- Published on
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.
- Published on
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.
- Published on
Emergency And Acute Medicine-Hyperemesis Gravidarum
Basics
Description Hyperemesis gravidarum is the most severe form of nausea and vomiting of pregnancy, also known as pernicious vomiting of pregnancy. It is characterized by persistent, unexplained vomiting leading to dehydration and metabolic disturbances. It occurs in approximately 0.3–2% of pregnancies and is a diagnosis of exclusion.
Etiology The exact cause is unknown. Proposed mechanisms include elevated levels of hCG and estradiol, thyrotoxicosis, upper gastrointestinal motility disorders, hepatic dysfunction, autonomic nervous system abnormalities, psychological factors, Helicobacter pylori infection, and genetic predisposition.
Diagnosis
Signs and symptoms Nausea and vomiting affect 50–90% of pregnancies, typically beginning between 4–10 weeks and resolving by 20 weeks. Symptoms peaking at 8–12 weeks are typical; onset after 20 weeks suggests an alternate diagnosis. Hyperemesis gravidarum is defined by severe, persistent vomiting, dehydration, and weight loss exceeding 5% of prepregnancy weight, often accompanied by ketonuria, ketonemia, electrolyte abnormalities, and elevated urine specific gravity.
History Assess onset and duration of vomiting, gestational age, prior similar pregnancies, last menstrual period, oral intake, urine output, presence of bloody or bilious emesis, abdominal pain, and vaginal bleeding. Risk factors include motion sickness, migraines, younger maternal age, low prepregnancy BMI, nulliparity, early-day symptom predominance, and a 15% recurrence risk in subsequent pregnancies.
Physical exam Evaluate hydration status and abdominal tenderness.
Essential workup Perform focused history and physical examination emphasizing hydration status and exclusion of alternative causes such as appendicitis or cholecystitis. Obtain uncontaminated urinalysis. If vomiting persists beyond 24 hours, obtain CBC, electrolytes, renal function tests, liver enzymes, bilirubin, and lipase.
Diagnosis tests and interpretation
Laboratory Urinalysis typically shows elevated specific gravity and ketonuria. Glucosuria warrants serum glucose testing; bilirubinuria prompts hepatobiliary evaluation. CBC may show hemoconcentration; WBC count is usually normal. Electrolytes may reveal elevated BUN, creatinine, hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis. Liver enzymes and bilirubin may be mildly elevated but should remain <100 IU/L and <4 mg/dL, respectively. Amylase may be elevated due to salivary origin; lipase is preferred to assess pancreatitis. TSH may be abnormal. Serum hCG levels are not indicated if an intrauterine pregnancy is confirmed.
Imaging Ultrasound is indicated if first-trimester imaging has not been performed to evaluate for molar pregnancy or multiple gestations.
Differential diagnosis Pyelonephritis, gastroenteritis, gastroparesis, bowel obstruction, Mallory–Weiss tear, hepatobiliary disease, pancreatitis, appendicitis, diabetic ketoacidosis, hyperthyroidism, hyperparathyroidism, uremia, and pseudotumor cerebri.
Treatment
Prehospital Initiate IV access and monitoring if significant volume depletion is suspected.
Initial stabilization/therapy Begin IV crystalloid hydration with normal saline or lactated Ringer’s solution.
Emergency department management Continue IV hydration; add dextrose to interrupt ketosis if indicated. Administer IV antiemetics to break the vomiting cycle. Transition to oral rehydration once symptoms improve. Thiamine 100 mg IV/IM/PO should be given to patients requiring IV fluids to prevent Wernicke encephalopathy. Antihistamines may be effective. Methylprednisolone may be considered as a last resort and should be avoided before 10 weeks’ gestation.
Medication First line Metoclopramide 10–20 mg IV; ondansetron 4–8 mg IV or 4 mg PO/ODT q8h; prochlorperazine 5–10 mg IV (max 40 mg/day); promethazine 12.5–25 mg IM. Outpatient options include meclizine 25 mg PO q6h PRN, metoclopramide 10 mg PO q6–8h PRN, prochlorperazine PO or PR, promethazine PO or PR, pyridoxine 25 mg PO TID, ginger supplements, doxylamine 12.5 mg PO q6–8h (often combined with pyridoxine), and thiamine 50 mg PO daily for symptoms lasting >3 weeks. Second line Methylprednisolone 16 mg IV or PO q8h for 3 days with taper, prescribed in consultation with obstetrics.
Follow-up and disposition
Admission criteria Inability to tolerate oral intake, persistent vomiting despite therapy, severe electrolyte or metabolic derangements, or early gestation (<8 weeks) with severe disease.
Discharge criteria Tolerance of oral intake, correction of dehydration, improvement in symptoms, and reduced ketonuria with reliable follow-up. Counsel patients on small, frequent meals rich in carbohydrates and low in fat; avoid spicy or irritant foods. Home IV therapy may be arranged if necessary.
Follow-up recommendations All patients should receive at least 3 mg of thiamine daily; 50 mg PO daily is recommended. The risk of first-trimester fetal loss is lower in women with hyperemesis gravidarum.
Key points Consider alternative diagnoses when nausea and vomiting begin after 9 weeks’ gestation. PICC lines are associated with increased maternal morbidity compared with enteral or medication-based management. Correct hyponatremia cautiously to avoid central pontine myelinolysis. Wernicke encephalopathy is a rare but severe complication and may present without classic features; administer thiamine promptly in any patient with confusion or apathy.
Basics
Description Hyperemesis gravidarum is the most severe form of nausea and vomiting of pregnancy, also known as pernicious vomiting of pregnancy. It is characterized by persistent, unexplained vomiting leading to dehydration and metabolic disturbances. It occurs in approximately 0.3–2% of pregnancies and is a diagnosis of exclusion.
