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Infectious Disease and Microbiology – Bronchiolitis
Bronchiolitis is an acute inflammatory disease of the lower respiratory tract that primarily affects the terminal and respiratory bronchioles. It most commonly results from viral infection, leading to inflammatory obstruction of small airways. In some cases, inflammation may extend to adjacent alveolar ducts and alveolar spaces. Although typically viral in origin, bacterial infections can occasionally cause bronchiolitis.
Bronchiolitis is most common in infants and young children, particularly during the first two years of life, with peak incidence around 6 months of age. In the United States, the incidence has been reported as high as 11 cases per 100 children per year during the first year of life. Approximately 6 per 1,000 infants under 6 months are hospitalized annually. Each year, an estimated 675,000 ambulatory visits and 75,000 hospitalizations occur in children younger than 2 years. Bronchiolitis is the most common cause of hospitalization in infants and follows a seasonal pattern, with peak incidence during winter and early spring months.
Risk factors include male sex, age between 3 and 6 months, lack of breastfeeding, exposure to cigarette smoke, crowded living conditions, child care attendance, prematurity, low birth weight, age less than 6–12 weeks, chronic lung disease, congenital heart disease, immunodeficiency, neurological disease, congenital airway abnormalities, and high altitude. Environmental exposures such as toxic fumes, mineral dust, tobacco smoke, and certain medications (e.g., penicillamine) have also been implicated. Bone marrow, lung, and heart–lung transplantation have been associated with bronchiolitis as well.
The pathophysiology involves viral penetration of bronchiolar epithelial cells, leading to direct cellular injury and inflammation. Edema, increased mucus production, and sloughed epithelial cells obstruct small airways, resulting in air trapping and atelectasis. This obstruction contributes to wheezing, impaired gas exchange, and respiratory distress.
The most common causative agent is respiratory syncytial virus (RSV), responsible for more than 50% of cases. Other viruses include parainfluenza, influenza, rhinovirus, rubeola, mumps, parvovirus, enterovirus, coronavirus, coxsackievirus, human metapneumovirus, and varicella zoster virus. In adults, rare cases have been associated with Mycoplasma pneumoniae and Legionella pneumophila. Histologically, bronchiolitis may present as inflammatory bronchiolitis, constrictive bronchiolitis obliterans, or proliferative bronchiolitis. Otitis media is a commonly associated condition.
Clinically, bronchiolitis often begins with mild upper respiratory symptoms such as nasal congestion, coryza, and sneezing, lasting several days and sometimes accompanied by decreased appetite. Fever typically ranges between 38.5°C and 39.0°C. As the illness progresses, lower respiratory symptoms develop, including cough, expiratory wheezing, tachypnea, grunting, retractions, increased respiratory effort, and air trapping. Infants may appear in significant respiratory distress. Wheezing is common, though crackles—particularly early in inspiration—are frequently heard.
Laboratory studies are generally not diagnostic; white blood cell counts are usually normal. In severe cases, viral testing may be performed. Chest radiographs often show hyperinflation and increased anteroposterior diameter, reflecting air trapping.
The differential diagnosis includes asthma, congestive heart failure, foreign body aspiration, pertussis, organophosphate poisoning, cystic fibrosis, and bronchopneumonia. A key distinguishing feature is that bronchiolitis typically represents the first episode of wheezing in an infant, whereas asthma is characterized by recurrent wheezing.
Management is primarily supportive. Oxygen therapy, hydration, and respiratory support are the mainstays of treatment. Infants with significant respiratory distress require hospitalization and are often placed in cool, humidified oxygen. The routine use of bronchodilators is not recommended, as evidence does not support consistent clinical benefit or reduction in hospitalization. Short-term improvement in oxygen saturation or clinical scores may occur with nebulized beta-agonists in some outpatient settings, but they are not recommended for routine use. Ribavirin has been used in select high-risk patients with RSV infection, though its use remains controversial.
Most infants recover with supportive care. However, some may progress to respiratory failure requiring ventilatory support. Long-term follow-up has shown that a proportion of infants with bronchiolitis may develop hyperreactive airways later in childhood. The overall case fatality rate is less than 1%, and mortality among high-risk infants remains below 3.5%.
Bronchiolitis is an acute inflammatory disease of the lower respiratory tract that primarily affects the terminal and respiratory bronchioles. It most commonly results from viral infection, leading to inflammatory obstruction of small airways. In some cases, inflammation may extend to adjacent alveolar ducts and alveolar spaces. Although typically viral in origin, bacterial infections can occasionally cause bronchiolitis.
Bronchiolitis is most common in infants and young children, particularly during the first two years of life, with peak incidence around 6 months of age. In the United States, the incidence has been reported as high as 11 cases per 100 children per year during the first year of life. Approximately 6 per 1,000 infants under 6 months are hospitalized annually. Each year, an estimated 675,000 ambulatory visits and 75,000 hospitalizations occur in children younger than 2 years. Bronchiolitis is the most common cause of hospitalization in infants and follows a seasonal pattern, with peak incidence during winter and early spring months.
Risk factors include male sex, age between 3 and 6 months, lack of breastfeeding, exposure to cigarette smoke, crowded living conditions, child care attendance, prematurity, low birth weight, age less than 6–12 weeks, chronic lung disease, congenital heart disease, immunodeficiency, neurological disease, congenital airway abnormalities, and high altitude. Environmental exposures such as toxic fumes, mineral dust, tobacco smoke, and certain medications (e.g., penicillamine) have also been implicated. Bone marrow, lung, and heart–lung transplantation have been associated with bronchiolitis as well.
The pathophysiology involves viral penetration of bronchiolar epithelial cells, leading to direct cellular injury and inflammation. Edema, increased mucus production, and sloughed epithelial cells obstruct small airways, resulting in air trapping and atelectasis. This obstruction contributes to wheezing, impaired gas exchange, and respiratory distress.
The most common causative agent is respiratory syncytial virus (RSV), responsible for more than 50% of cases. Other viruses include parainfluenza, influenza, rhinovirus, rubeola, mumps, parvovirus, enterovirus, coronavirus, coxsackievirus, human metapneumovirus, and varicella zoster virus. In adults, rare cases have been associated with Mycoplasma pneumoniae and Legionella pneumophila. Histologically, bronchiolitis may present as inflammatory bronchiolitis, constrictive bronchiolitis obliterans, or proliferative bronchiolitis. Otitis media is a commonly associated condition.
Clinically, bronchiolitis often begins with mild upper respiratory symptoms such as nasal congestion, coryza, and sneezing, lasting several days and sometimes accompanied by decreased appetite. Fever typically ranges between 38.5°C and 39.0°C. As the illness progresses, lower respiratory symptoms develop, including cough, expiratory wheezing, tachypnea, grunting, retractions, increased respiratory effort, and air trapping. Infants may appear in significant respiratory distress. Wheezing is common, though crackles—particularly early in inspiration—are frequently heard.
Laboratory studies are generally not diagnostic; white blood cell counts are usually normal. In severe cases, viral testing may be performed. Chest radiographs often show hyperinflation and increased anteroposterior diameter, reflecting air trapping.
The differential diagnosis includes asthma, congestive heart failure, foreign body aspiration, pertussis, organophosphate poisoning, cystic fibrosis, and bronchopneumonia. A key distinguishing feature is that bronchiolitis typically represents the first episode of wheezing in an infant, whereas asthma is characterized by recurrent wheezing.
Management is primarily supportive. Oxygen therapy, hydration, and respiratory support are the mainstays of treatment. Infants with significant respiratory distress require hospitalization and are often placed in cool, humidified oxygen. The routine use of bronchodilators is not recommended, as evidence does not support consistent clinical benefit or reduction in hospitalization. Short-term improvement in oxygen saturation or clinical scores may occur with nebulized beta-agonists in some outpatient settings, but they are not recommended for routine use. Ribavirin has been used in select high-risk patients with RSV infection, though its use remains controversial.
Most infants recover with supportive care. However, some may progress to respiratory failure requiring ventilatory support. Long-term follow-up has shown that a proportion of infants with bronchiolitis may develop hyperreactive airways later in childhood. The overall case fatality rate is less than 1%, and mortality among high-risk infants remains below 3.5%.
