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Emergency and Acute Medicine - Tendonitis
Tendonitis is a term historically used to describe painful tendon conditions, although the more accurate terms today are tendinopathy or tendinosis, reflecting the chronic degenerative rather than purely inflammatory nature of most tendon disorders. These conditions are typically part of an overuse syndrome characterized by chronic pain, tendon thickening, and impaired function. Acute irritation may last from 48 hours to 2 weeks, whereas chronic tendinopathy involves collagen degeneration, fibrosis, and disorganized healing that persists for more than 3 months. The underlying pathology involves repeated microtrauma to the musculotendinous unit, leading to failed repair and proliferation of abnormal tissue.
The primary cause of tendinopathy is mechanical overload or repetitive stress. Intrinsic factors such as poor flexibility, muscle weakness, or imbalance contribute to injury, while extrinsic factors include excessive activity, improper technique, or sudden increases in training intensity. At the cellular level, tendons show collagen disorganization, increased vascularity, and release of inflammatory mediators that contribute to pain and swelling, even in the absence of true inflammation.
Patients typically present with a history of repetitive activity or overuse involving a specific movement. Pain is the hallmark symptom and often follows a characteristic pattern: it improves briefly with initial movement but worsens after continued activity. Classic inflammatory signs such as warmth, redness, and swelling may be present. On examination, there is localized tenderness over the tendon, pain with movement, reduced range of motion, and sometimes instability. Differentiating between tendonitis and tenosynovitis can be difficult clinically, and both are generally grouped under tendinopathies.
Several common clinical syndromes are associated with tendinopathy. In the shoulder, supraspinatus tendinopathy results from impingement between the humerus and acromion, causing pain with overhead movement. Calcific tendonitis, often affecting the rotator cuff, involves calcium deposition within the tendon and may cause acute pain during resorption phases. Bicipital tendinopathy presents with anterior shoulder pain radiating down the arm and is worsened by resisted supination or forward flexion. Lateral epicondylitis, or tennis elbow, causes pain over the lateral elbow exacerbated by gripping or wrist extension, while medial epicondylitis affects the flexor tendons.
In the wrist and hand, De Quervain tenosynovitis involves inflammation of the thumb tendons and produces pain with thumb movement, especially during the Finkelstein test. Trigger finger occurs when thickening of the tendon sheath causes catching or locking of the finger during motion. In the lower limb, Achilles tendinopathy is a common overuse injury, particularly in active individuals, presenting with posterior ankle pain, stiffness, and reduced mobility. Achilles tendon rupture may present with a sudden “popping” sensation and inability to plantarflex, although it is sometimes missed initially.
Diagnosis is primarily clinical, based on history and physical examination. Imaging is used selectively to exclude other conditions. Radiographs may show calcifications or rule out fractures, while ultrasound is useful for detecting tendon thickening and fluid collections. MRI provides detailed assessment of tendon structure and surrounding tissues. Laboratory tests are generally unnecessary unless infection or systemic disease is suspected.
Management focuses on conservative treatment. Initial therapy includes rest, ice, and nonsteroidal anti-inflammatory drugs, along with temporary immobilization if needed. Gradual rehabilitation with range-of-motion and strengthening exercises, particularly eccentric loading exercises, is essential for recovery. Most cases improve over 6 to 12 weeks. Additional treatments may include local injections, splinting, or emerging therapies such as prolotherapy or shock-wave therapy for calcific tendonitis.
Specific conditions may require tailored management. De Quervain tenosynovitis responds well to thumb spica splinting and NSAIDs. Trigger finger may require corticosteroid injection or surgical release if persistent. Achilles tendon injuries require rest, orthotics, and in the case of rupture, immobilization and orthopedic referral.
Most patients can be managed as outpatients, with referral indicated for complete tendon rupture or failure of conservative therapy after several months. Prevention of recurrence is an important aspect of long-term care, including activity modification and correction of biomechanical factors. A key clinical point is that certain medications, particularly fluoroquinolone antibiotics, have been associated with increased risk of tendinopathy and tendon rupture.
Tendonitis is a term historically used to describe painful tendon conditions, although the more accurate terms today are tendinopathy or tendinosis, reflecting the chronic degenerative rather than purely inflammatory nature of most tendon disorders. These conditions are typically part of an overuse syndrome characterized by chronic pain, tendon thickening, and impaired function. Acute irritation may last from 48 hours to 2 weeks, whereas chronic tendinopathy involves collagen degeneration, fibrosis, and disorganized healing that persists for more than 3 months. The underlying pathology involves repeated microtrauma to the musculotendinous unit, leading to failed repair and proliferation of abnormal tissue.
The primary cause of tendinopathy is mechanical overload or repetitive stress. Intrinsic factors such as poor flexibility, muscle weakness, or imbalance contribute to injury, while extrinsic factors include excessive activity, improper technique, or sudden increases in training intensity. At the cellular level, tendons show collagen disorganization, increased vascularity, and release of inflammatory mediators that contribute to pain and swelling, even in the absence of true inflammation.
Patients typically present with a history of repetitive activity or overuse involving a specific movement. Pain is the hallmark symptom and often follows a characteristic pattern: it improves briefly with initial movement but worsens after continued activity. Classic inflammatory signs such as warmth, redness, and swelling may be present. On examination, there is localized tenderness over the tendon, pain with movement, reduced range of motion, and sometimes instability. Differentiating between tendonitis and tenosynovitis can be difficult clinically, and both are generally grouped under tendinopathies.
Several common clinical syndromes are associated with tendinopathy. In the shoulder, supraspinatus tendinopathy results from impingement between the humerus and acromion, causing pain with overhead movement. Calcific tendonitis, often affecting the rotator cuff, involves calcium deposition within the tendon and may cause acute pain during resorption phases. Bicipital tendinopathy presents with anterior shoulder pain radiating down the arm and is worsened by resisted supination or forward flexion. Lateral epicondylitis, or tennis elbow, causes pain over the lateral elbow exacerbated by gripping or wrist extension, while medial epicondylitis affects the flexor tendons.
In the wrist and hand, De Quervain tenosynovitis involves inflammation of the thumb tendons and produces pain with thumb movement, especially during the Finkelstein test. Trigger finger occurs when thickening of the tendon sheath causes catching or locking of the finger during motion. In the lower limb, Achilles tendinopathy is a common overuse injury, particularly in active individuals, presenting with posterior ankle pain, stiffness, and reduced mobility. Achilles tendon rupture may present with a sudden “popping” sensation and inability to plantarflex, although it is sometimes missed initially.
Diagnosis is primarily clinical, based on history and physical examination. Imaging is used selectively to exclude other conditions. Radiographs may show calcifications or rule out fractures, while ultrasound is useful for detecting tendon thickening and fluid collections. MRI provides detailed assessment of tendon structure and surrounding tissues. Laboratory tests are generally unnecessary unless infection or systemic disease is suspected.
Management focuses on conservative treatment. Initial therapy includes rest, ice, and nonsteroidal anti-inflammatory drugs, along with temporary immobilization if needed. Gradual rehabilitation with range-of-motion and strengthening exercises, particularly eccentric loading exercises, is essential for recovery. Most cases improve over 6 to 12 weeks. Additional treatments may include local injections, splinting, or emerging therapies such as prolotherapy or shock-wave therapy for calcific tendonitis.
Specific conditions may require tailored management. De Quervain tenosynovitis responds well to thumb spica splinting and NSAIDs. Trigger finger may require corticosteroid injection or surgical release if persistent. Achilles tendon injuries require rest, orthotics, and in the case of rupture, immobilization and orthopedic referral.
Most patients can be managed as outpatients, with referral indicated for complete tendon rupture or failure of conservative therapy after several months. Prevention of recurrence is an important aspect of long-term care, including activity modification and correction of biomechanical factors. A key clinical point is that certain medications, particularly fluoroquinolone antibiotics, have been associated with increased risk of tendinopathy and tendon rupture.