Etiology The exact cause is unknown. Proposed mechanisms include elevated levels of hCG and estradiol, thyrotoxicosis, upper gastrointestinal motility disorders, hepatic dysfunction, autonomic nervous system abnormalities, psychological factors, Helicobacter pylori infection, and genetic predisposition.
Diagnosis
Signs and symptoms Nausea and vomiting affect 50–90% of pregnancies, typically beginning between 4–10 weeks and resolving by 20 weeks. Symptoms peaking at 8–12 weeks are typical; onset after 20 weeks suggests an alternate diagnosis. Hyperemesis gravidarum is defined by severe, persistent vomiting, dehydration, and weight loss exceeding 5% of prepregnancy weight, often accompanied by ketonuria, ketonemia, electrolyte abnormalities, and elevated urine specific gravity.
History Assess onset and duration of vomiting, gestational age, prior similar pregnancies, last menstrual period, oral intake, urine output, presence of bloody or bilious emesis, abdominal pain, and vaginal bleeding. Risk factors include motion sickness, migraines, younger maternal age, low prepregnancy BMI, nulliparity, early-day symptom predominance, and a 15% recurrence risk in subsequent pregnancies.
Physical exam Evaluate hydration status and abdominal tenderness.
Essential workup Perform focused history and physical examination emphasizing hydration status and exclusion of alternative causes such as appendicitis or cholecystitis. Obtain uncontaminated urinalysis. If vomiting persists beyond 24 hours, obtain CBC, electrolytes, renal function tests, liver enzymes, bilirubin, and lipase.
Diagnosis tests and interpretation
Laboratory Urinalysis typically shows elevated specific gravity and ketonuria. Glucosuria warrants serum glucose testing; bilirubinuria prompts hepatobiliary evaluation. CBC may show hemoconcentration; WBC count is usually normal. Electrolytes may reveal elevated BUN, creatinine, hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis. Liver enzymes and bilirubin may be mildly elevated but should remain <100 IU/L and <4 mg/dL, respectively. Amylase may be elevated due to salivary origin; lipase is preferred to assess pancreatitis. TSH may be abnormal. Serum hCG levels are not indicated if an intrauterine pregnancy is confirmed.
Imaging Ultrasound is indicated if first-trimester imaging has not been performed to evaluate for molar pregnancy or multiple gestations.
Differential diagnosis Pyelonephritis, gastroenteritis, gastroparesis, bowel obstruction, Mallory–Weiss tear, hepatobiliary disease, pancreatitis, appendicitis, diabetic ketoacidosis, hyperthyroidism, hyperparathyroidism, uremia, and pseudotumor cerebri.
Treatment
Prehospital Initiate IV access and monitoring if significant volume depletion is suspected.
Initial stabilization/therapy Begin IV crystalloid hydration with normal saline or lactated Ringer’s solution.
Emergency department management Continue IV hydration; add dextrose to interrupt ketosis if indicated. Administer IV antiemetics to break the vomiting cycle. Transition to oral rehydration once symptoms improve. Thiamine 100 mg IV/IM/PO should be given to patients requiring IV fluids to prevent Wernicke encephalopathy. Antihistamines may be effective. Methylprednisolone may be considered as a last resort and should be avoided before 10 weeks’ gestation.
Medication First line Metoclopramide 10–20 mg IV; ondansetron 4–8 mg IV or 4 mg PO/ODT q8h; prochlorperazine 5–10 mg IV (max 40 mg/day); promethazine 12.5–25 mg IM. Outpatient options include meclizine 25 mg PO q6h PRN, metoclopramide 10 mg PO q6–8h PRN, prochlorperazine PO or PR, promethazine PO or PR, pyridoxine 25 mg PO TID, ginger supplements, doxylamine 12.5 mg PO q6–8h (often combined with pyridoxine), and thiamine 50 mg PO daily for symptoms lasting >3 weeks. Second line Methylprednisolone 16 mg IV or PO q8h for 3 days with taper, prescribed in consultation with obstetrics.
Follow-up and disposition
Admission criteria Inability to tolerate oral intake, persistent vomiting despite therapy, severe electrolyte or metabolic derangements, or early gestation (<8 weeks) with severe disease.
Discharge criteria Tolerance of oral intake, correction of dehydration, improvement in symptoms, and reduced ketonuria with reliable follow-up. Counsel patients on small, frequent meals rich in carbohydrates and low in fat; avoid spicy or irritant foods. Home IV therapy may be arranged if necessary.
Follow-up recommendations All patients should receive at least 3 mg of thiamine daily; 50 mg PO daily is recommended. The risk of first-trimester fetal loss is lower in women with hyperemesis gravidarum.
Key points Consider alternative diagnoses when nausea and vomiting begin after 9 weeks’ gestation. PICC lines are associated with increased maternal morbidity compared with enteral or medication-based management. Correct hyponatremia cautiously to avoid central pontine myelinolysis. Wernicke encephalopathy is a rare but severe complication and may present without classic features; administer thiamine promptly in any patient with confusion or apathy.
- Published on
Emergency And Acute Medicine – Immunosuppression
Basics
Description Immunosuppression is a congenital or acquired deficiency in host defense mechanisms, including impaired antibody production (B-cell), cellular immunity (T-cell), phagocytic dysfunction, complement deficiency, or disruption of skin and mucosal barriers.
Etiology
Congenital immune disorders. Immunosuppressive medications. Aging with immunosenescence, poor circulation, and impaired wound healing. Chronic diseases (lung, kidney, heart). HIV infection, with susceptibility related to CD4 count. Diabetes mellitus causing impaired immune response and vascular insufficiency. Malnutrition related to poverty, alcoholism, drug abuse, or eating disorders. Asplenia (functional in sickle cell disease or postsplenectomy) with increased risk from encapsulated organisms. Organ transplantation with immunosuppressive therapy; infections may be donor-derived, recipient-derived, or nosocomial, with timing since transplant guiding likely pathogens. Malignancy and chemotherapy with infection risk proportional to depth and duration of neutropenia. Neutropenia defined as ANC <500 />m³ or <1,000 />m³ with anticipated nadir <500 />m³. Gram-positive organisms are most common in the U.S.; gram-negative organisms are less common but often more virulent. Risk of fungal infection increases with prolonged neutropenia, prior broad-spectrum antibiotics, or intensive chemotherapy.
