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Hypothermia and Peripheral Cold Injuries¶

Chapter 477 | Part 15: Disorders Associated with Environmental Exposures · Parts 15-16 – Genetics, Genomics & Precision Medicine · Chapter 477

Key Clinical Points¶

Primary accidental hypothermia is defined as an unintentional drop in core temperature below 35°C (95°F).
J or Osborn waves at the QRS-ST junction are hallmark ECG findings; these are often misidentified as injury currents.
Paradoxical undressing occurs in moderate to severe hypothermia due to malfunctioning thermoregulation.
Active rewarming is mandatory for core temperatures <32°C, cardiovascular instability, or suspected secondary hypothermia.
Avoid direct heat to extremities in severe cases to prevent 'afterdrop' (peripheral vasodilation leading to a drop in core temperature).
Frostbite severity is indicated by the presence of vesicles; hemorrhagic vesicles signify serious microvascular injury.
Hypothermia masks signs of infection (fever, leukocytosis), and shivering may be confused with rigors.
Hematocrit values are falsely elevated by 2% for every 1°C drop in temperature.
Coagulation studies are often deceptively normal because they are performed at 37°C (99°F) during testing.
A history of asphyxia (e.g., avalanche) is a major negative predictor of survival.

DEFINITION & CLASSIFICATION¶

• Primary Accidental Hypothermia: Result of direct exposure of a previously healthy individual to the cold. • Secondary Hypothermia: Complication of a serious systemic disorder or injury.

Definition (Harrison's 22e): Primary accidental hypothermia is a result of the direct exposure of a previously healthy individual to the cold.

• Risk Factors (Table 477-1): Factors increasing susceptibility include: ◦ Age extremes: Elderly (diminished perception, immobility) and Neonates (high surface-to-mass ratio). ◦ Environmental: Occupational, sports-related, inadequate clothing, immersion. ◦ Toxicologic/Pharmacologic: Ethanol (vasodilation, impaired judgment), Anesthetics (block shivering), Antipsychotics, Antidepressants, Anxiolytics, Benzodiazepines, Neuromuscular blockers. ◦ Endocrine: Diabetes mellitus, Hypoglycemia, Hypothyroidism (reduced metabolism), Adrenal insufficiency, Hypopituitarism. ◦ Neurologic: CVA, Hypothalamic disorders, Parkinson's disease, Spinal cord injury. ◦ Multisystemic: Trauma, Sepsis, Shock, Hepatic/Renal failure, Carcinomatasis, Burns, Skin diseases (psoriasis, erythrodermas). ◦ Nutritional: Malnutrition (Marasmus, Kwashiorkor).

ETIOLOGY & PATHOPHYSIOLOGY¶

• Heat Loss Mechanisms: ◦ Radiation: 55–65% of total loss. ◦ Conduction: 10–15% (increased in cold water). ◦ Convection: Increased in wind. ◦ Respiration & Evaporation: Affected by ambient temperature and humidity.

• Thermoregulation Control: ◦ Immediate response: Autonomic nervous system (norepinephrine release, increased muscle tone, shivering). ◦ Delayed control: Endocrine system (thyroid axis stimulation to increase metabolic rate).

• Contributing Factors for Impaired Thermoregulation: ◦ Ethanol: Vasodilation → increased heat loss; reduced thermogenesis/gluconeogenesis. ◦ Medications: Antipsychotics, Benzodiazepines, etc., reduce central vasoconstriction; Anesthetics block shivering. ◦ Endocrine/Metabolic: Hypothyroidism (reduced metabolism), Hypoglycemia (neuroglycopenic effects), Uremia, DKA, Lactic acidosis. ◦ Neurologic Injury: Trauma, CVA, Subarachnoid hemorrhage, Hypothalamic lesions. ◦ Specific Syndromes: Shapiro's syndrome (Agenesis of the corpus callosum) → profuse perspiration followed by rapid temperature drop. ◦ Skin Conditions: Burns, psoriasis, erythrodermas → increased peripheral blood flow leads to excessive heat loss.

