Emergency and Acute Medicine – Human Bite


Overview
Human bites are the third most common type of bite injury, following dog and cat bites. Up to 75% occur during aggressive encounters, while 15–20% are related to sexual activity (“love nips”). Human bites carry a higher risk of infection than animal bites because of the dense oral bacterial flora.


Types of Human Bites
Occlusional bites occur when human teeth directly bite the skin, producing lacerations or crush injuries; these are more prone to infection than animal bites. Clenched-fist injuries (CFIs), also known as fight bites, are the most serious form. They typically present as small wounds over the metacarpophalangeal joints of the dominant hand and occur when a clenched fist strikes another person’s teeth. When the hand relaxes, the puncture site may seal, trapping oral bacteria within the joint. Tendons can carry bacteria into deeper potential spaces of the hand, markedly increasing the risk of deep and extensive infection.


Microbiology and Etiology
Human bite infections are polymicrobial, involving aerobic and anaerobic organisms. The most common pathogens are Streptococcus and Staphylococcus species. Other organisms include Eikenella corrodens, Haemophilus influenzae, Peptostreptococcus, and Corynebacterium. E. corrodens exhibits synergism with Streptococcus, Staphylococcus aureus, Bacteroides, and gram-negative organisms. Although rare, viral transmission through human bites has been reported, including hepatitis viruses, HIV, and herpes simplex virus.


Clinical Presentation
Most human bites involve the upper extremities (60–75%), followed by the head and neck (15–20%), trunk (10–20%), and lower extremities (approximately 5%). Common complications include cellulitis, deep-space infections such as septic arthritis and osteomyelitis, fractures, and tendon injuries. Hand bites have the highest infection rates.


History and Examination
History should include the time of injury, patient allergies, immune status, tetanus immunization status, and HIV or hepatitis B status of the person inflicting the bite, if known. On examination, carefully document wound location and extent, swelling, crush injury, devitalized tissue, range of motion, tendon and nerve function, signs of infection including regional adenopathy, and any joint or bone involvement.


Essential Evaluation
A meticulous examination is critical, especially for clenched-fist injuries. The deepest part of the wound must be examined while the fingers are taken through a full range of motion to identify extensor tendon lacerations or joint capsule violation.


Diagnostic Testing
Aerobic and anaerobic cultures should be obtained from clinically infected wounds; cultures are not indicated for noninfected bites. CBC is appropriate when there are signs of significant infection. Electrolytes, glucose, BUN, and creatinine should be checked in diabetic patients or those with severe infections. Imaging is usually unnecessary, but plain radiographs are indicated for suspected fractures, foreign bodies such as teeth, baseline evaluation when bone or joint space is violated, or infection near bone or joint spaces. Ultrasound may help differentiate abscess from cellulitis.


Differential Diagnosis and Special Considerations
Animal bites typically cause more punctures and lacerations, whereas human bites more often produce crush injuries. In suspected sexual abuse, look for central bruising or “hickeys,” linear abrasions or bruises on both dorsal and palmar or plantar surfaces, and multiple lesions on different extremities. An intercanine distance greater than 3 cm suggests permanent dentition and an attacker older than 8 years. If abuse is suspected, collect saliva using a saline-moistened swab placed in a paper envelope, obtain photographs, and notify authorities.


Prehospital and Initial Management
Control bleeding with direct pressure. Ensure airway patency and adequate tissue perfusion.


Emergency Department Management
Irrigate wounds copiously with normal saline using an 18-gauge needle or plastic catheter directed along the wound tract, avoiding forceful injection into tissues. Débride foreign material, necrotic tissue, and devitalized skin, but do not débride puncture wounds. Remove eschar to allow drainage and irrigation of underlying pus.


Clenched-fist injuries require immobilization and splinting in a functional position with bulky hand dressing, elevation, and early consultation with a hand surgeon for possible operative irrigation and exploration. Use a sling for outpatients and tubular stockinette suspension for inpatients. Do not perform primary repair of avulsion wounds.


Wound Closure
Primary closure increases infection risk and should be avoided in infected wounds or those older than 24 hours. Closure of wounds older than 8 hours is controversial. Facial wounds may be closed up to 24 hours after injury with counseling regarding infection risk. Infected wounds and those presenting after 24 hours should be left open, with possible delayed primary closure or approximation using Steri-Strips. Clenched-fist injuries should never be sutured.


Antibiotic Therapy and Prophylaxis
Prophylactic antibiotics are controversial for low-risk bites but are recommended for moderate to severe injuries, crush injuries with edema, bone or joint involvement, hand bites, wounds near prosthetic joints, and patients with diabetes, prior splenectomy, or immunosuppression. Tetanus prophylaxis should be updated as indicated. Refer patients for possible HIV testing and surveillance when appropriate.


Medications
First-line therapy includes amoxicillin–clavulanate orally, ampicillin–sulbactam IV, piperacillin–tazobactam IV, ticarcillin–clavulanate IV, or ceftriaxone plus metronidazole. Second-line regimens involve combination therapy with trimethoprim–sulfamethoxazole, penicillin VK, ciprofloxacin, or doxycycline, each combined with anaerobic coverage using clindamycin or metronidazole.


Disposition
Admission is indicated for infected wounds at presentation, severe or progressive cellulitis or lymphangitis, systemic infection, or failure of outpatient antibiotics. Healthy patients with localized infection may be discharged on antibiotics with 24-hour follow-up, while noninfected wounds require reassessment within 48 hours.


