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Emergency And Acute Medicine-Hyperkalemia
Basics
Description Potassium is primarily intracellular, with approximately 98% inside cells and 2% in the extracellular space. Normal serum potassium ranges from 3.5 to 5.0 mmol/L. Potassium excretion occurs mainly through the kidneys (≈90%) and to a lesser extent through the gastrointestinal tract (≈10%). Renal and extrarenal mechanisms regulate serum potassium via dietary intake, distal tubular function, acid–base balance, mineralocorticoids, insulin, catecholamines, osmolarity, and medications.
Etiology Decreased potassium excretion is the most common cause and is typically due to acute or chronic renal failure. Other causes include distal tubular disorders (acute interstitial nephritis, renal transplant rejection, sickle cell nephropathy, type IV renal tubular acidosis), mineralocorticoid deficiency (Addison disease, hypoaldosteronism), and medications such as ACE inhibitors, ARBs, beta-blockers, potassium-sparing diuretics, NSAIDs, cyclosporine, trimethoprim, and lithium. Intracellular to extracellular shifts occur with metabolic acidosis, hyperosmolar states, insulin deficiency, cell necrosis, rhabdomyolysis, hemolysis, chemotherapy, digitalis toxicity, succinylcholine, beta-blockers, alpha-agonists, and hyperkalemic periodic paralysis. Excess potassium load may result from trauma, tumor lysis, salt substitutes, oral potassium, potassium-containing antibiotics, or rapid transfusion of stored blood. Pseudohyperkalemia results from hemolysis during blood draw, thrombocytosis, extreme leukocytosis, or prolonged tourniquet use.
Diagnosis
Signs and symptoms Hyperkalemia is frequently asymptomatic, even at high levels. Neuromuscular manifestations include weakness that may progress to paralysis and dyspnea due to respiratory muscle involvement. Cardiac dysrhythmias may be the first presentation, with symptoms such as chest pain, palpitations, or syncope.
Physical exam Findings may include muscle weakness, paralysis in severe cases, and evidence of cardiac dysrhythmias.
Essential workup Serum potassium >5.0 mmol/L confirms hyperkalemia. Use a heparinized tube if pseudohyperkalemia is suspected.
Diagnosis tests and interpretation
Laboratory Obtain electrolytes, BUN, creatinine, and glucose. Renal failure typically shows elevated BUN and creatinine. Mineralocorticoid deficiency may present with hyponatremia. Type IV renal tubular acidosis causes mild metabolic acidosis. Arterial blood gases assess acid–base status. Creatine kinase should be checked if rhabdomyolysis is suspected. In patients with hyperkalemia and normal renal function, calculate the transtubular potassium gradient (TTKG); values >8 suggest extrarenal causes, while <6 indicate impaired renal excretion.
ECG Findings correlate imperfectly with potassium levels. Early changes include peaked T waves and shortened QT interval (5–6.5 mmol/L). Moderate elevations (6.5–8 mmol/L) may cause PR prolongation, loss of P waves, and QRS widening. Severe hyperkalemia (>8 mmol/L) can result in intraventricular blocks, bundle branch blocks, sine-wave patterns, and ventricular arrest. ECG may be normal despite life-threatening hyperkalemia.
Differential diagnosis Pseudohyperkalemia.
Treatment
Prehospital Treat suspected hyperkalemia-related dysrhythmias differently from standard ACLS. Administer inhaled beta-agonists, consider sodium bicarbonate in metabolic acidosis, and give calcium when hyperkalemia is suspected in unstable patients.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Establish IV access and initiate continuous cardiac monitoring.
Emergency department management With ECG changes or instability, immediately antagonize cardiac membrane effects using calcium gluconate (awake patient) or calcium chloride (cardiac arrest). To shift potassium intracellularly, administer insulin with glucose, inhaled albuterol, and sodium bicarbonate (especially if acidotic). To remove potassium, restrict exogenous potassium, discontinue contributing medications, use loop diuretics if renal function permits, administer cation exchange resins for non-emergent cases, and initiate hemodialysis in renal failure. Special situations include urgent dialysis in renal failure, cautious calcium use in digoxin toxicity, and hydrocortisone for mineralocorticoid deficiency.
Medication Calcium gluconate 10% 10 mL IV over 2–5 min or calcium chloride 10% 10 mL IV; regular insulin 10 U IV with 50 mL D50W; albuterol 10–20 mg nebulized; sodium bicarbonate 44–132 mEq IV; furosemide 40–80 mg IV; sodium or calcium polystyrene sulfonate PO or PR; hydrocortisone 100 mg IV when indicated.
Follow-up and disposition
Admission criteria Most patients require admission due to delayed potassium redistribution and ongoing risk of rebound hyperkalemia.
Discharge criteria Mild hyperkalemia (<5.5 mmol/L) with clear reversible cause, demonstrated response to therapy, no anticipated rebound, and reliable early follow-up.
Issues for referral Address the underlying cause, commonly chronic kidney disease requiring nephrology follow-up and possible dialysis.
Follow-up recommendations Close monitoring and access to dialysis are essential for discharged patients.
Key points Clinical and ECG effects are more important than the absolute potassium value. Do not delay treatment when ECG changes indicate a hyperkalemic emergency. Hyperkalemia is often silent until severe—obtain an ECG early in at-risk patients. Use sodium bicarbonate cautiously to avoid volume overload.
Basics
Description Potassium is primarily intracellular, with approximately 98% inside cells and 2% in the extracellular space. Normal serum potassium ranges from 3.5 to 5.0 mmol/L. Potassium excretion occurs mainly through the kidneys (≈90%) and to a lesser extent through the gastrointestinal tract (≈10%). Renal and extrarenal mechanisms regulate serum potassium via dietary intake, distal tubular function, acid–base balance, mineralocorticoids, insulin, catecholamines, osmolarity, and medications.
Etiology Decreased potassium excretion is the most common cause and is typically due to acute or chronic renal failure. Other causes include distal tubular disorders (acute interstitial nephritis, renal transplant rejection, sickle cell nephropathy, type IV renal tubular acidosis), mineralocorticoid deficiency (Addison disease, hypoaldosteronism), and medications such as ACE inhibitors, ARBs, beta-blockers, potassium-sparing diuretics, NSAIDs, cyclosporine, trimethoprim, and lithium. Intracellular to extracellular shifts occur with metabolic acidosis, hyperosmolar states, insulin deficiency, cell necrosis, rhabdomyolysis, hemolysis, chemotherapy, digitalis toxicity, succinylcholine, beta-blockers, alpha-agonists, and hyperkalemic periodic paralysis. Excess potassium load may result from trauma, tumor lysis, salt substitutes, oral potassium, potassium-containing antibiotics, or rapid transfusion of stored blood. Pseudohyperkalemia results from hemolysis during blood draw, thrombocytosis, extreme leukocytosis, or prolonged tourniquet use.
Diagnosis
Signs and symptoms Hyperkalemia is frequently asymptomatic, even at high levels. Neuromuscular manifestations include weakness that may progress to paralysis and dyspnea due to respiratory muscle involvement. Cardiac dysrhythmias may be the first presentation, with symptoms such as chest pain, palpitations, or syncope.
Physical exam Findings may include muscle weakness, paralysis in severe cases, and evidence of cardiac dysrhythmias.
Essential workup Serum potassium >5.0 mmol/L confirms hyperkalemia. Use a heparinized tube if pseudohyperkalemia is suspected.
Diagnosis tests and interpretation
Laboratory Obtain electrolytes, BUN, creatinine, and glucose. Renal failure typically shows elevated BUN and creatinine. Mineralocorticoid deficiency may present with hyponatremia. Type IV renal tubular acidosis causes mild metabolic acidosis. Arterial blood gases assess acid–base status. Creatine kinase should be checked if rhabdomyolysis is suspected. In patients with hyperkalemia and normal renal function, calculate the transtubular potassium gradient (TTKG); values >8 suggest extrarenal causes, while <6 indicate impaired renal excretion.
ECG Findings correlate imperfectly with potassium levels. Early changes include peaked T waves and shortened QT interval (5–6.5 mmol/L). Moderate elevations (6.5–8 mmol/L) may cause PR prolongation, loss of P waves, and QRS widening. Severe hyperkalemia (>8 mmol/L) can result in intraventricular blocks, bundle branch blocks, sine-wave patterns, and ventricular arrest. ECG may be normal despite life-threatening hyperkalemia.
Differential diagnosis Pseudohyperkalemia.
Treatment
Prehospital Treat suspected hyperkalemia-related dysrhythmias differently from standard ACLS. Administer inhaled beta-agonists, consider sodium bicarbonate in metabolic acidosis, and give calcium when hyperkalemia is suspected in unstable patients.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Establish IV access and initiate continuous cardiac monitoring.
Emergency department management With ECG changes or instability, immediately antagonize cardiac membrane effects using calcium gluconate (awake patient) or calcium chloride (cardiac arrest). To shift potassium intracellularly, administer insulin with glucose, inhaled albuterol, and sodium bicarbonate (especially if acidotic). To remove potassium, restrict exogenous potassium, discontinue contributing medications, use loop diuretics if renal function permits, administer cation exchange resins for non-emergent cases, and initiate hemodialysis in renal failure. Special situations include urgent dialysis in renal failure, cautious calcium use in digoxin toxicity, and hydrocortisone for mineralocorticoid deficiency.
Medication Calcium gluconate 10% 10 mL IV over 2–5 min or calcium chloride 10% 10 mL IV; regular insulin 10 U IV with 50 mL D50W; albuterol 10–20 mg nebulized; sodium bicarbonate 44–132 mEq IV; furosemide 40–80 mg IV; sodium or calcium polystyrene sulfonate PO or PR; hydrocortisone 100 mg IV when indicated.
Follow-up and disposition
Admission criteria Most patients require admission due to delayed potassium redistribution and ongoing risk of rebound hyperkalemia.
Discharge criteria Mild hyperkalemia (<5.5 mmol/L) with clear reversible cause, demonstrated response to therapy, no anticipated rebound, and reliable early follow-up.
Issues for referral Address the underlying cause, commonly chronic kidney disease requiring nephrology follow-up and possible dialysis.
Follow-up recommendations Close monitoring and access to dialysis are essential for discharged patients.
Key points Clinical and ECG effects are more important than the absolute potassium value. Do not delay treatment when ECG changes indicate a hyperkalemic emergency. Hyperkalemia is often silent until severe—obtain an ECG early in at-risk patients. Use sodium bicarbonate cautiously to avoid volume overload.
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Emergency And Acute Medicine: Hypernatremia
Basics
Description Hypernatremia is defined as a serum sodium concentration >145 mEq/L. Mild hypernatremia is 146–155 mEq/L, while severe hypernatremia is >155 mEq/L and is associated with high morbidity and mortality.
Etiology Hypernatremia is categorized by volume status. Hypovolemic hypernatremia is the most common and results from loss of water and sodium with proportionally greater water loss. Causes include renal failure, diuretics, lactulose, osmotic diuresis (mannitol, glucosuria, high-protein feeds), insensible losses (burns, sweating), respiratory losses, impaired thirst, lack of access to water, diarrhea, vomiting, and intubation. Isovolemic hypernatremia results from free water loss without sodium loss, commonly due to fever or diabetes insipidus. Central diabetes insipidus may follow head trauma, tumors, congenital disease, infection, granulomatous disease, stroke, or aneurysm. Nephrogenic diabetes insipidus may be congenital or drug-induced (lithium, amphotericin B, foscarnet, demeclocycline) or associated with obstructive uropathy, chronic tubulointerstitial disease, or electrolyte disturbances. Hypervolemic hypernatremia results from excess sodium gain exceeding water gain, most commonly iatrogenic from sodium bicarbonate, hypertonic IV fluids, parenteral nutrition, hypertonic dialysis, or sodium-containing medications; less common causes include endocrine disorders and seawater drowning.
Pediatric considerations Children are more susceptible to iatrogenic hypernatremia and have higher risk of death or permanent neurologic injury, with morbidity up to 50%. Neonates may present with irritability, lethargy, high-pitched cry, or muscle weakness; poor breastfeeding or improper formula preparation are common causes.
Geriatric considerations Older adults are at highest risk due to impaired thirst and renal concentrating ability; neglect should be considered when dehydration is unexplained.
Pregnancy considerations Transient diabetes insipidus of pregnancy may occur. Vasopressin and desmopressin are pregnancy category B. Physical examination is less reliable for assessing hydration.
Diagnosis
Signs and symptoms Clinical features often reflect the underlying cause and are more pronounced with acute elevations. Sodium ≥185 mEq/L is frequently fatal. Neurologic manifestations, typically seen at levels ≥160 mEq/L, include headache, irritability, tremor, ataxia, confusion, delirium, seizures, coma, hyperreflexia, asterixis, chorea, intracranial hemorrhage, and dural sinus thrombosis. Musculoskeletal findings include spasticity, weakness, and muscle twitching. Other features include anorexia, tachypnea, poor skin turgor, nausea, and vomiting. Hypovolemic hypernatremia presents with tachycardia, orthostasis, dry mucous membranes, oliguria, and azotemia. Hypervolemic hypernatremia may cause pulmonary and peripheral edema.
Physical exam Assess hydration using mucous membranes, skin turgor, neck veins, and orthostatic vitals. Perform and repeatedly reassess a full neurologic examination.
Essential workup Confirm with serum sodium measurement.
Diagnosis tests and interpretation
Laboratory Obtain electrolytes, BUN/creatinine, glucose, CBC, urinalysis with specific gravity, urine and serum osmolality, and urine sodium.
