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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.
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.
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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.
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.
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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.
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.
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Emergency and Acute Medicine – Calcium Channel Blocker Poisoning
Overview and Definitions
Calcium channel blocker (CCB) poisoning is a potentially life-threatening intoxication resulting from inhibition of calcium influx into cardiac and smooth muscle cells. This leads to impaired myocardial contractility, decreased vascular tone, and conduction abnormalities. CCB toxicity is associated with significant morbidity and mortality and requires early recognition and aggressive supportive care.
Three major classes of calcium channel blockers exist. Phenylalkylamines (verapamil) primarily affect the myocardium, producing negative chronotropic and inotropic effects with hypotension and bradycardia, without reflex tachycardia. Dihydropyridines (e.g., nifedipine) predominantly cause peripheral vasodilation leading to hypotension, often accompanied by reflex tachycardia. Benzothiazepines (diltiazem) have combined cardiac and vascular effects, with initial increases in heart rate and cardiac output followed by bradycardia and hypotension.
Calcium plays a critical role in cardiac and smooth muscle contraction and in insulin secretion from pancreatic beta cells. Blockade of calcium channels results in decreased contractility, impaired conduction, and reduced insulin release, leading to hyperglycemia, which is a hallmark of severe toxicity.
Etiology and Pathophysiology
CCB toxicity occurs following intentional overdose, medication errors, or accidental pediatric ingestion. Sustained-release formulations are particularly dangerous due to delayed onset and prolonged toxicity. Inhibition of calcium entry into myocardial cells reduces cardiac output and slows atrioventricular conduction, while vascular smooth muscle relaxation causes profound hypotension. Concurrent inhibition of insulin secretion leads to myocardial energy failure due to impaired carbohydrate utilization, contributing to shock and refractory hypotension.
Diagnosis
Signs and Symptoms
Cardiovascular manifestations include hypotension, bradycardia, reflex tachycardia (particularly with dihydropyridines), conduction delays, and high-grade heart blocks. Neurologic findings include altered mental status, agitation, seizures, and coma. Metabolic abnormalities include hyperglycemia and metabolic acidosis. Patients may appear warm rather than cool despite shock.
Essential Workup
A 12-lead ECG is mandatory to evaluate for bradycardia, QRS prolongation, and heart block. Continuous cardiac and hemodynamic monitoring is required.
Diagnostic Tests and Interpretation
Laboratory evaluation includes serum electrolytes, BUN, creatinine, glucose, CBC, and ionized calcium levels when calcium therapy is administered. Digoxin levels should be obtained in patients on digoxin prior to calcium administration. Hyperglycemia in the setting of bradycardia and hypotension strongly suggests CCB poisoning. Toxicology screening should be considered if co-ingestants are suspected.
Differential Diagnosis
β-blocker toxicity, clonidine toxicity, digoxin toxicity, and acute myocardial infarction with heart block.
Management
Prehospital Care
Transport all pill bottles to the emergency department. Administer calcium in unstable patients when CCB overdose is suspected.
Initial Stabilization and Therapy
Initial management follows ABC principles with early airway protection as needed. Supplemental oxygen, IV access with isotonic fluids, and continuous cardiac monitoring are essential.
Emergency Department Management
Therapeutic goals include maintaining heart rate above 60 beats/min, systolic blood pressure above 90 mm Hg, adequate urine output, and improving mental status. Syrup of ipecac is contraindicated. Activated charcoal may be considered early, particularly in sustained-release ingestions or co-ingestants.
Calcium therapy provides transient improvement. Calcium gluconate is preferred due to reduced tissue toxicity, while calcium chloride is more potent but risks extravasation injury. Calcium is contraindicated in digoxin toxicity. IV fluids should be administered cautiously. Atropine is usually ineffective.
High-dose insulin euglycemia therapy is a cornerstone of treatment, improving myocardial carbohydrate utilization and hemodynamics. Vasopressors such as dopamine, epinephrine, or norepinephrine may be required. Amrinone may improve inotropy. Electrical pacing is reserved for refractory cases. IV lipid emulsion and hypertonic sodium bicarbonate may be considered as rescue therapies.
Disposition and Follow-Up
Patients with symptoms or sustained-release ingestion require admission to a monitored setting. Asymptomatic patients who ingest immediate-release formulations may be discharged after 8 hours of observation. Psychiatric evaluation is required for intentional overdoses. Caregiver education is essential for pediatric exposures
Clinical Pearls and Pitfalls
Consider CCB toxicity in any patient presenting with unexplained hypotension, bradycardia, and hyperglycemia. Do not rely on atropine alone. Early initiation of high-dose insulin therapy improves outcomes. Sustained-release preparations may cause delayed and prolonged toxicity.
Overview and Definitions
Calcium channel blocker (CCB) poisoning is a potentially life-threatening intoxication resulting from inhibition of calcium influx into cardiac and smooth muscle cells. This leads to impaired myocardial contractility, decreased vascular tone, and conduction abnormalities. CCB toxicity is associated with significant morbidity and mortality and requires early recognition and aggressive supportive care.
Three major classes of calcium channel blockers exist. Phenylalkylamines (verapamil) primarily affect the myocardium, producing negative chronotropic and inotropic effects with hypotension and bradycardia, without reflex tachycardia. Dihydropyridines (e.g., nifedipine) predominantly cause peripheral vasodilation leading to hypotension, often accompanied by reflex tachycardia. Benzothiazepines (diltiazem) have combined cardiac and vascular effects, with initial increases in heart rate and cardiac output followed by bradycardia and hypotension.
Calcium plays a critical role in cardiac and smooth muscle contraction and in insulin secretion from pancreatic beta cells. Blockade of calcium channels results in decreased contractility, impaired conduction, and reduced insulin release, leading to hyperglycemia, which is a hallmark of severe toxicity.
Etiology and Pathophysiology
CCB toxicity occurs following intentional overdose, medication errors, or accidental pediatric ingestion. Sustained-release formulations are particularly dangerous due to delayed onset and prolonged toxicity. Inhibition of calcium entry into myocardial cells reduces cardiac output and slows atrioventricular conduction, while vascular smooth muscle relaxation causes profound hypotension. Concurrent inhibition of insulin secretion leads to myocardial energy failure due to impaired carbohydrate utilization, contributing to shock and refractory hypotension.
Diagnosis
Signs and Symptoms
Cardiovascular manifestations include hypotension, bradycardia, reflex tachycardia (particularly with dihydropyridines), conduction delays, and high-grade heart blocks. Neurologic findings include altered mental status, agitation, seizures, and coma. Metabolic abnormalities include hyperglycemia and metabolic acidosis. Patients may appear warm rather than cool despite shock.
Essential Workup
A 12-lead ECG is mandatory to evaluate for bradycardia, QRS prolongation, and heart block. Continuous cardiac and hemodynamic monitoring is required.
Diagnostic Tests and Interpretation
Laboratory evaluation includes serum electrolytes, BUN, creatinine, glucose, CBC, and ionized calcium levels when calcium therapy is administered. Digoxin levels should be obtained in patients on digoxin prior to calcium administration. Hyperglycemia in the setting of bradycardia and hypotension strongly suggests CCB poisoning. Toxicology screening should be considered if co-ingestants are suspected.
Differential Diagnosis
β-blocker toxicity, clonidine toxicity, digoxin toxicity, and acute myocardial infarction with heart block.
Management
Prehospital Care
Transport all pill bottles to the emergency department. Administer calcium in unstable patients when CCB overdose is suspected.
Initial Stabilization and Therapy
Initial management follows ABC principles with early airway protection as needed. Supplemental oxygen, IV access with isotonic fluids, and continuous cardiac monitoring are essential.
Emergency Department Management
Therapeutic goals include maintaining heart rate above 60 beats/min, systolic blood pressure above 90 mm Hg, adequate urine output, and improving mental status. Syrup of ipecac is contraindicated. Activated charcoal may be considered early, particularly in sustained-release ingestions or co-ingestants.
Calcium therapy provides transient improvement. Calcium gluconate is preferred due to reduced tissue toxicity, while calcium chloride is more potent but risks extravasation injury. Calcium is contraindicated in digoxin toxicity. IV fluids should be administered cautiously. Atropine is usually ineffective.
