Download - Decompression
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!