.

DCS also known as Caisson disease or the bends, it is caused by

several different factors as sited in this article review. This sickness was
also classified into two according to its symptoms; the DCS type I or the
less severe and DCS type II the severe type of decompression sickness.
Risk factors must be observe to avoid this kind of ailment. Several research
has been conducted for better understanding of DCS and for developing
treatment for this sickness.

Christina L. Javier
B.S Biology
3rd year
 Subtopics

I. Introduction and History

II. Epidemiology

III. Classification

IV. Causes

V. Signs and symptoms

VI. Pre deposing factors

VII. Mechanism

VIII. Diagnosis

IX. Prevention

X. Treatment

XI. Prognosis

XII. Conclusion
 I. INTRODUCTION

This review article was made to discuss what decompression sickness is,
when and where this illness starts, how it occurs and who is likely to have this kind of
sickness. Different references were collected and extracted its important part.

What is decompression sickness?

According to Naval Safety Center, decompression sickness also known as

caisson disease or the bends is a disorder in which nitrogen dissolved in the blood and
tissues by high pressure forms bubbles as pressures decreases (Leo, 2013).
Decompression Sickness begins with the formation and the size of extravascular and the
intravascular bubbles were increased then the sum of the dissolved gas tension such
oxygen, carbon dioxide, nitrogen and helium then water vapours exceeds its local
absolute pressure (Vann, 2010). Sickness is cause by several different factors such as
dive time, dive depth, surfacing method, diving too long and diving too quickly. This illness
may affect variety of organs and can range from mild to severe. It can occurs in divers,
compressed air workers, aviators and astronauts.

Where and when decompression sickness begin?

Humans are engaged in free diving since 4500 BCE to search for their
foods. To survive, many of humans before are just depending on oceans, rivers, and seas
to obtain food and some materials such as sponges, pearls and corals. Because of this,
few of them are engaging in deep diving at 100 feet depth or much deeper (Nestor, 2014).

The table on the next page represents the significant events in the history
of decompression sickness and cerebral arterial gas embolism (Acott, 1999).
 Early history

Archaeological evidences in some part

4,500 – 3,200 BC of Pacific, Atlantic and Indian oceans,
shows an ancient free diving cultures.

Divers were used for strategic purpose.

1,194 – 1,184 BC Breathe hold divers involved in Trojan
War wherein they cut the anchor ropes
or boring holes in the hull to sabotage
the ships of their enemy.

Early swimmers/divers used an air filled

900 BC balloon to serve as a device for
buoyancy. This buoyancy device is from
the palace of King Assur -Nasir Pal.

Aristotle made a reed snorkel that allows

350 BC the divers to breathe while head is
underwater and has been used
throughout the history until now.
 According to the book I’ve read,
Alexander the Great was trained by
Aristotle and they claimed that Aristotle
requested Alexander the Great to drop
356 – 323 BC him into the sea in a glass barrel, so that
he can explore under water.
Alexander the Great made used of
diving bell called “Colimphax”. Aristotle
described this bell as an upside down
kettle filled with air.

Siege of Syracuse was made by the

215 – 212 BC Greek divers to construct underwater
defensive obstacle
.

168 BC Commercial diving starts in

Mediterranean harbors.

Renaissance diving equipment

1450 A diving device that is similar to horses’

nosebag by Mariano Taccola.
 Leonardo Da Vinci sketched several
1500 s underwater aids and inventions but none
of its designs were established.

Enlightenment Age

A new diving bell was designed by

Franz Kessler. This new equipment has
an internal framework where it serves
1616 as a diver seat and it contains series of
tiny ports. Kessler’s invention was
negatively buoyant so divers can walk
on a sea bed.

1620 First submarine was invented by

Cornelius Drebbel.

Pascal principle was published.

1649 Principle state that the pressure applied
is equal to the liquid will be transmitted.

Henshaw used Domicilium that is

1662 pressurized by a large pair of bellows to
treat medical conditions. This device is
 a chamber that is an air tight room
where in air was compressed.

