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Emergency And Acute Medicine - Erysipelas
Basic description
Erysipelas is a superficial bacterial infection of the skin characterized by prominent involvement of the lymphatic system. Leukocytosis is common, and blood cultures are positive in approximately 3–5% of cases.
Etiology
Group A β-hemolytic streptococcus is the most common causative organism, with group C or G streptococci occurring less frequently.
Common portals of entry include skin ulcers, local trauma, abrasions, psoriatic or eczematous lesions, and fungal infections.
Pediatric considerations
Haemophilus influenzae type b can cause facial cellulitis in children that may resemble erysipelas and should be considered in unimmunized patients. Many of these children are bacteremic and require hospital admission with appropriate antibiotic coverage such as cefuroxime. This organism has become far less common with widespread Hib vaccination.
Group B streptococci may cause erysipelas in newborns, often arising from infection of the umbilical stump.
Pregnancy considerations
Erythema of the breast associated with puerperal mastitis is frequently caused by staphylococcal species; coverage for methicillin-resistant Staphylococcus aureus should be considered.
Diagnosis – signs and symptoms
The most commonly affected sites are the lower extremities (70–80%), followed by the face (5–20%) and ears. Facial involvement is often bilateral, whereas involvement elsewhere is typically unilateral. The skin appears intensely erythematous, giving rise to the historical term “Saint Anthony’s fire.”
Erysipelas occurs more often in infants, children, and the elderly. Systemic symptoms may include malaise, fever, chills, nausea, and vomiting. A traumatic portal of entry is not always evident. Rarely, periorbital cellulitis or cavernous sinus involvement may occur.
History
Facial erysipelas may follow nasopharyngeal infection or trauma. The condition has a predilection for areas of lymphatic obstruction, such as the upper extremity after radical mastectomy or the lower extremity after saphenous vein harvesting. It may be a marker of previously unrecognized lymphatic obstruction or congenital lymphedema, such as Milroy disease.
Recurrence occurs in approximately 30% of patients within three years, often due to lymphatic damage from prior episodes.
Physical examination
Affected skin is edematous, indurated with a peau d’orange appearance, painful, and sharply demarcated with raised borders. When involving the face, a classic butterfly distribution over the cheeks and nasal bridge may be seen. Vesicles or bullae can occur in more severe infections.
Essential workup
Diagnosis is clinical, based on characteristic skin findings and the clinical context. Needle aspirate or wound cultures are rarely helpful and are not routinely indicated.
Diagnosis tests and interpretation
Laboratory studies
Skin swabs are not useful, as they typically yield only normal skin flora.
CBC with differential and blood cultures should be obtained in high-risk patients, including those with diabetes, hypotension, or those requiring admission. Blood cultures are more likely to be positive in patients with lymphedema.
Glucose should be checked in diabetics.
Urinalysis may be performed to evaluate for proteinuria, hematuria, or red cell casts, which could suggest post-streptococcal glomerulonephritis, typically occurring about two weeks after infection onset.
Antistreptolysin O and anti-DNase B titers are not helpful in uncomplicated erysipelas and should not be routinely ordered.
Imaging
Routine imaging is not indicated. If deeper infection such as myositis is suspected, plain radiographs or CT may be used to assess for gas. Ultrasound can be helpful to evaluate for abscess or to exclude deep vein thrombosis in the lower extremity.
Differential diagnosis
Abscess
Acute bacterial sinusitis
Allergic inflammation
Cellulitis
Contact dermatitis
Deep vein thrombosis
Inflammatory breast carcinoma
Herpes zoster
Impetigo
Mastitis
Necrotizing fasciitis
Periorbital cellulitis
Systemic lupus erythematosus
Toxic shock syndrome
Venous stasis dermatitis
Viral exanthem
Treatment – prehospital
Use of gloves and appropriate hand hygiene is important to reduce transmission of streptococcal carriage.
Initial stabilization and therapy
Some patients may appear toxic and require intravenous fluids or hemodynamic support.
Emergency department treatment and procedures
Antibiotic therapy should be initiated promptly and continued for approximately 10 days. Patients with extensive disease typically require admission for intravenous antibiotics, with transition to oral therapy once clinically improved.
Mild cases may be treated as outpatients if the patient is nontoxic, reliable, and has close follow-up.
Penicillin is the treatment of choice when erysipelas is clearly diagnosed. If cellulitis cannot be excluded, add staphylococcal coverage with a penicillinase-resistant penicillin or first-generation cephalosporin.
In areas with high MRSA prevalence, vancomycin or other appropriate agents should be considered.
Acetaminophen may be used for fever.
Hospitalized patients should be placed on isolation precautions, as the condition is contagious.
Medication
Outpatient therapy
Penicillin V, amoxicillin, clindamycin, dicloxacillin, erythromycin, cephalexin, or cefuroxime for 10 days, with pediatric dosing adjusted by weight.
Inpatient therapy
Penicillin G IV or IM, clindamycin IV, or vancomycin IV depending on severity, allergy status, and local resistance patterns.
First-line therapy
Penicillin or a first-generation cephalosporin (oral or IV).
Clindamycin for penicillin-allergic patients.
Second-line therapy
Erythromycin.
Follow-up and disposition
Admission criteria
Extensive involvement, fever, toxic appearance, suspected orbital or periorbital cellulitis, inability to tolerate oral therapy, unreliable follow-up, or unimmunized children requiring coverage for H. influenzae.
Discharge criteria
Minimal facial involvement, nontoxic appearance, no immunosuppression, ability to tolerate oral therapy, reliable follow-up, and a clear diagnosis.
Issues for referral
Nephrology referral is indicated if urinalysis shows findings suggestive of post-streptococcal glomerulonephritis, particularly in children.
Infectious disease consultation is recommended for immunocompromised patients or unusual organisms.
Follow-up recommendations
Compression stockings may reduce recurrence in patients with lower-extremity lymphedema.
Treat underlying tinea pedis with topical antifungals to reduce relapse risk.
Clinical pearls and common missteps
Failure to improve or pain disproportionate to exam findings should prompt evaluation for necrotizing fasciitis or deeper infection.
Managing underlying lymphedema reduces recurrence risk.
Micropustules suggest staphylococcal infection rather than erysipelas and warrant broader antibiotic coverage.
Crepitus should raise concern for an alternative diagnosis.
Always assess tetanus immunization status and update as needed.
Consider prophylactic antibiotics in patients with frequent recurrences.
Basic description
Erysipelas is a superficial bacterial infection of the skin characterized by prominent involvement of the lymphatic system. Leukocytosis is common, and blood cultures are positive in approximately 3–5% of cases.
Etiology
Group A β-hemolytic streptococcus is the most common causative organism, with group C or G streptococci occurring less frequently.
Common portals of entry include skin ulcers, local trauma, abrasions, psoriatic or eczematous lesions, and fungal infections.
Pediatric considerations
Haemophilus influenzae type b can cause facial cellulitis in children that may resemble erysipelas and should be considered in unimmunized patients. Many of these children are bacteremic and require hospital admission with appropriate antibiotic coverage such as cefuroxime. This organism has become far less common with widespread Hib vaccination.
Group B streptococci may cause erysipelas in newborns, often arising from infection of the umbilical stump.
Pregnancy considerations
Erythema of the breast associated with puerperal mastitis is frequently caused by staphylococcal species; coverage for methicillin-resistant Staphylococcus aureus should be considered.
Diagnosis – signs and symptoms
The most commonly affected sites are the lower extremities (70–80%), followed by the face (5–20%) and ears. Facial involvement is often bilateral, whereas involvement elsewhere is typically unilateral. The skin appears intensely erythematous, giving rise to the historical term “Saint Anthony’s fire.”
Erysipelas occurs more often in infants, children, and the elderly. Systemic symptoms may include malaise, fever, chills, nausea, and vomiting. A traumatic portal of entry is not always evident. Rarely, periorbital cellulitis or cavernous sinus involvement may occur.
History
Facial erysipelas may follow nasopharyngeal infection or trauma. The condition has a predilection for areas of lymphatic obstruction, such as the upper extremity after radical mastectomy or the lower extremity after saphenous vein harvesting. It may be a marker of previously unrecognized lymphatic obstruction or congenital lymphedema, such as Milroy disease.
Recurrence occurs in approximately 30% of patients within three years, often due to lymphatic damage from prior episodes.
Physical examination
Affected skin is edematous, indurated with a peau d’orange appearance, painful, and sharply demarcated with raised borders. When involving the face, a classic butterfly distribution over the cheeks and nasal bridge may be seen. Vesicles or bullae can occur in more severe infections.
Essential workup
Diagnosis is clinical, based on characteristic skin findings and the clinical context. Needle aspirate or wound cultures are rarely helpful and are not routinely indicated.
Diagnosis tests and interpretation
Laboratory studies
Skin swabs are not useful, as they typically yield only normal skin flora.
CBC with differential and blood cultures should be obtained in high-risk patients, including those with diabetes, hypotension, or those requiring admission. Blood cultures are more likely to be positive in patients with lymphedema.
Glucose should be checked in diabetics.
Urinalysis may be performed to evaluate for proteinuria, hematuria, or red cell casts, which could suggest post-streptococcal glomerulonephritis, typically occurring about two weeks after infection onset.
Antistreptolysin O and anti-DNase B titers are not helpful in uncomplicated erysipelas and should not be routinely ordered.
Imaging
Routine imaging is not indicated. If deeper infection such as myositis is suspected, plain radiographs or CT may be used to assess for gas. Ultrasound can be helpful to evaluate for abscess or to exclude deep vein thrombosis in the lower extremity.
Differential diagnosis
Abscess
Acute bacterial sinusitis
Allergic inflammation
Cellulitis
Contact dermatitis
Deep vein thrombosis
Inflammatory breast carcinoma
Herpes zoster
Impetigo
Mastitis
Necrotizing fasciitis
Periorbital cellulitis
Systemic lupus erythematosus
Toxic shock syndrome
Venous stasis dermatitis
Viral exanthem
Treatment – prehospital
Use of gloves and appropriate hand hygiene is important to reduce transmission of streptococcal carriage.
Initial stabilization and therapy
Some patients may appear toxic and require intravenous fluids or hemodynamic support.
Emergency department treatment and procedures
Antibiotic therapy should be initiated promptly and continued for approximately 10 days. Patients with extensive disease typically require admission for intravenous antibiotics, with transition to oral therapy once clinically improved.
Mild cases may be treated as outpatients if the patient is nontoxic, reliable, and has close follow-up.
Penicillin is the treatment of choice when erysipelas is clearly diagnosed. If cellulitis cannot be excluded, add staphylococcal coverage with a penicillinase-resistant penicillin or first-generation cephalosporin.
In areas with high MRSA prevalence, vancomycin or other appropriate agents should be considered.
Acetaminophen may be used for fever.
Hospitalized patients should be placed on isolation precautions, as the condition is contagious.
Medication
Outpatient therapy
Penicillin V, amoxicillin, clindamycin, dicloxacillin, erythromycin, cephalexin, or cefuroxime for 10 days, with pediatric dosing adjusted by weight.
Inpatient therapy
Penicillin G IV or IM, clindamycin IV, or vancomycin IV depending on severity, allergy status, and local resistance patterns.
First-line therapy
Penicillin or a first-generation cephalosporin (oral or IV).
Clindamycin for penicillin-allergic patients.
Second-line therapy
Erythromycin.
Follow-up and disposition
Admission criteria
Extensive involvement, fever, toxic appearance, suspected orbital or periorbital cellulitis, inability to tolerate oral therapy, unreliable follow-up, or unimmunized children requiring coverage for H. influenzae.
Discharge criteria
Minimal facial involvement, nontoxic appearance, no immunosuppression, ability to tolerate oral therapy, reliable follow-up, and a clear diagnosis.
Issues for referral
Nephrology referral is indicated if urinalysis shows findings suggestive of post-streptococcal glomerulonephritis, particularly in children.
Infectious disease consultation is recommended for immunocompromised patients or unusual organisms.
Follow-up recommendations
Compression stockings may reduce recurrence in patients with lower-extremity lymphedema.
Treat underlying tinea pedis with topical antifungals to reduce relapse risk.
Clinical pearls and common missteps
Failure to improve or pain disproportionate to exam findings should prompt evaluation for necrotizing fasciitis or deeper infection.
Managing underlying lymphedema reduces recurrence risk.
Micropustules suggest staphylococcal infection rather than erysipelas and warrant broader antibiotic coverage.
Crepitus should raise concern for an alternative diagnosis.
Always assess tetanus immunization status and update as needed.
Consider prophylactic antibiotics in patients with frequent recurrences.
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Emergency And Acute Medicine - Epistaxis
Basic description
Epistaxis is a frequent emergency presentation that is typically mild and self-limited but can occasionally be life threatening. The lifetime incidence is approximately 60%, with most cases occurring in children younger than 10 years. Males are affected more often than females. Severe hemorrhage requiring surgical intervention is more common in patients older than 50 years.
Epistaxis occurs more frequently in low-humidity environments, during winter months, in northern climates, and at high altitude.
The nasal cavity receives blood supply from both the internal and external carotid arteries. Management depends on the location of bleeding.