Diagnosis
Signs And Symptoms Fever may be the only sign of severe infection. Symptoms are often subtle or absent. Review systems carefully for localizing complaints. Assess for recent hospitalization, nursing home exposure, sick contacts, and current or prophylactic antimicrobials that may alter pathogen spectrum.
Physical Exam Perform a thorough head-to-toe exam. Avoid digital rectal exam in febrile neutropenia. Infection may lack classic inflammatory signs (e.g., meningitis without nuchal rigidity, pneumonia without focal findings).
Essential Workup
Diagnostic evaluation must be individualized. Inflammatory responses may be blunted, leading to atypical presentations such as pneumonia without infiltrate, UTI without pyuria, or meningitis without CSF pleocytosis.
Diagnosis Tests And Interpretation
Labs CBC with differential to assess neutropenia or left shift. Blood cultures ×2 (include line cultures if present). Urinalysis and urine culture. Serum lactate for occult hypoperfusion. ABG if respiratory compromise or suspected Pneumocystis jirovecii pneumonia. Pregnancy test when appropriate.
Imaging Chest x-ray for neutropenic, hypoxic, or pulmonary findings; CT or MRI as guided by symptoms.
Procedures Lumbar puncture if meningitis suspected; check platelets and coagulation first. Consider cryptococcal antigen testing even without CSF pleocytosis.
Differential Diagnosis
Infectious sources (oropharynx, sinuses, lungs, GI tract, perineum, urinary tract, skin, bone, indwelling devices). Noninfectious causes of fever include drug fever, malignancy, graft rejection, vasculitis, rheumatologic disease, pulmonary embolism, thyroid disease, and transfusion reactions.
Treatment
Prehospital Establish IV access and begin IV fluids.
Initial Stabilization Aggressive fluid resuscitation for hypovolemia. Goal-directed therapy for sepsis. Use vasopressors for refractory hypotension (dopamine or norepinephrine).
Emergency Department Management Apply infection-control precautions. Obtain cultures promptly and administer empiric broad-spectrum antibiotics without delay. Most febrile neutropenic patients require admission; selected low-risk patients may be treated as outpatients.
Medication
Empiric broad-spectrum therapy should be individualized.
Oral (low-risk): Ciprofloxacin 750 mg PO BID plus amoxicillin–clavulanate 875 mg PO BID.
IV monotherapy options: Cefepime 2 g IV q8h; ceftazidime 2 g IV q8h; meropenem 1 g IV q8h; imipenem–cilastatin 500 mg IV q6h; piperacillin–tazobactam 4.5 g IV q6h.
Add aminoglycoside for high-risk patients if indicated.
Add vancomycin only for suspected line infection, MRSA, or severe skin/soft tissue infection.
Add anaerobic coverage (e.g., clindamycin) if oral, abdominal, or perianal source suspected.
Follow-Up And Disposition
Admission Criteria ANC <100 />m³, high-risk immunocompromised state, unstable vitals, significant comorbidities, or lack of reliable follow-up.
Discharge Criteria Low-risk, well-appearing patients tolerating oral therapy with reliable 24-hour follow-up, after discussion with the treating specialist.
Follow-Up Recommendations Reassessment within 24 hours to review cultures and clinical status.
Pearls And Pitfalls
Isolated fever may be the only sign of life-threatening infection. Do not delay antibiotics in febrile neutropenia. Review prior microbiology and resistance patterns. Involve oncology, transplant, or infectious disease specialists early.
Basics
Description Immunosuppression is a congenital or acquired deficiency in host defense mechanisms, including impaired antibody production (B-cell), cellular immunity (T-cell), phagocytic dysfunction, complement deficiency, or disruption of skin and mucosal barriers.
Etiology
Congenital immune disorders. Immunosuppressive medications. Aging with immunosenescence, poor circulation, and impaired wound healing. Chronic diseases (lung, kidney, heart). HIV infection, with susceptibility related to CD4 count. Diabetes mellitus causing impaired immune response and vascular insufficiency. Malnutrition related to poverty, alcoholism, drug abuse, or eating disorders. Asplenia (functional in sickle cell disease or postsplenectomy) with increased risk from encapsulated organisms. Organ transplantation with immunosuppressive therapy; infections may be donor-derived, recipient-derived, or nosocomial, with timing since transplant guiding likely pathogens. Malignancy and chemotherapy with infection risk proportional to depth and duration of neutropenia. Neutropenia defined as ANC <500 />m³ or <1,000 />m³ with anticipated nadir <500 />m³. Gram-positive organisms are most common in the U.S.; gram-negative organisms are less common but often more virulent. Risk of fungal infection increases with prolonged neutropenia, prior broad-spectrum antibiotics, or intensive chemotherapy.
Diagnosis
Signs And Symptoms Fever may be the only sign of severe infection. Symptoms are often subtle or absent. Review systems carefully for localizing complaints. Assess for recent hospitalization, nursing home exposure, sick contacts, and current or prophylactic antimicrobials that may alter pathogen spectrum.
Physical Exam Perform a thorough head-to-toe exam. Avoid digital rectal exam in febrile neutropenia. Infection may lack classic inflammatory signs (e.g., meningitis without nuchal rigidity, pneumonia without focal findings).
Essential Workup
Diagnostic evaluation must be individualized. Inflammatory responses may be blunted, leading to atypical presentations such as pneumonia without infiltrate, UTI without pyuria, or meningitis without CSF pleocytosis.
