23.2 Severe Burn Injury, Inhalation Injury & Environmental Emergencies

ABIM Critical Care Medicine Study Guide Exam

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1 Chapter 1: Exam Orientation: Format, Blueprint & Study Strategy

1.1 ABIM Critical Care Medicine Exam: Format, Blueprint & Study Strategy

2 Chapter 2: Acute Respiratory Failure & ARDS

2.1 ARDS Definition, Pathophysiology & Phenotypes 2.2 Lung-Protective Mechanical Ventilation 2.3 Refractory ARDS: Prone Positioning, Neuromuscular Blockade & VV-ECMO

3 Chapter 3: Obstructive Airways, Pulmonary Vascular & Pleural Emergencies

3.1 Severe Asthma & COPD Exacerbations in the ICU 3.2 Massive & Submassive Pulmonary Embolism 3.3 Pulmonary Hypertension & Right Ventricular Failure in the ICU 3.4 Massive Hemoptysis, Complex Pleural Effusions & Thoracic Drainage

4 Chapter 4: Airway, Parenchymal & Nonthrombotic Pulmonary Emergencies

4.1 Airway Management, Upper-Airway Obstruction & Artificial-Airway Complications 4.2 Diffuse Alveolar Hemorrhage, Interstitial Lung Disease, Pulmonary Vasculitis & Noncardiogenic Edema 4.3 Severe Community-Acquired & Viral Pneumonia 4.4 Nonthrombotic Embolism (Air, Fat, Amniotic Fluid, Tumor, Septic) & Acute Chest Syndrome

5 Chapter 5: Mechanical Ventilation Modes, Dyssynchrony & Liberation

5.1 Mechanical Ventilator Modes & Advanced Breath Delivery 5.2 Patient-Ventilator Dyssynchrony & Waveform Analysis 5.3 Ventilator Liberation, Spontaneous Breathing Trials & Post-Extubation Support

6 Chapter 6: Shock Syndromes & Hemodynamic Principles

6.1 Shock Classification, Cellular Pathophysiology & Biomarkers 6.2 Hemodynamic Monitoring: Arterial Lines, CVP & Pulmonary Artery Catheter 6.3 Dynamic Assessment of Fluid Responsiveness & Resuscitation Targets

7 Chapter 7: Vasoactive Therapies & Mechanical Circulatory Support

7.1 Vasopressors & Inotropes: Pharmacology & Clinical Titration 7.2 Temporary Mechanical Circulatory Support: IABP, Impella & TandemHeart 7.3 Venoarterial ECMO (VA-ECMO) & Differential Hypoxemia 7.4 Post-Cardiac Arrest Care, Targeted Temperature Management & Neuroprognostication

8 Chapter 8: Acute Kidney Injury & Renal Replacement Therapy

8.1 KDIGO AKI Classification, Etiologies & Diagnostic Evaluation 8.2 Continuous Renal Replacement Therapy (CRRT) vs Intermittent Hemodialysis 8.3 Indications & Timing for RRT in Critical Illness: AKIKI & STARRT-AKI

9 Chapter 9: Electrolyte, Acid-Base & Endocrine Emergencies

9.1 Severe Dysnatremias: Hyponatremia, Hypernatremia & Osmotic Demyelination 9.2 Potassium, Calcium, Magnesium & Phosphate Disorders 9.3 Complex & Mixed Acid-Base Disorders: Boston vs Copenhagen vs Stewart 9.4 Endocrine Crises: DKA, HHS, Thyroid Storm, Myxedema Coma & Adrenal Crisis

10 Chapter 10: Glycemic Control, Hyperammonemia, Pituitary & Adrenal Disorders

10.1 ICU Glycemic Control & Severe Hypoglycemia 10.2 Non-Hepatic Hyperammonemia & Metabolic Encephalopathy 10.3 Pituitary Emergencies, Adrenal Excess & Critical Illness-Related Corticosteroid Insufficiency

11 Chapter 11: Acute Coronary Syndromes & Cardiac Arrhythmias

11.1 Acute Coronary Syndromes & Mechanical Complications of Myocardial Infarction 11.2 Critical Tachyarrhythmias: Atrial Fibrillation with RVR, VT & VF 11.3 Critical Bradyarrhythmias, Conduction Blocks & Temporary Cardiac Pacing

12 Chapter 12: Acute Heart Failure, Valvular & Pericardial Emergencies

12.1 Acute Decompensated Heart Failure & Cardiogenic Pulmonary Edema 12.2 Acute Valvular Regurgitation & Prosthetic Valve Emergencies 12.3 Pericardial Tamponade & Acute Aortic Syndromes

