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Emergency And Acute Medicine – Rabies
Rabies is a viral infection of the central nervous system affecting mammals and has the highest case fatality rate of any known infectious disease once clinical symptoms develop. It is caused by a negative-stranded RNA virus in the genus Lyssavirus of the family Rhabdoviridae. Worldwide, rabies causes approximately 30,000–70,000 deaths annually, most commonly in Southeast Asia, the Philippines, Africa, South America, and the Indian subcontinent. In the United States, 2–3 human cases occur per year, most related to foreign travel or bat exposure. In the U.S., bats are the most common reservoir; globally, dogs are the primary reservoir. Other reservoirs include raccoons, skunks, foxes, woodchucks, and groundhogs. Small rodents such as squirrels and rats have not been documented to transmit rabies to humans.
Transmission occurs through contact with infected saliva, most commonly via animal bite. Nonbite transmission may occur through saliva exposure to mucous membranes or open wounds. Bat exposures may occur without a visible bite. Organ transplantation represents the only well-documented person-to-person transmission. Casual contact such as petting an animal or contact with blood, urine, or feces is not considered a transmission risk.
After inoculation, the virus replicates locally in muscle tissue and binds to nicotinic acetylcholine receptors, then enters peripheral nerves and travels via retrograde axonal transport toward the CNS at approximately 1–4 inches per day. Once in the CNS, rapid viral replication causes encephalitis. The virus then spreads centrifugally to peripheral nerves and salivary glands.
The disease progresses through five stages: incubation, prodrome, encephalitis, coma, and death (rarely recovery). The incubation period averages 1–3 months but may range from 10 days to 1 year, depending on viral load and proximity of the exposure to the CNS. The prodrome lasts 1–7 days and includes nonspecific symptoms such as fever, headache, malaise, myalgias, nausea, and sore throat. Paresthesias or fasciculations at the bite site are highly suggestive.
The encephalitic (classic) form accounts for approximately 80% of cases. Patients develop anxiety, agitation, hallucinations, confusion, seizures, muscle spasms, and autonomic instability. Hydrophobia—painful pharyngeal spasms triggered by attempts to swallow—and aerophobia—pharyngeal spasms induced by airflow—are pathognomonic. Brainstem involvement may cause diplopia and facial paralysis. Paralytic rabies (about 20%) presents with ascending paralysis resembling Guillain–Barré syndrome. Atypical forms, often associated with bat exposures, may present with neuropathic pain or movement disorders.
Once neurologic symptoms appear, rabies is almost universally fatal. Most patients die within two weeks of symptom onset due to respiratory failure or cardiovascular collapse. Rare survivors typically have significant neurologic deficits.
Diagnosis during life relies on detection of rabies RNA by RT-PCR in saliva, virus isolation, or detection of rabies antibodies in serum (if unvaccinated) or cerebrospinal fluid (CSF). CSF may show mild pleocytosis and elevated protein. Neuroimaging is often normal but may demonstrate cerebral edema. A high index of suspicion is essential, especially in patients with unexplained encephalitis and a history of animal exposure or travel to endemic areas.
Emergency management begins with thorough wound cleansing using soap and water, which significantly reduces viral load. Tetanus immunization should be updated as indicated. Determination of need for postexposure prophylaxis (PEP) should involve consultation with local public health authorities. For domestic animals, a 10-day observation period may be appropriate. For wild animals, the animal should be tested if available. If the animal cannot be tested or exposure is high risk, PEP should be initiated.
PEP consists of both passive and active immunization. Human rabies immune globulin (HRIG) is administered at 20 IU/kg, with as much as possible infiltrated around the wound and the remainder given intramuscularly at a site distant from vaccine administration. Rabies vaccine (1 mL IM in the deltoid in adults or anterolateral thigh in infants) is given on days 0, 3, 7, and 14, with an additional dose on day 28 for immunocompromised patients. Individuals previously vaccinated require only vaccine doses on days 0 and 3 and do not require HRIG. HRIG should not be administered more than 7 days after the first vaccine dose.
Pre-exposure prophylaxis consists of vaccination on days 0, 7, and either 21 or 28 and is recommended for veterinarians, animal handlers, laboratory workers, and travelers to endemic regions. Rabies vaccination and HRIG are considered safe in pregnancy.
Patients with clinical rabies require hospital admission and supportive care. Stable patients receiving PEP may be discharged with arrangements for completion of the vaccine series. Coordination with public health authorities is essential.
The key principle is that postexposure prophylaxis is the only proven effective intervention and must be administered promptly in all high-risk exposures. Once symptoms develop, rabies is almost universally fatal.
Rabies is a viral infection of the central nervous system affecting mammals and has the highest case fatality rate of any known infectious disease once clinical symptoms develop. It is caused by a negative-stranded RNA virus in the genus Lyssavirus of the family Rhabdoviridae. Worldwide, rabies causes approximately 30,000–70,000 deaths annually, most commonly in Southeast Asia, the Philippines, Africa, South America, and the Indian subcontinent. In the United States, 2–3 human cases occur per year, most related to foreign travel or bat exposure. In the U.S., bats are the most common reservoir; globally, dogs are the primary reservoir. Other reservoirs include raccoons, skunks, foxes, woodchucks, and groundhogs. Small rodents such as squirrels and rats have not been documented to transmit rabies to humans.
Transmission occurs through contact with infected saliva, most commonly via animal bite. Nonbite transmission may occur through saliva exposure to mucous membranes or open wounds. Bat exposures may occur without a visible bite. Organ transplantation represents the only well-documented person-to-person transmission. Casual contact such as petting an animal or contact with blood, urine, or feces is not considered a transmission risk.
After inoculation, the virus replicates locally in muscle tissue and binds to nicotinic acetylcholine receptors, then enters peripheral nerves and travels via retrograde axonal transport toward the CNS at approximately 1–4 inches per day. Once in the CNS, rapid viral replication causes encephalitis. The virus then spreads centrifugally to peripheral nerves and salivary glands.
The disease progresses through five stages: incubation, prodrome, encephalitis, coma, and death (rarely recovery). The incubation period averages 1–3 months but may range from 10 days to 1 year, depending on viral load and proximity of the exposure to the CNS. The prodrome lasts 1–7 days and includes nonspecific symptoms such as fever, headache, malaise, myalgias, nausea, and sore throat. Paresthesias or fasciculations at the bite site are highly suggestive.
The encephalitic (classic) form accounts for approximately 80% of cases. Patients develop anxiety, agitation, hallucinations, confusion, seizures, muscle spasms, and autonomic instability. Hydrophobia—painful pharyngeal spasms triggered by attempts to swallow—and aerophobia—pharyngeal spasms induced by airflow—are pathognomonic. Brainstem involvement may cause diplopia and facial paralysis. Paralytic rabies (about 20%) presents with ascending paralysis resembling Guillain–Barré syndrome. Atypical forms, often associated with bat exposures, may present with neuropathic pain or movement disorders.
Once neurologic symptoms appear, rabies is almost universally fatal. Most patients die within two weeks of symptom onset due to respiratory failure or cardiovascular collapse. Rare survivors typically have significant neurologic deficits.
Diagnosis during life relies on detection of rabies RNA by RT-PCR in saliva, virus isolation, or detection of rabies antibodies in serum (if unvaccinated) or cerebrospinal fluid (CSF). CSF may show mild pleocytosis and elevated protein. Neuroimaging is often normal but may demonstrate cerebral edema. A high index of suspicion is essential, especially in patients with unexplained encephalitis and a history of animal exposure or travel to endemic areas.
Emergency management begins with thorough wound cleansing using soap and water, which significantly reduces viral load. Tetanus immunization should be updated as indicated. Determination of need for postexposure prophylaxis (PEP) should involve consultation with local public health authorities. For domestic animals, a 10-day observation period may be appropriate. For wild animals, the animal should be tested if available. If the animal cannot be tested or exposure is high risk, PEP should be initiated.
PEP consists of both passive and active immunization. Human rabies immune globulin (HRIG) is administered at 20 IU/kg, with as much as possible infiltrated around the wound and the remainder given intramuscularly at a site distant from vaccine administration. Rabies vaccine (1 mL IM in the deltoid in adults or anterolateral thigh in infants) is given on days 0, 3, 7, and 14, with an additional dose on day 28 for immunocompromised patients. Individuals previously vaccinated require only vaccine doses on days 0 and 3 and do not require HRIG. HRIG should not be administered more than 7 days after the first vaccine dose.
Pre-exposure prophylaxis consists of vaccination on days 0, 7, and either 21 or 28 and is recommended for veterinarians, animal handlers, laboratory workers, and travelers to endemic regions. Rabies vaccination and HRIG are considered safe in pregnancy.
Patients with clinical rabies require hospital admission and supportive care. Stable patients receiving PEP may be discharged with arrangements for completion of the vaccine series. Coordination with public health authorities is essential.
The key principle is that postexposure prophylaxis is the only proven effective intervention and must be administered promptly in all high-risk exposures. Once symptoms develop, rabies is almost universally fatal.
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Emergency And Acute Medicine – QT Syndrome, Prolonged
Prolonged QT syndrome is a disorder of myocardial repolarization characterized by prolongation of the QT interval on electrocardiogram (ECG). It reflects delayed ventricular repolarization and predisposes patients to malignant ventricular arrhythmias, particularly torsades de pointes, ventricular tachycardia, and ventricular fibrillation. These arrhythmias may cause syncope, seizures, or sudden cardiac death.
The underlying pathophysiology involves abnormalities in cardiac sodium, potassium, or calcium ion channels and may also include imbalance in sympathetic innervation. QT prolongation may be “pause-dependent,” often following a short–long–short sequence, or “adrenergic-dependent,” particularly in congenital forms triggered by exercise, emotional stress, or loud auditory stimuli. Nocturnal bradycardia can also lengthen the QT interval, leading to sleep-related events. Prolonged QT is an independent risk factor for sudden cardiac death.
Congenital long QT syndrome is linked to mutations in at least 10 genes affecting cardiac ion channels. The autosomal recessive form associated with congenital deafness is known as Jervell and Lange-Nielsen syndrome, while the autosomal dominant form without deafness is Romano-Ward syndrome. The congenital form occurs in approximately 1 in 3,000–5,000 individuals, with mortality of about 6% by age 40 if untreated. Ten to fifteen percent of gene carriers may have a normal baseline QTc. Sudden death may occur without warning symptoms in some pediatric patients.
Acquired QT prolongation is most commonly drug-induced or secondary to metabolic abnormalities. Medications associated with QT prolongation include class Ia and III antiarrhythmics, certain antibiotics (e.g., erythromycin), antifungals, psychotropic agents (e.g., haloperidol), methadone, and others. Electrolyte abnormalities such as hypokalemia, hypomagnesemia, and hypocalcemia are common causes. Cardiac conditions (bradyarrhythmias, AV block, myocarditis, ischemia), CNS disorders (subarachnoid hemorrhage, stroke), hypothyroidism, hypothermia, anorexia nervosa, and severe fasting may also contribute.
Patients may present with palpitations, lightheadedness, dizziness, syncope, or seizure-like activity. A history of syncope during exercise or emotional stress is suggestive. Family history of sudden death or syncope and congenital deafness are important clues. Medication review is essential.
