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.

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.

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.

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.

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.

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.

Emergency and Acute Medicine – Patellar Injuries

Patellar injuries encompass a spectrum of conditions involving the patella and its associated extensor mechanism, including patellar dislocation, patellar fracture, patellar tendon rupture, and patellar tendinitis. These injuries commonly result from traumatic forces, sudden deceleration, or repetitive overuse and are frequently encountered in athletic and emergency settings. Accurate recognition is essential, as management ranges from conservative treatment to urgent surgical intervention.

Patellar dislocation most often occurs due to sudden knee flexion combined with external rotation of the tibia on the femur, accompanied by a strong contraction of the quadriceps muscle. Lateral dislocation is by far the most common type, with the patella displaced over the lateral femoral condyle. Direct trauma to the patella is a less frequent cause. Risk factors include genu valgum, patella alta, shallow femoral trochlea, weak vastus medialis, pes planus, and structural abnormalities of the patella. Dislocations are particularly common in adolescent athletes, especially females, and younger age at first dislocation is associated with higher recurrence rates.

Patients with patellar dislocation typically report a sensation of the knee “giving way,” often accompanied by a popping or tearing feeling, immediate pain, swelling, and difficulty bearing weight. On examination, there may be an obvious lateral deformity of the patella, although spontaneous reduction frequently occurs before ED evaluation. Tenderness along the patella and a positive apprehension test (Fairbanks sign) are characteristic findings.

Patellar fractures are most commonly caused by direct trauma such as a fall or direct blow to the knee, often resulting in comminuted or minimally displaced fractures. Indirect mechanisms involve excessive tension through the extensor mechanism, leading to transverse or displaced fractures. Transverse fractures account for the majority of cases, followed by comminuted, longitudinal, and osteochondral fractures. Patients present with anterior knee pain, swelling, hemarthrosis, difficulty ambulating, and impaired knee extension. Palpable defects or crepitus may be present.

Patellar tendon rupture usually results from a forceful eccentric contraction of the quadriceps on a flexed knee, such as during landing from a jump or heavy lifting. It occurs more often in older athletes and in patients with predisposing conditions such as chronic patellar tendinitis, diabetes mellitus, inflammatory arthropathies, prior steroid injections, or previous knee surgery. Clinically, patients experience abrupt severe pain, inability to maintain knee extension, and a high-riding patella on examination or imaging.

Patellar tendinitis, also known as “jumper’s knee,” is an overuse injury caused by repetitive microtrauma from activities involving frequent jumping or rapid acceleration and deceleration. It is common in volleyball players, basketball players, runners, and high jumpers. Patients typically report localized pain at the inferior pole of the patella or proximal patellar tendon that worsens with stair climbing or rising from a seated position.

Radiographic evaluation is essential in suspected patellar injuries. Standard anteroposterior, lateral, and sunrise (axial) views of the knee should be obtained. In patellar dislocations, postreduction radiographs are important to exclude associated osteochondral fractures. A bipartite patella may mimic fracture and should be distinguished with comparison views if needed. In patellar tendon rupture, imaging may reveal a superiorly displaced patella. Radiographs are often normal in early patellar tendinitis.

Management depends on the specific injury. Simple lateral patellar dislocations are typically reduced by gentle knee extension, sometimes with medial pressure on the patella. Procedural analgesia or sedation may be required. Other dislocation types (superior, medial, or intra-articular) should not be reduced in the ED and require orthopedic consultation. Patellar fractures warrant orthopedic evaluation; nondisplaced fractures with intact extensor function may be treated nonoperatively with immobilization, while displaced or open fractures require surgical management. Patellar tendon rupture requires early orthopedic consultation and surgical repair, typically within two to six weeks. Patellar tendinitis is managed conservatively with rest, activity modification, NSAIDs, and physical therapy.

Patients with successfully reduced lateral patellar dislocations and normal postreduction imaging may be discharged with a knee immobilizer, crutches, and close orthopedic follow-up. Admission is indicated for irreducible dislocations, associated fractures, open injuries, or compromised extensor mechanism. Important clinical pearls include recognizing that patellar dislocations may spontaneously reduce prior to evaluation and that swelling may obscure a palpable defect in patellar tendon rupture.