13 Chapter 13: Myocardial Disease, Hypertensive & Cardiac Device Emergencies

13.1 Fulminant Myocarditis, Stress & Peripartum Cardiomyopathy, and Hypertrophic Cardiomyopathy 13.2 Hypertensive Emergencies & Ruptured Abdominal Aortic Aneurysm 13.3 Implanted Cardiac Devices, LVAD Emergencies & Electrical Storm

14 Chapter 14: Sepsis & Systemic Infectious Diseases

14.1 Sepsis-3 Definitions & Surviving Sepsis Campaign 2026 Guidelines 14.2 Refractory Septic Shock & Adjunctive Therapies 14.3 Multidrug-Resistant Pathogens & Antimicrobial Stewardship in the ICU

15 Chapter 15: ICU-Acquired & Severe Focal Infections

15.1 Hospital-Acquired & Ventilator-Associated Pneumonia 15.2 Central Line-Associated Bloodstream Infections & Catheter-Associated UTIs 15.3 Intra-Abdominal Sepsis, Necrotizing Soft Tissue Infections & CNS Infections

16 Chapter 16: Focal, Special-Host & Systemic Infections

16.1 CNS Infections Beyond Bacterial Meningitis: Encephalitis, Brain Abscess & Epidural Abscess 16.2 Infections in the Immunocompromised Host, Tropical & Bioterror Infections 16.3 Infective Endocarditis, Device Infections & Other Focal Cardiovascular Infections 16.4 Antimicrobial Pharmacokinetics, Allergy, Toxicity & Infection Prevention 16.5 Gastrointestinal & Hepatobiliary Infections: Fulminant C. difficile, Typhlitis, CMV Colitis & Abscesses

17 Chapter 17: Neurocritical Care & Coma

17.1 Coma, Altered Mental Status & Acute Delirium in the ICU 17.2 Status Epilepticus & Non-Convulsive Status Epilepticus 17.3 Acute Ischemic Stroke & Intracranial Hemorrhage

18 Chapter 18: Cerebrovascular Syndromes, Encephalopathy & Withdrawal States

18.1 Cerebral Venous Sinus Thrombosis, PRES & Reversible Cerebral Vasoconstriction Syndrome 18.2 Alcohol & Sedative Withdrawal, Wernicke Encephalopathy & Drug-Induced Encephalopathy

19 Chapter 19: Intracranial Hypertension & Neuromuscular Weakness

19.1 Intracranial Pressure Monitoring, Cerebral Perfusion & Tiered ICP Management 19.2 Acute Neuromuscular Respiratory Failure, ICU-Acquired Weakness & Brain Death Determination

20 Chapter 20: Traumatic Brain Injury, Spinal Cord Injury & Toxin-Mediated Paralysis

20.1 Traumatic Brain Injury Management & Paroxysmal Sympathetic Hyperactivity 20.2 Acute Spinal Cord Injury, Neurogenic Shock & Autonomic Dysreflexia 20.3 Toxin-Mediated Paralysis & Neuromuscular Crises: Botulism, Tetanus, Tick Paralysis & Myasthenic Crisis

21 Chapter 21: Gastrointestinal, Hepatic & Abdominal Emergencies

21.1 Acute Upper & Lower Gastrointestinal Bleeding in the ICU 21.2 Acute Liver Failure & Severe Acute Pancreatitis 21.3 Abdominal Compartment Syndrome & Acute Mesenteric Ischemia

22 Chapter 22: Luminal GI Emergencies & Complications of Cirrhosis

22.1 Esophageal, Gastric & Bowel Emergencies: Perforation, Obstruction, Ogilvie Syndrome & Colonic Ischemia 22.2 Complications of Cirrhosis: Alcohol-Associated Hepatitis, Hepatorenal Syndrome & Pulmonary Vascular Syndromes

23 Chapter 23: Trauma, Burns & Perioperative Critical Care

23.1 Polytrauma Resuscitation, Damage Control & Massive Transfusion 23.2 Severe Burn Injury, Inhalation Injury & Environmental Emergencies 23.3 Perioperative Critical Care for High-Risk Surgical Patients

24 Chapter 24: Thoracic Trauma, Environmental Injury & Obstetric Critical Care

24.1 Thoracic Trauma: Flail Chest, Pulmonary Contusion, Great Vessel & Tracheobronchial Injury 24.2 Environmental Injury: Drowning, Diving, Altitude, Heat, Cold, Electrical & Radiation 24.3 Obstetric & Genitourinary Emergencies and the Physiology of Pregnancy

