of the air recompression therapies,
Tables 52, 53 and 55.
(2) Table 72 is applicable when multiple recompression of submarine survivors

is called for.
(3) Table 73 may be used in place of Table 55. Although somewhat more difficult
to accomplish, the smaller step size in the final 18 metres is preferred. The table
approximates the bleed rate of the final 18 metres of Tables 71 and 72. Medical
advice may recommend a period of O2 breathing during the shallower depths of this
table.
(4) These tables are applied with the following modifications for Tables 71 and
72.
(a) Maximum Pressure. Maximum pressure may be less than that quoted and
depends on the working pressure of the chamber available.
(b) Ascent. The ascent is to be conducted as follows:
i. It is to be a continuous bleed at the rates indicated.
ii. If the rate is slowed it is not to be compensated for by

subsequent acceleration.
(c) Oxygen. When using Tables 71 to 73, on the advice of a Diving Medical
Specialist, a 32½/67½ oxygen/nitrogen mixture may be administered at 50
metres with all the Tables, as can pure O2 at 18 metres or shallower. The
mixture or pure O2 will normally be breathed for 25 minute periods followed
by 5 minute intervals breathing chamber air. (See also Table 64). It should be
noted that where extra O2 has been administered in these long tables, care
should be exercised concerning pulmonary O2 toxicity. A calculation of total
units of pulmonary toxic dose of O2 should be used as a guideline.
S-13 ORIGINAL
RN Treatment Table 71 - Modified Air Recompression Therapy

(metres) Hours Mins (hours and mins) (metres/hour)
70 30 00:00 - 00:30
70 - 63 7 00:30 - 00:37 60
63 - 51 2 00:37 - 02:37 6
51 - 39 4 02:37 - 06:37 3
39 - 29 5 06:37 - 11:37 2
29 - 20 6 11:37 - 17:37 1.5
20 - 10 10 17:37 - 27:37 1
10 - 0 20 27:37 - 47:37 0.5
Surface 47:37

50 2 See Note 00:00 - 02:00
50 - 39 3 40 02:00 - 05:40 3
39 - 29 5 05:40 - 10:40 2
29 - 20 6 10:40 - 16:40 1.5
20 - 10 10 16:40 - 26:40 1
10 - 0 20 26:40 - 46:40 0.5
Surface 46:40
Note. The period of 2 hours can be reduced and decompression started earlier if the patient's
symptoms have cleared.
S-14 ORIGINAL

50 2 00:00 - 02:00
42 30 02:05 - 02:35
36 30 02:40 - 03:10
30 30 03:15 - 03:45
24 30 03:50 - 04:20
18 6 04:25 - 10:25
17 55 10:30 - 11:25
16 55 11:30 - 12:25 5 minutes
15 55 12:30 - 13:25 between stops
14 55 13:30 - 14:25 throughout
13 55 14:30 - 15:25
12 55 15:30 - 16:25
11 55 16:30 - 17:25
10 1 55 17:30 - 19:25
9 1 55 19:30 - 21:25
8 1 55 21:30 - 23:25
7 1 55 23:30 - 25:25
6 1 55 25:30 - 27:25
5 1 55 27:30 - 29:25
4 1 55 29:30 - 31:25
3 1 55 31:30 - 33:25
2 1 55 33:30 - 35:25
1 1 55 35:30 - 37:25
Surface 37:30
S-15 ORIGINAL
INTENTIONALLY BLANK
S-16 ORIGINAL
ANNEX T
UNITED STATES NAVY THERAPEUTIC RECOMPRESSION TABLES
1. US Navy Treatment Table 1A
a. This table is used when Oxygen is not available. It is used for the treatment of
symptoms using in-water decompression, Asymptomatic omitted decompression, Type
1 symptoms relieved at 66 feet or less and exceeded Sur ‘D’ surface intervals with no
symptoms.
(1) The patient breathes Air from the surface.
(2) The rate of descent must not exceed 25 feet per minute.
(3) The time of the treatment starts at leaving the surface.
(4) The attendant breathes chamber air throughout the entire treatment.
T-1 ORIGINAL
US Navy Treatment Table 1A
Gauge Depth Stops / Ascent Elapsed Time Rate of Ascent

(minutes) (hours & (feet / metres per
(feet) (metres)
100 30 30 (Air) 00:00 - 00:30

100 / 80 30 / 24 1 (Air) 00:30 - 00:31 1 minute between stops
80 24 12 (Air) 00:31 - 00:43
60 18 30 (Air) 00:44 - 01:14
50 15 30 (Air) 01:15 - 01:45
40 12 30 (Air) 01:46 - 02:16
30 9 60 (Air) 02:17 - 03:17
30 / 20 9/6 1 (Air) 03:17 - 03:18 1 minute between stops
20 6 60 (Air) 03:18 - 04:18
20 / 10 6/3 1 (Air) 04:18 - 04:19 1 minute between stops
10 3 120 (Air) 04:19 - 06:19
Surface 06:20
T-2 ORIGINAL
a. This table is used when oxygen is not available. It is used for the treatment of
asymptomatic omitted decompression and Type 1 symptoms relieved at deeper than 66
feet.
(3) The timing of the treatment starts at leaving the surface.
(1) Chamber Medical Equipment
(2) Meals and fluids for the duration of the treatment table
T-3 ORIGINAL

(minutes) (hours & mins) (feet/metres per minute)
(feet) (metres)
165 50 30 (Air) 00:00 - 00:30

