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Emergency and Acute Medicine – Iritis (Anterior Uveitis)
Basics and description
Iritis is an inflammatory condition of the anterior uveal tract and is synonymous with anterior uveitis. When the inflammation occurs after blunt or penetrating eye injury, it is referred to as traumatic iritis. The condition may present acutely or follow a chronic, relapsing course and can threaten vision if not recognized and treated appropriately.
Etiology
Most cases of iritis are idiopathic, but many are associated with trauma, systemic inflammatory diseases, infections, malignancies, or drug reactions. Noninfectious systemic associations include ankylosing spondylitis, reactive arthritis (Reiter syndrome), sarcoidosis, Behçet disease, inflammatory bowel disease, juvenile rheumatoid arthritis, Kawasaki syndrome, interstitial nephritis, IgA nephropathy, Sjögren syndrome, and psoriatic arthritis. Infectious causes include viral pathogens such as herpes simplex virus, herpes zoster virus, cytomegalovirus, HIV, rubella, measles, mumps, varicella, adenovirus, and West Nile virus; bacterial causes such as tuberculosis, syphilis, Lyme disease, chlamydia, gonorrhea, brucellosis, pertussis, rickettsial infections, and leprosy; and less commonly fungal infections. Other associations include leukemia, lymphoma, multiple sclerosis, malignant melanoma, cocaine use, pesticide exposure, corneal foreign bodies, and blunt ocular trauma.
Diagnosis and clinical presentation
Acute iritis typically presents with ocular pain, a red eye, photophobia (often consensual), tearing, and mildly decreased visual acuity. On examination, characteristic findings include ciliary flush (perilimbal injection), miosis, inflammatory cells and protein “flare” in the anterior chamber, and sometimes hypopyon. Posterior synechiae, which are adhesions between the iris and the lens, may develop. Intraocular pressure is often low but can occasionally be elevated. Chronic iritis may present with recurrent episodes and few acute symptoms, making diagnosis more challenging.
Essential workup and evaluation
A thorough history and review of systems are critical, as up to half of patients have an associated systemic disease. Slit-lamp examination is diagnostic and reveals leukocytes (“cells”) and protein leakage (“flare”) in the anterior chamber; these findings are best appreciated with a short, wide beam of light. Intraocular pressure should be measured. Relief of pain with topical anesthetic suggests a superficial process and makes iritis less likely.
Diagnostic tests and interpretation
Routine laboratory testing is usually not required in the emergency setting. Further outpatient evaluation should be guided by clinical suspicion and coordinated with ophthalmology and other specialists. Targeted testing may include inflammatory markers, HLA-B27 typing, autoimmune serologies, tuberculosis screening, syphilis testing, Lyme serologies, ACE levels, or imaging such as chest radiography or sacroiliac joint films, depending on suspected systemic disease. Ultrasound biomicroscopy may assist in selected cases.
Differential diagnosis
Conditions that can mimic iritis include acute angle-closure glaucoma, conjunctivitis, corneal abrasion or foreign body, episcleritis, keratitis, intraocular foreign body, posterior segment tumors, and traumatic globe rupture. These must be carefully excluded because management differs significantly.
Treatment and emergency management
The primary goals of treatment are to reduce inflammation, relieve pain, prevent posterior synechiae, and preserve vision. Cycloplegic agents are the cornerstone of initial therapy, as they decrease ciliary muscle spasm, relieve pain and photophobia, and prevent synechiae formation. Topical corticosteroids may be indicated but should only be started in consultation with an ophthalmologist because of the risk of worsening infectious keratitis, particularly herpes simplex virus infection. Secondary glaucoma should be treated if present. Supportive care includes warm compresses, dark glasses, and appropriate analgesia. Identification and treatment of any underlying systemic or infectious cause are essential.
Medications
Cyclopentolate 1–2% is commonly used for mild to moderate inflammation, typically one drop three times daily. Homatropine 2–5% may be used for moderate inflammation. Atropine 1% is reserved for moderate to severe cases and should only be used with ophthalmology guidance. Prednisolone acetate 1% topical drops may be used for inflammation under ophthalmologic supervision. Analgesics such as acetaminophen or acetaminophen with codeine may be given for pain control.
Pediatric considerations
Cycloplegic agents are generally not recommended in children under 6 years of age because of the risk of systemic anticholinergic toxicity, which may cause flushing, tachycardia, hypotension, blurred vision, and hallucinations.
Disposition and follow-up
Hospital admission is rarely required unless there is a significant associated systemic illness. All patients with suspected iritis should be referred to an ophthalmologist within 24 hours for confirmation of diagnosis, monitoring, and adjustment of therapy. Referral to rheumatology, gastroenterology, or other specialists may be necessary when a systemic disease is identified.
Pearls and pitfalls
If topical anesthetic relieves eye pain, iritis is unlikely. Iritis must be distinguished from other causes of painful red eye that can rapidly threaten vision, including keratitis, herpes simplex conjunctivitis, bacterial conjunctivitis, acute angle-closure glaucoma, and globe rupture. Early recognition and appropriate referral are critical to preventing complications and vision loss.
Basics and description
Iritis is an inflammatory condition of the anterior uveal tract and is synonymous with anterior uveitis. When the inflammation occurs after blunt or penetrating eye injury, it is referred to as traumatic iritis. The condition may present acutely or follow a chronic, relapsing course and can threaten vision if not recognized and treated appropriately.
Etiology
Most cases of iritis are idiopathic, but many are associated with trauma, systemic inflammatory diseases, infections, malignancies, or drug reactions. Noninfectious systemic associations include ankylosing spondylitis, reactive arthritis (Reiter syndrome), sarcoidosis, Behçet disease, inflammatory bowel disease, juvenile rheumatoid arthritis, Kawasaki syndrome, interstitial nephritis, IgA nephropathy, Sjögren syndrome, and psoriatic arthritis. Infectious causes include viral pathogens such as herpes simplex virus, herpes zoster virus, cytomegalovirus, HIV, rubella, measles, mumps, varicella, adenovirus, and West Nile virus; bacterial causes such as tuberculosis, syphilis, Lyme disease, chlamydia, gonorrhea, brucellosis, pertussis, rickettsial infections, and leprosy; and less commonly fungal infections. Other associations include leukemia, lymphoma, multiple sclerosis, malignant melanoma, cocaine use, pesticide exposure, corneal foreign bodies, and blunt ocular trauma.
Diagnosis and clinical presentation
Acute iritis typically presents with ocular pain, a red eye, photophobia (often consensual), tearing, and mildly decreased visual acuity. On examination, characteristic findings include ciliary flush (perilimbal injection), miosis, inflammatory cells and protein “flare” in the anterior chamber, and sometimes hypopyon. Posterior synechiae, which are adhesions between the iris and the lens, may develop. Intraocular pressure is often low but can occasionally be elevated. Chronic iritis may present with recurrent episodes and few acute symptoms, making diagnosis more challenging.
Essential workup and evaluation
A thorough history and review of systems are critical, as up to half of patients have an associated systemic disease. Slit-lamp examination is diagnostic and reveals leukocytes (“cells”) and protein leakage (“flare”) in the anterior chamber; these findings are best appreciated with a short, wide beam of light. Intraocular pressure should be measured. Relief of pain with topical anesthetic suggests a superficial process and makes iritis less likely.
Diagnostic tests and interpretation
Routine laboratory testing is usually not required in the emergency setting. Further outpatient evaluation should be guided by clinical suspicion and coordinated with ophthalmology and other specialists. Targeted testing may include inflammatory markers, HLA-B27 typing, autoimmune serologies, tuberculosis screening, syphilis testing, Lyme serologies, ACE levels, or imaging such as chest radiography or sacroiliac joint films, depending on suspected systemic disease. Ultrasound biomicroscopy may assist in selected cases.
Differential diagnosis
Conditions that can mimic iritis include acute angle-closure glaucoma, conjunctivitis, corneal abrasion or foreign body, episcleritis, keratitis, intraocular foreign body, posterior segment tumors, and traumatic globe rupture. These must be carefully excluded because management differs significantly.
Treatment and emergency management
The primary goals of treatment are to reduce inflammation, relieve pain, prevent posterior synechiae, and preserve vision. Cycloplegic agents are the cornerstone of initial therapy, as they decrease ciliary muscle spasm, relieve pain and photophobia, and prevent synechiae formation. Topical corticosteroids may be indicated but should only be started in consultation with an ophthalmologist because of the risk of worsening infectious keratitis, particularly herpes simplex virus infection. Secondary glaucoma should be treated if present. Supportive care includes warm compresses, dark glasses, and appropriate analgesia. Identification and treatment of any underlying systemic or infectious cause are essential.
Medications
Cyclopentolate 1–2% is commonly used for mild to moderate inflammation, typically one drop three times daily. Homatropine 2–5% may be used for moderate inflammation. Atropine 1% is reserved for moderate to severe cases and should only be used with ophthalmology guidance. Prednisolone acetate 1% topical drops may be used for inflammation under ophthalmologic supervision. Analgesics such as acetaminophen or acetaminophen with codeine may be given for pain control.
Pediatric considerations
Cycloplegic agents are generally not recommended in children under 6 years of age because of the risk of systemic anticholinergic toxicity, which may cause flushing, tachycardia, hypotension, blurred vision, and hallucinations.
Disposition and follow-up
Hospital admission is rarely required unless there is a significant associated systemic illness. All patients with suspected iritis should be referred to an ophthalmologist within 24 hours for confirmation of diagnosis, monitoring, and adjustment of therapy. Referral to rheumatology, gastroenterology, or other specialists may be necessary when a systemic disease is identified.
Pearls and pitfalls
If topical anesthetic relieves eye pain, iritis is unlikely. Iritis must be distinguished from other causes of painful red eye that can rapidly threaten vision, including keratitis, herpes simplex conjunctivitis, bacterial conjunctivitis, acute angle-closure glaucoma, and globe rupture. Early recognition and appropriate referral are critical to preventing complications and vision loss.
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Emergency And Acute Medicine – Intussusception
Basics
Description Intussusception occurs when a proximal segment of bowel telescopes into a distal segment, leading to bowel obstruction, ischemia, infarction, and possible gangrene. More than 80% of cases involve the ileocecal region. It is the most common cause of intestinal obstruction in the first 2 years of life. Mortality is less than 1% with prompt treatment, but morbidity increases significantly with delayed diagnosis.
Epidemiology Most cases occur between 5 and 9 months of age, with an incidence of approximately 2.4 per 1,000 live births. There is a male predominance of about 2:1. Children older than 2 years are more likely to have a pathologic lead point, and in children older than 6 years, lymphoma is the most common lead point. Adults almost always have an identifiable pathologic lead point.
Alert Any infant or child presenting with episodic abdominal pain, vomiting, lethargy or altered mental status, or heme-positive stool should be evaluated for intussusception.
Etiology Most cases, particularly in infants, are idiopathic. In older children and adults, intussusception is often caused by a lead point such as lymphoma, polyps, lipomas, hypertrophied lymphoid tissue, Meckel diverticulum, viral infections such as adenovirus or rotavirus, parasites, foreign bodies, Henoch–Schönlein purpura, or underlying conditions such as celiac disease or cystic fibrosis.
Diagnosis
Signs and symptoms The classic triad of abdominal pain, vomiting, and bloody “currant jelly” stools occurs in fewer than half of patients. Abdominal pain is typically sudden, severe, intermittent, and associated with screaming and drawing up of the legs. Vomiting may be bilious. Stools may be grossly bloody or only occult blood positive. Mental status changes such as irritability, lethargy, or listlessness are common and may precede abdominal findings. Fever and abdominal distention may occur as the disease progresses.
Physical exam The abdomen may be distended and tender, and a sausage-shaped mass is sometimes palpable in the right upper quadrant. The right lower quadrant may feel empty. Rectal examination may reveal blood or a mass. In advanced cases, signs of peritonitis or sepsis from bowel perforation may be present.
Essential workup The diagnosis is suggested by the clinical presentation and confirmed radiographically. A heme-positive stool can support the diagnosis, particularly in patients presenting with lethargy.
Diagnosis tests and interpretation Laboratory studies typically include a CBC, electrolytes, BUN, and type and cross-match if surgery is anticipated. Abdominal radiographs are abnormal in only 35–40% of cases but may show decreased gas in the right colon, bowel obstruction, or free air if perforation has occurred. Ultrasound is the preferred initial diagnostic test and is highly sensitive and specific, demonstrating a “target” or “donut” sign. Contrast or air enema is both diagnostic and therapeutic and is successful in approximately 75–80% of cases when performed within 24 hours of symptom onset. Enema reduction is contraindicated in patients with perforation, peritonitis, or hemodynamic instability. Surgical intervention is required when enema reduction fails or is contraindicated, or when a pathologic lead point is suspected.
Differential diagnosis Conditions to consider include acute gastroenteritis, appendicitis, pneumonia, pyelonephritis, colic, malrotation with volvulus, strangulated hernia, Hirschsprung disease, inflammatory bowel disease, Henoch–Schönlein purpura, trauma, and intestinal ischemia.