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Infectious Disease and Microbiology – Balanitis
Balanitis refers to inflammation and/or infection of the glans penis, while balanoposthitis involves both the glans and the foreskin. Infectious causes are common and may result from fungal, bacterial, viral, or parasitic pathogens. Sexual exposure plays an important role in transmission, particularly in men whose partners have Candida vaginitis. In young boys, balanitis may occur in association with diaper dermatitis.
Risk factors include being uncircumcised, diabetes mellitus (especially newly diagnosed diabetes), immunodeficiency, poor hygiene, use of broad-spectrum antibiotics, and increasing age in the case of Candida colonization. Circumcision and proper genital hygiene significantly reduce the risk. Treatment of sexual partners is important when Candida or Trichomonas infection is identified.
Infectious etiologies include Candida species (most common), Trichomonas species, anaerobic bacteria such as Bacteroides and Gardnerella vaginalis, Chlamydia, Neisseria gonorrhoeae, human papillomavirus (HPV), herpes simplex virus (HSV), Treponema pallidum, Mycoplasma, Mycobacterium (including Bacillus Calmette–Guérin), group A and B streptococci, Staphylococcus aureus, Borrelia burgdorferi, and Entamoeba histolytica.
Patients typically present with pain, tenderness, erythema, pruritus, edema, erosions, and sometimes pustules on the glans penis. Anaerobic infections may produce a characteristic foul odor.
Diagnosis is largely clinical but may be supported by laboratory testing. Fungal preparations often reveal Candida. Direct impression onto CHROMagar Candida medium has been shown to provide a higher yield than swab sampling. Wet mount examination may detect Trichomonas or Gardnerella. Urethral discharge should be tested for sexually transmitted infections. Serologic or culture testing for HIV, HPV, and HSV may be indicated based on risk factors. Blood glucose testing is recommended to evaluate for underlying diabetes mellitus.
The differential diagnosis includes numerous noninfectious conditions such as irritant dermatitis, trauma, contact dermatitis, lichen sclerosus, lichen planus, Zoon’s balanitis, erythroplasia of Queyrat, pemphigus, pemphigoid, Bowen’s disease, leukoplakia, fixed drug eruption, psoriasis (particularly inverse psoriasis), Paget’s disease, nummular eczema, scabies, and squamous cell carcinoma.
Management begins with good hygiene, including gentle washing of the glans after foreskin retraction. Candida balanitis is typically treated with topical imidazole antifungal agents, and 1% hydrocortisone cream may be added for symptomatic relief. Severe cases may require oral fluconazole. Trichomonas infection responds to metronidazole, and sexual partners should be treated simultaneously. Anaerobic infections may be managed with oral metronidazole, oral amoxicillin–clavulanate, or topical clindamycin cream.
Patients should be monitored for recurrence and evaluated for underlying diabetes if not previously diagnosed. Complications include phimosis, paraphimosis, fissuring of the prepuce, and scarring.
Balanitis refers to inflammation and/or infection of the glans penis, while balanoposthitis involves both the glans and the foreskin. Infectious causes are common and may result from fungal, bacterial, viral, or parasitic pathogens. Sexual exposure plays an important role in transmission, particularly in men whose partners have Candida vaginitis. In young boys, balanitis may occur in association with diaper dermatitis.
Risk factors include being uncircumcised, diabetes mellitus (especially newly diagnosed diabetes), immunodeficiency, poor hygiene, use of broad-spectrum antibiotics, and increasing age in the case of Candida colonization. Circumcision and proper genital hygiene significantly reduce the risk. Treatment of sexual partners is important when Candida or Trichomonas infection is identified.
Infectious etiologies include Candida species (most common), Trichomonas species, anaerobic bacteria such as Bacteroides and Gardnerella vaginalis, Chlamydia, Neisseria gonorrhoeae, human papillomavirus (HPV), herpes simplex virus (HSV), Treponema pallidum, Mycoplasma, Mycobacterium (including Bacillus Calmette–Guérin), group A and B streptococci, Staphylococcus aureus, Borrelia burgdorferi, and Entamoeba histolytica.
Patients typically present with pain, tenderness, erythema, pruritus, edema, erosions, and sometimes pustules on the glans penis. Anaerobic infections may produce a characteristic foul odor.
Diagnosis is largely clinical but may be supported by laboratory testing. Fungal preparations often reveal Candida. Direct impression onto CHROMagar Candida medium has been shown to provide a higher yield than swab sampling. Wet mount examination may detect Trichomonas or Gardnerella. Urethral discharge should be tested for sexually transmitted infections. Serologic or culture testing for HIV, HPV, and HSV may be indicated based on risk factors. Blood glucose testing is recommended to evaluate for underlying diabetes mellitus.
The differential diagnosis includes numerous noninfectious conditions such as irritant dermatitis, trauma, contact dermatitis, lichen sclerosus, lichen planus, Zoon’s balanitis, erythroplasia of Queyrat, pemphigus, pemphigoid, Bowen’s disease, leukoplakia, fixed drug eruption, psoriasis (particularly inverse psoriasis), Paget’s disease, nummular eczema, scabies, and squamous cell carcinoma.
Management begins with good hygiene, including gentle washing of the glans after foreskin retraction. Candida balanitis is typically treated with topical imidazole antifungal agents, and 1% hydrocortisone cream may be added for symptomatic relief. Severe cases may require oral fluconazole. Trichomonas infection responds to metronidazole, and sexual partners should be treated simultaneously. Anaerobic infections may be managed with oral metronidazole, oral amoxicillin–clavulanate, or topical clindamycin cream.
Patients should be monitored for recurrence and evaluated for underlying diabetes if not previously diagnosed. Complications include phimosis, paraphimosis, fissuring of the prepuce, and scarring.
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Infectious Disease and Microbiology – Bartonellosis (Oroya Fever/Verruga Peruana)
Bartonellosis is an infection caused by Bartonella bacilliformis, transmitted by sandflies of the genus Phlebotomus. It occurs in endemic areas and presents in two distinct clinical forms. Nonimmune individuals typically develop an acute febrile illness known as Oroya fever, characterized by profound hemolytic anemia. After recovery from the acute phase, a chronic cutaneous form called verruga peruana may develop, featuring angioproliferative skin lesions that resemble those seen in bacillary angiomatosis caused by other Bartonella species.
The disease is endemic to the Andean river valleys at altitudes between 600 and 2,500 meters in Peru, Ecuador, and Colombia. Oroya fever most commonly affects tourists or visitors who lack prior immunity, whereas verruga peruana is more frequently seen in the native population. Rare imported cases have been reported outside endemic regions. Risk factors include residence in or travel to endemic areas and exposure to the sandfly vector. Prevention focuses on vector control measures such as indoor and outdoor insecticide spraying, use of insect repellents, and bed nets.
Pathophysiologically, B. bacilliformis invades erythrocytes and endothelial cells. The bacteria multiply within intracellular vacuoles inside red blood cells, which are subsequently destroyed by the reticuloendothelial system, resulting in severe hemolytic anemia. The organism is a small, gram-negative bacillus closely related to Bartonella quintana.
The incubation period of Oroya fever averages about three weeks but can extend up to 100 days. The acute illness may begin gradually with low-grade fever, malaise, headache, and anorexia, or abruptly with high fever, chills, diaphoresis, altered mental status, and rapidly progressive anemia. Patients may experience dyspnea, chest discomfort, myalgias, arthralgias, and in severe cases, delirium or coma. Anasarca indicates a poor prognosis. During the convalescent phase, fever subsides and anemia improves.
Physical examination in Oroya fever reveals high fever, signs of profound anemia, generalized nontender lymphadenopathy, and occasionally thrombocytopenic purpura. Splenomegaly is uncommon and may suggest concurrent infection.
Verruga peruana develops weeks to months after recovery from the acute phase. Lesions appear in crops and may be miliary (1–4 mm papular erythematous lesions), nodular, or larger “mular” lesions exceeding 5 mm in diameter. They are typically bright red, bleed easily, and may involve skin, mucous membranes, or internal organs. Lesions are generally nontender unless secondarily infected and may be present at different stages simultaneously.
