This final lesson of the Pulmonary and Critical Care volume surveys the “grab bag” of critical care emergencies that every intensivist must manage: anaphylaxis, hyperthermic emergencies, accidental hypothermia, the major toxicologic emergencies (toxic alcohols, carbon monoxide, cyanide, drugs of abuse, and therapeutic drug overdoses), acute abdominal surgical emergencies, obstetric critical care, and anoxic brain injury. The unifying themes are early recognition, rapid reversal of the underlying insult, and disciplined supportive care.
Anaphylaxis
Anaphylaxis is a severe systemic reaction caused by acute release of inflammatory mediators into the circulation. Most episodes are triggered by IgE-mediated responses to foods, medications, insect venom, or latex, but some occur without an identifiable allergic trigger. The resulting capillary leak produces pruritus, urticaria, tissue swelling (angioedema), and hypotension; the distributive shock of anaphylaxis closely mimics septic shock. Symptom onset may be immediate or delayed by hours to days, although faster onset generally signals a more severe reaction. Airway-compromising angioedema is the most feared complication. Table 62 (as published in the source) summarizes organ involvement; a published case image (Figure 28) shows dramatic angioedema of the tongue, lower lip, and right side of the face.
| Organ system | Symptoms | Signs | Patients affected |
|---|---|---|---|
| Skin and mucosa | Pruritus of skin, oropharynx, genitals, palms, soles | Flushing, urticaria, morbilliform rash, angioedema | 85% |
| Respiratory | Dyspnea, chest and throat tightness, stridor, cough, hoarseness, sneezing, rhinorrhea | Wheeze, stridor, respiratory distress | 70% |
| Cardiovascular | Lightheadedness, chest pain, palpitations | Hypotension, tachycardia > bradycardia | 45% |
| Gastrointestinal | Abdominal pain, nausea, vomiting, diarrhea | — | 45% |
| Neurologic | Anxiety, headache | Encephalopathy | 15% |
Treatment is epinephrine, first and fast, given intramuscularly or intravenously. Antihistamines may be added for pruritus and rash, but they are adjuncts only; evidence supporting glucocorticoids is sparse. Some patients need repeated or continuous epinephrine to achieve stability. Provide supplemental oxygen, watch closely for airway compromise (intubation may be required), give fluid resuscitation with vasopressors as needed, and remove the precipitating antigen if exposure is ongoing. Anaphylaxis is rarely fatal, but survival depends on early recognition and prompt disease-reversing therapy, especially when shock or airway compromise is present.
Biphasic anaphylaxis — recurrence 1 to 72 hours after the initial episode resolves — is more likely after a severe initial episode or when more than one dose of epinephrine was required. When biphasic risk is present, or when fatality risk is elevated (coexisting cardiovascular disease, limited access to epinephrine or emergency services), extended observation of up to 6 hours or longer is warranted. After discharge, long-term management centers on strict trigger avoidance and education in self-administered epinephrine use; serum tryptase, which peaks 60–90 minutes after onset and remains measurable up to about 5 hours, can retrospectively document mast-cell activation when the diagnosis is uncertain.
Angioedema without an allergic trigger
Angioedema can be bradykinin-mediated rather than mast-cell mediated, occurring without allergic stimulus — notably in response to ACE inhibitors (even after years of uneventful use) and sometimes with no identifiable cause. Compared with anaphylaxis, nonallergic angioedema has a slower onset and is not accompanied by urticaria, pruritus, or hypotension, but the swelling can still threaten the airway and may require intubation.
Recurrent angioedema can be hereditary or acquired. Hereditary angioedema is distinct from mast cell–associated angioedema: it results from deficiency or dysfunction of C1 esterase inhibitor, with unregulated complement activation causing sporadic, localized edema of the head and neck. The absence of typical urticarial lesions distinguishes it clinically. Diagnosis relies on quantitative and functional C1 esterase inhibitor levels and C4 complement levels. Treatment is supportive, sometimes supplemented with agents that target bradykinin or complement pathways.