Special Populations
In geriatric patients, human bite marks rarely occur accidentally and should raise concern for elder abuse. In pediatric patients, human bite marks are also uncommon and suggest possible abuse; an intercanine distance greater than 3 cm indicates an adult attacker.


Follow-Up and Referral
All infected hand wounds require hand specialist follow-up. Suspected child abuse mandates referral to appropriate authorities.


Key Clinical Cautions
Always examine clenched-fist wounds through full finger motion to detect tendon or joint involvement. Early hand surgery consultation is essential for all clenched-fist injuries because of their high infection rate.

Emergency and Acute Medicine – Bladder Injury


Overview and Definitions
Bladder injury most commonly results from blunt trauma. Approximately 10% of patients with pelvic fractures sustain significant bladder injury, and 80–90% of bladder ruptures are associated with pelvic fractures. Overall mortality ranges from 17–22%, increasing to nearly 60% in combined intraperitoneal and extraperitoneal ruptures.


Etiology and Classification
Trauma accounts for about 82% of bladder injuries. Blunt mechanisms include motor vehicle accidents (87%), falls (7%), and assault (6%). Penetrating injuries are most often due to gunshot wounds (85%) and stabbings (15%). Iatrogenic causes account for 14% and include TURP, urologic, gynecologic, obstetric, abdominal, and orthopedic hip procedures, biopsies, indwelling Foley catheters, and IUD placement. Intoxication accounts for 2.9%, and spontaneous rupture occurs in less than 1%.
Extraperitoneal rupture (62%) is usually associated with pelvic fractures and results from blunt force or bone fragments. Intraperitoneal rupture (25%) occurs from direct compression of a distended bladder, typically involving the bladder dome. Combined intraperitoneal and extraperitoneal rupture (12%) carries the highest mortality due to associated injuries. Bladder contusion involves injury to the endothelial lining or muscularis with an intact bladder wall and may cause gross hematuria with normal imaging; it usually resolves without intervention.
In children, the bladder is intra-abdominal until late adolescence, making intraperitoneal rupture more common and overall bladder injury more frequent due to a less rigid pelvis.


Clinical Presentation
The classic triad includes gross hematuria, suprapubic pain, and difficulty voiding. History should focus on traumatic mechanism or recent procedures. On examination, the urethral meatus must be inspected; if blood is present, Foley catheter placement should be deferred until a retrograde urethrogram is performed, as concomitant urethral injury occurs in 10–29% of cases.


Evaluation and Diagnostic Testing
Initial evaluation includes urinalysis, which shows gross hematuria in 95–100% of significant injuries and microscopic hematuria in about 5%. BUN may be elevated due to intraperitoneal urine resorption, and electrolyte abnormalities such as hyperkalemia or hypernatremia may be present.
Retrograde cystography or CT cystography is the diagnostic modality of choice, with sensitivity around 95% and specificity near 100%. If urethral injury is suspected, a retrograde urethrogram is performed first. Proper cystography requires adequate bladder distension with diluted contrast and postdrainage imaging, as up to 10% of ruptures are detected only after bladder emptying. Extraperitoneal ruptures show teardrop- or star-shaped extravasation, whereas intraperitoneal ruptures demonstrate contrast outlining bowel loops or filling paracolic gutters. FAST examination showing free pelvic fluid should heighten suspicion for bladder injury.


Differential Diagnosis
Consider peritoneal trauma, urethral injury, and renal or ureteral trauma.


Management
Prehospital bladder catheterization should be avoided. Initial management follows standard ABCs with early urologic consultation. Extraperitoneal nonpenetrating ruptures may be managed with Foley catheter drainage (20F or larger) for approximately 14 days, with most lacerations sealing within 3 weeks; surgical repair is recommended if the patient is undergoing pelvic or abdominal surgery for other injuries. Intraperitoneal ruptures require surgical exploration and repair. Bladder contusions require no specific intervention. Broad-spectrum antibiotics are indicated for intraperitoneal rupture.


Disposition and Follow-Up
Admission is required for patients with associated major trauma or those needing surgical intervention. Bladder contusions without rupture and without other injuries may be discharged. Most bladder ruptures require admission, and discharge should occur only after urologic clearance. Urology follow-up is required for all outpatient-managed injuries, with Foley catheter removal typically at 14 days for conservatively managed extraperitoneal ruptures.


Clinical Insights and Common Errors
Free pelvic fluid on CT or ultrasound should prompt concern for bladder injury. Unresponsive, intoxicated, or altered patients require careful evaluation. Any penetrating injury to the lower abdomen with hematuria warrants cystography.

Emergency and Acute Medicine – Botulism


Overview And Definitions
Botulism is a rare but highly lethal neuroparalytic illness in the United States, with fewer than 200 cases annually, yet it carries major bioterrorism significance. It is caused by a heat-labile polypeptide exotoxin produced by Clostridium botulinum, recognized as the most potent toxin known. The toxin irreversibly inhibits acetylcholine release at presynaptic cholinergic nerve terminals, resulting in flaccid paralysis. Neurologic recovery depends on axonal sprouting and formation of new synapses, accounting for the prolonged and often incomplete recovery. Symptom onset typically occurs within 12–72 hours but may be delayed up to one week, and death may occur within 24 hours of symptom onset. Mortality approaches 60–70% without treatment and decreases to 3–10% with aggressive supportive care. The principal clinical forms include food-borne, wound, and infantile botulism, with toxin absorption occurring through mucosal surfaces or nonintact skin.


