Environmental Medicine, Bites, Envenomations, Thermal Injury & Dysbarism

Rewarming matches the severity tier: (1) Mild Hypothermia (32–35°C) is treated with Passive External Rewarming (remove wet clothing in a warm room and cover with dry insulating blankets so endogenous shivering generates heat); (2) Moderate Hypothermia (28–32°C) requires Active External and Minimally Invasive Rewarming (forced-air warming blankets [Bair Hugger] applied to the trunk first to prevent core temperature “afterdrop” from cold acidotic extremity blood returning to the heart, plus warmed humidified oxygen and warmed intravenous crystalloids at 40–42°C); and (3) Severe Hypothermia (<28°C) or Hypothermic Cardiac Arrest mandates Active Internal (Core) Rewarming—with Veno-Arterial Extracorporeal Membrane Oxygenation (VA-ECMO) or Cardiopulmonary Bypass as the gold-standard method (rewarming 5–10°C/hr while providing hemodynamic perfusion), or warm thoracic/peritoneal lavage if ECMO is unavailable. During hypothermic VF/VT arrest, perform high-quality CPR, limit shocks and vasoactive drugs (epinephrine/amiodarone are ineffective in a frozen myocardium <30°C and accumulate to toxic levels upon warming), and continue resuscitation until core temperature exceeds 32–35°C.

Frostbite is actual freezing of intracellular and extracellular tissue water into ice crystals combined with microvascular thrombosis when tissue temperatures drop below 0°C (affecting distal toes, fingers, nose, and ears). Superficial frostbite shows waxy white skin with clear blisters after rewarming, whereas deep frostbite forms hard, wooden, insensate gangrenous tissue with hemorrhagic (blood-filled) blisters. Immediate treatment is rapid rewarming in a circulating water bath strictly maintained at 37–39°C (98.6–102.2°F) for 15–30 minutes until the tissue is pliable and erythematous, paired with parenteral opioid analgesia, ibuprofen (inhibits thromboxane A2 dermal ischemia), tetanus prophylaxis, and intravenous/intra-arterial tPA thrombolysis (or iloprost) within 24 hours for severe digit-threatening ischemia. Never rewarm a frostbitten extremity if there is any possibility of refreezing in the field (thaw-refreeze cycles cause catastrophic tissue destruction), never rub with snow or use dry radiant heat, and delay surgical amputation for 1–3 months until dry gangrene fully demarcates (“Frostbite in January, amputate in July”). By contrast, Immersion (Trench) Foot results from prolonged wet, non-freezing cold exposure (1–15°C for days), and Chilblains (Pernio) presents with pruritic/painful violaceous inflammatory papules on the fingers/toes after cold-damp exposure (treated with nifedipine and warming).

Heat Stroke requires immediate rapid physical cooling (target core temperature ≤38.5–39.0°C within 30 minutes): for young patients with Exertional Heat Stroke, Cold/Ice-Water Immersion is the fastest, gold-standard method (lowest mortality); for elderly patients with Classic Heat Stroke (where immersion interferes with monitoring/CPR), use Evaporative Cooling (spraying the naked patient with lukewarm water while blowing high-flow fans across the skin) plus ice packs to the groin, axillae, and neck. Antipyretics (acetaminophen, aspirin/NSAIDs) and Dantrolene are completely ineffective and contraindicated in environmental heat stroke because hypothalamic prostaglandin set-point and ryanodine receptors are not the cause (and acetaminophen/NSAIDs worsen hepatic and renal injury!). Rapid ascent above 2,500 meters (8,000 feet) without acclimatization decreases inspired barometric oxygen pressure (PiO2), triggering hypobaric hypoxia: (1) Acute Mountain Sickness (AMS) presents within 6–24 hours with throbbing headache, anorexia, nausea, dizziness, and insomnia; prevent and treat with gradual ascent and Acetazolamide (a carbonic anhydrase inhibitor that induces a mild renal bicarbonate diuresis and metabolic acidosis, stimulating central medullary chemoreceptors to hyperventilate especially at night). (2) High-Altitude Pulmonary Edema (HAPE) is a noncardiogenic pulmonary edema caused by patchy hypoxic pulmonary vasoconstriction, which dramatically elevates pulmonary artery pressure and forces fluid across overperfused capillary beds; patients present 2–4 days after ascent with dry cough progressing to pink frothy sputum, dyspnea at rest, cyanosis, crackles, and patchy infiltrates; treatment is IMMEDIATE descent + supplemental oxygen + Nifedipine (a dihydropyridine calcium channel blocker that vasodilates the pulmonary arteries; portable hyperbaric Gamow bag or sildenafil/tadalafil if descent is delayed; loop diuretics are NOT indicated!). (3) High-Altitude Cerebral Edema (HACE) is vasogenic cerebral edema from hypoxia-induced cerebral vasodilation and blood-brain barrier breakdown, presenting with ataxia (the earliest and most sensitive sign), severe lethargy, confusion, papilledema, and coma; treatment is IMMEDIATE descent + supplemental oxygen + Dexamethasone.