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Emergency and Acute Medicine - Tenosynovitis
Tenosynovitis refers to inflammation of a tendon and its surrounding synovial sheath, which normally functions to lubricate and facilitate smooth tendon movement through osseofibrous tunnels. This condition may arise from overuse, inflammatory processes, or infection. The synovial sheath consists of visceral and parietal layers that nourish the tendon, but it also creates a confined space where infection can rapidly spread. Infection may occur through direct inoculation from a skin wound, penetrating injury, or high-pressure injection, or via hematogenous spread. Flexor tenosynovitis of the hand is particularly concerning and is most often infectious in origin, commonly resulting from penetrating injuries at the finger flexion creases. High-pressure injection injuries, such as those from paint sprayers or air tools, may appear minor externally but carry a high risk of severe underlying damage and infection.
The causes of tenosynovitis vary depending on the type. Overuse-related conditions such as De Quervain tenosynovitis involve inflammation of the abductor pollicis longus and extensor pollicis brevis tendons as they pass through a fibrous sheath at the radial styloid. Infectious causes include gonococcal tenosynovitis, typically seen in young adults and associated with disseminated infection, and nongonococcal infections, most commonly due to Staphylococcus aureus or Streptococcus species. Other organisms may be involved depending on the exposure, such as Pasteurella multocida in cat bites, Eikenella corrodens in human bites, Pseudomonas in immunocompromised or marine injuries, and even mycobacterial or fungal pathogens in specific settings.
The hallmark of infectious flexor tenosynovitis is the presence of the four Kanavel signs: fusiform swelling of the finger (often described as a “sausage digit”), tenderness along the course of the flexor tendon sheath, pain with passive extension of the finger, and a flexed resting posture of the digit. These findings indicate a surgical emergency. In contrast, inflammatory forms such as De Quervain tenosynovitis present with pain over the radial aspect of the wrist that worsens with thumb movement and improves with rest. The Finkelstein test reproduces pain when the thumb is flexed into the palm and the wrist is deviated ulnarly. Gonococcal tenosynovitis often presents with systemic symptoms such as fever, chills, and migratory joint pain, sometimes accompanied by characteristic skin lesions.
Diagnosis is primarily clinical, based on history and physical examination. It is essential to assess for risk factors such as recent trauma, puncture wounds, bites, high-pressure injuries, or sexually transmitted infections. Neurovascular status should always be documented. Laboratory studies, including complete blood count and inflammatory markers, may support the diagnosis of infection. Cultures are important in suspected gonococcal disease. Imaging is generally of limited utility but may help identify foreign bodies or complications; MRI can assist in uncertain cases but is rarely required in the emergency setting.
Management depends on the underlying cause and urgency of the condition. All suspected infectious flexor tenosynovitis cases require immediate consultation with a hand surgeon, initiation of broad-spectrum intravenous antibiotics, and often surgical intervention. Delays in treatment significantly increase the risk of permanent functional impairment. High-pressure injection injuries are also surgical emergencies requiring urgent evaluation and intervention.
Inflammatory tenosynovitis is typically managed conservatively with rest, immobilization, elevation, nonsteroidal anti-inflammatory drugs, and splinting, such as a thumb spica splint for De Quervain tenosynovitis. Corticosteroid injections may be considered for persistent symptoms. Gonococcal tenosynovitis requires hospital admission and intravenous antibiotic therapy, while nongonococcal infections require broad antimicrobial coverage tailored to likely pathogens and patient risk factors.
Disposition is determined by severity and etiology. Infectious and high-risk cases require hospital admission and often surgical management, whereas noninfectious inflammatory cases can usually be managed on an outpatient basis with close follow-up. Early recognition, especially of Kanavel signs and high-risk mechanisms, is critical, as prompt treatment significantly improves outcomes and preserves function.
Tenosynovitis refers to inflammation of a tendon and its surrounding synovial sheath, which normally functions to lubricate and facilitate smooth tendon movement through osseofibrous tunnels. This condition may arise from overuse, inflammatory processes, or infection. The synovial sheath consists of visceral and parietal layers that nourish the tendon, but it also creates a confined space where infection can rapidly spread. Infection may occur through direct inoculation from a skin wound, penetrating injury, or high-pressure injection, or via hematogenous spread. Flexor tenosynovitis of the hand is particularly concerning and is most often infectious in origin, commonly resulting from penetrating injuries at the finger flexion creases. High-pressure injection injuries, such as those from paint sprayers or air tools, may appear minor externally but carry a high risk of severe underlying damage and infection.
The causes of tenosynovitis vary depending on the type. Overuse-related conditions such as De Quervain tenosynovitis involve inflammation of the abductor pollicis longus and extensor pollicis brevis tendons as they pass through a fibrous sheath at the radial styloid. Infectious causes include gonococcal tenosynovitis, typically seen in young adults and associated with disseminated infection, and nongonococcal infections, most commonly due to Staphylococcus aureus or Streptococcus species. Other organisms may be involved depending on the exposure, such as Pasteurella multocida in cat bites, Eikenella corrodens in human bites, Pseudomonas in immunocompromised or marine injuries, and even mycobacterial or fungal pathogens in specific settings.
The hallmark of infectious flexor tenosynovitis is the presence of the four Kanavel signs: fusiform swelling of the finger (often described as a “sausage digit”), tenderness along the course of the flexor tendon sheath, pain with passive extension of the finger, and a flexed resting posture of the digit. These findings indicate a surgical emergency. In contrast, inflammatory forms such as De Quervain tenosynovitis present with pain over the radial aspect of the wrist that worsens with thumb movement and improves with rest. The Finkelstein test reproduces pain when the thumb is flexed into the palm and the wrist is deviated ulnarly. Gonococcal tenosynovitis often presents with systemic symptoms such as fever, chills, and migratory joint pain, sometimes accompanied by characteristic skin lesions.
Diagnosis is primarily clinical, based on history and physical examination. It is essential to assess for risk factors such as recent trauma, puncture wounds, bites, high-pressure injuries, or sexually transmitted infections. Neurovascular status should always be documented. Laboratory studies, including complete blood count and inflammatory markers, may support the diagnosis of infection. Cultures are important in suspected gonococcal disease. Imaging is generally of limited utility but may help identify foreign bodies or complications; MRI can assist in uncertain cases but is rarely required in the emergency setting.
Management depends on the underlying cause and urgency of the condition. All suspected infectious flexor tenosynovitis cases require immediate consultation with a hand surgeon, initiation of broad-spectrum intravenous antibiotics, and often surgical intervention. Delays in treatment significantly increase the risk of permanent functional impairment. High-pressure injection injuries are also surgical emergencies requiring urgent evaluation and intervention.
Inflammatory tenosynovitis is typically managed conservatively with rest, immobilization, elevation, nonsteroidal anti-inflammatory drugs, and splinting, such as a thumb spica splint for De Quervain tenosynovitis. Corticosteroid injections may be considered for persistent symptoms. Gonococcal tenosynovitis requires hospital admission and intravenous antibiotic therapy, while nongonococcal infections require broad antimicrobial coverage tailored to likely pathogens and patient risk factors.
Disposition is determined by severity and etiology. Infectious and high-risk cases require hospital admission and often surgical management, whereas noninfectious inflammatory cases can usually be managed on an outpatient basis with close follow-up. Early recognition, especially of Kanavel signs and high-risk mechanisms, is critical, as prompt treatment significantly improves outcomes and preserves function.
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Emergency and Acute Medicine - Testicular Torsion
Testicular torsion is a urologic emergency caused by rotation of the testicle around the spermatic cord, leading to vascular compromise and potential infarction. The degree of torsion can vary from partial rotation to complete twisting, and ischemic damage can occur rapidly. Testicular viability is highly time dependent, with salvage rates approaching 100% if treated within 6 hours, decreasing significantly after 12 hours, and becoming very low beyond that timeframe. Despite this, attempts at salvage are still recommended up to 24 hours after symptom onset. Prolonged ischemia can result in testicular atrophy and impaired fertility.
The condition demonstrates a bimodal age distribution, most commonly affecting neonates and adolescents, particularly between the ages of 12 and 18. It is rare but still possible in older adults. The underlying cause is typically a congenital anatomical abnormality, most notably the “bell-clapper” deformity, in which the testicle lacks normal fixation within the scrotum and can rotate freely. This abnormality is often bilateral, placing both testicles at risk.
