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Emergency And Acute Medicine – Foot Fracture
Basics Description
Foot fractures involve injury to the tarsal bones or metatarsals, including the calcaneus, talus, navicular, cuboid, cuneiforms, and metatarsals.
Etiology
The most common foot fractures involve the metatarsals and phalanges. The calcaneus is the most frequently fractured tarsal bone.
Calcaneus fractures usually result from high-velocity axial compression to the heel; approximately 75% are intra-articular and 50% are associated with other injuries, including spinal fractures, lower extremity trauma, bilateral involvement, or open wounds.
Metatarsal fractures may result from stress, twisting injuries, or direct trauma. The first metatarsal is often injured by direct force. The second and third metatarsals are most commonly affected by stress or twisting injuries. The fifth metatarsal commonly sustains avulsion fractures at the proximal apophysis (dancer’s fracture) or a Jones fracture at the metaphyseal–diaphyseal junction from inversion injury.
Talus fractures are typically caused by dorsiflexion with axial loading. Navicular fractures result from axial compression or stress. Cuboid and cuneiform fractures are rare and usually occur with associated injuries, particularly tarsometatarsal (Lisfranc) injuries. Lisfranc injuries are high-energy injuries caused by axial load on a plantar-flexed foot or forced eversion and are frequently missed on initial evaluation.
Pediatric considerations include a predominance of metatarsal fractures, often from direct trauma, with physeal injury possible. Calcaneal fractures in children are less commonly intra-articular and less often associated with spinal injury.
Diagnosis Signs And Symptoms
History usually reveals trauma; stress fractures may present with progressive pain related to repetitive activity.
Physical examination may show ecchymosis, swelling, deformity, localized tenderness, pain with weight bearing, or joint instability.
Essential Workup
A focused extremity examination is required to assess neurovascular status, skin integrity, swelling, deformity, and function. In suspected calcaneal fractures, evaluation of the spine is essential due to the risk of associated injury. Standard anteroposterior, lateral, and oblique foot radiographs are required.
Diagnosis Tests And Interpretation
Imaging may require special views depending on the suspected injury. Lisfranc injuries may require weight-bearing stress views, MRI for ligamentous assessment, or CT. Talar fractures may require oblique views or CT. Calcaneal fractures require axial views, with a Böhler angle less than 20° suggesting compression fracture, and often CT for further definition. Lumbar spine imaging is recommended in calcaneal fractures. Stress fractures may not be visible on initial radiographs and may require delayed imaging, bone scan, or CT.
Complications to assess include compartment syndrome, nonunion, avascular necrosis (especially with talar neck fractures), and sural nerve injury with calcaneal fractures.
Differential Diagnosis
Ankle sprain, foot contusion, talar dome injury, and Freiberg disease may mimic foot fractures.
Treatment
Prehospital care includes ice application, immobilization, and spinal precautions when calcaneal fracture is suspected.
Initial stabilization prioritizes management of associated injuries.
Emergency department management includes airway, breathing, and circulation assessment, neurovascular evaluation, prompt reduction of dislocations with reassessment, immobilization in a bulky splint, elevation, ice, and crutches. Circumferential casting should be delayed until swelling subsides. Pain control is essential. Compartment syndrome should be suspected with severe pain, swelling, or pain on passive toe movement. Early orthopedic consultation is required for displaced, open, or midfoot fractures.
Medication
Analgesics and sedatives may be used as indicated for pain control and procedural sedation. Antibiotics are indicated for open fractures.
Follow Up Disposition
Admission criteria include open fractures, compartment syndrome, neurovascular compromise, or need for immediate operative fixation.
Discharge criteria include stable patients with isolated, nondisplaced metatarsal fractures who can be managed with immobilization and close orthopedic follow-up.
Clinical Insights And Frequent Errors
Calcaneal fractures should prompt evaluation for spinal injury. Lisfranc injuries are commonly missed and require a high index of suspicion. Persistent pain or swelling despite normal initial imaging warrants reevaluation for occult or stress fractures.
Basics Description
Foot fractures involve injury to the tarsal bones or metatarsals, including the calcaneus, talus, navicular, cuboid, cuneiforms, and metatarsals.
Etiology
The most common foot fractures involve the metatarsals and phalanges. The calcaneus is the most frequently fractured tarsal bone.
Calcaneus fractures usually result from high-velocity axial compression to the heel; approximately 75% are intra-articular and 50% are associated with other injuries, including spinal fractures, lower extremity trauma, bilateral involvement, or open wounds.
Metatarsal fractures may result from stress, twisting injuries, or direct trauma. The first metatarsal is often injured by direct force. The second and third metatarsals are most commonly affected by stress or twisting injuries. The fifth metatarsal commonly sustains avulsion fractures at the proximal apophysis (dancer’s fracture) or a Jones fracture at the metaphyseal–diaphyseal junction from inversion injury.
Talus fractures are typically caused by dorsiflexion with axial loading. Navicular fractures result from axial compression or stress. Cuboid and cuneiform fractures are rare and usually occur with associated injuries, particularly tarsometatarsal (Lisfranc) injuries. Lisfranc injuries are high-energy injuries caused by axial load on a plantar-flexed foot or forced eversion and are frequently missed on initial evaluation.
Pediatric considerations include a predominance of metatarsal fractures, often from direct trauma, with physeal injury possible. Calcaneal fractures in children are less commonly intra-articular and less often associated with spinal injury.
Diagnosis Signs And Symptoms
History usually reveals trauma; stress fractures may present with progressive pain related to repetitive activity.
Physical examination may show ecchymosis, swelling, deformity, localized tenderness, pain with weight bearing, or joint instability.
Essential Workup
A focused extremity examination is required to assess neurovascular status, skin integrity, swelling, deformity, and function. In suspected calcaneal fractures, evaluation of the spine is essential due to the risk of associated injury. Standard anteroposterior, lateral, and oblique foot radiographs are required.
Diagnosis Tests And Interpretation
Imaging may require special views depending on the suspected injury. Lisfranc injuries may require weight-bearing stress views, MRI for ligamentous assessment, or CT. Talar fractures may require oblique views or CT. Calcaneal fractures require axial views, with a Böhler angle less than 20° suggesting compression fracture, and often CT for further definition. Lumbar spine imaging is recommended in calcaneal fractures. Stress fractures may not be visible on initial radiographs and may require delayed imaging, bone scan, or CT.
Complications to assess include compartment syndrome, nonunion, avascular necrosis (especially with talar neck fractures), and sural nerve injury with calcaneal fractures.
Differential Diagnosis
Ankle sprain, foot contusion, talar dome injury, and Freiberg disease may mimic foot fractures.
Treatment
Prehospital care includes ice application, immobilization, and spinal precautions when calcaneal fracture is suspected.
Initial stabilization prioritizes management of associated injuries.
Emergency department management includes airway, breathing, and circulation assessment, neurovascular evaluation, prompt reduction of dislocations with reassessment, immobilization in a bulky splint, elevation, ice, and crutches. Circumferential casting should be delayed until swelling subsides. Pain control is essential. Compartment syndrome should be suspected with severe pain, swelling, or pain on passive toe movement. Early orthopedic consultation is required for displaced, open, or midfoot fractures.
Medication
Analgesics and sedatives may be used as indicated for pain control and procedural sedation. Antibiotics are indicated for open fractures.
Follow Up Disposition
Admission criteria include open fractures, compartment syndrome, neurovascular compromise, or need for immediate operative fixation.
Discharge criteria include stable patients with isolated, nondisplaced metatarsal fractures who can be managed with immobilization and close orthopedic follow-up.
Clinical Insights And Frequent Errors
Calcaneal fractures should prompt evaluation for spinal injury. Lisfranc injuries are commonly missed and require a high index of suspicion. Persistent pain or swelling despite normal initial imaging warrants reevaluation for occult or stress fractures.
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Emergency And Acute Medicine - Extremity Trauma, Penetrating
Condition overview
Penetrating extremity trauma refers to injuries in which an object breaches the skin and underlying tissues of an arm or leg. These injuries range from minor puncture wounds to severe limb-threatening trauma involving vascular, neurologic, musculoskeletal, or compartment compromise.
Mechanisms of injury
Common mechanisms include stab or puncture wounds, gunshot wounds, lacerations, animal or human bites, and high-pressure injection injuries. High-muzzle-velocity gunshot wounds are particularly destructive, as the shock wave may cause extensive tissue damage beyond the visible wound tract, often with more damage at the exit wound than the entry site.
Clinical presentation
Findings may include entry and exit wounds, lacerations, or punctures. Vascular injury should be suspected with decreased or absent distal pulses, ischemic changes, expanding hematoma, or a bruit or thrill over the injury; the presence of a distal pulse does not exclude proximal vascular damage. Neurologic injury may present with paresthesias, weakness, or loss of sensation distal to the wound. Musculoskeletal injury may manifest as deformity, joint effusion, ligamentous laxity, or limited range of motion. Compartment syndrome is suggested by severe, constant pain, pain with passive stretch, compartment tenderness, weakness, and sensory deficits, with pallor and pulselessness being late findings.
History and examination priorities
Key historical elements include the mechanism and timing of injury, circumstances such as assault or self-harm, and comorbid conditions including diabetes, immunosuppression, peripheral vascular disease, valvular heart disease, or asplenia. Examination should document wound location, size, depth, and shape, and assess for exit wounds. Distal pulses should be compared bilaterally by palpation and Doppler. Capillary refill, motor and sensory function, joint stability, and signs of compartment syndrome must be evaluated. The wound should be carefully inspected for foreign bodies.