Diagnosis is based on ECG findings. QTc (corrected QT) is considered prolonged when >0.44 seconds in men and >0.46 seconds in women. The QT interval is measured from the beginning of the QRS complex to the end of the T wave and averaged over several beats. The Bazett formula (QT divided by the square root of the RR interval) is most commonly used for correction. ECG may also show T-wave abnormalities, U waves, increased QT variability, torsades de pointes, or ventricular arrhythmias. Laboratory evaluation should include serum electrolytes, calcium, magnesium, and toxicology screen. Echocardiography may be performed to exclude structural heart disease. Holter monitoring, stress testing, and genetic testing may be considered in suspected congenital cases.
Initial management focuses on stabilization and arrhythmia treatment. Patients should receive supplemental oxygen, IV access, and cardiac monitoring. Hemodynamically unstable patients with torsades de pointes require immediate synchronized cardioversion or defibrillation as indicated.
Magnesium sulfate is first-line therapy for torsades de pointes, even if serum magnesium levels are normal. A typical adult dose is 2 g IV over 2–3 minutes, followed by infusion if needed. Serum potassium should be corrected to high-normal levels (4.5–5.0 mEq/L). In recurrent torsades refractory to magnesium, temporary transvenous pacing at rates of 100–120 bpm may shorten the QT interval. IV isoproterenol may be used in acquired long QT cases associated with bradycardia but is generally ineffective in congenital forms. Offending medications must be discontinued and metabolic abnormalities corrected.
For congenital long QT syndrome, β-blockers reduce the risk of arrhythmic events by approximately 70% and are recommended in symptomatic patients under cardiology guidance. High-risk patients may require pacemaker placement, implantable cardioverter-defibrillator (ICD), or surgical sympathetic denervation.
Admission is indicated for symptomatic patients, those with syncope, ventricular arrhythmias, metabolic abnormalities, or suspected ischemia. Asymptomatic patients with incidental prolonged QT may be discharged after cardiology consultation if no high-risk features are present.
Prolonged QT should be suspected in any patient presenting with unexplained syncope or seizure-like activity. Prompt correction of electrolyte abnormalities and discontinuation of QT-prolonging medications are essential. Magnesium sulfate followed by pacing remains the cornerstone of treatment for torsades de pointes. All patients with newly identified prolonged QT require cardiology follow-up.
Prolonged QT syndrome is a disorder of myocardial repolarization characterized by prolongation of the QT interval on electrocardiogram (ECG). It reflects delayed ventricular repolarization and predisposes patients to malignant ventricular arrhythmias, particularly torsades de pointes, ventricular tachycardia, and ventricular fibrillation. These arrhythmias may cause syncope, seizures, or sudden cardiac death.
The underlying pathophysiology involves abnormalities in cardiac sodium, potassium, or calcium ion channels and may also include imbalance in sympathetic innervation. QT prolongation may be “pause-dependent,” often following a short–long–short sequence, or “adrenergic-dependent,” particularly in congenital forms triggered by exercise, emotional stress, or loud auditory stimuli. Nocturnal bradycardia can also lengthen the QT interval, leading to sleep-related events. Prolonged QT is an independent risk factor for sudden cardiac death.
Congenital long QT syndrome is linked to mutations in at least 10 genes affecting cardiac ion channels. The autosomal recessive form associated with congenital deafness is known as Jervell and Lange-Nielsen syndrome, while the autosomal dominant form without deafness is Romano-Ward syndrome. The congenital form occurs in approximately 1 in 3,000–5,000 individuals, with mortality of about 6% by age 40 if untreated. Ten to fifteen percent of gene carriers may have a normal baseline QTc. Sudden death may occur without warning symptoms in some pediatric patients.
Acquired QT prolongation is most commonly drug-induced or secondary to metabolic abnormalities. Medications associated with QT prolongation include class Ia and III antiarrhythmics, certain antibiotics (e.g., erythromycin), antifungals, psychotropic agents (e.g., haloperidol), methadone, and others. Electrolyte abnormalities such as hypokalemia, hypomagnesemia, and hypocalcemia are common causes. Cardiac conditions (bradyarrhythmias, AV block, myocarditis, ischemia), CNS disorders (subarachnoid hemorrhage, stroke), hypothyroidism, hypothermia, anorexia nervosa, and severe fasting may also contribute.
Patients may present with palpitations, lightheadedness, dizziness, syncope, or seizure-like activity. A history of syncope during exercise or emotional stress is suggestive. Family history of sudden death or syncope and congenital deafness are important clues. Medication review is essential.
Diagnosis is based on ECG findings. QTc (corrected QT) is considered prolonged when >0.44 seconds in men and >0.46 seconds in women. The QT interval is measured from the beginning of the QRS complex to the end of the T wave and averaged over several beats. The Bazett formula (QT divided by the square root of the RR interval) is most commonly used for correction. ECG may also show T-wave abnormalities, U waves, increased QT variability, torsades de pointes, or ventricular arrhythmias. Laboratory evaluation should include serum electrolytes, calcium, magnesium, and toxicology screen. Echocardiography may be performed to exclude structural heart disease. Holter monitoring, stress testing, and genetic testing may be considered in suspected congenital cases.
Initial management focuses on stabilization and arrhythmia treatment. Patients should receive supplemental oxygen, IV access, and cardiac monitoring. Hemodynamically unstable patients with torsades de pointes require immediate synchronized cardioversion or defibrillation as indicated.
Magnesium sulfate is first-line therapy for torsades de pointes, even if serum magnesium levels are normal. A typical adult dose is 2 g IV over 2–3 minutes, followed by infusion if needed. Serum potassium should be corrected to high-normal levels (4.5–5.0 mEq/L). In recurrent torsades refractory to magnesium, temporary transvenous pacing at rates of 100–120 bpm may shorten the QT interval. IV isoproterenol may be used in acquired long QT cases associated with bradycardia but is generally ineffective in congenital forms. Offending medications must be discontinued and metabolic abnormalities corrected.
For congenital long QT syndrome, β-blockers reduce the risk of arrhythmic events by approximately 70% and are recommended in symptomatic patients under cardiology guidance. High-risk patients may require pacemaker placement, implantable cardioverter-defibrillator (ICD), or surgical sympathetic denervation.
Admission is indicated for symptomatic patients, those with syncope, ventricular arrhythmias, metabolic abnormalities, or suspected ischemia. Asymptomatic patients with incidental prolonged QT may be discharged after cardiology consultation if no high-risk features are present.
Prolonged QT should be suspected in any patient presenting with unexplained syncope or seizure-like activity. Prompt correction of electrolyte abnormalities and discontinuation of QT-prolonging medications are essential. Magnesium sulfate followed by pacing remains the cornerstone of treatment for torsades de pointes. All patients with newly identified prolonged QT require cardiology follow-up.
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Emergency And Acute Medicine – Red Eye
Red eye is a common presentation caused by vascular engorgement of the conjunctiva and may result from nearly any ocular disorder. Although frequently benign, it can signal serious ocular or systemic disease. Conjunctivitis is the most common cause, but inflammatory, allergic, infectious, traumatic, and glaucomatous etiologies must be considered.
Inflammatory causes include uveitis (anterior or posterior), iritis with perilimbic injection, episcleritis (often idiopathic), and scleritis, which is commonly associated with systemic disease. Allergic conjunctivitis results from histamine-mediated vascular permeability and typically presents bilaterally with chemosis, watery discharge, and pruritus. Infectious causes include bacterial conjunctivitis with purulent discharge, viral conjunctivitis with watery discharge, and less commonly fungal infection. More severe infections include orbital cellulitis, dacryocystitis, canaliculitis, and endophthalmitis. Traumatic causes include corneal abrasion, subconjunctival hemorrhage, foreign body, and occult globe perforation. Other etiologies include pingueculitis, pterygium, blepharitis, dry eye syndrome, conjunctival tumors, ophthalmia neonatorum, and acute angle-closure glaucoma.
History should assess age, onset and duration of symptoms, chemical or allergen exposure, occupation (e.g., metal worker), contact lens use, associated systemic symptoms, and comorbidities. Key ocular symptoms include pain, foreign-body sensation, vision change, discharge, and pruritus. In neonates and patients over 50 years of age, particular caution is required.
Physical examination must include visual acuity in all patients. Assess for diffuse versus localized injection, lid involvement, discharge type, foreign body, proptosis, photophobia, pupil abnormalities, extraocular movements, and visual fields. Examine for preauricular lymphadenopathy and facial lesions suggestive of herpes infection. Slit-lamp examination with fluorescein is essential to evaluate for corneal abrasion, ulceration, dendritic lesions of herpes simplex virus, anterior chamber cell or flare, and foreign body. Lid eversion is required to exclude retained foreign material. Fundoscopy and tonometry should be performed when glaucoma is suspected.
Diagnostic testing is directed by suspected etiology. Culture of discharge may be indicated in dacryocystitis or severe bacterial conjunctivitis, especially if Neisseria gonorrhoeae is suspected, which requires special media such as Thayer–Martin agar. Corneal ulcers require scraping for culture, typically by ophthalmology. Neonatal conjunctivitis is most commonly due to Chlamydia trachomatis, while gonococcal infection presents early with copious purulent discharge and requires urgent treatment. Systemic workup may be necessary in suspected inflammatory or granulomatous uveitis and may include CBC, ESR, ANA, VDRL, FTA-ABS, ACE level, tuberculosis testing, Lyme titers, HLA-B27, and chest imaging. Orbital imaging with CT is indicated when orbital cellulitis, trauma, or foreign body is suspected.
Initial management includes removal of contact lenses and immediate irrigation for chemical injuries. Chemical exposure requires copious irrigation prior to detailed examination. Treatment is directed at the underlying cause. Eye patching is no longer recommended for corneal abrasions and may be contraindicated. Tetanus immunization should be updated in traumatic injuries. Patients should avoid contact lens use until cleared by an eye specialist.
Corneal abrasions in non–contact lens wearers are treated with erythromycin ointment or polymyxin B/trimethoprim drops. Contact lens wearers require antipseudomonal coverage such as ofloxacin, ciprofloxacin, or tobramycin drops. Cycloplegics such as cyclopentolate may reduce pain from associated iritis. Corneal ulcers require more aggressive antibiotic therapy, often with fluoroquinolone drops at frequent intervals, and urgent ophthalmology consultation. Severe or central ulcers may require intensive dosing and possible hospitalization.
Acute angle-closure glaucoma presents with severe eye pain, decreased vision, mid-dilated nonreactive pupil, nausea, vomiting, and elevated intraocular pressure above 21 mm Hg. This is an ophthalmologic emergency requiring pressure-lowering therapy and urgent consultation. Subconjunctival hemorrhage generally requires reassurance unless trauma suggests globe rupture. Herpes simplex or zoster keratitis requires antiviral therapy such as trifluridine drops or vidarabine ointment and ophthalmology consultation. Steroid use should only occur under specialist guidance.
Admission is required for endophthalmitis, perforated corneal ulcers, orbital cellulitis, significant trauma, or systemic involvement. Neonates with suspected gonococcal conjunctivitis require hospitalization and intravenous antibiotics. Urgent ophthalmology referral is necessary for dacryocystitis, corneal ulcer, scleritis, angle-closure glaucoma, uveitis, proptosis, orbital cellulitis, vision loss, uncertain diagnosis, and gonococcal or chlamydial conjunctivitis.
Failure to recognize corneal ulcer, herpetic infection, neonatal bacterial infection, angle-closure glaucoma, or penetrating trauma may result in permanent vision loss. Steroids should never be initiated without ophthalmologic consultation. Prompt reassessment is required if symptoms do not improve as expected.
Red eye is a common presentation caused by vascular engorgement of the conjunctiva and may result from nearly any ocular disorder. Although frequently benign, it can signal serious ocular or systemic disease. Conjunctivitis is the most common cause, but inflammatory, allergic, infectious, traumatic, and glaucomatous etiologies must be considered.
