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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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Emergency And Acute Medicine – Placental Abruption
Placental abruption is hemorrhage at the decidual–placental interface resulting in partial or complete separation of a normally implanted placenta before delivery of the fetus. It occurs in approximately 1% of all pregnancies and accounts for about 30% of bleeding episodes in the second half of pregnancy. It is responsible for 15% of fetal deaths, with neonatal mortality rates of 10–30%, and contributes to approximately 6% of maternal mortality. It is also referred to as abruptio placentae or accidental hemorrhage.
The primary cause is unknown, but the underlying process involves vascular injury with bleeding into the decidua basalis or mechanical shearing between the placenta and uterus, leading to clot formation and placental separation. Severe cases may result in disseminated intravascular coagulation (DIC) and significant maternal–fetal compromise. Many abruptions are thought to arise from chronic inflammatory or ischemic placental disease. Acute abruption may occur following trauma, rapid uterine decompression, or implantation over a uterine anomaly or fibroid.
Risk factors include prior abruption (10–20% recurrence risk), maternal hypertension and preeclampsia, advanced maternal age, increased parity, multiple gestation, uterine fibroids, tobacco use, cocaine abuse, trauma, premature rupture of membranes, oligohydramnios, polyhydramnios with rapid decompression, rapid delivery of the first twin, elevated second-trimester maternal serum alpha-fetoprotein, and thrombophilias. It is more common among African American and Caucasian women, with incidence increasing more rapidly among African American women.
Patients typically present after 20 weeks’ gestation with vaginal bleeding, which is painful in more than 80% of cases. However, bleeding may be absent in 20–25% due to concealed hemorrhage. Abdominal or back pain, uterine tenderness, frequent contractions, uterine tetany, nausea, vomiting, and unexplained preterm labor may occur. A history of trauma or cocaine use should be sought. On examination, uterine tenderness is common, and signs of hypotensive shock may appear late. Fetal distress may manifest as decreased fetal movement, bradycardia, or nonreassuring fetal heart rate tracings. Signs of DIC such as petechiae or bleeding from IV sites may be present. A sterile vaginal examination must be performed cautiously, particularly if placenta previa has not been excluded.
Diagnosis is primarily clinical. Immediate evaluation includes large-bore IV access, blood type and cross-match, rapid hemoglobin assessment, and continuous fetal and uterine monitoring. Laboratory studies include CBC, PT/PTT, fibrinogen level, and fibrin split products. Fibrinogen levels below 200 mg/dL and platelets below 100,000/μL strongly suggest abruption with coagulopathy. Kleihauer–Betke testing is indicated in Rh-negative patients. Ultrasound identifies abruption in only about 50% of cases, and a negative study does not exclude the diagnosis. MRI is sensitive but not practical in acute settings. CT performed for trauma evaluation may incidentally reveal abruption.
The differential diagnosis includes placenta previa, uterine rupture, preterm labor, vaginal or cervical lacerations, ovarian torsion, pyelonephritis, cholecystitis, appendicitis, and other intra-abdominal trauma.
Prehospital management includes transport in the left lateral recumbent position with full resuscitative measures if shock is suspected. Initial stabilization focuses on airway, breathing, and circulation with oxygen, cardiac monitoring, large-bore IV access, and aggressive crystalloid resuscitation. In the emergency department, continuous maternal cardiac and fetal monitoring is required. Blood products including packed red blood cells, fresh frozen plasma, cryoprecipitate, and platelets should be administered as indicated, often via a massive transfusion protocol. Immediate obstetric consultation is mandatory. Foley catheter placement allows close urine output monitoring. Tocolysis is generally contraindicated. In trauma-associated abruption, maternal stabilization takes priority.
Rh-immunoglobulin (300 μg IM at ≥12 weeks’ gestation) should be administered to Rh-negative patients, with dosing adjusted based on Kleihauer–Betke results. Corticosteroids for fetal lung maturity between 24 and 34 weeks and magnesium sulfate may be considered in consultation with obstetrics.
