Rabu, 23 Mei 2012

A tale of three divers: recompression therapy for divers with severe Type II decompression sickness with neurological deficits

Case Report
Singapore Med J 2009; 50(5) : e173
A tale of three divers: recompression
therapy for divers with severe Type II
decompression sickness with
neurological deficits
Liow M H L, Chong S J, Kang W L
Decompression sickness (DCS) is manifested in
a myriad of symptoms, and can affect any part of
the body. It is attributed to the formation of inert
gas bubbles in the blood and tissues. Following a
diving incident, the pathogenesis of DCS is a result
of mechanical obstruction caused by the inert gas
bubbles and the body’s immunological response
to the bubbles. Neurological DCS may present
with unusual sensory/motor symptoms that may
lead to paralysis. This report describes three
divers who suffered severe neurological Type II
DCS and underwent recompression therapy at
the Naval Hyperbaric Centre in 2007.
Keywords : decompression sickness, diving
hy p e r b a r i c
ox yg e n a t i o n ,
neurological deficits, recompression therapy
Singapore Med J 2009; 50(5): e173-e175
providing recompression therapy (RCT) as part of the
provision of underwater and hyperbaric medicine to both
military and civilian divers for the past 30 years. We
report three recent cases of severe Type II neurological
DCS with good recovery post-RCT at the NHC.
Case 1
Our first case was a 45-year-old Chinese man, an
experienced commercial diver with no past history of
DCS. He completed a single uncomplicated 37 m dive (20
minutes underwater) and adhered to the decompression
schedule as stated in United States Navy dive tables.
During the dive ascent, he experienced some left ankle/
left wrist pain which he initially attributed to physical
exertion. His symptoms did not resolve on surfacing, and
he subsequently developed musculoskeletal symptoms of
bilateral upper limb pain, left wrist swelling/pain and left
ankle pain. He also had suffered from numbness in his
left wrist. He was first seen at a local hospital emergency
department and was referred to the NHC for further
assessment. An examination revealed that his left wrist
was erythematous and swollen. He also had paraesthesia
on his left C6/C7/C8 dermatomes and a limited range of
motion in his left wrist. Generalised tenderness over his
bilateral shoulders, elbows, left wrist and left ankle was
noted. A diagnosis of Type II DCS (musculoskeletal and
neurological) was made on the basis of the presence of
peripheral paraesthesia coupled with limb/joint pains. He
underwent three courses of uncomplicated RCT (Three
× Royal Navy Treatment Table 62 [TT62]) and had
complete symptom resolution following his third RCT.
Case 2
Our second case was a 32-year-old man, a commercial
diver who presented to a local hospital after a boat salvage
dive off Changi Naval Base. He descended to 40 m for
30 minutes and did not adhere to the stipulated diving
decompression schedule on ascent. He presented initially
with bilateral upper/lower limb pain and numbness. At the
Diving Medicine
Naval Underwater
Medicine Centre,
Navy Medical
Republic of
Singapore Navy,
AFPN 6060,
126 Tanah Merah
Coast Road,
Singapore 498822
Medical Officer
and Head
Kang WL, MMed,
Chief Naval Medical
Medical Doctrine
and Training
Chong SJ, MMed,
Correspondence to:
Dr Liow M H
Tel: (65) 8139 1045
Fax: (65) 6750 5610
Email: lenenkie@
Decompression sickness (DCS) is a condition that
manifests in a myriad of symptoms that may affect any
part of the human body. It is attributed to the formation
of inert gas bubbles in the blood and tissues. DCS is a
potentially life-threatening disease, often requiring
recompression hyperbaric therapy. DCS is further
categorised as Type I (limb and/or joint pains or skin
rash) and Type II (cardiopulmonary and/or neurological
system involvements). The incidence of Type II DCS
is about 62% of all dive-related illnesses.(1) Type II
neurological DCS may present with sensory/motor
symptoms or paraparesis. Another important condition
to recognise in the treatment of decompression sickness
is cerebral arterial gas embolism (CAGE). CAGE causes
severe neurological deficits/coma due to the obstruction
of cerebral blood flow from air emboli which lodge
distally in smaller arteries and arterioles of the brain.