25 Chapter 25: Transplantation, Donor Management & Post-Cardiac Surgery Care

25.1 Solid Organ Transplant Recipients & Deceased Donor Management 25.2 Post-Cardiac Surgery Critical Care: Bleeding, Tamponade, Low Output & Vasoplegia

26 Chapter 26: Hematologic Emergencies, Toxicology, Critical Ultrasound & ICU Liberation

26.1 Hematologic Emergencies in the ICU: HIT, DIC, TMA & Anticoagulant Reversal 26.2 Critical Care Toxicology, Toxidromes & Specific Antidotes 26.3 Critical Care Point-of-Care Ultrasound (POCUS) 26.4 ICU Liberation, Analgosedation, Goals of Care & Critical Care Ethics

27 Chapter 27: Transfusion Medicine, Hematologic & Oncologic Disorders

27.1 Transfusion Medicine: Products, Thresholds, Reactions & Apheresis 27.2 Red and White Cell Disorders, Hemoglobinopathies, Factor Deficiencies & Hypercoagulable States 27.3 Oncologic Emergencies, Hematopoietic Cell Transplant Complications & Cellular Therapy Toxicity

28 Chapter 28: Clinical Pharmacology, Adverse Drug Reactions & Specific Poisonings

28.1 Pharmacokinetic Principles, Dose Adjustment & Drug Interactions in Critical Illness 28.2 Adverse Drug Reactions: Anaphylaxis, Severe Cutaneous Reactions & Hyperthermic Syndromes 28.3 Specific Poisonings: Sodium-Channel Blockers, Lithium, Valproate, Theophylline, Iron, Sulfonylureas & Methemoglobinemia

29 Chapter 29: Ethics, Research Methods, Administration & Abdominal Ultrasound

29.1 Advance Care Planning, Nonbeneficial Treatment, Informed Consent & Confidentiality 29.2 Critical Care Research Methods, Statistics, IRB Oversight & Quality Improvement 29.3 Abdominal, Vascular & Procedural Point-of-Care Ultrasound

23.2 Severe Burn Injury, Inhalation Injury & Environmental Emergencies

Key Takeaways Explain This Topic AI

The Wallace Rule of Nines estimates %TBSA for partial- and full-thickness burns in adults, excluding superficial first-degree erythema; the classic Parkland formula (4 mL x kg x %TBSA) and the American Burn Association Advanced Burn Life Support (ABLS) starting formula (2 mL x kg x %TBSA of Lactated Ringer's) provide starting infusion rates where half is given over the first 8 hours from injury.

Resuscitation fluids must be titrated hourly to physiological endpoints rather than fixed formulas; the standard adult urine output target is 0.5 mL/kg/h (30-50 mL/h), while high-voltage electrical injuries with pigmenturia require 1.0-1.5 mL/kg/h (75-100 mL/h) until clearing to prevent acute tubular necrosis.

'Fluid creep' resulting from excessive crystalloid resuscitation causes life-threatening intra-abdominal hypertension, abdominal compartment syndrome, extremity compartment syndrome, and acute pulmonary edema, worsening tissue ischemia.

Smoke inhalation carries dual lethal toxicities: carbon monoxide causes tissue hypoxia with falsely normal standard pulse oximetry requiring co-oximetry and 100% or hyperbaric oxygen; cyanide halts mitochondrial oxidative phosphorylation presenting with severe lactic acidosis (>= 8-10 mmol/L) and elevated ScvO2, requiring emergent hydroxocobalamin (5 g IV).

Severe accidental hypothermia (< 28°C) presents with Osborne J-waves, bradyarrhythmias, and refractory ventricular fibrillation where extracorporeal life support (ECLS/VA-ECMO) is the rewarming method of choice; heat stroke (core temp > 40°C with CNS dysfunction) mandates immediate rapid cooling to < 38.5-39°C within 30 minutes, where antipyretics are ineffective and contraindicated.

Last updated: October 2026

Burn Injury Classification and Surface Area Estimation

Care of the severely burned patient in the intensive care unit requires precise quantification of burn depth and Total Body Surface Area (%TBSA) to guide fluid resuscitation, wound care, and systemic organ support.

Classification of Burn Depth

Burn wounds are classified pathologically by the depth of cutaneous injury:

Superficial (First-Degree) : Involves the epidermis only. Manifests as painful erythema and dry skin without blistering (e.g., classic mild sunburn). Capillary refill is rapid. Heals within 3 to 6 days without scarring. Superficial burns are strictly EXCLUDED from %TBSA calculations for fluid resuscitation.

