Environmental Extremes: From Heat Stroke to Drowning

A Critical Care Perspective on Thermal and Immersion Emergencies

Dr Neeraj Manikath , claude.ai

Abstract

Environmental emergencies represent a spectrum of life-threatening conditions that demand rapid recognition and evidence-based intervention. This review examines the contemporary management of heat stroke, drowning, and severe hypothermia—conditions united by their time-sensitive nature and potential for complete recovery with optimal care. We synthesize current evidence on cooling strategies, drowning resuscitation, and rewarming techniques while highlighting practical clinical pearls for the intensivist.

Modern Cooling Techniques for Exertional and Classic Heat Stroke

Pathophysiological Foundations

Heat stroke represents the most severe form of heat-related illness, characterized by core temperature exceeding 40°C with central nervous system dysfunction. The distinction between exertional heat stroke (EHS) and classic heat stroke (CHS) carries therapeutic implications that extend beyond academic taxonomy.

Pearl #1: The "40°C threshold" is a clinical guide, not a diagnostic prerequisite. Patients with profound CNS dysfunction and history of heat exposure warrant aggressive cooling even if initial temperature is below 40°C—they may have already begun cooling during transport.

EHS typically affects younger, physically active individuals during strenuous exercise in hot environments, with preserved sweating mechanisms initially. The pathophysiology involves excessive endogenous heat production overwhelming dissipation capacity, leading to a systemic inflammatory response syndrome (SIRS) resembling sepsis. Cytokine release (IL-1β, IL-6, TNF-α) triggers endothelial activation, increased gut permeability, and endotoxemia—the "heat stroke cascade" that perpetuates injury even after cooling.

CHS predominantly affects vulnerable populations (elderly, chronically ill, socially isolated) during heat waves. Impaired thermoregulation, often compounded by medications (anticholinergics, diuretics, β-blockers), leads to passive heat accumulation. Unlike EHS, anhidrosis is common, and the onset is typically gradual over days.

Evidence-Based Cooling Strategies

The Golden Hour Principle: Mortality correlates directly with duration of hyperthermia. Target cooling to <39°C within 30 minutes of presentation—every minute counts.

Oyster #1: Delayed cooling while obtaining a complete history or "stabilizing" the patient is a critical error. Cooling IS stabilization in heat stroke.

Cold Water Immersion (CWI)

CWI remains the gold standard for EHS, achieving cooling rates of 0.15-0.35°C/min—superior to all other modalities. Immersion in 1-2°C water provides maximal thermal gradient, though practical implementation in emergency departments often favors 10-15°C water for patient comfort and staff safety.

Technique: Immerse the patient up to the neck in circulating cold water. Continuous core temperature monitoring (rectal or esophageal) is mandatory. Remove from bath at 38.5-39°C to prevent overshoot hypothermia.

Hack #1: If a dedicated immersion tub is unavailable, use a body bag or tarp laid in a stretcher, filled with ice water and towels for cushioning. This improvised solution can achieve near-equivalent cooling rates.

Contraindications are fewer than traditionally taught. Cardiovascular instability is not an absolute contraindication—vasoplegic shock often improves with cooling as the inflammatory cascade reverses. However, avoid CWI in patients requiring aggressive resuscitation where access would be compromised.

Evaporative Cooling

Evaporative methods involve spraying tepid water (15°C) on exposed skin with high-velocity fans. Cooling rates (0.05-0.31°C/min) approach CWI when optimized, making this the preferred method for CHS where immersion may be poorly tolerated.

Technical optimization:

Maximize skin exposure (remove all clothing)
Use atomizing sprayers for fine mist
Position fans at body level (not overhead)
Maintain room temperature at 25-26°C
Avoid overly cold water which causes vasoconstriction

Pearl #2: Shivering reduces cooling efficiency. Consider low-dose benzodiazepines (midazolam 2-5mg IV) to suppress shivering thermogenesis without the hemodynamic consequences of paralysis.

