SCUBA Diving Injuries: DCS and AGE

By admin On Oct 30, 2023

Ovid: 5-Minute Sports Medicine Consult, The

Paul B. McKee

Basics

Description

Decompression sickness (DCS): Formation of nitrogen gas bubbles in the blood and body tissues caused by inadequate elimination of the nitrogen gas. As a diver descends and breathes air, the tissues can become saturated with nitrogen due to the increased pressure. As the diver ascends, the excess nitrogen must be eliminated. If the nitrogen is not eliminated, it can become trapped in the tissue, thus resulting in the symptoms of DCS. The term DCS is used in a general sense to denote all forms of injury due to bubble formation occurring as a consequence of a sudden reduction in ambient pressure.
- Type I DCS is characterized by musculoskeletal pain (vague, intense pain), dermal complications (pruritus, rash, blebs), and constitutional symptoms (fatigue, malaise, anorexia). Extreme fatigue may be a sign or forerunner of a more severe decompression illness.
- Type II DCS is characterized by neurologic symptoms (paresthesias, weakness, poor sphincter control, paralysis), cardiorespiratory symptoms (dyspnea, nonproductive cough, hemoptysis), and vestibular symptoms (tinnitus, dizziness, hearing loss) (1)[C].
Arterial gas embolism (AGE): A CNS injury (usually cerebral) or systemic injury (usually cardiac) as a consequence of pulmonary barotrauma. Barotrauma refers to injury produced by mechanical forces caused by a change of pressure in a gas-filled space (the lungs). Air released from an overpressurized alveolus enters the pulmonary circulation and causes occlusion of the organ's blood supply. Venous gas emboli reach the arterial circulation paradoxically via a patent foramen ovale or a right to left shunt (2,3,4)[C]. AGE can be confused with type II DCS.
It is sometimes difficult to tell the difference between type II DCS and AGE, because both can cause similar symptoms. The time of onset of symptoms may be more informative. The time course of air embolism symptoms from lung overexpansion is usually short (immediately or within minutes after surfacing), whereas decompression sickness usually develops later after a dive (hours to days).
Some clinicians advocate grouping type II DCS and AGE into 1 clinical entity called decompression illness (DCI). The 2 are treated the same (recompression).
Synonym(s): The bends; Air embolism; Caisson disease; Decompression illness

Epidemiology

DCI is estimated to occur in ∼4 in 100,000 sport divers per year (Divers Alert Network statistics).
Predominant age is young adulthood (20–29 yrs).
Predominant sex is male; however, there is no evidence to suggest that men are more susceptible (5)[C].

Risk Factors

Rapid ascent from SCUBA diving
Flying too soon after SCUBA diving
Inexperienced divers (6)[C]
Multiple/repetitive dives
Tunnel work (Caisson disease)
Inadequate pressurization/denitrogenation when flying
Prolonged dive at depth of >33 ft
Taking a warm shower after diving
Obesity (nitrogen is lipid-soluble)
Fatigue
Dehydration
Poor physical conditioning
Acute illnesses (pulmonary or GI)
Breath-hold diving
Holding breath while ascending
Patent foramen ovale
Intracardiac septal defects
COPD (increases risk for pulmonary barotrauma)
Strenuous physical activity while diving (commercial diving)
Physical activity before or after diving
Panicking while diving
Diving in cold water
Rough sea conditions

General Prevention

Follow the dive profile.
Only dive nondecompression dives or perform adequate safety stops.
Avoid flying or traveling to higher altitudes for 24 hr after diving.
Maintain good hydration.
Avoid holding breath while diving.

Diagnosis

History

The history should include the dive profile, rate of ascent, time of onset of symptoms, and changes in the type or intensity of symptoms.
An independent account from a dive buddy or dive instructor is often useful, especially if the patient's consciousness is impaired.
Obtaining information from a dive computer (if the patient was using one) is also very useful.
Note any history of previous dives in the past few days, any exposure to altitude (which can precipitate decompression sickness), and any previous health problems.