Superficial Partial-Thickness (Superficial Second-Degree) : Involves the epidermis and the papillary dermis. Characterized by thin-walled, fluid-filled blisters, weeping erythematous bases, brisk capillary refill, and severe pain to air exposure. Typically heals in 1 to 3 weeks without grafting.

Deep Partial-Thickness (Deep Second-Degree) : Extends into the deeper reticular dermis. Appears mottled pink to waxy white, dry, with diminished or sluggish capillary refill. Sensation to light pinprick is diminished due to dermal nerve ending destruction, though pressure sensation remains intact. Often requires surgical excision and autografting to prevent hypertrophic scarring.

Full-Thickness (Third-Degree) : Destroys the entire epidermis and dermis into subcutaneous fat. The wound appears hard, leathery, charred, or porcelain white (eschar) with visible thrombosed thrombophlebitic subcutaneous vessels. It is completely insensate, dry, and lacks capillary blanching. Mandates early surgical tangential excision and skin grafting.

Fourth-Degree : Extends beyond subcutaneous tissue into underlying fascia, muscle, tendon, or bone. Commonly seen in high-voltage electrical injuries and prolonged entrapment.

Wallace Rule of Nines

In adult patients, %TBSA of partial- and full-thickness burns is estimated using the Wallace Rule of Nines :

• Head and Neck : 9 % 9\% 9% (anterior 4.5 % 4.5\% 4.5% , posterior 4.5 % 4.5\% 4.5% )
• Anterior Torso : 18 % 18\% 18% (chest 9 % 9\% 9% , abdomen 9 % 9\% 9% )
• Posterior Torso : 18 % 18\% 18% (upper back 9 % 9\% 9% , lower back/buttocks 9 % 9\% 9% )
• Each Upper Extremity : 9 % 9\% 9% (anterior 4.5 % 4.5\% 4.5% , posterior 4.5 % 4.5\% 4.5% )
• Each Lower Extremity : 18 % 18\% 18% (anterior 9 % 9\% 9% , posterior 9 % 9\% 9% )
• Perineum and Genitalia : 1 % 1\% 1%

For scattered, non-contiguous, or patchy burns, the Palmar Surface Method is utilized: the patient's entire hand (palm plus all five fingers held together) represents approximately 1 % 1\% 1% of their total body surface area .

• Burn Shock, Resuscitation Formulas, and Fluid Creep
• Pathophysiology of Burn Shock

Extensive burns ( > 20 % TBSA > 20\%\text{ TBSA} > 20% TBSA ) produce a biphasic hemodynamic response. The initial phase ( burn shock ) spans the first 24 to 48 hours and is a complex combination of hypovolemic, distributive, and cardiogenic shock. Thermal injury stimulates an overwhelming release of inflammatory mediators (histamine, prostaglandins, leukotrienes, thromboxane A 2 A_2 A 2 ​ , bradykinin, and reactive oxygen species), causing widespread disruption of microvascular endothelial tight junctions. Protein-rich plasma extravasates rapidly into the interstitial space—not only in burned tissue, but throughout the entire body—culminating in marked hypovolemia, hemoconcentration, and cellular ischemia.

Resuscitation Formulas: Parkland vs. Modern ABA Consensus

The Classic Parkland Formula : Total 24-Hour Volume (mL) = 4 mL × Weight (kg) × % TBSA \text{Total 24-Hour Volume (mL)} = 4\text{ mL} \times \text{Weight (kg)} \times \%\text{TBSA} Total 24-Hour Volume (mL) = 4 mL × Weight (kg) × % TBSA

Administered using a balanced crystalloid (Lactated Ringer's).

Timing : 50 % 50\% 50% of the calculated volume is infused over the first 8 hours from the exact time of injury (NOT from hospital arrival). The remaining 50 % 50\% 50% is infused over the subsequent 16 hours.

The Modern American Burn Association (ABA) Consensus Update :

Extensive clinical evidence demonstrated that rigid adherence to the 4 mL/kg/%TBSA 4\text{ mL/kg/\%TBSA} 4 mL/kg/%TBSA Parkland formula systematically over-resuscitates burn patients. Current ABA guidelines recommend a lower starting fluid rate:

Thermal and Chemical Burns in Adults : 2 mL × Weight (kg) × % TBSA 2\text{ mL} \times \text{Weight (kg)} \times \%\text{TBSA} 2 mL × Weight (kg) × % TBSA

High-Voltage Electrical Burns : 3 to 4 mL × Weight (kg) × % TBSA 3\text{ to }4\text{ mL} \times \text{Weight (kg)} \times \%\text{TBSA} 3 to 4 mL × Weight (kg) × % TBSA

Balanced crystalloid (Lactated Ringer's or Plasma-Lyte) is preferred; 0.9% normal saline should be avoided due to the development of severe hyperchloremic metabolic acidosis.