Anterior epistaxis accounts for about 90% of cases and is usually visualized directly in the anterior nasal cavity. The most common source is Kiesselbach plexus on the anteroinferior nasal septum. Less commonly, bleeding originates from the posterior nasal floor or septum.
Posterior epistaxis represents about 10% of cases and arises from vessels not directly visualized, most often branches of the sphenopalatine artery.
Etiology
Idiopathic causes include dry nasal mucosa related to low humidity.
Foreign bodies are common in children and in patients with psychiatric illness or developmental delay.
Infectious causes include rhinitis, sinusitis, nasal diphtheria, and nasal mucormycosis.
Allergic rhinitis is a frequent contributor.
Trauma includes nose picking, postoperative injury, facial trauma, and barotrauma.
Environmental irritants include ammonia, gasoline, sulfuric acid, and glutaraldehyde.
Intranasal neoplasms include papilloma and other tumors.
Coagulopathies include hemophilia A or B, von Willebrand disease, thrombocytopenia from liver disease, leukemia, chemotherapy, viral illness, or autoimmune disease.
Platelet dysfunction may occur with renal disease or chronic alcohol use.
Medication-related causes include salicylates, NSAIDs, heparin, and warfarin.
Other causes include hereditary hemorrhagic telangiectasia, atherosclerosis of nasal vessels, and endometriosis.
Diagnosis – signs and symptoms
History
Determine laterality, severity, and duration of bleeding.
Assess recurrence and prior episodes.
Ask about nasal obstruction, vomiting or coughing blood, known tumors, or bleeding disorders.
Easy bruising or unusual bleeding suggests an underlying coagulopathy.
Identify comorbid conditions that may be worsened by blood loss, such as coronary artery disease or chronic lung disease.
Physical examination
Assess vital signs for evidence of hemorrhagic shock.
Look for signs of coagulopathy including bruising, petechiae, or purpura.
Inspect the nasal cavity after topical anesthesia and vasoconstriction using a nasal speculum.
Evaluate for blood in the mouth or oropharynx.
Essential workup
Assess airway and hemodynamic stability.
Determine whether bleeding is anterior or posterior.
Evaluate for underlying bleeding disorders when indicated.
Diagnosis tests and interpretation
Laboratory studies
For severe bleeding or suspected coagulopathy consider CBC, type and cross-match, PT/INR, PTT, and BUN.
Diagnostic procedures
Direct visualization with nasal speculum after topical anesthetic and vasoconstrictor. Adequate lighting and suction are essential.
Differential diagnosis
Hematemesis
Hemoptysis
Pediatric considerations
Posterior epistaxis is uncommon in children and should prompt evaluation for bleeding disorders.
Consider foreign bodies or neoplasms such as juvenile angiofibroma.
Use of topical antiseptic ointment for four weeks reduces recurrent epistaxis.
Treatment – prehospital
Stable patients should lean forward, pinch the soft part of the nose, and spit out blood rather than swallow it.
Unstable patients require airway management, IV access, and crystalloid resuscitation.
Initial stabilization and therapy
Secure the airway in patients with altered mental status, facial trauma, or aspiration risk.
Treat hypotension with fluids and blood products as indicated.
Emergency department treatment and procedures
Use universal precautions.
For anterior bleeding, apply direct pressure for 15 minutes.
If bleeding persists, insert cotton pledgets soaked in anesthetic and vasoconstrictor.
Clear clots by gentle blowing, irrigation, or suction.
Cauterize the identified bleeding site with silver nitrate and consider absorbable hemostatic agents.
If cautery fails, anterior nasal packing or balloon devices may be used, ensuring adequate anesthesia and careful placement.
Petroleum-impregnated gauze packing is an alternative when commercial devices are unavailable.
Persistent bleeding after anterior packing suggests inadequate packing or a posterior source.
Posterior epistaxis may require posterior packing with commercial devices or a Foley catheter technique and mandates hospital admission with monitoring.
Posterior packs should not remain in place longer than three days due to infection risk.
Medication
Topical vasoactive agents include cocaine 4%, oxymetazoline with lidocaine, phenylephrine, or anesthetic–epinephrine mixtures.
Antibiotics are required while nasal packing is in place, including amoxicillin–clavulanate, cephalexin, clindamycin, or trimethoprim–sulfamethoxazole.
Follow-up and disposition
Admission criteria
Severe hemorrhage requiring transfusion.
Significant coagulopathy.
Posterior nasal packing, which requires admission, telemetry, oxygen, and specialist consultation.
Anterior packing without reliable follow-up.
Discharge criteria
Hemodynamically stable patients with controlled bleeding.
Use topical oxymetazoline for up to two days, humidification, nasal lubrication, and avoidance of nasal trauma.
All patients discharged with packing must receive antistaphylococcal antibiotics.
Issues for referral
All patients with nasal packing should see an otolaryngologist within 48 hours.
Recurrent unilateral bleeding, nasal obstruction, or suspicious lesions require specialist evaluation.
Follow-up recommendations
Return for uncontrolled bleeding, fever, breathing difficulty, or vomiting.
Avoid nose blowing for 12 hours after bleeding stops.
If bleeding recurs, lean forward and pinch the nose firmly for 10 minutes without interruption.
Use nasal ointment and home humidification as instructed.
Clinical pearls and common missteps
Suspect nasal foreign bodies in unilateral bleeding in children and cognitively impaired patients.
Avoid petroleum-based ointments on anterior nasal balloons due to risk of delayed rupture.
Do not overinflate balloons or pack too tightly, as this may cause tissue necrosis.
Patients with nasal packing should always receive prophylactic antibiotics.
Basic description
Epistaxis is a frequent emergency presentation that is typically mild and self-limited but can occasionally be life threatening. The lifetime incidence is approximately 60%, with most cases occurring in children younger than 10 years. Males are affected more often than females. Severe hemorrhage requiring surgical intervention is more common in patients older than 50 years.
Epistaxis occurs more frequently in low-humidity environments, during winter months, in northern climates, and at high altitude.
The nasal cavity receives blood supply from both the internal and external carotid arteries. Management depends on the location of bleeding.
Anterior epistaxis accounts for about 90% of cases and is usually visualized directly in the anterior nasal cavity. The most common source is Kiesselbach plexus on the anteroinferior nasal septum. Less commonly, bleeding originates from the posterior nasal floor or septum.
Posterior epistaxis represents about 10% of cases and arises from vessels not directly visualized, most often branches of the sphenopalatine artery.
Etiology
Idiopathic causes include dry nasal mucosa related to low humidity.
Foreign bodies are common in children and in patients with psychiatric illness or developmental delay.
Infectious causes include rhinitis, sinusitis, nasal diphtheria, and nasal mucormycosis.
Allergic rhinitis is a frequent contributor.
Trauma includes nose picking, postoperative injury, facial trauma, and barotrauma.
Environmental irritants include ammonia, gasoline, sulfuric acid, and glutaraldehyde.
Intranasal neoplasms include papilloma and other tumors.
Coagulopathies include hemophilia A or B, von Willebrand disease, thrombocytopenia from liver disease, leukemia, chemotherapy, viral illness, or autoimmune disease.
Platelet dysfunction may occur with renal disease or chronic alcohol use.
Medication-related causes include salicylates, NSAIDs, heparin, and warfarin.
Other causes include hereditary hemorrhagic telangiectasia, atherosclerosis of nasal vessels, and endometriosis.
Diagnosis – signs and symptoms
History
Determine laterality, severity, and duration of bleeding.
Assess recurrence and prior episodes.
Ask about nasal obstruction, vomiting or coughing blood, known tumors, or bleeding disorders.
Easy bruising or unusual bleeding suggests an underlying coagulopathy.
Identify comorbid conditions that may be worsened by blood loss, such as coronary artery disease or chronic lung disease.
Physical examination
Assess vital signs for evidence of hemorrhagic shock.
Look for signs of coagulopathy including bruising, petechiae, or purpura.
Inspect the nasal cavity after topical anesthesia and vasoconstriction using a nasal speculum.
Evaluate for blood in the mouth or oropharynx.
Essential workup
Assess airway and hemodynamic stability.
Determine whether bleeding is anterior or posterior.
Evaluate for underlying bleeding disorders when indicated.
Diagnosis tests and interpretation
Laboratory studies
For severe bleeding or suspected coagulopathy consider CBC, type and cross-match, PT/INR, PTT, and BUN.
Diagnostic procedures
Direct visualization with nasal speculum after topical anesthetic and vasoconstrictor. Adequate lighting and suction are essential.
Differential diagnosis
Hematemesis
Hemoptysis
Pediatric considerations
Posterior epistaxis is uncommon in children and should prompt evaluation for bleeding disorders.
Consider foreign bodies or neoplasms such as juvenile angiofibroma.
Use of topical antiseptic ointment for four weeks reduces recurrent epistaxis.
Treatment – prehospital
Stable patients should lean forward, pinch the soft part of the nose, and spit out blood rather than swallow it.
Unstable patients require airway management, IV access, and crystalloid resuscitation.
Initial stabilization and therapy
Secure the airway in patients with altered mental status, facial trauma, or aspiration risk.
Treat hypotension with fluids and blood products as indicated.
Emergency department treatment and procedures
Use universal precautions.
For anterior bleeding, apply direct pressure for 15 minutes.
If bleeding persists, insert cotton pledgets soaked in anesthetic and vasoconstrictor.
Clear clots by gentle blowing, irrigation, or suction.
Cauterize the identified bleeding site with silver nitrate and consider absorbable hemostatic agents.
If cautery fails, anterior nasal packing or balloon devices may be used, ensuring adequate anesthesia and careful placement.
Petroleum-impregnated gauze packing is an alternative when commercial devices are unavailable.
Persistent bleeding after anterior packing suggests inadequate packing or a posterior source.
Posterior epistaxis may require posterior packing with commercial devices or a Foley catheter technique and mandates hospital admission with monitoring.
Posterior packs should not remain in place longer than three days due to infection risk.
Medication
Topical vasoactive agents include cocaine 4%, oxymetazoline with lidocaine, phenylephrine, or anesthetic–epinephrine mixtures.
Antibiotics are required while nasal packing is in place, including amoxicillin–clavulanate, cephalexin, clindamycin, or trimethoprim–sulfamethoxazole.
Follow-up and disposition
Admission criteria
Severe hemorrhage requiring transfusion.
Significant coagulopathy.
Posterior nasal packing, which requires admission, telemetry, oxygen, and specialist consultation.
Anterior packing without reliable follow-up.
Discharge criteria
Hemodynamically stable patients with controlled bleeding.
Use topical oxymetazoline for up to two days, humidification, nasal lubrication, and avoidance of nasal trauma.
All patients discharged with packing must receive antistaphylococcal antibiotics.
Issues for referral
All patients with nasal packing should see an otolaryngologist within 48 hours.
Recurrent unilateral bleeding, nasal obstruction, or suspicious lesions require specialist evaluation.
Follow-up recommendations
Return for uncontrolled bleeding, fever, breathing difficulty, or vomiting.
Avoid nose blowing for 12 hours after bleeding stops.
If bleeding recurs, lean forward and pinch the nose firmly for 10 minutes without interruption.
Use nasal ointment and home humidification as instructed.
Clinical pearls and common missteps
Suspect nasal foreign bodies in unilateral bleeding in children and cognitively impaired patients.
Avoid petroleum-based ointments on anterior nasal balloons due to risk of delayed rupture.
Do not overinflate balloons or pack too tightly, as this may cause tissue necrosis.
Patients with nasal packing should always receive prophylactic antibiotics.
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Emergency And Acute Medicine - Epiphyseal Injuries
Basic description
Fractures involving the physis account for approximately 21–30% of pediatric long bone fractures, with up to 30% resulting in some degree of growth disturbance. These injuries most commonly affect the distal radius and ulna, distal tibia and fibula, and the phalanges.
Epiphyseal injuries are more common than ligamentous injuries in children because the tensile strength of pediatric bone is lower than that of adjacent ligaments, making the physis the weakest structural component. In adults, a similar mechanism more often produces a sprain.
These injuries are most frequent during periods of rapid growth: ages 9–12 years in females and 12–15 years in males. They are uncommon in infancy and early childhood because the epiphysis is not yet ossified and acts as a shock absorber. Overall incidence is about twice as high in males, as female bones mature earlier.
Salter–Harris classification
Introduced in 1963, this is the most widely used system for classifying physeal fractures.
Additional classification systems
Ogden expanded the Salter–Harris system to include injuries to surrounding structures such as the periosteum, perichondrium, and zone of Ranvier (Types VI and VII).
The Peterson classification (1994) identified fracture patterns not covered by Salter–Harris, including injuries where most force is transmitted through the metaphysis with minimal physeal disruption, as well as severe open injuries with loss of epiphysis, physis, and metaphysis.
Etiology
Common causes include competitive and recreational trauma, accidental injury, child abuse, extreme cold exposure, radiation injury, and underlying genetic, neurologic, or metabolic disorders.
Diagnosis – signs and symptoms
History
Most injuries occur after a fall or direct trauma. Less common mechanisms include cold injury and radiation exposure.