Hyperthermic Emergencies
A hyperthermic emergency is a core temperature elevation, usually above 40 °C (104 °F), causing end-organ dysfunction: altered mental status, seizures, kidney injury, muscle rigidity, rhabdomyolysis, acute respiratory distress syndrome, or disseminated intravascular coagulation (DIC). The three classic causes — heat stroke, malignant hyperthermia, and neuroleptic malignant syndrome — are all fatal if not recognized and treated appropriately. Predisposing factors extend well beyond hot weather: extremes of age, heart failure, dehydration, obesity, anticholinergic drugs, occlusive clothing, thyrotoxicosis, sepsis, sympathomimetic drugs, and withdrawal states all impair heat dissipation or increase heat production.
| Diagnosis | Suggestive history | Key examination findings | Treatment | Notes |
|---|---|---|---|---|
| Heat stroke | Environmental heat exposure | Encephalopathy and fever | Rapid active cooling (evaporative techniques in MKSAP; cold-water immersion prioritized by 2025 SCCM guidance) | Historically MKSAP cautioned against ice-water immersion in nonexertional cases |
| Malignant hyperthermia | Exposure to volatile anesthetic or succinylcholine | Masseter muscle rigidity; rising arterial PCO2 | Stop inciting drug; dantrolene | Monitor and treat hyperkalemia and rising PCO2 |
| Neuroleptic malignant syndrome | Typical > atypical antipsychotic; onset over days to weeks | Altered mentation, severe (“lead-pipe”) rigidity, tachycardia, hypertension, hyporeflexia, no clonus | Stop the inciting drug; dantrolene or bromocriptine | Resolves over days to weeks |
| Severe serotonin syndrome* | Within 24 h of starting or increasing an SSRI; gastrointestinal prodrome | Agitation, myoclonus, hyperreflexia, rigidity | Stop inciting drug; benzodiazepines; cyproheptadine | Resolves within 24 hours |
*Serotonin syndrome is not routinely considered a cause of severe hyperthermia but is commonly confused with neuroleptic malignant syndrome.
Heat stroke
Heat stroke occurs when the body’s thermal regulatory system is overwhelmed by environmental heat load, defined by core temperature above 40 °C (104 °F) plus encephalopathy. Elderly patients with comorbidities and predisposing medications are particularly vulnerable (classic/nonexertional heat stroke); exertional heat stroke strikes young, otherwise healthy individuals when high ambient temperature, physical activity, and humidity coincide. Untreated mortality reaches 60%. Extraneurologic complications include kidney and liver injury, DIC, and rhabdomyolysis. Hepatocytes are exquisitely heat-sensitive: aminotransferases are routinely elevated on presentation and may eventually exceed 100 times normal.
The two forms differ in useful ways. In classic heat stroke, sweating has often ceased (hot, dry skin), dehydration predominates, and fluid requirements can be deceptively modest. In exertional heat stroke, patients are frequently profusely diaphoretic despite dehydration, and rhabdomyolysis with its complications (hypocalcemia, hyperphosphatemia, hyperkalemia), acute kidney injury, and hyponatremia are common, demanding aggressive crystalloid resuscitation. Because peripheral vasoconstriction impedes heat loss, repeated isotonic fluid boluses are preferred over α-adrenergic vasopressors for initial hypotension. Above 42 °C (107.6 °F), direct cellular injury ensues: thermosensitive enzymes fail and oxidative phosphorylation uncouples, so the duration of hyperthermia drives morbidity and mortality — cooling is a race.
Centrally acting antipyretics (NSAIDs, acetaminophen) are not effective. For nonexertional heat stroke, evaporative cooling (water mist plus fans) with or without ice packs can lower core temperature to a safe target, usually about 38.5 °C (101 °F). For exertional heat stroke, evaporative cooling may suffice, but patients who remain severely symptomatic sometimes require immersion in ice water to bring the core temperature down rapidly; MKSAP 19 stated that because immersion may be complicated by hypothermia, it is not recommended as first-line treatment, and ice-water immersion should not be used in older patients with nonexertional hyperthermia. Active cooling should be stopped around 38–39 °C to avoid overshoot hypothermia. Seizures are common during cooling, and cold-induced tonic-clonic rigidity can mimic seizure activity; if intubation is needed, avoid depolarizing agents.
