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Emergency And Acute Medicine – Henoch–Schönlein Purpura
Basics And Description
Henoch–Schönlein purpura is a small-vessel vasculitis characterized by IgA-mediated inflammation affecting the skin, gastrointestinal tract, kidneys, joints, and, less commonly, the central nervous system. Multisystem involvement may lead to acute, life-threatening complications or long-term sequelae, particularly renal disease. Although often self-limited, careful evaluation and follow-up are essential.
Etiology
The underlying mechanism involves increased serum IgA with formation of circulating IgA immune complexes and mesangial IgA deposition in the glomeruli. The exact cause is unknown, but multiple associations have been identified. These include infections such as group A streptococcus, Mycoplasma, and viral illnesses including varicella and Epstein–Barr virus. Drug associations include penicillin, tetracycline, aspirin, sulfonamides, and erythromycin. Allergens such as insect bites and certain foods including chocolate, milk, and wheat have also been implicated. The condition most commonly affects school-aged children and young adults, occurs more frequently in males than females, is more common in white populations, and has a higher incidence in winter and spring.
Diagnosis – Signs And Symptoms
Patients are often well appearing despite extensive rash. Constitutional symptoms may include malaise, low-grade fever, and recent or current upper respiratory infection. Hypertension may be present when renal involvement develops. Infants younger than 3 months may present with skin findings alone, while children under 2 years may present with isolated facial edema.
Skin Manifestations
A purpuric rash is the hallmark and presenting feature in approximately half of patients, with eventual development in nearly all cases. Lesions begin as blanching pink papules and evolve within 24 hours into palpable purpura measuring 2–3 cm. The rash is typically symmetric, involves gravity-dependent areas such as the lower extremities and buttocks, and may extend to the trunk or upper extremities. Facial involvement is rare. Recurrence occurs in up to 40% of patients, usually within six weeks.
Abdominal Involvement
Abdominal pain occurs in 70–80% of cases and may range from colicky to severe. Gastrointestinal symptoms may precede the rash by up to four weeks. Gastrointestinal bleeding is common and ranges from occult blood loss to severe hemorrhage. Intussusception, usually ileoileal or ileocolic, is a serious complication.
Renal And Genitourinary Involvement
Asymptomatic hematuria is common and occurs in up to 80% of patients. Proteinuria suggests glomerulonephritis. Other manifestations include scrotal pain, testicular swelling, and, in severe cases, renal failure.
Musculoskeletal Involvement
Arthritis or arthralgia occurs in 70–80% of patients, is typically migratory, periarticular, and most commonly affects the knees and ankles. Angioedema may also occur.
Neurologic Involvement
Less common manifestations include headache, seizures, altered mental status, focal neurologic deficits, and visual or speech disturbances. Intracranial hemorrhage is rare but serious.
History
Key elements include recent infections, onset and progression of rash, presence of abdominal pain, vomiting, edema, joint symptoms, and timing and progression of multisystem complaints.
Physical Examination
Assessment should include vital signs with attention to blood pressure, cardiovascular perfusion, abdominal tenderness or distention, palpable masses, evidence of gastrointestinal bleeding, genitourinary examination for testicular involvement, careful skin inspection for nonblanching purpura, and a focused neurologic examination.
Essential Workup
The primary goal is to exclude life-threatening causes of purpura, abdominal pain, hematuria, and neurologic findings.
Diagnostic Tests And Interpretation
Laboratory studies typically show a normal platelet count and may reveal leukocytosis. Coagulation studies are indicated if bleeding is present or diagnosis is uncertain. Electrolytes, blood urea nitrogen, and creatinine should be obtained if hypertension or abnormal urinalysis is present. Urinalysis frequently shows hematuria, and proteinuria suggests renal involvement. Cultures may be obtained to exclude infectious triggers. Abdominal imaging with ultrasound, contrast enema, or CT is indicated for abdominal pain or gastrointestinal bleeding to evaluate for intussusception. Testicular ultrasound is indicated for scrotal symptoms. Head CT is required for neurologic findings. Lumbar puncture is performed only when clinically indicated.
Differential Diagnosis
Important considerations include gastroenteritis, appendicitis, inflammatory bowel disease, Meckel diverticulum, acute glomerulonephritis, systemic lupus erythematosus, polyarteritis nodosa, meningococcemia, bacterial sepsis, Rocky Mountain spotted fever, viral exanthems, thrombocytopenia, drug reactions, testicular torsion, and incarcerated hernia.
Treatment – Prehospital Care
Stabilization should be provided as clinically indicated.
Initial Stabilization And Therapy
Intravenous fluids are administered for shock. Packed red blood cells are indicated for massive gastrointestinal hemorrhage.
Emergency Department Treatment And Procedures
Life-threatening complications require immediate intervention. NSAIDs such as ibuprofen are used for arthralgia. Corticosteroids, typically prednisone, are indicated for severe abdominal pain after exclusion of surgical causes, painful subcutaneous edema, arthritis, significant renal involvement, or central nervous system disease. Severe nephritis may require high-dose pulse methylprednisolone. Immunosuppressive agents and intravenous immunoglobulin may be considered in severe, life-threatening disease, though evidence is limited.
Medications
First-line therapy includes ibuprofen 600 mg orally every 6 hours, or 5–10 mg/kg per dose in children. Second-line therapy includes prednisone 60 mg daily in adults or 1–2 mg/kg/day in children for 5–7 days.
Follow-Up And Disposition
Admission is required for severe abdominal pain, gastrointestinal bleeding, intussusception, central nervous system involvement, or evidence of renal failure. Patients may be discharged if platelet count and renal function are normal and abdominal pain is minimal or absent. Patients started on steroids should have follow-up within 24 hours.
Follow-Up Recommendations
Close follow-up with a primary care physician is required, with regular monitoring of blood pressure and repeat urinalysis and laboratory studies as indicated. In children, monitoring is recommended for at least six months.
Clinical Insights And Common Errors
Always exclude life-threatening causes of purpura and abdominal pain. NSAIDs are sufficient for most patients. Systemic corticosteroids do not alter the long-term prognosis of Henoch–Schönlein purpura nephritis and should be reserved for specific indications.
Basics And Description
Henoch–Schönlein purpura is a small-vessel vasculitis characterized by IgA-mediated inflammation affecting the skin, gastrointestinal tract, kidneys, joints, and, less commonly, the central nervous system. Multisystem involvement may lead to acute, life-threatening complications or long-term sequelae, particularly renal disease. Although often self-limited, careful evaluation and follow-up are essential.
Etiology
The underlying mechanism involves increased serum IgA with formation of circulating IgA immune complexes and mesangial IgA deposition in the glomeruli. The exact cause is unknown, but multiple associations have been identified. These include infections such as group A streptococcus, Mycoplasma, and viral illnesses including varicella and Epstein–Barr virus. Drug associations include penicillin, tetracycline, aspirin, sulfonamides, and erythromycin. Allergens such as insect bites and certain foods including chocolate, milk, and wheat have also been implicated. The condition most commonly affects school-aged children and young adults, occurs more frequently in males than females, is more common in white populations, and has a higher incidence in winter and spring.
Diagnosis – Signs And Symptoms
Patients are often well appearing despite extensive rash. Constitutional symptoms may include malaise, low-grade fever, and recent or current upper respiratory infection. Hypertension may be present when renal involvement develops. Infants younger than 3 months may present with skin findings alone, while children under 2 years may present with isolated facial edema.
Skin Manifestations
A purpuric rash is the hallmark and presenting feature in approximately half of patients, with eventual development in nearly all cases. Lesions begin as blanching pink papules and evolve within 24 hours into palpable purpura measuring 2–3 cm. The rash is typically symmetric, involves gravity-dependent areas such as the lower extremities and buttocks, and may extend to the trunk or upper extremities. Facial involvement is rare. Recurrence occurs in up to 40% of patients, usually within six weeks.
Abdominal Involvement
Abdominal pain occurs in 70–80% of cases and may range from colicky to severe. Gastrointestinal symptoms may precede the rash by up to four weeks. Gastrointestinal bleeding is common and ranges from occult blood loss to severe hemorrhage. Intussusception, usually ileoileal or ileocolic, is a serious complication.
Renal And Genitourinary Involvement
Asymptomatic hematuria is common and occurs in up to 80% of patients. Proteinuria suggests glomerulonephritis. Other manifestations include scrotal pain, testicular swelling, and, in severe cases, renal failure.
Musculoskeletal Involvement
Arthritis or arthralgia occurs in 70–80% of patients, is typically migratory, periarticular, and most commonly affects the knees and ankles. Angioedema may also occur.
Neurologic Involvement
Less common manifestations include headache, seizures, altered mental status, focal neurologic deficits, and visual or speech disturbances. Intracranial hemorrhage is rare but serious.
History
Key elements include recent infections, onset and progression of rash, presence of abdominal pain, vomiting, edema, joint symptoms, and timing and progression of multisystem complaints.
Physical Examination
Assessment should include vital signs with attention to blood pressure, cardiovascular perfusion, abdominal tenderness or distention, palpable masses, evidence of gastrointestinal bleeding, genitourinary examination for testicular involvement, careful skin inspection for nonblanching purpura, and a focused neurologic examination.
Essential Workup
The primary goal is to exclude life-threatening causes of purpura, abdominal pain, hematuria, and neurologic findings.
Diagnostic Tests And Interpretation
Laboratory studies typically show a normal platelet count and may reveal leukocytosis. Coagulation studies are indicated if bleeding is present or diagnosis is uncertain. Electrolytes, blood urea nitrogen, and creatinine should be obtained if hypertension or abnormal urinalysis is present. Urinalysis frequently shows hematuria, and proteinuria suggests renal involvement. Cultures may be obtained to exclude infectious triggers. Abdominal imaging with ultrasound, contrast enema, or CT is indicated for abdominal pain or gastrointestinal bleeding to evaluate for intussusception. Testicular ultrasound is indicated for scrotal symptoms. Head CT is required for neurologic findings. Lumbar puncture is performed only when clinically indicated.
Differential Diagnosis
Important considerations include gastroenteritis, appendicitis, inflammatory bowel disease, Meckel diverticulum, acute glomerulonephritis, systemic lupus erythematosus, polyarteritis nodosa, meningococcemia, bacterial sepsis, Rocky Mountain spotted fever, viral exanthems, thrombocytopenia, drug reactions, testicular torsion, and incarcerated hernia.
Treatment – Prehospital Care
Stabilization should be provided as clinically indicated.
Initial Stabilization And Therapy
Intravenous fluids are administered for shock. Packed red blood cells are indicated for massive gastrointestinal hemorrhage.
Emergency Department Treatment And Procedures
Life-threatening complications require immediate intervention. NSAIDs such as ibuprofen are used for arthralgia. Corticosteroids, typically prednisone, are indicated for severe abdominal pain after exclusion of surgical causes, painful subcutaneous edema, arthritis, significant renal involvement, or central nervous system disease. Severe nephritis may require high-dose pulse methylprednisolone. Immunosuppressive agents and intravenous immunoglobulin may be considered in severe, life-threatening disease, though evidence is limited.
Medications
First-line therapy includes ibuprofen 600 mg orally every 6 hours, or 5–10 mg/kg per dose in children. Second-line therapy includes prednisone 60 mg daily in adults or 1–2 mg/kg/day in children for 5–7 days.
Follow-Up And Disposition
Admission is required for severe abdominal pain, gastrointestinal bleeding, intussusception, central nervous system involvement, or evidence of renal failure. Patients may be discharged if platelet count and renal function are normal and abdominal pain is minimal or absent. Patients started on steroids should have follow-up within 24 hours.
Follow-Up Recommendations
Close follow-up with a primary care physician is required, with regular monitoring of blood pressure and repeat urinalysis and laboratory studies as indicated. In children, monitoring is recommended for at least six months.
Clinical Insights And Common Errors
Always exclude life-threatening causes of purpura and abdominal pain. NSAIDs are sufficient for most patients. Systemic corticosteroids do not alter the long-term prognosis of Henoch–Schönlein purpura nephritis and should be reserved for specific indications.
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Emergency And Acute Medicine – High-Altitude Illness
Basics
Description
High-altitude illness occurs due to hypobaric hypoxia following rapid ascent to higher elevations, typically above 8,000 ft (≈2,500 m), without adequate acclimatization. The incidence depends on the rate of ascent, final altitude reached, sleeping altitude, and duration of exposure.
Acute mountain sickness (AMS) occurs in up to 67% of individuals who ascend rapidly (1–2 days) to elevations above 14,000 ft. Among skiers sleeping at altitude, AMS occurs in approximately 22% at 7,000–9,000 ft and 40% at 10,000 ft.
High-altitude pulmonary edema (HAPE) occurs in fewer than 1–2% of exposed individuals, and high-altitude cerebral edema (HACE) occurs in less than 1%. HAPE and HACE are uncommon below 13,000 ft (≈4,000 m).
Risk Factors
Risk factors for AMS include a prior history of high-altitude illness, rapid ascent, physical exertion, younger age (<50 yr), obesity, and preexisting lung disease. physical fitness does not confer protection.< />pan>
Pregnancy Considerations
The relationship between pregnancy and high-altitude illness is not well defined. Pregnancy-induced hypertension, proteinuria, and peripheral edema are more common at altitude, likely related to maternal hypoxemia. There is no evidence of increased risk of spontaneous abortion or placental complications at moderate altitude. Travel above 13,000 ft should be approached cautiously, especially in complicated pregnancies.
