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Emergency and Acute Medicine – Patent Ductus Arteriosus
Patent ductus arteriosus (PDA) is a condition in which the fetal vessel connecting the pulmonary trunk to the descending aorta fails to close after birth. Normally, shortly after delivery, increased oxygen tension and changes in prostaglandin metabolism lead to ductal constriction, closure, and eventual fibrosis. In preterm infants, persistent patency may represent a physiologic and sometimes life-saving response related to hypoxia and immaturity. In contrast, persistence of the ductus in full-term infants represents a true congenital malformation due to structural deficiencies of the ductal wall.
As pulmonary vascular resistance falls after birth, blood is shunted from the aorta into the pulmonary artery, producing a left-to-right shunt. The magnitude of shunting depends on ductal size and the relative pulmonary and systemic vascular resistances, and in severe cases up to 70% of left ventricular output may pass through the ductus. Risk factors include prematurity, hypoxic conditions, high altitude, maternal rubella infection, and coexisting congenital heart disease, with a female predominance.
Clinical presentation varies with ductal size. Small PDAs may be asymptomatic, whereas larger shunts can lead to congestive heart failure, often within the first days of life. Typical findings include wide pulse pressure, a prominent apical impulse, a palpable thrill, and a characteristic continuous “machinery” murmur best heard at the second left intercostal space and radiating along the left sternal border. Additional features may include recurrent pulmonary infections and failure to thrive.
Diagnosis is primarily established through imaging. Chest radiography may be normal in infants but can show increased pulmonary vascular markings, cardiac chamber enlargement, and dilated great vessels in older patients. Electrocardiography may reveal left ventricular hypertrophy, with right ventricular hypertrophy indicating more severe disease. Echocardiography with Doppler is the diagnostic modality of choice, allowing visualization of ductal size, left atrial enlargement, and continuous aortic-to-pulmonary flow. Cardiac catheterization confirms shunting when needed and may be used therapeutically.
Management depends on patient age, symptoms, and ductal significance. Small, asymptomatic PDAs may be observed. In preterm infants, pharmacologic closure with prostaglandin synthesis inhibitors such as indomethacin is often effective during the first week of life. Full-term infants and children generally require definitive closure, as spontaneous resolution is rare; options include surgical ligation or transcatheter occlusion techniques. Supportive care includes oxygen for heart failure, fluid and sodium restriction, correction of anemia, and endocarditis prophylaxis when indicated.
Admission is required for patients with heart failure, pulmonary hypertension, or suspected endocarditis. Asymptomatic patients may be discharged with close cardiology follow-up and plans for elective closure. Key clinical points include recognition that heart failure may reduce renal perfusion and urine output, and that indomethacin therapy carries risks such as gastrointestinal bleeding.
Patent ductus arteriosus (PDA) is a condition in which the fetal vessel connecting the pulmonary trunk to the descending aorta fails to close after birth. Normally, shortly after delivery, increased oxygen tension and changes in prostaglandin metabolism lead to ductal constriction, closure, and eventual fibrosis. In preterm infants, persistent patency may represent a physiologic and sometimes life-saving response related to hypoxia and immaturity. In contrast, persistence of the ductus in full-term infants represents a true congenital malformation due to structural deficiencies of the ductal wall.
As pulmonary vascular resistance falls after birth, blood is shunted from the aorta into the pulmonary artery, producing a left-to-right shunt. The magnitude of shunting depends on ductal size and the relative pulmonary and systemic vascular resistances, and in severe cases up to 70% of left ventricular output may pass through the ductus. Risk factors include prematurity, hypoxic conditions, high altitude, maternal rubella infection, and coexisting congenital heart disease, with a female predominance.
Clinical presentation varies with ductal size. Small PDAs may be asymptomatic, whereas larger shunts can lead to congestive heart failure, often within the first days of life. Typical findings include wide pulse pressure, a prominent apical impulse, a palpable thrill, and a characteristic continuous “machinery” murmur best heard at the second left intercostal space and radiating along the left sternal border. Additional features may include recurrent pulmonary infections and failure to thrive.
Diagnosis is primarily established through imaging. Chest radiography may be normal in infants but can show increased pulmonary vascular markings, cardiac chamber enlargement, and dilated great vessels in older patients. Electrocardiography may reveal left ventricular hypertrophy, with right ventricular hypertrophy indicating more severe disease. Echocardiography with Doppler is the diagnostic modality of choice, allowing visualization of ductal size, left atrial enlargement, and continuous aortic-to-pulmonary flow. Cardiac catheterization confirms shunting when needed and may be used therapeutically.
Management depends on patient age, symptoms, and ductal significance. Small, asymptomatic PDAs may be observed. In preterm infants, pharmacologic closure with prostaglandin synthesis inhibitors such as indomethacin is often effective during the first week of life. Full-term infants and children generally require definitive closure, as spontaneous resolution is rare; options include surgical ligation or transcatheter occlusion techniques. Supportive care includes oxygen for heart failure, fluid and sodium restriction, correction of anemia, and endocarditis prophylaxis when indicated.
Admission is required for patients with heart failure, pulmonary hypertension, or suspected endocarditis. Asymptomatic patients may be discharged with close cardiology follow-up and plans for elective closure. Key clinical points include recognition that heart failure may reduce renal perfusion and urine output, and that indomethacin therapy carries risks such as gastrointestinal bleeding.
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Emergency and Acute Medicine – Paronychia
Paronychia is an inflammatory condition of the nail folds surrounding the nail plate that occurs when disruption of the protective seal between the nail plate and nail fold allows microorganisms to enter the eponychial space. This disruption commonly follows minor trauma and leads to localized infection and inflammation.
The etiology differs between acute and chronic paronychia. Acute paronychia is most commonly caused by *Staphylococcus aureus*, although streptococci, *Pseudomonas*, and anaerobic organisms may also be involved. Chronic paronychia is multifactorial and results from repeated exposure to allergens and irritants, with fungal organisms—most commonly *Candida albicans*—frequently coexisting alongside *Staphylococcus* species.
Clinically, paronychia presents with pain, warmth, swelling, and erythema of the proximal or lateral nail folds, usually developing two to five days after trauma. For symptoms to meet criteria for chronic paronychia, they must persist for more than six weeks. A careful history is important. Acute paronychia is often associated with nail biting, finger sucking, aggressive manicuring, or direct trauma. Chronic paronychia is commonly seen in individuals with occupations involving persistent moisture exposure, such as dishwashers or bartenders, and occurs more frequently in patients with diabetes or peripheral vascular disease. In children, infections often involve anaerobic oral flora due to nail biting.
On physical examination, early paronychia begins as localized erythema, swelling, and tenderness at the dorsolateral nail fold, which may bulge over the nail plate. As the condition progresses, a subcuticular or subungual abscess may form. Green discoloration of the nail suggests *Pseudomonas* infection, while nail plate hypertrophy raises concern for a fungal etiology.
The diagnosis of paronychia is primarily clinical and based on history and physical examination. Evaluation should include assessment for associated infections such as felon or cellulitis and confirmation of tetanus immunization status. Laboratory testing is generally not helpful, and cultures are not routinely indicated. If herpetic whitlow is suspected, a Tzanck smear or viral culture may be considered. Imaging with soft tissue radiographs is reserved for suspected foreign bodies or possible osteomyelitis. A digital pressure test, using opposing pressure between the thumb and affected finger, may help identify early subungual abscess formation.
Management depends on the stage and type of paronychia. Early acute paronychia without purulence can often be treated with warm-water soaks four times daily, with or without topical antibiotics or corticosteroids. If a superficial abscess is present, elevation of the eponychial fold using a small blade or needle may allow adequate drainage; local anesthesia or a digital nerve block may be required. When infection extends beneath the nail plate, partial nail removal may be necessary, while extensive subungual abscesses may require complete nail removal. Runaround abscesses involving both sides of the nail fold require partial proximal nail removal with packing to prevent re-adhesion.
Antibiotic therapy is recommended when there is cellulitis, abscess formation, or systemic signs of infection. Appropriate first-line oral agents include trimethoprim–sulfamethoxazole, dicloxacillin, or amoxicillin–clavulanate, typically for five to ten days depending on severity. Clindamycin or amoxicillin–clavulanate is preferred when infection is associated with nail biting or oral exposure. Chronic paronychia management focuses on avoidance of irritants and moisture, with topical corticosteroids considered first-line therapy, often combined with a broad-spectrum topical antifungal. Refractory cases may require surgical eponychial marsupialization or oral antifungal therapy.