165/140 50/42 1 (Air) 00:30 - 00:31 1 minute between stops
140 42 12 (Air) 00:31 - 00:43
120 36 12 (Air) 00:44 - 00:56
100 30 12 (Air) 00:57 - 01:09
80 24 12 (Air) 01:10 - 01:22
60 18 30 (Air) 01:23 - 01:53
50 15 30 (Air) 01:54 - 02:24
40 12 30 (Air) 02:25 - 02:55
30 9 120 (Air) 02:56 - 04:56
20 6 120 (Air) 04:57 - 06:57
10 3 240 (Air) 06:58 - 10:58
Surface 10:59
T-4 ORIGINAL
3. US Navy Treatment Table 3
a. This table is used when Oxygen is not available and to treat Type 11 or Arterial Gas
Embolism symptoms that are not relieved within 30 minutes at 165 feet / 50 metres.
(1) The patient breathes air from the surface.
c. Personnel requirements for this treatment table are:
1 x Qualified Chamber Attendant (preferably a Diving Medical Technician or

Diving Medical Officer).
T-5 ORIGINAL
US Navy Treatment Table 3

(feet) (metres)
165 50 30 (Air) 00:00 - 00:30

140 42 12 (Air) 00:31 - 00:43
120 36 12 (Air) 00:44 - 00:56
100 30 12 (Air) 00:57 - 01:09
80 24 12 (Air) 01:10 - 01:22
60 18 30 (Air) 01:23 - 01:53
50 15 30 (Air) 01:54 - 02:24
40 12 30 (Air) 02:25 - 02:55
30 9 720 (Air) 02:56 - 14:56
20 6 120 (Air) 14:57 - 16:57
10 3 120 (Air) 16:58 - 18:58
Surface 18:59
T-6 ORIGINAL
a. This table is used for the treatment of Arterial Gas Embolism and Type 11
symptoms at 165 feet where deterioration is noted after initial recompression to 60 feet.
Oxygen, if available, should be used whenever possible.
(3) The timing of the treatment starts from leaving the surface.
(4) If oxygen is available, the patient should begin breathing oxygen immediately
upon arrival at 60 feet.
(5) A minimum of 4 breathing periods of 25 minutes on oxygen and 5 minutes on

air are prescribed.
(6) The patient also breathes oxygen, if available, for at least 4 hours following the
prescribed oxygen breathing periods beginning no later than 2 hours before ascent
from 30 feet.
(7) Oxygen breathing periods may be divided up as convenient at 30 feet.
c. The chamber attendant breathes chamber air until 2 hours prior to leaving 30 feet
(9 metres), at this point the attendant will breathe 100% oxygen to the surface.
d. If oxygen is available, the chamber attendant must breathe oxygen for at least 4
hours at 30 feet. Oxygen breathing periods may be divided up as convenient at 30 feet.
e. Personnel requirements are as follows:
2 x Qualified Chamber Attendants
f. Other support requirements:
(1) Chamber Medical Equipment.
T-7 ORIGINAL

(feet) (metres)
165 50 30-120 (Air) See additional

165/140 50/42 1 (Air) instructions 1 minute between stops
140 42 30 (Air)
140/120 42/36 1 (Air) 1 minute between stops
120 36 30 (Air)
100 30 30 (Air)
80 24 30 (Air)
60 18 360 (Air)
50 15 360 (Air)
40 12 360 (Air)
30 9 720 (Air)
20 6 120 (Air)
10 3 120 (Air)
Surface
T-8 ORIGINAL
a. This table is used to treat Type 1 (Pain only) symptoms when a complete
neurological examination has been completed, all symptoms are relieved within 10
minutes and no other abnormalities are present. The table is used for the treatment of
omitted decompression of less than 30 minutes. It is also used for the treatment of
asymptomatic divers following exceeded surface interval from a Sur ‘D’ dive.
(1) The patient breathes Oxygen from the surface.
(3) The timing of the treatment starts on reaching 60 feet/18 metres.
c. If Oxygen breathing is interrupted at 60 feet/18 metres, change to a USN Treatment

Table 6 upon arrival at 30 feet/9 metres.
d. The attendant breathes chamber air at 60 feet/18 metres. The attendant should
breathe oxygen during the oxygen period at 30 feet/9 metres and during the ascent to the
surface.
e. Personnel requirements for this Treatment Table are as follows:
1 x Outside Tender / Chamber Operator
1 x Qualified Chamber Attendant.
f. Other support requirements:
(3) Built-in breathing system (BIBS) gas usage for the patient: 81 SCF
(4) Built-in breathing system (BIBS) gas usage: 29 SCF
T-9 ORIGINAL

(feet) (metres)
60 18 20 (Oxygen)) 00:00 - 00:20

60 18 5 (Air) 00:20 - 00:25
60 18 20 (Oxygen) 00:25 - 00:45
60 / 30 18 / 9 30 (Oxygen) 00:45 - 01:15 1 ft/min - 3 m/10 min
30 9 5 (Air) 01:15 - 01:20
30 9 20 (Oxygen) 01:20 - 01:40
30 9 5 (Air) 01:40 - 01:45
30 / 0 9/0 30 (Oxygen) 01:45 - 02:15 1 ft/min - 3 m/10 min
Surface 02:15
T-10 ORIGINAL
a. This table is used to treat Type 11 symptoms, arterial gas embolism responding to
treatment at 60 feet/18 metres and Type 1 symptoms not showing relief within 10
minutes after arriving at 60 feet/18 metres. May also be used for diver blow-up from
depths greater than 20 feet/6 metres when the diver is asymptomatic but more than 30
minutes of decompression has been omitted.
(1) The patient starts breathing Oxygen on the surface.
(3) The timing of the treatment starts on arrival at 60 feet/18 metres.
c. Treatment Table 6 may be extended for 2 additional oxygen breathing periods with
corresponding air breaks at 60 feet/18 metres and/or 30 feet/9 metres:
(1) Treatment Table 6 should be extended at 60 feet/18 metres if residual

symptoms, other than soreness around affected areas persists after the third oxygen
breathing period. If residual symptoms other than soreness persist at 30 feet/9
metres, Treatment Table 6 should be extended at 30 feet/9 metres.
d. Arterial Gas Embolism is also treated by initial compression to 60 feet/18 metres.

