Decompression Sickness Clinical Presentation
- Author: Stephen A Pulley, DO, MS, FACOEP; Chief Editor: Joe Alcock, MD, MS more...
When taking the history remember that symptoms or signs that appear during or following a dive are pressure-related until proven otherwise based on a diagnostic or therapeutic recompression via hyperbaric oxygen (HBO). Therefore, having the forethought to ask about pressure exposure aids in the diagnosis. Having a familiarity with diving aids the healthcare provider in raising concern for pressure-related injuries. However, some patients have symptoms temporally linked to diving that ultimately are determined to be nondiving-related issues. The take-home point is to consider decompression sickness (DCS) as a possibility but not to exclude others, especially if symptoms are atypical and the dive profile would not normally have been expected to cause a problem.
The following specifics about the dive should be elicited:
Location of the dive (eg, ocean, lake, river, quarry, or cave)
Timing of events during the dive and over the prior 72 hours (eg, time dives occurred, length of dives, surface intervals, safety stops, flying, and method of timing used [eg, watch with tables, dive computer])
Maximum dive depth and the rate of ascent
Approximate times spent at specific depths
Work of the patient during the dive (ie, consider currents, distance swam, water temperature, and primary activity [eg, wreck diving, artifact recovery, commercial work])
Gases and equipment used (ie, compressed air, rebreathing equipment, mixed gases, or none as in a free dive)
Problems encountered (eg, violation of no–decompression-limit dive tables, equipment, entanglement, dizziness, marine bites or stings)
Patient's physical condition before, during, and after the dive (eg, fatigue, hydration, drug or alcohol intake, fever, vertigo, nausea, overexertion, pulled muscles)
First aid delivered (ie, oxygen, positioning, medications, fluids)
Ask the patient about the following symptoms:
General symptoms of profound fatigue or heaviness, weakness, sweating, malaise, or anorexia
Musculoskeletal symptoms of joint pain, tendonitis, crepitus, back pain, or heaviness of extremities
Mental-status symptoms of confusion, unconsciousness, changes in personality
Eye and ear symptoms of scotomata (negative then positive), diplopia, tunnel vision, blurring, extraocular motor paresis, tinnitus, or partial hearing loss
Skin symptoms of pruritus or mottling
Pulmonary symptoms of dyspnea, nonproductive cough, or hemoptysis
Cardiac symptoms of inspiratory, substernal, or sharp or burning chest pain
Gastrointestinal symptoms of girdle abdominal pain, fecal incontinence, nausea, or vomiting
Genitourinary symptoms of urinary incontinence or urinary retention
Neurologic symptoms of paresthesia (general or over a joint), paresis, paralysis, migrainous headache, vertigo, dysarthria, or ataxia
Lymphatic symptoms of edema
Physical examination findings may include the following:
General - Fatigue, shock
Mental status - Disorientation, mental dullness
Eyes - Visual-field deficit, pupillary changes, air bubbles in the retinal vessels, or nystagmus
Mouth - Liebermeister sign (a sharply defined area of pallor in the tongue)
Pulmonary - Tachypnea, respiratory failure, respiratory distress, or hemoptysis
Cardiac - Tachycardia, hypotension, dysrhythmia, or Hamman sign (crackling sound heard over the heart during systole)
Gastrointestinal - Vomiting
Genitourinary - Urinary bladder distention, decreased urinary output
Neurologic - Hyperesthesia, hypoesthesia, paresis, anal sphincter weakness, loss of bulbocavernosus reflex, spotty motor or sensory deficits, focal seizure, generalized seizure, or ataxia
Musculoskeletal - Subjective joint pain without objective findings, or decreased range of motion because of muscle splinting of involved joint or tendon
Lymphatic - Lymphedema
Skin - Pruritus, mottling/marbling, hyperemia, violaceous color, cyanosis, or pallor
Pain, frequently musculoskeletal, occurs in 50-60% of decompression sickness (DCS) cases. Two specific maneuvers can aid the practitioner in diagnosing DCS.