Food-borne botulism results from ingestion of preformed toxin, most commonly associated with improperly canned or stored foods. Conditions required include contamination with spores, anaerobic conditions allowing germination, sufficient time for toxin production, inadequate heating, and ingestion by a susceptible host. Wound botulism presents after traumatic contamination of wounds, often without GI symptoms, and is frequently associated with intravenous drug use. Adult intestinal toxemia botulism occurs in individuals with altered gut flora due to structural abnormalities, immunocompromise, or prolonged antibiotic exposure and may recur. Inhalational botulism is rare but poses a significant bioterrorism risk. Iatrogenic botulism from cosmetic or therapeutic use is exceedingly uncommon.


Pediatric Considerations
Infantile botulism accounts for 50–76% of reported cases, with 90% occurring in infants younger than six months. It follows ingestion of C. botulinum spores that germinate within the immature gut, often associated with soil or dust exposure and weaning from breast milk. Presentation begins with constipation, followed by bulbar weakness and progressive descending flaccid paralysis. Honey is a known source of spores and should not be given to children under one year of age.


Etiology And Pathophysiology
Clostridium botulinum is a large, spore-forming, obligate anaerobic gram-positive bacillus ubiquitous in the environment. Seven antigenically distinct toxins (A–G) exist, with types A, B, E, and rarely F responsible for most human disease.


Clinical Features
Diagnosis is primarily clinical. Patients with classic food-borne botulism present with early bulbar palsies, including diplopia, dysphagia, dysarthria, and dysphonia, followed by symmetric descending paralysis. Sensation remains intact, and mentation is preserved. Progressive respiratory muscle weakness leads to ventilatory failure. Autonomic dysfunction is common and includes dry mouth, blurred vision, orthostatic hypotension, constipation, and urinary retention. Fever is typically absent. Wound botulism may be associated with fever. Infantile botulism presents with constipation, poor feeding, hypotonia, weak cry, lethargy, and respiratory compromise. Inhalational botulism mirrors food-borne disease but lacks gastrointestinal symptoms.


Evaluation And Diagnostic Testing
The diagnosis should prompt immediate notification of state health authorities or the CDC. Laboratory evaluation includes CBC, electrolytes, renal function, glucose, and arterial blood gas analysis to assess respiratory compromise. Confirmatory testing is performed via mouse bioassay on blood, stool, gastric contents, or suspected food sources, with results available in 6–96 hours. CSF analysis is normal, aiding distinction from Guillain–Barré syndrome. Neuroimaging is typically normal. Electrophysiologic studies show normal nerve conduction with reduced evoked muscle action potentials.


Differential Diagnosis
Consider myasthenia gravis, Lambert–Eaton syndrome, Guillain–Barré syndrome, tick paralysis, hypokalemic periodic paralysis, magnesium intoxication, diphtheritic neuropathy, poliomyelitis, and rare basilar stroke syndromes. In infants, sepsis, dehydration, metabolic disorders, and spinal muscular atrophy must be excluded.


Management Principles
Respiratory failure is the leading cause of death, making early airway protection and mechanical ventilation the cornerstone of management. Antitoxin therapy must be administered immediately once botulism is suspected, without waiting for laboratory confirmation. Wound botulism requires surgical débridement. Antibiotics are not effective for intestinal botulism and may worsen symptoms by increasing toxin release but may be used for secondary wound infections. Standard precautions are sufficient, as person-to-person transmission does not occur.


Pharmacologic Therapy
Infant botulism is treated with human-derived botulism immune globulin (BabyBIG®), which significantly reduces hospital stay. Adults require heptavalent botulinum antitoxin obtained through the CDC under emergency use protocols. Antibiotics are reserved for secondary infections. Vaccination with toxoid is limited to laboratory personnel.


Disposition And Follow-Up
All suspected cases require admission, with ICU care for any respiratory compromise. Discharge is appropriate only after prolonged, progressive neurologic recovery. Long-term follow-up often includes rehabilitation for persistent weakness, which may last up to one year, and psychological support for patients and families.


Clinical Insights And Common Errors
Botulism represents a public health emergency requiring rapid coordination with health authorities. Outbreaks involving multiple patients should heighten suspicion, as few alternative diagnoses present in clusters. Antitoxin halts disease progression but does not reverse established paralysis, emphasizing the importance of early administration before overt respiratory failure develops. Bulbar weakness may be misinterpreted as altered mental status, delaying diagnosis, and early respiratory insufficiency may be clinically subtle.

Emergency and Acute Medicine – Bursitis


Overview And Definitions
Bursae are synovial fluid–filled sacs, approximately 150 in number, located between bones, tendons, ligaments, muscles, and skin, where they function to reduce friction during movement. Bursitis refers to inflammation of a bursa and may result from acute trauma, repetitive overuse, infection, crystal deposition, or systemic inflammatory disease. Chronic inflammation can lead to proliferative thickening of the bursal wall. Frequently involved locations include the subacromial bursa of the shoulder, the olecranon bursa of the elbow, trochanteric and iliopsoas bursae of the hip, prepatellar and pes anserine bursae of the knee, and the calcaneal bursa of the foot, often related to footwear.


Etiology And Pathophysiology
Trauma and repetitive microtrauma are the most common causes, either from a single injury or chronic pressure and overuse. Infectious bursitis usually results from direct inoculation through skin disruption, sometimes microscopic, and is more common in patients with diabetes, chronic alcohol use, uremia, gout, or immunosuppression. Staphylococcus species account for the majority of septic cases. Crystal-induced inflammation may occur from calcium phosphate or monosodium urate deposition. Systemic inflammatory disorders such as rheumatoid arthritis, gout, ankylosing spondylitis, psoriatic arthritis, lupus, and rheumatic fever may also precipitate bursitis.


