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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 - 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 - 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.
- Published on
Emergency And Acute Medicine - Erythema Infectiosum
Basic description
Erythema infectiosum is a characteristic viral exanthem, also known as fifth disease, historically the fifth most commonly described childhood rash. It typically presents with a mild viral prodrome followed by a “slapped-cheek” facial rash and a subsequent diffuse, lacy, reticular eruption, with or without arthropathy. It most commonly affects school-aged children younger than 14 years and is usually self-limited with lifelong immunity. Chronic or severe disease is rare but may occur in patients with congenital anemias or immunosuppression. Infection during pregnancy carries a risk of serious fetal complications.
Etiology
The condition is caused by human parvovirus B19, a small single-stranded DNA virus that infects human erythroid progenitor cells and transiently suppresses erythropoiesis. Transmission occurs via respiratory droplets, blood products, and vertical maternal–fetal spread. It is most common in late winter and spring. The incubation period ranges from 4 to 21 days, and patients are most contagious during the week before rash onset. Most adults have serologic evidence of prior infection.
Diagnosis – signs and symptoms
Young children typically develop a bright erythematous “slapped-cheek” rash accompanied by low-grade fever and malaise. Four to fourteen days later, a diffuse, pruritic, lacy rash may appear, most prominent on the extremities and usually sparing the palms and soles. Adolescents and adults may develop symmetric polyarthropathy, particularly involving small joints, while children more commonly experience knee involvement. Many patients remain asymptomatic or experience only mild viral symptoms.
History
Symptoms often begin with mild constitutional complaints such as fever, headache, nasal congestion, nausea, or sore throat. Patients are contagious only before the facial rash appears.
Physical examination
Stage one consists of coalescent, warm, erythematous, edematous facial papules with circumoral pallor. Stage two features a diffuse, maculopapular, reticular rash that may persist for weeks. Stage three is marked by fading of the rash with recurrence triggered by heat, sunlight, stress, or exercise, eventually resolving without scarring.
Essential workup
Diagnosis is clinical and based on classic presentation.
Diagnosis tests and interpretation
Laboratory testing is usually unnecessary. A CBC and reticulocyte count are indicated if aplastic crisis is suspected. In immunocompromised or pregnant patients, confirmation may be obtained with parvovirus B19 PCR or serology. IgM antibodies indicate acute infection, while IgG antibodies confirm immunity. Pregnant patients may require ultrasound monitoring for hydrops fetalis.
Differential diagnosis
Allergic reaction, drug eruption, nonspecific viral exanthem, measles, rubella, roseola, scarlet fever, erysipelas, infectious mononucleosis, collagen vascular disease, rheumatoid arthritis, sunburn, and enteroviral infections.
Treatment
The disease is typically self-limited and requires no specific therapy.
Prehospital care
Supportive care and standard ABCs for severe presentations.
Initial stabilization and therapy
Airway, breathing, and circulation management as needed. Supplemental oxygen and intravenous fluids may be required for severe dehydration. Severe anemia should be treated with packed red blood cell transfusion. Analgesia may be provided for arthropathy.
Emergency department treatment and procedures
No antiviral therapy or vaccine is available. Management is supportive, including antipyretics for fever, NSAIDs for joint pain if renal function permits, antihistamines for pruritus, and IV fluids when indicated. Immunocompromised patients with chronic infection or red cell aplasia may benefit from IVIG in consultation with infectious disease specialists. Hospitalization is indicated for aplastic crisis or severe complications.
Medication
Acetaminophen or ibuprofen for fever and pain. Diphenhydramine may be used for pruritus with caution regarding sedation. IVIG is reserved for select cases under specialist guidance.
Follow-up and disposition
Admission criteria
Aplastic crisis, severe anemia, hydrops fetalis, severe immunosuppression, toxic appearance, or debilitating arthritis.
Discharge criteria
Most patients can be safely discharged. Once the facial rash appears, patients are no longer contagious and may return to school or work if clinically stable.
Issues for referral
Hematology referral for patients with hereditary anemias or aplastic crisis. Infectious disease consultation for immunocompromised patients. Obstetric referral for pregnant patients with confirmed or suspected acute infection.
Follow-up recommendations
Pregnant patients with new infection require serial ultrasounds for 10–12 weeks. Patients at risk for aplastic crisis should have repeat CBC testing within 1–2 days.
Patient education
There is no vaccine. Hand hygiene reduces transmission. Children are usually no longer contagious by the time the rash appears, so exclusion from school is generally unnecessary.
Complications
Transient aplastic crisis in patients with underlying anemias, chronic anemia in immunocompromised individuals, arthropathy in adults, rare neurologic or cardiac involvement, and pregnancy-related complications including hydrops fetalis and fetal loss.
Clinical pearls and common missteps
Parvovirus B19 infection is usually mild and self-limited. Patients are not contagious once the rash appears. Always evaluate patients with anemia or immunosuppression for complications. Confirm infection in pregnancy and ensure appropriate fetal monitoring.
Basic description
Erythema infectiosum is a characteristic viral exanthem, also known as fifth disease, historically the fifth most commonly described childhood rash. It typically presents with a mild viral prodrome followed by a “slapped-cheek” facial rash and a subsequent diffuse, lacy, reticular eruption, with or without arthropathy. It most commonly affects school-aged children younger than 14 years and is usually self-limited with lifelong immunity. Chronic or severe disease is rare but may occur in patients with congenital anemias or immunosuppression. Infection during pregnancy carries a risk of serious fetal complications.
Etiology
The condition is caused by human parvovirus B19, a small single-stranded DNA virus that infects human erythroid progenitor cells and transiently suppresses erythropoiesis. Transmission occurs via respiratory droplets, blood products, and vertical maternal–fetal spread. It is most common in late winter and spring. The incubation period ranges from 4 to 21 days, and patients are most contagious during the week before rash onset. Most adults have serologic evidence of prior infection.
Diagnosis – signs and symptoms
Young children typically develop a bright erythematous “slapped-cheek” rash accompanied by low-grade fever and malaise. Four to fourteen days later, a diffuse, pruritic, lacy rash may appear, most prominent on the extremities and usually sparing the palms and soles. Adolescents and adults may develop symmetric polyarthropathy, particularly involving small joints, while children more commonly experience knee involvement. Many patients remain asymptomatic or experience only mild viral symptoms.
History
Symptoms often begin with mild constitutional complaints such as fever, headache, nasal congestion, nausea, or sore throat. Patients are contagious only before the facial rash appears.
Physical examination
Stage one consists of coalescent, warm, erythematous, edematous facial papules with circumoral pallor. Stage two features a diffuse, maculopapular, reticular rash that may persist for weeks. Stage three is marked by fading of the rash with recurrence triggered by heat, sunlight, stress, or exercise, eventually resolving without scarring.
Essential workup
Diagnosis is clinical and based on classic presentation.
Diagnosis tests and interpretation
Laboratory testing is usually unnecessary. A CBC and reticulocyte count are indicated if aplastic crisis is suspected. In immunocompromised or pregnant patients, confirmation may be obtained with parvovirus B19 PCR or serology. IgM antibodies indicate acute infection, while IgG antibodies confirm immunity. Pregnant patients may require ultrasound monitoring for hydrops fetalis.
Differential diagnosis
Allergic reaction, drug eruption, nonspecific viral exanthem, measles, rubella, roseola, scarlet fever, erysipelas, infectious mononucleosis, collagen vascular disease, rheumatoid arthritis, sunburn, and enteroviral infections.
Treatment
The disease is typically self-limited and requires no specific therapy.
Prehospital care
Supportive care and standard ABCs for severe presentations.
Initial stabilization and therapy
Airway, breathing, and circulation management as needed. Supplemental oxygen and intravenous fluids may be required for severe dehydration. Severe anemia should be treated with packed red blood cell transfusion. Analgesia may be provided for arthropathy.
Emergency department treatment and procedures
No antiviral therapy or vaccine is available. Management is supportive, including antipyretics for fever, NSAIDs for joint pain if renal function permits, antihistamines for pruritus, and IV fluids when indicated. Immunocompromised patients with chronic infection or red cell aplasia may benefit from IVIG in consultation with infectious disease specialists. Hospitalization is indicated for aplastic crisis or severe complications.
Medication
Acetaminophen or ibuprofen for fever and pain. Diphenhydramine may be used for pruritus with caution regarding sedation. IVIG is reserved for select cases under specialist guidance.
Follow-up and disposition
Admission criteria
Aplastic crisis, severe anemia, hydrops fetalis, severe immunosuppression, toxic appearance, or debilitating arthritis.
Discharge criteria
Most patients can be safely discharged. Once the facial rash appears, patients are no longer contagious and may return to school or work if clinically stable.
Issues for referral
Hematology referral for patients with hereditary anemias or aplastic crisis. Infectious disease consultation for immunocompromised patients. Obstetric referral for pregnant patients with confirmed or suspected acute infection.