Malignant hyperthermia
Malignant hyperthermia occurs in people with a rare autosomal dominant derangement of intracellular calcium metabolism who are exposed to inhaled anesthetic agents (halothane, isoflurane) or the depolarizing paralytic succinylcholine. The response includes muscle rigidity, rhabdomyolysis, cardiac arrhythmias, and core temperatures of 45 °C (113 °F) or higher; mortality can reach 10%. Masseter muscle rigidity and an unexplained rise in end-tidal/arterial PCO2 are early clues in the perioperative setting. Treatment is immediate discontinuation of the triggering agent, active cooling, and dantrolene given every 5 to 10 minutes until rigidity and hyperthermia resolve, with monitoring for hyperkalemia. There is no dedicated Harrison’s chapter for this entity; the MKSAP framework and hyperthermia differential (Table 63) remain the reference point.
Neuroleptic malignant syndrome and serotonin syndrome
Neuroleptic malignant syndrome (NMS) is an idiosyncratic reaction classically linked to first-generation antipsychotics such as haloperidol, but it also occurs with newer antipsychotics and antiemetics. It is most common at initiation or dose escalation yet can occur after prolonged use; highlighting a pathogenetic role for dopamine receptor blockade, it has also followed rapid withdrawal of dopaminergic Parkinson disease medications. The tetrad is fever, mental status change, muscle rigidity, and dysautonomia; mortality may exceed 10%. Treatment is stopping the trigger (or reinstating the withdrawn dopaminergic agent), active cooling, and supportive care with IV fluids; evidence for benzodiazepines, dantrolene, and bromocriptine is anecdotal. Antipsychotics may be reintroduced after at least 2 weeks, at lower dose, avoiding dehydration and concomitant lithium. NMS resolves over days to weeks — a useful contrast with serotonin syndrome, which arises within 24 hours of starting or increasing a serotonergic drug (SSRIs most commonly), features hyperreflexia and myoclonus rather than hyporeflexia, and resolves within about 24 hours of drug removal; cyproheptadine is used off-label when benzodiazepines fail.
Accidental Hypothermia
Accidental hypothermia, defined by a core temperature below 35 °C (95 °F), is classically a winter diagnosis but occurs in temperate weather whenever exposure is sufficient (wet conditions are a classic setup). In mild hypothermia, shivering is an effective compensatory mechanism; early signs include tachycardia, hyperventilation, diuresis, and poor judgment. Below 32 °C (89.6 °F), shivering ceases, and hypotension, bradycardia and other arrhythmias, and progressive depression of consciousness follow, ending in coma. Moderate hypothermia brings paradoxical undressing and hallucinations; Osborne (J) waves may appear on the electrocardiogram (Figure 29) — a shoulder or “hump” at the junction of the QRS and ST segments, best seen in the inferior and lateral chest leads.
| Severity | Core temperature | Findings |
|---|---|---|
| Mild | 32.0–35.0 °C (89.6–95.0 °F) | ↑HR, ↑BP, ↑RR, shivering, alert, poor judgment |
| Moderate | 28.0–32.0 °C (82.4–89.6 °F) | ↓HR, ↓BP, ↓RR, ↓cardiac output, ↓O2 consumption, ↓kidney function, somnolence, no shivering, supraventricular arrhythmia |
| Severe | <28.0 °C (<82.4 °F) | Coma, absent reflexes, ventricular arrhythmia, asystole, apnea |
Management is staged by severity. A shivering patient removed from the cold and adequately insulated will passively rewarm. Once core temperature falls below 32 °C and shivering stops, active rewarming is required: surface methods (heating pads, forced-air warming) or invasive methods (peritoneal or pleural irrigation via peritoneal catheter or thoracostomy tube). Extracorporeal life support (ECLS), including cardiopulmonary bypass, is recommended for patients in cardiac arrest because it maximizes rewarming rate and provides hemodynamic support; venoarterial ECMO is increasingly favored over bypass because it reduces post-rewarming cardiorespiratory failure and improves neurologic outcome. During active rewarming, monitor core temperature with an esophageal probe — rectal and bladder temperatures lag behind the rising core. Hypothermic myocardium is irritable: pulses may be undetectable in a still-perfusing patient (maximize monitor gain before declaring pulselessness), and chest compressions that are not truly indicated can convert a perfusing rhythm into a nonperfusing one. Medications are largely ineffective in deep hypothermia and are generally withheld below 30 °C (86 °F); drug binding and clearance change, so residual doses given while cold can become toxic during rewarming. Atrial arrhythmias usually convert spontaneously during rewarming and are observed rather than treated, and remember that hypothermia masks infection — rigors can be mistaken for shivering.