Imaging Chest radiograph for infection, aspiration, or pulmonary edema. CT brain for altered mental status, venous sinus thrombosis, or intracranial hemorrhage.
Diagnostic procedures Consider Foley catheter placement for accurate intake and output monitoring.
Differential diagnosis Diabetic ketoacidosis, hyperosmolar hyperglycemic state, and primary CNS pathology.
Treatment
Prehospital Begin volume resuscitation if hypovolemia or hemodynamic instability is present.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Administer 0.9% normal saline bolus for hypotension. Treat altered mental status with glucose assessment and supportive measures.
Emergency department management Calculate free water deficit: Water deficit = 0.6 × weight (kg) × (1 − desired Na/actual Na). Avoid rapid correction; decrease serum sodium by no more than 0.5–0.7 mEq/L per hour to prevent seizures and cerebral edema. Hypovolemic hypernatremia requires initial volume resuscitation with normal saline, then transition to hypotonic fluids (D5W or 0.45% saline) once stable. Isovolemic hypernatremia is treated by replacing free water with D5W or hypotonic saline, correcting half the deficit in the first 24 hours and the remainder over 1–2 days. Hypervolemic hypernatremia requires removal of excess sodium and water with diuretics or dialysis, followed by cautious free water replacement once euvolemic. Diabetes insipidus management includes sodium restriction, desmopressin for central DI, adjunctive agents such as chlorpropamide or carbamazepine when appropriate, thiazide diuretics for nephrogenic DI, and discontinuation of offending drugs.
Medication Desmopressin 1–2 μg IV/SC q12h or 5–20 μg intranasally; chlorpropamide 100–500 mg/day. First line initial volume correction with normal saline if hypovolemic. Second line treat the underlying cause and correct free water deficit.
Follow-up and disposition
Admission criteria Newly diagnosed sodium >150 mEq/L, sodium >160 mEq/L, symptomatic patients, or those requiring close monitoring; ICU admission for severe or symptomatic cases.
Discharge criteria Sodium <150 mEq/L and asymptomatic, or chronically hypernatremic patients at baseline with no symptoms.
Follow-up recommendations Repeat serum sodium within one week or sooner based on clinical course.
Key points Acute hypernatremia carries a high risk of permanent neurologic injury; meticulous neurologic documentation is essential. Extremes of age and chronic illness increase vulnerability. Ongoing fluid losses require frequent reassessment and recalculation of water needs, with serial laboratory monitoring to ensure safe correction.
Basics
Description Hypernatremia is defined as a serum sodium concentration >145 mEq/L. Mild hypernatremia is 146–155 mEq/L, while severe hypernatremia is >155 mEq/L and is associated with high morbidity and mortality.
Etiology Hypernatremia is categorized by volume status. Hypovolemic hypernatremia is the most common and results from loss of water and sodium with proportionally greater water loss. Causes include renal failure, diuretics, lactulose, osmotic diuresis (mannitol, glucosuria, high-protein feeds), insensible losses (burns, sweating), respiratory losses, impaired thirst, lack of access to water, diarrhea, vomiting, and intubation. Isovolemic hypernatremia results from free water loss without sodium loss, commonly due to fever or diabetes insipidus. Central diabetes insipidus may follow head trauma, tumors, congenital disease, infection, granulomatous disease, stroke, or aneurysm. Nephrogenic diabetes insipidus may be congenital or drug-induced (lithium, amphotericin B, foscarnet, demeclocycline) or associated with obstructive uropathy, chronic tubulointerstitial disease, or electrolyte disturbances. Hypervolemic hypernatremia results from excess sodium gain exceeding water gain, most commonly iatrogenic from sodium bicarbonate, hypertonic IV fluids, parenteral nutrition, hypertonic dialysis, or sodium-containing medications; less common causes include endocrine disorders and seawater drowning.
Pediatric considerations Children are more susceptible to iatrogenic hypernatremia and have higher risk of death or permanent neurologic injury, with morbidity up to 50%. Neonates may present with irritability, lethargy, high-pitched cry, or muscle weakness; poor breastfeeding or improper formula preparation are common causes.
Geriatric considerations Older adults are at highest risk due to impaired thirst and renal concentrating ability; neglect should be considered when dehydration is unexplained.
Pregnancy considerations Transient diabetes insipidus of pregnancy may occur. Vasopressin and desmopressin are pregnancy category B. Physical examination is less reliable for assessing hydration.
Diagnosis
Signs and symptoms Clinical features often reflect the underlying cause and are more pronounced with acute elevations. Sodium ≥185 mEq/L is frequently fatal. Neurologic manifestations, typically seen at levels ≥160 mEq/L, include headache, irritability, tremor, ataxia, confusion, delirium, seizures, coma, hyperreflexia, asterixis, chorea, intracranial hemorrhage, and dural sinus thrombosis. Musculoskeletal findings include spasticity, weakness, and muscle twitching. Other features include anorexia, tachypnea, poor skin turgor, nausea, and vomiting. Hypovolemic hypernatremia presents with tachycardia, orthostasis, dry mucous membranes, oliguria, and azotemia. Hypervolemic hypernatremia may cause pulmonary and peripheral edema.
Physical exam Assess hydration using mucous membranes, skin turgor, neck veins, and orthostatic vitals. Perform and repeatedly reassess a full neurologic examination.
Essential workup Confirm with serum sodium measurement.
Diagnosis tests and interpretation
Laboratory Obtain electrolytes, BUN/creatinine, glucose, CBC, urinalysis with specific gravity, urine and serum osmolality, and urine sodium.
Imaging Chest radiograph for infection, aspiration, or pulmonary edema. CT brain for altered mental status, venous sinus thrombosis, or intracranial hemorrhage.
Diagnostic procedures Consider Foley catheter placement for accurate intake and output monitoring.
Differential diagnosis Diabetic ketoacidosis, hyperosmolar hyperglycemic state, and primary CNS pathology.
Treatment
Prehospital Begin volume resuscitation if hypovolemia or hemodynamic instability is present.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Administer 0.9% normal saline bolus for hypotension. Treat altered mental status with glucose assessment and supportive measures.
Emergency department management Calculate free water deficit: Water deficit = 0.6 × weight (kg) × (1 − desired Na/actual Na). Avoid rapid correction; decrease serum sodium by no more than 0.5–0.7 mEq/L per hour to prevent seizures and cerebral edema. Hypovolemic hypernatremia requires initial volume resuscitation with normal saline, then transition to hypotonic fluids (D5W or 0.45% saline) once stable. Isovolemic hypernatremia is treated by replacing free water with D5W or hypotonic saline, correcting half the deficit in the first 24 hours and the remainder over 1–2 days. Hypervolemic hypernatremia requires removal of excess sodium and water with diuretics or dialysis, followed by cautious free water replacement once euvolemic. Diabetes insipidus management includes sodium restriction, desmopressin for central DI, adjunctive agents such as chlorpropamide or carbamazepine when appropriate, thiazide diuretics for nephrogenic DI, and discontinuation of offending drugs.
Medication Desmopressin 1–2 μg IV/SC q12h or 5–20 μg intranasally; chlorpropamide 100–500 mg/day. First line initial volume correction with normal saline if hypovolemic. Second line treat the underlying cause and correct free water deficit.
Follow-up and disposition
Admission criteria Newly diagnosed sodium >150 mEq/L, sodium >160 mEq/L, symptomatic patients, or those requiring close monitoring; ICU admission for severe or symptomatic cases.
Discharge criteria Sodium <150 mEq/L and asymptomatic, or chronically hypernatremic patients at baseline with no symptoms.
Follow-up recommendations Repeat serum sodium within one week or sooner based on clinical course.
Key points Acute hypernatremia carries a high risk of permanent neurologic injury; meticulous neurologic documentation is essential. Extremes of age and chronic illness increase vulnerability. Ongoing fluid losses require frequent reassessment and recalculation of water needs, with serial laboratory monitoring to ensure safe correction.
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Emergency And Acute Medicine: Hyperosmolar Syndrome
Basics
Description Hyperosmolar syndrome results from relative insulin deficiency in undiagnosed or poorly controlled diabetes. Sustained hyperglycemia causes osmotic diuresis leading to profound dehydration; extracellular volume is maintained initially at the expense of intracellular dehydration, eventually resulting in severe total body water and electrolyte deficits (H₂O, Na⁺, Cl⁻, K⁺, PO₄⁻, Ca²⁺, Mg²⁺). Unlike diabetic ketoacidosis (DKA), severe ketoacidosis is absent because residual insulin suppresses lipolysis and ketone production.
Geriatric considerations Most common in elderly patients with type 2 diabetes, often precipitated by acute illness and reduced renal function; 30–40% present with new-onset diabetes.
Pediatric considerations Hyperosmolar hyperglycemic states are rare in children.
Etiology Precipitated by factors that impair insulin action, increase glucose load, or limit fluid replacement. Infection is the most common trigger (32–60%). Other causes include medication nonadherence, dietary indiscretion, pneumonia, UTI, sepsis, diuretics, beta-blockers, calcium channel blockers, phenytoin, cimetidine, amphetamines, ethanol, myocardial infarction, stroke, renal failure, heat stroke, pancreatitis, bowel obstruction, endocrine disorders, and burns.
Diagnosis
Signs and symptoms Develop over days to weeks and include polyuria, polydipsia, weight loss, dizziness, weakness, fatigue, blurred vision, and leg cramps.
Physical exam Marked dehydration with tachycardia, hypotension, orthostasis, dry mucous membranes, decreased skin turgor, sunken eyes, collapsed neck veins, preserved urine output until late, altered mental status ranging from lethargy to coma, seizures, focal neurologic deficits, and evidence of a precipitating illness.
Essential workup Diagnostic criteria include serum glucose ≥600 mg/dL (often >1,000 mg/dL), minimal ketosis, pH ≥7.30, bicarbonate ≥15 mEq/L, and effective serum osmolality >320 mOsm/kg (2 × Na⁺ + glucose/18).
Diagnosis tests and interpretation
Laboratory Obtain comprehensive studies to confirm diagnosis and identify triggers. Electrolytes may show elevated or normal potassium despite large total body deficit; mild anion gap acidosis may be present from lactic acid or renal insufficiency. Correct sodium for hyperglycemia: corrected Na⁺ = measured Na⁺ + 1.6 × [(glucose − 100)/100]. BUN and creatinine are elevated from prerenal and intrinsic renal causes. VBG or ABG assesses pH; ABG if mixed disorders suspected. Check serum ketones, β-hydroxybutyrate, lactate when pH <7.3 or anion gap is high. Measure serum osmolality. CBC may show leukocytosis and hemoconcentration. Lipase and amylase may be elevated with or without pancreatitis. Urinalysis evaluates glucose, ketones, and infection. Check magnesium, calcium, phosphate, blood cultures if septic, creatine kinase for rhabdomyolysis, pregnancy test when appropriate, and cardiac enzymes for ischemia.
Imaging Chest radiograph for pneumonia; head CT for altered mental status or focal deficits.
ECG Evaluate for electrolyte-related conduction abnormalities and ischemia.
Differential diagnosis Differentiate from DKA; mixed HHS/DKA occurs in up to one-third of cases. Evaluate other causes of metabolic acidosis if present (lactic acidosis, sepsis, hypoperfusion, postictal states).
Treatment
Prehospital Initiate IV fluids and stabilization.
Initial stabilization/therapy Secure airway in comatose patients, initiate cardiac monitoring, obtain IV access, check glucose, and give naloxone and thiamine when coma etiology is unclear. Restore hemodynamics with 0.9% normal saline 1–2 L in the first hour; larger volumes may be required to establish urine output.
Emergency department management Reassess volume status and mental state frequently. Check electrolytes and glucose hourly initially. Search for and treat precipitating illness. Fluids Begin with 0.9% normal saline 1–2 L over 1–2 hours to restore intravascular volume, then transition to 0.45% saline. Estimate total body water deficit: TBW deficit = 0.6 × weight (kg) × (1 − 140/corrected Na⁺); average deficit ≈9 L. Replace ~50% in the first 12 hours. Switch to D5 ½ NS when glucose <250 mg/dL. Potassium Anticipate large deficits (≈5–10 mEq/kg). Begin replacement after urine output is established and if K⁺ ≤5 mEq/L. If K⁺ 4–5 mEq/L, add 20–30 mEq to first liter, then ~20 mEq/hr. If K⁺ 3–4 mEq/L, give 40 mEq in first liter. If K⁺ <3 mEq/L, hold insulin and replete until >3.3 mEq/L. Monitor K⁺ every 1–2 hours. Insulin Not used early. Start only after hemodynamic stability and K⁺ >3.3 mEq/L; some patients improve with fluids alone. Use IV infusion (0.05–0.1 U/kg/hr), targeting glucose decline of 50–90 mg/dL/hr; faster correction increases cerebral edema risk. Reduce rate when glucose <250 mg/dL and maintain 150–200 mg/dL until bicarbonate >18 mEq/L and pH >7.3. Phosphate Replace only if <1 mg/dL. Magnesium Supplement cautiously, especially in renal failure. Anticoagulation Consider prophylactic heparin due to thrombotic risk; monitor for MI, PE, and mesenteric ischemia.
Medication Insulin infusion 0.05–0.1 U/kg/hr; magnesium sulfate as indicated; potassium phosphate IV or PO per level; naloxone 2 mg IV; thiamine 100 mg IV.
Follow-up and disposition
Admission criteria Nearly all cases require ICU admission for frequent labs and monitoring during the first 24 hours; select mild cases may be observed 12–24 hours.
Discharge criteria Patients meeting HHS criteria should not be discharged; only mild hyperglycemia with normal osmolality after correction may be considered.