Clinical Features
Patients may present with acute or chronic symptoms. Pain is typically localized and worsened by joint movement or direct pressure. Functional complaints such as limping or activity limitation are common. Localized swelling is often evident, especially in superficial bursae. In aseptic bursitis, tenderness is usually mild, with reduced active range of motion but preserved passive motion. Septic bursitis is suggested by warmth, erythema, swelling, marked tenderness, and sometimes fever. A history of gout, pseudogout, rheumatologic disease, recent procedures, injections, or aspirations involving the bursa should be elicited.


Evaluation And Diagnostic Approach
A careful examination of adjacent joints, tendons, and soft tissues is essential. Any suspicion of infection warrants diagnostic aspiration, particularly for olecranon and prepatellar bursae, using a lateral approach to avoid needle tract complications. Deep bursae such as the hip may require ultrasound guidance or specialist involvement.
Laboratory evaluation may include CBC with differential when infection is suspected and targeted tests for systemic disease such as uric acid, ESR, or CRP. Aspirated bursal fluid should be analyzed for cell count with differential, glucose, protein, crystals, Gram stain, and culture, with cultures sent in all cases. Imaging with plain radiographs may show soft tissue swelling, calcifications, or underlying arthropathy, particularly after trauma. Ultrasound, MRI, or CT may assist in evaluating deep or septic bursitis.


Differential Diagnosis
Conditions that may mimic bursitis include septic or inflammatory arthritis, osteoarthritis, gout and pseudogout, tendonitis, fasciitis, epicondylitis, fractures, ligament or tendon injury, contusion, osteomyelitis, and nerve entrapment. Hip pain may also arise from lumbar spine disease, sacroiliitis, or neuritis.


Management Principles
Initial care includes joint immobilization when pain is significant, with caution to avoid prolonged shoulder immobilization due to the risk of adhesive capsulitis.
Nonseptic bursitis is treated with rest, avoidance of aggravating activities, protective padding, ice therapy, and NSAIDs continued for several days beyond symptom resolution to reduce recurrence. Fluctuant bursae may be aspirated and compressed. If symptoms persist after infection is excluded, intrabursal corticosteroid injection combined with local anesthetic may be considered using strict sterile technique, with limits on frequency of injections.
Septic bursitis requires aspiration and appropriate antimicrobial therapy. Superficial infections may be managed with aspiration and oral antibiotics if close follow-up is ensured, while deeper or more severe infections may require drainage and IV antibiotics. Therapy should be guided by Gram stain results and local resistance patterns, with continued treatment beyond clinical resolution. Underlying conditions such as gout should be addressed concurrently.


Disposition And Follow-Up
Most patients can be managed as outpatients and improve within several days. Septic bursitis requires close follow-up and may necessitate repeated aspirations until cultures are sterile. Admission is indicated for systemic illness, extensive cellulitis, immunosuppression, inability to tolerate oral therapy, or failure of outpatient management. Referral to rheumatology or orthopedics is recommended for recurrent, refractory, or surgically managed cases.


Key Clinical Insights And Common Errors
Clinical examination alone may not reliably distinguish septic from nonseptic bursitis, making aspiration and fluid analysis critical. NSAID-related gastrointestinal bleeding and renal toxicity should be considered, particularly with ketorolac use. Although erythema, warmth, swelling, and pain strongly suggest infection, aspiration and culture remain essential. Care must be taken during aspiration to avoid introducing infection into adjacent joints.

Emergency and Acute Medicine – Burns


Overview And Definitions
Burns are acute injuries to skin and underlying tissues resulting from thermal, chemical, electrical, radiation, or mechanical energy transfer. Severity is determined by burn depth, total body surface area (TBSA) involved, anatomic location, and associated inhalation or systemic injury.


Etiology And Mechanisms
Burns are broadly classified into seven categories. Scald injuries result from hot liquids, grease, or steam. Contact burns arise from exposure to hot or cold surfaces. Thermal burns are caused by fire or open flames. Radiation burns occur from ionizing or nonionizing exposure. Chemical burns result from acids, alkalis, or other corrosive substances. Electrical burns occur from low- or high-voltage exposure and may cause deep tissue injury with minimal skin findings. Friction burns include road rash and rope burns.


Clinical Presentation And Associated Findings
Most burns demonstrate visible skin injury. Inhalation injury should be suspected with facial burns, pharyngeal erythema, singed nasal hair or eyelashes, carbonaceous sputum, and changes in respiratory mechanics such as wheezing, coughing, or tachypnea. Electrical and chemical burns may appear deceptively minor externally, sometimes showing only entry or exit wounds.
History should include an AMPLE assessment, burn source and environment, possibility of explosion, medical history, medications, allergies, and tetanus status. Carbon monoxide poisoning is the most common cause of death in fires and renders pulse oximetry unreliable. Cyanide poisoning should be considered when synthetic materials such as wool, nylon, silk, or polyurethane are involved.
Physical examination prioritizes airway assessment, followed by a full trauma survey. Evaluate the face, oropharynx, and nares for inhalation injury, assess the cervical spine when mechanism is concerning, examine the eyes for corneal burns, and estimate burn depth and surface area. In children, specific burn patterns may raise concern for nonaccidental injury.