Inflammatory causes include uveitis (anterior or posterior), iritis with perilimbic injection, episcleritis (often idiopathic), and scleritis, which is commonly associated with systemic disease. Allergic conjunctivitis results from histamine-mediated vascular permeability and typically presents bilaterally with chemosis, watery discharge, and pruritus. Infectious causes include bacterial conjunctivitis with purulent discharge, viral conjunctivitis with watery discharge, and less commonly fungal infection. More severe infections include orbital cellulitis, dacryocystitis, canaliculitis, and endophthalmitis. Traumatic causes include corneal abrasion, subconjunctival hemorrhage, foreign body, and occult globe perforation. Other etiologies include pingueculitis, pterygium, blepharitis, dry eye syndrome, conjunctival tumors, ophthalmia neonatorum, and acute angle-closure glaucoma.
History should assess age, onset and duration of symptoms, chemical or allergen exposure, occupation (e.g., metal worker), contact lens use, associated systemic symptoms, and comorbidities. Key ocular symptoms include pain, foreign-body sensation, vision change, discharge, and pruritus. In neonates and patients over 50 years of age, particular caution is required.
Physical examination must include visual acuity in all patients. Assess for diffuse versus localized injection, lid involvement, discharge type, foreign body, proptosis, photophobia, pupil abnormalities, extraocular movements, and visual fields. Examine for preauricular lymphadenopathy and facial lesions suggestive of herpes infection. Slit-lamp examination with fluorescein is essential to evaluate for corneal abrasion, ulceration, dendritic lesions of herpes simplex virus, anterior chamber cell or flare, and foreign body. Lid eversion is required to exclude retained foreign material. Fundoscopy and tonometry should be performed when glaucoma is suspected.
Diagnostic testing is directed by suspected etiology. Culture of discharge may be indicated in dacryocystitis or severe bacterial conjunctivitis, especially if Neisseria gonorrhoeae is suspected, which requires special media such as Thayer–Martin agar. Corneal ulcers require scraping for culture, typically by ophthalmology. Neonatal conjunctivitis is most commonly due to Chlamydia trachomatis, while gonococcal infection presents early with copious purulent discharge and requires urgent treatment. Systemic workup may be necessary in suspected inflammatory or granulomatous uveitis and may include CBC, ESR, ANA, VDRL, FTA-ABS, ACE level, tuberculosis testing, Lyme titers, HLA-B27, and chest imaging. Orbital imaging with CT is indicated when orbital cellulitis, trauma, or foreign body is suspected.
Initial management includes removal of contact lenses and immediate irrigation for chemical injuries. Chemical exposure requires copious irrigation prior to detailed examination. Treatment is directed at the underlying cause. Eye patching is no longer recommended for corneal abrasions and may be contraindicated. Tetanus immunization should be updated in traumatic injuries. Patients should avoid contact lens use until cleared by an eye specialist.
Corneal abrasions in non–contact lens wearers are treated with erythromycin ointment or polymyxin B/trimethoprim drops. Contact lens wearers require antipseudomonal coverage such as ofloxacin, ciprofloxacin, or tobramycin drops. Cycloplegics such as cyclopentolate may reduce pain from associated iritis. Corneal ulcers require more aggressive antibiotic therapy, often with fluoroquinolone drops at frequent intervals, and urgent ophthalmology consultation. Severe or central ulcers may require intensive dosing and possible hospitalization.
Acute angle-closure glaucoma presents with severe eye pain, decreased vision, mid-dilated nonreactive pupil, nausea, vomiting, and elevated intraocular pressure above 21 mm Hg. This is an ophthalmologic emergency requiring pressure-lowering therapy and urgent consultation. Subconjunctival hemorrhage generally requires reassurance unless trauma suggests globe rupture. Herpes simplex or zoster keratitis requires antiviral therapy such as trifluridine drops or vidarabine ointment and ophthalmology consultation. Steroid use should only occur under specialist guidance.
Admission is required for endophthalmitis, perforated corneal ulcers, orbital cellulitis, significant trauma, or systemic involvement. Neonates with suspected gonococcal conjunctivitis require hospitalization and intravenous antibiotics. Urgent ophthalmology referral is necessary for dacryocystitis, corneal ulcer, scleritis, angle-closure glaucoma, uveitis, proptosis, orbital cellulitis, vision loss, uncertain diagnosis, and gonococcal or chlamydial conjunctivitis.
Failure to recognize corneal ulcer, herpetic infection, neonatal bacterial infection, angle-closure glaucoma, or penetrating trauma may result in permanent vision loss. Steroids should never be initiated without ophthalmologic consultation. Prompt reassessment is required if symptoms do not improve as expected.
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Emergency And Acute Medicine – Rectal Trauma
Rectal trauma refers to injury of the rectal mucosa ranging from simple contusion to full-thickness laceration with extension into the peritoneum or perineum. Approximately two-thirds of the rectum is extraperitoneal, which influences management and risk of contamination. Injuries may result from penetrating, blunt, foreign body, or iatrogenic causes.
Penetrating trauma accounts for most severe injuries, with gunshot wounds responsible for approximately 80% of penetrating rectal trauma, followed by stab and impalement injuries. Blunt trauma may occur in motor vehicle collisions, hydrostatic injuries such as waterskiing accidents, or pelvic fractures where bone fragments penetrate the rectum. Rectal foreign bodies may be associated with autoerotic activity, assault, anal intercourse, or ingestion of sharp objects. Iatrogenic trauma is the most common overall cause and includes complications of barium enema, colonoscopy (particularly with polypectomy), hemorrhoidectomy, and urologic or obstetric procedures such as episiotomy. In children, rectal injury may result from thermometer insertion, and any rectal trauma in young children should raise concern for nonaccidental injury.
Patients may present with perineal, anal, or lower abdominal pain, rectal bleeding, obstipation, or signs of perforation and peritonitis such as guarding, rebound tenderness, and fever. A pelvic fracture increases suspicion for rectal injury. History should include mechanism, timing, and any anal manipulation or instrumentation. Rectal injury must be suspected in all patients with gunshot wounds, stab wounds, or impalement injuries involving the trunk, buttocks, perineum, or upper thigh.
Physical examination requires careful inspection and palpation of the buttocks, anus, and perineum. Entrance and exit wounds should be identified in penetrating trauma. Digital rectal examination assesses for gross blood or occult blood and evaluates prostate position. A high-riding prostate may indicate urethral injury. Female patients require speculum and bimanual examination, and male patients require thorough genitourinary examination.
Laboratory evaluation includes complete blood count to assess for blood loss and leukocytosis suggestive of peritonitis, type and screen if hemorrhage is suspected, and urinalysis to evaluate for genitourinary involvement. Imaging with upright and supine abdominal films and pelvic radiographs may identify pneumoperitoneum, extraperitoneal air, foreign bodies, or pelvic fractures. CT scan of the abdomen and pelvis with appropriate contrast is indicated in blunt trauma or when perforation is suspected. Retrograde urethrogram is required if urethral injury is suspected. Contrast enema with water-soluble contrast may be useful when perforation is uncertain.
Initial management follows trauma principles with airway, breathing, and circulation assessment, spinal precautions in blunt trauma, and fluid resuscitation for hypotension. Prehospital removal of rectal foreign bodies should not be attempted. In the emergency department, tetanus prophylaxis should be updated and broad-spectrum antibiotics covering gram-negative and anaerobic organisms administered when significant mucosal disruption or peritonitis is present. Foley catheter placement should be deferred until urethral injury is excluded.
Rectal foreign body removal may be attempted in the emergency department if the object is low and accessible. The patient is positioned in lithotomy, local anesthesia may be used, and gentle sphincter dilation performed. Obstetric forceps, ring forceps, biopsy forceps, or suction devices may assist extraction. Suprapubic pressure and patient Valsalva maneuver may help. A Foley catheter passed above the object with balloon inflation can relieve suction and facilitate removal. After extraction, sigmoidoscopy should be performed to evaluate for mucosal injury. Surgical consultation is required for peritonitis, full-thickness lacerations, high-riding or sharp objects, objects more than 10 cm from the anal verge, or failed extraction attempts.
Antibiotic regimens should provide gram-negative and anaerobic coverage. Options include ampicillin/sulbactam, cefotetan, cefoxitin, piperacillin/tazobactam, or combination therapy with ampicillin, gentamicin, and metronidazole. Clindamycin or metronidazole may be added for enhanced anaerobic coverage. Analgesia and sedation may include fentanyl and midazolam as needed.
Surgical intervention is indicated for perforation, torn anal sphincter, significant bleeding, high-riding or sharp foreign bodies requiring removal under general anesthesia, or hemodynamic instability. Laparotomy is reserved for severe or complicated cases.
Admission is required for perforation, significant bleeding, unstable vital signs, abdominal pain, torn sphincter, or foreign bodies requiring operative removal. Patients may be discharged if vital signs are stable, abdominal examination is benign, and sigmoidoscopy or anoscopy is normal. All discharged patients require repeat abdominal examination within 12–24 hours and strict return precautions for abdominal pain, vomiting, or fever.
A key pitfall is failure to recognize perforation after foreign body extraction. Approximately 60% of rectal foreign bodies can be removed in the emergency department. High suspicion for rectal injury is essential in patients presenting with abdominal pain after lower gastrointestinal or genitourinary procedures.
Rectal trauma refers to injury of the rectal mucosa ranging from simple contusion to full-thickness laceration with extension into the peritoneum or perineum. Approximately two-thirds of the rectum is extraperitoneal, which influences management and risk of contamination. Injuries may result from penetrating, blunt, foreign body, or iatrogenic causes.
Penetrating trauma accounts for most severe injuries, with gunshot wounds responsible for approximately 80% of penetrating rectal trauma, followed by stab and impalement injuries. Blunt trauma may occur in motor vehicle collisions, hydrostatic injuries such as waterskiing accidents, or pelvic fractures where bone fragments penetrate the rectum. Rectal foreign bodies may be associated with autoerotic activity, assault, anal intercourse, or ingestion of sharp objects. Iatrogenic trauma is the most common overall cause and includes complications of barium enema, colonoscopy (particularly with polypectomy), hemorrhoidectomy, and urologic or obstetric procedures such as episiotomy. In children, rectal injury may result from thermometer insertion, and any rectal trauma in young children should raise concern for nonaccidental injury.
Patients may present with perineal, anal, or lower abdominal pain, rectal bleeding, obstipation, or signs of perforation and peritonitis such as guarding, rebound tenderness, and fever. A pelvic fracture increases suspicion for rectal injury. History should include mechanism, timing, and any anal manipulation or instrumentation. Rectal injury must be suspected in all patients with gunshot wounds, stab wounds, or impalement injuries involving the trunk, buttocks, perineum, or upper thigh.
Physical examination requires careful inspection and palpation of the buttocks, anus, and perineum. Entrance and exit wounds should be identified in penetrating trauma. Digital rectal examination assesses for gross blood or occult blood and evaluates prostate position. A high-riding prostate may indicate urethral injury. Female patients require speculum and bimanual examination, and male patients require thorough genitourinary examination.
Laboratory evaluation includes complete blood count to assess for blood loss and leukocytosis suggestive of peritonitis, type and screen if hemorrhage is suspected, and urinalysis to evaluate for genitourinary involvement. Imaging with upright and supine abdominal films and pelvic radiographs may identify pneumoperitoneum, extraperitoneal air, foreign bodies, or pelvic fractures. CT scan of the abdomen and pelvis with appropriate contrast is indicated in blunt trauma or when perforation is suspected. Retrograde urethrogram is required if urethral injury is suspected. Contrast enema with water-soluble contrast may be useful when perforation is uncertain.