If symptoms stabilize within the first oxygen breathing period, treatment is continued
using Treatment Table 6. If during the first oxygen breathing period deterioration is
noted, compression to 165 feet should begin and Treatment Table 6A started. If a
Diving Medical Officer is on-scene or available for consultation, then treatment may
continue at 60 feet/18 metres.
e. The attendant breathes chamber air at 60 feet/18 metres. The attendant breathes
100% oxygen during the last 30 minutes at 30 feet/9 metres and during ascent to the
surface on an unmodified Treatment Table or where there has been only a single
extension at 30 or 60 feet. If there has been more than one extension the Oxygen
breathing is increased to 60 minutes. If the chamber attendant has had a hyperbaric
exposure in the past 12 hours an additional 60 minute oxygen period is taken at 30 feet/9
metres.
f. Personnel requirements for this Treatment Table are as follows:

T-11 ORIGINAL
g. Other support requirements:
Treatment Table 6 without extensions: 155 SCF Oxygen

metres: 257 SCF Oxygen
Treatment Table 6 without extensions: 52 SCF Oxygen

metres: 85 SCF Oxygen.

(minutes) (hours & (feet/metres per minute)
(feet) (metres)
60 18 20 (Oxygen)) 00:00 - 00:20

60 18 5 (Air) 00:20 - 00:25
60 18 20 (Oxygen) 00:25 - 00:45
60 18 5 (Air) 00:45 - 00:50
60 18 20 (Oxygen) 00:50 - 01:10
60 18 5 (Air) 01:10 - 01:15
60 / 30 18 / 9 30 (Oxygen) 01:15 - 01:45 1 ft/min - 3 m/10 min
30 9 15 (Air) 01:45 - 02:00
30 9 60 (Oxygen) 02:00 - 03:00
30 9 15 (Air) 03:00 - 03:15
30 9 60 (Oxygen) 03:15 - 04:15
30 / 0 9/0 30 (Oxygen) 04:15 - 04:45 1 ft/min - 3 m/10 min
Surface 04:45
T-12 ORIGINAL
a. This table is used to treat any worsening symptoms or Arterial Gas Embolism not
responding to initial compression to 60 feet/18 metres when complete relief of symptoms
is reached within 30 minutes at 165 feet/50 metres. This table may also be used for diver
blow-up from depths greater than 60 feet/18 metres when the diver has neurological
symptoms.
(1) The patient breathes air from the surface.
(4) Treatment Table 6A may be extended for 2 additional oxygen breathing

periods with corresponding air breaks at 60 feet/18 metres and/or 30 feet/9 metres.
(5) Treatment Table 6A should be extended at 60 feet/18 metres if residual

symptoms, other than soreness around affected areas persist at 30 feet/9 metres,
Treatment Table 6A should be extended at 30 feet/9 metres.
(6) If the chamber is equipped with a high O2 Nitrox mix it may be administered
at 165 feet and shallower as prescribed by a Diving Medical Officer.
(7) In patients who improve at 165 feet but do not obtain complete relief within
30 minutes, an additional 90 minutes should be spent at 165 feet and the patient
decompressed on Treatment Table 4. A Diving Medical Officer should be
consulted, if possible, before the shift is made.
c. The attendant breathes chamber air at 165 feet and during 60 feet/18 metres. The
attendant breathes 100% Oxygen during the last 60 minutes at 30 feet/9 metres and
during ascent to the surface at a minimum on all treatments. If the attendant has had a
hyperbaric exposure in the past 12 hours an additional 60 minute oxygen period is taken
at 30 feet/9 metres.
d. Personnel requirements for this Treatment Table are as follows:
1 x Qualified Chamber Attendant (Diving Medical Technician or Diving

Medical Officer if possible)
T-13 ORIGINAL
e. Other support requirements:
Treatment Table 6A without extensions: 155 SCF Oxygen
Treatment Table 6A with 2 extensions at 60 feet/18 metres and 30 feet/9

Treatment gas at 165 feet/50 metres: 52 SCF N2O2
Treatment Table 6A without extensions: 52 SCF Oxygen
Treatment Table 6A with 2 extensions at 60 feet/18 metres and 30 feet/9

T-14 ORIGINAL

(minutes) (hours & (feet/metres per minute)
(feet) (metres)
165 50 30 (Air) (N2O2) 00:00 - 00:30

165/60 50/18 4 (Air) (N2O2) 00:30 - 00:34 26 ft/min
60 18 20 (Oxygen) 00:34 - 00:54
60 18 5 (Air) 00:54 - 00:59
60 18 20 (Oxygen) 00:59 - 01:19
60 18 5 (Air) 01:19 - 01:24
60 18 20 (Oxygen) 01:24 - 01:44
60 18 5 (Air) 01:44 - 01:49
60/30 18/9 30 (Oxygen) 01:49 - 02:19 1 ft/min - 3 m/10 min
30 9 15 (Air) 02:19 - 02:34
30 9 60 (Oxygen) 02:34 - 03:34
30 9 15 (Air) 03:34 - 03:49
30 9 60 (Oxygen) 03:49 - 04:49
Surface 05:19
T-15 ORIGINAL
a. This table is an heroic measure used for the treatment of non-responding Arterial
Gas Embolism and life threatening decompression illness. Treatment Table 7 is an
extension at 60 feet/18 metres of USN Treatment Tables 6, 6A and 4.
(1) The patient breathes Oxygen upon arrival at 60 feet/18 metres.
(2) If the chamber is equipped with N2O2 it may be administered at the direction
of the Diving Medical Officer.
(3) Decompression begins with a 2 foot upward excursion from 60 to 58 feet.