This results in cerebral ischaemia, hypoxia and cerebral
oedema. The Naval Hyperbaric Centre (NHC) has been

Singapore Med J 2009; 50(5) : e174
emergency department, he was unable to ambulate and
was noted to have tetraparesis of power 3/5, affecting all
four limbs, associated with diminished sensation over the
C5–T1 and T10–S4 dermatomes. Anal tone was lax and
the patient was unable to void urine. He was given pain
relief at the hospital before he was transferred to NHC.
A diagnosis of Type II DCS (spinal and musculoskeletal)
was made and the patient underwent immediate RCT
A review post-recompression showed an immediate
improvement in the power of all four limbs from 3/5
to 4/5. He subsequently underwent a total of eight
uncomplicated RCTs (seven TT62, one TT61) with
concurrent intravenous steroids over a period of eight
days, with gradual recovery of symptoms. He regained
full motor power in his limbs (except in the left lower
limb) and was ambulating after four sessions of TT62.
However, he continued to have mild residual weakness of
his left lower limb and diminished sensation over left L5–
S4 dermatomes despite further RCT. Further investigation
at the hospital revealed a significantly prolapsed L4/L5
intervertebral disc on magnetic resonance imaging.
Case 3
Our third case was a 31-year-old Swedish man, a
recreational diver with a past history of gastroesophageal
reflux disease. He had just embarked on technical diving,
(technical dives may be defined as being either dives
to depths deeper than 40 m or dives in an overhead
environment with no direct access to the surface or
natural light. Such environments may include fresh and
saltwater caves and the interior of shipwrecks. In many
cases, technical dives also include planned decompression
carried out over a number of stages during a controlled
ascent to the surface at the end of the dive) and completed
six days of dives (total of 30 dives). On his seventh day,
he completed two Trimix (Trimix is a breathing gas,
consisting of oxygen, helium and nitrogen, and is often
used in deep commercial diving and during the deep phase
of dives carried out using technical diving techniques)
dives (67 m) of 25 minutes’ duration. He adhered to all the
decompression stops and surfaced with no complications.
He complained of rashes, dizziness and shortness of
breath, which started 20 minutes after surfacing. He also
vomited several times. In-water recompression at 72 feet
(22 m) was attempted, with marginal relief of symptoms,
before he was evacuated straight to the NHC.
Examination at the NHC revealed tetraparesis
with reduced motor power of all four limbs (power
4/5) with sensation unaffected. Deep tendon reflexes
were normal and plantars were downgoing bilaterally.
The patient complained of diplopia on left gaze with
no other significant cranial nerve deficits. He did not
exhibit any cerebellar signs or nystagmus. His vomitus
tested positive for blood (suspected Mallory-Weiss tear
from repeated vomiting). He was diagnosed with Type II
DCS (neurological) and underwent two sessions of RCT
(TT62) without complications. He regained full motor
power as well as resolution of left diplopia post-treatment.
He was subsequently referred to a local hospital for the
management of his suspected Mallory-Weiss tear.
The presentation of Type II neurological DCS is varied
and unpredictable. The patterns of weakness in a study
of divers with Type II DCS were as follows: paraparesis
27%; paraplegia 26%; lower extremity monoparesis
14%; lower extremity monoplegia 6%; quadriparesis
4%; hemiparesis 4%; hemiplegia 3%; and quadriplegia
2%.(2) In the three severe Type II cases reported above,
it is noted that they each presented with a unique set
of neurological deficits. Clinically, sensory and motor
neurological DCS usually present independently, and this
is attributed to sensory and motor deficit dissociation in
the spinal cord.(3) Hence, it is important to recognise the
signs and symptoms of decompression sickness and to
administer prompt treatment. The differential diagnosis
of decompression sickness includes cerebrovascular
accident and CAGE.
Emergency treatment of severe DCS on site includes
providing basic life support, horizontal positioning of the
victim, the administration of 100% normobaric oxygen,
followed by an early evacuation to the nearest hyperbaric
facility for definitive recompression treatment in order to
prevent serious neurological sequelae.(4,5) The subsequent
management of DCS should be guided by repeated
clinical neurological examination and assessment of
symptoms.(6) Ball reviewed 49 cases of spinal DCS from a
United States naval station and classified them according
to severity and time to recompression with oxygen.(4) A
delay in treatment was found in studies to worsen the
outcome for severely-injured divers. DCS occurs due to
the liberation of gas bubbles following an oversaturation
of tissues with inert gas. These bubbles can cause cerebral
blood flow obstruction leading to brain ischaemia. Several
other mechanisms have been postulated to explain the
pathophysiology behind Type II neurological DCS. They
include arterial bubble embolism in neural vasculature,
epidural venous obstruction leading to infarction and the
formation of autochthonous (formed in situ) bubbles.