Toxicology
Alcohol poisoning
Ethanol and other ingested alcohols activate γ-aminobutyric acid (GABA) receptors, the principal inhibitory system of the central nervous system, producing dose-dependent CNS depression — loss of consciousness and, at high doses, respiratory depression with respiratory failure or aspiration. Ethanol is the most commonly encountered toxicity; the other clinically important alcohols are ethylene glycol (antifreeze), methanol (wood alcohol), and isopropyl alcohol (rubbing alcohol).
The two toxic alcohols share a pattern. Ethylene glycol is metabolized by alcohol dehydrogenase to oxalic acid, which crystallizes in renal tubules and can cause permanent kidney damage; methanol is metabolized to formic acid, which is retinal-toxic and causes blindness. Both produce an increased anion gap metabolic acidosis plus an increased osmolal gap. Management is competitive inhibition of alcohol dehydrogenase with intravenous fomepizole (IV ethanol competes similarly if fomepizole is unavailable), plus hemodialysis, which rapidly removes the parent alcohols and should be performed as soon as possible in confirmed ethylene glycol or methanol poisoning or in suspected cases with high anion gap acidosis or end-organ damage (visual impairment or kidney injury). Isopropyl alcohol has no toxic metabolites: it raises the osmolal gap and produces ketones, but does not elevate the anion gap; treatment of ethanol and isopropyl alcohol toxicity is supportive.
| Alcohol | Common sources | Major findings | Anion gap | Osmolar gap | Antidote / treatment |
|---|---|---|---|---|---|
| Ethanol | Alcoholic beverages | CNS depression | Possible | Yes | Supportive care |
| Isopropyl alcohol | Rubbing alcohol, disinfectants | CNS depression, ketone elevation | No | Yes | Supportive care |
| Methanol | Antifreeze, windshield-wiper fluid, de-icing solutions, solvents, “moonshine” | CNS depression, vision loss, hypotension | Yes | Yes | Fomepizole (ethanol only if fomepizole unavailable); hemodialysis for severe acidemia, very large ingestions, severe CNS depression, or any visual impairment |
| Ethylene glycol | Antifreeze, de-icing solutions, solvents | CNS depression, acute kidney injury, hypocalcemia, hypotension | Yes | Yes | Fomepizole (ethanol only if fomepizole unavailable); hemodialysis for severe acidemia, very large ingestions, severe CNS depression, AKI, or systemic collapse |
Carbon monoxide poisoning
Carbon monoxide (CO) is a colorless, odorless product of hydrocarbon combustion that is readily absorbed when inhaled and binds avidly to hemoglobin to form carboxyhemoglobin, displacing oxygen and causing tissue hypoxia and ischemia; it also shifts the oxyhemoglobin dissociation curve to the left and binds myoglobin. Toxicity occurs almost exclusively in enclosed spaces with ongoing combustion and is usually accidental, though it may be intentional. Patients present with headache, nausea, malaise, confusion, syncope, seizures, or coma; those with coronary disease may develop cardiac ischemia.
Pulse oximetry is not helpful: current transcutaneous oximetry cannot differentiate oxyhemoglobin from carboxyhemoglobin, so readings are falsely reassuring. Diagnosis requires blood gas analysis with CO-oximetry. Carboxyhemoglobin is below 3% in normal individuals and may reach 10%–15% in smokers; higher levels are consistent with poisoning. Because oxygen and CO compete for hemoglobin, the primary treatment is supplemental oxygen: the carboxyhemoglobin half-life is 300 minutes on ambient air, 90 minutes on 100% oxygen, and about 30 minutes with hyperbaric oxygen (pressure gradually increased to 2–3 atmospheres). Patients with carboxyhemoglobin of 25% or greater plus evidence of organ ischemia should receive hyperbaric oxygen if possible. Beyond the acute hypoxic injury, roughly 40% of severe CO poisonings develop delayed neurologic sequelae — neurocognitive and personality defects that typically appear within 20 days (sometimes later) and may persist a year or longer, probably from ischemic damage to oxygen-sensitive brain regions; evidence that hyperbaric oxygen reduces these sequelae is weak.