Admission is rarely required for paronychia alone. Patients with uncomplicated infections may be discharged with appropriate wound care instructions and follow-up. Those with packing in place should be re-evaluated within 24 hours. Referral is indicated for chronic or recurrent paronychia that does not respond to standard therapy.
Key clinical pearls include recognizing that acute paronychia generally responds well to timely drainage with or without antibiotics, while chronic paronychia is usually driven by repeated exposure to irritants rather than infection alone. Conditions such as psoriasis, Reiter syndrome, and herpetic whitlow can mimic paronychia and should be considered in recurrent or atypical cases.
Paronychia is an inflammatory condition of the nail folds surrounding the nail plate that occurs when disruption of the protective seal between the nail plate and nail fold allows microorganisms to enter the eponychial space. This disruption commonly follows minor trauma and leads to localized infection and inflammation.
The etiology differs between acute and chronic paronychia. Acute paronychia is most commonly caused by *Staphylococcus aureus*, although streptococci, *Pseudomonas*, and anaerobic organisms may also be involved. Chronic paronychia is multifactorial and results from repeated exposure to allergens and irritants, with fungal organisms—most commonly *Candida albicans*—frequently coexisting alongside *Staphylococcus* species.
Clinically, paronychia presents with pain, warmth, swelling, and erythema of the proximal or lateral nail folds, usually developing two to five days after trauma. For symptoms to meet criteria for chronic paronychia, they must persist for more than six weeks. A careful history is important. Acute paronychia is often associated with nail biting, finger sucking, aggressive manicuring, or direct trauma. Chronic paronychia is commonly seen in individuals with occupations involving persistent moisture exposure, such as dishwashers or bartenders, and occurs more frequently in patients with diabetes or peripheral vascular disease. In children, infections often involve anaerobic oral flora due to nail biting.
On physical examination, early paronychia begins as localized erythema, swelling, and tenderness at the dorsolateral nail fold, which may bulge over the nail plate. As the condition progresses, a subcuticular or subungual abscess may form. Green discoloration of the nail suggests *Pseudomonas* infection, while nail plate hypertrophy raises concern for a fungal etiology.
The diagnosis of paronychia is primarily clinical and based on history and physical examination. Evaluation should include assessment for associated infections such as felon or cellulitis and confirmation of tetanus immunization status. Laboratory testing is generally not helpful, and cultures are not routinely indicated. If herpetic whitlow is suspected, a Tzanck smear or viral culture may be considered. Imaging with soft tissue radiographs is reserved for suspected foreign bodies or possible osteomyelitis. A digital pressure test, using opposing pressure between the thumb and affected finger, may help identify early subungual abscess formation.
Management depends on the stage and type of paronychia. Early acute paronychia without purulence can often be treated with warm-water soaks four times daily, with or without topical antibiotics or corticosteroids. If a superficial abscess is present, elevation of the eponychial fold using a small blade or needle may allow adequate drainage; local anesthesia or a digital nerve block may be required. When infection extends beneath the nail plate, partial nail removal may be necessary, while extensive subungual abscesses may require complete nail removal. Runaround abscesses involving both sides of the nail fold require partial proximal nail removal with packing to prevent re-adhesion.
Antibiotic therapy is recommended when there is cellulitis, abscess formation, or systemic signs of infection. Appropriate first-line oral agents include trimethoprim–sulfamethoxazole, dicloxacillin, or amoxicillin–clavulanate, typically for five to ten days depending on severity. Clindamycin or amoxicillin–clavulanate is preferred when infection is associated with nail biting or oral exposure. Chronic paronychia management focuses on avoidance of irritants and moisture, with topical corticosteroids considered first-line therapy, often combined with a broad-spectrum topical antifungal. Refractory cases may require surgical eponychial marsupialization or oral antifungal therapy.
Admission is rarely required for paronychia alone. Patients with uncomplicated infections may be discharged with appropriate wound care instructions and follow-up. Those with packing in place should be re-evaluated within 24 hours. Referral is indicated for chronic or recurrent paronychia that does not respond to standard therapy.
Key clinical pearls include recognizing that acute paronychia generally responds well to timely drainage with or without antibiotics, while chronic paronychia is usually driven by repeated exposure to irritants rather than infection alone. Conditions such as psoriasis, Reiter syndrome, and herpetic whitlow can mimic paronychia and should be considered in recurrent or atypical cases.
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Emergency and Acute Medicine – Pelvic Inflammatory Disease
Pelvic inflammatory disease (PID) is an acute, community-acquired, sexually transmitted infection involving the upper female genital tract, including the uterus, fallopian tubes, ovaries, and adjacent pelvic structures. It is one of the most common gynecologic reasons for emergency department visits, accounting for hundreds of thousands of cases annually. PID represents a spectrum of disease rather than a single entity, and there is no definitive diagnostic gold standard. Because delayed treatment increases the risk of infertility, chronic pelvic pain, and ectopic pregnancy, clinicians must maintain a low threshold for diagnosis and initiate empiric antibiotic therapy when PID is suspected. Progressive or untreated infection may result in complications such as tubo-ovarian abscess (TOA). An important associated condition is Fitz-Hugh–Curtis syndrome, a perihepatic capsular inflammation that presents with sharp right upper quadrant pain worsened by movement, coughing, or inspiration.
The most important risk factors for PID include age younger than 25 years, multiple or symptomatic sexual partners, a prior history of PID, nonbarrier contraception, and certain demographic factors such as African American ethnicity. The most common causative organisms are *Chlamydia trachomatis* and *Neisseria gonorrhoeae*, although PID is frequently polymicrobial. Other implicated pathogens include group A and B streptococci, staphylococci, gram-negative rods such as *Escherichia coli*, *Klebsiella* spp., *Proteus* spp., and various anaerobes. Because of this broad microbiologic spectrum, treatment regimens must provide wide antimicrobial coverage.
Clinically, PID most often presents with bilateral lower abdominal or pelvic pain, which may range from mild and subtle to severe. Pain that worsens during intercourse or occurs shortly after or during menses is particularly suggestive. Associated symptoms commonly include abnormal vaginal discharge, abnormal uterine bleeding, dysmenorrhea, dyspareunia, dysuria, nausea, vomiting, fever, and chills. On examination, only about half of patients are febrile. Abdominal examination typically reveals lower quadrant tenderness, often bilateral, with possible rebound tenderness and decreased bowel sounds. Pelvic examination may demonstrate purulent endocervical discharge, cervical motion tenderness, and uterine or adnexal tenderness. Right upper quadrant tenderness in the context of PID suggests Fitz-Hugh–Curtis syndrome. Importantly, the absence of prominent uterine or adnexal tenderness should prompt consideration of alternative diagnoses.
The diagnosis of PID is primarily clinical and based on history and physical examination, including a pelvic exam. A pregnancy test is mandatory in all patients to exclude ectopic pregnancy or complications of intrauterine pregnancy. Minimum diagnostic criteria include the presence of lower abdominal tenderness, uterine or adnexal tenderness, or cervical motion tenderness. Supportive findings include fever above 38.3°C, abnormal cervical or vaginal discharge, leukocytosis, elevated inflammatory markers such as ESR or C-reactive protein, and microbiologic evidence of gonococcal or chlamydial infection. Laboratory studies may include a complete blood count, nucleic acid amplification testing for *N. gonorrhoeae* and *C. trachomatis*, and microscopic evaluation of vaginal discharge. Imaging is not routinely required but transvaginal ultrasound is indicated when adnexal fullness or mass is present, when TOA is suspected, when pelvic examination is limited, or when outpatient therapy fails.
Management depends on disease severity and patient reliability for follow-up. Most patients with mild to moderate PID can be treated as outpatients with intramuscular ceftriaxone or cefoxitin (with probenecid) plus oral doxycycline, with the addition of metronidazole when anaerobic coverage is indicated. Inpatient therapy is reserved for patients with severe illness, pregnancy, suspected TOA, immunodeficiency, inability to tolerate oral medications, failure of outpatient therapy, or concern for noncompliance. Recommended inpatient regimens include doxycycline combined with cefoxitin or cefotetan, or alternatives such as gentamicin plus clindamycin or ampicillin/sulbactam plus doxycycline. Parenteral therapy should continue for at least 24 hours after clinical improvement, followed by oral antibiotics to complete a 14-day course. Sexual partners should be evaluated and treated, and patients should receive counseling and testing for other sexually transmitted infections, including HIV.