Treatment
Prehospital care Management includes establishing IV access and administering isotonic fluid boluses for hypovolemia when indicated. The diagnosis is rarely confirmed in the prehospital setting.
Initial stabilization In the emergency department, IV access is obtained, fluid resuscitation initiated, and a nasogastric tube placed for decompression if needed. Early surgical consultation is essential.
Emergency department management Stabilization of airway, breathing, and circulation is followed by imaging and radiologic reduction with air or contrast enema when appropriate. Broad-spectrum antibiotics are initiated if there is concern for perforation, peritonitis, or sepsis. Surgical reduction is required if nonoperative management fails.
Follow-up and disposition Patients who undergo successful enema reduction should be admitted for observation due to the risk of recurrence. All patients requiring surgery should be admitted. Discharge may be considered only after prolonged observation, complete resolution of symptoms, normal mental status, and reliable caregivers who understand the signs of recurrence.
Pearls and pitfalls Intussusception may present primarily with lethargy rather than abdominal pain, and the classic triad is often absent. Delayed diagnosis increases the risk of bowel necrosis, perforation, and sepsis. Recurrence occurs in up to 10% of cases and may still be amenable to repeat enema reduction.
Basics
Description Intussusception occurs when a proximal segment of bowel telescopes into a distal segment, leading to bowel obstruction, ischemia, infarction, and possible gangrene. More than 80% of cases involve the ileocecal region. It is the most common cause of intestinal obstruction in the first 2 years of life. Mortality is less than 1% with prompt treatment, but morbidity increases significantly with delayed diagnosis.
Epidemiology Most cases occur between 5 and 9 months of age, with an incidence of approximately 2.4 per 1,000 live births. There is a male predominance of about 2:1. Children older than 2 years are more likely to have a pathologic lead point, and in children older than 6 years, lymphoma is the most common lead point. Adults almost always have an identifiable pathologic lead point.
Alert Any infant or child presenting with episodic abdominal pain, vomiting, lethargy or altered mental status, or heme-positive stool should be evaluated for intussusception.
Etiology Most cases, particularly in infants, are idiopathic. In older children and adults, intussusception is often caused by a lead point such as lymphoma, polyps, lipomas, hypertrophied lymphoid tissue, Meckel diverticulum, viral infections such as adenovirus or rotavirus, parasites, foreign bodies, Henoch–Schönlein purpura, or underlying conditions such as celiac disease or cystic fibrosis.
Diagnosis
Signs and symptoms The classic triad of abdominal pain, vomiting, and bloody “currant jelly” stools occurs in fewer than half of patients. Abdominal pain is typically sudden, severe, intermittent, and associated with screaming and drawing up of the legs. Vomiting may be bilious. Stools may be grossly bloody or only occult blood positive. Mental status changes such as irritability, lethargy, or listlessness are common and may precede abdominal findings. Fever and abdominal distention may occur as the disease progresses.
Physical exam The abdomen may be distended and tender, and a sausage-shaped mass is sometimes palpable in the right upper quadrant. The right lower quadrant may feel empty. Rectal examination may reveal blood or a mass. In advanced cases, signs of peritonitis or sepsis from bowel perforation may be present.
Essential workup The diagnosis is suggested by the clinical presentation and confirmed radiographically. A heme-positive stool can support the diagnosis, particularly in patients presenting with lethargy.
Diagnosis tests and interpretation Laboratory studies typically include a CBC, electrolytes, BUN, and type and cross-match if surgery is anticipated. Abdominal radiographs are abnormal in only 35–40% of cases but may show decreased gas in the right colon, bowel obstruction, or free air if perforation has occurred. Ultrasound is the preferred initial diagnostic test and is highly sensitive and specific, demonstrating a “target” or “donut” sign. Contrast or air enema is both diagnostic and therapeutic and is successful in approximately 75–80% of cases when performed within 24 hours of symptom onset. Enema reduction is contraindicated in patients with perforation, peritonitis, or hemodynamic instability. Surgical intervention is required when enema reduction fails or is contraindicated, or when a pathologic lead point is suspected.
Differential diagnosis Conditions to consider include acute gastroenteritis, appendicitis, pneumonia, pyelonephritis, colic, malrotation with volvulus, strangulated hernia, Hirschsprung disease, inflammatory bowel disease, Henoch–Schönlein purpura, trauma, and intestinal ischemia.
Treatment
Prehospital care Management includes establishing IV access and administering isotonic fluid boluses for hypovolemia when indicated. The diagnosis is rarely confirmed in the prehospital setting.
Initial stabilization In the emergency department, IV access is obtained, fluid resuscitation initiated, and a nasogastric tube placed for decompression if needed. Early surgical consultation is essential.
Emergency department management Stabilization of airway, breathing, and circulation is followed by imaging and radiologic reduction with air or contrast enema when appropriate. Broad-spectrum antibiotics are initiated if there is concern for perforation, peritonitis, or sepsis. Surgical reduction is required if nonoperative management fails.
Follow-up and disposition Patients who undergo successful enema reduction should be admitted for observation due to the risk of recurrence. All patients requiring surgery should be admitted. Discharge may be considered only after prolonged observation, complete resolution of symptoms, normal mental status, and reliable caregivers who understand the signs of recurrence.
Pearls and pitfalls Intussusception may present primarily with lethargy rather than abdominal pain, and the classic triad is often absent. Delayed diagnosis increases the risk of bowel necrosis, perforation, and sepsis. Recurrence occurs in up to 10% of cases and may still be amenable to repeat enema reduction.
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Emergency And Acute Medicine – Intracerebral Hemorrhage
Basics
Description Intracerebral hemorrhage is bleeding into the brain parenchyma causing direct compression of brain tissue. Secondary injury results from cerebral edema, rising intracranial pressure, and risk of brain herniation.
Etiology
Intracerebral hemorrhage may be spontaneous or traumatic. Common causes include uncontrolled or acute hypertension (most common), vascular malformations (arteriovenous malformations, venous angiomas), ruptured cerebral aneurysms, intracranial neoplasms (especially melanoma and glioma), anticoagulant or thrombolytic therapy, illicit drug use (cocaine, amphetamines), bleeding disorders, cerebral amyloid angiopathy, and blunt or penetrating head trauma.
Diagnosis
Signs and symptoms Sudden severe headache, seizures, vomiting, neck stiffness, altered mental status, or coma. Neurologic deficits depend on hemorrhage location. Putaminal hemorrhage causes contralateral hemiparesis and sensory loss. Lobar hemorrhage causes variable focal deficits. Cerebellar hemorrhage presents with vomiting, ataxia, and nystagmus. Thalamic hemorrhage causes motor and sensory deficits with eye movement abnormalities. Pontine hemorrhage presents with quadriplegia and pinpoint pupils.
Essential workup
Secure airway if indicated and obtain immediate noncontrast CT of the head, which shows acute hemorrhage as a hyperdense lesion.
Diagnosis tests and interpretation
Lab CBC, electrolytes, BUN/creatinine, coagulation studies (PT, PTT, INR, platelets), pregnancy test when appropriate, ECG, and toxicology screen if indicated.
Imaging Noncontrast CT is diagnostic. CT angiography may identify an underlying vascular lesion and contrast extravasation (“spot sign”), which predicts hematoma expansion and worse outcomes. MRI may be useful later but is not first line in the ED.
Differential diagnosis
Seizure with postictal paralysis, ischemic stroke, CNS infection, intracranial mass, electrolyte or metabolic abnormalities, intoxication, migraine, transient ischemic attack, and traumatic intracranial hemorrhages.
Treatment
Prehospital Maintain cervical spine precautions if trauma suspected, elevate head with spinal alignment, and document neurologic deficits for comparison.
Initial stabilization Manage airway and breathing aggressively. Early neurosurgical and neurologic consultation is essential.
Emergency department management Control blood pressure cautiously to avoid reducing cerebral perfusion. Gradually lower diastolic blood pressure by approximately 10%, avoiding rapid normalization. Treat elevated intracranial pressure with head elevation, controlled ventilation, osmotic therapy, and fluid management. Reverse coagulopathies promptly using vitamin K, fresh frozen plasma, platelets, or prothrombin complex concentrates as indicated. Consider anticonvulsants for seizure management or prophylaxis.
Medication
Common agents include labetalol, nicardipine, esmolol, or enalapril for blood pressure control; mannitol or furosemide for intracranial pressure; phenytoin or fosphenytoin for seizures; and appropriate blood products for anticoagulation reversal.
Follow-up and disposition
Admission criteria All patients with intracerebral hemorrhage require admission. ICU care is indicated for altered mental status, intubation, or continuous blood pressure infusions.
Discharge criteria Discharge is not appropriate for intracerebral hemorrhage.
Follow-up recommendations Long-term blood pressure control, smoking and substance cessation, and rehabilitation planning are critical to reduce recurrence and improve functional recovery.
Key points
Early brain imaging is essential in patients with headache, hypertension, or altered mental status. Blood pressure reduction must be cautious to preserve cerebral perfusion. Delayed hemorrhage should be considered in anticoagulated patients with head trauma.
Basics
Description Intracerebral hemorrhage is bleeding into the brain parenchyma causing direct compression of brain tissue. Secondary injury results from cerebral edema, rising intracranial pressure, and risk of brain herniation.
Etiology
Intracerebral hemorrhage may be spontaneous or traumatic. Common causes include uncontrolled or acute hypertension (most common), vascular malformations (arteriovenous malformations, venous angiomas), ruptured cerebral aneurysms, intracranial neoplasms (especially melanoma and glioma), anticoagulant or thrombolytic therapy, illicit drug use (cocaine, amphetamines), bleeding disorders, cerebral amyloid angiopathy, and blunt or penetrating head trauma.
Diagnosis
Signs and symptoms Sudden severe headache, seizures, vomiting, neck stiffness, altered mental status, or coma. Neurologic deficits depend on hemorrhage location. Putaminal hemorrhage causes contralateral hemiparesis and sensory loss. Lobar hemorrhage causes variable focal deficits. Cerebellar hemorrhage presents with vomiting, ataxia, and nystagmus. Thalamic hemorrhage causes motor and sensory deficits with eye movement abnormalities. Pontine hemorrhage presents with quadriplegia and pinpoint pupils.
Essential workup
Secure airway if indicated and obtain immediate noncontrast CT of the head, which shows acute hemorrhage as a hyperdense lesion.
Diagnosis tests and interpretation
Lab CBC, electrolytes, BUN/creatinine, coagulation studies (PT, PTT, INR, platelets), pregnancy test when appropriate, ECG, and toxicology screen if indicated.
Imaging Noncontrast CT is diagnostic. CT angiography may identify an underlying vascular lesion and contrast extravasation (“spot sign”), which predicts hematoma expansion and worse outcomes. MRI may be useful later but is not first line in the ED.
Differential diagnosis
Seizure with postictal paralysis, ischemic stroke, CNS infection, intracranial mass, electrolyte or metabolic abnormalities, intoxication, migraine, transient ischemic attack, and traumatic intracranial hemorrhages.
Treatment
Prehospital Maintain cervical spine precautions if trauma suspected, elevate head with spinal alignment, and document neurologic deficits for comparison.
Initial stabilization Manage airway and breathing aggressively. Early neurosurgical and neurologic consultation is essential.
Emergency department management Control blood pressure cautiously to avoid reducing cerebral perfusion. Gradually lower diastolic blood pressure by approximately 10%, avoiding rapid normalization. Treat elevated intracranial pressure with head elevation, controlled ventilation, osmotic therapy, and fluid management. Reverse coagulopathies promptly using vitamin K, fresh frozen plasma, platelets, or prothrombin complex concentrates as indicated. Consider anticonvulsants for seizure management or prophylaxis.
Medication
Common agents include labetalol, nicardipine, esmolol, or enalapril for blood pressure control; mannitol or furosemide for intracranial pressure; phenytoin or fosphenytoin for seizures; and appropriate blood products for anticoagulation reversal.
Follow-up and disposition
Admission criteria All patients with intracerebral hemorrhage require admission. ICU care is indicated for altered mental status, intubation, or continuous blood pressure infusions.
Discharge criteria Discharge is not appropriate for intracerebral hemorrhage.
Follow-up recommendations Long-term blood pressure control, smoking and substance cessation, and rehabilitation planning are critical to reduce recurrence and improve functional recovery.
Key points
Early brain imaging is essential in patients with headache, hypertension, or altered mental status. Blood pressure reduction must be cautious to preserve cerebral perfusion. Delayed hemorrhage should be considered in anticoagulated patients with head trauma.
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Emergency And Acute Medicine – Influenza
Basics
Description Influenza is an acute, usually self-limited viral respiratory infection transmitted via small-particle aerosols from coughing, sneezing, or talking. The virus infects respiratory epithelium after deposition in the airway. Incubation is 1–4 days (average 2), with a mean illness duration of approximately 4 days in adults. Seasonal outbreaks peak most commonly in winter, often February. Mortality is largely due to pulmonary complications. Complications include primary viral pneumonia, secondary bacterial pneumonia, COPD exacerbations, otitis media and sinusitis in children, reactive airway disease, and rarely myositis, myocarditis, pericarditis, Guillain–Barré syndrome, aseptic meningitis, ARDS, and multisystem organ failure.