Boyle’s Law was published. Robert

1670 Boyle conducted an experiment (e.g.
viper in a vacuum) showing the
decreases on ambient pressure may
lead to bubble formation in tissues.

1677 First used of Cadaques bell.

1680 Rebreathing diving set was made by

Boreli.

Dr. Denise Papin designed a diving bell

1689 that has a constant pressure to supply
fresh air.

Two cases of unknown illness was seen

by Giovani Battista Morgagni. Air in
1769 cerebral circulation was observed by
G.B Morgagni, and he assume that the
death of the two divers was because of
it.
 Laplace’ Law was published. Laplace
principle state that the size of the vessel
1784 is directly proportional to the tension
required to withstand a specific internal
fluid pressure.

1787 Charles Law was formulated but not

published.

Modern diving bell was designed by

1788 John Smeaton. This equipment was not
intended to be submerge.

The effects of long exposure to

1789 normobaric oxygen in pulmonary was
observed by Sequin and Lavoisier.

J. Smeaton modified the design diving

1790 bell to allow this equipment to
submerge.

1801 Dalton’s Gas Law was published.

 Henry’s Law was published by William
Henry. Wherein the amount of gas
dissolves in a specific type and volume
1803 of liquid with a constant temperature, is
directly proportional to the partial
pressure of that gas in equilibrium with
specific liquid.

Fatal effect of small amount of air in

1829 cerebral circulation was demonstrated
by Bichat.

Hyperbaric chamber was constructed

1834 by Junod. This chamber used
hyperbaric air to treat pulmonary
diseases.

Trigger invented the Caisson and he

1841 also noted the first case of
decompression sickness in two miners.

In the study of Pol and Wattelle, they

observed caisson workers of Lordes.
The used of recompression as a
1847 treatment to the decompression illness
 was also reported. They conclude that
18 year olds were not capable of having
this kind of illness than older workers.

Twenty five construction workers of

Tamar bridge have cases of
decompression sickness. This study
was conducted by Littleton wherein he
1855 conclude that decompression sickness
is due to the release of air occasioning
pressure to the brain, and he
recommended that the step-by-step
reduction and application of pressure
must done.

1857 Sudden release of intravascular gas

may cause death - (Hoppe-Seyler)

Bucquoy advised a slow

decompression and he was able to
1861 publish a report on the hazards of
working in compressed air.

Recompression as a “true specific”

1863 treatment to decompression sickness.
This thoughts was recommended by
Foley.
 The major advancement in diving
activity starts when Rouquayrol and
1865 Denayrouze was constructed their
demand valve and diving rig. This aims
to increase the diver’s mobility
underwater.

A report was published by Bauer

wherein twenty five caisson workers
1870 were paralyzed and four of them were
died. The rest of them were recovered
after 4 weeks
.

Thirty of three hundred fifty two

compressed air employees of St. Louis
Eades bridge project were injured and
1871 12 of them were died. Dr. Alphonse
Jaminet, a physician, described his own
experience in decompression sickness.
His description was first recorded.

Gal’s description on neurological

1872 decompression sickness in divers was
published.
 An ENT surgeon, Andrew Smith was
the physician in charge in the Brooklyn
bridge project and he was the first to
use the term “caisson disease”. The
1873 said project employed 600 workers, 119
cases of decompression were observe
by Dr. Smith. Fourteen of them were
died. The surgeon did not used
recompression as treatment for caisson
disease because he thought that it is a
heroic mode of treatment.

The acute oxygen toxicity or the Paul

Bret Effect was established by Paul Bret
and his “La Pression Barometique” was
published. He used his pet (dog) to
1878 describe the association between
obesity and an increased susceptibility
to decompression illness. His dog
survives pressure exposure while its
body is thin, but when it became obese
the dog died in same pressure
exposure.

Frog used in experiment to study

1900 decompression caused bubbles and to
explain the process of recompression.
 Haldane was appointed by British
1905 Admiralty to make a safe
decompression procedures.

The risk of permanency of disability of

decompression sickness and its
1912 increasing number of death was
emphasized by Hill.

1913 L. Brauer was the first to use the term

“arterial gas embolism”.