Diagnostic evaluation
The physical examination guides further testing. Acute wound cultures are not routinely indicated. Plain radiographs with at least anteroposterior and lateral views are used to detect fractures or radiopaque foreign bodies. Ultrasound, fluoroscopy, or CT may help identify radiolucent foreign bodies. When vascular injury is suspected and immediate surgery is not required, arteriography may be indicated.
Management principles
Prehospital care focuses on hemorrhage control with direct pressure, limb elevation, pain control, neurovascular assessment, and stabilization of impaled objects in place. In the emergency department, airway and hemodynamic stabilization take priority. The wound should be fully exposed, constricting items removed, and bleeding controlled with direct pressure; blind clamping and prolonged tourniquet use are discouraged. After a full neurologic exam, pain control is provided. Visible debris and devitalized tissue are removed, with copious high-pressure saline irrigation as the cornerstone of wound care. Tetanus prophylaxis is essential.
Stab and gunshot wounds should receive a single dose of cefazolin in the emergency department. Extremities should be immobilized when vascular injury, fracture, tendon injury, or joint violation is suspected. Loss of distal pulse or signs of ischemia mandate emergent surgical consultation without delay for imaging. Clean lacerations seen within 6–8 hours may be closed primarily; puncture wounds and gunshot wounds should not be closed primarily, with delayed primary closure considered for contaminated or older wounds.
Special considerations
Plantar puncture wounds require careful inspection and removal of foreign material; aggressive probing or irrigation may worsen contamination. Prophylactic antibiotics are generally not recommended unless the patient is diabetic, immunocompromised, or the wound is highly contaminated or delayed in presentation. High-pressure injection injuries of the hand require immediate orthopedic evaluation, as surface wounds may underestimate deep tissue involvement. Small inert foreign bodies, including bullets, may be left in place if not near vital structures, whereas organic material should always be removed.
Disposition and follow-up
Admission and emergent surgical consultation are required for suspected vascular injury, compartment syndrome, joint penetration, high-velocity gunshot wounds, or contaminated wounds in high-risk patients. Stable patients without indications for surgery may be discharged after appropriate wound care with instructions for elevation, wound hygiene, and close follow-up within 24–48 hours.
Key clinical lessons
A normal distal pulse does not exclude significant vascular injury. High-pressure hand injuries and plantar puncture wounds are commonly underestimated. Failure of a puncture wound infection to improve with antibiotics should prompt concern for a retained foreign body.
Condition overview
Penetrating extremity trauma refers to injuries in which an object breaches the skin and underlying tissues of an arm or leg. These injuries range from minor puncture wounds to severe limb-threatening trauma involving vascular, neurologic, musculoskeletal, or compartment compromise.
Mechanisms of injury
Common mechanisms include stab or puncture wounds, gunshot wounds, lacerations, animal or human bites, and high-pressure injection injuries. High-muzzle-velocity gunshot wounds are particularly destructive, as the shock wave may cause extensive tissue damage beyond the visible wound tract, often with more damage at the exit wound than the entry site.
Clinical presentation
Findings may include entry and exit wounds, lacerations, or punctures. Vascular injury should be suspected with decreased or absent distal pulses, ischemic changes, expanding hematoma, or a bruit or thrill over the injury; the presence of a distal pulse does not exclude proximal vascular damage. Neurologic injury may present with paresthesias, weakness, or loss of sensation distal to the wound. Musculoskeletal injury may manifest as deformity, joint effusion, ligamentous laxity, or limited range of motion. Compartment syndrome is suggested by severe, constant pain, pain with passive stretch, compartment tenderness, weakness, and sensory deficits, with pallor and pulselessness being late findings.
History and examination priorities
Key historical elements include the mechanism and timing of injury, circumstances such as assault or self-harm, and comorbid conditions including diabetes, immunosuppression, peripheral vascular disease, valvular heart disease, or asplenia. Examination should document wound location, size, depth, and shape, and assess for exit wounds. Distal pulses should be compared bilaterally by palpation and Doppler. Capillary refill, motor and sensory function, joint stability, and signs of compartment syndrome must be evaluated. The wound should be carefully inspected for foreign bodies.
Diagnostic evaluation
The physical examination guides further testing. Acute wound cultures are not routinely indicated. Plain radiographs with at least anteroposterior and lateral views are used to detect fractures or radiopaque foreign bodies. Ultrasound, fluoroscopy, or CT may help identify radiolucent foreign bodies. When vascular injury is suspected and immediate surgery is not required, arteriography may be indicated.
Management principles
Prehospital care focuses on hemorrhage control with direct pressure, limb elevation, pain control, neurovascular assessment, and stabilization of impaled objects in place. In the emergency department, airway and hemodynamic stabilization take priority. The wound should be fully exposed, constricting items removed, and bleeding controlled with direct pressure; blind clamping and prolonged tourniquet use are discouraged. After a full neurologic exam, pain control is provided. Visible debris and devitalized tissue are removed, with copious high-pressure saline irrigation as the cornerstone of wound care. Tetanus prophylaxis is essential.
Stab and gunshot wounds should receive a single dose of cefazolin in the emergency department. Extremities should be immobilized when vascular injury, fracture, tendon injury, or joint violation is suspected. Loss of distal pulse or signs of ischemia mandate emergent surgical consultation without delay for imaging. Clean lacerations seen within 6–8 hours may be closed primarily; puncture wounds and gunshot wounds should not be closed primarily, with delayed primary closure considered for contaminated or older wounds.
Special considerations
Plantar puncture wounds require careful inspection and removal of foreign material; aggressive probing or irrigation may worsen contamination. Prophylactic antibiotics are generally not recommended unless the patient is diabetic, immunocompromised, or the wound is highly contaminated or delayed in presentation. High-pressure injection injuries of the hand require immediate orthopedic evaluation, as surface wounds may underestimate deep tissue involvement. Small inert foreign bodies, including bullets, may be left in place if not near vital structures, whereas organic material should always be removed.
Disposition and follow-up
Admission and emergent surgical consultation are required for suspected vascular injury, compartment syndrome, joint penetration, high-velocity gunshot wounds, or contaminated wounds in high-risk patients. Stable patients without indications for surgery may be discharged after appropriate wound care with instructions for elevation, wound hygiene, and close follow-up within 24–48 hours.
Key clinical lessons
A normal distal pulse does not exclude significant vascular injury. High-pressure hand injuries and plantar puncture wounds are commonly underestimated. Failure of a puncture wound infection to improve with antibiotics should prompt concern for a retained foreign body.
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Emergency And Acute Medicine – Foreign Body in the ear
Basics Description
Foreign bodies lodged in the external auditory canal are common, particularly in children younger than 8 years. The canal is a cartilaginous and bony passage lined with highly sensitive periosteum, making removal painful; small children may require procedural sedation or general anesthesia. Foreign bodies often lodge at the junction of the cartilaginous and bony canal or at the isthmus. The canal is innervated by the facial, glossopharyngeal, and vagus nerves.
Inanimate objects often present late because children may delay reporting. The right ear is more commonly involved due to right-handedness. Predisposing factors include cerumen impaction, pica, and psychiatric illness.
Complications include canal laceration, tympanic membrane perforation (often iatrogenic), otitis externa, temporomandibular joint erosion, parapharyngeal abscess, mastoiditis, meningitis, and brain abscess. Button batteries are particularly dangerous due to electrical injury and pressure necrosis, often causing rapid tissue destruction.
Etiology
Children commonly insert beads, stones, paper, seeds, popcorn kernels, beans, toys, and button batteries. Adults more often present with cotton-swab tips, earplugs, insects (cockroaches most common in the US), or concealed illicit drugs.
Diagnosis Signs And Symptoms
Symptoms include unilateral ear pain, fullness, decreased hearing, crying in infants, buzzing or movement sensation with live insects, nausea, dizziness, ipsilateral tearing, itching, bleeding, or purulent discharge.
History should include prior removal attempts and possible trauma.
Physical examination requires careful otoscopy before and after removal to identify the object type, assess swelling risk, evaluate for otitis externa, retained fragments, or tympanic membrane perforation. A bilateral ear exam and inspection of nostrils are essential, especially in children and psychiatric patients. Concerning findings such as vertigo, nystagmus, hearing loss, facial nerve weakness, or severe pain warrant ENT consultation.
Essential Workup
A careful otoscopic examination is the cornerstone. Identify the foreign body and minimize patient discomfort before attempting removal.
Diagnosis Tests And Interpretation
Laboratory studies are not indicated. CT imaging is reserved for suspected infectious, erosive, or intracranial complications. Otomicroscopy may assist when standard techniques fail.
Differential Diagnosis
Cerumen impaction, otitis externa, canal hematoma, granuloma, trauma, tympanic membrane perforation, residual inflammation after self-removal, and tumors.
Treatment
Prehospital care for suspected live insects includes instillation of warm lidocaine or mineral oil to immobilize the insect; field removal attempts are discouraged.
In the emergency department, ensure adequate lighting, proper head immobilization, and analgesia. Lidocaine (1–2%) may be instilled topically or injected into the canal walls. Procedural sedation is recommended for children or uncooperative adults and should be used early to prevent traumatic repeated attempts.
Removal techniques depend on object type: irrigation for non–button battery objects; forceps, hooks, suction, Fogarty catheter, or cyanoacrylate glue for selected cases; acetone for Styrofoam or adhesive materials. Vegetable matter should not be irrigated. Button batteries must never be irrigated and require urgent removal. Live insects should be killed first with lidocaine, alcohol, or mineral oil before extraction. Sharp objects and complicated cases require ENT referral.
Medication
Analgesia or sedation may include fentanyl, ketamine, or midazolam. Topical antibiotic-steroid drops are indicated if canal abrasion or infection is suspected. Oral antibiotics are reserved for tympanic membrane perforation or secondary infection.