Etiology
Influenza is caused primarily by influenza A or B viruses, with influenza A generally producing more severe disease. Influenza A is classified by hemagglutinin (H1, H2, H3) and neuraminidase subtypes. Annual epidemics result from antigenic drift, while pandemics result from antigenic shift. Waterfowl serve as the primary reservoir. Vaccine targets circulating subtype antigens.
Diagnosis
Signs and symptoms Influenza-like illness is defined as fever with cough or sore throat without another clear diagnosis. Fever and cough together are somewhat specific but insensitive. Children often have higher fevers, more lower respiratory involvement, calf myalgias, and febrile seizures. Elderly patients may present atypically with confusion, lassitude, or minimal respiratory symptoms. Local epidemic activity is the strongest predictor of disease.
Essential workup
Diagnosis is primarily clinical during influenza season when community prevalence is high.
Diagnosis tests and interpretation
Lab CBC may show normal or mildly decreased WBC count. Pulse oximetry or ABG is indicated for significant respiratory symptoms.
Imaging Chest radiograph is indicated for lower respiratory findings and may be normal or show bilateral interstitial infiltrates.
Diagnostic procedures Rapid antigen tests are specific but poorly sensitive. PCR testing is both sensitive and specific and can differentiate subtypes. Viral culture is not useful for ED decision-making.
Differential diagnosis
Other respiratory viral infections, bronchitis, atypical pneumonia, infectious mononucleosis, and rarely anthrax.
Treatment
Initial stabilization Provide supplemental oxygen, IV fluids, and ventilatory support as indicated.
Emergency department management Treatment is primarily supportive with antipyretics, hydration, and bronchodilators for bronchospasm. Avoid aspirin, especially in children. Neuraminidase inhibitors (oseltamivir, zanamivir) are most effective when started within 48 hours of symptom onset and reduce symptom duration by less than one day. Antivirals are recommended for severe illness, hospitalized patients, immunocompromised individuals, and those at high risk for complications.
Medication
Oseltamivir 75 mg PO BID for treatment or 75 mg PO daily for postexposure prophylaxis. Zanamivir inhalation 10 mg q12h. Albuterol for associated bronchospasm.
Prevention
Annual inactivated influenza vaccination is recommended for high-risk groups, health care workers, pregnant women, and children. Live attenuated intranasal vaccine is approved for healthy individuals aged 2–49 years but contraindicated in pregnancy, immunocompromise, and certain comorbidities. Chemoprophylaxis may be used in selected high-risk exposures.
Follow-up and disposition
Admission criteria Hypoxia, pneumonia, severe dehydration, altered mental status, or inability to tolerate oral intake.
Discharge criteria Stable patients tolerating fluids with mild disease.
Follow-up recommendations Outpatient follow-up and return precautions for worsening respiratory symptoms.
Pearls and pitfalls
Local influenza prevalence is the most important diagnostic clue. Most patients do not require testing or antivirals. Consider concurrent reactive airway disease in patients with wheezing or hypoxia. Stay updated with seasonal CDC guidance.
Basics
Description Influenza is an acute, usually self-limited viral respiratory infection transmitted via small-particle aerosols from coughing, sneezing, or talking. The virus infects respiratory epithelium after deposition in the airway. Incubation is 1–4 days (average 2), with a mean illness duration of approximately 4 days in adults. Seasonal outbreaks peak most commonly in winter, often February. Mortality is largely due to pulmonary complications. Complications include primary viral pneumonia, secondary bacterial pneumonia, COPD exacerbations, otitis media and sinusitis in children, reactive airway disease, and rarely myositis, myocarditis, pericarditis, Guillain–Barré syndrome, aseptic meningitis, ARDS, and multisystem organ failure.
Etiology
Influenza is caused primarily by influenza A or B viruses, with influenza A generally producing more severe disease. Influenza A is classified by hemagglutinin (H1, H2, H3) and neuraminidase subtypes. Annual epidemics result from antigenic drift, while pandemics result from antigenic shift. Waterfowl serve as the primary reservoir. Vaccine targets circulating subtype antigens.
Diagnosis
Signs and symptoms Influenza-like illness is defined as fever with cough or sore throat without another clear diagnosis. Fever and cough together are somewhat specific but insensitive. Children often have higher fevers, more lower respiratory involvement, calf myalgias, and febrile seizures. Elderly patients may present atypically with confusion, lassitude, or minimal respiratory symptoms. Local epidemic activity is the strongest predictor of disease.
Essential workup
Diagnosis is primarily clinical during influenza season when community prevalence is high.
Diagnosis tests and interpretation
Lab CBC may show normal or mildly decreased WBC count. Pulse oximetry or ABG is indicated for significant respiratory symptoms.
Imaging Chest radiograph is indicated for lower respiratory findings and may be normal or show bilateral interstitial infiltrates.
Diagnostic procedures Rapid antigen tests are specific but poorly sensitive. PCR testing is both sensitive and specific and can differentiate subtypes. Viral culture is not useful for ED decision-making.
Differential diagnosis
Other respiratory viral infections, bronchitis, atypical pneumonia, infectious mononucleosis, and rarely anthrax.
Treatment
Initial stabilization Provide supplemental oxygen, IV fluids, and ventilatory support as indicated.
Emergency department management Treatment is primarily supportive with antipyretics, hydration, and bronchodilators for bronchospasm. Avoid aspirin, especially in children. Neuraminidase inhibitors (oseltamivir, zanamivir) are most effective when started within 48 hours of symptom onset and reduce symptom duration by less than one day. Antivirals are recommended for severe illness, hospitalized patients, immunocompromised individuals, and those at high risk for complications.
Medication
Oseltamivir 75 mg PO BID for treatment or 75 mg PO daily for postexposure prophylaxis. Zanamivir inhalation 10 mg q12h. Albuterol for associated bronchospasm.
Prevention
Annual inactivated influenza vaccination is recommended for high-risk groups, health care workers, pregnant women, and children. Live attenuated intranasal vaccine is approved for healthy individuals aged 2–49 years but contraindicated in pregnancy, immunocompromise, and certain comorbidities. Chemoprophylaxis may be used in selected high-risk exposures.
Follow-up and disposition
Admission criteria Hypoxia, pneumonia, severe dehydration, altered mental status, or inability to tolerate oral intake.
Discharge criteria Stable patients tolerating fluids with mild disease.
Follow-up recommendations Outpatient follow-up and return precautions for worsening respiratory symptoms.
Pearls and pitfalls
Local influenza prevalence is the most important diagnostic clue. Most patients do not require testing or antivirals. Consider concurrent reactive airway disease in patients with wheezing or hypoxia. Stay updated with seasonal CDC guidance.
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Emergency And Acute Medicine – Inflammatory Bowel Disease
Basics
Description Inflammatory bowel disease (IBD) consists of idiopathic, chronic inflammatory disorders of the gastrointestinal tract with frequent extraintestinal involvement. It includes ulcerative colitis (UC), Crohn disease, and intermediate forms. Disease may present as new onset or as an acute exacerbation. Crohn disease often presents subtly and requires a high index of suspicion. In UC, inflammation is continuous, begins in the rectum, and is limited to the colon and submucosa. Crohn disease may affect any region from mouth to anus, is discontinuous, and involves transmural inflammation. Both conditions are associated with an increased risk of colon cancer after more than 10 years of disease. Age distribution is bimodal, with peaks in early adulthood and around 60 years of age. Pediatric cases may present early in life, often with prominent extraintestinal features.
Etiology
The cause is unknown. IBD is multifactorial, involving genetic susceptibility, environmental influences, and dysregulated immune responses. Family history is common. No definitive infectious cause has been identified, though psychosocial stress may exacerbate symptoms.
Diagnosis
Signs and symptoms Crohn disease may manifest as inflammatory, fibrostenotic, or fistulizing disease. Ulcerative colitis ranges from mild to fulminant colitis. Constitutional symptoms include fever, fatigue, night sweats, and weight loss, particularly in Crohn disease, with growth or pubertal delay in children. Gastrointestinal manifestations include abdominal pain, diarrhea, and bleeding. Crohn disease pain is often episodic and periumbilical or right lower quadrant, while UC pain is more generalized and often associated with defecation. Diarrhea in UC is typically bloody with mucus, urgency, and tenesmus. Extraintestinal manifestations include arthritis, uveitis, episcleritis, aphthous ulcers, erythema nodosum, and pyoderma gangrenosum. Perianal disease such as fissures, abscesses, and fistulas is characteristic of Crohn disease and absent in UC.
Essential workup
IBD should be considered in patients with chronic diarrhea, abdominal pain, weight loss, anemia, or extraintestinal inflammatory findings, especially with recurrent or unexplained presentations.
Diagnosis tests and interpretation
Lab No single diagnostic test exists. Common findings include anemia, elevated ESR, electrolyte abnormalities, and inflammatory markers. Stool studies should exclude infectious etiologies including Clostridioides difficile.
Imaging Upright abdominal and chest radiographs assess for toxic megacolon, obstruction, or perforation. CT or MRI of the abdomen helps identify abscesses, inflammatory masses, and complications, with MRI preferred when available to limit radiation exposure. Colonoscopy with biopsy confirms diagnosis but should be deferred in severe disease due to perforation risk.
Differential diagnosis
Infectious colitis, pseudomembranous colitis, appendicitis, diverticulitis, ischemic colitis, colorectal cancer, functional bowel disease, sexually transmitted proctitis, HIV, vasculitis, and lymphoma.
Treatment
Initial stabilization Provide IV isotonic fluids for dehydration and transfuse if there is significant blood loss.
Emergency department management Insert nasogastric tube if obstruction or toxic dilation is suspected. Administer broad-spectrum antibiotics in fulminant disease, suspected perforation, or sepsis. Stress-dose steroids may be required in patients recently on chronic steroids. Surgical consultation is mandatory for perforation, uncontrolled hemorrhage, obstruction, or toxic megacolon. Medical therapy is generally continued or resumed rather than initiated in the ED unless previously established, with gastroenterology consultation recommended.
Medication
Therapies depend on disease severity and prior diagnosis and may include aminosalicylates, corticosteroids, antibiotics such as metronidazole or ciprofloxacin for Crohn disease, and immunomodulators or biologics under specialist guidance.
Follow-up and disposition
Admission criteria Indications include perforation, obstruction, toxic megacolon, massive bleeding, severe pain, dehydration, electrolyte imbalance, high fever, or severe flare requiring intensive therapy.
Discharge criteria Mild symptoms without toxicity, obstruction, significant bleeding, or dehydration, with reliable follow-up and established care.
Follow-up recommendations Gastroenterology follow-up is essential, with surgical consultation for complications or refractory disease.
Pearls and pitfalls
Always exclude toxic megacolon in severe flares. Avoid antidiarrheal agents in severe ulcerative colitis. Consider Crohn disease in children with growth delay or perianal disease. Always rule out C. difficile during disease exacerbations.
Basics
Description Inflammatory bowel disease (IBD) consists of idiopathic, chronic inflammatory disorders of the gastrointestinal tract with frequent extraintestinal involvement. It includes ulcerative colitis (UC), Crohn disease, and intermediate forms. Disease may present as new onset or as an acute exacerbation. Crohn disease often presents subtly and requires a high index of suspicion. In UC, inflammation is continuous, begins in the rectum, and is limited to the colon and submucosa. Crohn disease may affect any region from mouth to anus, is discontinuous, and involves transmural inflammation. Both conditions are associated with an increased risk of colon cancer after more than 10 years of disease. Age distribution is bimodal, with peaks in early adulthood and around 60 years of age. Pediatric cases may present early in life, often with prominent extraintestinal features.
Etiology
The cause is unknown. IBD is multifactorial, involving genetic susceptibility, environmental influences, and dysregulated immune responses. Family history is common. No definitive infectious cause has been identified, though psychosocial stress may exacerbate symptoms.
Diagnosis
Signs and symptoms Crohn disease may manifest as inflammatory, fibrostenotic, or fistulizing disease. Ulcerative colitis ranges from mild to fulminant colitis. Constitutional symptoms include fever, fatigue, night sweats, and weight loss, particularly in Crohn disease, with growth or pubertal delay in children. Gastrointestinal manifestations include abdominal pain, diarrhea, and bleeding. Crohn disease pain is often episodic and periumbilical or right lower quadrant, while UC pain is more generalized and often associated with defecation. Diarrhea in UC is typically bloody with mucus, urgency, and tenesmus. Extraintestinal manifestations include arthritis, uveitis, episcleritis, aphthous ulcers, erythema nodosum, and pyoderma gangrenosum. Perianal disease such as fissures, abscesses, and fistulas is characteristic of Crohn disease and absent in UC.