Diagnosis in the acute phase is made by identifying numerous bacteria attached to red blood cells on Giemsa- or Wright-stained peripheral blood smears or by positive blood or bone marrow cultures. Peripheral smear may also reveal macrocytosis, poikilocytosis, Howell–Jolly bodies, nucleated red blood cells, and immature myeloid cells. Profound anemia with a negative Coombs’ test is typical. In subacute cases, smears may initially be negative, and blood cultures are required. In the chronic phase, organisms can be demonstrated in cultures from skin lesions or bone marrow. Serologic tests such as ELISA or indirect immunofluorescence can support the diagnosis. Skin biopsy may show increased angiogenesis and characteristic endothelial inclusions (Rocha-Lima inclusions).
The acute phase must be differentiated from other endemic febrile illnesses such as malaria, typhoid fever, and leptospirosis. Verruga lesions resemble bacillary angiomatosis, Kaposi’s sarcoma, and certain neoplasms; epidemiologic context is a key diagnostic clue.
Treatment of Oroya fever consists of chloramphenicol (500 mg orally or intravenously every 6 hours) combined with a second antimicrobial, preferably a beta-lactam such as penicillin, for 14 days. Chloramphenicol also provides coverage against salmonellosis, a common secondary infection. Doxycycline is an alternative agent, while fluoroquinolones are generally not recommended due to resistance. Verruga peruana is treated with rifampin (10 mg/kg daily, maximum 600 mg daily) for 10–14 days. Streptomycin is a second-line option. Supportive care, including blood transfusion for severe anemia, is essential in the acute phase. Large or secondarily infected skin lesions may require surgical excision.
Patients with Oroya fever typically require inpatient management, whereas those with verruga peruana can often be managed as outpatients. Monitoring during the acute phase should include hydration status, complete blood counts, and surveillance for secondary infections such as salmonellosis, malaria, or tuberculosis.
Untreated Oroya fever carries a mortality rate of 50–88%. With appropriate therapy, fever usually resolves within 24 hours, though bacteremia may persist longer. Complications include secondary bacterial infections during convalescence and ulceration or bleeding of verruga lesions.
Bartonellosis is an infection caused by Bartonella bacilliformis, transmitted by sandflies of the genus Phlebotomus. It occurs in endemic areas and presents in two distinct clinical forms. Nonimmune individuals typically develop an acute febrile illness known as Oroya fever, characterized by profound hemolytic anemia. After recovery from the acute phase, a chronic cutaneous form called verruga peruana may develop, featuring angioproliferative skin lesions that resemble those seen in bacillary angiomatosis caused by other Bartonella species.
The disease is endemic to the Andean river valleys at altitudes between 600 and 2,500 meters in Peru, Ecuador, and Colombia. Oroya fever most commonly affects tourists or visitors who lack prior immunity, whereas verruga peruana is more frequently seen in the native population. Rare imported cases have been reported outside endemic regions. Risk factors include residence in or travel to endemic areas and exposure to the sandfly vector. Prevention focuses on vector control measures such as indoor and outdoor insecticide spraying, use of insect repellents, and bed nets.
Pathophysiologically, B. bacilliformis invades erythrocytes and endothelial cells. The bacteria multiply within intracellular vacuoles inside red blood cells, which are subsequently destroyed by the reticuloendothelial system, resulting in severe hemolytic anemia. The organism is a small, gram-negative bacillus closely related to Bartonella quintana.
The incubation period of Oroya fever averages about three weeks but can extend up to 100 days. The acute illness may begin gradually with low-grade fever, malaise, headache, and anorexia, or abruptly with high fever, chills, diaphoresis, altered mental status, and rapidly progressive anemia. Patients may experience dyspnea, chest discomfort, myalgias, arthralgias, and in severe cases, delirium or coma. Anasarca indicates a poor prognosis. During the convalescent phase, fever subsides and anemia improves.
Physical examination in Oroya fever reveals high fever, signs of profound anemia, generalized nontender lymphadenopathy, and occasionally thrombocytopenic purpura. Splenomegaly is uncommon and may suggest concurrent infection.
Verruga peruana develops weeks to months after recovery from the acute phase. Lesions appear in crops and may be miliary (1–4 mm papular erythematous lesions), nodular, or larger “mular” lesions exceeding 5 mm in diameter. They are typically bright red, bleed easily, and may involve skin, mucous membranes, or internal organs. Lesions are generally nontender unless secondarily infected and may be present at different stages simultaneously.
Diagnosis in the acute phase is made by identifying numerous bacteria attached to red blood cells on Giemsa- or Wright-stained peripheral blood smears or by positive blood or bone marrow cultures. Peripheral smear may also reveal macrocytosis, poikilocytosis, Howell–Jolly bodies, nucleated red blood cells, and immature myeloid cells. Profound anemia with a negative Coombs’ test is typical. In subacute cases, smears may initially be negative, and blood cultures are required. In the chronic phase, organisms can be demonstrated in cultures from skin lesions or bone marrow. Serologic tests such as ELISA or indirect immunofluorescence can support the diagnosis. Skin biopsy may show increased angiogenesis and characteristic endothelial inclusions (Rocha-Lima inclusions).
The acute phase must be differentiated from other endemic febrile illnesses such as malaria, typhoid fever, and leptospirosis. Verruga lesions resemble bacillary angiomatosis, Kaposi’s sarcoma, and certain neoplasms; epidemiologic context is a key diagnostic clue.
Treatment of Oroya fever consists of chloramphenicol (500 mg orally or intravenously every 6 hours) combined with a second antimicrobial, preferably a beta-lactam such as penicillin, for 14 days. Chloramphenicol also provides coverage against salmonellosis, a common secondary infection. Doxycycline is an alternative agent, while fluoroquinolones are generally not recommended due to resistance. Verruga peruana is treated with rifampin (10 mg/kg daily, maximum 600 mg daily) for 10–14 days. Streptomycin is a second-line option. Supportive care, including blood transfusion for severe anemia, is essential in the acute phase. Large or secondarily infected skin lesions may require surgical excision.
Patients with Oroya fever typically require inpatient management, whereas those with verruga peruana can often be managed as outpatients. Monitoring during the acute phase should include hydration status, complete blood counts, and surveillance for secondary infections such as salmonellosis, malaria, or tuberculosis.
Untreated Oroya fever carries a mortality rate of 50–88%. With appropriate therapy, fever usually resolves within 24 hours, though bacteremia may persist longer. Complications include secondary bacterial infections during convalescence and ulceration or bleeding of verruga lesions.
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Infectious Disease and Microbiology – Bell’s Palsy
Bell’s palsy is defined as an acute, idiopathic, unilateral paralysis of the facial nerve (cranial nerve VII). Approximately half of all facial nerve palsies are classified as Bell’s palsy. Bilateral involvement is rare, occurring in about 0.3% of cases. Although termed “idiopathic,” viral etiologies are strongly suspected, particularly herpes simplex virus. Other infectious associations include herpes zoster (including herpes zoster oticus). Rarely, Bell’s palsy has been reported as an adverse event following immunization.
The incidence in the United States ranges from 13 to 34 cases per 100,000 persons annually. The condition most commonly affects individuals aged 20–35 years and those over 70 years of age. Males and females are equally affected. Bell’s palsy is the most common cause of seventh nerve palsy in children. Risk factors include pregnancy, diabetes mellitus, and hypertension in individuals older than 40 years. Currently, there is no known preventive measure.
Clinically, Bell’s palsy presents with acute onset over one to two days and rapid progression to partial or complete unilateral facial paralysis. Patients may experience decreased tear and saliva production on the affected side, hyperacusis (increased sensitivity to sound), dysgeusia (altered taste), and retroauricular pain. The diagnosis is primarily clinical.