Decompress with stops every 2 feet for times shown in the profile below. Ascent
between stops is 30 seconds. Stop begins with ascent from deeper to next shallower
stop. Stop at 4 feet/1 metre for 4 hours and then ascend directly to the surface in 1
minute.
(4) Consultation with a Diving Medical Officer shall begin as soon as possible
following committment to a Treatment Table 7.
c. The attendant breathes chamber air throughout the treatment.
d. Personnel requirements for this Treatment Table are as follows:
2 x Qualified Chamber Attendants (Diving Medical Officer if possible)
Provision should be made for additional personnel because of the length of the
treatment table.
e. Other support requirements are as follows:
(3) Built-in Breathing System (BIBS) gas usage for the patient will vary. The
patient begins breathing Oxygen immediately upon arrival at 60 feet / 18 metres.
Breathing periods of 25 minutes on Oxygen and 5 minutes ofn Air are prescribed.
Time at 60 feet/18 metres will be determined by patient response and/or the
recommendation of the Diving Medical Officer.
T-16 ORIGINAL
Gauge Depth Stops / Ascent Elapsed Rate of Ascent

(hours & minutes) Time
(feet) (metres)
60 18 12 hours minimum See

(No maximum) additional
60/40 18/12 Linear decompression instructions: 3 ft/hour - 2 ft/ 40
minutes
40/20 12/6 Linear decompression 2 ft/hour - 2 ft/60
minutes
20/4 6/1 Linear decompression
4 1 4 hours 4 ft/minute
4/0 1/0
Surface
T-17 ORIGINAL
a. This table is an adaptation of Royal Navy Treatment Table 65. It is used mainly for
deep blow-up when more than 60 minutes of decompression is missed. Treatment Table
8 can also be used when recompression deeper than 165 feet is required. Treatment
Table schedule is the same as Treatment Table 7 from 60 feet.
(1) The rate of descent should be as fast as the patient and chamber attendant can
tolerate.
(2) The patient begins breathing HE02/N2O2 or Air at treatment depth.
(4) If the chamber is equipped with HE02 or N2O2 it may be administered by

direction of a Diving Medical Officer.
(5) Decompression begins with a 2 or 3 foot up-ward excursion from treatment

depth. Decompress with stops every 2 feet for the times shown in the profile below.
Ascent between stops is 30 seconds. Stop begins with ascent from deeper to next
shallower stop. Stop at 4 feet for 4 hours and ascend directly to the surface in 1
minute.
(6) The patient begins breathing Oxygen upon arrival at 60 feet for 4 breathing
periods of 25 minutes on Oxygen and 5 minutes on Air.
(7) The time at depth will be determined by patient response and/or Diving
Medical Officer recommendation.
(8) Treatment Table 8 must not be started without consultation with a Diving
Medical Officer.
c. Personnel required to complete this Treatment Table are as follows:
2 x Qualified Chamber Attendants (Diving Medical Officer if possible)
Provisions for additional personnel must be made because of the length and severity
of treatment.
T-18 ORIGINAL
d. Other support requirements:
(3) Built-in Breathing System (BIBS) gas usage for the patient will vary
according to the time at depth which is determined by patient response and/or
Diving Medical Officer recommendation.
(4) Built-in Breathing System (BIBS) gas usage for the attendant: None.
Gauge Depth Stops / Ascent Elapsed Rate of Ascent

(hours & minutes) Time
(feet) (metres)
225 70 30 min (Maximum) See each 2ft / 5 minutes

165 50 3 hours (Maximum) additional each 2ft / 12 mins
140 42 5 hours (Maximum) instructions: each 2ft / 15 minutes
120 36 8 hours (Maximum) each 2ft / 20 mins
100 30 11 hours (Maximum) each 2ft / 25 minutes
80 24 15 hours (Maximum) each 2ft / 30 mins
60 18 12 hours minimum 3ft/hour - 2ft/40 mins
(No maximum)
60/40 18/12 Linear decompression 2ft/hour - 2ft/60 mins
40/20 12/6 Linear decompression 1ft/hour - 2ft/120 mins
20/4 6/1 Linear decompression
4 1 4 hours 4 ft / minute
4 ft / minute
Surface
T-19 ORIGINAL
INTENTIONALLY BLANK
T-20 ORIGINAL
ANNEX U
MEDICAL EQUIPMENT FOR RECOMPRESSION THERAPY
1. The following list of medical equipment is considered to be the minimum scale held for
use by a Diving Medical Officer/Non-specialist Medical Officer at a Recompression facility.
a. Diagnostic Equipment
(1) 1 Stethoscope
(2) 1 Reflex hammer
(3) 1 Torch
(4) 1 Mirror, headband (optional)
(5) 1 Otoscope
(6) 1 Clinical thermometer (non-mercury type for chamber use)
(7) 1 Sphygnomanometer, aneroid
(8) 1 Tuning Fork
b. Surgical Equipment and Instruments
(1) 1 Breathing apparatus
(2) 1 Airway Resuscitation
(3) 1 Suction apparatus (foot operated with catheters)
(4) 1 Intubation set, large
(5) 1 Mouth gag
(6) 1 Paracentesis needle
(7) 1 Tourniquet, non-pneumatic
(8) Assortment of syringes and needles
(9) Intracardiac Injection Set
U-1 ORIGINAL
(10) Set of surgical instruments, necessary for haemostatics, incision, sutures,