All confirmed or suspected cases require admission for maternal and fetal monitoring. ICU care is indicated for DIC, amniotic fluid embolism, or severe hemorrhage. Stable trauma patients without evidence of abruption after 4–6 hours of normal monitoring may be discharged in consultation with obstetrics, with instructions for pelvic rest and close follow-up.
Placental abruption remains a clinical diagnosis, as no single test reliably confirms or excludes it. Hypotension is often a late finding in pregnant patients with hypovolemia. Early anticipation of consumptive coagulopathy and prompt blood product administration are critical. Severe preeclampsia may mask hypovolemia, resulting in a normotensive but critically ill patient, and should be considered in any severe or unexplained abruption.
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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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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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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.
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Emergency And Acute Medicine – Placenta Previa
Placenta previa is defined as placental tissue overlying or positioned close to the internal cervical os. As the uterus enlarges and the cervix begins to dilate, placental vessels near the cervix may tear, resulting in vaginal bleeding. More than 90% of placenta previa diagnosed before 20 weeks’ gestation will resolve as the placenta “migrates” upward with uterine growth. However, if the placenta overlaps the internal os by more than 20 mm, previa is highly likely to persist at delivery. Greater degrees of overlap (15–23 mm or more) strongly predict persistence at term. Placenta previa accounts for approximately 20% of antepartum hemorrhage cases.
Placenta previa is classified into four types: complete (placenta completely covers the cervical os), partial (partially covers the os), marginal (placental edge reaches the margin of the os), and low-lying placenta (placental edge lies within 2 cm of the os). The overall incidence at term is approximately 0.4% of pregnancies. Maternal mortality is low (around 0.03%), but perinatal morbidity and mortality are increased—largely due to preterm delivery.
The exact etiology is unknown. Factors affecting implantation location include prior uterine curettage, abnormal endometrial vascularization, and delayed ovulation. Risk factors include multiparity (especially grand multiparity), multiple gestation, prior cesarean section (risk increases with number of previous C-sections), advanced maternal age, prior placenta previa, smoking, assisted reproduction, Asian maternal race, high-altitude residence, male fetus, and elevated maternal serum alpha-fetoprotein. Placenta previa is also associated with congenital anomalies, abnormal fetal presentation, preterm premature rupture of membranes, and amniotic fluid embolism. Placenta accreta spectrum disorders (accreta, increta, percreta) occur in 5–10% of patients with previa and may require cesarean hysterectomy due to severe bleeding.
The hallmark presentation is painless bright red vaginal bleeding after 20 weeks’ gestation. Seventy percent of patients present with painless bleeding, while about 20% may have associated uterine contractions. The first bleeding episode typically occurs between 27 and 32 weeks. Bleeding may range from minor spotting to massive hemorrhage, and recurrence is common. The severity or number of bleeding episodes does not necessarily correlate with the degree of placental coverage. Intercourse or heavy exercise may precipitate bleeding, though often there is no clear inciting event.
On examination, digital vaginal examination must never be performed in second- or third-trimester bleeding until placenta previa has been excluded by ultrasound, as this may precipitate severe hemorrhage. A sterile speculum exam is safe and may help identify whether bleeding originates from the cervical os, vagina, or another lesion. Signs of significant bleeding include blood pooling at the patient’s feet and vital sign instability such as tachycardia or hypotension. Continuous fetal heart rate monitoring is essential.
Diagnosis is made primarily by ultrasound. Transabdominal ultrasound is 93–98% accurate but may have false negatives (e.g., obesity, posterior placenta) and false positives (e.g., overdistended bladder). If placenta previa is suspected or findings are uncertain, transvaginal ultrasound should be performed, as it is essentially 100% accurate and does not increase bleeding risk. Color Doppler ultrasound may help identify placenta accreta. MRI can assist in evaluating invasive placental disorders.
Laboratory evaluation includes CBC, platelets, type and screen (or cross-match if transfusion anticipated), and Rh status. Kleihauer–Betke testing is performed in Rh-negative patients to detect fetomaternal hemorrhage. Coagulation studies are obtained if coagulopathy is suspected.