The differential diagnosis is broad and includes infectious causes such as Lyme disease, HIV infection (particularly during seroconversion), otitis media, mastoiditis, tuberculosis, syphilis, infectious meningitis, rubella, tetanus, Mycoplasma infection, and enteroviral infections. Noninfectious causes include sarcoidosis, Sjögren’s syndrome, systemic lupus erythematosus, tumors (parotid gland tumors, melanoma, meningioma), cerebral aneurysm, Guillain-Barré syndrome, trauma, iatrogenic injury, and others. In cases of bilateral facial paralysis, Lyme disease and sarcoidosis should be strongly considered.
Electrodiagnostic studies such as electromyography (EMG) or electroneurography may be useful in selected cases, particularly if recovery is incomplete. Patients with a typical presentation and early recovery usually do not require further testing. Imaging with CT or MRI is indicated if the presentation is atypical, if symptoms progress slowly, or if there is no improvement within six months, to exclude intracranial or middle ear pathology. Recent evidence suggests that ultrasound measurement of the distal facial nerve diameter may help predict recovery at three months.
Early treatment significantly improves outcomes. Prednisolone should be initiated within three days of symptom onset, at a dose of 60–80 mg daily for one week, as it increases the likelihood of complete recovery at three and nine months. Antiviral therapy may be added in severe cases of facial palsy. Eye protection is essential, including artificial tears during the day and lubricating ointment at night, to prevent corneal injury. The role of surgical decompression remains controversial.
Ongoing care focuses on eye protection and psychological support. Complications include incomplete recovery in approximately one-third of patients, keratitis, corneal abrasions, and recurrence in 7–15% of cases.
Bell’s palsy is defined as an acute, idiopathic, unilateral paralysis of the facial nerve (cranial nerve VII). Approximately half of all facial nerve palsies are classified as Bell’s palsy. Bilateral involvement is rare, occurring in about 0.3% of cases. Although termed “idiopathic,” viral etiologies are strongly suspected, particularly herpes simplex virus. Other infectious associations include herpes zoster (including herpes zoster oticus). Rarely, Bell’s palsy has been reported as an adverse event following immunization.
The incidence in the United States ranges from 13 to 34 cases per 100,000 persons annually. The condition most commonly affects individuals aged 20–35 years and those over 70 years of age. Males and females are equally affected. Bell’s palsy is the most common cause of seventh nerve palsy in children. Risk factors include pregnancy, diabetes mellitus, and hypertension in individuals older than 40 years. Currently, there is no known preventive measure.
Clinically, Bell’s palsy presents with acute onset over one to two days and rapid progression to partial or complete unilateral facial paralysis. Patients may experience decreased tear and saliva production on the affected side, hyperacusis (increased sensitivity to sound), dysgeusia (altered taste), and retroauricular pain. The diagnosis is primarily clinical.
The differential diagnosis is broad and includes infectious causes such as Lyme disease, HIV infection (particularly during seroconversion), otitis media, mastoiditis, tuberculosis, syphilis, infectious meningitis, rubella, tetanus, Mycoplasma infection, and enteroviral infections. Noninfectious causes include sarcoidosis, Sjögren’s syndrome, systemic lupus erythematosus, tumors (parotid gland tumors, melanoma, meningioma), cerebral aneurysm, Guillain-Barré syndrome, trauma, iatrogenic injury, and others. In cases of bilateral facial paralysis, Lyme disease and sarcoidosis should be strongly considered.
Electrodiagnostic studies such as electromyography (EMG) or electroneurography may be useful in selected cases, particularly if recovery is incomplete. Patients with a typical presentation and early recovery usually do not require further testing. Imaging with CT or MRI is indicated if the presentation is atypical, if symptoms progress slowly, or if there is no improvement within six months, to exclude intracranial or middle ear pathology. Recent evidence suggests that ultrasound measurement of the distal facial nerve diameter may help predict recovery at three months.
Early treatment significantly improves outcomes. Prednisolone should be initiated within three days of symptom onset, at a dose of 60–80 mg daily for one week, as it increases the likelihood of complete recovery at three and nine months. Antiviral therapy may be added in severe cases of facial palsy. Eye protection is essential, including artificial tears during the day and lubricating ointment at night, to prevent corneal injury. The role of surgical decompression remains controversial.
Ongoing care focuses on eye protection and psychological support. Complications include incomplete recovery in approximately one-third of patients, keratitis, corneal abrasions, and recurrence in 7–15% of cases.
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Infectious Disease and Microbiology – Blastomycosis
Blastomycosis is an acute or chronic infection caused by Blastomyces dermatitidis, a dimorphic fungus found in soil. The organism exists as mold in the environment and converts to yeast in human tissue. The annual incidence ranges from 0.3 to 1.8 cases per 100,000 population, with up to 7.4 hospital admissions per 1 million people in endemic regions. The infection is endemic in areas near bodies of water in the southeastern United States and along the Mississippi, Ohio, and St. Lawrence River valleys. It is also found along the Mediterranean coast, in South America, Mexico, and parts of Africa. Although previously thought to affect middle-aged men more commonly, this is likely related to environmental exposure patterns rather than gender predisposition. Immunocompromised individuals are at risk for more severe disease and poorer outcomes. Prevention focuses on minimizing exposure in endemic regions, including the use of respiratory protection for individuals at occupational risk.
Infection occurs through inhalation of conidia from the environment, with potential for hematogenous dissemination to other organs. The immune system more effectively clears the conidial form; however, once inside the host, the organism converts into a broad-based budding yeast form that is less susceptible to immune clearance. Reactivation may occur in immunocompromised patients.
Clinically, blastomycosis most commonly presents as pulmonary disease. Acute pneumonia presents with fever, night sweats, productive cough, dyspnea, and pleuritic chest pain, and may be accompanied by rash. Chronic pneumonia resembles pulmonary tuberculosis, with subacute onset of fever, night sweats, weight loss, mild productive cough, and sometimes hemoptysis. Disseminated disease can involve the skin, bones, genitourinary tract, central nervous system, or other organs. Skin lesions are typically non-tender papules, nodules, or plaques that may become verrucous or ulcerated. Soft tissue swelling may occur and can form draining tracts. CNS involvement may manifest as meningitis or focal neurologic deficits.
Diagnosis relies primarily on culture and direct visualization. Serologic testing is limited due to cross-reactivity with other endemic mycoses. Urine antigen testing is available but also limited by cross-reactivity. Chest radiography may reveal masses, nodules, lobar infiltrates, or cavitary lesions; lymphadenopathy is uncommon. Culture is positive in approximately 86% of sputum samples and 92% of bronchoalveolar lavage specimens. Wet mount preparations using potassium hydroxide or calcofluor white have about 46% sensitivity. The characteristic finding is a large yeast (8–15 μm) with a single broad-based bud. Histopathology shows pyogranulomas, and fungal elements are more easily visualized with methenamine silver or periodic acid–Schiff stains. The differential diagnosis includes atypical pneumonia, lung cancer, mycobacterial disease, and squamous cell carcinoma for cutaneous lesions.
Treatment depends on severity and organ involvement. For pulmonary or disseminated non-CNS disease, amphotericin B (or a lipid/liposomal formulation) is administered for two weeks, followed by itraconazole 200 mg three times daily for three days, then 200 mg twice daily for 6–12 months. Mild to moderate disease may be treated with itraconazole alone for 6–12 months. CNS disease requires lipid/liposomal amphotericin B (3–5 mg/kg IV for 4–6 weeks), followed by at least 12 months of oral azole therapy (itraconazole, fluconazole, or voriconazole). Immunocompromised patients should receive amphotericin B followed by itraconazole for at least 12 months, and lifelong suppressive therapy may be considered. In children with mild disease, itraconazole (10 mg/kg/day) is recommended for 6–12 months; severe disease requires amphotericin followed by itraconazole. In pregnancy, amphotericin B is the treatment of choice, as azoles are contraindicated.
Patients require close monitoring for antifungal toxicity. Therapeutic drug monitoring of itraconazole is recommended after two weeks of therapy, with target levels greater than 1.0 μg/mL and less than 10 μg/mL. Liver function tests should be monitored at least every three months during azole therapy. Itraconazole should be taken with food to enhance absorption. Follow-up for approximately six months after completion of therapy is recommended due to relapse risk.
