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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.
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Emergency And Acute Medicine - Erysipelas
Basic description
Erysipelas is a superficial bacterial infection of the skin characterized by prominent involvement of the lymphatic system. Leukocytosis is common, and blood cultures are positive in approximately 3–5% of cases.
Etiology
Group A β-hemolytic streptococcus is the most common causative organism, with group C or G streptococci occurring less frequently.
Common portals of entry include skin ulcers, local trauma, abrasions, psoriatic or eczematous lesions, and fungal infections.
Pediatric considerations
Haemophilus influenzae type b can cause facial cellulitis in children that may resemble erysipelas and should be considered in unimmunized patients. Many of these children are bacteremic and require hospital admission with appropriate antibiotic coverage such as cefuroxime. This organism has become far less common with widespread Hib vaccination.
Group B streptococci may cause erysipelas in newborns, often arising from infection of the umbilical stump.
Pregnancy considerations
Erythema of the breast associated with puerperal mastitis is frequently caused by staphylococcal species; coverage for methicillin-resistant Staphylococcus aureus should be considered.
Diagnosis – signs and symptoms
The most commonly affected sites are the lower extremities (70–80%), followed by the face (5–20%) and ears. Facial involvement is often bilateral, whereas involvement elsewhere is typically unilateral. The skin appears intensely erythematous, giving rise to the historical term “Saint Anthony’s fire.”
Erysipelas occurs more often in infants, children, and the elderly. Systemic symptoms may include malaise, fever, chills, nausea, and vomiting. A traumatic portal of entry is not always evident. Rarely, periorbital cellulitis or cavernous sinus involvement may occur.
History
Facial erysipelas may follow nasopharyngeal infection or trauma. The condition has a predilection for areas of lymphatic obstruction, such as the upper extremity after radical mastectomy or the lower extremity after saphenous vein harvesting. It may be a marker of previously unrecognized lymphatic obstruction or congenital lymphedema, such as Milroy disease.
Recurrence occurs in approximately 30% of patients within three years, often due to lymphatic damage from prior episodes.
Physical examination
Affected skin is edematous, indurated with a peau d’orange appearance, painful, and sharply demarcated with raised borders. When involving the face, a classic butterfly distribution over the cheeks and nasal bridge may be seen. Vesicles or bullae can occur in more severe infections.
Essential workup
Diagnosis is clinical, based on characteristic skin findings and the clinical context. Needle aspirate or wound cultures are rarely helpful and are not routinely indicated.
Diagnosis tests and interpretation
Laboratory studies
Skin swabs are not useful, as they typically yield only normal skin flora.
CBC with differential and blood cultures should be obtained in high-risk patients, including those with diabetes, hypotension, or those requiring admission. Blood cultures are more likely to be positive in patients with lymphedema.
Glucose should be checked in diabetics.
Urinalysis may be performed to evaluate for proteinuria, hematuria, or red cell casts, which could suggest post-streptococcal glomerulonephritis, typically occurring about two weeks after infection onset.
Antistreptolysin O and anti-DNase B titers are not helpful in uncomplicated erysipelas and should not be routinely ordered.
Imaging
Routine imaging is not indicated. If deeper infection such as myositis is suspected, plain radiographs or CT may be used to assess for gas. Ultrasound can be helpful to evaluate for abscess or to exclude deep vein thrombosis in the lower extremity.
Differential diagnosis
Abscess
Acute bacterial sinusitis
Allergic inflammation
Cellulitis
Contact dermatitis
Deep vein thrombosis
Inflammatory breast carcinoma
Herpes zoster
Impetigo
Mastitis
Necrotizing fasciitis
Periorbital cellulitis
Systemic lupus erythematosus
Toxic shock syndrome
Venous stasis dermatitis
Viral exanthem
Treatment – prehospital
Use of gloves and appropriate hand hygiene is important to reduce transmission of streptococcal carriage.
Initial stabilization and therapy
Some patients may appear toxic and require intravenous fluids or hemodynamic support.
Emergency department treatment and procedures
Antibiotic therapy should be initiated promptly and continued for approximately 10 days. Patients with extensive disease typically require admission for intravenous antibiotics, with transition to oral therapy once clinically improved.
Mild cases may be treated as outpatients if the patient is nontoxic, reliable, and has close follow-up.
Penicillin is the treatment of choice when erysipelas is clearly diagnosed. If cellulitis cannot be excluded, add staphylococcal coverage with a penicillinase-resistant penicillin or first-generation cephalosporin.
In areas with high MRSA prevalence, vancomycin or other appropriate agents should be considered.
Acetaminophen may be used for fever.
Hospitalized patients should be placed on isolation precautions, as the condition is contagious.
Medication
Outpatient therapy
Penicillin V, amoxicillin, clindamycin, dicloxacillin, erythromycin, cephalexin, or cefuroxime for 10 days, with pediatric dosing adjusted by weight.
Inpatient therapy
Penicillin G IV or IM, clindamycin IV, or vancomycin IV depending on severity, allergy status, and local resistance patterns.
First-line therapy
Penicillin or a first-generation cephalosporin (oral or IV).
Clindamycin for penicillin-allergic patients.
Second-line therapy
Erythromycin.
Follow-up and disposition
Admission criteria
Extensive involvement, fever, toxic appearance, suspected orbital or periorbital cellulitis, inability to tolerate oral therapy, unreliable follow-up, or unimmunized children requiring coverage for H. influenzae.
Discharge criteria
Minimal facial involvement, nontoxic appearance, no immunosuppression, ability to tolerate oral therapy, reliable follow-up, and a clear diagnosis.
Issues for referral
Nephrology referral is indicated if urinalysis shows findings suggestive of post-streptococcal glomerulonephritis, particularly in children.
Infectious disease consultation is recommended for immunocompromised patients or unusual organisms.
Follow-up recommendations
Compression stockings may reduce recurrence in patients with lower-extremity lymphedema.
Treat underlying tinea pedis with topical antifungals to reduce relapse risk.
Clinical pearls and common missteps
Failure to improve or pain disproportionate to exam findings should prompt evaluation for necrotizing fasciitis or deeper infection.
Managing underlying lymphedema reduces recurrence risk.
Micropustules suggest staphylococcal infection rather than erysipelas and warrant broader antibiotic coverage.
Crepitus should raise concern for an alternative diagnosis.
Always assess tetanus immunization status and update as needed.
Consider prophylactic antibiotics in patients with frequent recurrences.
Basic description
Erysipelas is a superficial bacterial infection of the skin characterized by prominent involvement of the lymphatic system. Leukocytosis is common, and blood cultures are positive in approximately 3–5% of cases.
Etiology
Group A β-hemolytic streptococcus is the most common causative organism, with group C or G streptococci occurring less frequently.
Common portals of entry include skin ulcers, local trauma, abrasions, psoriatic or eczematous lesions, and fungal infections.
Pediatric considerations
Haemophilus influenzae type b can cause facial cellulitis in children that may resemble erysipelas and should be considered in unimmunized patients. Many of these children are bacteremic and require hospital admission with appropriate antibiotic coverage such as cefuroxime. This organism has become far less common with widespread Hib vaccination.
Group B streptococci may cause erysipelas in newborns, often arising from infection of the umbilical stump.
Pregnancy considerations
Erythema of the breast associated with puerperal mastitis is frequently caused by staphylococcal species; coverage for methicillin-resistant Staphylococcus aureus should be considered.
Diagnosis – signs and symptoms
The most commonly affected sites are the lower extremities (70–80%), followed by the face (5–20%) and ears. Facial involvement is often bilateral, whereas involvement elsewhere is typically unilateral. The skin appears intensely erythematous, giving rise to the historical term “Saint Anthony’s fire.”
Erysipelas occurs more often in infants, children, and the elderly. Systemic symptoms may include malaise, fever, chills, nausea, and vomiting. A traumatic portal of entry is not always evident. Rarely, periorbital cellulitis or cavernous sinus involvement may occur.
History
Facial erysipelas may follow nasopharyngeal infection or trauma. The condition has a predilection for areas of lymphatic obstruction, such as the upper extremity after radical mastectomy or the lower extremity after saphenous vein harvesting. It may be a marker of previously unrecognized lymphatic obstruction or congenital lymphedema, such as Milroy disease.
Recurrence occurs in approximately 30% of patients within three years, often due to lymphatic damage from prior episodes.
Physical examination
Affected skin is edematous, indurated with a peau d’orange appearance, painful, and sharply demarcated with raised borders. When involving the face, a classic butterfly distribution over the cheeks and nasal bridge may be seen. Vesicles or bullae can occur in more severe infections.
Essential workup
Diagnosis is clinical, based on characteristic skin findings and the clinical context. Needle aspirate or wound cultures are rarely helpful and are not routinely indicated.