CLINICAL FEATURES¶

• General Presentation: Diagnosis is often straightforward based on exposure history; however, in urban settings, it may be subtle and mimic other conditions.

• Severity-Based Manifestations (Table 477-2): ◦ Mild (35°C–32.2°C): → CNS: Linear depression of cerebral metabolism, amnesia, apathy, dysarthria, impaired judgment. → Cardiovascular: Tachycardia → progressive bradycardia; vasoconstriction; increased cardiac output/BP. → Respiratory: Tachypnea → decreased respiratory minute volume; bronchorrhea, bronchospasm. → Renal/Endocrine: Diuresis; increased catecholamines, steroids, T3, and T4. → Neuromuscular: Increased preshivering muscle tone → fatigue.

◦ Moderate (<32.2°C–28°C): → CNS: EEG abnormalities, decreased consciousness, pupillary dilation, paradoxical undressing, hallucinations. → Cardiovascular: Decreased pulse/cardiac output; arrhythmias; J-wave ECG changes. → Respiratory: Hypoventilation (50% decrease in CO_2 production per 8°C drop); loss of airway reflexes. → Renal/Endocrine: → 50% increase in renal blood flow; intact autoregulation; impaired insulin action. → Neuromuscular: Hyporeflexia, rigidity.

◦ Severe (<28°C): → CNS: Loss of cerebrovascular autoregulation; coma; loss of ocular reflexes; severe EEG abnormalities. → Cardiovascular: Decreased BP/HR/Cardiac output; reentrant dysrhythmias; high risk of VF; asystole. → Respiratory: Pulmonic congestion/edema; 75% decrease in O_2 consumption; apnea. → Renal/Endocrine: Decreased renal blood flow (parallels cardiac output); extreme oliguria; poikilothermia; 80% decrease in basal metabolism. → Neuromuscular: No motion; decreased nerve-conduction velocity; peripheral areflexia; no corneal/oculocephalic reflexes.

• Physical Examination Findings: ◦ Paradoxical Undressing: Removal of clothing due to cold stress (maladaptive behavior). ◦ J or Osborn Wave: Located at the junction of QRS and ST segment; often misdiagnosed as injury current by automated systems. ◦ Pulse Oximetry: Often unreliable due to vasoconstriction. ◦ Frostbite: → Symptoms: Sensory deficiency (touch, pain, temperature); 'chunk of wood' sensation. → Appearance: Waxy, mottled, yellow, or violaceous-white; presence of edema and erythema. → Severity: Vesiculation → deeper involvement; Hemorrhagic vesicles → severe microvascular injury. ◦ Chilblain (Pernio): Result of repeated exposure to damp cold >0^circ C; common in young females with Raynaud's. ◦ Immersion (Trench) Foot: Nonfreezing cold injury from wet cold >0^circ C. ◦ Myxedema: Prolonged relaxation phase of Achilles reflex (> contraction phase).

DIFFERENTIAL DIAGNOSIS¶

• Secondary Hypothermia (Distinguishing Features): ◦ Hypoglycemia: → Neuroglycopenic effects on hypothalamus. ◦ Hypovolemia: → Tachycardia disproportionate to core temperature. ◦ Toxin Overdose: → Tachycardia disproportionate to core temperature. ◦ Infection/Sepsis: → Shaking rigors may be mistaken for shivering; hypothermia in sepsis is a poor prognostic sign.

• Clinical Mimickers: ◦ Spinal Cord Lesion: Can cause areflexia (mimicking severe hypothermia). ◦ Acute Abdomen: Cold-induced ileus and abdominal rectus spasm can mask/mimic acute abdomen. ◦ Psychiatric Disorders: Should be considered in urban settings with subtle presentations.