Physical Exam

Gas deposition in joints and soft tissues may manifest as a “pain only” syndrome (limb bends), or simple pruritus (cutis marmorata), blebs (or skin bends), fatigue, or vague soreness.
Gas deposition in the cerebral circulation causes strokelike symptoms (cerebral bends).
Gas deposition in the spinal cord (or autochthonous bubbles) can cause transverse paresis (spinal cord bends or spinal decompression sickness).
Development of bubbles in the inner ear can cause deafness or equilibrium dysfunction, nausea, vomiting, and nystagmus (inner ear bends or “staggers”).
Excessive venous bubbles develop and release vasoactive substances causing pulmonary irritation and bronchoconstriction. Symptoms may include chest pain, dyspnea, and cough (lung bends or “chokes”).
Other symptoms include headache, ataxia, delirium, coma, convulsions, confusion, patchy numbness, coughing paroxysms (Behnken's sign), arrhythmias, cardiac arrest, tachy- or bradycardia, vertigo, aphasia, blindness, and rapidly ascending paraplegia.
Skin lesions: Painful, pruritic, red rash on torso; burning blebs on skin; lymphedema. Also palpate skin for SC emphysema.
Joints: Erythema and edema on periarticular surfaces. There is usually pain with movement.
Neurologic: Various manifestations of a cerebrovascular accident, including numbness, weakness, aphasia, paresthesias, paralysis, paraplegia, confusion, personality changes, etc.
Cardiac: Arrhythmias, tachy- or bradycardia, findings of congestive heart failure
Pulmonary: Decreased breath sounds if pneumothorax present

Diagnostic Tests & Interpretation

Imaging

Chest radiography to look for pneumothorax, mediastinal emphysema, heart enlargement
CT scan of the brain to look for cerebral abnormalities
US to look for gas bubbles in joints, tendons, bursae, muscles
Diagnostic repressurization (place the patient in a hyperbaric chamber, descend to 60 ft or 2.8 ATA; symptoms should improve within 15 min if DCS is truly the correct diagnosis)

Differential Diagnosis

Traumatic injury to extremity
Cerebrovascular accident
Acute myocardial infarction
Musculoskeletal strains
Urticaria/anaphylaxis
Malingering
Contaminated breathing gas (carbon monoxide)
Near drowning and hypoxic brain injury
Seafood toxin poisoning (ciguatera, puffer fish, paralytic shellfish, sea snake, cone shell)
Migraine
Guillain-Barre syndrome
Multiple sclerosis
Transverse myelitis
Spinal cord compression (from disk protrusion, hematoma, or tumor)

P.525

Middle ear or sinus barotrauma with cranial nerve compression
Inner ear barotrauma
Unrelated seizure (hypoglycemia, epilepsy) and postictal state from unrelated seizure
Cold water immersion pulmonary edema

Treatment

DCS type I: Mild cases of DCS type I may be treated by breathing 100% oxygen via a nonrebreather mask. Close observation is necessary, and if conservative measures fail to alleviate symptoms, strong consideration for hyperbaric oxygen therapy (HBOT) should be considered.
DCS type II: Definitive treatment of DCS type II and unresolved DCS type I after conservative treatment is recompression in a hyperbaric oxygen chamber. HBOT involves compression of the nitrogen gas bubbles that caused the symptoms of DCS while the oxygen administered replaces the nitrogen in the blood. The nitrogen gas then defuses slowly out of the affected tissues over time, thereby alleviating the symptoms. Treatment is administered based on the U.S. Navy treatment protocols arranged in a table format. Tables 5 and 6 are the most commonly used methods and take ∼3–4.5 hr, respectively, to complete. Treatment should continue until symptoms completely resolve. Patients often experience significant improvement of symptoms as the trapped nitrogen gas bubbles shrink, which generally occurs soon after the patient arrives to depth of 60 ft (2.8 ATA).
AGE: Initial treatment is the same as any emergency: Airway, breathing, and circulation. Once ABCs have been accounted for, 100% oxygen via a nonrebreather mask is indicated. Position the patient in left lateral decubitus position and begin HBOT treatment using U.S. Navy Table 6 (100% oxygen at 2.8 ATA). Table 6 may be preceded by a 30-min period of (40–50% oxygen at 6 ATA) for those whose symptoms don't improve significantly at the traditional 2.8 ATA. Less oxygen is used in order to prevent oxygen toxicity. Treatment is continued until symptoms resolve or plateau.