Diagnosis tests and interpretation
Laboratory studies
Skin swabs are not useful, as they typically yield only normal skin flora.
CBC with differential and blood cultures should be obtained in high-risk patients, including those with diabetes, hypotension, or those requiring admission. Blood cultures are more likely to be positive in patients with lymphedema.
Glucose should be checked in diabetics.
Urinalysis may be performed to evaluate for proteinuria, hematuria, or red cell casts, which could suggest post-streptococcal glomerulonephritis, typically occurring about two weeks after infection onset.
Antistreptolysin O and anti-DNase B titers are not helpful in uncomplicated erysipelas and should not be routinely ordered.
Imaging
Routine imaging is not indicated. If deeper infection such as myositis is suspected, plain radiographs or CT may be used to assess for gas. Ultrasound can be helpful to evaluate for abscess or to exclude deep vein thrombosis in the lower extremity.
Differential diagnosis
Abscess
Acute bacterial sinusitis
Allergic inflammation
Cellulitis
Contact dermatitis
Deep vein thrombosis
Inflammatory breast carcinoma
Herpes zoster
Impetigo
Mastitis
Necrotizing fasciitis
Periorbital cellulitis
Systemic lupus erythematosus
Toxic shock syndrome
Venous stasis dermatitis
Viral exanthem
Treatment – prehospital
Use of gloves and appropriate hand hygiene is important to reduce transmission of streptococcal carriage.
Initial stabilization and therapy
Some patients may appear toxic and require intravenous fluids or hemodynamic support.
Emergency department treatment and procedures
Antibiotic therapy should be initiated promptly and continued for approximately 10 days. Patients with extensive disease typically require admission for intravenous antibiotics, with transition to oral therapy once clinically improved.
Mild cases may be treated as outpatients if the patient is nontoxic, reliable, and has close follow-up.
Penicillin is the treatment of choice when erysipelas is clearly diagnosed. If cellulitis cannot be excluded, add staphylococcal coverage with a penicillinase-resistant penicillin or first-generation cephalosporin.
In areas with high MRSA prevalence, vancomycin or other appropriate agents should be considered.
Acetaminophen may be used for fever.
Hospitalized patients should be placed on isolation precautions, as the condition is contagious.
Medication
Outpatient therapy
Penicillin V, amoxicillin, clindamycin, dicloxacillin, erythromycin, cephalexin, or cefuroxime for 10 days, with pediatric dosing adjusted by weight.
Inpatient therapy
Penicillin G IV or IM, clindamycin IV, or vancomycin IV depending on severity, allergy status, and local resistance patterns.
First-line therapy
Penicillin or a first-generation cephalosporin (oral or IV).
Clindamycin for penicillin-allergic patients.
Second-line therapy
Erythromycin.
Follow-up and disposition
Admission criteria
Extensive involvement, fever, toxic appearance, suspected orbital or periorbital cellulitis, inability to tolerate oral therapy, unreliable follow-up, or unimmunized children requiring coverage for H. influenzae.
Discharge criteria
Minimal facial involvement, nontoxic appearance, no immunosuppression, ability to tolerate oral therapy, reliable follow-up, and a clear diagnosis.
Issues for referral
Nephrology referral is indicated if urinalysis shows findings suggestive of post-streptococcal glomerulonephritis, particularly in children.
Infectious disease consultation is recommended for immunocompromised patients or unusual organisms.
Follow-up recommendations
Compression stockings may reduce recurrence in patients with lower-extremity lymphedema.
Treat underlying tinea pedis with topical antifungals to reduce relapse risk.
Clinical pearls and common missteps
Failure to improve or pain disproportionate to exam findings should prompt evaluation for necrotizing fasciitis or deeper infection.
Managing underlying lymphedema reduces recurrence risk.
Micropustules suggest staphylococcal infection rather than erysipelas and warrant broader antibiotic coverage.
Crepitus should raise concern for an alternative diagnosis.
Always assess tetanus immunization status and update as needed.
Consider prophylactic antibiotics in patients with frequent recurrences.
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Emergency And Acute Medicine - Epistaxis
Basic description
Epistaxis is a frequent emergency presentation that is typically mild and self-limited but can occasionally be life threatening. The lifetime incidence is approximately 60%, with most cases occurring in children younger than 10 years. Males are affected more often than females. Severe hemorrhage requiring surgical intervention is more common in patients older than 50 years.
Epistaxis occurs more frequently in low-humidity environments, during winter months, in northern climates, and at high altitude.
The nasal cavity receives blood supply from both the internal and external carotid arteries. Management depends on the location of bleeding.
Anterior epistaxis accounts for about 90% of cases and is usually visualized directly in the anterior nasal cavity. The most common source is Kiesselbach plexus on the anteroinferior nasal septum. Less commonly, bleeding originates from the posterior nasal floor or septum.
Posterior epistaxis represents about 10% of cases and arises from vessels not directly visualized, most often branches of the sphenopalatine artery.
Etiology
Idiopathic causes include dry nasal mucosa related to low humidity.
Foreign bodies are common in children and in patients with psychiatric illness or developmental delay.
Infectious causes include rhinitis, sinusitis, nasal diphtheria, and nasal mucormycosis.
Allergic rhinitis is a frequent contributor.
Trauma includes nose picking, postoperative injury, facial trauma, and barotrauma.
Environmental irritants include ammonia, gasoline, sulfuric acid, and glutaraldehyde.
Intranasal neoplasms include papilloma and other tumors.
Coagulopathies include hemophilia A or B, von Willebrand disease, thrombocytopenia from liver disease, leukemia, chemotherapy, viral illness, or autoimmune disease.
Platelet dysfunction may occur with renal disease or chronic alcohol use.
Medication-related causes include salicylates, NSAIDs, heparin, and warfarin.
Other causes include hereditary hemorrhagic telangiectasia, atherosclerosis of nasal vessels, and endometriosis.
Diagnosis – signs and symptoms
History
Determine laterality, severity, and duration of bleeding.
Assess recurrence and prior episodes.
Ask about nasal obstruction, vomiting or coughing blood, known tumors, or bleeding disorders.
Easy bruising or unusual bleeding suggests an underlying coagulopathy.
Identify comorbid conditions that may be worsened by blood loss, such as coronary artery disease or chronic lung disease.
Physical examination
Assess vital signs for evidence of hemorrhagic shock.
Look for signs of coagulopathy including bruising, petechiae, or purpura.
Inspect the nasal cavity after topical anesthesia and vasoconstriction using a nasal speculum.
Evaluate for blood in the mouth or oropharynx.
Essential workup
Assess airway and hemodynamic stability.
Determine whether bleeding is anterior or posterior.
Evaluate for underlying bleeding disorders when indicated.
Diagnosis tests and interpretation
Laboratory studies
For severe bleeding or suspected coagulopathy consider CBC, type and cross-match, PT/INR, PTT, and BUN.
Diagnostic procedures
Direct visualization with nasal speculum after topical anesthetic and vasoconstrictor. Adequate lighting and suction are essential.
Differential diagnosis
Hematemesis
Hemoptysis
Pediatric considerations
Posterior epistaxis is uncommon in children and should prompt evaluation for bleeding disorders.
Consider foreign bodies or neoplasms such as juvenile angiofibroma.
Use of topical antiseptic ointment for four weeks reduces recurrent epistaxis.
Treatment – prehospital
Stable patients should lean forward, pinch the soft part of the nose, and spit out blood rather than swallow it.
Unstable patients require airway management, IV access, and crystalloid resuscitation.
Initial stabilization and therapy
Secure the airway in patients with altered mental status, facial trauma, or aspiration risk.
Treat hypotension with fluids and blood products as indicated.
Emergency department treatment and procedures
Use universal precautions.
For anterior bleeding, apply direct pressure for 15 minutes.
If bleeding persists, insert cotton pledgets soaked in anesthetic and vasoconstrictor.
Clear clots by gentle blowing, irrigation, or suction.
Cauterize the identified bleeding site with silver nitrate and consider absorbable hemostatic agents.
If cautery fails, anterior nasal packing or balloon devices may be used, ensuring adequate anesthesia and careful placement.
Petroleum-impregnated gauze packing is an alternative when commercial devices are unavailable.
Persistent bleeding after anterior packing suggests inadequate packing or a posterior source.
Posterior epistaxis may require posterior packing with commercial devices or a Foley catheter technique and mandates hospital admission with monitoring.
Posterior packs should not remain in place longer than three days due to infection risk.
Medication
Topical vasoactive agents include cocaine 4%, oxymetazoline with lidocaine, phenylephrine, or anesthetic–epinephrine mixtures.