Patients who do not meet admission criteria may be safely discharged with close follow-up arranged within 48–72 hours to ensure clinical improvement. Failure to improve within this timeframe warrants reassessment and possible inpatient management. Key clinical principles include recognizing that PID exists along a disease continuum, that early empiric treatment is essential to prevent long-term sequelae, and that quinolones and oral cephalosporins are no longer recommended in the United States for gonorrhea-related infections due to resistance. Comprehensive patient education, partner treatment, and reliable follow-up are critical components of effective PID management.
Pelvic inflammatory disease (PID) is an acute, community-acquired, sexually transmitted infection involving the upper female genital tract, including the uterus, fallopian tubes, ovaries, and adjacent pelvic structures. It is one of the most common gynecologic reasons for emergency department visits, accounting for hundreds of thousands of cases annually. PID represents a spectrum of disease rather than a single entity, and there is no definitive diagnostic gold standard. Because delayed treatment increases the risk of infertility, chronic pelvic pain, and ectopic pregnancy, clinicians must maintain a low threshold for diagnosis and initiate empiric antibiotic therapy when PID is suspected. Progressive or untreated infection may result in complications such as tubo-ovarian abscess (TOA). An important associated condition is Fitz-Hugh–Curtis syndrome, a perihepatic capsular inflammation that presents with sharp right upper quadrant pain worsened by movement, coughing, or inspiration.
The most important risk factors for PID include age younger than 25 years, multiple or symptomatic sexual partners, a prior history of PID, nonbarrier contraception, and certain demographic factors such as African American ethnicity. The most common causative organisms are *Chlamydia trachomatis* and *Neisseria gonorrhoeae*, although PID is frequently polymicrobial. Other implicated pathogens include group A and B streptococci, staphylococci, gram-negative rods such as *Escherichia coli*, *Klebsiella* spp., *Proteus* spp., and various anaerobes. Because of this broad microbiologic spectrum, treatment regimens must provide wide antimicrobial coverage.
Clinically, PID most often presents with bilateral lower abdominal or pelvic pain, which may range from mild and subtle to severe. Pain that worsens during intercourse or occurs shortly after or during menses is particularly suggestive. Associated symptoms commonly include abnormal vaginal discharge, abnormal uterine bleeding, dysmenorrhea, dyspareunia, dysuria, nausea, vomiting, fever, and chills. On examination, only about half of patients are febrile. Abdominal examination typically reveals lower quadrant tenderness, often bilateral, with possible rebound tenderness and decreased bowel sounds. Pelvic examination may demonstrate purulent endocervical discharge, cervical motion tenderness, and uterine or adnexal tenderness. Right upper quadrant tenderness in the context of PID suggests Fitz-Hugh–Curtis syndrome. Importantly, the absence of prominent uterine or adnexal tenderness should prompt consideration of alternative diagnoses.
The diagnosis of PID is primarily clinical and based on history and physical examination, including a pelvic exam. A pregnancy test is mandatory in all patients to exclude ectopic pregnancy or complications of intrauterine pregnancy. Minimum diagnostic criteria include the presence of lower abdominal tenderness, uterine or adnexal tenderness, or cervical motion tenderness. Supportive findings include fever above 38.3°C, abnormal cervical or vaginal discharge, leukocytosis, elevated inflammatory markers such as ESR or C-reactive protein, and microbiologic evidence of gonococcal or chlamydial infection. Laboratory studies may include a complete blood count, nucleic acid amplification testing for *N. gonorrhoeae* and *C. trachomatis*, and microscopic evaluation of vaginal discharge. Imaging is not routinely required but transvaginal ultrasound is indicated when adnexal fullness or mass is present, when TOA is suspected, when pelvic examination is limited, or when outpatient therapy fails.
Management depends on disease severity and patient reliability for follow-up. Most patients with mild to moderate PID can be treated as outpatients with intramuscular ceftriaxone or cefoxitin (with probenecid) plus oral doxycycline, with the addition of metronidazole when anaerobic coverage is indicated. Inpatient therapy is reserved for patients with severe illness, pregnancy, suspected TOA, immunodeficiency, inability to tolerate oral medications, failure of outpatient therapy, or concern for noncompliance. Recommended inpatient regimens include doxycycline combined with cefoxitin or cefotetan, or alternatives such as gentamicin plus clindamycin or ampicillin/sulbactam plus doxycycline. Parenteral therapy should continue for at least 24 hours after clinical improvement, followed by oral antibiotics to complete a 14-day course. Sexual partners should be evaluated and treated, and patients should receive counseling and testing for other sexually transmitted infections, including HIV.
Patients who do not meet admission criteria may be safely discharged with close follow-up arranged within 48–72 hours to ensure clinical improvement. Failure to improve within this timeframe warrants reassessment and possible inpatient management. Key clinical principles include recognizing that PID exists along a disease continuum, that early empiric treatment is essential to prevent long-term sequelae, and that quinolones and oral cephalosporins are no longer recommended in the United States for gonorrhea-related infections due to resistance. Comprehensive patient education, partner treatment, and reliable follow-up are critical components of effective PID management.
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Emergency and Acute Medicine – Pelvic Fracture
Pelvic fractures account for approximately 3% of all bony fractures but are associated with disproportionately high morbidity and mortality. The pelvis consists of the sacrum and two innominate bones, each formed by the ilium, ischium, and pubis. Stability of the pelvic ring depends on strong ligamentous, muscular, and soft tissue support. The anterior pelvis is stabilized by the symphysis pubis and pubic rami, while posterior stability is provided by the sacroiliac (SI) complex and pelvic floor. Because the pelvis protects major vascular structures as well as genitourinary, gastrointestinal, gynecologic, neurologic, and musculoskeletal systems, fractures often coexist with life-threatening injuries and require urgent recognition and management.
Most pelvic fractures result from high-energy trauma. Approximately 65% are caused by vehicular mechanisms, including pedestrians struck by automobiles, while falls and crush injuries account for another 20%. Athletic, penetrating, and nontraumatic causes are less common. Mortality ranges from 6–19% and increases significantly in open fractures or when hemorrhagic shock is present. Unstable fractures, particularly those involving the posterior pelvis, are prone to severe hemorrhage due to disruption of arterial branches and venous plexuses, often with associated retroperitoneal hematoma. In children, hemorrhage may be more severe, and nonaccidental trauma must be considered. In pregnancy, pelvic fractures pose additional risk to the gravid uterus, including uterine rupture.
Clinically, patients typically present with pelvic, hip, groin, or lower back pain, often accompanied by swelling, ecchymosis, and tenderness. Many have associated injuries involving the abdomen, genitourinary tract, neurologic system, or vascular structures. Signs of pelvic instability, deformity, limb shortening or rotation, and inability to bear weight are concerning. In severe cases, hemorrhagic shock may dominate the presentation, with tachycardia, hypotension, altered mental status, and cool, pale extremities. Bleeding from the urethra, rectum, or vagina, as well as open wounds over the pelvis, suggests an open pelvic fracture.
Initial evaluation follows standard trauma principles. A single anteroposterior (AP) pelvic radiograph is the most important early diagnostic test and should be obtained promptly when pelvic fracture is suspected. Additional views such as inlet, outlet, or Judet oblique projections may further define injury patterns, particularly involving the posterior pelvis or acetabulum. Computed tomography (CT) provides detailed assessment of fracture anatomy, retroperitoneal hematoma, and associated visceral injuries, and CT angiography can identify arterial bleeding in hemodynamically stable patients. Focused abdominal sonography for trauma (FAST) may help detect intraperitoneal bleeding but has limited ability to distinguish pelvic from abdominal sources. Laboratory studies include type and cross-match, hemoglobin and hematocrit, platelet count, and coagulation profile.
Pelvic fractures are commonly categorized using the Tile classification system, which helps guide management. Type A fractures are stable and include avulsion injuries, isolated pubic rami fractures, and transverse sacral fractures. Type B fractures are rotationally unstable but vertically stable, such as open-book and lateral compression injuries. Type C fractures are both rotationally and vertically unstable, including vertical shear (Malgaigne) fractures, and are associated with the highest risk of hemorrhage and mortality. Acetabular fractures represent a distinct subgroup requiring specialized orthopedic evaluation.