Issues for referral Arrange endocrinology and primary care follow-up within one week for long-term glycemic management.
Key points Always identify and treat the precipitating cause. Avoid rapid glucose correction to prevent hypotension and cerebral edema. Transition fluids appropriately to prevent hypernatremia or cellular edema. Prevent hypokalemia proactively. Avoid phenytoin for seizures as it inhibits endogenous insulin release.
Basics
Description Hyperosmolar syndrome results from relative insulin deficiency in undiagnosed or poorly controlled diabetes. Sustained hyperglycemia causes osmotic diuresis leading to profound dehydration; extracellular volume is maintained initially at the expense of intracellular dehydration, eventually resulting in severe total body water and electrolyte deficits (H₂O, Na⁺, Cl⁻, K⁺, PO₄⁻, Ca²⁺, Mg²⁺). Unlike diabetic ketoacidosis (DKA), severe ketoacidosis is absent because residual insulin suppresses lipolysis and ketone production.
Geriatric considerations Most common in elderly patients with type 2 diabetes, often precipitated by acute illness and reduced renal function; 30–40% present with new-onset diabetes.
Pediatric considerations Hyperosmolar hyperglycemic states are rare in children.
Etiology Precipitated by factors that impair insulin action, increase glucose load, or limit fluid replacement. Infection is the most common trigger (32–60%). Other causes include medication nonadherence, dietary indiscretion, pneumonia, UTI, sepsis, diuretics, beta-blockers, calcium channel blockers, phenytoin, cimetidine, amphetamines, ethanol, myocardial infarction, stroke, renal failure, heat stroke, pancreatitis, bowel obstruction, endocrine disorders, and burns.
Diagnosis
Signs and symptoms Develop over days to weeks and include polyuria, polydipsia, weight loss, dizziness, weakness, fatigue, blurred vision, and leg cramps.
Physical exam Marked dehydration with tachycardia, hypotension, orthostasis, dry mucous membranes, decreased skin turgor, sunken eyes, collapsed neck veins, preserved urine output until late, altered mental status ranging from lethargy to coma, seizures, focal neurologic deficits, and evidence of a precipitating illness.
Essential workup Diagnostic criteria include serum glucose ≥600 mg/dL (often >1,000 mg/dL), minimal ketosis, pH ≥7.30, bicarbonate ≥15 mEq/L, and effective serum osmolality >320 mOsm/kg (2 × Na⁺ + glucose/18).
Diagnosis tests and interpretation
Laboratory Obtain comprehensive studies to confirm diagnosis and identify triggers. Electrolytes may show elevated or normal potassium despite large total body deficit; mild anion gap acidosis may be present from lactic acid or renal insufficiency. Correct sodium for hyperglycemia: corrected Na⁺ = measured Na⁺ + 1.6 × [(glucose − 100)/100]. BUN and creatinine are elevated from prerenal and intrinsic renal causes. VBG or ABG assesses pH; ABG if mixed disorders suspected. Check serum ketones, β-hydroxybutyrate, lactate when pH <7.3 or anion gap is high. Measure serum osmolality. CBC may show leukocytosis and hemoconcentration. Lipase and amylase may be elevated with or without pancreatitis. Urinalysis evaluates glucose, ketones, and infection. Check magnesium, calcium, phosphate, blood cultures if septic, creatine kinase for rhabdomyolysis, pregnancy test when appropriate, and cardiac enzymes for ischemia.
Imaging Chest radiograph for pneumonia; head CT for altered mental status or focal deficits.
ECG Evaluate for electrolyte-related conduction abnormalities and ischemia.
Differential diagnosis Differentiate from DKA; mixed HHS/DKA occurs in up to one-third of cases. Evaluate other causes of metabolic acidosis if present (lactic acidosis, sepsis, hypoperfusion, postictal states).
Treatment
Prehospital Initiate IV fluids and stabilization.
Initial stabilization/therapy Secure airway in comatose patients, initiate cardiac monitoring, obtain IV access, check glucose, and give naloxone and thiamine when coma etiology is unclear. Restore hemodynamics with 0.9% normal saline 1–2 L in the first hour; larger volumes may be required to establish urine output.
Emergency department management Reassess volume status and mental state frequently. Check electrolytes and glucose hourly initially. Search for and treat precipitating illness. Fluids Begin with 0.9% normal saline 1–2 L over 1–2 hours to restore intravascular volume, then transition to 0.45% saline. Estimate total body water deficit: TBW deficit = 0.6 × weight (kg) × (1 − 140/corrected Na⁺); average deficit ≈9 L. Replace ~50% in the first 12 hours. Switch to D5 ½ NS when glucose <250 mg/dL. Potassium Anticipate large deficits (≈5–10 mEq/kg). Begin replacement after urine output is established and if K⁺ ≤5 mEq/L. If K⁺ 4–5 mEq/L, add 20–30 mEq to first liter, then ~20 mEq/hr. If K⁺ 3–4 mEq/L, give 40 mEq in first liter. If K⁺ <3 mEq/L, hold insulin and replete until >3.3 mEq/L. Monitor K⁺ every 1–2 hours. Insulin Not used early. Start only after hemodynamic stability and K⁺ >3.3 mEq/L; some patients improve with fluids alone. Use IV infusion (0.05–0.1 U/kg/hr), targeting glucose decline of 50–90 mg/dL/hr; faster correction increases cerebral edema risk. Reduce rate when glucose <250 mg/dL and maintain 150–200 mg/dL until bicarbonate >18 mEq/L and pH >7.3. Phosphate Replace only if <1 mg/dL. Magnesium Supplement cautiously, especially in renal failure. Anticoagulation Consider prophylactic heparin due to thrombotic risk; monitor for MI, PE, and mesenteric ischemia.
Medication Insulin infusion 0.05–0.1 U/kg/hr; magnesium sulfate as indicated; potassium phosphate IV or PO per level; naloxone 2 mg IV; thiamine 100 mg IV.
Follow-up and disposition
Admission criteria Nearly all cases require ICU admission for frequent labs and monitoring during the first 24 hours; select mild cases may be observed 12–24 hours.
Discharge criteria Patients meeting HHS criteria should not be discharged; only mild hyperglycemia with normal osmolality after correction may be considered.
Issues for referral Arrange endocrinology and primary care follow-up within one week for long-term glycemic management.
Key points Always identify and treat the precipitating cause. Avoid rapid glucose correction to prevent hypotension and cerebral edema. Transition fluids appropriately to prevent hypernatremia or cellular edema. Prevent hypokalemia proactively. Avoid phenytoin for seizures as it inhibits endogenous insulin release.
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Emergency And Acute Medicine: Hyperparathyroidism
Basics
Description Hyperparathyroidism is characterized by excess parathyroid hormone (PTH) leading to metabolic effects including decreased urinary calcium excretion, increased urinary phosphate loss, increased renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, and increased calcium and phosphate release from bone. Hypercalcemia is the primary metabolic abnormality. Despite reduced renal calcium excretion, hypercalciuria occurs due to elevated serum calcium, often accompanied by urinary magnesium loss. Magnesium is essential for both PTH secretion and peripheral PTH action; hypomagnesemia may blunt PTH effects. Genetic associations include multiple endocrine neoplasia (MEN) syndromes: MEN 1 (hyperparathyroidism, pancreatic islet tumors, pituitary disease) and MEN 2 (hyperparathyroidism in MEN 2A, medullary thyroid carcinoma, pheochromocytoma, and mucosal neuromas in MEN 2B).
Etiology Primary hyperparathyroidism results from parathyroid adenoma (≈85%), hyperplasia (≈14%), or rarely carcinoma (<1%). Secondary hyperparathyroidism is a compensatory response to vitamin D deficiency or chronic kidney disease with hyperphosphatemia; calcium levels are low or normal with elevated PTH.
Diagnosis
Signs and symptoms Classic features include renal stones, bone pain, gastrointestinal complaints, and neuropsychiatric changes. Alert Hypercalcemic crisis presents with anorexia, nausea, vomiting, and progressive mental status depression.
History Symptoms correlate with severity and rapidity of hypercalcemia.
Pediatric considerations Neonates born to hypoparathyroid mothers may present with hypotonia, weakness, and lethargy; hypercalcemic infants may have distinctive facial features including broad forehead, epicanthal folds, underdeveloped nasal bridge, and prominent upper lip.
Physical exam Findings may include dehydration, hypertension despite volume depletion, cardiac conduction abnormalities (bradyarrhythmias, bundle branch block, complete heart block, asystole), shortened QT interval, potentiation of digoxin toxicity, neurologic deficits (decreased reflexes, proximal weakness, lethargy, coma), psychiatric symptoms (depression, anxiety, psychosis), gastrointestinal symptoms (anorexia, constipation, peptic ulcer disease, pancreatitis), musculoskeletal pain, gout or pseudogout, and renal manifestations including nephrolithiasis and nephrocalcinosis.
Essential workup Measure serum calcium and albumin to assess corrected calcium. Evaluate for symptoms of severe hypercalcemia or impending parathyroid crisis. If asymptomatic with normal ECG and corrected calcium <14 mg/dL, no further ED testing is required. If symptomatic or calcium ≥14 mg/dL, obtain ionized calcium, electrolytes, BUN/creatinine, phosphorus, magnesium, alkaline phosphatase, ESR, TSH, CBC, and chest radiograph.
Diagnosis tests and interpretation
Laboratory Correct calcium for albumin: corrected Ca (mg/dL) = measured Ca + 0.8 × (4 − albumin). Acidosis increases ionized calcium by reducing albumin binding. Phosphorus is typically low in primary hyperparathyroidism and elevated in secondary disease. Chloride-to-phosphate ratio >33 favors hyperparathyroidism; <30 suggests malignancy. Alkaline phosphatase is elevated in ~50% of cases. ESR and anemia are usually normal in hyperparathyroidism but elevated in malignancy or granulomatous disease. Magnesium is often low or low-normal. PTH is elevated in primary and secondary hyperparathyroidism. PTH-related peptide suggests malignancy-associated hypercalcemia.
Imaging Chest radiograph evaluates volume status and screens for malignancy or granulomatous disease.
Diagnostic procedures Definitive diagnosis and treatment are established with parathyroidectomy.
Differential diagnosis PTH-mediated causes include primary or secondary hyperparathyroidism and familial hypocalciuric hypercalcemia. Non-PTH causes include malignancy, vitamin D excess or granulomatous disease, immobilization (e.g., Paget disease), and drug-induced hypercalcemia (thiazides, lithium, vitamin A, aluminum antacids, estrogens, androgens, tamoxifen).
Treatment
Prehospital May present primarily with psychiatric manifestations.
Initial stabilization/therapy Place on cardiac monitor if symptomatic or calcium >14 mg/dL. Begin IV hydration with 0.9% normal saline and correct acidosis.
Emergency department management Treat hypercalcemia with aggressive isotonic saline hydration (≥250 mL/hr unless limited by heart failure) targeting urine output ≥100 mL/hr. After adequate hydration, add loop diuretics to enhance calciuresis; avoid thiazides. Consider glucocorticoids in vitamin D–mediated or granulomatous disease. Initiate bisphosphonates in coordination with endocrinology. Treat dysrhythmias conventionally and use extreme caution with digoxin. Stop contributing medications and monitor closely for heart failure and electrolyte disturbances. Use calcitonin when hydration is contraindicated and initiate dialysis for refractory hypercalcemia with renal failure.
Medication First line Normal saline infusion; furosemide 40 mg IV q2–4h after rehydration; prednisone 40–60 mg PO or hydrocortisone 100 mg IV. Second line (with endocrinology) Calcitonin salmon 4 U/kg SC q12h; pamidronate 60–90 mg IV depending on calcium level; zoledronic acid 4 mg IV; cinacalcet 30 mg PO daily or BID for secondary hyperparathyroidism or carcinoma.
Follow-up and disposition
Admission criteria Corrected calcium >14 mg/dL, symptomatic hypercalcemia, or cardiac conduction abnormalities.
Discharge criteria Asymptomatic patients with calcium <14 mg/dL who can maintain hydration.
Issues for referral Endocrinology referral for PTH evaluation and definitive management.
Follow-up recommendations Arrange outpatient PTH testing, reinforce hydration, and discontinue medications that increase calcium levels.
Key points Hyperparathyroid-related hypercalcemia is often mild and rarely exceeds 14 mg/dL; higher levels suggest malignancy. Measure ionized or albumin-corrected calcium. Administering loop diuretics before adequate hydration worsens hypercalcemia and is a common management error.
Basics
Description Hyperparathyroidism is characterized by excess parathyroid hormone (PTH) leading to metabolic effects including decreased urinary calcium excretion, increased urinary phosphate loss, increased renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, and increased calcium and phosphate release from bone. Hypercalcemia is the primary metabolic abnormality. Despite reduced renal calcium excretion, hypercalciuria occurs due to elevated serum calcium, often accompanied by urinary magnesium loss. Magnesium is essential for both PTH secretion and peripheral PTH action; hypomagnesemia may blunt PTH effects. Genetic associations include multiple endocrine neoplasia (MEN) syndromes: MEN 1 (hyperparathyroidism, pancreatic islet tumors, pituitary disease) and MEN 2 (hyperparathyroidism in MEN 2A, medullary thyroid carcinoma, pheochromocytoma, and mucosal neuromas in MEN 2B).
Etiology Primary hyperparathyroidism results from parathyroid adenoma (≈85%), hyperplasia (≈14%), or rarely carcinoma (<1%). Secondary hyperparathyroidism is a compensatory response to vitamin D deficiency or chronic kidney disease with hyperphosphatemia; calcium levels are low or normal with elevated PTH.