Antibiotics are required while nasal packing is in place, including amoxicillin–clavulanate, cephalexin, clindamycin, or trimethoprim–sulfamethoxazole.
Follow-up and disposition
Admission criteria
Severe hemorrhage requiring transfusion.
Significant coagulopathy.
Posterior nasal packing, which requires admission, telemetry, oxygen, and specialist consultation.
Anterior packing without reliable follow-up.
Discharge criteria
Hemodynamically stable patients with controlled bleeding.
Use topical oxymetazoline for up to two days, humidification, nasal lubrication, and avoidance of nasal trauma.
All patients discharged with packing must receive antistaphylococcal antibiotics.
Issues for referral
All patients with nasal packing should see an otolaryngologist within 48 hours.
Recurrent unilateral bleeding, nasal obstruction, or suspicious lesions require specialist evaluation.
Follow-up recommendations
Return for uncontrolled bleeding, fever, breathing difficulty, or vomiting.
Avoid nose blowing for 12 hours after bleeding stops.
If bleeding recurs, lean forward and pinch the nose firmly for 10 minutes without interruption.
Use nasal ointment and home humidification as instructed.
Clinical pearls and common missteps
Suspect nasal foreign bodies in unilateral bleeding in children and cognitively impaired patients.
Avoid petroleum-based ointments on anterior nasal balloons due to risk of delayed rupture.
Do not overinflate balloons or pack too tightly, as this may cause tissue necrosis.
Patients with nasal packing should always receive prophylactic antibiotics.
Basic description
Epistaxis is a frequent emergency presentation that is typically mild and self-limited but can occasionally be life threatening. The lifetime incidence is approximately 60%, with most cases occurring in children younger than 10 years. Males are affected more often than females. Severe hemorrhage requiring surgical intervention is more common in patients older than 50 years.
Epistaxis occurs more frequently in low-humidity environments, during winter months, in northern climates, and at high altitude.
The nasal cavity receives blood supply from both the internal and external carotid arteries. Management depends on the location of bleeding.
Anterior epistaxis accounts for about 90% of cases and is usually visualized directly in the anterior nasal cavity. The most common source is Kiesselbach plexus on the anteroinferior nasal septum. Less commonly, bleeding originates from the posterior nasal floor or septum.
Posterior epistaxis represents about 10% of cases and arises from vessels not directly visualized, most often branches of the sphenopalatine artery.
Etiology
Idiopathic causes include dry nasal mucosa related to low humidity.
Foreign bodies are common in children and in patients with psychiatric illness or developmental delay.
Infectious causes include rhinitis, sinusitis, nasal diphtheria, and nasal mucormycosis.
Allergic rhinitis is a frequent contributor.
Trauma includes nose picking, postoperative injury, facial trauma, and barotrauma.
Environmental irritants include ammonia, gasoline, sulfuric acid, and glutaraldehyde.
Intranasal neoplasms include papilloma and other tumors.
Coagulopathies include hemophilia A or B, von Willebrand disease, thrombocytopenia from liver disease, leukemia, chemotherapy, viral illness, or autoimmune disease.
Platelet dysfunction may occur with renal disease or chronic alcohol use.
Medication-related causes include salicylates, NSAIDs, heparin, and warfarin.
Other causes include hereditary hemorrhagic telangiectasia, atherosclerosis of nasal vessels, and endometriosis.
Diagnosis – signs and symptoms
History
Determine laterality, severity, and duration of bleeding.
Assess recurrence and prior episodes.
Ask about nasal obstruction, vomiting or coughing blood, known tumors, or bleeding disorders.
Easy bruising or unusual bleeding suggests an underlying coagulopathy.
Identify comorbid conditions that may be worsened by blood loss, such as coronary artery disease or chronic lung disease.
Physical examination
Assess vital signs for evidence of hemorrhagic shock.
Look for signs of coagulopathy including bruising, petechiae, or purpura.
Inspect the nasal cavity after topical anesthesia and vasoconstriction using a nasal speculum.
Evaluate for blood in the mouth or oropharynx.
Essential workup
Assess airway and hemodynamic stability.
Determine whether bleeding is anterior or posterior.
Evaluate for underlying bleeding disorders when indicated.
Diagnosis tests and interpretation
Laboratory studies
For severe bleeding or suspected coagulopathy consider CBC, type and cross-match, PT/INR, PTT, and BUN.
Diagnostic procedures
Direct visualization with nasal speculum after topical anesthetic and vasoconstrictor. Adequate lighting and suction are essential.
Differential diagnosis
Hematemesis
Hemoptysis
Pediatric considerations
Posterior epistaxis is uncommon in children and should prompt evaluation for bleeding disorders.
Consider foreign bodies or neoplasms such as juvenile angiofibroma.
Use of topical antiseptic ointment for four weeks reduces recurrent epistaxis.
Treatment – prehospital
Stable patients should lean forward, pinch the soft part of the nose, and spit out blood rather than swallow it.
Unstable patients require airway management, IV access, and crystalloid resuscitation.
Initial stabilization and therapy
Secure the airway in patients with altered mental status, facial trauma, or aspiration risk.
Treat hypotension with fluids and blood products as indicated.
Emergency department treatment and procedures
Use universal precautions.
For anterior bleeding, apply direct pressure for 15 minutes.
If bleeding persists, insert cotton pledgets soaked in anesthetic and vasoconstrictor.
Clear clots by gentle blowing, irrigation, or suction.
Cauterize the identified bleeding site with silver nitrate and consider absorbable hemostatic agents.
If cautery fails, anterior nasal packing or balloon devices may be used, ensuring adequate anesthesia and careful placement.
Petroleum-impregnated gauze packing is an alternative when commercial devices are unavailable.
Persistent bleeding after anterior packing suggests inadequate packing or a posterior source.
Posterior epistaxis may require posterior packing with commercial devices or a Foley catheter technique and mandates hospital admission with monitoring.
Posterior packs should not remain in place longer than three days due to infection risk.
Medication
Topical vasoactive agents include cocaine 4%, oxymetazoline with lidocaine, phenylephrine, or anesthetic–epinephrine mixtures.
Antibiotics are required while nasal packing is in place, including amoxicillin–clavulanate, cephalexin, clindamycin, or trimethoprim–sulfamethoxazole.
Follow-up and disposition
Admission criteria
Severe hemorrhage requiring transfusion.
Significant coagulopathy.
Posterior nasal packing, which requires admission, telemetry, oxygen, and specialist consultation.
Anterior packing without reliable follow-up.
Discharge criteria
Hemodynamically stable patients with controlled bleeding.
Use topical oxymetazoline for up to two days, humidification, nasal lubrication, and avoidance of nasal trauma.
All patients discharged with packing must receive antistaphylococcal antibiotics.
Issues for referral
All patients with nasal packing should see an otolaryngologist within 48 hours.
Recurrent unilateral bleeding, nasal obstruction, or suspicious lesions require specialist evaluation.
Follow-up recommendations
Return for uncontrolled bleeding, fever, breathing difficulty, or vomiting.
Avoid nose blowing for 12 hours after bleeding stops.
If bleeding recurs, lean forward and pinch the nose firmly for 10 minutes without interruption.
Use nasal ointment and home humidification as instructed.
Clinical pearls and common missteps
Suspect nasal foreign bodies in unilateral bleeding in children and cognitively impaired patients.
Avoid petroleum-based ointments on anterior nasal balloons due to risk of delayed rupture.
Do not overinflate balloons or pack too tightly, as this may cause tissue necrosis.
Patients with nasal packing should always receive prophylactic antibiotics.
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Emergency And Acute Medicine - Adult Epiglottitis
Basic description
Epiglottitis is a rapidly progressive inflammation of the epiglottis and surrounding supraglottic tissues that can lead to acute airway compromise. Although often more indolent in adults than in children, adults may still deteriorate abruptly with complete airway obstruction. While the incidence of pediatric epiglottitis has declined, adult cases are increasing.
Inflammation primarily involves the epiglottis, where edema poses the greatest airway risk, but may also extend to adjacent structures including the vallecula and arytenoids. The incidence in adults is approximately 1–4 per 100,000 per year and is rising. It is more common in men, with a ratio of 3:1, and most frequently affects patients in their fifth decade of life. Adult mortality is approximately 7%, compared with less than 1% in children.
Immunocompromised patients may present with fulminant disease, minimal early symptoms, and atypical organisms such as Candida or Pseudomonas aeruginosa. Potential complications include total airway obstruction, retropharyngeal abscess, acute respiratory distress syndrome, pneumonia, and empyema.
Etiology
Infectious causes include Haemophilus influenzae type B as well as type A and nontypeable strains, Haemophilus parainfluenzae, Streptococcus pneumoniae, Staphylococcus aureus, group A Streptococcus, Neisseria meningitidis, herpes simplex virus, cytomegalovirus, and Pseudomonas aeruginosa.