Assessment Of Burn Severity
Burn size is expressed as a percentage of TBSA. In adults, the rule of nines estimates surface area: head and neck 9%, each arm 9%, each leg 18%, anterior trunk 18%, posterior trunk 18%, and perineum or palm 1%. In infants and children, the head accounts for a larger percentage and the legs for less.
The Lund and Browder chart provides age-adjusted estimates and is more accurate. The palm method, where the patient’s palm and fingers equal approximately 1% TBSA, is useful for scattered burns.
Depth classification includes superficial (first-degree) burns involving only the epidermis with erythema and pain, healing without scarring. Partial-thickness (second-degree) burns involve the dermis and may be superficial or deep. Superficial partial-thickness burns are pink, moist, painful, and heal within weeks with minimal scarring. Deep partial-thickness burns have pale dermis, reduced sensation, and often result in scarring or contractures. Full-thickness (third-degree) burns extend through the dermis, producing leathery, insensate skin and requiring surgical management. Fourth-degree burns involve deeper structures such as fascia, muscle, or bone and cause significant disability.


Diagnostic Evaluation
Severe burns require laboratory evaluation including CBC, electrolytes, renal function, glucose, coagulation studies, type and crossmatch, and pregnancy testing when appropriate. Arterial blood gas with carboxyhemoglobin level is indicated for suspected inhalation injury. Cyanide levels may be obtained selectively. Imaging may include chest radiography. Bronchoscopy is useful to evaluate inhalation injury, and ECG monitoring is important in electrical burns and in older patients.


Prehospital And Initial Management
Immediate care focuses on stopping the burning process, removing contaminated clothing or jewelry, keeping the patient warm, and cooling burned areas when appropriate. Airway protection with early oxygen administration is essential, with prompt intubation for respiratory compromise. Early IV access and fluid resuscitation are critical in burns exceeding 20% TBSA. Adequate analgesia should be provided, wounds covered with clean materials, and patients transported promptly to a burn center when indicated.


Emergency Department Management
Airway control remains the top priority, with early intubation for upper airway involvement or circumferential neck burns. Provide supplemental oxygen, IV access, continuous monitoring, analgesia, and assessment for associated injuries.
Fluid resuscitation for partial- and full-thickness burns greater than 20% TBSA is guided by the Parkland formula in adults: 4 mL/kg/%TBSA using lactated Ringer solution, with half administered in the first 8 hours and the remainder over the next 16 hours. Urine output goals are 0.5 mL/kg/hr in adults and 1 mL/kg/hr in children.
Escharotomy is indicated for circumferential burns causing vascular or respiratory compromise. Wound care includes topical antibiotics, nonadherent dressings, and avoidance of prophylactic systemic antibiotics. Transfer to a burn center should not be delayed for wound care. Minor burns may be managed as outpatients with careful cleansing, blister management, topical therapy, and daily dressing changes.


Special Populations
Children require modified fluid resuscitation, with the Galveston formula providing more accurate estimates. They are at higher risk of hypothermia and hypoglycemia and require close monitoring. Nonaccidental trauma must be considered.
In pregnancy, maternal and fetal risks are significant, fluid needs may be higher, and early obstetric consultation and fetal monitoring are recommended.


Disposition And Follow-Up
Admission is required for moderate to severe burns, suspected abuse, inability to manage wounds, or need for specialized care. Burn center referral is indicated for extensive burns, involvement of critical areas, electrical or chemical burns, inhalation injury, or significant comorbidities.
Patients with minor, noncritical burns may be discharged if reliable, with close follow-up arranged within 1–2 days to reassess wound status, pain control, and infection.


Clinical Insights And Common Errors
Early airway protection and aggressive fluid resuscitation are critical determinants of outcome. Delayed recognition of inhalation injury can be fatal. Adequate pain control should never be deferred. Children require vigilant monitoring for hypoglycemia and hypothermia, and fluid needs must be reassessed frequently.

Emergency and Acute Medicine – Bundle Branch Blocks


Overview And Definitions
Bundle branch blocks (BBBs) result from impaired intraventricular conduction through the right or left bundle branches. In complete BBB, conduction is absent or markedly delayed in one bundle while the other conducts normally, causing the affected ventricle to depolarize via slower muscle-to-muscle transmission. This produces a widened, disorganized QRS complex ≥120 msec.
Incomplete BBB represents delayed but not fully blocked conduction, with QRS duration between 100 and 120 msec.
Right bundle branch block (RBBB) reflects delayed right ventricular depolarization, whereas left bundle branch block (LBBB) reflects delayed left ventricular depolarization. LBBB may result from delay in the main left bundle or both left fascicles and leads to early right septal activation with loss of normal septal Q waves on ECG.


Anatomic And Conduction Considerations
The left bundle divides into two fascicles. The left anterior fascicle conducts impulses inferiorly, anteriorly, and to the right; its blockage alters frontal plane axis. The left posterior fascicle activates the midseptum and inferior–posterior walls; isolated block is rare.
Bifascicular block refers to RBBB combined with either left anterior or left posterior fascicular block.


Etiology And Pathophysiology
Common causes include myocardial infarction, cardiomyopathy, chronic hypertension, valvular heart disease, age-related fibrosis of the Purkinje system, and postoperative changes after cardiac surgery. Congenital heart disease such as atrial septal defect may be associated. Exercise-induced BBBs can occur.
Certain diseases and conditions are notable, including Brugada syndrome (typically presenting with RBBB pattern and associated with sudden cardiac death) and Chagas disease, particularly in Central and South America.
Medications may contribute, including β-blockers, calcium channel blockers, tricyclic antidepressants, class Ia and Ic antiarrhythmics, and digoxin.