Prognosis is favorable in immunocompetent individuals, with cure rates of 90–97% when treated appropriately with amphotericin. Mortality approaches 40% in immunocompromised patients, particularly those with bone marrow transplantation or AIDS. Outcomes in pregnant women can be excellent if diagnosed early, though they are at increased risk for severe disease. Complications include respiratory failure (acute respiratory distress syndrome), CNS involvement, and relapse.
Blastomycosis is an acute or chronic infection caused by Blastomyces dermatitidis, a dimorphic fungus found in soil. The organism exists as mold in the environment and converts to yeast in human tissue. The annual incidence ranges from 0.3 to 1.8 cases per 100,000 population, with up to 7.4 hospital admissions per 1 million people in endemic regions. The infection is endemic in areas near bodies of water in the southeastern United States and along the Mississippi, Ohio, and St. Lawrence River valleys. It is also found along the Mediterranean coast, in South America, Mexico, and parts of Africa. Although previously thought to affect middle-aged men more commonly, this is likely related to environmental exposure patterns rather than gender predisposition. Immunocompromised individuals are at risk for more severe disease and poorer outcomes. Prevention focuses on minimizing exposure in endemic regions, including the use of respiratory protection for individuals at occupational risk.
Infection occurs through inhalation of conidia from the environment, with potential for hematogenous dissemination to other organs. The immune system more effectively clears the conidial form; however, once inside the host, the organism converts into a broad-based budding yeast form that is less susceptible to immune clearance. Reactivation may occur in immunocompromised patients.
Clinically, blastomycosis most commonly presents as pulmonary disease. Acute pneumonia presents with fever, night sweats, productive cough, dyspnea, and pleuritic chest pain, and may be accompanied by rash. Chronic pneumonia resembles pulmonary tuberculosis, with subacute onset of fever, night sweats, weight loss, mild productive cough, and sometimes hemoptysis. Disseminated disease can involve the skin, bones, genitourinary tract, central nervous system, or other organs. Skin lesions are typically non-tender papules, nodules, or plaques that may become verrucous or ulcerated. Soft tissue swelling may occur and can form draining tracts. CNS involvement may manifest as meningitis or focal neurologic deficits.
Diagnosis relies primarily on culture and direct visualization. Serologic testing is limited due to cross-reactivity with other endemic mycoses. Urine antigen testing is available but also limited by cross-reactivity. Chest radiography may reveal masses, nodules, lobar infiltrates, or cavitary lesions; lymphadenopathy is uncommon. Culture is positive in approximately 86% of sputum samples and 92% of bronchoalveolar lavage specimens. Wet mount preparations using potassium hydroxide or calcofluor white have about 46% sensitivity. The characteristic finding is a large yeast (8–15 μm) with a single broad-based bud. Histopathology shows pyogranulomas, and fungal elements are more easily visualized with methenamine silver or periodic acid–Schiff stains. The differential diagnosis includes atypical pneumonia, lung cancer, mycobacterial disease, and squamous cell carcinoma for cutaneous lesions.
Treatment depends on severity and organ involvement. For pulmonary or disseminated non-CNS disease, amphotericin B (or a lipid/liposomal formulation) is administered for two weeks, followed by itraconazole 200 mg three times daily for three days, then 200 mg twice daily for 6–12 months. Mild to moderate disease may be treated with itraconazole alone for 6–12 months. CNS disease requires lipid/liposomal amphotericin B (3–5 mg/kg IV for 4–6 weeks), followed by at least 12 months of oral azole therapy (itraconazole, fluconazole, or voriconazole). Immunocompromised patients should receive amphotericin B followed by itraconazole for at least 12 months, and lifelong suppressive therapy may be considered. In children with mild disease, itraconazole (10 mg/kg/day) is recommended for 6–12 months; severe disease requires amphotericin followed by itraconazole. In pregnancy, amphotericin B is the treatment of choice, as azoles are contraindicated.
Patients require close monitoring for antifungal toxicity. Therapeutic drug monitoring of itraconazole is recommended after two weeks of therapy, with target levels greater than 1.0 μg/mL and less than 10 μg/mL. Liver function tests should be monitored at least every three months during azole therapy. Itraconazole should be taken with food to enhance absorption. Follow-up for approximately six months after completion of therapy is recommended due to relapse risk.
Prognosis is favorable in immunocompetent individuals, with cure rates of 90–97% when treated appropriately with amphotericin. Mortality approaches 40% in immunocompromised patients, particularly those with bone marrow transplantation or AIDS. Outcomes in pregnant women can be excellent if diagnosed early, though they are at increased risk for severe disease. Complications include respiratory failure (acute respiratory distress syndrome), CNS involvement, and relapse.
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Infectious Disease and Microbiology – Blepharitis and Chalazion
Blepharitis is an infection and inflammation of the eyelid margins. It may be classified as anterior (involving inflammation at the base of the eyelashes), posterior (affecting the inner portion of the eyelid and meibomian glands), or granulomatous. Chalazion, in contrast, is a painless granulomatous inflammation of a meibomian gland that produces a localized nodule within the eyelid. Blepharitis is a common condition encountered by both primary care physicians and ophthalmologists. Posterior blepharitis is frequently associated with rosacea and seborrheic dermatitis.
Risk factors include dermatologic conditions such as atopic dermatitis, with more than three-fourths of such patients demonstrating positive cultures for Staphylococcus aureus. However, a positive culture does not always indicate active infection, and clinical correlation is essential. The pathophysiology involves bacterial colonization and inflammation that alter meibomian gland secretions, contributing to gland dysfunction and chronic irritation.
The most common causative organisms are Staphylococcus species, particularly S. aureus. Numerous other pathogens have been reported, including bacteria, fungi, viruses, and parasites, although these are less common. Organisms capable of colonizing adjacent skin areas such as the scalp or nares may spread to the eyelids and contribute to infection. Blepharitis is commonly associated with rosacea and seborrheic dermatitis.
Patients typically report chronic irritation, burning sensation, mild redness, and occasional pruritus of the eyelids. Some may experience blurred vision. On physical examination, acute blepharitis may present with collections of pus and ulceration at the lid margin. Chronic blepharitis often shows misdirected or missing eyelashes, telangiectasia, and a swollen lid margin. Superficial lid involvement usually presents with hyperemia and telangiectasia. Slit-lamp examination by an ophthalmologist may assist in evaluation.
Management focuses primarily on conservative measures. Warm compresses and strict eyelid hygiene are foundational treatments. Gentle massage of the eyelids using a diluted mixture of baby shampoo and water applied with a cotton-tipped applicator helps improve meibomian gland drainage. Topical ophthalmic antibiotics such as bacitracin or erythromycin (twice to four times daily for approximately two weeks) are commonly used for staphylococcal blepharitis. Gentamicin and 1% mercuric oxide preparations may also be used. In chronic or refractory cases, cultures should be obtained, and systemic antibiotics such as dicloxacillin, quinolones, or azithromycin may be considered.
For chalazion, persistent and nontender lesions may require incision and curettage. This involves removal of inflammatory debris via conjunctival incision. If infection is absent, intralesional corticosteroid injection may be considered. In rare cases of necrotizing fasciitis involving the eyelids, urgent surgical debridement is required.
Follow-up is important for nonhealing or ulcerative eyelid lesions, as basal cell carcinoma, squamous cell carcinoma, or meibomian gland carcinoma must be excluded. Complications include the development of hordeolum (stye). An external hordeolum results from staphylococcal infection of the glands of Zeis or Moll at the eyelid margin, whereas an internal hordeolum involves suppurative infection of the meibomian glands within the tarsal plate.
Blepharitis is an infection and inflammation of the eyelid margins. It may be classified as anterior (involving inflammation at the base of the eyelashes), posterior (affecting the inner portion of the eyelid and meibomian glands), or granulomatous. Chalazion, in contrast, is a painless granulomatous inflammation of a meibomian gland that produces a localized nodule within the eyelid. Blepharitis is a common condition encountered by both primary care physicians and ophthalmologists. Posterior blepharitis is frequently associated with rosacea and seborrheic dermatitis.