Geriatric Considerations
Although older adults often have comorbidities such as hypertension, COPD, or coronary artery disease, individuals older than 55 years appear to have a lower risk of AMS than younger adults.
Etiology
The primary cause of high-altitude illness is rapid ascent without acclimatization. Susceptibility varies between individuals, and illness is influenced by ascent rate, altitude attained, sleeping altitude, and physiologic response to hypoxia.
Diagnosis
Signs and Symptoms
Acute Mountain Sickness (AMS)
AMS is defined by headache plus at least one of the following: nausea or vomiting, fatigue or lassitude, dizziness, or difficulty sleeping. Symptoms typically begin 4–12 hours after ascent and are usually self-limited but may become debilitating.
High-Altitude Pulmonary Edema (HAPE)
HAPE usually develops 2–4 days after ascent, often on the second night. It is potentially life-threatening and presents with dry cough progressing to productive cough, dyspnea at rest, and decreased exercise tolerance.
High-Altitude Cerebral Edema (HACE)
HACE is life-threatening and typically occurs in patients with AMS and/or HAPE. Onset usually requires 2–4 days but may occur as early as 12 hours after AMS symptoms. Findings include severe headache, nausea and vomiting, altered mental status, and ataxia.
Pediatric Considerations
In infants and young children, AMS may present as irritability, decreased playfulness, reduced appetite, vomiting, and sleep disturbances. HAPE occurs more frequently in individuals younger than 20 years, and cases have not been reported in children younger than 4 years.
Physical Examination
Essential Workup
Diagnosis is primarily clinical in the setting of recent altitude gain.
Diagnostic Tests and Interpretation
Differential Diagnosis
Treatment
Prehospital Care
Severe cases require immediate descent. Further ascent is contraindicated in symptomatic individuals. Supplemental oxygen or simulated descent using a portable hyperbaric chamber (e.g., Gamow bag) may be lifesaving when evacuation is delayed.
Initial Stabilization and Therapy
For HAPE and HACE, prioritize airway, breathing, and circulation. Provide supplemental oxygen, establish IV access, and monitor closely. Endotracheal intubation may be required for respiratory failure or airway protection. CPAP may be beneficial in HAPE.
Emergency Department Treatment and Procedures
AMS
Mild cases are usually self-limited. Management includes halting ascent, symptomatic treatment, acetazolamide for moderate to severe symptoms, analgesics for headache, antiemetics for nausea, and oxygen for severe cases. Descent is required if symptoms persist or worsen.
HAPE
Immediate descent is mandatory for moderate to severe disease. Mild cases may be managed at altitude only if oxygen and close monitoring are available. Bed rest, high-flow supplemental oxygen, and avoidance of exertion are critical. Nifedipine may be used when oxygen or descent is unavailable. Hyperbaric therapy may be used when descent is impossible.
HACE
Immediate evacuation to lower altitude is essential. Administer oxygen and dexamethasone. Maintain bed rest with head elevation and manage elevated intracranial pressure aggressively in severe cases.
Medications
First-Line Therapy
Acetazolamide for AMS, nifedipine for HAPE
Second-Line Therapy
Dexamethasone
Use of multiple medications concurrently is not supported by current evidence.
Follow-Up and Disposition
Admission Criteria
HAPE, HACE, or persistent symptoms after descent and observation require admission.
Discharge Criteria
Patients may be discharged after clinical improvement with oxygen saturation >95% on room air at sea level or appropriate baseline saturation at altitude.
Issues for Referral
Patients with recurrent AMS may benefit from acetazolamide prophylaxis for future ascents. Those with prior HAPE may benefit from nifedipine prophylaxis.
Clinical Pearls and Pitfalls
High-altitude illness often mimics viral syndromes, leading to missed diagnosis. Once symptoms develop, further ascent is contraindicated until complete resolution. Ataxia and dyspnea at rest are early warning signs of HACE and HAPE, respectively. When descent is not possible, hyperbaric therapy and adjunctive medications should be considered promptly.
Basics
Description
High-altitude illness occurs due to hypobaric hypoxia following rapid ascent to higher elevations, typically above 8,000 ft (≈2,500 m), without adequate acclimatization. The incidence depends on the rate of ascent, final altitude reached, sleeping altitude, and duration of exposure.
Acute mountain sickness (AMS) occurs in up to 67% of individuals who ascend rapidly (1–2 days) to elevations above 14,000 ft. Among skiers sleeping at altitude, AMS occurs in approximately 22% at 7,000–9,000 ft and 40% at 10,000 ft.
High-altitude pulmonary edema (HAPE) occurs in fewer than 1–2% of exposed individuals, and high-altitude cerebral edema (HACE) occurs in less than 1%. HAPE and HACE are uncommon below 13,000 ft (≈4,000 m).
Risk Factors
Risk factors for AMS include a prior history of high-altitude illness, rapid ascent, physical exertion, younger age (<50 yr), obesity, and preexisting lung disease. physical fitness does not confer protection.< />pan>
Pregnancy Considerations
The relationship between pregnancy and high-altitude illness is not well defined. Pregnancy-induced hypertension, proteinuria, and peripheral edema are more common at altitude, likely related to maternal hypoxemia. There is no evidence of increased risk of spontaneous abortion or placental complications at moderate altitude. Travel above 13,000 ft should be approached cautiously, especially in complicated pregnancies.
Geriatric Considerations
Although older adults often have comorbidities such as hypertension, COPD, or coronary artery disease, individuals older than 55 years appear to have a lower risk of AMS than younger adults.
Etiology
The primary cause of high-altitude illness is rapid ascent without acclimatization. Susceptibility varies between individuals, and illness is influenced by ascent rate, altitude attained, sleeping altitude, and physiologic response to hypoxia.
Diagnosis
Signs and Symptoms
Acute Mountain Sickness (AMS)
AMS is defined by headache plus at least one of the following: nausea or vomiting, fatigue or lassitude, dizziness, or difficulty sleeping. Symptoms typically begin 4–12 hours after ascent and are usually self-limited but may become debilitating.
High-Altitude Pulmonary Edema (HAPE)
HAPE usually develops 2–4 days after ascent, often on the second night. It is potentially life-threatening and presents with dry cough progressing to productive cough, dyspnea at rest, and decreased exercise tolerance.
High-Altitude Cerebral Edema (HACE)
HACE is life-threatening and typically occurs in patients with AMS and/or HAPE. Onset usually requires 2–4 days but may occur as early as 12 hours after AMS symptoms. Findings include severe headache, nausea and vomiting, altered mental status, and ataxia.
Pediatric Considerations
In infants and young children, AMS may present as irritability, decreased playfulness, reduced appetite, vomiting, and sleep disturbances. HAPE occurs more frequently in individuals younger than 20 years, and cases have not been reported in children younger than 4 years.
Physical Examination
- AMS: Often normal examination; mild cases may mimic viral illness or alcohol hangover.
- HAPE: Tachypnea, rales, cyanosis, possible fever, and signs of respiratory distress.
- HACE: Ataxia, altered mental status, papilledema, retinal hemorrhages, seizures (rare), and coma in severe cases.
Essential Workup
Diagnosis is primarily clinical in the setting of recent altitude gain.
Diagnostic Tests and Interpretation
- AMS: No laboratory or imaging studies required.
- HAPE:
- Arterial blood gas: Hypoxemia (PaO₂ 30–50 mm Hg) with respiratory alkalosis
- Chest radiograph: Patchy alveolar infiltrates with areas of sparing; cardiomegaly and classic signs of cardiogenic pulmonary edema are typically absent
- ECG: Tachycardia, possible right-heart strain
- HACE:
- CT or MRI: Vasogenic edema of the cerebral white matter
Differential Diagnosis
- AMS: Viral syndrome, alcohol hangover, carbon monoxide poisoning, meningitis, encephalitis, exhaustion
- HAPE: Pneumonia, pulmonary embolism (typically more acute with pleuritic chest pain), high-altitude bronchitis
- HACE: Stroke or transient ischemic attack (focal deficits suggest vascular etiology)
Treatment
Prehospital Care
Severe cases require immediate descent. Further ascent is contraindicated in symptomatic individuals. Supplemental oxygen or simulated descent using a portable hyperbaric chamber (e.g., Gamow bag) may be lifesaving when evacuation is delayed.
Initial Stabilization and Therapy
For HAPE and HACE, prioritize airway, breathing, and circulation. Provide supplemental oxygen, establish IV access, and monitor closely. Endotracheal intubation may be required for respiratory failure or airway protection. CPAP may be beneficial in HAPE.
Emergency Department Treatment and Procedures
AMS
Mild cases are usually self-limited. Management includes halting ascent, symptomatic treatment, acetazolamide for moderate to severe symptoms, analgesics for headache, antiemetics for nausea, and oxygen for severe cases. Descent is required if symptoms persist or worsen.
HAPE
Immediate descent is mandatory for moderate to severe disease. Mild cases may be managed at altitude only if oxygen and close monitoring are available. Bed rest, high-flow supplemental oxygen, and avoidance of exertion are critical. Nifedipine may be used when oxygen or descent is unavailable. Hyperbaric therapy may be used when descent is impossible.
HACE
Immediate evacuation to lower altitude is essential. Administer oxygen and dexamethasone. Maintain bed rest with head elevation and manage elevated intracranial pressure aggressively in severe cases.
Medications
- Acetazolamide:
- AMS treatment: 250–500 mg PO BID (peds: 5 mg/kg PO BID)
- AMS prophylaxis: 250 mg PO BID starting 24 hr before ascent
- Dexamethasone: 8 mg IV, then 4 mg PO/IV QID
- Ibuprofen: 800 mg PO TID (peds: 5–10 mg/kg)
- Nifedipine: 10 mg PO, then 30 mg sustained release PO daily
- Promethazine: 12.5–25 mg PO/IM/PR q4–6h
First-Line Therapy
Acetazolamide for AMS, nifedipine for HAPE
Second-Line Therapy
Dexamethasone
Use of multiple medications concurrently is not supported by current evidence.
Follow-Up and Disposition
Admission Criteria
HAPE, HACE, or persistent symptoms after descent and observation require admission.
Discharge Criteria
Patients may be discharged after clinical improvement with oxygen saturation >95% on room air at sea level or appropriate baseline saturation at altitude.
Issues for Referral
Patients with recurrent AMS may benefit from acetazolamide prophylaxis for future ascents. Those with prior HAPE may benefit from nifedipine prophylaxis.
Clinical Pearls and Pitfalls
High-altitude illness often mimics viral syndromes, leading to missed diagnosis. Once symptoms develop, further ascent is contraindicated until complete resolution. Ataxia and dyspnea at rest are early warning signs of HACE and HAPE, respectively. When descent is not possible, hyperbaric therapy and adjunctive medications should be considered promptly.
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Emergency And Acute Medicine – Hiccups
Basics
Description
Hiccups are sudden, involuntary contractions of the diaphragm (usually unilateral) and other inspiratory muscles, abruptly terminated by closure of the glottis. The medical term is singultus. Episodes typically occur at a frequency of 4–60 per minute and result from stimulation of the hiccup reflex arc involving irritation of the vagus and phrenic nerves. The hiccup center is believed to be located in the upper spinal cord or brainstem.
Classification includes hiccup bouts lasting less than 48 hours, persistent hiccups lasting 48 hours to 1 month, and intractable hiccups persisting longer than 1 month. Hiccups are more common in males than females (approximately 4:1).
Etiology
Gastrointestinal causes include gastric distention, overeating, rapid eating, gastroesophageal reflux disease, achalasia, candida esophagitis, esophageal or gastric cancer, ulcers, hepatitis, hepatoma, pancreatitis, pancreatic pseudocyst or cancer, bowel obstruction, inflammatory bowel disease, cholelithiasis, cholecystitis, appendicitis, abdominal aortic aneurysm, and postoperative or post–abdominal procedures.
Diaphragmatic irritation may result from hiatal hernia, intra-abdominal mass, pericarditis, diaphragmatic eventration, splenomegaly, hepatomegaly, or peritonitis.
Central nervous system causes include ischemic or hemorrhagic stroke, head trauma, arteriovenous malformations, encephalitis, meningitis, abscess, malignancy, Parkinson disease, multiple sclerosis, hydrocephalus, and ventriculoperitoneal shunts.
Thoracic causes include pneumonia, tuberculosis, myocardial infarction, pericarditis, aortic aneurysm, malignancy, and mediastinal lymphadenopathy.
Head and neck causes include otic foreign bodies irritating the tympanic membrane, pharyngitis, laryngitis, goiter, retropharyngeal or peritonsillar abscess, and neck masses.
Metabolic causes include uremia, hyponatremia, hypocalcemia, gout, and diabetes mellitus.
Toxic and drug-related causes include alcohol, tobacco, α-methyldopa, benzodiazepines, steroids, barbiturates, narcotics, chemotherapeutic agents, antibiotics, and general anesthesia.
Psychogenic causes include stress, excitement, grief, malingering, and conversion disorder. Many cases remain idiopathic.
Diagnosis
Signs And Symptoms
Hiccups produce a characteristic sound that abruptly ends an inspiratory effort. Attacks usually occur at brief intervals and last seconds to minutes. Episodes persisting longer than 48 hours or continuing during sleep strongly suggest an underlying organic cause.
History
A targeted history should assess the severity and duration of the current episode, prior episodes, previous treatment attempts, and associated symptoms that may suggest an underlying etiology.