Scuba diving emergencies follow Boyle's Law (P1 x V1 = P2 x V2) and Henry's Law (gas solubility is proportional to pressure): (1) Decompression Sickness (DCS / Caisson Disease / “The Bends”) occurs 1 to 24 hours after surfacing (or flying in an commercial airplane too soon after a deep/prolonged dive) when dissolved inert nitrogen gas comes out of solution and forms microbubbles in venous blood and tissues: Type I DCS causes deep periarticular joint/muscle pain (shoulder/elbow/knee “the bends”) and mottled skin (cutis marmorata), while Type II DCS causes spinal cord ischemia (paresthesias, paraparesis, urinary retention) and vestibular vertigo (“the staggers”) or cardiopulmonary “chokes.” (2) Arterial Gas Embolism (AGE) occurs immediately (within 1–10 minutes of surfacing) when a panicked diver ascends while holding their breath; expanding alveolar air ruptures pulmonary capillaries (pulmonary barotrauma/pneumothorax), allowing gas bubbles to enter the pulmonary veins → left atrium → systemic arterial circulation to occlude cerebral or coronary arteries (presenting as an acute stroke, seizure, coma, or STEMI the moment the diver breaks the surface). Both DCS and AGE are treated immediately with 100% FiO2 via non-rebreather mask and urgent Recompression in a Hyperbaric Oxygen (HBO) Chamber! In Submersion / Drowning injury, laryngospasm and water aspiration wash out alveolar surfactant, causing noncardiogenic pulmonary edema/ARDS and hypoxic brain injury; management prioritizes immediate rescue breathing/ventilation and Lung-Protective PEEP (both freshwater and saltwater drowning have identical clinical management; prophylactic antibiotics, steroids, and the Heimlich maneuver to expel water are ineffective). In Electrical & Lightning Injuries: low-voltage Alternating Current (AC household) causes tetanic muscle contraction (“let-go” phenomenon) and Ventricular Fibrillation, whereas high-voltage Direct Current (DC / Lightning) causes a single massive depolarization with Asystole, respiratory arrest from medullary respiratory center paralysis (perform reverse triage in mass-casualty lightning strikes: resuscitate apneic/pulseless victims FIRST because spontaneous circulation often returns once brief artificial ventilation bridges medullary apnea!), fern-like cutaneous Lichtenberg figures (pathognomonic of lightning), tympanic membrane rupture, cataracts, and deep muscle rhabdomyolysis with compartment syndrome.