Essential workup
IBD should be considered in patients with chronic diarrhea, abdominal pain, weight loss, anemia, or extraintestinal inflammatory findings, especially with recurrent or unexplained presentations.
Diagnosis tests and interpretation
Lab No single diagnostic test exists. Common findings include anemia, elevated ESR, electrolyte abnormalities, and inflammatory markers. Stool studies should exclude infectious etiologies including Clostridioides difficile.
Imaging Upright abdominal and chest radiographs assess for toxic megacolon, obstruction, or perforation. CT or MRI of the abdomen helps identify abscesses, inflammatory masses, and complications, with MRI preferred when available to limit radiation exposure. Colonoscopy with biopsy confirms diagnosis but should be deferred in severe disease due to perforation risk.
Differential diagnosis
Infectious colitis, pseudomembranous colitis, appendicitis, diverticulitis, ischemic colitis, colorectal cancer, functional bowel disease, sexually transmitted proctitis, HIV, vasculitis, and lymphoma.
Treatment
Initial stabilization Provide IV isotonic fluids for dehydration and transfuse if there is significant blood loss.
Emergency department management Insert nasogastric tube if obstruction or toxic dilation is suspected. Administer broad-spectrum antibiotics in fulminant disease, suspected perforation, or sepsis. Stress-dose steroids may be required in patients recently on chronic steroids. Surgical consultation is mandatory for perforation, uncontrolled hemorrhage, obstruction, or toxic megacolon. Medical therapy is generally continued or resumed rather than initiated in the ED unless previously established, with gastroenterology consultation recommended.
Medication
Therapies depend on disease severity and prior diagnosis and may include aminosalicylates, corticosteroids, antibiotics such as metronidazole or ciprofloxacin for Crohn disease, and immunomodulators or biologics under specialist guidance.
Follow-up and disposition
Admission criteria Indications include perforation, obstruction, toxic megacolon, massive bleeding, severe pain, dehydration, electrolyte imbalance, high fever, or severe flare requiring intensive therapy.
Discharge criteria Mild symptoms without toxicity, obstruction, significant bleeding, or dehydration, with reliable follow-up and established care.
Follow-up recommendations Gastroenterology follow-up is essential, with surgical consultation for complications or refractory disease.
Pearls and pitfalls
Always exclude toxic megacolon in severe flares. Avoid antidiarrheal agents in severe ulcerative colitis. Consider Crohn disease in children with growth delay or perianal disease. Always rule out C. difficile during disease exacerbations.
- Published on
Emergency And Acute Medicine: Hyperthyroidism
Basics
Description Hyperthyroidism is caused by excessive thyroid hormone production, producing a continuum of disease due to direct metabolic effects of thyroid hormones and increased sensitivity to catecholamines. Clinical states range from subclinical or mild hyperthyroidism to thyrotoxicosis and, in 1–2% of cases, life-threatening thyroid storm. Thyroid regulation occurs through hypothalamic TRH stimulating pituitary TSH release, which increases thyroidal secretion of T4 and T3. Most circulating hormone is T4, which is peripherally converted to the more biologically active T3. Genetic predisposition plays a role, particularly in Graves disease, which is associated with HLA-B8 and HLA-DR3, and in some familial cases of nontoxic goiter with autosomal dominant inheritance.
Etiology Primary hyperthyroidism includes Graves disease, toxic multinodular or uninodular goiter, iodine-induced hyperthyroidism, and thyroiditis (postpartum, radiation, subacute de Quervain, and chronic lymphocytic). Other causes include metastatic thyroid cancer, ectopic thyroid tissue such as struma ovarii, pituitary adenoma, drug-induced hyperthyroidism (amiodarone, lithium, interferon, interleukin-2, iodinated contrast), factitious thyrotoxicosis from excess hormone ingestion, and aspirin overdose.
Diagnosis
Alert Thyroid storm is a medical emergency and may be precipitated by infection, trauma, surgery, diabetic ketoacidosis, myocardial infarction, stroke, chemotherapy, organophosphate intoxication, or abrupt withdrawal of antithyroid medications.
Signs and symptoms Findings reflect heightened end-organ responsiveness to thyroid hormone. Common signs include fever, tachycardia with widened pulse pressure, diaphoresis, tremor, hyperreflexia, goiter, thyromegaly, thyroid bruit, exophthalmos, lid lag, pretibial myxedema, congestive heart failure, shock, and psychosis. Symptoms include weight loss despite increased appetite, palpitations, chest pain, heat intolerance, diarrhea, vomiting, weakness, anxiety, insomnia, menstrual irregularities, and fatigue. Thyroid storm presents with exaggerated manifestations including extreme tachyarrhythmias, heart failure, shock, delirium, coma, seizures, and thromboembolic events.
Geriatric considerations Apathetic hyperthyroidism often presents with subtle findings such as refractory atrial fibrillation, heart failure, weight loss, depression, tremor, and emotional lability rather than classic hyperadrenergic features.
History Typically reveals gradual onset of symptoms.
Physical exam May show fever, tachycardia, systolic hypertension with widened pulse pressure, tachypnea, alopecia, fine diaphoretic skin, irregularly irregular rhythm, lung rales, RUQ tenderness, jaundice, proximal muscle weakness, tremor, and altered mental status.
Essential workup Identify underlying cause and precipitating factors. Plasma TSH is the preferred initial test; a normal TSH generally excludes hyperthyroidism. Low TSH with normal T4 requires T3 measurement to rule out T3 thyrotoxicosis. If laboratory testing is delayed or unavailable, strong clinical suspicion should prompt treatment.
Diagnosis tests and interpretation
Laboratory TSH is typically suppressed, with elevated free T4. Approximately 5% of patients have isolated T3 thyrotoxicosis. Additional testing may include CBC, chemistry panel, liver enzymes, ABG, glucose, and cardiac markers to evaluate complications or precipitants.
Imaging Chest radiograph is useful in heart failure or infection.
Diagnostic procedures ECG commonly shows sinus tachycardia or new-onset atrial fibrillation and helps identify ischemia as a precipitating factor.
Differential diagnosis Pheochromocytoma, sepsis, sympathomimetic intoxication, psychosis, heat stroke, delirium tremens, malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome, hypothalamic stroke, hypothyroidism with apathetic presentation, and factitious thyrotoxicosis.
Treatment
Prehospital Supportive care and stabilization.
Initial stabilization/therapy Manage airway, breathing, and circulation. Initiate cardiac monitoring, provide oxygen and IV fluids, and begin cooling measures. Use acetaminophen for fever and avoid aspirin, which increases free thyroid hormone levels.
Emergency department management Identify and treat precipitating causes. In suspected thyroid storm, initiate treatment based on clinical suspicion without delay. Inhibit hormone synthesis with thioamides, preferably propylthiouracil, which also reduces peripheral T4-to-T3 conversion; methimazole is an alternative. Block hormone release with iodine preparations only after thioamide administration and at least one hour later. Block peripheral effects using beta-blockers, with propranolol preferred due to inhibition of T4-to-T3 conversion; esmolol may be used when beta-1 selectivity is needed. Reduce peripheral conversion with corticosteroids. Adjunctive therapies include cholestyramine to reduce enterohepatic circulation of thyroid hormone and lithium if iodine is contraindicated. Manage heart failure, dehydration, hyperthermia, and associated conditions concurrently.
Medication Propylthiouracil, propranolol, iodine solutions (Lugol), methimazole, esmolol, hydrocortisone or dexamethasone, cholestyramine, lithium, guanethidine, and reserpine as indicated based on clinical context.
Pregnancy considerations Physiologic changes may mimic hyperthyroidism. Poorly controlled disease increases risks of hyperemesis gravidarum, preeclampsia, preterm labor, low birth weight, miscarriage, and stillbirth. PTU is preferred at the lowest effective dose; propranolol may be used cautiously. Radioactive iodine is contraindicated. Thyroidectomy is an option when medications are not tolerated. Postpartum thyroiditis occurs in up to 10% of patients and often resolves within one year.
Follow-up and disposition
Admission criteria Thyroid storm, need for IV rate control, or significant instability.
Discharge criteria Mild symptoms responsive to oral therapy with reliable follow-up.
Follow-up recommendations Arrange timely primary care or endocrinology follow-up.
Key points Thyroid storm is highly lethal without prompt treatment and often requires empiric therapy. Never administer iodine before blocking hormone synthesis with a thioamide. Radioactive iodine is contraindicated in pregnancy.
Basics
Description Hyperthyroidism is caused by excessive thyroid hormone production, producing a continuum of disease due to direct metabolic effects of thyroid hormones and increased sensitivity to catecholamines. Clinical states range from subclinical or mild hyperthyroidism to thyrotoxicosis and, in 1–2% of cases, life-threatening thyroid storm. Thyroid regulation occurs through hypothalamic TRH stimulating pituitary TSH release, which increases thyroidal secretion of T4 and T3. Most circulating hormone is T4, which is peripherally converted to the more biologically active T3. Genetic predisposition plays a role, particularly in Graves disease, which is associated with HLA-B8 and HLA-DR3, and in some familial cases of nontoxic goiter with autosomal dominant inheritance.
Etiology Primary hyperthyroidism includes Graves disease, toxic multinodular or uninodular goiter, iodine-induced hyperthyroidism, and thyroiditis (postpartum, radiation, subacute de Quervain, and chronic lymphocytic). Other causes include metastatic thyroid cancer, ectopic thyroid tissue such as struma ovarii, pituitary adenoma, drug-induced hyperthyroidism (amiodarone, lithium, interferon, interleukin-2, iodinated contrast), factitious thyrotoxicosis from excess hormone ingestion, and aspirin overdose.
Diagnosis
Alert Thyroid storm is a medical emergency and may be precipitated by infection, trauma, surgery, diabetic ketoacidosis, myocardial infarction, stroke, chemotherapy, organophosphate intoxication, or abrupt withdrawal of antithyroid medications.
Signs and symptoms Findings reflect heightened end-organ responsiveness to thyroid hormone. Common signs include fever, tachycardia with widened pulse pressure, diaphoresis, tremor, hyperreflexia, goiter, thyromegaly, thyroid bruit, exophthalmos, lid lag, pretibial myxedema, congestive heart failure, shock, and psychosis. Symptoms include weight loss despite increased appetite, palpitations, chest pain, heat intolerance, diarrhea, vomiting, weakness, anxiety, insomnia, menstrual irregularities, and fatigue. Thyroid storm presents with exaggerated manifestations including extreme tachyarrhythmias, heart failure, shock, delirium, coma, seizures, and thromboembolic events.
Geriatric considerations Apathetic hyperthyroidism often presents with subtle findings such as refractory atrial fibrillation, heart failure, weight loss, depression, tremor, and emotional lability rather than classic hyperadrenergic features.
History Typically reveals gradual onset of symptoms.
Physical exam May show fever, tachycardia, systolic hypertension with widened pulse pressure, tachypnea, alopecia, fine diaphoretic skin, irregularly irregular rhythm, lung rales, RUQ tenderness, jaundice, proximal muscle weakness, tremor, and altered mental status.
Essential workup Identify underlying cause and precipitating factors. Plasma TSH is the preferred initial test; a normal TSH generally excludes hyperthyroidism. Low TSH with normal T4 requires T3 measurement to rule out T3 thyrotoxicosis. If laboratory testing is delayed or unavailable, strong clinical suspicion should prompt treatment.
Diagnosis tests and interpretation
Laboratory TSH is typically suppressed, with elevated free T4. Approximately 5% of patients have isolated T3 thyrotoxicosis. Additional testing may include CBC, chemistry panel, liver enzymes, ABG, glucose, and cardiac markers to evaluate complications or precipitants.
Imaging Chest radiograph is useful in heart failure or infection.
Diagnostic procedures ECG commonly shows sinus tachycardia or new-onset atrial fibrillation and helps identify ischemia as a precipitating factor.
Differential diagnosis Pheochromocytoma, sepsis, sympathomimetic intoxication, psychosis, heat stroke, delirium tremens, malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome, hypothalamic stroke, hypothyroidism with apathetic presentation, and factitious thyrotoxicosis.
Treatment
Prehospital Supportive care and stabilization.
Initial stabilization/therapy Manage airway, breathing, and circulation. Initiate cardiac monitoring, provide oxygen and IV fluids, and begin cooling measures. Use acetaminophen for fever and avoid aspirin, which increases free thyroid hormone levels.
Emergency department management Identify and treat precipitating causes. In suspected thyroid storm, initiate treatment based on clinical suspicion without delay. Inhibit hormone synthesis with thioamides, preferably propylthiouracil, which also reduces peripheral T4-to-T3 conversion; methimazole is an alternative. Block hormone release with iodine preparations only after thioamide administration and at least one hour later. Block peripheral effects using beta-blockers, with propranolol preferred due to inhibition of T4-to-T3 conversion; esmolol may be used when beta-1 selectivity is needed. Reduce peripheral conversion with corticosteroids. Adjunctive therapies include cholestyramine to reduce enterohepatic circulation of thyroid hormone and lithium if iodine is contraindicated. Manage heart failure, dehydration, hyperthermia, and associated conditions concurrently.