Physical Examination
A focused examination should evaluate the head and neck, chest, abdomen, and neurologic system to identify potential causes.
Essential Workup
For persistent or intractable hiccups, further evaluation is guided by findings from the history and physical examination.
Diagnostic Tests And Interpretation
Laboratory evaluation may include a complete blood count with differential and measurement of electrolytes, blood urea nitrogen, and creatinine. A chest radiograph is commonly obtained. Additional imaging or testing should be based on clinical suspicion and is often appropriate for outpatient evaluation.
Differential Diagnosis
Eructation (belching).
Treatment
Emergency Department Treatment And Procedures
Specific causes should be treated when identified, such as removal of an ear foreign body or decompression of gastric distention with a nasogastric tube.
Nonpharmacologic maneuvers include posterior pharyngeal stimulation with a catheter or cotton swab, direct uvular stimulation, supraorbital pressure, carotid sinus massage, digital rectal massage, and suboccipital release with gentle traction and pressure to the posterior neck.
Pharmacologic therapy includes chlorpromazine, the only FDA-approved medication for hiccups. Other agents used include gabapentin, metoclopramide, baclofen, haloperidol, nebulized lidocaine, amitriptyline, and phenytoin.
Medications
Amitriptyline 10 mg PO TID
Baclofen 10 mg PO TID
Chlorpromazine 25–50 mg IV or IM, or 25–50 mg PO BID–TID
Gabapentin 100 mg PO TID–QID
Haloperidol 2–5 mg IM
Lidocaine 4% solution, 3 mL nebulized, may repeat
Metoclopramide 10 mg IV or IM, or 10–20 mg PO QID
Phenytoin 200 mg IV
Follow-Up And Disposition
Admission Criteria
Admission is indicated when hiccups interfere with daily activities or lead to complications such as poor oral intake, aspiration, insomnia, or wound dehiscence.
Discharge Criteria
Patients may be discharged if hiccups last less than 48 hours and evaluation does not suggest an underlying organic cause.
Issues For Referral
Referral is recommended for intractable hiccups requiring further investigation or advanced therapies such as phrenic nerve block or transection, hypnosis, behavioral modification, acupuncture, or psychiatric intervention.
Follow-Up Recommendations
Patients may try home remedies for recurrence, including swallowing a spoonful of sugar, sucking on hard candy, swallowing peanut butter, breath holding or Valsalva maneuver, biting a lemon, tongue traction, lifting the uvula with a cold spoon, drinking from the far side of a glass, applying noxious stimuli, or rebreathing into a paper bag.
Clinical Insights And Common Pitfalls
Prolonged or persistent hiccups are strongly suggestive of an underlying organic disease and should not be dismissed as benign without appropriate evaluation.
Basics
Description
Hiccups are sudden, involuntary contractions of the diaphragm (usually unilateral) and other inspiratory muscles, abruptly terminated by closure of the glottis. The medical term is singultus. Episodes typically occur at a frequency of 4–60 per minute and result from stimulation of the hiccup reflex arc involving irritation of the vagus and phrenic nerves. The hiccup center is believed to be located in the upper spinal cord or brainstem.
Classification includes hiccup bouts lasting less than 48 hours, persistent hiccups lasting 48 hours to 1 month, and intractable hiccups persisting longer than 1 month. Hiccups are more common in males than females (approximately 4:1).
Etiology
Gastrointestinal causes include gastric distention, overeating, rapid eating, gastroesophageal reflux disease, achalasia, candida esophagitis, esophageal or gastric cancer, ulcers, hepatitis, hepatoma, pancreatitis, pancreatic pseudocyst or cancer, bowel obstruction, inflammatory bowel disease, cholelithiasis, cholecystitis, appendicitis, abdominal aortic aneurysm, and postoperative or post–abdominal procedures.
Diaphragmatic irritation may result from hiatal hernia, intra-abdominal mass, pericarditis, diaphragmatic eventration, splenomegaly, hepatomegaly, or peritonitis.
Central nervous system causes include ischemic or hemorrhagic stroke, head trauma, arteriovenous malformations, encephalitis, meningitis, abscess, malignancy, Parkinson disease, multiple sclerosis, hydrocephalus, and ventriculoperitoneal shunts.
Thoracic causes include pneumonia, tuberculosis, myocardial infarction, pericarditis, aortic aneurysm, malignancy, and mediastinal lymphadenopathy.
Head and neck causes include otic foreign bodies irritating the tympanic membrane, pharyngitis, laryngitis, goiter, retropharyngeal or peritonsillar abscess, and neck masses.
Metabolic causes include uremia, hyponatremia, hypocalcemia, gout, and diabetes mellitus.
Toxic and drug-related causes include alcohol, tobacco, α-methyldopa, benzodiazepines, steroids, barbiturates, narcotics, chemotherapeutic agents, antibiotics, and general anesthesia.
Psychogenic causes include stress, excitement, grief, malingering, and conversion disorder. Many cases remain idiopathic.
Diagnosis
Signs And Symptoms
Hiccups produce a characteristic sound that abruptly ends an inspiratory effort. Attacks usually occur at brief intervals and last seconds to minutes. Episodes persisting longer than 48 hours or continuing during sleep strongly suggest an underlying organic cause.
History
A targeted history should assess the severity and duration of the current episode, prior episodes, previous treatment attempts, and associated symptoms that may suggest an underlying etiology.
Physical Examination
A focused examination should evaluate the head and neck, chest, abdomen, and neurologic system to identify potential causes.
Essential Workup
For persistent or intractable hiccups, further evaluation is guided by findings from the history and physical examination.
Diagnostic Tests And Interpretation
Laboratory evaluation may include a complete blood count with differential and measurement of electrolytes, blood urea nitrogen, and creatinine. A chest radiograph is commonly obtained. Additional imaging or testing should be based on clinical suspicion and is often appropriate for outpatient evaluation.
Differential Diagnosis
Eructation (belching).
Treatment
Emergency Department Treatment And Procedures
Specific causes should be treated when identified, such as removal of an ear foreign body or decompression of gastric distention with a nasogastric tube.
Nonpharmacologic maneuvers include posterior pharyngeal stimulation with a catheter or cotton swab, direct uvular stimulation, supraorbital pressure, carotid sinus massage, digital rectal massage, and suboccipital release with gentle traction and pressure to the posterior neck.
Pharmacologic therapy includes chlorpromazine, the only FDA-approved medication for hiccups. Other agents used include gabapentin, metoclopramide, baclofen, haloperidol, nebulized lidocaine, amitriptyline, and phenytoin.
Medications
Amitriptyline 10 mg PO TID
Baclofen 10 mg PO TID
Chlorpromazine 25–50 mg IV or IM, or 25–50 mg PO BID–TID
Gabapentin 100 mg PO TID–QID
Haloperidol 2–5 mg IM
Lidocaine 4% solution, 3 mL nebulized, may repeat
Metoclopramide 10 mg IV or IM, or 10–20 mg PO QID
Phenytoin 200 mg IV
Follow-Up And Disposition
Admission Criteria
Admission is indicated when hiccups interfere with daily activities or lead to complications such as poor oral intake, aspiration, insomnia, or wound dehiscence.
Discharge Criteria
Patients may be discharged if hiccups last less than 48 hours and evaluation does not suggest an underlying organic cause.
Issues For Referral
Referral is recommended for intractable hiccups requiring further investigation or advanced therapies such as phrenic nerve block or transection, hypnosis, behavioral modification, acupuncture, or psychiatric intervention.
Follow-Up Recommendations
Patients may try home remedies for recurrence, including swallowing a spoonful of sugar, sucking on hard candy, swallowing peanut butter, breath holding or Valsalva maneuver, biting a lemon, tongue traction, lifting the uvula with a cold spoon, drinking from the far side of a glass, applying noxious stimuli, or rebreathing into a paper bag.
Clinical Insights And Common Pitfalls
Prolonged or persistent hiccups are strongly suggestive of an underlying organic disease and should not be dismissed as benign without appropriate evaluation.
- Published on
Emergency And Acute Medicine – Genital Herpes
Overview And Definition
Genital herpes is a lifelong, recurrent viral infection caused by herpes simplex virus (HSV). Approximately one in four Americans older than 30 years are seropositive for HSV-2, though most are asymptomatic. The infection is characterized by periods of latency and reactivation, with viral shedding that can occur even in the absence of visible lesions, contributing to ongoing transmission.
Disease Course And Natural History
Primary infection has an incubation period of approximately 2–12 days, with symptoms typically peaking 8–10 days after onset and lesions healing within about three weeks. Primary disease may present with a more severe clinical syndrome and complications such as meningitis, encephalitis, or hepatitis. Importantly, more than half of first recognized episodes are not true primary infections, as earlier asymptomatic exposure is common.
Recurrent infection results from viral reactivation in the dorsal root ganglia. The average patient experiences about four recurrences per year. Recurrences are generally milder, involve fewer lesions, and resolve within 10 days. HSV-1 genital infections recur significantly less often than HSV-2.
Asymptomatic infection is common, with intermittent viral shedding that frequently leads to transmission by individuals without symptoms or lesions.
Etiology And Risk Factors
Most cases (70–90%) of genital herpes are caused by HSV-2, with the remainder caused by HSV-1. Genital HSV-1 infections are increasing in prevalence, likely due to higher rates of oral–genital contact and reduced childhood exposure to HSV-1, leaving more adolescents and adults susceptible. Acquisition of HSV-2 in individuals with prior HSV-1 infection tends to be less symptomatic, whereas acquisition of HSV-1 in those with HSV-2 is uncommon.
Genital herpes is strongly associated with HIV and other sexually transmitted infections. HSV infection increases both susceptibility to HIV and HIV viral shedding during HSV reactivation. Despite extensive research, no effective HSV vaccine is currently available.
Clinical Manifestations
Patients commonly report local pain, itching, or burning. A prodrome of tingling, itching, or pain may occur 1–2 days before lesion eruption and can sometimes mimic radicular pain such as sciatica. Lesions typically begin as macules and papules, progress to vesicles and pustules, and then ulcerate by approximately day five. Skin lesions crust over, whereas mucosal lesions heal without crusting.
Associated manifestations may include herpetic cervicitis, vaginitis, or urethritis, presenting with dysuria, urinary hesitancy or retention, vaginal discharge, or pelvic pain. Systemic symptoms such as fever, malaise, headache, myalgias, photophobia, anorexia, and lymphadenopathy are more common during primary infection.
Physical Examination Findings
Examination may reveal grouped vesicles on an erythematous base involving the vulva, vagina, cervix, perineum, buttocks, penile shaft, or glans. On moist mucosal surfaces, ulcers may predominate. Atypical findings include localized edema, erythema, fissures, or crusts.
Special Populations
Pediatric patients with genital herpes require careful evaluation, as neonatal infection is often disseminated or involves the central nervous system and carries high morbidity and mortality. Congenital HSV infection without vesicles may resemble other congenital infections. Sexual abuse must be considered in children with genital HSV, and evaluation for other sexually transmitted infections is recommended.
Pregnancy is a high-risk context, particularly with primary infection, which is associated with significant neonatal morbidity. Suppressive antiviral therapy after 36 weeks’ gestation reduces lesion recurrence at delivery and lowers cesarean section rates.
Diagnostic Approach
Diagnosis is usually clinical, based on history and examination. Laboratory testing is useful when confirmation is needed or in atypical or severe cases. Viral culture from vesicle fluid or ulcer base is positive in most early lesions but loses sensitivity as lesions heal. PCR testing is more sensitive and is the diagnostic test of choice, especially for central nervous system involvement. Serologic testing detects prior exposure but is not useful for diagnosing acute disease, as it cannot distinguish recent from chronic infection.
Differential Diagnosis
Important considerations include syphilis, chancroid, lymphogranuloma venereum, granuloma inguinale, candidiasis, and Behçet syndrome.
Emergency Management
Treatment reduces symptom severity and duration but does not eradicate latent virus or prevent future recurrences once therapy is stopped.
Episodic therapy for recurrences shortens lesion duration if started during the prodrome or within one day of lesion onset.
Suppressive therapy, recommended for patients with frequent recurrences (six or more per year), reduces recurrence frequency by approximately 75% and decreases viral shedding.
Severe disease, systemic involvement, or infection in immunocompromised patients requires intravenous antiviral therapy. Resistance to acyclovir occurs in a minority of immunocompromised patients, in which case foscarnet may be effective. Women with urinary retention may require bladder catheterization due to sacral nerve involvement.
Pharmacologic Treatment
First-episode, recurrent, suppressive, and HIV-associated genital herpes are treated with oral or intravenous acyclovir, valacyclovir, or famciclovir, with regimen selection based on severity, immune status, and recurrence pattern. Dosing adjustments may be necessary in renal impairment.
Disposition And Counseling
Hospital admission is indicated for patients with central nervous system involvement, disseminated disease, severe pain or urinary retention, or significant immunosuppression. Immunocompetent patients without systemic involvement can be managed as outpatients.
Discharge counseling is essential and should emphasize avoidance of sexual contact during prodrome and active lesions, consistent use of barrier protection even when asymptomatic, and the lifelong nature of infection. Patients should be informed about the likelihood of recurrence and the option of suppressive therapy.
Key Clinical Pearls
Primary genital herpes may be severe and should be treated promptly. Always consider sexual abuse in children presenting with genital HSV. Genital herpes is lifelong, with intermittent asymptomatic shedding that plays a major role in transmission.