Adjunctive and Invasive Methods

Ice pack application to high-flow vascular areas (axillae, groins, neck) provides minimal benefit as monotherapy (0.03-0.08°C/min) but supplements other methods. The traditional teaching of avoiding peripheral vasoconstriction is overemphasized—core cooling takes precedence.

Cold intravenous fluids (4°C crystalloid, 30 mL/kg) contribute approximately 0.03°C core temperature reduction per liter—modest but beneficial when combined with surface cooling. Avoid aggressive fluid resuscitation beyond initial bolus unless hypovolemia is evident; heat stroke patients often develop pulmonary edema.

Intravascular cooling catheters and extracorporeal circuits (continuous veno-venous hemofiltration, extracorporeal membrane oxygenation) are reserved for refractory cases or patients with contraindications to surface cooling. These provide controlled cooling (0.5-2°C/min) but delay to implementation often negates their theoretical advantage.

Hack #2: For rapid cooling in resource-limited settings, combine gastric and bladder lavage with iced saline (500mL aliquots) alongside surface cooling. While labor-intensive, this achieves meaningful core temperature reduction.

Pharmacologic Adjuncts: What Doesn't Work

Oyster #2: Antipyretics (acetaminophen, NSAIDs) are ineffective and potentially harmful in heat stroke. Hyperthermia results from failed thermoregulation, not elevated hypothalamic set-point. Additionally, hepatotoxicity risk is increased in heat stroke victims.

Dantrolene, despite theoretical appeal for reducing muscle heat production, shows no mortality benefit in human studies and may worsen hepatic injury.

Post-Cooling Management

Heat stroke is a multi-system disease requiring intensive monitoring for 24-72 hours:

Neurologic: Cerebral edema may peak 24-48 hours post-event. Maintain MAP >65 mmHg, avoid hyperthermia recurrence, consider hypertonic saline for refractory intracranial hypertension.
Renal: Acute kidney injury from rhabdomyolysis and direct thermal injury affects 25-30% of patients. Aggressive hydration (target urine output 200-300 mL/hr initially) and early renal replacement therapy if indicated.
Hepatic: Transaminitis peaks at 48-72 hours. Fulminant hepatic failure occurs in 5% of severe cases—monitor coagulation parameters and encephalopathy closely.
Coagulation: Disseminated intravascular coagulation develops in 30-40% of severe heat stroke. Early recognition and supportive care are essential.

Pearl #3: Temperature afterdrop and rebound hyperthermia can occur 6-12 hours post-cooling. Continue temperature monitoring and have rapid cooling protocols readily available.

The Pathophysiology and Management of the Drowning Victim

Redefining Drowning

The 2002 World Congress on Drowning established uniform terminology: drowning is "the process of experiencing respiratory impairment from submersion/immersion in liquid." Outcomes include survival (with or without morbidity) or death. Terms like "near-drowning," "wet/dry drowning," and "secondary drowning" should be abandoned as they create confusion.

The Pathophysiology Cascade

Oyster #3: The traditional "dry drowning" (laryngospasm without aspiration) concept is largely mythological. Autopsy studies demonstrate that >95% of drowning victims aspirate some water. Initial laryngospasm relaxes as hypoxemia progresses.

The primary injury mechanism is hypoxemia, not the aspirated fluid itself. Within seconds of submersion, panic and struggle lead to breath-holding (30-90 seconds in adults), followed by involuntary gasping and aspiration.

Freshwater vs. Seawater: A Clinical Distinction Without Difference

Historical teaching emphasized different pathophysiology based on water type—hyponatremia and hemolysis with freshwater; hypernatremia and hemoconcentration with seawater. Modern evidence reveals that insufficient water is typically aspirated to cause these theoretical electrolyte shifts. The median aspirated volume is 2-4 mL/kg—far below the quantities used in animal models that established this dogma.

Pearl #4: Do not delay resuscitation to determine water type or check electrolytes. Management is identical regardless of salinity.