1915 The United States Navy (USN) Diving

table were first issued.

The RN and US Department of Mines

1919 used air decompression schedules that
results in high incidence of
decompression sickness.
 Hyperbaric air was used by Dr. O.
1921 Cunningham in treating diabetes and
several type of illness.

1924 Standard recompression procedures

was first issued by the USN.

1929 Davis decompression chamber was

created.

USN Submarine escape was

1930’s discovered that arterial gas embolism
and decompression sickness are not
the same disorder.

Gagnan and J. Cousteau invented the

1943 “aqua lung”. This device was evaluated
by Gagnan to use in gas powered cars.

Decompression illness in divers,

1955 caisson workers and aviators were
identical. This study was issued by
Haymaker et al.
 Decompression sickness was divided
into two categories; type I (mild pain)
1960 and type II (serious). This classification
was done by Golding et al. and it was
supported by USN.

USN printed a procedure for the

1985 analysis of the Central Nervous System
in its Diving Manual.

This compilation of significant event in the study of decompression sickness

was collected in several references. The evolution of the knowledge in this illness is
chronologically arranged in order to emphasize the progress in the investigation of DCS.

II. EPIDEMIOLOGY

The occurrence of Decompression sickness (DCS) is very rare and the total
number of worldwide active diver is unknown. According to South Pacific Underwater
Medicine Society (SPUMS) and the European Underwater and Baromedical Society in
their recently issued Diving and Hyperbaric Medicine, the estimated rate of having
decompression sickness is about 2.8 cases out of 10,000 dives. They noticed that the
incidence in cave divers is lower than the expected number of cases. Appropriate diving
practice and training must be consider for the prevention of DCS.
 In the research of Jersey SL et al. they explained a near-fatal case of
neurological decompression sickness happened throughout the combat mission. The
pilot suffered a severe brain injury during the flight and it was nearly fatal that leads to a
permanent mental disability. Decompression sickness in divers and aviators are not
comparable. DCS in divers are commonly damaged the spinal cord, while DCS in aviators
the brain is normally injured. General risk factors such as higher altitude, longer exposure,
greater in flight activity and lack of pre-oxygenation may increase the predisposition to
aviation DCS.
Every year, Divers Alert Network or DAN is publishing an annual diving
report. This report is a compilation of surveys and cases such as divers’ injuries and
deaths. Recently, DAN receives a report about an old man. This 58 year old diver was
diagnosed a cardiovascular disease and he decided to give up is diving career, but after
his valve replacement surgery he resumed to cave diving. He emerged from a dive to 56
mfw. As a result, he suffered symptoms similar to decompression sickness. The diver
was tried to cure in a hyperbaric chamber but, he died.

Another incidence of death was recorded in annual diving report of DAN

but, the cause of the death is still unexplained. This experienced diver and instructor is a
29 year old male that has a medical history of asthma. He completed his dive without any
symptoms however, he complained of nausea and prickly limbs. He also experienced 30
seconds of seizures, shortness of breath and dizziness, then he was admitted to local
emergency room and shifted to a hyperbaric chamber for treatment but, suddenly he died.
Severe decompression sickness was also recorded in 64 year old professional diver. The
cause of his death is DCS and AGE.

III. Classification
 Decompression sickness in diving occurs when a nitrogen gas
accumulates in body tissues in a positive pressure environment and after subsequent
reduction of the ambient pressure that escapes into the body fluids and will form
buubles (Vann et al. 2011).

a) Type I decompression sickness (less severe/the bends)

Type I DCS is the less severe type or mild form of the illness and it’s
commonly produces pain that usually occurs in the joint such as arms, legs, back, or
muscles. It is categorized by one or a mixture of musculoskeletal DCS or bends, skin
DCS or creeps and lymphatic DCS. This mild pain starts within 10 minutes after surfacing
though, other textbooks says it starts within 15 minutes. This tooth ache like of pain
usually in joint and tissue but sometimes, it is hard to locate where pain occurs.