Overview And Definition
Genital herpes is a lifelong, recurrent viral infection caused by herpes simplex virus (HSV). Approximately one in four Americans older than 30 years are seropositive for HSV-2, though most are asymptomatic. The infection is characterized by periods of latency and reactivation, with viral shedding that can occur even in the absence of visible lesions, contributing to ongoing transmission.
Disease Course And Natural History
Primary infection has an incubation period of approximately 2–12 days, with symptoms typically peaking 8–10 days after onset and lesions healing within about three weeks. Primary disease may present with a more severe clinical syndrome and complications such as meningitis, encephalitis, or hepatitis. Importantly, more than half of first recognized episodes are not true primary infections, as earlier asymptomatic exposure is common.
Recurrent infection results from viral reactivation in the dorsal root ganglia. The average patient experiences about four recurrences per year. Recurrences are generally milder, involve fewer lesions, and resolve within 10 days. HSV-1 genital infections recur significantly less often than HSV-2.
Asymptomatic infection is common, with intermittent viral shedding that frequently leads to transmission by individuals without symptoms or lesions.
Etiology And Risk Factors
Most cases (70–90%) of genital herpes are caused by HSV-2, with the remainder caused by HSV-1. Genital HSV-1 infections are increasing in prevalence, likely due to higher rates of oral–genital contact and reduced childhood exposure to HSV-1, leaving more adolescents and adults susceptible. Acquisition of HSV-2 in individuals with prior HSV-1 infection tends to be less symptomatic, whereas acquisition of HSV-1 in those with HSV-2 is uncommon.
Genital herpes is strongly associated with HIV and other sexually transmitted infections. HSV infection increases both susceptibility to HIV and HIV viral shedding during HSV reactivation. Despite extensive research, no effective HSV vaccine is currently available.
Clinical Manifestations
Patients commonly report local pain, itching, or burning. A prodrome of tingling, itching, or pain may occur 1–2 days before lesion eruption and can sometimes mimic radicular pain such as sciatica. Lesions typically begin as macules and papules, progress to vesicles and pustules, and then ulcerate by approximately day five. Skin lesions crust over, whereas mucosal lesions heal without crusting.
Associated manifestations may include herpetic cervicitis, vaginitis, or urethritis, presenting with dysuria, urinary hesitancy or retention, vaginal discharge, or pelvic pain. Systemic symptoms such as fever, malaise, headache, myalgias, photophobia, anorexia, and lymphadenopathy are more common during primary infection.
Physical Examination Findings
Examination may reveal grouped vesicles on an erythematous base involving the vulva, vagina, cervix, perineum, buttocks, penile shaft, or glans. On moist mucosal surfaces, ulcers may predominate. Atypical findings include localized edema, erythema, fissures, or crusts.
Special Populations
Pediatric patients with genital herpes require careful evaluation, as neonatal infection is often disseminated or involves the central nervous system and carries high morbidity and mortality. Congenital HSV infection without vesicles may resemble other congenital infections. Sexual abuse must be considered in children with genital HSV, and evaluation for other sexually transmitted infections is recommended.
Pregnancy is a high-risk context, particularly with primary infection, which is associated with significant neonatal morbidity. Suppressive antiviral therapy after 36 weeks’ gestation reduces lesion recurrence at delivery and lowers cesarean section rates.
Diagnostic Approach
Diagnosis is usually clinical, based on history and examination. Laboratory testing is useful when confirmation is needed or in atypical or severe cases. Viral culture from vesicle fluid or ulcer base is positive in most early lesions but loses sensitivity as lesions heal. PCR testing is more sensitive and is the diagnostic test of choice, especially for central nervous system involvement. Serologic testing detects prior exposure but is not useful for diagnosing acute disease, as it cannot distinguish recent from chronic infection.
Differential Diagnosis
Important considerations include syphilis, chancroid, lymphogranuloma venereum, granuloma inguinale, candidiasis, and Behçet syndrome.
Emergency Management
Treatment reduces symptom severity and duration but does not eradicate latent virus or prevent future recurrences once therapy is stopped.
Episodic therapy for recurrences shortens lesion duration if started during the prodrome or within one day of lesion onset.
Suppressive therapy, recommended for patients with frequent recurrences (six or more per year), reduces recurrence frequency by approximately 75% and decreases viral shedding.
Severe disease, systemic involvement, or infection in immunocompromised patients requires intravenous antiviral therapy. Resistance to acyclovir occurs in a minority of immunocompromised patients, in which case foscarnet may be effective. Women with urinary retention may require bladder catheterization due to sacral nerve involvement.
Pharmacologic Treatment
First-episode, recurrent, suppressive, and HIV-associated genital herpes are treated with oral or intravenous acyclovir, valacyclovir, or famciclovir, with regimen selection based on severity, immune status, and recurrence pattern. Dosing adjustments may be necessary in renal impairment.
Disposition And Counseling
Hospital admission is indicated for patients with central nervous system involvement, disseminated disease, severe pain or urinary retention, or significant immunosuppression. Immunocompetent patients without systemic involvement can be managed as outpatients.
Discharge counseling is essential and should emphasize avoidance of sexual contact during prodrome and active lesions, consistent use of barrier protection even when asymptomatic, and the lifelong nature of infection. Patients should be informed about the likelihood of recurrence and the option of suppressive therapy.
Key Clinical Pearls
Primary genital herpes may be severe and should be treated promptly. Always consider sexual abuse in children presenting with genital HSV. Genital herpes is lifelong, with intermittent asymptomatic shedding that plays a major role in transmission.
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Emergency And Acute Medicine – Herpes Simplex
Definition And Overview
Herpes simplex is a viral disease characterized by recurrent, painful vesicular lesions involving mucocutaneous surfaces. Commonly affected sites include the lips, oral cavity, genitalia, rectum, hands, and eyes. Infection occurs in two phases: a primary phase during which the virus establishes latency within sensory nerve ganglia, and a secondary phase marked by recurrent reactivation at the same anatomic site. The incubation period is approximately four days after exposure. Viral shedding lasts about 7–10 days in primary infection (up to 23 days) and 3–4 days during recurrences. Neonatal infection may occur in utero, intrapartum (most commonly), or postnatally, with an incidence of approximately 1 in 3,500 births annually in the United States. Transmission is human-to-human, and 60–90% of the population is infected with herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2). Infection is more common in Black populations than White populations under 40 years of age, and females are affected more frequently than males.
Etiology And Virology
HSV-1 and HSV-2 are DNA viruses belonging to the Herpesviridae family. Transmission occurs through contact with infected secretions via mucous membranes or abraded skin, as well as through respiratory droplets. Recurrent asymptomatic mucosal shedding can transmit infection. HSV-1 most commonly causes oral infections, while HSV-2 more frequently causes genital disease, though either virus may infect oral or genital mucosa. Recurrence rates vary depending on viral type and anatomic location; HSV-2 genital infections recur more frequently than HSV-1 genital infections, and HSV-1 oral infections recur more often than genital HSV-1 infections.
Clinical Manifestations
Many primary infections are subclinical and detected only by serologic evidence of antibodies. Symptomatic disease typically presents with grouped 1–2 mm vesicles on an erythematous base, containing clear or cloudy fluid or appearing pustular.
Orofacial Disease
Primary orofacial infection often manifests as gingivostomatitis or pharyngitis with ulcerative lesions of the gingiva and mucosa. Associated symptoms include fever, malaise, irritability, headache, myalgias, and cervical lymphadenopathy. Symptoms may last two to four weeks and usually heal without scarring. Pain may limit oral intake, increasing the risk of dehydration.
Recurrent disease typically involves the lips, especially the vermilion border, and is often preceded by a prodrome of tingling, itching, burning, or throbbing. Triggers include sunlight, stress, heat, trauma, and immunosuppression. Lesions progress from erythema to vesicle, ulcer, crusting, and healing. Transmission can occur even without visible lesions.
Cutaneous Disease
Herpetic whitlow involves infection of the fingers, most commonly caused by HSV-2, and presents with vesicles on the pulp or lateral finger. It may occur from autoinoculation or occupational exposure and can last three to four weeks.
Traumatic herpes may develop after cosmetic, surgical, dental procedures, sun exposure, or burns.
Herpes gladiatorum is a cutaneous infection seen in athletes, particularly wrestlers, affecting the face, chest, and hands.
Eczema herpeticum is a disseminated HSV infection occurring in patients with atopic dermatitis, often associated with fever, headache, fatigue, and risk of secondary bacterial infection.
Ocular Disease
HSV is the most common cause of corneal blindness in developed countries. Infection may result from direct inoculation or spread from facial lesions. Symptoms include eye pain, photophobia, blurry vision, conjunctivitis, chemosis, and periauricular lymphadenopathy. Dendritic corneal lesions are seen on fluorescein examination. Vesicles on the tip of the nose (Hutchinson sign) suggest involvement of the nasociliary nerve and increased risk of ocular disease.
Central Nervous System Involvement
HSV encephalitis is the most common cause of severe sporadic encephalitis in the Western world, usually due to HSV-1 reactivation. Patients may present with altered mental status, seizures, focal neurologic deficits, or coma, with or without a history of mucocutaneous herpes.
Special Populations
In neonates, up to 60–80% of infected infants are born to mothers without known genital herpes. Vesicular lesions may be absent initially. Primary maternal genital infection carries the highest risk of neonatal transmission.
In children, primary infection often occurs early in life, with gingivostomatitis being the most common presentation in those under five years of age.
In pregnancy, suppressive antiviral therapy near term may reduce recurrence and viral shedding.
Diagnostic Evaluation
Diagnosis is often clinical based on history and examination. Definitive testing is indicated in severe disease, immunocompromised patients, suspected abuse, ocular involvement, or CNS disease. PCR testing of vesicular fluid is the most sensitive and specific diagnostic method. Viral culture, fluorescent antibody detection, and Tzanck smear may also be used.
Ocular disease requires fluorescein examination, and CNS disease requires lumbar puncture with CSF PCR, along with neuroimaging.
Differential Diagnosis
Conditions to consider include bacterial pharyngitis, Stevens–Johnson syndrome, herpes zoster, varicella, impetigo, syphilis, contact dermatitis, conjunctivitis, corneal abrasion, glaucoma, and other causes of encephalitis.
Emergency Management
Supportive care with hydration and analgesia is sufficient for mild primary infections in immunocompetent patients. Antiviral therapy is indicated for severe primary disease, recurrent infections with significant symptoms, immunocompromised patients, ocular disease, neonatal infection, and encephalitis. Incision and drainage of herpetic lesions should be avoided. Ocular involvement requires urgent ophthalmology consultation, and corticosteroids should not be used.
Pharmacologic Therapy
First-line treatment includes acyclovir, valacyclovir, or famciclovir. Acyclovir is preferred in children and severe disease. Encephalitis requires high-dose IV acyclovir for 14–21 days. Long-term suppressive therapy may be used for frequent recurrences. Antiviral dosing should be adjusted in renal impairment.
Disposition And Follow-Up
Hospital admission is required for encephalitis, neonatal infection, disseminated disease, severe dehydration, immunocompromised patients, and significant ocular involvement. Uncomplicated localized disease may be managed on an outpatient basis. Patients should be counseled on transmission risk, avoidance of contact with lesions, and indications for suppressive therapy.
Clinical Pearls And Pitfalls
Failure to recognize HSV encephalitis or ocular herpes can result in significant morbidity. Transmission may occur without visible lesions. Patients should be warned about autoinoculation and spread to others, especially during outbreaks. Avoid topical or systemic steroids unless specifically indicated and supervised.
Definition And Overview
Herpes simplex is a viral disease characterized by recurrent, painful vesicular lesions involving mucocutaneous surfaces. Commonly affected sites include the lips, oral cavity, genitalia, rectum, hands, and eyes. Infection occurs in two phases: a primary phase during which the virus establishes latency within sensory nerve ganglia, and a secondary phase marked by recurrent reactivation at the same anatomic site. The incubation period is approximately four days after exposure. Viral shedding lasts about 7–10 days in primary infection (up to 23 days) and 3–4 days during recurrences. Neonatal infection may occur in utero, intrapartum (most commonly), or postnatally, with an incidence of approximately 1 in 3,500 births annually in the United States. Transmission is human-to-human, and 60–90% of the population is infected with herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2). Infection is more common in Black populations than White populations under 40 years of age, and females are affected more frequently than males.
Etiology And Virology
HSV-1 and HSV-2 are DNA viruses belonging to the Herpesviridae family. Transmission occurs through contact with infected secretions via mucous membranes or abraded skin, as well as through respiratory droplets. Recurrent asymptomatic mucosal shedding can transmit infection. HSV-1 most commonly causes oral infections, while HSV-2 more frequently causes genital disease, though either virus may infect oral or genital mucosa. Recurrence rates vary depending on viral type and anatomic location; HSV-2 genital infections recur more frequently than HSV-1 genital infections, and HSV-1 oral infections recur more often than genital HSV-1 infections.
Clinical Manifestations
Many primary infections are subclinical and detected only by serologic evidence of antibodies. Symptomatic disease typically presents with grouped 1–2 mm vesicles on an erythematous base, containing clear or cloudy fluid or appearing pustular.
Orofacial Disease
Primary orofacial infection often manifests as gingivostomatitis or pharyngitis with ulcerative lesions of the gingiva and mucosa. Associated symptoms include fever, malaise, irritability, headache, myalgias, and cervical lymphadenopathy. Symptoms may last two to four weeks and usually heal without scarring. Pain may limit oral intake, increasing the risk of dehydration.