Cyanide poisoning
Cyanide is among the most lethal poisons known. It inhibits cellular respiration by binding cytochrome oxidase c in the mitochondria, blocking aerobic metabolism — producing clinical hypoxia despite a normal oxyhemoglobin saturation. Exposure occurs by ingestion or inhalation; inhalation is common in house fires, where burning vinyl generates cyanide that is aerosolized alongside CO (a frequent co-exposure). Prolonged nitroprusside infusion can also cause cyanide toxicity. Symptoms include headache, anxiety, nausea, and a metallic or bitter-almond odor/taste; severe exposure produces coma, seizures, vomiting, liver or kidney injury, ischemic pain, rhabdomyolysis, and death. Serum lactate is a sensitive but nonspecific marker; a normal lactate effectively rules out significant exposure.
Successful treatment depends on early recognition, elimination of ongoing exposure (including removal of contaminated clothing), and an antidote. Hydroxocobalamin avidly binds cyanide to form cyanocobalamin — soluble, nontoxic, and readily excreted — at a usual adult dose of 5 g, and is the most commonly recommended antidote because of its ease and safety. Alternatives include nitrites (amyl nitrite, sodium nitrite), which induce methemoglobin that in turn binds cyanide, and sodium thiosulfate, which donates sulfur to convert cyanide to harmless thiocyanate. Because inducing methemoglobinemia is unsafe in smoke-inhalation victims who may already carry high carboxyhemoglobin levels, nitrites should be avoided in that setting.
Toxicity of drugs of abuse
Drugs of abuse may be taken singly or in combination, and an accurate history is often impossible — altered mental status, reluctance to disclose, and unknown adulteration all conspire against it. Instead, recognize clinical toxic syndromes (toxidromes), which point to the offending drug class and its management.
| Syndrome | Manifestations | Representative drugs |
|---|---|---|
| Sympathomimetic | Tachycardia, hypertension, diaphoresis, agitation, seizures, mydriasis | Cocaine, amphetamines, ephedrine, caffeine |
| Cholinergic | “SLUDGE” (salivation, lacrimation, urination and defecation, gastrointestinal upset, emesis), bronchorrhea, bradycardia, miosis | Organophosphates (insecticides, sarin), carbamates, nicotine |
| Anticholinergic | Dry skin and mucous membranes, agitation/delirium, mydriasis, hyperthermia, tachycardia, hypertension, urinary retention | Antihistamines, tricyclic antidepressants, anti-Parkinson agents, atropine, scopolamine |
| Opioid | Miosis, respiratory depression, lethargy/confusion, hypothermia, bradycardia, hypotension | Morphine, fentanyl, oxycodone and related drugs, heroin |
Care is primarily supportive: airway patency and ventilation come first in any patient with depressed mental status, with intubation as needed to protect against aspiration or treat respiratory failure. An early empiric trial of naloxone is warranted when opioid overdose is suspected, titrated to an adequate respiratory rate — not to full mental status recovery. Naloxone’s half-life is very short, so its effects usually wear off before the opioid’s do; observe for continued or recurrent respiratory depression requiring repeat dosing, and expect opioid withdrawal, which is not fatal and requires only supportive care. For suspected benzodiazepine overdose, flumazenil is problematic: reversing benzodiazepines can trigger life-threatening CNS activation including seizures, especially in chronic users, so the safer course is ventilator support and allowing time for elimination. In sympathomimetic toxicity (cocaine, amphetamines), benzodiazepines are the cornerstone of agitation management, and β-blockers should be avoided — blocking β receptors leaves activated α receptors unopposed, theoretically precipitating severe hypertension. Hallucinogens have no antidote; support the airway, ventilation, and hemodynamics, and use physical restraints or sedation when agitation is extreme. Selected agents: cocaine intoxication is brief (~30 minutes) with prominent myocardial infarction risk; methamphetamine causes violent agitation and hyponatremia with a ~20-hour duration (and haloperidol may worsen hyperthermia); MDMA causes hyponatremia and serotonin syndrome; bath salts and synthetic cannabinoids produce violent agitation with negative routine urine drug screens; PCP causes variable mental status with nystagmus.