drainage and venotomy.
(11) Set for Catheterisation
(12) Scissors, bandage
(13) Several pairs of sterile gloves of different sizes
(14) 1 Intravenous administration set
c. Drugs and Dressing Material
(1) Anaesthetics
Local/regional anaesthetics
(2) Narcotics/Analgesics
(a) Morphine, injectable, Morphine substitutes
(b) Analgesics, oral
(3) Hypnotics, Sedatives, Tranquillisers
Diazepam.
(4) Drugs Affecting the Sympathetic Nervous System
(a) Atropine, injectable
(b) Vasoconstrictors, peripheral, injectable
(c) Cardiac drugs, injectable
(d) Sympatholytics
(5) Antibiotics and Chemotherapeutic Agents
(6) Blood Substitutes/Infusion Material, Sterile
(a) Plasma expanders (or national substitutes/equivalents)
(b) Electrolytes
U-2 ORIGINAL
(c) Dextrose Solution
(d) Infusion sets, sterile, disposable
(7) Biologicals
(a) Corticosteroids, injectable
(b) Heparin
(8) Diuretics
(9) Surgical Dressing Material
(a) Bandage, Gauze rollers
(b) First Aid Dressings
(c) Gauze, absorbent
(d) Cotton Wool, absorbent
(e) Adhesive plaster
(f) Sterile compresses
(g) Safety pins
(10) Disinfectants/Antiseptics
Cetrimide or Chlorhexidine
(11) Nursing Equipment
(a) 2 Blankets
(b) 1 Urinal
(c) 1 Bed-pan with cover
(d) 1 Covered pail for waster disposal
(e) 1 Feeding cup (invalid's cup)
U-3 ORIGINAL
INTENTIONALLY BLANK
U-4 ORIGINAL
ANNEX V
NATIONAL SPECIALISTS FOR DIVING ACCIDENT AUTOPSIES

NATION NAME AND ADDRESS TELEPHONE/FAX
BE See Note 1.
CA The Consultant in Diving Medicine Tel: (416) 635 2079.
Defence and Civil Institute of
Environmental Medicine (DCIEM)
North York
Ontario M3M 3B9
Canada
DA Institute of Forensic Medicine

University of Copenhagen
Frederik V’s vej 11 Tel: 35 32 61 80
DK 2100 Copenhagen O. (24 hour duty)
Institute of Forensic Medicine

University of Odense
Winslowparken 17
DK 5000 Odense C. Tel: 66 11 1586. Ext 4000
FR
GE Institute fuer Rechstmedizin Tele: 0451-500-2750
den Medizinischen
Prof. Dr. Manfred Oehmichen
23562 Luebeck, Kahlhorststrasse 31-35
Institut fuer Rechstmedizin Tele: 0404-717-2130

der Universitaet Hamburg
Prof. Dr. Pueschel
22529 Hamburg, Butenfeld 34
GR
IT
NL See Note 2.
NO Professor Sverre Mørk
Haukeland Hospital
Dept. of Pathology
N5021 Bergen Tel: (Switchboard)
Norway +44-55 29 80 60
PO
V-1 Original
NATION NAME AND ADDRESS TELEPHONE/FAX

SP INSTITUTO ANATOMICA FORENSE Tele: 968/ 521 753/860
PALACIO DE JUSTICA +34/ 968/ 521 753
Calle ANGEL BTUNA 21 Bajo
CARTAGENA 30205 ESPANA
See Note 2
TU
UK Dr Ian Calder Tel: + 44 223 277220
Surgeon Generals Dept Mobile: + 44 07850 327613
Room 9379
MOD Main Building
Whitehall
London
SW1A 2HB
US Armed Forces Medical Examiner Tele: +01 301-319-0000
(AFIP-CME)
Armed Forces Institute of Pathology
Washington, D.C. 20306-6000
Notes:
1. There are no Pathologists trained in the specialist techniques for autopsy on divers for
the following Nations. BE, NE, IT, FR.
2. The Spanish Navy does not have a Forensic Surgeon. When necessary autopsies are
conducted by a Specialist Surgeon from the ‘Instituto Anatomico Forense.
V-2 Original
ANNEX W
NATIONAL DEPTH - TIME LIMITS FOR CEREBRAL O2 TOXICITY
Oxygen Mixtures
Country
Depth Time Time
(metres) (minutes) Mix Depth (metres) (minutes)
SIVA:
BE 60%O2/40%N2 24m
40%O2/60%N2 42m
32.5%O2/67.5N2 54m
SIVA plus:
O2/He 70m
The Belgian Armed Forces use two types of diving equipment for Oxygen
Diving; OXYGERS and the S10. The depth and time limits are as
mentioned in the DCIEM diving tables.
CA Canadian Depth/Time limits for ‘Cerebral’, or Central Nervous System
Oxygen toxicity vary according to the environment. There are five
identifiable situations. Four involve resting divers where the allowable PO2
is higher. The fifth situation pertains to active working divers so the limit is
lower:
1. Recompression Chambers (RCC) Treatment Tables - patients may be

recompressed to 60 fsw (18 m) on 100% O2. The PO2 at 60 fsw is 2.8
atmospheres absolute (ATA). A maximum of four x 20 minute oxygen
periods may be used at 60 fsw, separated by 5 minute air breaks. At 30 fsw
(9 m) which is 1.9 ATA, a maximum of nine x 20 minute oxygen periods
may be used, separated by 5 minute air breaks.
2. RCC Surface Decompression Tables - For Normal Exposure to