Noninfectious causes include chemical or thermal burns, toxic or illicit drug inhalation, trauma, and airway instrumentation.
Diagnosis – signs and symptoms
History
General symptoms include fever and upper respiratory tract complaints, though a prodrome may be absent. Head and neck symptoms commonly include dysphagia, muffled or “hot potato” voice, hoarseness, foreign body sensation in the throat, drooling, and associated tonsillar, peritonsillar, or uvular findings. Respiratory complaints include a subjective sense of airway obstruction and shortness of breath.
Physical examination
Patients may appear toxic and febrile and often sit upright in a tripod position. The classic “cherry red” epiglottis may be seen, though up to half of patients have a pale, edematous epiglottis instead. Gentle palpation of the hyoid or thyroid cartilage may be painful, and lateral movement of the larynx (“tracheal rock”) can elicit pain. Cervical lymphadenopathy may be present. Respiratory findings include stridor, accessory muscle use, and sudden airway loss.
Alert
Any patient with respiratory distress is at high risk for rapid progression to complete airway obstruction. Emergent surgical airway management may be required.
Essential workup
In patients with significant respiratory distress, invasive diagnostic procedures should be avoided. Management should prioritize empiric antibiotics and airway control before further diagnostic evaluation.
Diagnosis tests and interpretation
Laboratory studies
Obtain a complete blood count with differential and blood cultures. Pharyngeal cultures should be obtained only if there are no signs of respiratory distress.
Imaging
In patients with moderate to severe respiratory distress, airway control must precede imaging. A portable lateral soft tissue neck radiograph may show the epiglottic “thumb sign,” loss of the normal vallecular contour, swelling of the arytenoids or aryepiglottic folds, and prevertebral soft tissue swelling. False-negative rates are significant; negative imaging does not exclude the diagnosis.
CT imaging is reserved for cases in which laryngoscopy cannot be performed or when complications such as abscess are suspected.
Diagnostic procedures
Nasopharyngoscopy or indirect laryngoscopy may confirm the diagnosis but should not be performed prior to securing the airway if stridor or respiratory distress is present.
Differential diagnosis
Croup, airway foreign body, anaphylaxis, paradoxical vocal cord dysfunction, angioedema, laryngitis, pharyngitis, peritonsillar or retropharyngeal abscess, bacterial tracheitis, congenital airway anomalies, and meningitis.
Treatment – prehospital
Transport the patient in a position of comfort. Provide supplemental oxygen as tolerated while minimizing anxiety. Intubation should be attempted only in severe respiratory distress, as airway manipulation carries a high risk of worsening obstruction. Inhaled agents, racemic epinephrine, and β-agonists have no proven benefit.
Initial stabilization and therapy
Follow airway, breathing, and circulation priorities. Be fully prepared for definitive airway management, including surgical airway capability, from first contact until the diagnosis is excluded or the patient is transferred to intensive care. Airway examination itself can precipitate obstruction.
Orotracheal intubation is indicated for patients with significant respiratory distress or impending airway failure. Early ENT or surgical consultation is recommended when feasible. Needle jet ventilation may be a life-saving temporizing measure if intubation fails and a surgical airway is not immediately available.
Emergency department treatment
Provide humidified oxygen, establish IV access, and initiate empiric intravenous antibiotics. The role of corticosteroids remains controversial.
Medication
First line
Cefotaxime 2 g IV every 8 hours
or
Ceftriaxone 2 g IV every 24 hours
Second line or alternative regimens
Ampicillin–sulbactam 3 g IV initially, then 200–300 mg/kg/day in four divided doses plus vancomycin 1 g IV every 12 hours
Trimethoprim–sulfamethoxazole 320 mg IV initially, then 4–5 mg/kg IV every 12 hours
Additional coverage for Staphylococcus aureus
Nafcillin 150–200 mg/kg/day IV in four divided doses
or
Clindamycin 600–900 mg IV every 8 hours
Prophylaxis for close contacts
Rifampin 600 mg PO daily for 4 days in adults
Follow-up and disposition
Admission criteria
All patients with suspected or confirmed epiglottitis require admission to an intensive care unit for airway monitoring and intravenous antibiotics.
Discharge criteria
Patients should not be discharged unless epiglottitis has been definitively excluded by direct visualization of the supraglottic structures by an experienced clinician.
Issues for referral
Early otolaryngology consultation is recommended in all suspected cases.
Clinical pearls and common missteps
Delayed airway control is the most common cause of poor outcome. Avoid unnecessary interventions until the airway is secured. Adult epiglottitis carries a mortality rate of approximately 7%, underscoring the need for early recognition and decisive management.
Basic description
Epiglottitis is a rapidly progressive inflammation of the epiglottis and surrounding supraglottic tissues that can lead to acute airway compromise. Although often more indolent in adults than in children, adults may still deteriorate abruptly with complete airway obstruction. While the incidence of pediatric epiglottitis has declined, adult cases are increasing.
Inflammation primarily involves the epiglottis, where edema poses the greatest airway risk, but may also extend to adjacent structures including the vallecula and arytenoids. The incidence in adults is approximately 1–4 per 100,000 per year and is rising. It is more common in men, with a ratio of 3:1, and most frequently affects patients in their fifth decade of life. Adult mortality is approximately 7%, compared with less than 1% in children.
Immunocompromised patients may present with fulminant disease, minimal early symptoms, and atypical organisms such as Candida or Pseudomonas aeruginosa. Potential complications include total airway obstruction, retropharyngeal abscess, acute respiratory distress syndrome, pneumonia, and empyema.
Etiology
Infectious causes include Haemophilus influenzae type B as well as type A and nontypeable strains, Haemophilus parainfluenzae, Streptococcus pneumoniae, Staphylococcus aureus, group A Streptococcus, Neisseria meningitidis, herpes simplex virus, cytomegalovirus, and Pseudomonas aeruginosa.
Noninfectious causes include chemical or thermal burns, toxic or illicit drug inhalation, trauma, and airway instrumentation.
Diagnosis – signs and symptoms
History
General symptoms include fever and upper respiratory tract complaints, though a prodrome may be absent. Head and neck symptoms commonly include dysphagia, muffled or “hot potato” voice, hoarseness, foreign body sensation in the throat, drooling, and associated tonsillar, peritonsillar, or uvular findings. Respiratory complaints include a subjective sense of airway obstruction and shortness of breath.
Physical examination
Patients may appear toxic and febrile and often sit upright in a tripod position. The classic “cherry red” epiglottis may be seen, though up to half of patients have a pale, edematous epiglottis instead. Gentle palpation of the hyoid or thyroid cartilage may be painful, and lateral movement of the larynx (“tracheal rock”) can elicit pain. Cervical lymphadenopathy may be present. Respiratory findings include stridor, accessory muscle use, and sudden airway loss.
Alert
Any patient with respiratory distress is at high risk for rapid progression to complete airway obstruction. Emergent surgical airway management may be required.
Essential workup
In patients with significant respiratory distress, invasive diagnostic procedures should be avoided. Management should prioritize empiric antibiotics and airway control before further diagnostic evaluation.
Diagnosis tests and interpretation
Laboratory studies
Obtain a complete blood count with differential and blood cultures. Pharyngeal cultures should be obtained only if there are no signs of respiratory distress.
Imaging
In patients with moderate to severe respiratory distress, airway control must precede imaging. A portable lateral soft tissue neck radiograph may show the epiglottic “thumb sign,” loss of the normal vallecular contour, swelling of the arytenoids or aryepiglottic folds, and prevertebral soft tissue swelling. False-negative rates are significant; negative imaging does not exclude the diagnosis.
CT imaging is reserved for cases in which laryngoscopy cannot be performed or when complications such as abscess are suspected.
Diagnostic procedures
Nasopharyngoscopy or indirect laryngoscopy may confirm the diagnosis but should not be performed prior to securing the airway if stridor or respiratory distress is present.
Differential diagnosis
Croup, airway foreign body, anaphylaxis, paradoxical vocal cord dysfunction, angioedema, laryngitis, pharyngitis, peritonsillar or retropharyngeal abscess, bacterial tracheitis, congenital airway anomalies, and meningitis.
Treatment – prehospital
Transport the patient in a position of comfort. Provide supplemental oxygen as tolerated while minimizing anxiety. Intubation should be attempted only in severe respiratory distress, as airway manipulation carries a high risk of worsening obstruction. Inhaled agents, racemic epinephrine, and β-agonists have no proven benefit.