The True Pathophysiologic Triad:

Surfactant washout and dysfunction → alveolar instability → atelectasis
Inflammatory response → increased capillary permeability → pulmonary edema
Ventilation-perfusion mismatch → shunt physiology → refractory hypoxemia

This creates a clinical picture resembling acute respiratory distress syndrome (ARDS), explaining why drowning victims may deteriorate hours after initial stability.

Scene and Initial Management

The Five-Minute Window: Neurological outcome correlates inversely with submersion duration. Submersion <5 minutes: favorable prognosis. >10 minutes: high morbidity/mortality risk. However, never assume death at the scene—exceptions exist, particularly with cold water (see hypothermia section).

In-Water Rescue Breathing: For trained rescuers, ventilation during rescue improves outcomes compared to rescue-then-ventilate approaches. Even 2-5 breaths can be lifesaving during extended retrieval.

Hack #3: Spinal immobilization is not routinely indicated unless obvious trauma, diving incident, or signs of injury. Universal c-spine precautions delay critical interventions and lack supporting evidence in drowning victims.

Hospital Resuscitation

Airway and Breathing

Most drowning victims present with either respiratory distress or arrest. The clinical spectrum:

Mild: Coughing, dyspnea, SpO₂ >92% on room air
Moderate: Respiratory distress, SpO₂ 85-92% requiring supplemental oxygen
Severe: Respiratory failure, SpO₂ <85%, altered mental status, requiring positive pressure ventilation

Oxygenation Strategy:

Start with high-flow nasal cannula (HFNC) for mild-moderate cases
Progress to non-invasive ventilation (NIV) if HFNC insufficient
Low threshold for early intubation in severe cases

Pearl #5: Drowning victims are at extreme aspiration risk. If intubation is required, use rapid sequence intubation with optimal head elevation and suction immediately available.

Mechanical Ventilation Principles:

Apply ARDS-net low tidal volume strategy (6 mL/kg ideal body weight)
Target plateau pressure <30 cmH₂O
Use adequate PEEP (typically 8-15 cmH₂O) to recruit collapsed alveoli
Accept permissive hypercapnia if needed to limit ventilator-induced lung injury
Consider prone positioning for refractory hypoxemia

Oyster #4: Routine prophylactic antibiotics are not indicated. Drowning-associated pneumonia is uncommon (<10%) and typically develops 48-72 hours post-event. Reserve antibiotics for clinical signs of infection or grossly contaminated water exposure.

Circulation

Most drowning victims who achieve return of spontaneous circulation (ROSC) are normovolemic or hypervolemic. Aggressive fluid resuscitation worsens pulmonary edema.

Fluid Strategy:

Initial bolus: 10-20 mL/kg if hypotensive
Transition to maintenance fluids (0.5-1 mL/kg/hr)
Use vasopressors (norepinephrine first-line) to maintain MAP >65 mmHg rather than volume loading

Neurologic Care

Hypoxic brain injury determines long-term outcome in most survivors. Therapeutic hypothermia showed initial promise but recent evidence is equivocal.

Post-Cardiac Arrest Care:

Targeted temperature management: maintain 36°C (normothermia) and avoid hyperthermia
Maintain CPP >60 mmHg (MAP minus ICP if monitored)
Treat seizures aggressively—EEG monitoring for 24-48 hours in comatose patients
Defer prognostication for at least 72 hours post-arrest

Hack #4: For comatose drowning victims, early EEG can identify subclinical seizures in up to 20% of patients, allowing targeted treatment that may improve outcomes.

Disposition and Observation

Who needs admission?

Any patient requiring supplemental oxygen beyond initial stabilization
Abnormal chest radiograph
Altered mental status
Initial SpO₂ <95% on room air
Hemodynamic instability

Pearl #6: The "asymptomatic drowning victim" is a clinical dilemma. Most authorities recommend 4-6 hour observation for patients who were symptomatic at scene but completely asymptomatic in ED with normal examination, chest X-ray, and pulse oximetry. Delayed deterioration beyond 8 hours is exceptionally rare.