Follow-up recommendations
Pregnant patients with new infection require serial ultrasounds for 10–12 weeks. Patients at risk for aplastic crisis should have repeat CBC testing within 1–2 days.
Patient education
There is no vaccine. Hand hygiene reduces transmission. Children are usually no longer contagious by the time the rash appears, so exclusion from school is generally unnecessary.
Complications
Transient aplastic crisis in patients with underlying anemias, chronic anemia in immunocompromised individuals, arthropathy in adults, rare neurologic or cardiac involvement, and pregnancy-related complications including hydrops fetalis and fetal loss.
Clinical pearls and common missteps
Parvovirus B19 infection is usually mild and self-limited. Patients are not contagious once the rash appears. Always evaluate patients with anemia or immunosuppression for complications. Confirm infection in pregnancy and ensure appropriate fetal monitoring.
- Published on
Emergency And Acute Medicine - Erythema multiforme
Basic description
Erythema multiforme is a rash caused by a hypersensitivity reaction that may occur in response to medications, infections, or other illnesses.
Erythema multiforme minor is characterized by typical target lesions and edematous papules, usually distributed peripherally. It is a benign, self-limited condition and is generally not associated with serious acute illness.
Erythema multiforme major, also referred to as bullous erythema multiforme, presents with similar target lesions and edematous papules in a peripheral distribution but includes involvement of one or more mucous membranes with less than 10% total body surface area epidermal detachment.
It is important to differentiate erythema multiforme from Stevens–Johnson syndrome, which also involves less than 10% total body surface area epidermal detachment but typically presents with more widespread blistering over the trunk and face and prominent mucosal involvement, and from toxic epidermal necrolysis, which involves more than 30% total body surface area detachment.
Erythema multiforme is now considered a distinct entity separate from Stevens–Johnson syndrome and toxic epidermal necrolysis. It most commonly affects children and young adults, with more than half of cases occurring in patients younger than 20 years. Males are affected more often than females.
Etiology
Erythema multiforme is a hypersensitivity reaction, likely related to a transient autoimmune defect. Herpes simplex virus is the most common precipitating factor, accounting for more than 70% of cases. Other causes include idiopathic disease, medications such as penicillins, sulfa-based drugs, phenytoin, barbiturates, and NSAIDs, vaccines including diphtheria–tetanus, hepatitis B, and smallpox, as well as malignancy and infections such as HIV, cytomegalovirus, hepatitis C, and Mycoplasma infections.
Diagnosis – signs and symptoms
Patients may have a mild prodrome with low-grade fever or malaise, although systemic symptoms are infrequent. A history of antecedent herpes simplex infection within three weeks is common. The condition is usually not associated with severe systemic illness.
Physical examination
The characteristic rash consists of symmetric dull red macules and papules that evolve into round, well-demarcated target lesions with central clearing. There is no epidermal necrosis in erythema multiforme minor. The term “multiforme” reflects the presence of lesions at various stages of evolution simultaneously.
Lesions are typically distributed on the extremities, especially the dorsal hands and feet, extensor surfaces, elbows, and knees, and erythema multiforme is one of the few rashes that may involve the palms and soles. The rash often spreads from the extremities toward the trunk.
Mucosal involvement, when present, usually consists of minor blistering or erosions affecting a single mucosal surface, most commonly the lips or oral cavity. The duration of illness is usually one to four weeks, although recurrent or chronic cases may occur.
Essential workup
Evaluation consists of a complete history and physical examination, with particular attention to skin findings, recent infections, medication exposure, and genitourinary involvement.
Diagnosis tests and interpretation
No specific laboratory tests or imaging studies are required. Skin biopsy, when performed, shows a mononuclear cell infiltrate around superficial dermal blood vessels without leukocytoclastic vasculitis or epidermal keratinocyte necrosis. Biopsy is not necessary in most cases.
Differential diagnosis
Systemic lupus erythematosus, fixed drug eruption, pityriasis rosea, secondary syphilis, erythema migrans, urticaria, viral exanthem, vasculitis, Stevens–Johnson syndrome, and toxic epidermal necrolysis.
Treatment
Prehospital care
Erythema multiforme is not contagious and does not require isolation or postexposure prophylaxis.
Initial stabilization and therapy
The condition is generally benign and self-limited and does not require acute stabilization.
Emergency department treatment and procedures
Management focuses on identifying and removing the underlying cause when possible. Treatment is primarily symptomatic and includes cool compresses and antipruritic measures.
Medication
Antiviral therapy may be considered in acute herpes-associated erythema multiforme if initiated within 48 hours of onset, although it may not significantly alter the clinical course. Acyclovir may be used for prevention of recurrent disease.
Antipruritic agents such as cetirizine, diphenhydramine, or hydroxyzine can be used for symptomatic relief.
Topical corticosteroids of low to medium potency are first-line therapy for skin lesions, with low-potency agents reserved for the face or intertriginous areas.
Oral corticosteroids are reserved for severe mucosal disease. Topical anesthetic mouth rinses may be used for painful oral lesions.
Follow-up and disposition
Admission criteria
Admission is rarely required and is generally limited to patients unable to tolerate oral intake due to severe mucosal involvement or those requiring hospitalization for another concurrent condition.
Discharge criteria
Most patients can be safely discharged, as erythema multiforme is typically a benign and self-limited disorder.
Issues for referral
Referral to dermatology is recommended if the diagnosis is uncertain or if the rash is atypical or severe. Immediate ophthalmology referral is required for any ocular involvement.
Follow-up recommendations
Patients should follow up with a primary care physician within one week to assess progression or resolution of the rash and to evaluate for underlying triggers such as infection, medications, or malignancy. Dermatology follow-up within one week is appropriate if diagnostic uncertainty remains.
Clinical pearls and common pitfalls
Severe systemic illness should prompt consideration of alternative diagnoses such as Stevens–Johnson syndrome or toxic epidermal necrolysis. Most patients with erythema multiforme have an underlying herpes simplex infection. Secondary syphilis may produce similar lesions on the palms and soles. Reassurance is important, as erythema multiforme is usually benign and self-limited.
Basic description
Erythema multiforme is a rash caused by a hypersensitivity reaction that may occur in response to medications, infections, or other illnesses.
Erythema multiforme minor is characterized by typical target lesions and edematous papules, usually distributed peripherally. It is a benign, self-limited condition and is generally not associated with serious acute illness.
Erythema multiforme major, also referred to as bullous erythema multiforme, presents with similar target lesions and edematous papules in a peripheral distribution but includes involvement of one or more mucous membranes with less than 10% total body surface area epidermal detachment.
It is important to differentiate erythema multiforme from Stevens–Johnson syndrome, which also involves less than 10% total body surface area epidermal detachment but typically presents with more widespread blistering over the trunk and face and prominent mucosal involvement, and from toxic epidermal necrolysis, which involves more than 30% total body surface area detachment.
Erythema multiforme is now considered a distinct entity separate from Stevens–Johnson syndrome and toxic epidermal necrolysis. It most commonly affects children and young adults, with more than half of cases occurring in patients younger than 20 years. Males are affected more often than females.
Etiology
Erythema multiforme is a hypersensitivity reaction, likely related to a transient autoimmune defect. Herpes simplex virus is the most common precipitating factor, accounting for more than 70% of cases. Other causes include idiopathic disease, medications such as penicillins, sulfa-based drugs, phenytoin, barbiturates, and NSAIDs, vaccines including diphtheria–tetanus, hepatitis B, and smallpox, as well as malignancy and infections such as HIV, cytomegalovirus, hepatitis C, and Mycoplasma infections.
Diagnosis – signs and symptoms
Patients may have a mild prodrome with low-grade fever or malaise, although systemic symptoms are infrequent. A history of antecedent herpes simplex infection within three weeks is common. The condition is usually not associated with severe systemic illness.
Physical examination
The characteristic rash consists of symmetric dull red macules and papules that evolve into round, well-demarcated target lesions with central clearing. There is no epidermal necrosis in erythema multiforme minor. The term “multiforme” reflects the presence of lesions at various stages of evolution simultaneously.
Lesions are typically distributed on the extremities, especially the dorsal hands and feet, extensor surfaces, elbows, and knees, and erythema multiforme is one of the few rashes that may involve the palms and soles. The rash often spreads from the extremities toward the trunk.
Mucosal involvement, when present, usually consists of minor blistering or erosions affecting a single mucosal surface, most commonly the lips or oral cavity. The duration of illness is usually one to four weeks, although recurrent or chronic cases may occur.
Essential workup
Evaluation consists of a complete history and physical examination, with particular attention to skin findings, recent infections, medication exposure, and genitourinary involvement.
Diagnosis tests and interpretation
No specific laboratory tests or imaging studies are required. Skin biopsy, when performed, shows a mononuclear cell infiltrate around superficial dermal blood vessels without leukocytoclastic vasculitis or epidermal keratinocyte necrosis. Biopsy is not necessary in most cases.
