Decompression sickness

Caribbean Emergency Care Conference 2011

J. van Leeuwen MD Surgeon

IntroductionClassification DS is classified by symptoms

The earliest descriptions of DS used the terms: "bends" for joint or skeletal pain

"chokes" for breathing problems

"staggers" for neurological problems

DS in a nutshell

IntroductionType I ('simple’)

for symptoms involving only the skin, musculoskeletal system, or lymphatic syste

Type II ('serious’)

for symptoms where other organs (such as the central nervous system) are involved

IntroductionType II DCS

is considered more serious and usually has worse outcomes

Signs and symptoms

Bubbles can form

anywhere in the body

Most

frequently observed in the shoulders, elbows, knees, and ankles. Joint pain ("the bends") accounts for about 60% to 70% of DS cases, with the shoulder being the most common site

Musculoskeletal (mostly joints)

Localized deep pain, ranging from mild to excruciating

Red rash in skin

Sometimes a dull ache, but rarely a sharp pain. Active and passive motion of the joint aggravates the pain

Itching, usually around the ears, face, neck, arms, and upper torso

Sensation of tiny insects crawling over the skin

Mottled or marbled skin usually around the shoulders, upper chest and abdomen, with itching

Swelling of the skin, accompanied by tiny scar-like skin depressions (pitting edema)

Cutaneous Type I DS

Neurologic (brain)Type II DS

Altered sensation, tingling or numbness paresthesia, increased sensitivity hyperesthesia

Confusion or memory loss (amnesia)

Visual abnormalities

Unexplained mood or behaviour changes

Seizures, unconsciousness

Neurologic (spinal cord)

Ascending weakness or paralysis in the legs

Girdling abdominal or chest pain

Urinary incontinence and fecal incontinence

Constitutional (whole body)

Headache

Unexplained fatigue

Generalised malaise, poorly localised aches

Audiovestibulair (inner ear)

Loss of balance

Dizziness, vertigo, nausea, vomiting

Hearing loss

Pulmonary Dry persistent cough

Burning chest pain under the sternum, aggravated by breathing

Shortness of breath

Frequency symptomsJoint pain 89%

Arm symptoms 70%

Leg symptoms 30%

Dizziness 5.3%

Paralysis 2.3%

Shortness of breath 1.6%

Extreme fatigue 1.3%

Collapse/unconsciousness 0.5%

Onset of DS

within 1 hour 42%

within 3 hours 60%

within 8 hours 83%

within 24 hours 98%

within 48 hours 100%

Although onset of DS can occur rapidly after a dive, in extreme cases even before a dive has been completed, in more than half of all cases symptoms do not begin to present until over an hour following the dive

What causes DS

A reduction in ambient pressure that results in the formation of bubbles of inert gases within tissues of the body

It may happen when leaving a high-pressure environment, ascending from depth, or ascending to altitude

Predisposing factors

Although the occurrence of DS is not easily predictable, many predisposing factors are known

environmental

individual

Environmental (to increase risk)

The magnitude of the pressure reduction ratio and duration 

Repetitive exposures – repetitive dives within a short period of time (a few hours)

Repetitive ascents to altitudes above 5,500 metres

The US Navy Dive Manual indicates that ascent rates greater than about 20 m/min (66 ft/min) when diving increase the chance of DS, while recreational dive tables require an ascent rate of 10 m/min (33 ft/min) with the last 6 m (20 ft) taking at least one minute

IndividualAge 

Previous injury – there is some indication that recent joint or limb injuries to developing decompression-related bubbles

Ambient temperature – exposure to very cold ambient temperatures may increase the risk of altitude DS

High body fat content is at greater risk of DS. This is due to nitrogen's five times greater solubility in fat than in water

Alcohol consumption and dehydration 

Maintaining proper hydration is recommended.

Patent foramen ovale 

Venous blood with microbubbles of inert gas bypass the lungs, where the bubbles would otherwise be filtered out by the lung capillary system, and return directly to arteries to the brain, spinal cord and heart

In the arterial system, bubbles (arterial gas embolism) are far more dangerous because they block circulation and cause infarction (tissue death, due to local loss of blood flow). In the brain, results in stroke, and in the spinal cord results in paralysis

MechanismDepressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body. These bubbles produce the symptoms of decompression sickness

Bubbles may form whenever the body experiences a reduction in pressure, but not all bubbles result in DS

On ascent from a dive, inert gas comes out of solution in a process called "outgassing" or "offgassing". Under normal conditions, most offgassing occurs by gas exchange in the lungs. If inert gas comes out of solution too quickly to allow outgassing in the lungs then bubbles may form in the blood

The formation of bubbles in the skin or joints results in milder symptoms, while large numbers of bubbles in the venous blood can cause lung damage

DiagnosisDS should be suspected if any of the symptoms associated with the condition occurs following a drop in pressure, in particular, within 24 hours of diving

In 1995, 95% of all cases reported to Divers Alert Network had shown symptoms within 24 hours

The diagnosis is confirmed if the symptoms are relieved by recompression

PreventionTo prevent ascend 10 metres (33 ft) per minute, and carry out a decompression schedule as necessary

This schedule requires the diver to ascend to a particular depth, and remain at that depth until sufficient gas has been eliminated from the body to allow further ascent

Dives that contain no decompression stops are called "no-stop dives", but divers usually schedule a short "safety stop" at 3 metres (10 ft), 4.6 metres (15 ft), or 6 metres (20 ft), depending on the training agency

Treatment100% oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a high-pressure chamber) can be provided

Mild cases of the "bends" and some skin symptoms may disappear during descent from high altitude