Two venomous spiders are tested on board examinations: (1) Black Widow Spider (Latrodectus mactans; shiny black body with a red-orange ventral hourglass marking): its venom contains alpha-latrotoxin, which binds presynaptic neurexin receptors and triggers massive, uncontrolled exocytosis of acetylcholine and norepinephrine from motor and autonomic nerve terminals. Within 1 hour of a pinprick bite (which shows only a faint targetoid halo and minimal local necrosis), the patient develops severe cramping muscle spasms spreading from the extremity to the back and abdomen—producing board-like abdominal wall rigidity that closely mimics an acute surgical abdomen (but without peritonitis on imaging!), accompanied by diaphoresis, hypertension, and tachycardia; treat with parenteral opioids, benzodiazepines (lorazepam/diazepam) for muscle spasm, and Latrodectus antivenom for severe refractory cases. (2) Brown Recluse Spider (Loxosceles reclusa; violin-shaped dorsal cephalothorax marking, endemic to the South-Central US): its venom contains sphingomyelinase D, a cytotoxic and hemolytic enzyme that activates complement and neutrophils. An initially painless bite evolves over 24–72 hours into a painful erythematous/violaceous blister with a pale ischemic halo (“red, white, and blue sign”) that ulcerates into a sunken black necrotic eschar over 1–2 weeks (rarely causing systemic intravascular hemolysis, DIC, and renal failure known as loxoscelism); treatment is conservative local wound care, tetanus prophylaxis, dapsone/antibiotics only if secondary infection occurs, and delayed surgical excision only after the necrotic eschar has fully demarcated (early wide debridement worsens scarring!). In the Desert Southwest (Arizona), the Bark Scorpion (Centruroides sculpturatus) sting opens neuronal sodium channels, causing severe local pain (positive “tap test” without swelling), cranial nerve/somatic motor hyperactivity (roving conjugate/disconjugate eye movements, opsoclonus, tongue fasciculations, stridor, hypersalivation), and sympathetically mediated hypertension/tachycardia in children (treated with Centruroides-specific equine Fab2 antivenom [Anascorp] and midazolam). For Marine Envenomations: Stingray, Lionfish, and Stonefish spines contain heat-labile proteinaceous toxins → immediately immerse the wound in hot water (40–45°C / 104–113°F) for 30–90 minutes to denature the venom and relieve pain; whereas Cnidarian (Jellyfish / Portuguese Man-of-War) nematocyst tentacles are treated with vinegar (5% acetic acid) and tentacle removal (never rinse with fresh water, which osmotically triggers nematocyst firing!).

Mammalian bite wounds carry polymicrobial oral flora: Cat and Dog bites (where deep puncture cat bites have an >80% infection rate and predisposition to flexor tenosynovitis/osteomyelitis) are most commonly infected within 12–24 hours by Pasteurella multocida (a small Gram-negative coccobacillus causing rapid cellulitis), whereas Dog bites in asplenic, cirrhotic, or immunocompromised hosts also carry Capnocytophaga canimorsus (causing fulminant sepsis, DIC, and symmetrical peripheral gangrene). Human bites—classically a “clenched-fist injury” (“fight bite”) where a punch strikes an opponent's tooth, inoculating the 3rd or 4th MCP joint capsule—introduce Eikenella corrodens (a facultative Gram-negative rod resistant to clindamycin and metronidazole), Staphylococcus aureus, and oral anaerobes. For all cat bites, human bites, deep dog bites, and bites on the hands, feet, face, or genitals, prescribe first-line oral Amoxicillin-Clavulanate (Augmentin) (or IV Ampicillin-Sulbactam if hospitalized) for 3–5 days prophylaxis (5–14 days for active infection), update tetanus, and leave puncture wounds, cat bites, human bites, and hand/foot bites OPEN to heal by secondary intention (only clean facial lacerations are loosely sutured primarily for cosmesis!). Rabies Post-Exposure Prophylaxis (PEP) is a medical emergency because clinical rabies encephalitis (hydrophobia, aerophobia, pharyngeal spasms, agitation, coma, Negri bodies in hippocampal pyramidal neurons and cerebellar Purkinje cells) is virtually 100% fatal. Indications for Rabies PEP depend on the animal species: (1) High-risk wild reservoir reservoirs (Bats, Raccoons, Skunks, Foxes, Coyotes): ANY bite, scratch, or even awakening in a room with a bat present (or finding a bat in a room with an unattended infant, intoxicated person, or mentally impaired individual, because bat teeth are microscopic!) mandates immediate Rabies PEP (unless the wild animal is captured and brain-biopsy negative); (2) Domestic Dogs, Cats, and Ferrets: if the animal is healthy and available, quarantine and observe the animal for 10 days (do not give PEP unless the animal develops signs of rabies; if the animal is stray/escaped or rabid, start PEP immediately); and (3) Small Rodents (mice, rats, squirrels, hamsters) and Lagomorphs (rabbits, hares): almost never transmit rabies and do NOT require PEP. For a previously unvaccinated patient, Rabies PEP consists of: (1) Immediate thorough soap-and-water wound cleansing, (2) Human Rabies Immune Globulin (HRIG, 20 IU/kg) infiltrated directly into and around the wound (with any remaining volume injected IM at a site distant from the vaccine), and (3) 4 doses of Inactivated Rabies Vaccine administered IM in the deltoid on Days 0, 3, 7, and 14 (add a 5th dose on Day 28 if the patient is immunocompromised; if the patient was previously vaccinated against rabies, give NO HRIG and only 2 vaccine doses on Days 0 and 3!).

