KembaraXtra-Medicine – Anaphylaxis




Anaphylaxis is a severe, rapid-onset, life-threatening allergic reaction. It occurs when IgE-mediated and non–IgE-mediated systemic mast cell degranulation leads to release of inflammatory mediators, producing respiratory, cardiovascular, gastrointestinal, and/or mucocutaneous symptoms. A common synonym is anaphylactic reaction. Relevant ICD-10CM codes include T78.2 (anaphylactic shock, unspecified, initial encounter), T78.00XA (anaphylactic reaction due to unspecified food, initial encounter), T80.52XA (anaphylactic reaction due to vaccination, initial encounter), and T63.94XA (toxic effect of contact with unspecified venomous animal, undetermined, initial encounter).


In the United States, the incidence is estimated at 50 to 2000 episodes per 100,000 persons, with a lifetime prevalence of 1.6% to 5.1%. Emergency department visits for anaphylaxis increased by 101% from 2005 to 2014, yet fatalities have remained stable at about 0.7 per million adults per year. In adults, medications and insect stings are leading triggers, while in children and adolescents, foods and insect stings are the leading triggers.


Risk factors depend on the trigger and severity. Atopy increases risk for anaphylaxis triggered by food, exercise, and latex. Risk factors for severe anaphylaxis include cardiovascular disease, asthma, older age, mast cell disorder, beta-blocker use, and ACE inhibitor use.


Clinical presentation commonly includes involvement across multiple systems. Mucocutaneous findings include urticaria, pruritus, flushing, and angioedema. Respiratory symptoms include dyspnea, cough, wheezing, hypoxia, stridor, and rhinitis. Cardiovascular features include hypotension, tachycardia, weakness, dizziness, syncope, malaise, and vascular collapse. Gastrointestinal symptoms include nausea, vomiting, diarrhea, dysphagia, and abdominal pain.


Anaphylaxis results from a sudden systemic release of histamine and other mediators from basophils and mast cells via IgE-dependent and non–IgE-dependent mechanisms, and almost any substance can trigger it. In acute settings, the cause is often not identified, accounting for 30% to 60% of cases. Common triggers include foods and additives (notably peanuts, tree nuts, eggs, shellfish, fish, cow’s milk, fruits, soy). A notable food-related mechanism is alpha-gal syndrome, where a lone star tick bite can cause IgE sensitization to alpha-1,3-galactose, leading to delayed anaphylaxis after eating mammalian (red meat) products. Medication triggers include antibiotics (especially penicillins and sulfa agents), insulin, allergen extracts, opiates, vaccines, NSAIDs, contrast media, streptokinase, immunomodulators, and IV iron. Environmental exposures include bee/wasp stings, snake venom, and fire ant venom. Other triggers include blood products (plasma, immunoglobulin, cryoprecipitate, whole blood), latex, and exercise. Mechanistically, immune (often IgE-mediated) triggers include foods, venoms, many medications, latex, seminal fluid, and sometimes radiocontrast; IgE-independent immune triggers include radiocontrast (in most cases), dextrans, some monoclonal antibodies (e.g., rituximab), and some medications; and nonimmunologic triggers include certain drugs such as opioids and protamine. “Idiopathic” anaphylaxis refers to cases where known causes (including mastocytosis) have been excluded. Non–IgE mechanisms may involve complement activation, kinin production, potentiation, or direct mediator release, and more than one mechanism can occur together (for example, exercise-induced reactions following food). ACE inhibitors are a notable cause of unexplained angioedema, occurring in up to 1 in 200 users and may occur at any time after starting the medication.


The differential diagnosis is broad and includes allergic reactions without anaphylaxis, other causes of shock such as sepsis or pulmonary embolism, endocrine conditions such as carcinoid, adrenal crisis, paradoxical pheochromocytoma, systemic mastocytosis, serum sickness, severe asthma (distinguished by abrupt onset in anaphylaxis versus progressive worsening), scombroid poisoning, localized angioedema, acute urticaria, vasovagal/presyncopal syndromes, airway foreign body, vocal cord dysfunction, and anxiety-related symptoms such as globus hystericus.


Workup is mainly aimed at excluding mimics, but treatment should never be delayed because anaphylaxis can be rapidly fatal. Diagnosis is primarily clinical. Laboratory testing is generally not helpful in the emergency setting, though serum/urine histamine and serum tryptase (drawn 30 minutes to 2 hours after symptom onset and compared with baseline) may support the diagnosis; importantly, normal levels do not exclude anaphylaxis and these tests may not be readily available. Imaging is usually not helpful; chest radiography is considered when evaluating foreign body aspiration or pulmonary pathology in acute respiratory compromise. An ECG should be considered in patients with sudden loss of consciousness, chest pain, dyspnea, and in elderly patients; ECG typically shows sinus tachycardia.


