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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.
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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.
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Emergency And Acute Medicine – Hypothyroidism
Basics
Description Decreased effective circulating thyroid hormone causes reduced metabolic rate and diminished catecholamine sensitivity. More common in women and the elderly. Myxedema coma is a rare, life-threatening decompensation marked by altered mental status and impaired thermoregulation precipitated by stress in a hypothyroid patient.
Etiology
Primary causes include idiopathic, congenital, autoimmune thyroiditis (Hashimoto disease), iodine deficiency (most common worldwide), neoplasm, infection, and iatrogenic causes (thyroid surgery, radioiodine, external radiation). Drug induced causes include iodides, lithium, amiodarone, sunitinib, bexarotene, interferons, narcotics, and sedatives. Central hypothyroidism is rare and due to pituitary or hypothalamic dysfunction, often with other hormone deficiencies.
Myxedema coma is triggered by infection, hypothermia, intoxication, drugs, stroke, heart failure, trauma, or pregnancy.
Diagnosis
Signs And Symptoms
History: Fatigue, cold intolerance, weight gain, constipation, depression, cognitive slowing, headaches, myalgias, muscle weakness, menorrhagia, infertility, carpal tunnel syndrome.
Physical exam: Periorbital edema, coarse sparse hair, brittle nails, loss of lateral third of eyebrows, hoarse voice, goiter, dry pale cool skin, nonpitting edema, prolonged relaxation of deep tendon reflexes.
Myxedema coma: Altered mental status, hypothermia, hypotension, bradycardia, respiratory failure.
Pediatric And Geriatric Considerations
Congenital hypothyroidism largely prevented by newborn screening. Childhood disease usually due to Hashimoto thyroiditis and may impair growth and development. Elderly patients may present atypically, mimicking normal aging.
Essential Workup
Laboratory confirmation may not be immediately available; treatment should be initiated based on clinical suspicion in severe cases.
Diagnosis Tests And Interpretation
Labs: Low total and free T4 and T3. TSH elevated in primary hypothyroidism, normal or low in central causes. Associated findings include anemia, hyponatremia, hypoglycemia, hypoxemia, hypercapnia, respiratory acidosis, elevated CK, LDH, cholesterol, and creatinine.
Imaging: Chest radiograph may show cardiomegaly from pericardial effusion.
ECG: Sinus bradycardia, low voltage, PR prolongation, bundle branch blocks, QT prolongation, nonspecific ST–T changes; Osborn waves if profoundly hypothermic.
Differential Diagnosis
Chronic kidney disease, heart failure, depression, hypoalbuminemia, pernicious anemia, nephrotic syndrome, sepsis.
Alert Euthyroid sick syndrome may cause abnormal thyroid tests during acute illness.
Treatment
Initial Stabilization/Therapy ABCs with airway protection and ventilation as needed. Cardiac monitoring, oxygen supplementation, cautious passive rewarming. Avoid aggressive rewarming.
Emergency Department Treatment/Procedures
Mild hypothyroidism: Outpatient oral thyroid hormone replacement.
Myxedema coma: Medical emergency. Initiate IV thyroid hormone replacement immediately on suspicion. Use lower doses and avoid aggressive T3 in elderly or cardiac patients. Administer hydrocortisone to prevent adrenal crisis. Treat hypoglycemia with dextrose, hypotension with IV fluids (pressors often ineffective until thyroid hormone given), severe hyponatremia with hypertonic saline if indicated. Identify and treat precipitating cause.
Medication
First line thyroid hormone therapy:
• T4 IV load ~2 μg/kg (ideal body weight) then 10–40 μg IV or PO daily
• Optional T3 IV 10 μg load then 10 μg IV q8–12h (avoid in elderly/cardiac patients)
Second line/supportive: Hydrocortisone 100 mg IV q6–8h, dextrose IV for hypoglycemia.
Follow-Up And Disposition
Admission Criteria All patients with myxedema coma require ICU admission.
Discharge Criteria Uncomplicated hypothyroidism suitable for outpatient management.
Follow-Up Recommendations Primary care or endocrinology follow-up for long-term thyroid hormone management. Pregnant, elderly, and cardiac patients require cautious dose titration.
Key Points And Cautions
Symptoms are nonspecific and easily overlooked. Myxedema coma has high mortality and requires prompt treatment. Do not delay therapy awaiting lab confirmation. Avoid aggressive T3 use in elderly or patients with ischemic heart disease.
Basics
Description Decreased effective circulating thyroid hormone causes reduced metabolic rate and diminished catecholamine sensitivity. More common in women and the elderly. Myxedema coma is a rare, life-threatening decompensation marked by altered mental status and impaired thermoregulation precipitated by stress in a hypothyroid patient.
Etiology
Primary causes include idiopathic, congenital, autoimmune thyroiditis (Hashimoto disease), iodine deficiency (most common worldwide), neoplasm, infection, and iatrogenic causes (thyroid surgery, radioiodine, external radiation). Drug induced causes include iodides, lithium, amiodarone, sunitinib, bexarotene, interferons, narcotics, and sedatives. Central hypothyroidism is rare and due to pituitary or hypothalamic dysfunction, often with other hormone deficiencies.
Myxedema coma is triggered by infection, hypothermia, intoxication, drugs, stroke, heart failure, trauma, or pregnancy.
Diagnosis
Signs And Symptoms
History: Fatigue, cold intolerance, weight gain, constipation, depression, cognitive slowing, headaches, myalgias, muscle weakness, menorrhagia, infertility, carpal tunnel syndrome.
Physical exam: Periorbital edema, coarse sparse hair, brittle nails, loss of lateral third of eyebrows, hoarse voice, goiter, dry pale cool skin, nonpitting edema, prolonged relaxation of deep tendon reflexes.
Myxedema coma: Altered mental status, hypothermia, hypotension, bradycardia, respiratory failure.
Pediatric And Geriatric Considerations
Congenital hypothyroidism largely prevented by newborn screening. Childhood disease usually due to Hashimoto thyroiditis and may impair growth and development. Elderly patients may present atypically, mimicking normal aging.
Essential Workup
Laboratory confirmation may not be immediately available; treatment should be initiated based on clinical suspicion in severe cases.
Diagnosis Tests And Interpretation
Labs: Low total and free T4 and T3. TSH elevated in primary hypothyroidism, normal or low in central causes. Associated findings include anemia, hyponatremia, hypoglycemia, hypoxemia, hypercapnia, respiratory acidosis, elevated CK, LDH, cholesterol, and creatinine.
Imaging: Chest radiograph may show cardiomegaly from pericardial effusion.