Initial management follows trauma principles with airway, breathing, and circulation assessment, spinal precautions in blunt trauma, and fluid resuscitation for hypotension. Prehospital removal of rectal foreign bodies should not be attempted. In the emergency department, tetanus prophylaxis should be updated and broad-spectrum antibiotics covering gram-negative and anaerobic organisms administered when significant mucosal disruption or peritonitis is present. Foley catheter placement should be deferred until urethral injury is excluded.
Rectal foreign body removal may be attempted in the emergency department if the object is low and accessible. The patient is positioned in lithotomy, local anesthesia may be used, and gentle sphincter dilation performed. Obstetric forceps, ring forceps, biopsy forceps, or suction devices may assist extraction. Suprapubic pressure and patient Valsalva maneuver may help. A Foley catheter passed above the object with balloon inflation can relieve suction and facilitate removal. After extraction, sigmoidoscopy should be performed to evaluate for mucosal injury. Surgical consultation is required for peritonitis, full-thickness lacerations, high-riding or sharp objects, objects more than 10 cm from the anal verge, or failed extraction attempts.
Antibiotic regimens should provide gram-negative and anaerobic coverage. Options include ampicillin/sulbactam, cefotetan, cefoxitin, piperacillin/tazobactam, or combination therapy with ampicillin, gentamicin, and metronidazole. Clindamycin or metronidazole may be added for enhanced anaerobic coverage. Analgesia and sedation may include fentanyl and midazolam as needed.
Surgical intervention is indicated for perforation, torn anal sphincter, significant bleeding, high-riding or sharp foreign bodies requiring removal under general anesthesia, or hemodynamic instability. Laparotomy is reserved for severe or complicated cases.
Admission is required for perforation, significant bleeding, unstable vital signs, abdominal pain, torn sphincter, or foreign bodies requiring operative removal. Patients may be discharged if vital signs are stable, abdominal examination is benign, and sigmoidoscopy or anoscopy is normal. All discharged patients require repeat abdominal examination within 12–24 hours and strict return precautions for abdominal pain, vomiting, or fever.
A key pitfall is failure to recognize perforation after foreign body extraction. Approximately 60% of rectal foreign bodies can be removed in the emergency department. High suspicion for rectal injury is essential in patients presenting with abdominal pain after lower gastrointestinal or genitourinary procedures.
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Emergency And Acute Medicine – Rectal Prolapse
Rectal prolapse is a full-thickness evagination of the rectal wall outside the anal opening. Three types are recognized: full-thickness prolapse, which is the most common and involves protrusion of the rectal wall through the anal canal; partial thickness (mucosal) prolapse, where only mucosa protrudes; and occult (internal) prolapse or rectal intussusception, where prolapse occurs without external protrusion and may be difficult to diagnose.
The cause is unclear and likely multifactorial. Contributing factors include chronic constipation and excessive straining, laxity or weakness of the pelvic floor and sphincter (often related to pelvic floor trauma or childbearing), and neurologic disease. It is more common in women, with a peak incidence in the seventh decade. In children, true rectal prolapse is unusual after age four; pediatric cases should prompt consideration of contributing conditions such as chronic diarrhea, parasitic infection, cystic fibrosis, or malnutrition.
Patients typically present with a dark red mass protruding from the rectum, sometimes with mucous or bloody discharge. They may report a sensation of rectal fullness or mass, tenesmus, constipation, or fecal incontinence. History should focus on duration, progression, and any evidence of bowel obstruction. Early prolapse may reduce spontaneously but often becomes progressively more frequent and persistent.
Diagnosis is clinical and relies on careful physical examination. True rectal prolapse appears as a dark red mass at the anal verge with circumferential circular folds in the beefy mucosa. Mucosal prolapse is usually only a few centimeters and lacks the circular folds of the muscular layer. Internal hemorrhoids have folds that radiate like spokes rather than circular rings. Prolapsed hemorrhoids and polyps do not involve the entire rectal mucosa and do not have a central lumen-like opening. Intussusception may present with intermittent severe abdominal pain and a more ill-appearing patient; on exam, a finger can be passed between the apex of the prolapsed bowel and the anal sphincter, whereas in rectal prolapse the protruding mucosa is continuous with perianal skin.
No laboratory tests or imaging are required for uncomplicated prolapse. Preoperative evaluation may be needed if the prolapse is incarcerated and the patient is heading to the operating room.
Prehospital care includes placing the patient in a position of comfort, preventing mucosal drying with moist gauze, and avoiding trauma to the exposed tissue. Most simple prolapse does not require extensive stabilization. If the prolapse is incarcerated or ischemic, keep the patient NPO, provide IV fluids, and prepare for possible surgery.
Emergency department management focuses on manual reduction. Position the patient in a knee-chest position and apply gentle, steady pressure for 5–15 minutes, inverting the mucosa back through the lumen from distal to proximal. Sedation can be used if needed to relax the sphincter, and a finger in the rectum can help guide reduction. For large or difficult reductions, applying about one-half to one cup of sugar to the prolapsed tissue can reduce edema and facilitate reduction. If the prolapse immediately recurs after reduction, a pressure dressing with lubricant, gauze, and tape can be applied, and the buttocks may be taped together for several hours. If the prolapse is ischemic or incarcerated, if reduction fails, or if prolapse frequently recurs, admission for emergent surgical management is indicated.
A key danger is constriction of blood flow by the anal sphincter, which can cause ischemia, venous obstruction, thrombosis, and full-thickness necrosis with potential loss of bowel. Timely reduction decreases risk, and ischemic mucosa requires surgical intervention. Common complications after reduction include localized pain and self-limited mucosal bleeding.
Patients can be discharged if the prolapse is reduced, they are stable and tolerating oral intake, and they receive instructions to address contributing factors, especially constipation management with stool softeners, increased fluids, higher dietary fiber, and avoiding prolonged sitting or straining. Follow-up with colorectal surgery is recommended, especially for recurrent prolapse or evaluation for a possible leading lesion. In children, evaluation for cystic fibrosis should be considered as part of follow-up.
Rectal prolapse is a full-thickness evagination of the rectal wall outside the anal opening. Three types are recognized: full-thickness prolapse, which is the most common and involves protrusion of the rectal wall through the anal canal; partial thickness (mucosal) prolapse, where only mucosa protrudes; and occult (internal) prolapse or rectal intussusception, where prolapse occurs without external protrusion and may be difficult to diagnose.
The cause is unclear and likely multifactorial. Contributing factors include chronic constipation and excessive straining, laxity or weakness of the pelvic floor and sphincter (often related to pelvic floor trauma or childbearing), and neurologic disease. It is more common in women, with a peak incidence in the seventh decade. In children, true rectal prolapse is unusual after age four; pediatric cases should prompt consideration of contributing conditions such as chronic diarrhea, parasitic infection, cystic fibrosis, or malnutrition.
Patients typically present with a dark red mass protruding from the rectum, sometimes with mucous or bloody discharge. They may report a sensation of rectal fullness or mass, tenesmus, constipation, or fecal incontinence. History should focus on duration, progression, and any evidence of bowel obstruction. Early prolapse may reduce spontaneously but often becomes progressively more frequent and persistent.
Diagnosis is clinical and relies on careful physical examination. True rectal prolapse appears as a dark red mass at the anal verge with circumferential circular folds in the beefy mucosa. Mucosal prolapse is usually only a few centimeters and lacks the circular folds of the muscular layer. Internal hemorrhoids have folds that radiate like spokes rather than circular rings. Prolapsed hemorrhoids and polyps do not involve the entire rectal mucosa and do not have a central lumen-like opening. Intussusception may present with intermittent severe abdominal pain and a more ill-appearing patient; on exam, a finger can be passed between the apex of the prolapsed bowel and the anal sphincter, whereas in rectal prolapse the protruding mucosa is continuous with perianal skin.
No laboratory tests or imaging are required for uncomplicated prolapse. Preoperative evaluation may be needed if the prolapse is incarcerated and the patient is heading to the operating room.
Prehospital care includes placing the patient in a position of comfort, preventing mucosal drying with moist gauze, and avoiding trauma to the exposed tissue. Most simple prolapse does not require extensive stabilization. If the prolapse is incarcerated or ischemic, keep the patient NPO, provide IV fluids, and prepare for possible surgery.
Emergency department management focuses on manual reduction. Position the patient in a knee-chest position and apply gentle, steady pressure for 5–15 minutes, inverting the mucosa back through the lumen from distal to proximal. Sedation can be used if needed to relax the sphincter, and a finger in the rectum can help guide reduction. For large or difficult reductions, applying about one-half to one cup of sugar to the prolapsed tissue can reduce edema and facilitate reduction. If the prolapse immediately recurs after reduction, a pressure dressing with lubricant, gauze, and tape can be applied, and the buttocks may be taped together for several hours. If the prolapse is ischemic or incarcerated, if reduction fails, or if prolapse frequently recurs, admission for emergent surgical management is indicated.
A key danger is constriction of blood flow by the anal sphincter, which can cause ischemia, venous obstruction, thrombosis, and full-thickness necrosis with potential loss of bowel. Timely reduction decreases risk, and ischemic mucosa requires surgical intervention. Common complications after reduction include localized pain and self-limited mucosal bleeding.
Patients can be discharged if the prolapse is reduced, they are stable and tolerating oral intake, and they receive instructions to address contributing factors, especially constipation management with stool softeners, increased fluids, higher dietary fiber, and avoiding prolonged sitting or straining. Follow-up with colorectal surgery is recommended, especially for recurrent prolapse or evaluation for a possible leading lesion. In children, evaluation for cystic fibrosis should be considered as part of follow-up.
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Emergency And Acute Medicine – Reactive Arthritis
Reactive arthritis is an inflammatory syndrome classically described by the triad of conjunctivitis, urethritis, and arthritis. Historically referred to as Reiter syndrome, the eponym is no longer favored. The condition is commonly remembered by the phrase “can’t see, can’t pee, can’t climb a tree,” although only about one-third of patients present with the full triad.
The exact incidence is difficult to determine due to the absence of standardized diagnostic criteria. Two main forms are recognized. The postdysentery type follows gastrointestinal infections, most commonly caused by Salmonella, Shigella, Campylobacter, Yersinia, or Clostridium difficile. The venereal type follows genitourinary infections, most often Chlamydia trachomatis and less commonly Neisseria gonorrhoeae. Reactive arthritis has also been described after upper respiratory infections, urinary tract infections, and intravesical BCG therapy for bladder carcinoma. It is more common in males than females, approximately 5:1, and most often occurs in the third decade of life.
Symptoms typically develop within four weeks of the inciting infection but may be delayed up to one year. Urogenital symptoms occur in more than 90% of cases and may include urethritis, cervicitis, or prostatitis. The arthritis is usually asymmetric and polyarticular, most commonly affecting the knees and ankles, but it may also involve fingers, the back, and sacroiliac joints. Achilles tendonitis occurs in approximately 40% of patients, and dactylitis, or “sausage digit,” is present in about 15%. Ophthalmologic involvement occurs in 30–60% of cases. Conjunctivitis is most common and is typically bilateral with mild irritation or mucopurulent discharge. Uveitis and keratitis are less common, usually unilateral, and may cause eye pain, redness, and photophobia.