Clinical criteria make anaphylaxis highly likely when any one of the following is met: (1) an acute illness with skin/mucosal involvement plus either respiratory compromise or reduced blood pressure/end-organ dysfunction symptoms; (2) rapid onset of two or more after exposure to a likely allergen--skin/mucosal involvement, respiratory compromise, reduced blood pressure, or persistent GI symptoms such as crampy abdominal pain/vomiting; or (3) reduced blood pressure after exposure to a known allergen--age-specific hypotension or >30% systolic BP decrease in infants/children, or systolic BP <90 mm hg or>30% decrease from baseline in adults.


Immediate nonpharmacologic treatment begins with removing the trigger, rapidly establishing and protecting the airway, providing supplemental oxygen if needed, obtaining IV access, giving IV fluids (normal saline), and placing the patient on cardiac monitoring.


The cornerstone medication is intramuscular epinephrine. Adults and children >30 kg should receive 0.3 to 0.5 mg IM epinephrine (1:1000 concentration) in the anterolateral thigh; anyone >50 kg should receive 0.5 mg IM. Children <30 kg should receive 0.01 mg />g IM epinephrine (1:1000 concentration). IM administration is preferred because it produces a faster and more reliable rise to effective plasma levels, and the dose can be repeated within minutes if symptoms do not improve. Adjunct therapies include H1 and H2 antihistamines such as diphenhydramine and famotidine to improve itching and erythema, but they do not reverse airway obstruction, respiratory compromise, or hypotension, and their onset is delayed 1–2 hours. Corticosteroids do not help acutely because of slow onset and have not been shown to prevent prolonged or biphasic anaphylaxis, but they are commonly used as secondary treatment. Aerosolized beta-agonists help treat bronchospasm. If hypotension or cardiovascular collapse persists despite fluids and IM epinephrine, IV epinephrine (1:10,000 concentration) is used as vasopressor therapy, and small IV boluses may be used in the peri-arrest state. Patients on beta-blockers may respond poorly to initial treatment; in these cases, IV glucagon should be considered.


Disposition depends on severity and risk of recurrence. Patients with mild episodes should be observed for 1 hour after symptom resolution. Patients with severe symptoms—including cyanosis, pulse oximetry <92%, systolic bp <90 mm hg, confusion, loss of consciousness, or incontinence—those needing more than one epinephrine dose, those with a wide pulse pressure, unknown trigger, cutaneous signs />ymptoms, or a medication trigger in children should be observed for at least 6 hours to watch for biphasic anaphylaxis.


For discharge planning and chronic management, patients who are stable and remain asymptomatic should be prescribed two epinephrine autoinjectors, with clear instructions on when and how to use them. Referral to an allergist is helpful when the trigger is unclear in the emergency setting. Patient education is essential: a prior history of anaphylaxis or known triggers is the most reliable way to identify risk. Patients should be instructed to carry an epinephrine device at all times; school-aged children should have an additional autoinjector available at school with appropriate staff. Patients should also be advised to wear or carry MedicAlert identification listing substances that have triggered anaphylaxis. People with prior contrast reactions should avoid radiologic contrast when possible; however, pretreatment regimens with methylprednisolone or diphenhydramine may be used when contrast is unavoidable. For insect-sting anaphylaxis, venom immunotherapy initiated after the event is effective and is recommended for up to 5 years after the incident.

Emergency And Acute Medicine – Inborn Errors Of Metabolism


Basics
Description Inborn errors of metabolism are inherited defects in metabolic pathways that lead to abnormal accumulation or deficiency of metabolites. More than 400 disorders are described, most presenting in infancy or childhood with variable and often nonspecific findings. Incidence ranges from 1:10,000 to 1:200,000 births. Major categories include amino acid disorders, urea cycle defects, organic acidemias, fatty acid oxidation defects, mitochondrial disorders, carbohydrate disorders, lysosomal storage diseases, peroxisomal disorders, and disorders of protein glycosylation. Pathophysiology relates directly to enzymatic or transport defects within metabolic pathways.
Etiology Genetic deficiency of enzymes or membrane transport systems involved in intermediary metabolism.


Diagnosis
Signs and symptoms Presentation may be acute and catastrophic or chronic and indolent. Neonates may initially be asymptomatic or present with hypothermia (mitochondrial defects), hypotonia or hypertonia (peroxisomal disorders), apnea (urea cycle defects, organic acidemias), seizures, vomiting, poor feeding, jaundice, hypoglycemia, dysmorphic features, or coma. Older untreated children may present with failure to thrive, dehydration, recurrent vomiting or diarrhea, food intolerance, lethargy, ataxia, seizures, or developmental delay.
History Review newborn screening results, dietary history, family history, consanguinity, and intercurrent illness.
Physical exam May reveal abnormal odor, altered mental status, tachypnea, dysmorphic facies, cataracts, cardiomyopathy, hepatosplenomegaly, dermatitis, or jaundice.