Place a large blood pressure (BP) cuff over the area of pain and inflate it to 150-250 mm Hg. In patients with nitrogen bubbling in the joint or tendons, this increase can force some of the nitrogen back into solution, resulting in a temporary decrease in pain.
Milking the muscle toward the affected joint may increase pain by pushing more nitrogen bubbles toward the joint.
Differentiating between arterial gas embolization (AGE) and DCS
For AGE, (1) any type of dive can cause AGE, (2) the onset is immediate (< 10-120 min), and (3) neurologic deficits manifest in only the brain.
For DCS, (1) the dive must be of sufficient duration to saturate tissues, (2) the onset is latent (0-36 h), and (3) neurologic deficits manifest in spinal cord and brain.
Differentiating carbon monoxide poisoning
The symptoms of carbon monoxide poisoning (eg, dyspnea, headache, fatigue, dizziness, visual changes, unconsciousness) can mimic DCS or AGE. Sources for this carbon monoxide can include improper filling of tanks or boat engine exhausts, among others. Failure to recognize carbon monoxide poisoning is not a serious omission as long as the patient is recognized as having a diving injury. The hyperbaric treatment of DCS and AGE is also the treatment of choice for carbon monoxide poisoning. Also see Carbon Monoxide Toxicity and Carbon Monoxide Screening.
Predisposing causes of DCS include the following:
Inadequate decompression or surpassing no-decompression limits: This includes increased depth and duration of the dives and repeated dives.
Inadequate surface intervals (ie, failure to decrease accumulated nitrogen)
Failure to take recommended safety stops
Flying or going to higher altitude soon (12-24 h) after diving (increases the pressure gradient) 
A principal cause of DCS is rapid ascent. A major cause of rapid ascent may be panic. Anxiety traits can be identified during instruction.
Individual predisposing physiologic characteristics include the following:
Obesity: Obesity had been thought to be a risk factor because nitrogen is lipid soluble. However, studies have shown that neither body fat or body mass index (BMI) correlates with venous gas embolism and resultant DCS. [103, 104]
Age and poor aerobic conditioning: These do appear to influence risk of venous gas embolism and DCS. [103, 104]
High-fat meal 
Illness affecting lung or circulatory efficiency
Prior musculoskeletal injury (scar tissue decreases diffusion)
Predisposing environmental factors are as follows:
Cold water (vasoconstriction decreases nitrogen offloading)
Heavy work (vacuum effect in which tendon use causes gas pockets)
Rough sea conditions
Heated diving suits (leads to dehydration and increases nitrogen upload) [73, 106, 107]
Divers who have been chilled on decompression dives (or dives near the no-decompression limit) and take very hot baths or showers may stimulate bubble formation.
Improper use of decompression tables may increase the diver's risk. DCS may occur even if the decompression tables and no-decompression limits are strictly observed. The decompression tables and no-decompression limits list the maximum time allowed for a dive based on the maximum depth achieved (see the comment below about the US Navy tables). The limits take into consideration nitrogen saturation of lipid tissues. According to the Henry law, once nitrogen has saturated tissues, a standard ascent to the surface with decreasing ambient pressure can allow nitrogen to bubble out of solution. Once the no-decompression limit has been passed, one or more decompression stops are required during ascent to allow delayed diffusion of nitrogen out of the lipid tissues back into the blood. Nitrogen is then exhaled through the lungs. Current recommendations are for routine decompression stops, even if within the times of the tables. These tables also include calculations based on the surface interval between dives and residual nitrogen offloading during the time between dives.
The original tables have three problems. First, the tables are based on young, healthy, and fit US Navy volunteers. Since many civilian divers do not fit this profile, the tables have limitations. Second, the rapidly expanding use of dive computers takes into account the actual time spent at each depth, rather than just the maximum depth. This allows for more time under water and removes a built-in factor (the shorter maximum depth time) that helps keep divers in the conservative range. Third, the number of casual divers is increasing. This can lead to mistakes from lack of practice of the stringent routine/adherence to safety principles needed
See the discussion under Prevention for more information.
Residual paralysis, myocardial necrosis, and other ischemic injuries may occur without immediate recompression. These may occur even in adequately treated patients.
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