Initial stabilization and therapy
Follow airway, breathing, and circulation priorities. Be fully prepared for definitive airway management, including surgical airway capability, from first contact until the diagnosis is excluded or the patient is transferred to intensive care. Airway examination itself can precipitate obstruction.
Orotracheal intubation is indicated for patients with significant respiratory distress or impending airway failure. Early ENT or surgical consultation is recommended when feasible. Needle jet ventilation may be a life-saving temporizing measure if intubation fails and a surgical airway is not immediately available.
Emergency department treatment
Provide humidified oxygen, establish IV access, and initiate empiric intravenous antibiotics. The role of corticosteroids remains controversial.
Medication
First line
Cefotaxime 2 g IV every 8 hours
or
Ceftriaxone 2 g IV every 24 hours
Second line or alternative regimens
Ampicillin–sulbactam 3 g IV initially, then 200–300 mg/kg/day in four divided doses plus vancomycin 1 g IV every 12 hours
Trimethoprim–sulfamethoxazole 320 mg IV initially, then 4–5 mg/kg IV every 12 hours
Additional coverage for Staphylococcus aureus
Nafcillin 150–200 mg/kg/day IV in four divided doses
or
Clindamycin 600–900 mg IV every 8 hours
Prophylaxis for close contacts
Rifampin 600 mg PO daily for 4 days in adults
Follow-up and disposition
Admission criteria
All patients with suspected or confirmed epiglottitis require admission to an intensive care unit for airway monitoring and intravenous antibiotics.
Discharge criteria
Patients should not be discharged unless epiglottitis has been definitively excluded by direct visualization of the supraglottic structures by an experienced clinician.
Issues for referral
Early otolaryngology consultation is recommended in all suspected cases.
Clinical pearls and common missteps
Delayed airway control is the most common cause of poor outcome. Avoid unnecessary interventions until the airway is secured. Adult epiglottitis carries a mortality rate of approximately 7%, underscoring the need for early recognition and decisive management.
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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 - Epidural Abscess
Basic Overview
Spinal epidural abscess is an uncommon but serious pyogenic infection involving the epidural space of the spinal canal, with an estimated incidence of 2–25 cases per 100,000 hospital admissions. The thoracic spine is most frequently affected, followed by the lumbar and cervical regions.
Causative Mechanisms
Infection typically originates from a distant focus and reaches the epidural space via hematogenous spread in approximately half of cases, while direct extension accounts for others. In about one third of patients, no clear source is identified. Skin and soft tissue infections are the most common sources, though any pyogenic infection can be responsible.
Staphylococcus aureus causes more than half of cases, with a significant proportion due to methicillin-resistant strains. Streptococci are the second most common pathogens. Other causative organisms include Haemophilus influenzae, gram-negative bacilli, mycobacteria, anaerobes, coagulase-negative staphylococci, fungi, and mixed flora. Epidural abscess may also complicate epidural catheter placement, spinal surgery, or rarely lumbar puncture, particularly after multiple attempts.
Special Considerations In Children
Pediatric patients often present similarly to adults with back pain, fever, and neurologic deficits, though younger children and infants may exhibit nonspecific symptoms such as irritability, fever, or meningitis. Sphincter dysfunction is common. Most pediatric cases arise from hematogenous spread, with pathogen distribution and spinal location similar to adults.
Clinical Features And Presentation
The combination of fever and severe back pain is a critical warning sign. Radicular pain or neurologic abnormalities significantly increase suspicion for epidural abscess. The classic triad consists of progressive back pain, fever, and neurologic deficits such as weakness, paralysis, sensory level changes, or sphincter dysfunction. Some patients present primarily with sepsis and minimal back pain.
The condition affects all age groups, with peak incidence between 60 and 70 years. Most patients have identifiable risk factors, including intravenous drug use, diabetes mellitus, malignancy, chronic steroid use, alcoholism, recent spinal instrumentation or surgery, and indwelling vascular catheters. However, epidural abscess can occur without predisposing conditions.
History And Physical Findings
Patients may report back pain, fever, weakness, paresthesias, or bowel and bladder dysfunction. Examination often reveals fever, focal spinal tenderness or erythema, neurologic deficits, and signs of systemic infection. Evidence of intravenous drug use or other risk factors may be present.
Key Diagnostic Priorities
Evaluation should emphasize identifying predisposing conditions, localizing spinal tenderness, and detecting neurologic deficits such as saddle anesthesia, sphincter tone reduction, and lower extremity weakness. Measurement of postvoid residual urine volume can help identify urinary retention. Magnetic resonance imaging with and without gadolinium contrast is the diagnostic modality of choice and should be obtained emergently. Computed tomography with contrast or myelography may be used if MRI is unavailable.
Diagnostic Studies And Interpretation
Laboratory evaluation typically reveals an elevated erythrocyte sedimentation rate, which is highly sensitive but nonspecific. A normal ESR makes epidural abscess unlikely. C-reactive protein is also usually elevated. Blood cultures are positive in approximately 60% of cases, and leukocytosis with left shift is common. Cerebrospinal fluid analysis is often abnormal but nonspecific; lumbar puncture should generally be avoided due to the risk of spreading infection.
MRI has a sensitivity exceeding 90% and typically demonstrates high-intensity lesions on T2-weighted images. CT with contrast or CT myelography may be used when MRI is not available, though these carry additional risks.
Alternative Diagnoses To Consider
Because symptoms are often nonspecific, diagnosis is frequently delayed. Epidural abscess is commonly misdiagnosed as benign musculoskeletal back pain. Other considerations include vertebral osteomyelitis, spinal tumors, meningitis, discitis, pyelonephritis, spinal cord compression, ischemia, and disc herniation. In children, fever with back pain should prompt urgent imaging.
Prehospital And Early Management
Spinal immobilization is recommended when trauma or fracture is suspected.
Initial Stabilization Strategy
Prompt initiation of broad-spectrum intravenous antibiotics is essential and should cover Staphylococcus aureus, streptococci, and gram-negative organisms. Vancomycin combined with a third-generation cephalosporin is an appropriate initial regimen. Coverage for Pseudomonas species is indicated in patients with intravenous drug use. Anaerobic coverage may be added when clinically indicated.
Emergency Department Management
Urgent imaging is mandatory once epidural abscess is suspected, as delays worsen neurologic outcomes. If the level of infection cannot be localized clinically, imaging of the entire spine should be considered. Neurosurgical consultation or transfer to a facility with neurosurgical capability is required. Surgical decompression is often definitive, though select patients may be managed conservatively with prolonged intravenous antibiotics.
Antimicrobial Therapy
Common empiric regimens include vancomycin with ceftazidime, with metronidazole added if anaerobic infection is suspected. Antibiotic therapy should be adjusted based on culture results.
Disposition And Hospitalization
All patients with confirmed or strongly suspected epidural abscess require hospital admission. Emergent MRI and neurosurgical evaluation are mandatory. Discharge from the emergency department is not appropriate in these cases.
Referral And Transfer Considerations
Patients should be managed at centers with MRI availability and neurosurgical expertise. If transfer is required, blood cultures should be obtained and antibiotics initiated prior to transfer unless this would delay care.
Clinical Insights And Common Errors
Epidural abscess may recur, particularly in immunocompromised patients. Any patient with staphylococcal bacteremia and back pain or neurologic symptoms should be evaluated for epidural abscess. Failure to image the correct spinal region is a frequent error; careful neurologic and spinal examination can guide imaging, but when localization is unclear, imaging the entire spine is warranted.
Basic Overview
Spinal epidural abscess is an uncommon but serious pyogenic infection involving the epidural space of the spinal canal, with an estimated incidence of 2–25 cases per 100,000 hospital admissions. The thoracic spine is most frequently affected, followed by the lumbar and cervical regions.
Causative Mechanisms
Infection typically originates from a distant focus and reaches the epidural space via hematogenous spread in approximately half of cases, while direct extension accounts for others. In about one third of patients, no clear source is identified. Skin and soft tissue infections are the most common sources, though any pyogenic infection can be responsible.
Staphylococcus aureus causes more than half of cases, with a significant proportion due to methicillin-resistant strains. Streptococci are the second most common pathogens. Other causative organisms include Haemophilus influenzae, gram-negative bacilli, mycobacteria, anaerobes, coagulase-negative staphylococci, fungi, and mixed flora. Epidural abscess may also complicate epidural catheter placement, spinal surgery, or rarely lumbar puncture, particularly after multiple attempts.
Special Considerations In Children
Pediatric patients often present similarly to adults with back pain, fever, and neurologic deficits, though younger children and infants may exhibit nonspecific symptoms such as irritability, fever, or meningitis. Sphincter dysfunction is common. Most pediatric cases arise from hematogenous spread, with pathogen distribution and spinal location similar to adults.