Mucocutaneous manifestations are more frequent in patients who are HLA-B27 positive. Keratoderma blennorrhagicum presents as erythematous macules and vesicles on the palms and soles that progress to pustules and hyperkeratotic plaques resembling pustular psoriasis. Circinate balanitis occurs in more than half of affected males and presents as plaques or vesicles on the glans penis. Oral lesions, nail dystrophy, and periungual pustules may also be seen. Systemic symptoms such as fever, fatigue, malaise, and weight loss may be present.
The diagnosis is clinical and based on characteristic findings and a recent history of gastrointestinal or genitourinary infection. No laboratory test confirms the diagnosis. Laboratory studies may show leukocytosis, mild anemia, and elevated ESR or CRP. Urinalysis may demonstrate sterile pyuria. Imaging studies are not diagnostic but may be used to exclude other conditions; plain radiographs may show joint effusion. Arthrocentesis should be performed if septic arthritis is a concern. Synovial fluid typically shows leukocytosis with polymorphonuclear predominance, and crystals are absent.
The differential diagnosis includes septic arthritis, gonococcal arthritis, chlamydial urethritis, syphilis, gout, rheumatoid arthritis, pustular psoriasis, Behçet disease, contact dermatitis, and Kawasaki disease in children. Exclusion of life- or limb-threatening conditions such as septic arthritis is essential.
Management in the emergency setting is primarily symptomatic after serious infections have been excluded. Nonsteroidal anti-inflammatory drugs are first-line therapy for arthritis, along with rest, ice, and elevation. The role of antibiotics in reactive arthritis itself is unclear, as studies have not shown consistent long-term benefit once arthritis is established, although the initial infection should be treated if still present. Short courses of systemic corticosteroids may be considered in severe or prolonged cases. Conjunctivitis may be managed with topical agents for symptomatic relief, and severe uveitis requires urgent ophthalmology referral.
Most patients can be managed as outpatients with follow-up through primary care. Severe uveitis warrants ophthalmology follow-up. The course is often prolonged, lasting three to twelve months, and approximately 25% of patients experience recurrent episodes.
A key pitfall is failure to exclude serious conditions such as septic arthritis, gonococcal arthritis, or Kawasaki disease in children. Careful evaluation and appropriate exclusion of emergent diagnoses are critical before attributing symptoms to reactive arthritis.
Reactive arthritis is an inflammatory syndrome classically described by the triad of conjunctivitis, urethritis, and arthritis. Historically referred to as Reiter syndrome, the eponym is no longer favored. The condition is commonly remembered by the phrase “can’t see, can’t pee, can’t climb a tree,” although only about one-third of patients present with the full triad.
The exact incidence is difficult to determine due to the absence of standardized diagnostic criteria. Two main forms are recognized. The postdysentery type follows gastrointestinal infections, most commonly caused by Salmonella, Shigella, Campylobacter, Yersinia, or Clostridium difficile. The venereal type follows genitourinary infections, most often Chlamydia trachomatis and less commonly Neisseria gonorrhoeae. Reactive arthritis has also been described after upper respiratory infections, urinary tract infections, and intravesical BCG therapy for bladder carcinoma. It is more common in males than females, approximately 5:1, and most often occurs in the third decade of life.
Symptoms typically develop within four weeks of the inciting infection but may be delayed up to one year. Urogenital symptoms occur in more than 90% of cases and may include urethritis, cervicitis, or prostatitis. The arthritis is usually asymmetric and polyarticular, most commonly affecting the knees and ankles, but it may also involve fingers, the back, and sacroiliac joints. Achilles tendonitis occurs in approximately 40% of patients, and dactylitis, or “sausage digit,” is present in about 15%. Ophthalmologic involvement occurs in 30–60% of cases. Conjunctivitis is most common and is typically bilateral with mild irritation or mucopurulent discharge. Uveitis and keratitis are less common, usually unilateral, and may cause eye pain, redness, and photophobia.
Mucocutaneous manifestations are more frequent in patients who are HLA-B27 positive. Keratoderma blennorrhagicum presents as erythematous macules and vesicles on the palms and soles that progress to pustules and hyperkeratotic plaques resembling pustular psoriasis. Circinate balanitis occurs in more than half of affected males and presents as plaques or vesicles on the glans penis. Oral lesions, nail dystrophy, and periungual pustules may also be seen. Systemic symptoms such as fever, fatigue, malaise, and weight loss may be present.
The diagnosis is clinical and based on characteristic findings and a recent history of gastrointestinal or genitourinary infection. No laboratory test confirms the diagnosis. Laboratory studies may show leukocytosis, mild anemia, and elevated ESR or CRP. Urinalysis may demonstrate sterile pyuria. Imaging studies are not diagnostic but may be used to exclude other conditions; plain radiographs may show joint effusion. Arthrocentesis should be performed if septic arthritis is a concern. Synovial fluid typically shows leukocytosis with polymorphonuclear predominance, and crystals are absent.
The differential diagnosis includes septic arthritis, gonococcal arthritis, chlamydial urethritis, syphilis, gout, rheumatoid arthritis, pustular psoriasis, Behçet disease, contact dermatitis, and Kawasaki disease in children. Exclusion of life- or limb-threatening conditions such as septic arthritis is essential.
Management in the emergency setting is primarily symptomatic after serious infections have been excluded. Nonsteroidal anti-inflammatory drugs are first-line therapy for arthritis, along with rest, ice, and elevation. The role of antibiotics in reactive arthritis itself is unclear, as studies have not shown consistent long-term benefit once arthritis is established, although the initial infection should be treated if still present. Short courses of systemic corticosteroids may be considered in severe or prolonged cases. Conjunctivitis may be managed with topical agents for symptomatic relief, and severe uveitis requires urgent ophthalmology referral.
Most patients can be managed as outpatients with follow-up through primary care. Severe uveitis warrants ophthalmology follow-up. The course is often prolonged, lasting three to twelve months, and approximately 25% of patients experience recurrent episodes.
A key pitfall is failure to exclude serious conditions such as septic arthritis, gonococcal arthritis, or Kawasaki disease in children. Careful evaluation and appropriate exclusion of emergent diagnoses are critical before attributing symptoms to reactive arthritis.
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Emergency And Acute Medicine – Rash, Pediatric
Pediatric rashes are common and range from benign self-limited viral exanthems to life-threatening infectious or systemic diseases. Accurate diagnosis relies on identifying lesion morphology, configuration, distribution, associated systemic findings, and progression over time. Primary lesions include macules (flat color changes), papules (<5 mm elevated lesions), plaques (>5 mm elevated lesions), nodules (deeper solid lesions), wheals (transient edematous lesions), vesicles (<5 mm fluid-filled), bullae (>5 mm fluid-filled), pustules, and purpura or petechiae (nonblanching lesions due to extravasated red blood cells). Secondary changes such as scaling, lichenification, excoriation, erosion, and ulceration reflect progression or manipulation of primary lesions. Color changes may reflect vascular dilation, hemorrhage, pigment alteration, or inflammatory proliferation.
Etiologies vary by morphology. Papulosquamous eruptions are commonly infectious, allergic, or autoimmune. Purpura and petechiae raise concern for platelet disorders, coagulation abnormalities, vasculitis, or overwhelming infection. Vesiculobullous lesions may result from viral infection, drug reactions, or autoimmune disease. Ulcers may reflect infection or vascular insufficiency. Age influences presentation, as distribution and severity differ between neonates, infants, and adolescents.
History should include age, onset, evolution, progression pattern, whether lesions are synchronous or asynchronous, associated symptoms such as fever, pruritus, abdominal pain, or joint pain, and prodromal symptoms such as cough or rhinorrhea. Immunization status, recent travel, insect exposures, medications, and family history are essential. Underlying dermatoses such as atopic dermatitis or psoriasis should be noted.
Physical examination must assess systemic stability. Fever with purpura suggests possible sepsis. Cardiac murmurs may indicate endocarditis. Hepatosplenomegaly can suggest systemic infection or hematologic disease. The rash should be classified as papulosquamous, vesiculobullous, or purpuric, and distribution should be documented, including palm and sole involvement.
Laboratory testing is guided by presentation. Purpuric rashes require complete blood count with platelet count and coagulation studies to evaluate for thrombocytopenia or disseminated intravascular coagulation. Febrile children may require CBC, electrolytes, renal function tests, blood cultures, and lactate if sepsis is suspected. Lumbar puncture is indicated when meningitis or encephalitis is suspected. Viral cultures or titers may assist in diagnosing exanthems. Potassium hydroxide preparations help identify fungal infections in scaling lesions, and scabies scrapings may be performed for pruritic linear lesions. Chest radiography is indicated if pulmonary involvement is suspected.
Differential diagnosis depends on morphology. Maculopapular rashes include viral exanthems such as measles, rubella, roseola, and erythema infectiosum, as well as scarlet fever, Kawasaki disease, and early varicella. Purpuric rashes include meningococcemia, pneumococcemia, gonococcemia, endocarditis, Rocky Mountain spotted fever, Henoch–Schönlein purpura, idiopathic thrombocytopenic purpura, leukemia, and disseminated intravascular coagulation. Scaling red lesions may represent tinea, pityriasis rosea, eczema, seborrheic dermatitis, or secondary syphilis. Vesiculobullous eruptions include varicella, herpes simplex, hand-foot-and-mouth disease, scabies, impetigo, drug hypersensitivity reactions, toxic epidermal necrolysis, and staphylococcal scalded skin syndrome.
Management prioritizes stabilization in children with systemic instability. Any child with purpura and fever requires immediate evaluation and empiric intravenous antibiotics targeting meningococcemia and other invasive bacterial infections. Airway support, intravenous access, fluid resuscitation, and vasopressors may be required in shock. Diphenhydramine is appropriate for suspected allergic reactions. Specific antimicrobial therapy should be directed toward the underlying cause. Acetaminophen may be used for fever control.
Admission decisions depend on the underlying diagnosis and systemic involvement. Children with systemic illness, unstable vital signs, staphylococcal scalded skin syndrome, severe varicella, or other high-risk conditions require hospitalization. Stable children with self-limited exanthems may be discharged with close follow-up. Return precautions should include rapidly spreading rash, new petechiae or bleeding, changes in rash morphology, new fever, neck stiffness, or systemic deterioration.
Careful attention to the initial appearance and spread of the rash, along with associated systemic symptoms, is critical. Meningococcemia must always be considered in a child with fever and purpura, as early recognition and treatment are lifesaving.
Pediatric rashes are common and range from benign self-limited viral exanthems to life-threatening infectious or systemic diseases. Accurate diagnosis relies on identifying lesion morphology, configuration, distribution, associated systemic findings, and progression over time. Primary lesions include macules (flat color changes), papules (<5 mm elevated lesions), plaques (>5 mm elevated lesions), nodules (deeper solid lesions), wheals (transient edematous lesions), vesicles (<5 mm fluid-filled), bullae (>5 mm fluid-filled), pustules, and purpura or petechiae (nonblanching lesions due to extravasated red blood cells). Secondary changes such as scaling, lichenification, excoriation, erosion, and ulceration reflect progression or manipulation of primary lesions. Color changes may reflect vascular dilation, hemorrhage, pigment alteration, or inflammatory proliferation.
Etiologies vary by morphology. Papulosquamous eruptions are commonly infectious, allergic, or autoimmune. Purpura and petechiae raise concern for platelet disorders, coagulation abnormalities, vasculitis, or overwhelming infection. Vesiculobullous lesions may result from viral infection, drug reactions, or autoimmune disease. Ulcers may reflect infection or vascular insufficiency. Age influences presentation, as distribution and severity differ between neonates, infants, and adolescents.