Risk factors include dermatologic conditions such as atopic dermatitis, with more than three-fourths of such patients demonstrating positive cultures for Staphylococcus aureus. However, a positive culture does not always indicate active infection, and clinical correlation is essential. The pathophysiology involves bacterial colonization and inflammation that alter meibomian gland secretions, contributing to gland dysfunction and chronic irritation.
The most common causative organisms are Staphylococcus species, particularly S. aureus. Numerous other pathogens have been reported, including bacteria, fungi, viruses, and parasites, although these are less common. Organisms capable of colonizing adjacent skin areas such as the scalp or nares may spread to the eyelids and contribute to infection. Blepharitis is commonly associated with rosacea and seborrheic dermatitis.
Patients typically report chronic irritation, burning sensation, mild redness, and occasional pruritus of the eyelids. Some may experience blurred vision. On physical examination, acute blepharitis may present with collections of pus and ulceration at the lid margin. Chronic blepharitis often shows misdirected or missing eyelashes, telangiectasia, and a swollen lid margin. Superficial lid involvement usually presents with hyperemia and telangiectasia. Slit-lamp examination by an ophthalmologist may assist in evaluation.
Management focuses primarily on conservative measures. Warm compresses and strict eyelid hygiene are foundational treatments. Gentle massage of the eyelids using a diluted mixture of baby shampoo and water applied with a cotton-tipped applicator helps improve meibomian gland drainage. Topical ophthalmic antibiotics such as bacitracin or erythromycin (twice to four times daily for approximately two weeks) are commonly used for staphylococcal blepharitis. Gentamicin and 1% mercuric oxide preparations may also be used. In chronic or refractory cases, cultures should be obtained, and systemic antibiotics such as dicloxacillin, quinolones, or azithromycin may be considered.
For chalazion, persistent and nontender lesions may require incision and curettage. This involves removal of inflammatory debris via conjunctival incision. If infection is absent, intralesional corticosteroid injection may be considered. In rare cases of necrotizing fasciitis involving the eyelids, urgent surgical debridement is required.
Follow-up is important for nonhealing or ulcerative eyelid lesions, as basal cell carcinoma, squamous cell carcinoma, or meibomian gland carcinoma must be excluded. Complications include the development of hordeolum (stye). An external hordeolum results from staphylococcal infection of the glands of Zeis or Moll at the eyelid margin, whereas an internal hordeolum involves suppurative infection of the meibomian glands within the tarsal plate.
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Emergency And Acute Medicine – Pityriasis Rosea
Pityriasis rosea is a self-limited inflammatory skin eruption of unknown origin that primarily affects children and young adults. The condition often begins with a single lesion known as a herald patch, which is an ovoid, erythematous, slightly raised plaque usually located on the trunk or proximal extremities. Within 7–14 days, a secondary eruption develops, consisting of multiple smaller, salmon-colored, elliptic papules with fine scaling. These lesions typically align along Langer lines on the trunk in a symmetric “Christmas tree” distribution. Nearly 80% of cases resolve spontaneously within 1–2 months.
The exact cause is unknown, although weak evidence suggests a viral association, particularly with human herpesvirus types 6 and 7. Several medications have been linked to pityriasis-like eruptions, including barbiturates, captopril, clonidine, gold, isotretinoin, metronidazole, bismuth, interferon, imatinib (Gleevec), and the hepatitis B vaccine. There are weak associations with eczema, asthma, and underlying malignancies.
Many patients report mild prodromal symptoms in the days preceding the rash, including malaise, gastrointestinal upset, or upper respiratory symptoms. On examination, the herald patch is typically 2–10 cm in diameter and seen in 50–90% of cases. The secondary eruption follows, appearing symmetrically along cleavage lines, predominantly on the trunk and proximal extremities. Pruritus is common and may vary in severity. Inverse pityriasis rosea, characterized by lesions on the face and distal extremities with minimal trunk involvement, is more frequently observed in children. Rare pediatric cases may include oral lesions such as punctate hemorrhages or ulcerations.
Diagnosis is clinical and based on characteristic history and physical findings. No routine laboratory testing is required. However, when the herald patch is absent or the presentation is atypical, alternative diagnoses must be considered. Secondary syphilis can mimic the rash and should prompt testing with a rapid plasma reagin (RPR) in patients with risk factors. A potassium hydroxide (KOH) preparation may help distinguish tinea corporis or tinea versicolor.
The differential diagnosis for the herald patch includes nummular eczema and tinea corporis. The secondary eruption may resemble secondary syphilis, drug eruption, guttate psoriasis, lichen planus, seborrheic dermatitis, scabies, dermatomyositis, cutaneous lymphoma, lupus, Kaposi sarcoma, or occult malignancy. Toxic appearance or mucous membrane involvement should prompt reconsideration of the diagnosis.
No stabilization is required in the emergency setting. Pityriasis rosea is self-limiting, and treatment is directed toward symptomatic relief, particularly for pruritus. Topical corticosteroids such as hydrocortisone 1% cream applied three times daily and oral antihistamines such as diphenhydramine may provide relief. In more severe cases, short courses of oral prednisone may be used. Erythromycin has also been reported to reduce symptom duration in some patients.
Hospital admission is not required. Patients with a clear diagnosis may be discharged with reassurance that the condition is benign and typically resolves within 1–2 months. Dermatology referral may be considered for severe, persistent, or atypical cases, especially if pruritus is refractory.
Pityriasis rosea most commonly affects the trunk and proximal extremities. Involvement of mucous membranes, distal extremities, or a toxic clinical appearance should prompt evaluation for alternative diagnoses.
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Emergency And Acute Medicine – Pheochromocytoma
Pheochromocytoma is a catecholamine-producing tumor arising from chromaffin tissue of the sympathetic nervous system. Most tumors originate in the adrenal medulla, with approximately 80% being solitary adrenal tumors (more commonly right-sided), 10% bilateral (often inherited), and 10% extra-adrenal (paragangliomas) located in the abdomen, thorax, neck, or bladder. About 10% are malignant. The condition is rare, occurring in approximately 2–8 per million people per year, and accounts for 0.2–0.4% of hypertensive patients, although it is more common in those with severe or refractory hypertension. It typically presents between the third and fifth decades of life, affects males and females equally, and is diagnosed postmortem in nearly half of cases. Approximately 10% are asymptomatic and discovered incidentally on imaging.
Up to 25% of cases are inherited in an autosomal dominant pattern and are associated with syndromes such as Multiple Endocrine Neoplasia type 2A, Multiple Endocrine Neoplasia type 2B, and von Hippel–Lindau disease. MEN 2A includes medullary thyroid carcinoma, pheochromocytoma, and hyperparathyroidism. MEN 2B includes medullary thyroid carcinoma, pheochromocytoma, mucosal neuromas, and skeletal abnormalities. Von Hippel–Lindau disease is associated with retinal and CNS hemangioblastomas, renal and pancreatic cysts, and pheochromocytoma. Other associations include neurofibromatosis, tuberous sclerosis, and paragangliomas.
The tumor synthesizes and stores catecholamines similarly to the normal adrenal medulla, predominantly secreting norepinephrine and, less commonly, epinephrine. Some epinephrine-predominant tumors may cause hypotensive episodes. Catecholamine release may occur spontaneously due to tumor necrosis or changes in blood flow, or may be triggered by trauma, exercise, surgery, anesthesia, glucagon, metoclopramide, steroids, tyramine-containing foods, iodinated contrast, tricyclic antidepressants, β-blockers, or sympathomimetics.
Hypertension is the most common manifestation and may be paroxysmal, sustained, or sustained with superimposed paroxysms. Classic paroxysms consist of abrupt episodes of severe hypertension, throbbing bilateral headache, tachycardia or palpitations, diaphoresis, pallor, anxiety, and tremulousness. Episodes typically last minutes to hours and increase in frequency and severity over time. Some patients are normotensive, particularly those with small tumors or familial disease. Chronic symptoms may include orthostatic hypotension due to reduced plasma volume, constipation or ileus from decreased peristalsis, weight loss, glucose intolerance, anxiety, and fatigue.