Follow Up Disposition
Admission is required for button batteries that cannot be removed.
Discharge is appropriate once the foreign body is removed or if a nonhazardous object cannot be safely removed in the ED.
ENT referral is indicated for failed removal, complications, immunocompromised patients, or significant trauma.
Follow Up Recommendations
Advise patients not to insert objects into the ear. Provide short-term analgesia after traumatic removal. Treat otitis externa with topical antimicrobials. Avoid water submersion if trauma or infection is present and arrange ENT follow-up when indicated.
Key Practice Insights And Avoidable Errors
Early use of procedural sedation improves success and reduces complications. Never irrigate an ear containing a button battery, as this can rapidly worsen tissue necrosis.
Basics Description
Foreign bodies lodged in the external auditory canal are common, particularly in children younger than 8 years. The canal is a cartilaginous and bony passage lined with highly sensitive periosteum, making removal painful; small children may require procedural sedation or general anesthesia. Foreign bodies often lodge at the junction of the cartilaginous and bony canal or at the isthmus. The canal is innervated by the facial, glossopharyngeal, and vagus nerves.
Inanimate objects often present late because children may delay reporting. The right ear is more commonly involved due to right-handedness. Predisposing factors include cerumen impaction, pica, and psychiatric illness.
Complications include canal laceration, tympanic membrane perforation (often iatrogenic), otitis externa, temporomandibular joint erosion, parapharyngeal abscess, mastoiditis, meningitis, and brain abscess. Button batteries are particularly dangerous due to electrical injury and pressure necrosis, often causing rapid tissue destruction.
Etiology
Children commonly insert beads, stones, paper, seeds, popcorn kernels, beans, toys, and button batteries. Adults more often present with cotton-swab tips, earplugs, insects (cockroaches most common in the US), or concealed illicit drugs.
Diagnosis Signs And Symptoms
Symptoms include unilateral ear pain, fullness, decreased hearing, crying in infants, buzzing or movement sensation with live insects, nausea, dizziness, ipsilateral tearing, itching, bleeding, or purulent discharge.
History should include prior removal attempts and possible trauma.
Physical examination requires careful otoscopy before and after removal to identify the object type, assess swelling risk, evaluate for otitis externa, retained fragments, or tympanic membrane perforation. A bilateral ear exam and inspection of nostrils are essential, especially in children and psychiatric patients. Concerning findings such as vertigo, nystagmus, hearing loss, facial nerve weakness, or severe pain warrant ENT consultation.
Essential Workup
A careful otoscopic examination is the cornerstone. Identify the foreign body and minimize patient discomfort before attempting removal.
Diagnosis Tests And Interpretation
Laboratory studies are not indicated. CT imaging is reserved for suspected infectious, erosive, or intracranial complications. Otomicroscopy may assist when standard techniques fail.
Differential Diagnosis
Cerumen impaction, otitis externa, canal hematoma, granuloma, trauma, tympanic membrane perforation, residual inflammation after self-removal, and tumors.
Treatment
Prehospital care for suspected live insects includes instillation of warm lidocaine or mineral oil to immobilize the insect; field removal attempts are discouraged.
In the emergency department, ensure adequate lighting, proper head immobilization, and analgesia. Lidocaine (1–2%) may be instilled topically or injected into the canal walls. Procedural sedation is recommended for children or uncooperative adults and should be used early to prevent traumatic repeated attempts.
Removal techniques depend on object type: irrigation for non–button battery objects; forceps, hooks, suction, Fogarty catheter, or cyanoacrylate glue for selected cases; acetone for Styrofoam or adhesive materials. Vegetable matter should not be irrigated. Button batteries must never be irrigated and require urgent removal. Live insects should be killed first with lidocaine, alcohol, or mineral oil before extraction. Sharp objects and complicated cases require ENT referral.
Medication
Analgesia or sedation may include fentanyl, ketamine, or midazolam. Topical antibiotic-steroid drops are indicated if canal abrasion or infection is suspected. Oral antibiotics are reserved for tympanic membrane perforation or secondary infection.
Follow Up Disposition
Admission is required for button batteries that cannot be removed.
Discharge is appropriate once the foreign body is removed or if a nonhazardous object cannot be safely removed in the ED.
ENT referral is indicated for failed removal, complications, immunocompromised patients, or significant trauma.
Follow Up Recommendations
Advise patients not to insert objects into the ear. Provide short-term analgesia after traumatic removal. Treat otitis externa with topical antimicrobials. Avoid water submersion if trauma or infection is present and arrange ENT follow-up when indicated.
Key Practice Insights And Avoidable Errors
Early use of procedural sedation improves success and reduces complications. Never irrigate an ear containing a button battery, as this can rapidly worsen tissue necrosis.
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Emergency And Acute Medicine – Shaft and Distal Forearm Fractures
Basics Description
Forearm shaft fractures may involve one or both bones and are frequently displaced due to muscular contraction. These injuries may be associated with joint dislocations, including Galeazzi fractures, which involve a distal radius fracture with distal radioulnar joint dislocation, and Monteggia fractures, which involve a proximal ulna fracture with radial head dislocation.
Distal forearm fractures include several classic patterns. Colles fractures result from hyperextension with dorsal displacement of the distal radius fragment and are often associated with ulnar styloid injury. Smith fractures occur with hyperflexion and result in volar displacement. Barton fractures are intra-articular fractures of the dorsal rim of the distal radius and may involve carpal dislocation. Hutchinson fractures involve the radial styloid.
In children, shaft fractures commonly present as torus fractures, greenstick fractures, or plastic deformities. Distal fractures in pediatric patients frequently involve Salter–Harris growth plate injuries.
Etiology
Common mechanisms include direct blows to the forearm, longitudinal compression such as falls on an outstretched hand, horizontal force, and excessive pronation, supination, hyperextension, or hyperflexion.
Diagnosis Signs And Symptoms
Patients typically present with pain, deformity, swelling, and limited function. History should include mechanism of injury, hand dominance, occupational or repetitive stress factors, and prior bone disease or fractures.
Physical examination focuses on deformity, tenderness, crepitus, edema, ecchymosis, joint effusions at the elbow or wrist, abnormal mobility, and careful assessment of neurovascular status. Findings concerning for compartment syndrome require urgent attention.
Essential Workup
Suspected forearm fractures require anteroposterior and lateral radiographs that include the wrist, forearm, and elbow to evaluate joints above and below the injury.
Diagnosis Tests And Interpretation
Imaging may include CT for complex or intra-articular fractures. Compartment pressure measurement is indicated when compartment syndrome is suspected. Laboratory studies are generally reserved for preoperative evaluation.
Differential Diagnosis
Consider muscle or ligament injury, elbow or wrist dislocations, contusions or hematomas, infection, tumors, osteomyelitis, vascular or neurologic injury, arthritis, and in children, normal growth plates or nutrient vessels that may mimic fractures.
Treatment
Prehospital care includes elevation, splinting, and immobilization of the elbow and wrist. Open fractures should be covered with sterile dressings and not reduced in the field.
In the emergency department, nondisplaced shaft fractures are treated with long-arm splinting and orthopedic referral. Displaced shaft fractures often require orthopedic consultation and operative fixation.
Nondisplaced distal fractures are managed with sugar-tong or anteroposterior splints and referral. Simple Colles or Smith fractures may be reduced in the emergency department and splinted, while complicated patterns require orthopedic consultation. Barton and Hutchinson fractures are splinted and referred, with operative management as needed.
Open fractures require antibiotics, tetanus prophylaxis, splinting, and immediate orthopedic consultation. Any fracture associated with neurovascular compromise or compartment syndrome requires urgent specialist evaluation.
In pediatric patients, minimally angulated torus or greenstick fractures may be splinted and referred, while plastic deformities and Salter–Harris fractures require orthopedic consultation.
Medication
Pain control is achieved with acetaminophen, NSAIDs, or opioids as appropriate. Open fractures require parenteral antibiotics such as first-generation cephalosporins, with additional coverage for contaminated wounds. Tetanus prophylaxis should be updated as indicated.
Follow Up Disposition
Admission is required for open fractures, compartment syndrome, neurovascular compromise, fractures requiring immediate surgery, or suspected nonaccidental trauma.
Discharge is appropriate after adequate reduction and immobilization, confirmation of intact neurovascular status, effective pain control, and ensured orthopedic follow-up with clear splint and cast care instructions.
Clinical Insights And Common Pitfalls
Always evaluate for a second fracture or associated joint dislocation. Reassess neurovascular status frequently and maintain a high index of suspicion for evolving compartment syndrome.
Basics Description
Forearm shaft fractures may involve one or both bones and are frequently displaced due to muscular contraction. These injuries may be associated with joint dislocations, including Galeazzi fractures, which involve a distal radius fracture with distal radioulnar joint dislocation, and Monteggia fractures, which involve a proximal ulna fracture with radial head dislocation.
Distal forearm fractures include several classic patterns. Colles fractures result from hyperextension with dorsal displacement of the distal radius fragment and are often associated with ulnar styloid injury. Smith fractures occur with hyperflexion and result in volar displacement. Barton fractures are intra-articular fractures of the dorsal rim of the distal radius and may involve carpal dislocation. Hutchinson fractures involve the radial styloid.
In children, shaft fractures commonly present as torus fractures, greenstick fractures, or plastic deformities. Distal fractures in pediatric patients frequently involve Salter–Harris growth plate injuries.
Etiology
Common mechanisms include direct blows to the forearm, longitudinal compression such as falls on an outstretched hand, horizontal force, and excessive pronation, supination, hyperextension, or hyperflexion.