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.

Emergency and Acute Medicine – Parkinson Disease

Parkinson disease (PD) is a gradually progressive neurodegenerative disorder that typically affects individuals in middle or late life. It is characterized by degeneration of dopaminergic neurons in the substantia nigra, formation of Lewy bodies in remaining neurons, and accelerated cortical atrophy. Although symptoms often begin unilaterally, the disease usually progresses to symmetric involvement. Parkinson disease affects approximately 1% of people over 60 years of age and up to 4% of those over 80. Importantly, nonspecific symptoms such as fatigue, constipation, and hyposmia may precede the diagnosis by many years, sometimes up to two decades.

The etiology of Parkinson disease is most often sporadic or idiopathic. However, several other conditions can present with parkinsonism and must be considered, especially in the emergency setting. These include drug-induced causes such as neuroleptics and sudden withdrawal of dopaminergic medications leading to parkinsonism–hyperpyrexia syndrome, as well as exposure to toxins like carbon monoxide, methanol, cyanide, organophosphates, and MPTP. Structural brain lesions involving the basal ganglia or midbrain, hydrocephalus, infections such as viral encephalitis or Mycoplasma, and other neurologic conditions like central pontine myelinolysis and encephalitis lethargica can also produce parkinsonian features.

Clinical manifestations of Parkinson disease are divided into nonmotor and motor symptoms. Nonmotor symptoms include orthostatic hypotension, constipation, delayed gastric emptying, dysphagia, pain and sensory disturbances, depression, hallucinations, dementia, and sleep disorders. Motor symptoms are classically defined by resting “pill-rolling” tremor, cogwheel rigidity due to increased muscle tone, bradykinesia with marked slowness of movement, postural instability, stooped posture, and a reduced facial expression often described as a “masked face.” A sudden change in baseline motor function or mental status in a patient with known PD may be the only sign of an underlying systemic illness such as infection.

History is the cornerstone of diagnosis and emergency assessment. Important elements include the onset and progression of symptoms, whether the presentation was gradual or sudden, medication adherence, and exposure to drugs or toxins that may cause parkinsonism. Sudden withdrawal or noncompliance with dopaminergic therapy can precipitate parkinsonism–hyperpyrexia syndrome, a life-threatening condition marked by rigidity, hyperthermia, reduced consciousness, autonomic instability, and complications such as acute renal failure, rhabdomyolysis, venous thrombosis, and disseminated intravascular coagulation.

Physical examination typically reveals cogwheel rigidity, resting tremor, bradykinesia, and postural abnormalities. Diagnosis of Parkinson disease is primarily clinical, and no specific laboratory test is required to confirm it. In the emergency department, investigations are directed toward identifying alternative diagnoses, complications, or precipitants of deterioration. Laboratory studies may be indicated if parkinsonism–hyperpyrexia syndrome or infection is suspected. Neuroimaging with CT or MRI is not required to diagnose PD but may be performed to evaluate dementia or exclude other neurologic conditions. Chest radiography may be useful when respiratory infection is suspected.

The differential diagnosis of Parkinson disease is broad and includes essential tremor, benign familial tremor, major depression, Wilson disease, Huntington disease, Alzheimer disease, dementia with Lewy bodies, Creutzfeldt–Jakob disease, vitamin B12 deficiency, hypothyroidism, hydrocephalus, multi-infarct dementia, and toxic exposures such as carbon monoxide poisoning. Careful clinical assessment is essential to avoid misdiagnosis.

Management in the emergency department focuses on symptom control, identification and treatment of triggers, and prevention of complications. Antiparkinsonian medications may be initiated or adjusted in consultation with neurology. Patients with mild disease may not require immediate pharmacologic therapy, while those with moderate disease often benefit from dopaminergic or anticholinergic agents. Underlying infections or metabolic disturbances should be treated promptly. Parkinsonism–hyperpyrexia syndrome requires urgent replacement of dopaminergic therapy, supportive care, and management of associated complications.