DIAGNOSTIC APPROACH¶

Core Temperature Measurement: → Essential for diagnosis; use esophageal probe (lower third) if feasible. → Continuous monitoring is required.
ECG Monitoring: → Identify J or Osborn waves; monitor atrial arrhythmias (usually resolve spontaneously during rewarming).
Pulse Oximetry: → Use with caution as it is often unreliable due to vasoconstriction.
Laboratory Analysis: → Hematocrit: Correct for temperature (Hct increases 2% per 1°C drop). → Coagulation Studies: Note that these are performed at 37°C; they may appear normal despite in vivo coagulopathy. → Arterial Blood Gases: Do not correct for temperature. → Target: pH of 7.42 and PCO_2 of 40 mmHg (reflects appropriate ventilation). → Electrolytes: Monitor for hypokalemia or hyperkalemia; note that ECG changes may be masked.
Supportive Monitoring: → ETCO2 monitoring to prevent over-zealous hyperventilation. → Gastric tube to prevent dilation from decreased motility. → Bladder catheter for diuresis monitoring and temperature tracking.

MANAGEMENT & TREATMENT¶

Initial Rewarming Decision: → Passive External Rewarming: Use for mild primary hypothermia (rate 0.5–2°C/hr). → Active Rewarming: Required for core temperature <32^circ C, cardiovascular instability, age extremes, CNS dysfunction, hormone insufficiency, or suspected secondary hypothermia.
Specific Techniques: → Truncal Heat Application: Preferred to reduce risk of 'afterdrop'. → Avoid Extremity Heating: In severe cases, avoid direct heat to limbs → prevents peripheral vasodilation and subsequent drop in core temperature. → Fluid Management: IV/IO crystalloid bolus; Normal Saline preferred over Lactated Ringer's (liver cannot metabolize lactate efficiently in hypothermia).
Extracorporeal Life Support (Table 477-3): → Continuous venovenous (CVV) rewarming: → Circuit: CV catheter to CV, dual-lumen CV, or peripheral. → No oxygenator/circulatory support required. → Flow rates: 150–400 mL/min. → Rate of Rewarming (ROR): 2°–3°C (4.4°–6.6°F)/h. → Continuous arteriovenous rewarming (CAVR): → Circuit: percutaneous 8.5-Fr femoral catheters. → Requirement: Systolic blood pressure ≥ 60 mmHg. → No perfusionist/pump/anticoagulation required. → Flow rates: 225–375 mL/min. → ROR: 3°–4°C (6.6°–8.8°F)/h. → Venoarterial extracorporeal membrane oxygenation (VA-ECMO): → Benefit: Decreased risk of post-rewarming cardiorespiratory failure; improved neurologic outcome.

PROGNOSIS & COMPLICATIONS¶

• Prognostic Indicators: ◦ Survival can occur with cardiac arrest time >7 hours. ◦ Negative Predictor: History of asphyxia (e.g., avalanche) followed by secondary cooling is the most significant predictor of poor outcome.

• Complications: ◦ Afterdrop: Core temperature continues to fall after removal from cold due to peripheral vasodilation. ◦ Coagulopathy: Common due to inhibited enzymatic reactions and impaired platelet function (thromboxane B production is temperature-dependent). ◦ Pulmonary Edema: Risk increases in severe hypothermia.

SPECIAL POPULATIONS¶

• Age Extremes: → Elderly: High risk due to impaired thermoregulation and comorbidities. → Neonates: High surface-to-mass ratio leads to rapid heat loss.

• Myxedema: → Characterized by prolonged relaxation phase of Achilles reflex.

KEY PEARLS & HIGH-YIELD POINTS¶

• Clinical Traps: → Do not assume areflexia is only due to hypothermia; consider spinal cord lesions. → Do not trust standard coagulation tests for in vivo status (they are performed at 37°C). → Be wary of 'afterdrop' when treating severe cases; focus heat on the trunk.

• Diagnostic Clues: → J-waves = Hypothermia. → Paradoxical undressing = Severe hypothermia. → Tachycardia with low core temp = Suggests secondary causes (hypoglycemia, tox_in, etc.). → High Hematocrit eq high hemoglobin; it is a result of volume loss and temperature-induced concentration.