ECG: Sinus bradycardia, low voltage, PR prolongation, bundle branch blocks, QT prolongation, nonspecific ST–T changes; Osborn waves if profoundly hypothermic.
Differential Diagnosis
Chronic kidney disease, heart failure, depression, hypoalbuminemia, pernicious anemia, nephrotic syndrome, sepsis.
Alert Euthyroid sick syndrome may cause abnormal thyroid tests during acute illness.
Treatment
Initial Stabilization/Therapy ABCs with airway protection and ventilation as needed. Cardiac monitoring, oxygen supplementation, cautious passive rewarming. Avoid aggressive rewarming.
Emergency Department Treatment/Procedures
Mild hypothyroidism: Outpatient oral thyroid hormone replacement.
Myxedema coma: Medical emergency. Initiate IV thyroid hormone replacement immediately on suspicion. Use lower doses and avoid aggressive T3 in elderly or cardiac patients. Administer hydrocortisone to prevent adrenal crisis. Treat hypoglycemia with dextrose, hypotension with IV fluids (pressors often ineffective until thyroid hormone given), severe hyponatremia with hypertonic saline if indicated. Identify and treat precipitating cause.
Medication
First line thyroid hormone therapy:
• T4 IV load ~2 μg/kg (ideal body weight) then 10–40 μg IV or PO daily
• Optional T3 IV 10 μg load then 10 μg IV q8–12h (avoid in elderly/cardiac patients)
Second line/supportive: Hydrocortisone 100 mg IV q6–8h, dextrose IV for hypoglycemia.
Follow-Up And Disposition
Admission Criteria All patients with myxedema coma require ICU admission.
Discharge Criteria Uncomplicated hypothyroidism suitable for outpatient management.
Follow-Up Recommendations Primary care or endocrinology follow-up for long-term thyroid hormone management. Pregnant, elderly, and cardiac patients require cautious dose titration.
Key Points And Cautions
Symptoms are nonspecific and easily overlooked. Myxedema coma has high mortality and requires prompt treatment. Do not delay therapy awaiting lab confirmation. Avoid aggressive T3 use in elderly or patients with ischemic heart disease.
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Emergency And Acute Medicine – Hypothermia
Basics
Description Core body temperature <35°c. risk factors include impaired thermoregulation (infants, elderly), comorbid illness, intoxication, and environmental exposure. heat loss occurs via radiation (most significant), conduction, convection, evaporation, respiration. production relies on shivering, nonshivering thermogenesis, increased thyroxine epinephrine.< />pan>
Etiology
Dermal disease (burns, exfoliative dermatitis, severe psoriasis). Drug induced (ethanol, phenothiazines, sedative–hypnotics). Environmental exposure (immersion, nonimmersion). Iatrogenic causes (aggressive fluid resuscitation, heat stroke treatment). Metabolic disorders (hypothyroidism, hypopituitarism, hypoadrenalism). Neurologic conditions (spinal cord injury, head trauma, stroke, tumor, Wernicke disease). Neuromuscular inefficiency (extremes of age, impaired shivering, lack of acclimatization). Sepsis. Pediatric patients are at higher risk because of increased surface area to mass ratio; consider nonaccidental trauma.
Diagnosis
Signs And Symptoms
Mild (35–32.2°C): Hypertension, shivering, tachycardia progressing to bradycardia, tachypnea, vasoconstriction, apathy, ataxia, cold diuresis, impaired judgment.
Moderate (32.2–28°C): Atrial dysrhythmias, bradycardia refractory to atropine, decreased level of consciousness, hypoventilation with CO₂ retention, dilated pupils, diminished gag reflex, cessation of shivering, hyporeflexia, hypotension, J (Osborn) waves.
Severe (<28°c): apnea, coma, minimal eeg activity, nonreactive pupils, oliguria, pulmonary edema, ventricular dysrhythmias or asystole.< />pan>
History Duration and circumstances of cold exposure or submersion.
Physical Exam Pulse and blood pressure may be difficult to detect; pupils often dilated at very low temperatures.
Essential Workup Accurate core temperature measurement.
Diagnosis Tests And Interpretation
Lab Fingerstick glucose, ABG (no temperature correction), CBC (hemoconcentration), electrolytes, BUN/creatinine, potassium, CPK, lactate, coagulation studies, toxicology screen.
Imaging CXR for pneumonia.
ECG Bradyarrhythmias, atrial fibrillation, ventricular fibrillation, prolonged PR/QRS/QT, Osborn waves.
Differential Diagnosis Environmental exposure, sepsis, CNS pathology, metabolic disorders, drug toxicity.
Treatment
Prehospital Patient is not dead until “warm and dead.” Prolonged pulse checks (30–45 s). CPR during transport if indicated.
Initial Stabilization/Therapy ABCs, supplemental oxygen, safe intubation if needed, cardiac monitoring, warmed IV fluids (D5NS preferred), remove wet clothing, passive rewarming, naloxone, dextrose, and thiamine for altered mental status, stress-dose steroids if adrenal insufficiency suspected.
Emergency Department Treatment/Procedures Handle gently to avoid precipitating ventricular fibrillation. Most dysrhythmias resolve with rewarming alone. Defibrillate up to 1–3 times below 28–30°C, then defer until rewarmed. Active rewarming is required for core temperature <32°c. use passive external rewarming for mild cases, active (forced warm air, trunk first) moderate and core (humidified oxygen, warmed iv fluids, peritoneal or pleural lavage, extracorporeal including hemodialysis cardiopulmonary bypass) severe hypothermia cardiac arrest. faster rates (1–2°c />r) are associated with better outcomes.
Medication Amiodarone for persistent ventricular dysrhythmias after rewarming, dextrose for hypoglycemia, hydrocortisone or methylprednisolone if adrenal insufficiency suspected, levothyroxine only for myxedema coma, naloxone, thiamine.
Follow-Up And Disposition
Admission Criteria Moderate to severe hypothermia (<32°c).< />pan>
Discharge Criteria Young, healthy patients with very mild hypothermia who normalize and have a safe, warm environment.
Follow-Up Recommendations Social services involvement for patients at risk of recurrent cold exposure.
Key Points And Cautions Defibrillation is rarely effective below 28–30°C. Atrial fibrillation often resolves with rewarming alone. Beware afterdrop and rewarming shock. Gentle handling and adequate volume resuscitation are essential.