Patients usually present with sudden onset of severe unilateral testicular pain, often accompanied by scrotal swelling and redness. Pain may also radiate to the lower abdomen or inguinal region. Nausea and vomiting are common, and some patients report prior intermittent episodes of similar pain, suggesting intermittent torsion and spontaneous detorsion. Symptoms of urinary tract infection are typically absent.
On physical examination, the affected testicle may be high-riding and lie in a transverse orientation rather than its normal vertical position. One of the most important clinical findings is the absence of the cremasteric reflex on the affected side, which is highly sensitive for torsion. Differentiating torsion from other causes of acute scrotum, such as epididymitis, may be difficult in advanced cases due to swelling. The Prehn sign, which assesses pain relief with testicular elevation, is unreliable. Torsion of the appendix testis may present with a “blue dot” sign and is typically less severe.
Diagnosis requires rapid evaluation. While laboratory tests are nonspecific, imaging plays a key role when time allows. Color Doppler ultrasound is the preferred modality, demonstrating reduced or absent blood flow in the affected testicle, whereas inflammatory conditions like epididymitis show increased flow. However, imaging should not delay surgical intervention if clinical suspicion is high. In uncertain cases or when imaging is unavailable or inconclusive, immediate surgical exploration is warranted.
Management is time critical and centers on urgent urologic consultation and surgical intervention. Initial supportive care includes analgesia and intravenous fluids. If definitive surgical treatment is delayed, manual detorsion may be attempted by rotating the testicle laterally (the “open book” maneuver), as torsion typically occurs medially. Successful detorsion may relieve pain and restore blood flow, but surgical exploration is still required afterward to prevent recurrence.
All confirmed cases require surgical exploration and bilateral orchiopexy to secure both testicles and prevent future torsion. Patients with inconclusive imaging or persistent suspicion must also undergo exploration. Those with alternative diagnoses or normal imaging may be discharged with appropriate follow-up, but they should be educated on the risk of recurrence and instructed to return immediately if symptoms recur.
A key clinical principle is that testicular torsion must always be considered in any patient presenting with acute scrotal pain, especially adolescents. It can mimic other conditions such as appendicitis, and delays in diagnosis can result in loss of the testicle. The phrase “time is testicle” underscores the urgency of prompt recognition and management.
Testicular torsion is a urologic emergency caused by rotation of the testicle around the spermatic cord, leading to vascular compromise and potential infarction. The degree of torsion can vary from partial rotation to complete twisting, and ischemic damage can occur rapidly. Testicular viability is highly time dependent, with salvage rates approaching 100% if treated within 6 hours, decreasing significantly after 12 hours, and becoming very low beyond that timeframe. Despite this, attempts at salvage are still recommended up to 24 hours after symptom onset. Prolonged ischemia can result in testicular atrophy and impaired fertility.
The condition demonstrates a bimodal age distribution, most commonly affecting neonates and adolescents, particularly between the ages of 12 and 18. It is rare but still possible in older adults. The underlying cause is typically a congenital anatomical abnormality, most notably the “bell-clapper” deformity, in which the testicle lacks normal fixation within the scrotum and can rotate freely. This abnormality is often bilateral, placing both testicles at risk.
Patients usually present with sudden onset of severe unilateral testicular pain, often accompanied by scrotal swelling and redness. Pain may also radiate to the lower abdomen or inguinal region. Nausea and vomiting are common, and some patients report prior intermittent episodes of similar pain, suggesting intermittent torsion and spontaneous detorsion. Symptoms of urinary tract infection are typically absent.
On physical examination, the affected testicle may be high-riding and lie in a transverse orientation rather than its normal vertical position. One of the most important clinical findings is the absence of the cremasteric reflex on the affected side, which is highly sensitive for torsion. Differentiating torsion from other causes of acute scrotum, such as epididymitis, may be difficult in advanced cases due to swelling. The Prehn sign, which assesses pain relief with testicular elevation, is unreliable. Torsion of the appendix testis may present with a “blue dot” sign and is typically less severe.
Diagnosis requires rapid evaluation. While laboratory tests are nonspecific, imaging plays a key role when time allows. Color Doppler ultrasound is the preferred modality, demonstrating reduced or absent blood flow in the affected testicle, whereas inflammatory conditions like epididymitis show increased flow. However, imaging should not delay surgical intervention if clinical suspicion is high. In uncertain cases or when imaging is unavailable or inconclusive, immediate surgical exploration is warranted.
Management is time critical and centers on urgent urologic consultation and surgical intervention. Initial supportive care includes analgesia and intravenous fluids. If definitive surgical treatment is delayed, manual detorsion may be attempted by rotating the testicle laterally (the “open book” maneuver), as torsion typically occurs medially. Successful detorsion may relieve pain and restore blood flow, but surgical exploration is still required afterward to prevent recurrence.
All confirmed cases require surgical exploration and bilateral orchiopexy to secure both testicles and prevent future torsion. Patients with inconclusive imaging or persistent suspicion must also undergo exploration. Those with alternative diagnoses or normal imaging may be discharged with appropriate follow-up, but they should be educated on the risk of recurrence and instructed to return immediately if symptoms recur.
A key clinical principle is that testicular torsion must always be considered in any patient presenting with acute scrotal pain, especially adolescents. It can mimic other conditions such as appendicitis, and delays in diagnosis can result in loss of the testicle. The phrase “time is testicle” underscores the urgency of prompt recognition and management.
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Emergency and Acute Medicine - Tendon Laceration
Tendon laceration is an important traumatic injury that can significantly impair function if not properly identified and treated. Any laceration near a tendon must be carefully explored through a full range of motion to exclude injury, as even partial disruptions can lead to long-term disability. These injuries may result from external trauma such as penetrating injuries from knives, glass, gunshot wounds, or foreign bodies, as well as blunt trauma causing crushing or avulsion forces. Less commonly, tendon damage may occur internally due to entrapment or laceration from fractures. Upper-extremity injuries are more commonly associated with workplace accidents, home injuries, assaults, or self-harm, while lower-extremity injuries are often related to occupational incidents or motor vehicle accidents.
Pain is the most consistent presenting symptom, often accompanied by functional deficits such as weakness or inability to move a joint. Associated soft tissue findings may include swelling, bruising, visible lacerations, and bleeding. Abnormal resting posture of a limb or joint instability should raise suspicion for tendon injury. A detailed history is essential, including mechanism of injury, timing, hand dominance, and tetanus immunization status.
Physical examination plays a critical role in diagnosis. The resting position of the hand should be assessed, noting the natural cascade of finger flexion. Each tendon must be evaluated individually, with testing against resistance to detect subtle injuries. Flexor tendon injuries may present with inability to flex specific joints, such as loss of distal interphalangeal flexion in flexor digitorum profundus injuries or proximal interphalangeal flexion in flexor digitorum superficialis injuries. Extensor tendon injuries are suggested by weakness or inability to extend the digits. Direct visualization of the tendon through the wound, ideally in a well-lit and bloodless field after local anesthesia, is essential, and the tendon should be examined throughout its full range of motion.
Investigations are guided by clinical suspicion. Radiographs are commonly used to detect fractures or radiopaque foreign bodies. Ultrasound can help identify complete tendon lacerations, although partial injuries are more difficult to visualize. MRI may be used in selected cases. Wounds presenting late or showing signs of infection should be cultured. Differential diagnoses include associated fractures, foreign bodies, and specific tendon-related deformities such as boutonnière deformity, mallet finger, and jersey finger.
Initial management focuses on hemorrhage control, immobilization, and preservation of neurovascular function. In the emergency setting, treatment includes adequate analgesia, tetanus prophylaxis, and thorough irrigation of the wound. Antibiotics, typically a first-generation cephalosporin such as cefazolin, are administered, with broader coverage required for contaminated wounds such as human bites. Devitalized tissue should be debrided, and foreign bodies removed.
Partial tendon lacerations involving more than 20% of the tendon cross-sectional area require repair. Simple extensor tendon injuries may be repaired in the emergency department using nonabsorbable sutures, while flexor tendon injuries and those involving the wrist or forearm require prompt consultation with a hand surgeon, ideally within 12 hours. If surgical repair is not immediately available, the wound should be irrigated, the skin loosely closed, and the limb immobilized in a functional position using a splint.