Medication Propylthiouracil, propranolol, iodine solutions (Lugol), methimazole, esmolol, hydrocortisone or dexamethasone, cholestyramine, lithium, guanethidine, and reserpine as indicated based on clinical context.
Pregnancy considerations Physiologic changes may mimic hyperthyroidism. Poorly controlled disease increases risks of hyperemesis gravidarum, preeclampsia, preterm labor, low birth weight, miscarriage, and stillbirth. PTU is preferred at the lowest effective dose; propranolol may be used cautiously. Radioactive iodine is contraindicated. Thyroidectomy is an option when medications are not tolerated. Postpartum thyroiditis occurs in up to 10% of patients and often resolves within one year.
Follow-up and disposition
Admission criteria Thyroid storm, need for IV rate control, or significant instability.
Discharge criteria Mild symptoms responsive to oral therapy with reliable follow-up.
Follow-up recommendations Arrange timely primary care or endocrinology follow-up.
Key points Thyroid storm is highly lethal without prompt treatment and often requires empiric therapy. Never administer iodine before blocking hormone synthesis with a thioamide. Radioactive iodine is contraindicated in pregnancy.
- Published on
Emergency And Acute Medicine: Hyperthermia
Basics
Description Hyperthermia represents a spectrum of heat-related illness caused by progressively overwhelming heat stress, ranging from dehydration and electrolyte abnormalities to thermoregulatory failure and multisystem organ dysfunction. Normal body temperature is maintained by balancing heat production and dissipation. At temperatures above 42°C (108°F), oxidative phosphorylation becomes uncoupled and critical enzymes fail. Heat stroke is defined by a core temperature >105°F (40.5°C) with failure of thermoregulation, severe CNS dysfunction, and multisystem organ failure. Classic heat stroke is nonexertional, typically affecting the elderly, very young, or debilitated patients who cannot escape a hot environment; it develops over days to weeks and is associated with severe dehydration and hot, often dry skin. Exertional heat stroke occurs in younger, healthy individuals under intense physical exertion, develops over hours, and may occur despite ongoing sweating. Heat exhaustion involves moderate temperature elevation, usually <104°F (40°C), preserved thermoregulation and CNS function, and fluid or salt depletion; without treatment it may progress to heat stroke.
Etiology Predisposing factors impair heat dissipation or increase heat production. Medical conditions include extremes of age, dehydration, cardiovascular disease, obesity, diabetes, hyperthyroidism, pheochromocytoma, febrile illness, and skin disorders limiting sweating. Pharmacologic contributors include sympathomimetics, cocaine, PCP, LSD, MAO inhibitors, antipsychotics, anxiolytics, anticholinergics, antihistamines, beta-blockers, diuretics, laxatives, and drug or alcohol withdrawal. Environmental risks include high heat and humidity, prolonged exertion, immobility, lack of air conditioning, poor acclimatization, and occlusive clothing.
Pediatric considerations Children are at increased risk due to higher body surface area–to–mass ratio and reduced sweating capacity.
Diagnosis
Signs and symptoms Heat stroke presents with the classic triad of hyperthermia, CNS dysfunction, and hot skin. Core temperature exceeds 105°F (40.5°C). Neurologic findings include delirium, coma, seizures, ataxia, and confusion. Cardiovascular findings include tachycardia, hypotension, wide pulse pressure, and conduction abnormalities. Pulmonary findings include tachypnea, respiratory alkalosis, hypoxemia, and noncardiogenic pulmonary edema. GI symptoms include nausea, vomiting, and diarrhea. Renal failure, rhabdomyolysis, hepatic failure with extreme transaminase elevation, and coagulopathy including DIC may occur and indicate poor prognosis. Heat exhaustion causes headache, fatigue, malaise, impaired judgment, nausea, vomiting, tachycardia, dehydration, tachypnea, and profuse sweating without severe CNS dysfunction. Heat cramps cause painful muscle cramps after heavy sweating and hypotonic fluid replacement, leading to hyponatremia. Heat edema presents as dependent lower-extremity swelling in nonacclimatized individuals. Heat syncope presents as transient loss of consciousness during heat exposure, especially in the elderly. Prickly heat causes a pruritic maculopapular or vesicular rash due to sweat duct obstruction.
Essential workup Measure accurate core temperature using a rectal or esophageal probe. Establish history of heat exposure. Heat exhaustion is a diagnosis of exclusion. Heat stroke requires both core temperature >40.5°C and severe CNS dysfunction.
Diagnosis tests and interpretation
Laboratory Obtain CBC (leukocytosis, hemoconcentration), electrolytes, BUN, creatinine, glucose, urinalysis (myoglobin), creatine kinase for rhabdomyolysis, ABG (acidosis and elevated lactate common in exertional heat stroke), blood and urine cultures if sepsis is considered, toxicology screen, PT/PTT and DIC panel, liver function tests, and troponin (elevation suggests poor prognosis).
Imaging ECG in elderly or cardiac risk patients. Chest radiograph for ARDS or aspiration. Head CT for altered mental status. Lumbar puncture may be required to exclude CNS infection.
Differential diagnosis Sepsis, thyroid storm, pheochromocytoma, stimulant or anticholinergic toxicity, meningitis or encephalitis, cerebral malaria, delirium tremens, neuroleptic malignant syndrome, malignant hyperthermia, and serotonin syndrome.
Treatment
Prehospital Remove patient from heat source, disrobe, and initiate cooling with wet sheets.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Begin continuous core temperature monitoring. Initiate rapid cooling if temperature >104°F (40°C). Give IV 0.9% normal saline bolus if hypotensive. For altered mental status, administer glucose, thiamine, and naloxone as indicated.
Emergency department management Cooling is the priority. Use evaporative cooling with misted warm water and high airflow; combine with ice packs to groin and axilla. Cold-water immersion is effective but often impractical. Advanced techniques such as cold peritoneal lavage, extracorporeal circulation, or cold dialysis may be considered for refractory cases. Stop cooling at 102°F (39°C) to prevent hypothermia. Antipyretics are ineffective and alcohol sponge baths should be avoided. Supportive care includes aggressive isotonic fluid resuscitation while avoiding fluid overload. Insert Foley catheter to monitor urine output; target >2 mL/kg/hr if rhabdomyolysis is present. Treat seizures, agitation, and shivering with benzodiazepines. Avoid vasopressors and antiarrhythmics until adequate cooling, as many arrhythmias resolve with temperature normalization. Treat associated heat syndromes with appropriate hydration, electrolyte replacement, elevation or compression, and topical therapy as indicated.
Medication Benzodiazepines such as diazepam or lorazepam for seizures or agitation; naloxone when opioid toxicity is suspected.
Follow-up and disposition
Admission criteria All patients with heat stroke require ICU admission. Heat exhaustion requires admission if severe electrolyte abnormalities, renal failure, rhabdomyolysis, or advanced age are present.
Discharge criteria Patients without heat stroke or severe heat exhaustion who normalize clinically after treatment may be discharged with counseling.
Key points Heat stroke cannot be diagnosed without both core temperature >40.5°C and severe CNS dysfunction. Rapid cooling and supportive care are the cornerstones of management. Continuous core temperature monitoring is standard of care, and evaporative cooling is the preferred first-line method.
Basics
Description Hyperthermia represents a spectrum of heat-related illness caused by progressively overwhelming heat stress, ranging from dehydration and electrolyte abnormalities to thermoregulatory failure and multisystem organ dysfunction. Normal body temperature is maintained by balancing heat production and dissipation. At temperatures above 42°C (108°F), oxidative phosphorylation becomes uncoupled and critical enzymes fail. Heat stroke is defined by a core temperature >105°F (40.5°C) with failure of thermoregulation, severe CNS dysfunction, and multisystem organ failure. Classic heat stroke is nonexertional, typically affecting the elderly, very young, or debilitated patients who cannot escape a hot environment; it develops over days to weeks and is associated with severe dehydration and hot, often dry skin. Exertional heat stroke occurs in younger, healthy individuals under intense physical exertion, develops over hours, and may occur despite ongoing sweating. Heat exhaustion involves moderate temperature elevation, usually <104°F (40°C), preserved thermoregulation and CNS function, and fluid or salt depletion; without treatment it may progress to heat stroke.
Etiology Predisposing factors impair heat dissipation or increase heat production. Medical conditions include extremes of age, dehydration, cardiovascular disease, obesity, diabetes, hyperthyroidism, pheochromocytoma, febrile illness, and skin disorders limiting sweating. Pharmacologic contributors include sympathomimetics, cocaine, PCP, LSD, MAO inhibitors, antipsychotics, anxiolytics, anticholinergics, antihistamines, beta-blockers, diuretics, laxatives, and drug or alcohol withdrawal. Environmental risks include high heat and humidity, prolonged exertion, immobility, lack of air conditioning, poor acclimatization, and occlusive clothing.
Pediatric considerations Children are at increased risk due to higher body surface area–to–mass ratio and reduced sweating capacity.
Diagnosis
Signs and symptoms Heat stroke presents with the classic triad of hyperthermia, CNS dysfunction, and hot skin. Core temperature exceeds 105°F (40.5°C). Neurologic findings include delirium, coma, seizures, ataxia, and confusion. Cardiovascular findings include tachycardia, hypotension, wide pulse pressure, and conduction abnormalities. Pulmonary findings include tachypnea, respiratory alkalosis, hypoxemia, and noncardiogenic pulmonary edema. GI symptoms include nausea, vomiting, and diarrhea. Renal failure, rhabdomyolysis, hepatic failure with extreme transaminase elevation, and coagulopathy including DIC may occur and indicate poor prognosis. Heat exhaustion causes headache, fatigue, malaise, impaired judgment, nausea, vomiting, tachycardia, dehydration, tachypnea, and profuse sweating without severe CNS dysfunction. Heat cramps cause painful muscle cramps after heavy sweating and hypotonic fluid replacement, leading to hyponatremia. Heat edema presents as dependent lower-extremity swelling in nonacclimatized individuals. Heat syncope presents as transient loss of consciousness during heat exposure, especially in the elderly. Prickly heat causes a pruritic maculopapular or vesicular rash due to sweat duct obstruction.
Essential workup Measure accurate core temperature using a rectal or esophageal probe. Establish history of heat exposure. Heat exhaustion is a diagnosis of exclusion. Heat stroke requires both core temperature >40.5°C and severe CNS dysfunction.
Diagnosis tests and interpretation
Laboratory Obtain CBC (leukocytosis, hemoconcentration), electrolytes, BUN, creatinine, glucose, urinalysis (myoglobin), creatine kinase for rhabdomyolysis, ABG (acidosis and elevated lactate common in exertional heat stroke), blood and urine cultures if sepsis is considered, toxicology screen, PT/PTT and DIC panel, liver function tests, and troponin (elevation suggests poor prognosis).
Imaging ECG in elderly or cardiac risk patients. Chest radiograph for ARDS or aspiration. Head CT for altered mental status. Lumbar puncture may be required to exclude CNS infection.
Differential diagnosis Sepsis, thyroid storm, pheochromocytoma, stimulant or anticholinergic toxicity, meningitis or encephalitis, cerebral malaria, delirium tremens, neuroleptic malignant syndrome, malignant hyperthermia, and serotonin syndrome.
Treatment
Prehospital Remove patient from heat source, disrobe, and initiate cooling with wet sheets.
Initial stabilization/therapy Ensure airway, breathing, and circulation. Begin continuous core temperature monitoring. Initiate rapid cooling if temperature >104°F (40°C). Give IV 0.9% normal saline bolus if hypotensive. For altered mental status, administer glucose, thiamine, and naloxone as indicated.
Emergency department management Cooling is the priority. Use evaporative cooling with misted warm water and high airflow; combine with ice packs to groin and axilla. Cold-water immersion is effective but often impractical. Advanced techniques such as cold peritoneal lavage, extracorporeal circulation, or cold dialysis may be considered for refractory cases. Stop cooling at 102°F (39°C) to prevent hypothermia. Antipyretics are ineffective and alcohol sponge baths should be avoided. Supportive care includes aggressive isotonic fluid resuscitation while avoiding fluid overload. Insert Foley catheter to monitor urine output; target >2 mL/kg/hr if rhabdomyolysis is present. Treat seizures, agitation, and shivering with benzodiazepines. Avoid vasopressors and antiarrhythmics until adequate cooling, as many arrhythmias resolve with temperature normalization. Treat associated heat syndromes with appropriate hydration, electrolyte replacement, elevation or compression, and topical therapy as indicated.
Medication Benzodiazepines such as diazepam or lorazepam for seizures or agitation; naloxone when opioid toxicity is suspected.
Follow-up and disposition
Admission criteria All patients with heat stroke require ICU admission. Heat exhaustion requires admission if severe electrolyte abnormalities, renal failure, rhabdomyolysis, or advanced age are present.
Discharge criteria Patients without heat stroke or severe heat exhaustion who normalize clinically after treatment may be discharged with counseling.
