Hyperbaric and Diving Medicine¶
Chapter 476 | Part 15: Disorders Associated with Environmental Exposures
KEY CLINICAL POINTS¶
- Hyperbaric oxygen therapy (HBOT) is indicated for 15 conditions, including air/gas embolism, carbon monoxide poisoning, and radiation tissue injury.
- Decompression sickness (DCS) is caused by inert gas bubble formation during rapid decompression, with management requiring recompression to 2.8 ATA.
- Barotrauma risks include middle-ear and inner-ear injuries, pulmonary barotrauma, and cerebral arterial gas embolism (CAGE).
- HBOT mechanisms include anti-inflammatory effects, enhanced angiogenesis, and oxygen delivery to hypoxic tissues.
- Chronic mountain sickness and high-altitude pulmonary hypertension are distinct conditions with different pathophysiology and treatments.
1. DEFINITION & OVERVIEW¶
Hyperbaric medicine involves treating disorders with whole-body exposure to pressures >101.3 kPa (1 atmosphere absolute). Diving medicine addresses risks from underwater environments, including decompression sickness and barotrauma.
Table 476-1: Current List of Indications for Hyperbaric Oxygen Therapy¶
| Indication |
|---|
| Air or gas embolism |
| Carbon monoxide poisoning |
| Clostridial myositis and myonecrosis |
| Crush injury, compartment syndrome |
| Decompression sickness |
| Arterial insufficiency |
| Severe anemia |
| Intracranial abscess |
| Necrotizing soft tissue infections |
| Osteomyelitis (refractory) |
| Delayed radiation injury |
| Skin grafts and flaps |
| Acute thermal burn injury |
1.1 Hyperbaric Medicine¶
HBOT uses pressurized oxygen (2–2.8 ATA) to enhance oxygen delivery, reduce edema, and stimulate angiogenesis. Indications include carbon monoxide poisoning, radiation injury, and nonhealing wounds.
1.2 Diving Medicine¶
Diving involves risks of barotrauma, decompression sickness (DCS), and gas embolism. Management includes pressure equalization techniques, recompression therapy, and oxygen administration.
2. EPIDEMIOLOGY¶
DCS incidence in recreational diving is ~1 in 5000–10,000 dives. Chronic mountain sickness affects high-altitude populations like Andean and Tibetan communities. Radiation tissue injury occurs in 5–10% of long-term cancer survivors.
Table 476-2: Manifestations of Decompression Sickness¶
| Organ System | Manifestations |
|---|---|
| Musculoskeletal | Limb pain, girdle pain |
| Neurologic | Cerebral confusion, spinal paralysis, vertigo |
| Pulmonary | Cough, dyspnea |
| Cardiovascular | Hemoconcentration, coagulopathy |
| Cutaneous | Rash, itch, cutaneous erythema |
2.1 Diving Risks¶
DCS risk increases with depth, duration, and rapid ascent. Commercial diving and saturation dives carry higher risks due to prolonged exposure.
2.2 High-Altitude Populations¶
Chronic mountain sickness (Monge’s disease) affects 16% of cirrhotic patients and 32% with hepatopulmonary syndrome. High-altitude pulmonary hypertension is common in Andean and Tibetan populations.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
HBOT mechanisms include oxygen toxicity reduction, anti-inflammatory effects, and enhanced angiogenesis. DCS results from inert gas bubble formation due to supersaturation during decompression.
3.1 Hyperbaric Oxygen Therapy¶
HBOT increases dissolved oxygen in plasma, reduces edema, and stimulates fibroblast activity. Mechanisms include ROS/RNS signaling, antioxidant defenses, and vascular endothelial growth factor (VEGF) upregulation.
3.2 Decompression Sickness¶
Inert gas (N I ) dissolves in tissues during compression. Rapid decompression causes supersaturation, leading to bubble formation in venous circulation. Bubbles can occlude microvasculature and trigger inflammatory cascades.
4. CLINICAL FEATURES¶
DCS presents with musculoskeletal pain, neurologic deficits, and pulmonary symptoms. HBOT indications include radiation necrosis, crush injuries, and carbon monoxide poisoning. Barotrauma manifests as middle-ear pain, inner-ear damage, or pulmonary complications.