Disposition depends on the severity and type of injury. Infected tendon lacerations or those caused by human bites require hospital admission and operative management. Significant flexor tendon injuries often require admission or transfer for surgical repair. Selected uncomplicated extensor tendon injuries that are repaired and properly splinted may be discharged with close surgical follow-up.
A key clinical point is that partial tendon lacerations are frequently missed because patients may retain near-normal range of motion. Strength testing is therefore essential, as significant injuries can still demonstrate preserved motion. Any laceration over the metacarpophalangeal joint should be considered a potential human bite until proven otherwise. Early recognition, careful examination, and appropriate referral are critical to prevent long-term functional impairment.
Tendon laceration is an important traumatic injury that can significantly impair function if not properly identified and treated. Any laceration near a tendon must be carefully explored through a full range of motion to exclude injury, as even partial disruptions can lead to long-term disability. These injuries may result from external trauma such as penetrating injuries from knives, glass, gunshot wounds, or foreign bodies, as well as blunt trauma causing crushing or avulsion forces. Less commonly, tendon damage may occur internally due to entrapment or laceration from fractures. Upper-extremity injuries are more commonly associated with workplace accidents, home injuries, assaults, or self-harm, while lower-extremity injuries are often related to occupational incidents or motor vehicle accidents.
Pain is the most consistent presenting symptom, often accompanied by functional deficits such as weakness or inability to move a joint. Associated soft tissue findings may include swelling, bruising, visible lacerations, and bleeding. Abnormal resting posture of a limb or joint instability should raise suspicion for tendon injury. A detailed history is essential, including mechanism of injury, timing, hand dominance, and tetanus immunization status.
Physical examination plays a critical role in diagnosis. The resting position of the hand should be assessed, noting the natural cascade of finger flexion. Each tendon must be evaluated individually, with testing against resistance to detect subtle injuries. Flexor tendon injuries may present with inability to flex specific joints, such as loss of distal interphalangeal flexion in flexor digitorum profundus injuries or proximal interphalangeal flexion in flexor digitorum superficialis injuries. Extensor tendon injuries are suggested by weakness or inability to extend the digits. Direct visualization of the tendon through the wound, ideally in a well-lit and bloodless field after local anesthesia, is essential, and the tendon should be examined throughout its full range of motion.
Investigations are guided by clinical suspicion. Radiographs are commonly used to detect fractures or radiopaque foreign bodies. Ultrasound can help identify complete tendon lacerations, although partial injuries are more difficult to visualize. MRI may be used in selected cases. Wounds presenting late or showing signs of infection should be cultured. Differential diagnoses include associated fractures, foreign bodies, and specific tendon-related deformities such as boutonnière deformity, mallet finger, and jersey finger.
Initial management focuses on hemorrhage control, immobilization, and preservation of neurovascular function. In the emergency setting, treatment includes adequate analgesia, tetanus prophylaxis, and thorough irrigation of the wound. Antibiotics, typically a first-generation cephalosporin such as cefazolin, are administered, with broader coverage required for contaminated wounds such as human bites. Devitalized tissue should be debrided, and foreign bodies removed.
Partial tendon lacerations involving more than 20% of the tendon cross-sectional area require repair. Simple extensor tendon injuries may be repaired in the emergency department using nonabsorbable sutures, while flexor tendon injuries and those involving the wrist or forearm require prompt consultation with a hand surgeon, ideally within 12 hours. If surgical repair is not immediately available, the wound should be irrigated, the skin loosely closed, and the limb immobilized in a functional position using a splint.
Disposition depends on the severity and type of injury. Infected tendon lacerations or those caused by human bites require hospital admission and operative management. Significant flexor tendon injuries often require admission or transfer for surgical repair. Selected uncomplicated extensor tendon injuries that are repaired and properly splinted may be discharged with close surgical follow-up.
A key clinical point is that partial tendon lacerations are frequently missed because patients may retain near-normal range of motion. Strength testing is therefore essential, as significant injuries can still demonstrate preserved motion. Any laceration over the metacarpophalangeal joint should be considered a potential human bite until proven otherwise. Early recognition, careful examination, and appropriate referral are critical to prevent long-term functional impairment.
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Emergency and Acute Medicine: Stridor
Stridor is a high-pitched, harsh, vibratory sound predominantly heard during inspiration and indicates obstruction of airflow through the upper airway. It reflects narrowing at the level of the larynx or trachea and is a clinical sign of potentially serious airway compromise. Because it signifies upper airway obstruction, stridor must always be approached as an emergency, especially in children where deterioration can be rapid.
The causes of stridor are diverse and can be broadly divided into congenital, infectious, structural, and obstructive categories. Congenital causes include conditions such as laryngomalacia, vocal cord abnormalities, and subglottic stenosis. Infectious causes are particularly important in acute presentations and include viral croup, epiglottitis, bacterial tracheitis, and deep neck space infections like peritonsillar or retropharyngeal abscesses. Extrinsic compression from trauma, hematoma, or vascular anomalies may also compromise the airway. Intraluminal obstruction can occur due to foreign bodies, tumors, cysts, or tracheomalacia, while conditions like angioedema can cause rapid airway swelling.
Patients typically present with breathing difficulty and audible noisy respiration that worsens with agitation, crying, feeding, or lying supine. Associated symptoms may include hoarseness, a muffled “hot potato” voice, drooling, sore throat, cough, and dysphagia. Infants may have feeding difficulties, apnea, or cyanotic episodes. On examination, signs of respiratory distress are common, including tachypnea, nasal flaring, intercostal and subcostal retractions, and use of accessory muscles. Cyanosis and paradoxical breathing are late and concerning findings. Certain features, such as trismus, may suggest deep neck infections.
Diagnosis is primarily clinical, and unnecessary investigations should be avoided if they risk agitating the patient, particularly children. Imaging is reserved for very mild or unclear cases. Definitive evaluation is achieved through direct visualization of the airway, typically with laryngoscopy. However, this must only be performed in a controlled setting, such as an operating room, with immediate availability of a surgical airway, as manipulation can precipitate complete obstruction.
Management focuses first on airway stabilization. In prehospital and early care, the patient—especially a child—should be kept calm, given oxygen, and monitored closely. Agitation must be minimized as it can worsen airway obstruction. In the emergency setting, stridor is treated as a difficult airway, and clinicians must be prepared for rapid deterioration.
If intubation is required, it should ideally be performed in a controlled environment with experienced personnel. A smaller endotracheal tube is recommended due to airway narrowing. Ketamine is often preferred for induction because it preserves spontaneous breathing. Blind nasotracheal intubation should be avoided. If intubation fails or the airway is lost, an emergency surgical airway such as cricothyrotomy or tracheostomy is required.
Adjunctive treatments depend on the underlying cause. Nebulized epinephrine and corticosteroids such as dexamethasone are commonly used in conditions like croup. Antibiotics, such as ceftriaxone, are indicated when a bacterial infection is suspected. Sedation and paralysis may be required after securing the airway.
All patients with unresolved stridor require hospital admission for monitoring and further evaluation. Discharge is only appropriate when symptoms have completely resolved and a non-threatening cause is identified. Early involvement of specialists such as otolaryngologists or pediatric surgeons is essential.
A key clinical pitfall is attempting airway examination without adequate preparation for emergency airway intervention. Stridor should always prompt urgent evaluation and careful airway management, as delay or improper handling can lead to sudden and catastrophic airway obstruction.
Stridor is a high-pitched, harsh, vibratory sound predominantly heard during inspiration and indicates obstruction of airflow through the upper airway. It reflects narrowing at the level of the larynx or trachea and is a clinical sign of potentially serious airway compromise. Because it signifies upper airway obstruction, stridor must always be approached as an emergency, especially in children where deterioration can be rapid.
The causes of stridor are diverse and can be broadly divided into congenital, infectious, structural, and obstructive categories. Congenital causes include conditions such as laryngomalacia, vocal cord abnormalities, and subglottic stenosis. Infectious causes are particularly important in acute presentations and include viral croup, epiglottitis, bacterial tracheitis, and deep neck space infections like peritonsillar or retropharyngeal abscesses. Extrinsic compression from trauma, hematoma, or vascular anomalies may also compromise the airway. Intraluminal obstruction can occur due to foreign bodies, tumors, cysts, or tracheomalacia, while conditions like angioedema can cause rapid airway swelling.