Clinical Features And Presentation
The combination of fever and severe back pain is a critical warning sign. Radicular pain or neurologic abnormalities significantly increase suspicion for epidural abscess. The classic triad consists of progressive back pain, fever, and neurologic deficits such as weakness, paralysis, sensory level changes, or sphincter dysfunction. Some patients present primarily with sepsis and minimal back pain.
The condition affects all age groups, with peak incidence between 60 and 70 years. Most patients have identifiable risk factors, including intravenous drug use, diabetes mellitus, malignancy, chronic steroid use, alcoholism, recent spinal instrumentation or surgery, and indwelling vascular catheters. However, epidural abscess can occur without predisposing conditions.
History And Physical Findings
Patients may report back pain, fever, weakness, paresthesias, or bowel and bladder dysfunction. Examination often reveals fever, focal spinal tenderness or erythema, neurologic deficits, and signs of systemic infection. Evidence of intravenous drug use or other risk factors may be present.
Key Diagnostic Priorities
Evaluation should emphasize identifying predisposing conditions, localizing spinal tenderness, and detecting neurologic deficits such as saddle anesthesia, sphincter tone reduction, and lower extremity weakness. Measurement of postvoid residual urine volume can help identify urinary retention. Magnetic resonance imaging with and without gadolinium contrast is the diagnostic modality of choice and should be obtained emergently. Computed tomography with contrast or myelography may be used if MRI is unavailable.
Diagnostic Studies And Interpretation
Laboratory evaluation typically reveals an elevated erythrocyte sedimentation rate, which is highly sensitive but nonspecific. A normal ESR makes epidural abscess unlikely. C-reactive protein is also usually elevated. Blood cultures are positive in approximately 60% of cases, and leukocytosis with left shift is common. Cerebrospinal fluid analysis is often abnormal but nonspecific; lumbar puncture should generally be avoided due to the risk of spreading infection.
MRI has a sensitivity exceeding 90% and typically demonstrates high-intensity lesions on T2-weighted images. CT with contrast or CT myelography may be used when MRI is not available, though these carry additional risks.
Alternative Diagnoses To Consider
Because symptoms are often nonspecific, diagnosis is frequently delayed. Epidural abscess is commonly misdiagnosed as benign musculoskeletal back pain. Other considerations include vertebral osteomyelitis, spinal tumors, meningitis, discitis, pyelonephritis, spinal cord compression, ischemia, and disc herniation. In children, fever with back pain should prompt urgent imaging.
Prehospital And Early Management
Spinal immobilization is recommended when trauma or fracture is suspected.
Initial Stabilization Strategy
Prompt initiation of broad-spectrum intravenous antibiotics is essential and should cover Staphylococcus aureus, streptococci, and gram-negative organisms. Vancomycin combined with a third-generation cephalosporin is an appropriate initial regimen. Coverage for Pseudomonas species is indicated in patients with intravenous drug use. Anaerobic coverage may be added when clinically indicated.
Emergency Department Management
Urgent imaging is mandatory once epidural abscess is suspected, as delays worsen neurologic outcomes. If the level of infection cannot be localized clinically, imaging of the entire spine should be considered. Neurosurgical consultation or transfer to a facility with neurosurgical capability is required. Surgical decompression is often definitive, though select patients may be managed conservatively with prolonged intravenous antibiotics.
Antimicrobial Therapy
Common empiric regimens include vancomycin with ceftazidime, with metronidazole added if anaerobic infection is suspected. Antibiotic therapy should be adjusted based on culture results.
Disposition And Hospitalization
All patients with confirmed or strongly suspected epidural abscess require hospital admission. Emergent MRI and neurosurgical evaluation are mandatory. Discharge from the emergency department is not appropriate in these cases.
Referral And Transfer Considerations
Patients should be managed at centers with MRI availability and neurosurgical expertise. If transfer is required, blood cultures should be obtained and antibiotics initiated prior to transfer unless this would delay care.
Clinical Insights And Common Errors
Epidural abscess may recur, particularly in immunocompromised patients. Any patient with staphylococcal bacteremia and back pain or neurologic symptoms should be evaluated for epidural abscess. Failure to image the correct spinal region is a frequent error; careful neurologic and spinal examination can guide imaging, but when localization is unclear, imaging the entire spine is warranted.
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Emergency And Acute Medicine - Epidural Hematoma
Fundamental Overview
An epidural hematoma results from direct trauma to the skull, where inward deformation of the calvarium causes separation of the dura from the inner skull surface and subsequent bleeding. The middle meningeal artery is responsible for more than half of cases, while meningeal venous bleeding accounts for approximately one third. Skull fractures are present in about 75% of patients, though they are less common in children.
More than half of patients have epidural hematoma as an isolated head injury, but it is frequently associated with subdural hematoma or cerebral contusion. On noncontrast CT imaging, the classic appearance is a lenticular (biconvex), unilateral collection, most often in the temporal region. The hematoma typically does not cross suture lines, though midline extension may occur.
Causation And Epidemiology
Epidural hematoma accounts for approximately 1.5% of traumatic brain injuries. The condition is more common in males, with a male-to-female ratio of about 3:1, and peak incidence occurs in the second and third decades of life. Motor vehicle collisions, assaults, and falls are the most frequent causes, with assault having the highest association with intracranial injury requiring neurosurgical intervention.
The condition is uncommon in very young children under five years of age and in elderly patients. Overall mortality is approximately 12% and is strongly correlated with the patient’s neurologic status prior to surgical intervention.
Pediatric-Specific Considerations
Head injury remains the leading cause of death and acquired disability in children. Falls and pedestrian or bicycle-related accidents are common mechanisms, while the most severe injuries are typically related to motor vehicle accidents. Nonaccidental trauma must always be considered.
Less than half of children with epidural hematoma present with altered consciousness. If epidural hematoma is part of the differential diagnosis, CT imaging is warranted regardless of mental status. Pediatric bleeding is more often venous in origin, and posterior fossa epidural hematomas occur more frequently than in adults. Children younger than five years generally have excellent outcomes, with recovery rates approaching 95%.
Clinical Manifestations
Patients often present with altered or progressively worsening level of consciousness. Approximately 85% experience loss of consciousness at some point during their clinical course, though only 11–30% demonstrate a classic lucid interval. Nausea and vomiting occur in roughly 40% of cases.
Unique Pediatric Presentations
In infants, the most notable sign may be a significant drop in hematocrit, sometimes as high as 40%. A bulging fontanelle accompanied by vomiting, seizures, or lethargy is highly suggestive. Fewer than half of pediatric patients lose consciousness at the time of injury.
Examination Findings
Ipsilateral pupillary dilation is seen in 20–40% of patients, most commonly on the same side as the hematoma. Hemiparesis occurs in more than one third of cases and is typically contralateral to the lesion.
Essential Diagnostic Priorities
Prompt neuroimaging is mandatory when epidural hematoma is suspected.
Diagnostic Studies And Interpretation
Laboratory evaluation may include arterial blood gas, complete blood count, serum chemistries, and coagulation studies, along with toxicology screening when appropriate.
Noncontrast CT of the head is the diagnostic modality of choice, typically revealing a smooth-bordered, biconvex hematoma. Mixed-density lesions suggest active bleeding. Temporal and parietal regions are most commonly involved. CT with bone windows is useful for detecting associated skull fractures. Additional imaging and trauma evaluation should be guided by clinical findings.
In infants with open fontanelles, ultrasound may be used as an adjunct diagnostic tool.
Conditions To Differentiate From
Recent head trauma strongly supports the diagnosis, though trauma may appear minor in infants and toddlers. Other considerations include subdural hematoma, cerebral concussion or contusion, intracerebral hemorrhage, diffuse axonal injury, subdural hygroma, abusive head trauma, and toxic, metabolic, or infectious etiologies.
Prehospital Management Principles
Patients with head injury demonstrate improved survival when transported to designated trauma centers. Spinal immobilization is essential, and adequate oxygenation must be ensured during transport. Airway protection and intubation may be required.
Initial Stabilization Approach
Avoidance of hypoxia and hypotension is critical. Rapid-sequence intubation is indicated for neurologic deterioration or signs of increased intracranial pressure. Controlled ventilation should target a PaCO₂ of 35–40 mm Hg, with hyperventilation reserved for impending herniation. Agents known to increase intracranial pressure should be avoided.
The head of the bed should be elevated 20–30 degrees after volume resuscitation. A rapid neurologic assessment including Glasgow Coma Scale scoring is required. Associated injuries are common and should be identified during secondary survey.
Emergency Department Interventions
Early neurosurgical intervention, ideally within four hours, significantly improves survival in comatose patients. Burr hole placement is often performed at the fracture site or ipsilateral to pupillary dilation, with craniectomy reserved for uncontrolled bleeding.