Diagnosis Signs And Symptoms
Patients typically present with pain, deformity, swelling, and limited function. History should include mechanism of injury, hand dominance, occupational or repetitive stress factors, and prior bone disease or fractures.
Physical examination focuses on deformity, tenderness, crepitus, edema, ecchymosis, joint effusions at the elbow or wrist, abnormal mobility, and careful assessment of neurovascular status. Findings concerning for compartment syndrome require urgent attention.
Essential Workup
Suspected forearm fractures require anteroposterior and lateral radiographs that include the wrist, forearm, and elbow to evaluate joints above and below the injury.
Diagnosis Tests And Interpretation
Imaging may include CT for complex or intra-articular fractures. Compartment pressure measurement is indicated when compartment syndrome is suspected. Laboratory studies are generally reserved for preoperative evaluation.
Differential Diagnosis
Consider muscle or ligament injury, elbow or wrist dislocations, contusions or hematomas, infection, tumors, osteomyelitis, vascular or neurologic injury, arthritis, and in children, normal growth plates or nutrient vessels that may mimic fractures.
Treatment
Prehospital care includes elevation, splinting, and immobilization of the elbow and wrist. Open fractures should be covered with sterile dressings and not reduced in the field.
In the emergency department, nondisplaced shaft fractures are treated with long-arm splinting and orthopedic referral. Displaced shaft fractures often require orthopedic consultation and operative fixation.
Nondisplaced distal fractures are managed with sugar-tong or anteroposterior splints and referral. Simple Colles or Smith fractures may be reduced in the emergency department and splinted, while complicated patterns require orthopedic consultation. Barton and Hutchinson fractures are splinted and referred, with operative management as needed.
Open fractures require antibiotics, tetanus prophylaxis, splinting, and immediate orthopedic consultation. Any fracture associated with neurovascular compromise or compartment syndrome requires urgent specialist evaluation.
In pediatric patients, minimally angulated torus or greenstick fractures may be splinted and referred, while plastic deformities and Salter–Harris fractures require orthopedic consultation.
Medication
Pain control is achieved with acetaminophen, NSAIDs, or opioids as appropriate. Open fractures require parenteral antibiotics such as first-generation cephalosporins, with additional coverage for contaminated wounds. Tetanus prophylaxis should be updated as indicated.
Follow Up Disposition
Admission is required for open fractures, compartment syndrome, neurovascular compromise, fractures requiring immediate surgery, or suspected nonaccidental trauma.
Discharge is appropriate after adequate reduction and immobilization, confirmation of intact neurovascular status, effective pain control, and ensured orthopedic follow-up with clear splint and cast care instructions.
Clinical Insights And Common Pitfalls
Always evaluate for a second fracture or associated joint dislocation. Reassess neurovascular status frequently and maintain a high index of suspicion for evolving compartment syndrome.
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IEmergency And Acute Medicine – Duodenal Trauma
Basics Description
The duodenum is a 12-inch long, C-shaped structure extending from the pylorus to the ligament of Treitz and is divided into four sections. The distal portion of the first section and the remaining three sections are retroperitoneal. It lies mostly over the first three lumbar vertebrae, with the second portion being the most commonly injured. Types of injury include duodenal wall hematoma, wall perforation, hemorrhage including retroperitoneal bleeding, and crush injury. Duodenal trauma accounts for 3–5% of all traumatic abdominal injuries. Penetrating trauma causes approximately 75% of cases, with mortality ranging from 13–28%, often due to exsanguination. Blunt trauma carries higher mortality because of greater injury force and delayed diagnosis related to the retroperitoneal location. If diagnosed within 24 hours, mortality is approximately 11%; if delayed beyond 24 hours, mortality approaches 40%, with late deaths commonly due to sepsis.
Pediatric Considerations
Most pediatric duodenal injuries result from recreational trauma such as bicycle handlebar injuries. Intramural duodenal hematomas may be associated with nonaccidental trauma; suspected cases require immediate referral to child protective services. In children, hematomas most commonly involve the first portion of the duodenum.
Pregnancy Considerations
Retroperitoneal hemorrhage is more common due to increased abdominal and pelvic vascularity. The enlarged uterus may provide partial protection from bowel injury, and peritoneal irritation may be blunted, necessitating a higher index of suspicion.
Etiology
Blunt trauma mechanisms include shear strain from rapid acceleration–deceleration at points of fixation and tensile strain from direct compression or stretching. Penetrating trauma is the most common cause overall and may create cavitation with subsequent infection.
Diagnosis Signs And Symptoms
Symptoms may be minimal and nonspecific, including vague abdominal, flank, or back pain. High gastrointestinal obstruction may occur with duodenal hematomas.
History
Penetrating or blunt abdominal trauma.
Physical-Exam
Retroperitoneal injury may present subtly with right upper quadrant pain, nausea, vomiting, tachycardia, and fever. Intraperitoneal involvement presents with signs of peritonitis.
Essential Workup
Obtain basic laboratory studies including amylase. Perform an acute abdominal series or CT imaging. Diagnostic peritoneal lavage or exploratory laparotomy is indicated in unstable patients with high clinical suspicion.
Diagnosis Tests And Interpretation
Laboratory studies are generally nonspecific; approximately 50% of patients have elevated serum amylase, and rising leukocytosis may suggest missed injury. FAST examination is validated for hemoperitoneum but is unreliable for duodenal injury, with one-third of retroperitoneal injuries having a normal FAST. Upright chest and abdominal radiographs may show intraperitoneal or retroperitoneal air, air in the biliary tree, rightward scoliosis, loss of psoas shadow, or air around the right kidney. Air insufflation via nasogastric tube may enhance detection of retroperitoneal air. Intramural hematomas may show a coiled-spring appearance. CT with oral and IV contrast is the preferred diagnostic modality, identifying retroperitoneal gas, contrast extravasation, duodenal wall thickening, periduodenal fluid, sentinel clot, or sausage-shaped intramural masses. Exploratory laparotomy remains the definitive diagnostic test when suspicion persists despite negative studies. Diagnostic peritoneal lavage may reveal blood, bile, or bowel contents but has a false-negative rate of up to 65%.
Differential Diagnosis
Hollow viscus injuries involving stomach or intestines, liver and biliary injuries, vascular injuries including aortic or mesenteric vessels, and postoperative complications such as infection or suture dehiscence.
Treatment Pre Hospital
Follow standard trauma protocols. Clear documentation of mechanism of injury and transport to an appropriate trauma center are essential.
Initial Stabilization And Therapy
Secure the airway and initiate resuscitation as needed. Provide aggressive fluid resuscitation with warmed crystalloids and transfuse blood products when indicated. Place central venous access in unstable patients. Initiate nasogastric decompression and obtain early trauma surgery consultation.
Emergency Department Treatment And Procedures
Administer tetanus prophylaxis and broad-spectrum antibiotics for penetrating injuries. Definitive management typically requires laparotomy with duodenal exploration. Low-grade blunt injuries (grade I or II) are often managed nonoperatively, though up to 10% may fail conservative therapy. Antibiotics are essential in cases of perforation to prevent sepsis.
Medication
Cefoxitin 2 g IV every 6 hours (pediatric dose 40 mg/kg) or levofloxacin 750 mg IV or ciprofloxacin 400 mg IV daily combined with metronidazole 500 mg IV every 8 hours.
Follow-Up And Disposition
All patients with duodenal injury require admission to a trauma surgical service. Minor hematomas may require nasogastric decompression for obstruction for up to seven days with close observation for expansion or rupture. No patient with confirmed duodenal trauma should be discharged from the emergency department. Complications include intra-abdominal abscess, duodenal fistula, pancreatic fistula, and sepsis.
Issues For Referral
Duodenal injuries are graded using the American Association for the Surgery of Trauma Duodenal Injury Scale, with most injuries being grade II or III. Approximately 80% are managed with primary repair.
Follow-Up Recommendations
All confirmed injuries require inpatient management. If diagnostic studies are negative, arrange follow-up with a primary care physician within 24–48 hours. Begin with clear liquids and advance diet as tolerated.
Pearls And Pitfalls
Delayed or missed diagnosis significantly increases morbidity and mortality. Physical examination may be misleading due to the retroperitoneal location of the duodenum. Persistent clinical suspicion warrants immediate surgical consultation even with negative diagnostic tests.
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Emergency and Acute Medicine – Domestic Violence
Basics
Description
Intimate partner violence (IPV) is physical, sexual, or psychological abuse by a current or former partner. It occurs in adult and adolescent intimate relationships across all socioeconomic groups.
Etiology
Most victims are women injured by male perpetrators, but men and individuals in same-sex relationships may also be victims. Risk factors include female sex, young age (20–24 years), and separation from a partner or spouse.
Diagnosis
Directly asking about IPV increases identification of victims.
Signs and symptoms
Traumatic injuries include a wide range of presentations. Unwitnessed head, neck, and facial injuries are common. Forearm bruises or fractures may suggest defensive posture. Injuries may be in various stages of healing.
Psychiatric and medical associations include chronic pain syndromes, depression, somatization, anxiety, suicidality, and substance abuse.
Alert
Clinical clues include discrepancies between history and physical findings, a partner refusing to leave the patient alone with the provider, delay in seeking care, any injury during pregnancy, concerning patient–partner interactions, and multiple symptoms without clear physical findings.
History
Screening questions can identify IPV. Evidence is mixed regarding improved outcomes, but IPV screening is required by the Joint Commission and supported by some professional organizations. Screening should be direct, nonjudgmental, supportive, and private. Computer-based ED screening may be effective. Consider IPV in patients with substance abuse or intoxication, who may be at higher risk and under-identified.
Physical examination
Perform a careful examination for traumatic injuries and a mental status assessment.