Acute crisis may present with prolonged severe hypertension or shock, hyperpyrexia, lactic acidosis, multiorgan failure, pulmonary edema from stress cardiomyopathy (including Takotsubo), stroke, myocardial infarction, aortic dissection, or acute abdomen due to tumor necrosis or mesenteric infarction. Physical findings often include severe hypertension with orthostatic changes, tachycardia, diaphoresis, pallor, tremor, mydriasis, and signs of hypertensive retinopathy. Café-au-lait spots or thyroid nodules may suggest associated syndromes. Tumors are usually not palpable.
Initial evaluation includes accurate blood pressure measurement with orthostatic readings and ECG to assess for ischemia or dysrhythmia. Laboratory findings may show elevated hemoglobin from hemoconcentration, leukocytosis from demargination, hyperglycemia, lactic acidosis, renal dysfunction, or hypercalcemia (in MEN 2A). The best screening test is plasma-free fractionated metanephrines, which are highly sensitive but may yield false positives. A normal result effectively excludes the diagnosis. Confirmation is typically performed with 24-hour urine collection for catecholamines and metanephrines, including creatinine to confirm adequate sampling. Numerous medications and substances can interfere with results.
Imaging with CT or MRI is used to localize tumors once biochemical confirmation is obtained. MRI is particularly useful for extra-adrenal lesions. Metaiodobenzylguanidine (MIBG) scanning has high specificity but limited sensitivity. Fine-needle aspiration is contraindicated due to risk of catecholamine surge.
Management of hypertensive crisis requires prompt α-adrenergic blockade. Phentolamine is traditionally used as an IV bolus followed by infusion, with aggressive fluid resuscitation to counteract vasodilation-induced hypotension. Alternatively, nicardipine or nitroprusside infusions may be used. β-blockers may be added only after adequate α-blockade to control reflex tachycardia. β-blockade must never be initiated before α-blockade, as unopposed α-stimulation can precipitate severe hypertension. Ventricular arrhythmias may require lidocaine or esmolol.
For preoperative or chronic management, phenoxybenzamine is initiated at least 7 days prior to surgery and titrated gradually. Selective α1-blockers such as doxazosin or terazosin are alternatives. β-blockers are added after adequate α-blockade if tachycardia persists. Calcium-channel blockers may also be used. Metyrosine can inhibit catecholamine synthesis in refractory cases.
Patients with suspected pheochromocytoma and labile blood pressure, hypertensive crisis, arrhythmias, or end-organ damage require admission. Stable patients with mild hypertension may be discharged with close follow-up and initiation of appropriate antihypertensive therapy. Plasma-free metanephrines should ideally be drawn during a hypertensive episode for maximal sensitivity.
Clinically, the combination of paroxysmal severe hypertension, headache, palpitations, and intense diaphoresis is highly suggestive of pheochromocytoma. Pallor rather than flushing is typical. Orthostatic hypotension is common and may worsen after α-blockade if volume repletion is inadequate. The diagnosis should be considered in unexplained shock, cardiomyopathy, recurrent hypertensive crises, or new-onset glucose intolerance with weight loss. Under no circumstances should β-blockers be administered before adequate α-blockade in suspected pheochromocytoma.
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Emergency And Acute Medicine – Phimosis
Phimosis is the inability to retract the foreskin (prepuce) over the glans penis. True (pathologic) phimosis results from scarring and fibrosis of the preputial opening, preventing retraction. It is important to distinguish this from physiologic phimosis, which is normal in young children due to natural adhesions between the glans and the inner prepuce. At birth, the foreskin is rarely retractable. Approximately 90% of foreskins are retractable by age 3 years and 99% by age 17, as smegma-producing epithelial cells shed and adhesions separate naturally. Parents should be instructed never to forcibly retract a child’s foreskin, as this may cause trauma and scarring.
True phimosis may develop from trauma due to forcible retraction, recurrent diaper dermatitis, repeated episodes of balanoposthitis (inflammation of the glans and foreskin), poor hygiene, poorly performed circumcision, or congenital anomalies. Chronic inflammation leads to fibrosis and narrowing of the preputial opening.
Patients may present with dysuria, hematuria, poor urinary stream, or ballooning of the foreskin during urination in severe cases. Examination may reveal a whitish, narrowed preputial orifice, along with edema, erythema, and tenderness of the foreskin. Associated balanoposthitis may be present. In extreme cases, obstructive uropathy or vascular compromise of the glans can occur, though these are uncommon.
In most cases, no laboratory or imaging workup is necessary. If severe stenosis causes suspected obstructive uropathy, evaluation of kidney function with BUN and creatinine and renal ultrasonography should be performed. When phimosis occurs secondary to recurrent balanoposthitis, screening for diabetes mellitus with urinalysis, serum glucose, or hemoglobin A1C is appropriate.
The main differential diagnosis is physiologic preputial adhesions in young children, which are normal and do not require intervention. Balanoposthitis without true phimosis should also be considered.
Pre-hospital personnel and caregivers should not attempt to retract the foreskin before medical evaluation, as this may worsen scarring or precipitate the more urgent condition of paraphimosis. Most patients require no immediate stabilization.
If obstructive uropathy is present, bladder decompression with urethral catheterization or suprapubic aspiration may be required. If vascular compromise of the glans occurs, an urgent dorsal slit procedure is necessary after adequate anesthesia, although this situation is rare in phimosis. Topical corticosteroids are often effective and represent first-line therapy. Betamethasone dipropionate 0.05–0.1% applied to the preputial orifice twice daily for 4–6 weeks has a high success rate in reducing phimosis. In pediatric patients requiring foreskin incision, procedural sedation is typically preferred over penile block.
Admission is indicated for obstructive uropathy or severe balanoposthitis with ischemia or necrosis. Patients who can void normally and have reliable urologic follow-up may be discharged. Referral to urology is recommended for evaluation of response to steroid therapy, possible dilation, operative repair, or elective circumcision if needed.
Physiologic phimosis should be managed with reassurance, age-appropriate expectations, and proper hygiene. Forced retraction should be avoided in children, especially between ages 3 and 17, when nonretractability may still be normal. Any signs of vascular compromise of the glans require urgent intervention to prevent necrosis.
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Infectious Disease and Microbiology – Brain Abscess
Brain abscess is a focal collection of purulent material within the brain parenchyma caused by bacterial, fungal, or protozoal infection. It may present as a well-formed abscess with a defined capsule or as an early inflammatory stage known as cerebritis. This is a rare condition, identified in 0.2–1.3% of large autopsy series and approximately 1 in 10,000 hospital admissions. About 25% of cases occur in children, and the median age at diagnosis is 30–45 years.
Risk factors include sinusitis, otitis media, poor dental hygiene, infective endocarditis, bacteremia from indwelling central lines or intravenous drug use, Osler–Weber–Rendu disease, preexisting brain injury, immunodeficiency, cyanotic congenital heart disease, and intrapulmonary shunting due to arteriovenous malformations. Preventive strategies involve prompt treatment of sinus and ear infections and maintaining good dental hygiene, particularly management of upper molar abscesses.
Infection reaches the brain through direct extension from adjacent structures (sinuses, middle ear, mastoid, orbit, teeth, meninges), following trauma or neurosurgery, or via hematogenous spread. The causative organisms often reflect the source. Otogenic, sinus, and odontogenic infections commonly involve mixed flora including anaerobes, microaerophilic and viridans streptococci, Streptococcus milleri, Haemophilus species, Fusobacterium, Prevotella, Enterobacteriaceae, and Pseudomonas. Post-traumatic or postoperative infections frequently involve Staphylococcus aureus, Pseudomonas, other gram-negative bacilli, and Propionibacterium. Hematogenous spread may involve S. aureus, streptococci, Salmonella, Listeria, Klebsiella pneumoniae, Escherichia coli, Proteus, Pseudomonas, Bacteroides species, Actinomyces, and fungi. In immunocompromised hosts, pathogens include Toxoplasma gondii, Listeria, Rhodococcus equi, Nocardia asteroides, Aspergillus, Cryptococcus neoformans, Coccidioides immitis, Candida, Zygomycetes, Cladosporium, and Curvularia. In immigrants from endemic areas, parasitic causes such as Taenia solium, Entamoeba histolytica, Schistosoma japonicum, and Paragonimus species should be considered.