History should include age, onset, evolution, progression pattern, whether lesions are synchronous or asynchronous, associated symptoms such as fever, pruritus, abdominal pain, or joint pain, and prodromal symptoms such as cough or rhinorrhea. Immunization status, recent travel, insect exposures, medications, and family history are essential. Underlying dermatoses such as atopic dermatitis or psoriasis should be noted.
Physical examination must assess systemic stability. Fever with purpura suggests possible sepsis. Cardiac murmurs may indicate endocarditis. Hepatosplenomegaly can suggest systemic infection or hematologic disease. The rash should be classified as papulosquamous, vesiculobullous, or purpuric, and distribution should be documented, including palm and sole involvement.
Laboratory testing is guided by presentation. Purpuric rashes require complete blood count with platelet count and coagulation studies to evaluate for thrombocytopenia or disseminated intravascular coagulation. Febrile children may require CBC, electrolytes, renal function tests, blood cultures, and lactate if sepsis is suspected. Lumbar puncture is indicated when meningitis or encephalitis is suspected. Viral cultures or titers may assist in diagnosing exanthems. Potassium hydroxide preparations help identify fungal infections in scaling lesions, and scabies scrapings may be performed for pruritic linear lesions. Chest radiography is indicated if pulmonary involvement is suspected.
Differential diagnosis depends on morphology. Maculopapular rashes include viral exanthems such as measles, rubella, roseola, and erythema infectiosum, as well as scarlet fever, Kawasaki disease, and early varicella. Purpuric rashes include meningococcemia, pneumococcemia, gonococcemia, endocarditis, Rocky Mountain spotted fever, Henoch–Schönlein purpura, idiopathic thrombocytopenic purpura, leukemia, and disseminated intravascular coagulation. Scaling red lesions may represent tinea, pityriasis rosea, eczema, seborrheic dermatitis, or secondary syphilis. Vesiculobullous eruptions include varicella, herpes simplex, hand-foot-and-mouth disease, scabies, impetigo, drug hypersensitivity reactions, toxic epidermal necrolysis, and staphylococcal scalded skin syndrome.
Management prioritizes stabilization in children with systemic instability. Any child with purpura and fever requires immediate evaluation and empiric intravenous antibiotics targeting meningococcemia and other invasive bacterial infections. Airway support, intravenous access, fluid resuscitation, and vasopressors may be required in shock. Diphenhydramine is appropriate for suspected allergic reactions. Specific antimicrobial therapy should be directed toward the underlying cause. Acetaminophen may be used for fever control.
Admission decisions depend on the underlying diagnosis and systemic involvement. Children with systemic illness, unstable vital signs, staphylococcal scalded skin syndrome, severe varicella, or other high-risk conditions require hospitalization. Stable children with self-limited exanthems may be discharged with close follow-up. Return precautions should include rapidly spreading rash, new petechiae or bleeding, changes in rash morphology, new fever, neck stiffness, or systemic deterioration.
Careful attention to the initial appearance and spread of the rash, along with associated systemic symptoms, is critical. Meningococcemia must always be considered in a child with fever and purpura, as early recognition and treatment are lifesaving.
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Emergency And Acute Medicine – Rash
Rash refers to abnormal skin lesions resulting from inflammatory, infectious, vascular, autoimmune, allergic, or malignant processes. In emergency medicine, careful attention to morphology, distribution, associated systemic symptoms, and evolution is essential. Warning signs of a dermatologic emergency include erythroderma, blistering or desquamation, purpura, skin pain out of proportion to findings, and systemic symptoms such as fever or hypotension.
Rashes are classified by morphology. Vesiculobullous lesions are fluid-filled elevations caused by disruption of epidermal or dermal integrity and include vesicles (<5 mm) and bullae (>5 mm). Serious causes include toxic epidermal necrolysis, Stevens–Johnson syndrome, pemphigus vulgaris, bullous pemphigoid, disseminated herpes infections, and severe drug reactions. Purpura and petechiae result from vascular or hemostatic failure and do not blanch with pressure; life-threatening causes include meningococcemia, disseminated intravascular coagulation, Rocky Mountain spotted fever, and vasculitis. Erythema is caused by superficial vascular dilation and blanches with pressure; erythroderma involves ≥90% of body surface area and may occur with toxic shock syndrome, severe drug reactions, psoriasis, or cutaneous lymphoma. Papulosquamous eruptions include psoriasis, pityriasis rosea, secondary syphilis, and dermatitis. Nodules may represent granulomatous disease, infection, panniculitis, cysts, or malignancy.
History should address age, immune status, medication changes, recent infections, travel, tick exposure, environmental factors, sick contacts, and prior similar episodes. Associated symptoms such as fever, pruritus, arthralgias, abdominal pain, or prodromal viral symptoms help narrow the diagnosis. A detailed drug history is critical, particularly for possible drug reactions with eosinophilia and systemic symptoms (DRESS) or Stevens–Johnson syndrome.
Physical examination must assess vital signs and systemic stability. Fever, hypotension, respiratory distress, or altered mental status suggest a potentially life-threatening condition. Skin pain disproportionate to findings raises concern for necrotizing infection. Lymphadenopathy may suggest systemic drug reaction or infection. Primary lesion type, distribution (central vs peripheral, mucosal involvement, palm/sole involvement), and secondary changes such as scaling, crusting, ulceration, or necrosis should be documented.
Workup depends on severity and suspected cause. Patients with fever or systemic symptoms require laboratory evaluation including CBC with differential, electrolytes, renal function, and blood cultures when infection is suspected. Purpuric rashes require platelet count and coagulation studies to evaluate for thrombocytopenia or DIC. Viral lesions may be evaluated with PCR or direct fluorescent antibody testing. Suspected syphilis warrants rapid plasma reagin testing. Autoimmune conditions may require inflammatory markers and specialized serologies in consultation with specialists. Skin scrapings may identify fungal infection or scabies. Skin biopsy under dermatologic consultation may be required for unclear or severe cases. The Nikolsky sign, in which lateral pressure causes epidermal sloughing, suggests epidermal detachment disorders.
Management prioritizes stabilization and early treatment of life-threatening conditions. Patients with petechiae or purpura and fever should receive immediate empiric antibiotics covering meningococcemia and Rocky Mountain spotted fever. Diffuse erythema with hypotension should prompt treatment for toxic shock syndrome. Disseminated bullous or exfoliative disorders should be managed similarly to severe burns, with attention to fluid balance, wound care, and infection prevention. Symptomatic treatment for pruritus includes antihistamines such as diphenhydramine or hydroxyzine. Systemic corticosteroids are reserved for confirmed allergic reactions, steroid-responsive disease, or specialist guidance. Severe allergic reactions require antihistamines, corticosteroids, and epinephrine if airway compromise is present.
Admission is indicated for patients with significant bullous or exfoliative disease, purpura with systemic symptoms, erythroderma with instability, or evidence of sepsis. Patients with limited, stable lesions and no systemic signs may be discharged with close follow-up. Clear return precautions should include worsening rash, spreading redness, increasing pain, joint pain, fever, severe headache, confusion, or signs of anaphylaxis such as difficulty breathing or tongue swelling.
Rapid progression of a rash with systemic symptoms signals potential emergency. Empiric antibiotics are critical in febrile patients with purpura or erythroderma and hemodynamic instability. Hyperpigmented scaly papules on the palms and soles should prompt evaluation for secondary syphilis. Careful assessment and timely intervention are essential to prevent morbidity and mortality.
Rash refers to abnormal skin lesions resulting from inflammatory, infectious, vascular, autoimmune, allergic, or malignant processes. In emergency medicine, careful attention to morphology, distribution, associated systemic symptoms, and evolution is essential. Warning signs of a dermatologic emergency include erythroderma, blistering or desquamation, purpura, skin pain out of proportion to findings, and systemic symptoms such as fever or hypotension.
Rashes are classified by morphology. Vesiculobullous lesions are fluid-filled elevations caused by disruption of epidermal or dermal integrity and include vesicles (<5 mm) and bullae (>5 mm). Serious causes include toxic epidermal necrolysis, Stevens–Johnson syndrome, pemphigus vulgaris, bullous pemphigoid, disseminated herpes infections, and severe drug reactions. Purpura and petechiae result from vascular or hemostatic failure and do not blanch with pressure; life-threatening causes include meningococcemia, disseminated intravascular coagulation, Rocky Mountain spotted fever, and vasculitis. Erythema is caused by superficial vascular dilation and blanches with pressure; erythroderma involves ≥90% of body surface area and may occur with toxic shock syndrome, severe drug reactions, psoriasis, or cutaneous lymphoma. Papulosquamous eruptions include psoriasis, pityriasis rosea, secondary syphilis, and dermatitis. Nodules may represent granulomatous disease, infection, panniculitis, cysts, or malignancy.
History should address age, immune status, medication changes, recent infections, travel, tick exposure, environmental factors, sick contacts, and prior similar episodes. Associated symptoms such as fever, pruritus, arthralgias, abdominal pain, or prodromal viral symptoms help narrow the diagnosis. A detailed drug history is critical, particularly for possible drug reactions with eosinophilia and systemic symptoms (DRESS) or Stevens–Johnson syndrome.
Physical examination must assess vital signs and systemic stability. Fever, hypotension, respiratory distress, or altered mental status suggest a potentially life-threatening condition. Skin pain disproportionate to findings raises concern for necrotizing infection. Lymphadenopathy may suggest systemic drug reaction or infection. Primary lesion type, distribution (central vs peripheral, mucosal involvement, palm/sole involvement), and secondary changes such as scaling, crusting, ulceration, or necrosis should be documented.
Workup depends on severity and suspected cause. Patients with fever or systemic symptoms require laboratory evaluation including CBC with differential, electrolytes, renal function, and blood cultures when infection is suspected. Purpuric rashes require platelet count and coagulation studies to evaluate for thrombocytopenia or DIC. Viral lesions may be evaluated with PCR or direct fluorescent antibody testing. Suspected syphilis warrants rapid plasma reagin testing. Autoimmune conditions may require inflammatory markers and specialized serologies in consultation with specialists. Skin scrapings may identify fungal infection or scabies. Skin biopsy under dermatologic consultation may be required for unclear or severe cases. The Nikolsky sign, in which lateral pressure causes epidermal sloughing, suggests epidermal detachment disorders.
Management prioritizes stabilization and early treatment of life-threatening conditions. Patients with petechiae or purpura and fever should receive immediate empiric antibiotics covering meningococcemia and Rocky Mountain spotted fever. Diffuse erythema with hypotension should prompt treatment for toxic shock syndrome. Disseminated bullous or exfoliative disorders should be managed similarly to severe burns, with attention to fluid balance, wound care, and infection prevention. Symptomatic treatment for pruritus includes antihistamines such as diphenhydramine or hydroxyzine. Systemic corticosteroids are reserved for confirmed allergic reactions, steroid-responsive disease, or specialist guidance. Severe allergic reactions require antihistamines, corticosteroids, and epinephrine if airway compromise is present.
Admission is indicated for patients with significant bullous or exfoliative disease, purpura with systemic symptoms, erythroderma with instability, or evidence of sepsis. Patients with limited, stable lesions and no systemic signs may be discharged with close follow-up. Clear return precautions should include worsening rash, spreading redness, increasing pain, joint pain, fever, severe headache, confusion, or signs of anaphylaxis such as difficulty breathing or tongue swelling.