The PECARN rule stratifies pediatric minor head trauma (GCS 14–15) into three risk tiers: (1) High-Risk Criteria (Obtain Immediate Non-Contrast Head CT; ~4.4% ciTBI risk): for children <2 years old, any of GCS ≤14, other signs of altered mental status (agitation, somnolence, repetitive questioning, slow response), OR palpable skull fracture; for children ≥2 years old, any of GCS ≤14, other signs of altered mental status, OR clinical signs of basilar skull fracture (hemotympanum, periorbital “raccoon eyes,” retroauricular “Battle sign,” or CSF rhinorrhea/otorrhea). (2) Intermediate-Risk Criteria (ED Observation for 4–6 hours vs. Head CT based on parental preference, worsening symptoms, or multiple factors; ~0.9% risk): for children <2 years old, any of non-frontal (occipital, parietal, or temporal) scalp hematoma, loss of consciousness (LOC) ≥5 seconds, severe mechanism of injury (fall >3 feet [0.9 m], MVC with ejection/rollover/fatality, struck by high-impact object), or not acting normally per parent; for children ≥2 years old, any of any loss of consciousness, history of vomiting, severe mechanism of injury (fall >5 feet [1.5 m]), or severe headache. (3) Very Low-Risk Criteria (Zero High- or Intermediate-Risk predictors present; <0.02–0.05% risk): DO NOT obtain a Head CT—reassure parents and discharge home with return precautions!

Three classic hemoglobin/cytochrome asphyxiants are tested on emergency medicine boards: (1) Carbon Monoxide (CO) Poisoning (winter space heaters, indoor charcoal grills, automobile exhaust, house fires): CO binds hemoglobin with >200 times the affinity of oxygen to form carboxyhemoglobin (COHb), shifting the oxygen-hemoglobin dissociation curve to the LEFT (preventing O2 unloading to tissues) and inhibiting mitochondrial Complex IV. Patients present with headache, dizziness, nausea, confusion, cherry-red skin/mucosa, and bilateral globus pallidus necrosis on brain MRI; standard pulse oximetry (SpO2) is falsely normal (~98–100%) because two-wavelength pulse oximeters cannot distinguish COHb from oxyhemoglobin—diagnose via arterial/venous Co-Oximetry (COHb >3% in nonsmokers, >10% in smokers) and treat with 100% high-flow normobaric oxygen (reduces COHb half-life from 5 hours to 90 minutes) or Hyperbaric Oxygen (HBO) (reduces half-life to 25 minutes; indicated for COHb >25% [>15% in pregnancy], syncope, coma, seizures, or myocardial ischemia). (2) Cyanide Poisoning (burning wool/silk/polyurethane plastics in house fires or prolonged sodium nitroprusside infusion): inhibits ferric iron (Fe3+) in cytochrome c oxidase (Complex IV), halting aerobic respiration so cells cannot extract O2 from blood—causing arterialization of venous blood (narrowed arteriovenous O2 difference), bitter almond breath, coma, hypotension, and severe high-anion-gap lactic acidosis (lactate >10 mmol/L); treat immediately with intravenous Hydroxocobalamin (Vitamin B12a, which binds cyanide to form nontoxic cyanocobalamin excreted in urine) plus sodium thiosulfate. (3) Methemoglobinemia (caused by oxidizing drugs: dapsone, topical benzocaine/lidocaine anesthetics, nitrates/nitrites, primaquine, phenazopyridine, or well-water nitrates in infants): oxidizes hemoglobin iron from ferrous (Fe2+) to ferric (Fe3+), which cannot bind O2 and shifts the remaining curve to the left; patients present with dusky slate-gray central cyanosis refractory to 100% oxygen, a classic pulse oximetry reading clamped at ~85% despite a normal arterial PaO2 (>100 mmHg) on ABG (“saturation gap”), and chocolate-brown blood on filter paper; treat immediately with intravenous Methylene Blue (which uses NADPH from G6PD to reduce Fe3+ back to Fe2+; if the patient has G6PD deficiency, methylene blue is ineffective and triggers hemolysis—use high-dose Vitamin C [ascorbic acid] or exchange transfusion instead!).

