Environmental & Allergic Emergencies
Epinephrine, cooling, rewarming, and descent
Anaphylaxis and angioedema
Anaphylaxis is a rapid, multisystem IgE-mediated reaction (skin, airway, GI, circulation), or hypotension alone after exposure to a known allergen. Give intramuscular epinephrine into the anterolateral thigh IMMEDIATELY and repeat every 5–15 minutes as needed. There is no absolute contraindication, and epinephrine is the only therapy that reduces mortality.
Delayed epinephrine is the leading preventable cause of anaphylaxis death; give it before antihistamines or steroids.
Adjuncts. After epinephrine, lay the patient supine and give IV fluids for hypotension, H1 (diphenhydramine) plus H2 antihistamines, corticosteroids, and albuterol for bronchospasm. Refractory shock needs an IV epinephrine infusion; patients on β-blockers who resist epinephrine may respond to glucagon. An elevated serum tryptase supports the diagnosis. Observe for a biphasic reaction, which can recur hours later without re-exposure, and discharge with an epinephrine auto-injector and allergy referral.
Angioedema without hives suggests bradykinin, not histamine. Absent urticaria and itch is the tip-off, though anaphylaxis can occasionally lack hives, and these swellings respond poorly to epinephrine, antihistamines, and steroids.
| Feature | Allergic | ACE-inhibitor | Hereditary (HAE) |
|---|---|---|---|
| Mediator | Histamine (IgE, mast cells) | Bradykinin (reduced breakdown) | Bradykinin (C1-esterase inhibitor deficiency) |
| Urticaria, itch | Present | Absent | Absent |
| Timing | Minutes after exposure | Any time, even years into therapy | Recurrent attacks, often triggered by trauma, dental work, or stress |
| Labs | Tryptase may rise | Normal C4 | Low C4 |
| Treatment | Epinephrine, antihistamines, steroids | Stop the ACE inhibitor; secure the airway | C1-inhibitor concentrate, icatibant (B2 antagonist), ecallantide |
Heat illness
Heat stroke is a core temperature above 40 °C (104 °F) WITH central nervous system dysfunction (confusion, seizures, coma). Cool rapidly, ideally by cold-water or ice-water immersion for exertional cases, and stop at about 39 °C to avoid overshoot. Classic (nonexertional) heat stroke strikes the elderly during heat waves and is often cooled by evaporation (misting plus fans). Antipyretics do NOT work because there is no hypothalamic set-point shift, and dantrolene has no role. Watch for rhabdomyolysis, AKI, liver injury, and DIC.
Heat exhaustion is a core temperature under 40 °C with intact mentation, heavy sweating, and a normal neurologic exam; rest, cooling, and fluids suffice. CNS dysfunction with a temperature over 40 °C is what upgrades it to life-threatening heat stroke.
| Feature | Heat exhaustion | Heat stroke |
|---|---|---|
| Core temperature | <40 °C | >40 °C |
| Mental status | Normal | Confusion, seizures, coma |
| Treatment | Rest, cooling, oral or IV fluids | Emergency rapid cooling (ice-water immersion) |
Cold injury and drowning
Hypothermia. Mild hypothermia (32–35 °C) causes shivering; moderate (28–32 °C) brings confusion, loss of shivering, and Osborn (J) waves at the QRS-ST junction, which grow as the temperature falls; severe (<28 °C) brings bradycardia and arrhythmias. Rewarm by severity: passive or active external rewarming for mild cases, and active core rewarming (warm IV fluids, lavage, ECMO) for severe hypothermia or arrest.
Not dead until warm and dead. Continue resuscitation until the core is rewarmed to at least 32–35 °C before declaring death; the cold myocardium responds poorly to shocks and drugs.
Handle severely hypothermic patients gently; rough movement can trigger ventricular fibrillation.
Afterdrop. During rewarming, cold peripheral blood returning to the core can drop the temperature further and cause hypotension. Rewarm the core, give warmed fluids, and monitor for arrhythmia.
Frostbite is rewarmed rapidly in a 37–39 °C water bath, not by rubbing, and only when refreezing can be prevented.
Drowning injures by hypoxemia; the fresh-versus-salt-water distinction is not clinically important. Prioritize oxygenation and ventilation, not abdominal thrusts, and observe survivors for delayed pulmonary edema or ARDS over the following hours.
High-altitude illness
Descent is the universal cure. Acute mountain sickness (AMS) causes headache and nausea; high-altitude cerebral edema (HACE) adds ataxia and encephalopathy; high-altitude pulmonary edema (HAPE) causes dyspnea, cough, and hypoxia and is the leading cause of altitude death. Gradual ascent is the best prevention.
| Syndrome | Features | Treatment |
|---|---|---|
| AMS | Headache, nausea | Acetazolamide, descent |
| HACE (brain) | Ataxia, encephalopathy | Descent, dexamethasone, oxygen |
| HAPE (lung) | Dyspnea, cough, hypoxia | Descent, oxygen, nifedipine |
Acetazolamide (a carbonic anhydrase inhibitor) speeds acclimatization by producing a mild metabolic acidosis that stimulates ventilation.
Bites, stings, and electrical injury
Pit vipers. North American crotalid (rattlesnake) bites cause local tissue necrosis and coagulopathy. Treat with antivenom (CroFab), immobilization, and supportive care, following swelling and coagulation studies. Do NOT apply a tourniquet or ice, incise, or suction; these increase local injury without benefit.
Black widow (Latrodectus) envenomation causes severe muscle cramps and abdominal rigidity that can mimic an acute abdomen; treat with opioid analgesics plus benzodiazepines, and antivenom for severe envenomation refractory to these.
Electrical injury damages deep tissue far beyond the visible surface burns, causing rhabdomyolysis, compartment syndrome, and arrhythmias; monitor the ECG and give IV fluids to protect the kidneys.
Lightning commonly causes asystole or respiratory arrest with good recovery if resuscitation starts promptly, so mass-casualty lightning strikes use REVERSE triage: resuscitate the apparently dead first.