Oyster #5: Parents often inquire about "secondary drowning"—delayed respiratory failure in previously well children. While rare, it reflects progressive pulmonary edema from initial injury. Educate families to monitor for 24 hours post-discharge for respiratory distress signs, but avoid creating undue anxiety about this uncommon scenario.

Cold Water Immersion and Severe Hypothermia: Resuscitation and Rewarming

Pathophysiology of Hypothermia

Hypothermia (core temperature <35°C) exists on a continuum with progressively deranged physiology:

Mild (32-35°C): Shivering, tachycardia, confusion
Moderate (28-32°C): Shivering cessation, bradycardia, arrhythmias, stupor
Severe (<28°C): Areflexia, pulmonary edema, ventricular arrhythmias, coma
Profound (<24°C): Appears clinically dead, maximum neuroprotection

Pearl #7: "No one is dead until warm and dead." The cerebral protective effects of hypothermia allow survival with intact neurological function after prolonged cardiac arrest—cases of survival after >6 hours of cardiac arrest exist.

The Cold Water Drowning Paradox

Cold water drowning presents a unique scenario where two potentially fatal conditions create a survival advantage. Rapid cooling (particularly in children with high surface area-to-mass ratio) induces profound hypothermia before terminal hypoxemia, reducing cerebral metabolic demand by ~50% at 28°C and ~75% at 20°C.

Key Determinants of Outcome:

Water temperature (<6°C optimal for neuroprotection)
Submersion duration
Victim age (children better outcomes)
Rapidity of cooling (faster is better)
Cleanliness of water (aspiration of contaminants worsens prognosis)

Hack #5: In ambiguous situations (unknown submersion duration, witnessed collapse into icy water), presume hypothermia preceded arrest and pursue aggressive resuscitation. Neurological recovery has occurred after submersion times exceeding 60 minutes.

Field Management and Rescue

Critical Decision Point: Differentiate between:

Cold water immersion (submersion in cold water)
Cold exposure (environmental hypothermia without submersion)

Management principles overlap but submersion victims require drowning-specific interventions.

Rescue and Initial Care:

Handle extremely gently—rough handling precipitates ventricular fibrillation (VF) in severely hypothermic patients
Horizontal position during extraction (prevents afterdrop from peripheral blood return)
Remove wet clothing, insulate from further heat loss
Do not delay CPR to check pulse—if no signs of life, begin CPR immediately

Oyster #6: The teaching to "check pulse for 1 minute" in hypothermia is impractical in field settings. If trained rescuers cannot detect signs of life within 10 seconds, begin CPR. Ultrasound confirmation of cardiac activity, if immediately available, guides decision-making.

CPR Modifications:

Continue standard compression rates and depths
Modified drug dosing: withhold medications until core temperature >30°C (below this, medications accumulate without metabolism)
Defibrillation: attempt 3 shocks; if unsuccessful, defer further shocks until >30°C

Hospital Rewarming Strategies

Rewarming rate depends on cardiovascular stability—unstable patients require rapid active core rewarming; stable patients tolerate gradual methods.

Passive External Rewarming

Application: Mild hypothermia (>32°C) in stable patients

Technique: Remove cold/wet clothing, insulate with blankets in warm environment. Rewarming rate: 0.5-2°C/hr through endogenous heat production.

Limitation: Ineffective when shivering mechanism is exhausted (<32°C) or patient is cardiovascularly unstable.

Active External Rewarming (AER)

Application: Moderate hypothermia or mild hypothermia requiring faster rewarming

Techniques:

Forced-air warming blankets (Bair Hugger): 1-2.5°C/hr
Warm water immersion (40-42°C): 2-4°C/hr

Hack #6: If commercial forced-air warmers are unavailable, use warm IV fluid bags placed in axillae and groins, changed every 10 minutes. Less efficient but better than passive measures alone.

Concern: Afterdrop phenomenon—core temperature decreases during initial rewarming as cold peripheral blood returns centrally. Typically 1-2°C drop over 15-30 minutes. Anticipate this, but don't allow it to prevent AER in appropriate patients.