Helium/Oxygen (He/O2) Surface Supplied Diving operations employing
decompression in an RCC, CA Tables have a maximum of 82 minutes at 40
fsw, with a five minute air break after every 30 minutes on oxygen.
3. In-water Decompression Tables - Oxygen is allowed for an in-water

decompression stop at 30 fsw. The maximum time for a Normal Exposure
He/O2 dive is 96 minutes, with air breaks every 30 minutes.
4. Rebreather Decompression - The Canadian Underwater MCM Apparatus

(CUMA) allows for RCC and in-water decompression. CA CUMA Tables
have a maximum of 77 minutes at 40 fsw in the RCC, with a five minute air
break after every 30 minutes on O2. For in-water decompression, the CA
Table has a maximum of 58 minutes at 30 fsw breathing pure O2. No in-
water air breaks are taken.
5. In-water Oxygen Diving - The normal active diving PO2 limit is 1.6
ATA. This applies to surface supplied and rebreather diving. Exposure to
this PO2 does not normally exceed two hours, in addition to oxygen
exposure during decompression.
W-1 ORIGINAL
Oxygen Mixtures
Country
Depth Time Time
DA Denmark follows the US Navy recommended depth/time limits for
oxygen diving.
FR 7 240 60%O2/40%N2 25
40%O2/60%N2 45
With special authorisation: 32.5%O2/67.5%N2 55
23%O2/37%He/40%N2 80
10 10 18%O2/41%He/41%N2 80
18 3
GE Germany follows the Royal Navy depth/time and mixture limits,
with the exception of the following notation for O2/N2 mixtures:
60%O2/40%N2-Mixture “B”
40%O2/60%N2-Mixture “C”
32.5%O2/67.5%N2 -Mixture “D”
GR
IT Italy follows the Royal Navy depth/time limits to 12 metres, but does not
include the 15 metre limits.
60%O2/40%N2 24
40%O2/60%N2 42
32.5%O2/67.5%N2 54
17.5%O2/82.5%He 110
12.5%O2/87.5%He 150
NL 7 200 B-Mixture - 24 -
9 60 C-Mixture - 42 -
11 25 D-Mixture - 54 -
12 15
14 10
NO
PO
SP A toxicity limit of 1.7 Bar must not be exceeded with the exception of the
following:
a. When carrying out surface decompression using oxygen.

b. When using treatment tables.
c. When conducting oxygen tolerance testing at 18 m.
d. When using PO-68 in exceptional conditions.
e. When using DC-55 with the 60% O2 mixture within authorised
limits.
f. When completing decompression stops with the 30% O2
mixture.
g. He/ O2 dives having O2 decompression stops.
W-2 ORIGINAL
Oxygen Mixtures
Country
Depth Time Time
TU
UK 7 240 60/40 O2/N2 - 24 -
8 240 40/60 O2/N2 - 42 -
9 80 32½/67½ O2/N2 - 54 -
11 25
12 15
15 10
US Single depth-time limits for oxygen are as follows
Depth Maximum Oxygen Time
20 fsw / 6 msw 240 minutes

W-3 ORIGINAL
INTENTIONALLY BLANK
W-4 ORIGINAL
ANNEX X
BIBLIOGRAPHY
1. Established Medical Texts
La Pression Barometric (Barometric Pressure) by Paul Bert (1878). The Hitchcock

translation has been reprinted for The Undersea Medical Society, Bethesda MD.
Caisson Sickness and the Physiology of Work in Compressed Air (1912) by Sir Leonard
Hill, Edward Arnold, London.
Respiration (1935) by J S Haldane and J G Priestley, Clarendon Press, Oxford.
Decompression Sickness (1951) edited by J F Fulton, Saunders, London.
Deep Diving and Submarine Operations (1955) by R H Davis, Siebe, Gorman and Co
Ltd, London.
Key Documents of the Biomedical Aspects of Deep Sea Diving (1983). A selection from
the world’s literature 1608-1982. Published by The Undersea Medical Society,
Bethesda, MD.
2. Current Medical Texts
Diving and Subaquatic Medicine, 3rd edn (1991) by C Edmonds, C Lowry and J
Pennefather, Butterworth, London ISBN 0-7506-0259-7.
Diving Medicine 3nd edn (1997) by A A Bove and J C Davis, Saunders, Philadelphia
etc. ISBN 0-7216-6056-8.
Case Histories of Diving and Hyperbaric Accidents (1988) edited by C L Waite for the
Undersea and Hyperbaric Medical Society, Bethesda MD.
Medical Examination of Sports Scuba Divers (1986) 2nd edn, edited by J C Davis, Best
Publishers., San Pedro, CAO.
3. First Aid
Diver’s Medical Manual (1991) by C Edmonds, R L Thomas and B J McKenzie, Diving