Essential workup Consider in any child with unexplained neurologic deterioration, persistent vomiting, metabolic acidosis, hypoglycemia, shock unresponsive to resuscitation, or failure to thrive.


Diagnosis tests and interpretation
Lab Bedside glucose, electrolytes, BUN/creatinine, CBC, calcium, liver function tests, bilirubin, coagulation studies, blood gas, lactate, pyruvate, uric acid, urinalysis, ammonia, serum amino acids, urine organic acids, and cultures as indicated.
Imaging CT head for altered mental status; chest radiograph as indicated.
Procedures Lumbar puncture when infection is a concern.


Differential diagnosis Sepsis, meningitis, encephalitis, dehydration, toxic ingestion, nonaccidental trauma, Reye syndrome, hepatic encephalopathy, endocrine disorders, renal failure, renal tubular acidosis, CNS mass lesions.


Treatment
Prehospital Prioritize ABCs and bedside glucose. Start IV glucose immediately; do not delay for fluids unless in shock. Avoid lactated Ringer solution. Keep patient NPO.
Initial stabilization Administer glucose (after Accu-Chek and thiamine when appropriate) and naloxone for altered mental status.
Emergency department management Secure airway, breathing, and circulation. Use normal saline for fluid boluses and avoid hypotonic fluids and lactated Ringer. Initiate IV glucose at 8–10 mg/kg/min (D10 at 1.5× maintenance) to prevent catabolism. Treat severe hypoglycemia with D25 bolus. Correct dehydration and acid–base abnormalities; consider bicarbonate only if pH <7.0. initiate dialysis for refractory severe acidosis or hyperammonemia. stop all oral intake initially. treat hyperammonemia urgently with ammonia-scavenging agents (arginine, sodium benzoate, phenylacetate, phenylbutyrate) in consultation a metabolic specialist. identify and precipitating infections.< />pan>


Medication D25 2–4 mL/kg IV for hypoglycemia, sodium bicarbonate 1–2 mEq/kg IV for severe acidosis, disease-specific therapies such as levocarnitine or pyridoxine as indicated.
First line IV glucose infusion with normal saline as needed for shock.
Second line Bicarbonate therapy for pH <7.0 and hemodialysis when indicated.< />pan>


Follow-up and disposition
Admission criteria All infants and children with suspected inborn errors of metabolism, significant ketosis, inability to tolerate oral intake, altered mental status, severe or persistent acidosis, refractory hypoglycemia, or hyperammonemia; ICU care for severe presentations. Transfer to a specialized pediatric center is often required.
Discharge criteria Normal mental status, adequate hydration, reassuring laboratory results, no significant intercurrent illness, and close follow-up arranged.
Follow-up recommendations Ongoing care with a metabolic disease specialist and primary care physician.


Pearls and pitfalls Always consider metabolic disease in unexplained pediatric decompensation. Do not delay glucose infusion. Avoid lactated Ringer solution. Use bicarbonate cautiously and only for severe acidosis. Early dialysis can be lifesaving in hyperammonemia.

Emergency And Acute Medicine – Impetigo


Basics
Description Impetigo is a common superficial bacterial skin infection. It may be a primary infection of minor skin breaks or a secondary infection of preexisting dermatoses (impetiginization). It is most prevalent in children aged 2–5 years and occurs more often in warm, humid climates and summer months. Predisposing factors include minor trauma (especially around the nose), insect bites, burns, diabetes mellitus, HIV infection, varicella, and chronic skin disease. Complications include acute poststreptococcal glomerulonephritis (1–5% of nonbullous cases), cellulitis, sepsis, endocarditis, toxic shock syndrome, and staphylococcal scalded skin syndrome.


Etiology
Classic (nonbullous) impetigo results from bacterial entry through disrupted skin and is caused by Staphylococcus aureus, group A β-hemolytic streptococci, or both. Bullous impetigo is caused exclusively by S. aureus producing exfoliative toxins (A, B, D) that cleave desmoglein 1, leading to intraepidermal blistering.


Diagnosis
Signs and symptoms Nonbullous impetigo begins as erythematous macules or papules that evolve into vesicles or pustules, which rupture and form characteristic honey-colored crusts. Lesions are highly contagious and often pruritic. Regional lymphadenopathy may occur; systemic symptoms are uncommon. Bullous impetigo presents with flaccid bullae containing clear or yellow fluid that rupture easily, leaving erythematous bases; Nikolsky sign is absent. Fever and systemic symptoms are rare.
Physical exam Lesions most commonly involve the face, extremities, and scalp. Diagnosis is clinical based on appearance and distribution.