Diagnosis Tests And Interpretation
Labs CBC with differential to assess neutropenia or left shift. Blood cultures ×2 (include line cultures if present). Urinalysis and urine culture. Serum lactate for occult hypoperfusion. ABG if respiratory compromise or suspected Pneumocystis jirovecii pneumonia. Pregnancy test when appropriate.
Imaging Chest x-ray for neutropenic, hypoxic, or pulmonary findings; CT or MRI as guided by symptoms.
Procedures Lumbar puncture if meningitis suspected; check platelets and coagulation first. Consider cryptococcal antigen testing even without CSF pleocytosis.
Differential Diagnosis
Infectious sources (oropharynx, sinuses, lungs, GI tract, perineum, urinary tract, skin, bone, indwelling devices). Noninfectious causes of fever include drug fever, malignancy, graft rejection, vasculitis, rheumatologic disease, pulmonary embolism, thyroid disease, and transfusion reactions.
Treatment
Prehospital Establish IV access and begin IV fluids.
Initial Stabilization Aggressive fluid resuscitation for hypovolemia. Goal-directed therapy for sepsis. Use vasopressors for refractory hypotension (dopamine or norepinephrine).
Emergency Department Management Apply infection-control precautions. Obtain cultures promptly and administer empiric broad-spectrum antibiotics without delay. Most febrile neutropenic patients require admission; selected low-risk patients may be treated as outpatients.
Medication
Empiric broad-spectrum therapy should be individualized.
Oral (low-risk): Ciprofloxacin 750 mg PO BID plus amoxicillin–clavulanate 875 mg PO BID.
IV monotherapy options: Cefepime 2 g IV q8h; ceftazidime 2 g IV q8h; meropenem 1 g IV q8h; imipenem–cilastatin 500 mg IV q6h; piperacillin–tazobactam 4.5 g IV q6h.
Add aminoglycoside for high-risk patients if indicated.
Add vancomycin only for suspected line infection, MRSA, or severe skin/soft tissue infection.
Add anaerobic coverage (e.g., clindamycin) if oral, abdominal, or perianal source suspected.
Follow-Up And Disposition
Admission Criteria ANC <100 />m³, high-risk immunocompromised state, unstable vitals, significant comorbidities, or lack of reliable follow-up.
Discharge Criteria Low-risk, well-appearing patients tolerating oral therapy with reliable 24-hour follow-up, after discussion with the treating specialist.
Follow-Up Recommendations Reassessment within 24 hours to review cultures and clinical status.
Pearls And Pitfalls
Isolated fever may be the only sign of life-threatening infection. Do not delay antibiotics in febrile neutropenia. Review prior microbiology and resistance patterns. Involve oncology, transplant, or infectious disease specialists early.
- Published on
Emergency And Acute Medicine – Immunizations
Basics
Description Immunization enhances resistance to infectious diseases through passive or active mechanisms. Passive immunization involves administration of antibodies or maternal antibody transfer via placenta or breast milk. Active immunization stimulates the immune system, producing IgM antibodies within 7–10 days followed by IgG antibodies peaking at 2–6 weeks. Oral and nasal vaccines induce mucosal IgA, whereas parenteral vaccines primarily induce systemic immunity. Improper storage, dosing, or administration route can reduce effectiveness.
Etiology
Live attenuated vaccines (e.g., measles, mumps, rubella, varicella, rotavirus) replicate in the host and may cause severe disease in immunocompromised patients. Inactivated vaccines (e.g., IPV, hepatitis A, influenza, pertussis) are safe in immunocompromised patients. Toxoid, subunit, and conjugate vaccines (e.g., tetanus, diphtheria, Hib, pneumococcus, meningococcus, HPV) use antigenic components to stimulate immunity. Hepatitis B vaccines are produced using recombinant DNA technology. Combination vaccines reduce injection burden but increase cost.
Epidemiology
Widespread immunization has markedly reduced many life-threatening infections. Polio has been eliminated from the Western Hemisphere. Hib, diphtheria, and tetanus are now rare in North America. Measles, rubella, and varicella persist mainly in unimmunized populations and travelers. Conjugate pneumococcal vaccines have reduced invasive disease by more than 90% for vaccine serotypes. Rotavirus vaccines reduce severe gastroenteritis. Annual influenza vaccines are produced based on global surveillance. Immunization schedules are tailored by age, pregnancy status, comorbidities, travel, occupation, and immune status.
Diagnosis
Signs And Symptoms Adverse events are usually mild and self-limited. Common reactions include local pain, swelling, erythema, and low-grade fever. Fever is seen after rotavirus, pneumococcal, HPV, MMR/MMRV, meningococcal, and influenza vaccines. Rash may follow varicella or MMR vaccines. Neurologic adverse events are rare and include febrile seizures, hypotonic–hyporesponsive episodes, and very rarely encephalopathy or Guillain–Barré syndrome. Gastrointestinal symptoms may occur after rotavirus vaccine. Live attenuated intranasal influenza vaccine may cause mild respiratory symptoms.
Essential Workup
Review immunization status during ED visits. Determine reasons for incomplete vaccination. Identify true contraindications, including prior anaphylaxis to a vaccine or specific components (e.g., yeast for HepB, egg protein for influenza, neomycin or gelatin for MMR). Assess for conditions requiring deferral, such as moderate to severe acute illness, immunodeficiency, pregnancy (for live vaccines), or recent immune globulin administration.
Treatment
Prehospital And Initial Stabilization Focus on airway, breathing, and circulation.
Emergency Department Management Treat anaphylaxis with epinephrine, antihistamines, bronchodilators, and IV fluids. Manage local reactions with cold compresses and analgesics. Treat fever, myalgias, and arthralgias with acetaminophen or ibuprofen. Manage seizures with benzodiazepines. Provide active or passive immunization as indicated for wound management or exposure prophylaxis. Avoid salicylates for 6 weeks after varicella vaccination in children.
Medication
Acetaminophen 15 mg/kg/dose PO q4–6h.
Ibuprofen 10 mg/kg/dose PO q6–8h.