Clinical Presentation
Many patients are asymptomatic. RBBB may be associated with a split S2 that persists with expiration, while LBBB produces a paradoxical or reversed split S2. When symptoms occur, they may include syncope or presyncope, chest pain, or manifestations related to the underlying cardiac disease.


Initial Evaluation And Essential Workup
A 12-lead ECG is central to diagnosis. Careful clinical assessment is required to identify ischemia, syncope, or associated dysrhythmias.


Electrocardiographic Features
RBBB shows a QRS duration ≥0.12 sec when complete and 0.10–0.12 sec when incomplete, with rsrʹ, rsRʹ, or rSRʹ (“M-shaped”) complexes in V1–V2 and a wide, deep S wave in V5–V6. Brugada syndrome presents with RBBB morphology plus ST-segment elevation in V1–V3.
LBBB is characterized by broad, slurred R waves in leads V5–V6, I, and aVL; small or absent R waves with deep S waves in V1–V2; and absence of normal septal Q waves in V5–V6 and I.
Left anterior fascicular block shows a QRS <120 msec with left-axis deviation (approximately −45° to −90°), deep s waves in ii, iii, and avf, qr complexes i avl.< />pan>
Left posterior fascicular block shows QRS <120 msec with right-axis deviation (≥120°), rs complexes in i and avl, qr ii, iii, avf, after excluding other causes of deviation.< />pan>


Diagnostic Testing
Laboratory testing may include electrolytes when metabolic disturbances are suspected and cardiac enzymes if ischemia is a concern. Chest radiography can reveal cardiomegaly or congestive heart failure. Electrophysiologic testing may be indicated in patients with unexplained syncope and structural heart disease as part of inpatient evaluation.


Differential Diagnosis
Consider ventricular tachycardia, myocardial infarction, ventricular hypertrophy, hyperkalemia, and drug-induced conduction abnormalities. In patients with LBBB, myocardial infarction assessment relies on criteria such as the Sgarbossa criteria, including concordant ST elevation or depression and excessive discordant ST elevation.


Management In The Emergency Setting
Isolated bundle branch block itself does not require specific therapy. Management focuses on treating associated conditions such as ischemia, heart failure, or syncope. Continuous monitoring is important, as BBBs can complicate rhythm interpretation and mimic ventricular tachycardia or ischemia.
Patients with symptomatic bifascicular block or high-grade atrioventricular block should have transcutaneous pacing pads applied, with sedation and analgesia as needed. Transvenous pacing is indicated for bifascicular block with type II second-degree or third-degree AV block, or for alternating LBBB and RBBB. New BBB with symptoms suggestive of myocardial infarction warrants urgent reperfusion therapy or catheterization.


Disposition And Follow-Up
Admission is required for patients with suspected myocardial ischemia, syncope, dysrhythmias, or BBB associated with high-grade AV block. Asymptomatic patients or those with incidental findings may be discharged with appropriate counseling. Referral to a cardiologist is recommended to evaluate for underlying cardiac disease.


Clinical Pearls And Pitfalls
New conduction abnormalities should always prompt consideration of myocardial ischemia. Specific ECG criteria help identify infarction in the presence of bundle branch block. Careful rhythm interpretation is essential to avoid misdiagnosing ventricular tachycardia or missing acute ischemia.

Emergency and Acute Medicine – Brugada Syndrome


Overview And Definitions
Brugada syndrome is an inherited cardiac channelopathy caused by mutations in cardiac sodium (Na⁺) channels, occurring in the absence of structural heart disease. It carries a very high risk of sudden cardiac death, typically due to ventricular fibrillation. Two-year mortality approaches 30% without intervention. The condition accounts for 40–60% of cases previously labeled idiopathic ventricular fibrillation. It is more prevalent in men, particularly those of Southeast Asian descent, but can affect all ages, sexes, and races.


Etiology And Pathophysiology
Brugada syndrome is inherited in an autosomal dominant pattern in approximately 50% of cases, with variable penetrance. More than 70 sodium channel mutations have been identified, most involving the SCN5A gene, which accounts for roughly 20% of cases. The abnormal sodium current predisposes to malignant ventricular dysrhythmias, especially under triggering conditions such as fever, metabolic derangements, or drug exposure.


Clinical Presentation
Patients most commonly present with syncope, near-syncope, palpitations, or sudden cardiac arrest due to polymorphic ventricular tachycardia or ventricular fibrillation. Episodes often occur at rest or during sleep. A history may reveal nocturnal agonal respirations, fever-associated symptoms, cocaine use, or exposure to tricyclic antidepressants or psychotropic drugs. Family history is critical and may include unexplained drowning, early or sudden cardiac death, or known Brugada syndrome in relatives. Physical examination is usually normal but should focus on excluding alternative causes of syncope or dysrhythmia.


Diagnostic Evaluation
A 12-lead ECG is essential. Toxicology screening and careful history and family assessment are required. Laboratory studies should evaluate electrolytes, metabolic abnormalities, and ischemia when appropriate.


Electrocardiographic Findings
Diagnosis is based on characteristic ECG patterns in the right precordial leads (V1–V3), often with right bundle branch block or incomplete right bundle branch block morphology and ST-segment elevation.
Type 1 (coved pattern) shows ≥2 mm ST elevation with a downsloping, concave ST segment and a negative symmetric T wave, without QRS duration mismatch between V1 and V6.
Type 2 (saddleback pattern) shows an r′ ≥2 mm followed by convex ST elevation and a QRS duration mismatch between V1 and V6. ST elevation may be limited to V1 and rarely extends to V3.