Patients typically present with breathing difficulty and audible noisy respiration that worsens with agitation, crying, feeding, or lying supine. Associated symptoms may include hoarseness, a muffled “hot potato” voice, drooling, sore throat, cough, and dysphagia. Infants may have feeding difficulties, apnea, or cyanotic episodes. On examination, signs of respiratory distress are common, including tachypnea, nasal flaring, intercostal and subcostal retractions, and use of accessory muscles. Cyanosis and paradoxical breathing are late and concerning findings. Certain features, such as trismus, may suggest deep neck infections.
Diagnosis is primarily clinical, and unnecessary investigations should be avoided if they risk agitating the patient, particularly children. Imaging is reserved for very mild or unclear cases. Definitive evaluation is achieved through direct visualization of the airway, typically with laryngoscopy. However, this must only be performed in a controlled setting, such as an operating room, with immediate availability of a surgical airway, as manipulation can precipitate complete obstruction.
Management focuses first on airway stabilization. In prehospital and early care, the patient—especially a child—should be kept calm, given oxygen, and monitored closely. Agitation must be minimized as it can worsen airway obstruction. In the emergency setting, stridor is treated as a difficult airway, and clinicians must be prepared for rapid deterioration.
If intubation is required, it should ideally be performed in a controlled environment with experienced personnel. A smaller endotracheal tube is recommended due to airway narrowing. Ketamine is often preferred for induction because it preserves spontaneous breathing. Blind nasotracheal intubation should be avoided. If intubation fails or the airway is lost, an emergency surgical airway such as cricothyrotomy or tracheostomy is required.
Adjunctive treatments depend on the underlying cause. Nebulized epinephrine and corticosteroids such as dexamethasone are commonly used in conditions like croup. Antibiotics, such as ceftriaxone, are indicated when a bacterial infection is suspected. Sedation and paralysis may be required after securing the airway.
All patients with unresolved stridor require hospital admission for monitoring and further evaluation. Discharge is only appropriate when symptoms have completely resolved and a non-threatening cause is identified. Early involvement of specialists such as otolaryngologists or pediatric surgeons is essential.
A key clinical pitfall is attempting airway examination without adequate preparation for emergency airway intervention. Stridor should always prompt urgent evaluation and careful airway management, as delay or improper handling can lead to sudden and catastrophic airway obstruction.
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Emergency and Acute Medicine: Stevens–Johnson Syndrome
Stevens–Johnson syndrome (SJS) is a rare but severe mucocutaneous disorder characterized by widespread skin and mucosal injury. It involves blistering and epidermal detachment affecting less than 10% of the body surface area, distinguishing it from more extensive conditions such as toxic epidermal necrolysis. The disease almost always involves mucous membranes, typically affecting at least two sites such as the oral cavity, eyes, or genitalia. Skin lesions often begin on the face, neck, and trunk and may rapidly become confluent over hours to days. Although part of a spectrum with toxic epidermal necrolysis, SJS is considered a distinct clinical entity.
The condition is most commonly triggered by medications or infections. Drugs such as antibiotics (especially sulfonamides and penicillins), anticonvulsants, nonsteroidal anti-inflammatory drugs, and allopurinol are frequent culprits. Infectious causes include Mycoplasma pneumoniae and herpes simplex virus. The underlying mechanism involves an immune-mediated process in which cytotoxic T cells target keratinocytes expressing drug-related antigens, leading to widespread apoptosis of skin cells and systemic inflammation.
Patients typically present with a prodrome resembling a viral illness, occurring one to three days before the rash. Symptoms include fever, malaise, headache, upper respiratory symptoms, and sometimes joint or muscle pain. This is followed by skin tenderness, burning, and the development of erythematous or purpuric macules that may evolve into target-like lesions or flaccid blisters. These lesions can detach with slight pressure, demonstrating the Nikolsky sign. Painful mucosal involvement is a hallmark feature, leading to symptoms such as difficulty swallowing, urination discomfort, and eye irritation or conjunctivitis. Ocular involvement is common and may progress to serious complications such as corneal damage.
Diagnosis is primarily clinical and based on history, examination, and the extent of skin involvement. A careful medication history is crucial, as symptoms typically develop within two weeks of drug exposure, or more rapidly upon re-exposure. Laboratory tests may reveal nonspecific findings such as anemia or lymphopenia, while skin biopsy can confirm the diagnosis by showing full-thickness epidermal necrosis and subepidermal separation.
Management focuses on early recognition, withdrawal of the offending agent, and supportive care. Patients should be treated similarly to burn victims, especially those with significant skin involvement. Fluid resuscitation is essential due to fluid losses from denuded skin. Pain control is critical, as mucosal lesions can be extremely painful. Monitoring and treatment of secondary infections are vital, as sepsis—particularly from gram-negative organisms—is the leading cause of death. Advanced therapies such as intravenous immunoglobulin or corticosteroids may be considered, although their use remains controversial.
All patients with SJS require hospital admission, and those with extensive skin involvement should be managed in a burn unit or intensive care setting. Airway protection and ventilatory support may be necessary in severe cases. Long-term follow-up is important, particularly for ocular and dermatologic complications. Patients must be clearly educated about the causative drug and advised to avoid it permanently, as re-exposure can lead to rapid and more severe recurrence.
A key challenge is early recognition, as SJS often begins with nonspecific flu-like symptoms. Clinicians must maintain a high index of suspicion in patients presenting with mucocutaneous lesions and recent drug exposure. Prompt diagnosis and aggressive supportive care significantly improve outcomes.
Stevens–Johnson syndrome (SJS) is a rare but severe mucocutaneous disorder characterized by widespread skin and mucosal injury. It involves blistering and epidermal detachment affecting less than 10% of the body surface area, distinguishing it from more extensive conditions such as toxic epidermal necrolysis. The disease almost always involves mucous membranes, typically affecting at least two sites such as the oral cavity, eyes, or genitalia. Skin lesions often begin on the face, neck, and trunk and may rapidly become confluent over hours to days. Although part of a spectrum with toxic epidermal necrolysis, SJS is considered a distinct clinical entity.
The condition is most commonly triggered by medications or infections. Drugs such as antibiotics (especially sulfonamides and penicillins), anticonvulsants, nonsteroidal anti-inflammatory drugs, and allopurinol are frequent culprits. Infectious causes include Mycoplasma pneumoniae and herpes simplex virus. The underlying mechanism involves an immune-mediated process in which cytotoxic T cells target keratinocytes expressing drug-related antigens, leading to widespread apoptosis of skin cells and systemic inflammation.
Patients typically present with a prodrome resembling a viral illness, occurring one to three days before the rash. Symptoms include fever, malaise, headache, upper respiratory symptoms, and sometimes joint or muscle pain. This is followed by skin tenderness, burning, and the development of erythematous or purpuric macules that may evolve into target-like lesions or flaccid blisters. These lesions can detach with slight pressure, demonstrating the Nikolsky sign. Painful mucosal involvement is a hallmark feature, leading to symptoms such as difficulty swallowing, urination discomfort, and eye irritation or conjunctivitis. Ocular involvement is common and may progress to serious complications such as corneal damage.
Diagnosis is primarily clinical and based on history, examination, and the extent of skin involvement. A careful medication history is crucial, as symptoms typically develop within two weeks of drug exposure, or more rapidly upon re-exposure. Laboratory tests may reveal nonspecific findings such as anemia or lymphopenia, while skin biopsy can confirm the diagnosis by showing full-thickness epidermal necrosis and subepidermal separation.
Management focuses on early recognition, withdrawal of the offending agent, and supportive care. Patients should be treated similarly to burn victims, especially those with significant skin involvement. Fluid resuscitation is essential due to fluid losses from denuded skin. Pain control is critical, as mucosal lesions can be extremely painful. Monitoring and treatment of secondary infections are vital, as sepsis—particularly from gram-negative organisms—is the leading cause of death. Advanced therapies such as intravenous immunoglobulin or corticosteroids may be considered, although their use remains controversial.