Recurrent disease typically involves the lips, especially the vermilion border, and is often preceded by a prodrome of tingling, itching, burning, or throbbing. Triggers include sunlight, stress, heat, trauma, and immunosuppression. Lesions progress from erythema to vesicle, ulcer, crusting, and healing. Transmission can occur even without visible lesions.
Cutaneous Disease
Herpetic whitlow involves infection of the fingers, most commonly caused by HSV-2, and presents with vesicles on the pulp or lateral finger. It may occur from autoinoculation or occupational exposure and can last three to four weeks.
Traumatic herpes may develop after cosmetic, surgical, dental procedures, sun exposure, or burns.
Herpes gladiatorum is a cutaneous infection seen in athletes, particularly wrestlers, affecting the face, chest, and hands.
Eczema herpeticum is a disseminated HSV infection occurring in patients with atopic dermatitis, often associated with fever, headache, fatigue, and risk of secondary bacterial infection.
Ocular Disease
HSV is the most common cause of corneal blindness in developed countries. Infection may result from direct inoculation or spread from facial lesions. Symptoms include eye pain, photophobia, blurry vision, conjunctivitis, chemosis, and periauricular lymphadenopathy. Dendritic corneal lesions are seen on fluorescein examination. Vesicles on the tip of the nose (Hutchinson sign) suggest involvement of the nasociliary nerve and increased risk of ocular disease.
Central Nervous System Involvement
HSV encephalitis is the most common cause of severe sporadic encephalitis in the Western world, usually due to HSV-1 reactivation. Patients may present with altered mental status, seizures, focal neurologic deficits, or coma, with or without a history of mucocutaneous herpes.
Special Populations
In neonates, up to 60–80% of infected infants are born to mothers without known genital herpes. Vesicular lesions may be absent initially. Primary maternal genital infection carries the highest risk of neonatal transmission.
In children, primary infection often occurs early in life, with gingivostomatitis being the most common presentation in those under five years of age.
In pregnancy, suppressive antiviral therapy near term may reduce recurrence and viral shedding.
Diagnostic Evaluation
Diagnosis is often clinical based on history and examination. Definitive testing is indicated in severe disease, immunocompromised patients, suspected abuse, ocular involvement, or CNS disease. PCR testing of vesicular fluid is the most sensitive and specific diagnostic method. Viral culture, fluorescent antibody detection, and Tzanck smear may also be used.
Ocular disease requires fluorescein examination, and CNS disease requires lumbar puncture with CSF PCR, along with neuroimaging.
Differential Diagnosis
Conditions to consider include bacterial pharyngitis, Stevens–Johnson syndrome, herpes zoster, varicella, impetigo, syphilis, contact dermatitis, conjunctivitis, corneal abrasion, glaucoma, and other causes of encephalitis.
Emergency Management
Supportive care with hydration and analgesia is sufficient for mild primary infections in immunocompetent patients. Antiviral therapy is indicated for severe primary disease, recurrent infections with significant symptoms, immunocompromised patients, ocular disease, neonatal infection, and encephalitis. Incision and drainage of herpetic lesions should be avoided. Ocular involvement requires urgent ophthalmology consultation, and corticosteroids should not be used.
Pharmacologic Therapy
First-line treatment includes acyclovir, valacyclovir, or famciclovir. Acyclovir is preferred in children and severe disease. Encephalitis requires high-dose IV acyclovir for 14–21 days. Long-term suppressive therapy may be used for frequent recurrences. Antiviral dosing should be adjusted in renal impairment.
Disposition And Follow-Up
Hospital admission is required for encephalitis, neonatal infection, disseminated disease, severe dehydration, immunocompromised patients, and significant ocular involvement. Uncomplicated localized disease may be managed on an outpatient basis. Patients should be counseled on transmission risk, avoidance of contact with lesions, and indications for suppressive therapy.
Clinical Pearls And Pitfalls
Failure to recognize HSV encephalitis or ocular herpes can result in significant morbidity. Transmission may occur without visible lesions. Patients should be warned about autoinoculation and spread to others, especially during outbreaks. Avoid topical or systemic steroids unless specifically indicated and supervised.
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Emergency And Acute Medicine – Herpes Zoster
Definition And Overview
Herpes zoster, commonly known as shingles, is characterized by a unilateral eruption of painful vesicles distributed along a single dermatome. It results from reactivation of latent varicella zoster virus (VZV) in dorsal root ganglia. Dissemination is rare in immunocompetent hosts but occurs more frequently in immunocompromised patients. The disease is most common in individuals with impaired cell-mediated immunity, particularly adults older than 50 years, patients with malignancy, and those receiving immunosuppressive therapy.
Etiology And Risk Factors
Herpes zoster is caused by reactivation of VZV, a DNA virus in the Herpesviridae family. Most cases occur in individuals with a history of primary varicella (chickenpox), and only rarely in vaccinated individuals. Declining cell-mediated immunity with aging or immunosuppression is the primary risk factor.
Pregnancy is not associated with an increased risk of congenital varicella syndrome. In children, herpes zoster may occur following in utero exposure or primary varicella infection during the first six months of life.
Clinical Features
Dermatomal zoster typically begins with a prodrome of pain, paresthesias, or pruritus in the affected dermatome, occurring in approximately 75% of patients. Pain may be sharp, burning, tingling, or severe. The classic rash consists of grouped vesicles on an erythematous base, which progress to crusting over 7–10 days, with complete resolution in 2–3 weeks. Thoracic and lumbar dermatomes are most commonly involved, followed by trigeminal and cervical distributions.
Zoster sine herpete presents with dermatomal pain without rash and can be diagnostically challenging.
Herpes zoster ophthalmicus results from involvement of the ophthalmic division of the trigeminal nerve. Hutchinson sign, defined as vesicles on the tip of the nose, suggests nasociliary nerve involvement and increased risk of ocular complications. Ocular findings may include punctate keratitis or corneal pseudodendrites, which are less ulcerative and show less fluorescein uptake than HSV dendrites.
Ramsay Hunt syndrome is caused by involvement of cranial nerves VII and VIII and presents with vesicles in the external auditory canal, peripheral facial palsy, vertigo, and altered sensation of the anterior two-thirds of the tongue.
Disseminated disease may occur, particularly in immunocompromised patients, and can involve the central nervous system, liver, or lungs, leading to complications such as meningoencephalitis, myelitis, hepatitis, pneumonitis, and peripheral neuropathy.
Postherpetic neuralgia is defined as pain persisting at the site of zoster lesions for more than three months after cutaneous healing. It occurs in 10–70% of patients, with risk increasing in those older than 50 years and in patients with severe initial rash or pain.
Diagnostic Evaluation
Diagnosis is primarily clinical in typical presentations. Laboratory testing is reserved for atypical cases, disseminated disease, or immunocompromised patients. Tzanck smear may show multinucleated giant cells but cannot distinguish VZV from HSV and has low sensitivity. PCR testing from vesicle fluid, blood, cerebrospinal fluid, or bronchoalveolar lavage is the preferred diagnostic method due to high sensitivity and specificity. Serologic testing is less reliable in the acute setting, and viral culture is slow and insensitive.
Differential Diagnosis
Conditions to consider include primary varicella, herpes simplex infection, cellulitis, allergic contact dermatitis, bullous impetigo, molluscum contagiosum, insect bites, trigeminal neuralgia, radiculopathy, biliary or renal colic, Bell palsy, peripheral vertigo, conjunctivitis, and HSV keratitis.
Emergency Management
Herpes zoster is usually self-limited. Management focuses on reducing pain, shortening disease duration, and preventing postherpetic neuralgia. Lesions should be covered, and universal precautions maintained, as zoster can transmit varicella to nonimmune individuals.
In immunocompetent patients, oral antiviral therapy should be initiated within 72 hours of rash onset, though treatment may still be beneficial if new lesions are forming. Valacyclovir is preferred for ease of dosing, though acyclovir or famciclovir are acceptable alternatives. Analgesia should be tailored to pain severity, ranging from nonsteroidal anti-inflammatory drugs to opioids. Corticosteroids remain controversial and may modestly improve acute pain and rash healing but do not prevent postherpetic neuralgia.
Immunocompromised patients require intravenous acyclovir and close monitoring.
Herpes zoster ophthalmicus requires urgent ophthalmology consultation. Oral antivirals are indicated, with intravenous therapy for immunocompromised patients or those with cranial nerve involvement.
Postherpetic neuralgia is managed with analgesics, tricyclic antidepressants, gabapentin or pregabalin, and topical lidocaine; antivirals are not effective once PHN is established.
Postexposure Prophylaxis And Prevention
Varicella zoster immune globulin (VariZIG) is recommended within 72 hours of exposure for immunocompromised patients, pregnant individuals, and certain neonates. The live-attenuated zoster vaccine is recommended for adults over 60 years of age but is contraindicated in pregnancy and immunocompromised patients. Vaccination does not treat active disease or prevent postherpetic neuralgia in those with established zoster.
Disposition And Follow-Up
Most patients can be managed as outpatients. Admission is indicated for immunocompromised patients, disseminated disease, severe or intractable pain, neonatal infection, or herpes zoster ophthalmicus with cranial nerve involvement. Patients should be advised to avoid contact with pregnant or immunocompromised individuals until all lesions have crusted. Long-term follow-up may be required for management of postherpetic neuralgia.
Clinical Pearls And Pitfalls
Always assess for ocular involvement when lesions appear on the tip of the nose. Consider herpes zoster in patients with unexplained dermatomal pain, even in the absence of rash. Fully expose the skin in patients presenting with chest or abdominal pain. Counsel patients early about the risk and chronic nature of postherpetic neuralgia.
Definition And Overview
Herpes zoster, commonly known as shingles, is characterized by a unilateral eruption of painful vesicles distributed along a single dermatome. It results from reactivation of latent varicella zoster virus (VZV) in dorsal root ganglia. Dissemination is rare in immunocompetent hosts but occurs more frequently in immunocompromised patients. The disease is most common in individuals with impaired cell-mediated immunity, particularly adults older than 50 years, patients with malignancy, and those receiving immunosuppressive therapy.
Etiology And Risk Factors
Herpes zoster is caused by reactivation of VZV, a DNA virus in the Herpesviridae family. Most cases occur in individuals with a history of primary varicella (chickenpox), and only rarely in vaccinated individuals. Declining cell-mediated immunity with aging or immunosuppression is the primary risk factor.
Pregnancy is not associated with an increased risk of congenital varicella syndrome. In children, herpes zoster may occur following in utero exposure or primary varicella infection during the first six months of life.
Clinical Features
Dermatomal zoster typically begins with a prodrome of pain, paresthesias, or pruritus in the affected dermatome, occurring in approximately 75% of patients. Pain may be sharp, burning, tingling, or severe. The classic rash consists of grouped vesicles on an erythematous base, which progress to crusting over 7–10 days, with complete resolution in 2–3 weeks. Thoracic and lumbar dermatomes are most commonly involved, followed by trigeminal and cervical distributions.
Zoster sine herpete presents with dermatomal pain without rash and can be diagnostically challenging.
Herpes zoster ophthalmicus results from involvement of the ophthalmic division of the trigeminal nerve. Hutchinson sign, defined as vesicles on the tip of the nose, suggests nasociliary nerve involvement and increased risk of ocular complications. Ocular findings may include punctate keratitis or corneal pseudodendrites, which are less ulcerative and show less fluorescein uptake than HSV dendrites.
Ramsay Hunt syndrome is caused by involvement of cranial nerves VII and VIII and presents with vesicles in the external auditory canal, peripheral facial palsy, vertigo, and altered sensation of the anterior two-thirds of the tongue.
Disseminated disease may occur, particularly in immunocompromised patients, and can involve the central nervous system, liver, or lungs, leading to complications such as meningoencephalitis, myelitis, hepatitis, pneumonitis, and peripheral neuropathy.
Postherpetic neuralgia is defined as pain persisting at the site of zoster lesions for more than three months after cutaneous healing. It occurs in 10–70% of patients, with risk increasing in those older than 50 years and in patients with severe initial rash or pain.
Diagnostic Evaluation
Diagnosis is primarily clinical in typical presentations. Laboratory testing is reserved for atypical cases, disseminated disease, or immunocompromised patients. Tzanck smear may show multinucleated giant cells but cannot distinguish VZV from HSV and has low sensitivity. PCR testing from vesicle fluid, blood, cerebrospinal fluid, or bronchoalveolar lavage is the preferred diagnostic method due to high sensitivity and specificity. Serologic testing is less reliable in the acute setting, and viral culture is slow and insensitive.
Differential Diagnosis
Conditions to consider include primary varicella, herpes simplex infection, cellulitis, allergic contact dermatitis, bullous impetigo, molluscum contagiosum, insect bites, trigeminal neuralgia, radiculopathy, biliary or renal colic, Bell palsy, peripheral vertigo, conjunctivitis, and HSV keratitis.
Emergency Management
Herpes zoster is usually self-limited. Management focuses on reducing pain, shortening disease duration, and preventing postherpetic neuralgia. Lesions should be covered, and universal precautions maintained, as zoster can transmit varicella to nonimmune individuals.