Neurological symptoms, pulmonary symptoms, and mottled or marbled skin lesions should be treated with hyperbaric oxygen therapy if seen within 10 to 14 days of development

TreatmentOxygen first aid has been used as an emergency treatment

If given within the first four hours of surfacing, it increases the success of recompression therapy as well as a decrease the number of recompression treatments required

TreatmentGive fluids, as this reduces dehydration

In the past, both the Trendelenburg position and the left lateral decubitus position have been beneficial where air emboli are suspected

PrognosisImmediate treatment with 100% oxygen, followed by recompression in a hyperbaric chamber, will in most cases result in no long term effects

Three-month follow-ups on diving accidents reported to DAN in 1987 showed 14.3% of the 268 divers surveyed still had residual signs and symptoms from Type II DS and 7% from Type I DS

EpidemiologyThe incidence of decompression sickness is rare, estimated at 2.8 cases per 10,000 dives, with the risk 2.6 times greater for males than females

DS affects approximately 1,000 U.S. scuba divers per year

From 1998 to 2002, they recorded 50,150 dives, from which 28 recompressions were required — 0.05%

Treatment principles

HBOT lies in its ability to drastically increase partial pressure of oxygen in the tissues of the body. The oxygen partial pressures achievable using HBOT are much higher than those achievable while breathing pure oxygen at normobaric conditions

Under normal atmospheric pressure, oxygen transport is limited by the oxygen binding capacity of hemoglobin in red blood cells and very little oxygen is transported by blood plasma.

Because the hemoglobin of the red blood cells is almost saturated with oxygen under atmospheric pressure, this transport cannot be used any further.

Oxygen transport by plasma, however is significantly increased using HBOT

IndicationsAir or gas embolism

Carbon monoxide poisoning

Clostridal myositis and myonecrosis (gas gangrene)

Crush injury, compartment syndrome, and other acute traumatic ischemias

Decompression sickness

Hyperbaric Oxygen Therapy

Involves intermittently breathing pure oxygen at greater than ambient pressure

Think of oxygen as a drug and the hyperbaric chamber as a dosing device

Elevating tissue oxygen tension is the primary effect

Hyperbaric Oxygen Therapy

Primary therapy for:Decompression sickness

Air embolism

Carbon monoxide poisoning

Adjunct therapy for:Surgical intervention

Antibiotics

Accepted IndicationsAir or gas embolism

Carbon monoxide poisoning

Clostridial myositis and myonecrosis

Crush injury, compartment syndrome, acute traumatic ischemias

Decompression sickness

Enhance healing of wounds

Necrotizing fasciitis

Chronic osteomyelitis

Radiation necrosis, brown recluse spider bites

Thermal burns

Basic MechanismsBoyle’s Law – pressure and volume inversely proportional under constant temperature

By increasing ambient pressure to 2 atm, decreases the volume by ½

Henry’s Law – at a given temperature, the amount of gas dissolved in solute is directly proportional to the partial pressure of the gas.

By increasing ambient pressure, more oxygen can be dissolved in the plasma

Mechanism of action

Angiogenesis in ischemic tissues

Bacteriostatic/bactericidal actions

Carboxyhemoglobin dissociation hastened

Clostridium perfringens alpha toxin synthesis inhibited

Vasoconstriction

Temporary inhibition of neutrophil Beta 2 integrin adhesion

Monoplace (1 person) or multiplace (2-14 patients) chamber

Pressures applied inside the chamber are usually 2-3 x atm pressure, plus may have an additional hydrostatic pressure equivalent of 1-2 atm.

Treatments last from 2-8 hours

ComplicationsMiddle ear barotrauma

Middle ear barotrauma is the most common adverse effect of HBO treatmentHemorrhage or serous effusion developsPrevention: teaching patient auto-insufflation technique or use of decongestantsIf auto-insufflation fails, tympanostomy tubes are placed.

Complications

Pulmonary barotraumaRare

Suspect if pulmonary or hemodynamic changes occur during or shortly after decompression

Place chest tube if pneumothorax develops

ComplicationsOxygen Toxicity

Can impair elasticity, vital capacity, and gas exchange.

CNS toxicity

Seizure Risk is higher in hypercapnic, acidotic, or septic patients

Eyes Progressive myopia has been reported in patients undergoing repetitive daily therapy

CO Poisoning

Leading cause of injury and death by poisoning in the world

Affinity of CO for hemoglobin (forming carboxyhemoglobin) is 200 times that of oxygen

Clostridial Myonecrosis(gas gangrene)

Mortality rates of 11-52%

Diffused oxygen which raises capillary p02 levels at the wound site, stimulates capillary budding and granulation of new, healthy tissue

Necrotizing Fasciitis andFournier’s gangrene

Addition of HBO to surgical and antibiotic treatment reduced mortality versus surgery and antibiotics alone

May suppress growth of anaerobic organisms

May increase leukocyte function and suppress bacterial growth

Crush injuryReduces infection and wound dehiscence and improves healing

Improves oxygenation to hypoperfused tissue

Causes arterial hyperoxia causing vasoconstriction and decreased edema formation.

Also, intermittent pressure stimulates circulation and reduces edema

Early use of HBO may reduce compartment pressures enough to avoid fasciotomy

Prevention

Don’t push your limits and do all required decompression stops

Keep physically fit and within a healthy weight range

Don't exercise within 12 hours of diving

Don't ascend to altitude or fly immediately after diving

Make sure you're adequately hydrated before every dive

Don't drink alcohol before or after diving and never dive when hungover

Get checked out by a doctor to find out if you have a PFO

MASHA DANKI!