Active Core Rewarming (ACR)

Indications:

Severe hypothermia (<28°C)
Cardiac arrest
Hemodynamic instability
Inadequate response to less invasive methods

Modalities in ascending invasiveness:

1. Heated Humidified Oxygen (42-46°C)

Minimal contribution (~0.5-1°C/hr) but no downside
Standard of care for intubated patients

2. Warmed Intravenous Fluids (40-42°C)

Limited efficacy (~0.5°C/hr per 500mL)
Use 0.9% saline (lactated Ringer's may not be metabolized)
Fluid warmers essential—microwave warming risks burns and uneven heating

3. Body Cavity Lavage

Gastric lavage: modest effect, aspiration risk
Bladder irrigation: technically simple, limited efficacy
Thoracic lavage (open or closed): 3-5°C/hr rewarming
Peritoneal dialysis: 1-3°C/hr, technically simple

Pearl #8: Closed thoracic lavage via bilateral chest tubes (warm saline infused into one hemithorax, drained from the other) achieves similar rewarming rates to open thoracotomy with lower morbidity. Consider this before proceeding to ECMO if available expertise exists.

4. Extracorporeal Rewarming: The Gold Standard

Extracorporeal Membrane Oxygenation (ECMO) represents the definitive treatment for severe hypothermic cardiac arrest. Rewarming rates of 9-10°C/hr allow rapid restoration of physiologic temperature.

Advantages:

Simultaneous circulatory support and oxygenation
Controlled rewarming rate
Electrolyte/acid-base management
Highest survival rates (up to 100% in select case series)

The HOPE Score (Hypothermia Outcome Prediction after ECLS) predicts survival likelihood:

Poor prognostic factors: Asphyxia prior to cooling, serum potassium >12 mmol/L, core temperature <24°C with submersion, obvious lethal injury/illness
Favorable factors: Witnessed collapse, short duration to CPR initiation, K⁺ <12 mmol/L

Hack #7: If ECMO is not immediately available but the patient warrants aggressive rewarming, initiate continuous veno-venous hemofiltration (CVVH) with warmed dialysate while arranging transfer. CVVH provides 2-3°C/hr rewarming—bridging therapy until ECMO is accessible.

Oyster #7: Serum potassium >12 mmol/L in hypothermic cardiac arrest indicates severe cellular injury and is associated with near-zero survival regardless of rewarming method. This helps identify futile cases, though some experts advocate for ECMO trial if other factors are favorable.

Termination of Resuscitation

The unique neuroprotective potential of hypothermia mandates prolonged resuscitation attempts. Traditional criteria do not apply.

Consider termination when:

Core temperature >32°C achieved without ROSC
Serum K⁺ >12 mmol/L (some controversy remains)
Obvious lethal trauma
Chest cannot be compressed (frozen)
Safety risks to rescuers prohibit continued effort

In-hospital: Continue CPR until core temperature ≥32-35°C or decision made for ECMO. Survival cases exist after >6 hours of CPR.

Post-Rewarming Care

Cardiovascular: Hemodynamic instability common due to "rewarming shock"—vasodilation, relative hypovolemia, myocardial dysfunction. Titrate vasopressors and volume carefully.

Renal: Cold diuresis during hypothermia causes significant volume depletion. Post-rewarming volume requirements may be substantial.

Infection: Immunosuppression is common—"cold sepsis" can emerge 24-48 hours post-rewarming. Consider empiric broad-spectrum antibiotics in severely hypothermic patients.

Neurologic: Post-rewarming neurological assessment should be deferred 72 hours minimum. Many patients with initial deep coma achieve full recovery.

Conclusion

Environmental emergencies demand aggressive, time-sensitive interventions guided by pathophysiologic principles rather than dogma. Modern cooling techniques have transformed heat stroke outcomes, drowning management continues to evolve beyond historical misconceptions, and hypothermia resuscitation pushes the boundaries of what we consider salvageable. The intensivist armed with these contemporary approaches and practical clinical pearls can optimize outcomes in these challenging scenarios where minutes matter and complete recovery remains possible.

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Disclosure: The author reports no conflicts of interest.

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