Physical examination
Findings include focal tenderness over the physis, swelling, limited range of motion, and possible non–weight-bearing status if the lower extremity is involved. Apparent joint laxity may reflect physeal injury rather than ligament damage.
Essential workup
Obtain radiographs to assess and classify the injury. Always evaluate distal pulses, capillary refill, motor and sensory function, and skin integrity. Identify and manage associated injuries.
Diagnosis tests and interpretation
Imaging
Differential diagnosis
Strain, sprain, and contusion.
Treatment – prehospital
Immobilize the limb in the position found if there is no vascular compromise. Apply ice or cold packs and assess neurovascular status. Consider the possibility of associated injuries.
Initial stabilization and therapy
Provide analgesia. Control bleeding and cover open wounds with sterile dressings.
Emergency department treatment
Displaced fractures require reduction to restore anatomic alignment. Immediate intervention is required if there is vascular or neurologic compromise.
All suspected or confirmed physeal injuries should be immobilized with a splint that stabilizes the joints above and below the injury in neutral alignment.
Open fractures require IV antibiotics, copious irrigation, sterile dressing, and urgent orthopedic consultation. Consultation is also indicated for displaced Salter–Harris type II injuries and all type III or higher injuries.
Medication
First line (analgesia)
If open fracture
Follow-up and disposition
Admission criteria
Open fractures, fractures requiring operative reduction, and consideration for higher-grade (type III–V) injuries.
Discharge criteria
Low-grade fractures, or higher-grade fractures with reliable follow-up, may be discharged with splinting, analgesia, ice, elevation, and orthopedic follow-up within one week.
Issues for referral
All physeal injuries require follow-up with a musculoskeletal specialist.
Follow-up recommendations
Ongoing monitoring is often necessary, particularly for higher-grade injuries, to assess for limb-length discrepancy or angular deformity through periodic examination and imaging.
Clinical pearls and common missteps
Growth plate injuries can result in limb-length discrepancy if the entire physis is affected, or angular deformity if only part is involved. When a Salter–Harris injury is suspected clinically but radiographs are normal, immobilization with short-interval follow-up is appropriate.
Basic description
Fractures involving the physis account for approximately 21–30% of pediatric long bone fractures, with up to 30% resulting in some degree of growth disturbance. These injuries most commonly affect the distal radius and ulna, distal tibia and fibula, and the phalanges.
Epiphyseal injuries are more common than ligamentous injuries in children because the tensile strength of pediatric bone is lower than that of adjacent ligaments, making the physis the weakest structural component. In adults, a similar mechanism more often produces a sprain.
These injuries are most frequent during periods of rapid growth: ages 9–12 years in females and 12–15 years in males. They are uncommon in infancy and early childhood because the epiphysis is not yet ossified and acts as a shock absorber. Overall incidence is about twice as high in males, as female bones mature earlier.
Salter–Harris classification
Introduced in 1963, this is the most widely used system for classifying physeal fractures.
- Type I: Fracture confined to the physis with complete separation of the epiphysis from the metaphysis. If the periosteum remains intact, displacement may be minimal. Diagnosis is often clinical, based on focal physeal tenderness. Growth disturbance is rare.
- Type II: The most common pattern (≈80%). The fracture extends along the physis with an associated metaphyseal fragment (Thurston–Holland sign). Growth disturbance is uncommon.
- Type III: Rare. The fracture extends through part of the physis and into the epiphysis, most often affecting the distal tibia. Anatomic reduction is required if displaced. Growth disturbance may occur due to vascular compromise.
- Type IV: Fracture crosses the articular surface, physis, and metaphysis. Commonly affects the distal humerus. Accurate anatomic reduction is essential, and displaced fractures usually require operative fixation. Growth arrest is common even with optimal care.
- Type V: Crush injury to the physis. Often radiographically occult initially and typically diagnosed in retrospect. Growth disturbance is inevitable.
Additional classification systems
Ogden expanded the Salter–Harris system to include injuries to surrounding structures such as the periosteum, perichondrium, and zone of Ranvier (Types VI and VII).
The Peterson classification (1994) identified fracture patterns not covered by Salter–Harris, including injuries where most force is transmitted through the metaphysis with minimal physeal disruption, as well as severe open injuries with loss of epiphysis, physis, and metaphysis.
Etiology
Common causes include competitive and recreational trauma, accidental injury, child abuse, extreme cold exposure, radiation injury, and underlying genetic, neurologic, or metabolic disorders.
Diagnosis – signs and symptoms
History
Most injuries occur after a fall or direct trauma. Less common mechanisms include cold injury and radiation exposure.
Physical examination
Findings include focal tenderness over the physis, swelling, limited range of motion, and possible non–weight-bearing status if the lower extremity is involved. Apparent joint laxity may reflect physeal injury rather than ligament damage.
Essential workup
Obtain radiographs to assess and classify the injury. Always evaluate distal pulses, capillary refill, motor and sensory function, and skin integrity. Identify and manage associated injuries.
Diagnosis tests and interpretation
Imaging
- Plain radiographs:
- Type I injuries may appear normal; subtle physeal widening or joint effusion may be present. Comparison views can be helpful.
- Types II–IV are usually evident on initial imaging.
- Type V injuries often appear normal initially; later imaging may show premature physeal closure.
- Ultrasound: Useful in infants with unossified cartilage.
- CT: Helpful for defining fragment orientation and comminution.
- MRI: Most sensitive in the acute phase; can identify physeal arrest lines and is recommended when diagnosis is uncertain and would alter management.
Differential diagnosis
Strain, sprain, and contusion.
Treatment – prehospital
Immobilize the limb in the position found if there is no vascular compromise. Apply ice or cold packs and assess neurovascular status. Consider the possibility of associated injuries.
Initial stabilization and therapy
Provide analgesia. Control bleeding and cover open wounds with sterile dressings.
Emergency department treatment
Displaced fractures require reduction to restore anatomic alignment. Immediate intervention is required if there is vascular or neurologic compromise.
All suspected or confirmed physeal injuries should be immobilized with a splint that stabilizes the joints above and below the injury in neutral alignment.
Open fractures require IV antibiotics, copious irrigation, sterile dressing, and urgent orthopedic consultation. Consultation is also indicated for displaced Salter–Harris type II injuries and all type III or higher injuries.
Medication
First line (analgesia)
- Fentanyl 2–3 μg/kg IV or transmucosal formulation 5–15 μg/kg (maximum 400 μg; avoid if <10 kg)< />pan>
- Morphine 0.1 mg/kg IV or IM
If open fracture
- Cefazolin 25–50 mg/kg/day IV or IM divided every 6–8 hours
- Penicillin G 100,000–300,000 U/kg/day IV or IM divided every 4–6 hours for farm-related injuries
- Gentamicin 5–7.5 mg/kg/day for heavily contaminated wounds
Follow-up and disposition
Admission criteria
Open fractures, fractures requiring operative reduction, and consideration for higher-grade (type III–V) injuries.
Discharge criteria
Low-grade fractures, or higher-grade fractures with reliable follow-up, may be discharged with splinting, analgesia, ice, elevation, and orthopedic follow-up within one week.
Issues for referral
All physeal injuries require follow-up with a musculoskeletal specialist.
Follow-up recommendations
Ongoing monitoring is often necessary, particularly for higher-grade injuries, to assess for limb-length discrepancy or angular deformity through periodic examination and imaging.
Clinical pearls and common missteps
Growth plate injuries can result in limb-length discrepancy if the entire physis is affected, or angular deformity if only part is involved. When a Salter–Harris injury is suspected clinically but radiographs are normal, immobilization with short-interval follow-up is appropriate.
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Emergency And Acute Medicine - Epiglottitis, Pediatric
Basic description
Pediatric epiglottitis is an inflammation of the epiglottis and nearby supraglottic tissues that can become rapidly fatal because of progressive upper-airway obstruction. Children are especially vulnerable because their upper airway has a smaller cross-sectional diameter, the mucosa is more loosely attached and highly vascular (so swelling develops quickly), and the airway can collapse dynamically during distress.
After widespread Haemophilus influenzae type b (Hib) vaccination, childhood epiglottitis became far less common; however, rare cases can still occur, including vaccine failure. In the post-Hib era, the average age has shifted upward, and the condition is now seen more often in adolescents and adults than in toddlers or young school-aged children. Cases may occur year-round.
Alert
Any child with suspected epiglottitis requires continuous intensive monitoring and urgent readiness for airway intervention because obstruction can progress suddenly.
Etiology
Infectious causes include H. influenzae type b, Streptococcus pneumoniae, group A β-hemolytic Streptococcus, Staphylococcus aureus, and viruses. Less common pathogens include Klebsiella, Pseudomonas, and Candida.
Noninfectious causes include caustic injury, thermal injury, trauma, post-transplant lymphoproliferative disorder, and hereditary angioedema.
Diagnosis – signs and symptoms
History
Presentation is typically abrupt and severe without a preceding viral prodrome. Common features include irritability, intense throat pain (often described as the worst sore throat), fever, noisy breathing, and rapidly worsening toxicity or respiratory distress. Adolescents may resemble adult presentations, including repeated prior visits before diagnosis.
Physical examination
Children often appear toxic with high fever and quickly progressive symptoms. Key throat findings include drooling, dysphagia, and a muffled “hot potato” voice. Respiratory distress may evolve rapidly; the child usually prefers to sit upright, leaning forward with the mouth open (tripod/sniffing position) to optimize airflow. Stridor may be subtle early and progress later. Severe complications include complete airway obstruction, epiglottic abscess, pneumonia, and atelectasis.
Essential workup
Epiglottitis is primarily a clinical diagnosis. Attempts to directly visualize the epiglottis in an awake child (including indirect laryngoscopy) should be avoided unless performed in a controlled environment with full airway capability. In adolescents without impending obstruction, fiberoptic nasopharyngoscopy may be appropriate. If infection is suspected, cultures of the epiglottis should be obtained during laryngoscopy only after the airway is secured.
Diagnosis tests and interpretation
Laboratory studies
Defer lab tests until the airway is controlled. After stabilization, obtain throat cultures and blood cultures (blood cultures are often positive when Hib is the cause).
Imaging
Lateral soft tissue neck radiographs are usually unnecessary and can be dangerous because they may delay airway control, agitate the child, and remove the patient to a less controlled setting. If imaging is obtained, the child must be accompanied and airway equipment and skilled personnel must be immediately available. Possible findings include a normal film, epiglottic swelling (“thumbprint sign”), supraglottic swelling, a ballooned hypopharynx, obliteration of the vallecula, and an epiglottic width to C3 vertebral body width ratio greater than 0.5.
Diagnostic procedures
Laryngoscopy should be performed in a controlled setting whenever possible. The epiglottis typically appears swollen, erythematous, and inflamed. Cultures obtained after airway control can help target therapy.
Differential diagnosis
Bacterial tracheitis, retropharyngeal abscess, peritonsillar abscess, croup (with age overlap), pertussis, mononucleosis, Ludwig angina, diphtheria, anaphylaxis with angioedema, hereditary angioedema, upper-airway foreign body, laryngeal trauma, laryngospasm, toxic inhalation/aspiration (e.g., hydrocarbons), airway burns, hyperventilation, and CNS disorders.
Treatment – prehospital
Intervention should match the degree of obstruction, transport time, and provider capability. Notify the receiving facility early and coordinate transport with minimal agitation of the child.
Initial stabilization and therapy
Prioritize airway management if the child is in extremis. Bag-valve-mask ventilation with 100% oxygen and cricoid pressure may provide adequate ventilation and time to move to a controlled setting (often the operating room).
For intubation, use an endotracheal tube one to two sizes smaller than usual for age/length. Gentle anterior neck compression may help identify air bubbles at the narrowed glottic opening. Difficult-airway adjuncts may be needed.
If oral intubation fails, proceed to emergent surgical airway options: cricothyrotomy or needle cricothyrotomy may be used in older children (typically >10–12 years), while needle cricothyrotomy is preferred in younger children.
Emergency department treatment
Provide 100% oxygen as tolerated. Keep the child in the position of comfort and avoid forcing supine positioning. While not definitively proven, nebulized racemic epinephrine or L-epinephrine may temporarily reduce symptoms while definitive airway planning proceeds, but use cautiously to avoid agitation.
Avoid agitating procedures such as IV placement and blood draws until airway plans are finalized. Consider early definitive airway management for rapidly worsening distress, increasing tachypnea, escalating throat pain, tachycardia, hypoxemia, or in children at high risk of sudden obstruction (e.g., immunodeficiency).
When possible, intubate in the operating room or similarly controlled environment by the most experienced clinician, often using inhalational anesthesia. Have multiple tube sizes available. Surgical backup must be present or immediately available for emergent tracheotomy or cricothyrotomy.
Start IV antibiotics promptly; second- or third-generation cephalosporins are effective against β-lactamase–producing H. influenzae. Steroids are controversial but often used, especially for chemical or thermal causes.