Key points Heat stroke cannot be diagnosed without both core temperature >40.5°C and severe CNS dysfunction. Rapid cooling and supportive care are the cornerstones of management. Continuous core temperature monitoring is standard of care, and evaporative cooling is the preferred first-line method.
- Published on
Emergency And Acute Medicine: Hypertensive Emergencies
Basics
Description Hypertensive crisis refers to severe blood pressure elevation, typically SBP >179 mm Hg or DBP >109 mm Hg. Hypertensive urgency is severe BP elevation without acute end-organ injury. Hypertensive emergency is severe BP elevation with acute target-organ damage. In hypertensive emergency, autoregulation fails: arterioles initially constrict to protect capillary beds, but extreme pressures overwhelm this response, causing endothelial injury, increased permeability, platelet and coagulation activation, and fibrin deposition. Sympathetic and renin–angiotensin activation further increase vasoconstriction and inflammation, worsening ischemia and perpetuating a vicious cycle. Commonly affected organs include brain (encephalopathy, ischemic stroke, intracerebral hemorrhage), retina (hemorrhage, papilledema), heart (ACS, acute heart failure, aortic dissection), kidneys (acute renal failure), and placenta (preeclampsia/eclampsia).
Etiology Causes include essential hypertension; renal vascular or parenchymal disease; coarctation of the aorta; CNS injury (head trauma, stroke/ICH, tumor, spinal cord injury); endocrine disorders (pheochromocytoma, Cushing syndrome, primary hyperaldosteronism, renin-secreting tumors); drugs and toxins (cocaine, PCP, amphetamines, erythropoietin, tacrolimus, cyclosporine, corticosteroids, oral contraceptives, MAOI interactions, lead); withdrawal of antihypertensives; autonomic hyperreactivity (Guillain–Barré, acute intermittent porphyria); postoperative pain or anesthetic complications; and pregnancy-related disease (preeclampsia/eclampsia).
Diagnosis
History Review prescribed and OTC medications, antihypertensive adherence or withdrawal, duration and control of baseline hypertension, prior end-organ disease, comorbidities (CAD, diabetes, obesity), and recreational drug use. Screen for end-organ injury, commonly dyspnea, chest pain, headache, confusion, and focal neurologic deficits.
Physical exam Measure BP in both arms using appropriate cuff size. Assess for neurologic deficits and mental status changes, perform funduscopic exam for hemorrhages or papilledema, evaluate cardiovascular status (JVP, crackles, S3, aortic regurg murmur), and check for pulse asymmetry.
Essential workup Obtain a 12-lead ECG for ischemia and LVH, and assess kidney function because acute renal failure may be clinically silent.
Diagnosis tests and interpretation
Laboratory CBC (anemia and thrombocytopenia may indicate thrombotic microangiopathy), BMP including BUN/creatinine and electrolytes (hypokalemia suggests mineralocorticoid excess), urinalysis (protein, blood, casts), urine toxicology when drug use is suspected, and pregnancy test when appropriate. Use standard chest pain protocols when indicated.
Imaging Chest radiograph for cardiopulmonary symptoms, head CT for headache, confusion, or focal deficits, and CTA chest/abdomen if aortic dissection is suspected.
Procedures Consider arterial line monitoring in unstable cases. Lumbar puncture may be used to evaluate for subarachnoid hemorrhage after appropriate imaging.
Differential diagnosis ACS, acute heart failure, aortic dissection, ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, preeclampsia/eclampsia, withdrawal syndromes (beta-blocker, clonidine), and catecholamine excess states (pheochromocytoma, sympathomimetic intoxication, tyramine reaction with MAOIs).
Treatment
Prehospital Support ABCs and consider cautious BP reduction only when clearly indicated.
Initial stabilization/therapy Provide oxygen as needed, establish IV access, monitor ECG and pulse oximetry.
Emergency department management Hypertensive urgency does not require IV reduction; give missed home medications, use oral agents only, and lower BP gradually over 24–48 hours with close follow-up. Hypertensive emergency requires IV therapy guided by the end-organ injury rather than the absolute BP. Reduce MAP by no more than 20–25% in the first hour, then target roughly SBP ~160 and DBP ~100 over 2–6 hours, transitioning to oral agents within 6–12 hours once stable. Lower more gradually in acute CNS injury, but more rapidly in aortic dissection. Hypertensive encephalopathy: lower MAP up to 20% or DBP to 100–110 within the first hour, then normalize over 48–72 hours using nicardipine, clevidipine, or labetalol. Ischemic stroke: treat only if SBP >220 or DBP >120, or if thrombolysis planned (target <185/110 pre-tPA, then <180/105); avoid reducing MAP more than 15–20% in the first 24 hours; preferred agents are nicardipine, clevidipine, or labetalol. ICH/SAH: treat if SBP >180 or DBP >100; aim SBP 140–160 or MAP down 20–25% in the first hour; avoid nitroglycerin and nitroprusside due to cerebral vasodilation and ICP effects; use nicardipine, clevidipine, or labetalol. ACS: target MAP 60–100 using labetalol or esmolol with nitroglycerin; avoid hydralazine and nitroprusside. Acute heart failure: target MAP 60–100 with nitroprusside or nitroglycerin plus ACE inhibitor and/or loop diuretic. Acute renal failure or microangiopathy: reduce MAP 20–25% in the first hour using nicardipine, clevidipine, or fenoldopam; ACE inhibitors are preferred for scleroderma renal crisis. Aortic dissection: reduce shear force by lowering HR and BP; beta-blockade must come first; target SBP 100–120 and HR <65 within 20 minutes using esmolol plus a vasodilator (dihydropyridine CCB or nitroprusside); obtain urgent surgical consultation for type A.
Sympathomimetic crisis: avoid pure beta-blockade; use phentolamine or calcium channel blocker plus benzodiazepines; use clonidine for clonidine withdrawal.
Pregnancy considerations Preeclampsia is SBP >140 or DBP >90 with proteinuria after 20 weeks to 4 weeks postpartum, often with headache, visual changes, edema, or RUQ pain; target SBP 130–150 and DBP 80–100 using labetalol, nicardipine, hydralazine, and magnesium, with obstetric consultation.
Medication Clevidipine 1–16 mg/h infusion; nicardipine 2–15 mg/h infusion; labetalol 20–80 mg IV q10 min (max 300 mg) or 0.5–2 mg/min infusion; esmolol 80 mg IV bolus then 150 μg/kg/min infusion; nitroglycerin 5–100 μg/min infusion; nitroprusside 0.25–10 μg/kg/min infusion; hydralazine 10–20 mg IV bolus; fenoldopam 0.1–0.6 μg/kg/min infusion; enalaprilat 1.25–5 mg IV q6h; phentolamine 5–15 mg IV q5–15 min.
Follow-up and disposition
Admission criteria Any patient with acute end-organ injury requires admission; ICU monitoring is indicated for hypertensive emergency.
Discharge criteria No end-organ injury, reliable follow-up, known hypertension, reversible trigger such as medication nonadherence, and ability to resume a safe outpatient regimen; provide strict return precautions for chest pain, neurologic symptoms, or severe headache.
Follow-up recommendations Ensure timely primary care follow-up for medication initiation or adjustment and long-term BP control.
Key points Do not use IV agents for hypertensive urgency. In hypertensive emergency, the initial goal is controlled MAP reduction of 20–25% in the first hour, except for ischemic stroke and aortic dissection where targets differ. Avoid precipitous BP drops that can worsen ischemia. In aortic dissection prevent reflex tachycardia by starting beta-blockade first. In catecholamine excess avoid unopposed alpha stimulation by avoiding pure beta-blockers.
Basics
Description Hypertensive crisis refers to severe blood pressure elevation, typically SBP >179 mm Hg or DBP >109 mm Hg. Hypertensive urgency is severe BP elevation without acute end-organ injury. Hypertensive emergency is severe BP elevation with acute target-organ damage. In hypertensive emergency, autoregulation fails: arterioles initially constrict to protect capillary beds, but extreme pressures overwhelm this response, causing endothelial injury, increased permeability, platelet and coagulation activation, and fibrin deposition. Sympathetic and renin–angiotensin activation further increase vasoconstriction and inflammation, worsening ischemia and perpetuating a vicious cycle. Commonly affected organs include brain (encephalopathy, ischemic stroke, intracerebral hemorrhage), retina (hemorrhage, papilledema), heart (ACS, acute heart failure, aortic dissection), kidneys (acute renal failure), and placenta (preeclampsia/eclampsia).
Etiology Causes include essential hypertension; renal vascular or parenchymal disease; coarctation of the aorta; CNS injury (head trauma, stroke/ICH, tumor, spinal cord injury); endocrine disorders (pheochromocytoma, Cushing syndrome, primary hyperaldosteronism, renin-secreting tumors); drugs and toxins (cocaine, PCP, amphetamines, erythropoietin, tacrolimus, cyclosporine, corticosteroids, oral contraceptives, MAOI interactions, lead); withdrawal of antihypertensives; autonomic hyperreactivity (Guillain–Barré, acute intermittent porphyria); postoperative pain or anesthetic complications; and pregnancy-related disease (preeclampsia/eclampsia).
Diagnosis
History Review prescribed and OTC medications, antihypertensive adherence or withdrawal, duration and control of baseline hypertension, prior end-organ disease, comorbidities (CAD, diabetes, obesity), and recreational drug use. Screen for end-organ injury, commonly dyspnea, chest pain, headache, confusion, and focal neurologic deficits.
Physical exam Measure BP in both arms using appropriate cuff size. Assess for neurologic deficits and mental status changes, perform funduscopic exam for hemorrhages or papilledema, evaluate cardiovascular status (JVP, crackles, S3, aortic regurg murmur), and check for pulse asymmetry.
Essential workup Obtain a 12-lead ECG for ischemia and LVH, and assess kidney function because acute renal failure may be clinically silent.
Diagnosis tests and interpretation
Laboratory CBC (anemia and thrombocytopenia may indicate thrombotic microangiopathy), BMP including BUN/creatinine and electrolytes (hypokalemia suggests mineralocorticoid excess), urinalysis (protein, blood, casts), urine toxicology when drug use is suspected, and pregnancy test when appropriate. Use standard chest pain protocols when indicated.
Imaging Chest radiograph for cardiopulmonary symptoms, head CT for headache, confusion, or focal deficits, and CTA chest/abdomen if aortic dissection is suspected.
Procedures Consider arterial line monitoring in unstable cases. Lumbar puncture may be used to evaluate for subarachnoid hemorrhage after appropriate imaging.
Differential diagnosis ACS, acute heart failure, aortic dissection, ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, preeclampsia/eclampsia, withdrawal syndromes (beta-blocker, clonidine), and catecholamine excess states (pheochromocytoma, sympathomimetic intoxication, tyramine reaction with MAOIs).
Treatment
Prehospital Support ABCs and consider cautious BP reduction only when clearly indicated.
Initial stabilization/therapy Provide oxygen as needed, establish IV access, monitor ECG and pulse oximetry.
Emergency department management Hypertensive urgency does not require IV reduction; give missed home medications, use oral agents only, and lower BP gradually over 24–48 hours with close follow-up. Hypertensive emergency requires IV therapy guided by the end-organ injury rather than the absolute BP. Reduce MAP by no more than 20–25% in the first hour, then target roughly SBP ~160 and DBP ~100 over 2–6 hours, transitioning to oral agents within 6–12 hours once stable. Lower more gradually in acute CNS injury, but more rapidly in aortic dissection. Hypertensive encephalopathy: lower MAP up to 20% or DBP to 100–110 within the first hour, then normalize over 48–72 hours using nicardipine, clevidipine, or labetalol. Ischemic stroke: treat only if SBP >220 or DBP >120, or if thrombolysis planned (target <185/110 pre-tPA, then <180/105); avoid reducing MAP more than 15–20% in the first 24 hours; preferred agents are nicardipine, clevidipine, or labetalol. ICH/SAH: treat if SBP >180 or DBP >100; aim SBP 140–160 or MAP down 20–25% in the first hour; avoid nitroglycerin and nitroprusside due to cerebral vasodilation and ICP effects; use nicardipine, clevidipine, or labetalol. ACS: target MAP 60–100 using labetalol or esmolol with nitroglycerin; avoid hydralazine and nitroprusside. Acute heart failure: target MAP 60–100 with nitroprusside or nitroglycerin plus ACE inhibitor and/or loop diuretic. Acute renal failure or microangiopathy: reduce MAP 20–25% in the first hour using nicardipine, clevidipine, or fenoldopam; ACE inhibitors are preferred for scleroderma renal crisis. Aortic dissection: reduce shear force by lowering HR and BP; beta-blockade must come first; target SBP 100–120 and HR <65 within 20 minutes using esmolol plus a vasodilator (dihydropyridine CCB or nitroprusside); obtain urgent surgical consultation for type A.
Sympathomimetic crisis: avoid pure beta-blockade; use phentolamine or calcium channel blocker plus benzodiazepines; use clonidine for clonidine withdrawal.