Additional Testing
Laboratory testing includes serum chemistries, cardiac biomarkers if ischemia is suspected, CBC in syncope evaluation, and D-dimer when pulmonary embolism is considered. Chest radiography assesses cardiomegaly, and CT angiography is used selectively. Electrophysiology testing with sodium channel blocker challenge may unmask diagnostic ECG changes. Implantable cardioverter-defibrillator (ICD) placement dramatically reduces mortality.


Differential Diagnosis
Consider other causes of syncope and dysrhythmia, including vasovagal syncope, hypovolemia, pregnancy, atrial and ventricular tachyarrhythmias, Wolff–Parkinson–White syndrome, long QT syndromes, high-grade AV block, symptomatic bradycardia, and drug overdose (especially TCAs). ECG mimics include isolated RBBB, athletic heart changes, septal hypertrophy, pectus excavatum, arrhythmogenic right ventricular cardiomyopathy, STEMI, myocarditis, pericarditis, electrolyte disorders, and pulmonary embolism.


Management And Emergency Care
Initial management follows standard airway, breathing, and circulation principles, with full ACLS protocols for arrest or unstable dysrhythmias. Continuous cardiac monitoring is required. Cardiology consultation for electrophysiology evaluation is essential. Electrolyte and metabolic abnormalities should be corrected promptly. Antiarrhythmic medications are generally ineffective. Management of asymptomatic patients remains controversial, though EP evaluation is recommended.


Disposition And Follow-Up
Patients with concerning ECG findings, unexplained syncope, ongoing dysrhythmias, or inability to obtain urgent cardiology follow-up should be admitted. Discharge may be considered only if the patient is asymptomatic, hemodynamically stable, and cleared by cardiology, including appropriate ICD interrogation if present. All patients with suspected or confirmed Brugada syndrome require electrophysiology follow-up.


Key Clinical Insights And Diagnostic Traps
Maintain suspicion for Brugada syndrome in cases of unexplained syncope or sudden cardiac death, particularly with a relevant family history. The ECG pattern—RBBB or incomplete RBBB with ST elevation isolated to V1–V3—is central to diagnosis, but several mimics exist. Fever, systemic illness, or drugs may unmask the Brugada pattern. Early cardiology involvement is critical, as ICD implantation is the only proven therapy that nearly eliminates the risk of sudden cardiac death.

Emergency and Acute Medicine – Acute Bronchitis


Overview And Definitions
Acute bronchitis is an inflammatory condition of the bronchial airways characterized by mucosal hyperemia, edema, and excess mucus production. Impairment of ciliary function and local immune defenses leads to airway obstruction caused by edema, secretions, and bronchial smooth muscle spasm. The condition is usually self-limited and most often follows an upper respiratory tract infection.


Etiology And Pathophysiology
Acute bronchitis is predominantly viral in origin. Common pathogens include parainfluenza, influenza A and B, respiratory syncytial virus, human metapneumovirus, adenovirus, coronavirus, rhinovirus, echovirus, coxsackievirus, and, less commonly, measles and herpes viruses, which may cause severe disease. Certain organisms are associated with more prolonged or severe illness, including Mycoplasma pneumoniae, Chlamydia pneumoniae, and Bordetella pertussis. Pertussis incidence is increasing even among immunized individuals due to waning immunity. Bacterial causes are otherwise uncommon except in patients with chronic lung disease.


Clinical Presentation
Patients often describe a prodrome of malaise, chills, myalgias, coryza, and sore throat, followed by cough that is initially dry and later becomes mucoid or mucopurulent. Mild dyspnea and chest discomfort or burning related to coughing are common. Symptoms typically improve after 3–5 days, though cough and fatigue may persist for 1–3 weeks. Physical examination may reveal low-grade fever, tachypnea, rhonchi or wheezing, and occasional crackles. Mild hemoptysis can occur.


Diagnostic Evaluation
Diagnosis is primarily clinical. Routine laboratory testing is generally unnecessary. Influenza A and B testing may be useful when results would alter management or reporting. Pertussis should be considered in patients with cough lasting 14 days or longer, especially with paroxysms, post-tussive vomiting, inspiratory whoop, or known outbreak exposure. Chest radiography is not routinely indicated but should be obtained in patients with hypoxia, dyspnea, chest pain, tachycardia, tachypnea, fever ≥38°C, focal lung findings, advanced age, or significant comorbid disease. Imaging typically shows no consolidation in uncomplicated bronchitis.


Differential Diagnosis
Important alternatives include pneumonia, reactive airway disease or asthma, aspiration, acute sinusitis, and, in chronic cases, gastroesophageal reflux disease, chronic bronchitis, bronchiectasis, ACE inhibitor–related cough, malignancy, heart failure, sarcoidosis, and psychogenic cough.


Management And Emergency Care
Treatment is supportive. Oxygen is administered for hypoxia, and fluids are given if dehydration is present. Bronchodilators may benefit patients with wheezing or evidence of airflow obstruction. Antitussives and antipyretics can be used for symptomatic relief. Antiviral therapy such as oseltamivir or zanamivir may be considered for early influenza-related illness, and amantadine may be used selectively during influenza A outbreaks, accounting for resistance patterns. Antibiotics are generally not recommended, even with purulent sputum, due to minimal benefit and risks of resistance and adverse effects. They may be considered if fever recurs after initial improvement or if pertussis is confirmed. Smoking cessation should be encouraged but does not alone justify antibiotic use.