Physiological Titration: Urine Output Targets

Resuscitation formulas provide only an initial estimate of fluid requirements. Once initiated, the crystalloid rate must be adjusted upward or downward by 10 % to 20 % 10\%\text{ to }20\% 10% to 20% hourly based strictly on physiological endpoints:

Standard Adult Target : 0.5 mL/kg/h 0.5\text{ mL/kg/h} 0.5 mL/kg/h ( 30 to 50 mL/h 30\text{ to }50\text{ mL/h} 30 to 50 mL/h ).

High-Voltage Electrical Injury / Pigmenturia : High-voltage currents traverse deep muscular tissue, generating intense internal heat that induces extensive rhabdomyolysis and myoglobinuria. To prevent myoglobin precipitation in renal tubules and acute tubular necrosis, target a higher urine output of 1.0 to 1.5 mL/kg/h 1.0\text{ to }1.5\text{ mL/kg/h} 1.0 to 1.5 mL/kg/h ( 75 to 100 mL/h 75\text{ to }100\text{ mL/h} 75 to 100 mL/h ) until the urine clears gross pigment.

The Hazard of "Fluid Creep"

Fluid creep refers to the insidious administration of crystalloids far exceeding calculated physiological requirements, commonly driven by automated infusion protocols, reliance on CVP rather than urine output, or treating transient oliguria with excessive fluid boluses. Fluid creep precipitates disastrous complications:

Abdominal Compartment Syndrome (ACS) : Retroperitoneal and visceral edema markedly increases intra-abdominal pressure ( > 20 mmHg > 20\text{ mmHg} > 20 mmHg ), compromising renal perfusion and elevating diaphragms to impair lung compliance.

Extremity Compartment Syndrome : Severe interstitial swelling within unburned limbs enclosed by rigid muscular fascia.

Acute Respiratory Failure : Alveolar-capillary barrier disruption causing non-cardiogenic pulmonary edema.

Wound Conversion : Elevated interstitial pressures compress dermal capillary venules, converting viable partial-thickness burns into ischemic full-thickness wounds.

Resuscitation Parameter Traditional Parkland Formula Modern ABA Consensus Guideline High-Voltage Electrical Burn

Starting Formula 4 mL × kg × % TBSA 4\text{ mL} \times \text{kg} \times \%\text{TBSA} 4 mL × kg × % TBSA 2 mL × kg × % TBSA 2\text{ mL} \times \text{kg} \times \%\text{TBSA} 2 mL × kg × % TBSA 3 to 4 mL × kg × % TBSA 3\text{ to }4\text{ mL} \times \text{kg} \times \%\text{TBSA} 3 to 4 mL × kg × % TBSA

Fluid Selection Lactated Ringer's Lactated Ringer's or balanced crystalloid Lactated Ringer's (avoid 0.9% NS)

Infusion Schedule 50 % 50\% 50% over first 8 h from injury, 50 % 50\% 50% over next 16 h 50 % 50\% 50% over first 8 h from injury, 50 % 50\% 50% over next 16 h Hourly titration based on pigmenturia

Target Adult Urine Output 0.5 mL/kg/h 0.5\text{ mL/kg/h} 0.5 mL/kg/h ( 30 to 50 mL/h 30\text{ to }50\text{ mL/h} 30 to 50 mL/h ) 0.5 mL/kg/h 0.5\text{ mL/kg/h} 0.5 mL/kg/h ( 30 to 50 mL/h 30\text{ to }50\text{ mL/h} 30 to 50 mL/h ) 1.0 to 1.5 mL/kg/h 1.0\text{ to }1.5\text{ mL/kg/h} 1.0 to 1.5 mL/kg/h ( 75 to 100 mL/h 75\text{ to }100\text{ mL/h} 75 to 100 mL/h )

Colloid Rescue Role None in first 24 hours 5% Albumin considered after 12–24 h if fluid creep occurs Albumin infusion if massive volumes required

Inhalation Injury and Airway Management

Inhalation injury independently doubles the mortality of thermal burns and increases the risk of ARDS and pneumonia by up to 20-fold. It encompasses three distinct clinical pathophysiological entities:

1. Supraglottic Thermal Injury

The upper airway possesses tremendous heat-exchange capacity; therefore, true thermal heat injury is almost exclusively confined to structures above the vocal cords (pharynx, larynx, epiglottis). Superheated gases cause acute thermal injury that triggers progressive laryngeal edema. Airway edema develops rapidly over 12 to 24 hours, even if the patient appears comfortable on initial presentation.