All patients with SJS require hospital admission, and those with extensive skin involvement should be managed in a burn unit or intensive care setting. Airway protection and ventilatory support may be necessary in severe cases. Long-term follow-up is important, particularly for ocular and dermatologic complications. Patients must be clearly educated about the causative drug and advised to avoid it permanently, as re-exposure can lead to rapid and more severe recurrence.
A key challenge is early recognition, as SJS often begins with nonspecific flu-like symptoms. Clinicians must maintain a high index of suspicion in patients presenting with mucocutaneous lesions and recent drug exposure. Prompt diagnosis and aggressive supportive care significantly improve outcomes.
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Emergency and Acute Medicine: Bee Sting (Hymenoptera Envenomation)
Bee stings are a common form of envenomation caused by insects from the order Hymenoptera, which includes bees, wasps, hornets, and fire ants. Their venom triggers the release of biologically active substances that can produce a range of reactions, from mild local irritation to life-threatening systemic responses. Most reactions are IgE-mediated type I hypersensitivity reactions, although less commonly, delayed immune responses such as type III (Arthus) reactions may occur.
Clinical presentation varies widely depending on the individual’s immune response and the amount of venom delivered. The most common reaction is a localized response, characterized by immediate pain, redness, and swelling at the sting site, typically resolving within a few hours. Larger local reactions may involve an entire limb, peak within 48 hours, and persist for several days, sometimes accompanied by mild fever.
Systemic reactions represent true allergic responses and can progress to anaphylaxis, which is potentially fatal. Symptoms usually develop within 15–20 minutes and may include respiratory distress (wheezing, stridor, shortness of breath), cardiovascular instability (hypotension, tachycardia, shock), gastrointestinal symptoms (nausea, vomiting, diarrhea), and skin manifestations such as urticaria, flushing, and angioedema. Toxic reactions can occur after multiple stings due to a large venom load and may mimic anaphylaxis. Rare delayed or unusual immune-mediated complications include vasculitis, nephropathy, serum sickness, and neurologic involvement.
Diagnosis is primarily clinical, based on history and physical examination. There are no specific laboratory or imaging tests required for uncomplicated cases. However, investigations such as blood tests or ECG may be warranted in patients with significant systemic involvement, particularly those with underlying cardiovascular disease.
Management depends on the severity of the reaction. Immediate priorities in severe systemic reactions include airway stabilization, oxygen administration, intravenous access, and prompt use of epinephrine, which is the first-line treatment for anaphylaxis. Antihistamines (both H1 and H2 blockers), corticosteroids, and inhaled β-agonists are used as adjunct therapies. Persistent hypotension requires aggressive fluid resuscitation and possibly vasopressor support.
For local reactions, treatment is supportive and includes removal of the stinger (preferably by scraping rather than squeezing to avoid further venom release), application of cold compresses, limb elevation, and use of oral or topical antihistamines or corticosteroids. Pain control and avoidance of constrictive items such as rings or tight clothing are also important.
Patients with systemic reactions should be observed for at least 6 hours, while those with severe or life-threatening reactions may require admission and prolonged monitoring. Discharge is appropriate for patients with mild local reactions or resolved systemic symptoms after observation. Importantly, individuals who experience systemic reactions should be prescribed an epinephrine auto-injector and referred to an allergist for further evaluation and possible immunotherapy.
A key clinical point is that most fatal outcomes occur within the first hour due to airway compromise or circulatory collapse. Rapid recognition and early administration of epinephrine are critical. Patients with a history of severe reactions must be educated on avoidance strategies and emergency self-treatment to reduce the risk of recurrence.
Bee stings are a common form of envenomation caused by insects from the order Hymenoptera, which includes bees, wasps, hornets, and fire ants. Their venom triggers the release of biologically active substances that can produce a range of reactions, from mild local irritation to life-threatening systemic responses. Most reactions are IgE-mediated type I hypersensitivity reactions, although less commonly, delayed immune responses such as type III (Arthus) reactions may occur.
Clinical presentation varies widely depending on the individual’s immune response and the amount of venom delivered. The most common reaction is a localized response, characterized by immediate pain, redness, and swelling at the sting site, typically resolving within a few hours. Larger local reactions may involve an entire limb, peak within 48 hours, and persist for several days, sometimes accompanied by mild fever.
Systemic reactions represent true allergic responses and can progress to anaphylaxis, which is potentially fatal. Symptoms usually develop within 15–20 minutes and may include respiratory distress (wheezing, stridor, shortness of breath), cardiovascular instability (hypotension, tachycardia, shock), gastrointestinal symptoms (nausea, vomiting, diarrhea), and skin manifestations such as urticaria, flushing, and angioedema. Toxic reactions can occur after multiple stings due to a large venom load and may mimic anaphylaxis. Rare delayed or unusual immune-mediated complications include vasculitis, nephropathy, serum sickness, and neurologic involvement.
Diagnosis is primarily clinical, based on history and physical examination. There are no specific laboratory or imaging tests required for uncomplicated cases. However, investigations such as blood tests or ECG may be warranted in patients with significant systemic involvement, particularly those with underlying cardiovascular disease.
Management depends on the severity of the reaction. Immediate priorities in severe systemic reactions include airway stabilization, oxygen administration, intravenous access, and prompt use of epinephrine, which is the first-line treatment for anaphylaxis. Antihistamines (both H1 and H2 blockers), corticosteroids, and inhaled β-agonists are used as adjunct therapies. Persistent hypotension requires aggressive fluid resuscitation and possibly vasopressor support.
For local reactions, treatment is supportive and includes removal of the stinger (preferably by scraping rather than squeezing to avoid further venom release), application of cold compresses, limb elevation, and use of oral or topical antihistamines or corticosteroids. Pain control and avoidance of constrictive items such as rings or tight clothing are also important.
Patients with systemic reactions should be observed for at least 6 hours, while those with severe or life-threatening reactions may require admission and prolonged monitoring. Discharge is appropriate for patients with mild local reactions or resolved systemic symptoms after observation. Importantly, individuals who experience systemic reactions should be prescribed an epinephrine auto-injector and referred to an allergist for further evaluation and possible immunotherapy.
A key clinical point is that most fatal outcomes occur within the first hour due to airway compromise or circulatory collapse. Rapid recognition and early administration of epinephrine are critical. Patients with a history of severe reactions must be educated on avoidance strategies and emergency self-treatment to reduce the risk of recurrence.
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Emergency and Acute Medicine: Scorpion Sting (Envenomation)
Scorpion envenomation is a potentially serious condition caused by injection of neurotoxic venom, which affects sodium channels and leads to prolonged neuronal firing. This results in widespread stimulation of autonomic, somatic, and cranial nerves. Symptoms typically begin within minutes of the sting and can last from several hours up to 72 hours. The severity of illness varies depending on the species and the patient, with children at significantly higher risk of severe toxicity and complications.
The most clinically significant species in North America is Centruroides sculpturatus (bark scorpion), found in parts of the southern United States, Mexico, and Central America. Globally, many dangerous species exist across Asia, Africa, the Middle East, and South America. Pediatric patients are especially vulnerable due to lower body mass and may present with symptoms that mimic seizures, poisoning, or central nervous system infections.
Clinical manifestations develop rapidly, usually peaking within 1–2 hours. Local findings are often minimal, typically limited to pain and heightened sensitivity without significant redness or swelling. Systemic toxicity is more prominent and includes autonomic disturbances such as tachycardia, hypertension, sweating, agitation, and hyperthermia from sympathetic activation, as well as bradycardia, hypotension, and excessive salivation from parasympathetic effects. Neuromuscular symptoms include restlessness, involuntary muscle jerking, and severe agitation. Cranial nerve involvement may lead to abnormal eye movements, blurred vision, tongue fasciculations, and impaired swallowing or airway control.
Severity is classified into four grades. Mild cases (grades I and II) involve only local or regional symptoms, while severe envenomation (grades III and IV) includes neuromuscular dysfunction and combined autonomic and cranial nerve involvement. Severe cases may progress to respiratory compromise, requiring urgent intervention.
Diagnosis is clinical and based on symptom recognition, especially in endemic areas. Identification of the scorpion is not necessary. Laboratory tests are generally not required for mild cases but may be indicated in severe envenomation to assess complications such as electrolyte imbalance, renal injury, or rhabdomyolysis. Imaging and ECG may be used when cardiopulmonary symptoms are present.