Management priorities focus on rapid resuscitation, hemorrhage control, and stabilization. Early application of a pelvic binder or improvised sheet wrap at the level of the greater trochanters is critical in suspected unstable fractures, as it reduces pelvic volume and limits bleeding. Fluid resuscitation with crystalloids and early blood transfusion is indicated for shock, avoiding lower extremity IV access when possible. External fixation, angiographic embolization, or surgical pelvic packing may be required for ongoing hemorrhage. Type A fractures are generally managed conservatively with analgesia and mobilization as tolerated, whereas Type B and C fractures require urgent orthopedic and trauma consultation, close monitoring, and often operative intervention.
Patients with hemodynamic instability, unstable pelvic fractures, acetabular fractures, pelvic hemorrhage, or associated injuries should be admitted, frequently to the intensive care unit. Hemodynamically stable patients with isolated, stable Type A fractures and no other injuries may be discharged with appropriate analgesia and close orthopedic follow-up. A key clinical principle is that pelvic fractures signal high-energy trauma; clinicians must maintain a high index of suspicion for associated abdominal, genitourinary, vascular, and neurologic injuries. Early stabilization of the pelvis and management decisions guided by hemodynamic status are essential to improving outcomes.
Pelvic fractures account for approximately 3% of all bony fractures but are associated with disproportionately high morbidity and mortality. The pelvis consists of the sacrum and two innominate bones, each formed by the ilium, ischium, and pubis. Stability of the pelvic ring depends on strong ligamentous, muscular, and soft tissue support. The anterior pelvis is stabilized by the symphysis pubis and pubic rami, while posterior stability is provided by the sacroiliac (SI) complex and pelvic floor. Because the pelvis protects major vascular structures as well as genitourinary, gastrointestinal, gynecologic, neurologic, and musculoskeletal systems, fractures often coexist with life-threatening injuries and require urgent recognition and management.
Most pelvic fractures result from high-energy trauma. Approximately 65% are caused by vehicular mechanisms, including pedestrians struck by automobiles, while falls and crush injuries account for another 20%. Athletic, penetrating, and nontraumatic causes are less common. Mortality ranges from 6–19% and increases significantly in open fractures or when hemorrhagic shock is present. Unstable fractures, particularly those involving the posterior pelvis, are prone to severe hemorrhage due to disruption of arterial branches and venous plexuses, often with associated retroperitoneal hematoma. In children, hemorrhage may be more severe, and nonaccidental trauma must be considered. In pregnancy, pelvic fractures pose additional risk to the gravid uterus, including uterine rupture.
Clinically, patients typically present with pelvic, hip, groin, or lower back pain, often accompanied by swelling, ecchymosis, and tenderness. Many have associated injuries involving the abdomen, genitourinary tract, neurologic system, or vascular structures. Signs of pelvic instability, deformity, limb shortening or rotation, and inability to bear weight are concerning. In severe cases, hemorrhagic shock may dominate the presentation, with tachycardia, hypotension, altered mental status, and cool, pale extremities. Bleeding from the urethra, rectum, or vagina, as well as open wounds over the pelvis, suggests an open pelvic fracture.
Initial evaluation follows standard trauma principles. A single anteroposterior (AP) pelvic radiograph is the most important early diagnostic test and should be obtained promptly when pelvic fracture is suspected. Additional views such as inlet, outlet, or Judet oblique projections may further define injury patterns, particularly involving the posterior pelvis or acetabulum. Computed tomography (CT) provides detailed assessment of fracture anatomy, retroperitoneal hematoma, and associated visceral injuries, and CT angiography can identify arterial bleeding in hemodynamically stable patients. Focused abdominal sonography for trauma (FAST) may help detect intraperitoneal bleeding but has limited ability to distinguish pelvic from abdominal sources. Laboratory studies include type and cross-match, hemoglobin and hematocrit, platelet count, and coagulation profile.
Pelvic fractures are commonly categorized using the Tile classification system, which helps guide management. Type A fractures are stable and include avulsion injuries, isolated pubic rami fractures, and transverse sacral fractures. Type B fractures are rotationally unstable but vertically stable, such as open-book and lateral compression injuries. Type C fractures are both rotationally and vertically unstable, including vertical shear (Malgaigne) fractures, and are associated with the highest risk of hemorrhage and mortality. Acetabular fractures represent a distinct subgroup requiring specialized orthopedic evaluation.
Management priorities focus on rapid resuscitation, hemorrhage control, and stabilization. Early application of a pelvic binder or improvised sheet wrap at the level of the greater trochanters is critical in suspected unstable fractures, as it reduces pelvic volume and limits bleeding. Fluid resuscitation with crystalloids and early blood transfusion is indicated for shock, avoiding lower extremity IV access when possible. External fixation, angiographic embolization, or surgical pelvic packing may be required for ongoing hemorrhage. Type A fractures are generally managed conservatively with analgesia and mobilization as tolerated, whereas Type B and C fractures require urgent orthopedic and trauma consultation, close monitoring, and often operative intervention.
Patients with hemodynamic instability, unstable pelvic fractures, acetabular fractures, pelvic hemorrhage, or associated injuries should be admitted, frequently to the intensive care unit. Hemodynamically stable patients with isolated, stable Type A fractures and no other injuries may be discharged with appropriate analgesia and close orthopedic follow-up. A key clinical principle is that pelvic fractures signal high-energy trauma; clinicians must maintain a high index of suspicion for associated abdominal, genitourinary, vascular, and neurologic injuries. Early stabilization of the pelvis and management decisions guided by hemodynamic status are essential to improving outcomes.
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Emergency and Acute Medicine – Pelvic Fracture
Pelvic fractures account for approximately 3% of all bony fractures but are associated with disproportionately high morbidity and mortality. The pelvis consists of the sacrum and two innominate bones, each formed by the ilium, ischium, and pubis. Stability of the pelvic ring depends on strong ligamentous, muscular, and soft tissue support. The anterior pelvis is stabilized by the symphysis pubis and pubic rami, while posterior stability is provided by the sacroiliac (SI) complex and pelvic floor. Because the pelvis protects major vascular structures as well as genitourinary, gastrointestinal, gynecologic, neurologic, and musculoskeletal systems, fractures often coexist with life-threatening injuries and require urgent recognition and management.
Most pelvic fractures result from high-energy trauma. Approximately 65% are caused by vehicular mechanisms, including pedestrians struck by automobiles, while falls and crush injuries account for another 20%. Athletic, penetrating, and nontraumatic causes are less common. Mortality ranges from 6–19% and increases significantly in open fractures or when hemorrhagic shock is present. Unstable fractures, particularly those involving the posterior pelvis, are prone to severe hemorrhage due to disruption of arterial branches and venous plexuses, often with associated retroperitoneal hematoma. In children, hemorrhage may be more severe, and nonaccidental trauma must be considered. In pregnancy, pelvic fractures pose additional risk to the gravid uterus, including uterine rupture.
Clinically, patients typically present with pelvic, hip, groin, or lower back pain, often accompanied by swelling, ecchymosis, and tenderness. Many have associated injuries involving the abdomen, genitourinary tract, neurologic system, or vascular structures. Signs of pelvic instability, deformity, limb shortening or rotation, and inability to bear weight are concerning. In severe cases, hemorrhagic shock may dominate the presentation, with tachycardia, hypotension, altered mental status, and cool, pale extremities. Bleeding from the urethra, rectum, or vagina, as well as open wounds over the pelvis, suggests an open pelvic fracture.
Initial evaluation follows standard trauma principles. A single anteroposterior (AP) pelvic radiograph is the most important early diagnostic test and should be obtained promptly when pelvic fracture is suspected. Additional views such as inlet, outlet, or Judet oblique projections may further define injury patterns, particularly involving the posterior pelvis or acetabulum. Computed tomography (CT) provides detailed assessment of fracture anatomy, retroperitoneal hematoma, and associated visceral injuries, and CT angiography can identify arterial bleeding in hemodynamically stable patients. Focused abdominal sonography for trauma (FAST) may help detect intraperitoneal bleeding but has limited ability to distinguish pelvic from abdominal sources. Laboratory studies include type and cross-match, hemoglobin and hematocrit, platelet count, and coagulation profile.
Pelvic fractures are commonly categorized using the Tile classification system, which helps guide management. Type A fractures are stable and include avulsion injuries, isolated pubic rami fractures, and transverse sacral fractures. Type B fractures are rotationally unstable but vertically stable, such as open-book and lateral compression injuries. Type C fractures are both rotationally and vertically unstable, including vertical shear (Malgaigne) fractures, and are associated with the highest risk of hemorrhage and mortality. Acetabular fractures represent a distinct subgroup requiring specialized orthopedic evaluation.