Essential workup
After IPV identification, perform a directed evaluation for traumatic injuries and acute medical or behavioral health conditions. Assess risk for future injury or victimization.
Differential diagnosis
Maintain a high index of suspicion for IPV in patients with traumatic injuries, behavioral health complaints, and medical presentations such as genitourinary or gynecologic complaints and multiple somatic symptoms.
Treatment
Prehospital
Provide standard trauma evaluation and treatment. Incorporate accurate EMS descriptions into the medical record.
Initial stabilization and therapy
Provide timely medical care and ongoing emotional support throughout evaluation and treatment.
Emergency department treatment and procedures
Interview the patient privately without family members present. Use a professional medical interpreter when needed. Document thoroughly using the patient’s exact words; careful documentation is admissible in court. Record extent and location of injuries; diagrams or photographs are helpful.
If stable for discharge, assess lethality risk, including escalating violence, threats of homicide or suicide, and access to lethal weapons. Collaborate with the patient to create a discharge plan aligned with their wishes. Arrange referrals for victim services, emergency shelter information, hotlines, restraining order information, and legal services.
Mandatory reporting varies by state and may increase risk or pose ethical challenges. Inform patients of reporting requirements and potential outcomes.
Medication
Acetaminophen 650–975 mg PO.
Morphine sulfate 0.1 mg/kg/dose IV or IM.
Follow-up and disposition
Admission criteria
Use standard admission guidelines based on injury severity. Medically stable patients with imminent safety risk may require hospitalization until a safe plan is established.
Discharge criteria
Patients whose safety is ensured and whose injuries are manageable as an outpatient may be discharged.
Issues for referral
Advocacy services availability varies by region.
Follow-up recommendations
Provide information on outpatient services and emergency shelter options.
Pearls and pitfalls
Failure to consider IPV in the differential diagnosis. Inadequate, nonobjective documentation of assault details and exam findings. Failure to assess discharge safety and arrange appropriate referrals. Mandatory reporting laws remain controversial and may have unintended consequences.
Basics
Description
Intimate partner violence (IPV) is physical, sexual, or psychological abuse by a current or former partner. It occurs in adult and adolescent intimate relationships across all socioeconomic groups.
Etiology
Most victims are women injured by male perpetrators, but men and individuals in same-sex relationships may also be victims. Risk factors include female sex, young age (20–24 years), and separation from a partner or spouse.
Diagnosis
Directly asking about IPV increases identification of victims.
Signs and symptoms
Traumatic injuries include a wide range of presentations. Unwitnessed head, neck, and facial injuries are common. Forearm bruises or fractures may suggest defensive posture. Injuries may be in various stages of healing.
Psychiatric and medical associations include chronic pain syndromes, depression, somatization, anxiety, suicidality, and substance abuse.
Alert
Clinical clues include discrepancies between history and physical findings, a partner refusing to leave the patient alone with the provider, delay in seeking care, any injury during pregnancy, concerning patient–partner interactions, and multiple symptoms without clear physical findings.
History
Screening questions can identify IPV. Evidence is mixed regarding improved outcomes, but IPV screening is required by the Joint Commission and supported by some professional organizations. Screening should be direct, nonjudgmental, supportive, and private. Computer-based ED screening may be effective. Consider IPV in patients with substance abuse or intoxication, who may be at higher risk and under-identified.
Physical examination
Perform a careful examination for traumatic injuries and a mental status assessment.
Essential workup
After IPV identification, perform a directed evaluation for traumatic injuries and acute medical or behavioral health conditions. Assess risk for future injury or victimization.
Differential diagnosis
Maintain a high index of suspicion for IPV in patients with traumatic injuries, behavioral health complaints, and medical presentations such as genitourinary or gynecologic complaints and multiple somatic symptoms.
Treatment
Prehospital
Provide standard trauma evaluation and treatment. Incorporate accurate EMS descriptions into the medical record.
Initial stabilization and therapy
Provide timely medical care and ongoing emotional support throughout evaluation and treatment.
Emergency department treatment and procedures
Interview the patient privately without family members present. Use a professional medical interpreter when needed. Document thoroughly using the patient’s exact words; careful documentation is admissible in court. Record extent and location of injuries; diagrams or photographs are helpful.
If stable for discharge, assess lethality risk, including escalating violence, threats of homicide or suicide, and access to lethal weapons. Collaborate with the patient to create a discharge plan aligned with their wishes. Arrange referrals for victim services, emergency shelter information, hotlines, restraining order information, and legal services.
Mandatory reporting varies by state and may increase risk or pose ethical challenges. Inform patients of reporting requirements and potential outcomes.
Medication
Acetaminophen 650–975 mg PO.
Morphine sulfate 0.1 mg/kg/dose IV or IM.
Follow-up and disposition
Admission criteria
Use standard admission guidelines based on injury severity. Medically stable patients with imminent safety risk may require hospitalization until a safe plan is established.
Discharge criteria
Patients whose safety is ensured and whose injuries are manageable as an outpatient may be discharged.
Issues for referral
Advocacy services availability varies by region.
Follow-up recommendations
Provide information on outpatient services and emergency shelter options.
Pearls and pitfalls
Failure to consider IPV in the differential diagnosis. Inadequate, nonobjective documentation of assault details and exam findings. Failure to assess discharge safety and arrange appropriate referrals. Mandatory reporting laws remain controversial and may have unintended consequences.
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Emergency And Acute Medicine – Drowning
Basics Description
Drowning is a process resulting in primary respiratory impairment from submersion or immersion in a liquid medium. Fatal drowning refers to death at any time as a result of the drowning process, while nonfatal drowning occurs when the victim survives after interruption of submersion. Water rescue describes submersion or immersion without respiratory impairment. All drowning victims aspirate some amount of liquid; previously used terms such as “wet” and “dry” drowning are obsolete. The final common pathway is hypoxia, with no clinically significant difference between freshwater and saltwater drowning.
Pathophysiology
Aspiration of small volumes of water decreases lung compliance, causing ventilation–perfusion mismatch and intrapulmonary shunting, usually without major electrolyte disturbances. Grossly contaminated water increases the risk of pulmonary infection. Hypoxemia leads to lactic acidosis, multisystem organ dysfunction, noncardiogenic pulmonary edema, myocardial dysrhythmias, coagulation abnormalities including disseminated intravascular coagulation, acute renal failure, and cerebral hypoxia resulting in cerebral edema and increased intracranial pressure.
Pediatric Considerations
Hypothermia is more common in children due to a higher body surface area–to–mass ratio and may be neuroprotective by lowering metabolic rate. The diving reflex, particularly in young children exposed to cold water, causes bradycardia and preferential blood flow to the heart and brain, delaying hypoxic injury.
Alert
Risk factors include inadequate supervision, alcohol or drug use, limited swimming ability, trauma, seizure disorder, risky behavior, pre-existing medical conditions, suicide attempt, and poor water safety education.
Diagnosis Signs And Symptoms
Findings include cardiopulmonary arrest, cyanosis, dyspnea, copious pulmonary secretions, altered mental status or loss of consciousness, hypothermia, cerebral edema or neurologic injury, and evidence of trauma. Cervical spine injury is rare.
Essential Workup
Obtain witness and EMS information, initiate early airway management and cardiopulmonary resuscitation when indicated, and measure core temperature to assess hypothermia.
Diagnostic Tests And Interpretation
Laboratory studies include arterial blood gas, complete blood count, electrolytes, blood urea nitrogen, creatinine, glucose, and alcohol or toxicology screening. Imaging includes chest radiography, which may show infiltrates or acute respiratory distress syndrome but can be normal initially, electrocardiography showing bradyarrhythmias or tachyarrhythmias, and computed tomography of the brain or cervical spine when indicated.
Differential Diagnosis
Consider dysrhythmias such as long QT syndrome, myocardial infarction, seizure, syncope, trauma, or suicide attempt as causes of submersion. In pediatric patients, always consider abuse or neglect, particularly in bathtub incidents.
Treatment Prehospital
Address airway, breathing, and circulation, avoid further aspiration, secure the airway, initiate early cardiopulmonary resuscitation, apply cervical spine precautions when indicated, and begin rewarming. Abdominal thrusts are not recommended as they delay effective resuscitation and increase aspiration risk.
Initial Stabilization And Therapy
Manage airway and oxygenation, remove wet clothing, initiate rewarming, and support circulation.
Emergency Department Treatment
Correct hypoxemia, intubate with positive end-expiratory pressure if needed, treat acidosis, and evaluate for traumatic injuries. In cardiac arrest, follow advanced cardiac life support protocols and continue resuscitation until core temperature exceeds 32°C or return of spontaneous circulation occurs. Corticosteroids have no proven benefit. Poor prognostic indicators include prolonged submersion, severe acidosis, need for cardiopulmonary resuscitation, low oxygen saturation, and low Glasgow Coma Scale score.
Medication
Epinephrine, vasopressin, lidocaine, and sodium bicarbonate may be administered when clinically indicated.
Follow-Up And Disposition
Patients with respiratory symptoms, neurologic abnormalities, abnormal imaging or laboratory findings, or those requiring ventilatory support should be admitted, often to intensive care. Symptomatic patients or those with significant submersion history require observation. Patients may be discharged only after at least eight hours of observation with no respiratory distress, no neurologic impairment, and reliable caregivers.
Pearls And Pitfalls
All drowning patients require observation for delayed complications. Hypothermia may be protective. Prevention through supervision and water safety education is essential.