Medication
First line
Ampicillin/sulbactam 200–300 mg/kg/day IV divided every 6 hours
or
Cefotaxime 150 mg/kg/day IV divided every 6–8 hours
or
Ceftriaxone 100 mg/kg/day IV divided every 12 hours
Second line and selected options
Ampicillin 100–200 mg/kg/day IV divided every 6 hours plus chloramphenicol
Chloramphenicol 75–100 mg/kg/day IV divided every 6 hours
Meropenem 120 mg/kg/day IV divided every 8 hours (maximum 6 g/day)
Dexamethasone 0.6 mg/kg/day IV (maximum 10 mg); use remains controversial
Racemic epinephrine 0.05 mL/kg (maximum 0.5 mL) in 2.5 mL normal saline via nebulizer every 30 minutes as needed
L-epinephrine 1:1,000 at 0.5 mL/kg (maximum 5 mL) via nebulizer every 30 minutes as needed
Rifampin for household contact prophylaxis: 20 mg/kg (maximum 600 mg) daily for 4 days
If hereditary angioedema is suspected: C1 esterase inhibitor concentrate (or fresh frozen plasma if unavailable) with expert consultation
Follow-up and disposition
Admission criteria
All suspected or confirmed cases require ICU admission after airway stabilization, antibiotics, and supportive care.
Discharge criteria
Patients are not discharged from the ED with suspected epiglottitis. Public health actions and prophylaxis may be required for close contacts when Hib is confirmed, especially in households with infants under 12 months, unimmunized or incompletely immunized children, or immunosuppressed contacts. Child care contacts may need prophylaxis when multiple cases occur within 60 days. Invasive H. influenzae disease should be reported to local or state public health authorities.
Issues for referral
Critical care consultation is required; pulmonary and ENT involvement is commonly appropriate depending on local practice and airway course.
Clinical pearls and common missteps
This is a true airway emergency. The child must be continuously monitored and never left unattended, including during transport or any imaging, and must always be accompanied by personnel capable of immediate airway stabilization.
Basic description
Pediatric epiglottitis is an inflammation of the epiglottis and nearby supraglottic tissues that can become rapidly fatal because of progressive upper-airway obstruction. Children are especially vulnerable because their upper airway has a smaller cross-sectional diameter, the mucosa is more loosely attached and highly vascular (so swelling develops quickly), and the airway can collapse dynamically during distress.
After widespread Haemophilus influenzae type b (Hib) vaccination, childhood epiglottitis became far less common; however, rare cases can still occur, including vaccine failure. In the post-Hib era, the average age has shifted upward, and the condition is now seen more often in adolescents and adults than in toddlers or young school-aged children. Cases may occur year-round.
Alert
Any child with suspected epiglottitis requires continuous intensive monitoring and urgent readiness for airway intervention because obstruction can progress suddenly.
Etiology
Infectious causes include H. influenzae type b, Streptococcus pneumoniae, group A β-hemolytic Streptococcus, Staphylococcus aureus, and viruses. Less common pathogens include Klebsiella, Pseudomonas, and Candida.
Noninfectious causes include caustic injury, thermal injury, trauma, post-transplant lymphoproliferative disorder, and hereditary angioedema.
Diagnosis – signs and symptoms
History
Presentation is typically abrupt and severe without a preceding viral prodrome. Common features include irritability, intense throat pain (often described as the worst sore throat), fever, noisy breathing, and rapidly worsening toxicity or respiratory distress. Adolescents may resemble adult presentations, including repeated prior visits before diagnosis.
Physical examination
Children often appear toxic with high fever and quickly progressive symptoms. Key throat findings include drooling, dysphagia, and a muffled “hot potato” voice. Respiratory distress may evolve rapidly; the child usually prefers to sit upright, leaning forward with the mouth open (tripod/sniffing position) to optimize airflow. Stridor may be subtle early and progress later. Severe complications include complete airway obstruction, epiglottic abscess, pneumonia, and atelectasis.
Essential workup
Epiglottitis is primarily a clinical diagnosis. Attempts to directly visualize the epiglottis in an awake child (including indirect laryngoscopy) should be avoided unless performed in a controlled environment with full airway capability. In adolescents without impending obstruction, fiberoptic nasopharyngoscopy may be appropriate. If infection is suspected, cultures of the epiglottis should be obtained during laryngoscopy only after the airway is secured.
Diagnosis tests and interpretation
Laboratory studies
Defer lab tests until the airway is controlled. After stabilization, obtain throat cultures and blood cultures (blood cultures are often positive when Hib is the cause).
Imaging
Lateral soft tissue neck radiographs are usually unnecessary and can be dangerous because they may delay airway control, agitate the child, and remove the patient to a less controlled setting. If imaging is obtained, the child must be accompanied and airway equipment and skilled personnel must be immediately available. Possible findings include a normal film, epiglottic swelling (“thumbprint sign”), supraglottic swelling, a ballooned hypopharynx, obliteration of the vallecula, and an epiglottic width to C3 vertebral body width ratio greater than 0.5.
Diagnostic procedures
Laryngoscopy should be performed in a controlled setting whenever possible. The epiglottis typically appears swollen, erythematous, and inflamed. Cultures obtained after airway control can help target therapy.
Differential diagnosis
Bacterial tracheitis, retropharyngeal abscess, peritonsillar abscess, croup (with age overlap), pertussis, mononucleosis, Ludwig angina, diphtheria, anaphylaxis with angioedema, hereditary angioedema, upper-airway foreign body, laryngeal trauma, laryngospasm, toxic inhalation/aspiration (e.g., hydrocarbons), airway burns, hyperventilation, and CNS disorders.
Treatment – prehospital
Intervention should match the degree of obstruction, transport time, and provider capability. Notify the receiving facility early and coordinate transport with minimal agitation of the child.
Initial stabilization and therapy
Prioritize airway management if the child is in extremis. Bag-valve-mask ventilation with 100% oxygen and cricoid pressure may provide adequate ventilation and time to move to a controlled setting (often the operating room).
For intubation, use an endotracheal tube one to two sizes smaller than usual for age/length. Gentle anterior neck compression may help identify air bubbles at the narrowed glottic opening. Difficult-airway adjuncts may be needed.
If oral intubation fails, proceed to emergent surgical airway options: cricothyrotomy or needle cricothyrotomy may be used in older children (typically >10–12 years), while needle cricothyrotomy is preferred in younger children.
Emergency department treatment
Provide 100% oxygen as tolerated. Keep the child in the position of comfort and avoid forcing supine positioning. While not definitively proven, nebulized racemic epinephrine or L-epinephrine may temporarily reduce symptoms while definitive airway planning proceeds, but use cautiously to avoid agitation.
Avoid agitating procedures such as IV placement and blood draws until airway plans are finalized. Consider early definitive airway management for rapidly worsening distress, increasing tachypnea, escalating throat pain, tachycardia, hypoxemia, or in children at high risk of sudden obstruction (e.g., immunodeficiency).
When possible, intubate in the operating room or similarly controlled environment by the most experienced clinician, often using inhalational anesthesia. Have multiple tube sizes available. Surgical backup must be present or immediately available for emergent tracheotomy or cricothyrotomy.
Start IV antibiotics promptly; second- or third-generation cephalosporins are effective against β-lactamase–producing H. influenzae. Steroids are controversial but often used, especially for chemical or thermal causes.
Medication
First line
Ampicillin/sulbactam 200–300 mg/kg/day IV divided every 6 hours
or
Cefotaxime 150 mg/kg/day IV divided every 6–8 hours
or
Ceftriaxone 100 mg/kg/day IV divided every 12 hours
Second line and selected options
Ampicillin 100–200 mg/kg/day IV divided every 6 hours plus chloramphenicol
Chloramphenicol 75–100 mg/kg/day IV divided every 6 hours
Meropenem 120 mg/kg/day IV divided every 8 hours (maximum 6 g/day)
Dexamethasone 0.6 mg/kg/day IV (maximum 10 mg); use remains controversial
Racemic epinephrine 0.05 mL/kg (maximum 0.5 mL) in 2.5 mL normal saline via nebulizer every 30 minutes as needed
L-epinephrine 1:1,000 at 0.5 mL/kg (maximum 5 mL) via nebulizer every 30 minutes as needed
Rifampin for household contact prophylaxis: 20 mg/kg (maximum 600 mg) daily for 4 days
If hereditary angioedema is suspected: C1 esterase inhibitor concentrate (or fresh frozen plasma if unavailable) with expert consultation
Follow-up and disposition
Admission criteria
All suspected or confirmed cases require ICU admission after airway stabilization, antibiotics, and supportive care.
Discharge criteria
Patients are not discharged from the ED with suspected epiglottitis. Public health actions and prophylaxis may be required for close contacts when Hib is confirmed, especially in households with infants under 12 months, unimmunized or incompletely immunized children, or immunosuppressed contacts. Child care contacts may need prophylaxis when multiple cases occur within 60 days. Invasive H. influenzae disease should be reported to local or state public health authorities.
Issues for referral
Critical care consultation is required; pulmonary and ENT involvement is commonly appropriate depending on local practice and airway course.
Clinical pearls and common missteps
This is a true airway emergency. The child must be continuously monitored and never left unattended, including during transport or any imaging, and must always be accompanied by personnel capable of immediate airway stabilization.
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Emergency And Acute Medicine - Adult Epiglottitis
Basic description
Epiglottitis is a rapidly progressive inflammation of the epiglottis and surrounding supraglottic tissues that can lead to acute airway compromise. Although often more indolent in adults than in children, adults may still deteriorate abruptly with complete airway obstruction. While the incidence of pediatric epiglottitis has declined, adult cases are increasing.
Inflammation primarily involves the epiglottis, where edema poses the greatest airway risk, but may also extend to adjacent structures including the vallecula and arytenoids. The incidence in adults is approximately 1–4 per 100,000 per year and is rising. It is more common in men, with a ratio of 3:1, and most frequently affects patients in their fifth decade of life. Adult mortality is approximately 7%, compared with less than 1% in children.
Immunocompromised patients may present with fulminant disease, minimal early symptoms, and atypical organisms such as Candida or Pseudomonas aeruginosa. Potential complications include total airway obstruction, retropharyngeal abscess, acute respiratory distress syndrome, pneumonia, and empyema.
Etiology
Infectious causes include Haemophilus influenzae type B as well as type A and nontypeable strains, Haemophilus parainfluenzae, Streptococcus pneumoniae, Staphylococcus aureus, group A Streptococcus, Neisseria meningitidis, herpes simplex virus, cytomegalovirus, and Pseudomonas aeruginosa.
Noninfectious causes include chemical or thermal burns, toxic or illicit drug inhalation, trauma, and airway instrumentation.
Diagnosis – signs and symptoms
History
General symptoms include fever and upper respiratory tract complaints, though a prodrome may be absent. Head and neck symptoms commonly include dysphagia, muffled or “hot potato” voice, hoarseness, foreign body sensation in the throat, drooling, and associated tonsillar, peritonsillar, or uvular findings. Respiratory complaints include a subjective sense of airway obstruction and shortness of breath.
Physical examination
Patients may appear toxic and febrile and often sit upright in a tripod position. The classic “cherry red” epiglottis may be seen, though up to half of patients have a pale, edematous epiglottis instead. Gentle palpation of the hyoid or thyroid cartilage may be painful, and lateral movement of the larynx (“tracheal rock”) can elicit pain. Cervical lymphadenopathy may be present. Respiratory findings include stridor, accessory muscle use, and sudden airway loss.
Alert
Any patient with respiratory distress is at high risk for rapid progression to complete airway obstruction. Emergent surgical airway management may be required.
Essential workup
In patients with significant respiratory distress, invasive diagnostic procedures should be avoided. Management should prioritize empiric antibiotics and airway control before further diagnostic evaluation.
Diagnosis tests and interpretation
Laboratory studies
Obtain a complete blood count with differential and blood cultures. Pharyngeal cultures should be obtained only if there are no signs of respiratory distress.
Imaging
In patients with moderate to severe respiratory distress, airway control must precede imaging. A portable lateral soft tissue neck radiograph may show the epiglottic “thumb sign,” loss of the normal vallecular contour, swelling of the arytenoids or aryepiglottic folds, and prevertebral soft tissue swelling. False-negative rates are significant; negative imaging does not exclude the diagnosis.
CT imaging is reserved for cases in which laryngoscopy cannot be performed or when complications such as abscess are suspected.
Diagnostic procedures
Nasopharyngoscopy or indirect laryngoscopy may confirm the diagnosis but should not be performed prior to securing the airway if stridor or respiratory distress is present.
Differential diagnosis
Croup, airway foreign body, anaphylaxis, paradoxical vocal cord dysfunction, angioedema, laryngitis, pharyngitis, peritonsillar or retropharyngeal abscess, bacterial tracheitis, congenital airway anomalies, and meningitis.
Treatment – prehospital
Transport the patient in a position of comfort. Provide supplemental oxygen as tolerated while minimizing anxiety. Intubation should be attempted only in severe respiratory distress, as airway manipulation carries a high risk of worsening obstruction. Inhaled agents, racemic epinephrine, and β-agonists have no proven benefit.
Initial stabilization and therapy
Follow airway, breathing, and circulation priorities. Be fully prepared for definitive airway management, including surgical airway capability, from first contact until the diagnosis is excluded or the patient is transferred to intensive care. Airway examination itself can precipitate obstruction.
Orotracheal intubation is indicated for patients with significant respiratory distress or impending airway failure. Early ENT or surgical consultation is recommended when feasible. Needle jet ventilation may be a life-saving temporizing measure if intubation fails and a surgical airway is not immediately available.