Differential diagnosis
Systemic lupus erythematosus, fixed drug eruption, pityriasis rosea, secondary syphilis, erythema migrans, urticaria, viral exanthem, vasculitis, Stevens–Johnson syndrome, and toxic epidermal necrolysis.
Treatment
Prehospital care
Erythema multiforme is not contagious and does not require isolation or postexposure prophylaxis.
Initial stabilization and therapy
The condition is generally benign and self-limited and does not require acute stabilization.
Emergency department treatment and procedures
Management focuses on identifying and removing the underlying cause when possible. Treatment is primarily symptomatic and includes cool compresses and antipruritic measures.
Medication
Antiviral therapy may be considered in acute herpes-associated erythema multiforme if initiated within 48 hours of onset, although it may not significantly alter the clinical course. Acyclovir may be used for prevention of recurrent disease.
Antipruritic agents such as cetirizine, diphenhydramine, or hydroxyzine can be used for symptomatic relief.
Topical corticosteroids of low to medium potency are first-line therapy for skin lesions, with low-potency agents reserved for the face or intertriginous areas.
Oral corticosteroids are reserved for severe mucosal disease. Topical anesthetic mouth rinses may be used for painful oral lesions.
Follow-up and disposition
Admission criteria
Admission is rarely required and is generally limited to patients unable to tolerate oral intake due to severe mucosal involvement or those requiring hospitalization for another concurrent condition.
Discharge criteria
Most patients can be safely discharged, as erythema multiforme is typically a benign and self-limited disorder.
Issues for referral
Referral to dermatology is recommended if the diagnosis is uncertain or if the rash is atypical or severe. Immediate ophthalmology referral is required for any ocular involvement.
Follow-up recommendations
Patients should follow up with a primary care physician within one week to assess progression or resolution of the rash and to evaluate for underlying triggers such as infection, medications, or malignancy. Dermatology follow-up within one week is appropriate if diagnostic uncertainty remains.
Clinical pearls and common pitfalls
Severe systemic illness should prompt consideration of alternative diagnoses such as Stevens–Johnson syndrome or toxic epidermal necrolysis. Most patients with erythema multiforme have an underlying herpes simplex infection. Secondary syphilis may produce similar lesions on the palms and soles. Reassurance is important, as erythema multiforme is usually benign and self-limited.
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Emergency And Acute Medicine - Esophageal trauma
Basic description
The adult esophagus is approximately 25–30 cm in length and lies in close proximity to the mediastinum, with potential access to the pleural space. It begins at the hypopharynx posterior to the larynx at the level of the cricoid cartilage. On either side are the piriform recesses, which are common sites for foreign body lodgment.
Physiologic narrowing occurs at the cricopharyngeal muscle (upper esophageal sphincter), at the crossover of the left mainstem bronchus and aortic arch, and at the gastroesophageal junction (lower esophageal sphincter). Additional narrowing may occur in areas of disease such as malignancy, webs, or Schatzki rings.
The upper third of the esophagus consists of striated muscle and initiates swallowing. The middle third contains both striated and smooth muscle, and the distal third is composed entirely of smooth muscle. Although relatively fixed, the esophagus may be displaced by adjacent structures such as goiter, enlarged atria, or mediastinal masses.
Etiology
Esophageal trauma may result from external or internal forces.
External mechanisms include penetrating injuries such as stab or missile wounds, direct perforation from foreign bodies, pressure necrosis, chemical or radiation injury, and iatrogenic trauma from instrumentation. Blunt trauma, most commonly from motor vehicle collisions, may also cause injury.
Internal mechanisms include caustic ingestions, infections, medication-induced injury, swallowed foreign bodies, iatrogenic causes, and barotrauma.
Caustic ingestions include alkali substances, which cause liquefaction necrosis and deep tissue penetration, and acids, which cause coagulation necrosis and thermal injury. Chlorine bleach typically causes mucosal edema and superficial erythema.
Infectious causes include viral infections such as CMV, HPV, and HSV, and fungal infections in immunocompromised patients.
Medication-related injury has been reported with agents such as alendronate, doxycycline, NSAIDs, and mycophenolate mofetil.
Swallowed foreign bodies include food bolus impaction, coins, bones, pins, and button batteries. Meat impaction is the most common type in adults, particularly among prisoners, psychiatric patients, intoxicated individuals, and edentulous patients.
Iatrogenic injury accounts for more than half of cases, most commonly due to endoscopy, nasogastric tube placement, or nasotracheal intubation.
Increased intraluminal pressure from vomiting or retching may result in Mallory–Weiss tears, which are mucosal lacerations with bleeding, or Boerhaave syndrome, which is a spontaneous full-thickness rupture of the distal esophagus.
Pediatric considerations
Foreign body ingestion accounts for most cases of esophageal trauma in children, particularly in those aged 18–48 months. Perforations are most often iatrogenic. Caustic ingestions are more common in children younger than five years. Button batteries lodged in the esophagus require urgent removal due to their highly alkaline nature. Single-use laundry detergent packets are an increasingly common hazard.
Diagnosis – signs and symptoms
Common symptoms include dysphagia, odynophagia, chest pain that may be pleuritic and severe, hoarseness, and dyspnea.
Tears or perforations may present with bleeding or hematemesis.
Foreign body ingestion may cause drooling, choking, gagging, vomiting, stridor, wheezing, or inability to tolerate oral intake.
Caustic ingestion may produce oral pain, abdominal pain, vomiting, and drooling.
History
Key historical elements include the type, amount, and timing of ingestions; history of prolonged vomiting; sudden inability to swallow after eating; foreign body sensation; penetrating trauma; or prior cancer therapy.
Physical examination
Findings suggestive of perforation include subcutaneous emphysema at the base of the neck, a Hamman crunch due to mediastinal air, signs of shock, septicemia, or peritonitis.
Penetrating trauma may be associated with injuries to the trachea, neck, chest, or abdomen.
Caustic ingestions may cause airway edema with stridor and visible oral burns.
Essential workup
A high index of suspicion and early diagnosis are critical. Mortality for esophageal perforation is less than 5% if repaired within 24 hours but increases dramatically with delayed diagnosis. Early endoscopy is indicated for caustic ingestions. Chest and lateral neck radiographs are part of the initial evaluation.
Diagnosis tests and interpretation
Laboratory studies may include complete blood count, type and crossmatch for significant bleeding, coagulation studies, electrolytes for prolonged vomiting or retained foreign body, and arterial blood gas analysis in acid ingestions.
Imaging includes chest radiography to assess for pneumomediastinum, pneumothorax, widened mediastinum, or pleural effusion. Lateral cervical spine radiographs may reveal retropharyngeal air or fluid.
Esophagram is useful for suspected perforation, with water-soluble contrast preferred initially. Endoscopy is indicated for suspected perforation, caustic injury, or foreign body removal. CT with dilute oral contrast may aid in identifying perforation and associated complications.
Differential diagnosis
Pulmonary causes include tracheal injury and pneumothorax. Cardiovascular causes include myocardial infarction and aortic dissection. Other esophageal conditions include strictures, neoplasm, Schatzki ring, diverticula, achalasia, esophageal spasm, gastroesophageal reflux, and medication-induced esophagitis.
Treatment
Prehospital care
Chest pain should be presumed cardiac until proven otherwise. Airway protection, suctioning of secretions, intravenous fluids for hypotension or bleeding, and analgesia are indicated. Neutralizing agents and large volumes of oral fluids should be avoided in caustic ingestions.
Initial stabilization and therapy
Airway management and resuscitation are priorities. Establish intravenous access, initiate monitoring, and consider early intubation for penetrating neck or chest injuries.
Emergency department treatment and procedures
Most foreign bodies pass spontaneously, but endoscopic removal is required in a significant minority. Pharmacologic measures such as glucagon, nitroglycerin, or benzodiazepines may be attempted for food impaction. Gastroenterology consultation is indicated if these measures fail.
Caustic ingestions require avoidance of emesis and lavage, cautious dilution with milk, and early endoscopy for prognostication. Corticosteroids are not recommended.
Partial-thickness tears generally heal spontaneously. Full-thickness perforations require surgical consultation, broad-spectrum intravenous antibiotics, and possible operative repair.
Medication
For food impaction, glucagon, nitroglycerin, or diazepam may be used selectively.
For perforation, broad-spectrum intravenous antibiotics such as cefoxitin with gentamicin are indicated. Steroids are not indicated in caustic injury.
Follow-up and disposition
Admission criteria
Indications for admission include caustic ingestion, sharp foreign bodies, airway compromise, penetrating neck or chest trauma, evidence of sepsis or mediastinitis, esophageal perforation, significant bleeding, and inability to tolerate oral intake.
Discharge criteria
Patients may be discharged if bleeding from a partial-thickness tear is self-limited or if a foreign body or food bolus has passed beyond the lower esophageal sphincter without complications.