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Emergency and Acute Medicine – Dizziness
Basics
Description
Patient descriptions of dizziness (vertigo, lightheadedness, disequilibrium, or nonspecific terms) are often unreliable and should not guide decision making. A safer approach emphasizes associated symptoms, timing, and triggers, followed by a focused physical examination for diagnostic clues. Dizziness is categorized using a “timing and triggers” framework. Acute vestibular syndrome presents with abrupt onset of persistent dizziness. Episodic vestibular syndrome consists of spontaneous episodes lasting minutes to hours. Positional vestibular syndrome causes very brief episodes, typically 20–50 seconds, triggered by head or body position changes. Chronic vestibular syndrome has a gradual onset and persists for weeks to months or longer.
Etiology
General medical causes account for nearly half of cases and include arrhythmias, hypoglycemia and other metabolic disturbances, hypovolemia, sepsis, infections, and low cardiac output states. Otologic or vestibular causes represent about one third and include benign paroxysmal positional vertigo, labyrinthitis, and vestibular neuritis. Neurologic causes include stroke, transient ischemic attack, and vestibular migraine. Psychiatric causes such as anxiety and depression account for a smaller proportion.
Diagnosis
Signs and symptoms
History should define the timing and trigger pattern and assess for red flags. Key questions address onset, persistence versus intermittence, duration of episodes, positional triggers, associated hearing or neurologic symptoms, recent head injury, and new medications. Review of systems should focus on clues to serious disease, including headache suggesting stroke or dissection, ear pain suggesting otitis or mastoiditis, hearing changes suggesting Ménière disease or labyrinthitis, neck pain suggesting vertebral dissection, fever suggesting infection, dyspnea suggesting pulmonary embolism or anemia, chest pain suggesting acute coronary syndrome, fluid losses suggesting hypovolemia, and pregnancy-related complications.
Exacerbation with head motion occurs in both central and peripheral causes; however, dizziness only with head motion in an otherwise asymptomatic patient suggests a peripheral etiology.
Physical examination
Vital signs are assessed, including orthostatic testing. Otoscopic examination, cardiac examination, and a complete neurologic examination are essential. Cranial nerves II–XII should be evaluated with special attention to nystagmus. Gait observation and cerebellar testing are performed. The Dix–Hallpike maneuver is reserved for intermittent symptoms.
The HINTS examination is used only in patients with acute vestibular syndrome and consists of head impulse testing, nystagmus assessment, and testing for skew deviation. In the first 48 hours of symptoms, this exam can be more sensitive than MRI for detecting stroke. A normal head impulse test without corrective saccade suggests a central cause, whereas a corrective saccade suggests a peripheral cause. Direction-changing, vertical, or torsional nystagmus suggests a central etiology, while direction-fixed nystagmus suggests a peripheral cause. A vertical corrective saccade on alternate cover testing indicates a central process. Any concerning component should prompt concern for stroke.
Essential workup
History and physical examination are mandatory and often sufficient. Triage focuses on abnormal vital signs, altered mentation, or focal deficits. The evaluation is guided by timing, triggers, and telltale signs such as HINTS findings in acute dizziness.
Diagnosis tests and interpretation
Laboratory testing may include serum glucose, hematocrit if anemia is suspected, electrolytes, renal function tests, venous blood gas when carbon monoxide or hypercapnia is considered, urinalysis for infection, and toxicology screening when exposure is suspected.
Imaging includes noncontrast head CT when acute hemorrhage is suspected, recognizing limited sensitivity for posterior circulation ischemia. MRI is indicated when no alternative etiology is found and the HINTS exam is concerning.
Diagnostic procedures may include Dix–Hallpike testing, head thrust testing, and skew deviation assessment. Electrocardiography is used to detect arrhythmia or myocardial ischemia. Lumbar puncture is considered for unexplained headache or infectious signs.
Differential diagnosis
Acute vestibular syndrome includes benign causes such as vestibular neuritis and labyrinthitis and dangerous causes such as cerebellar or brainstem stroke. Episodic vestibular syndrome includes vestibular migraine and transient ischemic attack. Positional vestibular syndrome includes benign paroxysmal positional vertigo and, rarely, central paroxysmal positional vertigo from posterior fossa mass. Chronic vestibular syndrome includes psychiatric causes, medication effects, and rarely posterior fossa tumors.
Treatment
Initial stabilization and therapy
Stabilization is directed by abnormal vital signs or associated systemic illness. Management depends on classification of dizziness and suspected etiology.
Emergency department treatment and procedures
Symptomatic control is provided while evaluation proceeds. If benign paroxysmal positional vertigo is suspected, the Epley maneuver should be performed.
Medication
Symptomatic medications include ondansetron, diazepam, diphenhydramine, meclizine for short-term use only, and promethazine. Response to these agents does not establish etiology.
Follow-up and disposition
Admission criteria
Admission decisions depend on the underlying cause and associated symptoms, particularly concern for stroke, cardiac disease, or systemic illness.
Discharge criteria
Patients with isolated dizziness, normal neurologic and oculomotor examinations, and ability to function safely at home may be discharged with instructions.
Issues for referral
Outpatient referral may be to primary care, otolaryngology, or neurology depending on the suspected cause.
Follow-up recommendations
Patients should avoid driving or operating machinery while symptomatic and rise slowly from sitting or lying positions. They should seek immediate care for new neurologic deficits, signs of infection, acute cardiopulmonary symptoms, or significant fluid losses.
Pearls and pitfalls
The timing-and-triggers approach improves diagnostic accuracy. Advanced age and vascular risk factors increase stroke likelihood. Noncontrast CT is insensitive for acute cerebellar stroke, and cerebellar infarction may present with isolated dizziness. A negative head impulse test is concerning for central pathology. The treatment for benign paroxysmal positional vertigo is the Epley maneuver, not vestibular suppressants.
Basics
Description
Patient descriptions of dizziness (vertigo, lightheadedness, disequilibrium, or nonspecific terms) are often unreliable and should not guide decision making. A safer approach emphasizes associated symptoms, timing, and triggers, followed by a focused physical examination for diagnostic clues. Dizziness is categorized using a “timing and triggers” framework. Acute vestibular syndrome presents with abrupt onset of persistent dizziness. Episodic vestibular syndrome consists of spontaneous episodes lasting minutes to hours. Positional vestibular syndrome causes very brief episodes, typically 20–50 seconds, triggered by head or body position changes. Chronic vestibular syndrome has a gradual onset and persists for weeks to months or longer.
Etiology
General medical causes account for nearly half of cases and include arrhythmias, hypoglycemia and other metabolic disturbances, hypovolemia, sepsis, infections, and low cardiac output states. Otologic or vestibular causes represent about one third and include benign paroxysmal positional vertigo, labyrinthitis, and vestibular neuritis. Neurologic causes include stroke, transient ischemic attack, and vestibular migraine. Psychiatric causes such as anxiety and depression account for a smaller proportion.
Diagnosis
Signs and symptoms
History should define the timing and trigger pattern and assess for red flags. Key questions address onset, persistence versus intermittence, duration of episodes, positional triggers, associated hearing or neurologic symptoms, recent head injury, and new medications. Review of systems should focus on clues to serious disease, including headache suggesting stroke or dissection, ear pain suggesting otitis or mastoiditis, hearing changes suggesting Ménière disease or labyrinthitis, neck pain suggesting vertebral dissection, fever suggesting infection, dyspnea suggesting pulmonary embolism or anemia, chest pain suggesting acute coronary syndrome, fluid losses suggesting hypovolemia, and pregnancy-related complications.
Exacerbation with head motion occurs in both central and peripheral causes; however, dizziness only with head motion in an otherwise asymptomatic patient suggests a peripheral etiology.
Physical examination
Vital signs are assessed, including orthostatic testing. Otoscopic examination, cardiac examination, and a complete neurologic examination are essential. Cranial nerves II–XII should be evaluated with special attention to nystagmus. Gait observation and cerebellar testing are performed. The Dix–Hallpike maneuver is reserved for intermittent symptoms.
The HINTS examination is used only in patients with acute vestibular syndrome and consists of head impulse testing, nystagmus assessment, and testing for skew deviation. In the first 48 hours of symptoms, this exam can be more sensitive than MRI for detecting stroke. A normal head impulse test without corrective saccade suggests a central cause, whereas a corrective saccade suggests a peripheral cause. Direction-changing, vertical, or torsional nystagmus suggests a central etiology, while direction-fixed nystagmus suggests a peripheral cause. A vertical corrective saccade on alternate cover testing indicates a central process. Any concerning component should prompt concern for stroke.
Essential workup
History and physical examination are mandatory and often sufficient. Triage focuses on abnormal vital signs, altered mentation, or focal deficits. The evaluation is guided by timing, triggers, and telltale signs such as HINTS findings in acute dizziness.
Diagnosis tests and interpretation
Laboratory testing may include serum glucose, hematocrit if anemia is suspected, electrolytes, renal function tests, venous blood gas when carbon monoxide or hypercapnia is considered, urinalysis for infection, and toxicology screening when exposure is suspected.
Imaging includes noncontrast head CT when acute hemorrhage is suspected, recognizing limited sensitivity for posterior circulation ischemia. MRI is indicated when no alternative etiology is found and the HINTS exam is concerning.
Diagnostic procedures may include Dix–Hallpike testing, head thrust testing, and skew deviation assessment. Electrocardiography is used to detect arrhythmia or myocardial ischemia. Lumbar puncture is considered for unexplained headache or infectious signs.
Differential diagnosis
Acute vestibular syndrome includes benign causes such as vestibular neuritis and labyrinthitis and dangerous causes such as cerebellar or brainstem stroke. Episodic vestibular syndrome includes vestibular migraine and transient ischemic attack. Positional vestibular syndrome includes benign paroxysmal positional vertigo and, rarely, central paroxysmal positional vertigo from posterior fossa mass. Chronic vestibular syndrome includes psychiatric causes, medication effects, and rarely posterior fossa tumors.