Common medications used in Parkinson disease include carbidopa/levodopa as first-line therapy, dopamine agonists such as pramipexole and ropinirole, MAO-B inhibitors like selegiline and rasagiline, anticholinergics such as benztropine for tremor-dominant disease, and amantadine to stimulate dopamine release. Adjunctive agents like entacapone may be used to enhance levodopa bioavailability. In parkinsonism–hyperpyrexia syndrome, intravenous or enteral levodopa and bromocriptine are essential.

Admission is indicated for patients with Parkinson disease who present with serious medical conditions such as infection, trauma, cardiovascular or cerebrovascular emergencies, electrolyte disturbances, altered mental status, medication complications, failure to thrive, or suspected abuse. Patients with depression and suicidal intent or complications related to deep brain stimulation devices also require inpatient care. Stable patients with mild to moderate disease may be discharged with medications and urgent outpatient neurology follow-up.

Key clinical pearls include recognizing that Parkinson disease can be difficult to diagnose and is frequently confused with other neurologic conditions. Sudden withdrawal of dopaminergic medications is a medical emergency and must be avoided. In the emergency setting, vigilance for systemic illness, medication noncompliance, and life-threatening complications is critical to optimal patient outcomes.

Emergency and Acute Medicine – Paraphimosis

Paraphimosis is a urologic emergency defined by entrapment of the retracted foreskin proximal to the glans penis. This entrapment leads to progressive lymphatic congestion and venous obstruction, which can ultimately compromise arterial blood flow to the glans. If not promptly recognized and treated, paraphimosis may result in ischemia, necrosis, and permanent penile injury.

The condition most commonly occurs when the foreskin is retracted and not returned to its normal position. Predisposing factors include phimosis, inflammation, trauma, and sexual inexperience, particularly in individuals unaware of the need to reduce the foreskin after intercourse. Paraphimosis is frequently iatrogenic, occurring after physical examination, urinary catheterization, cystoscopy, or genital hygiene when the foreskin is left retracted.

Patients typically present with penile pain, a visibly retracted foreskin, and a swollen, edematous glans. The glans may appear erythematous, dusky, or cyanotic as venous congestion progresses. Local cellulitis may be present, and in advanced or untreated cases, necrosis of the glans can develop. Physical examination should include careful inspection of the entire penis to exclude constricting foreign bodies or bands, such as hair tourniquets, wire, or string, which can mimic paraphimosis.

The diagnosis of paraphimosis is clinical and should be made based on history and physical examination alone. Treatment must not be delayed for laboratory or imaging studies. Imaging is generally unnecessary unless a foreign body is suspected, in which case radiographs may be obtained after restoration of adequate perfusion.

Initial management focuses on rapid reduction of edema and prompt return of the foreskin to its normal position to restore blood flow. Pain control is essential and may require local anesthesia, a penile nerve block, systemic analgesia, or conscious sedation, especially in children. Ice packs may be applied to the glans to reduce swelling while preparations for reduction are made. Manual reduction is the first-line treatment and involves circumferential compression of the edematous glans while simultaneously applying traction to advance the foreskin distally over the glans.

If manual reduction is unsuccessful, additional techniques may be employed to reduce edema. These include the multiple puncture technique, in which small-gauge needle punctures are made in the swollen foreskin to allow expression of edema fluid, followed by another attempt at manual reduction. Osmotic methods, such as application of gauze soaked in 50% dextrose, may also help decrease edema if immediate reduction is delayed. When noninvasive methods fail, a dorsal slit of the foreskin may be required to release the constricting ring. In some cases, suturing may be necessary after reduction if the incision is extensive.

Antibiotics are generally not required unless there is associated cellulitis or balanoposthitis. Once reduction is successful and symptoms resolve, most patients can be discharged with close urologic follow-up. Admission is indicated for patients with penile necrosis, severe infection, or inability to achieve reduction. Urologic consultation is recommended in all cases, and circumcision may be considered to prevent recurrence, although this remains a topic of clinical debate.

Patient education is essential to prevent recurrence. Patients should be instructed on proper foreskin hygiene and the importance of returning the foreskin to its normal position after retraction for cleaning, sexual activity, or medical procedures. Early recognition and prompt management are key to preventing serious complications of paraphimosis.