High-dose insulin euglycemia therapy is a cornerstone of treatment, improving myocardial carbohydrate utilization and hemodynamics. Vasopressors such as dopamine, epinephrine, or norepinephrine may be required. Amrinone may improve inotropy. Electrical pacing is reserved for refractory cases. IV lipid emulsion and hypertonic sodium bicarbonate may be considered as rescue therapies.
Disposition and Follow-Up
Patients with symptoms or sustained-release ingestion require admission to a monitored setting. Asymptomatic patients who ingest immediate-release formulations may be discharged after 8 hours of observation. Psychiatric evaluation is required for intentional overdoses. Caregiver education is essential for pediatric exposures
Clinical Pearls and Pitfalls
Consider CCB toxicity in any patient presenting with unexplained hypotension, bradycardia, and hyperglycemia. Do not rely on atropine alone. Early initiation of high-dose insulin therapy improves outcomes. Sustained-release preparations may cause delayed and prolonged toxicity.
- Published on
Emergency and Acute Medicine – Atrial Flutter
Clinical Overview
Atrial flutter is an atrial dysrhythmia affecting approximately 200,000 new patients annually. It is most commonly caused by a macroreentrant circuit within the right atrium and is considered the atrial arrhythmia most sensitive to cardioversion. Atrial flutter rarely occurs in the absence of underlying structural or organic heart disease and is less common than supraventricular tachycardia or atrial fibrillation. Episodes are typically paroxysmal, lasting seconds to hours, and atrial flutter is present in roughly 25–35% of patients who also have atrial fibrillation. When untreated, it may contribute to the development of tachycardia-induced cardiomyopathy.
Etiology And Predisposing Conditions
Common causes include alcoholism, cardiomyopathies, myocarditis, congestive heart failure, electrolyte disturbances, ischemic heart disease, pulmonary embolism and other pulmonary diseases, valvular heart disease, postoperative states following cardiac surgery—most frequently during the first postoperative week—and thyrotoxicosis.
In pediatric patients, atrial flutter may occur and is often asymptomatic. Mortality is highest during the neonatal period. It is commonly associated with congenital heart disease or infectious causes such as rheumatic fever or myocarditis. Toxic ingestions must be considered in children presenting with new atrioventricular conduction abnormalities.
Clinical Presentation
Patients may experience palpitations, syncope or presyncope, chest pain, fatigue, dyspnea, reduced exercise tolerance, and tachycardia often exceeding 150 beats per minute. Severe presentations may include hypotension or heart failure.
Infants tolerate atrial flutter poorly because the atrioventricular node may conduct very rapidly, leading to extreme ventricular rates that can result in shock or congestive heart failure. Atrial flutter can occur in fetuses and neonates without associated cardiac defects and often does not recur beyond the neonatal period. In contrast, older children usually have structural heart disease, with higher recurrence rates and more difficult rhythm control.
Initial Evaluation
Essential evaluation includes electrocardiography, laboratory studies, and chest radiography. The ECG confirms the diagnosis and guides management. Laboratory testing should include electrolytes and mineral panels, cardiac enzymes, digoxin levels when relevant, and coagulation studies. Chest radiography may reveal cardiomyopathy or evidence of heart failure. Echocardiography is useful for identifying regional wall motion abnormalities or valvular dysfunction.
Differential Diagnosis
Important considerations include supraventricular tachycardia, sinus tachycardia, atrial fibrillation, multifocal atrial tachycardia, and ventricular tachycardia.
Prehospital And Immediate Management
Initial management includes oxygen administration, cardiac monitoring, and intravenous access. Hemodynamically unstable patients should undergo immediate synchronized cardioversion in the field, typically starting at 100 joules.
Emergency Department Management
Unstable patients require immediate synchronized cardioversion. Current guidelines recommend beginning at 150–200 joules to improve first-shock success and reduce cumulative energy exposure.
Rate control should be achieved before administering antidysrhythmic agents to prevent 1:1 atrioventricular conduction and possible hemodynamic collapse, though adequate rate control can be challenging. Anticoagulation follows the same principles as atrial fibrillation, with therapeutic anticoagulation for at least three weeks prior to cardioversion when symptom duration exceeds 48 hours or is unknown, and continuation afterward even if transesophageal echocardiography is negative. Thromboembolic risk ranges from 1.7% to 7%.
Stroke risk stratification using the CHADS₂ score guides anticoagulation decisions. Patients with valvular disease, fluctuating atrial fibrillation/flutter, left ventricular dysfunction, prior stroke or thromboembolism, or symptom duration longer than 48 hours carry higher embolic risk.
Pharmacologic And Rhythm Control Options
Adenosine rarely terminates atrial flutter but may help unmask flutter waves diagnostically. Amiodarone is useful for rate control in pre-excited atrial arrhythmias and is preferred in patients with severe ventricular dysfunction, though hypotension and bradycardia may occur with rapid infusion. Calcium channel blockers and beta-blockers are effective for rate control, with verapamil associated with higher rates of hypotension and limited to narrow-complex arrhythmias. Magnesium sulfate may assist with rate control, though evidence is limited. Digoxin is a third-line agent with delayed onset but may benefit patients with ventricular dysfunction.
For rhythm control, procainamide is preferred in patients with Wolff–Parkinson–White syndrome and preserved ventricular function, though caution is required in QT prolongation. Sotalol and ibutilide may be used for rhythm conversion when arrhythmia duration is 48 hours or less and ventricular function is preserved. Ibutilide requires correction of electrolytes prior to use and post-administration monitoring due to the risk of torsades de pointes. Electrical cardioversion remains the safest and most effective method for restoring sinus rhythm.
Maintenance of sinus rhythm is challenging due to a high recurrence rate approaching 50% at one year. Amiodarone is the most effective pharmacologic agent. Catheter ablation offers acute success rates exceeding 95% with low complication rates and is recommended for recurrent, drug-resistant atrial flutter, medication intolerance, or patient preference to avoid long-term pharmacotherapy.
Pediatric Management Considerations
Verapamil is contraindicated in infants and young children due to the risk of severe cardiovascular compromise. Digoxin is the first-line pharmacologic therapy in pediatric atrial flutter. Cardioversion is often the preferred initial treatment in neonates.
Disposition And Follow-Up
Admission is indicated for new-onset atrial flutter requiring antidysrhythmic therapy, persistent symptoms, heart failure, or need for cardioversion. Discharge may be appropriate when rhythm or rate is controlled, underlying causes are addressed, anticoagulation is initiated, and reliable follow-up is arranged. Chronic atrial flutter patients with stable control and anticoagulation may be managed as outpatients. Cardiology follow-up is recommended, with catheter ablation increasingly serving as definitive therapy.
Key Clinical Insights And Safety Considerations
Wolff–Parkinson–White syndrome must always be excluded, as adenosine, beta-blockers, calcium channel blockers, and digoxin can precipitate ventricular fibrillation in these patients. Cardioversion should never be delayed in unstable patients for intravenous access. Beta-blockers must be used cautiously in those with pulmonary disease or heart failure. Management priorities include rate control, prevention of systemic embolization, restoration of sinus rhythm, and maintenance of long-term rhythm stability.
Clinical Overview
Atrial flutter is an atrial dysrhythmia affecting approximately 200,000 new patients annually. It is most commonly caused by a macroreentrant circuit within the right atrium and is considered the atrial arrhythmia most sensitive to cardioversion. Atrial flutter rarely occurs in the absence of underlying structural or organic heart disease and is less common than supraventricular tachycardia or atrial fibrillation. Episodes are typically paroxysmal, lasting seconds to hours, and atrial flutter is present in roughly 25–35% of patients who also have atrial fibrillation. When untreated, it may contribute to the development of tachycardia-induced cardiomyopathy.
Etiology And Predisposing Conditions
Common causes include alcoholism, cardiomyopathies, myocarditis, congestive heart failure, electrolyte disturbances, ischemic heart disease, pulmonary embolism and other pulmonary diseases, valvular heart disease, postoperative states following cardiac surgery—most frequently during the first postoperative week—and thyrotoxicosis.