Treatment
Initial stabilization and therapy
Stabilization is directed by abnormal vital signs or associated systemic illness. Management depends on classification of dizziness and suspected etiology.
Emergency department treatment and procedures
Symptomatic control is provided while evaluation proceeds. If benign paroxysmal positional vertigo is suspected, the Epley maneuver should be performed.
Medication
Symptomatic medications include ondansetron, diazepam, diphenhydramine, meclizine for short-term use only, and promethazine. Response to these agents does not establish etiology.
Follow-up and disposition
Admission criteria
Admission decisions depend on the underlying cause and associated symptoms, particularly concern for stroke, cardiac disease, or systemic illness.
Discharge criteria
Patients with isolated dizziness, normal neurologic and oculomotor examinations, and ability to function safely at home may be discharged with instructions.
Issues for referral
Outpatient referral may be to primary care, otolaryngology, or neurology depending on the suspected cause.
Follow-up recommendations
Patients should avoid driving or operating machinery while symptomatic and rise slowly from sitting or lying positions. They should seek immediate care for new neurologic deficits, signs of infection, acute cardiopulmonary symptoms, or significant fluid losses.
Pearls and pitfalls
The timing-and-triggers approach improves diagnostic accuracy. Advanced age and vascular risk factors increase stroke likelihood. Noncontrast CT is insensitive for acute cerebellar stroke, and cerebellar infarction may present with isolated dizziness. A negative head impulse test is concerning for central pathology. The treatment for benign paroxysmal positional vertigo is the Epley maneuver, not vestibular suppressants.
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Emergency And Acute Medicine – Dysfunctional Uterine Bleeding
Basics Description
Abnormal uterine bleeding refers to an alteration in the pattern or volume of normal menses. Typical menstrual blood loss is 30–80 mL, with a normal cycle interval of 28 ± 7 days. Abnormal uterine bleeding is classified into dysfunctional uterine bleeding (DUB) and organic uterine bleeding. Dysfunctional uterine bleeding is hormonally mediated, divided into anovulatory and ovulatory categories, is not due to organic or iatrogenic causes, and is therefore a diagnosis of exclusion. Organic uterine bleeding is related to systemic illness or disease of the reproductive tract.
Etiology
Anovulatory bleeding, the most common cause, results from unopposed estrogen stimulation of the proliferative endometrium. Neuroendocrine dysfunction may be associated with polycystic ovarian syndrome, very low-calorie diets, rapid weight changes, intense exercise, anorexia, psychological stress, obesity, medications, hypothyroidism, or primary hypothalamic dysfunction. Ovulatory bleeding is caused by inadequate uterine prostaglandin F2α, increased uterine contractility, or excessive prostacycline production, which diminishes platelet function and increases uterine vasodilation.
Pediatric Considerations
Anovulatory bleeding is common during adolescence due to immaturity of the hypothalamic–pituitary–ovarian axis.
Diagnosis Signs And Symptoms
Patients present with abnormal uterine bleeding in the absence of systemic or structural disease. It is most common in perimenarcheal and perimenopausal women and is typically painless. Anovulatory patterns include metrorrhagia with irregular bleeding between periods, menorrhagia with regular cycles and excessive flow greater than 80 mL or lasting more than 7 days, oligomenorrhea with cycles longer than 35 days, and menometrorrhagia with heavy and irregular bleeding.
History
History focuses on bleeding pattern, duration, volume, associated symptoms, medication use, and risk factors for pregnancy or systemic disease.
Physical-Exam
Acne, hirsutism, and obesity suggest polycystic ovarian syndrome. Pelvic examination typically reveals mild to moderate bleeding. Pallor, tachycardia, hypotension, and orthostasis indicate severe blood loss. Evaluate for trauma or foreign bodies.
Alert
Hemodynamic instability is rare in dysfunctional uterine bleeding; if present, consider ectopic pregnancy or another cause of acute hemorrhage.
Essential Workup
A pregnancy test is mandatory.
Diagnosis Tests And Interpretation
Laboratory evaluation includes pregnancy test, complete blood count, and coagulation studies. Iron studies, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, prolactin, and cervical cultures are typically deferred for outpatient follow-up. Pelvic ultrasound may identify uterine, tubal, or ovarian pathology and help exclude organic causes. Dilation and curettage may be required for heavy bleeding unresponsive to therapy. Endometrial biopsy is recommended for patients older than 35 years.
Differential Diagnosis
Pregnancy-related causes include threatened, incomplete, or spontaneous abortion, ectopic pregnancy, and molar pregnancy. Infectious causes include vaginitis, cervicitis, and pelvic inflammatory disease. Coagulopathies include von Willebrand disease, idiopathic thrombocytopenic purpura, platelet disorders, and thalassemia. Medication-related causes include warfarin, aspirin, oral contraceptives, tricyclic antidepressants, and antipsychotics. Systemic illnesses include adrenal, hepatic, renal, thyroid disease, diabetes, and other endocrinopathies. Anatomic causes include fibroids, endometriosis, polyps, endometrial hyperplasia, malignancy, intrauterine devices, and trauma.
Treatment Pre Hospital
Administer intravenous crystalloids as needed for hypotension or tachycardia secondary to heavy bleeding.
Initial Stabilization And Therapy
Follow ABCs. Transfuse packed red blood cells for significant bleeding unresponsive to crystalloid resuscitation.
Emergency Department Treatment And Procedures
Observation is usually sufficient for mild bleeding. Administer intravenous fluids or packed red blood cells for continued bleeding or hemodynamic instability. Obtain gynecology consultation for severe bleeding unresponsive to medical therapy. Dilation and curettage may be necessary for instability. Endometrial ablation or hysterectomy is reserved for refractory cases.
Medication
Conjugated estrogen is indicated for heavy bleeding with hemodynamic instability at 2.5 mg orally every 6 hours or 25 mg intravenously, repeatable after 3 hours if needed. Ibuprofen 400–800 mg orally every 8 hours reduces prostaglandin synthesis. Medroxyprogesterone acetate 5–10 mg orally daily is added once bleeding subsides. Combined oral contraceptives containing ethinyl estradiol 35 μg and norethindrone 1 mg may be given four times daily for one week. Tranexamic acid 1,300 mg orally three times daily for five days may be used, though limited by gastrointestinal side effects and allergy risk. Medications may be deferred in mild cases with outpatient gynecology referral.
Follow-Up And Disposition
Admission is required for significant blood loss, continued bleeding, or hemodynamic instability requiring aggressive resuscitation or operative intervention. Most patients may be discharged once bleeding is controlled and vital signs are stable, with gynecology follow-up arranged.
Issues For Referral
Endometrial biopsy is indicated for patients older than 35 years. Follow-up with gynecology or primary care is essential to evaluate for ongoing blood loss or malignancy.
Pearls And Pitfalls
Dysfunctional uterine bleeding is a diagnosis of exclusion. Only 2% of endometrial carcinomas occur before age 40. Hemodynamic instability makes DUB an unlikely primary diagnosis.
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Emergency And Acute Medicine – Dysphagia
Basics Description
Dysphagia is defined as difficulty swallowing and may result from neuromuscular or mechanical causes. It can involve impairment at the oropharyngeal or esophageal level, and careful clinical distinction is essential because etiologies, workup, and urgency differ significantly.
Etiology
Oropharyngeal (transfer) dysphagia is characterized by difficulty initiating a swallow and impaired transfer of food from the mouth to the proximal esophagus. Patients often swallow solids more easily than liquids and develop symptoms immediately upon swallowing. Associated features include nasal or oral regurgitation, coughing, choking, drooling, and aspiration. This form is usually due to neuromuscular disorders causing bulbar muscle weakness or impaired coordination.
Esophageal (transport) dysphagia results from failure of normal transit through the esophagus and is associated with a retrosternal sticking sensation occurring seconds after swallowing. Patients may experience nocturnal regurgitation, aspiration, or regurgitation of undigested food, which is characteristic of esophageal obstruction. Causes include motility disorders and mechanical obstruction.
Functional dysphagia is a diagnosis of exclusion after a full evaluation shows no mechanical or neuromuscular pathology, with symptoms lasting longer than 12 weeks.
Odynophagia refers to pain with swallowing and is a separate but often related condition. Pain localization is generally poor; upper esophageal pain is better localized due to somatic innervation, while lower esophageal visceral pain is poorly localized and may mimic acute coronary syndrome.
Pediatric Considerations
In infants and newborns, common causes include prematurity, congenital malformations, neuromuscular disease, infection such as candidiasis, and inflammation. Foreign body aspiration must always be considered. Other pediatric causes include caustic ingestions, infections, neurologic disorders, and sequelae of head injury. Acquired tracheoesophageal fistula may occur after disk battery or caustic ingestion or prior surgery. Life-threatening pediatric causes include epiglottitis, retropharyngeal abscess, central nervous system infection, botulism, esophageal perforation, and diphtheria.
Diagnosis Signs And Symptoms
Symptoms include difficulty initiating swallowing, sensation of food sticking after swallowing, coughing or choking after eating, impaired gag reflex, dysphonia, drooling, dysarthria, and chest pain.
History
Determine whether dysphagia occurs with solids, liquids, or both. Difficulty with both solids and liquids suggests a neuromuscular disorder, whereas solids alone or progression from solids to liquids suggests mechanical obstruction. Immediate symptoms indicate oropharyngeal dysphagia, while delayed symptoms suggest esophageal involvement. Intermittent symptoms suggest rings or webs, whereas progressive symptoms raise concern for peptic or malignant strictures. Acute onset is concerning for life-threatening causes, with food impaction being the most common. Associated symptoms such as nasal regurgitation, choking, heartburn, or weight loss should be elicited.