Disposition And Follow-Up
Most patients can be safely discharged if there is no significant respiratory compromise. Admission is reserved for those with hypoxia, significant cardiopulmonary disease, severe illness, or diagnostic uncertainty. Patients should be advised that cough may persist for several weeks and instructed to return for worsening symptoms, new dyspnea, or lack of improvement after 2–3 weeks. Routine follow-up is unnecessary if symptoms resolve.


Key Clinical Insights And Common Errors
High fever, hypoxia, or focal pulmonary findings should prompt evaluation for pneumonia. Acute bronchitis is most often viral, and unnecessary antibiotic use is a frequent error. Immunocompromised patients may develop more severe disease and warrant closer monitoring and coordination with their primary physician.

Emergency and Acute Medicine – Bronchiolitis


Overview and Definitions
Bronchiolitis is a lower respiratory tract infection characterized by airway inflammation, bronchoconstriction, wheezing, tachypnea, and varying degrees of respiratory distress, typically preceded by an upper respiratory prodrome.


Etiology and Pathophysiology
Respiratory syncytial virus is responsible for approximately 85–90% of cases. Other causative viruses include influenza, parainfluenza, and adenovirus. Disease incidence peaks during winter months. Viral infection leads to mucosal edema, increased mucus production, and small airway obstruction, resulting in impaired ventilation and increased work of breathing.


Clinical Presentation
Bronchiolitis primarily affects children younger than 2 years, most commonly infants under 1 year. Initial symptoms include nasal congestion with marked rhinorrhea, followed by cough that may be associated with posttussive vomiting. Wheezing, crackles, and rhonchi are common on auscultation. Respiratory distress manifests as tachypnea, nasal flaring, retractions, and grunting, often worsening over 1–3 days. Fever is usually low-grade (<39.5°c). hypoxemia is typically mild, and cyanosis rare. decreased oral intake common, though frank dehydration uncommon. apnea may occur, particularly in premature or very young infants. high-risk children receive monthly intramuscular palivizumab during rsv season to reduce infection risk.< />pan>


Essential Evaluation
Diagnosis is clinical. Assessment focuses on respiratory effort, oxygenation, and hydration status. Pulse oximetry is useful for confirming oxygenation and trending disease progression. Identification of the viral cause may assist with inpatient cohorting but rarely alters acute management.


Diagnostic Tests and Interpretation
Most patients require no laboratory testing beyond pulse oximetry. Nasopharyngeal aspirates or washes for viral studies may be considered in critically ill children, febrile infants under 3 months, those with atypical features, suspected alternative diagnoses (e.g., pertussis or chlamydia), significant comorbidities (chronic lung or cardiac disease), or prematurity. Chest radiographs typically show hyperinflation, peribronchial thickening, atelectasis, or variable infiltrates; atelectasis in young infants suggests more severe disease. Imaging is not routinely indicated and is reserved for atypical presentations, lack of improvement after 2–3 weeks, concern for alternative diagnoses, or impending respiratory failure. Septic evaluation may be required in febrile neonates, and urine testing should be considered in febrile infants 1–3 months old.


Differential Diagnosis
Asthma or recurrent virus-induced wheezing, pertussis (paroxysmal cough without wheeze between spells), bacterial pneumonia (toxic appearance, focal consolidation), foreign body aspiration (sudden onset, often afebrile), and congestive heart failure (feeding difficulty, failure to thrive).


Prehospital Care
Young infants have limited respiratory reserve and may deteriorate rapidly. Continuous cardiorespiratory monitoring and oxygen supplementation are indicated when saturations fall below 90–92% or distress is severe. Vigilance for apnea is critical, especially in infants under 7 weeks, weight <4 kg, or with marked tachypnea comorbidities. bag-mask ventilation may be required for recurrent apneas.< />pan>


Initial Stabilization in the ED
Management follows pediatric advanced life support principles with attention to airway, ventilation, and hydration. Early intubation is indicated for recurrent apnea or impending respiratory failure.


Emergency Department Management
Supplemental oxygen is provided for hypoxemia. Parenteral hydration is used when oral intake is inadequate or respiratory distress is significant. Most children do not benefit from routine pharmacotherapy. Bronchodilators may be trialed in moderate to severe disease, continued only if a clear reduction in work of breathing is observed. Corticosteroids alone generally do not alter outcomes; however, combined nebulized epinephrine with oral dexamethasone may reduce admissions in moderate to severe cases, likely due to synergistic effects. Antibiotics are not indicated unless there is evidence of bacterial infection. Ribavirin has no role in ED management.


Medications
Therapeutic trials may include nebulized albuterol or levalbuterol, nebulized epinephrine, and dexamethasone in selected patients. Most children require no medications, and bronchodilators after discharge are ineffective unless clear benefit was demonstrated prior to discharge.


Disposition
Admission is indicated for hypoxemia requiring oxygen, inability to maintain hydration, significant or persistent respiratory distress, apnea, severe comorbidities, failure to improve after therapy, or unreliable home monitoring. Discharge may be considered when feeding is adequate, oxygenation is acceptable on room air, respiratory distress has resolved, and close follow-up is assured.


Follow-Up Care
Because bronchiolitis often worsens early in its course, close outpatient follow-up within 24 hours is essential. Caregivers should be counseled regarding signs of worsening respiratory distress, dehydration, and apnea. Symptoms may persist for 2–3 weeks, and small, frequent feeds are recommended.


Key Clinical Insights and Common Errors
Infants with bronchiolitis frequently present with a combination of respiratory distress, hypoxia, dehydration, and apnea. Underestimating the potential for rapid deterioration is a common error; vigilant monitoring and early supportive care are critical to preventing adverse outcomes.