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

ABSTRACT

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

complication,

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 REPORTS

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 Section, Naval Underwater Medicine Centre, Navy Medical Service, Republic of Singapore Navy, AFPN 6060, 126 Tanah Merah Coast Road, Singapore 498822

Liow MHL, MBBS, DFD Medical Officer and Head

Kang WL, MMed, MRCSE, FAMS Chief Naval Medical Officer

Medical Doctrine and Training Branch

Chong SJ, MMed, MRCSE, MRCSI Head

Correspondence to: Dr Liow M H Lincoln Tel: (65) 8139 1045 Fax: (65) 6750 5610 Email: lenenkie@ gmail.com

INTRODUCTION

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

(TT62).

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.

DISCUSSION

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)

Currently,

besides

DCS,

hyperbaric

oxygen

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.

ACKNOWLEDGEMENTS

The authors would like to thank the Navy Medical

Service and the Naval Hyperbaric Centre for providing

the information regarding the three divers.

REFERENCES

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