In pediatric patients, atrial flutter may occur and is often asymptomatic. Mortality is highest during the neonatal period. It is commonly associated with congenital heart disease or infectious causes such as rheumatic fever or myocarditis. Toxic ingestions must be considered in children presenting with new atrioventricular conduction abnormalities.
Clinical Presentation
Patients may experience palpitations, syncope or presyncope, chest pain, fatigue, dyspnea, reduced exercise tolerance, and tachycardia often exceeding 150 beats per minute. Severe presentations may include hypotension or heart failure.
Infants tolerate atrial flutter poorly because the atrioventricular node may conduct very rapidly, leading to extreme ventricular rates that can result in shock or congestive heart failure. Atrial flutter can occur in fetuses and neonates without associated cardiac defects and often does not recur beyond the neonatal period. In contrast, older children usually have structural heart disease, with higher recurrence rates and more difficult rhythm control.
Initial Evaluation
Essential evaluation includes electrocardiography, laboratory studies, and chest radiography. The ECG confirms the diagnosis and guides management. Laboratory testing should include electrolytes and mineral panels, cardiac enzymes, digoxin levels when relevant, and coagulation studies. Chest radiography may reveal cardiomyopathy or evidence of heart failure. Echocardiography is useful for identifying regional wall motion abnormalities or valvular dysfunction.
Differential Diagnosis
Important considerations include supraventricular tachycardia, sinus tachycardia, atrial fibrillation, multifocal atrial tachycardia, and ventricular tachycardia.
Prehospital And Immediate Management
Initial management includes oxygen administration, cardiac monitoring, and intravenous access. Hemodynamically unstable patients should undergo immediate synchronized cardioversion in the field, typically starting at 100 joules.
Emergency Department Management
Unstable patients require immediate synchronized cardioversion. Current guidelines recommend beginning at 150–200 joules to improve first-shock success and reduce cumulative energy exposure.
Rate control should be achieved before administering antidysrhythmic agents to prevent 1:1 atrioventricular conduction and possible hemodynamic collapse, though adequate rate control can be challenging. Anticoagulation follows the same principles as atrial fibrillation, with therapeutic anticoagulation for at least three weeks prior to cardioversion when symptom duration exceeds 48 hours or is unknown, and continuation afterward even if transesophageal echocardiography is negative. Thromboembolic risk ranges from 1.7% to 7%.
Stroke risk stratification using the CHADS₂ score guides anticoagulation decisions. Patients with valvular disease, fluctuating atrial fibrillation/flutter, left ventricular dysfunction, prior stroke or thromboembolism, or symptom duration longer than 48 hours carry higher embolic risk.
Pharmacologic And Rhythm Control Options
Adenosine rarely terminates atrial flutter but may help unmask flutter waves diagnostically. Amiodarone is useful for rate control in pre-excited atrial arrhythmias and is preferred in patients with severe ventricular dysfunction, though hypotension and bradycardia may occur with rapid infusion. Calcium channel blockers and beta-blockers are effective for rate control, with verapamil associated with higher rates of hypotension and limited to narrow-complex arrhythmias. Magnesium sulfate may assist with rate control, though evidence is limited. Digoxin is a third-line agent with delayed onset but may benefit patients with ventricular dysfunction.
For rhythm control, procainamide is preferred in patients with Wolff–Parkinson–White syndrome and preserved ventricular function, though caution is required in QT prolongation. Sotalol and ibutilide may be used for rhythm conversion when arrhythmia duration is 48 hours or less and ventricular function is preserved. Ibutilide requires correction of electrolytes prior to use and post-administration monitoring due to the risk of torsades de pointes. Electrical cardioversion remains the safest and most effective method for restoring sinus rhythm.
Maintenance of sinus rhythm is challenging due to a high recurrence rate approaching 50% at one year. Amiodarone is the most effective pharmacologic agent. Catheter ablation offers acute success rates exceeding 95% with low complication rates and is recommended for recurrent, drug-resistant atrial flutter, medication intolerance, or patient preference to avoid long-term pharmacotherapy.
Pediatric Management Considerations
Verapamil is contraindicated in infants and young children due to the risk of severe cardiovascular compromise. Digoxin is the first-line pharmacologic therapy in pediatric atrial flutter. Cardioversion is often the preferred initial treatment in neonates.
Disposition And Follow-Up
Admission is indicated for new-onset atrial flutter requiring antidysrhythmic therapy, persistent symptoms, heart failure, or need for cardioversion. Discharge may be appropriate when rhythm or rate is controlled, underlying causes are addressed, anticoagulation is initiated, and reliable follow-up is arranged. Chronic atrial flutter patients with stable control and anticoagulation may be managed as outpatients. Cardiology follow-up is recommended, with catheter ablation increasingly serving as definitive therapy.
Key Clinical Insights And Safety Considerations
Wolff–Parkinson–White syndrome must always be excluded, as adenosine, beta-blockers, calcium channel blockers, and digoxin can precipitate ventricular fibrillation in these patients. Cardioversion should never be delayed in unstable patients for intravenous access. Beta-blockers must be used cautiously in those with pulmonary disease or heart failure. Management priorities include rate control, prevention of systemic embolization, restoration of sinus rhythm, and maintenance of long-term rhythm stability.
- Published on
Emergency And Acute Medicine - Ankylosing Spondylitis
Core Overview: Ankylosing spondylitis (AS) is a chronic inflammatory condition that primarily targets the axial skeleton, with a strong predilection for the sacroiliac (SI) joints and spine (SI joints ~100%, cervical ~75%, thoracic ~70%, lumbosacral ~50%; hips and shoulders each ~30%). Inflammation begins at vertebral entheses (outer annulus fibrosus insertions); progressive ossification with syndesmophyte formation can lead to fusion (ankylosis) and the classic brittle “bamboo spine” appearance on imaging. Typical onset is age 15–35 years, with a male predominance (about 2–3:1). ALERT: Patients with AS have markedly increased risk of spinal fracture and paralysis—serious injury can occur after relatively minor trauma.
Risk Profile: Genetics are strongly associated with AS; HLA-B27 is present in roughly 80–90% of affected patients.
Likely Cause: AS is thought to be triggered by environmental factors (often presumed infectious exposures) in genetically predisposed individuals.
Clinical Presentation: The most common presentation is inflammatory low back pain with sacroiliitis—often worse with rest and improved with movement/exercise, and may wake the patient in the second half of the night. Because the spine may be rigid and brittle, patients are at higher risk for major injury from low-energy mechanisms. Extraspinal inflammatory manifestations may occur and sometimes precede spinal symptoms, including uveitis (common; often acute, unilateral, alternating), mild increased CAD risk and valvular disease over time, restrictive lung disease from limited chest expansion and fibrosis, GI associations (notably inflammatory bowel disease in a minority), and renal risks (IgA nephropathy/amyloidosis and NSAID-related nephropathy). Enthesitis is common, frequently presenting as Achilles tendinopathy or plantar fasciitis.
History And Examination: History often features insidious back pain for >3 months in patients <40 years, radiating into the gluteal region from si area and gradually involving more of spine; ask about prior uveitis, ibd, pulmonary restriction, enthesitis, or migrating />olyarthritis. On exam, SI joint tenderness may be reproduced with direct pressure over both ASIS simultaneously; additional findings can include enthesitis or dactylitis, loss of lumbar lordosis, increased thoracic kyphosis, reduced spinal mobility, and decreased chest expansion. Pediatric Note: Juvenile AS (often boys, late childhood/adolescence) may be mistaken for recurrent sprains; it more commonly involves extraspinal joints and lower-extremity entheses—look for asymmetric pauciarthritis and ankle/knee/tarsal enthesitis, plantar fasciitis, and Achilles tendinopathy.
Key Emergency Evaluation: In any patient with known or suspected AS who develops new spinal pain (even without clear trauma), prioritize exclusion of fracture and neurologic injury; also exclude sepsis or septic joint when clinically suspected. Sacroiliitis can be assessed with pelvic compression (“pelvic rock”) or Patrick/FABER-type maneuvers that stress the SI region.