At first, victim with DCS type I will be experiencing slightly pain however,
this mild pain gently become an intense pain. The shoulders, wrist, elbow, hand, knee
and ankle are the most frequent site of mild pains according to Dr. S. Pulley a clinical
professor of Department of Emergency Medicine.

b) Type II decompression sickness (more severe)

Type II DCS is the more severe type of the illness and may lead to
neurological problems, paraplegia, blindness and sometimes death. It is categorized
according to the symptoms; the spinal cord and peripheral nervous system DCS, inner
ear DCS wherein it is commonly occurred in helium – oxygen diving, and pulmonary DCS
that may develop due to the blockage of lung circulation. The common site affected by
this type is the spinal cord. Victims with DCS type II may experience shortness of breath
or chokes, chest pain, severe head ache, and altered mental status. Severe cases on this
type that are rare may result in shock and death.

IV. Cause of Decompression sickness

During decompression the gas bubbles form into tissues and when the
difference between the inert gas pressure in tissues and also the ambient pressure
exceeds tolerable limits. Different rates of blood supply to the organs and corresponding
times of exposure is multiply by the varying half valve. This two event may cause an
autochtonous gas bubbles in the various organs. Blow up of decompression needs a high
pressure exposure and this will result in an explosive decompression where in the gas
bubbles will simultaneously combines in the arterial blood and in the tissues. The
combination of arterial gas embolism and autochtonous gas bubbles that will cause DCS.
(Bulmann 1984).

Its symptomatology is recognized by the organ that is affected by the

capillary obstruction. Increase in volume of the gas bubbles is a relevant event in
developing of decompression sickness. Further, there are secondary factors such as
platelets aggregation, intravasal coagulation and also the perifocal edema with
hemorrhage and displacement of fluid located in extravasal space. (Bulmann 1984).

DCS may also cause by many factors. One of these, is the formation of
bubbles in blood or tissue throughout or after a decrease in environmental pressure.
Working in compressed air area can also lead to decompression sickness. According to
Naval Safety Center written by Ms. Kelsey Leo, dive time such as diving too long and
diving too quickly can trigger this ailment. One of the major reason of rapid ascent is
maybe due to panic. The controlled ascent must not more than 10 meters per minute to
avoid DCS. When surfacing too quickly, it can result to high pressure then nitrogen
bubbles formed in blood. After the formation of nitrogen bubbles from the blood will
expand and gather into joints, tissues and other parts of the body. Bubbles may block the
circulation of blood that will cause death.

Therefore, the sign and symptoms of DCS will immediately begin.

V. Sign and Symptoms

Signs of this condition are numbness of the limbs, mild pain in joint or
muscle, Symptoms of Decompression sickness are depending on what type of DCS is,
and generates symptoms related to the effect of bubble formation on blood The
symptoms usually begins within 6 hours. The first symptoms that possibly patient/victim
may feel are fatigue, headache, loss of appetite and undistinguishable feeling of ailment.

a) Type I symptoms (mild pain)

The symptoms of this condition are arrange according to their categories in the recent
page of this review. DCS type I symptoms are the following:

Musculoskeletal DCS
- localized deep pain and dull aches in joints and tissues

Skin DCS
- itching of the skin
- the feeling of insect crawling around the skin
- scar like lesion
 - cutis marmorata (a pink marble like mottling of the skin)
- purplish rush

Lymphatic DCS
- swelling of lymph nodes
- same symptoms occurs in Skin DCS
- some physician considered anorexia and excessive fatigue after a dive
(Finlayson and Saniei 2012)

b) Type II symptoms
This type of DCS is the severe type however, symptoms are not observable. Type I
symptoms possibly occur in this type. The following symptoms are listed below:

Spinal cord and peripheral nervous system DCS

- pain in abdominal, thoracic area and sometimes hips (visceral pain)
- joint pain between the ribs and sternum or ribs and spinal column
- radicular or girdle pain
- electric sensation on the skin
- decreased sensation to touch
- muscle weakness
- paralysis
- mental status changes that can result to personality changes and strange
behavior
- malfunction of urinary system
- coordination deficiency
- amnesia