Prehospital management involves transport to a facility capable of managing high-risk or preterm deliveries. If hypotensive, the patient should be positioned in the left lateral recumbent position. Oxygen and IV access should be established. Initial stabilization includes airway, breathing, and circulation assessment, two large-bore IV lines, crystalloid resuscitation, and blood transfusion as needed. Blood transfusion is indicated for significant hypotension or hematocrit less than 30%. Fresh frozen plasma may be required for coagulopathy. Continuous fetal monitoring and immediate obstetric consultation are mandatory for symptomatic patients.
In the emergency department, patients with active bleeding require emergent obstetric consultation. Maintain NPO status and bed rest until obstetrics determines stability. Rh-negative patients should receive Rho(D) immune globulin (300 μg IM), with additional dosing guided by Kleihauer–Betke results. Magnesium sulfate may be used for preterm contractions when delivery is not indicated. Antenatal corticosteroids (e.g., betamethasone 12 mg IM every 24 hours for two doses) are recommended between 24 and 34 weeks to promote fetal lung maturity. Emergency cesarean delivery is indicated for ongoing hemorrhage or fetal compromise.
All patients with active bleeding from placenta previa should be admitted, as this condition constitutes a potential obstetric emergency. Selected stable patients whose bleeding has resolved may be managed outpatient in consultation with obstetrics. Asymptomatic patients with incidental findings may not require admission but should follow strict instructions, including pelvic rest and prompt reporting of any bleeding or contractions. If the placenta overlies the os by more than 20 mm, cesarean delivery is typically planned at 36–37 weeks.
Painless vaginal bleeding after 20 weeks’ gestation should be considered placenta previa until proven otherwise, whereas painful vaginal bleeding suggests placental abruption. Importantly, both conditions can coexist. Digital vaginal examination must be avoided until previa is excluded, while sterile speculum examination and transvaginal ultrasound are safe and appropriate diagnostic tools.
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Infectious Disease and Microbiology – Botulism
Botulism is a potentially life-threatening neuroparalytic syndrome caused by neurotoxins produced by Clostridium botulinum. Botulinum neurotoxin (BoNT) is among the most potent toxins known. There are five epidemiologic forms of botulism: foodborne, infant botulism, wound botulism, intestinal colonization (adult infectious botulism), and inhalational botulism. Symptoms typically develop 12–36 hours after ingestion of preformed toxin.
Botulism is rare but can occur in small outbreaks, often associated with commercially or home-canned foods. In the United States, most cases occur in infants, approximately one-fourth are foodborne, and a smaller number are related to wounds. Risk factors include improper home canning of low-acid foods such as corn, asparagus, beans, and beets. The fatality rate is higher among patients older than 60 years. Honey ingestion is a well-established risk factor for infant botulism due to gastrointestinal colonization and in situ toxin production. Wound botulism should be suspected in intravenous drug users. Iatrogenic cases have been reported following injection of unlicensed botulinum toxin preparations.
Prevention focuses on proper food preservation techniques. Home-canned foods should be boiled for at least 10 minutes before consumption. Infants under one year of age should not be given honey. Bulging cans should be discarded. Rapid identification of suspected cases is essential to prevent outbreaks.
C. botulinum is an anaerobic, gram-positive, spore-forming rod. It produces toxins classified from types A to G, based on antigenic differences. Human disease is most commonly associated with toxin types A, B, E, and F. Type A is frequently found in the western United States and China, type B in the eastern United States and Europe, and type F worldwide, often linked to fish products. The spores are widely present in soil and marine sediments. While spores are resistant to boiling, they can be destroyed by heating to 120°C. Because of its extreme toxicity, botulinum toxin is considered a potential biological warfare agent.
Clinically, botulism presents with bilateral cranial neuropathies followed by symmetric descending weakness. Patients typically remain afebrile, awake, and alert despite progressive paralysis. Sensory function remains intact. Early manifestations may include diplopia, ptosis, dysarthria, dysphagia, and dry mouth. As paralysis progresses, respiratory failure may occur. Clinical suspicion is critical, as early diagnosis significantly impacts outcomes.