Diagnosis
Signs and symptoms Classic features include renal stones, bone pain, gastrointestinal complaints, and neuropsychiatric changes. Alert Hypercalcemic crisis presents with anorexia, nausea, vomiting, and progressive mental status depression.
History Symptoms correlate with severity and rapidity of hypercalcemia.
Pediatric considerations Neonates born to hypoparathyroid mothers may present with hypotonia, weakness, and lethargy; hypercalcemic infants may have distinctive facial features including broad forehead, epicanthal folds, underdeveloped nasal bridge, and prominent upper lip.
Physical exam Findings may include dehydration, hypertension despite volume depletion, cardiac conduction abnormalities (bradyarrhythmias, bundle branch block, complete heart block, asystole), shortened QT interval, potentiation of digoxin toxicity, neurologic deficits (decreased reflexes, proximal weakness, lethargy, coma), psychiatric symptoms (depression, anxiety, psychosis), gastrointestinal symptoms (anorexia, constipation, peptic ulcer disease, pancreatitis), musculoskeletal pain, gout or pseudogout, and renal manifestations including nephrolithiasis and nephrocalcinosis.
Essential workup Measure serum calcium and albumin to assess corrected calcium. Evaluate for symptoms of severe hypercalcemia or impending parathyroid crisis. If asymptomatic with normal ECG and corrected calcium <14 mg/dL, no further ED testing is required. If symptomatic or calcium ≥14 mg/dL, obtain ionized calcium, electrolytes, BUN/creatinine, phosphorus, magnesium, alkaline phosphatase, ESR, TSH, CBC, and chest radiograph.
Diagnosis tests and interpretation
Laboratory Correct calcium for albumin: corrected Ca (mg/dL) = measured Ca + 0.8 × (4 − albumin). Acidosis increases ionized calcium by reducing albumin binding. Phosphorus is typically low in primary hyperparathyroidism and elevated in secondary disease. Chloride-to-phosphate ratio >33 favors hyperparathyroidism; <30 suggests malignancy. Alkaline phosphatase is elevated in ~50% of cases. ESR and anemia are usually normal in hyperparathyroidism but elevated in malignancy or granulomatous disease. Magnesium is often low or low-normal. PTH is elevated in primary and secondary hyperparathyroidism. PTH-related peptide suggests malignancy-associated hypercalcemia.
Imaging Chest radiograph evaluates volume status and screens for malignancy or granulomatous disease.
Diagnostic procedures Definitive diagnosis and treatment are established with parathyroidectomy.
Differential diagnosis PTH-mediated causes include primary or secondary hyperparathyroidism and familial hypocalciuric hypercalcemia. Non-PTH causes include malignancy, vitamin D excess or granulomatous disease, immobilization (e.g., Paget disease), and drug-induced hypercalcemia (thiazides, lithium, vitamin A, aluminum antacids, estrogens, androgens, tamoxifen).
Treatment
Prehospital May present primarily with psychiatric manifestations.
Initial stabilization/therapy Place on cardiac monitor if symptomatic or calcium >14 mg/dL. Begin IV hydration with 0.9% normal saline and correct acidosis.
Emergency department management Treat hypercalcemia with aggressive isotonic saline hydration (≥250 mL/hr unless limited by heart failure) targeting urine output ≥100 mL/hr. After adequate hydration, add loop diuretics to enhance calciuresis; avoid thiazides. Consider glucocorticoids in vitamin D–mediated or granulomatous disease. Initiate bisphosphonates in coordination with endocrinology. Treat dysrhythmias conventionally and use extreme caution with digoxin. Stop contributing medications and monitor closely for heart failure and electrolyte disturbances. Use calcitonin when hydration is contraindicated and initiate dialysis for refractory hypercalcemia with renal failure.
Medication First line Normal saline infusion; furosemide 40 mg IV q2–4h after rehydration; prednisone 40–60 mg PO or hydrocortisone 100 mg IV. Second line (with endocrinology) Calcitonin salmon 4 U/kg SC q12h; pamidronate 60–90 mg IV depending on calcium level; zoledronic acid 4 mg IV; cinacalcet 30 mg PO daily or BID for secondary hyperparathyroidism or carcinoma.
Follow-up and disposition
Admission criteria Corrected calcium >14 mg/dL, symptomatic hypercalcemia, or cardiac conduction abnormalities.
Discharge criteria Asymptomatic patients with calcium <14 mg/dL who can maintain hydration.
Issues for referral Endocrinology referral for PTH evaluation and definitive management.
Follow-up recommendations Arrange outpatient PTH testing, reinforce hydration, and discontinue medications that increase calcium levels.
Key points Hyperparathyroid-related hypercalcemia is often mild and rarely exceeds 14 mg/dL; higher levels suggest malignancy. Measure ionized or albumin-corrected calcium. Administering loop diuretics before adequate hydration worsens hypercalcemia and is a common management error.
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Emergency And Acute Medicine: Hypertensive Emergencies
Basics
Description Hypertensive crisis refers to severe blood pressure elevation, typically SBP >179 mm Hg or DBP >109 mm Hg. Hypertensive urgency is severe BP elevation without acute end-organ injury. Hypertensive emergency is severe BP elevation with acute target-organ damage. In hypertensive emergency, autoregulation fails: arterioles initially constrict to protect capillary beds, but extreme pressures overwhelm this response, causing endothelial injury, increased permeability, platelet and coagulation activation, and fibrin deposition. Sympathetic and renin–angiotensin activation further increase vasoconstriction and inflammation, worsening ischemia and perpetuating a vicious cycle. Commonly affected organs include brain (encephalopathy, ischemic stroke, intracerebral hemorrhage), retina (hemorrhage, papilledema), heart (ACS, acute heart failure, aortic dissection), kidneys (acute renal failure), and placenta (preeclampsia/eclampsia).
Etiology Causes include essential hypertension; renal vascular or parenchymal disease; coarctation of the aorta; CNS injury (head trauma, stroke/ICH, tumor, spinal cord injury); endocrine disorders (pheochromocytoma, Cushing syndrome, primary hyperaldosteronism, renin-secreting tumors); drugs and toxins (cocaine, PCP, amphetamines, erythropoietin, tacrolimus, cyclosporine, corticosteroids, oral contraceptives, MAOI interactions, lead); withdrawal of antihypertensives; autonomic hyperreactivity (Guillain–Barré, acute intermittent porphyria); postoperative pain or anesthetic complications; and pregnancy-related disease (preeclampsia/eclampsia).
Diagnosis
History Review prescribed and OTC medications, antihypertensive adherence or withdrawal, duration and control of baseline hypertension, prior end-organ disease, comorbidities (CAD, diabetes, obesity), and recreational drug use. Screen for end-organ injury, commonly dyspnea, chest pain, headache, confusion, and focal neurologic deficits.
Physical exam Measure BP in both arms using appropriate cuff size. Assess for neurologic deficits and mental status changes, perform funduscopic exam for hemorrhages or papilledema, evaluate cardiovascular status (JVP, crackles, S3, aortic regurg murmur), and check for pulse asymmetry.
Essential workup Obtain a 12-lead ECG for ischemia and LVH, and assess kidney function because acute renal failure may be clinically silent.
Diagnosis tests and interpretation
Laboratory CBC (anemia and thrombocytopenia may indicate thrombotic microangiopathy), BMP including BUN/creatinine and electrolytes (hypokalemia suggests mineralocorticoid excess), urinalysis (protein, blood, casts), urine toxicology when drug use is suspected, and pregnancy test when appropriate. Use standard chest pain protocols when indicated.
Imaging Chest radiograph for cardiopulmonary symptoms, head CT for headache, confusion, or focal deficits, and CTA chest/abdomen if aortic dissection is suspected.
Procedures Consider arterial line monitoring in unstable cases. Lumbar puncture may be used to evaluate for subarachnoid hemorrhage after appropriate imaging.
Differential diagnosis ACS, acute heart failure, aortic dissection, ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, preeclampsia/eclampsia, withdrawal syndromes (beta-blocker, clonidine), and catecholamine excess states (pheochromocytoma, sympathomimetic intoxication, tyramine reaction with MAOIs).
Treatment
Prehospital Support ABCs and consider cautious BP reduction only when clearly indicated.
Initial stabilization/therapy Provide oxygen as needed, establish IV access, monitor ECG and pulse oximetry.
Emergency department management Hypertensive urgency does not require IV reduction; give missed home medications, use oral agents only, and lower BP gradually over 24–48 hours with close follow-up. Hypertensive emergency requires IV therapy guided by the end-organ injury rather than the absolute BP. Reduce MAP by no more than 20–25% in the first hour, then target roughly SBP ~160 and DBP ~100 over 2–6 hours, transitioning to oral agents within 6–12 hours once stable. Lower more gradually in acute CNS injury, but more rapidly in aortic dissection. Hypertensive encephalopathy: lower MAP up to 20% or DBP to 100–110 within the first hour, then normalize over 48–72 hours using nicardipine, clevidipine, or labetalol. Ischemic stroke: treat only if SBP >220 or DBP >120, or if thrombolysis planned (target <185/110 pre-tPA, then <180/105); avoid reducing MAP more than 15–20% in the first 24 hours; preferred agents are nicardipine, clevidipine, or labetalol. ICH/SAH: treat if SBP >180 or DBP >100; aim SBP 140–160 or MAP down 20–25% in the first hour; avoid nitroglycerin and nitroprusside due to cerebral vasodilation and ICP effects; use nicardipine, clevidipine, or labetalol. ACS: target MAP 60–100 using labetalol or esmolol with nitroglycerin; avoid hydralazine and nitroprusside. Acute heart failure: target MAP 60–100 with nitroprusside or nitroglycerin plus ACE inhibitor and/or loop diuretic. Acute renal failure or microangiopathy: reduce MAP 20–25% in the first hour using nicardipine, clevidipine, or fenoldopam; ACE inhibitors are preferred for scleroderma renal crisis. Aortic dissection: reduce shear force by lowering HR and BP; beta-blockade must come first; target SBP 100–120 and HR <65 within 20 minutes using esmolol plus a vasodilator (dihydropyridine CCB or nitroprusside); obtain urgent surgical consultation for type A.
Sympathomimetic crisis: avoid pure beta-blockade; use phentolamine or calcium channel blocker plus benzodiazepines; use clonidine for clonidine withdrawal.
Pregnancy considerations Preeclampsia is SBP >140 or DBP >90 with proteinuria after 20 weeks to 4 weeks postpartum, often with headache, visual changes, edema, or RUQ pain; target SBP 130–150 and DBP 80–100 using labetalol, nicardipine, hydralazine, and magnesium, with obstetric consultation.
Medication Clevidipine 1–16 mg/h infusion; nicardipine 2–15 mg/h infusion; labetalol 20–80 mg IV q10 min (max 300 mg) or 0.5–2 mg/min infusion; esmolol 80 mg IV bolus then 150 μg/kg/min infusion; nitroglycerin 5–100 μg/min infusion; nitroprusside 0.25–10 μg/kg/min infusion; hydralazine 10–20 mg IV bolus; fenoldopam 0.1–0.6 μg/kg/min infusion; enalaprilat 1.25–5 mg IV q6h; phentolamine 5–15 mg IV q5–15 min.
Follow-up and disposition
Admission criteria Any patient with acute end-organ injury requires admission; ICU monitoring is indicated for hypertensive emergency.
Discharge criteria No end-organ injury, reliable follow-up, known hypertension, reversible trigger such as medication nonadherence, and ability to resume a safe outpatient regimen; provide strict return precautions for chest pain, neurologic symptoms, or severe headache.
Follow-up recommendations Ensure timely primary care follow-up for medication initiation or adjustment and long-term BP control.
Key points Do not use IV agents for hypertensive urgency. In hypertensive emergency, the initial goal is controlled MAP reduction of 20–25% in the first hour, except for ischemic stroke and aortic dissection where targets differ. Avoid precipitous BP drops that can worsen ischemia. In aortic dissection prevent reflex tachycardia by starting beta-blockade first. In catecholamine excess avoid unopposed alpha stimulation by avoiding pure beta-blockers.
Basics
Description Hypertensive crisis refers to severe blood pressure elevation, typically SBP >179 mm Hg or DBP >109 mm Hg. Hypertensive urgency is severe BP elevation without acute end-organ injury. Hypertensive emergency is severe BP elevation with acute target-organ damage. In hypertensive emergency, autoregulation fails: arterioles initially constrict to protect capillary beds, but extreme pressures overwhelm this response, causing endothelial injury, increased permeability, platelet and coagulation activation, and fibrin deposition. Sympathetic and renin–angiotensin activation further increase vasoconstriction and inflammation, worsening ischemia and perpetuating a vicious cycle. Commonly affected organs include brain (encephalopathy, ischemic stroke, intracerebral hemorrhage), retina (hemorrhage, papilledema), heart (ACS, acute heart failure, aortic dissection), kidneys (acute renal failure), and placenta (preeclampsia/eclampsia).
Etiology Causes include essential hypertension; renal vascular or parenchymal disease; coarctation of the aorta; CNS injury (head trauma, stroke/ICH, tumor, spinal cord injury); endocrine disorders (pheochromocytoma, Cushing syndrome, primary hyperaldosteronism, renin-secreting tumors); drugs and toxins (cocaine, PCP, amphetamines, erythropoietin, tacrolimus, cyclosporine, corticosteroids, oral contraceptives, MAOI interactions, lead); withdrawal of antihypertensives; autonomic hyperreactivity (Guillain–Barré, acute intermittent porphyria); postoperative pain or anesthetic complications; and pregnancy-related disease (preeclampsia/eclampsia).
