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Hyperbaric and Diving Medicine

Chapter 476 | Part 15: Disorders Associated with Environmental Exposures · Parts 15-16 – Genetics, Genomics & Precision Medicine · Chapter 476

Key Clinical Points

  1. HBOT is defined by the UHMS as a medical procedure requiring a physician's prescription where the patient's entire body is placed within a hard-sided hyperbaric chamber breathing 100% oxygen at pressures typically between 2.0 and 2.8 ATA.
  2. The UHMS recognizes 15 accepted indications for HBOT, including air/gas embolism, carbon monoxide poisoning, clostridial myositis, decompression sickness, and delayed radiation injury.
  3. HBOT reduces the half-life of carboxyhemoglobin (COHb) from ≈5.5 hours at sea level to ≈21 minutes at 2.0 ATA; it is indicated for moderate to severe poisoning, metabolic acidosis, or loss of consciousness.
  4. Transcutaneous oxygen tension (PtcO_2) mapping is used to select patients for HBOT: PtcO_2 > 40 mmHg on air suggests the wound is not hypoxic (consider alternatives), while PtcO_2 < 35 mmHg is a contraindication.
  5. Untreated pneumothorax is an absolute contraindication to HBOT due to risk of expansion and tension; patients must have a patent chest drain in place prior to compression.
  6. Common side effects include barotrauma (middle ear pain in ≈30% of cases) and myopic shift (up to 75% of patients after 30 treatments at 2 ATA, typically resolving in 6–12 weeks).
  7. Chronic mountain sickness (Monge's disease) is characterized by excessive erythrocytosis and pulmonary hypertension; high-altitude pulmonary hypertension (HAPE) is characterized by pulmonary hypertension without erythrocytosis.
  8. Acetazolamide is the drug of choice for altitude sickness but is contraindicated in patients with preexisting metabolic acidosis or chronic kidney disease with GFR <10 mL/min (dose adjusted if GFR <50 mL/min).
  9. Barotrauma is the most common complication of HBOT; prevention involves slower compression and training in Eustachian tube insufflation.
  10. HBOT is generally well tolerated, but risks include oxygen toxicity (seizures), barotrauma, and potential acceleration of cataract maturation.

DEFINITION & OVERVIEW

• Hyperbaric Medicine: Treatment of certain health disorders using whole-body exposure to pressures >101.3 kPa (1 atmosphere or 760 mmHg). • HBOT Definition: A medical procedure requiring a physician's prescription and oversight in which patients must have their entire body placed within a hard-sided hyperbaric chamber that meets ASME-PVHO-1 and NFPA 99 code and standards, at a pressure of not less than 2.0 atmospheres absolute (ATA) while breathing physician prescribed medical grade oxygen for an amount of time that is typically between 90–120 minutes per treatment. • Chamber Types: ◦ Monoplace: Designed for a single patient; the chamber atmosphere may be pressurized with oxygen or air (if the patient uses a delivery system). ◦ Multiplace: Designed for multiple patients and attendants; the chamber is pressurized with air while patients breathe 100% oxygen via a mask, head tent, or endotracheal tube.

EPIDEMIOLOGY

• High-Altitude Populations: ◦ Primary locations: South American Andes, Tibetan Plateau, and parts of Ethiopia. ◦ Specific populations: Han Chinese in Tibet; residents of Colorado. • Carbon Monoxide (CO) Poisoning Statistics: ◦ US Emergency Department visits: >50,000 per year. ◦ US Deaths: ≈2000 per year. ◦ Source distribution: 50% of nonlethal exposures are self-harm; others include defective heaters, house fires, industrial exposure, and motor vehicles. • Wound Epidemiology: ◦ Prevalence: 1% of population in industrialized countries. ◦ Economic impact: U.S. $25 billion per year.