Investigations And Interpretation: CBC may show mild leukocytosis, mild–moderate anemia, and thrombocytosis; BMP can help assess renal involvement, and ESR/CRP may be elevated but are not reliably decisive in the ED. HLA-B27 testing is typically arranged by specialists and a negative result does not exclude AS. Pelvic radiographs are appropriate when undiagnosed AS is suspected; early sacroiliitis may appear as iliac-side subchondral erosions that later progress to sclerosis and bony proliferation—if plain films are unrevealing and suspicion remains, MRI should be considered. For any new spinal pain, obtain spine imaging to exclude fracture; CT is often needed to further evaluate suspected fractures, and MRI is urgent when neurologic deficits are present. CXR may show apical fibrosis or patchy inflammatory changes. ECG is reasonable with ACS symptoms or arrhythmia concerns (including AV block), and echocardiography is indicated for a new murmur or new heart-failure evidence given the increased risk of aortic insufficiency over time.
Conditions To Distinguish From AS: Consider juvenile AS (onset <20 with more enthesitis />xtraspinal involvement), reactive arthritis, enteropathic arthritis (Crohn/UC-associated), psoriatic arthritis (rash; dactylitis), septic arthritis (arthrocentesis if suspected monoarthritis), mechanical low back pain (improves with rest; worsens with exertion; lacks systemic inflammatory features), spinal epidural abscess (often constant, severe, may have fever/IVDA/immunosuppression), and neoplastic back pain (older age, night pain, persistent/unremitting).
Prehospital Priorities: ALERT: Because minor trauma can cause unstable spinal injury, immobilization should avoid forcing the spine into a neutral position; cushioning and transport in the position of comfort (e.g., scoop stretcher with padding) may be safer than rigid collar/backboard alone. Anticipate difficult airway management due to cervical/TMJ limitation—fiberoptic techniques are often preferred; consider temporizing strategies (e.g., LMA or BVM with airway adjunct) until a definitive airway can be secured safely. Ventilation may be challenging due to chest-wall restriction and fibrosis, and CPR may carry higher rib-fracture risk.
Emergency Department Management: If cord compression is suspected, obtain MRI urgently. For any new spinal pain, aggressively evaluate for fracture—CT may be required even when initial radiographs are unrevealing. If infection is a concern, pursue labs and arthrocentesis as indicated. Treat pain and inflammation, typically starting with NSAIDs when appropriate.
Medications: Use nonselective NSAIDs such as ibuprofen, indomethacin (often limited by GI/CNS adverse effects), or naproxen; COX-2 inhibitors (e.g., celecoxib) can be considered, especially when GI bleeding risk is elevated. TNF-α inhibitors (e.g., adalimumab, etanercept) are disease-modifying options typically initiated in specialist care. In pregnancy, avoid NSAIDs when possible—use acetaminophen first-line and opioids second-line if needed. In older adults, weigh NSAID risks (CV, GI bleed, renal injury, hypertension) and consider gastroprotection (H2 blocker/PPI) or COX-2 selection when appropriate. If NSAIDs/acetaminophen are ineffective at appropriate doses, second-line options may include opioid analgesics, muscle relaxants, or short courses of low-dose steroids in select cases.
Disposition Planning: Admit for acute neurologic deficits, uncontrolled pain, or when sepsis/septic joint cannot be excluded. Discharge may be reasonable when serious injury and neurologic deficit have been ruled out and pain is controlled to a safe level.
Referral And Follow-Up: Encourage a medical alert bracelet due to high trauma risk. Arrange rheumatology referral for suspected new AS or for escalation to immunomodulating therapy, and consider physical medicine/rehab for splints and orthoses (e.g., heel cushioning to unload Achilles enthesis). Advise primary care reassessment within 1–2 weeks to gauge response, with earlier review for patients at higher risk of NSAID complications (elderly, hypertensive, high GI-bleed risk).
Clinical Tips And Common Traps: Anticipate a difficult airway and avoid neck repositioning because cervical instability and severe rigidity can make standard techniques hazardous—use airway adjuncts and pursue fiberoptic intubation when feasible. Immobilization should prioritize the patient’s position of comfort with padding rather than forcing standard collar/backboard alignment. Maintain high suspicion for fracture and cord injury after even low-energy trauma, as seemingly minor mechanisms can cause catastrophic spinal injury in AS.
Core Overview: Ankylosing spondylitis (AS) is a chronic inflammatory condition that primarily targets the axial skeleton, with a strong predilection for the sacroiliac (SI) joints and spine (SI joints ~100%, cervical ~75%, thoracic ~70%, lumbosacral ~50%; hips and shoulders each ~30%). Inflammation begins at vertebral entheses (outer annulus fibrosus insertions); progressive ossification with syndesmophyte formation can lead to fusion (ankylosis) and the classic brittle “bamboo spine” appearance on imaging. Typical onset is age 15–35 years, with a male predominance (about 2–3:1). ALERT: Patients with AS have markedly increased risk of spinal fracture and paralysis—serious injury can occur after relatively minor trauma.
Risk Profile: Genetics are strongly associated with AS; HLA-B27 is present in roughly 80–90% of affected patients.
Likely Cause: AS is thought to be triggered by environmental factors (often presumed infectious exposures) in genetically predisposed individuals.
Clinical Presentation: The most common presentation is inflammatory low back pain with sacroiliitis—often worse with rest and improved with movement/exercise, and may wake the patient in the second half of the night. Because the spine may be rigid and brittle, patients are at higher risk for major injury from low-energy mechanisms. Extraspinal inflammatory manifestations may occur and sometimes precede spinal symptoms, including uveitis (common; often acute, unilateral, alternating), mild increased CAD risk and valvular disease over time, restrictive lung disease from limited chest expansion and fibrosis, GI associations (notably inflammatory bowel disease in a minority), and renal risks (IgA nephropathy/amyloidosis and NSAID-related nephropathy). Enthesitis is common, frequently presenting as Achilles tendinopathy or plantar fasciitis.
History And Examination: History often features insidious back pain for >3 months in patients <40 years, radiating into the gluteal region from si area and gradually involving more of spine; ask about prior uveitis, ibd, pulmonary restriction, enthesitis, or migrating />olyarthritis. On exam, SI joint tenderness may be reproduced with direct pressure over both ASIS simultaneously; additional findings can include enthesitis or dactylitis, loss of lumbar lordosis, increased thoracic kyphosis, reduced spinal mobility, and decreased chest expansion. Pediatric Note: Juvenile AS (often boys, late childhood/adolescence) may be mistaken for recurrent sprains; it more commonly involves extraspinal joints and lower-extremity entheses—look for asymmetric pauciarthritis and ankle/knee/tarsal enthesitis, plantar fasciitis, and Achilles tendinopathy.
Key Emergency Evaluation: In any patient with known or suspected AS who develops new spinal pain (even without clear trauma), prioritize exclusion of fracture and neurologic injury; also exclude sepsis or septic joint when clinically suspected. Sacroiliitis can be assessed with pelvic compression (“pelvic rock”) or Patrick/FABER-type maneuvers that stress the SI region.
Investigations And Interpretation: CBC may show mild leukocytosis, mild–moderate anemia, and thrombocytosis; BMP can help assess renal involvement, and ESR/CRP may be elevated but are not reliably decisive in the ED. HLA-B27 testing is typically arranged by specialists and a negative result does not exclude AS. Pelvic radiographs are appropriate when undiagnosed AS is suspected; early sacroiliitis may appear as iliac-side subchondral erosions that later progress to sclerosis and bony proliferation—if plain films are unrevealing and suspicion remains, MRI should be considered. For any new spinal pain, obtain spine imaging to exclude fracture; CT is often needed to further evaluate suspected fractures, and MRI is urgent when neurologic deficits are present. CXR may show apical fibrosis or patchy inflammatory changes. ECG is reasonable with ACS symptoms or arrhythmia concerns (including AV block), and echocardiography is indicated for a new murmur or new heart-failure evidence given the increased risk of aortic insufficiency over time.
Conditions To Distinguish From AS: Consider juvenile AS (onset <20 with more enthesitis />xtraspinal involvement), reactive arthritis, enteropathic arthritis (Crohn/UC-associated), psoriatic arthritis (rash; dactylitis), septic arthritis (arthrocentesis if suspected monoarthritis), mechanical low back pain (improves with rest; worsens with exertion; lacks systemic inflammatory features), spinal epidural abscess (often constant, severe, may have fever/IVDA/immunosuppression), and neoplastic back pain (older age, night pain, persistent/unremitting).