Diagnosis
History Review prescribed and OTC medications, antihypertensive adherence or withdrawal, duration and control of baseline hypertension, prior end-organ disease, comorbidities (CAD, diabetes, obesity), and recreational drug use. Screen for end-organ injury, commonly dyspnea, chest pain, headache, confusion, and focal neurologic deficits.
Physical exam Measure BP in both arms using appropriate cuff size. Assess for neurologic deficits and mental status changes, perform funduscopic exam for hemorrhages or papilledema, evaluate cardiovascular status (JVP, crackles, S3, aortic regurg murmur), and check for pulse asymmetry.
Essential workup Obtain a 12-lead ECG for ischemia and LVH, and assess kidney function because acute renal failure may be clinically silent.
Diagnosis tests and interpretation
Laboratory CBC (anemia and thrombocytopenia may indicate thrombotic microangiopathy), BMP including BUN/creatinine and electrolytes (hypokalemia suggests mineralocorticoid excess), urinalysis (protein, blood, casts), urine toxicology when drug use is suspected, and pregnancy test when appropriate. Use standard chest pain protocols when indicated.
Imaging Chest radiograph for cardiopulmonary symptoms, head CT for headache, confusion, or focal deficits, and CTA chest/abdomen if aortic dissection is suspected.
Procedures Consider arterial line monitoring in unstable cases. Lumbar puncture may be used to evaluate for subarachnoid hemorrhage after appropriate imaging.
Differential diagnosis ACS, acute heart failure, aortic dissection, ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, preeclampsia/eclampsia, withdrawal syndromes (beta-blocker, clonidine), and catecholamine excess states (pheochromocytoma, sympathomimetic intoxication, tyramine reaction with MAOIs).
Treatment
Prehospital Support ABCs and consider cautious BP reduction only when clearly indicated.
Initial stabilization/therapy Provide oxygen as needed, establish IV access, monitor ECG and pulse oximetry.
Emergency department management Hypertensive urgency does not require IV reduction; give missed home medications, use oral agents only, and lower BP gradually over 24–48 hours with close follow-up. Hypertensive emergency requires IV therapy guided by the end-organ injury rather than the absolute BP. Reduce MAP by no more than 20–25% in the first hour, then target roughly SBP ~160 and DBP ~100 over 2–6 hours, transitioning to oral agents within 6–12 hours once stable. Lower more gradually in acute CNS injury, but more rapidly in aortic dissection. Hypertensive encephalopathy: lower MAP up to 20% or DBP to 100–110 within the first hour, then normalize over 48–72 hours using nicardipine, clevidipine, or labetalol. Ischemic stroke: treat only if SBP >220 or DBP >120, or if thrombolysis planned (target <185/110 pre-tPA, then <180/105); avoid reducing MAP more than 15–20% in the first 24 hours; preferred agents are nicardipine, clevidipine, or labetalol. ICH/SAH: treat if SBP >180 or DBP >100; aim SBP 140–160 or MAP down 20–25% in the first hour; avoid nitroglycerin and nitroprusside due to cerebral vasodilation and ICP effects; use nicardipine, clevidipine, or labetalol. ACS: target MAP 60–100 using labetalol or esmolol with nitroglycerin; avoid hydralazine and nitroprusside. Acute heart failure: target MAP 60–100 with nitroprusside or nitroglycerin plus ACE inhibitor and/or loop diuretic. Acute renal failure or microangiopathy: reduce MAP 20–25% in the first hour using nicardipine, clevidipine, or fenoldopam; ACE inhibitors are preferred for scleroderma renal crisis. Aortic dissection: reduce shear force by lowering HR and BP; beta-blockade must come first; target SBP 100–120 and HR <65 within 20 minutes using esmolol plus a vasodilator (dihydropyridine CCB or nitroprusside); obtain urgent surgical consultation for type A.
Sympathomimetic crisis: avoid pure beta-blockade; use phentolamine or calcium channel blocker plus benzodiazepines; use clonidine for clonidine withdrawal.
Pregnancy considerations Preeclampsia is SBP >140 or DBP >90 with proteinuria after 20 weeks to 4 weeks postpartum, often with headache, visual changes, edema, or RUQ pain; target SBP 130–150 and DBP 80–100 using labetalol, nicardipine, hydralazine, and magnesium, with obstetric consultation.
Medication Clevidipine 1–16 mg/h infusion; nicardipine 2–15 mg/h infusion; labetalol 20–80 mg IV q10 min (max 300 mg) or 0.5–2 mg/min infusion; esmolol 80 mg IV bolus then 150 μg/kg/min infusion; nitroglycerin 5–100 μg/min infusion; nitroprusside 0.25–10 μg/kg/min infusion; hydralazine 10–20 mg IV bolus; fenoldopam 0.1–0.6 μg/kg/min infusion; enalaprilat 1.25–5 mg IV q6h; phentolamine 5–15 mg IV q5–15 min.
Follow-up and disposition
Admission criteria Any patient with acute end-organ injury requires admission; ICU monitoring is indicated for hypertensive emergency.
Discharge criteria No end-organ injury, reliable follow-up, known hypertension, reversible trigger such as medication nonadherence, and ability to resume a safe outpatient regimen; provide strict return precautions for chest pain, neurologic symptoms, or severe headache.
Follow-up recommendations Ensure timely primary care follow-up for medication initiation or adjustment and long-term BP control.
Key points Do not use IV agents for hypertensive urgency. In hypertensive emergency, the initial goal is controlled MAP reduction of 20–25% in the first hour, except for ischemic stroke and aortic dissection where targets differ. Avoid precipitous BP drops that can worsen ischemia. In aortic dissection prevent reflex tachycardia by starting beta-blockade first. In catecholamine excess avoid unopposed alpha stimulation by avoiding pure beta-blockers.
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Emergency And Acute Medicine: Hyperthermia
Basics
Description Hyperthermia represents a spectrum of heat-related illness caused by progressively overwhelming heat stress, ranging from dehydration and electrolyte abnormalities to thermoregulatory failure and multisystem organ dysfunction. Normal body temperature is maintained by balancing heat production and dissipation. At temperatures above 42°C (108°F), oxidative phosphorylation becomes uncoupled and critical enzymes fail. Heat stroke is defined by a core temperature >105°F (40.5°C) with failure of thermoregulation, severe CNS dysfunction, and multisystem organ failure. Classic heat stroke is nonexertional, typically affecting the elderly, very young, or debilitated patients who cannot escape a hot environment; it develops over days to weeks and is associated with severe dehydration and hot, often dry skin. Exertional heat stroke occurs in younger, healthy individuals under intense physical exertion, develops over hours, and may occur despite ongoing sweating. Heat exhaustion involves moderate temperature elevation, usually <104°F (40°C), preserved thermoregulation and CNS function, and fluid or salt depletion; without treatment it may progress to heat stroke.
Etiology Predisposing factors impair heat dissipation or increase heat production. Medical conditions include extremes of age, dehydration, cardiovascular disease, obesity, diabetes, hyperthyroidism, pheochromocytoma, febrile illness, and skin disorders limiting sweating. Pharmacologic contributors include sympathomimetics, cocaine, PCP, LSD, MAO inhibitors, antipsychotics, anxiolytics, anticholinergics, antihistamines, beta-blockers, diuretics, laxatives, and drug or alcohol withdrawal. Environmental risks include high heat and humidity, prolonged exertion, immobility, lack of air conditioning, poor acclimatization, and occlusive clothing.
Pediatric considerations Children are at increased risk due to higher body surface area–to–mass ratio and reduced sweating capacity.
Diagnosis
Signs and symptoms Heat stroke presents with the classic triad of hyperthermia, CNS dysfunction, and hot skin. Core temperature exceeds 105°F (40.5°C). Neurologic findings include delirium, coma, seizures, ataxia, and confusion. Cardiovascular findings include tachycardia, hypotension, wide pulse pressure, and conduction abnormalities. Pulmonary findings include tachypnea, respiratory alkalosis, hypoxemia, and noncardiogenic pulmonary edema. GI symptoms include nausea, vomiting, and diarrhea. Renal failure, rhabdomyolysis, hepatic failure with extreme transaminase elevation, and coagulopathy including DIC may occur and indicate poor prognosis. Heat exhaustion causes headache, fatigue, malaise, impaired judgment, nausea, vomiting, tachycardia, dehydration, tachypnea, and profuse sweating without severe CNS dysfunction. Heat cramps cause painful muscle cramps after heavy sweating and hypotonic fluid replacement, leading to hyponatremia. Heat edema presents as dependent lower-extremity swelling in nonacclimatized individuals. Heat syncope presents as transient loss of consciousness during heat exposure, especially in the elderly. Prickly heat causes a pruritic maculopapular or vesicular rash due to sweat duct obstruction.
Essential workup Measure accurate core temperature using a rectal or esophageal probe. Establish history of heat exposure. Heat exhaustion is a diagnosis of exclusion. Heat stroke requires both core temperature >40.5°C and severe CNS dysfunction.
Diagnosis tests and interpretation
Laboratory Obtain CBC (leukocytosis, hemoconcentration), electrolytes, BUN, creatinine, glucose, urinalysis (myoglobin), creatine kinase for rhabdomyolysis, ABG (acidosis and elevated lactate common in exertional heat stroke), blood and urine cultures if sepsis is considered, toxicology screen, PT/PTT and DIC panel, liver function tests, and troponin (elevation suggests poor prognosis).
Imaging ECG in elderly or cardiac risk patients. Chest radiograph for ARDS or aspiration. Head CT for altered mental status. Lumbar puncture may be required to exclude CNS infection.
Differential diagnosis Sepsis, thyroid storm, pheochromocytoma, stimulant or anticholinergic toxicity, meningitis or encephalitis, cerebral malaria, delirium tremens, neuroleptic malignant syndrome, malignant hyperthermia, and serotonin syndrome.
Treatment
Prehospital Remove patient from heat source, disrobe, and initiate cooling with wet sheets.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Begin continuous core temperature monitoring. Initiate rapid cooling if temperature >104°F (40°C). Give IV 0.9% normal saline bolus if hypotensive. For altered mental status, administer glucose, thiamine, and naloxone as indicated.
Emergency department management Cooling is the priority. Use evaporative cooling with misted warm water and high airflow; combine with ice packs to groin and axilla. Cold-water immersion is effective but often impractical. Advanced techniques such as cold peritoneal lavage, extracorporeal circulation, or cold dialysis may be considered for refractory cases. Stop cooling at 102°F (39°C) to prevent hypothermia. Antipyretics are ineffective and alcohol sponge baths should be avoided. Supportive care includes aggressive isotonic fluid resuscitation while avoiding fluid overload. Insert Foley catheter to monitor urine output; target >2 mL/kg/hr if rhabdomyolysis is present. Treat seizures, agitation, and shivering with benzodiazepines. Avoid vasopressors and antiarrhythmics until adequate cooling, as many arrhythmias resolve with temperature normalization. Treat associated heat syndromes with appropriate hydration, electrolyte replacement, elevation or compression, and topical therapy as indicated.
Medication Benzodiazepines such as diazepam or lorazepam for seizures or agitation; naloxone when opioid toxicity is suspected.
Follow-up and disposition
Admission criteria All patients with heat stroke require ICU admission. Heat exhaustion requires admission if severe electrolyte abnormalities, renal failure, rhabdomyolysis, or advanced age are present.
Discharge criteria Patients without heat stroke or severe heat exhaustion who normalize clinically after treatment may be discharged with counseling.
Key points Heat stroke cannot be diagnosed without both core temperature >40.5°C and severe CNS dysfunction. Rapid cooling and supportive care are the cornerstones of management. Continuous core temperature monitoring is standard of care, and evaporative cooling is the preferred first-line method.
Basics
Description Hyperthermia represents a spectrum of heat-related illness caused by progressively overwhelming heat stress, ranging from dehydration and electrolyte abnormalities to thermoregulatory failure and multisystem organ dysfunction. Normal body temperature is maintained by balancing heat production and dissipation. At temperatures above 42°C (108°F), oxidative phosphorylation becomes uncoupled and critical enzymes fail. Heat stroke is defined by a core temperature >105°F (40.5°C) with failure of thermoregulation, severe CNS dysfunction, and multisystem organ failure. Classic heat stroke is nonexertional, typically affecting the elderly, very young, or debilitated patients who cannot escape a hot environment; it develops over days to weeks and is associated with severe dehydration and hot, often dry skin. Exertional heat stroke occurs in younger, healthy individuals under intense physical exertion, develops over hours, and may occur despite ongoing sweating. Heat exhaustion involves moderate temperature elevation, usually <104°F (40°C), preserved thermoregulation and CNS function, and fluid or salt depletion; without treatment it may progress to heat stroke.
Etiology Predisposing factors impair heat dissipation or increase heat production. Medical conditions include extremes of age, dehydration, cardiovascular disease, obesity, diabetes, hyperthyroidism, pheochromocytoma, febrile illness, and skin disorders limiting sweating. Pharmacologic contributors include sympathomimetics, cocaine, PCP, LSD, MAO inhibitors, antipsychotics, anxiolytics, anticholinergics, antihistamines, beta-blockers, diuretics, laxatives, and drug or alcohol withdrawal. Environmental risks include high heat and humidity, prolonged exertion, immobility, lack of air conditioning, poor acclimatization, and occlusive clothing.
Pediatric considerations Children are at increased risk due to higher body surface area–to–mass ratio and reduced sweating capacity.