Emergency department treatment
Provide humidified oxygen, establish IV access, and initiate empiric intravenous antibiotics. The role of corticosteroids remains controversial.
Medication
First line
Cefotaxime 2 g IV every 8 hours
or
Ceftriaxone 2 g IV every 24 hours
Second line or alternative regimens
Ampicillin–sulbactam 3 g IV initially, then 200–300 mg/kg/day in four divided doses plus vancomycin 1 g IV every 12 hours
Trimethoprim–sulfamethoxazole 320 mg IV initially, then 4–5 mg/kg IV every 12 hours
Additional coverage for Staphylococcus aureus
Nafcillin 150–200 mg/kg/day IV in four divided doses
or
Clindamycin 600–900 mg IV every 8 hours
Prophylaxis for close contacts
Rifampin 600 mg PO daily for 4 days in adults
Follow-up and disposition
Admission criteria
All patients with suspected or confirmed epiglottitis require admission to an intensive care unit for airway monitoring and intravenous antibiotics.
Discharge criteria
Patients should not be discharged unless epiglottitis has been definitively excluded by direct visualization of the supraglottic structures by an experienced clinician.
Issues for referral
Early otolaryngology consultation is recommended in all suspected cases.
Clinical pearls and common missteps
Delayed airway control is the most common cause of poor outcome. Avoid unnecessary interventions until the airway is secured. Adult epiglottitis carries a mortality rate of approximately 7%, underscoring the need for early recognition and decisive management.
Basic description
Epiglottitis is a rapidly progressive inflammation of the epiglottis and surrounding supraglottic tissues that can lead to acute airway compromise. Although often more indolent in adults than in children, adults may still deteriorate abruptly with complete airway obstruction. While the incidence of pediatric epiglottitis has declined, adult cases are increasing.
Inflammation primarily involves the epiglottis, where edema poses the greatest airway risk, but may also extend to adjacent structures including the vallecula and arytenoids. The incidence in adults is approximately 1–4 per 100,000 per year and is rising. It is more common in men, with a ratio of 3:1, and most frequently affects patients in their fifth decade of life. Adult mortality is approximately 7%, compared with less than 1% in children.
Immunocompromised patients may present with fulminant disease, minimal early symptoms, and atypical organisms such as Candida or Pseudomonas aeruginosa. Potential complications include total airway obstruction, retropharyngeal abscess, acute respiratory distress syndrome, pneumonia, and empyema.
Etiology
Infectious causes include Haemophilus influenzae type B as well as type A and nontypeable strains, Haemophilus parainfluenzae, Streptococcus pneumoniae, Staphylococcus aureus, group A Streptococcus, Neisseria meningitidis, herpes simplex virus, cytomegalovirus, and Pseudomonas aeruginosa.
Noninfectious causes include chemical or thermal burns, toxic or illicit drug inhalation, trauma, and airway instrumentation.
Diagnosis – signs and symptoms
History
General symptoms include fever and upper respiratory tract complaints, though a prodrome may be absent. Head and neck symptoms commonly include dysphagia, muffled or “hot potato” voice, hoarseness, foreign body sensation in the throat, drooling, and associated tonsillar, peritonsillar, or uvular findings. Respiratory complaints include a subjective sense of airway obstruction and shortness of breath.
Physical examination
Patients may appear toxic and febrile and often sit upright in a tripod position. The classic “cherry red” epiglottis may be seen, though up to half of patients have a pale, edematous epiglottis instead. Gentle palpation of the hyoid or thyroid cartilage may be painful, and lateral movement of the larynx (“tracheal rock”) can elicit pain. Cervical lymphadenopathy may be present. Respiratory findings include stridor, accessory muscle use, and sudden airway loss.
Alert
Any patient with respiratory distress is at high risk for rapid progression to complete airway obstruction. Emergent surgical airway management may be required.
Essential workup
In patients with significant respiratory distress, invasive diagnostic procedures should be avoided. Management should prioritize empiric antibiotics and airway control before further diagnostic evaluation.
Diagnosis tests and interpretation
Laboratory studies
Obtain a complete blood count with differential and blood cultures. Pharyngeal cultures should be obtained only if there are no signs of respiratory distress.
Imaging
In patients with moderate to severe respiratory distress, airway control must precede imaging. A portable lateral soft tissue neck radiograph may show the epiglottic “thumb sign,” loss of the normal vallecular contour, swelling of the arytenoids or aryepiglottic folds, and prevertebral soft tissue swelling. False-negative rates are significant; negative imaging does not exclude the diagnosis.
CT imaging is reserved for cases in which laryngoscopy cannot be performed or when complications such as abscess are suspected.
Diagnostic procedures
Nasopharyngoscopy or indirect laryngoscopy may confirm the diagnosis but should not be performed prior to securing the airway if stridor or respiratory distress is present.
Differential diagnosis
Croup, airway foreign body, anaphylaxis, paradoxical vocal cord dysfunction, angioedema, laryngitis, pharyngitis, peritonsillar or retropharyngeal abscess, bacterial tracheitis, congenital airway anomalies, and meningitis.
Treatment – prehospital
Transport the patient in a position of comfort. Provide supplemental oxygen as tolerated while minimizing anxiety. Intubation should be attempted only in severe respiratory distress, as airway manipulation carries a high risk of worsening obstruction. Inhaled agents, racemic epinephrine, and β-agonists have no proven benefit.
Initial stabilization and therapy
Follow airway, breathing, and circulation priorities. Be fully prepared for definitive airway management, including surgical airway capability, from first contact until the diagnosis is excluded or the patient is transferred to intensive care. Airway examination itself can precipitate obstruction.
Orotracheal intubation is indicated for patients with significant respiratory distress or impending airway failure. Early ENT or surgical consultation is recommended when feasible. Needle jet ventilation may be a life-saving temporizing measure if intubation fails and a surgical airway is not immediately available.
Emergency department treatment
Provide humidified oxygen, establish IV access, and initiate empiric intravenous antibiotics. The role of corticosteroids remains controversial.
Medication
First line
Cefotaxime 2 g IV every 8 hours
or
Ceftriaxone 2 g IV every 24 hours
Second line or alternative regimens
Ampicillin–sulbactam 3 g IV initially, then 200–300 mg/kg/day in four divided doses plus vancomycin 1 g IV every 12 hours
Trimethoprim–sulfamethoxazole 320 mg IV initially, then 4–5 mg/kg IV every 12 hours
Additional coverage for Staphylococcus aureus
Nafcillin 150–200 mg/kg/day IV in four divided doses
or
Clindamycin 600–900 mg IV every 8 hours
Prophylaxis for close contacts
Rifampin 600 mg PO daily for 4 days in adults
Follow-up and disposition
Admission criteria
All patients with suspected or confirmed epiglottitis require admission to an intensive care unit for airway monitoring and intravenous antibiotics.
Discharge criteria
Patients should not be discharged unless epiglottitis has been definitively excluded by direct visualization of the supraglottic structures by an experienced clinician.
Issues for referral
Early otolaryngology consultation is recommended in all suspected cases.
Clinical pearls and common missteps
Delayed airway control is the most common cause of poor outcome. Avoid unnecessary interventions until the airway is secured. Adult epiglottitis carries a mortality rate of approximately 7%, underscoring the need for early recognition and decisive management.
- Published on
Emergency And Acute Medicine - Epidural Hematoma
Fundamental Overview
An epidural hematoma results from direct trauma to the skull, where inward deformation of the calvarium causes separation of the dura from the inner skull surface and subsequent bleeding. The middle meningeal artery is responsible for more than half of cases, while meningeal venous bleeding accounts for approximately one third. Skull fractures are present in about 75% of patients, though they are less common in children.
More than half of patients have epidural hematoma as an isolated head injury, but it is frequently associated with subdural hematoma or cerebral contusion. On noncontrast CT imaging, the classic appearance is a lenticular (biconvex), unilateral collection, most often in the temporal region. The hematoma typically does not cross suture lines, though midline extension may occur.
Causation And Epidemiology
Epidural hematoma accounts for approximately 1.5% of traumatic brain injuries. The condition is more common in males, with a male-to-female ratio of about 3:1, and peak incidence occurs in the second and third decades of life. Motor vehicle collisions, assaults, and falls are the most frequent causes, with assault having the highest association with intracranial injury requiring neurosurgical intervention.
The condition is uncommon in very young children under five years of age and in elderly patients. Overall mortality is approximately 12% and is strongly correlated with the patient’s neurologic status prior to surgical intervention.
Pediatric-Specific Considerations
Head injury remains the leading cause of death and acquired disability in children. Falls and pedestrian or bicycle-related accidents are common mechanisms, while the most severe injuries are typically related to motor vehicle accidents. Nonaccidental trauma must always be considered.
Less than half of children with epidural hematoma present with altered consciousness. If epidural hematoma is part of the differential diagnosis, CT imaging is warranted regardless of mental status. Pediatric bleeding is more often venous in origin, and posterior fossa epidural hematomas occur more frequently than in adults. Children younger than five years generally have excellent outcomes, with recovery rates approaching 95%.
Clinical Manifestations
Patients often present with altered or progressively worsening level of consciousness. Approximately 85% experience loss of consciousness at some point during their clinical course, though only 11–30% demonstrate a classic lucid interval. Nausea and vomiting occur in roughly 40% of cases.
Unique Pediatric Presentations
In infants, the most notable sign may be a significant drop in hematocrit, sometimes as high as 40%. A bulging fontanelle accompanied by vomiting, seizures, or lethargy is highly suggestive. Fewer than half of pediatric patients lose consciousness at the time of injury.
Examination Findings
Ipsilateral pupillary dilation is seen in 20–40% of patients, most commonly on the same side as the hematoma. Hemiparesis occurs in more than one third of cases and is typically contralateral to the lesion.
Essential Diagnostic Priorities
Prompt neuroimaging is mandatory when epidural hematoma is suspected.
Diagnostic Studies And Interpretation
Laboratory evaluation may include arterial blood gas, complete blood count, serum chemistries, and coagulation studies, along with toxicology screening when appropriate.
Noncontrast CT of the head is the diagnostic modality of choice, typically revealing a smooth-bordered, biconvex hematoma. Mixed-density lesions suggest active bleeding. Temporal and parietal regions are most commonly involved. CT with bone windows is useful for detecting associated skull fractures. Additional imaging and trauma evaluation should be guided by clinical findings.
In infants with open fontanelles, ultrasound may be used as an adjunct diagnostic tool.
Conditions To Differentiate From
Recent head trauma strongly supports the diagnosis, though trauma may appear minor in infants and toddlers. Other considerations include subdural hematoma, cerebral concussion or contusion, intracerebral hemorrhage, diffuse axonal injury, subdural hygroma, abusive head trauma, and toxic, metabolic, or infectious etiologies.
Prehospital Management Principles
Patients with head injury demonstrate improved survival when transported to designated trauma centers. Spinal immobilization is essential, and adequate oxygenation must be ensured during transport. Airway protection and intubation may be required.
Initial Stabilization Approach
Avoidance of hypoxia and hypotension is critical. Rapid-sequence intubation is indicated for neurologic deterioration or signs of increased intracranial pressure. Controlled ventilation should target a PaCO₂ of 35–40 mm Hg, with hyperventilation reserved for impending herniation. Agents known to increase intracranial pressure should be avoided.
The head of the bed should be elevated 20–30 degrees after volume resuscitation. A rapid neurologic assessment including Glasgow Coma Scale scoring is required. Associated injuries are common and should be identified during secondary survey.
Emergency Department Interventions
Early neurosurgical intervention, ideally within four hours, significantly improves survival in comatose patients. Burr hole placement is often performed at the fracture site or ipsilateral to pupillary dilation, with craniectomy reserved for uncontrolled bleeding.
Conservative management in asymptomatic patients carries a high risk of deterioration, with more than 30% ultimately requiring surgery. Patients should be maintained euvolemic with isotonic fluids, and continuous end-tidal CO₂ monitoring is recommended. Arterial line placement and Foley catheterization facilitate close physiologic monitoring.
Intracranial pressure control includes adequate sedation, neuromuscular blockade when intubated, and osmotic therapy once euvolemia is achieved. Blood pressure and glucose control are essential, and seizure prophylaxis or treatment should be initiated. Steroids, prophylactic antibiotics, routine hyperventilation, and calcium channel blockers have not shown benefit.
Outcome Predictors
Poor prognosis is associated with age over 40 years, large or rapidly expanding hematomas, significant midline shift, low admission Glasgow Coma Scale score, prolonged pupillary asymmetry, elevated postoperative intracranial pressure, and associated brain or systemic injuries.
Medication Therapy
Commonly used agents include benzodiazepines for seizure control, antiepileptic drugs for prophylaxis, osmotic diuretics for intracranial pressure reduction, antihypertensives for blood pressure control, sedatives, neuromuscular blockers, and induction agents appropriate for neurocritical care. Hypertonic saline has shown benefit in selected pediatric patients.