Prehospital Priorities: ALERT: Because minor trauma can cause unstable spinal injury, immobilization should avoid forcing the spine into a neutral position; cushioning and transport in the position of comfort (e.g., scoop stretcher with padding) may be safer than rigid collar/backboard alone. Anticipate difficult airway management due to cervical/TMJ limitation—fiberoptic techniques are often preferred; consider temporizing strategies (e.g., LMA or BVM with airway adjunct) until a definitive airway can be secured safely. Ventilation may be challenging due to chest-wall restriction and fibrosis, and CPR may carry higher rib-fracture risk.
Emergency Department Management: If cord compression is suspected, obtain MRI urgently. For any new spinal pain, aggressively evaluate for fracture—CT may be required even when initial radiographs are unrevealing. If infection is a concern, pursue labs and arthrocentesis as indicated. Treat pain and inflammation, typically starting with NSAIDs when appropriate.
Medications: Use nonselective NSAIDs such as ibuprofen, indomethacin (often limited by GI/CNS adverse effects), or naproxen; COX-2 inhibitors (e.g., celecoxib) can be considered, especially when GI bleeding risk is elevated. TNF-α inhibitors (e.g., adalimumab, etanercept) are disease-modifying options typically initiated in specialist care. In pregnancy, avoid NSAIDs when possible—use acetaminophen first-line and opioids second-line if needed. In older adults, weigh NSAID risks (CV, GI bleed, renal injury, hypertension) and consider gastroprotection (H2 blocker/PPI) or COX-2 selection when appropriate. If NSAIDs/acetaminophen are ineffective at appropriate doses, second-line options may include opioid analgesics, muscle relaxants, or short courses of low-dose steroids in select cases.
Disposition Planning: Admit for acute neurologic deficits, uncontrolled pain, or when sepsis/septic joint cannot be excluded. Discharge may be reasonable when serious injury and neurologic deficit have been ruled out and pain is controlled to a safe level.
Referral And Follow-Up: Encourage a medical alert bracelet due to high trauma risk. Arrange rheumatology referral for suspected new AS or for escalation to immunomodulating therapy, and consider physical medicine/rehab for splints and orthoses (e.g., heel cushioning to unload Achilles enthesis). Advise primary care reassessment within 1–2 weeks to gauge response, with earlier review for patients at higher risk of NSAID complications (elderly, hypertensive, high GI-bleed risk).
Clinical Tips And Common Traps: Anticipate a difficult airway and avoid neck repositioning because cervical instability and severe rigidity can make standard techniques hazardous—use airway adjuncts and pursue fiberoptic intubation when feasible. Immobilization should prioritize the patient’s position of comfort with padding rather than forcing standard collar/backboard alignment. Maintain high suspicion for fracture and cord injury after even low-energy trauma, as seemingly minor mechanisms can cause catastrophic spinal injury in AS.
- Published on
Emergency and Acute Medicine – Pediatric Apnea
Definition and Clinical Overview
Pediatric apnea is defined as the absence of effective respiratory airflow for ≥20 seconds or a shorter pause associated with bradycardia or oxygen desaturation. It represents a medical emergency that may signal underlying neurologic, respiratory, cardiac, metabolic, infectious, or traumatic pathology. Apnea may present as an isolated event or as part of an apparent life-threatening event (ALTE), which describes a clinical presentation rather than a definitive diagnosis.
Pathophysiologic Mechanisms
Central apnea results from impaired respiratory drive due to dysfunction of the brainstem or neuromuscular pathways. Obstructive apnea occurs when respiratory effort persists but airflow is blocked because of upper airway obstruction, often accompanied by paradoxical chest wall motion. Mixed apnea combines both mechanisms. ALTEs involve apnea associated with color change, altered tone, choking, or gagging and require careful evaluation to identify the underlying cause.
Etiologic Considerations
Apnea has a broad differential diagnosis. Infectious causes include sepsis, meningitis, encephalitis, pneumonia, pertussis, chlamydia, RSV, and other viral infections. Respiratory causes include enlarged tonsils or adenoids, vocal cord dysfunction, laryngotracheomalacia, vascular rings, foreign bodies, craniofacial abnormalities, and choanal atresia or stenosis, as well as functional airway collapse in premature or ill infants. Neurologic etiologies include seizures, intracranial hemorrhage, increased intracranial pressure, tumors, congenital CNS malformations, and hypoxic injury. Cardiac causes include dysrhythmias, congenital heart disease, myocarditis, cardiomyopathy, and heart failure. Gastrointestinal causes include gastroesophageal reflux, volvulus, and intussusception. Additional considerations include ingestions or toxins, metabolic and endocrine disorders, neuromuscular disease, child abuse, transient choking episodes, laryngospasm, periodic breathing, and breath-holding spells.
Clinical Presentation
Apnea may be ongoing, reported historically, or impending. The presentation may range from brief self-limited events to prolonged respiratory arrest requiring immediate intervention.
History Assessment
Key elements include duration and frequency of apnea, state at onset (sleeping, awake, crying), relationship to feeding or positioning, degree of respiratory effort, presence and distribution of color change, eye position, abnormal movements or tone changes, and caregiver interventions. Antecedent symptoms such as fever, cough, or trauma should be elicited, along with prior medical history including prematurity, cardiopulmonary disease, neurologic disorders, gastrointestinal conditions, and prior ALTEs in the patient or family.
Physical Examination
Evaluation includes vital signs with temperature, growth trends, and continuous pulse oximetry. Airway and lung examination should assess for stridor, abnormal respiratory rates, accessory muscle use, and adventitious sounds. Cardiac examination focuses on rhythm abnormalities, murmurs, and signs of heart failure. A focused neurologic examination assesses mental status, tone, reflexes, seizure activity, signs of trauma, and funduscopic findings.
Initial Evaluation Priorities
A complete history and physical examination guide diagnostic testing and management. Immediate priorities include ensuring airway patency, clearing secretions or obstructions, and maintaining proper head and neck positioning, especially when occult trauma is a concern.
Diagnostic Studies
Laboratory evaluation is directed by clinical presentation and may include bedside glucose, CBC, urinalysis, blood, urine, and CSF cultures, CSF analysis, electrolytes including calcium, renal function tests, blood gas analysis, respiratory viral testing, pertussis and chlamydia studies, toxicology screening, liver function tests, and ammonia levels. Imaging may include chest radiography, head CT or MRI, ECG, and GI studies when indicated. EEG or polysomnography is typically reserved for follow-up evaluation. Skeletal survey should be considered when nonaccidental trauma is suspected.
Differential Diagnosis
The differential diagnosis is extensive and reflects the wide range of etiologies. Breath-holding spells are reflexive expiratory events seen in otherwise healthy children. Periodic breathing may be a normal finding in neonates. In newborns, occult infection—particularly sepsis—must always be strongly considered.
Prehospital and Emergency Management
If apnea is present, intervention must begin immediately. Management includes airway clearance, high-flow oxygen, bag-valve-mask ventilation, and endotracheal intubation if apnea persists. IV access and cardiac monitoring should be established, and empiric therapy initiated when indicated. Supportive care and caregiver counseling are essential components of management.
Disposition and Follow-Up
Most children with confirmed or suspected apnea require hospital admission for monitoring, particularly those with abnormal vital signs, concerning medical histories, or recurrent events. Intensive care is indicated for persistent instability. Discharge may be considered only in carefully selected low-risk patients who remain asymptomatic during observation and have reliable caregivers and clearly defined follow-up. Referral to primary care and appropriate subspecialists should be based on the suspected etiology.
Key Clinical Considerations and Common Pitfalls
Always maintain a high index of suspicion for hidden infection, especially neonatal sepsis. Unexplained apnea should also prompt careful evaluation for unrecognized trauma, as presentations may be subtle and easily overlooked.
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Emergency And Acute Medicine – Aphthous Ulcers
Overview:
Painful, ovoid or round ulcerations of the mucous membranes of the mouth, tongue, or genitals, commonly referred to as canker sores.