In a mass-casualty Lightning Strike, standard trauma triage is inverted into “Reverse Triage” (resuscitate the “dead” first!): victims who are awake, moaning, or breathing spontaneously have already survived the initial electrical discharge and will likely live, whereas victims who appear clinically dead (apneic and pulseless) often suffer from transient medullary respiratory center paralysis after spontaneous cardiac automaticity has resumed—unless immediate bag-valve-mask ventilation is provided, they will suffer a secondary hypoxic cardiac arrest and die! Cutaneous hallmarks of lightning include pathognomonic ferning, arborescent erythematous marks (Lichtenberg figures, which are NOT true thermal burns and fade within 24–48 hours), tympanic membrane rupture (from the acoustic blast wave), and delayed cataracts. In high-voltage industrial electrical injuries (>1,000 V), superficial entry/exit skin burns look deceptively small (“tip of the iceberg”) while deep periosseous skeletal muscle undergoes massive coagulative necrosis—releasing myoglobin, potassium, and intracellular phosphate to cause life-threatening hyperkalemia, pigment-induced acute kidney injury (rhabdomyolysis), and extremity compartment syndrome (requiring aggressive isotonic crystalloid resuscitation titrated to a urine output of 1–1.5 mL/kg/hr and low-threshold decompressive fasciotomy). In pediatric oral electrical burns (a toddler biting an electrical cord at the oral commissure), advise parents that severe delayed labial artery hemorrhage occurs 5 to 14 days later when the necrotic eschar sloughs off (instruct parents to compress the lip corner between finger and thumb and return to the ED immediately).

Whole-body exposure to penetrating ionizing radiation (>1 Gray [Gy] / 100 rads) preferentially destroys rapidly dividing stem cells according to the Law of Bergonie and Tribondeau, producing Acute Radiation Syndrome (ARS) across four chronological phases (Prodromal nausea/vomiting → Latent symptom-free period → Manifest illness → Recovery or death) and three dose-dependent organ subsyndromes: (1) Hematopoietic Subsyndrome (1–6 Gy): bone marrow hypoplasia causes a rapid drop in the Absolute Lymphocyte Count (ALC) within 24–48 hours, followed 2–4 weeks later by neutropenia (infection) and thrombocytopenia (hemorrhage); (2) Gastrointestinal Subsyndrome (6–15 Gy): denudation of intestinal crypt stem cells causes severe secretory/bloody diarrhea, mucosal sloughing, gram-negative bacteremia, and hypovolemic shock within 5–10 days; and (3) Cerebrovascular / CNS Subsyndrome (>20–30 Gy): rapid cerebral edema, ataxia, seizures, coma, and 100% mortality within 24–72 hours. The two most sensitive biologic biodosimeters predicting radiation dose and survival are: (1) Time to onset of emesis (vomiting within <1–2 hours of exposure indicates a severe/potentially lethal dose >4 Gy), and (2) the rate of decline of the Absolute Lymphocyte Count (ALC) over the first 24–48 hours (Andrews lymphocyte nomogram). Management includes external decontamination (removing clothing removes 90% of radioactive dust), reverse isolation, G-CSF (filgrastim) for marrow stimulation, and specific radionuclide decorporation agents: Potassium Iodide (KI) to block thyroid uptake of Radioactive Iodine-131, Prussian Blue for Cesium-137 or Thallium, and DTPA for Plutonium/Americium.