Clinical pearls and common pitfalls
Time to diagnosis and definitive therapy is the most important predictor of outcome, with intervention within 24 hours significantly reducing mortality. Cervical injuries have better outcomes than thoracic or abdominal injuries. Spontaneous perforation carries the highest mortality, followed by iatrogenic and then traumatic causes.
Basic description
The adult esophagus is approximately 25–30 cm in length and lies in close proximity to the mediastinum, with potential access to the pleural space. It begins at the hypopharynx posterior to the larynx at the level of the cricoid cartilage. On either side are the piriform recesses, which are common sites for foreign body lodgment.
Physiologic narrowing occurs at the cricopharyngeal muscle (upper esophageal sphincter), at the crossover of the left mainstem bronchus and aortic arch, and at the gastroesophageal junction (lower esophageal sphincter). Additional narrowing may occur in areas of disease such as malignancy, webs, or Schatzki rings.
The upper third of the esophagus consists of striated muscle and initiates swallowing. The middle third contains both striated and smooth muscle, and the distal third is composed entirely of smooth muscle. Although relatively fixed, the esophagus may be displaced by adjacent structures such as goiter, enlarged atria, or mediastinal masses.
Etiology
Esophageal trauma may result from external or internal forces.
External mechanisms include penetrating injuries such as stab or missile wounds, direct perforation from foreign bodies, pressure necrosis, chemical or radiation injury, and iatrogenic trauma from instrumentation. Blunt trauma, most commonly from motor vehicle collisions, may also cause injury.
Internal mechanisms include caustic ingestions, infections, medication-induced injury, swallowed foreign bodies, iatrogenic causes, and barotrauma.
Caustic ingestions include alkali substances, which cause liquefaction necrosis and deep tissue penetration, and acids, which cause coagulation necrosis and thermal injury. Chlorine bleach typically causes mucosal edema and superficial erythema.
Infectious causes include viral infections such as CMV, HPV, and HSV, and fungal infections in immunocompromised patients.
Medication-related injury has been reported with agents such as alendronate, doxycycline, NSAIDs, and mycophenolate mofetil.
Swallowed foreign bodies include food bolus impaction, coins, bones, pins, and button batteries. Meat impaction is the most common type in adults, particularly among prisoners, psychiatric patients, intoxicated individuals, and edentulous patients.
Iatrogenic injury accounts for more than half of cases, most commonly due to endoscopy, nasogastric tube placement, or nasotracheal intubation.
Increased intraluminal pressure from vomiting or retching may result in Mallory–Weiss tears, which are mucosal lacerations with bleeding, or Boerhaave syndrome, which is a spontaneous full-thickness rupture of the distal esophagus.
Pediatric considerations
Foreign body ingestion accounts for most cases of esophageal trauma in children, particularly in those aged 18–48 months. Perforations are most often iatrogenic. Caustic ingestions are more common in children younger than five years. Button batteries lodged in the esophagus require urgent removal due to their highly alkaline nature. Single-use laundry detergent packets are an increasingly common hazard.
Diagnosis – signs and symptoms
Common symptoms include dysphagia, odynophagia, chest pain that may be pleuritic and severe, hoarseness, and dyspnea.
Tears or perforations may present with bleeding or hematemesis.
Foreign body ingestion may cause drooling, choking, gagging, vomiting, stridor, wheezing, or inability to tolerate oral intake.
Caustic ingestion may produce oral pain, abdominal pain, vomiting, and drooling.
History
Key historical elements include the type, amount, and timing of ingestions; history of prolonged vomiting; sudden inability to swallow after eating; foreign body sensation; penetrating trauma; or prior cancer therapy.
Physical examination
Findings suggestive of perforation include subcutaneous emphysema at the base of the neck, a Hamman crunch due to mediastinal air, signs of shock, septicemia, or peritonitis.
Penetrating trauma may be associated with injuries to the trachea, neck, chest, or abdomen.
Caustic ingestions may cause airway edema with stridor and visible oral burns.
Essential workup
A high index of suspicion and early diagnosis are critical. Mortality for esophageal perforation is less than 5% if repaired within 24 hours but increases dramatically with delayed diagnosis. Early endoscopy is indicated for caustic ingestions. Chest and lateral neck radiographs are part of the initial evaluation.
Diagnosis tests and interpretation
Laboratory studies may include complete blood count, type and crossmatch for significant bleeding, coagulation studies, electrolytes for prolonged vomiting or retained foreign body, and arterial blood gas analysis in acid ingestions.
Imaging includes chest radiography to assess for pneumomediastinum, pneumothorax, widened mediastinum, or pleural effusion. Lateral cervical spine radiographs may reveal retropharyngeal air or fluid.
Esophagram is useful for suspected perforation, with water-soluble contrast preferred initially. Endoscopy is indicated for suspected perforation, caustic injury, or foreign body removal. CT with dilute oral contrast may aid in identifying perforation and associated complications.
Differential diagnosis
Pulmonary causes include tracheal injury and pneumothorax. Cardiovascular causes include myocardial infarction and aortic dissection. Other esophageal conditions include strictures, neoplasm, Schatzki ring, diverticula, achalasia, esophageal spasm, gastroesophageal reflux, and medication-induced esophagitis.
Treatment
Prehospital care
Chest pain should be presumed cardiac until proven otherwise. Airway protection, suctioning of secretions, intravenous fluids for hypotension or bleeding, and analgesia are indicated. Neutralizing agents and large volumes of oral fluids should be avoided in caustic ingestions.
Initial stabilization and therapy
Airway management and resuscitation are priorities. Establish intravenous access, initiate monitoring, and consider early intubation for penetrating neck or chest injuries.
Emergency department treatment and procedures
Most foreign bodies pass spontaneously, but endoscopic removal is required in a significant minority. Pharmacologic measures such as glucagon, nitroglycerin, or benzodiazepines may be attempted for food impaction. Gastroenterology consultation is indicated if these measures fail.
Caustic ingestions require avoidance of emesis and lavage, cautious dilution with milk, and early endoscopy for prognostication. Corticosteroids are not recommended.
Partial-thickness tears generally heal spontaneously. Full-thickness perforations require surgical consultation, broad-spectrum intravenous antibiotics, and possible operative repair.
Medication
For food impaction, glucagon, nitroglycerin, or diazepam may be used selectively.
For perforation, broad-spectrum intravenous antibiotics such as cefoxitin with gentamicin are indicated. Steroids are not indicated in caustic injury.
Follow-up and disposition
Admission criteria
Indications for admission include caustic ingestion, sharp foreign bodies, airway compromise, penetrating neck or chest trauma, evidence of sepsis or mediastinitis, esophageal perforation, significant bleeding, and inability to tolerate oral intake.
Discharge criteria
Patients may be discharged if bleeding from a partial-thickness tear is self-limited or if a foreign body or food bolus has passed beyond the lower esophageal sphincter without complications.
Clinical pearls and common pitfalls
Time to diagnosis and definitive therapy is the most important predictor of outcome, with intervention within 24 hours significantly reducing mortality. Cervical injuries have better outcomes than thoracic or abdominal injuries. Spontaneous perforation carries the highest mortality, followed by iatrogenic and then traumatic causes.
- Published on
Emergency And Acute Medicine - Esophageal trauma
Basic description
The adult esophagus is approximately 25–30 cm in length and lies in close proximity to the mediastinum, with potential access to the pleural space. It begins at the hypopharynx posterior to the larynx at the level of the cricoid cartilage. On either side are the piriform recesses, which are common sites for foreign body lodgment.
Physiologic narrowing occurs at the cricopharyngeal muscle (upper esophageal sphincter), at the crossover of the left mainstem bronchus and aortic arch, and at the gastroesophageal junction (lower esophageal sphincter). Additional narrowing may occur in areas of disease such as malignancy, webs, or Schatzki rings.
The upper third of the esophagus consists of striated muscle and initiates swallowing. The middle third contains both striated and smooth muscle, and the distal third is composed entirely of smooth muscle. Although relatively fixed, the esophagus may be displaced by adjacent structures such as goiter, enlarged atria, or mediastinal masses.
Etiology
Esophageal trauma may result from external or internal forces.
External mechanisms include penetrating injuries such as stab or missile wounds, direct perforation from foreign bodies, pressure necrosis, chemical or radiation injury, and iatrogenic trauma from instrumentation. Blunt trauma, most commonly from motor vehicle collisions, may also cause injury.
Internal mechanisms include caustic ingestions, infections, medication-induced injury, swallowed foreign bodies, iatrogenic causes, and barotrauma.
Caustic ingestions include alkali substances, which cause liquefaction necrosis and deep tissue penetration, and acids, which cause coagulation necrosis and thermal injury. Chlorine bleach typically causes mucosal edema and superficial erythema.
Infectious causes include viral infections such as CMV, HPV, and HSV, and fungal infections in immunocompromised patients.