Management priorities focus on rapid resuscitation, hemorrhage control, and stabilization. Early application of a pelvic binder or improvised sheet wrap at the level of the greater trochanters is critical in suspected unstable fractures, as it reduces pelvic volume and limits bleeding. Fluid resuscitation with crystalloids and early blood transfusion is indicated for shock, avoiding lower extremity IV access when possible. External fixation, angiographic embolization, or surgical pelvic packing may be required for ongoing hemorrhage. Type A fractures are generally managed conservatively with analgesia and mobilization as tolerated, whereas Type B and C fractures require urgent orthopedic and trauma consultation, close monitoring, and often operative intervention.
Patients with hemodynamic instability, unstable pelvic fractures, acetabular fractures, pelvic hemorrhage, or associated injuries should be admitted, frequently to the intensive care unit. Hemodynamically stable patients with isolated, stable Type A fractures and no other injuries may be discharged with appropriate analgesia and close orthopedic follow-up. A key clinical principle is that pelvic fractures signal high-energy trauma; clinicians must maintain a high index of suspicion for associated abdominal, genitourinary, vascular, and neurologic injuries. Early stabilization of the pelvis and management decisions guided by hemodynamic status are essential to improving outcomes.
Pelvic fractures account for approximately 3% of all bony fractures but are associated with disproportionately high morbidity and mortality. The pelvis consists of the sacrum and two innominate bones, each formed by the ilium, ischium, and pubis. Stability of the pelvic ring depends on strong ligamentous, muscular, and soft tissue support. The anterior pelvis is stabilized by the symphysis pubis and pubic rami, while posterior stability is provided by the sacroiliac (SI) complex and pelvic floor. Because the pelvis protects major vascular structures as well as genitourinary, gastrointestinal, gynecologic, neurologic, and musculoskeletal systems, fractures often coexist with life-threatening injuries and require urgent recognition and management.
Most pelvic fractures result from high-energy trauma. Approximately 65% are caused by vehicular mechanisms, including pedestrians struck by automobiles, while falls and crush injuries account for another 20%. Athletic, penetrating, and nontraumatic causes are less common. Mortality ranges from 6–19% and increases significantly in open fractures or when hemorrhagic shock is present. Unstable fractures, particularly those involving the posterior pelvis, are prone to severe hemorrhage due to disruption of arterial branches and venous plexuses, often with associated retroperitoneal hematoma. In children, hemorrhage may be more severe, and nonaccidental trauma must be considered. In pregnancy, pelvic fractures pose additional risk to the gravid uterus, including uterine rupture.
Clinically, patients typically present with pelvic, hip, groin, or lower back pain, often accompanied by swelling, ecchymosis, and tenderness. Many have associated injuries involving the abdomen, genitourinary tract, neurologic system, or vascular structures. Signs of pelvic instability, deformity, limb shortening or rotation, and inability to bear weight are concerning. In severe cases, hemorrhagic shock may dominate the presentation, with tachycardia, hypotension, altered mental status, and cool, pale extremities. Bleeding from the urethra, rectum, or vagina, as well as open wounds over the pelvis, suggests an open pelvic fracture.
Initial evaluation follows standard trauma principles. A single anteroposterior (AP) pelvic radiograph is the most important early diagnostic test and should be obtained promptly when pelvic fracture is suspected. Additional views such as inlet, outlet, or Judet oblique projections may further define injury patterns, particularly involving the posterior pelvis or acetabulum. Computed tomography (CT) provides detailed assessment of fracture anatomy, retroperitoneal hematoma, and associated visceral injuries, and CT angiography can identify arterial bleeding in hemodynamically stable patients. Focused abdominal sonography for trauma (FAST) may help detect intraperitoneal bleeding but has limited ability to distinguish pelvic from abdominal sources. Laboratory studies include type and cross-match, hemoglobin and hematocrit, platelet count, and coagulation profile.
Pelvic fractures are commonly categorized using the Tile classification system, which helps guide management. Type A fractures are stable and include avulsion injuries, isolated pubic rami fractures, and transverse sacral fractures. Type B fractures are rotationally unstable but vertically stable, such as open-book and lateral compression injuries. Type C fractures are both rotationally and vertically unstable, including vertical shear (Malgaigne) fractures, and are associated with the highest risk of hemorrhage and mortality. Acetabular fractures represent a distinct subgroup requiring specialized orthopedic evaluation.
Management priorities focus on rapid resuscitation, hemorrhage control, and stabilization. Early application of a pelvic binder or improvised sheet wrap at the level of the greater trochanters is critical in suspected unstable fractures, as it reduces pelvic volume and limits bleeding. Fluid resuscitation with crystalloids and early blood transfusion is indicated for shock, avoiding lower extremity IV access when possible. External fixation, angiographic embolization, or surgical pelvic packing may be required for ongoing hemorrhage. Type A fractures are generally managed conservatively with analgesia and mobilization as tolerated, whereas Type B and C fractures require urgent orthopedic and trauma consultation, close monitoring, and often operative intervention.
Patients with hemodynamic instability, unstable pelvic fractures, acetabular fractures, pelvic hemorrhage, or associated injuries should be admitted, frequently to the intensive care unit. Hemodynamically stable patients with isolated, stable Type A fractures and no other injuries may be discharged with appropriate analgesia and close orthopedic follow-up. A key clinical principle is that pelvic fractures signal high-energy trauma; clinicians must maintain a high index of suspicion for associated abdominal, genitourinary, vascular, and neurologic injuries. Early stabilization of the pelvis and management decisions guided by hemodynamic status are essential to improving outcomes.
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Emergency and Acute Medicine – Pediatric Trauma
Pediatric trauma accounts for a significant cause of morbidity and mortality, with blunt trauma representing approximately 80% of cases and head injury present in most multisystem trauma. Trauma remains the leading cause of death and disability in children older than one year in developed countries. Young children are particularly vulnerable, with a high proportion of abuse-related injuries occurring in those younger than three years, especially infants under six months of age.
Most pediatric trauma results from single-system, minor blunt injuries. Common mechanisms include motor vehicle collisions, bicycle accidents, pedestrian versus vehicle incidents, and falls from height. Penetrating trauma is uncommon in younger children. Risk factors include inadequate supervision, developmental immaturity, poor judgment, risk-taking behaviors, and exposure to drugs or alcohol. Inconsistent history or injury patterns should raise concern for nonaccidental trauma.
History is typically obtained from caregivers, witnesses, or emergency personnel. Discrepancies between the history and observed injuries should prompt evaluation for abuse. Mechanism of injury alone is a poor predictor of severity, although certain factors such as handlebar injuries, intrusion into passenger space, lack of restraints, or absence of helmet use increase the likelihood of serious injury. A complete AMPLE history, including allergies, medications, past medical history, last oral intake, and events surrounding the injury, is essential.
Evaluation follows a structured primary survey using the ABCDE approach, addressing airway, breathing, circulation, disability, and exposure. Children may maintain compensation until significant blood loss occurs, after which rapid decompensation may follow. Unique anatomic features include a proportionally larger head, smaller blood volume, flexible chest wall, larger solid abdominal organs, and an intra-abdominal bladder in young children. Secondary survey focuses on detailed head-to-toe examination, including neurologic status, cervical spine assessment, chest and abdominal findings, extremity injuries, and skin evaluation. Certain injury patterns, such as lap belt syndrome or handlebar injuries, suggest specific internal injuries.
History and a thorough, age-appropriate physical examination are the cornerstone of evaluation. Routine trauma panels and blanket imaging are not evidence based in children and should be avoided. Laboratory testing and imaging should be individualized. Normal initial hemoglobin does not exclude hemorrhage. Elevated liver enzymes may guide abdominal imaging but should not be the sole determinant. Gross hematuria is concerning for genitourinary injury, while microscopic hematuria alone is not. Imaging decisions should be selective, with CT reserved for specific indications such as abnormal mental status, focal neurologic deficits, significant abdominal findings, or concerning mechanisms.
Prehospital priorities include rapid transport, airway stabilization, cervical spine immobilization, and hemorrhage control. In the emergency department, most children remain stable but require close monitoring. Management includes early oxygen, intravenous access with isotonic fluid resuscitation, pain control, blood transfusion if indicated, airway management when necessary, and treatment of identified injuries. Reassessment is critical, and family presence during resuscitation is encouraged when appropriate.