Rapid progression of a rash with systemic symptoms signals potential emergency. Empiric antibiotics are critical in febrile patients with purpura or erythroderma and hemodynamic instability. Hyperpigmented scaly papules on the palms and soles should prompt evaluation for secondary syphilis. Careful assessment and timely intervention are essential to prevent morbidity and mortality.
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Emergency And Acute Medicine – Pulmonary Embolism
Pulmonary embolism (PE) occurs when thrombi—most commonly originating in the deep veins of the lower extremities or pelvis—travel to and obstruct the pulmonary arterial circulation. Thrombi may also arise from renal or upper extremity veins. The size and location of the embolus determine the severity of clinical manifestations, ranging from mild dyspnea to cardiovascular collapse.
Most patients with PE have identifiable risk factors. Common acquired risks include recent surgery, immobilization, pregnancy, prior DVT or PE, stroke or paraplegia, malignancy, age over 50 years, obesity, smoking, oral contraceptive use, and major trauma. Inherited thrombophilias include Factor V Leiden mutation, protein C or S deficiency, antithrombin III deficiency, antiphospholipid antibody syndrome, and lupus anticoagulant. In children, PE is rare and usually associated with central venous catheters, immobility, congenital heart disease, trauma, malignancy, surgery, or infection.
Clinical presentation is variable and often nonspecific. The most common symptoms are dyspnea, pleuritic chest pain, and tachypnea. Patients may also report cough or hemoptysis (rarely massive). Cardiovascular findings can include tachycardia, syncope, or hypotension in massive PE. Fever is uncommon and usually low grade. Physical exam may reveal cyanosis, signs of DVT (unilateral leg swelling, tenderness), or evidence of thrombophlebitis. In elderly patients, symptoms may be subtle.
Initial evaluation includes chest radiography and ECG primarily to rule out alternative diagnoses. Chest x-ray is often normal in PE but may show nonspecific findings such as atelectasis or pleural effusion. Classic but uncommon signs include Hampton hump (pleural-based opacity) and Westermark sign (regional oligemia). ECG is usually normal or shows sinus tachycardia. Other possible findings include nonspecific ST–T changes, right bundle branch block, or S1Q3T3 pattern (neither sensitive nor specific).
Risk stratification tools assist in diagnostic decision-making. The modified Wells criteria assign points based on clinical features such as signs of DVT, heart rate >100 bpm, recent surgery or immobilization, prior DVT/PE, hemoptysis, malignancy, and whether PE is the most likely diagnosis. A score <4 combined with a negative d-dimer confers <2% risk of pe. the pulmonary embolism rule-out criteria (perc) may exclude pe in low-risk patients if all are (age <50, hr <100, o₂ saturation ≥95%, no hemoptysis, estrogen use, prior dvt />E, no unilateral leg swelling, no recent surgery/trauma). A PERC-negative patient with low clinical suspicion has <1% risk of pe within 45 days.< />pan>
Laboratory studies are nonspecific. Arterial blood gas may show hypoxemia, hypocapnia, respiratory alkalosis, or elevated alveolar–arterial gradient, but can be normal. CBC may reveal anemia. D-dimer testing (enzyme-linked immunosorbent assay) has high sensitivity but low specificity; a negative d-dimer in a low-risk patient effectively rules out PE. D-dimer is frequently elevated in malignancy or recent surgery.
Imaging is central to diagnosis. CT pulmonary angiography (CTPA) is the preferred diagnostic modality and can also detect alternative causes of symptoms. It is highly accurate for proximal emboli, with positive and negative predictive values around 96% in appropriate pretest probability groups. Ventilation–perfusion (V/Q) scanning remains useful, particularly in patients with contraindications to contrast. A normal V/Q scan effectively excludes PE, whereas a high-probability V/Q scan combined with high clinical suspicion confers approximately 96% probability of PE. Lower-extremity duplex ultrasound may identify DVT; a positive study supports anticoagulation, though a negative result does not exclude PE. Echocardiography assesses right ventricular strain and may guide management in unstable patients. Pulmonary angiography remains the gold standard but is reserved for cases where noninvasive imaging is inconclusive.
Management begins with airway, breathing, and circulation. Supplemental oxygen, IV access, and cardiac monitoring are initiated. In hypotensive patients, IV fluids should be administered cautiously, as excessive volume may worsen right ventricular failure. Vasopressors may be required if hypotension persists.
Anticoagulation is the cornerstone of treatment, preventing further clot formation and stabilizing existing thrombus. Unfractionated heparin requires close monitoring with target activated partial thromboplastin time 1.5–2.5 times control. Low-molecular-weight heparin (e.g., enoxaparin 1 mg/kg SC every 12 hours) is at least as effective and easier to administer. Long-term therapy includes warfarin (target INR 2–3) or direct oral anticoagulants such as rivaroxaban (15 mg twice daily for 3 weeks, then 20 mg daily). Rivaroxaban does not require routine monitoring but is not recommended in renal or hepatic insufficiency or pregnancy.
Thrombolysis (e.g., alteplase 100 mg IV over 2 hours) is indicated in hemodynamically unstable patients with confirmed PE and may be considered in selected stable patients with massive PE, severe hypoxemia, or right ventricular dysfunction. Inferior vena cava filters are reserved for patients with contraindications to anticoagulation or recurrent PE despite therapeutic anticoagulation. Surgical or catheter-directed embolectomy may be considered in select unstable patients.
All patients diagnosed with PE require hospital admission for monitoring and anticoagulation. In selected stable patients with high suspicion and no contraindications, empiric anticoagulation may be started while awaiting definitive imaging if diagnostic resources are temporarily unavailable.
The clinical presentation of PE is highly variable and often mimics other conditions such as myocardial infarction, pneumonia, asthma, pneumothorax, or anxiety. Maintaining a high index of suspicion is essential. Patients with malignancy are at increased risk of recurrent PE despite therapeutic anticoagulation. Early risk stratification and prompt treatment significantly reduce morbidity and mortality.
Pulmonary embolism (PE) occurs when thrombi—most commonly originating in the deep veins of the lower extremities or pelvis—travel to and obstruct the pulmonary arterial circulation. Thrombi may also arise from renal or upper extremity veins. The size and location of the embolus determine the severity of clinical manifestations, ranging from mild dyspnea to cardiovascular collapse.
Most patients with PE have identifiable risk factors. Common acquired risks include recent surgery, immobilization, pregnancy, prior DVT or PE, stroke or paraplegia, malignancy, age over 50 years, obesity, smoking, oral contraceptive use, and major trauma. Inherited thrombophilias include Factor V Leiden mutation, protein C or S deficiency, antithrombin III deficiency, antiphospholipid antibody syndrome, and lupus anticoagulant. In children, PE is rare and usually associated with central venous catheters, immobility, congenital heart disease, trauma, malignancy, surgery, or infection.
Clinical presentation is variable and often nonspecific. The most common symptoms are dyspnea, pleuritic chest pain, and tachypnea. Patients may also report cough or hemoptysis (rarely massive). Cardiovascular findings can include tachycardia, syncope, or hypotension in massive PE. Fever is uncommon and usually low grade. Physical exam may reveal cyanosis, signs of DVT (unilateral leg swelling, tenderness), or evidence of thrombophlebitis. In elderly patients, symptoms may be subtle.
Initial evaluation includes chest radiography and ECG primarily to rule out alternative diagnoses. Chest x-ray is often normal in PE but may show nonspecific findings such as atelectasis or pleural effusion. Classic but uncommon signs include Hampton hump (pleural-based opacity) and Westermark sign (regional oligemia). ECG is usually normal or shows sinus tachycardia. Other possible findings include nonspecific ST–T changes, right bundle branch block, or S1Q3T3 pattern (neither sensitive nor specific).
Risk stratification tools assist in diagnostic decision-making. The modified Wells criteria assign points based on clinical features such as signs of DVT, heart rate >100 bpm, recent surgery or immobilization, prior DVT/PE, hemoptysis, malignancy, and whether PE is the most likely diagnosis. A score <4 combined with a negative d-dimer confers <2% risk of pe. the pulmonary embolism rule-out criteria (perc) may exclude pe in low-risk patients if all are (age <50, hr <100, o₂ saturation ≥95%, no hemoptysis, estrogen use, prior dvt />E, no unilateral leg swelling, no recent surgery/trauma). A PERC-negative patient with low clinical suspicion has <1% risk of pe within 45 days.< />pan>
Laboratory studies are nonspecific. Arterial blood gas may show hypoxemia, hypocapnia, respiratory alkalosis, or elevated alveolar–arterial gradient, but can be normal. CBC may reveal anemia. D-dimer testing (enzyme-linked immunosorbent assay) has high sensitivity but low specificity; a negative d-dimer in a low-risk patient effectively rules out PE. D-dimer is frequently elevated in malignancy or recent surgery.
Imaging is central to diagnosis. CT pulmonary angiography (CTPA) is the preferred diagnostic modality and can also detect alternative causes of symptoms. It is highly accurate for proximal emboli, with positive and negative predictive values around 96% in appropriate pretest probability groups. Ventilation–perfusion (V/Q) scanning remains useful, particularly in patients with contraindications to contrast. A normal V/Q scan effectively excludes PE, whereas a high-probability V/Q scan combined with high clinical suspicion confers approximately 96% probability of PE. Lower-extremity duplex ultrasound may identify DVT; a positive study supports anticoagulation, though a negative result does not exclude PE. Echocardiography assesses right ventricular strain and may guide management in unstable patients. Pulmonary angiography remains the gold standard but is reserved for cases where noninvasive imaging is inconclusive.
Management begins with airway, breathing, and circulation. Supplemental oxygen, IV access, and cardiac monitoring are initiated. In hypotensive patients, IV fluids should be administered cautiously, as excessive volume may worsen right ventricular failure. Vasopressors may be required if hypotension persists.
Anticoagulation is the cornerstone of treatment, preventing further clot formation and stabilizing existing thrombus. Unfractionated heparin requires close monitoring with target activated partial thromboplastin time 1.5–2.5 times control. Low-molecular-weight heparin (e.g., enoxaparin 1 mg/kg SC every 12 hours) is at least as effective and easier to administer. Long-term therapy includes warfarin (target INR 2–3) or direct oral anticoagulants such as rivaroxaban (15 mg twice daily for 3 weeks, then 20 mg daily). Rivaroxaban does not require routine monitoring but is not recommended in renal or hepatic insufficiency or pregnancy.
Thrombolysis (e.g., alteplase 100 mg IV over 2 hours) is indicated in hemodynamically unstable patients with confirmed PE and may be considered in selected stable patients with massive PE, severe hypoxemia, or right ventricular dysfunction. Inferior vena cava filters are reserved for patients with contraindications to anticoagulation or recurrent PE despite therapeutic anticoagulation. Surgical or catheter-directed embolectomy may be considered in select unstable patients.
All patients diagnosed with PE require hospital admission for monitoring and anticoagulation. In selected stable patients with high suspicion and no contraindications, empiric anticoagulation may be started while awaiting definitive imaging if diagnostic resources are temporarily unavailable.
The clinical presentation of PE is highly variable and often mimics other conditions such as myocardial infarction, pneumonia, asthma, pneumothorax, or anxiety. Maintaining a high index of suspicion is essential. Patients with malignancy are at increased risk of recurrent PE despite therapeutic anticoagulation. Early risk stratification and prompt treatment significantly reduce morbidity and mortality.