Physical-Exam
Findings are often subtle or normal. Perform careful oropharyngeal inspection, pulmonary and cardiac auscultation, and a complete neurologic examination with emphasis on cranial nerves V, VII, IX, X, and XII.
Essential Workup
Ensure adequate airway evaluation and perform a thorough neurologic examination.
Diagnosis Tests And Interpretation
Electrocardiogram should be obtained when chest discomfort raises concern for cardiac etiology. No routine laboratory studies are indicated. Chest radiograph may show dilated esophagus in achalasia, aspiration pneumonitis, or extrinsic compression. Lateral neck radiograph may be helpful in selected cases. Modified barium swallow or videofluoroscopy assesses anatomy and function but should not be performed if endoscopy is anticipated. CT or MRI of the head is indicated for new-onset neuromuscular dysphagia. Upper endoscopy allows relief of obstruction, direct visualization, and biopsy when indicated. Esophageal manometry and fiberoptic nasopharyngeal laryngoscopy are usually performed in the outpatient setting.
Differential Diagnosis
Oropharyngeal causes include infections such as botulism and central nervous system infections, mechanical causes including congenital abnormalities and malignancy, medication-induced injury, and neuromuscular disorders such as stroke, amyotrophic lateral sclerosis, Guillain–Barré syndrome, myasthenia gravis, Parkinson disease, multiple sclerosis, and traumatic brain injury. Esophageal causes include mechanical obstruction from diverticula, webs, foreign bodies, neoplasms, strictures, rings, radiation injury, and postsurgical changes; motility disorders such as achalasia and diffuse esophageal spasm; inflammatory conditions including eosinophilic or pill esophagitis; and extrinsic compression from cardiovascular or mediastinal abnormalities.
Treatment Pre Hospital
Maintain vigilant airway monitoring and position the patient comfortably with suction readily available.
Initial Stabilization And Therapy
Maintain airway vigilance and keep the patient NPO. Administer intravenous fluids with 0.9% normal saline for dehydration. Evaluate urgently for life-threatening causes including retropharyngeal abscess or hematoma, epiglottitis, foreign body, upper airway obstruction, and cardiovascular etiologies.
Emergency Department Treatment And Procedures
Nitroglycerin may be used for esophageal spasm. Glucagon may be attempted for food impaction. Treat complications such as airway obstruction, aspiration pneumonia, dehydration, and malnutrition. Endoscopy is indicated when obstruction persists. Dietary modifications include thickened liquids for neuromuscular disorders and thin liquids for mechanical causes.
Medication
Glucagon 1 mg IV may be administered for food impaction, with a second 1 mg dose after 5 minutes if no improvement; pediatric dosing is 0.02–0.03 mg/kg, not exceeding 0.5 mg. Calcium channel blockers and nitrates may be considered for esophageal motility disorders such as achalasia.
Follow-Up And Disposition
Admission is required for persistent esophageal obstruction, inability to protect the airway, inability to tolerate secretions, or compromised hydration or nutrition. Patients who are stable and well hydrated may be discharged with urgent referral to neurology, otolaryngology, or gastroenterology.
Issues For Referral
Next-day follow-up with primary care, ENT, or gastroenterology is recommended.
Follow-Up Recommendations
Clear liquid diet until specialist evaluation. Return immediately for shortness of breath, chest pain, or inability to tolerate secretions.
Pearls And Pitfalls
Always consider foreign body aspiration in children. Dysphagia is a common presentation of stroke and should be considered in patients with recurrent pneumonia. Life-threatening causes must be excluded before deferring evaluation to the outpatient setting.
Basics Description
Dysphagia is defined as difficulty swallowing and may result from neuromuscular or mechanical causes. It can involve impairment at the oropharyngeal or esophageal level, and careful clinical distinction is essential because etiologies, workup, and urgency differ significantly.
Etiology
Oropharyngeal (transfer) dysphagia is characterized by difficulty initiating a swallow and impaired transfer of food from the mouth to the proximal esophagus. Patients often swallow solids more easily than liquids and develop symptoms immediately upon swallowing. Associated features include nasal or oral regurgitation, coughing, choking, drooling, and aspiration. This form is usually due to neuromuscular disorders causing bulbar muscle weakness or impaired coordination.
Esophageal (transport) dysphagia results from failure of normal transit through the esophagus and is associated with a retrosternal sticking sensation occurring seconds after swallowing. Patients may experience nocturnal regurgitation, aspiration, or regurgitation of undigested food, which is characteristic of esophageal obstruction. Causes include motility disorders and mechanical obstruction.
Functional dysphagia is a diagnosis of exclusion after a full evaluation shows no mechanical or neuromuscular pathology, with symptoms lasting longer than 12 weeks.
Odynophagia refers to pain with swallowing and is a separate but often related condition. Pain localization is generally poor; upper esophageal pain is better localized due to somatic innervation, while lower esophageal visceral pain is poorly localized and may mimic acute coronary syndrome.
Pediatric Considerations
In infants and newborns, common causes include prematurity, congenital malformations, neuromuscular disease, infection such as candidiasis, and inflammation. Foreign body aspiration must always be considered. Other pediatric causes include caustic ingestions, infections, neurologic disorders, and sequelae of head injury. Acquired tracheoesophageal fistula may occur after disk battery or caustic ingestion or prior surgery. Life-threatening pediatric causes include epiglottitis, retropharyngeal abscess, central nervous system infection, botulism, esophageal perforation, and diphtheria.
Diagnosis Signs And Symptoms
Symptoms include difficulty initiating swallowing, sensation of food sticking after swallowing, coughing or choking after eating, impaired gag reflex, dysphonia, drooling, dysarthria, and chest pain.
History
Determine whether dysphagia occurs with solids, liquids, or both. Difficulty with both solids and liquids suggests a neuromuscular disorder, whereas solids alone or progression from solids to liquids suggests mechanical obstruction. Immediate symptoms indicate oropharyngeal dysphagia, while delayed symptoms suggest esophageal involvement. Intermittent symptoms suggest rings or webs, whereas progressive symptoms raise concern for peptic or malignant strictures. Acute onset is concerning for life-threatening causes, with food impaction being the most common. Associated symptoms such as nasal regurgitation, choking, heartburn, or weight loss should be elicited.
Physical-Exam
Findings are often subtle or normal. Perform careful oropharyngeal inspection, pulmonary and cardiac auscultation, and a complete neurologic examination with emphasis on cranial nerves V, VII, IX, X, and XII.
Essential Workup
Ensure adequate airway evaluation and perform a thorough neurologic examination.
Diagnosis Tests And Interpretation
Electrocardiogram should be obtained when chest discomfort raises concern for cardiac etiology. No routine laboratory studies are indicated. Chest radiograph may show dilated esophagus in achalasia, aspiration pneumonitis, or extrinsic compression. Lateral neck radiograph may be helpful in selected cases. Modified barium swallow or videofluoroscopy assesses anatomy and function but should not be performed if endoscopy is anticipated. CT or MRI of the head is indicated for new-onset neuromuscular dysphagia. Upper endoscopy allows relief of obstruction, direct visualization, and biopsy when indicated. Esophageal manometry and fiberoptic nasopharyngeal laryngoscopy are usually performed in the outpatient setting.
Differential Diagnosis
Oropharyngeal causes include infections such as botulism and central nervous system infections, mechanical causes including congenital abnormalities and malignancy, medication-induced injury, and neuromuscular disorders such as stroke, amyotrophic lateral sclerosis, Guillain–Barré syndrome, myasthenia gravis, Parkinson disease, multiple sclerosis, and traumatic brain injury. Esophageal causes include mechanical obstruction from diverticula, webs, foreign bodies, neoplasms, strictures, rings, radiation injury, and postsurgical changes; motility disorders such as achalasia and diffuse esophageal spasm; inflammatory conditions including eosinophilic or pill esophagitis; and extrinsic compression from cardiovascular or mediastinal abnormalities.
Treatment Pre Hospital
Maintain vigilant airway monitoring and position the patient comfortably with suction readily available.
Initial Stabilization And Therapy
Maintain airway vigilance and keep the patient NPO. Administer intravenous fluids with 0.9% normal saline for dehydration. Evaluate urgently for life-threatening causes including retropharyngeal abscess or hematoma, epiglottitis, foreign body, upper airway obstruction, and cardiovascular etiologies.
Emergency Department Treatment And Procedures
Nitroglycerin may be used for esophageal spasm. Glucagon may be attempted for food impaction. Treat complications such as airway obstruction, aspiration pneumonia, dehydration, and malnutrition. Endoscopy is indicated when obstruction persists. Dietary modifications include thickened liquids for neuromuscular disorders and thin liquids for mechanical causes.
Medication
Glucagon 1 mg IV may be administered for food impaction, with a second 1 mg dose after 5 minutes if no improvement; pediatric dosing is 0.02–0.03 mg/kg, not exceeding 0.5 mg. Calcium channel blockers and nitrates may be considered for esophageal motility disorders such as achalasia.
Follow-Up And Disposition
Admission is required for persistent esophageal obstruction, inability to protect the airway, inability to tolerate secretions, or compromised hydration or nutrition. Patients who are stable and well hydrated may be discharged with urgent referral to neurology, otolaryngology, or gastroenterology.
Issues For Referral
Next-day follow-up with primary care, ENT, or gastroenterology is recommended.
Follow-Up Recommendations
Clear liquid diet until specialist evaluation. Return immediately for shortness of breath, chest pain, or inability to tolerate secretions.
Pearls And Pitfalls
Always consider foreign body aspiration in children. Dysphagia is a common presentation of stroke and should be considered in patients with recurrent pneumonia. Life-threatening causes must be excluded before deferring evaluation to the outpatient setting.