Admission is required for children with altered mental status, airway compromise, hemodynamic instability, significant imaging findings, operative injuries, suspected abuse, or lack of a reliable caregiver. Children with normal mental status, reassuring examinations, and negative indicated imaging may be safely discharged to reliable caregivers with appropriate instructions. Follow-up should be tailored to injuries sustained, with attention to potential post-traumatic stress, neurologic sequelae, and psychosocial needs.
Pediatric trauma accounts for a significant cause of morbidity and mortality, with blunt trauma representing approximately 80% of cases and head injury present in most multisystem trauma. Trauma remains the leading cause of death and disability in children older than one year in developed countries. Young children are particularly vulnerable, with a high proportion of abuse-related injuries occurring in those younger than three years, especially infants under six months of age.
Most pediatric trauma results from single-system, minor blunt injuries. Common mechanisms include motor vehicle collisions, bicycle accidents, pedestrian versus vehicle incidents, and falls from height. Penetrating trauma is uncommon in younger children. Risk factors include inadequate supervision, developmental immaturity, poor judgment, risk-taking behaviors, and exposure to drugs or alcohol. Inconsistent history or injury patterns should raise concern for nonaccidental trauma.
History is typically obtained from caregivers, witnesses, or emergency personnel. Discrepancies between the history and observed injuries should prompt evaluation for abuse. Mechanism of injury alone is a poor predictor of severity, although certain factors such as handlebar injuries, intrusion into passenger space, lack of restraints, or absence of helmet use increase the likelihood of serious injury. A complete AMPLE history, including allergies, medications, past medical history, last oral intake, and events surrounding the injury, is essential.
Evaluation follows a structured primary survey using the ABCDE approach, addressing airway, breathing, circulation, disability, and exposure. Children may maintain compensation until significant blood loss occurs, after which rapid decompensation may follow. Unique anatomic features include a proportionally larger head, smaller blood volume, flexible chest wall, larger solid abdominal organs, and an intra-abdominal bladder in young children. Secondary survey focuses on detailed head-to-toe examination, including neurologic status, cervical spine assessment, chest and abdominal findings, extremity injuries, and skin evaluation. Certain injury patterns, such as lap belt syndrome or handlebar injuries, suggest specific internal injuries.
History and a thorough, age-appropriate physical examination are the cornerstone of evaluation. Routine trauma panels and blanket imaging are not evidence based in children and should be avoided. Laboratory testing and imaging should be individualized. Normal initial hemoglobin does not exclude hemorrhage. Elevated liver enzymes may guide abdominal imaging but should not be the sole determinant. Gross hematuria is concerning for genitourinary injury, while microscopic hematuria alone is not. Imaging decisions should be selective, with CT reserved for specific indications such as abnormal mental status, focal neurologic deficits, significant abdominal findings, or concerning mechanisms.
Prehospital priorities include rapid transport, airway stabilization, cervical spine immobilization, and hemorrhage control. In the emergency department, most children remain stable but require close monitoring. Management includes early oxygen, intravenous access with isotonic fluid resuscitation, pain control, blood transfusion if indicated, airway management when necessary, and treatment of identified injuries. Reassessment is critical, and family presence during resuscitation is encouraged when appropriate.
Admission is required for children with altered mental status, airway compromise, hemodynamic instability, significant imaging findings, operative injuries, suspected abuse, or lack of a reliable caregiver. Children with normal mental status, reassuring examinations, and negative indicated imaging may be safely discharged to reliable caregivers with appropriate instructions. Follow-up should be tailored to injuries sustained, with attention to potential post-traumatic stress, neurologic sequelae, and psychosocial needs.
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Emergency and Acute Medicine – Pediculosis
Pediculosis is an infestation caused by lice that live in close association with humans. Bites are typically painless, and symptoms arise from the host’s inflammatory response to saliva and anticoagulants injected during feeding. Transmission occurs through direct contact and fomites such as combs, pillows, hats, and clothing. Head lice spread primarily through head-to-head contact and are more common in children and females. Pubic lice are usually transmitted through sexual contact. All lice are obligate human parasites and generally cannot survive away from a host for more than 7–10 days.
The condition is caused by three main species. *Pediculus capitis* (head lice) is the most common and affects all socioeconomic groups. *Pediculus corporis* (body lice) is associated with poor hygiene, poverty, and overcrowding, living primarily in clothing seams and transferring to the skin for feeding. *Phthirus pubis* (pubic or crab lice) typically infests coarse hair in the pubic region and is sexually transmitted. In children, pubic lice should raise concern for possible sexual abuse.
Clinical presentation varies by type. Head lice may cause scalp pruritus or be asymptomatic, often mistaken for dandruff. Body lice present with pruritus and excoriations, especially along clothing seams. Pubic lice cause intense itching, often worse at night. Physical examination focuses on identifying live lice or nits cemented to hair shafts, which cannot be easily brushed off. Empty nits alone do not confirm active infestation. Findings may include erythema, excoriations, secondary bacterial infection, posterior cervical lymphadenopathy, or bluish macules (maculae ceruleae) in pubic lice. Body lice are confirmed by finding nits in clothing seams rather than on the skin.
Diagnosis is clinical, based on careful history and physical examination with universal precautions. Laboratory testing is rarely necessary, although nits may be visualized under low-power microscopy and may fluoresce under a Wood lamp. Imaging has no role. Differential diagnoses include scabies, contact or allergic dermatitis, seborrheic dermatitis, and bed bug bites.
Management is primarily outpatient and supportive. Pruritus may be relieved with oral antihistamines or topical steroids. Head lice are treated with topical pediculicides such as permethrin 1% cream rinse or pyrethrin-based products, with nit removal using a fine-toothed comb. Reapplication in 7–10 days is usually required due to incomplete ovicidal activity. All household contacts should be examined, and infested individuals treated. Clothing, bedding, towels, and headgear should be washed and dried using hot cycles, and personal items such as combs and brushes disinfected.
Body lice management emphasizes hygiene, laundering clothing and bedding at high temperatures, and applying topical pediculicides when needed. Pubic lice are treated with topical pediculicides applied to affected hair-bearing areas, with simultaneous treatment of sexual contacts. Eyelash involvement is managed with petrolatum applied twice daily for several days. Second-line agents such as ivermectin or spinosad may be used for resistant cases.
Admission is rarely required and is reserved for patients with extensive bacterial superinfection or severe hypersensitivity reactions. Most patients can be discharged after treatment with appropriate education. Children may return to school after initial therapy, provided repeat treatment is completed. Follow-up is recommended to ensure eradication and to address social or safeguarding concerns when indicated.
Key points include confirming diagnosis by direct visualization, repeating treatment after 7–10 days, thorough environmental decontamination, and awareness of increasing resistance to first-line agents. Lindane is no longer recommended due to toxicity, and second-line treatments are effective but more costly.
Pediculosis is an infestation caused by lice that live in close association with humans. Bites are typically painless, and symptoms arise from the host’s inflammatory response to saliva and anticoagulants injected during feeding. Transmission occurs through direct contact and fomites such as combs, pillows, hats, and clothing. Head lice spread primarily through head-to-head contact and are more common in children and females. Pubic lice are usually transmitted through sexual contact. All lice are obligate human parasites and generally cannot survive away from a host for more than 7–10 days.
The condition is caused by three main species. *Pediculus capitis* (head lice) is the most common and affects all socioeconomic groups. *Pediculus corporis* (body lice) is associated with poor hygiene, poverty, and overcrowding, living primarily in clothing seams and transferring to the skin for feeding. *Phthirus pubis* (pubic or crab lice) typically infests coarse hair in the pubic region and is sexually transmitted. In children, pubic lice should raise concern for possible sexual abuse.
Clinical presentation varies by type. Head lice may cause scalp pruritus or be asymptomatic, often mistaken for dandruff. Body lice present with pruritus and excoriations, especially along clothing seams. Pubic lice cause intense itching, often worse at night. Physical examination focuses on identifying live lice or nits cemented to hair shafts, which cannot be easily brushed off. Empty nits alone do not confirm active infestation. Findings may include erythema, excoriations, secondary bacterial infection, posterior cervical lymphadenopathy, or bluish macules (maculae ceruleae) in pubic lice. Body lice are confirmed by finding nits in clothing seams rather than on the skin.