Overdose of therapeutic drugs
Patients may overdose on prescribed medications inadvertently or intentionally, often ingesting several drugs together with alcohol. Reconstructing the event — suicidal ideation or intent, the patient’s and family’s prescriptions, filled prescriptions, bystander accounts, and the clinical syndrome — guides management. If the patient is alert and cooperative enough to protect the airway, activated charcoal may be beneficial within 1 to 2 hours of ingestion (it adsorbs most substances best when given early, but not charged compounds such as lithium or iron salts). Acetaminophen and salicylate overdoses are covered in the gastroenterology/hepatology and nephrology contexts respectively; the remaining common overdoses are summarized below.
| Medication | Key clinical findings | Treatment | Notes |
|---|---|---|---|
| Acetaminophen | ↑liver chemistry studies, ↑creatinine, ↑INR, encephalopathy, cerebral edema, vomiting | N-acetylcysteine | Transfer to a liver transplant center if severe |
| Salicylates | Mixed respiratory alkalosis/anion gap metabolic acidosis, tinnitus, agitation, confusion, hyperthermia | Bicarbonate infusion, glucose, forced diuresis | Target urine pH 7.5–8.0; hemodialysis for acute kidney injury or severe toxicity |
| β-Blocker / calcium channel blocker | ↓HR, ↓BP, heart block; altered mental status with β-blockers | Atropine (1 mg IV up to 3 doses), glucagon, calcium chloride, vasopressors, pacing if indicated, high-dose insulin + glucose, IV lipid emulsion | Therapies may be added sequentially or simultaneously based on severity and response |
| Digoxin | ↓HR, arrhythmia, nausea/emesis, abdominal pain, confusion, weakness | Digoxin-specific antibody | Antibody lowers potassium; hemodialysis is ineffective |
| Tricyclic antidepressants | ↓BP, sedation, seizures, anticholinergic signs, prolonged QRS, arrhythmia | Bicarbonate infusion titrated to QRS; benzodiazepines for seizures | Physostigmine contraindicated |
| Antihistamines | Anticholinergic signs including agitation and seizures | Benzodiazepines; physostigmine for isolated anticholinergic overdose | Physostigmine requires continuous cardiac monitoring and bedside atropine |
| Sulfonylurea | ↓glucose, confusion, seizure, anxiety, diaphoresis, tremor | IV glucose + octreotide; IM glucagon as temporizing | Monitor glucose for 48 h after large ingestions |
| Metformin | ↑lactate, abdominal pain | Hemodialysis for severe acidosis or acute kidney injury | Glucose usually normal with isolated ingestion |
| Lithium | GI distress, confusion, ataxia, tremor, myoclonic jerks, diabetes insipidus | Hemodialysis if level >4 mEq/L (4 mmol/L) or severe toxicity | Serum level confirms diagnosis and guides dialysis |
| SSRI/SNRI | Agitation, myoclonus, ↑reflexes, rigidity, fever, tachycardia | Benzodiazepines; cyproheptadine if severe | Venlafaxine carries increased cardiac toxicity |
Acute Abdominal Surgical Emergencies
Many causes of abdominal pain, distention, and rigidity can and should be managed medically, but some require surgery, and timely diagnosis followed by prompt intervention is what saves lives. Imaging decisions should be driven by history and examination and must not delay intervention.