Diagnosis
Signs and symptoms Heat stroke presents with the classic triad of hyperthermia, CNS dysfunction, and hot skin. Core temperature exceeds 105°F (40.5°C). Neurologic findings include delirium, coma, seizures, ataxia, and confusion. Cardiovascular findings include tachycardia, hypotension, wide pulse pressure, and conduction abnormalities. Pulmonary findings include tachypnea, respiratory alkalosis, hypoxemia, and noncardiogenic pulmonary edema. GI symptoms include nausea, vomiting, and diarrhea. Renal failure, rhabdomyolysis, hepatic failure with extreme transaminase elevation, and coagulopathy including DIC may occur and indicate poor prognosis. Heat exhaustion causes headache, fatigue, malaise, impaired judgment, nausea, vomiting, tachycardia, dehydration, tachypnea, and profuse sweating without severe CNS dysfunction. Heat cramps cause painful muscle cramps after heavy sweating and hypotonic fluid replacement, leading to hyponatremia. Heat edema presents as dependent lower-extremity swelling in nonacclimatized individuals. Heat syncope presents as transient loss of consciousness during heat exposure, especially in the elderly. Prickly heat causes a pruritic maculopapular or vesicular rash due to sweat duct obstruction.
Essential workup Measure accurate core temperature using a rectal or esophageal probe. Establish history of heat exposure. Heat exhaustion is a diagnosis of exclusion. Heat stroke requires both core temperature >40.5°C and severe CNS dysfunction.
Diagnosis tests and interpretation
Laboratory Obtain CBC (leukocytosis, hemoconcentration), electrolytes, BUN, creatinine, glucose, urinalysis (myoglobin), creatine kinase for rhabdomyolysis, ABG (acidosis and elevated lactate common in exertional heat stroke), blood and urine cultures if sepsis is considered, toxicology screen, PT/PTT and DIC panel, liver function tests, and troponin (elevation suggests poor prognosis).
Imaging ECG in elderly or cardiac risk patients. Chest radiograph for ARDS or aspiration. Head CT for altered mental status. Lumbar puncture may be required to exclude CNS infection.
Differential diagnosis Sepsis, thyroid storm, pheochromocytoma, stimulant or anticholinergic toxicity, meningitis or encephalitis, cerebral malaria, delirium tremens, neuroleptic malignant syndrome, malignant hyperthermia, and serotonin syndrome.
Treatment
Prehospital Remove patient from heat source, disrobe, and initiate cooling with wet sheets.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Begin continuous core temperature monitoring. Initiate rapid cooling if temperature >104°F (40°C). Give IV 0.9% normal saline bolus if hypotensive. For altered mental status, administer glucose, thiamine, and naloxone as indicated.
Emergency department management Cooling is the priority. Use evaporative cooling with misted warm water and high airflow; combine with ice packs to groin and axilla. Cold-water immersion is effective but often impractical. Advanced techniques such as cold peritoneal lavage, extracorporeal circulation, or cold dialysis may be considered for refractory cases. Stop cooling at 102°F (39°C) to prevent hypothermia. Antipyretics are ineffective and alcohol sponge baths should be avoided. Supportive care includes aggressive isotonic fluid resuscitation while avoiding fluid overload. Insert Foley catheter to monitor urine output; target >2 mL/kg/hr if rhabdomyolysis is present. Treat seizures, agitation, and shivering with benzodiazepines. Avoid vasopressors and antiarrhythmics until adequate cooling, as many arrhythmias resolve with temperature normalization. Treat associated heat syndromes with appropriate hydration, electrolyte replacement, elevation or compression, and topical therapy as indicated.
Medication Benzodiazepines such as diazepam or lorazepam for seizures or agitation; naloxone when opioid toxicity is suspected.
Follow-up and disposition
Admission criteria All patients with heat stroke require ICU admission. Heat exhaustion requires admission if severe electrolyte abnormalities, renal failure, rhabdomyolysis, or advanced age are present.
Discharge criteria Patients without heat stroke or severe heat exhaustion who normalize clinically after treatment may be discharged with counseling.
Key points Heat stroke cannot be diagnosed without both core temperature >40.5°C and severe CNS dysfunction. Rapid cooling and supportive care are the cornerstones of management. Continuous core temperature monitoring is standard of care, and evaporative cooling is the preferred first-line method.
- Published on
Emergency And Acute Medicine: Hyperthyroidism
Basics
Description Hyperthyroidism is caused by excessive thyroid hormone production, producing a continuum of disease due to direct metabolic effects of thyroid hormones and increased sensitivity to catecholamines. Clinical states range from subclinical or mild hyperthyroidism to thyrotoxicosis and, in 1–2% of cases, life-threatening thyroid storm. Thyroid regulation occurs through hypothalamic TRH stimulating pituitary TSH release, which increases thyroidal secretion of T4 and T3. Most circulating hormone is T4, which is peripherally converted to the more biologically active T3. Genetic predisposition plays a role, particularly in Graves disease, which is associated with HLA-B8 and HLA-DR3, and in some familial cases of nontoxic goiter with autosomal dominant inheritance.
Etiology Primary hyperthyroidism includes Graves disease, toxic multinodular or uninodular goiter, iodine-induced hyperthyroidism, and thyroiditis (postpartum, radiation, subacute de Quervain, and chronic lymphocytic). Other causes include metastatic thyroid cancer, ectopic thyroid tissue such as struma ovarii, pituitary adenoma, drug-induced hyperthyroidism (amiodarone, lithium, interferon, interleukin-2, iodinated contrast), factitious thyrotoxicosis from excess hormone ingestion, and aspirin overdose.
Diagnosis
Alert Thyroid storm is a medical emergency and may be precipitated by infection, trauma, surgery, diabetic ketoacidosis, myocardial infarction, stroke, chemotherapy, organophosphate intoxication, or abrupt withdrawal of antithyroid medications.
Signs and symptoms Findings reflect heightened end-organ responsiveness to thyroid hormone. Common signs include fever, tachycardia with widened pulse pressure, diaphoresis, tremor, hyperreflexia, goiter, thyromegaly, thyroid bruit, exophthalmos, lid lag, pretibial myxedema, congestive heart failure, shock, and psychosis. Symptoms include weight loss despite increased appetite, palpitations, chest pain, heat intolerance, diarrhea, vomiting, weakness, anxiety, insomnia, menstrual irregularities, and fatigue. Thyroid storm presents with exaggerated manifestations including extreme tachyarrhythmias, heart failure, shock, delirium, coma, seizures, and thromboembolic events.
Geriatric considerations Apathetic hyperthyroidism often presents with subtle findings such as refractory atrial fibrillation, heart failure, weight loss, depression, tremor, and emotional lability rather than classic hyperadrenergic features.
History Typically reveals gradual onset of symptoms.
Physical exam May show fever, tachycardia, systolic hypertension with widened pulse pressure, tachypnea, alopecia, fine diaphoretic skin, irregularly irregular rhythm, lung rales, RUQ tenderness, jaundice, proximal muscle weakness, tremor, and altered mental status.
Essential workup Identify underlying cause and precipitating factors. Plasma TSH is the preferred initial test; a normal TSH generally excludes hyperthyroidism. Low TSH with normal T4 requires T3 measurement to rule out T3 thyrotoxicosis. If laboratory testing is delayed or unavailable, strong clinical suspicion should prompt treatment.
Diagnosis tests and interpretation
Laboratory TSH is typically suppressed, with elevated free T4. Approximately 5% of patients have isolated T3 thyrotoxicosis. Additional testing may include CBC, chemistry panel, liver enzymes, ABG, glucose, and cardiac markers to evaluate complications or precipitants.
Imaging Chest radiograph is useful in heart failure or infection.
Diagnostic procedures ECG commonly shows sinus tachycardia or new-onset atrial fibrillation and helps identify ischemia as a precipitating factor.
Differential diagnosis Pheochromocytoma, sepsis, sympathomimetic intoxication, psychosis, heat stroke, delirium tremens, malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome, hypothalamic stroke, hypothyroidism with apathetic presentation, and factitious thyrotoxicosis.
Treatment
Prehospital Supportive care and stabilization.
Initial stabilization/therapy Manage airway, breathing, and circulation. Initiate cardiac monitoring, provide oxygen and IV fluids, and begin cooling measures. Use acetaminophen for fever and avoid aspirin, which increases free thyroid hormone levels.
Emergency department management Identify and treat precipitating causes. In suspected thyroid storm, initiate treatment based on clinical suspicion without delay. Inhibit hormone synthesis with thioamides, preferably propylthiouracil, which also reduces peripheral T4-to-T3 conversion; methimazole is an alternative. Block hormone release with iodine preparations only after thioamide administration and at least one hour later. Block peripheral effects using beta-blockers, with propranolol preferred due to inhibition of T4-to-T3 conversion; esmolol may be used when beta-1 selectivity is needed. Reduce peripheral conversion with corticosteroids. Adjunctive therapies include cholestyramine to reduce enterohepatic circulation of thyroid hormone and lithium if iodine is contraindicated. Manage heart failure, dehydration, hyperthermia, and associated conditions concurrently.
Medication Propylthiouracil, propranolol, iodine solutions (Lugol), methimazole, esmolol, hydrocortisone or dexamethasone, cholestyramine, lithium, guanethidine, and reserpine as indicated based on clinical context.
Pregnancy considerations Physiologic changes may mimic hyperthyroidism. Poorly controlled disease increases risks of hyperemesis gravidarum, preeclampsia, preterm labor, low birth weight, miscarriage, and stillbirth. PTU is preferred at the lowest effective dose; propranolol may be used cautiously. Radioactive iodine is contraindicated. Thyroidectomy is an option when medications are not tolerated. Postpartum thyroiditis occurs in up to 10% of patients and often resolves within one year.
Follow-up and disposition
Admission criteria Thyroid storm, need for IV rate control, or significant instability.
Discharge criteria Mild symptoms responsive to oral therapy with reliable follow-up.
Follow-up recommendations Arrange timely primary care or endocrinology follow-up.
Key points Thyroid storm is highly lethal without prompt treatment and often requires empiric therapy. Never administer iodine before blocking hormone synthesis with a thioamide. Radioactive iodine is contraindicated in pregnancy.
Basics
Description Hyperthyroidism is caused by excessive thyroid hormone production, producing a continuum of disease due to direct metabolic effects of thyroid hormones and increased sensitivity to catecholamines. Clinical states range from subclinical or mild hyperthyroidism to thyrotoxicosis and, in 1–2% of cases, life-threatening thyroid storm. Thyroid regulation occurs through hypothalamic TRH stimulating pituitary TSH release, which increases thyroidal secretion of T4 and T3. Most circulating hormone is T4, which is peripherally converted to the more biologically active T3. Genetic predisposition plays a role, particularly in Graves disease, which is associated with HLA-B8 and HLA-DR3, and in some familial cases of nontoxic goiter with autosomal dominant inheritance.
Etiology Primary hyperthyroidism includes Graves disease, toxic multinodular or uninodular goiter, iodine-induced hyperthyroidism, and thyroiditis (postpartum, radiation, subacute de Quervain, and chronic lymphocytic). Other causes include metastatic thyroid cancer, ectopic thyroid tissue such as struma ovarii, pituitary adenoma, drug-induced hyperthyroidism (amiodarone, lithium, interferon, interleukin-2, iodinated contrast), factitious thyrotoxicosis from excess hormone ingestion, and aspirin overdose.
Diagnosis
Alert Thyroid storm is a medical emergency and may be precipitated by infection, trauma, surgery, diabetic ketoacidosis, myocardial infarction, stroke, chemotherapy, organophosphate intoxication, or abrupt withdrawal of antithyroid medications.
Signs and symptoms Findings reflect heightened end-organ responsiveness to thyroid hormone. Common signs include fever, tachycardia with widened pulse pressure, diaphoresis, tremor, hyperreflexia, goiter, thyromegaly, thyroid bruit, exophthalmos, lid lag, pretibial myxedema, congestive heart failure, shock, and psychosis. Symptoms include weight loss despite increased appetite, palpitations, chest pain, heat intolerance, diarrhea, vomiting, weakness, anxiety, insomnia, menstrual irregularities, and fatigue. Thyroid storm presents with exaggerated manifestations including extreme tachyarrhythmias, heart failure, shock, delirium, coma, seizures, and thromboembolic events.
Geriatric considerations Apathetic hyperthyroidism often presents with subtle findings such as refractory atrial fibrillation, heart failure, weight loss, depression, tremor, and emotional lability rather than classic hyperadrenergic features.
History Typically reveals gradual onset of symptoms.
Physical exam May show fever, tachycardia, systolic hypertension with widened pulse pressure, tachypnea, alopecia, fine diaphoretic skin, irregularly irregular rhythm, lung rales, RUQ tenderness, jaundice, proximal muscle weakness, tremor, and altered mental status.
Essential workup Identify underlying cause and precipitating factors. Plasma TSH is the preferred initial test; a normal TSH generally excludes hyperthyroidism. Low TSH with normal T4 requires T3 measurement to rule out T3 thyrotoxicosis. If laboratory testing is delayed or unavailable, strong clinical suspicion should prompt treatment.
Diagnosis tests and interpretation
Laboratory TSH is typically suppressed, with elevated free T4. Approximately 5% of patients have isolated T3 thyrotoxicosis. Additional testing may include CBC, chemistry panel, liver enzymes, ABG, glucose, and cardiac markers to evaluate complications or precipitants.
Imaging Chest radiograph is useful in heart failure or infection.
Diagnostic procedures ECG commonly shows sinus tachycardia or new-onset atrial fibrillation and helps identify ischemia as a precipitating factor.
Differential diagnosis Pheochromocytoma, sepsis, sympathomimetic intoxication, psychosis, heat stroke, delirium tremens, malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome, hypothalamic stroke, hypothyroidism with apathetic presentation, and factitious thyrotoxicosis.