ETIOLOGY & PATHOPHYSIOLOGY

• HBOT Mechanisms (Figure 3): ◦ Physical/Chemical: Hydrostatic compression, enhanced inert gas diffusion gradients (between bubble, tissue, and lungs), high arterial pO_2 (at 2.8 ATA, pO_2 can reach ≈270 kPa / ≈2025 mmHg; dissolved oxygen in plasma reaches ≈60 mL/L). ◦ Physiological: Bubble volume reduction, enhanced O_2 diffusion, osmotic effect, generation of ROS and RNS. ◦ Biological: Restoration of tissue normoxia, edema reduction, hyperoxic vasoconstriction, anti-inflammatory effects (e.g., β 1 integrins), enhanced angiogenesis/fibroblast activity, stem cell mobilization. • Carbon Monoxide Pathophysiology: ◦ Binding: Binds to hemoglobin with affinity >200 times that of oxygen; reduces oxygen-carrying capacity and shifts the oxyhemoglobin dissociation curve to the left. ◦ Additional effects: Acts as an anesthetic agent, disrupts cellular oxidative processes, binds to heme proteins (cytochrome a/a3), causes brain lipid peroxidation. ◦ Target Organs: Brain and heart are most sensitive due to high blood flow and low tolerance for hypoxia. • Radiation Tissue Injury Pathophysiology: ◦ Primary mechanism: Initial exposure leads to fibrosis and obliterative endarteritis → hypovascular hypoxic state. ◦ Alternative model: Overexpression of inflammatory cytokines (triggered by oxidative stress/mitochondrial dysfunction) promotes fibrosis; tissue hypoxia is a secondary provocation.

CLINICAL FEATURES

• Carbon Monoxide Poisoning: ◦ Minor exposure: Asymptomatic or vague symptoms (headache, lethargy, nausea). ◦ High dose: Poor concentration/cognition, short-term memory loss, confusion, seizures, loss of consciousness. ◦ Long-term sequelae: Motor disturbances, peripheral neuropathy, hearing loss, vestibular abnormalities, dementia, psychosis. ◦ Risk factors for poor outcome: Age >35 years, exposure >24 h, acidosis, loss of consciousness. • High-Altitude Illness: ◦ Chronic Mountain Sickness (Monge's): Excessive erythrocytosis, moderate to severe pulmonary hypertension → cor pulmonale. ◦ High-Altitude Pulmonary Hypertension (HAPE): Pulmonary hypertension (without erythrocytosis) → heart failure. • HBOT Adverse Effects: ◦ Barotrauma: Middle ear pain in ≈30% of patients; usually minor but requires slower compression and training. ◦ Myopic Shift: Alteration in refractive index due to lens damage; affects up to 75% of patients after 30 treatments at 2 ATA (usually resolves in 6–12 weeks). ◦ Pulmonary Barotrauma: Rare; associated with gas trapping lesions like bullae. ◦ Cataract maturation: Occasionally accelerated by HBOT.

DIFFERENTIAL DIAGNOSIS

• Wound Healing Failure: ◦ Must distinguish between: Microvascular disease, tissue edema (responsive to HBOT) vs. critical arterial stenosis, infection, or need for surgical reconstruction.

INVESTIGATIONS & DIAGNOSIS

• HBOT Suitability Assessment (Figure 4): 1. Initial Screening: Assess if wound is suitable for compression and check for contraindications (e.g., critical major vessel disease). 2. Transcutaneous Wound Mapping (on air): - PtcO_2 > 40 mmHg → Not hypoxic → Consider alternatives. - PtcO_2 < 35 mmHg → Contraindication. - PtcO_2 ≤ 40 mmHg → Proceed to oxygen challenge. 3. Oxygen Challenge (100% O2): - At 1 ATA: - PtcO_2 > 100 mmHg → HBOT unlikely to be effective. - PtcO_2 ≤ 100 mmHg → Proceed to higher pressure assessment. - At 2.4 ATA: - PtcO_2 > 200 mmHg → HBOT unlikely to be effective. - PtcO_2 between 35–100 mmHg → Case-by-case basis. - PtcO_2 ≤ 100 mmHg → HBOT indicated. • CO Poisoning Assessment: 1. Confirm exposure via Carboxyhemoglobin (COHb) levels. 2. Assess risk factors for poor outcome: Age >35, duration >24h, acidosis, loss of consciousness.