Conservative management in asymptomatic patients carries a high risk of deterioration, with more than 30% ultimately requiring surgery. Patients should be maintained euvolemic with isotonic fluids, and continuous end-tidal CO₂ monitoring is recommended. Arterial line placement and Foley catheterization facilitate close physiologic monitoring.
Intracranial pressure control includes adequate sedation, neuromuscular blockade when intubated, and osmotic therapy once euvolemia is achieved. Blood pressure and glucose control are essential, and seizure prophylaxis or treatment should be initiated. Steroids, prophylactic antibiotics, routine hyperventilation, and calcium channel blockers have not shown benefit.
Outcome Predictors
Poor prognosis is associated with age over 40 years, large or rapidly expanding hematomas, significant midline shift, low admission Glasgow Coma Scale score, prolonged pupillary asymmetry, elevated postoperative intracranial pressure, and associated brain or systemic injuries.
Medication Therapy
Commonly used agents include benzodiazepines for seizure control, antiepileptic drugs for prophylaxis, osmotic diuretics for intracranial pressure reduction, antihypertensives for blood pressure control, sedatives, neuromuscular blockers, and induction agents appropriate for neurocritical care. Hypertonic saline has shown benefit in selected pediatric patients.
Disposition And Monitoring
All patients with epidural hematoma or altered consciousness require admission to an intensive care setting with frequent neurologic assessments. Repeat CT imaging should be performed within 12–24 hours or sooner if clinical deterioration occurs. Patients at highest risk include those with skull fractures, rapid bleeding, low Glasgow Coma Scale scores, or focal neurologic deficits.
Discharge from the emergency department is not appropriate for patients with epidural hematoma.
Fundamental Overview
An epidural hematoma results from direct trauma to the skull, where inward deformation of the calvarium causes separation of the dura from the inner skull surface and subsequent bleeding. The middle meningeal artery is responsible for more than half of cases, while meningeal venous bleeding accounts for approximately one third. Skull fractures are present in about 75% of patients, though they are less common in children.
More than half of patients have epidural hematoma as an isolated head injury, but it is frequently associated with subdural hematoma or cerebral contusion. On noncontrast CT imaging, the classic appearance is a lenticular (biconvex), unilateral collection, most often in the temporal region. The hematoma typically does not cross suture lines, though midline extension may occur.
Causation And Epidemiology
Epidural hematoma accounts for approximately 1.5% of traumatic brain injuries. The condition is more common in males, with a male-to-female ratio of about 3:1, and peak incidence occurs in the second and third decades of life. Motor vehicle collisions, assaults, and falls are the most frequent causes, with assault having the highest association with intracranial injury requiring neurosurgical intervention.
The condition is uncommon in very young children under five years of age and in elderly patients. Overall mortality is approximately 12% and is strongly correlated with the patient’s neurologic status prior to surgical intervention.
Pediatric-Specific Considerations
Head injury remains the leading cause of death and acquired disability in children. Falls and pedestrian or bicycle-related accidents are common mechanisms, while the most severe injuries are typically related to motor vehicle accidents. Nonaccidental trauma must always be considered.
Less than half of children with epidural hematoma present with altered consciousness. If epidural hematoma is part of the differential diagnosis, CT imaging is warranted regardless of mental status. Pediatric bleeding is more often venous in origin, and posterior fossa epidural hematomas occur more frequently than in adults. Children younger than five years generally have excellent outcomes, with recovery rates approaching 95%.
Clinical Manifestations
Patients often present with altered or progressively worsening level of consciousness. Approximately 85% experience loss of consciousness at some point during their clinical course, though only 11–30% demonstrate a classic lucid interval. Nausea and vomiting occur in roughly 40% of cases.
Unique Pediatric Presentations
In infants, the most notable sign may be a significant drop in hematocrit, sometimes as high as 40%. A bulging fontanelle accompanied by vomiting, seizures, or lethargy is highly suggestive. Fewer than half of pediatric patients lose consciousness at the time of injury.
Examination Findings
Ipsilateral pupillary dilation is seen in 20–40% of patients, most commonly on the same side as the hematoma. Hemiparesis occurs in more than one third of cases and is typically contralateral to the lesion.
Essential Diagnostic Priorities
Prompt neuroimaging is mandatory when epidural hematoma is suspected.
Diagnostic Studies And Interpretation
Laboratory evaluation may include arterial blood gas, complete blood count, serum chemistries, and coagulation studies, along with toxicology screening when appropriate.
Noncontrast CT of the head is the diagnostic modality of choice, typically revealing a smooth-bordered, biconvex hematoma. Mixed-density lesions suggest active bleeding. Temporal and parietal regions are most commonly involved. CT with bone windows is useful for detecting associated skull fractures. Additional imaging and trauma evaluation should be guided by clinical findings.
In infants with open fontanelles, ultrasound may be used as an adjunct diagnostic tool.
Conditions To Differentiate From
Recent head trauma strongly supports the diagnosis, though trauma may appear minor in infants and toddlers. Other considerations include subdural hematoma, cerebral concussion or contusion, intracerebral hemorrhage, diffuse axonal injury, subdural hygroma, abusive head trauma, and toxic, metabolic, or infectious etiologies.
Prehospital Management Principles
Patients with head injury demonstrate improved survival when transported to designated trauma centers. Spinal immobilization is essential, and adequate oxygenation must be ensured during transport. Airway protection and intubation may be required.
Initial Stabilization Approach
Avoidance of hypoxia and hypotension is critical. Rapid-sequence intubation is indicated for neurologic deterioration or signs of increased intracranial pressure. Controlled ventilation should target a PaCO₂ of 35–40 mm Hg, with hyperventilation reserved for impending herniation. Agents known to increase intracranial pressure should be avoided.
The head of the bed should be elevated 20–30 degrees after volume resuscitation. A rapid neurologic assessment including Glasgow Coma Scale scoring is required. Associated injuries are common and should be identified during secondary survey.
Emergency Department Interventions
Early neurosurgical intervention, ideally within four hours, significantly improves survival in comatose patients. Burr hole placement is often performed at the fracture site or ipsilateral to pupillary dilation, with craniectomy reserved for uncontrolled bleeding.
Conservative management in asymptomatic patients carries a high risk of deterioration, with more than 30% ultimately requiring surgery. Patients should be maintained euvolemic with isotonic fluids, and continuous end-tidal CO₂ monitoring is recommended. Arterial line placement and Foley catheterization facilitate close physiologic monitoring.
Intracranial pressure control includes adequate sedation, neuromuscular blockade when intubated, and osmotic therapy once euvolemia is achieved. Blood pressure and glucose control are essential, and seizure prophylaxis or treatment should be initiated. Steroids, prophylactic antibiotics, routine hyperventilation, and calcium channel blockers have not shown benefit.
Outcome Predictors
Poor prognosis is associated with age over 40 years, large or rapidly expanding hematomas, significant midline shift, low admission Glasgow Coma Scale score, prolonged pupillary asymmetry, elevated postoperative intracranial pressure, and associated brain or systemic injuries.
Medication Therapy
Commonly used agents include benzodiazepines for seizure control, antiepileptic drugs for prophylaxis, osmotic diuretics for intracranial pressure reduction, antihypertensives for blood pressure control, sedatives, neuromuscular blockers, and induction agents appropriate for neurocritical care. Hypertonic saline has shown benefit in selected pediatric patients.
Disposition And Monitoring
All patients with epidural hematoma or altered consciousness require admission to an intensive care setting with frequent neurologic assessments. Repeat CT imaging should be performed within 12–24 hours or sooner if clinical deterioration occurs. Patients at highest risk include those with skull fractures, rapid bleeding, low Glasgow Coma Scale scores, or focal neurologic deficits.
Discharge from the emergency department is not appropriate for patients with epidural hematoma.
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Emergency And Acute Medicine - 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 – Failure To Thrive
Overview And Definitions
Failure to thrive (FTT) is not a single diagnosis but a descriptive term encompassing a spectrum of conditions characterized by inadequate physical growth, most often identified before two years of age. It is broadly categorized into organic causes, in which an underlying medical condition is present, and nonorganic causes, where no identifiable medical etiology exists. Although FTT occurs across all socioeconomic groups, poverty significantly increases risk. Early-life FTT, particularly in the first few months, may lead to long-term growth impairment as well as behavioral and developmental consequences.
Etiology And Pathophysiology
Failure to thrive results from one or more fundamental mechanisms including insufficient caloric intake, impaired caloric absorption or malabsorption, or excessive caloric expenditure. These mechanisms are frequently secondary to chronic medical conditions but may also arise from psychosocial or environmental factors.