Treatment
Prehospital Supportive care and stabilization.
Initial stabilization/therapy Manage airway, breathing, and circulation. Initiate cardiac monitoring, provide oxygen and IV fluids, and begin cooling measures. Use acetaminophen for fever and avoid aspirin, which increases free thyroid hormone levels.
Emergency department management Identify and treat precipitating causes. In suspected thyroid storm, initiate treatment based on clinical suspicion without delay. Inhibit hormone synthesis with thioamides, preferably propylthiouracil, which also reduces peripheral T4-to-T3 conversion; methimazole is an alternative. Block hormone release with iodine preparations only after thioamide administration and at least one hour later. Block peripheral effects using beta-blockers, with propranolol preferred due to inhibition of T4-to-T3 conversion; esmolol may be used when beta-1 selectivity is needed. Reduce peripheral conversion with corticosteroids. Adjunctive therapies include cholestyramine to reduce enterohepatic circulation of thyroid hormone and lithium if iodine is contraindicated. Manage heart failure, dehydration, hyperthermia, and associated conditions concurrently.
Medication Propylthiouracil, propranolol, iodine solutions (Lugol), methimazole, esmolol, hydrocortisone or dexamethasone, cholestyramine, lithium, guanethidine, and reserpine as indicated based on clinical context.
Pregnancy considerations Physiologic changes may mimic hyperthyroidism. Poorly controlled disease increases risks of hyperemesis gravidarum, preeclampsia, preterm labor, low birth weight, miscarriage, and stillbirth. PTU is preferred at the lowest effective dose; propranolol may be used cautiously. Radioactive iodine is contraindicated. Thyroidectomy is an option when medications are not tolerated. Postpartum thyroiditis occurs in up to 10% of patients and often resolves within one year.
Follow-up and disposition
Admission criteria Thyroid storm, need for IV rate control, or significant instability.
Discharge criteria Mild symptoms responsive to oral therapy with reliable follow-up.
Follow-up recommendations Arrange timely primary care or endocrinology follow-up.
Key points Thyroid storm is highly lethal without prompt treatment and often requires empiric therapy. Never administer iodine before blocking hormone synthesis with a thioamide. Radioactive iodine is contraindicated in pregnancy.
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Emergency And Acute Medicine – Hypothermia
Basics
Description Core body temperature <35°c. risk factors include impaired thermoregulation (infants, elderly), comorbid illness, intoxication, and environmental exposure. heat loss occurs via radiation (most significant), conduction, convection, evaporation, respiration. production relies on shivering, nonshivering thermogenesis, increased thyroxine epinephrine.< />pan>
Etiology
Dermal disease (burns, exfoliative dermatitis, severe psoriasis). Drug induced (ethanol, phenothiazines, sedative–hypnotics). Environmental exposure (immersion, nonimmersion). Iatrogenic causes (aggressive fluid resuscitation, heat stroke treatment). Metabolic disorders (hypothyroidism, hypopituitarism, hypoadrenalism). Neurologic conditions (spinal cord injury, head trauma, stroke, tumor, Wernicke disease). Neuromuscular inefficiency (extremes of age, impaired shivering, lack of acclimatization). Sepsis. Pediatric patients are at higher risk because of increased surface area to mass ratio; consider nonaccidental trauma.
Diagnosis
Signs And Symptoms
Mild (35–32.2°C): Hypertension, shivering, tachycardia progressing to bradycardia, tachypnea, vasoconstriction, apathy, ataxia, cold diuresis, impaired judgment.
Moderate (32.2–28°C): Atrial dysrhythmias, bradycardia refractory to atropine, decreased level of consciousness, hypoventilation with CO₂ retention, dilated pupils, diminished gag reflex, cessation of shivering, hyporeflexia, hypotension, J (Osborn) waves.
Severe (<28°c): apnea, coma, minimal eeg activity, nonreactive pupils, oliguria, pulmonary edema, ventricular dysrhythmias or asystole.< />pan>
History Duration and circumstances of cold exposure or submersion.
Physical Exam Pulse and blood pressure may be difficult to detect; pupils often dilated at very low temperatures.
Essential Workup Accurate core temperature measurement.
Diagnosis Tests And Interpretation
Lab Fingerstick glucose, ABG (no temperature correction), CBC (hemoconcentration), electrolytes, BUN/creatinine, potassium, CPK, lactate, coagulation studies, toxicology screen.
Imaging CXR for pneumonia.
ECG Bradyarrhythmias, atrial fibrillation, ventricular fibrillation, prolonged PR/QRS/QT, Osborn waves.
Differential Diagnosis Environmental exposure, sepsis, CNS pathology, metabolic disorders, drug toxicity.
Treatment
Prehospital Patient is not dead until “warm and dead.” Prolonged pulse checks (30–45 s). CPR during transport if indicated.
Initial Stabilization/Therapy ABCs, supplemental oxygen, safe intubation if needed, cardiac monitoring, warmed IV fluids (D5NS preferred), remove wet clothing, passive rewarming, naloxone, dextrose, and thiamine for altered mental status, stress-dose steroids if adrenal insufficiency suspected.
Emergency Department Treatment/Procedures Handle gently to avoid precipitating ventricular fibrillation. Most dysrhythmias resolve with rewarming alone. Defibrillate up to 1–3 times below 28–30°C, then defer until rewarmed. Active rewarming is required for core temperature <32°c. use passive external rewarming for mild cases, active (forced warm air, trunk first) moderate and core (humidified oxygen, warmed iv fluids, peritoneal or pleural lavage, extracorporeal including hemodialysis cardiopulmonary bypass) severe hypothermia cardiac arrest. faster rates (1–2°c />r) are associated with better outcomes.
Medication Amiodarone for persistent ventricular dysrhythmias after rewarming, dextrose for hypoglycemia, hydrocortisone or methylprednisolone if adrenal insufficiency suspected, levothyroxine only for myxedema coma, naloxone, thiamine.
Follow-Up And Disposition
Admission Criteria Moderate to severe hypothermia (<32°c).< />pan>
Discharge Criteria Young, healthy patients with very mild hypothermia who normalize and have a safe, warm environment.
Follow-Up Recommendations Social services involvement for patients at risk of recurrent cold exposure.
Key Points And Cautions Defibrillation is rarely effective below 28–30°C. Atrial fibrillation often resolves with rewarming alone. Beware afterdrop and rewarming shock. Gentle handling and adequate volume resuscitation are essential.
Basics
Description Core body temperature <35°c. risk factors include impaired thermoregulation (infants, elderly), comorbid illness, intoxication, and environmental exposure. heat loss occurs via radiation (most significant), conduction, convection, evaporation, respiration. production relies on shivering, nonshivering thermogenesis, increased thyroxine epinephrine.< />pan>
Etiology
Dermal disease (burns, exfoliative dermatitis, severe psoriasis). Drug induced (ethanol, phenothiazines, sedative–hypnotics). Environmental exposure (immersion, nonimmersion). Iatrogenic causes (aggressive fluid resuscitation, heat stroke treatment). Metabolic disorders (hypothyroidism, hypopituitarism, hypoadrenalism). Neurologic conditions (spinal cord injury, head trauma, stroke, tumor, Wernicke disease). Neuromuscular inefficiency (extremes of age, impaired shivering, lack of acclimatization). Sepsis. Pediatric patients are at higher risk because of increased surface area to mass ratio; consider nonaccidental trauma.
Diagnosis
Signs And Symptoms
Mild (35–32.2°C): Hypertension, shivering, tachycardia progressing to bradycardia, tachypnea, vasoconstriction, apathy, ataxia, cold diuresis, impaired judgment.
Moderate (32.2–28°C): Atrial dysrhythmias, bradycardia refractory to atropine, decreased level of consciousness, hypoventilation with CO₂ retention, dilated pupils, diminished gag reflex, cessation of shivering, hyporeflexia, hypotension, J (Osborn) waves.
Severe (<28°c): apnea, coma, minimal eeg activity, nonreactive pupils, oliguria, pulmonary edema, ventricular dysrhythmias or asystole.< />pan>
History Duration and circumstances of cold exposure or submersion.
Physical Exam Pulse and blood pressure may be difficult to detect; pupils often dilated at very low temperatures.
Essential Workup Accurate core temperature measurement.
Diagnosis Tests And Interpretation
Lab Fingerstick glucose, ABG (no temperature correction), CBC (hemoconcentration), electrolytes, BUN/creatinine, potassium, CPK, lactate, coagulation studies, toxicology screen.
Imaging CXR for pneumonia.
ECG Bradyarrhythmias, atrial fibrillation, ventricular fibrillation, prolonged PR/QRS/QT, Osborn waves.
Differential Diagnosis Environmental exposure, sepsis, CNS pathology, metabolic disorders, drug toxicity.
Treatment
Prehospital Patient is not dead until “warm and dead.” Prolonged pulse checks (30–45 s). CPR during transport if indicated.
Initial Stabilization/Therapy ABCs, supplemental oxygen, safe intubation if needed, cardiac monitoring, warmed IV fluids (D5NS preferred), remove wet clothing, passive rewarming, naloxone, dextrose, and thiamine for altered mental status, stress-dose steroids if adrenal insufficiency suspected.
Emergency Department Treatment/Procedures Handle gently to avoid precipitating ventricular fibrillation. Most dysrhythmias resolve with rewarming alone. Defibrillate up to 1–3 times below 28–30°C, then defer until rewarmed. Active rewarming is required for core temperature <32°c. use passive external rewarming for mild cases, active (forced warm air, trunk first) moderate and core (humidified oxygen, warmed iv fluids, peritoneal or pleural lavage, extracorporeal including hemodialysis cardiopulmonary bypass) severe hypothermia cardiac arrest. faster rates (1–2°c />r) are associated with better outcomes.
Medication Amiodarone for persistent ventricular dysrhythmias after rewarming, dextrose for hypoglycemia, hydrocortisone or methylprednisolone if adrenal insufficiency suspected, levothyroxine only for myxedema coma, naloxone, thiamine.
Follow-Up And Disposition
Admission Criteria Moderate to severe hypothermia (<32°c).< />pan>
Discharge Criteria Young, healthy patients with very mild hypothermia who normalize and have a safe, warm environment.
Follow-Up Recommendations Social services involvement for patients at risk of recurrent cold exposure.
Key Points And Cautions Defibrillation is rarely effective below 28–30°C. Atrial fibrillation often resolves with rewarming alone. Beware afterdrop and rewarming shock. Gentle handling and adequate volume resuscitation are essential.
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Emergency And Acute Medicine – Hypothyroidism
Basics
Description Decreased effective circulating thyroid hormone causes reduced metabolic rate and diminished catecholamine sensitivity. More common in women and the elderly. Myxedema coma is a rare, life-threatening decompensation marked by altered mental status and impaired thermoregulation precipitated by stress in a hypothyroid patient.
Etiology
Primary causes include idiopathic, congenital, autoimmune thyroiditis (Hashimoto disease), iodine deficiency (most common worldwide), neoplasm, infection, and iatrogenic causes (thyroid surgery, radioiodine, external radiation). Drug induced causes include iodides, lithium, amiodarone, sunitinib, bexarotene, interferons, narcotics, and sedatives. Central hypothyroidism is rare and due to pituitary or hypothalamic dysfunction, often with other hormone deficiencies.
Myxedema coma is triggered by infection, hypothermia, intoxication, drugs, stroke, heart failure, trauma, or pregnancy.
Diagnosis
Signs And Symptoms
History: Fatigue, cold intolerance, weight gain, constipation, depression, cognitive slowing, headaches, myalgias, muscle weakness, menorrhagia, infertility, carpal tunnel syndrome.
Physical exam: Periorbital edema, coarse sparse hair, brittle nails, loss of lateral third of eyebrows, hoarse voice, goiter, dry pale cool skin, nonpitting edema, prolonged relaxation of deep tendon reflexes.
Myxedema coma: Altered mental status, hypothermia, hypotension, bradycardia, respiratory failure.
Pediatric And Geriatric Considerations
Congenital hypothyroidism largely prevented by newborn screening. Childhood disease usually due to Hashimoto thyroiditis and may impair growth and development. Elderly patients may present atypically, mimicking normal aging.
Essential Workup
Laboratory confirmation may not be immediately available; treatment should be initiated based on clinical suspicion in severe cases.
Diagnosis Tests And Interpretation
Labs: Low total and free T4 and T3. TSH elevated in primary hypothyroidism, normal or low in central causes. Associated findings include anemia, hyponatremia, hypoglycemia, hypoxemia, hypercapnia, respiratory acidosis, elevated CK, LDH, cholesterol, and creatinine.
Imaging: Chest radiograph may show cardiomegaly from pericardial effusion.
ECG: Sinus bradycardia, low voltage, PR prolongation, bundle branch blocks, QT prolongation, nonspecific ST–T changes; Osborn waves if profoundly hypothermic.
Differential Diagnosis
Chronic kidney disease, heart failure, depression, hypoalbuminemia, pernicious anemia, nephrotic syndrome, sepsis.
Alert Euthyroid sick syndrome may cause abnormal thyroid tests during acute illness.
Treatment
Initial Stabilization/Therapy ABCs with airway protection and ventilation as needed. Cardiac monitoring, oxygen supplementation, cautious passive rewarming. Avoid aggressive rewarming.
Emergency Department Treatment/Procedures
Mild hypothyroidism: Outpatient oral thyroid hormone replacement.
Myxedema coma: Medical emergency. Initiate IV thyroid hormone replacement immediately on suspicion. Use lower doses and avoid aggressive T3 in elderly or cardiac patients. Administer hydrocortisone to prevent adrenal crisis. Treat hypoglycemia with dextrose, hypotension with IV fluids (pressors often ineffective until thyroid hormone given), severe hyponatremia with hypertonic saline if indicated. Identify and treat precipitating cause.