Management begins with stabilization of airway, breathing, and circulation. Oxygen and intravenous access should be established early. Mild envenomations are treated with supportive care, including oral analgesics and tetanus prophylaxis. Severe envenomations require close monitoring and may necessitate airway protection, sedation (e.g., midazolam for agitation), and cardiovascular support.
Antivenom (Anascorp) is the definitive treatment for severe cases and works rapidly to reverse neurologic symptoms. It is administered intravenously, with initial dosing followed by reassessment and additional doses if needed. Importantly, the same dosing is used in both adults and children, as it is based on venom load rather than body weight.
Patients with severe envenomation should be admitted to an intensive care setting. Those who respond well to antivenom and remain stable after observation may be discharged with instructions regarding delayed reactions such as serum sickness. Mild cases can be safely discharged after a short observation period if symptoms do not progress.
A critical clinical point is maintaining a high index of suspicion in endemic regions, especially in children presenting with unexplained neurologic or autonomic symptoms. Early recognition and timely administration of antivenom can significantly reduce morbidity and prevent life-threatening complications.
Scorpion envenomation is a potentially serious condition caused by injection of neurotoxic venom, which affects sodium channels and leads to prolonged neuronal firing. This results in widespread stimulation of autonomic, somatic, and cranial nerves. Symptoms typically begin within minutes of the sting and can last from several hours up to 72 hours. The severity of illness varies depending on the species and the patient, with children at significantly higher risk of severe toxicity and complications.
The most clinically significant species in North America is Centruroides sculpturatus (bark scorpion), found in parts of the southern United States, Mexico, and Central America. Globally, many dangerous species exist across Asia, Africa, the Middle East, and South America. Pediatric patients are especially vulnerable due to lower body mass and may present with symptoms that mimic seizures, poisoning, or central nervous system infections.
Clinical manifestations develop rapidly, usually peaking within 1–2 hours. Local findings are often minimal, typically limited to pain and heightened sensitivity without significant redness or swelling. Systemic toxicity is more prominent and includes autonomic disturbances such as tachycardia, hypertension, sweating, agitation, and hyperthermia from sympathetic activation, as well as bradycardia, hypotension, and excessive salivation from parasympathetic effects. Neuromuscular symptoms include restlessness, involuntary muscle jerking, and severe agitation. Cranial nerve involvement may lead to abnormal eye movements, blurred vision, tongue fasciculations, and impaired swallowing or airway control.
Severity is classified into four grades. Mild cases (grades I and II) involve only local or regional symptoms, while severe envenomation (grades III and IV) includes neuromuscular dysfunction and combined autonomic and cranial nerve involvement. Severe cases may progress to respiratory compromise, requiring urgent intervention.
Diagnosis is clinical and based on symptom recognition, especially in endemic areas. Identification of the scorpion is not necessary. Laboratory tests are generally not required for mild cases but may be indicated in severe envenomation to assess complications such as electrolyte imbalance, renal injury, or rhabdomyolysis. Imaging and ECG may be used when cardiopulmonary symptoms are present.
Management begins with stabilization of airway, breathing, and circulation. Oxygen and intravenous access should be established early. Mild envenomations are treated with supportive care, including oral analgesics and tetanus prophylaxis. Severe envenomations require close monitoring and may necessitate airway protection, sedation (e.g., midazolam for agitation), and cardiovascular support.
Antivenom (Anascorp) is the definitive treatment for severe cases and works rapidly to reverse neurologic symptoms. It is administered intravenously, with initial dosing followed by reassessment and additional doses if needed. Importantly, the same dosing is used in both adults and children, as it is based on venom load rather than body weight.
Patients with severe envenomation should be admitted to an intensive care setting. Those who respond well to antivenom and remain stable after observation may be discharged with instructions regarding delayed reactions such as serum sickness. Mild cases can be safely discharged after a short observation period if symptoms do not progress.
A critical clinical point is maintaining a high index of suspicion in endemic regions, especially in children presenting with unexplained neurologic or autonomic symptoms. Early recognition and timely administration of antivenom can significantly reduce morbidity and prevent life-threatening complications.
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Emergency and Acute Medicine - Subarachnoid Hemorrhage
Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space and cerebrospinal fluid, most commonly due to rupture of a cerebral aneurysm. It is a life-threatening neurologic emergency with high mortality, ranging from 30–50%. It typically affects adults, with peak incidence in the sixth decade, and is rare before the third decade. Important risk factors include hypertension, smoking, alcohol abuse, stimulant drug use such as cocaine, female sex, and a family history of SAH. Certain genetic conditions, including polycystic kidney disease and connective tissue disorders, further increase risk.
The most common cause of spontaneous SAH is rupture of a saccular (berry) aneurysm, accounting for 80–90% of cases, usually occurring at arterial bifurcations within the circle of Willis. Other causes include arteriovenous malformations, arterial dissections, intracranial tumors, and mycotic aneurysms. Traumatic SAH is also seen in severe head injuries.
Patients classically present with a sudden, severe headache often described as a “thunderclap headache” or the “worst headache of life,” reaching maximal intensity within seconds. This headache is typically different from prior headaches. Associated features include vomiting, transient loss of consciousness, seizures, neck stiffness, and focal neurologic deficits. A “sentinel headache,” representing a minor bleed, may occur days to weeks before the major event in up to half of patients.
On examination, patients may have nuchal rigidity, altered mental status, and focal neurologic deficits. Cranial nerve involvement, particularly third nerve palsy presenting as a “down and out” eye, may be seen. Retinal hemorrhage can occasionally be the only clue, especially in comatose patients.
Diagnosis begins with an emergent noncontrast CT scan of the head, which detects SAH in up to 98% of cases if performed within 12 hours of symptom onset. If the CT scan is negative but clinical suspicion remains high, a lumbar puncture must be performed. The presence of red blood cells in the cerebrospinal fluid or xanthochromia confirms the diagnosis. Further imaging, such as CT angiography or digital subtraction angiography, is used to identify the source of bleeding, while transcranial Doppler may be used to monitor for vasospasm.
Management is focused on rapid stabilization and prevention of complications. Initial priorities include airway protection, oxygenation, cardiac monitoring, and establishing intravenous access. Blood pressure must be carefully controlled to reduce the risk of rebleeding while maintaining adequate cerebral perfusion, with a target systolic pressure below 160 mmHg. Measures to reduce intracranial pressure include head elevation, avoidance of straining, and use of antiemetics and stool softeners. In selected cases, mannitol and controlled ventilation may be required.
All patients should receive Nimodipine to reduce the risk of delayed cerebral vasospasm and improve neurologic outcomes. Seizures should be treated promptly with benzodiazepines, and metabolic abnormalities should be corrected. Definitive management involves urgent neurosurgical intervention, either by surgical clipping or endovascular coiling of the aneurysm.
All patients with confirmed or suspected SAH require admission to an intensive care unit. Early recognition and treatment are critical, as mortality is high and many patients deteriorate rapidly. A key pitfall is failure to consider SAH in patients presenting with acute severe headache, or stopping evaluation after a negative CT scan without proceeding to lumbar puncture when indicated.
Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space and cerebrospinal fluid, most commonly due to rupture of a cerebral aneurysm. It is a life-threatening neurologic emergency with high mortality, ranging from 30–50%. It typically affects adults, with peak incidence in the sixth decade, and is rare before the third decade. Important risk factors include hypertension, smoking, alcohol abuse, stimulant drug use such as cocaine, female sex, and a family history of SAH. Certain genetic conditions, including polycystic kidney disease and connective tissue disorders, further increase risk.
The most common cause of spontaneous SAH is rupture of a saccular (berry) aneurysm, accounting for 80–90% of cases, usually occurring at arterial bifurcations within the circle of Willis. Other causes include arteriovenous malformations, arterial dissections, intracranial tumors, and mycotic aneurysms. Traumatic SAH is also seen in severe head injuries.