Basics
Description Core body temperature <35°c. risk factors include impaired thermoregulation (infants, elderly), comorbid illness, intoxication, and environmental exposure. heat loss occurs via radiation (most significant), conduction, convection, evaporation, respiration. production relies on shivering, nonshivering thermogenesis, increased thyroxine epinephrine.< />pan>
Etiology
Dermal disease (burns, exfoliative dermatitis, severe psoriasis). Drug induced (ethanol, phenothiazines, sedative–hypnotics). Environmental exposure (immersion, nonimmersion). Iatrogenic causes (aggressive fluid resuscitation, heat stroke treatment). Metabolic disorders (hypothyroidism, hypopituitarism, hypoadrenalism). Neurologic conditions (spinal cord injury, head trauma, stroke, tumor, Wernicke disease). Neuromuscular inefficiency (extremes of age, impaired shivering, lack of acclimatization). Sepsis. Pediatric patients are at higher risk because of increased surface area to mass ratio; consider nonaccidental trauma.
Diagnosis
Signs And Symptoms
Mild (35–32.2°C): Hypertension, shivering, tachycardia progressing to bradycardia, tachypnea, vasoconstriction, apathy, ataxia, cold diuresis, impaired judgment.
Moderate (32.2–28°C): Atrial dysrhythmias, bradycardia refractory to atropine, decreased level of consciousness, hypoventilation with CO₂ retention, dilated pupils, diminished gag reflex, cessation of shivering, hyporeflexia, hypotension, J (Osborn) waves.
Severe (<28°c): apnea, coma, minimal eeg activity, nonreactive pupils, oliguria, pulmonary edema, ventricular dysrhythmias or asystole.< />pan>
History Duration and circumstances of cold exposure or submersion.
Physical Exam Pulse and blood pressure may be difficult to detect; pupils often dilated at very low temperatures.
Essential Workup Accurate core temperature measurement.
Diagnosis Tests And Interpretation
Lab Fingerstick glucose, ABG (no temperature correction), CBC (hemoconcentration), electrolytes, BUN/creatinine, potassium, CPK, lactate, coagulation studies, toxicology screen.
Imaging CXR for pneumonia.
ECG Bradyarrhythmias, atrial fibrillation, ventricular fibrillation, prolonged PR/QRS/QT, Osborn waves.
Differential Diagnosis Environmental exposure, sepsis, CNS pathology, metabolic disorders, drug toxicity.
Treatment
Prehospital Patient is not dead until “warm and dead.” Prolonged pulse checks (30–45 s). CPR during transport if indicated.
Initial Stabilization/Therapy ABCs, supplemental oxygen, safe intubation if needed, cardiac monitoring, warmed IV fluids (D5NS preferred), remove wet clothing, passive rewarming, naloxone, dextrose, and thiamine for altered mental status, stress-dose steroids if adrenal insufficiency suspected.
Emergency Department Treatment/Procedures Handle gently to avoid precipitating ventricular fibrillation. Most dysrhythmias resolve with rewarming alone. Defibrillate up to 1–3 times below 28–30°C, then defer until rewarmed. Active rewarming is required for core temperature <32°c. use passive external rewarming for mild cases, active (forced warm air, trunk first) moderate and core (humidified oxygen, warmed iv fluids, peritoneal or pleural lavage, extracorporeal including hemodialysis cardiopulmonary bypass) severe hypothermia cardiac arrest. faster rates (1–2°c />r) are associated with better outcomes.
Medication Amiodarone for persistent ventricular dysrhythmias after rewarming, dextrose for hypoglycemia, hydrocortisone or methylprednisolone if adrenal insufficiency suspected, levothyroxine only for myxedema coma, naloxone, thiamine.
Follow-Up And Disposition
Admission Criteria Moderate to severe hypothermia (<32°c).< />pan>
Discharge Criteria Young, healthy patients with very mild hypothermia who normalize and have a safe, warm environment.
Follow-Up Recommendations Social services involvement for patients at risk of recurrent cold exposure.
Key Points And Cautions Defibrillation is rarely effective below 28–30°C. Atrial fibrillation often resolves with rewarming alone. Beware afterdrop and rewarming shock. Gentle handling and adequate volume resuscitation are essential.
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Emergency And Acute Medicine: 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.
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Emergency And Acute Medicine: Hyphema
Basics
Description Blood in the anterior chamber of the eye between the iris and cornea. Hyphema refers to grossly visible layered blood. Microhyphema refers to suspended red blood cells seen only on slit-lamp exam. Genetic predisposition is related to hereditary blood dyscrasias.
Etiology Blunt trauma is the most common cause (70–80%) due to anteroposterior compression with equatorial globe expansion causing rupture of iris or ciliary body vessels. Penetrating trauma causes direct vessel injury or sudden ocular decompression. Spontaneous causes include ocular tumors (melanoma, retinoblastoma, xanthogranuloma, metastatic tumors), blood dyscrasias (hemophilia, leukemia, thrombocytopenia, von Willebrand disease), anticoagulant or antiplatelet use (aspirin, warfarin, heparin), iris neovascularization (proliferative diabetic retinopathy, retinal vein occlusion, carotid stenosis), and postsurgical causes such as cataract extraction, trabeculectomy, or vitrectomy. In children without trauma, suspect nonaccidental injury.
Diagnosis
Signs And Symptoms Photophobia, blurred vision, decreased visual acuity, ocular pain, nausea, and vomiting.
History Assess prior visual acuity, prior ocular surgery or glaucoma treatment, bleeding disorders including sickle cell disease, mechanism and timing of injury, onset of visual loss, and history of excessive tearing (suggestive of open globe injury).
Physical Exam Perform full trauma exam. Look for periorbital ecchymosis, eyelid lacerations, enophthalmos, limited ocular movement with diplopia, or proptosis. Ocular exam includes visual acuity, exclusion of open globe injury before tonometry, pupillary response, slit-lamp exam, and dilated fundus exam without pressure on the globe. Hyphema grading: Grade I <1/3 AC, Grade II 1/3–1/2 AC, Grade III >1/2 AC, Grade IV total (“8-ball” hyphema). Higher grades have increased risk of rebleeding, glaucoma, corneal staining, and poor visual recovery.
Diagnosis Tests And Interpretation
Lab Obtain platelet count, PT/PTT if bleeding disorder or anticoagulant use is suspected. Screen for sickle cell disease when indicated.
Imaging CT orbits for suspected open globe, intraocular foreign body, or orbital fracture. B-scan ultrasound only if globe integrity is confirmed and posterior structures cannot be visualized.
Essential Workup Visual acuity, globe integrity, intraocular pressure, assessment for associated injuries, targeted labs, and imaging when indicated.
Differential Diagnosis Uveitis, endophthalmitis.
Treatment
Prehospital Place eye shield if open globe is suspected.
Initial Stabilization/Therapy Keep head elevated, limit activity, avoid straining, place rigid eye shield, and avoid eye patching.