Clinical manifestations are often subtle and nonspecific. Headache of less than two weeks’ duration occurs in approximately 75% of patients. Other symptoms include neck stiffness (25%), mental status changes, nausea, vomiting, low-grade fever (45–50%), focal neurological deficits (50%), and seizures (25%), which may prompt initial neuroimaging. Signs of increased intracranial pressure such as papilledema and third or sixth cranial nerve palsies suggest significant cerebral edema. Presentation varies depending on abscess location, pathogen, and underlying disease.
Laboratory findings may show leukocytosis in 60–70% of patients and elevated ESR in up to 90%. Lumbar puncture is generally contraindicated in patients with focal neurological signs due to risk of herniation. Blood cultures may be positive. Definitive microbiological diagnosis is achieved through stereotactic aspiration with Gram stain, culture, special stains, and increasingly 16S ribosomal RNA sequencing. Serologic testing may assist in suspected toxoplasmosis or neurocysticercosis.
Neuroimaging with CT or MRI is essential. Gadolinium-enhanced MRI provides superior visualization, especially in the brainstem, and diffusion-weighted imaging helps distinguish abscesses from neoplastic lesions. Ring-enhancing lesions may persist for several months despite adequate therapy. Serial imaging is necessary to monitor response to treatment.
Stereotactic aspiration is the procedure of choice for abscesses larger than 2.5 cm and that are surgically accessible. Craniotomy with aspiration may be required when vascular structures must be directly visualized. Differential diagnosis includes epidural or subdural empyema, septic dural sinus thrombosis, mycotic aneurysms, septic emboli with infarction, necrotizing encephalitis, primary or metastatic brain tumors, pyogenic meningitis, hematoma, and radiation necrosis.
Management requires prompt initiation of empiric intravenous antibiotics after appropriate cultures are obtained. For abscesses arising from oral, sinus, or otogenic sources, cefotaxime or ceftriaxone combined with metronidazole is recommended. Alternatively, penicillin G plus metronidazole may be used for oral sources. For suspected hematogenous spread, vancomycin combined with metronidazole and a third-generation cephalosporin is advised. Postsurgical infections should be treated with vancomycin plus ceftazidime or cefepime. If methicillin-sensitive S. aureus is identified, vancomycin should be replaced with nafcillin or oxacillin for improved CNS penetration. Therapy typically continues for 6–8 weeks or longer, guided by clinical and radiographic response. Corticosteroids may be used in cases of significant mass effect and depressed mental status. Surgical intervention is both diagnostic and therapeutic, relieving intracranial pressure and providing material for microbiologic diagnosis.
Complications include cerebral herniation (15–20%), persistent neurological deficits such as hemiparesis (up to 50%), epilepsy (fewer than 50%), and significant morbidity. Mortality is strongly influenced by neurological status at presentation. Long-term follow-up with serial CT or MRI scans for at least one year after completion of antibiotics is recommended to monitor for recurrence or residual disease.
Brain abscess is a focal collection of purulent material within the brain parenchyma caused by bacterial, fungal, or protozoal infection. It may present as a well-formed abscess with a defined capsule or as an early inflammatory stage known as cerebritis. This is a rare condition, identified in 0.2–1.3% of large autopsy series and approximately 1 in 10,000 hospital admissions. About 25% of cases occur in children, and the median age at diagnosis is 30–45 years.
Risk factors include sinusitis, otitis media, poor dental hygiene, infective endocarditis, bacteremia from indwelling central lines or intravenous drug use, Osler–Weber–Rendu disease, preexisting brain injury, immunodeficiency, cyanotic congenital heart disease, and intrapulmonary shunting due to arteriovenous malformations. Preventive strategies involve prompt treatment of sinus and ear infections and maintaining good dental hygiene, particularly management of upper molar abscesses.
Infection reaches the brain through direct extension from adjacent structures (sinuses, middle ear, mastoid, orbit, teeth, meninges), following trauma or neurosurgery, or via hematogenous spread. The causative organisms often reflect the source. Otogenic, sinus, and odontogenic infections commonly involve mixed flora including anaerobes, microaerophilic and viridans streptococci, Streptococcus milleri, Haemophilus species, Fusobacterium, Prevotella, Enterobacteriaceae, and Pseudomonas. Post-traumatic or postoperative infections frequently involve Staphylococcus aureus, Pseudomonas, other gram-negative bacilli, and Propionibacterium. Hematogenous spread may involve S. aureus, streptococci, Salmonella, Listeria, Klebsiella pneumoniae, Escherichia coli, Proteus, Pseudomonas, Bacteroides species, Actinomyces, and fungi. In immunocompromised hosts, pathogens include Toxoplasma gondii, Listeria, Rhodococcus equi, Nocardia asteroides, Aspergillus, Cryptococcus neoformans, Coccidioides immitis, Candida, Zygomycetes, Cladosporium, and Curvularia. In immigrants from endemic areas, parasitic causes such as Taenia solium, Entamoeba histolytica, Schistosoma japonicum, and Paragonimus species should be considered.
Clinical manifestations are often subtle and nonspecific. Headache of less than two weeks’ duration occurs in approximately 75% of patients. Other symptoms include neck stiffness (25%), mental status changes, nausea, vomiting, low-grade fever (45–50%), focal neurological deficits (50%), and seizures (25%), which may prompt initial neuroimaging. Signs of increased intracranial pressure such as papilledema and third or sixth cranial nerve palsies suggest significant cerebral edema. Presentation varies depending on abscess location, pathogen, and underlying disease.
Laboratory findings may show leukocytosis in 60–70% of patients and elevated ESR in up to 90%. Lumbar puncture is generally contraindicated in patients with focal neurological signs due to risk of herniation. Blood cultures may be positive. Definitive microbiological diagnosis is achieved through stereotactic aspiration with Gram stain, culture, special stains, and increasingly 16S ribosomal RNA sequencing. Serologic testing may assist in suspected toxoplasmosis or neurocysticercosis.
Neuroimaging with CT or MRI is essential. Gadolinium-enhanced MRI provides superior visualization, especially in the brainstem, and diffusion-weighted imaging helps distinguish abscesses from neoplastic lesions. Ring-enhancing lesions may persist for several months despite adequate therapy. Serial imaging is necessary to monitor response to treatment.
Stereotactic aspiration is the procedure of choice for abscesses larger than 2.5 cm and that are surgically accessible. Craniotomy with aspiration may be required when vascular structures must be directly visualized. Differential diagnosis includes epidural or subdural empyema, septic dural sinus thrombosis, mycotic aneurysms, septic emboli with infarction, necrotizing encephalitis, primary or metastatic brain tumors, pyogenic meningitis, hematoma, and radiation necrosis.
Management requires prompt initiation of empiric intravenous antibiotics after appropriate cultures are obtained. For abscesses arising from oral, sinus, or otogenic sources, cefotaxime or ceftriaxone combined with metronidazole is recommended. Alternatively, penicillin G plus metronidazole may be used for oral sources. For suspected hematogenous spread, vancomycin combined with metronidazole and a third-generation cephalosporin is advised. Postsurgical infections should be treated with vancomycin plus ceftazidime or cefepime. If methicillin-sensitive S. aureus is identified, vancomycin should be replaced with nafcillin or oxacillin for improved CNS penetration. Therapy typically continues for 6–8 weeks or longer, guided by clinical and radiographic response. Corticosteroids may be used in cases of significant mass effect and depressed mental status. Surgical intervention is both diagnostic and therapeutic, relieving intracranial pressure and providing material for microbiologic diagnosis.
Complications include cerebral herniation (15–20%), persistent neurological deficits such as hemiparesis (up to 50%), epilepsy (fewer than 50%), and significant morbidity. Mortality is strongly influenced by neurological status at presentation. Long-term follow-up with serial CT or MRI scans for at least one year after completion of antibiotics is recommended to monitor for recurrence or residual disease.