Four marine foodborne toxidromes are high-yield on emergency medicine and internal medicine boards: (1) Scombroid Fish Poisoning: caused by eating improperly refrigerated dark-meat fish (tuna, mahi-mahi, mackerel, bonito, skipjack) in which surface bacteria decarboxylate flesh histidine into massive quantities of histamine. Within 10–60 minutes of eating fish that may taste peppery or metallic, diners develop bright red facial/neck flushing, throbbing headache, palpitations, wheezing, and diarrhea resembling acute anaphylaxis; treat immediately with H1 and H2 antihistamines (diphenhydramine + famotidine) (epinephrine if bronchospasm/hypotension occurs; note that the patient is not allergic to fish and does not need to avoid properly refrigerated fish in the future!). (2) Ciguatera Fish Poisoning: caused by eating large tropical predatory reef fish (barracuda, grouper, red snapper, amberjack, moray eel) that bioaccumulate dinoflagellate (Gambierdiscus toxicus) ciguatoxin, which opens voltage-gated sodium channels. Patients develop acute gastroenteritis followed by perioral paresthesias, bradycardia/hypotension, and the pathognomonic neurological symptom of cold allodynia / temperature reversal (cold objects or cold drinks feel burning hot, or teeth feel loose; managed supportively with IV fluids, atropine for bradycardia, and IV Mannitol for severe neurological symptoms). (3) Pufferfish (Fugu) Poisoning (Tetrodotoxin) and (4) Paralytic Shellfish Poisoning (Saxitoxin from “red tide” dinoflagellate blooms in mussels/clams/oysters): both toxins block voltage-gated sodium channels in peripheral nerves, causing rapid onset (within 30 minutes) of perioral numbness, floating sensation, cranial nerve palsies, and ascending flaccid diaphragmatic paralysis requiring emergent endotracheal intubation and mechanical ventilation until the toxin is renally excreted.

Four environmental heavy metal toxidromes require specific chelation regimens: (1) Lead (Pb) Poisoning (peeling pre-1978 house paint chips/dust in toddlers, battery recycling, moonshine, retained bullet fragments): Lead inhibits two heme synthesis enzymes—delta-ALA dehydratase and ferrochelatase—leading to elevated erythrocyte protoporphyrin and microcytic sideroblastic anemia with coarse basophilic stippling on blood smear. Clinically, remember LEAD: Lead lines on gingiva (Burton lines) and tibial metaphyses on pediatric knee X-ray, Encephalopathy / developmental cognitive regression and Erythrocyte basophilic stippling, Abdominal colic and sideroblastic Anemia, and Drops (wrist drop [radial nerve] and foot drop [peroneal nerve] motor neuropathy). Confirm capillary screening with a venous Blood Lead Level (BLL): remove environmental source for BLL ≥3.5 mcg/dL; administer oral Succimer (DMSA) for BLL 45–69 mcg/dL in children; and administer parenteral Dimercaprol (BAL) PLUS Calcium Disodium EDTA for BLL ≥70 mcg/dL or acute Lead Encephalopathy (always give BAL first before CaNa2-EDTA to prevent EDTA from redistributing lead into the brain!). (2) Arsenic (As) Poisoning (contaminated groundwater, wood preservatives, pesticides, smelting): trivalent arsenic binds sulfhydryl (lipoic acid) groups of pyruvate dehydrogenase; acute poisoning causes garlic breath, hemorrhagic “rice-water” gastroenteritis, QTc prolongation (torsades de pointes), and shock, while chronic poisoning causes stocking-glove painful peripheral neuropathy, palmoplantar hyperkeratosis, transverse white fingernail striae (Mees lines), and skin/lung/bladder cancer; chelate with Dimercaprol (BAL) or Succimer. (3) Mercury (Hg) Poisoning (thermometers, batteries, artisanal gold mining, methylmercury in predatory fish): causes intention tremor, erethism (“Mad Hatter” neuropsychiatric irritability/shyness), gingivostomatitis, visual/auditory loss (Minamata disease), and membranous nephropathy (chelate with Dimercaprol or Succimer). (4) Acute Iron (Fe) Overdose (toddlers ingesting maternal prenatal vitamins): causes corrosive hemorrhagic gastroenteritis (radiopaque pills visible on abdominal X-ray!), high-anion-gap metabolic acidosis, shock, hepatic necrosis, and late gastric outlet scarring; chelate with intravenous Deferoxamine (which binds ferric iron to form renally excreted ferrioxamine, turning urine a classic vin rose [pinkish-red] color).