Medication-related injury has been reported with agents such as alendronate, doxycycline, NSAIDs, and mycophenolate mofetil.
Swallowed foreign bodies include food bolus impaction, coins, bones, pins, and button batteries. Meat impaction is the most common type in adults, particularly among prisoners, psychiatric patients, intoxicated individuals, and edentulous patients.
Iatrogenic injury accounts for more than half of cases, most commonly due to endoscopy, nasogastric tube placement, or nasotracheal intubation.
Increased intraluminal pressure from vomiting or retching may result in Mallory–Weiss tears, which are mucosal lacerations with bleeding, or Boerhaave syndrome, which is a spontaneous full-thickness rupture of the distal esophagus.
Pediatric considerations
Foreign body ingestion accounts for most cases of esophageal trauma in children, particularly in those aged 18–48 months. Perforations are most often iatrogenic. Caustic ingestions are more common in children younger than five years. Button batteries lodged in the esophagus require urgent removal due to their highly alkaline nature. Single-use laundry detergent packets are an increasingly common hazard.
Diagnosis – signs and symptoms
Common symptoms include dysphagia, odynophagia, chest pain that may be pleuritic and severe, hoarseness, and dyspnea.
Tears or perforations may present with bleeding or hematemesis.
Foreign body ingestion may cause drooling, choking, gagging, vomiting, stridor, wheezing, or inability to tolerate oral intake.
Caustic ingestion may produce oral pain, abdominal pain, vomiting, and drooling.
History
Key historical elements include the type, amount, and timing of ingestions; history of prolonged vomiting; sudden inability to swallow after eating; foreign body sensation; penetrating trauma; or prior cancer therapy.
Physical examination
Findings suggestive of perforation include subcutaneous emphysema at the base of the neck, a Hamman crunch due to mediastinal air, signs of shock, septicemia, or peritonitis.
Penetrating trauma may be associated with injuries to the trachea, neck, chest, or abdomen.
Caustic ingestions may cause airway edema with stridor and visible oral burns.
Essential workup
A high index of suspicion and early diagnosis are critical. Mortality for esophageal perforation is less than 5% if repaired within 24 hours but increases dramatically with delayed diagnosis. Early endoscopy is indicated for caustic ingestions. Chest and lateral neck radiographs are part of the initial evaluation.
Diagnosis tests and interpretation
Laboratory studies may include complete blood count, type and crossmatch for significant bleeding, coagulation studies, electrolytes for prolonged vomiting or retained foreign body, and arterial blood gas analysis in acid ingestions.
Imaging includes chest radiography to assess for pneumomediastinum, pneumothorax, widened mediastinum, or pleural effusion. Lateral cervical spine radiographs may reveal retropharyngeal air or fluid.
Esophagram is useful for suspected perforation, with water-soluble contrast preferred initially. Endoscopy is indicated for suspected perforation, caustic injury, or foreign body removal. CT with dilute oral contrast may aid in identifying perforation and associated complications.
Differential diagnosis
Pulmonary causes include tracheal injury and pneumothorax. Cardiovascular causes include myocardial infarction and aortic dissection. Other esophageal conditions include strictures, neoplasm, Schatzki ring, diverticula, achalasia, esophageal spasm, gastroesophageal reflux, and medication-induced esophagitis.
Treatment
Prehospital care
Chest pain should be presumed cardiac until proven otherwise. Airway protection, suctioning of secretions, intravenous fluids for hypotension or bleeding, and analgesia are indicated. Neutralizing agents and large volumes of oral fluids should be avoided in caustic ingestions.
Initial stabilization and therapy
Airway management and resuscitation are priorities. Establish intravenous access, initiate monitoring, and consider early intubation for penetrating neck or chest injuries.
Emergency department treatment and procedures
Most foreign bodies pass spontaneously, but endoscopic removal is required in a significant minority. Pharmacologic measures such as glucagon, nitroglycerin, or benzodiazepines may be attempted for food impaction. Gastroenterology consultation is indicated if these measures fail.
Caustic ingestions require avoidance of emesis and lavage, cautious dilution with milk, and early endoscopy for prognostication. Corticosteroids are not recommended.
Partial-thickness tears generally heal spontaneously. Full-thickness perforations require surgical consultation, broad-spectrum intravenous antibiotics, and possible operative repair.
Medication
For food impaction, glucagon, nitroglycerin, or diazepam may be used selectively.
For perforation, broad-spectrum intravenous antibiotics such as cefoxitin with gentamicin are indicated. Steroids are not indicated in caustic injury.
Follow-up and disposition
Admission criteria
Indications for admission include caustic ingestion, sharp foreign bodies, airway compromise, penetrating neck or chest trauma, evidence of sepsis or mediastinitis, esophageal perforation, significant bleeding, and inability to tolerate oral intake.
Discharge criteria
Patients may be discharged if bleeding from a partial-thickness tear is self-limited or if a foreign body or food bolus has passed beyond the lower esophageal sphincter without complications.
Clinical pearls and common pitfalls
Time to diagnosis and definitive therapy is the most important predictor of outcome, with intervention within 24 hours significantly reducing mortality. Cervical injuries have better outcomes than thoracic or abdominal injuries. Spontaneous perforation carries the highest mortality, followed by iatrogenic and then traumatic causes.
Basic description
The adult esophagus is approximately 25–30 cm in length and lies in close proximity to the mediastinum, with potential access to the pleural space. It begins at the hypopharynx posterior to the larynx at the level of the cricoid cartilage. On either side are the piriform recesses, which are common sites for foreign body lodgment.
Physiologic narrowing occurs at the cricopharyngeal muscle (upper esophageal sphincter), at the crossover of the left mainstem bronchus and aortic arch, and at the gastroesophageal junction (lower esophageal sphincter). Additional narrowing may occur in areas of disease such as malignancy, webs, or Schatzki rings.
The upper third of the esophagus consists of striated muscle and initiates swallowing. The middle third contains both striated and smooth muscle, and the distal third is composed entirely of smooth muscle. Although relatively fixed, the esophagus may be displaced by adjacent structures such as goiter, enlarged atria, or mediastinal masses.
Etiology
Esophageal trauma may result from external or internal forces.
External mechanisms include penetrating injuries such as stab or missile wounds, direct perforation from foreign bodies, pressure necrosis, chemical or radiation injury, and iatrogenic trauma from instrumentation. Blunt trauma, most commonly from motor vehicle collisions, may also cause injury.
Internal mechanisms include caustic ingestions, infections, medication-induced injury, swallowed foreign bodies, iatrogenic causes, and barotrauma.
Caustic ingestions include alkali substances, which cause liquefaction necrosis and deep tissue penetration, and acids, which cause coagulation necrosis and thermal injury. Chlorine bleach typically causes mucosal edema and superficial erythema.
Infectious causes include viral infections such as CMV, HPV, and HSV, and fungal infections in immunocompromised patients.
Medication-related injury has been reported with agents such as alendronate, doxycycline, NSAIDs, and mycophenolate mofetil.
Swallowed foreign bodies include food bolus impaction, coins, bones, pins, and button batteries. Meat impaction is the most common type in adults, particularly among prisoners, psychiatric patients, intoxicated individuals, and edentulous patients.
Iatrogenic injury accounts for more than half of cases, most commonly due to endoscopy, nasogastric tube placement, or nasotracheal intubation.
Increased intraluminal pressure from vomiting or retching may result in Mallory–Weiss tears, which are mucosal lacerations with bleeding, or Boerhaave syndrome, which is a spontaneous full-thickness rupture of the distal esophagus.
Pediatric considerations
Foreign body ingestion accounts for most cases of esophageal trauma in children, particularly in those aged 18–48 months. Perforations are most often iatrogenic. Caustic ingestions are more common in children younger than five years. Button batteries lodged in the esophagus require urgent removal due to their highly alkaline nature. Single-use laundry detergent packets are an increasingly common hazard.
Diagnosis – signs and symptoms
Common symptoms include dysphagia, odynophagia, chest pain that may be pleuritic and severe, hoarseness, and dyspnea.
Tears or perforations may present with bleeding or hematemesis.
Foreign body ingestion may cause drooling, choking, gagging, vomiting, stridor, wheezing, or inability to tolerate oral intake.
Caustic ingestion may produce oral pain, abdominal pain, vomiting, and drooling.
History
Key historical elements include the type, amount, and timing of ingestions; history of prolonged vomiting; sudden inability to swallow after eating; foreign body sensation; penetrating trauma; or prior cancer therapy.
Physical examination
Findings suggestive of perforation include subcutaneous emphysema at the base of the neck, a Hamman crunch due to mediastinal air, signs of shock, septicemia, or peritonitis.
Penetrating trauma may be associated with injuries to the trachea, neck, chest, or abdomen.
Caustic ingestions may cause airway edema with stridor and visible oral burns.