Follow-Up And Disposition
Admission Criteria Serious adverse reactions such as anaphylaxis, encephalopathy, or severe neurologic symptoms.
Discharge Criteria Routine postimmunization reactions without complications.
Follow-Up Recommendations Arrange primary care follow-up to complete immunization schedules. Report unexpected adverse events to the Vaccine Adverse Event Reporting System.
Key Points And Cautions
Most vaccine reactions are mild and self-limited. True contraindications are rare. Failure to recognize contraindications or to continue antihistamines after allergic reactions may lead to complications. Immunization remains one of the most effective preventive interventions in emergency and acute medicine.
Basics
Description Immunization enhances resistance to infectious diseases through passive or active mechanisms. Passive immunization involves administration of antibodies or maternal antibody transfer via placenta or breast milk. Active immunization stimulates the immune system, producing IgM antibodies within 7–10 days followed by IgG antibodies peaking at 2–6 weeks. Oral and nasal vaccines induce mucosal IgA, whereas parenteral vaccines primarily induce systemic immunity. Improper storage, dosing, or administration route can reduce effectiveness.
Etiology
Live attenuated vaccines (e.g., measles, mumps, rubella, varicella, rotavirus) replicate in the host and may cause severe disease in immunocompromised patients. Inactivated vaccines (e.g., IPV, hepatitis A, influenza, pertussis) are safe in immunocompromised patients. Toxoid, subunit, and conjugate vaccines (e.g., tetanus, diphtheria, Hib, pneumococcus, meningococcus, HPV) use antigenic components to stimulate immunity. Hepatitis B vaccines are produced using recombinant DNA technology. Combination vaccines reduce injection burden but increase cost.
Epidemiology
Widespread immunization has markedly reduced many life-threatening infections. Polio has been eliminated from the Western Hemisphere. Hib, diphtheria, and tetanus are now rare in North America. Measles, rubella, and varicella persist mainly in unimmunized populations and travelers. Conjugate pneumococcal vaccines have reduced invasive disease by more than 90% for vaccine serotypes. Rotavirus vaccines reduce severe gastroenteritis. Annual influenza vaccines are produced based on global surveillance. Immunization schedules are tailored by age, pregnancy status, comorbidities, travel, occupation, and immune status.
Diagnosis
Signs And Symptoms Adverse events are usually mild and self-limited. Common reactions include local pain, swelling, erythema, and low-grade fever. Fever is seen after rotavirus, pneumococcal, HPV, MMR/MMRV, meningococcal, and influenza vaccines. Rash may follow varicella or MMR vaccines. Neurologic adverse events are rare and include febrile seizures, hypotonic–hyporesponsive episodes, and very rarely encephalopathy or Guillain–Barré syndrome. Gastrointestinal symptoms may occur after rotavirus vaccine. Live attenuated intranasal influenza vaccine may cause mild respiratory symptoms.
Essential Workup
Review immunization status during ED visits. Determine reasons for incomplete vaccination. Identify true contraindications, including prior anaphylaxis to a vaccine or specific components (e.g., yeast for HepB, egg protein for influenza, neomycin or gelatin for MMR). Assess for conditions requiring deferral, such as moderate to severe acute illness, immunodeficiency, pregnancy (for live vaccines), or recent immune globulin administration.
Treatment
Prehospital And Initial Stabilization Focus on airway, breathing, and circulation.
Emergency Department Management Treat anaphylaxis with epinephrine, antihistamines, bronchodilators, and IV fluids. Manage local reactions with cold compresses and analgesics. Treat fever, myalgias, and arthralgias with acetaminophen or ibuprofen. Manage seizures with benzodiazepines. Provide active or passive immunization as indicated for wound management or exposure prophylaxis. Avoid salicylates for 6 weeks after varicella vaccination in children.
Medication
Acetaminophen 15 mg/kg/dose PO q4–6h.
Ibuprofen 10 mg/kg/dose PO q6–8h.
Follow-Up And Disposition
Admission Criteria Serious adverse reactions such as anaphylaxis, encephalopathy, or severe neurologic symptoms.
Discharge Criteria Routine postimmunization reactions without complications.
Follow-Up Recommendations Arrange primary care follow-up to complete immunization schedules. Report unexpected adverse events to the Vaccine Adverse Event Reporting System.
Key Points And Cautions
Most vaccine reactions are mild and self-limited. True contraindications are rare. Failure to recognize contraindications or to continue antihistamines after allergic reactions may lead to complications. Immunization remains one of the most effective preventive interventions in emergency and acute medicine.
- 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.
- Published on
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 – 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.
- Published on
Emergency And Acute Medicine: Hypoparathyroidism
Basics
Description Hypoparathyroidism results from deficiency of parathyroid hormone (PTH), whereas pseudohypoparathyroidism is due to end-organ resistance to PTH. PTH reduces urinary calcium loss, increases urinary phosphate loss, stimulates renal conversion of vitamin D to its active form, and mobilizes calcium and phosphate from bone. Hypocalcemia is the primary metabolic abnormality. Calcitonin promotes deposition of calcium and phosphate into bone. Magnesium is required for both PTH production and peripheral PTH action. Primary hypoparathyroidism reflects intrinsic gland failure, while pseudohypoparathyroidism features elevated PTH with tissue resistance and is often associated with hypothyroidism and hypogonadism. Genetic associations include congenital absence (DiGeorge syndrome), autoimmune polyglandular syndrome type I, Wilson disease, and Albright hereditary osteodystrophy.
Etiology
Failure of parathyroid function due to autoimmune destruction, surgical removal or vascular disruption, radiation injury, or severe hypomagnesemia. Pseudohypoparathyroidism is caused by end-organ resistance to PTH.