Note: Any type of neurological symptom after surfacing is not normal, it

must be considered a Type II decompression sickness symptom.
 Inner ear DCS
- tinnitus
- vertigo
- hearing damage / partial deafness
- dizziness
- nausea
- vomiting

Pulmonary DCS
- breathing rate increase
- loss of consciousness
- total circulatory collapse
- death (if not immediately treated)

Further, other symptoms in decompression sickness in water experienced

by divers are similar to altitude decompression sickness of aviators except for the
symptoms of spinal cord involvement. The altitude DCS spinal cord indication is less
common and symptoms of brain involvement are more frequent in it than the DCS in
water. This information was sited in U.S NAVY Diving Manual - volume 5.

VI. Predisposing factors

The predisposing factors of DCS in the research of Pulley (2012) it

categorize according to the influence of the following; the influence of physiological trait
and environmental influence.
 Physiological trait influence includes the following:
- Age
 - Dehydration
- Circulatory deficiency
- Obesity / body fat
- Fatigue
- Poor of physical condition
- Previous musculoskeletal injury

 Environmental factors includes;

- Cold water
- Heated diving suits
- Rough sea condition
- Heavy work

On Clinical presentation of Medscape, they include diver error as one of the

factors that causes decompression sickness. Below are the lists of usual error of the diver
(Leo, 2013).
Several daily dives
Not following the dive tables
Breath holding
Travelling to high altitude within 24 hours after diving may lead to
decompression sickness

VII. Mechanism of Decompression Sickness

Dr. Simon Mitchell defined decompression illness as a disorder produced

by formation of bubbles in blood or in the body tissues. Dr. S. Mitchell discussed the
mechanism of decompression sickness in his article “The Mechanism of Decompression
Sickness”. He said to his article that bubbles have two potential sources, the first source
is the dissolved form of bubbles in tissues. This bubble formation is due to nitrogen
dissolves in blood stream during the dive. Gas bubbles are not the casual mechanism of
DCS but, it is an exacerbating factor (Madden and Laden, 2009). Increasing the pressure
while breathing the air may cause nitrogen molecules that came from the air you breathe
dissolves into blood. Then this nitrogen will enter the lung capillary bed and after passing
through the left heart, arteries will spread it to the tissues. The head and body in the
capillary beds, as the nitrogen departs the blood and spreads into tissues. Diving to deep,
the faster nitrogen is taken up from the air we breathe, and diving too long, the further
time it has to accumulate in the tissues (Mitchell, 2006).

Throughout the subsequent ascent, less nitrogen can remain dissolved in

the tissues and pressure reduces. When pressure is reduces, the nitrogen disperses out
of the tissues and into the venous blood in the capillary beds of the body. Then carried in
the veins back to the lungs for elimination process. This process happens fast enough to
disintegrate the nitrogen molecules without any formation of bubbles occur. Yet, in tissues
that cannot take free of their nitrogen very quickly, the dissolved nitrogen pressure will
surpass the ambient pressure at the same point during the ascent. This process is
referred to as super saturation, and the dissolved nitrogen molecules might not be able
to resist the physical stimulus in bubble formation (Mitchell, 2006).

Dr. Mitchel explained also the fast and slow tissues of these processes.
These two terms of tissues is used to describe the speed with which a particular tissue
takes up and nitrogen elimination. Faster type of tissue uptakes the nitrogen and
elimination of nitrogen is quick. Relative solubility in the tissue and blood is also faster.
Fast tissues are resistant to bubble formation as long as the ascent is made at the correct
rate. Spinal cord white matter is example of fast tissues. Usually short duration sport dives
are active in this type. If the bottom time was long and a little fast ascent, it can accumulate
a large nitrogen load sensibly quickly (Mitchell, 2006).
 Slower tissues like tendons are often not a problem after a short dive,
although it is deep, since they don’t have sufficient time to accumulate significant
quantities of the nitrogen. Nitrogen can build up over a long time once they become more
significant during long dives/repetitive dive (Mitchell, 2006).