Disposition And Monitoring
All patients with epidural hematoma or altered consciousness require admission to an intensive care setting with frequent neurologic assessments. Repeat CT imaging should be performed within 12–24 hours or sooner if clinical deterioration occurs. Patients at highest risk include those with skull fractures, rapid bleeding, low Glasgow Coma Scale scores, or focal neurologic deficits.
Discharge from the emergency department is not appropriate for patients with epidural hematoma.
Fundamental Overview
An epidural hematoma results from direct trauma to the skull, where inward deformation of the calvarium causes separation of the dura from the inner skull surface and subsequent bleeding. The middle meningeal artery is responsible for more than half of cases, while meningeal venous bleeding accounts for approximately one third. Skull fractures are present in about 75% of patients, though they are less common in children.
More than half of patients have epidural hematoma as an isolated head injury, but it is frequently associated with subdural hematoma or cerebral contusion. On noncontrast CT imaging, the classic appearance is a lenticular (biconvex), unilateral collection, most often in the temporal region. The hematoma typically does not cross suture lines, though midline extension may occur.
Causation And Epidemiology
Epidural hematoma accounts for approximately 1.5% of traumatic brain injuries. The condition is more common in males, with a male-to-female ratio of about 3:1, and peak incidence occurs in the second and third decades of life. Motor vehicle collisions, assaults, and falls are the most frequent causes, with assault having the highest association with intracranial injury requiring neurosurgical intervention.
The condition is uncommon in very young children under five years of age and in elderly patients. Overall mortality is approximately 12% and is strongly correlated with the patient’s neurologic status prior to surgical intervention.
Pediatric-Specific Considerations
Head injury remains the leading cause of death and acquired disability in children. Falls and pedestrian or bicycle-related accidents are common mechanisms, while the most severe injuries are typically related to motor vehicle accidents. Nonaccidental trauma must always be considered.
Less than half of children with epidural hematoma present with altered consciousness. If epidural hematoma is part of the differential diagnosis, CT imaging is warranted regardless of mental status. Pediatric bleeding is more often venous in origin, and posterior fossa epidural hematomas occur more frequently than in adults. Children younger than five years generally have excellent outcomes, with recovery rates approaching 95%.
Clinical Manifestations
Patients often present with altered or progressively worsening level of consciousness. Approximately 85% experience loss of consciousness at some point during their clinical course, though only 11–30% demonstrate a classic lucid interval. Nausea and vomiting occur in roughly 40% of cases.
Unique Pediatric Presentations
In infants, the most notable sign may be a significant drop in hematocrit, sometimes as high as 40%. A bulging fontanelle accompanied by vomiting, seizures, or lethargy is highly suggestive. Fewer than half of pediatric patients lose consciousness at the time of injury.
Examination Findings
Ipsilateral pupillary dilation is seen in 20–40% of patients, most commonly on the same side as the hematoma. Hemiparesis occurs in more than one third of cases and is typically contralateral to the lesion.
Essential Diagnostic Priorities
Prompt neuroimaging is mandatory when epidural hematoma is suspected.
Diagnostic Studies And Interpretation
Laboratory evaluation may include arterial blood gas, complete blood count, serum chemistries, and coagulation studies, along with toxicology screening when appropriate.
Noncontrast CT of the head is the diagnostic modality of choice, typically revealing a smooth-bordered, biconvex hematoma. Mixed-density lesions suggest active bleeding. Temporal and parietal regions are most commonly involved. CT with bone windows is useful for detecting associated skull fractures. Additional imaging and trauma evaluation should be guided by clinical findings.
In infants with open fontanelles, ultrasound may be used as an adjunct diagnostic tool.
Conditions To Differentiate From
Recent head trauma strongly supports the diagnosis, though trauma may appear minor in infants and toddlers. Other considerations include subdural hematoma, cerebral concussion or contusion, intracerebral hemorrhage, diffuse axonal injury, subdural hygroma, abusive head trauma, and toxic, metabolic, or infectious etiologies.
Prehospital Management Principles
Patients with head injury demonstrate improved survival when transported to designated trauma centers. Spinal immobilization is essential, and adequate oxygenation must be ensured during transport. Airway protection and intubation may be required.
Initial Stabilization Approach
Avoidance of hypoxia and hypotension is critical. Rapid-sequence intubation is indicated for neurologic deterioration or signs of increased intracranial pressure. Controlled ventilation should target a PaCO₂ of 35–40 mm Hg, with hyperventilation reserved for impending herniation. Agents known to increase intracranial pressure should be avoided.
The head of the bed should be elevated 20–30 degrees after volume resuscitation. A rapid neurologic assessment including Glasgow Coma Scale scoring is required. Associated injuries are common and should be identified during secondary survey.
Emergency Department Interventions
Early neurosurgical intervention, ideally within four hours, significantly improves survival in comatose patients. Burr hole placement is often performed at the fracture site or ipsilateral to pupillary dilation, with craniectomy reserved for uncontrolled bleeding.
Conservative management in asymptomatic patients carries a high risk of deterioration, with more than 30% ultimately requiring surgery. Patients should be maintained euvolemic with isotonic fluids, and continuous end-tidal CO₂ monitoring is recommended. Arterial line placement and Foley catheterization facilitate close physiologic monitoring.
Intracranial pressure control includes adequate sedation, neuromuscular blockade when intubated, and osmotic therapy once euvolemia is achieved. Blood pressure and glucose control are essential, and seizure prophylaxis or treatment should be initiated. Steroids, prophylactic antibiotics, routine hyperventilation, and calcium channel blockers have not shown benefit.
Outcome Predictors
Poor prognosis is associated with age over 40 years, large or rapidly expanding hematomas, significant midline shift, low admission Glasgow Coma Scale score, prolonged pupillary asymmetry, elevated postoperative intracranial pressure, and associated brain or systemic injuries.
Medication Therapy
Commonly used agents include benzodiazepines for seizure control, antiepileptic drugs for prophylaxis, osmotic diuretics for intracranial pressure reduction, antihypertensives for blood pressure control, sedatives, neuromuscular blockers, and induction agents appropriate for neurocritical care. Hypertonic saline has shown benefit in selected pediatric patients.
Disposition And Monitoring
All patients with epidural hematoma or altered consciousness require admission to an intensive care setting with frequent neurologic assessments. Repeat CT imaging should be performed within 12–24 hours or sooner if clinical deterioration occurs. Patients at highest risk include those with skull fractures, rapid bleeding, low Glasgow Coma Scale scores, or focal neurologic deficits.
Discharge from the emergency department is not appropriate for patients with epidural hematoma.
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Emergency And Acute Medicine - Epidural Abscess
Basic Overview
Spinal epidural abscess is an uncommon but serious pyogenic infection involving the epidural space of the spinal canal, with an estimated incidence of 2–25 cases per 100,000 hospital admissions. The thoracic spine is most frequently affected, followed by the lumbar and cervical regions.
Causative Mechanisms
Infection typically originates from a distant focus and reaches the epidural space via hematogenous spread in approximately half of cases, while direct extension accounts for others. In about one third of patients, no clear source is identified. Skin and soft tissue infections are the most common sources, though any pyogenic infection can be responsible.
Staphylococcus aureus causes more than half of cases, with a significant proportion due to methicillin-resistant strains. Streptococci are the second most common pathogens. Other causative organisms include Haemophilus influenzae, gram-negative bacilli, mycobacteria, anaerobes, coagulase-negative staphylococci, fungi, and mixed flora. Epidural abscess may also complicate epidural catheter placement, spinal surgery, or rarely lumbar puncture, particularly after multiple attempts.
Special Considerations In Children
Pediatric patients often present similarly to adults with back pain, fever, and neurologic deficits, though younger children and infants may exhibit nonspecific symptoms such as irritability, fever, or meningitis. Sphincter dysfunction is common. Most pediatric cases arise from hematogenous spread, with pathogen distribution and spinal location similar to adults.
Clinical Features And Presentation
The combination of fever and severe back pain is a critical warning sign. Radicular pain or neurologic abnormalities significantly increase suspicion for epidural abscess. The classic triad consists of progressive back pain, fever, and neurologic deficits such as weakness, paralysis, sensory level changes, or sphincter dysfunction. Some patients present primarily with sepsis and minimal back pain.
The condition affects all age groups, with peak incidence between 60 and 70 years. Most patients have identifiable risk factors, including intravenous drug use, diabetes mellitus, malignancy, chronic steroid use, alcoholism, recent spinal instrumentation or surgery, and indwelling vascular catheters. However, epidural abscess can occur without predisposing conditions.
History And Physical Findings
Patients may report back pain, fever, weakness, paresthesias, or bowel and bladder dysfunction. Examination often reveals fever, focal spinal tenderness or erythema, neurologic deficits, and signs of systemic infection. Evidence of intravenous drug use or other risk factors may be present.
Key Diagnostic Priorities
Evaluation should emphasize identifying predisposing conditions, localizing spinal tenderness, and detecting neurologic deficits such as saddle anesthesia, sphincter tone reduction, and lower extremity weakness. Measurement of postvoid residual urine volume can help identify urinary retention. Magnetic resonance imaging with and without gadolinium contrast is the diagnostic modality of choice and should be obtained emergently. Computed tomography with contrast or myelography may be used if MRI is unavailable.
Diagnostic Studies And Interpretation
Laboratory evaluation typically reveals an elevated erythrocyte sedimentation rate, which is highly sensitive but nonspecific. A normal ESR makes epidural abscess unlikely. C-reactive protein is also usually elevated. Blood cultures are positive in approximately 60% of cases, and leukocytosis with left shift is common. Cerebrospinal fluid analysis is often abnormal but nonspecific; lumbar puncture should generally be avoided due to the risk of spreading infection.
MRI has a sensitivity exceeding 90% and typically demonstrates high-intensity lesions on T2-weighted images. CT with contrast or CT myelography may be used when MRI is not available, though these carry additional risks.
Alternative Diagnoses To Consider
Because symptoms are often nonspecific, diagnosis is frequently delayed. Epidural abscess is commonly misdiagnosed as benign musculoskeletal back pain. Other considerations include vertebral osteomyelitis, spinal tumors, meningitis, discitis, pyelonephritis, spinal cord compression, ischemia, and disc herniation. In children, fever with back pain should prompt urgent imaging.
Prehospital And Early Management
Spinal immobilization is recommended when trauma or fracture is suspected.
Initial Stabilization Strategy
Prompt initiation of broad-spectrum intravenous antibiotics is essential and should cover Staphylococcus aureus, streptococci, and gram-negative organisms. Vancomycin combined with a third-generation cephalosporin is an appropriate initial regimen. Coverage for Pseudomonas species is indicated in patients with intravenous drug use. Anaerobic coverage may be added when clinically indicated.
Emergency Department Management
Urgent imaging is mandatory once epidural abscess is suspected, as delays worsen neurologic outcomes. If the level of infection cannot be localized clinically, imaging of the entire spine should be considered. Neurosurgical consultation or transfer to a facility with neurosurgical capability is required. Surgical decompression is often definitive, though select patients may be managed conservatively with prolonged intravenous antibiotics.
Antimicrobial Therapy
Common empiric regimens include vancomycin with ceftazidime, with metronidazole added if anaerobic infection is suspected. Antibiotic therapy should be adjusted based on culture results.
Disposition And Hospitalization
All patients with confirmed or strongly suspected epidural abscess require hospital admission. Emergent MRI and neurosurgical evaluation are mandatory. Discharge from the emergency department is not appropriate in these cases.
Referral And Transfer Considerations
Patients should be managed at centers with MRI availability and neurosurgical expertise. If transfer is required, blood cultures should be obtained and antibiotics initiated prior to transfer unless this would delay care.
Clinical Insights And Common Errors
Epidural abscess may recur, particularly in immunocompromised patients. Any patient with staphylococcal bacteremia and back pain or neurologic symptoms should be evaluated for epidural abscess. Failure to image the correct spinal region is a frequent error; careful neurologic and spinal examination can guide imaging, but when localization is unclear, imaging the entire spine is warranted.
Basic Overview
Spinal epidural abscess is an uncommon but serious pyogenic infection involving the epidural space of the spinal canal, with an estimated incidence of 2–25 cases per 100,000 hospital admissions. The thoracic spine is most frequently affected, followed by the lumbar and cervical regions.
Causative Mechanisms
Infection typically originates from a distant focus and reaches the epidural space via hematogenous spread in approximately half of cases, while direct extension accounts for others. In about one third of patients, no clear source is identified. Skin and soft tissue infections are the most common sources, though any pyogenic infection can be responsible.
Staphylococcus aureus causes more than half of cases, with a significant proportion due to methicillin-resistant strains. Streptococci are the second most common pathogens. Other causative organisms include Haemophilus influenzae, gram-negative bacilli, mycobacteria, anaerobes, coagulase-negative staphylococci, fungi, and mixed flora. Epidural abscess may also complicate epidural catheter placement, spinal surgery, or rarely lumbar puncture, particularly after multiple attempts.
Special Considerations In Children
Pediatric patients often present similarly to adults with back pain, fever, and neurologic deficits, though younger children and infants may exhibit nonspecific symptoms such as irritability, fever, or meningitis. Sphincter dysfunction is common. Most pediatric cases arise from hematogenous spread, with pathogen distribution and spinal location similar to adults.