Etiology And Risk Factors:
The cause is unknown and likely multifactorial. Associations include immunologic dysfunction with altered cell-mediated immunity, infections, food hypersensitivities (e.g., gluten), vitamin deficiencies, pregnancy, menstruation, trauma, stress, ethnicity, immunodeficiency, and medications such as β-blockers and anti-inflammatory agents. Aphthous ulcers most commonly affect children and young adults, with peak onset between 10–19 years. They are the most common inflammatory ulcerative condition of the oral cavity, affecting 20–40% of the population, occur more frequently in women, and may be familial.
Clinical Features:
Minor aphthous ulcers account for 70–90% of cases and are typically <5 mm in diameter, painful, shallow, with necrotic centers, raised margins, erythematous halos, and a gray-white pseudomembrane. they affect non-keratinized mucosa of the anterior oral cavity heal within 10–14 days without scarring.< />pan>
Major aphthous ulcers (Sutton disease) are larger, deeper, more painful, last weeks to months, may scar, and are often associated with systemic disease.
Herpetiform aphthous ulcers present as clusters of numerous small ulcers that may coalesce; despite appearance, herpes simplex virus is not isolated.
History And Examination:
Patients often report a prodrome of burning or pricking 1–2 days before ulcer appearance. History should explore autoimmune disease, inflammatory bowel disease, Behçet disease, reactive arthritis, gluten sensitivity, HIV, malignancy, sexual history, and medication use. Examination focuses on oral lesions, hydration status, secondary infection, and signs of systemic disease.
Evaluation:
Diagnosis is clinical. Further workup is reserved for ulcers persisting longer than three weeks, recurrent severe disease, or associated systemic symptoms. Directed laboratory testing and biopsy may be indicated based on clinical suspicion.
Differential Considerations:
Trauma, medication reactions, viral and bacterial infections, erythema multiforme, autoimmune disease, inflammatory bowel disease, hematologic disorders, and malignancy must be considered, particularly in atypical or persistent cases.
Management Approach:
Treatment is guided by severity and duration, with the primary goal of pain control and inflammation reduction.
Therapeutic Options:
Mild to moderate disease is managed with avoidance of oral trauma and acidic foods, topical anesthetics, protective bioadhesives, topical anti-inflammatory agents, and antimicrobial mouth rinses.
Severe disease may require short courses of systemic corticosteroids or, in refractory cases, specialist-guided immunomodulatory therapy.
Disposition And Follow-Up:
Admission is reserved for patients unable to maintain oral intake, those with dehydration, or abnormal vital signs. Most patients may be discharged once pain is controlled and fluids are tolerated. Persistent lesions beyond two weeks warrant outpatient follow-up and further evaluation.
Clinical Pearls And Pitfalls:
Most aphthous ulcers are benign and self-limited, requiring only symptomatic care. Emergency clinicians should remain vigilant for underlying systemic disease in patients with severe, atypical, or persistent ulcerations.
Overview:
Painful, ovoid or round ulcerations of the mucous membranes of the mouth, tongue, or genitals, commonly referred to as canker sores.
Etiology And Risk Factors:
The cause is unknown and likely multifactorial. Associations include immunologic dysfunction with altered cell-mediated immunity, infections, food hypersensitivities (e.g., gluten), vitamin deficiencies, pregnancy, menstruation, trauma, stress, ethnicity, immunodeficiency, and medications such as β-blockers and anti-inflammatory agents. Aphthous ulcers most commonly affect children and young adults, with peak onset between 10–19 years. They are the most common inflammatory ulcerative condition of the oral cavity, affecting 20–40% of the population, occur more frequently in women, and may be familial.
Clinical Features:
Minor aphthous ulcers account for 70–90% of cases and are typically <5 mm in diameter, painful, shallow, with necrotic centers, raised margins, erythematous halos, and a gray-white pseudomembrane. they affect non-keratinized mucosa of the anterior oral cavity heal within 10–14 days without scarring.< />pan>
Major aphthous ulcers (Sutton disease) are larger, deeper, more painful, last weeks to months, may scar, and are often associated with systemic disease.
Herpetiform aphthous ulcers present as clusters of numerous small ulcers that may coalesce; despite appearance, herpes simplex virus is not isolated.
History And Examination:
Patients often report a prodrome of burning or pricking 1–2 days before ulcer appearance. History should explore autoimmune disease, inflammatory bowel disease, Behçet disease, reactive arthritis, gluten sensitivity, HIV, malignancy, sexual history, and medication use. Examination focuses on oral lesions, hydration status, secondary infection, and signs of systemic disease.
Evaluation:
Diagnosis is clinical. Further workup is reserved for ulcers persisting longer than three weeks, recurrent severe disease, or associated systemic symptoms. Directed laboratory testing and biopsy may be indicated based on clinical suspicion.
Differential Considerations:
Trauma, medication reactions, viral and bacterial infections, erythema multiforme, autoimmune disease, inflammatory bowel disease, hematologic disorders, and malignancy must be considered, particularly in atypical or persistent cases.
Management Approach:
Treatment is guided by severity and duration, with the primary goal of pain control and inflammation reduction.
Therapeutic Options:
Mild to moderate disease is managed with avoidance of oral trauma and acidic foods, topical anesthetics, protective bioadhesives, topical anti-inflammatory agents, and antimicrobial mouth rinses.
Severe disease may require short courses of systemic corticosteroids or, in refractory cases, specialist-guided immunomodulatory therapy.
Disposition And Follow-Up:
Admission is reserved for patients unable to maintain oral intake, those with dehydration, or abnormal vital signs. Most patients may be discharged once pain is controlled and fluids are tolerated. Persistent lesions beyond two weeks warrant outpatient follow-up and further evaluation.
Clinical Pearls And Pitfalls:
Most aphthous ulcers are benign and self-limited, requiring only symptomatic care. Emergency clinicians should remain vigilant for underlying systemic disease in patients with severe, atypical, or persistent ulcerations.
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Emergency And Acute Medicine – Traumatic Aortic Rupture (Traumatic Aortic Injury)
Core Overview:
Traumatic aortic rupture, also termed traumatic aortic injury (TAI), is responsible for approximately 20% of deaths from fatal motor vehicle collisions. Nearly 85% of affected patients die at the scene. Those who reach the emergency department typically have a contained rupture, with hemorrhage temporarily tamponaded by the adventitia. Without intervention, mortality remains extremely high: nearly half die within 24 hours and up to 90% within four months. The mean patient age is 33 years, with a strong male predominance. Aortic tears are most often transverse and may be partial or circumferential.
Mechanisms Of Injury:
High-speed motor vehicle collisions exceeding 30 mph are the most common cause, particularly involving unrestrained occupants, drivers impacted by the steering column, or ejected passengers. Other mechanisms include pedestrian–vehicle collisions, aviation crashes, falls greater than 10 feet, blast injuries, crush injuries, and direct chest trauma. Proposed pathophysiologic mechanisms include shear stress from rapid deceleration between the fixed descending aorta and mobile arch, bending forces at the aortic isthmus, torsional stretching of the arch, compression between osseous structures and the vertebral column, and acute intravascular pressure surges (“waterhammer” effect).
Clinical Presentation:
Despite the severity of injury, manifestations are frequently subtle or absent, especially in polytrauma patients. Up to half have no external signs of chest trauma. Substernal chest pain occurs in only about one-quarter of cases. Dyspnea, hoarseness, and stridor may result from mediastinal hematoma compressing adjacent structures. Examination findings are neither sensitive nor specific. Patients may exhibit hypertension due to sympathetic stimulation, a harsh systolic murmur, signs of distal ischemia, oliguria, paraplegia, or neck base swelling. Acute coarctation physiology may develop, producing upper-extremity hypertension with reduced lower-extremity pressures.
Initial Evaluation Priorities:
Plain chest radiography is the primary screening tool and is highly sensitive, though poorly specific. A widened mediastinum is the most sensitive radiographic sign. Because false-negative radiographs occur in up to 10% of cases, high-risk mechanisms warrant advanced imaging even with a normal chest x-ray.
Diagnostic Assessment:
Laboratory studies include CBC, chemistry panel, coagulation studies, and type and crossmatch.
Chest radiography findings may include mediastinal widening, obscured aortic knob, left apical cap, abnormal paratracheal stripes, or displaced nasogastric tube.
CT angiography of the chest is the preferred confirmatory test in hemodynamically stable patients, with near-perfect sensitivity and specificity, and has largely replaced aortography.
