8.3 Submersion, Diving Emergencies & Envenomation/HazMat

Submersion, Diving Emergencies & Envenomation/HazMat

Critical care transport paramedics encounter specialized environmental and toxicological hazards requiring advanced application of gas laws, envenomation pharmacology, and hazardous materials containment. This section details submersion injury pulmonary mechanics, SCUBA diving barotrauma, antivenom administration, and HazMat transport protocols.

Submersion Injuries & Near-Drowning Mechanics

Submersion injury begins with hypoxemia resulting from primary asphyxia while submerged. Fluid aspiration occurs in over 90% of submersion victims, while 10% experience dry drowning secondary to persistent reflex laryngospasm.

Pulmonary Pathophysiology

Historically, drowning management distinguished between fresh water aspiration (hypotonic, causing rapid alveolar absorption, intravascular hypervolemia, and hemolysis) and salt water aspiration (hypertonic, drawing fluid into alveoli and causing severe hypovolemia). In clinical practice, human aspiration volumes rarely exceed 22 mL/kg required to cause electrolyte derangements; the distinction between fresh and salt water drowning is clinically irrelevant.

Fluid Aspiration ──► Surfactant Destruction / Washout ──► Alveolar Collapse & Atelectasis
                 ──► Capillary Membrane Breakdown   ──► Non-Cardiogenic Pulmonary Edema
                 ──► Massive Intrapulmonary Shunting ──► Severe Hypoxemia & ARDS

• Surfactant Disruption: Aspiration of liquid washes out and inactivates endogenous pulmonary surfactant. This leads to increased alveolar surface tension, widespread atelectasis, decreased pulmonary compliance, and severe ventilation-perfusion (V/Q) mismatching.
• Non-Cardiogenic Pulmonary Edema: Capillary-alveolar membrane damage leads to fluid accumulation in the alveoli, resulting in acute lung injury (ALI) and Acute Respiratory Distress Syndrome (ARDS).

Critical Care Transport Management

1. Oxygenation & Airway Management: Administer high-flow 100% FiO2. Early endotracheal intubation is indicated for GCS ≤ 8, severe respiratory distress, or persistent hypoxemia (PaO2/FiO2 ratio < 200).
2. PEEP Titration: Apply Positive End-Expiratory Pressure (PEEP) of 10 to 15 cmH2O to recruit collapsed alveoli, increase functional residual capacity (FRC), and displace alveolar edema fluid back into the interstitial space.
3. Ventilator Strategy: Follow ARDSNet protective ventilation guidelines: tidal volumes of 6 mL/kg predicted body weight (PBW) and plateau pressure target Pplat < 30 cmH2O.
4. Prophylactic Interventions: Routine prophylactic administration of antibiotics or systemic corticosteroids is strictly NOT recommended—it provides no clinical benefit and selects for resistant pulmonary pathogens.

Diving Medicine: Barotrauma, AGE & Decompression Sickness

SCUBA diving subjects the human body to rapid ambient pressure changes governed by physical gas laws.

Gas Laws in Diving Medicine

• Boyle's Law ($P_1 V_1 = P_2 V_2$): At a constant temperature, volume is inversely proportional to pressure. As a diver ascends, ambient barometric pressure decreases, causing gas in closed compartments (lungs, middle ear) to expand. Breath-holding during ascent causes pulmonary barotrauma.
• Henry's Law ($C = k \cdot P$): The amount of gas dissolved in a liquid is proportional to the partial pressure of that gas above the liquid. Under high ambient pressure at depth, inert gas (nitrogen) dissolves into blood and fatty tissues. Rapid ascent reduces ambient pressure, causing dissolved nitrogen to come out of solution as gas bubbles in tissue and vasculature.

ASCENT ──► Decreased Ambient Pressure ──► Boyle's Law: Gas Volume Expands ──► Pulmonary Barotrauma / AGE
       ──► Decreased Solubilty     ──► Henry's Law: Nitrogen Bubbles   ──► Decompression Sickness (DCS)

Arterial Gas Embolism (AGE) vs. Decompression Sickness (DCS)

Decompression Sickness Classification

• Type I DCS ("Bends"): Mild, non-life-threatening. Characterized by deep, aching joint pain (elbows, shoulders, knees), lymphatic obstruction, and skin lesions (cutis marmorata—mottled, purpuric skin rash).
• Type II DCS (Systemic / Severe):
  • Spinal Cord DCS: Bubble formation in venous plexus of spinal cord causing lower extremity weakness, numbness, paraplegia, and loss of sphincter control.
  • Pulmonary DCS ("Chokes"): Microembolization to pulmonary circulation causing substernal chest pain, dyspnea, cough, and non-cardiogenic pulmonary edema.
  • Vestibular DCS ("Staggers"): Nitrogen bubbles in inner ear causing severe vertigo, nystagmus, ataxia, and sensorineural hearing loss.