MANAGEMENT & TREATMENT

• HBOT Protocols: 1. General Treatment (e.g., LRTI): 30–60 sessions; 202.6–243.1 kPa (2–2.4 ATA) for 1.5–2 h each session. 2. Carbon Monoxide Poisoning: - Goal: Reduce risk of neurocognitive deficits. - Protocol: 2–3 sessions to 2–2.8 ATA for 1.5–2 h each; first two should be delivered within 24 h of exposure. • Altitude Management: 1. Chronic Mountain Sickness: Venesection and acetazolamide. 2. High-Altitude Pulmonary Hypertension: Descent to lower altitude; consider sustained-release nifedipine (30 mg twice a day). 3. Acetazolamide Administration: - Contraindication: Preexisting metabolic acidosis. - Adjustment: If GFR <50 mL/min → adjust dose. - Absolute Contraindication: If GFR <10 mL/min → do not use. 4. Cirrhosis at Altitude: Screen for portopulmonary arterial hypertension (16%) and hepatopulmonary syndrome (32%). Note: Acetazolamide may be inadvisable due to risk of hepatic encephalopathy. 5. Diabetes at Altitude: Use Continuous Glucose Monitor (CGM) and a reliable glucometer. 6. Lung Disease: Provide supplemental oxygen if predicted PaO_2 for altitude <50–55 mmHg. • Pre-treatment Safety Checks: 1. Pneumothorax: Must have patent chest drain in place before compression. 2. Bullae/Gas Trapping: Perform risk/benefit analysis before treatment.

COMPLICATIONS & PROGNOSIS

• Wound Healing Outcomes: ◦ 6 months post-treatment, ≈70% of indolergic ulcers improved or healed. ◦ Diabetic foot ulcers: HBOT increases chance of healing (RR 2.35) and reduces major amputations (OR 0.41). • HBOT Specific Risks: ◦ Barotrauma: Most common complication (≈30%). ◦ Myopic Shift: Common after 30 treatments at 2 ATA; usually reversible in 6–12 weeks. ◦ Pulmonary Toxicity: Risk is higher in patients with prior bleomycin or mitomycin C exposure.

SPECIAL CONSIDERATIONS

• Cirrhosis: ◦ 16% may have portopulmonary arterial hypertension. ◦ 32% may have hepatopulmonary syndrome (can cause exaggerated hypoxemia). ◦ Note: Acetazolamide may be inadvisable due to risk of hepatic encephalopathy. • Malignancy/Radiation: ◦ Carotid body dysfunction (from neck radiation or paraganglioma) can reduce acclimatization. ◦ Bleomycin/Mitomycin C: Can cause pneumonitis in ≈20% of patients; may increase susceptibility to oxygen toxicity.

KEY PEARLS & CLINICAL TRAPS

• Table 476-1 (Accepted Indications): Includes air/gas embolism, CO poisoning, clostridial myositis, crush injury, decompression sickness, arterial insufficiency, severe anemia, intracranial abscess, necrotizing soft tissue infections, osteomyelitis, delayed radiation injury, skin grafts/flaps, acute thermal burns, sudden sensorineural hearing loss, and avascular necrosis. • Table 476-2 (Decompression Sickness): ◦ Musculoskeletal: Limb pain. ◦ Pulmonary: Cough, Dyspnea. ◦ Cutaneous: Rash, itch. ◦ Constitutional: Fatigue and malaise. • Absolute Contraindication: Untreated pneumothorax; must have a patent chest drain before compression. • CO Poisoning Rule: HBOT is used to reduce neurocognitive deficits by addressing tissue hypoxia beyond just clearing COHb.

Reference Tables

Harrison's 22e, p.3762

    1. Air or gas embolism (includes diving-related, iatrogenic, and accidental
      causes)
      2. Carbon monoxide poisoning (including poisoning complicated by cyanide
      poisoning)
      3. Clostridial myositis and myonecrosis (gas gangrene)
      4. Crush injury, compartment syndrome, and acute traumatic ischemias
      5. Decompression sickness
      6. Arterial insufficiency including central retinal arterial occlusion and problem
      wounds
      7. Severe anemia
      8. Intracranial abscess
      9. Necrotizing soft tissue infections (e.g., Fournier’s gangrene)
      10. Osteomyelitis (refractory to other therapy)
      11. Delayed radiation injury (soft tissue injury and bony necrosis)
      12. Skin grafts and flaps (compromised)
      13. Acute thermal burn injury
      14. Sudden sensorineural hearing loss
      15. Avascular necrosis (aseptic osteonecrosis)

TABLE 476-2 Manifestations of Decompression Sickness

Harrison's 22e, p.3767

ORGAN SYSTEM MANIFESTATIONS
Musculoskeletal Limb pain
Pulmonary Cough
Dyspnea
Cutaneous Rash, itch
Constitutional Fatigue and malaise