Essential workup
A high index of suspicion and early diagnosis are critical. Mortality for esophageal perforation is less than 5% if repaired within 24 hours but increases dramatically with delayed diagnosis. Early endoscopy is indicated for caustic ingestions. Chest and lateral neck radiographs are part of the initial evaluation.
Diagnosis tests and interpretation
Laboratory studies may include complete blood count, type and crossmatch for significant bleeding, coagulation studies, electrolytes for prolonged vomiting or retained foreign body, and arterial blood gas analysis in acid ingestions.
Imaging includes chest radiography to assess for pneumomediastinum, pneumothorax, widened mediastinum, or pleural effusion. Lateral cervical spine radiographs may reveal retropharyngeal air or fluid.
Esophagram is useful for suspected perforation, with water-soluble contrast preferred initially. Endoscopy is indicated for suspected perforation, caustic injury, or foreign body removal. CT with dilute oral contrast may aid in identifying perforation and associated complications.
Differential diagnosis
Pulmonary causes include tracheal injury and pneumothorax. Cardiovascular causes include myocardial infarction and aortic dissection. Other esophageal conditions include strictures, neoplasm, Schatzki ring, diverticula, achalasia, esophageal spasm, gastroesophageal reflux, and medication-induced esophagitis.
Treatment
Prehospital care
Chest pain should be presumed cardiac until proven otherwise. Airway protection, suctioning of secretions, intravenous fluids for hypotension or bleeding, and analgesia are indicated. Neutralizing agents and large volumes of oral fluids should be avoided in caustic ingestions.
Initial stabilization and therapy
Airway management and resuscitation are priorities. Establish intravenous access, initiate monitoring, and consider early intubation for penetrating neck or chest injuries.
Emergency department treatment and procedures
Most foreign bodies pass spontaneously, but endoscopic removal is required in a significant minority. Pharmacologic measures such as glucagon, nitroglycerin, or benzodiazepines may be attempted for food impaction. Gastroenterology consultation is indicated if these measures fail.
Caustic ingestions require avoidance of emesis and lavage, cautious dilution with milk, and early endoscopy for prognostication. Corticosteroids are not recommended.
Partial-thickness tears generally heal spontaneously. Full-thickness perforations require surgical consultation, broad-spectrum intravenous antibiotics, and possible operative repair.
Medication
For food impaction, glucagon, nitroglycerin, or diazepam may be used selectively.
For perforation, broad-spectrum intravenous antibiotics such as cefoxitin with gentamicin are indicated. Steroids are not indicated in caustic injury.
Follow-up and disposition
Admission criteria
Indications for admission include caustic ingestion, sharp foreign bodies, airway compromise, penetrating neck or chest trauma, evidence of sepsis or mediastinitis, esophageal perforation, significant bleeding, and inability to tolerate oral intake.
Discharge criteria
Patients may be discharged if bleeding from a partial-thickness tear is self-limited or if a foreign body or food bolus has passed beyond the lower esophageal sphincter without complications.
Clinical pearls and common pitfalls
Time to diagnosis and definitive therapy is the most important predictor of outcome, with intervention within 24 hours significantly reducing mortality. Cervical injuries have better outcomes than thoracic or abdominal injuries. Spontaneous perforation carries the highest mortality, followed by iatrogenic and then traumatic causes.
- Published on
Emergency And Acute Medicine - Ethylene glycol poisoning
Basic description
Peak serum concentration occurs in 1–4 hr. The half-life is 2.5–4.5 hr, and less than 20% is excreted unchanged by the kidneys.
Ethylene glycol is metabolized by hepatic alcohol dehydrogenase and aldehyde dehydrogenase to acidic metabolites that ultimately form oxalic acid. Aldehyde and acid metabolites are directly toxic to the CNS, heart, and kidneys.
Etiology
Exposure is typically from ethylene-glycol–containing products such as antifreeze and certain solvents. The minimum reported lethal dose is approximately 30 mL of 100% ethylene glycol.
Diagnosis – signs and symptoms
Cardiovascular: tachycardia, bradycardia, dysrhythmias, hypertension, hypotension.
Cns: inebriation, irritability, ataxia, obtundation, coma, cerebral edema, seizures; may also have peripheral nervous system findings including cranial nerve abnormalities.
Gi: nausea, vomiting, abdominal pain.
Pulmonary: tachypnea, hyperventilation, Kussmaul respirations, pulmonary edema.
Renal: crystalluria and acute renal failure.
Three overlapping stages may be seen:
History
Intentional or unintentional ingestion may be reported. Consider this diagnosis even without a clear history when there is an unexplained high anion gap metabolic acidosis and/or an elevated, unexplained osmol gap.
Physical examination
Tachypnea and altered mental status are common.
Essential workup
Obtain a complete ingestion history. Draw the following simultaneously:
Diagnosis tests and interpretation
Calculate the anion gap: (Na⁺) − (Cl⁻ + HCO₃⁻); normal is approximately 8–12.
Calculate the osmol gap: measured osmolality − calculated osmolarity; an increased gap is generally >10.
Calculated osmolarity: 2(Na⁺) + glucose/18 + BUN/2.8 + ethanol (mg/dL)/4.6.
The osmol gap is most useful early after ingestion (and may be larger with concurrent ethanol ingestion, with less severe acidosis). A normal osmol gap does not exclude ethylene glycol poisoning, especially with late presentation when metabolites drive an anion gap acidosis.
Urinalysis may show envelope-shaped calcium oxalate crystals (specific but insensitive). Absence of crystals does not rule out exposure.
Wood lamp inspection of urine or gastric contents may show fluorescein from antifreeze, but this is insensitive and nonspecific.
Differential diagnosis
Elevated osmol gap: methanol, ethanol, isopropyl alcohol, mannitol/glycerin/propylene glycol/sorbitol, acetone/ammonia, propylene glycol.
Elevated anion gap metabolic acidosis: alcoholic ketoacidosis, toxic asphyxiants (e.g., cyanide/CO/H₂S), acetaminophen-related causes, antiretrovirals (NRTIs), toluene, metformin, uremia, DKA, iron/INH, lactic acidosis, salicylates, starvation ketosis, methanol, ethylene glycol.
Treatment
Prehospital care
Bring containers of suspected substances. Monitor airway and mental status. For dermal exposure, remove contaminated clothing/jewelry and irrigate with soap and water.
Initial stabilization and therapy
ABCs. Provide supplemental oxygen, cardiac monitoring, and IV access with 0.9% saline. For altered mental status, check glucose and consider dextrose, naloxone, and thiamine as appropriate.
Emergency department treatment and procedures
Pregnancy considerations
Fomepizole is class C in pregnancy. Ethanol is not recommended.
Pediatric considerations
Ethanol can cause significant CNS depression and hypoglycemia in children.
Medication
Activated charcoal: 1 g/kg PO.
Dextrose: D50W 25 g IV (peds: D25W 2–4 mL/kg).
Ethanol: oral (via NG) or IV 10% ethanol in D5W per dosing protocols; adjust during hemodialysis.
Fomepizole: 15 mg/kg IV load over 30 min, then 10 mg/kg q12h ×4 doses, then 15 mg/kg q12h until level <25 mg />L; dose adjustments required during hemodialysis.
Magnesium: 25–50 mg/kg IV once (max 2 g).
Naloxone: 2 mg IV/IM (peds: 0.1 mg/kg).
Pyridoxine: 100 mg daily for 2 days.
Sodium bicarbonate: 1–2 mEq/kg IV in D5W.
Thiamine: 100 mg daily for 2 days (peds: 50 mg).
Follow-up and disposition
Admission criteria
Admit all patients with significant suspected or confirmed ethylene glycol ingestion, even if initially asymptomatic. ICU admission is indicated for serious illness, metabolic acidosis, or renal failure. Transfer if fomepizole or hemodialysis is indicated but not available.
Discharge criteria
An asymptomatic patient with isolated exposure may be discharged only if ethylene glycol concentration is undetectable and there is no metabolic acidosis.
Follow-up recommendations
Psychiatric evaluation is indicated after intentional ingestion.
Clinical pearls and common pitfalls
An osmol gap <10 does not exclude ethylene glycol poisoning. treat early with fomepizole when the diagnosis is on table and confirm serum levels available. presentations may show only an osmol gap, while late anion gap. do use absence of urinary crystals or lack fluorescence under a wood lamp to rule out exposure. if confirmation, antidote availability, 24 /> hemodialysis capability is uncertain, transfer to a facility that has all of these resources.
Basic description
Peak serum concentration occurs in 1–4 hr. The half-life is 2.5–4.5 hr, and less than 20% is excreted unchanged by the kidneys.
Ethylene glycol is metabolized by hepatic alcohol dehydrogenase and aldehyde dehydrogenase to acidic metabolites that ultimately form oxalic acid. Aldehyde and acid metabolites are directly toxic to the CNS, heart, and kidneys.