Emergency Department Treatment/Procedures Provide mild analgesia (avoid NSAIDs) and antiemetics. Use cycloplegics (atropine 1% or cyclopentolate 1%) and topical steroids (prednisolone acetate 1%). Aminocaproic acid may be used in consultation with ophthalmology. Oral prednisone may be indicated in selected high-risk cases. Manage elevated intraocular pressure with topical beta-blockers first, then alpha-agonists, carbonic anhydrase inhibitors, and systemic agents if needed. Avoid carbonic anhydrase inhibitors and mannitol in sickle cell disease. Surgical evacuation is indicated for uncontrolled intraocular pressure.
Medications
First Line Atropine 1% TID, prednisolone acetate 1% QID.
Second Line Timolol or levobunolol, brimonidine or apraclonidine, dorzolamide or brinzolamide, acetazolamide.
Follow-Up And Disposition
Admission Criteria Uncontrolled intraocular pressure, open globe injury, noncompliance, associated injuries, children <7 years, or high-risk conditions such as sickle cell disease or hemophilia.
Discharge Criteria Controlled intraocular pressure and absence of admission criteria.
Follow-Up Recommendations Daily ophthalmology follow-up for the first 3 days to monitor for rebleeding, corneal staining, and pressure elevation.
Pearls And Pitfalls Always exclude ruptured globe before tonometry or treatment. Intraocular pressure reduction is not immediate. Screen for sickle cell disease in at-risk populations.
Basics
Description Blood in the anterior chamber of the eye between the iris and cornea. Hyphema refers to grossly visible layered blood. Microhyphema refers to suspended red blood cells seen only on slit-lamp exam. Genetic predisposition is related to hereditary blood dyscrasias.
Etiology Blunt trauma is the most common cause (70–80%) due to anteroposterior compression with equatorial globe expansion causing rupture of iris or ciliary body vessels. Penetrating trauma causes direct vessel injury or sudden ocular decompression. Spontaneous causes include ocular tumors (melanoma, retinoblastoma, xanthogranuloma, metastatic tumors), blood dyscrasias (hemophilia, leukemia, thrombocytopenia, von Willebrand disease), anticoagulant or antiplatelet use (aspirin, warfarin, heparin), iris neovascularization (proliferative diabetic retinopathy, retinal vein occlusion, carotid stenosis), and postsurgical causes such as cataract extraction, trabeculectomy, or vitrectomy. In children without trauma, suspect nonaccidental injury.
Diagnosis
Signs And Symptoms Photophobia, blurred vision, decreased visual acuity, ocular pain, nausea, and vomiting.
History Assess prior visual acuity, prior ocular surgery or glaucoma treatment, bleeding disorders including sickle cell disease, mechanism and timing of injury, onset of visual loss, and history of excessive tearing (suggestive of open globe injury).
Physical Exam Perform full trauma exam. Look for periorbital ecchymosis, eyelid lacerations, enophthalmos, limited ocular movement with diplopia, or proptosis. Ocular exam includes visual acuity, exclusion of open globe injury before tonometry, pupillary response, slit-lamp exam, and dilated fundus exam without pressure on the globe. Hyphema grading: Grade I <1/3 AC, Grade II 1/3–1/2 AC, Grade III >1/2 AC, Grade IV total (“8-ball” hyphema). Higher grades have increased risk of rebleeding, glaucoma, corneal staining, and poor visual recovery.
Diagnosis Tests And Interpretation
Lab Obtain platelet count, PT/PTT if bleeding disorder or anticoagulant use is suspected. Screen for sickle cell disease when indicated.
Imaging CT orbits for suspected open globe, intraocular foreign body, or orbital fracture. B-scan ultrasound only if globe integrity is confirmed and posterior structures cannot be visualized.
Essential Workup Visual acuity, globe integrity, intraocular pressure, assessment for associated injuries, targeted labs, and imaging when indicated.
Differential Diagnosis Uveitis, endophthalmitis.
Treatment
Prehospital Place eye shield if open globe is suspected.
Initial Stabilization/Therapy Keep head elevated, limit activity, avoid straining, place rigid eye shield, and avoid eye patching.
Emergency Department Treatment/Procedures Provide mild analgesia (avoid NSAIDs) and antiemetics. Use cycloplegics (atropine 1% or cyclopentolate 1%) and topical steroids (prednisolone acetate 1%). Aminocaproic acid may be used in consultation with ophthalmology. Oral prednisone may be indicated in selected high-risk cases. Manage elevated intraocular pressure with topical beta-blockers first, then alpha-agonists, carbonic anhydrase inhibitors, and systemic agents if needed. Avoid carbonic anhydrase inhibitors and mannitol in sickle cell disease. Surgical evacuation is indicated for uncontrolled intraocular pressure.
Medications
First Line Atropine 1% TID, prednisolone acetate 1% QID.
Second Line Timolol or levobunolol, brimonidine or apraclonidine, dorzolamide or brinzolamide, acetazolamide.
Follow-Up And Disposition
Admission Criteria Uncontrolled intraocular pressure, open globe injury, noncompliance, associated injuries, children <7 years, or high-risk conditions such as sickle cell disease or hemophilia.
Discharge Criteria Controlled intraocular pressure and absence of admission criteria.
Follow-Up Recommendations Daily ophthalmology follow-up for the first 3 days to monitor for rebleeding, corneal staining, and pressure elevation.
Pearls And Pitfalls Always exclude ruptured globe before tonometry or treatment. Intraocular pressure reduction is not immediate. Screen for sickle cell disease in at-risk populations.
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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.
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KembaraXtra-Emergency And Acute Medicine: Hypoglycemia
Basics
Description
Hypoglycemia results from deficiency of counterregulatory hormones (glucagon, epinephrine, cortisol, growth hormone) or excessive insulin response. Defined as serum glucose <70 mg />L.
Risk Factors
Strict glycemic control with insulin, prior hypoglycemia, hypoglycemia unawareness, impaired counterregulation (<5 years or elderly), renal disease, malnutrition, coronary artery liver congenital metabolic endocrine disorders, hyperinsulinism, and neonatal diabetes mellitus.< />pan>
Etiology
Increased insulin levels due to insulin or oral hypoglycemic overdose, sepsis, insulinoma, autoimmune hypoglycemia, alimentary hyperinsulinism, renal failure, or liver cirrhosis. Decreased glucose production from alcohol use, drugs (salicylates, β-blockers including eye drops, SSRIs, some antibiotics), adrenal insufficiency, malnutrition, dehydration, cerebral edema, extremes of age, heart failure, endocrine disorders, and pregnancy-related substrate deficiency.