Pregnancy considerations Preeclampsia is SBP >140 or DBP >90 with proteinuria after 20 weeks to 4 weeks postpartum, often with headache, visual changes, edema, or RUQ pain; target SBP 130–150 and DBP 80–100 using labetalol, nicardipine, hydralazine, and magnesium, with obstetric consultation.
Medication Clevidipine 1–16 mg/h infusion; nicardipine 2–15 mg/h infusion; labetalol 20–80 mg IV q10 min (max 300 mg) or 0.5–2 mg/min infusion; esmolol 80 mg IV bolus then 150 μg/kg/min infusion; nitroglycerin 5–100 μg/min infusion; nitroprusside 0.25–10 μg/kg/min infusion; hydralazine 10–20 mg IV bolus; fenoldopam 0.1–0.6 μg/kg/min infusion; enalaprilat 1.25–5 mg IV q6h; phentolamine 5–15 mg IV q5–15 min.
Follow-up and disposition
Admission criteria Any patient with acute end-organ injury requires admission; ICU monitoring is indicated for hypertensive emergency.
Discharge criteria No end-organ injury, reliable follow-up, known hypertension, reversible trigger such as medication nonadherence, and ability to resume a safe outpatient regimen; provide strict return precautions for chest pain, neurologic symptoms, or severe headache.
Follow-up recommendations Ensure timely primary care follow-up for medication initiation or adjustment and long-term BP control.
Key points Do not use IV agents for hypertensive urgency. In hypertensive emergency, the initial goal is controlled MAP reduction of 20–25% in the first hour, except for ischemic stroke and aortic dissection where targets differ. Avoid precipitous BP drops that can worsen ischemia. In aortic dissection prevent reflex tachycardia by starting beta-blockade first. In catecholamine excess avoid unopposed alpha stimulation by avoiding pure beta-blockers.
- Published on
Emergency And Acute Medicine: Hyperparathyroidism
Basics
Description Hyperparathyroidism is characterized by excess parathyroid hormone (PTH) leading to metabolic effects including decreased urinary calcium excretion, increased urinary phosphate loss, increased renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, and increased calcium and phosphate release from bone. Hypercalcemia is the primary metabolic abnormality. Despite reduced renal calcium excretion, hypercalciuria occurs due to elevated serum calcium, often accompanied by urinary magnesium loss. Magnesium is essential for both PTH secretion and peripheral PTH action; hypomagnesemia may blunt PTH effects. Genetic associations include multiple endocrine neoplasia (MEN) syndromes: MEN 1 (hyperparathyroidism, pancreatic islet tumors, pituitary disease) and MEN 2 (hyperparathyroidism in MEN 2A, medullary thyroid carcinoma, pheochromocytoma, and mucosal neuromas in MEN 2B).
Etiology Primary hyperparathyroidism results from parathyroid adenoma (≈85%), hyperplasia (≈14%), or rarely carcinoma (<1%). Secondary hyperparathyroidism is a compensatory response to vitamin D deficiency or chronic kidney disease with hyperphosphatemia; calcium levels are low or normal with elevated PTH.
Diagnosis
Signs and symptoms Classic features include renal stones, bone pain, gastrointestinal complaints, and neuropsychiatric changes. Alert Hypercalcemic crisis presents with anorexia, nausea, vomiting, and progressive mental status depression.
History Symptoms correlate with severity and rapidity of hypercalcemia.
Pediatric considerations Neonates born to hypoparathyroid mothers may present with hypotonia, weakness, and lethargy; hypercalcemic infants may have distinctive facial features including broad forehead, epicanthal folds, underdeveloped nasal bridge, and prominent upper lip.
Physical exam Findings may include dehydration, hypertension despite volume depletion, cardiac conduction abnormalities (bradyarrhythmias, bundle branch block, complete heart block, asystole), shortened QT interval, potentiation of digoxin toxicity, neurologic deficits (decreased reflexes, proximal weakness, lethargy, coma), psychiatric symptoms (depression, anxiety, psychosis), gastrointestinal symptoms (anorexia, constipation, peptic ulcer disease, pancreatitis), musculoskeletal pain, gout or pseudogout, and renal manifestations including nephrolithiasis and nephrocalcinosis.
Essential workup Measure serum calcium and albumin to assess corrected calcium. Evaluate for symptoms of severe hypercalcemia or impending parathyroid crisis. If asymptomatic with normal ECG and corrected calcium <14 mg/dL, no further ED testing is required. If symptomatic or calcium ≥14 mg/dL, obtain ionized calcium, electrolytes, BUN/creatinine, phosphorus, magnesium, alkaline phosphatase, ESR, TSH, CBC, and chest radiograph.
Diagnosis tests and interpretation
Laboratory Correct calcium for albumin: corrected Ca (mg/dL) = measured Ca + 0.8 × (4 − albumin). Acidosis increases ionized calcium by reducing albumin binding. Phosphorus is typically low in primary hyperparathyroidism and elevated in secondary disease. Chloride-to-phosphate ratio >33 favors hyperparathyroidism; <30 suggests malignancy. Alkaline phosphatase is elevated in ~50% of cases. ESR and anemia are usually normal in hyperparathyroidism but elevated in malignancy or granulomatous disease. Magnesium is often low or low-normal. PTH is elevated in primary and secondary hyperparathyroidism. PTH-related peptide suggests malignancy-associated hypercalcemia.
Imaging Chest radiograph evaluates volume status and screens for malignancy or granulomatous disease.
Diagnostic procedures Definitive diagnosis and treatment are established with parathyroidectomy.
Differential diagnosis PTH-mediated causes include primary or secondary hyperparathyroidism and familial hypocalciuric hypercalcemia. Non-PTH causes include malignancy, vitamin D excess or granulomatous disease, immobilization (e.g., Paget disease), and drug-induced hypercalcemia (thiazides, lithium, vitamin A, aluminum antacids, estrogens, androgens, tamoxifen).
Treatment
Prehospital May present primarily with psychiatric manifestations.
Initial stabilization/therapy Place on cardiac monitor if symptomatic or calcium >14 mg/dL. Begin IV hydration with 0.9% normal saline and correct acidosis.
Emergency department management Treat hypercalcemia with aggressive isotonic saline hydration (≥250 mL/hr unless limited by heart failure) targeting urine output ≥100 mL/hr. After adequate hydration, add loop diuretics to enhance calciuresis; avoid thiazides. Consider glucocorticoids in vitamin D–mediated or granulomatous disease. Initiate bisphosphonates in coordination with endocrinology. Treat dysrhythmias conventionally and use extreme caution with digoxin. Stop contributing medications and monitor closely for heart failure and electrolyte disturbances. Use calcitonin when hydration is contraindicated and initiate dialysis for refractory hypercalcemia with renal failure.
Medication First line Normal saline infusion; furosemide 40 mg IV q2–4h after rehydration; prednisone 40–60 mg PO or hydrocortisone 100 mg IV. Second line (with endocrinology) Calcitonin salmon 4 U/kg SC q12h; pamidronate 60–90 mg IV depending on calcium level; zoledronic acid 4 mg IV; cinacalcet 30 mg PO daily or BID for secondary hyperparathyroidism or carcinoma.
Follow-up and disposition
Admission criteria Corrected calcium >14 mg/dL, symptomatic hypercalcemia, or cardiac conduction abnormalities.
Discharge criteria Asymptomatic patients with calcium <14 mg/dL who can maintain hydration.
Issues for referral Endocrinology referral for PTH evaluation and definitive management.
Follow-up recommendations Arrange outpatient PTH testing, reinforce hydration, and discontinue medications that increase calcium levels.
Key points Hyperparathyroid-related hypercalcemia is often mild and rarely exceeds 14 mg/dL; higher levels suggest malignancy. Measure ionized or albumin-corrected calcium. Administering loop diuretics before adequate hydration worsens hypercalcemia and is a common management error.
Basics
Description Hyperparathyroidism is characterized by excess parathyroid hormone (PTH) leading to metabolic effects including decreased urinary calcium excretion, increased urinary phosphate loss, increased renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, and increased calcium and phosphate release from bone. Hypercalcemia is the primary metabolic abnormality. Despite reduced renal calcium excretion, hypercalciuria occurs due to elevated serum calcium, often accompanied by urinary magnesium loss. Magnesium is essential for both PTH secretion and peripheral PTH action; hypomagnesemia may blunt PTH effects. Genetic associations include multiple endocrine neoplasia (MEN) syndromes: MEN 1 (hyperparathyroidism, pancreatic islet tumors, pituitary disease) and MEN 2 (hyperparathyroidism in MEN 2A, medullary thyroid carcinoma, pheochromocytoma, and mucosal neuromas in MEN 2B).
Etiology Primary hyperparathyroidism results from parathyroid adenoma (≈85%), hyperplasia (≈14%), or rarely carcinoma (<1%). Secondary hyperparathyroidism is a compensatory response to vitamin D deficiency or chronic kidney disease with hyperphosphatemia; calcium levels are low or normal with elevated PTH.
Diagnosis
Signs and symptoms Classic features include renal stones, bone pain, gastrointestinal complaints, and neuropsychiatric changes. Alert Hypercalcemic crisis presents with anorexia, nausea, vomiting, and progressive mental status depression.
History Symptoms correlate with severity and rapidity of hypercalcemia.
Pediatric considerations Neonates born to hypoparathyroid mothers may present with hypotonia, weakness, and lethargy; hypercalcemic infants may have distinctive facial features including broad forehead, epicanthal folds, underdeveloped nasal bridge, and prominent upper lip.
Physical exam Findings may include dehydration, hypertension despite volume depletion, cardiac conduction abnormalities (bradyarrhythmias, bundle branch block, complete heart block, asystole), shortened QT interval, potentiation of digoxin toxicity, neurologic deficits (decreased reflexes, proximal weakness, lethargy, coma), psychiatric symptoms (depression, anxiety, psychosis), gastrointestinal symptoms (anorexia, constipation, peptic ulcer disease, pancreatitis), musculoskeletal pain, gout or pseudogout, and renal manifestations including nephrolithiasis and nephrocalcinosis.
Essential workup Measure serum calcium and albumin to assess corrected calcium. Evaluate for symptoms of severe hypercalcemia or impending parathyroid crisis. If asymptomatic with normal ECG and corrected calcium <14 mg/dL, no further ED testing is required. If symptomatic or calcium ≥14 mg/dL, obtain ionized calcium, electrolytes, BUN/creatinine, phosphorus, magnesium, alkaline phosphatase, ESR, TSH, CBC, and chest radiograph.
Diagnosis tests and interpretation
Laboratory Correct calcium for albumin: corrected Ca (mg/dL) = measured Ca + 0.8 × (4 − albumin). Acidosis increases ionized calcium by reducing albumin binding. Phosphorus is typically low in primary hyperparathyroidism and elevated in secondary disease. Chloride-to-phosphate ratio >33 favors hyperparathyroidism; <30 suggests malignancy. Alkaline phosphatase is elevated in ~50% of cases. ESR and anemia are usually normal in hyperparathyroidism but elevated in malignancy or granulomatous disease. Magnesium is often low or low-normal. PTH is elevated in primary and secondary hyperparathyroidism. PTH-related peptide suggests malignancy-associated hypercalcemia.
Imaging Chest radiograph evaluates volume status and screens for malignancy or granulomatous disease.
Diagnostic procedures Definitive diagnosis and treatment are established with parathyroidectomy.
Differential diagnosis PTH-mediated causes include primary or secondary hyperparathyroidism and familial hypocalciuric hypercalcemia. Non-PTH causes include malignancy, vitamin D excess or granulomatous disease, immobilization (e.g., Paget disease), and drug-induced hypercalcemia (thiazides, lithium, vitamin A, aluminum antacids, estrogens, androgens, tamoxifen).
Treatment
Prehospital May present primarily with psychiatric manifestations.
Initial stabilization/therapy Place on cardiac monitor if symptomatic or calcium >14 mg/dL. Begin IV hydration with 0.9% normal saline and correct acidosis.
Emergency department management Treat hypercalcemia with aggressive isotonic saline hydration (≥250 mL/hr unless limited by heart failure) targeting urine output ≥100 mL/hr. After adequate hydration, add loop diuretics to enhance calciuresis; avoid thiazides. Consider glucocorticoids in vitamin D–mediated or granulomatous disease. Initiate bisphosphonates in coordination with endocrinology. Treat dysrhythmias conventionally and use extreme caution with digoxin. Stop contributing medications and monitor closely for heart failure and electrolyte disturbances. Use calcitonin when hydration is contraindicated and initiate dialysis for refractory hypercalcemia with renal failure.
Medication First line Normal saline infusion; furosemide 40 mg IV q2–4h after rehydration; prednisone 40–60 mg PO or hydrocortisone 100 mg IV. Second line (with endocrinology) Calcitonin salmon 4 U/kg SC q12h; pamidronate 60–90 mg IV depending on calcium level; zoledronic acid 4 mg IV; cinacalcet 30 mg PO daily or BID for secondary hyperparathyroidism or carcinoma.