| Diagnosis | Presentation | Diagnostic imaging | Notes |
|---|---|---|---|
| Acute cholecystitis / cholangitis | Persistent peritoneal RUQ or epigastric pain, fever, emesis, positive Murphy sign | Ultrasonography | ↑alkaline phosphatase and bilirubin suggest cholangitis (typically not cholecystitis); EUS/ERCP diagnose and treat cholangitis |
| Bowel obstruction | Cramping pain, emesis, distention, obstipation, dehydration | Radiography: dilated loops with air-fluid levels; CT identifies cause and complications | Top causes: incarcerated hernia, adhesions, volvulus, intussusception |
| Acute appendicitis | Classic periumbilical → RLQ pain, emesis, leukocytosis | Often unnecessary; CT if unclear | Pain quality and location vary with appendix position |
| Peptic ulcer perforation | Abrupt peritoneal pain, later distention and hypovolemia | Radiography: free air | — |
| Acute mesenteric ischemia | Pain out of proportion to examination, vomiting, hypotension; thrombotic/embolic risk factors | CT angiography or conventional arteriography; CT/ultrasound if unclear | Surgery necessary in the majority; plain CT and lactate can be normal early; ↑amylase and ↑phosphate are common |
| Toxic megacolon | Pain, diarrhea, fever, tachycardia, hypotension, confusion | Radiography: dilated colon with air-fluid levels; CT if unclear | Causes: inflammatory bowel disease, Clostridioides difficile infection |
| Ruptured abdominal aortic aneurysm | ↓BP, abdominal and/or flank pain, pulsatile mass | Unnecessary if high suspicion and unstable; CT/ultrasound if unclear | Risk factors: older age, male sex, smoking, hypertension, family history; high mortality without early surgery |
| Ectopic pregnancy with tubal rupture | ↓BP, ↓hemoglobin, ↑hCG, abdominal pain, vaginal bleeding | Transvaginal ultrasonography; unnecessary if high suspicion and unstable | — |
Fat embolism syndrome deserves mention in the trauma context: fat globules commonly enter the circulation after long-bone fractures, but the syndrome itself is a rare, potentially lethal complication in which emboli lodge in capillaries and arterioles. It is a clinical diagnosis centered on the triad of respiratory insufficiency, neurologic dysfunction, and petechial rash in the appropriate setting; high-resolution CT findings are nonspecific and imaging may be normal. There is no definitive therapy — treatment is supportive, and most patients recover spontaneously and completely, though mortality can reach 5%–20%.
Obstetric Critical Care Emergencies
The physiologic changes of pregnancy make critical care management uniquely challenging: maternal physiology must be optimized without compromising the fetus, medication pharmacology must account for placental transfer, and care requires a multidisciplinary team of intensivist, obstetrician-gynecologist, and neonatologist. The most frequent emergencies are summarized below.
| Presentation | Causes | Key treatment principles |
|---|---|---|
| Dyspnea | Status asthmaticus | Inhaled glucocorticoids (preferentially budesonide or fluticasone); short-acting β2-agonists and short systemic glucocorticoid courses are acceptable; intubation/mechanical ventilation if needed |
| Venous thromboembolism | Ultrasonography if DVT suspected, V/Q scan, or CT pulmonary angiography; low-molecular-weight heparin preferred | |
| Pneumonia | Chest radiography; avoid fluoroquinolones and tetracyclines; treat influenza exposure with oseltamivir | |
| Pulmonary edema (preeclampsia, tocolytic therapy, peripartum cardiomyopathy) | Chest radiography, echocardiogram, invasive hemodynamic monitoring if needed; furosemide; nitroglycerin, hydralazine, or calcium channel blockers for preload/afterload reduction; intubation if needed | |
| ARDS (consider amniotic fluid embolism, acute fatty liver of pregnancy, intrauterine infection) | Evaluate for delivery; no controlled data on safety of permissive hypercapnia, fluid-restrictive strategy, or prone positioning in pregnancy | |
| Hemorrhage | Antepartum: abruptio placentae (clinical: abrupt vaginal bleeding, back pain, contractions), placenta previa (ultrasound), uterine rupture (clinical: bleeding, pain, shock, fetal compromise during labor) | Resuscitation with fluids and blood products; correct coagulopathy; consider delivery; refractory bleeding → embolization/surgical exploration; hysterectomy |
| Postpartum: uterine atony, retained placenta | ||
| Hypertension | Preeclampsia (hypertension with proteinuria after 20 weeks’ gestation; severe = end-organ dysfunction) | Consider delivery; magnesium sulfate to prevent eclampsia; antihypertensives (labetalol, hydralazine, nifedipine) |
| Seizure | Eclampsia (new-onset seizures in a patient with preeclampsia) | Maternal hemodynamic and respiratory support; magnesium sulfate; antihypertensives (labetalol, hydralazine, nicardipine); delivery |
Encephalopathy: Coma and Anoxic Brain Injury
Altered mental status is common in the ICU, driven both by critical illness and by an environment that disrupts sleep and strips away orienting cues. Among the many causes, three matter most in critical care: delirium (addressed in Principles of Critical Care), coma, and anoxic brain injury.