Medical Centre, St Leonards 2065, Australia (in press).
The DAN Emergency Handbook, revised 2nd edn (1989) by J Lippman and S Bugg, JL
Publications Carnegie, Victoria ISBN 0-9590306-1-1.
X-1 ORIGINAL
SCUBA Diving Safety (1978) by C W Ducker, World Publications. Mountain View, CA.
ISBN 0-89037-135-0.
Field Guide for the Diver Medic (1983) by C G Daugherty, distributed by the National
Association of Diver Medical Technicians, Houston, TX.
4. Specialist Texts
The Physiology and Medicine of Diving 3rd edition (1982) edited by P B Bennett and
D H Elliott, Bailliere Tindall and Cassell, London. ISBN 0-941-332-020. 4th edn in
press.
Hyperbaric Oxygen Therapy (1977) edited by J C Davis and T K Hunt, Undersea

Biomedical Society, Bethesda, MD. ISBN 0-930406-01-X.
Decompression Sickness: The Biophysical Basis of Prevention and Treatment by B A

Hills, Wiley, New York. ISBN 0-471-99-457-X.
Decompression-Recompression Sickness (1981) by A A Buhlmann, Springer-Verlag,

Berlin. ISBN 3-387-13308-9.
Stress and Performance in Diving (1987) by A J Bachrach and G H Egstrom. Best

Publishers, San Pedro. ISBN 0-941332-06-3.
Accidental Hypothermia (1977) by D Maclean and D Emslie-Smith, Blackwell, Oxford.

ISBN 0-632-00831-8.
The Nature and Treatment of Hypothermia (1983) edited by R S Pozos and L E

Wittmers, University of Minnesota Press, Minneapolis. ISBN 0-8166-1154-8.
Dangerous Marine Creatures (1989) by C Edmonds. Reid Books, Sydney. ISBN 0-

7301-02149.
Poisonous and Venomous Marine Animals of the World (1978) by B W Halstead,

Darwin Press, New Jersey.
A Medical Guide to Hazardous Marine Life (1987) P S Auerbach, Progressive Printing,

Jacksonville, FA.
Australian Animal Toxins (1983) by S K Sutherland, Oxford University Press, Oxford.

ISBN 0-19-55-4367X.
5. Journals
Undersea and Hyperbaric Medicine. Undersea and Hyperbaric Medical Society. ISSN
1066-2936.
X-2 ORIGINAL
Journal of Hyperbaric Medicine (first published as Hyperbaric Oxygen Review).

Undersea and Hyperbaric Medical Society. ISSN 00884-1225.
Pressure Undersea and Hyperbaric Medical Society. ISSN 0889-0242.
Aviation, Space and Environmental Medicine. Aerospace Medical Association ISSN

0095-6562.
EUBS (European Undersea Biomedical Society) Newsletter.
SPUMS Journal, South Pacific Underwater Medicine Society. ISSN 0813-1988.
6. Indexes
Underwater and Hyperbaric Medicine: Abstracts from the Literature. Undersea and
Hyperbaric Medical Society, ISSN 0886-3474.
A Bibliographic Sourcebook of Compressed Air Diving and Submarine Medicine. E C

Hoff and L J Greenbaum, 3 vols covering the period up to 1961, Dept of the Navy,
Washington.
An Annotated Bibliography of Diving and Submarine Medicine (1971) C W Shilling and

M F Wertz, covering the period 1962-69, Gordon and Breach, New York.
Underwater Medicine and Related Sciences: A guide to the literature Five volumes
covering the period 1967-79. C W Shilling et al. The Undersea Medical Society,
Bethesda, MD.
7. Conferences and Proceedings

The Undersea and Hyperbaric Medical Society, The European Undersea Biomedical
Society and the South Pacific Underwater Medicine Society host regular conferences. The
proceedings of each are published in full or abstract form. The Undersea and Hyperbaric Medical
Society also hosts workshops on specialised topics. Details of these may be obtained from the
respective societies.
8. Diving Manuals
US Navy NAVSEA 0994-LP-001-9010.
UK Miliary Diving Manual BR 2606.
NOAA (National Oceanographic and Atmospheric Administration), US Government

Printing Office, Washington USA.
BSAC (British Sub-Aqua CLub), London, UK.
X-3 ORIGINAL
9. Professional Societies
The Undersea and Hyperbaric Medical Society, 9650 Rockville Pike, Bethesda,
Maryland 20014. This is probably the most important organisation with world-wide
membership.
The European Undersea Baromedical Society, currently c/o National Hyperbaric Centre
Aberdeen, AB2 5FA, UK.
Divers Alert Network DAN Box 3823. Duke University Medical Center, Durham,
North Carolina 27710, USA Tel. (919) 684 8111. This organisation is based in the USA,
but has extensions in Europe and Japan. It collates data on diving accidents and analyses
this in regular reports. It also supplies emergency and routine information to divers,
diving physicians and others. It distributes diving safety texts and runs courses in diving
medicine. It also assists in insurance and emergency transport for divers.
Societe Francaise de Medecine Subaquatique et Hyperbare (France).
Societa Italiana di Medicina Subacquea Iperbarica (Italy).
Barologia (South Africa).
The South Pacific Underwater Medicine Society, membership mainly from South East
Asia, Australia, New Zealand. c/o The Australian College of Occupational Medicine,
PO Box 2090, St Kilda, West Victoria 3182, Australia.
X-4 ORIGINAL
LIST OF EFFECTIVE PAGES

(LEP)
Subject Page Status Protective Marking

Title Page i/ii Original Unclassified
NATO Letter of Promulgation iii/iv Original Unclassified
Reservations v/vi Original Unclassified
Title Page (NATO) vii/viii Original Unclassified
Record of Changes ix/x Original Unclassified
Table of Contents xi/xviii Original Unclassified
Preface xix/xx Original Unclassified
Chapter 1 Divider Original Unclassified