Follow-up and disposition
Admission criteria Corrected calcium >14 mg/dL, symptomatic hypercalcemia, or cardiac conduction abnormalities.
Discharge criteria Asymptomatic patients with calcium <14 mg/dL who can maintain hydration.
Issues for referral Endocrinology referral for PTH evaluation and definitive management.
Follow-up recommendations Arrange outpatient PTH testing, reinforce hydration, and discontinue medications that increase calcium levels.
Key points Hyperparathyroid-related hypercalcemia is often mild and rarely exceeds 14 mg/dL; higher levels suggest malignancy. Measure ionized or albumin-corrected calcium. Administering loop diuretics before adequate hydration worsens hypercalcemia and is a common management error.
- Published on
Emergency And Acute Medicine: Hyperosmolar Syndrome
Basics
Description Hyperosmolar syndrome results from relative insulin deficiency in undiagnosed or poorly controlled diabetes. Sustained hyperglycemia causes osmotic diuresis leading to profound dehydration; extracellular volume is maintained initially at the expense of intracellular dehydration, eventually resulting in severe total body water and electrolyte deficits (H₂O, Na⁺, Cl⁻, K⁺, PO₄⁻, Ca²⁺, Mg²⁺). Unlike diabetic ketoacidosis (DKA), severe ketoacidosis is absent because residual insulin suppresses lipolysis and ketone production.
Geriatric considerations Most common in elderly patients with type 2 diabetes, often precipitated by acute illness and reduced renal function; 30–40% present with new-onset diabetes.
Pediatric considerations Hyperosmolar hyperglycemic states are rare in children.
Etiology Precipitated by factors that impair insulin action, increase glucose load, or limit fluid replacement. Infection is the most common trigger (32–60%). Other causes include medication nonadherence, dietary indiscretion, pneumonia, UTI, sepsis, diuretics, beta-blockers, calcium channel blockers, phenytoin, cimetidine, amphetamines, ethanol, myocardial infarction, stroke, renal failure, heat stroke, pancreatitis, bowel obstruction, endocrine disorders, and burns.
Diagnosis
Signs and symptoms Develop over days to weeks and include polyuria, polydipsia, weight loss, dizziness, weakness, fatigue, blurred vision, and leg cramps.
Physical exam Marked dehydration with tachycardia, hypotension, orthostasis, dry mucous membranes, decreased skin turgor, sunken eyes, collapsed neck veins, preserved urine output until late, altered mental status ranging from lethargy to coma, seizures, focal neurologic deficits, and evidence of a precipitating illness.
Essential workup Diagnostic criteria include serum glucose ≥600 mg/dL (often >1,000 mg/dL), minimal ketosis, pH ≥7.30, bicarbonate ≥15 mEq/L, and effective serum osmolality >320 mOsm/kg (2 × Na⁺ + glucose/18).
Diagnosis tests and interpretation
Laboratory Obtain comprehensive studies to confirm diagnosis and identify triggers. Electrolytes may show elevated or normal potassium despite large total body deficit; mild anion gap acidosis may be present from lactic acid or renal insufficiency. Correct sodium for hyperglycemia: corrected Na⁺ = measured Na⁺ + 1.6 × [(glucose − 100)/100]. BUN and creatinine are elevated from prerenal and intrinsic renal causes. VBG or ABG assesses pH; ABG if mixed disorders suspected. Check serum ketones, β-hydroxybutyrate, lactate when pH <7.3 or anion gap is high. Measure serum osmolality. CBC may show leukocytosis and hemoconcentration. Lipase and amylase may be elevated with or without pancreatitis. Urinalysis evaluates glucose, ketones, and infection. Check magnesium, calcium, phosphate, blood cultures if septic, creatine kinase for rhabdomyolysis, pregnancy test when appropriate, and cardiac enzymes for ischemia.
Imaging Chest radiograph for pneumonia; head CT for altered mental status or focal deficits.
ECG Evaluate for electrolyte-related conduction abnormalities and ischemia.
Differential diagnosis Differentiate from DKA; mixed HHS/DKA occurs in up to one-third of cases. Evaluate other causes of metabolic acidosis if present (lactic acidosis, sepsis, hypoperfusion, postictal states).
Treatment
Prehospital Initiate IV fluids and stabilization.
Initial stabilization/therapy Secure airway in comatose patients, initiate cardiac monitoring, obtain IV access, check glucose, and give naloxone and thiamine when coma etiology is unclear. Restore hemodynamics with 0.9% normal saline 1–2 L in the first hour; larger volumes may be required to establish urine output.
Emergency department management Reassess volume status and mental state frequently. Check electrolytes and glucose hourly initially. Search for and treat precipitating illness. Fluids Begin with 0.9% normal saline 1–2 L over 1–2 hours to restore intravascular volume, then transition to 0.45% saline. Estimate total body water deficit: TBW deficit = 0.6 × weight (kg) × (1 − 140/corrected Na⁺); average deficit ≈9 L. Replace ~50% in the first 12 hours. Switch to D5 ½ NS when glucose <250 mg/dL. Potassium Anticipate large deficits (≈5–10 mEq/kg). Begin replacement after urine output is established and if K⁺ ≤5 mEq/L. If K⁺ 4–5 mEq/L, add 20–30 mEq to first liter, then ~20 mEq/hr. If K⁺ 3–4 mEq/L, give 40 mEq in first liter. If K⁺ <3 mEq/L, hold insulin and replete until >3.3 mEq/L. Monitor K⁺ every 1–2 hours. Insulin Not used early. Start only after hemodynamic stability and K⁺ >3.3 mEq/L; some patients improve with fluids alone. Use IV infusion (0.05–0.1 U/kg/hr), targeting glucose decline of 50–90 mg/dL/hr; faster correction increases cerebral edema risk. Reduce rate when glucose <250 mg/dL and maintain 150–200 mg/dL until bicarbonate >18 mEq/L and pH >7.3. Phosphate Replace only if <1 mg/dL. Magnesium Supplement cautiously, especially in renal failure. Anticoagulation Consider prophylactic heparin due to thrombotic risk; monitor for MI, PE, and mesenteric ischemia.
Medication Insulin infusion 0.05–0.1 U/kg/hr; magnesium sulfate as indicated; potassium phosphate IV or PO per level; naloxone 2 mg IV; thiamine 100 mg IV.
Follow-up and disposition
Admission criteria Nearly all cases require ICU admission for frequent labs and monitoring during the first 24 hours; select mild cases may be observed 12–24 hours.
Discharge criteria Patients meeting HHS criteria should not be discharged; only mild hyperglycemia with normal osmolality after correction may be considered.
Issues for referral Arrange endocrinology and primary care follow-up within one week for long-term glycemic management.
Key points Always identify and treat the precipitating cause. Avoid rapid glucose correction to prevent hypotension and cerebral edema. Transition fluids appropriately to prevent hypernatremia or cellular edema. Prevent hypokalemia proactively. Avoid phenytoin for seizures as it inhibits endogenous insulin release.
Basics
Description Hyperosmolar syndrome results from relative insulin deficiency in undiagnosed or poorly controlled diabetes. Sustained hyperglycemia causes osmotic diuresis leading to profound dehydration; extracellular volume is maintained initially at the expense of intracellular dehydration, eventually resulting in severe total body water and electrolyte deficits (H₂O, Na⁺, Cl⁻, K⁺, PO₄⁻, Ca²⁺, Mg²⁺). Unlike diabetic ketoacidosis (DKA), severe ketoacidosis is absent because residual insulin suppresses lipolysis and ketone production.
Geriatric considerations Most common in elderly patients with type 2 diabetes, often precipitated by acute illness and reduced renal function; 30–40% present with new-onset diabetes.
Pediatric considerations Hyperosmolar hyperglycemic states are rare in children.
Etiology Precipitated by factors that impair insulin action, increase glucose load, or limit fluid replacement. Infection is the most common trigger (32–60%). Other causes include medication nonadherence, dietary indiscretion, pneumonia, UTI, sepsis, diuretics, beta-blockers, calcium channel blockers, phenytoin, cimetidine, amphetamines, ethanol, myocardial infarction, stroke, renal failure, heat stroke, pancreatitis, bowel obstruction, endocrine disorders, and burns.
Diagnosis
Signs and symptoms Develop over days to weeks and include polyuria, polydipsia, weight loss, dizziness, weakness, fatigue, blurred vision, and leg cramps.
Physical exam Marked dehydration with tachycardia, hypotension, orthostasis, dry mucous membranes, decreased skin turgor, sunken eyes, collapsed neck veins, preserved urine output until late, altered mental status ranging from lethargy to coma, seizures, focal neurologic deficits, and evidence of a precipitating illness.
Essential workup Diagnostic criteria include serum glucose ≥600 mg/dL (often >1,000 mg/dL), minimal ketosis, pH ≥7.30, bicarbonate ≥15 mEq/L, and effective serum osmolality >320 mOsm/kg (2 × Na⁺ + glucose/18).
Diagnosis tests and interpretation
Laboratory Obtain comprehensive studies to confirm diagnosis and identify triggers. Electrolytes may show elevated or normal potassium despite large total body deficit; mild anion gap acidosis may be present from lactic acid or renal insufficiency. Correct sodium for hyperglycemia: corrected Na⁺ = measured Na⁺ + 1.6 × [(glucose − 100)/100]. BUN and creatinine are elevated from prerenal and intrinsic renal causes. VBG or ABG assesses pH; ABG if mixed disorders suspected. Check serum ketones, β-hydroxybutyrate, lactate when pH <7.3 or anion gap is high. Measure serum osmolality. CBC may show leukocytosis and hemoconcentration. Lipase and amylase may be elevated with or without pancreatitis. Urinalysis evaluates glucose, ketones, and infection. Check magnesium, calcium, phosphate, blood cultures if septic, creatine kinase for rhabdomyolysis, pregnancy test when appropriate, and cardiac enzymes for ischemia.
Imaging Chest radiograph for pneumonia; head CT for altered mental status or focal deficits.
ECG Evaluate for electrolyte-related conduction abnormalities and ischemia.
Differential diagnosis Differentiate from DKA; mixed HHS/DKA occurs in up to one-third of cases. Evaluate other causes of metabolic acidosis if present (lactic acidosis, sepsis, hypoperfusion, postictal states).
Treatment
Prehospital Initiate IV fluids and stabilization.
Initial stabilization/therapy Secure airway in comatose patients, initiate cardiac monitoring, obtain IV access, check glucose, and give naloxone and thiamine when coma etiology is unclear. Restore hemodynamics with 0.9% normal saline 1–2 L in the first hour; larger volumes may be required to establish urine output.
Emergency department management Reassess volume status and mental state frequently. Check electrolytes and glucose hourly initially. Search for and treat precipitating illness. Fluids Begin with 0.9% normal saline 1–2 L over 1–2 hours to restore intravascular volume, then transition to 0.45% saline. Estimate total body water deficit: TBW deficit = 0.6 × weight (kg) × (1 − 140/corrected Na⁺); average deficit ≈9 L. Replace ~50% in the first 12 hours. Switch to D5 ½ NS when glucose <250 mg/dL. Potassium Anticipate large deficits (≈5–10 mEq/kg). Begin replacement after urine output is established and if K⁺ ≤5 mEq/L. If K⁺ 4–5 mEq/L, add 20–30 mEq to first liter, then ~20 mEq/hr. If K⁺ 3–4 mEq/L, give 40 mEq in first liter. If K⁺ <3 mEq/L, hold insulin and replete until >3.3 mEq/L. Monitor K⁺ every 1–2 hours. Insulin Not used early. Start only after hemodynamic stability and K⁺ >3.3 mEq/L; some patients improve with fluids alone. Use IV infusion (0.05–0.1 U/kg/hr), targeting glucose decline of 50–90 mg/dL/hr; faster correction increases cerebral edema risk. Reduce rate when glucose <250 mg/dL and maintain 150–200 mg/dL until bicarbonate >18 mEq/L and pH >7.3. Phosphate Replace only if <1 mg/dL. Magnesium Supplement cautiously, especially in renal failure. Anticoagulation Consider prophylactic heparin due to thrombotic risk; monitor for MI, PE, and mesenteric ischemia.
Medication Insulin infusion 0.05–0.1 U/kg/hr; magnesium sulfate as indicated; potassium phosphate IV or PO per level; naloxone 2 mg IV; thiamine 100 mg IV.
Follow-up and disposition
Admission criteria Nearly all cases require ICU admission for frequent labs and monitoring during the first 24 hours; select mild cases may be observed 12–24 hours.
Discharge criteria Patients meeting HHS criteria should not be discharged; only mild hyperglycemia with normal osmolality after correction may be considered.
Issues for referral Arrange endocrinology and primary care follow-up within one week for long-term glycemic management.
Key points Always identify and treat the precipitating cause. Avoid rapid glucose correction to prevent hypotension and cerebral edema. Transition fluids appropriately to prevent hypernatremia or cellular edema. Prevent hypokalemia proactively. Avoid phenytoin for seizures as it inhibits endogenous insulin release.