Blood and tissues may both have bubble formation from the dissolved gas.
Bubbles forming in the blood prepare so in the capillaries on the venous side of the head
and body circulation. Nitrogen molecules from the tissues are trying to get back in the
lungs during ascent to be ready for elimination this thoughts has been explain earlier. As
they pass in the blood in the capillary beds of the head and body and appear susceptible
for the formation of bubbles there. These bubbles are then transported back to the right
side of the heart in the veins and next to the capillary bed of the lungs. The lung capillary
bed is serve as the first network of small blood vessels wherein bubbles are more likely
to trap. Certainly the lung appears to be a good filter for venous bubbles, and seems
capable to tolerate a significant proportion of its capillaries being obstructed by bubbles
without opposing effects.” Many of these bubbles might obtain their way into the arterial
circulation because of these “lung capillary filter where they can do more harm. The fact
that blood bypasses the lungs in the circulation of a foetus in which it is not filtered in this
way, and become one of the concerns over diving during pregnancy (Mitchell, 2006).

The Doppler bubble monitoring it is the mode of detection of these venous

nitrogen bubbles using a Doppler ultrasound. Dr. Mitchell suggest that bubble counts
made using this technique do not always associate with the risk of DCI because in the
lung capillary bed most of these venous bubbles will be filtered out so, it may not harmful.
In contrast, the real antagonist might be the bubbles forming in the tissues themselves,
and these bubbles cannot count by Doppler techniques (Mitchell, 2006).

Another potential source of bubbles in Decompression sickness or

sometimes they called it as a caisson disease is the lung over expansion due to the
introduction of air bubbles to the arterial circulation. And this time, it has nothing to solve
with dissolved nitrogen, even time and depth for that scenario. Actually, this crisis can
arise during ascent from depths as shallow as 1 – 2 meters. The most important rule in
scuba diving is “normal breathing and do not conduct a breath holding” this taught serve
as the guiding principle of open water trainees. Any air that trapped in the lungs during
breath holding, will cause expansion as pressure reduces. If there is enough over-
expansion of the lung it may break some of the small airways and the associated blood
vessels. This injury is signified to as pulmonary barotrauma and may result in the insertion
of air bubbles to the lung capillary circulation. These bubbles from lung capillaries are
then transported back to the left side of the heart from in which they are pumped out into
the arteries. The capillary beds of various tissues in the head and body is the first network
of small blood vessels where these bubbles are possible to trap. Some of the organs
theoretically influenced in this way, for instance, the brain are much less tolerant of
bubbles blocking blood vessels than are the lungs. Indeed, stroke-like symptoms is
caused by these bubbles arriving in the circulation of the brain and these arterial bubbles
are therefore considered a life threatening (Mitchell, 2006).

Dr. Mitchell also conclude that the bubbles forming from dissolved nitrogen
in the veins are less dangerous than bubbles introduced to the arteries by lung pulmonary
barotrauma. In this scenario, the lung filters venous bubbles while arterial bubbles act as
an armor that blocks blood vessels in vital structures such as the brain. Yet, the having a
persistent “patent foramen ovale” (PFO), it refers to a hole between the two upper
chambers of the heart which usually closes at birth, may let the venous nitrogen bubbles
to traverse into the arterial circulation, bypassing the lung capillary filter (Mitchell, 2006).
PFO size may increase when recompression treatment is applied to DCI patient (Torti et
al. 2004).
Therefore, the mechanism of Decompression illness is still difficult to
distinguish which of the two sources of bubbles is responsible for the symptoms in some
cases of DCI.
 VIII. Diagnosis