Warning

Early Preemptive Endotracheal Intubation Triggers :

Waiting for hypoxemic respiratory failure before intubating an inhalation injury patient is a lethal mistake; massive glottic edema will distort anatomical landmarks and render subsequent intubation or bag-mask ventilation impossible. Immediate preemptive intubation is indicated for:

• Audible stridor, hoarseness, or brassy cough
• Extensive full-thickness facial burns crossing the perioral region
• Blistering or severe edema of the palate, posterior pharynx, or tongue
• Carbonaceous sputum with significant respiratory distress
• Elevated Carboxyhemoglobin ( > 10 % > 10\% > 10% ) following closed-space fire entrapment

Large burns ( > 40 % to 50 % TBSA > 40\%\text{ to }50\%\text{ TBSA} > 40% to 50% TBSA ) prior to aggressive fluid resuscitation swelling

2. Subglottic Chemical Injury

Combustion of synthetic materials produces toxic aldehydes, sulfur dioxide, acrolein, and hydrogen chloride. These water-soluble chemicals react with respiratory mucosal moisture to form strong acids and bases below the vocal cords. The result is extensive tracheobronchial mucosal sloughing, ciliary paralysis, impaired mucous clearance, and the formation of obstructive fibrin-cellular airway casts. This precipitates severe atelectasis, distal air trapping, and profound ventilation-perfusion ( V A / Q V_A/Q V A ​ / Q ) mismatch.

Management : Lung-protective ventilation, aggressive pulmonary hygiene, therapeutic bronchoscopy for airway cast removal, and aerosolized nebulized heparin (5,000–10,000 units) combined with N-acetylcysteine (NAC 20%) every 4 hours to dissolve casts.

Carbon Monoxide vs. Cyanide Toxicity

Patients trapped in structural fires are frequently exposed to two deadly systemic asphyxiants: Carbon Monoxide (CO) and Hydrogen Cyanide (HCN) .

Carbon Monoxide Toxicity

Mechanism : Carbon monoxide binds to hemoglobin with an affinity approximately 200 to 250 times greater than oxygen , producing Carboxyhemoglobin (COHb) . COHb shifts the oxyhemoglobin dissociation curve sharply to the left, impairing oxygen unloading to tissues. Additionally, CO binds directly to intracellular myoglobin and mitochondrial cytochrome c oxidase, inducing cellular hypoxia and free-radical generation.

Diagnostic Trap : Standard dual-wavelength pulse oximetry ( SpO 2 \text{SpO}_2 SpO 2 ​ ) measures light absorption at 660 nm and 940 nm; it cannot distinguish between oxyhemoglobin and carboxyhemoglobin. A patient with a lethal COHb level of 50% will display a falsely reassuring SpO 2 \text{SpO}_2 SpO 2 ​ of 99 % to 100 % 99\%\text{ to }100\% 99% to 100% . Arterial blood gas with co-oximetry is mandatory to directly measure COHb.

Treatment : Immediate high-flow 100 % O 2 100\%\text{ O}_2 100% O 2 ​ via non-rebreather mask or endotracheal tube. Oxygen competes with CO for hemoglobin binding sites, reducing the elimination half-life of CO from 320 minutes on room air down to 60 to 90 minutes on 100 % O 2 100\%\text{ O}_2 100% O 2 ​ .

Hyperbaric Oxygen (HBO at 2.5–3.0 ATA) further reduces the half-life to 20 to 30 minutes and reduces delayed neurological sequelae. Indications for HBO include:

COHb > 25 % \text{COHb} > 25\% COHb > 25% (or > 15 % to 20 % > 15\%\text{ to }20\% > 15% to 20% in pregnant patients due to fetal hemoglobin affinity)

• Loss of consciousness or transient syncope
• Persistent neurological deficits or altered mental status
• Acute myocardial ischemia or ischemic ECG changes
• Severe, unexplained metabolic acidosis
• Cyanide Poisoning

Mechanism : Cyanide is produced during the combustion of nitrogen-containing synthetic polymers (plastics, polyurethane foam, nylon, wool). Inhaled cyanide gas binds with extreme affinity to the ferric ( Fe 3 + {\text{Fe}}^{3+} Fe 3 + ) iron of cytochrome a 3 a_3 a 3 ​ within cytochrome c oxidase (Complex IV) of the mitochondrial electron transport chain. This halts aerobic oxidative phosphorylation, completely arresting cellular ATP production. Cells convert immediately to anaerobic metabolism despite normal or high arterial oxygen tension.