Transport & Hyperbaric Referral Protocol

1. High-Flow 100% FiO2: Administer 100% FiO2 immediately via non-rebreather mask or endotracheal tube. Oxygen eliminates nitrogen partial pressure in the lungs, creating a steep gradient that accelerates nitrogen bubble resorption from blood and tissues.
2. Isotonic Fluid Resuscitation: Administer IV 0.9% Normal Saline at 150 to 250 mL/hr. Intravascular bubble formation causes endothelial damage, plasma leakage, and hemoconcentration; aggressive hydration maintains microvascular perfusion.
3. Patient Positioning: Maintain the patient in a flat supine position. Avoid Trendelenburg or left-lateral decubitus positions, which are obsolete and increase cerebral edema.
4. Transport Altitude Restrictions: Ground transport is strongly preferred. If air transport is mandatory:
   • Fixed-Wing Aircraft: Must maintain cabin pressurization to 1 atmosphere absolute (1 ATA).
   • Unpressurized Aircraft / Helicopters: Must maintain flight altitude strictly below 1,000 feet (300 meters) MSL above terrain. Higher altitudes decrease ambient pressure, expanding nitrogen bubbles and exacerbating AGE/DCS.
5. Definitive Treatment: Immediate transfer to a hyperbaric facility for Hyperbaric Oxygen Therapy (HBOT) (recompression chamber utilizing US Navy Treatment Table 6).

Envenomation Emergencies & Hazardous Materials Transport

Pit Viper vs. Coral Snake Envenomation

Pit Viper Envenomation (Subfamily Crotalinae)

Includes rattlesnakes, copperheads, and cottonmouths (water moccasins). Identified by elliptical pupils, heat-sensing facial pits, and retractable fangs.

• Venom Pathophysiology: Metalloproteinases, hyaluronidase, and phospholipases cause tissue necrosis, severe local swelling, third-spacing, and systemic consumptive coagulopathy (thrombocytopenia, hypofibrinogenemia, hemoxytosis, elevated PT/INR).
• Antidote: Crotalidae Polyvalent Immune Fab (CroFab) or Crotalidae Immune F(ab')2 (Anavip).
  • Indications: Progressive local tissue involvement (swelling crossing a major joint), systemic signs (hypotension, altered mental status), or severe coagulopathy (platelets < 100,000/mcG, fibrinogen < 100 mg/dL).
  • Initial Dosing: Reconstitute 4 to 6 vials of CroFab in 250 mL 0.9% Normal Saline and infuse IV over 1 hour (start at 25-50 mL/hr for 10 minutes to observe for anaphylaxis).
  • Re-evaluation: Evaluate control at 1 hour post-infusion. If control is not achieved, administer a second dose of 4 to 6 vials. Once initial control is established, administer maintenance dosing of 2 vials every 6 hours for 3 doses.
  • Field Contraindications: Do NOT apply tourniquets, arterial constriction bands, ice packs, or electrical shock, and do NOT attempt incision and suction.

Coral Snake Envenomation (Family Elapidae)

Identified by red-on-yellow bands ("Red touch yellow, kill a fellow; red touch black, venom lack").

• Venom Pathophysiology: Potent neurotoxins cause post-synaptic neuromuscular blockade. Local swelling and pain are minimal or absent.
• Clinical Presentation: Delayed onset (up to 12 hours). Progressive cranial nerve palsies, ptosis, diplopia, dysarthria, dysphagia, and sudden respiratory muscle paralysis leading to asphyxia.
• Antidote: Administer Eastern Coral Snake Antivenom (5 vials IV) immediately upon suspected envenomation, prior to the onset of respiratory distress, as neurotoxicity is difficult to reverse once bound.

Hazardous Materials (HazMat) & PPE Levels in Transport

Critical care transport personnel must identify Personal Protective Equipment (PPE) levels and enforce warm-zone decontamination protocols to prevent secondary contamination during ground or air transport.

Transport Decontamination Protocol

1. Mandatory Warm-Zone Decontamination: Patients exposed to hazardous chemicals MUST undergo primary decontamination in the Warm Zone prior to loading into an ambulance or aircraft. Transporting an undecontaminated patient traps volatile gases in an enclosed cabin, incapacitating crew members and contaminating medical equipment.
2. Decontamination Technique: Copious water lavage with mild soap is the primary method of chemical removal. Do NOT attempt chemical neutralization on patient skin (e.g., applying acid to alkali), as exothermic neutralization reactions cause severe thermal burns.