Etiology
Exposure is typically from ethylene-glycol–containing products such as antifreeze and certain solvents. The minimum reported lethal dose is approximately 30 mL of 100% ethylene glycol.
Diagnosis – signs and symptoms
Cardiovascular: tachycardia, bradycardia, dysrhythmias, hypertension, hypotension.
Cns: inebriation, irritability, ataxia, obtundation, coma, cerebral edema, seizures; may also have peripheral nervous system findings including cranial nerve abnormalities.
Gi: nausea, vomiting, abdominal pain.
Pulmonary: tachypnea, hyperventilation, Kussmaul respirations, pulmonary edema.
Renal: crystalluria and acute renal failure.
Three overlapping stages may be seen:
- First stage (1–12 hr): CNS depression, GI symptoms, worsening acidosis, coma, seizures, cerebral edema, tetany or myoclonus from hypocalcemia.
- Second stage (12–36 hr): cardiopulmonary manifestations; many deaths occur in this period.
- Third stage (36–72 hr): oliguria, flank pain, acute renal failure.
History
Intentional or unintentional ingestion may be reported. Consider this diagnosis even without a clear history when there is an unexplained high anion gap metabolic acidosis and/or an elevated, unexplained osmol gap.
Physical examination
Tachypnea and altered mental status are common.
Essential workup
Obtain a complete ingestion history. Draw the following simultaneously:
- Arterial blood gas
- Serum ethylene glycol, methanol, isopropyl alcohol, and ethanol concentrations
- Electrolytes, BUN/creatinine, glucose
- Measured serum osmolality (freezing point depression)
- Serum calcium, phosphorus, magnesium
Diagnosis tests and interpretation
Calculate the anion gap: (Na⁺) − (Cl⁻ + HCO₃⁻); normal is approximately 8–12.
Calculate the osmol gap: measured osmolality − calculated osmolarity; an increased gap is generally >10.
Calculated osmolarity: 2(Na⁺) + glucose/18 + BUN/2.8 + ethanol (mg/dL)/4.6.
The osmol gap is most useful early after ingestion (and may be larger with concurrent ethanol ingestion, with less severe acidosis). A normal osmol gap does not exclude ethylene glycol poisoning, especially with late presentation when metabolites drive an anion gap acidosis.
Urinalysis may show envelope-shaped calcium oxalate crystals (specific but insensitive). Absence of crystals does not rule out exposure.
Wood lamp inspection of urine or gastric contents may show fluorescein from antifreeze, but this is insensitive and nonspecific.
Differential diagnosis
Elevated osmol gap: methanol, ethanol, isopropyl alcohol, mannitol/glycerin/propylene glycol/sorbitol, acetone/ammonia, propylene glycol.
Elevated anion gap metabolic acidosis: alcoholic ketoacidosis, toxic asphyxiants (e.g., cyanide/CO/H₂S), acetaminophen-related causes, antiretrovirals (NRTIs), toluene, metformin, uremia, DKA, iron/INH, lactic acidosis, salicylates, starvation ketosis, methanol, ethylene glycol.
Treatment
Prehospital care
Bring containers of suspected substances. Monitor airway and mental status. For dermal exposure, remove contaminated clothing/jewelry and irrigate with soap and water.
Initial stabilization and therapy
ABCs. Provide supplemental oxygen, cardiac monitoring, and IV access with 0.9% saline. For altered mental status, check glucose and consider dextrose, naloxone, and thiamine as appropriate.
Emergency department treatment and procedures
- Limit absorption: gastric lavage may be considered only in select cases (<1 hr since ingestion, coma, or reported large ingestion). activated charcoal may be given for coingestants but adsorbs ethylene glycol poorly.< />pan>
- Block toxic metabolism: initiate fomepizole promptly when a potentially toxic ingestion is suspected (intentional ingestion, more than a “sip,” or unexplained osmol gap and/or anion gap acidosis with concerning presentation). Do not wait for confirmatory levels if suspicion is high.
- Alternative antidote: ethanol is second-line if fomepizole is unavailable, targeting a serum ethanol level of 100–150 mg/dL, and continuing until ethylene glycol level is ~25 mg/dL.
- Adjunct cofactors: thiamine, pyridoxine, and magnesium may be given to support metabolism toward less toxic pathways (human outcome data are limited).
- Hemodialysis: use to accelerate clearance of ethylene glycol and metabolites. Consider for severe acidosis, persistent metabolic derangements, renal insufficiency, pulmonary edema, cerebral edema, or ethylene glycol concentration >25 mg/dL; continue until level approaches 25 mg/dL and acidosis resolves.
- Correct complications: ensure urine output with IV fluids. Use sodium bicarbonate for severe acidemia (commonly when pH <7.1) to maintain ph in the normal range. monitor and replace calcium as needed because oxalate formation can lower serum calcium.< />pan>
Pregnancy considerations
Fomepizole is class C in pregnancy. Ethanol is not recommended.
Pediatric considerations
Ethanol can cause significant CNS depression and hypoglycemia in children.
Medication
Activated charcoal: 1 g/kg PO.
Dextrose: D50W 25 g IV (peds: D25W 2–4 mL/kg).
Ethanol: oral (via NG) or IV 10% ethanol in D5W per dosing protocols; adjust during hemodialysis.
Fomepizole: 15 mg/kg IV load over 30 min, then 10 mg/kg q12h ×4 doses, then 15 mg/kg q12h until level <25 mg />L; dose adjustments required during hemodialysis.
Magnesium: 25–50 mg/kg IV once (max 2 g).
Naloxone: 2 mg IV/IM (peds: 0.1 mg/kg).
Pyridoxine: 100 mg daily for 2 days.
Sodium bicarbonate: 1–2 mEq/kg IV in D5W.
Thiamine: 100 mg daily for 2 days (peds: 50 mg).
Follow-up and disposition
Admission criteria
Admit all patients with significant suspected or confirmed ethylene glycol ingestion, even if initially asymptomatic. ICU admission is indicated for serious illness, metabolic acidosis, or renal failure. Transfer if fomepizole or hemodialysis is indicated but not available.
Discharge criteria
An asymptomatic patient with isolated exposure may be discharged only if ethylene glycol concentration is undetectable and there is no metabolic acidosis.
Follow-up recommendations
Psychiatric evaluation is indicated after intentional ingestion.
Clinical pearls and common pitfalls
An osmol gap <10 does not exclude ethylene glycol poisoning. treat early with fomepizole when the diagnosis is on table and confirm serum levels available. presentations may show only an osmol gap, while late anion gap. do use absence of urinary crystals or lack fluorescence under a wood lamp to rule out exposure. if confirmation, antidote availability, 24 /> hemodialysis capability is uncertain, transfer to a facility that has all of these resources.
- Published on
Emergency And Acute Medicine - External Ear Chondritis And Abscess
Condition overview
This condition involves inflammation and/or infection of the auricular cartilage of the pinna. Because the cartilage of the external ear has minimal subcutaneous tissue, limited blood supply, and is exposed, it is particularly vulnerable to injury and infection. Chondritis often develops as a delayed complication after trauma or burns, sometimes appearing after the ear seems to have healed. Inadequate or delayed treatment can lead to cartilage avascular necrosis and permanent deformity of the pinna, ranging from a cauliflower-like ear to near-total loss of the external ear with possible narrowing of the auditory canal.
Underlying causes
Damage to the auricular cartilage may result from chemical or thermal burns, frostbite, auricular hematomas, blunt or penetrating trauma, human or insect bites, deep abrasions, otitis externa, and high ear piercings—especially when performed with poor technique, hygiene, or aftercare. Common causative organisms include Pseudomonas aeruginosa, Staphylococcus species, and Proteus species.
Clinical presentation
Symptoms often begin with a dull ache that progressively worsens. Fever and chills may occur in more advanced cases. Patients frequently report a history of ear trauma or recent ear piercing. On examination, the pinna is painful with marked tenderness, erythema, and warmth. Swelling leads to loss of normal auricular contours, typically sparing the lobule. The auriculocephalic angle may increase. As infection progresses, fluctuance can develop, followed by skin breakdown and purulent drainage.
Diagnostic approach
The diagnosis is primarily clinical, based on characteristic physical findings and a compatible history. Laboratory testing is reserved for patients with systemic signs of infection and may include a complete blood count and blood cultures. When drainage is performed for abscess or advanced chondritis, local cultures should be obtained to guide antibiotic therapy.
Conditions to consider
Important alternatives include allergic reactions, mastoiditis, dermatitis, and auricular hematoma.
Management principles
Early prevention and treatment are critical to avoid permanent deformity. Pressure to the injured ear should be avoided. Eschars and crusts should not be aggressively debrided. The ear should be gently cleansed twice daily with antibacterial soap and water, thoroughly dried, and treated with topical antibiotics if the skin barrier is disrupted. Hair should be kept away from the affected ear. Mild, early infections limited to the lobule may be treated with oral antibiotics. Established chondritis or abscess formation requires parenteral antibiotics and prompt surgical drainage.