Diagnosis is clinical, based on careful history and physical examination with universal precautions. Laboratory testing is rarely necessary, although nits may be visualized under low-power microscopy and may fluoresce under a Wood lamp. Imaging has no role. Differential diagnoses include scabies, contact or allergic dermatitis, seborrheic dermatitis, and bed bug bites.
Management is primarily outpatient and supportive. Pruritus may be relieved with oral antihistamines or topical steroids. Head lice are treated with topical pediculicides such as permethrin 1% cream rinse or pyrethrin-based products, with nit removal using a fine-toothed comb. Reapplication in 7–10 days is usually required due to incomplete ovicidal activity. All household contacts should be examined, and infested individuals treated. Clothing, bedding, towels, and headgear should be washed and dried using hot cycles, and personal items such as combs and brushes disinfected.
Body lice management emphasizes hygiene, laundering clothing and bedding at high temperatures, and applying topical pediculicides when needed. Pubic lice are treated with topical pediculicides applied to affected hair-bearing areas, with simultaneous treatment of sexual contacts. Eyelash involvement is managed with petrolatum applied twice daily for several days. Second-line agents such as ivermectin or spinosad may be used for resistant cases.
Admission is rarely required and is reserved for patients with extensive bacterial superinfection or severe hypersensitivity reactions. Most patients can be discharged after treatment with appropriate education. Children may return to school after initial therapy, provided repeat treatment is completed. Follow-up is recommended to ensure eradication and to address social or safeguarding concerns when indicated.
Key points include confirming diagnosis by direct visualization, repeating treatment after 7–10 days, thorough environmental decontamination, and awareness of increasing resistance to first-line agents. Lindane is no longer recommended due to toxicity, and second-line treatments are effective but more costly.
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KembaraXtra – Medicine – Molluscum Contagiosum
Molluscum contagiosum is a generally benign viral skin disease characterized by multiple small, painless, pearly papules. The infection is confined to the skin and mucous membranes and spreads through close personal contact or autoinoculation. It occurs worldwide with an estimated incidence of 2–8% and is more prevalent in tropical regions. Coinfection is common in immunocompromised patients, with up to 5–20% of individuals with HIV affected.
The condition is caused by a double-stranded DNA poxvirus of the Molluscipox genus. In children, transmission most commonly occurs through direct skin-to-skin contact, shared objects, or exposure to contaminated water such as swimming pools or baths. In adults, infection is most often acquired through sexual contact, although autoinoculation can occur at any age. Rarely, vertical transmission during childbirth has been reported.
After an incubation period of approximately 14–50 days, patients typically present with asymptomatic lesions, though mild pruritus or tenderness may occur. An eczematous reaction surrounding the lesions is seen in up to one-quarter of cases. In immunocompetent individuals, untreated lesions usually resolve spontaneously within several months but may persist for years. On examination, lesions appear as smooth, firm, dome-shaped papules measuring 2–6 mm in diameter. They may be flesh-colored, white, translucent, or light yellow and often contain a waxy, curd-like core composed of virion-rich material. A central umbilication is a classic feature, though it may be absent in some cases. Children most often have lesions on the face, trunk, and extremities, whereas healthy adults commonly have genital or lower abdominal involvement. In patients with HIV, lesions may be larger, disseminated, persistent, and involve the face, neck, and trunk, sometimes worsening with immune reconstitution after initiation of antiretroviral therapy.
Diagnosis is primarily clinical, based on history and characteristic skin findings. Skin biopsy may be performed when the diagnosis is uncertain. Adult men presenting with molluscum contagiosum should be evaluated for possible immunocompromise. In children, the condition is rarely associated with underlying immunodeficiency and typically does not require further investigation. Laboratory testing for immunosuppression, including HIV testing, may be indicated when lesions are extensive, atypical, or unexplained. Anogenital lesions warrant evaluation for other sexually transmitted infections.
Management is directed toward destruction or removal of infected epithelial cells to reduce autoinoculation and transmission. Active treatment is not always required, as lesions are self-limited in immunocompetent hosts. Immunocompromised patients are at higher risk for prolonged disease and secondary bacterial infection and more often require intervention. Physical treatment methods such as curettage, cryotherapy, or topical destructive agents are generally the most effective options. Patients should be advised to avoid scratching, shaving over lesions, sharing towels, contact sports, and swimming pools until lesions resolve. Sexual partners should be examined when genital involvement is present. Treated patients should be re-evaluated every 2–4 weeks, as multiple treatment sessions are often required.
Hospital admission is rarely necessary and is reserved for immunocompromised patients with extensive disease complicated by severe secondary infection. Most patients can be managed safely as outpatients, with dermatology referral considered when diagnosis is uncertain or disease is refractory to initial therapy. A key clinical pitfall is unnecessary aggressive treatment in immunocompetent patients, as observation alone is often appropriate, while failure to recognize underlying immunosuppression can delay appropriate management.
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Emergency and Acute Medicine – Myasthenia Gravis
Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder characterized by painless, fluctuating, and fatigable skeletal muscle weakness. Weakness typically worsens with repeated activity and improves with rest. The disease may present in an ocular form or as generalized myasthenia gravis. Ocular involvement, affecting the eyelids and extraocular muscles, is the most common initial presentation and accounts for approximately 60% of cases. Although symptoms may initially be limited to the eyes, nearly 80% of patients with ocular MG will progress to generalized disease within two years.
Generalized myasthenia gravis involves proximal limb muscles, axial musculature, and bulbar muscles, including those responsible for speech, chewing, and swallowing. The disease often follows an acute or subacute course with relapses and remissions. Thymic abnormalities are common, with thymic hyperplasia present in approximately 65% of patients and thymoma in about 15%. A life-threatening complication, known as myasthenic crisis, occurs when respiratory muscle weakness or bulbar dysfunction leads to respiratory failure or inability to protect the airway. Common triggers include infection, surgery, trauma, pregnancy, and medication changes, particularly rapid tapering of corticosteroids.
The pathophysiology of myasthenia gravis involves antibodies directed against nicotinic acetylcholine receptors at the neuromuscular junction, resulting in impaired neuromuscular transmission. Up to 20% of patients may be seronegative for acetylcholine receptor antibodies. Certain medications can induce or worsen myasthenic weakness, including aminoglycosides, macrolides, fluoroquinolones, beta-blockers, calcium-channel blockers, anticonvulsants, antipsychotics, and neuromuscular blocking agents. Penicillamine is a well-recognized cause of drug-induced MG.
Clinically, patients report fluctuating weakness that worsens with activity. Ocular symptoms include ptosis and diplopia, often noted during prolonged visual tasks such as reading or driving. Bulbar involvement leads to slurred or nasal speech, difficulty chewing, swallowing, and maintaining jaw closure. Limb weakness commonly affects proximal muscles, causing difficulty climbing stairs, rising from a seated position, or lifting objects overhead. On physical examination, ptosis, diplopia, and facial weakness may be evident, while reflexes and sensation remain normal. Repetitive testing of affected muscle groups typically reproduces weakness.
Emergency evaluation focuses on identifying respiratory compromise and precipitating factors such as infection. Diagnostic testing includes basic laboratory studies, thyroid function tests, and antibody testing for acetylcholine receptor antibodies. Imaging of the chest with CT is essential to evaluate for thymoma. Bedside diagnostic tools include the ice test, in which application of ice to the eyelid transiently improves ptosis, supporting the diagnosis. The edrophonium (Tensilon) test may produce short-lived improvement in strength but requires cardiac monitoring and atropine availability due to the risk of bradycardia and increased secretions.
Management in the emergency setting prioritizes airway protection and respiratory support. Patients in myasthenic crisis require early intubation and mechanical ventilation. Objective indicators of impending respiratory failure include reduced vital capacity and weak inspiratory pressures. In crisis, acetylcholinesterase inhibitors are typically withheld, and treatment includes plasmapheresis or intravenous immunoglobulin (IVIG), along with high-dose corticosteroids. Infections and other triggers must be identified and treated aggressively. Atropine may be used to counteract muscarinic effects in suspected cholinergic crisis.
Hospital admission is required for new-onset disease, diagnostic uncertainty, worsening weakness, or any evidence of respiratory compromise. Intensive care admission is mandatory for myasthenic crisis or borderline respiratory status. Patients who demonstrate improvement and have stable respiratory function may be discharged in consultation with neurology, with close outpatient follow-up arranged.