Clinical Presentation : Suspect cyanide toxicity in any closed-space smoke inhalation victim who presents with:

Severe Lactic Acidosis : Serum lactate ≥ 8 to 10 mmol/L \ge 8\text{ to }10\text{ mmol/L} ≥ 8 to 10 mmol/L (a lactate ≥ 10 mmol/L \ge 10\text{ mmol/L} ≥ 10 mmol/L in closed-space smoke exposure has > 85 % > 85\% > 85% sensitivity for toxic cyanide levels).

Refractory Hypotension and Shock : Bradycardia, cardiovascular collapse, and seizures.

Arterialization of Venous Blood : Because tissues are unable to extract oxygen from hemoglobin, central venous and mixed venous oxygen saturation are markedly elevated ( ScvO 2 > 85 % to 90 % \text{ScvO}_2 > 85\%\text{ to }90\% ScvO 2 ​ > 85% to 90% ), narrowing the arteriovenous oxygen content difference.

Definitive Antidote: Hydroxocobalamin (Cyanokit) :

Administer 5 g 5\text{ g} 5 g IV infusion over 15 minutes (may repeat once to a total of 10 g 10\text{ g} 10 g ). Hydroxocobalamin contains a cobalt center that binds cyanide with higher affinity than cytochrome a 3 a_3 a 3 ​ , forming non-toxic cyanocobalamin (Vitamin B 12 \text{B}_{12} B 12 ​ ) , which is excreted harmlessly in the urine.

Tip

Antidote Selection in Smoke Inhalation : Unlike sodium nitrite, hydroxocobalamin does not induce methemoglobinemia. Sodium nitrite forms methemoglobin to bind cyanide, but in fire victims with concurrent carbon monoxide poisoning, producing methemoglobin catastrophically compromises residual oxygen delivery and can precipitate fatal tissue hypoxia. Hydroxocobalamin is the safe, preferred first-line agent.

Diagnostic / Clinical Feature Carbon Monoxide (CO) Poisoning Cyanide (HCN) Poisoning

Mechanism of Hypoxia Impaired O 2 \text{O}_2 O 2 ​ carrying capacity & left-shift of Hb curve Blockade of mitochondrial Cytochrome c Oxidase (Complex IV)

Standard Pulse Oximetry ( SpO 2 \text{SpO}_2 SpO 2 ​ ) Falsely normal ( 98 % to 100 % 98\%\text{ to }100\% 98% to 100% ); requires co-oximetry Normal (reflects dissolved/bound arterial O 2 \text{O}_2 O 2 ​ )

Arterial Lactate Mild-to-moderate elevation Marked elevation ( ≥ 8 to 10 mmol/L \ge 8\text{ to }10\text{ mmol/L} ≥ 8 to 10 mmol/L )

Venous Oxygen Saturation ( ScvO 2 \text{ScvO}_2 ScvO 2 ​ ) Normal or low Abnormally high ( ScvO 2 > 85 % to 90 % \text{ScvO}_2 > 85\%\text{ to }90\% ScvO 2 ​ > 85% to 90% )

Primary Biomarker Carboxyhemoglobin (COHb level on co-oximeter) Whole blood cyanide level (delayed; treat empirically)

First-Line Antidote 100 % O 2 100\%\text{ O}_2 100% O 2 ​ (Hyperbaric O 2 \text{O}_2 O 2 ​ for severe cases) Hydroxocobalamin ( 5 g 5\text{ g} 5 g IV over 15 min)

Contraindicated Therapy Normobaric room air; delay in oxygen delivery Sodium Nitrite (if concurrent CO poisoning present)

• Environmental Emergencies: Accidental Hypothermia and Heat Stroke
• Accidental Hypothermia

Defined as an involuntary drop in core body temperature < 35 ∘ C < 35^\circ\text{C} < 3 5 ∘ C ( < 95 ∘ F < 95^\circ\text{F} < 9 5 ∘ F ). Core temperature must be measured using a low-reading esophageal, bladder, or rectal probe (esophageal is most accurate in intubated patients):

Mild ( 32 ∘ C to 35 ∘ C 32^\circ\text{C}\text{ to }35^\circ\text{C} 3 2 ∘ C to 3 5 ∘ C ) : Vigorous shivering, tachycardia, tachypnea, ataxia, cold diuresis.

Moderate ( 28 ∘ C to 32 ∘ C 28^\circ\text{C}\text{ to }32^\circ\text{C} 2 8 ∘ C to 3 2 ∘ C ) : Shivering ceases, altered mental status, hyporeflexia, bradycardia, hypotension.