Diagnosis
Signs And Symptoms The most common symptomatic presentation occurs postoperatively after parathyroid or thyroid surgery. Neonates may have transient disease with neurodevelopmental consequences proportional to hypocalcemia duration. Symptoms relate to hypocalcemia severity and acuity. Neuromuscular findings include circumoral and distal paresthesias, carpopedal spasm, tetany, positive Chvostek and Trousseau signs, laryngospasm, bronchospasm, muscle cramps, and seizures. Cardiovascular manifestations include prolonged QT interval, heart block, heart failure, ventricular arrhythmias, and vasoconstriction. Neuropsychiatric features include confusion, hallucinations, memory impairment, dementia, extrapyramidal symptoms, and raised intracranial pressure with papilledema. Dermatologic findings include brittle hair and nails, psoriasis, hyperpigmentation, and lenticular cataracts.
Essential Workup
In asymptomatic hypocalcemia, check albumin and correct total calcium. If symptomatic with normal total calcium, evaluate for alkalosis and obtain ionized calcium. Symptomatic low ionized calcium warrants PTH measurement.
Diagnosis Tests And Interpretation
Lab Corrected calcium = measured calcium + 0.8(4 − albumin). Obtain ionized calcium if symptomatic. Check electrolytes, BUN, creatinine, glucose, magnesium, phosphorus, and ABG if alkalosis suspected. Ionized calcium decreases by 3–8% for every 0.1 pH unit increase. Phosphate is typically elevated except in vitamin D deficiency.
Diagnostic Procedures ECG shows QT prolongation due to ST-segment lengthening.
Differential Diagnosis
Pseudohypocalcemia from hypoalbuminemia, alkalosis-related reduction in ionized calcium, hypomagnesemia, congenital PTH resistance, vitamin D deficiency, renal failure, sepsis, pancreatitis, rhabdomyolysis, acute hyperphosphatemia, and chelation from citrate or toxins.
Treatment
Prehospital Consider calcium administration for refractory ventricular fibrillation or status epilepticus in known or suspected hypocalcemia.
Initial Stabilization/Therapy Secure airway if laryngospasm is present. Initiate cardiac monitoring and seizure precautions. Administer IV calcium for unstable rhythms or tetany.
Emergency Department Treatment/Procedures Life-threatening hypocalcemia requires IV calcium chloride or calcium gluconate. Non–life-threatening cases should receive slow calcium infusion with frequent monitoring. Avoid rapid correction unless unstable. Replace magnesium if deficient. Maintain calcium at the lowest asymptomatic level, then transition to oral therapy. Bind phosphate when elevated and supplement vitamin D, preferably with calcitriol. Avoid high-phosphate beverages and evaluate for associated endocrinopathies.
Medication
First Line Calcium gluconate IV for most cases; calcium chloride reserved for life-threatening instability. Magnesium sulfate IV if deficient.
Second Line Oral calcium salts (carbonate or acetate), phosphate binders (sevelamer), magnesium oxide, vitamin D or calcitriol, and thiazide diuretics to reduce urinary calcium loss.
Follow-Up And Disposition
Admission Criteria Symptomatic hypocalcemia, ECG abnormalities, inability to tolerate oral therapy, or markedly low corrected calcium.
Discharge Criteria Asymptomatic patients without admission criteria.
Follow-Up Recommendations Repeat calcium, phosphorus, and magnesium levels within 1–2 days for patients requiring treatment.
Key Points And Cautions
Postoperative hypocalcemia is the most common symptomatic presentation. Symptoms are often mistaken for anxiety or hyperventilation. Exclude sepsis or rhabdomyolysis in nonoperative cases. Except in life-threatening situations, avoid rapid IV calcium administration to prevent complications.
Basics
Description Hypoparathyroidism results from deficiency of parathyroid hormone (PTH), whereas pseudohypoparathyroidism is due to end-organ resistance to PTH. PTH reduces urinary calcium loss, increases urinary phosphate loss, stimulates renal conversion of vitamin D to its active form, and mobilizes calcium and phosphate from bone. Hypocalcemia is the primary metabolic abnormality. Calcitonin promotes deposition of calcium and phosphate into bone. Magnesium is required for both PTH production and peripheral PTH action. Primary hypoparathyroidism reflects intrinsic gland failure, while pseudohypoparathyroidism features elevated PTH with tissue resistance and is often associated with hypothyroidism and hypogonadism. Genetic associations include congenital absence (DiGeorge syndrome), autoimmune polyglandular syndrome type I, Wilson disease, and Albright hereditary osteodystrophy.
Etiology
Failure of parathyroid function due to autoimmune destruction, surgical removal or vascular disruption, radiation injury, or severe hypomagnesemia. Pseudohypoparathyroidism is caused by end-organ resistance to PTH.
Diagnosis
Signs And Symptoms The most common symptomatic presentation occurs postoperatively after parathyroid or thyroid surgery. Neonates may have transient disease with neurodevelopmental consequences proportional to hypocalcemia duration. Symptoms relate to hypocalcemia severity and acuity. Neuromuscular findings include circumoral and distal paresthesias, carpopedal spasm, tetany, positive Chvostek and Trousseau signs, laryngospasm, bronchospasm, muscle cramps, and seizures. Cardiovascular manifestations include prolonged QT interval, heart block, heart failure, ventricular arrhythmias, and vasoconstriction. Neuropsychiatric features include confusion, hallucinations, memory impairment, dementia, extrapyramidal symptoms, and raised intracranial pressure with papilledema. Dermatologic findings include brittle hair and nails, psoriasis, hyperpigmentation, and lenticular cataracts.
Essential Workup
In asymptomatic hypocalcemia, check albumin and correct total calcium. If symptomatic with normal total calcium, evaluate for alkalosis and obtain ionized calcium. Symptomatic low ionized calcium warrants PTH measurement.
Diagnosis Tests And Interpretation
Lab Corrected calcium = measured calcium + 0.8(4 − albumin). Obtain ionized calcium if symptomatic. Check electrolytes, BUN, creatinine, glucose, magnesium, phosphorus, and ABG if alkalosis suspected. Ionized calcium decreases by 3–8% for every 0.1 pH unit increase. Phosphate is typically elevated except in vitamin D deficiency.