In immunocompetent patients, oral antiviral therapy should be initiated within 72 hours of rash onset, though treatment may still be beneficial if new lesions are forming. Valacyclovir is preferred for ease of dosing, though acyclovir or famciclovir are acceptable alternatives. Analgesia should be tailored to pain severity, ranging from nonsteroidal anti-inflammatory drugs to opioids. Corticosteroids remain controversial and may modestly improve acute pain and rash healing but do not prevent postherpetic neuralgia.
Immunocompromised patients require intravenous acyclovir and close monitoring.
Herpes zoster ophthalmicus requires urgent ophthalmology consultation. Oral antivirals are indicated, with intravenous therapy for immunocompromised patients or those with cranial nerve involvement.
Postherpetic neuralgia is managed with analgesics, tricyclic antidepressants, gabapentin or pregabalin, and topical lidocaine; antivirals are not effective once PHN is established.
Postexposure Prophylaxis And Prevention
Varicella zoster immune globulin (VariZIG) is recommended within 72 hours of exposure for immunocompromised patients, pregnant individuals, and certain neonates. The live-attenuated zoster vaccine is recommended for adults over 60 years of age but is contraindicated in pregnancy and immunocompromised patients. Vaccination does not treat active disease or prevent postherpetic neuralgia in those with established zoster.
Disposition And Follow-Up
Most patients can be managed as outpatients. Admission is indicated for immunocompromised patients, disseminated disease, severe or intractable pain, neonatal infection, or herpes zoster ophthalmicus with cranial nerve involvement. Patients should be advised to avoid contact with pregnant or immunocompromised individuals until all lesions have crusted. Long-term follow-up may be required for management of postherpetic neuralgia.
Clinical Pearls And Pitfalls
Always assess for ocular involvement when lesions appear on the tip of the nose. Consider herpes zoster in patients with unexplained dermatomal pain, even in the absence of rash. Fully expose the skin in patients presenting with chest or abdominal pain. Counsel patients early about the risk and chronic nature of postherpetic neuralgia.
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Emergency And Acute Medicine – Hernias
Definition And Classification
A hernia is the protrusion of an organ or bodily structure through a defect in the tissues that normally contain it. Hernias are classified as external when the protrusion is visible outside the body, internal when herniated contents remain within a body cavity, and interparietal when the hernial sac lies within the abdominal wall layers. Abdominal wall hernias result from weakness or disruption of the fibromuscular layers of the abdominal wall. Groin hernias include inguinal (direct and indirect) and femoral hernias, while ventral hernias include epigastric, umbilical, spigelian, and incisional hernias.
Types Of Hernias
Indirect inguinal hernias arise from persistence of the processus vaginalis, allowing peritoneal contents to pass through the internal inguinal ring. They are more common on the right side and carry a lifetime repair risk of approximately 27% in men and 3% in women.
Direct inguinal hernias occur due to weakness in the transversalis fascia within Hesselbach’s triangle, bounded by the inguinal ligament inferiorly, inferior epigastric vessels laterally, and the rectus abdominis medially.
Femoral hernias result from herniation through the femoral canal beneath the inguinal ligament and have a high risk of incarceration due to their narrow neck.
Incisional hernias occur from failure of prior surgical fascial closure.
Umbilical hernias arise from congenital failure of the umbilical ring to close or acquired weakness at the umbilicus; they frequently incarcerate in adults but often close spontaneously in infants.
Epigastric hernias occur along the midline between the xiphoid and umbilicus.
Spigelian hernias protrude through the oblique fascia lateral to the rectus abdominis muscle.
Obturator hernias pass through the obturator membrane and may compress the obturator nerve, causing medial thigh pain.
Lumbar hernias occur through defects in the posterior abdominal wall and have a relatively high incarceration rate.
Epidemiology
Herniorrhaphy is one of the most common general surgical procedures, with over 750,000 repairs performed annually in the United States. Hernias affect approximately 5% of the population. Groin and femoral hernias account for about 85% of cases, while umbilical and incisional hernias comprise most of the remainder.
Pathophysiology And Hernia States
A reducible hernia can be manually returned to the abdominal cavity. An incarcerated hernia cannot be reduced and may lead to obstruction. A strangulated hernia involves compromised blood supply to entrapped bowel, resulting in ischemia, necrosis, and potential gangrene. Hernias with small necks and large sacs are at particularly high risk. Symptoms of bowel obstruction or ischemia, including nausea, vomiting, fever, and leukocytosis, may be present.
Clinical Presentation
Patients typically report localized pain and swelling at the hernia site. Pain may worsen with straining or positional changes and improve with rest. Persistent pain, vomiting, or fever suggests incarceration or strangulation. Vital signs are often normal but may show tachycardia, hypotension, or fever in complicated cases. Physical examination may reveal skin color changes, tenderness, or irreducibility. Inguinal hernias may present as scrotal swelling in men or a groin or labial bulge in women. Femoral hernias appear inferior to the inguinal ligament. Obturator hernias may present with intermittent bowel obstruction and medial thigh pain worsened by hip extension.
Special Populations
In children, hernias may be intermittent and difficult to detect, with incarceration rates as high as 10–20%, particularly in infants younger than six months. Umbilical hernias in children usually close spontaneously.
During pregnancy, hernias are uncommon but may pose diagnostic challenges; emergent surgical consultation is required if incarceration or strangulation is suspected.
Older adults have a higher risk of bowel resection and postoperative complications when hernias become incarcerated.
Diagnostic Evaluation
Diagnosis is primarily clinical, based on careful history and physical examination, often aided by examination during standing or Valsalva maneuver. Laboratory studies may reveal leukocytosis in strangulation or electrolyte abnormalities with dehydration. Imaging is reserved for unclear cases or suspected complications. Ultrasound is useful for groin and abdominal wall hernias, while CT is preferred for obturator or spigelian hernias and in obese or complex cases.
Emergency Management
Initial management includes assessment of airway, breathing, and circulation, with intravenous fluid resuscitation for dehydration, obstruction, or sepsis. Incarcerated or strangulated hernias require urgent surgical consultation. Nasogastric decompression is indicated for bowel obstruction. Manual reduction may be attempted in selected patients without signs of strangulation, using gentle, sustained pressure with adequate analgesia and sedation. Reduction should not be attempted in patients with fever, leukocytosis, or signs of ischemia.
Medications
Analgesia is provided with opioids such as morphine or fentanyl. Sedation with benzodiazepines may be used to facilitate reduction when appropriate. Broad-spectrum antibiotics are considered in cases of suspected strangulation or sepsis.
Disposition And Follow-Up
Strangulated hernias require immediate surgical intervention and admission. Incarcerated hernias generally require admission for urgent surgery. Patients may be discharged after successful reduction if asymptomatic, with clear instructions and surgical follow-up. All patients should be referred for elective surgical evaluation.
Clinical Pearls And Pitfalls
Failure to recognize incarceration or strangulation can lead to bowel ischemia and sepsis. Forcing reduction in the presence of strangulation may return necrotic bowel to the abdomen, delaying diagnosis and worsening outcomes. Early surgical consultation is essential when complications are suspected.
Definition And Classification
A hernia is the protrusion of an organ or bodily structure through a defect in the tissues that normally contain it. Hernias are classified as external when the protrusion is visible outside the body, internal when herniated contents remain within a body cavity, and interparietal when the hernial sac lies within the abdominal wall layers. Abdominal wall hernias result from weakness or disruption of the fibromuscular layers of the abdominal wall. Groin hernias include inguinal (direct and indirect) and femoral hernias, while ventral hernias include epigastric, umbilical, spigelian, and incisional hernias.
Types Of Hernias
Indirect inguinal hernias arise from persistence of the processus vaginalis, allowing peritoneal contents to pass through the internal inguinal ring. They are more common on the right side and carry a lifetime repair risk of approximately 27% in men and 3% in women.
Direct inguinal hernias occur due to weakness in the transversalis fascia within Hesselbach’s triangle, bounded by the inguinal ligament inferiorly, inferior epigastric vessels laterally, and the rectus abdominis medially.
Femoral hernias result from herniation through the femoral canal beneath the inguinal ligament and have a high risk of incarceration due to their narrow neck.
Incisional hernias occur from failure of prior surgical fascial closure.
Umbilical hernias arise from congenital failure of the umbilical ring to close or acquired weakness at the umbilicus; they frequently incarcerate in adults but often close spontaneously in infants.
Epigastric hernias occur along the midline between the xiphoid and umbilicus.
Spigelian hernias protrude through the oblique fascia lateral to the rectus abdominis muscle.
Obturator hernias pass through the obturator membrane and may compress the obturator nerve, causing medial thigh pain.
Lumbar hernias occur through defects in the posterior abdominal wall and have a relatively high incarceration rate.
Epidemiology
Herniorrhaphy is one of the most common general surgical procedures, with over 750,000 repairs performed annually in the United States. Hernias affect approximately 5% of the population. Groin and femoral hernias account for about 85% of cases, while umbilical and incisional hernias comprise most of the remainder.
Pathophysiology And Hernia States
A reducible hernia can be manually returned to the abdominal cavity. An incarcerated hernia cannot be reduced and may lead to obstruction. A strangulated hernia involves compromised blood supply to entrapped bowel, resulting in ischemia, necrosis, and potential gangrene. Hernias with small necks and large sacs are at particularly high risk. Symptoms of bowel obstruction or ischemia, including nausea, vomiting, fever, and leukocytosis, may be present.
Clinical Presentation
Patients typically report localized pain and swelling at the hernia site. Pain may worsen with straining or positional changes and improve with rest. Persistent pain, vomiting, or fever suggests incarceration or strangulation. Vital signs are often normal but may show tachycardia, hypotension, or fever in complicated cases. Physical examination may reveal skin color changes, tenderness, or irreducibility. Inguinal hernias may present as scrotal swelling in men or a groin or labial bulge in women. Femoral hernias appear inferior to the inguinal ligament. Obturator hernias may present with intermittent bowel obstruction and medial thigh pain worsened by hip extension.
Special Populations
In children, hernias may be intermittent and difficult to detect, with incarceration rates as high as 10–20%, particularly in infants younger than six months. Umbilical hernias in children usually close spontaneously.
During pregnancy, hernias are uncommon but may pose diagnostic challenges; emergent surgical consultation is required if incarceration or strangulation is suspected.
Older adults have a higher risk of bowel resection and postoperative complications when hernias become incarcerated.
Diagnostic Evaluation
Diagnosis is primarily clinical, based on careful history and physical examination, often aided by examination during standing or Valsalva maneuver. Laboratory studies may reveal leukocytosis in strangulation or electrolyte abnormalities with dehydration. Imaging is reserved for unclear cases or suspected complications. Ultrasound is useful for groin and abdominal wall hernias, while CT is preferred for obturator or spigelian hernias and in obese or complex cases.
Emergency Management
Initial management includes assessment of airway, breathing, and circulation, with intravenous fluid resuscitation for dehydration, obstruction, or sepsis. Incarcerated or strangulated hernias require urgent surgical consultation. Nasogastric decompression is indicated for bowel obstruction. Manual reduction may be attempted in selected patients without signs of strangulation, using gentle, sustained pressure with adequate analgesia and sedation. Reduction should not be attempted in patients with fever, leukocytosis, or signs of ischemia.
Medications
Analgesia is provided with opioids such as morphine or fentanyl. Sedation with benzodiazepines may be used to facilitate reduction when appropriate. Broad-spectrum antibiotics are considered in cases of suspected strangulation or sepsis.
Disposition And Follow-Up
Strangulated hernias require immediate surgical intervention and admission. Incarcerated hernias generally require admission for urgent surgery. Patients may be discharged after successful reduction if asymptomatic, with clear instructions and surgical follow-up. All patients should be referred for elective surgical evaluation.
Clinical Pearls And Pitfalls
Failure to recognize incarceration or strangulation can lead to bowel ischemia and sepsis. Forcing reduction in the presence of strangulation may return necrotic bowel to the abdomen, delaying diagnosis and worsening outcomes. Early surgical consultation is essential when complications are suspected.
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Emergency And Acute Medicine - Globe Rupture
Basics Description
A globe rupture is a full-thickness injury of the cornea or sclera caused by trauma. Blunt trauma results in a sudden diffuse rise in intraocular pressure, leading to rupture at the weakest points of the eye such as the extraocular muscle insertions, corneoscleral junction, or limbus where the sclera is thinnest. Penetrating injuries occur when sharp objects or projectiles directly lacerate the sclera or anterior eye and are most commonly anterior due to protection from the bony orbit. Posterior injuries may occur with orbital fractures or penetrating trauma through the eyelid or eyebrow. Prognosis is worse with large lacerations, injuries posterior to rectus muscle insertions, blunt mechanisms, intraocular foreign bodies (especially organic), vitreous extrusion, lens damage, hyphema, retinal detachment, poor initial visual acuity, afferent pupillary defect, and delays to operative repair.
Etiology
Common causes include falls, blunt impact injuries, sports-related trauma, indirect concussive injuries such as explosions, sharp or stabbing injuries (accidental or intentional), and projectile injuries from industrial accidents, firearms, BB pellets, or blast-related shrapnel such as glass.
Diagnosis Signs And Symptoms
Patients may present with eye pain, localized swelling and ecchymosis, scleral or corneal laceration, extrusion of intraocular contents, markedly decreased visual acuity, restricted extraocular movements, hyphema, severe circumferential subconjunctival hemorrhage with bloody chemosis, abnormally deep or shallow anterior chamber, irregular pupil pointing toward the lesion, lens subluxation, commotio retinae, and low intraocular pressure. Tonometry should not be performed if globe rupture is suspected.