A key clinical pearl is that any patient with known myasthenia gravis presenting to the emergency department should be carefully evaluated for signs of myasthenic crisis and secondary precipitants. Early recognition and aggressive supportive management are essential to prevent respiratory failure and improve outcomes.
Myasthenia gravis (MG) is an antibody-mediated autoimmune disorder characterized by painless, fluctuating, and fatigable skeletal muscle weakness. Weakness typically worsens with repeated activity and improves with rest. The disease may present in an ocular form or as generalized myasthenia gravis. Ocular involvement, affecting the eyelids and extraocular muscles, is the most common initial presentation and accounts for approximately 60% of cases. Although symptoms may initially be limited to the eyes, nearly 80% of patients with ocular MG will progress to generalized disease within two years.
Generalized myasthenia gravis involves proximal limb muscles, axial musculature, and bulbar muscles, including those responsible for speech, chewing, and swallowing. The disease often follows an acute or subacute course with relapses and remissions. Thymic abnormalities are common, with thymic hyperplasia present in approximately 65% of patients and thymoma in about 15%. A life-threatening complication, known as myasthenic crisis, occurs when respiratory muscle weakness or bulbar dysfunction leads to respiratory failure or inability to protect the airway. Common triggers include infection, surgery, trauma, pregnancy, and medication changes, particularly rapid tapering of corticosteroids.
The pathophysiology of myasthenia gravis involves antibodies directed against nicotinic acetylcholine receptors at the neuromuscular junction, resulting in impaired neuromuscular transmission. Up to 20% of patients may be seronegative for acetylcholine receptor antibodies. Certain medications can induce or worsen myasthenic weakness, including aminoglycosides, macrolides, fluoroquinolones, beta-blockers, calcium-channel blockers, anticonvulsants, antipsychotics, and neuromuscular blocking agents. Penicillamine is a well-recognized cause of drug-induced MG.
Clinically, patients report fluctuating weakness that worsens with activity. Ocular symptoms include ptosis and diplopia, often noted during prolonged visual tasks such as reading or driving. Bulbar involvement leads to slurred or nasal speech, difficulty chewing, swallowing, and maintaining jaw closure. Limb weakness commonly affects proximal muscles, causing difficulty climbing stairs, rising from a seated position, or lifting objects overhead. On physical examination, ptosis, diplopia, and facial weakness may be evident, while reflexes and sensation remain normal. Repetitive testing of affected muscle groups typically reproduces weakness.
Emergency evaluation focuses on identifying respiratory compromise and precipitating factors such as infection. Diagnostic testing includes basic laboratory studies, thyroid function tests, and antibody testing for acetylcholine receptor antibodies. Imaging of the chest with CT is essential to evaluate for thymoma. Bedside diagnostic tools include the ice test, in which application of ice to the eyelid transiently improves ptosis, supporting the diagnosis. The edrophonium (Tensilon) test may produce short-lived improvement in strength but requires cardiac monitoring and atropine availability due to the risk of bradycardia and increased secretions.
Management in the emergency setting prioritizes airway protection and respiratory support. Patients in myasthenic crisis require early intubation and mechanical ventilation. Objective indicators of impending respiratory failure include reduced vital capacity and weak inspiratory pressures. In crisis, acetylcholinesterase inhibitors are typically withheld, and treatment includes plasmapheresis or intravenous immunoglobulin (IVIG), along with high-dose corticosteroids. Infections and other triggers must be identified and treated aggressively. Atropine may be used to counteract muscarinic effects in suspected cholinergic crisis.
Hospital admission is required for new-onset disease, diagnostic uncertainty, worsening weakness, or any evidence of respiratory compromise. Intensive care admission is mandatory for myasthenic crisis or borderline respiratory status. Patients who demonstrate improvement and have stable respiratory function may be discharged in consultation with neurology, with close outpatient follow-up arranged.
A key clinical pearl is that any patient with known myasthenia gravis presenting to the emergency department should be carefully evaluated for signs of myasthenic crisis and secondary precipitants. Early recognition and aggressive supportive management are essential to prevent respiratory failure and improve outcomes.
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Emergency and Acute Medicine – Myocarditis
Myocarditis is an inflammatory disease of the heart muscle characterized by myocyte necrosis and subsequent myocardial destruction. The condition typically results from a direct cytotoxic injury to cardiac myocytes by an infectious or toxic agent, followed by a secondary immune-mediated response that worsens myocardial damage. The true incidence is unknown because many cases are mild or asymptomatic; however, autopsy studies suggest myocarditis is present in 1–7% of the general population and in more than 50% of patients with HIV. It is more common in males than females, with an average age at diagnosis of approximately 42 years, and is a major cause of unexpected sudden death in individuals younger than 40 years.
The etiology of myocarditis is broad and includes infectious, toxic, autoimmune, and hypersensitivity causes. Viral infections are the most common etiology, particularly enteroviruses such as coxsackievirus B, adenovirus, influenza, herpesviruses, hepatitis C, HIV, Epstein–Barr virus, and cytomegalovirus. Bacterial causes include diphtheria, tuberculosis, meningococcus, mycoplasma, and group A streptococcus. Parasitic infections such as Trypanosoma cruzi (Chagas disease) represent the most common global cause of myocarditis and heart failure, especially in Central and South America. Additional causes include fungal, rickettsial, helminthic infections, medications (notably anthracyclines, cocaine, and certain antibiotics), toxins, radiation, autoimmune diseases, and envenomation from insects or snakes.
Clinical presentation is variable and ranges from mild viral-like illness to fulminant heart failure and sudden cardiac death. Common symptoms include dyspnea, chest pain, palpitations, and fatigue. Chest pain is often pleuritic or sharp and may mimic acute coronary syndrome due to local inflammation or coronary spasm. Dyspnea on exertion is frequent, and orthopnea or paroxysmal nocturnal dyspnea suggests the development of congestive heart failure. Syncope is concerning and may indicate malignant ventricular dysrhythmias or high-grade conduction block. In children, myocarditis is the most common cause of heart failure in previously healthy patients and often presents with nonspecific findings such as poor feeding, respiratory distress, sweating with feeds, or new murmurs.
Physical examination findings depend on severity and may include fever, tachycardia disproportionate to fever, hypotension, cyanosis, jugular venous distention, bibasilar crackles, peripheral edema, hepatomegaly, ascites, and gallop rhythms. A diminished S1, murmurs of mitral or tricuspid regurgitation, or a pericardial friction rub may be present, particularly when myocarditis is associated with pericarditis. Hypotension and cardiogenic shock are uncommon early but indicate a poor prognosis when present.
Evaluation in the emergency setting includes electrocardiography, chest radiography, and targeted laboratory testing. ECG findings are often nonspecific and commonly show sinus tachycardia, ST- and T-wave changes, atrial or ventricular dysrhythmias, and conduction delays; up to 20% of patients may develop heart block or bundle branch block. Cardiac biomarkers may be elevated, reflecting myocardial necrosis, though normal values do not exclude myocarditis. Echocardiography is essential to assess ventricular function, wall-motion abnormalities, pericardial effusion, and intracardiac thrombus. Cardiac MRI with gadolinium enhancement is increasingly valuable, as it can identify myocardial inflammation and necrosis with high diagnostic accuracy. Endomyocardial biopsy is reserved for select cases, such as transplant recipients or patients with unexplained, rapidly progressive disease.
Management is largely supportive and focused on treating complications. All patients require close monitoring with attention to airway, breathing, and circulation. Dysrhythmias should be treated promptly, and patients with Mobitz II or complete heart block require pacing. Heart failure is managed with oxygen, diuretics, ACE inhibitors, and cautious use of digoxin. NSAIDs are contraindicated in the acute phase due to potential worsening of myocardial injury. Anticoagulation is indicated in patients with severe left ventricular dysfunction or documented intracardiac thrombus. In pediatric viral myocarditis, intravenous immunoglobulin has been shown to improve ventricular function and outcomes. Sympathomimetic agents and β-blockers should generally be avoided in the acute setting.
Disposition depends on severity. All symptomatic patients, particularly those with dysrhythmias, new-onset heart failure, conduction abnormalities, thromboembolic events, or cardiogenic shock, require hospital admission, often to a monitored or intensive care setting. Asymptomatic patients without evidence of cardiac dysfunction or arrhythmia may be considered for discharge with close follow-up. Early recognition and careful monitoring are critical, as myocarditis carries significant morbidity and mortality, and progression to chronic cardiomyopathy or need for cardiac transplantation can occur despite initial stabilization.