Diagnostic Procedures ECG shows QT prolongation due to ST-segment lengthening.
Differential Diagnosis
Pseudohypocalcemia from hypoalbuminemia, alkalosis-related reduction in ionized calcium, hypomagnesemia, congenital PTH resistance, vitamin D deficiency, renal failure, sepsis, pancreatitis, rhabdomyolysis, acute hyperphosphatemia, and chelation from citrate or toxins.
Treatment
Prehospital Consider calcium administration for refractory ventricular fibrillation or status epilepticus in known or suspected hypocalcemia.
Initial Stabilization/Therapy Secure airway if laryngospasm is present. Initiate cardiac monitoring and seizure precautions. Administer IV calcium for unstable rhythms or tetany.
Emergency Department Treatment/Procedures Life-threatening hypocalcemia requires IV calcium chloride or calcium gluconate. Non–life-threatening cases should receive slow calcium infusion with frequent monitoring. Avoid rapid correction unless unstable. Replace magnesium if deficient. Maintain calcium at the lowest asymptomatic level, then transition to oral therapy. Bind phosphate when elevated and supplement vitamin D, preferably with calcitriol. Avoid high-phosphate beverages and evaluate for associated endocrinopathies.
Medication
First Line Calcium gluconate IV for most cases; calcium chloride reserved for life-threatening instability. Magnesium sulfate IV if deficient.
Second Line Oral calcium salts (carbonate or acetate), phosphate binders (sevelamer), magnesium oxide, vitamin D or calcitriol, and thiazide diuretics to reduce urinary calcium loss.
Follow-Up And Disposition
Admission Criteria Symptomatic hypocalcemia, ECG abnormalities, inability to tolerate oral therapy, or markedly low corrected calcium.
Discharge Criteria Asymptomatic patients without admission criteria.
Follow-Up Recommendations Repeat calcium, phosphorus, and magnesium levels within 1–2 days for patients requiring treatment.
Key Points And Cautions
Postoperative hypocalcemia is the most common symptomatic presentation. Symptoms are often mistaken for anxiety or hyperventilation. Exclude sepsis or rhabdomyolysis in nonoperative cases. Except in life-threatening situations, avoid rapid IV calcium administration to prevent complications.
- Published on
Emergency And Acute Medicine: Hyponatremia
Basics
Description Hyponatremia is defined as serum sodium <136 meq /> and is the most common electrolyte disturbance, occurring in 1–4% of hospitalized patients.
Etiology
Pseudohyponatremia Low measured sodium with normal serum osmolality due to displacement of sodium in the aqueous phase; seen with hyperlipidemia or hyperproteinemia (e.g., multiple myeloma).
Hyponatremia With Normal Osmolarity And Fluid Overload Inappropriate water retention seen in CHF, cirrhosis, renal failure, and nephrotic syndrome.
Hyponatremia With Normal Osmolarity And Euvolemia Dilutional hyponatremia with increased total body water and minimal edema. Causes include hypothyroidism, stress, SIADH (pulmonary disease, CNS disorders, malignancy, HIV), water intoxication, postoperative states, beer potomania, MDMA use, and mineralocorticoid abnormalities.
Hyponatremia With Normal Osmolarity And Hypovolemia Total body sodium and water loss with sodium loss predominating; causes include GI losses, sweating, burns, cerebral salt wasting, cystic fibrosis, salt-wasting nephropathies, and diuretics.
Drug Induced ADH stimulation (amiodarone, carbamazepine, cyclophosphamide, opiates, vincristine), increased ADH sensitivity (chlorpropamide, NSAIDs), or increased thirst (SSRIs, antipsychotics, MDMA).
Hyponatremia With Hyperosmolarity Due to osmotically active substances, most commonly hyperglycemia. Corrected Na = measured Na + 0.016 × (glucose − 100). Also seen with mannitol, maltose, or glycine.
Pediatric Considerations Higher risk of water intoxication and iatrogenic hyponatremia.
Pregnancy Considerations Vasopressin antagonists are pregnancy class C.
Geriatric Considerations Increased symptom burden due to impaired free water excretion and low sodium intake.
Diagnosis
Signs And Symptoms Mild (Na >120): headache, nausea, vomiting, weakness, anorexia, cramps. Moderate (110–120): confusion, hallucinations, bizarre behavior, incontinence, gait disturbance. Severe (<110): seizures, coma, herniation signs, respiratory arrest. chronic hyponatremia may be asymptomatic.< />pan>
History And Exam Review medications and assess volume status. Perform full neurologic examination.
Essential Workup Confirm serum sodium level with repeat testing.
Diagnosis Tests And Interpretation
Lab Electrolytes, BUN, creatinine, glucose (correct sodium if hyperglycemic), serum and urine osmolality, urine sodium, thyroid and adrenal function, CPK if rhabdomyolysis suspected. Plasma osmolality = 2 × Na + glucose/18 + BUN/2.8.
Imaging CXR for CHF, infection, or malignancy. CT head if altered mental status.
Differential Diagnosis Pseudohyponatremia from hyperglycemia, hyperlipidemia, hyperproteinemia, or radiocontrast exposure.
Treatment
Prehospital Supportive care and IV access.
Initial Stabilization/Therapy ABCs, IV 0.9% NS, naloxone, thiamine, and D50W for altered mental status.
Emergency Department Treatment/Procedures Management depends on severity, chronicity, and cause. Chronic hyponatremia requires slow correction to prevent osmotic demyelination; limit correction to 10-12 mEq/L in 24 hr. Acute severe hyponatremia with seizures requires hypertonic saline to raise sodium 8-10 mEq/L over 4-6 hr or to >120–125 mEq/L, then slow or stop correction. Typical dose is 200–400 mL of 3% saline over 2 hr or 1–2 mL/kg/hr.