DCS diagnosis is made on the basis of signs after dive or altitude exposure
that may lead to DCS symptoms for diagnosis of the sickness (Francis et al. 2003). A
rapid decompression to altitude such as a military jet, hypobaric chamber and during flight
in a commercial air craft that accidently loss its pressure may increase the risk of having
Decompression sickness (Freiberger 2002; Vann et al. 2000). Specialist may recognize
the occurrence of decompression sickness by the nature of its symptoms (Leo 2013),
symptoms may occur after the dive or pressure exposure (U.S Diving Manual Vol. 5). It
is important to remember the first symptoms/signs appeared during/after the exposure on
pressure or dive until it was confirmed by diagnostic or therapeutic recompression. (Pulley
2012). Tomography CT or magnetic resonance imaging MRI are used to recognize
decompression sickness yet, this machines are not reliable though it shows brain or spinal
cord abnormalities. The recompression therapy applied first before the MRI or CT results
but in some scenario in which the diver’s condition is stable. X-rays are used to diagnose
the dysbaric osteonercrosis (late effect of decompression sickness involves the
destruction of bone tissues mostly in shoulder and hip) (Bove, 2015). In selected case
chest radio grapy which is prior to hyberbaric oxygen (HBO2) may be useful to excluded
pneumothorax that requires a tube thorax costomy placement before sufficiently enough
to detect anatomic correlated of DCS with in Neurological type (Gempp et al. 2008).

In the study of Pulley (2012), the list below must be consider in analyzing
the patient with decompression sickness.

Determine the dive location such as ocean, lake, river, quarry, and cave.
Knowing the timing of events throughout dive plus over the prior of 72 hours for
example distance of dive, time dives occurred, surface intervals, method of timing
used safety stops, and flying.
Rate of ascent and maximum depth of dive
 Approximate period of time spent at specific depths.
Patient’s work during the dive; consider also the currents, swam distance, primary
activity and the temperature of water.
Utilization of equipment like, rebreathing equipment and gases like compressed
air and mixed gas.
Physical condition of the patient before and after diving or exposed in compressed
air.
Application of first aid such as positioning of patient, oxygen, medications and
fluids.
The physician must ask if the patience experience the following:
- Symptoms of intense heaviness or fatigue, weakness, sweating and
anorexia.
- Musculoskeletal symptoms like tendonitis, joint pain etc…
- Mental status symptoms like confusion and changes in personality.
- Eye and ear symptoms like tunnel vision, partial hearing loss and etc…
- Skin symptoms like itching and mottling.
- Pulmonary symptoms like nonproductive cough
- Cardiac symptoms like burning of chest
- Abdominal pain or gastrointestinal symptoms
- Neurologic symptoms
- Lymphatic symptoms of edema

IX. Prevention

DCS can be prevented in many ways, thus US Navy dive Manual

recommend several information inhibiting the decompression sickness. Their
recommendations are written below.
 1. Selection of diver. Repetitive case of DCS in divers may lead to disqualification of
his/her duty.
2. Pre-dive. Hydration in warm water due to immersion in it and may cause diuresis.
During and after diving inert gas may damage the elimination. It is recommended
that maintaining the normal degree of hydration during or after diving.
3. Dive depth limits: Maximum depth for SCUBA diving is 130 ft., the surface
interval requires to be consider as “Clean” in the next dive is 20 hours 20 minutes
(group of Alpha) and 15 hours 50 minutes (group of Zulu).
4. During the dive. Thirty feet per minute is recommended.
5. Post-dive. Both aerobic and anaerobic exercise have an exercise limits. After
compressed gas dive, may increase the risk of having DCS. Prevention of
strenuous exercise during this 4 hours exercise is recommended except if it is
required by the operational necessity.

In compressed air the nitrogen concentration is 78% that limits bottom time.
It requires a longer surface intervals between dives and lessen the dives that is normally
performed (Culic et. al 2014). Strategies are made to reduce the risk of DCS and extends
their dive time. Nitrox can reduces nitrogen uptake in the tissues and also it can extend
the time. It can also lessen the bubble formation during decompression, however it is
important to follow the depth limits required to avoid oxygen toxicity (Culic et al. 2014).