Pharmacologic therapy
Antibiotic regimens must include coverage for Pseudomonas. Oral options for mild cases include ciprofloxacin, cephalexin, or dicloxacillin, adjusted for age and weight in pediatric patients. Severe infections require intravenous antibiotics. Topical antibiotics are indicated when there is a break in the skin.
Disposition and follow-up
Admission is indicated for patients with significant edema, erythema, marked tenderness, systemic toxicity, fever, chills, or immunocompromise. Stable patients without systemic signs may be discharged with close otolaryngology follow-up. ENT consultation is recommended for all cases of chondritis, abscess, or cartilage necrosis, and early surgical drainage is essential when abscess is present.
Key clinical lessons
Prompt and aggressive early management is essential to prevent severe and permanent ear deformity. Antibiotic therapy should always include reliable antipseudomonal coverage.
Condition overview
This condition involves inflammation and/or infection of the auricular cartilage of the pinna. Because the cartilage of the external ear has minimal subcutaneous tissue, limited blood supply, and is exposed, it is particularly vulnerable to injury and infection. Chondritis often develops as a delayed complication after trauma or burns, sometimes appearing after the ear seems to have healed. Inadequate or delayed treatment can lead to cartilage avascular necrosis and permanent deformity of the pinna, ranging from a cauliflower-like ear to near-total loss of the external ear with possible narrowing of the auditory canal.
Underlying causes
Damage to the auricular cartilage may result from chemical or thermal burns, frostbite, auricular hematomas, blunt or penetrating trauma, human or insect bites, deep abrasions, otitis externa, and high ear piercings—especially when performed with poor technique, hygiene, or aftercare. Common causative organisms include Pseudomonas aeruginosa, Staphylococcus species, and Proteus species.
Clinical presentation
Symptoms often begin with a dull ache that progressively worsens. Fever and chills may occur in more advanced cases. Patients frequently report a history of ear trauma or recent ear piercing. On examination, the pinna is painful with marked tenderness, erythema, and warmth. Swelling leads to loss of normal auricular contours, typically sparing the lobule. The auriculocephalic angle may increase. As infection progresses, fluctuance can develop, followed by skin breakdown and purulent drainage.
Diagnostic approach
The diagnosis is primarily clinical, based on characteristic physical findings and a compatible history. Laboratory testing is reserved for patients with systemic signs of infection and may include a complete blood count and blood cultures. When drainage is performed for abscess or advanced chondritis, local cultures should be obtained to guide antibiotic therapy.
Conditions to consider
Important alternatives include allergic reactions, mastoiditis, dermatitis, and auricular hematoma.
Management principles
Early prevention and treatment are critical to avoid permanent deformity. Pressure to the injured ear should be avoided. Eschars and crusts should not be aggressively debrided. The ear should be gently cleansed twice daily with antibacterial soap and water, thoroughly dried, and treated with topical antibiotics if the skin barrier is disrupted. Hair should be kept away from the affected ear. Mild, early infections limited to the lobule may be treated with oral antibiotics. Established chondritis or abscess formation requires parenteral antibiotics and prompt surgical drainage.
Pharmacologic therapy
Antibiotic regimens must include coverage for Pseudomonas. Oral options for mild cases include ciprofloxacin, cephalexin, or dicloxacillin, adjusted for age and weight in pediatric patients. Severe infections require intravenous antibiotics. Topical antibiotics are indicated when there is a break in the skin.
Disposition and follow-up
Admission is indicated for patients with significant edema, erythema, marked tenderness, systemic toxicity, fever, chills, or immunocompromise. Stable patients without systemic signs may be discharged with close otolaryngology follow-up. ENT consultation is recommended for all cases of chondritis, abscess, or cartilage necrosis, and early surgical drainage is essential when abscess is present.
Key clinical lessons
Prompt and aggressive early management is essential to prevent severe and permanent ear deformity. Antibiotic therapy should always include reliable antipseudomonal coverage.
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Emergency And Acute Medicine – Pediatric Fever
Basics Description
Fever in children is defined as a rectal temperature of 38°C (100.4°F) or higher. Oral and tympanic temperatures are typically 0.6°C to 1°C lower than rectal measurements, and tympanic readings are unreliable in infants younger than six months. Axillary temperatures are generally inaccurate. Children who present afebrile but have a reliable history of documented fever should be considered febrile to the reported degree.
Etiology
Common causes of pediatric fever include bacteremia, viral illnesses often associated with exanthems, and localized infections. Vaccination against Haemophilus influenzae type B and Streptococcus pneumoniae has significantly reduced invasive disease caused by these organisms. Central nervous system causes include meningitis and encephalitis. Head and neck sources include otitis media, pharyngitis, cervical adenitis, sinusitis, mastoiditis, periorbital cellulitis, and deep neck space abscesses. Respiratory causes include croup, bronchiolitis, pneumonia, empyema, influenza, and epiglottitis. Additional etiologies include cardiac infections, urinary tract infections, gastrointestinal disease, osteomyelitis, septic arthritis, cellulitis, Kawasaki disease, neonatal herpes simplex virus infection, malignancy, drug reactions, heat-related illness, endocrine disorders, and inflammatory or autoimmune disease.
Diagnosis Signs And Symptoms
Clinical appearance is the most important factor in assessment. Airway, breathing, and circulation must be evaluated carefully, with special attention to hydration and perfusion. Toxic features include lethargy, poor feeding, delayed capillary refill, abnormal respirations, weak cry, hypotonia, and petechial or purpuric rash. Tachycardia and tachypnea may be the only early signs of serious illness. Fever increases heart rate by approximately ten beats per minute per degree Fahrenheit. Temperatures above 40°C are associated with increased bacteremia risk in children younger than twenty-four months, while temperatures above 42°C are more often noninfectious. Altered mental status may present as lethargy, irritability, or impaired interaction. Pneumonia should be suspected with tachypnea or hypoxia, and urinary tract infection should be considered in young females, uncircumcised males, and children with fever without a source. Febrile seizures may occur, and serious infection can be present even without fever. Antipyretics may improve clinical appearance without affecting underlying pathology, which can aid assessment. Approximately twenty percent of children will have fever without an identifiable source after initial evaluation.
Essential Workup
Oxygen saturation should be considered a mandatory vital sign. Resuscitation is initiated as needed. A focused history should include duration and pattern of fever, antipyretic use, immunization status, medical history, medications, birth history for infants younger than six months, exposures, feeding and elimination patterns, travel history, and review of systems. A thorough physical examination is performed to identify a source, and antipyretic therapy is initiated.
Diagnosis Tests And Interpretation
Laboratory evaluation may include a complete blood count with differential and urinalysis with culture in all male infants younger than six months, uncircumcised males younger than twelve months, and females younger than two years, using catheterized or suprapubic specimens. Blood cultures are obtained when bacteremia is suspected. Cerebrospinal fluid analysis is required for toxic children and neonates and considered selectively in older infants. Stool studies are indicated when bacterial diarrhea is suspected. Inflammatory markers such as C-reactive protein, erythrocyte sedimentation rate, and procalcitonin may provide supportive information. Chest radiography is indicated for tachypnea, hypoxia, or respiratory findings, with additional imaging guided by suspected source.
Treatment
Prehospital care focuses on stabilization and early antipyretic administration. Initial emergency department management prioritizes treatment of life-threatening conditions. Antipyretics are administered, while evaporative cooling has a limited role. Toxic-appearing children require immediate sepsis evaluation and empiric antibiotics. Neonates younger than twenty-eight days require full sepsis workup and admission with empiric antimicrobial therapy. Infants aged twenty-nine to ninety days are managed based on risk stratification, with selective laboratory evaluation, antibiotic use, and close follow-up. Children three months to three years of age are evaluated selectively, with focused testing based on clinical findings. Immunocompromised children, those with petechiae or purpura, sickle cell disease, malignancy, indwelling devices, or incomplete immunizations require aggressive evaluation and management.
Follow Up Disposition
Admission is required for toxic patients, neonates with fever, higher-risk infants who do not meet low-risk criteria, immunocompromised children, and those with unreliable follow-up. Discharge may be considered for well-appearing infants meeting low-risk criteria and older children who are nontoxic with reliable caregivers and follow-up. Clear return precautions and re-evaluation within twenty-four to forty-eight hours are essential.
Follow Up Recommendations
Children discharged with fever require close follow-up with a primary care provider and explicit instructions for return if symptoms worsen or new signs develop.
Key Clinical Insights And Common Errors
Fever is the most frequent presenting complaint in pediatric patients and may indicate life-threatening disease. Neonates require empiric treatment until serious infection is excluded. Older children may appear well despite significant illness, making subtle findings such as tachycardia, tachypnea, or altered mental status critically important. Inadequate follow-up and failure to recognize early signs of serious infection are common sources of error.