History
Assessment should include the mechanism of injury, concern for retained intraocular foreign body, prior eye surgery, preinjury visual acuity, tetanus status, and time of last oral intake.
Physical Exam
A careful penlight or slit-lamp examination should be performed to look for signs of rupture. Once a globe rupture is suspected or identified, further ocular examination should be deferred until surgical repair to avoid pressure on the eye and extrusion of contents. If rupture is excluded, a full ophthalmologic exam including visual acuity, slit-lamp evaluation, fundus exam, Seidel test, and intraocular pressure measurement may be performed. Ultrasound should only be used if rupture is not suspected.
Essential Workup
If globe rupture is suspected or confirmed, minimize examination and manipulation of the eye until operative repair.
Diagnosis Tests And Interpretation
Preoperative laboratory studies include CBC, electrolytes, and coagulation tests. Imaging may include orbital radiographs to identify metallic foreign bodies and CT of the orbits with axial and coronal views. MRI is contraindicated until metallic foreign bodies are excluded. B-scan ultrasound may be used only when rupture is not suspected.
Differential Diagnosis
Intraocular foreign body, hyphema, severe subconjunctival hemorrhage with chemosis, partial corneal laceration, and partial scleral laceration.
Treatment Pre Hospital
Place a rigid eye shield without applying pressure to the globe. If no shield is available, a protective cup may be used.
Initial Stabilization Therapy
Avoid manipulation of the eye and prevent activities that increase intraocular pressure such as coughing, vomiting, or straining.
Ed Treatment Procedures
Immediate ophthalmologic consultation is required for surgical management. Maintain NPO status, elevate the head of the bed, provide antiemetics, and apply a protective eye shield without pressure. Update tetanus immunization. Administer broad-spectrum IV antibiotics targeting skin flora and injury-specific contaminants, commonly vancomycin with ceftazidime or ciprofloxacin. Identify and manage associated injuries. Succinylcholine is relatively contraindicated but may be used with appropriate precautions if necessary for airway control.
In pediatric patients, consider nonaccidental trauma and minimize crying or agitation to prevent extrusion of ocular contents.
Medication
Commonly used agents include vancomycin, ceftazidime, ciprofloxacin, clindamycin, tobramycin, and antiemetics such as ondansetron or prochlorperazine.
Follow-Up Disposition
All patients with globe rupture or penetrating eye injury require admission. Discharge is appropriate only if globe penetration has been definitively excluded.
Issues For Referral
Emergent ophthalmologic consultation is essential, as delays increase the risk of infection and poor visual outcomes. Patients should be counseled on protective eyewear to prevent recurrence when appropriate.
Follow-Up Recommendations
Postoperative follow-up with ophthalmology is mandatory.
Key Clinical Insights And Avoidable Errors
Do not manipulate the eye when globe rupture is suspected or confirmed. Always place a protective eye shield without pressure. Treat nausea and vomiting aggressively to prevent increases in intraocular pressure. Ensure tetanus prophylaxis and initiate empiric antibiotics tailored to the injury mechanism promptly.
Basics Description
A globe rupture is a full-thickness injury of the cornea or sclera caused by trauma. Blunt trauma results in a sudden diffuse rise in intraocular pressure, leading to rupture at the weakest points of the eye such as the extraocular muscle insertions, corneoscleral junction, or limbus where the sclera is thinnest. Penetrating injuries occur when sharp objects or projectiles directly lacerate the sclera or anterior eye and are most commonly anterior due to protection from the bony orbit. Posterior injuries may occur with orbital fractures or penetrating trauma through the eyelid or eyebrow. Prognosis is worse with large lacerations, injuries posterior to rectus muscle insertions, blunt mechanisms, intraocular foreign bodies (especially organic), vitreous extrusion, lens damage, hyphema, retinal detachment, poor initial visual acuity, afferent pupillary defect, and delays to operative repair.
Etiology
Common causes include falls, blunt impact injuries, sports-related trauma, indirect concussive injuries such as explosions, sharp or stabbing injuries (accidental or intentional), and projectile injuries from industrial accidents, firearms, BB pellets, or blast-related shrapnel such as glass.
Diagnosis Signs And Symptoms
Patients may present with eye pain, localized swelling and ecchymosis, scleral or corneal laceration, extrusion of intraocular contents, markedly decreased visual acuity, restricted extraocular movements, hyphema, severe circumferential subconjunctival hemorrhage with bloody chemosis, abnormally deep or shallow anterior chamber, irregular pupil pointing toward the lesion, lens subluxation, commotio retinae, and low intraocular pressure. Tonometry should not be performed if globe rupture is suspected.
History
Assessment should include the mechanism of injury, concern for retained intraocular foreign body, prior eye surgery, preinjury visual acuity, tetanus status, and time of last oral intake.
Physical Exam
A careful penlight or slit-lamp examination should be performed to look for signs of rupture. Once a globe rupture is suspected or identified, further ocular examination should be deferred until surgical repair to avoid pressure on the eye and extrusion of contents. If rupture is excluded, a full ophthalmologic exam including visual acuity, slit-lamp evaluation, fundus exam, Seidel test, and intraocular pressure measurement may be performed. Ultrasound should only be used if rupture is not suspected.
Essential Workup
If globe rupture is suspected or confirmed, minimize examination and manipulation of the eye until operative repair.
Diagnosis Tests And Interpretation
Preoperative laboratory studies include CBC, electrolytes, and coagulation tests. Imaging may include orbital radiographs to identify metallic foreign bodies and CT of the orbits with axial and coronal views. MRI is contraindicated until metallic foreign bodies are excluded. B-scan ultrasound may be used only when rupture is not suspected.
Differential Diagnosis
Intraocular foreign body, hyphema, severe subconjunctival hemorrhage with chemosis, partial corneal laceration, and partial scleral laceration.
Treatment Pre Hospital
Place a rigid eye shield without applying pressure to the globe. If no shield is available, a protective cup may be used.
Initial Stabilization Therapy
Avoid manipulation of the eye and prevent activities that increase intraocular pressure such as coughing, vomiting, or straining.
Ed Treatment Procedures
Immediate ophthalmologic consultation is required for surgical management. Maintain NPO status, elevate the head of the bed, provide antiemetics, and apply a protective eye shield without pressure. Update tetanus immunization. Administer broad-spectrum IV antibiotics targeting skin flora and injury-specific contaminants, commonly vancomycin with ceftazidime or ciprofloxacin. Identify and manage associated injuries. Succinylcholine is relatively contraindicated but may be used with appropriate precautions if necessary for airway control.
In pediatric patients, consider nonaccidental trauma and minimize crying or agitation to prevent extrusion of ocular contents.
Medication
Commonly used agents include vancomycin, ceftazidime, ciprofloxacin, clindamycin, tobramycin, and antiemetics such as ondansetron or prochlorperazine.
Follow-Up Disposition
All patients with globe rupture or penetrating eye injury require admission. Discharge is appropriate only if globe penetration has been definitively excluded.
Issues For Referral
Emergent ophthalmologic consultation is essential, as delays increase the risk of infection and poor visual outcomes. Patients should be counseled on protective eyewear to prevent recurrence when appropriate.
Follow-Up Recommendations
Postoperative follow-up with ophthalmology is mandatory.
Key Clinical Insights And Avoidable Errors
Do not manipulate the eye when globe rupture is suspected or confirmed. Always place a protective eye shield without pressure. Treat nausea and vomiting aggressively to prevent increases in intraocular pressure. Ensure tetanus prophylaxis and initiate empiric antibiotics tailored to the injury mechanism promptly.
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Emergency And Acute Medicine - Giardiasis
Basics Description
Giardiasis is a noninvasive diarrheal illness caused by a protozoan parasite and is found worldwide. Prevalence ranges from 2–15% in developed countries and 20–40% in developing nations. It accounts for approximately 5% of travelers’ diarrhea and is the most common intestinal parasitic infection in the United States. Incidence peaks in early summer through fall, with highest rates in children aged 1–9 years and adults aged 30–39 years. Transmission occurs via the fecal–oral route. Humans are the primary reservoir, but domestic and wild mammals and contaminated surface water also serve as reservoirs. Populations at increased risk include travelers to endemic or wilderness areas, children in day care centers and their contacts, institutionalized individuals, and those engaging in anal sexual practices.
Etiology
Giardia lamblia is a flagellated protozoan, also known as Giardia intestinalis or Giardia duodenalis. After ingestion, organisms attach to intestinal villi and disrupt brush-border enzymes, leading to impaired digestion of lactose and other carbohydrates. No toxin is produced.
Diagnosis Signs And Symptoms
Symptoms typically begin 1–2 weeks after exposure. Infection is often asymptomatic. Symptomatic disease usually presents with acute-onset diarrhea that is foul-smelling, nonbloody, and frequently associated with steatorrhea. Illness is usually self-limited within 2–4 weeks but may be more severe in immunocompromised patients or those with underlying bowel disease. Common associated symptoms include flatulence, bloating, abdominal cramping, nausea, vomiting, malaise, anorexia, and weight loss. Fever is uncommon.
Thirty to fifty percent of patients develop chronic infection lasting longer than four weeks, characterized by fat malabsorption, secondary lactase deficiency, and macrocytic anemia due to folate deficiency. Pediatric patients may develop severe dehydration in acute disease and failure to thrive, growth retardation, or cognitive impairment in chronic infection. Physical examination is often benign. Extraintestinal manifestations include polyarthritis, urticaria, aphthous ulcers, maculopapular rash, and biliary tract disease.
Essential Workup
Evaluation should focus on exposure history, travel, high-risk group membership, and hydration status. The presence of gross or occult blood on rectal examination makes giardiasis unlikely.
Diagnosis Tests And Interpretation
Stool microscopy for ova and parasites has a sensitivity of 50–70% with one sample and up to 85–90% with three samples collected over several days. Specificity approaches 100%. Stool antigen detection by ELISA or immunofluorescent assay is highly sensitive and specific but does not detect other parasites. Stool PCR offers near-perfect sensitivity and specificity. Fecal leukocytes and stool cultures are unnecessary unless invasive bacterial infection is suspected. CBC may show macrocytic anemia in chronic disease. Electrolytes and renal function should be assessed if dehydration is present. Imaging studies are nonspecific and rarely required.
Differential Diagnosis
Viral gastroenteritis, bacterial enteritis, other protozoal infections, inflammatory bowel disease, irritable bowel syndrome, lactase deficiency, tropical sprue, medication or toxin-induced diarrhea, endocrine disorders, and gastrointestinal malignancy.
Treatment Initial Stabilization Therapy
Assess airway, breathing, and circulation. Administer intravenous isotonic fluids for significant dehydration. Children with severe dehydration require rapid fluid boluses and glucose monitoring.
Ed Treatment Procedures
Oral rehydration is sufficient for mild dehydration. Correct electrolyte abnormalities. Obtain stool studies when possible. If stool testing is negative but suspicion remains high, empiric treatment with metronidazole may be considered, and gastroenterology referral arranged for persistent symptoms.
Medication
First-line therapy includes metronidazole or tinidazole, each achieving cure rates near 90%. Metronidazole is given for 5–10 days, while tinidazole is administered as a single dose. Second-line agents include albendazole, nitazoxanide, quinacrine, paromomycin, or furazolidone when first-line therapy fails. Treatment choice should consider age, pregnancy status, renal function, and G6PD deficiency. Immunocompromised patients may require combination or prolonged therapy.
Follow-Up Disposition
Admission is indicated for patients with hemodynamic instability, severe electrolyte imbalance, inability to tolerate oral intake, or significant comorbid illness. Most patients can be discharged once hydration is adequate and symptoms are controlled.
Follow-Up Recommendations
Gastroenterology referral is recommended for persistent symptoms beyond four weeks despite therapy. Patients should be counseled regarding possible prolonged lactose intolerance and postinfectious fatigue.
Clinical Insights And Common Errors
Diagnosis is the primary challenge. Giardiasis should be considered in all patients with diarrhea, even without classic risk factors. A single stool specimen is often insufficient to exclude infection. Failure to recognize chronic disease and malabsorption can delay appropriate treatment.
Basics Description
Giardiasis is a noninvasive diarrheal illness caused by a protozoan parasite and is found worldwide. Prevalence ranges from 2–15% in developed countries and 20–40% in developing nations. It accounts for approximately 5% of travelers’ diarrhea and is the most common intestinal parasitic infection in the United States. Incidence peaks in early summer through fall, with highest rates in children aged 1–9 years and adults aged 30–39 years. Transmission occurs via the fecal–oral route. Humans are the primary reservoir, but domestic and wild mammals and contaminated surface water also serve as reservoirs. Populations at increased risk include travelers to endemic or wilderness areas, children in day care centers and their contacts, institutionalized individuals, and those engaging in anal sexual practices.
Etiology
Giardia lamblia is a flagellated protozoan, also known as Giardia intestinalis or Giardia duodenalis. After ingestion, organisms attach to intestinal villi and disrupt brush-border enzymes, leading to impaired digestion of lactose and other carbohydrates. No toxin is produced.
Diagnosis Signs And Symptoms
Symptoms typically begin 1–2 weeks after exposure. Infection is often asymptomatic. Symptomatic disease usually presents with acute-onset diarrhea that is foul-smelling, nonbloody, and frequently associated with steatorrhea. Illness is usually self-limited within 2–4 weeks but may be more severe in immunocompromised patients or those with underlying bowel disease. Common associated symptoms include flatulence, bloating, abdominal cramping, nausea, vomiting, malaise, anorexia, and weight loss. Fever is uncommon.