X. Treatment

Recompression is the commonly treatment applied in patient having

decompression sickness. This treatment is indicate for all patient except for patients with
symptoms are limited to itching, skin molting and fatigue, deterioration must be observed
in this type of symptoms (Bove, 2015). The used of recompression with air as a specific
treatment for DCS was first discover in 1896 (Moir, 1896). The first aid for DCS cases are
fluid resuscitation air way protection, blood pressure maintenance and also the
administration of 100% of oxygen. This first aid may serve as the general supportive
measures in treating DCS. Though, the treatment for altitude induced DCS is done by
normobaric oxygen (Kimbrell 1996; Krause and Pilmanis, 2000).
Treatments in this kind of disease is according to what type of
decompression sickness the patient has, it is because type I DCS and Type II DCS are
not the same (U.S Navy Diving Manual vol. 5)
Treatment of DCS type 1 is done by diagnosis of patient if he/she is positive
or negative in DCS type 1. If the symptoms where not completely relief during the first 10
minutes at 60 feet, this action needs an immediate recompression and must be instituted
before undergoing neurological examination. Treatment for this type must consider the
descent rate of 20 ft/min, ascent rate must not exceed to 1ft/min. Do not compensate for
slower ascent rates rather compensate for faster by halting the ascent. The arrival begins
at 60 feet and it indicates the time where oxygen begins. In case of patient experiencing
CNS oxygen toxicity, the oxygen breathing must be interrupted and allow first to settle for
15 minutes after the reactions, and resume the schedule at point of interruption.

Procedures in the event of CNS oxygen toxicity are the following:

1. Removed from oxygen and allow to breathe in a chambered air.

2. Resume the oxygen breathing after 15 minutes when all the symptoms have
lessen.
3. If the symptom begins with a convulsion or if CNS oxygen toxicity symptoms were
redeveloped patient should be removed his mask, then after the completion of all
symptoms and have been diminished, decompress 10 feet at a rate of 1 fsw/min.
in case of convulsion, start the travel if the patient is completely relaxed and
maintain his normal breathing. At shallower depth where the point of interruption,
oxygen breathing must be continued.
 Treatment to DCS type II is done by the initial compression to 60 fsw.
Improvements of symptoms within the initial oxygen period, then treatment will be
administer. Severe symptoms occurs within the first 20 minutes at 60 fsw such as
paralysis, major weakness and memory loss. Treatment in this type is the same as the
treatment enumerated in type 1 DCS (U.S Navy Diving Manual vol. 5).

Aspirin is usually given in diving accident as antiplatelet activity for non-

bleeding patient (Pulley 2012). However, administration of aspirin may increase the
bleeding propensity that may lead to complication in health of the patient with DCS
(Westerweel et al. 2013).

One of the treatment for DCS is by using a Hyperbaric treatment but this
treatment may only be used when needed or it will depended on patient’s initial response.
Repetitive treatments are recommended until it achieves the clinical stability. The HBO2
treatment should be repetitively administered until improvement will occurs that is based
on documented symptoms and physical findings. If treatment results is not improving or
completely resolution of symptoms with two consecutive trials of this may indicate to the
end point of the treatment (Moon, 2014).

The most important therapeutic measures are voluminal substitution with

plasma expanders and the prescription of steroids and aggregation inhibitors. Yet, this
additional measures in therapeutic side can still cannot replace the recompression
therapy especially if patient with DCS is affecting the nervous system, inner ear and joints
(Bulmann, 1984).

XI. Prognosis
 DCS is treated by 100 % oxygen, then recompression treatment will
followed in a hyperbaric chamber, yet this may result in no long-term effects. Though
permanent long term injury of patient may possible to occur (Benneth et al. 2010). In
medical review of Zipser (2015) he said that people may develop bends depends with the
following factors:
= First is the prognosis with oxygen treatment is good.
= Postpone of treatment in hyperbaric oxygen, and this can cause a damage
that is irreversible, though studies revealed that victims can do well after days of
experiencing symptoms.
= Severity of symptoms may indicate by inability to urinate.
= Older patient can’t tolerate to this disease but young and healthy people
can tolerate DCS.

XII. Conclusion

To sum up, decompression sickness is a disorder produced by formation of

bubbles in blood or in the body tissues. This illness is caused by several different factors.
Divers, miners, astronauts and pilots are some of the person that is more likely to acquire
this sickness. Research advancement in studying the cause and effect of decompression
sickness were conducted by different researchers around the world. Has mention above,
significant events in the development of the study on DCS shows that the evolution from
passed year up to now is improving. Several treatments for this illness are now available.

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