Laboratory confirmation involves detection of toxin in serum, stool, or implicated food samples. The traditional mouse bioassay has limited sensitivity, particularly in wound botulism. However, treatment should not be delayed pending laboratory confirmation when clinical suspicion is high.
The differential diagnosis includes myasthenia gravis, Lambert–Eaton syndrome, tick paralysis, the Miller Fisher variant of Guillain–Barré syndrome, stroke, poliomyelitis, and heavy metal intoxication.
Management is primarily supportive, with close monitoring of respiratory function and mechanical ventilation if required. Equine-derived antitoxin covering toxin types A, B, and E should be administered as early as possible to neutralize circulating toxin. In cases of wound botulism, appropriate antibiotics should be given after antitoxin administration. In infants, intravenous human botulism immune globulin (BIG-IV) is recommended early in the course of illness. Patients often require prolonged rehabilitation. Even after recovery, some individuals may report persistent fatigue, weakness, dizziness, and respiratory difficulty.
Botulism is a potentially life-threatening neuroparalytic syndrome caused by neurotoxins produced by Clostridium botulinum. Botulinum neurotoxin (BoNT) is among the most potent toxins known. There are five epidemiologic forms of botulism: foodborne, infant botulism, wound botulism, intestinal colonization (adult infectious botulism), and inhalational botulism. Symptoms typically develop 12–36 hours after ingestion of preformed toxin.
Botulism is rare but can occur in small outbreaks, often associated with commercially or home-canned foods. In the United States, most cases occur in infants, approximately one-fourth are foodborne, and a smaller number are related to wounds. Risk factors include improper home canning of low-acid foods such as corn, asparagus, beans, and beets. The fatality rate is higher among patients older than 60 years. Honey ingestion is a well-established risk factor for infant botulism due to gastrointestinal colonization and in situ toxin production. Wound botulism should be suspected in intravenous drug users. Iatrogenic cases have been reported following injection of unlicensed botulinum toxin preparations.
Prevention focuses on proper food preservation techniques. Home-canned foods should be boiled for at least 10 minutes before consumption. Infants under one year of age should not be given honey. Bulging cans should be discarded. Rapid identification of suspected cases is essential to prevent outbreaks.
C. botulinum is an anaerobic, gram-positive, spore-forming rod. It produces toxins classified from types A to G, based on antigenic differences. Human disease is most commonly associated with toxin types A, B, E, and F. Type A is frequently found in the western United States and China, type B in the eastern United States and Europe, and type F worldwide, often linked to fish products. The spores are widely present in soil and marine sediments. While spores are resistant to boiling, they can be destroyed by heating to 120°C. Because of its extreme toxicity, botulinum toxin is considered a potential biological warfare agent.
Clinically, botulism presents with bilateral cranial neuropathies followed by symmetric descending weakness. Patients typically remain afebrile, awake, and alert despite progressive paralysis. Sensory function remains intact. Early manifestations may include diplopia, ptosis, dysarthria, dysphagia, and dry mouth. As paralysis progresses, respiratory failure may occur. Clinical suspicion is critical, as early diagnosis significantly impacts outcomes.
Laboratory confirmation involves detection of toxin in serum, stool, or implicated food samples. The traditional mouse bioassay has limited sensitivity, particularly in wound botulism. However, treatment should not be delayed pending laboratory confirmation when clinical suspicion is high.
The differential diagnosis includes myasthenia gravis, Lambert–Eaton syndrome, tick paralysis, the Miller Fisher variant of Guillain–Barré syndrome, stroke, poliomyelitis, and heavy metal intoxication.
Management is primarily supportive, with close monitoring of respiratory function and mechanical ventilation if required. Equine-derived antitoxin covering toxin types A, B, and E should be administered as early as possible to neutralize circulating toxin. In cases of wound botulism, appropriate antibiotics should be given after antitoxin administration. In infants, intravenous human botulism immune globulin (BIG-IV) is recommended early in the course of illness. Patients often require prolonged rehabilitation. Even after recovery, some individuals may report persistent fatigue, weakness, dizziness, and respiratory difficulty.