Hypovolemic Hyponatremia Restore volume with 0.9% NS.
Euvolemic Or Hypervolemic Hyponatremia Water restriction (<1 l />ay), high salt intake, or 0.9% NS with loop diuretics. Maximum correction rate 0.5 mEq/L/hr.
Medication
First Line 500 mL–1 L isotonic saline bolus.
Adjuncts Furosemide 20–40 mg IV.
Second Line Conivaptan IV or tolvaptan PO for euvolemic or hypervolemic hyponatremia only.
Follow-Up And Disposition
Admission Criteria Symptomatic hyponatremia, sodium <120 meq />, or comorbid risk factors.
Discharge Criteria Sodium >130 mEq/L and asymptomatic, or stable chronic mild hyponatremia with close follow-up.
Follow-Up Recommendations Repeat sodium within one week, especially if diuretic-related.
Pearls And Pitfalls Avoid rapid correction to prevent osmotic demyelination syndrome, especially in women, alcoholics, malnourished patients, those with hypokalemia, or liver transplant history. Perform serial neurologic exams. Beware of falsely low sodium from blood draws near hypotonic IV lines. Thiazide-induced hyponatremia may persist up to two weeks after discontinuation.
Basics
Description Hyponatremia is defined as serum sodium <136 meq /> and is the most common electrolyte disturbance, occurring in 1–4% of hospitalized patients.
Etiology
Pseudohyponatremia Low measured sodium with normal serum osmolality due to displacement of sodium in the aqueous phase; seen with hyperlipidemia or hyperproteinemia (e.g., multiple myeloma).
Hyponatremia With Normal Osmolarity And Fluid Overload Inappropriate water retention seen in CHF, cirrhosis, renal failure, and nephrotic syndrome.
Hyponatremia With Normal Osmolarity And Euvolemia Dilutional hyponatremia with increased total body water and minimal edema. Causes include hypothyroidism, stress, SIADH (pulmonary disease, CNS disorders, malignancy, HIV), water intoxication, postoperative states, beer potomania, MDMA use, and mineralocorticoid abnormalities.
Hyponatremia With Normal Osmolarity And Hypovolemia Total body sodium and water loss with sodium loss predominating; causes include GI losses, sweating, burns, cerebral salt wasting, cystic fibrosis, salt-wasting nephropathies, and diuretics.
Drug Induced ADH stimulation (amiodarone, carbamazepine, cyclophosphamide, opiates, vincristine), increased ADH sensitivity (chlorpropamide, NSAIDs), or increased thirst (SSRIs, antipsychotics, MDMA).
Hyponatremia With Hyperosmolarity Due to osmotically active substances, most commonly hyperglycemia. Corrected Na = measured Na + 0.016 × (glucose − 100). Also seen with mannitol, maltose, or glycine.
Pediatric Considerations Higher risk of water intoxication and iatrogenic hyponatremia.
Pregnancy Considerations Vasopressin antagonists are pregnancy class C.
Geriatric Considerations Increased symptom burden due to impaired free water excretion and low sodium intake.
Diagnosis
Signs And Symptoms Mild (Na >120): headache, nausea, vomiting, weakness, anorexia, cramps. Moderate (110–120): confusion, hallucinations, bizarre behavior, incontinence, gait disturbance. Severe (<110): seizures, coma, herniation signs, respiratory arrest. chronic hyponatremia may be asymptomatic.< />pan>
History And Exam Review medications and assess volume status. Perform full neurologic examination.
Essential Workup Confirm serum sodium level with repeat testing.
Diagnosis Tests And Interpretation
Lab Electrolytes, BUN, creatinine, glucose (correct sodium if hyperglycemic), serum and urine osmolality, urine sodium, thyroid and adrenal function, CPK if rhabdomyolysis suspected. Plasma osmolality = 2 × Na + glucose/18 + BUN/2.8.
Imaging CXR for CHF, infection, or malignancy. CT head if altered mental status.
Differential Diagnosis Pseudohyponatremia from hyperglycemia, hyperlipidemia, hyperproteinemia, or radiocontrast exposure.
Treatment
Prehospital Supportive care and IV access.
Initial Stabilization/Therapy ABCs, IV 0.9% NS, naloxone, thiamine, and D50W for altered mental status.
Emergency Department Treatment/Procedures Management depends on severity, chronicity, and cause. Chronic hyponatremia requires slow correction to prevent osmotic demyelination; limit correction to 10-12 mEq/L in 24 hr. Acute severe hyponatremia with seizures requires hypertonic saline to raise sodium 8-10 mEq/L over 4-6 hr or to >120–125 mEq/L, then slow or stop correction. Typical dose is 200–400 mL of 3% saline over 2 hr or 1–2 mL/kg/hr.
Hypovolemic Hyponatremia Restore volume with 0.9% NS.
Euvolemic Or Hypervolemic Hyponatremia Water restriction (<1 l />ay), high salt intake, or 0.9% NS with loop diuretics. Maximum correction rate 0.5 mEq/L/hr.
Medication
First Line 500 mL–1 L isotonic saline bolus.
Adjuncts Furosemide 20–40 mg IV.
Second Line Conivaptan IV or tolvaptan PO for euvolemic or hypervolemic hyponatremia only.
Follow-Up And Disposition
Admission Criteria Symptomatic hyponatremia, sodium <120 meq />, or comorbid risk factors.
Discharge Criteria Sodium >130 mEq/L and asymptomatic, or stable chronic mild hyponatremia with close follow-up.
Follow-Up Recommendations Repeat sodium within one week, especially if diuretic-related.
Pearls And Pitfalls Avoid rapid correction to prevent osmotic demyelination syndrome, especially in women, alcoholics, malnourished patients, those with hypokalemia, or liver transplant history. Perform serial neurologic exams. Beware of falsely low sodium from blood draws near hypotonic IV lines. Thiazide-induced hyponatremia may persist up to two weeks after discontinuation.