Chapter 1 1-1 to 1-10 Original Unclassified







LEP-1 ORIGINAL
LEP-2 ORIGINAL
LIST OF EFFECTIVE PAGES

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Annexes Divider Original Unclassified
Annex A A-1 to A-6 Original Unclassified
Annex B B-1 to B-2 Original Unclassified
Annex C C-1 to C-12 Original Unclassified
Annex D D-1 to D-6 Original Unclassified
Annex E E-1 to E-6 Original Unclassified
Annex F F-1 to F-4 Original Unclassified
Annex G G-1 to G-2 Original Unclassified
Annex H H-1 to H-16 Original Unclassified
Annex I I-1 to I-2 Original Unclassified
Annex J J-1 to J-6 Original Unclassified
Annex K K-1 to K-8 Original Unclassified
Annex L L-1 to L-2 Original Unclassified
Annex M M-1 to M-2 Original Unclassified
Annex N N-1 to N-2 Original Unclassified
Annex O O-1 to O-2 Original Unclassified
Annex P P-1 to P-2 Original Unclassified
Annex Q Q-1 to Q-2 Original Unclassified
Annex R R-1 to R-2 Original Unclassified
Annex S S-1 to S-16 Original Unclassified
Annex T T-1 to T-20 Original Unclassified
Annex U U-1 to U-4 Original Unclassified
Annex V V-1 to V-2 Original Unclassified
Annex W W-1 to W-4 Original Unclassified
Annex X X-1 to X-4 Original Unclassified
List of Effective Pages LEP-1 to LEP-4 Original Unclassified
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ADivP 02 (A) Med

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ADivP-2(A)/MDivP-2(A)

PUBLICATION NOTICE ROUTING

1. ADivP-2(A)/MDivP-2(A), MULTINATIONAL GUIDE TO DIVING _________________

Navy Warfare Library Custodian

Navy warfare library publications must be made readily

Note to Navy Warfare Library Custodian

IIa (Reverse Blank) ORIGINAL

NORTH ATLANTIC TREATY ORGANIZATION

MILITARY AGENCY FOR STANDARDIZATION (MAS)

NATO LETTER OF PROMULGATION

1. ADivP-2(A)/MDivP-2(A), MULTINATIONAL GUIDE TO DIVING OPERATIONS is

2. ADivP-2(A)/MDivP-2(A) is effective on receipt. It supercedes ADivP-2, which shall

3. This MM may be released to a non-NATO nation by a NATO nation or command, on a

a. Providing updates of the publication to receiving nations as required.

b. Informing MAS when distributing this MM to other nations.

CHAPTER RECORD OF RESERVATIONS BY NATIONS

NATION SPECIFIC RESERVATIONS

Change date Date Entered Effective Date By Whom Entered

CHAPTER 1 FITNESS TO DIVE

CHAPTER 2 BREATHING GAS DISORDERS

SECTION 1 - RESPIRATORY GASES

SECTION 2 - INERT GASES

SECTION 3 - CARBON MONOXIDE

SECTION 2 - EAR, NOSE AND THROAT BAROTRAUMA

ENT Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0302

Alternobaric Vertigo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0306

SECTION 3 - PULMONARY BAROTRAUMA

Pulmonary Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0311

SECTION 4 - BAROTRAUMA OF OTHER TISSUES

Face Mask Barotrauma of Descent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0317

CHAPTER 4 ACUTE DECOMPRESSION ILLNESS

CHAPTER 5 MANAGEMENT OF DIVING ACCIDENTS

SECTION 2 - MEDICAL SUPPORT OF DIVING OPERATIONS

Provision of Medical Support . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0502

SECTION 3 - FIRST AID MEASURES

Command and Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0510

SECTION 5 - INVESTIGATION OF DIVING ACCIDENTS

CHAPTER 6 THERAPEUTIC RECOMPRESSION

SECTION 2 - GUIDELINES FOR HYPERBARIC THERAPY

Hyperbaric Treatment Facilities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0605

SECTION 3 - TREATMENT SCHEDULES

Omitted Decompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0608

SECTION 4 - CARE IN THE RECOMPRESSION CHAMBER

Chamber Attendants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0615

SECTION 5 - MANAGEMENT AFTER INITIAL RECOMPRESSION

CHAPTER 7 THE LONG TERM HEALTH EFFECTS OF DIVING

CHAPTER 8 OPERATIONAL HAZARDS

SECTION 1 - THERMAL PROBLEMS

SECTION 2 - DIVING IN POLLUTED WATER

SECTION 3 - HAZARDOUS MARINE LIFE

SECTION 4 - OTHER HAZARDS

Near Drowning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0814

ANNEX A National Authorities Responsible for Initiating Treatment of Diving

ANNEX B Diving Casualty Signal Status Report Code.

ANNEX C NATO Diving Incident Medical Record Form.

ANNEX D Neurological Examination.

ANNEX E National Authorities for Guidance on the Hazards of Pollution.

ANNEX F Glossary of Medical Terminology.

ANNEX G Belgian Navy Therapeutic Recompression Tables.

ANNEX H Canadian Navy Therapeutic Recompression Tables.

ANNEX I Danish Navy Therapeutic Recompression Tables.

ANNEX J French Navy (Gers) Therapeutic Recompression Tables.

ANNEX K German Navy Therapeutic Recompression Tables.