4.1 Decompression Sickness¶
Symptoms appear 15–120 minutes post-decompression. Common manifestations include joint pain, neurological deficits, and pulmonary issues. Severe cases may present with paralysis or respiratory failure.
4.2 Barotrauma¶
Middle-ear barotrauma (MEBT) causes pain and tympanic membrane rupture. Inner-ear barotrauma (IEBT) leads to vertigo and sensorineural hearing loss. Pulmonary barotrauma risks include pneumothorax and gas embolism.
5. DIFFERENTIAL DIAGNOSIS¶
DCS must be differentiated from cerebral arterial gas embolism (CAGE), pulmonary embolism, and stroke. HBOT indications should be distinguished from other wound healing disorders and infections.
5.1 DCS vs. CAGE¶
Both conditions share neurologic symptoms but differ in onset (DCS within 60 minutes vs. CAGE immediately post-injury). DCS is managed with recompression, while CAGE requires immediate oxygenation.
5.2 HBOT Indications¶
HBOT should be considered for nonhealing wounds, radiation necrosis, and carbon monoxide poisoning. Differential diagnoses include diabetes-related ulcers and infections.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis of DCS relies on dive history, clinical symptoms, and exclusion of alternative causes. HBOT response is assessed via wound healing metrics and transcutaneous oxygen measurements.
6.1 DCS Diagnosis¶
Clinical evaluation of dive profile, symptom timing, and physical exam. No specific lab tests, but imaging may show pulmonary emboli or spinal cord abnormalities.
6.2 HBOT Response¶
Transcutaneous oxygen tension (PtcO I ) measurements guide HBOT eligibility. Wound healing metrics and patient-reported outcomes assess treatment efficacy.
7. MANAGEMENT & TREATMENT¶
DCS is treated with recompression to 2.8 ATA and 100% oxygen. HBOT protocols vary by indication, with 20–40 sessions at 2–2.4 ATA. Barotrauma management includes pressure equalization and oxygen therapy.
7.1 Decompression Sickness¶
Recompression using U.S. Navy Table 6 protocol (4 h 45 min). Adjuncts include IV fluids, oxygen, and anti-inflammatory agents. Severe cases require immediate recompression.
7.2 HBOT Protocols¶
Standard regimens: 20–40 sessions at 2–2.4 ATA, 1.5–2 h per session. Oxygen toxicity risk is mitigated by limiting inspired PO I <161 kPa (1.6 ATA).
7.3 Barotrauma¶
MEBT: Valsalva maneuvers, decongestants. IEBT: Otologic evaluation. Pulmonary barotrauma: Avoid breath-holding, manage asthma with bronchodilators.
8. PROGNOSIS & COMPLICATIONS¶
DCS prognosis depends on severity and treatment timing. HBOT improves healing in 70% of chronic wounds but carries risks of oxygen toxicity and cataract formation. Long-term complications include pulmonary hypertension and neurocognitive deficits.
8.1 DCS Outcomes¶
Early treatment reduces disability risk. Severe spinal cord involvement may result in permanent paralysis. Late complications include chronic pain and neurologic deficits.
8.2 HBOT Risks¶
Oxygen toxicity (seizures at >161 kPa), cataract formation, and transient visual changes. Prolonged use may increase oxidative stress and retinal damage.
9. SPECIAL CONSIDERATIONS¶
HBOT is contraindicated in untreated pneumothorax and recent bleomycin/mitomycin C use. Diving contraindications include asthma, ischemic heart disease, and recent surgery. Pregnancy requires careful monitoring due to oxygen toxicity risks.
9.1 Contraindications¶
Absolute contraindications: Untreated pneumothorax, recent bleomycin exposure. Relative contraindications: Seizure disorders, severe hypertension.
9.2 Diving Restrictions¶
Asthmatics and ischemic heart disease patients face increased barotrauma risk. Diving after recent surgery or trauma requires 24–48 h recovery.
10. KEY POINTS & CLINICAL PEARLS¶
HBOT is indicated for 15 conditions, with 20–40 sessions at 2–2.4 ATA. DCS management requires immediate recompression. Barotrauma prevention involves pressure equalization techniques. Transcutaneous oximetry guides HBOT eligibility. Oxygen toxicity risk is minimized by limiting inspired PO I <161 kPa.