Pediatric considerations
Most common cause in first 3 months of life is persistent hyperinsulinemic hypoglycemia of infancy, especially in infants of diabetic mothers.
Diagnosis
Signs And Symptoms Adrenergic symptoms include diaphoresis, anxiety, tachycardia, hunger, paresthesias, chest pain, and ischemic ECG changes. Neuroglycopenic symptoms include dizziness, confusion, behavioral changes, slurred speech, focal deficits, seizures, hemiplegia, coma, and CVA mimic. Neonates may present with poor feeding, irritability, tremors, seizures, or bradycardia.
Alert
Patients with hypoglycemia unawareness may present only with late findings such as seizures or coma.
History
Assess diabetes status, renal or liver disease, alcohol use, medication exposure, and possible overdose.
Physical Exam Findings reflect adrenergic or neuroglycopenic manifestations.
Essential Workup Diagnosis requires neuroglycopenic symptoms, documented low glucose, and symptom resolution after glucose administration.
Diagnosis Tests And Interpretation
Lab Blood glucose (pre- and post-treatment), electrolytes, BUN/creatinine, PT, urinalysis, cultures if infection suspected, C-peptide if exogenous insulin overdose suspected.
Imaging CXR for aspiration or pneumonia if indicated.
ECG Evaluate for ischemia or dysrhythmias.
Differential Diagnosis
Stroke/TIA, seizure, intoxication, hypoxia, sepsis, metabolic or endocrine disorders, psychiatric disease.
Pediatric Growth hormone deficiency, inborn errors of metabolism, ketotic hypoglycemia, Reye syndrome, salicylate ingestion.
Treatment
Prehospital Check finger-stick glucose. Give IV dextrose if possible, oral glucose if awake, or glucagon if IV access unavailable.
Initial Stabilization/Therapy ABCs with seizure and aspiration precautions.
Emergency Department Treatment/Procedures Give D50W 50 mL IV for altered mental status; repeat as needed. Start continuous dextrose infusion (D5–D20) if persistent hypoglycemia or unable to eat. Use octreotide for sulfonylurea-induced or refractory hypoglycemia. Use glucagon if IV access delayed (ineffective in alcohol-related hypoglycemia or severe liver disease). Give hydrocortisone if adrenal insufficiency suspected.
Geriatric considerations Recovery may be prolonged despite correction.
Medications
First Line D50W 25 g IVP (Zimmerman rule: adults 1 mL/kg D50W; children 2 mL/kg D25W; infants 5 mL/kg D10W).
Second Line Octreotide 50 μg IV bolus then infusion or SC dosing; glucagon 0.5–2 mg IV/IM/SC; hydrocortisone 100 mg IV. Oral glucose 20 g if awake and safe.
Follow-Up And Disposition
Admission Criteria Long-acting insulin or sulfonylurea overdose, recurrent hypoglycemia, inability to tolerate oral intake, suicidal intent, persistent neurologic symptoms, or elderly patients with severe episodes.
Discharge Criteria Mild, resolved hypoglycemia with normal glucose, symptom resolution, oral tolerance, and observation for ≥3 hr.
Issues For Referral Primary care follow-up for medication or dietary adjustment.
Follow-Up Recommendations Re-evaluation within 48 hr.
Pearls And Pitfalls
IV dextrose is preferred over oral glucose. Multiple D50 boluses are often required. Do not rely solely on D10/D20. Consider hypoglycemia in all neurologic or psychiatric presentations. Recurrent episodes may require prolonged recovery.
Basics
Description
Hypoglycemia results from deficiency of counterregulatory hormones (glucagon, epinephrine, cortisol, growth hormone) or excessive insulin response. Defined as serum glucose <70 mg />L.
Risk Factors
Strict glycemic control with insulin, prior hypoglycemia, hypoglycemia unawareness, impaired counterregulation (<5 years or elderly), renal disease, malnutrition, coronary artery liver congenital metabolic endocrine disorders, hyperinsulinism, and neonatal diabetes mellitus.< />pan>
Etiology
Increased insulin levels due to insulin or oral hypoglycemic overdose, sepsis, insulinoma, autoimmune hypoglycemia, alimentary hyperinsulinism, renal failure, or liver cirrhosis. Decreased glucose production from alcohol use, drugs (salicylates, β-blockers including eye drops, SSRIs, some antibiotics), adrenal insufficiency, malnutrition, dehydration, cerebral edema, extremes of age, heart failure, endocrine disorders, and pregnancy-related substrate deficiency.
Pediatric considerations
Most common cause in first 3 months of life is persistent hyperinsulinemic hypoglycemia of infancy, especially in infants of diabetic mothers.
Diagnosis
Signs And Symptoms Adrenergic symptoms include diaphoresis, anxiety, tachycardia, hunger, paresthesias, chest pain, and ischemic ECG changes. Neuroglycopenic symptoms include dizziness, confusion, behavioral changes, slurred speech, focal deficits, seizures, hemiplegia, coma, and CVA mimic. Neonates may present with poor feeding, irritability, tremors, seizures, or bradycardia.
Alert
Patients with hypoglycemia unawareness may present only with late findings such as seizures or coma.
History
Assess diabetes status, renal or liver disease, alcohol use, medication exposure, and possible overdose.
Physical Exam Findings reflect adrenergic or neuroglycopenic manifestations.
Essential Workup Diagnosis requires neuroglycopenic symptoms, documented low glucose, and symptom resolution after glucose administration.
Diagnosis Tests And Interpretation
Lab Blood glucose (pre- and post-treatment), electrolytes, BUN/creatinine, PT, urinalysis, cultures if infection suspected, C-peptide if exogenous insulin overdose suspected.
Imaging CXR for aspiration or pneumonia if indicated.
ECG Evaluate for ischemia or dysrhythmias.
Differential Diagnosis
Stroke/TIA, seizure, intoxication, hypoxia, sepsis, metabolic or endocrine disorders, psychiatric disease.
Pediatric Growth hormone deficiency, inborn errors of metabolism, ketotic hypoglycemia, Reye syndrome, salicylate ingestion.
Treatment
Prehospital Check finger-stick glucose. Give IV dextrose if possible, oral glucose if awake, or glucagon if IV access unavailable.
Initial Stabilization/Therapy ABCs with seizure and aspiration precautions.
Emergency Department Treatment/Procedures Give D50W 50 mL IV for altered mental status; repeat as needed. Start continuous dextrose infusion (D5–D20) if persistent hypoglycemia or unable to eat. Use octreotide for sulfonylurea-induced or refractory hypoglycemia. Use glucagon if IV access delayed (ineffective in alcohol-related hypoglycemia or severe liver disease). Give hydrocortisone if adrenal insufficiency suspected.