Clinical Features And Presentation
The combination of fever and severe back pain is a critical warning sign. Radicular pain or neurologic abnormalities significantly increase suspicion for epidural abscess. The classic triad consists of progressive back pain, fever, and neurologic deficits such as weakness, paralysis, sensory level changes, or sphincter dysfunction. Some patients present primarily with sepsis and minimal back pain.
The condition affects all age groups, with peak incidence between 60 and 70 years. Most patients have identifiable risk factors, including intravenous drug use, diabetes mellitus, malignancy, chronic steroid use, alcoholism, recent spinal instrumentation or surgery, and indwelling vascular catheters. However, epidural abscess can occur without predisposing conditions.
History And Physical Findings
Patients may report back pain, fever, weakness, paresthesias, or bowel and bladder dysfunction. Examination often reveals fever, focal spinal tenderness or erythema, neurologic deficits, and signs of systemic infection. Evidence of intravenous drug use or other risk factors may be present.
Key Diagnostic Priorities
Evaluation should emphasize identifying predisposing conditions, localizing spinal tenderness, and detecting neurologic deficits such as saddle anesthesia, sphincter tone reduction, and lower extremity weakness. Measurement of postvoid residual urine volume can help identify urinary retention. Magnetic resonance imaging with and without gadolinium contrast is the diagnostic modality of choice and should be obtained emergently. Computed tomography with contrast or myelography may be used if MRI is unavailable.
Diagnostic Studies And Interpretation
Laboratory evaluation typically reveals an elevated erythrocyte sedimentation rate, which is highly sensitive but nonspecific. A normal ESR makes epidural abscess unlikely. C-reactive protein is also usually elevated. Blood cultures are positive in approximately 60% of cases, and leukocytosis with left shift is common. Cerebrospinal fluid analysis is often abnormal but nonspecific; lumbar puncture should generally be avoided due to the risk of spreading infection.
MRI has a sensitivity exceeding 90% and typically demonstrates high-intensity lesions on T2-weighted images. CT with contrast or CT myelography may be used when MRI is not available, though these carry additional risks.
Alternative Diagnoses To Consider
Because symptoms are often nonspecific, diagnosis is frequently delayed. Epidural abscess is commonly misdiagnosed as benign musculoskeletal back pain. Other considerations include vertebral osteomyelitis, spinal tumors, meningitis, discitis, pyelonephritis, spinal cord compression, ischemia, and disc herniation. In children, fever with back pain should prompt urgent imaging.
Prehospital And Early Management
Spinal immobilization is recommended when trauma or fracture is suspected.
Initial Stabilization Strategy
Prompt initiation of broad-spectrum intravenous antibiotics is essential and should cover Staphylococcus aureus, streptococci, and gram-negative organisms. Vancomycin combined with a third-generation cephalosporin is an appropriate initial regimen. Coverage for Pseudomonas species is indicated in patients with intravenous drug use. Anaerobic coverage may be added when clinically indicated.
Emergency Department Management
Urgent imaging is mandatory once epidural abscess is suspected, as delays worsen neurologic outcomes. If the level of infection cannot be localized clinically, imaging of the entire spine should be considered. Neurosurgical consultation or transfer to a facility with neurosurgical capability is required. Surgical decompression is often definitive, though select patients may be managed conservatively with prolonged intravenous antibiotics.
Antimicrobial Therapy
Common empiric regimens include vancomycin with ceftazidime, with metronidazole added if anaerobic infection is suspected. Antibiotic therapy should be adjusted based on culture results.
Disposition And Hospitalization
All patients with confirmed or strongly suspected epidural abscess require hospital admission. Emergent MRI and neurosurgical evaluation are mandatory. Discharge from the emergency department is not appropriate in these cases.
Referral And Transfer Considerations
Patients should be managed at centers with MRI availability and neurosurgical expertise. If transfer is required, blood cultures should be obtained and antibiotics initiated prior to transfer unless this would delay care.
Clinical Insights And Common Errors
Epidural abscess may recur, particularly in immunocompromised patients. Any patient with staphylococcal bacteremia and back pain or neurologic symptoms should be evaluated for epidural abscess. Failure to image the correct spinal region is a frequent error; careful neurologic and spinal examination can guide imaging, but when localization is unclear, imaging the entire spine is warranted.
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Emergency And Acute Medicine - Epididymitis And Orchitis
Basic Overview
Epididymitis refers to inflammation or infection of the epididymis and is uncommon in prepubertal boys. The disease process typically begins with cellular inflammation in the vas deferens that descends into the epididymis. In the acute phase, the epididymis becomes swollen and indurated, often involving both upper and lower poles, with associated thickening of the spermatic cord. Secondary testicular edema may occur due to passive congestion or inflammatory spread. Resolution may be complete, though peritubular fibrosis can develop and lead to ductal obstruction. Testicular atrophy occurs in up to two thirds of affected men due to partial vascular thrombosis of the testicular artery. Abscess formation and infarction are uncommon. Infertility risk is uncertain with unilateral disease but approaches 50% with bilateral involvement.
Orchitis is defined as inflammation or infection of the testicle and most often results from direct extension of epididymal infection. Isolated orchitis is rare and may occur through hematogenous bacterial spread or viral infection, particularly mumps. Bacterial orchitis is typically pyogenic and secondary to epididymitis. Viral orchitis, most commonly due to mumps, occurs in 20–30% of postpubertal males with mumps infection, usually several days after parotitis, though it may occur independently. The disease is unilateral in most cases and usually resolves within 6–10 days, though residual testicular atrophy is common. Granulomatous orchitis is associated with syphilis, mycobacterial, or fungal infections and is more common in immunocompromised patients.
Causes And Predisposing Factors
In children, epididymitis is most common in infants younger than one year and adolescents aged 12–15 years. A specific etiology is identified in only a minority of prepubertal cases and often involves coliform or pseudomonal urinary tract infections, frequently associated with structural urinary abnormalities. Sexually transmitted infections are rare in this age group.
In men younger than 35 years, epididymitis is most often sexually transmitted. Chlamydia trachomatis is the most common pathogen, followed by Neisseria gonorrhoeae. Coliform bacteria are less common but tend to cause more destructive infections with higher risk of abscess formation, particularly in individuals engaging in insertive anal intercourse. Ureaplasma urealyticum may also be implicated.
In men older than 35 years, epididymitis is frequently associated with underlying urologic pathology such as benign prostatic hypertrophy, prostate cancer, or urethral strictures. Coliform organisms predominate, often following urinary tract instrumentation. Drug-induced epididymitis may occur with amiodarone, particularly at supratherapeutic levels. Granulomatous causes include tuberculosis, syphilis, and fungal infections, especially in patients with HIV. Vasculitic conditions such as polyarteritis nodosa, Behçet disease, and Henoch–Schönlein purpura are rare causes.
Orchitis may be caused by pyogenic bacteria such as Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, staphylococci, and streptococci. Viral causes include mumps and less commonly coxsackievirus and lymphocytic choriomeningitis virus. Granulomatous and fungal orchitis should be considered in immunocompromised hosts. Post-traumatic orchitis may occur due to inflammatory response following injury.
Clinical Presentation
Patients typically report gradual onset of unilateral scrotal or testicular pain that progresses over hours to days. Scrotal swelling and erythema are common. Dysuria may be present, often with a history of urinary tract infection or abnormal bladder function. Urethral discharge may be absent even in gonococcal infections. Fever occurs in a minority of cases. Recent urethral instrumentation or catheterization may be noted.
Physical Examination Findings
Examination often reveals tenderness in the groin, lower abdomen, or scrotum. The scrotal skin is frequently warm and erythematous. Early in the course, the epididymis may feel swollen and indurated, while later stages may make differentiation between epididymis and testis difficult. The spermatic cord may be edematous, and the cremasteric reflex is typically intact. Pain relief with testicular elevation may occur but is not diagnostic. Pyogenic orchitis is associated with acute systemic illness, marked testicular swelling, severe pain, fever, and often a reactive hydrocele.
Key Evaluation Priorities
Excluding testicular torsion is critical in all cases of acute scrotal pain. Immediate urologic consultation is required if torsion is suspected.
Diagnostic Studies And Interpretation
Laboratory evaluation may reveal leukocytosis. Urinalysis and urine culture may demonstrate pyuria or bacteriuria, though many patients have normal findings. Urethral testing for chlamydia and gonorrhea using nucleic acid amplification or culture is recommended in postpubertal and sexually active patients. Blood cultures are indicated in systemically ill individuals.
Color Doppler ultrasonography is the preferred imaging modality and demonstrates increased blood flow and hyperemia in epididymo-orchitis, helping to differentiate it from testicular torsion, which shows reduced or absent perfusion. Testicular scintigraphy may be used where available but is less commonly performed.
Alternative Diagnoses To Consider
The differential diagnosis includes testicular torsion, testicular tumor, torsion of testicular appendages, scrotal trauma, incarcerated hernia, acute hydrocele, and scrotal abscess.
Initial Management Approach
Prehospital and initial emergency department care includes intravenous access and fluid resuscitation for systemically ill patients.
Emergency Department Management
Treatment consists of empiric antibiotic therapy based on age and suspected etiology, along with bed rest, scrotal elevation, ice application, analgesics, and anti-inflammatory medications. Sexually transmitted causes should be covered in younger or sexually active patients, while coliform organisms should be targeted in older men or those with urinary tract pathology.
Medication Therapy
For sexually active men younger than 35 years, recommended therapy includes ceftriaxone intramuscularly combined with doxycycline for 10 days, with azithromycin as an alternative if doxycycline is contraindicated. For men older than 35 years, those with enteric organisms, or those unable to receive cephalosporins or tetracyclines, fluoroquinolones such as levofloxacin or ofloxacin are appropriate. In children with concurrent urinary tract infection, trimethoprim–sulfamethoxazole may be used, avoiding quinolones and tetracyclines.
Disposition And Follow-Up
Hospital admission is indicated for patients with suspected torsion, scrotal abscess, systemic illness, intractable pain, or inability to tolerate oral therapy. Stable patients with reliable follow-up may be discharged on oral antibiotics.
Follow-Up Guidance
Failure to improve within three days of initiating therapy requires urologic reassessment. Persistent symptoms after completion of antibiotics necessitate evaluation for alternative diagnoses such as tuberculosis, fungal infection, abscess, tumor, or infarction. Sexual partners should be evaluated and treated when sexually transmitted infection is suspected. Children require urologic evaluation for underlying structural abnormalities.
Clinical Insights And Common Errors
Testicular torsion must be excluded in all patients with acute scrotal pain. In sexually active men younger than 35 years, epididymitis is most commonly due to sexually transmitted pathogens, whereas coliform bacteria predominate in older men. Empiric antibiotic therapy should be initiated promptly based on clinical presentation.
Basic Overview
Epididymitis refers to inflammation or infection of the epididymis and is uncommon in prepubertal boys. The disease process typically begins with cellular inflammation in the vas deferens that descends into the epididymis. In the acute phase, the epididymis becomes swollen and indurated, often involving both upper and lower poles, with associated thickening of the spermatic cord. Secondary testicular edema may occur due to passive congestion or inflammatory spread. Resolution may be complete, though peritubular fibrosis can develop and lead to ductal obstruction. Testicular atrophy occurs in up to two thirds of affected men due to partial vascular thrombosis of the testicular artery. Abscess formation and infarction are uncommon. Infertility risk is uncertain with unilateral disease but approaches 50% with bilateral involvement.
Orchitis is defined as inflammation or infection of the testicle and most often results from direct extension of epididymal infection. Isolated orchitis is rare and may occur through hematogenous bacterial spread or viral infection, particularly mumps. Bacterial orchitis is typically pyogenic and secondary to epididymitis. Viral orchitis, most commonly due to mumps, occurs in 20–30% of postpubertal males with mumps infection, usually several days after parotitis, though it may occur independently. The disease is unilateral in most cases and usually resolves within 6–10 days, though residual testicular atrophy is common. Granulomatous orchitis is associated with syphilis, mycobacterial, or fungal infections and is more common in immunocompromised patients.
Causes And Predisposing Factors
In children, epididymitis is most common in infants younger than one year and adolescents aged 12–15 years. A specific etiology is identified in only a minority of prepubertal cases and often involves coliform or pseudomonal urinary tract infections, frequently associated with structural urinary abnormalities. Sexually transmitted infections are rare in this age group.
In men younger than 35 years, epididymitis is most often sexually transmitted. Chlamydia trachomatis is the most common pathogen, followed by Neisseria gonorrhoeae. Coliform bacteria are less common but tend to cause more destructive infections with higher risk of abscess formation, particularly in individuals engaging in insertive anal intercourse. Ureaplasma urealyticum may also be implicated.
In men older than 35 years, epididymitis is frequently associated with underlying urologic pathology such as benign prostatic hypertrophy, prostate cancer, or urethral strictures. Coliform organisms predominate, often following urinary tract instrumentation. Drug-induced epididymitis may occur with amiodarone, particularly at supratherapeutic levels. Granulomatous causes include tuberculosis, syphilis, and fungal infections, especially in patients with HIV. Vasculitic conditions such as polyarteritis nodosa, Behçet disease, and Henoch–Schönlein purpura are rare causes.