Thirty to fifty percent of patients develop chronic infection lasting longer than four weeks, characterized by fat malabsorption, secondary lactase deficiency, and macrocytic anemia due to folate deficiency. Pediatric patients may develop severe dehydration in acute disease and failure to thrive, growth retardation, or cognitive impairment in chronic infection. Physical examination is often benign. Extraintestinal manifestations include polyarthritis, urticaria, aphthous ulcers, maculopapular rash, and biliary tract disease.
Essential Workup
Evaluation should focus on exposure history, travel, high-risk group membership, and hydration status. The presence of gross or occult blood on rectal examination makes giardiasis unlikely.
Diagnosis Tests And Interpretation
Stool microscopy for ova and parasites has a sensitivity of 50–70% with one sample and up to 85–90% with three samples collected over several days. Specificity approaches 100%. Stool antigen detection by ELISA or immunofluorescent assay is highly sensitive and specific but does not detect other parasites. Stool PCR offers near-perfect sensitivity and specificity. Fecal leukocytes and stool cultures are unnecessary unless invasive bacterial infection is suspected. CBC may show macrocytic anemia in chronic disease. Electrolytes and renal function should be assessed if dehydration is present. Imaging studies are nonspecific and rarely required.
Differential Diagnosis
Viral gastroenteritis, bacterial enteritis, other protozoal infections, inflammatory bowel disease, irritable bowel syndrome, lactase deficiency, tropical sprue, medication or toxin-induced diarrhea, endocrine disorders, and gastrointestinal malignancy.
Treatment Initial Stabilization Therapy
Assess airway, breathing, and circulation. Administer intravenous isotonic fluids for significant dehydration. Children with severe dehydration require rapid fluid boluses and glucose monitoring.
Ed Treatment Procedures
Oral rehydration is sufficient for mild dehydration. Correct electrolyte abnormalities. Obtain stool studies when possible. If stool testing is negative but suspicion remains high, empiric treatment with metronidazole may be considered, and gastroenterology referral arranged for persistent symptoms.
Medication
First-line therapy includes metronidazole or tinidazole, each achieving cure rates near 90%. Metronidazole is given for 5–10 days, while tinidazole is administered as a single dose. Second-line agents include albendazole, nitazoxanide, quinacrine, paromomycin, or furazolidone when first-line therapy fails. Treatment choice should consider age, pregnancy status, renal function, and G6PD deficiency. Immunocompromised patients may require combination or prolonged therapy.
Follow-Up Disposition
Admission is indicated for patients with hemodynamic instability, severe electrolyte imbalance, inability to tolerate oral intake, or significant comorbid illness. Most patients can be discharged once hydration is adequate and symptoms are controlled.
Follow-Up Recommendations
Gastroenterology referral is recommended for persistent symptoms beyond four weeks despite therapy. Patients should be counseled regarding possible prolonged lactose intolerance and postinfectious fatigue.
Clinical Insights And Common Errors
Diagnosis is the primary challenge. Giardiasis should be considered in all patients with diarrhea, even without classic risk factors. A single stool specimen is often insufficient to exclude infection. Failure to recognize chronic disease and malabsorption can delay appropriate treatment.
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Emergency And Acute Medicine - Glaucoma
Basics Description
Glaucoma is a group of disorders characterized by elevated intraocular pressure, progressive optic neuropathy, and irreversible vision loss if untreated.
Etiology
Primary glaucoma includes open-angle and angle-closure forms. Primary open-angle glaucoma has a normal anterior chamber angle, insidious onset, and chronic elevation of intraocular pressure. It accounts for approximately 90% of glaucoma cases in the United States and is a leading cause of blindness in African Americans. Risk factors include African American race, age over 40 years, family history, myopia, diabetes, and hypertension.
Primary angle-closure glaucoma results from narrowing or closure of the anterior chamber angle, preventing normal aqueous humor outflow through the trabecular meshwork. It presents abruptly with a sudden rise in intraocular pressure. Risk factors include Asian and Eskimo ethnicity, hyperopia, increasing age, female sex, and family history.
Secondary glaucoma may be open or closed angle and occurs due to other conditions such as ocular disease, trauma, systemic illness, or medications. Common drug causes include steroids, sertraline, bronchodilators, and topiramate. Associated diseases include uveitis, neovascularization, neurofibromatosis, intraocular tumors, trauma, and rapid correction of hyperglycemia.
Diagnosis Signs And Symptoms
Open-angle glaucoma typically causes painless, gradual loss of peripheral vision and may present late. Angle-closure glaucoma classically presents with painful loss of vision and a fixed, mid-dilated pupil.
History in open-angle disease includes slow bilateral visual decline or night blindness without pain. Angle-closure disease presents with severe eye pain, ipsilateral headache, nausea, vomiting, decreased visual acuity, halos around lights, and visual clouding. Symptoms may be triggered by dim lighting or medications such as anticholinergics, sympathomimetics, antihistamines, antipsychotics, tricyclic antidepressants, and sulfonamides like topiramate.
Physical examination in angle-closure glaucoma reveals decreased visual acuity, a mid-dilated nonreactive pupil, corneal edema with hazy appearance, conjunctival injection with ciliary flush, and a firm globe on palpation.
Essential Workup
A complete ocular examination is required, including visual acuity testing, tonometry, and slit-lamp examination.
Diagnosis Tests And Interpretation
Normal intraocular pressure ranges from 10–21 mm Hg. In open-angle glaucoma, pressure elevation is variable and may be normal in up to 30% of patients. In angle-closure glaucoma, any elevation is abnormal and values are often greater than 40 mm Hg. Slit-lamp examination evaluates the anterior chamber and excludes other ocular pathology. Gonioscopy provides direct assessment of the chamber angle and confirms angle closure.
Differential Diagnosis
Cavernous sinus thrombosis, acute iritis or uveitis, retinal artery or vein occlusion, temporal arteritis, retinal detachment, conjunctivitis, and corneal abrasion.
Treatment Pre Hospital
No specific prehospital ocular intervention is required. Provide analgesia as needed and stabilize other injuries if trauma is involved.
Initial Stabilization Therapy
In suspected acute angle-closure glaucoma, immediately initiate measures to reduce intraocular pressure and discontinue precipitating medications when applicable.
Ed Treatment Procedures
Open-angle glaucoma requires recognition and urgent ophthalmology referral. Long-term management typically involves topical beta-blockers or prostaglandin analogs.
Acute angle-closure glaucoma is an ophthalmologic emergency. Immediate treatment includes topical beta-blockers and alpha-2 agonists to reduce aqueous humor production, carbonic anhydrase inhibitors such as acetazolamide, and hyperosmotic agents like mannitol in severe cases. Once intraocular pressure is below 40 mm Hg, pilocarpine is used to constrict the pupil and open the trabecular meshwork. Topical corticosteroids reduce inflammation. Emergent ophthalmology consultation is required for definitive management, often with laser iridectomy. Adequate analgesia and antiemetics should be provided.
Medication
Common agents include acetazolamide, mannitol, pilocarpine, prednisolone acetate, topical beta-blockers (timolol, betaxolol), alpha-agonists (apraclonidine, brimonidine), carbonic anhydrase inhibitors (dorzolamide, brinzolamide), and prostaglandin analogs (latanoprost, bimatoprost, travoprost). Prostaglandin analogs are first-line for open-angle glaucoma due to favorable side-effect profiles, though cost may limit use.
Follow-Up Disposition
Admission is indicated for severe pain, nausea, vomiting, need for parenteral therapy, or lack of improvement in intraocular pressure. Patients with symptom resolution and improved pressures may be discharged after ophthalmology evaluation with close follow-up within 24 hours.
Issues For Referral
If ophthalmology is unavailable, initiate treatment and transfer the patient to a facility with ophthalmologic services.
Follow-Up Recommendations
Open-angle glaucoma requires urgent outpatient ophthalmology follow-up. Angle-closure glaucoma requires immediate specialist intervention.
Key Clinical Insights And Avoidable Errors
Delayed reduction of intraocular pressure can lead to permanent vision loss. Eye pain or headache associated with abdominal symptoms should prompt ocular evaluation to avoid missed diagnosis. Patients using topical beta-blockers may develop systemic adverse effects such as bradycardia, hypotension, or syncope, which can complicate presentation and management.
Basics Description
Glaucoma is a group of disorders characterized by elevated intraocular pressure, progressive optic neuropathy, and irreversible vision loss if untreated.
Etiology
Primary glaucoma includes open-angle and angle-closure forms. Primary open-angle glaucoma has a normal anterior chamber angle, insidious onset, and chronic elevation of intraocular pressure. It accounts for approximately 90% of glaucoma cases in the United States and is a leading cause of blindness in African Americans. Risk factors include African American race, age over 40 years, family history, myopia, diabetes, and hypertension.
Primary angle-closure glaucoma results from narrowing or closure of the anterior chamber angle, preventing normal aqueous humor outflow through the trabecular meshwork. It presents abruptly with a sudden rise in intraocular pressure. Risk factors include Asian and Eskimo ethnicity, hyperopia, increasing age, female sex, and family history.
Secondary glaucoma may be open or closed angle and occurs due to other conditions such as ocular disease, trauma, systemic illness, or medications. Common drug causes include steroids, sertraline, bronchodilators, and topiramate. Associated diseases include uveitis, neovascularization, neurofibromatosis, intraocular tumors, trauma, and rapid correction of hyperglycemia.
Diagnosis Signs And Symptoms
Open-angle glaucoma typically causes painless, gradual loss of peripheral vision and may present late. Angle-closure glaucoma classically presents with painful loss of vision and a fixed, mid-dilated pupil.
History in open-angle disease includes slow bilateral visual decline or night blindness without pain. Angle-closure disease presents with severe eye pain, ipsilateral headache, nausea, vomiting, decreased visual acuity, halos around lights, and visual clouding. Symptoms may be triggered by dim lighting or medications such as anticholinergics, sympathomimetics, antihistamines, antipsychotics, tricyclic antidepressants, and sulfonamides like topiramate.
Physical examination in angle-closure glaucoma reveals decreased visual acuity, a mid-dilated nonreactive pupil, corneal edema with hazy appearance, conjunctival injection with ciliary flush, and a firm globe on palpation.
Essential Workup
A complete ocular examination is required, including visual acuity testing, tonometry, and slit-lamp examination.
Diagnosis Tests And Interpretation
Normal intraocular pressure ranges from 10–21 mm Hg. In open-angle glaucoma, pressure elevation is variable and may be normal in up to 30% of patients. In angle-closure glaucoma, any elevation is abnormal and values are often greater than 40 mm Hg. Slit-lamp examination evaluates the anterior chamber and excludes other ocular pathology. Gonioscopy provides direct assessment of the chamber angle and confirms angle closure.
Differential Diagnosis
Cavernous sinus thrombosis, acute iritis or uveitis, retinal artery or vein occlusion, temporal arteritis, retinal detachment, conjunctivitis, and corneal abrasion.
Treatment Pre Hospital
No specific prehospital ocular intervention is required. Provide analgesia as needed and stabilize other injuries if trauma is involved.
Initial Stabilization Therapy
In suspected acute angle-closure glaucoma, immediately initiate measures to reduce intraocular pressure and discontinue precipitating medications when applicable.
Ed Treatment Procedures
Open-angle glaucoma requires recognition and urgent ophthalmology referral. Long-term management typically involves topical beta-blockers or prostaglandin analogs.
Acute angle-closure glaucoma is an ophthalmologic emergency. Immediate treatment includes topical beta-blockers and alpha-2 agonists to reduce aqueous humor production, carbonic anhydrase inhibitors such as acetazolamide, and hyperosmotic agents like mannitol in severe cases. Once intraocular pressure is below 40 mm Hg, pilocarpine is used to constrict the pupil and open the trabecular meshwork. Topical corticosteroids reduce inflammation. Emergent ophthalmology consultation is required for definitive management, often with laser iridectomy. Adequate analgesia and antiemetics should be provided.
Medication
Common agents include acetazolamide, mannitol, pilocarpine, prednisolone acetate, topical beta-blockers (timolol, betaxolol), alpha-agonists (apraclonidine, brimonidine), carbonic anhydrase inhibitors (dorzolamide, brinzolamide), and prostaglandin analogs (latanoprost, bimatoprost, travoprost). Prostaglandin analogs are first-line for open-angle glaucoma due to favorable side-effect profiles, though cost may limit use.
Follow-Up Disposition
Admission is indicated for severe pain, nausea, vomiting, need for parenteral therapy, or lack of improvement in intraocular pressure. Patients with symptom resolution and improved pressures may be discharged after ophthalmology evaluation with close follow-up within 24 hours.
Issues For Referral
If ophthalmology is unavailable, initiate treatment and transfer the patient to a facility with ophthalmologic services.
Follow-Up Recommendations
Open-angle glaucoma requires urgent outpatient ophthalmology follow-up. Angle-closure glaucoma requires immediate specialist intervention.
Key Clinical Insights And Avoidable Errors
Delayed reduction of intraocular pressure can lead to permanent vision loss. Eye pain or headache associated with abdominal symptoms should prompt ocular evaluation to avoid missed diagnosis. Patients using topical beta-blockers may develop systemic adverse effects such as bradycardia, hypotension, or syncope, which can complicate presentation and management.