Coma is absent cortical function with intact brainstem function, whether from illness, trauma, or medication; patients do not respond to external stimuli. Severity is graded with the Glasgow Coma Scale across three stimulus-response categories (eye, verbal, motor): a score of 15 is a normal, fully arousable patient and 3 is no response at all. Brainstem findings (pupillary or eye-movement abnormalities) and motor posturing help localize the lesion; lumbar puncture and CNS imaging (MRI or CT) help identify the cause. Treatment is supportive, with efforts to reverse the specific cause where possible.
| Response | Score |
|---|---|
| Eyes: does not open eyes / opens to pain / opens to voice / opens spontaneously | 1 / 2 / 3 / 4 |
| Verbal: no sound / incomprehensible sounds / inappropriate words / confused, disoriented / oriented, chats normally | 1 / 2 / 3 / 4 / 5 |
| Motor: no movement / extension to pain / abnormal flexion to pain / flexion-withdrawal to pain / localizes pain / obeys commands | 1 / 2 / 3 / 4 / 5 / 6 |
| Total (Eyes + Verbal + Motor) → classification: coma 3–8; moderate brain injury 9–12; mild brain injury 13–15 | 3–15 |
Anoxic brain injury is CNS damage caused by prolonged, profound tissue hypoxia — from near-drowning, seizures, obstructed airway, lung disease, cardiac arrest, asphyxiation, or other inhalational injury. Brain imaging shows edema and loss of gray-white matter demarcation. EEG ranges from diffuse slowing (typical of many encephalopathies) to burst suppression or seizure activity (indicating more severe injury) to electrical silence (which can indicate brain death).
Key Points Recap
Anaphylaxis & angioedema: Initial treatment of anaphylaxis is epinephrine (IM or IV); hereditary angioedema results from C1 esterase inhibitor deficiency/dysfunction. Hyperthermia: Nonexertional heat stroke is cooled with evaporative techniques (2025 SCCM guidance now prioritizes cold-water immersion for both forms, against dantrolene and antipyretics); exertional cases may need ice-water immersion. NMS is treated by stopping the trigger, cooling, and rehydration. Hypothermia: Continue CPR until the patient is rewarmed; ECLS for arrest, with HOPE-score-guided triage. Toxic alcohols: Ethylene glycol and methanol cause anion gap + osmolal gap acidosis — treat with fomepizole and early hemodialysis. CO poisoning: Pulse oximetry is unreliable; hyperbaric oxygen for carboxyhemoglobin ≥25% with organ dysfunction. Cyanide: Early recognition, exposure elimination, and hydroxocobalamin. Anoxic brain injury: Prognosis requires 3–5 days or more of supportive care before irreversibility can be declared.
References
- MKSAP 19 — Pulmonary and Critical Care Medicine American College of Physicians (2022). "Critical Care Medicine: Specific Critical Care Topics," pp. 80-89.
- Harrison's Principles of Internal Medicine, 22e McGraw-Hill (2024). Ch.364 "Anaphylaxis" (Hong/Boyce); Ch.470 "Poisoning and Drug Overdose" (Mycyk); Ch.477 "Hypothermia and Peripheral Cold Injuries" (Danzl); Ch.478 "Heat-Related Illnesses" (Danzl).
- Neffy: first intranasal epinephrine approved for anaphylaxis (FDA, Aug 2024) US FDA. Press announcement, Aug 9, 2024; see also Greenhawt M, Lieberman J, Blaiss M, et al. J Allergy Clin Immunol Pract 2024;12(12):3274-3282.e2.
- SCCM guidelines for the treatment of heat stroke (2025) Barletta JF, Palmieri TL, Toomey SA, et al. Crit Care Med 2025;53(2):e490-e500.
- HOPE score for ECLS rewarming in hypothermic cardiac arrest (2025 validation) Hall N, Métrailler-Mermoud J, Rousson V, et al. Scand J Trauma Resusc Emerg Med 2025;33:132.
- Xylazine adulteration in illicit fentanyl; OTC naloxone context Marshall SA, Nelson LA. J Pharm Pract 2025;38(2):264-269.