Severe ( < 28 ∘ C < 28^\circ\text{C} < 2 8 ∘ C ) : Coma, severe bradycardia, pulmonary edema, ventricular fibrillation, asystole.

Electrocardiographic Hallmarks

Osborne (J) Waves : A distinctive, positive deflection at the junction of the QRS complex and the ST segment, most prominent in the precordial leads. The height of the J-wave is proportional to the degree of hypothermia.

Prolongation of all ECG conduction intervals (PR, QRS, and QTc intervals).

Bradyarrhythmias, junctional rhythms, "slow" atrial fibrillation, and ventricular fibrillation (VF).

Rewarming Strategies and Arrest Protocols

Mild-to-Moderate : Passive external rewarming (warm blankets, ambient room temperature) and active external rewarming (forced warm air blankets).

Severe / Hemodynamically Unstable : Active internal/core rewarming: warmed IV fluids ( 40 ∘ C to 42 ∘ C 40^\circ\text{C}\text{ to }42^\circ\text{C} 4 0 ∘ C to 4 2 ∘ C ), warm humidified ventilator circuit ( 42 ∘ C 42^\circ\text{C} 4 2 ∘ C ), and warm bladder, pleural, or peritoneal irrigation.

Hypothermic Cardiac Arrest : The cold myocardium is refractory to defibrillation and pharmacological cardioversion. Deliver up to 3 initial defibrillation shocks and withhold repeated epinephrine until core temperature reaches > 30 ∘ C > 30^\circ\text{C} > 3 0 ∘ C , as medications accumulate and cause lethal rebound toxicity when the patient rewarms. Continue chest compressions continuously.

Extracorporeal Life Support (ECLS / VA-ECMO) : The gold standard for hypothermic arrest or refractory shock with core temperature < 28 ∘ C < 28^\circ\text{C} < 2 8 ∘ C . ECMO provides complete circulatory support and rapid rewarming ( 1 ∘ C to 2 ∘ C 1^\circ\text{C}\text{ to }2^\circ\text{C} 1 ∘ C to 2 ∘ C per hour).

Note

Resuscitation Principle in Accidental Hypothermia : The cold myocardium is profoundly resistant to electrical cardioversion and inotropic stimulation. Antiarrhythmics and vasopressors administered at temperatures < 30 ∘ C < 30^\circ\text{C} < 3 0 ∘ C undergo minimal hepatic clearance and accumulate to toxic levels. Core rewarming via VA-ECMO or active internal modalities must accompany CPR: "A patient is not dead until warm and dead" (rewarm to ≥ 32 ∘ C to 35 ∘ C \ge 32^\circ\text{C}\text{ to }35^\circ\text{C} ≥ 3 2 ∘ C to 3 5 ∘ C before terminating resuscitation).

Heat Stroke

Heat stroke is a medical emergency defined by a core body temperature > 40 ∘ C > 40^\circ\text{C} > 4 0 ∘ C ( > 104 ∘ F > 104^\circ\text{F} > 10 4 ∘ F ) accompanied by central nervous system dysfunction (delirium, ataxia, seizures, or coma).

Classic (Non-Exertional) Heat Stroke : Occurs during environmental heat waves in elderly, unhoused, or chronically ill individuals with impaired thermoregulation; anhidrosis (dry skin) is common.

Exertional Heat Stroke : Occurs in young athletes or military recruits performing strenuous exertion in hot, humid weather; diaphoresis is frequently preserved.

Complications and Emergency Management

Heat stroke causes widespread systemic inflammatory response, endothelial injury, rhabdomyolysis, acute kidney injury, disseminated intravascular coagulation (DIC), and acute liver failure.

Immediate Rapid Cooling : The cornerstone of therapy; mortality is directly correlated with the duration of hyperthermia. Cool immediately to a target core temperature of < 38.5 ∘ C to 39 ∘ C < 38.5^\circ\text{C}\text{ to }39^\circ\text{C} < 38. 5 ∘ C to 3 9 ∘ C within 30 minutes .

Exertional : Cold-water immersion is the most effective modality, achieving cooling rates > 0.2 ∘ C/min > 0.2^\circ\text{C/min} > 0. 2 ∘ C/min .

Classic / Frail : Evaporative and convective cooling (spraying lukewarm water over the exposed body while high-velocity industrial fans blow continuously).

Pharmacological Contraindications : Antipyretics (acetaminophen, NSAIDs) are completely ineffective and strictly contraindicated. The hypothalamic thermoregulatory set-point in heat stroke is normal (unlike fever); antipyretics do not reduce temperature and worsen hepatic necrosis and coagulopathy. Shivering should be treated with low-dose intravenous benzodiazepines to prevent endogenous heat production.