- Published on
Emergency And Acute Medicine – Pulmonary Edema
Pulmonary edema is the accumulation of fluid within the interstitium and alveoli due to imbalance in Starling forces, resulting in leakage of fluid from pulmonary capillaries. It is broadly categorized as cardiogenic or noncardiogenic. Cardiogenic pulmonary edema results from abnormal cardiac function leading to inadequate forward flow and elevated hydrostatic pressures, often seen in acute decompensated heart failure (AHF). Noncardiogenic pulmonary edema results from increased alveolar–capillary membrane permeability without primary cardiac dysfunction and includes acute lung injury and acute respiratory distress syndrome (ARDS), defined by a PaO₂/FiO₂ ratio ≤200 mm Hg.
Heart failure affects approximately 5.8 million people in the United States and increases with age, affecting about 10% of individuals over 75 years old. Thirty to forty percent of patients with heart failure are hospitalized annually, with an 11% one-month mortality following admission for acute heart failure.
Cardiogenic causes include systolic dysfunction (ischemic heart disease, cardiomyopathy, myocarditis), pressure overload (aortic stenosis, systemic hypertension), volume overload (mitral or aortic regurgitation), diastolic dysfunction (mitral stenosis, hypertrophic cardiomyopathy), and high-output states such as anemia, hyperthyroidism, arteriovenous fistula, or wet beriberi. Noncardiogenic causes include sepsis, aspiration, inhalation injury, near drowning, disseminated intravascular coagulation, pancreatitis, pulmonary contusion, severe trauma, uremia, high-altitude pulmonary edema, neurogenic pulmonary edema, drug overdose (e.g., narcotics, salicylates), pulmonary embolism, fat embolism, and transfusion-related acute lung injury.
Patients typically present with progressive dyspnea, initially on exertion and later at rest. Orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, cough, weakness, and acute weight gain are common in cardiogenic causes. Physical examination may reveal tachypnea, hypoxia, diaphoresis, cyanosis, jugular venous distention, rales, wheezing, S3 or S4 gallop, tachycardia, and peripheral edema. Patients may be hypertensive or hypotensive. Noncardiogenic edema produces similar pulmonary findings but usually lacks peripheral signs of volume overload.
Evaluation includes ECG to assess for ischemia or dysrhythmias and chest radiography to confirm diagnosis and evaluate severity. Laboratory studies typically include BNP or NT-proBNP, cardiac troponins, renal function, and electrolytes. BNP <100 pg />L makes heart failure unlikely, whereas >500 pg/mL strongly suggests cardiogenic pulmonary edema. Values between 100–500 pg/mL are indeterminate. BNP may be falsely elevated in renal failure and may not rise immediately in very acute heart failure. Troponin elevation occurs in about 20% of AHF cases and carries negative prognostic implications. Hyponatremia and elevated creatinine indicate severe disease and worse prognosis.
Chest radiography in cardiogenic edema may demonstrate cardiomegaly, cephalization of pulmonary vessels, Kerley B lines, pleural effusions, and bilateral perihilar “butterfly” alveolar edema. In noncardiogenic edema, bilateral infiltrates are present without cardiomegaly. Radiographs may be normal early in the disease. Bedside ultrasonography can reveal bilateral B-lines (comet-tail artifacts), supporting the diagnosis. Echocardiography evaluates ventricular function and structural abnormalities.
Differential diagnoses include COPD exacerbation, asthma, pneumonia, pulmonary embolism, pneumothorax, pleural effusion, pericardial tamponade, anaphylaxis, metabolic acidosis, and hyperventilation syndrome.
Management begins with airway, breathing, and circulation assessment. Prehospital care includes oxygen via nonrebreather mask, IV access, cardiac monitoring, pulse oximetry, and sublingual nitrates if blood pressure permits. In severe cases, positive-pressure ventilation or intubation may be required.
In the emergency department, the patient should be positioned upright. Supplemental oxygen and close monitoring are essential. Noninvasive ventilation (CPAP or BiPAP) improves oxygenation, reduces work of breathing, decreases left ventricular afterload, and reduces intubation rates and mortality in AHF. CPAP and BiPAP are similarly effective. In noncardiogenic edema and ARDS, low tidal volume ventilation (6 mL/kg) with adequate positive end-expiratory pressure (PEEP) is recommended.
Treatment differs by hemodynamic status. Normotensive or hypertensive patients benefit from nitrates (sublingual or IV nitroglycerin; nitroprusside in select cases) to reduce preload and afterload. Diuretics such as furosemide or bumetanide are typically administered after initial stabilization. ACE inhibitors may also be considered. Hypotensive patients with evidence of end-organ hypoperfusion require inotropic or vasopressor support, such as dobutamine, dopamine, norepinephrine, or milrinone, and should avoid nitrates and aggressive vasodilators. Unstable atrial fibrillation may require direct cardioversion. Noncardiogenic edema requires treatment of the underlying cause.
Medications commonly used include nitroglycerin (SL or IV), furosemide 20–80 mg IV, bumetanide 1–3 mg IV, dobutamine infusion, dopamine infusion, norepinephrine infusion, milrinone, and ACE inhibitors such as captopril or enalapril. Aspirin should be administered if myocardial infarction is suspected.
Most patients with pulmonary edema require hospital admission. ICU admission is indicated for those requiring positive-pressure ventilation, inotropic support, ARDS management, or treatment of acute myocardial infarction. Patients with new-onset pulmonary edema, ECG changes, advanced age, renal dysfunction, hypotension, digoxin use, or anemia should be admitted to a monitored unit. Discharge may be considered only in select low-risk patients with mild disease that resolves completely in the ED and reliable follow-up.
Nitrates are first-line therapy in normotensive or hypertensive cardiogenic pulmonary edema to reduce preload. BNP is useful in differentiating AHF from other causes of dyspnea. Chest radiographic findings may be absent early in the course. Early aggressive treatment with nitrates, diuretics, and noninvasive ventilation can rapidly improve outcomes and reduce mortality.
Pulmonary edema is the accumulation of fluid within the interstitium and alveoli due to imbalance in Starling forces, resulting in leakage of fluid from pulmonary capillaries. It is broadly categorized as cardiogenic or noncardiogenic. Cardiogenic pulmonary edema results from abnormal cardiac function leading to inadequate forward flow and elevated hydrostatic pressures, often seen in acute decompensated heart failure (AHF). Noncardiogenic pulmonary edema results from increased alveolar–capillary membrane permeability without primary cardiac dysfunction and includes acute lung injury and acute respiratory distress syndrome (ARDS), defined by a PaO₂/FiO₂ ratio ≤200 mm Hg.
Heart failure affects approximately 5.8 million people in the United States and increases with age, affecting about 10% of individuals over 75 years old. Thirty to forty percent of patients with heart failure are hospitalized annually, with an 11% one-month mortality following admission for acute heart failure.
Cardiogenic causes include systolic dysfunction (ischemic heart disease, cardiomyopathy, myocarditis), pressure overload (aortic stenosis, systemic hypertension), volume overload (mitral or aortic regurgitation), diastolic dysfunction (mitral stenosis, hypertrophic cardiomyopathy), and high-output states such as anemia, hyperthyroidism, arteriovenous fistula, or wet beriberi. Noncardiogenic causes include sepsis, aspiration, inhalation injury, near drowning, disseminated intravascular coagulation, pancreatitis, pulmonary contusion, severe trauma, uremia, high-altitude pulmonary edema, neurogenic pulmonary edema, drug overdose (e.g., narcotics, salicylates), pulmonary embolism, fat embolism, and transfusion-related acute lung injury.
Patients typically present with progressive dyspnea, initially on exertion and later at rest. Orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, cough, weakness, and acute weight gain are common in cardiogenic causes. Physical examination may reveal tachypnea, hypoxia, diaphoresis, cyanosis, jugular venous distention, rales, wheezing, S3 or S4 gallop, tachycardia, and peripheral edema. Patients may be hypertensive or hypotensive. Noncardiogenic edema produces similar pulmonary findings but usually lacks peripheral signs of volume overload.
Evaluation includes ECG to assess for ischemia or dysrhythmias and chest radiography to confirm diagnosis and evaluate severity. Laboratory studies typically include BNP or NT-proBNP, cardiac troponins, renal function, and electrolytes. BNP <100 pg />L makes heart failure unlikely, whereas >500 pg/mL strongly suggests cardiogenic pulmonary edema. Values between 100–500 pg/mL are indeterminate. BNP may be falsely elevated in renal failure and may not rise immediately in very acute heart failure. Troponin elevation occurs in about 20% of AHF cases and carries negative prognostic implications. Hyponatremia and elevated creatinine indicate severe disease and worse prognosis.
Chest radiography in cardiogenic edema may demonstrate cardiomegaly, cephalization of pulmonary vessels, Kerley B lines, pleural effusions, and bilateral perihilar “butterfly” alveolar edema. In noncardiogenic edema, bilateral infiltrates are present without cardiomegaly. Radiographs may be normal early in the disease. Bedside ultrasonography can reveal bilateral B-lines (comet-tail artifacts), supporting the diagnosis. Echocardiography evaluates ventricular function and structural abnormalities.
Differential diagnoses include COPD exacerbation, asthma, pneumonia, pulmonary embolism, pneumothorax, pleural effusion, pericardial tamponade, anaphylaxis, metabolic acidosis, and hyperventilation syndrome.
Management begins with airway, breathing, and circulation assessment. Prehospital care includes oxygen via nonrebreather mask, IV access, cardiac monitoring, pulse oximetry, and sublingual nitrates if blood pressure permits. In severe cases, positive-pressure ventilation or intubation may be required.
In the emergency department, the patient should be positioned upright. Supplemental oxygen and close monitoring are essential. Noninvasive ventilation (CPAP or BiPAP) improves oxygenation, reduces work of breathing, decreases left ventricular afterload, and reduces intubation rates and mortality in AHF. CPAP and BiPAP are similarly effective. In noncardiogenic edema and ARDS, low tidal volume ventilation (6 mL/kg) with adequate positive end-expiratory pressure (PEEP) is recommended.
Treatment differs by hemodynamic status. Normotensive or hypertensive patients benefit from nitrates (sublingual or IV nitroglycerin; nitroprusside in select cases) to reduce preload and afterload. Diuretics such as furosemide or bumetanide are typically administered after initial stabilization. ACE inhibitors may also be considered. Hypotensive patients with evidence of end-organ hypoperfusion require inotropic or vasopressor support, such as dobutamine, dopamine, norepinephrine, or milrinone, and should avoid nitrates and aggressive vasodilators. Unstable atrial fibrillation may require direct cardioversion. Noncardiogenic edema requires treatment of the underlying cause.
Medications commonly used include nitroglycerin (SL or IV), furosemide 20–80 mg IV, bumetanide 1–3 mg IV, dobutamine infusion, dopamine infusion, norepinephrine infusion, milrinone, and ACE inhibitors such as captopril or enalapril. Aspirin should be administered if myocardial infarction is suspected.
Most patients with pulmonary edema require hospital admission. ICU admission is indicated for those requiring positive-pressure ventilation, inotropic support, ARDS management, or treatment of acute myocardial infarction. Patients with new-onset pulmonary edema, ECG changes, advanced age, renal dysfunction, hypotension, digoxin use, or anemia should be admitted to a monitored unit. Discharge may be considered only in select low-risk patients with mild disease that resolves completely in the ED and reliable follow-up.
Nitrates are first-line therapy in normotensive or hypertensive cardiogenic pulmonary edema to reduce preload. BNP is useful in differentiating AHF from other causes of dyspnea. Chest radiographic findings may be absent early in the course. Early aggressive treatment with nitrates, diuretics, and noninvasive ventilation can rapidly improve outcomes and reduce mortality.