Pre-Hospital

Administer 100% oxygen by nonrebreather mask.
Give IV fluids; isotonic solutions are preferred. Glucose solutions may worsen neurologic outcome in patients with CNS conditions and should be avoided unless treating known hypoglycemia.
Trendelenburg position or left lateral decubitus (Durant's maneuver) if CNS is affected in DCS type II or AGE.
Give diazepam 5–15 mg IV for inner ear bends (symptomatic relief from vertigo, nausea, and vomiting).
Transport (via ground preferably) to nearest hyperbaric facility. Aircraft that can be pressurized to sea level also can be used for transport.

Additional Treatment

General Measures

Deep venous thrombosis and pulmonary embolism prophylaxis are recommended for patients with severe CNS bends with leg weakness.
Do not give NSAIDs to patients with pain-only symptoms of DCS until hyperbaric treatment has been instituted.
The cause of a fever in a patient with DCS should be determined and vigorously treated (outcome is significantly worsened by hyperthermia).

Additional Therapies

Call the Diver's Alert Network [DAN; (919) 684–4326] for referral to nearest hyperbaric facility for recompression.
DAN Latin American Hotline [DAN; 1–919–684–9111]
Patients may be sent home if only cutaneous symptoms are present and the patient responded to conservative therapy administered in the emergency department.
Rehabilitation of the injured diver is more successful than that of the patient with a traumatic spinal cord injury or stroke. The patient may continue to improve slowly after recompression treatments for up to 2 yrs.

Ongoing Care

Follow-Up Recommendations

Referral to the nearest hyperbaric chamber facility should be done as soon as possible.
Follow-up should be made with a physician knowledgeable in dive medicine.

Prognosis

The prognosis is excellent for early symptomatic presentation, referral, and treatment.
The duration and severity of symptoms prior to presentation and treatment negatively affects outcome.

Complications

Oxygen toxicity
Myopia due to oxygen toxicity to the lens (older patients) generally resolves in about 6 wks.
Residual neurologic deficits in CNS bends (46–75%) despite treatment
Residual paralysis may occur if recompression is not carried out immediately.
Residual paralysis may occur even in adequately treated patients if initial presentation is severe.

References

1. Newton HB. Neurologic complications of scuba diving. Am Fam Phys. 2001;63:2211–2218, 2225–2226.

2. Gerriets, T, Tetzlaff, K, Hutzelmann A, et al. Association between right-to-left shunts and brain lesions in sport divers. Aviation Space Environ Med. 2003;74:1058.

3. Gerriets T, Tetzlaff K, Liceni T, et al. Arteriovenous bubbles following cold water sport dives: relation to right-to-left shunting. Neurology. 2000;55:1741.

4. Schwerzmann M, Seller C, Lipp E, et al. Relation between directly detected patent foramen ovale and ischemic brain lesions in sport divers. Ann Intern Med. 2001;134:21.

5. St Leger, Dowse M, Bryson P, et al. Comparative data from 2250 male and female sports divers: diving patterns and decompression sickness. Aviation Space Environ Med. 2002;73:743.

6. Klingmann C, et al. Decompression illness reported in a survey of 429 recreational divers. Aviation Space Environ Med. 2008;79:123.

Additional Reading

USN Dive Manual Revision 6

Codes

ICD9

993.3 Caisson disease
958.0 Air embolism as an early complication of trauma

Clinical Pearls

DCS should be at the top of the differential diagnosis in any patient with recent history of diving and clinical symptoms.
HBOT is the definitive treatment for any patient diagnosed with DCS.
Proper diagnosis of DCS is supported if the patient's symptoms improve within a relatively short period of time after recompression.
Table 6 is the preferred method of treatment.
- In general, 24 hr is recommended as a safe duration to flying after any dive.
- After suffering from decompression sickness, those diagnosed with type I DCS characterized by musculoskeletal pain, dermal complications, and/or constitutional symptoms, 2 wks is recommended before returning to diving. For those diagnosed with type II DCS characterized by only minor neurologic symptoms, 6 wks is recommended before returning to diving. For those diagnosed with type II DCS characterized by severe neurologic symptoms, diving is no longer recommended.
- After treatment of DCS or AGE, exposure to altitude can precipitate symptoms. After reaching a clinical plateau with treatment, an additional period of 3–4 days at sea-level pressure is usually sufficient. In-flight oxygen supplementation may prevent a treated patient from developing reoccurring symptoms.