Patients classically present with a sudden, severe headache often described as a “thunderclap headache” or the “worst headache of life,” reaching maximal intensity within seconds. This headache is typically different from prior headaches. Associated features include vomiting, transient loss of consciousness, seizures, neck stiffness, and focal neurologic deficits. A “sentinel headache,” representing a minor bleed, may occur days to weeks before the major event in up to half of patients.
On examination, patients may have nuchal rigidity, altered mental status, and focal neurologic deficits. Cranial nerve involvement, particularly third nerve palsy presenting as a “down and out” eye, may be seen. Retinal hemorrhage can occasionally be the only clue, especially in comatose patients.
Diagnosis begins with an emergent noncontrast CT scan of the head, which detects SAH in up to 98% of cases if performed within 12 hours of symptom onset. If the CT scan is negative but clinical suspicion remains high, a lumbar puncture must be performed. The presence of red blood cells in the cerebrospinal fluid or xanthochromia confirms the diagnosis. Further imaging, such as CT angiography or digital subtraction angiography, is used to identify the source of bleeding, while transcranial Doppler may be used to monitor for vasospasm.
Management is focused on rapid stabilization and prevention of complications. Initial priorities include airway protection, oxygenation, cardiac monitoring, and establishing intravenous access. Blood pressure must be carefully controlled to reduce the risk of rebleeding while maintaining adequate cerebral perfusion, with a target systolic pressure below 160 mmHg. Measures to reduce intracranial pressure include head elevation, avoidance of straining, and use of antiemetics and stool softeners. In selected cases, mannitol and controlled ventilation may be required.
All patients should receive Nimodipine to reduce the risk of delayed cerebral vasospasm and improve neurologic outcomes. Seizures should be treated promptly with benzodiazepines, and metabolic abnormalities should be corrected. Definitive management involves urgent neurosurgical intervention, either by surgical clipping or endovascular coiling of the aneurysm.
All patients with confirmed or suspected SAH require admission to an intensive care unit. Early recognition and treatment are critical, as mortality is high and many patients deteriorate rapidly. A key pitfall is failure to consider SAH in patients presenting with acute severe headache, or stopping evaluation after a negative CT scan without proceeding to lumbar puncture when indicated.
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Emergency and Acute Medicine - Sudden Infant Death Syndrome (SIDS)
Sudden infant death syndrome (SIDS) is defined as the sudden, unexpected death of an infant younger than 1 year of age that remains unexplained after thorough investigation, including autopsy, examination of the death scene, and review of medical and family history. It is a diagnosis of exclusion and remains the leading cause of death in infants between 1 month and 1 year of age. The peak incidence occurs between 1 and 4 months of age, with 90% of cases occurring before 6 months. The incidence has declined significantly following public health campaigns promoting supine sleeping, such as the “Back to Sleep” initiative.
The etiology of SIDS is thought to be multifactorial, involving a vulnerable infant exposed to internal and external stressors during a critical developmental period. Potential contributing factors include underlying abnormalities such as cardiac dysrhythmias, metabolic disorders, infections, neurologic immaturity, or impaired arousal mechanisms. Maternal risk factors include smoking, alcohol or drug use, poor prenatal care, young maternal age, and short interpregnancy intervals. Infant-related risk factors include prematurity, low birth weight, male gender, exposure to secondhand smoke, overheating, soft bedding, and bed sharing. Protective factors include placing infants in a supine sleeping position, breastfeeding, and pacifier use. Home monitoring has not been shown to prevent SIDS.
Clinically, SIDS is typically silent and unpredictable. Infants are usually found unresponsive during sleep, having appeared healthy when last placed to bed. There are no preceding warning signs. A related entity, known as an apparent life-threatening event (ALTE), involves episodes of apnea, color change, altered muscle tone, or choking and may be associated with an increased risk of SIDS. Infants who experience such events often appear normal upon evaluation but require careful monitoring.
The evaluation of suspected SIDS cases focuses on excluding other causes of death. This includes a detailed investigation of the death scene, including sleep position, bedding, environmental conditions, and possible bed sharing. A thorough review of prenatal, perinatal, and postnatal history, as well as family medical and social history, is essential. Autopsy is mandatory in most jurisdictions and plays a critical role in identifying alternative causes such as congenital heart disease, infections, metabolic disorders, or nonaccidental trauma. Additional investigations may include laboratory studies, toxicology screening, imaging, and assessment for familial conditions such as prolonged QT syndrome.
Management in the emergency setting involves immediate resuscitation according to pediatric advanced life support protocols. Airway, breathing, and circulation should be assessed and supported, with medications administered as indicated. If resuscitation is unsuccessful and no clear cause is identified, clinicians should avoid prematurely labeling the death as SIDS until a full investigation is complete. Equally important is providing compassionate support to the family, who may experience profound grief, guilt, and confusion. Allowing family presence during resuscitation and offering opportunities to spend time with the infant afterward can be beneficial.
All surviving infants who experience ALTE should be admitted for observation and further evaluation, particularly if episodes are recurrent or associated with concerning features. Follow-up with pediatric specialists is recommended. A key aspect of care is family education on safe sleep practices, including placing infants on their backs, using a firm sleep surface, avoiding soft bedding, and preventing overheating. A major pitfall is failure to conduct a thorough investigation, as SIDS cannot be diagnosed without excluding other potentially preventable or treatable causes.
Sudden infant death syndrome (SIDS) is defined as the sudden, unexpected death of an infant younger than 1 year of age that remains unexplained after thorough investigation, including autopsy, examination of the death scene, and review of medical and family history. It is a diagnosis of exclusion and remains the leading cause of death in infants between 1 month and 1 year of age. The peak incidence occurs between 1 and 4 months of age, with 90% of cases occurring before 6 months. The incidence has declined significantly following public health campaigns promoting supine sleeping, such as the “Back to Sleep” initiative.
The etiology of SIDS is thought to be multifactorial, involving a vulnerable infant exposed to internal and external stressors during a critical developmental period. Potential contributing factors include underlying abnormalities such as cardiac dysrhythmias, metabolic disorders, infections, neurologic immaturity, or impaired arousal mechanisms. Maternal risk factors include smoking, alcohol or drug use, poor prenatal care, young maternal age, and short interpregnancy intervals. Infant-related risk factors include prematurity, low birth weight, male gender, exposure to secondhand smoke, overheating, soft bedding, and bed sharing. Protective factors include placing infants in a supine sleeping position, breastfeeding, and pacifier use. Home monitoring has not been shown to prevent SIDS.
Clinically, SIDS is typically silent and unpredictable. Infants are usually found unresponsive during sleep, having appeared healthy when last placed to bed. There are no preceding warning signs. A related entity, known as an apparent life-threatening event (ALTE), involves episodes of apnea, color change, altered muscle tone, or choking and may be associated with an increased risk of SIDS. Infants who experience such events often appear normal upon evaluation but require careful monitoring.
The evaluation of suspected SIDS cases focuses on excluding other causes of death. This includes a detailed investigation of the death scene, including sleep position, bedding, environmental conditions, and possible bed sharing. A thorough review of prenatal, perinatal, and postnatal history, as well as family medical and social history, is essential. Autopsy is mandatory in most jurisdictions and plays a critical role in identifying alternative causes such as congenital heart disease, infections, metabolic disorders, or nonaccidental trauma. Additional investigations may include laboratory studies, toxicology screening, imaging, and assessment for familial conditions such as prolonged QT syndrome.
Management in the emergency setting involves immediate resuscitation according to pediatric advanced life support protocols. Airway, breathing, and circulation should be assessed and supported, with medications administered as indicated. If resuscitation is unsuccessful and no clear cause is identified, clinicians should avoid prematurely labeling the death as SIDS until a full investigation is complete. Equally important is providing compassionate support to the family, who may experience profound grief, guilt, and confusion. Allowing family presence during resuscitation and offering opportunities to spend time with the infant afterward can be beneficial.
All surviving infants who experience ALTE should be admitted for observation and further evaluation, particularly if episodes are recurrent or associated with concerning features. Follow-up with pediatric specialists is recommended. A key aspect of care is family education on safe sleep practices, including placing infants on their backs, using a firm sleep surface, avoiding soft bedding, and preventing overheating. A major pitfall is failure to conduct a thorough investigation, as SIDS cannot be diagnosed without excluding other potentially preventable or treatable causes.