Clinical Presentation
There is no universally accepted definition of failure to thrive. Common criteria include weight below two standard deviations for age and sex, adjusted for prematurity, or a downward crossing of two major percentile lines on standardized growth charts. A change in growth velocity affecting one or more parameters is typical. Weight is usually affected first, followed by length or height, and finally head circumference in cases of prolonged caloric deficiency. Isolated linear growth failure often suggests endocrine disease, while impaired head circumference growth points toward a primary neurologic condition. Physical manifestations may include muscle wasting, loss of subcutaneous fat, alopecia, dermatitis, chronic illness states such as marasmus or kwashiorkor, endocrinologic abnormalities, developmental delay, and increased susceptibility to infection.
History And Physical Examination
A detailed feeding history is essential, including breast-feeding practices, formula type and preparation, feeding frequency, volume, and introduction of solids. Associated vomiting, urine and stool output, and blood in stool should be assessed. Prenatal and birth history should include maternal illness, substance exposure, gestational age, birth weight, and congenital anomalies. Developmental progress, temperament, and psychosocial context including family support, stressors, maternal depression, and possible abuse or neglect must be evaluated. Physical examination requires accurate measurement and plotting of weight, length or height, and head circumference on appropriate growth charts, ideally with multiple prior data points. Examination should assess for dysmorphic features, signs of cardiac, pulmonary, gastrointestinal, or neurologic disease, and indicators of maltreatment.
Essential Evaluation
Evaluation centers on a thorough history and physical examination, accurate growth chart analysis, direct observation of feeding, and assessment of caregiver–child interaction. Initial laboratory testing may include complete blood count, inflammatory markers, electrolytes, urinalysis and culture, and lead level when indicated.
Diagnostic Studies And Interpretation
Laboratory evaluation may reveal anemia, infection, malignancy, metabolic derangements, renal disease, endocrine disorders, or lead toxicity. Review of newborn screening results is often informative. Additional testing may include blood gas analysis, HIV testing, stool studies, imaging such as chest radiography, bone age assessment, and targeted diagnostic procedures including pH probe studies, sweat chloride testing, or tuberculin skin testing based on clinical suspicion.
Differential Diagnosis
Organic causes include gastrointestinal disorders such as malabsorption, celiac disease, cystic fibrosis, inflammatory bowel disease, anatomic obstruction, gastroesophageal reflux, and nutritional deficiencies; cardiac disease; chronic pulmonary disease; hematologic or oncologic conditions; renal disease; neurologic disorders; immunodeficiency; endocrine abnormalities; infectious etiologies; genetic syndromes; and toxic exposures. Nonorganic causes include feeding technique errors, inadequate food availability, psychosocial stressors, caregiver mental illness or substance use, parent–child interaction disorders, neglect, and fabricated illness by proxy.
Management And Initial Therapy
Initial management includes assessment for hypoglycemia and dehydration with prompt correction when present. A supportive, nonjudgmental approach is essential. Emergency department care focuses on identifying FTT, excluding urgent organic pathology, engaging social services when appropriate, and providing feeding support including lactation consultation.
Disposition And Follow Up
Hospital admission is indicated for children with significant organic disease, severe malnutrition, dehydration, electrolyte imbalance, suspected abuse or neglect, or when observation of feeding and caregiver interaction is required. Infants younger than three to six months warrant a lower threshold for admission due to neurodevelopmental vulnerability. Discharge is appropriate when close outpatient follow-up is assured and growth monitoring can be reliably maintained. Referral to appropriate subspecialists should be arranged based on the suspected etiology.
Key Clinical Insights And Common Errors
Failure to thrive is a descriptive finding rather than a diagnosis and often reflects an underlying medical or psychosocial issue. Weight loss typically precedes declines in length and head circumference. Normal laboratory results do not exclude serious nonorganic causes. Abrupt changes in growth trajectory should raise concern for organic disease. Early recognition and intervention are critical to prevent long-term developmental sequelae, and clinicians must remain vigilant for neglect or abuse while maintaining a supportive and unbiased approach.
Overview And Definitions
Failure to thrive (FTT) is not a single diagnosis but a descriptive term encompassing a spectrum of conditions characterized by inadequate physical growth, most often identified before two years of age. It is broadly categorized into organic causes, in which an underlying medical condition is present, and nonorganic causes, where no identifiable medical etiology exists. Although FTT occurs across all socioeconomic groups, poverty significantly increases risk. Early-life FTT, particularly in the first few months, may lead to long-term growth impairment as well as behavioral and developmental consequences.
Etiology And Pathophysiology
Failure to thrive results from one or more fundamental mechanisms including insufficient caloric intake, impaired caloric absorption or malabsorption, or excessive caloric expenditure. These mechanisms are frequently secondary to chronic medical conditions but may also arise from psychosocial or environmental factors.
Clinical Presentation
There is no universally accepted definition of failure to thrive. Common criteria include weight below two standard deviations for age and sex, adjusted for prematurity, or a downward crossing of two major percentile lines on standardized growth charts. A change in growth velocity affecting one or more parameters is typical. Weight is usually affected first, followed by length or height, and finally head circumference in cases of prolonged caloric deficiency. Isolated linear growth failure often suggests endocrine disease, while impaired head circumference growth points toward a primary neurologic condition. Physical manifestations may include muscle wasting, loss of subcutaneous fat, alopecia, dermatitis, chronic illness states such as marasmus or kwashiorkor, endocrinologic abnormalities, developmental delay, and increased susceptibility to infection.
History And Physical Examination
A detailed feeding history is essential, including breast-feeding practices, formula type and preparation, feeding frequency, volume, and introduction of solids. Associated vomiting, urine and stool output, and blood in stool should be assessed. Prenatal and birth history should include maternal illness, substance exposure, gestational age, birth weight, and congenital anomalies. Developmental progress, temperament, and psychosocial context including family support, stressors, maternal depression, and possible abuse or neglect must be evaluated. Physical examination requires accurate measurement and plotting of weight, length or height, and head circumference on appropriate growth charts, ideally with multiple prior data points. Examination should assess for dysmorphic features, signs of cardiac, pulmonary, gastrointestinal, or neurologic disease, and indicators of maltreatment.
Essential Evaluation
Evaluation centers on a thorough history and physical examination, accurate growth chart analysis, direct observation of feeding, and assessment of caregiver–child interaction. Initial laboratory testing may include complete blood count, inflammatory markers, electrolytes, urinalysis and culture, and lead level when indicated.
Diagnostic Studies And Interpretation
Laboratory evaluation may reveal anemia, infection, malignancy, metabolic derangements, renal disease, endocrine disorders, or lead toxicity. Review of newborn screening results is often informative. Additional testing may include blood gas analysis, HIV testing, stool studies, imaging such as chest radiography, bone age assessment, and targeted diagnostic procedures including pH probe studies, sweat chloride testing, or tuberculin skin testing based on clinical suspicion.
Differential Diagnosis
Organic causes include gastrointestinal disorders such as malabsorption, celiac disease, cystic fibrosis, inflammatory bowel disease, anatomic obstruction, gastroesophageal reflux, and nutritional deficiencies; cardiac disease; chronic pulmonary disease; hematologic or oncologic conditions; renal disease; neurologic disorders; immunodeficiency; endocrine abnormalities; infectious etiologies; genetic syndromes; and toxic exposures. Nonorganic causes include feeding technique errors, inadequate food availability, psychosocial stressors, caregiver mental illness or substance use, parent–child interaction disorders, neglect, and fabricated illness by proxy.
Management And Initial Therapy
Initial management includes assessment for hypoglycemia and dehydration with prompt correction when present. A supportive, nonjudgmental approach is essential. Emergency department care focuses on identifying FTT, excluding urgent organic pathology, engaging social services when appropriate, and providing feeding support including lactation consultation.
Disposition And Follow Up
Hospital admission is indicated for children with significant organic disease, severe malnutrition, dehydration, electrolyte imbalance, suspected abuse or neglect, or when observation of feeding and caregiver interaction is required. Infants younger than three to six months warrant a lower threshold for admission due to neurodevelopmental vulnerability. Discharge is appropriate when close outpatient follow-up is assured and growth monitoring can be reliably maintained. Referral to appropriate subspecialists should be arranged based on the suspected etiology.
Key Clinical Insights And Common Errors
Failure to thrive is a descriptive finding rather than a diagnosis and often reflects an underlying medical or psychosocial issue. Weight loss typically precedes declines in length and head circumference. Normal laboratory results do not exclude serious nonorganic causes. Abrupt changes in growth trajectory should raise concern for organic disease. Early recognition and intervention are critical to prevent long-term developmental sequelae, and clinicians must remain vigilant for neglect or abuse while maintaining a supportive and unbiased approach.
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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.