RCT involves the inhalation of 100% oxygen at
pressures greater than atmospheric pressure. Inhalation

Singapore Med J 2009; 50(5) : e175
of pressurised oxygen will bring the arterial partial
pressure of oxygen to 1,500 mmHg at a pressure
equivalent to two absolute atmospheres. The delivery
of high levels of oxygen is important to counteract the
ischaemic and hypoxic effects of vascular obstruction.
This process will also create a pressure gradient which
forces the inert gases back into solution (Fick’s Law).
According to Boyle’s law, the volume of a gas is inversely
proportional to the amount of pressure exerted on the
gas. RCT reduces the size/surface area of the bubbles
to decrease the inflammatory effect at the bubble-blood
interface. Using standard treatment tables and adherence
to decompression stops, the inert gases are gradually
displaced out of the tissues, and eventually transported
to the lungs to be removed. Hyperbaric oxygen treatment
also helps to relieve hypoxia, improves microcirculation,
decreases cerebral oedema by vasoconstriction and
prevents secondary brain damage in Type II neurological
DCS. Currently, the value of adjunctive medication, such
as intravenous steroids, remains controversial.(7)
treatment is also approved by the Undersea and
Hyperbaric Medical Society (UHMS) as a recommended
therapy for conditions such as arterial gas embolism,
acute carbon monoxide poisoning, acute necrotising
infections, clostridial myonecrosis (gas gangrene),
crush injury/compartment syndrome and other traumatic
ischaemias, exceptional anaemia resulting from blood
loss, refractory osteomyelitis, radiation tissue damage
(osteoradionecrosis), compromised skin grafts/flaps
and thermal burns.(8) In conclusion, we have described
three cases of severe DCS that responded well to early
RCT. It is important to note that taking a complete diving
history and its correlation to the symptoms remains
key to establishing the clinical diagnosis of DCS. The
favourable response to subsequent RCT further confirms
the diagnosis and we need to emphasise that early RCT
improves the overall prognosis of DCS.
The authors would like to thank the Navy Medical
Service and the Naval Hyperbaric Centre for providing
the information regarding the three divers.
1. Andrić D, Petri NM, Stipancević H, Petri LV, Kovacević H. Change
   of occurrence of type 1 and type 2 decompression sickness of divers
   treated at the Croatian Naval Medical Institute in the period from
   1967 to 2000. Int Marit Health 2003; 54:127-34.
2. Barratt DM, Van Meter K. Decompression sickness in Miskito
   Indian lobster divers: review of 229 cases. Aviat Space Environ Med
   2004; 75:350-3.
3. Togawa S, Maruyama M, Yamami N, et al. Dissociation of
   neurological deficits in spinal decompression illness. Undersea
   Hyperb Med 2006; 33:265-70.
4. Ball R. Effect of severity, time to recompression with oxygen,
   and re-treatment on outcome in forty-nine cases of spinal cord
   decompression sickness. Undersea Hyperb Med 1993; 20:133-45.
5. Beuster W, van Laak U. [Severe decompression sickness in divers].
   Wien Med Wochenschr 1999; 151:111-6. German.
6. Schröder S, Lier H, Wiese S. [Diving accidents. Emergency
   treatment of serious diving accidents]. Anaesthesist 2004; 53:1093-
   102. German.
7. Grønning M, Risberg J, Skeidsvoll H, et al. Electroencephalography
   and magnetic resonance imaging in neurological decompression
   sickness. Undersea Hyperb Med 2005; 32:397-402.
8. Uses of HBO approved by the Undersea and Hyperbaric Medical
   Society. In: Jain KK. Textbook of Hyperbaric Medicine. 4th ed.
   Toronto: Hogrefe & Huber Publishers, 2004: 75.
di tayangkan ulang oleh dr.Erick Supondha (hyperbaric&Diving medicine Consultant) Jakarta Indonesia 021 99070050 ,http//:wwwindodivinghealth.com