Transesophageal echocardiography can be performed rapidly in the ED and is useful when CT is not immediately available. MRI and intravascular ultrasound are accurate but limited by availability and monitoring constraints.
Important Diagnostic Alternatives:
False-positive mediastinal widening on supine films, mediastinal hematoma from non-aortic sources, mediastinal tumors or lymphadenopathy, and age-related or hypertensive aortic tortuosity.
Prehospital Considerations:
Key scene details include collision speed, restraint use, steering column damage, and whether the patient was ejected.
Early Stabilization Strategy:
Follow standard trauma protocols with priority given to life-threatening intracranial, intra-abdominal, or retroperitoneal injuries. Establish IV access and initiate monitoring promptly.
Definitive Emergency Management:
Immediate trauma and cardiothoracic or vascular surgery consultation is mandatory. Avoid actions that increase intrathoracic pressure. Aggressive control of heart rate and blood pressure is critical to minimize shearing forces and prevent rupture progression. Target heart rate is approximately 60 bpm with systolic blood pressure between 100–120 mm Hg. β-blockers are first-line agents, with calcium-channel blockers as alternatives when β-blockade is contraindicated. Vasodilators may be added only after adequate negative inotropy is achieved. Hypotension should be treated with blood products and vasopressors as needed.
Disposition Planning:
All patients with traumatic aortic injury require ICU admission or immediate operative management.
Clinical Pearls And Pitfalls:
Maintain a high index of suspicion for traumatic aortic injury in any patient exposed to rapid deceleration mechanisms, even when symptoms are minimal or absent. Physical findings are unreliable, making imaging essential for diagnosis. Careful evaluation of the mediastinum on chest radiography is critical, but a normal x-ray does not exclude injury. Early, controlled reduction of heart rate and blood pressure significantly lowers the risk of sudden rupture and improves outcomes once the diagnosis is established.
Core Overview:
Traumatic aortic rupture, also termed traumatic aortic injury (TAI), is responsible for approximately 20% of deaths from fatal motor vehicle collisions. Nearly 85% of affected patients die at the scene. Those who reach the emergency department typically have a contained rupture, with hemorrhage temporarily tamponaded by the adventitia. Without intervention, mortality remains extremely high: nearly half die within 24 hours and up to 90% within four months. The mean patient age is 33 years, with a strong male predominance. Aortic tears are most often transverse and may be partial or circumferential.
Mechanisms Of Injury:
High-speed motor vehicle collisions exceeding 30 mph are the most common cause, particularly involving unrestrained occupants, drivers impacted by the steering column, or ejected passengers. Other mechanisms include pedestrian–vehicle collisions, aviation crashes, falls greater than 10 feet, blast injuries, crush injuries, and direct chest trauma. Proposed pathophysiologic mechanisms include shear stress from rapid deceleration between the fixed descending aorta and mobile arch, bending forces at the aortic isthmus, torsional stretching of the arch, compression between osseous structures and the vertebral column, and acute intravascular pressure surges (“waterhammer” effect).
Clinical Presentation:
Despite the severity of injury, manifestations are frequently subtle or absent, especially in polytrauma patients. Up to half have no external signs of chest trauma. Substernal chest pain occurs in only about one-quarter of cases. Dyspnea, hoarseness, and stridor may result from mediastinal hematoma compressing adjacent structures. Examination findings are neither sensitive nor specific. Patients may exhibit hypertension due to sympathetic stimulation, a harsh systolic murmur, signs of distal ischemia, oliguria, paraplegia, or neck base swelling. Acute coarctation physiology may develop, producing upper-extremity hypertension with reduced lower-extremity pressures.
Initial Evaluation Priorities:
Plain chest radiography is the primary screening tool and is highly sensitive, though poorly specific. A widened mediastinum is the most sensitive radiographic sign. Because false-negative radiographs occur in up to 10% of cases, high-risk mechanisms warrant advanced imaging even with a normal chest x-ray.
Diagnostic Assessment:
Laboratory studies include CBC, chemistry panel, coagulation studies, and type and crossmatch.
Chest radiography findings may include mediastinal widening, obscured aortic knob, left apical cap, abnormal paratracheal stripes, or displaced nasogastric tube.
CT angiography of the chest is the preferred confirmatory test in hemodynamically stable patients, with near-perfect sensitivity and specificity, and has largely replaced aortography.
Transesophageal echocardiography can be performed rapidly in the ED and is useful when CT is not immediately available. MRI and intravascular ultrasound are accurate but limited by availability and monitoring constraints.
Important Diagnostic Alternatives:
False-positive mediastinal widening on supine films, mediastinal hematoma from non-aortic sources, mediastinal tumors or lymphadenopathy, and age-related or hypertensive aortic tortuosity.
Prehospital Considerations:
Key scene details include collision speed, restraint use, steering column damage, and whether the patient was ejected.
Early Stabilization Strategy:
Follow standard trauma protocols with priority given to life-threatening intracranial, intra-abdominal, or retroperitoneal injuries. Establish IV access and initiate monitoring promptly.
Definitive Emergency Management:
Immediate trauma and cardiothoracic or vascular surgery consultation is mandatory. Avoid actions that increase intrathoracic pressure. Aggressive control of heart rate and blood pressure is critical to minimize shearing forces and prevent rupture progression. Target heart rate is approximately 60 bpm with systolic blood pressure between 100–120 mm Hg. β-blockers are first-line agents, with calcium-channel blockers as alternatives when β-blockade is contraindicated. Vasodilators may be added only after adequate negative inotropy is achieved. Hypotension should be treated with blood products and vasopressors as needed.
Disposition Planning:
All patients with traumatic aortic injury require ICU admission or immediate operative management.
Clinical Pearls And Pitfalls:
Maintain a high index of suspicion for traumatic aortic injury in any patient exposed to rapid deceleration mechanisms, even when symptoms are minimal or absent. Physical findings are unreliable, making imaging essential for diagnosis. Careful evaluation of the mediastinum on chest radiography is critical, but a normal x-ray does not exclude injury. Early, controlled reduction of heart rate and blood pressure significantly lowers the risk of sudden rupture and improves outcomes once the diagnosis is established.
- Published on
Emergency And Acute Medicine – Antidepressant Poisoning
Core Overview: Antidepressants are among the most commonly prescribed psychiatric medications in the United States. Overdose presentations often involve selective serotonin reuptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs), or atypical antidepressants, frequently in combination with atypical antipsychotics or mood stabilizers. These agents are also prescribed for chronic pain, anxiety disorders, eating disorders, substance use disorders, and sleep disturbances. Tricyclic antidepressants are discussed separately.
Mechanisms And Causes:
SSRIs increase synaptic serotonin by inhibiting presynaptic reuptake (e.g., fluoxetine, paroxetine, sertraline, citalopram, escitalopram).
SNRIs inhibit reuptake of both serotonin and norepinephrine (e.g., venlafaxine, desvenlafaxine, duloxetine) and may be more toxic in overdose than initially assumed.
Atypical antidepressants have variable effects on serotonin, norepinephrine, and dopamine and include bupropion, trazodone, and mirtazapine.
Atypical antipsychotics act primarily on dopamine receptors with additional serotonergic, α-adrenergic, histaminic, and muscarinic effects. Many psychiatric medications can block potassium and sodium channels, resulting in QT or QRS prolongation and cardiotoxicity.
Clinical Features:
SSRIs commonly cause sedation and serotonin syndrome; most are benign in single-agent overdose, except citalopram and escitalopram, which may cause QTc prolongation, seizures, and delayed toxicity up to 12 hours.
SNRIs may cause somnolence, vomiting, tachycardia, seizures, and QTc prolongation, especially with venlafaxine and desvenlafaxine.
Atypical antidepressants: bupropion is associated with seizures and QRS/QTc prolongation; trazodone causes sedation, hypotension, QTc prolongation, and priapism; mirtazapine causes sedation and QTc prolongation, with rare neutropenia in chronic use.
Atypical antipsychotics typically cause sedation, tachycardia, and miosis, with drug-specific risks such as agranulocytosis and cardiomyopathy (clozapine), anticholinergic delirium (olanzapine, quetiapine), hypotension (quetiapine), QTc prolongation (ziprasidone), or prolonged CNS effects (aripiprazole).