Geriatric considerations Recovery may be prolonged despite correction.
Medications
First Line D50W 25 g IVP (Zimmerman rule: adults 1 mL/kg D50W; children 2 mL/kg D25W; infants 5 mL/kg D10W).
Second Line Octreotide 50 μg IV bolus then infusion or SC dosing; glucagon 0.5–2 mg IV/IM/SC; hydrocortisone 100 mg IV. Oral glucose 20 g if awake and safe.
Follow-Up And Disposition
Admission Criteria Long-acting insulin or sulfonylurea overdose, recurrent hypoglycemia, inability to tolerate oral intake, suicidal intent, persistent neurologic symptoms, or elderly patients with severe episodes.
Discharge Criteria Mild, resolved hypoglycemia with normal glucose, symptom resolution, oral tolerance, and observation for ≥3 hr.
Issues For Referral Primary care follow-up for medication or dietary adjustment.
Follow-Up Recommendations Re-evaluation within 48 hr.
Pearls And Pitfalls
IV dextrose is preferred over oral glucose. Multiple D50 boluses are often required. Do not rely solely on D10/D20. Consider hypoglycemia in all neurologic or psychiatric presentations. Recurrent episodes may require prolonged recovery.
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Emergency And Acute Medicine: Hypocalcemia
Basics
Description Hypocalcemia is defined as a total plasma calcium level <8.7 mg/dL. Ionized calcium may be normal and therefore asymptomatic. Normal total serum calcium is 8.7–10.5 mg/dL.
Etiology Incidence is ~0.6% in the general population. Mechanisms include increased calcium loss from or decreased entry into the circulation. Circulating calcium exists as protein bound (45–50%, mainly albumin), complexed to anions (5–10%), and ionized free calcium (45–50%, physiologically active). Calcium homeostasis is regulated by parathyroid hormone, vitamin D (1,25-dihydroxyvitamin D), and calcitonin. Hypoalbuminemia is the most common cause; for each 1 g/dL decrease in albumin, total calcium decreases by ~0.8 mg/dL while ionized calcium remains unchanged.
Pediatric considerations Children have higher normal calcium levels (9.2–11 mg/dL). Neonatal hypocalcemia is defined as total calcium <7.5 mg/dL or ionized calcium <4 mg/dL and may present with jitteriness, tachypnea, apnea with cyanosis, and vomiting.
Diagnosis
Signs And Symptoms Occur when ionized calcium <3.2 mg/dL and depend on severity and rate of decline. Neuromuscular findings include paresthesias, hyperreflexia, muscle spasms, tetany, Chvostek sign, Trousseau sign, laryngeal stridor, seizures, and choreoathetosis. Cardiovascular effects include torsades de pointes, heart block, hypotension, impaired contractility, bradycardia, QT and ST prolongation, and T-wave abnormalities. Psychiatric manifestations include anxiety, irritability, depression, psychosis, confusion, and movement disorders. Ocular findings include papilledema and cataracts in acute cases.
Essential Workup Confirm diagnosis with serum ionized calcium level.
Diagnosis Tests And Interpretation
Lab ABG (pH changes affect ionized calcium), serum albumin, electrolytes, BUN/creatinine, glucose, magnesium, phosphate, PTH, and vitamin D metabolites as indicated.
ECG Prolonged QT interval and possible heart block.
Differential Diagnosis Impaired PTH secretion or action (post-surgical hypoparathyroidism, autoimmune or congenital hypoparathyroidism, pseudohypoparathyroidism), impaired vitamin D synthesis or action (malabsorption, renal disease), calcium sequestration or complexing (hyperphosphatemia, transfusion citrate, pancreatitis, rhabdomyolysis, alkalosis), hypomagnesemia, medications (bisphosphonates, calcitonin, phenytoin, cisplatin, PPIs), malignancy, sepsis, burns, and hungry bone syndrome after parathyroidectomy.
Treatment
Initial Stabilization/Therapy ABCs, IV access, and cardiac monitoring.
Emergency Department Treatment/Procedures Treat symptomatic hypocalcemia as an emergency. Give IV calcium gluconate 1–2 g in 50 mL D5W over 20 min. Faster infusion may cause dysrhythmias. Follow bolus with continuous infusion (0.5–1.5 mg/kg/hr elemental calcium). Do not mix calcium with bicarbonate or phosphate. Monitor calcium every 1–4 hr and titrate to symptoms or ECG changes. Correct hypomagnesemia if present (Mg 2 g IV). Use caution in patients on digoxin.
Chronic management Oral calcium 1.5–2 g/day (up to 4 g/day if malabsorption) plus vitamin D supplementation. Calcitriol is preferred for rapid onset.
Medications
IV calcium Calcium gluconate, calcium chloride, or calcium gluceptate (dose by elemental calcium).
Oral calcium Calcium carbonate, citrate, gluconate, lactate, or glubionate.
Vitamin D Calcitriol, ergocalciferol, or related preparations as indicated.
Follow-Up And Disposition
Admission Criteria Symptomatic hypocalcemia, ionized calcium <3.2 mg/dL, or need for continuous IV calcium.
Discharge Criteria Asymptomatic patients with ionized calcium >3.2 mg/dL and no significant comorbidities.
Follow-Up Recommendations Endocrinology follow-up for disorders of PTH or vitamin D metabolism.
Pearls And Pitfalls Hypocalcemia has multiple causes; treatment depends on severity and etiology. Severe symptoms require IV calcium. Hypocalcemia will not correct if magnesium deficiency is not treated first.
Basics
Description Hypocalcemia is defined as a total plasma calcium level <8.7 mg/dL. Ionized calcium may be normal and therefore asymptomatic. Normal total serum calcium is 8.7–10.5 mg/dL.
Etiology Incidence is ~0.6% in the general population. Mechanisms include increased calcium loss from or decreased entry into the circulation. Circulating calcium exists as protein bound (45–50%, mainly albumin), complexed to anions (5–10%), and ionized free calcium (45–50%, physiologically active). Calcium homeostasis is regulated by parathyroid hormone, vitamin D (1,25-dihydroxyvitamin D), and calcitonin. Hypoalbuminemia is the most common cause; for each 1 g/dL decrease in albumin, total calcium decreases by ~0.8 mg/dL while ionized calcium remains unchanged.
Pediatric considerations Children have higher normal calcium levels (9.2–11 mg/dL). Neonatal hypocalcemia is defined as total calcium <7.5 mg/dL or ionized calcium <4 mg/dL and may present with jitteriness, tachypnea, apnea with cyanosis, and vomiting.