Medication
First line thyroid hormone therapy:
• T4 IV load ~2 μg/kg (ideal body weight) then 10–40 μg IV or PO daily
• Optional T3 IV 10 μg load then 10 μg IV q8–12h (avoid in elderly/cardiac patients)
Second line/supportive: Hydrocortisone 100 mg IV q6–8h, dextrose IV for hypoglycemia.
Follow-Up And Disposition
Admission Criteria All patients with myxedema coma require ICU admission.
Discharge Criteria Uncomplicated hypothyroidism suitable for outpatient management.
Follow-Up Recommendations Primary care or endocrinology follow-up for long-term thyroid hormone management. Pregnant, elderly, and cardiac patients require cautious dose titration.
Key Points And Cautions
Symptoms are nonspecific and easily overlooked. Myxedema coma has high mortality and requires prompt treatment. Do not delay therapy awaiting lab confirmation. Avoid aggressive T3 use in elderly or patients with ischemic heart disease.
Basics
Description Decreased effective circulating thyroid hormone causes reduced metabolic rate and diminished catecholamine sensitivity. More common in women and the elderly. Myxedema coma is a rare, life-threatening decompensation marked by altered mental status and impaired thermoregulation precipitated by stress in a hypothyroid patient.
Etiology
Primary causes include idiopathic, congenital, autoimmune thyroiditis (Hashimoto disease), iodine deficiency (most common worldwide), neoplasm, infection, and iatrogenic causes (thyroid surgery, radioiodine, external radiation). Drug induced causes include iodides, lithium, amiodarone, sunitinib, bexarotene, interferons, narcotics, and sedatives. Central hypothyroidism is rare and due to pituitary or hypothalamic dysfunction, often with other hormone deficiencies.
Myxedema coma is triggered by infection, hypothermia, intoxication, drugs, stroke, heart failure, trauma, or pregnancy.
Diagnosis
Signs And Symptoms
History: Fatigue, cold intolerance, weight gain, constipation, depression, cognitive slowing, headaches, myalgias, muscle weakness, menorrhagia, infertility, carpal tunnel syndrome.
Physical exam: Periorbital edema, coarse sparse hair, brittle nails, loss of lateral third of eyebrows, hoarse voice, goiter, dry pale cool skin, nonpitting edema, prolonged relaxation of deep tendon reflexes.
Myxedema coma: Altered mental status, hypothermia, hypotension, bradycardia, respiratory failure.
Pediatric And Geriatric Considerations
Congenital hypothyroidism largely prevented by newborn screening. Childhood disease usually due to Hashimoto thyroiditis and may impair growth and development. Elderly patients may present atypically, mimicking normal aging.
Essential Workup
Laboratory confirmation may not be immediately available; treatment should be initiated based on clinical suspicion in severe cases.
Diagnosis Tests And Interpretation
Labs: Low total and free T4 and T3. TSH elevated in primary hypothyroidism, normal or low in central causes. Associated findings include anemia, hyponatremia, hypoglycemia, hypoxemia, hypercapnia, respiratory acidosis, elevated CK, LDH, cholesterol, and creatinine.
Imaging: Chest radiograph may show cardiomegaly from pericardial effusion.
ECG: Sinus bradycardia, low voltage, PR prolongation, bundle branch blocks, QT prolongation, nonspecific ST–T changes; Osborn waves if profoundly hypothermic.
Differential Diagnosis
Chronic kidney disease, heart failure, depression, hypoalbuminemia, pernicious anemia, nephrotic syndrome, sepsis.
Alert Euthyroid sick syndrome may cause abnormal thyroid tests during acute illness.
Treatment
Initial Stabilization/Therapy ABCs with airway protection and ventilation as needed. Cardiac monitoring, oxygen supplementation, cautious passive rewarming. Avoid aggressive rewarming.
Emergency Department Treatment/Procedures
Mild hypothyroidism: Outpatient oral thyroid hormone replacement.
Myxedema coma: Medical emergency. Initiate IV thyroid hormone replacement immediately on suspicion. Use lower doses and avoid aggressive T3 in elderly or cardiac patients. Administer hydrocortisone to prevent adrenal crisis. Treat hypoglycemia with dextrose, hypotension with IV fluids (pressors often ineffective until thyroid hormone given), severe hyponatremia with hypertonic saline if indicated. Identify and treat precipitating cause.
Medication
First line thyroid hormone therapy:
• T4 IV load ~2 μg/kg (ideal body weight) then 10–40 μg IV or PO daily
• Optional T3 IV 10 μg load then 10 μg IV q8–12h (avoid in elderly/cardiac patients)
Second line/supportive: Hydrocortisone 100 mg IV q6–8h, dextrose IV for hypoglycemia.
Follow-Up And Disposition
Admission Criteria All patients with myxedema coma require ICU admission.
Discharge Criteria Uncomplicated hypothyroidism suitable for outpatient management.
Follow-Up Recommendations Primary care or endocrinology follow-up for long-term thyroid hormone management. Pregnant, elderly, and cardiac patients require cautious dose titration.
Key Points And Cautions
Symptoms are nonspecific and easily overlooked. Myxedema coma has high mortality and requires prompt treatment. Do not delay therapy awaiting lab confirmation. Avoid aggressive T3 use in elderly or patients with ischemic heart disease.
- Published on
Emergency And Acute Medicine – Idiopathic Thrombocytopenic Purpura
Basics
Description Idiopathic thrombocytopenic purpura (ITP) is isolated thrombocytopenia without an identifiable cause and with normal other cell lines. Incidence is approximately 2–5 per 100,000 per year. Acute ITP commonly affects children, with about 80% recovering within 8 weeks with or without therapy. Chronic ITP occurs mainly in adults, particularly young women, and often requires treatment to achieve remission. Refractory chronic ITP is characterized by fluctuating platelet counts and poor response to therapy.
Etiology
Immune-mediated platelet destruction due to autoantibodies, primarily IgG, leading to splenic and hepatic macrophage clearance. Some patients lack detectable autoantibodies, suggesting T-cell–mediated cytotoxicity. Complement activation may contribute. Decreased platelet production may occur in chronic or refractory disease. Eradication of Helicobacter pylori has been associated with platelet recovery in some patients.
Diagnosis
Signs And Symptoms
History: Mucocutaneous bleeding is most common, including epistaxis, gingival bleeding, menorrhagia, and conjunctival hemorrhage. Gastrointestinal bleeding, hemarthrosis, hematuria, and hematomas are uncommon. Pediatric cases often follow viral illness by 2–3 weeks. Adults typically have insidious onset; up to one-quarter are asymptomatic.
Physical exam: Petechiae and nonpalpable purpura are common. Spleen size is normal; splenomegaly suggests an alternate diagnosis. Intracranial hemorrhage is the most serious complication and leading cause of death, with risk increasing with age.
Essential Workup
Diagnosis of exclusion. CBC with differential and peripheral smear. PT and PTT if bleeding. Renal and liver function tests. Type and screen if bleeding. Pregnancy test when appropriate. Consider HIV testing.
Diagnosis Tests And Interpretation
Labs: Isolated thrombocytopenia with increased mean platelet volume. Normal RBC and WBC morphology. Normal coagulation studies and liver function.
Imaging: Noncontrast CT head if headache, neurologic deficits, trauma, or concern for intracranial hemorrhage.
Procedures: Bone marrow biopsy in patients >60 years, atypical cases, refractory disease, or prior to splenectomy. Antibody testing is not clinically useful.
Differential Diagnosis
Bone marrow failure or infiltration, splenic sequestration, thrombotic microangiopathies, disseminated intravascular coagulation, HELLP syndrome, valvular disease, and drug-induced thrombocytopenia.
Treatment
Prehospital And Initial Stabilization ABCs with attention to airway in severe mucosal bleeding or CNS hemorrhage. Establish IV access. Control bleeding with direct pressure.
Emergency Department Management Management depends on platelet count, bleeding severity, duration, age, and comorbidities. Observation is appropriate for children without bleeding or profound thrombocytopenia. Life-threatening bleeding requires high-dose IV corticosteroids, IVIG, and platelet transfusions (given after steroids or IVIG). Platelet transfusions alone are often ineffective. Aminocaproic acid may be considered for mucosal bleeding.
Medication
First line: High-dose glucocorticoids (dexamethasone 40 mg daily or prednisone 1–2 mg/kg/day), IVIG 1–2 g/kg for critical bleeding or urgent platelet rise, Anti-D immunoglobulin in Rh-positive patients.
Second line: Immunosuppressive agents, rituximab, thrombopoietin receptor agonists, or splenectomy for refractory disease.
Pregnancy Considerations
Differentiate from gestational thrombocytopenia and HELLP syndrome. Maternal platelet count does not predict neonatal thrombocytopenia. Mode of delivery is based on obstetric indications. Neonates should be screened and treated if thrombocytopenic.
Follow-Up And Disposition
Admission Criteria Life-threatening bleeding, any bleeding with platelets <20,000 />micro;L, asymptomatic patients with platelets <20,000 />micro;L and unreliable follow-up.
Discharge Criteria Asymptomatic patients or minor bleeding with platelets >30,000/µL.
Follow-Up Recommendations Hematology follow-up is required in all cases.
Key Points And Cautions
Exclude pseudothrombocytopenia before diagnosis. Spontaneous bleeding is uncommon until platelets fall below 10,000/µL. Intracranial hemorrhage risk increases with age and mandates urgent evaluation.
Basics
Description Idiopathic thrombocytopenic purpura (ITP) is isolated thrombocytopenia without an identifiable cause and with normal other cell lines. Incidence is approximately 2–5 per 100,000 per year. Acute ITP commonly affects children, with about 80% recovering within 8 weeks with or without therapy. Chronic ITP occurs mainly in adults, particularly young women, and often requires treatment to achieve remission. Refractory chronic ITP is characterized by fluctuating platelet counts and poor response to therapy.
Etiology
Immune-mediated platelet destruction due to autoantibodies, primarily IgG, leading to splenic and hepatic macrophage clearance. Some patients lack detectable autoantibodies, suggesting T-cell–mediated cytotoxicity. Complement activation may contribute. Decreased platelet production may occur in chronic or refractory disease. Eradication of Helicobacter pylori has been associated with platelet recovery in some patients.
Diagnosis
Signs And Symptoms
History: Mucocutaneous bleeding is most common, including epistaxis, gingival bleeding, menorrhagia, and conjunctival hemorrhage. Gastrointestinal bleeding, hemarthrosis, hematuria, and hematomas are uncommon. Pediatric cases often follow viral illness by 2–3 weeks. Adults typically have insidious onset; up to one-quarter are asymptomatic.
Physical exam: Petechiae and nonpalpable purpura are common. Spleen size is normal; splenomegaly suggests an alternate diagnosis. Intracranial hemorrhage is the most serious complication and leading cause of death, with risk increasing with age.
Essential Workup
Diagnosis of exclusion. CBC with differential and peripheral smear. PT and PTT if bleeding. Renal and liver function tests. Type and screen if bleeding. Pregnancy test when appropriate. Consider HIV testing.
Diagnosis Tests And Interpretation
Labs: Isolated thrombocytopenia with increased mean platelet volume. Normal RBC and WBC morphology. Normal coagulation studies and liver function.
Imaging: Noncontrast CT head if headache, neurologic deficits, trauma, or concern for intracranial hemorrhage.
Procedures: Bone marrow biopsy in patients >60 years, atypical cases, refractory disease, or prior to splenectomy. Antibody testing is not clinically useful.
Differential Diagnosis
Bone marrow failure or infiltration, splenic sequestration, thrombotic microangiopathies, disseminated intravascular coagulation, HELLP syndrome, valvular disease, and drug-induced thrombocytopenia.
Treatment
Prehospital And Initial Stabilization ABCs with attention to airway in severe mucosal bleeding or CNS hemorrhage. Establish IV access. Control bleeding with direct pressure.
Emergency Department Management Management depends on platelet count, bleeding severity, duration, age, and comorbidities. Observation is appropriate for children without bleeding or profound thrombocytopenia. Life-threatening bleeding requires high-dose IV corticosteroids, IVIG, and platelet transfusions (given after steroids or IVIG). Platelet transfusions alone are often ineffective. Aminocaproic acid may be considered for mucosal bleeding.
Medication
First line: High-dose glucocorticoids (dexamethasone 40 mg daily or prednisone 1–2 mg/kg/day), IVIG 1–2 g/kg for critical bleeding or urgent platelet rise, Anti-D immunoglobulin in Rh-positive patients.
Second line: Immunosuppressive agents, rituximab, thrombopoietin receptor agonists, or splenectomy for refractory disease.
Pregnancy Considerations
Differentiate from gestational thrombocytopenia and HELLP syndrome. Maternal platelet count does not predict neonatal thrombocytopenia. Mode of delivery is based on obstetric indications. Neonates should be screened and treated if thrombocytopenic.
Follow-Up And Disposition
Admission Criteria Life-threatening bleeding, any bleeding with platelets <20,000 />micro;L, asymptomatic patients with platelets <20,000 />micro;L and unreliable follow-up.
Discharge Criteria Asymptomatic patients or minor bleeding with platelets >30,000/µL.
Follow-Up Recommendations Hematology follow-up is required in all cases.
Key Points And Cautions
Exclude pseudothrombocytopenia before diagnosis. Spontaneous bleeding is uncommon until platelets fall below 10,000/µL. Intracranial hemorrhage risk increases with age and mandates urgent evaluation.