Initial Assessment: Determine the specific agents, dose, timing, and possible coingestants. Check bedside glucose in patients with altered mental status.
Diagnostic Evaluation:
Laboratory drug levels are rarely helpful acutely. Obtain ECG to assess QRS and QTc intervals. Order electrolytes, renal function, glucose, urine pregnancy test when appropriate, urine drug screen (limited impact on management), acetaminophen and salicylate levels, and serum ethanol. CT brain imaging is reserved for unexplained depressed mental status; chest radiograph is indicated if intubated or hypoxic.
Key Differentials: TCA toxicity, ethanol or sedative–hypnotic overdose, isoniazid toxicity, hypoglycemia, hypoxemia, electrolyte disturbances, withdrawal syndromes, serotonin syndrome, head trauma, opioid intoxication, mood stabilizer or antiepileptic overdose, and diabetic ketoacidosis.
Prehospital Priorities: Transport all medication containers with the patient. Support airway, breathing, and circulation. Administer IV fluids for hypotension and benzodiazepines for seizures.
Early Stabilization: Provide oxygen, continuous cardiac monitoring, IV access, and pulse oximetry. Intubate if airway protection is needed. Check rapid glucose; administer naloxone or dextrose as clinically indicated. Flumazenil is not recommended in mixed or unknown overdoses or in patients with seizure risk. Treat extrapyramidal symptoms with diphenhydramine or benztropine.
Emergency Department Management: Avoid GI decontamination if the airway is unprotected; do not intubate solely for charcoal. Activated charcoal may be considered early after ingestion. Treat QRS widening with IV sodium bicarbonate boluses (continuous infusions are ineffective). Manage hypotension refractory to fluids with norepinephrine rather than dopamine. Treat seizures with benzodiazepines, escalating to barbiturates if refractory. Address serotonin syndrome with benzodiazepines and active cooling.
Medication Options: Activated charcoal 50–75 g PO (up to 100 g); benzodiazepines (diazepam or lorazepam) for seizures/agitation; diphenhydramine or benztropine for EPS; naloxone as indicated; norepinephrine infusion for hypotension; phenobarbital for refractory seizures; sodium bicarbonate 1 mEq/kg IV bolus for QRS widening.
Disposition Planning:
Admit for 24-hour telemetry after ingestion of citalopram, escitalopram, venlafaxine, desvenlafaxine, or bupropion, even if initially asymptomatic. Admit patients with coma, persistent altered mental status, ECG abnormalities, hemodynamic instability, or neuroleptic malignant syndrome. Suicidal patients require 1:1 observation.
Asymptomatic patients more than 6 hours after ingestion of less toxic antidepressants may be medically cleared for psychiatric admission if not suicidal.
Follow-Up Care: Psychiatry referral is required for intentional overdoses.
Clinical Pearls And Pitfalls: Administer IV sodium bicarbonate promptly for QRS widening. Overdoses involving citalopram, venlafaxine, and bupropion are more likely to cause severe toxicity and delayed complications, warranting medical observation before psychiatric clearance.
Core Overview: Antidepressants are among the most commonly prescribed psychiatric medications in the United States. Overdose presentations often involve selective serotonin reuptake inhibitors (SSRIs), serotonin–norepinephrine reuptake inhibitors (SNRIs), or atypical antidepressants, frequently in combination with atypical antipsychotics or mood stabilizers. These agents are also prescribed for chronic pain, anxiety disorders, eating disorders, substance use disorders, and sleep disturbances. Tricyclic antidepressants are discussed separately.
Mechanisms And Causes:
SSRIs increase synaptic serotonin by inhibiting presynaptic reuptake (e.g., fluoxetine, paroxetine, sertraline, citalopram, escitalopram).
SNRIs inhibit reuptake of both serotonin and norepinephrine (e.g., venlafaxine, desvenlafaxine, duloxetine) and may be more toxic in overdose than initially assumed.
Atypical antidepressants have variable effects on serotonin, norepinephrine, and dopamine and include bupropion, trazodone, and mirtazapine.
Atypical antipsychotics act primarily on dopamine receptors with additional serotonergic, α-adrenergic, histaminic, and muscarinic effects. Many psychiatric medications can block potassium and sodium channels, resulting in QT or QRS prolongation and cardiotoxicity.
Clinical Features:
SSRIs commonly cause sedation and serotonin syndrome; most are benign in single-agent overdose, except citalopram and escitalopram, which may cause QTc prolongation, seizures, and delayed toxicity up to 12 hours.
SNRIs may cause somnolence, vomiting, tachycardia, seizures, and QTc prolongation, especially with venlafaxine and desvenlafaxine.
Atypical antidepressants: bupropion is associated with seizures and QRS/QTc prolongation; trazodone causes sedation, hypotension, QTc prolongation, and priapism; mirtazapine causes sedation and QTc prolongation, with rare neutropenia in chronic use.
Atypical antipsychotics typically cause sedation, tachycardia, and miosis, with drug-specific risks such as agranulocytosis and cardiomyopathy (clozapine), anticholinergic delirium (olanzapine, quetiapine), hypotension (quetiapine), QTc prolongation (ziprasidone), or prolonged CNS effects (aripiprazole).
Initial Assessment: Determine the specific agents, dose, timing, and possible coingestants. Check bedside glucose in patients with altered mental status.
Diagnostic Evaluation:
Laboratory drug levels are rarely helpful acutely. Obtain ECG to assess QRS and QTc intervals. Order electrolytes, renal function, glucose, urine pregnancy test when appropriate, urine drug screen (limited impact on management), acetaminophen and salicylate levels, and serum ethanol. CT brain imaging is reserved for unexplained depressed mental status; chest radiograph is indicated if intubated or hypoxic.
Key Differentials: TCA toxicity, ethanol or sedative–hypnotic overdose, isoniazid toxicity, hypoglycemia, hypoxemia, electrolyte disturbances, withdrawal syndromes, serotonin syndrome, head trauma, opioid intoxication, mood stabilizer or antiepileptic overdose, and diabetic ketoacidosis.
Prehospital Priorities: Transport all medication containers with the patient. Support airway, breathing, and circulation. Administer IV fluids for hypotension and benzodiazepines for seizures.
Early Stabilization: Provide oxygen, continuous cardiac monitoring, IV access, and pulse oximetry. Intubate if airway protection is needed. Check rapid glucose; administer naloxone or dextrose as clinically indicated. Flumazenil is not recommended in mixed or unknown overdoses or in patients with seizure risk. Treat extrapyramidal symptoms with diphenhydramine or benztropine.
Emergency Department Management: Avoid GI decontamination if the airway is unprotected; do not intubate solely for charcoal. Activated charcoal may be considered early after ingestion. Treat QRS widening with IV sodium bicarbonate boluses (continuous infusions are ineffective). Manage hypotension refractory to fluids with norepinephrine rather than dopamine. Treat seizures with benzodiazepines, escalating to barbiturates if refractory. Address serotonin syndrome with benzodiazepines and active cooling.
Medication Options: Activated charcoal 50–75 g PO (up to 100 g); benzodiazepines (diazepam or lorazepam) for seizures/agitation; diphenhydramine or benztropine for EPS; naloxone as indicated; norepinephrine infusion for hypotension; phenobarbital for refractory seizures; sodium bicarbonate 1 mEq/kg IV bolus for QRS widening.
Disposition Planning:
Admit for 24-hour telemetry after ingestion of citalopram, escitalopram, venlafaxine, desvenlafaxine, or bupropion, even if initially asymptomatic. Admit patients with coma, persistent altered mental status, ECG abnormalities, hemodynamic instability, or neuroleptic malignant syndrome. Suicidal patients require 1:1 observation.
Asymptomatic patients more than 6 hours after ingestion of less toxic antidepressants may be medically cleared for psychiatric admission if not suicidal.
Follow-Up Care: Psychiatry referral is required for intentional overdoses.
Clinical Pearls And Pitfalls: Administer IV sodium bicarbonate promptly for QRS widening. Overdoses involving citalopram, venlafaxine, and bupropion are more likely to cause severe toxicity and delayed complications, warranting medical observation before psychiatric clearance.