Diagnosis
Signs And Symptoms Occur when ionized calcium <3.2 mg/dL and depend on severity and rate of decline. Neuromuscular findings include paresthesias, hyperreflexia, muscle spasms, tetany, Chvostek sign, Trousseau sign, laryngeal stridor, seizures, and choreoathetosis. Cardiovascular effects include torsades de pointes, heart block, hypotension, impaired contractility, bradycardia, QT and ST prolongation, and T-wave abnormalities. Psychiatric manifestations include anxiety, irritability, depression, psychosis, confusion, and movement disorders. Ocular findings include papilledema and cataracts in acute cases.
Essential Workup Confirm diagnosis with serum ionized calcium level.
Diagnosis Tests And Interpretation
Lab ABG (pH changes affect ionized calcium), serum albumin, electrolytes, BUN/creatinine, glucose, magnesium, phosphate, PTH, and vitamin D metabolites as indicated.
ECG Prolonged QT interval and possible heart block.
Differential Diagnosis Impaired PTH secretion or action (post-surgical hypoparathyroidism, autoimmune or congenital hypoparathyroidism, pseudohypoparathyroidism), impaired vitamin D synthesis or action (malabsorption, renal disease), calcium sequestration or complexing (hyperphosphatemia, transfusion citrate, pancreatitis, rhabdomyolysis, alkalosis), hypomagnesemia, medications (bisphosphonates, calcitonin, phenytoin, cisplatin, PPIs), malignancy, sepsis, burns, and hungry bone syndrome after parathyroidectomy.
Treatment
Initial Stabilization/Therapy ABCs, IV access, and cardiac monitoring.
Emergency Department Treatment/Procedures Treat symptomatic hypocalcemia as an emergency. Give IV calcium gluconate 1–2 g in 50 mL D5W over 20 min. Faster infusion may cause dysrhythmias. Follow bolus with continuous infusion (0.5–1.5 mg/kg/hr elemental calcium). Do not mix calcium with bicarbonate or phosphate. Monitor calcium every 1–4 hr and titrate to symptoms or ECG changes. Correct hypomagnesemia if present (Mg 2 g IV). Use caution in patients on digoxin.
Chronic management Oral calcium 1.5–2 g/day (up to 4 g/day if malabsorption) plus vitamin D supplementation. Calcitriol is preferred for rapid onset.
Medications
IV calcium Calcium gluconate, calcium chloride, or calcium gluceptate (dose by elemental calcium).
Oral calcium Calcium carbonate, citrate, gluconate, lactate, or glubionate.
Vitamin D Calcitriol, ergocalciferol, or related preparations as indicated.
Follow-Up And Disposition
Admission Criteria Symptomatic hypocalcemia, ionized calcium <3.2 mg/dL, or need for continuous IV calcium.
Discharge Criteria Asymptomatic patients with ionized calcium >3.2 mg/dL and no significant comorbidities.
Follow-Up Recommendations Endocrinology follow-up for disorders of PTH or vitamin D metabolism.
Pearls And Pitfalls Hypocalcemia has multiple causes; treatment depends on severity and etiology. Severe symptoms require IV calcium. Hypocalcemia will not correct if magnesium deficiency is not treated first.
- Published on
Emergency And Acute Medicine: Hyperviscosity Syndrome
Basics
Description Hyperviscosity syndrome is the clinical consequence of increased blood viscosity leading to impaired microcirculatory flow and reduced tissue oxygen delivery. As viscosity rises, greater cardiac output is required to maintain perfusion, yet oxygen delivery worsens because blood transit through the microcirculation slows. The classic clinical presentation is a triad of mucosal bleeding, visual disturbances, and neurologic symptoms.
Etiology Hyperviscosity results from elevation of cellular or acellular blood components. Acellular (protein) hyperviscosity is the most common cause (85–90%) and is usually due to increased gamma globulins from monoclonal gammopathies such as Waldenström macroglobulinemia and multiple myeloma; polyclonal gammopathies from rheumatologic disease are rare. Cellular hyperviscosity (10–15%) occurs with markedly increased blood cells, including erythrocytosis in polycythemia vera, extreme leukocytosis (>100,000) in acute or chronic leukemia, and severe thrombocytosis.
Diagnosis
Signs and symptoms The classic triad includes bleeding, visual changes, and neurologic dysfunction. Hematologic manifestations are most common and include epistaxis, gingival, rectal, or uterine bleeding, prolonged postprocedural bleeding, and pruritus. Ocular findings include blurred vision, diplopia, visual loss, and characteristic funduscopic changes such as the “link-sausage” appearance of retinal veins, retinal hemorrhages, exudates, microaneurysms, and papilledema. Neurologic symptoms include headache, dizziness, vertigo, ataxia, tinnitus, hearing loss, paresthesias, peripheral neuropathy, seizures, altered mental status, coma, and intracranial hemorrhage. Renal manifestations include hematuria, sterile pyuria, and nephritic or nephrotic syndromes. Cardiovascular findings may include angina, myocardial infarction, dysrhythmias, and heart failure. Dermatologic features include Raynaud phenomenon, livedo reticularis, palpable purpura, digital infarcts, and peripheral gangrene.
History Suspect hyperviscosity syndrome in patients with the classic triad, known immunoglobulin-producing disorders, or hypercellular hematologic diseases presenting with microvascular ischemia or cardiac decompensation.
Physical exam No pathognomonic findings exist; exam reflects end-organ involvement such as mucosal bleeding, petechiae, focal neurologic deficits, heart failure signs, or abnormal funduscopic findings.
Essential workup Assess for bleeding and end-organ ischemia. Measure serum or whole blood viscosity when available. Suspect the diagnosis when laboratory processing is difficult due to serum stasis or analyzer obstruction from viscous samples.
Diagnosis tests and interpretation
Laboratory Obtain CBC with differential to assess anemia, erythrocytosis, leukocytosis, or thrombocytosis; normocytic normochromic anemia is common. Peripheral smear may show rouleaux formation, a key diagnostic clue. Check electrolytes, BUN, creatinine, and glucose; renal dysfunction is common, and pseudohyponatremia or hypercalcemia may occur in multiple myeloma. Urinalysis may show proteinuria or hematuria. Obtain coagulation studies. Perform serum and urine protein electrophoresis. Serum viscosity measurement (when available) is diagnostic; normal relative viscosity is 1.4–1.8, and symptoms usually develop at ≥4 centipoise.
Imaging Head CT is indicated in patients with neurologic symptoms to exclude intracranial hemorrhage.
Differential diagnosis Platelet disorders, inherited or acquired coagulation factor deficiencies, liver disease, vitamin K deficiency, and disseminated intravascular coagulation.