Orchitis may be caused by pyogenic bacteria such as Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, staphylococci, and streptococci. Viral causes include mumps and less commonly coxsackievirus and lymphocytic choriomeningitis virus. Granulomatous and fungal orchitis should be considered in immunocompromised hosts. Post-traumatic orchitis may occur due to inflammatory response following injury.
Clinical Presentation
Patients typically report gradual onset of unilateral scrotal or testicular pain that progresses over hours to days. Scrotal swelling and erythema are common. Dysuria may be present, often with a history of urinary tract infection or abnormal bladder function. Urethral discharge may be absent even in gonococcal infections. Fever occurs in a minority of cases. Recent urethral instrumentation or catheterization may be noted.
Physical Examination Findings
Examination often reveals tenderness in the groin, lower abdomen, or scrotum. The scrotal skin is frequently warm and erythematous. Early in the course, the epididymis may feel swollen and indurated, while later stages may make differentiation between epididymis and testis difficult. The spermatic cord may be edematous, and the cremasteric reflex is typically intact. Pain relief with testicular elevation may occur but is not diagnostic. Pyogenic orchitis is associated with acute systemic illness, marked testicular swelling, severe pain, fever, and often a reactive hydrocele.
Key Evaluation Priorities
Excluding testicular torsion is critical in all cases of acute scrotal pain. Immediate urologic consultation is required if torsion is suspected.
Diagnostic Studies And Interpretation
Laboratory evaluation may reveal leukocytosis. Urinalysis and urine culture may demonstrate pyuria or bacteriuria, though many patients have normal findings. Urethral testing for chlamydia and gonorrhea using nucleic acid amplification or culture is recommended in postpubertal and sexually active patients. Blood cultures are indicated in systemically ill individuals.
Color Doppler ultrasonography is the preferred imaging modality and demonstrates increased blood flow and hyperemia in epididymo-orchitis, helping to differentiate it from testicular torsion, which shows reduced or absent perfusion. Testicular scintigraphy may be used where available but is less commonly performed.
Alternative Diagnoses To Consider
The differential diagnosis includes testicular torsion, testicular tumor, torsion of testicular appendages, scrotal trauma, incarcerated hernia, acute hydrocele, and scrotal abscess.
Initial Management Approach
Prehospital and initial emergency department care includes intravenous access and fluid resuscitation for systemically ill patients.
Emergency Department Management
Treatment consists of empiric antibiotic therapy based on age and suspected etiology, along with bed rest, scrotal elevation, ice application, analgesics, and anti-inflammatory medications. Sexually transmitted causes should be covered in younger or sexually active patients, while coliform organisms should be targeted in older men or those with urinary tract pathology.
Medication Therapy
For sexually active men younger than 35 years, recommended therapy includes ceftriaxone intramuscularly combined with doxycycline for 10 days, with azithromycin as an alternative if doxycycline is contraindicated. For men older than 35 years, those with enteric organisms, or those unable to receive cephalosporins or tetracyclines, fluoroquinolones such as levofloxacin or ofloxacin are appropriate. In children with concurrent urinary tract infection, trimethoprim–sulfamethoxazole may be used, avoiding quinolones and tetracyclines.
Disposition And Follow-Up
Hospital admission is indicated for patients with suspected torsion, scrotal abscess, systemic illness, intractable pain, or inability to tolerate oral therapy. Stable patients with reliable follow-up may be discharged on oral antibiotics.
Follow-Up Guidance
Failure to improve within three days of initiating therapy requires urologic reassessment. Persistent symptoms after completion of antibiotics necessitate evaluation for alternative diagnoses such as tuberculosis, fungal infection, abscess, tumor, or infarction. Sexual partners should be evaluated and treated when sexually transmitted infection is suspected. Children require urologic evaluation for underlying structural abnormalities.
Clinical Insights And Common Errors
Testicular torsion must be excluded in all patients with acute scrotal pain. In sexually active men younger than 35 years, epididymitis is most commonly due to sexually transmitted pathogens, whereas coliform bacteria predominate in older men. Empiric antibiotic therapy should be initiated promptly based on clinical presentation.
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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.
- Published on
Emergency And Acute Medicine – Flail Chest
Basics Description
Flail chest is defined by a free-floating segment of the chest wall created when three or more adjacent ribs are fractured in two or more locations. It may also occur with rib fractures combined with sternal fractures or costochondral separations. The unstable segment characteristically moves inward during inspiration and outward during expiration (paradoxical motion). The primary clinical problem in flail chest is not the chest wall instability itself but the associated pulmonary contusion, which leads to impaired gas exchange rather than altered ventilatory mechanics.
Etiology
Flail chest results from high-energy blunt thoracic trauma, most commonly motor vehicle collisions, falls from height, assaults, or missile injuries. Rib fractures usually occur at the point of impact or at the posterior rib angle, with ribs 4–9 most frequently involved. Energy transfer to adjacent lung tissue disrupts the alveolocapillary membrane, producing pulmonary contusion, ventilation–perfusion mismatch, arteriovenous shunting, hypoxemia, and potential respiratory failure.
Pediatric considerations: Children have more elastic chest walls, making rib fractures less common; when present, they imply severe energy transfer.
Geriatric considerations: Older adults are more susceptible to rib fractures, often from low-energy mechanisms, and outcomes are worsened by osteoporosis.
Diagnosis Signs And Symptoms
History typically includes significant blunt chest trauma with localized chest wall pain that worsens with inspiration, coughing, or movement. Patients may report pleuritic chest pain, dyspnea, or hemoptysis.
Physical examination may reveal paradoxical chest wall motion, which can be subtle or absent early due to muscle spasm and splinting. Additional findings include multiple rib fractures with tenderness, crepitus, ecchymosis, edema, and bony step-offs. Respiratory findings range from tachypnea and splinting respirations to cyanosis, hypoxia, tachycardia, hypotension, and progressive crackles or diminished breath sounds as pulmonary contusion evolves.
Essential Workup
Diagnosis is primarily clinical and supported by imaging. Continuous monitoring of oxygenation and respiratory status is essential.
Diagnosis Tests And Interpretation
Laboratory studies may include arterial blood gas analysis demonstrating hypoxemia and an elevated alveolar–arterial gradient.
Chest radiography may show rib fractures and associated intrathoracic injuries such as pneumothorax, hemothorax, pneumomediastinum, or pulmonary contusion, which often becomes radiographically apparent within 6–12 hours.
Thoracic CT is more sensitive than plain radiographs and frequently identifies additional rib fractures and associated injuries not seen on initial chest X-ray.
Differential Diagnosis
Chest wall contusion, intercostal muscle strain, costochondral separation, sternal fracture or dislocation, and pulmonary conditions such as ARDS, pulmonary laceration, embolism, heart failure, pneumonia, or noncardiogenic pulmonary edema.
Treatment
Prehospital care includes positioning the patient with the injured side down to stabilize the chest wall and improve ventilation of the unaffected lung. Patients with significant thoracic trauma should be transported to a trauma center.
Initial stabilization follows airway, breathing, and circulation priorities with supplemental oxygen, IV access, cardiac monitoring, and pulse oximetry. Endotracheal intubation is indicated for severe hypoxemia, significant underlying lung disease, or impending respiratory failure.
Emergency department management focuses on maintaining adequate oxygenation and ventilation. High-flow oxygen is first-line in alert patients; noninvasive positive pressure ventilation may be used if oxygenation remains inadequate. Early invasive mechanical ventilation is indicated when noninvasive measures fail, providing physiologic internal stabilization of the flail segment. External fixation of the chest wall is not recommended.
Aggressive pain control is critical to prevent hypoventilation, atelectasis, and pneumonia. Intercostal nerve blocks with bupivacaine can provide effective temporary analgesia. Careful fluid management is essential to avoid worsening pulmonary edema in the presence of contusion. Prophylactic antibiotics are not indicated.
Medication
Analgesia may include acetaminophen–opioid combinations, IV or oral opioids such as morphine or hydromorphone, patient-controlled analgesia, and regional techniques. Bupivacaine 0.5% may be used for intercostal nerve blocks. Thoracic epidural analgesia should be considered in patients with severe pain or opioid-related hypoventilation. NSAIDs are generally discouraged due to bleeding risk. Acetaminophen dosing should not exceed recommended daily limits.
Follow Up Disposition
All patients with flail chest require admission to a critical care or closely monitored setting for respiratory observation and pain management. Discharge from the emergency department is not appropriate.
Clinical Takeaways And Common Pitfalls
Early and adequate pain control is essential to prevent respiratory complications. Always assess for associated injuries, particularly pulmonary contusion and pneumothorax. Elderly patients have markedly worse outcomes and require vigilant monitoring and aggressive supportive care.
Basics Description
Flail chest is defined by a free-floating segment of the chest wall created when three or more adjacent ribs are fractured in two or more locations. It may also occur with rib fractures combined with sternal fractures or costochondral separations. The unstable segment characteristically moves inward during inspiration and outward during expiration (paradoxical motion). The primary clinical problem in flail chest is not the chest wall instability itself but the associated pulmonary contusion, which leads to impaired gas exchange rather than altered ventilatory mechanics.
Etiology
Flail chest results from high-energy blunt thoracic trauma, most commonly motor vehicle collisions, falls from height, assaults, or missile injuries. Rib fractures usually occur at the point of impact or at the posterior rib angle, with ribs 4–9 most frequently involved. Energy transfer to adjacent lung tissue disrupts the alveolocapillary membrane, producing pulmonary contusion, ventilation–perfusion mismatch, arteriovenous shunting, hypoxemia, and potential respiratory failure.
Pediatric considerations: Children have more elastic chest walls, making rib fractures less common; when present, they imply severe energy transfer.
Geriatric considerations: Older adults are more susceptible to rib fractures, often from low-energy mechanisms, and outcomes are worsened by osteoporosis.
Diagnosis Signs And Symptoms
History typically includes significant blunt chest trauma with localized chest wall pain that worsens with inspiration, coughing, or movement. Patients may report pleuritic chest pain, dyspnea, or hemoptysis.
Physical examination may reveal paradoxical chest wall motion, which can be subtle or absent early due to muscle spasm and splinting. Additional findings include multiple rib fractures with tenderness, crepitus, ecchymosis, edema, and bony step-offs. Respiratory findings range from tachypnea and splinting respirations to cyanosis, hypoxia, tachycardia, hypotension, and progressive crackles or diminished breath sounds as pulmonary contusion evolves.
Essential Workup
Diagnosis is primarily clinical and supported by imaging. Continuous monitoring of oxygenation and respiratory status is essential.
Diagnosis Tests And Interpretation
Laboratory studies may include arterial blood gas analysis demonstrating hypoxemia and an elevated alveolar–arterial gradient.
Chest radiography may show rib fractures and associated intrathoracic injuries such as pneumothorax, hemothorax, pneumomediastinum, or pulmonary contusion, which often becomes radiographically apparent within 6–12 hours.
Thoracic CT is more sensitive than plain radiographs and frequently identifies additional rib fractures and associated injuries not seen on initial chest X-ray.
Differential Diagnosis
Chest wall contusion, intercostal muscle strain, costochondral separation, sternal fracture or dislocation, and pulmonary conditions such as ARDS, pulmonary laceration, embolism, heart failure, pneumonia, or noncardiogenic pulmonary edema.
Treatment
Prehospital care includes positioning the patient with the injured side down to stabilize the chest wall and improve ventilation of the unaffected lung. Patients with significant thoracic trauma should be transported to a trauma center.
Initial stabilization follows airway, breathing, and circulation priorities with supplemental oxygen, IV access, cardiac monitoring, and pulse oximetry. Endotracheal intubation is indicated for severe hypoxemia, significant underlying lung disease, or impending respiratory failure.
Emergency department management focuses on maintaining adequate oxygenation and ventilation. High-flow oxygen is first-line in alert patients; noninvasive positive pressure ventilation may be used if oxygenation remains inadequate. Early invasive mechanical ventilation is indicated when noninvasive measures fail, providing physiologic internal stabilization of the flail segment. External fixation of the chest wall is not recommended.
Aggressive pain control is critical to prevent hypoventilation, atelectasis, and pneumonia. Intercostal nerve blocks with bupivacaine can provide effective temporary analgesia. Careful fluid management is essential to avoid worsening pulmonary edema in the presence of contusion. Prophylactic antibiotics are not indicated.
Medication
Analgesia may include acetaminophen–opioid combinations, IV or oral opioids such as morphine or hydromorphone, patient-controlled analgesia, and regional techniques. Bupivacaine 0.5% may be used for intercostal nerve blocks. Thoracic epidural analgesia should be considered in patients with severe pain or opioid-related hypoventilation. NSAIDs are generally discouraged due to bleeding risk. Acetaminophen dosing should not exceed recommended daily limits.
Follow Up Disposition
All patients with flail chest require admission to a critical care or closely monitored setting for respiratory observation and pain management. Discharge from the emergency department is not appropriate.
Clinical Takeaways And Common Pitfalls
Early and adequate pain control is essential to prevent respiratory complications. Always assess for associated injuries, particularly pulmonary contusion and pneumothorax. Elderly patients have markedly worse outcomes and require vigilant monitoring and aggressive supportive care.