Reference Tables¶

TABLE 477-1 Risk Factors for Hypothermia Age extremes¶

Harrison's 22e, p.3768

Age extremes Elderly Neonates Environmental exposure Occupational Sports-related Inadequate clothing Immersion Toxicologic and pharmacologic Ethanol Anesthetics Antipsychotics Antidepressants Anxiolytics Benzodiazepines Neuromuscular blockers Insufficient fuel Malnutrition Marasmus Kwashiorkor	Endocrine-related Diabetes mellitus Hypoglycemia Hypothyroidism Adrenal insufficiency Hypopituitarism Neurologic Cerebrovascular accident Hypothalamic disorders Parkinson’s disease Spinal cord injury Multisystemic Trauma Sepsis Shock Hepatic or renal failure Carcinomatosis Burns and exfoliative dermatologic disorders Immobility or debilitation
477	Hypothermia and Peripheral Cold Injuries Daniel F. Danzl

TABLE 477-2 Physiologic Changes Associated with Accidental Hypothermia SEVERITY Mild¶

Harrison's 22e, p.3769

SEVERITY	BODY TEMPERATURE	CENTRAL NERVOUS SYSTEM	CARDIOVASCULAR	RESPIRATORY	RENAL AND ENDOCRINE	NEUROMUSCULAR
Mild	35°C (95°F)– 32.2°C (90°F)	Linear depression of cerebral metabolism; amnesia; apathy; dysarthria; impaired judgment; maladaptive behavior	Tachycardia, then progressive bradycardia; cardiac cycle prolongation; vasoconstriction; increase in cardiac output and blood pressure	Tachypnea, then progressive decrease in respiratory minute volume; declining oxygen consumption; bronchorrhea; bronchospasm	Diuresis; increase in catecholamines, adrenal steroids, triiodothyronine, and thyroxine; increase in metabolism with shivering	Increased preshivering muscle tone, then fatiguing
	<32.2°C (90°F)– 28°C (82.4°F)	EEG abnormalities; progressive depression of level of consciousness; pupillary dilation; paradoxical undressing; hallucinations	Progressive decrease in pulse and cardiac output; increased atrial and ventricular arrhythmias; suggestive (J-wave) ECG changes	Hypoventilation: 50% decrease in carbon dioxide production per 8°C (17.6°F) drop in temperature; absence of protective airway reflexes	50% increase in renal blood flow; renal autoregulation intact; impaired insulin action
Severe	<28°C (<82.4°F)	Loss of cerebrovascular autoregulation; decline in cerebral blood flow; coma; loss of ocular reflexes; progressive decrease in EEG abnormalities	Progressive decrease in blood pressure, heart rate, and cardiac output; reentrant dysrhythmias; maximal risk of ventricular fibrillation; asystole	Pulmonic congestion and edema; 75% decrease in oxygen consumption; apnea	Decrease in renal blood flow that parallels decrease in cardiac output; extreme oliguria; poikilothermia; 80% decrease in basal metabolism	No motion; decreased nerve-conduction velocity; peripheral areflexia; no corneal or oculocephalic reflexes

TABLE 477-3 Options for Extracorporeal Life Support¶

Harrison's 22e, p.3770

EXTRACORPOREAL REWARMING TECHNIQUE	CONSIDERATIONS
Continuous venovenous (CVV) rewarming	Circuit: CV catheter to CV, dual-lumen CV, or peripheral catheter No oxygenator/circulatory support Flow rates 150–400 mL/min ROR 2°–3°C (4.4°–6.6°F)/h
Continuous arteriovenous rewarming (CAVR)	Circuit: percutaneous 8.5-Fr femoral catheters Requires systolic blood pressure of 60 mmHg No perfusionist/pump/anticoagulation Flow rates 225–375 mL/min ROR 3°–4°C (6.6°–8.8°F)/h
Venoarterial extracorporeal membrane oxygenation (VA-ECMO)	Decreased risk of post-rewarming cardiorespiratory failure Improved neurologic outcome