Treatment
Prehospital Initiate IV fluid resuscitation in patients with bleeding or suspected hypovolemia.
Initial stabilization/therapy Rehydrate with isotonic saline. Bleeding or ischemia often does not respond to routine therapy and requires viscosity reduction. In patients with anemia and leukemia, avoid transfusion before plasmapheresis as it may worsen viscosity.
Emergency department management Provide supportive care and obtain early hematology consultation. Phlebotomy is a temporizing measure in severe cases with coma or seizures when plasmapheresis is not immediately available; remove 100–200 mL of whole blood and replace with isotonic saline, ideally after consultation, and is first-line in polycythemia vera. Plasmapheresis or leukapheresis is definitive therapy; typical volumes are 40 mL/kg in stable patients and up to 60 mL/kg in critically ill patients. Multiple sessions are often required. Monitor for hypocalcemia from citrate anticoagulation and rare dysrhythmias. Leukapheresis is preferred for hyperleukocytosis. ED clinicians may assist by establishing large-bore central access with caution due to bleeding risk.
Follow-up and disposition
Admission criteria Admit all patients with symptomatic hyperviscosity or evidence of bleeding or end-organ ischemia; ICU admission is indicated for hemorrhage, altered mental status, or acute myocardial infarction.
Discharge criteria Discharge only after definitive treatment of the underlying disorder and symptom resolution.
Issues for referral All patients require hematology consultation.
Key points Avoid diuretics as they can worsen viscosity. The hallmark triad consists of visual disturbances, bleeding, and neurologic symptoms. Early recognition and rapid viscosity reduction are critical to prevent irreversible end-organ damage.
Basics
Description Hyperviscosity syndrome is the clinical consequence of increased blood viscosity leading to impaired microcirculatory flow and reduced tissue oxygen delivery. As viscosity rises, greater cardiac output is required to maintain perfusion, yet oxygen delivery worsens because blood transit through the microcirculation slows. The classic clinical presentation is a triad of mucosal bleeding, visual disturbances, and neurologic symptoms.
Etiology Hyperviscosity results from elevation of cellular or acellular blood components. Acellular (protein) hyperviscosity is the most common cause (85–90%) and is usually due to increased gamma globulins from monoclonal gammopathies such as Waldenström macroglobulinemia and multiple myeloma; polyclonal gammopathies from rheumatologic disease are rare. Cellular hyperviscosity (10–15%) occurs with markedly increased blood cells, including erythrocytosis in polycythemia vera, extreme leukocytosis (>100,000) in acute or chronic leukemia, and severe thrombocytosis.
Diagnosis
Signs and symptoms The classic triad includes bleeding, visual changes, and neurologic dysfunction. Hematologic manifestations are most common and include epistaxis, gingival, rectal, or uterine bleeding, prolonged postprocedural bleeding, and pruritus. Ocular findings include blurred vision, diplopia, visual loss, and characteristic funduscopic changes such as the “link-sausage” appearance of retinal veins, retinal hemorrhages, exudates, microaneurysms, and papilledema. Neurologic symptoms include headache, dizziness, vertigo, ataxia, tinnitus, hearing loss, paresthesias, peripheral neuropathy, seizures, altered mental status, coma, and intracranial hemorrhage. Renal manifestations include hematuria, sterile pyuria, and nephritic or nephrotic syndromes. Cardiovascular findings may include angina, myocardial infarction, dysrhythmias, and heart failure. Dermatologic features include Raynaud phenomenon, livedo reticularis, palpable purpura, digital infarcts, and peripheral gangrene.
History Suspect hyperviscosity syndrome in patients with the classic triad, known immunoglobulin-producing disorders, or hypercellular hematologic diseases presenting with microvascular ischemia or cardiac decompensation.
Physical exam No pathognomonic findings exist; exam reflects end-organ involvement such as mucosal bleeding, petechiae, focal neurologic deficits, heart failure signs, or abnormal funduscopic findings.
Essential workup Assess for bleeding and end-organ ischemia. Measure serum or whole blood viscosity when available. Suspect the diagnosis when laboratory processing is difficult due to serum stasis or analyzer obstruction from viscous samples.
Diagnosis tests and interpretation
Laboratory Obtain CBC with differential to assess anemia, erythrocytosis, leukocytosis, or thrombocytosis; normocytic normochromic anemia is common. Peripheral smear may show rouleaux formation, a key diagnostic clue. Check electrolytes, BUN, creatinine, and glucose; renal dysfunction is common, and pseudohyponatremia or hypercalcemia may occur in multiple myeloma. Urinalysis may show proteinuria or hematuria. Obtain coagulation studies. Perform serum and urine protein electrophoresis. Serum viscosity measurement (when available) is diagnostic; normal relative viscosity is 1.4–1.8, and symptoms usually develop at ≥4 centipoise.
Imaging Head CT is indicated in patients with neurologic symptoms to exclude intracranial hemorrhage.
Differential diagnosis Platelet disorders, inherited or acquired coagulation factor deficiencies, liver disease, vitamin K deficiency, and disseminated intravascular coagulation.
Treatment
Prehospital Initiate IV fluid resuscitation in patients with bleeding or suspected hypovolemia.
Initial stabilization/therapy Rehydrate with isotonic saline. Bleeding or ischemia often does not respond to routine therapy and requires viscosity reduction. In patients with anemia and leukemia, avoid transfusion before plasmapheresis as it may worsen viscosity.
Emergency department management Provide supportive care and obtain early hematology consultation. Phlebotomy is a temporizing measure in severe cases with coma or seizures when plasmapheresis is not immediately available; remove 100–200 mL of whole blood and replace with isotonic saline, ideally after consultation, and is first-line in polycythemia vera. Plasmapheresis or leukapheresis is definitive therapy; typical volumes are 40 mL/kg in stable patients and up to 60 mL/kg in critically ill patients. Multiple sessions are often required. Monitor for hypocalcemia from citrate anticoagulation and rare dysrhythmias. Leukapheresis is preferred for hyperleukocytosis. ED clinicians may assist by establishing large-bore central access with caution due to bleeding risk.
Follow-up and disposition
Admission criteria Admit all patients with symptomatic hyperviscosity or evidence of bleeding or end-organ ischemia; ICU admission is indicated for hemorrhage, altered mental status, or acute myocardial infarction.
Discharge criteria Discharge only after definitive treatment of the underlying disorder and symptom resolution.
Issues for referral All patients require hematology consultation.
Key points Avoid diuretics as they can worsen viscosity. The hallmark triad consists of visual disturbances, bleeding, and neurologic symptoms. Early recognition and rapid viscosity reduction are critical to prevent irreversible end-organ damage.