Essential workup
Routine laboratory testing is not required. Consider bacterial culture of bullae or pustules for refractory disease, outbreak investigation, or suspected methicillin-resistant S. aureus.


Diagnosis tests and interpretation
Lab Anti–DNase B titers may be elevated in poststreptococcal glomerulonephritis. Urinalysis is indicated if hematuria or edema suggests nephritis.
Imaging and procedures Not routinely indicated; biopsy is rarely necessary.


Differential diagnosis
Herpes simplex, varicella zoster, atopic or contact dermatitis, dermatophytosis, candidiasis, scabies, folliculitis, erysipelas, bullous pemphigoid, pemphigus vulgaris, staphylococcal scalded skin syndrome, Stevens–Johnson syndrome, thermal burns, toxic epidermal necrolysis, and cutaneous anthrax.


Treatment
Prehospital Cover lesions and use universal precautions to prevent transmission.
Initial stabilization Impetigo is rarely life-threatening in otherwise healthy patients.
Emergency department management Local care includes gentle cleansing, removal of crusts, and wet dressings. Small, localized nonbullous lesions may be treated with topical antibiotics alone. Extensive disease, bullous impetigo, lymphadenopathy, systemic symptoms, or outbreak settings require systemic antibiotics. Empiric therapy should cover S. aureus and streptococci; adjust for MRSA based on local resistance patterns.


Medication
Topical (nonbullous only): mupirocin 2% TID for 10 days or retapamulin 1% BID for 5 days.
Oral options (10 days unless noted): amoxicillin–clavulanate, cephalexin, dicloxacillin, clindamycin, azithromycin (5-day course), or trimethoprim–sulfamethoxazole when MRSA suspected. Doxycycline may be used for MRSA in patients ≥8 years.


Follow-up and disposition
Admission criteria Rare; consider for widespread disease, extensive bullae or denuded skin, dehydration, treatment failure, toxic appearance, immunocompromise, or neonates.
Discharge criteria Nontoxic patients with reliable caregivers and ability to comply with therapy.
Follow-up recommendations Primary care follow-up to ensure resolution. Return for lack of improvement or signs of nephritis (hematuria, periorbital or leg edema).


Pearls and pitfalls
Use systemic antibiotics for bullous disease or lymphadenopathy. Rising antibiotic resistance limits older regimens; suspect mupirocin resistance with treatment failure and switch agents. Treat affected household contacts simultaneously to prevent reinfection.

​Emergency and Acute Medicine – Isopropanol poisoning
Isopropanol is a central nervous system depressant that is two to three times more potent than ethanol. It is rapidly absorbed after ingestion and is metabolized by alcohol dehydrogenase to acetone, which is also a CNS depressant. Unlike other toxic alcohols, isopropanol is ketogenic but does not cause a significant metabolic acidosis. Acetone is eliminated by the lungs and kidneys. The half-life of isopropanol ranges from 3 to 16 hours, while acetone has a longer half-life of 7.5 to 26 hours. Concomitant ethanol ingestion prolongs the half-life of isopropanol but not acetone.
Isopropanol is a clear, colorless, volatile liquid with a faint acetone odor and bitter taste, commonly found as 70% rubbing alcohol. It is present in many household and industrial products including disinfectants, hand sanitizers, solvents, window cleaners, paint removers, detergents, antifreeze, and toiletries. The typical adult patient is a chronic alcoholic who ingests isopropanol after depleting ethanol supplies. Dermal, inhalational, and rectal exposures can also cause systemic toxicity. Accidental ingestions are common in young children.
Symptoms usually develop within 30 to 60 minutes of exposure. Neurologic manifestations include lethargy, inebriation, vertigo, ataxia, headache, weakness, respiratory depression, coma, and apnea, without the initial excitatory phase seen with ethanol. Gastrointestinal findings include nausea, vomiting, abdominal pain, gastritis, and hematemesis. Cardiovascular effects include hypotension, tachycardia, myocardial depression, and peripheral vasodilation. Pulmonary findings include respiratory depression and hemorrhagic tracheobronchitis. Skin and eye exposure may cause irritation or chemical burns.
Diagnosis is based on history of exposure and the characteristic odor of isopropanol or acetone on the breath. Laboratory evaluation typically shows ketosis without significant acidosis unless end-organ hypoperfusion is present. Hypoglycemia may occur, particularly in children. Acetone can falsely elevate serum creatinine, which normalizes as acetone is metabolized. Urinalysis shows ketones, and an elevated osmolar gap is common. Coma is associated with serum isopropanol levels greater than 150 mg/dL. Imaging is guided by clinical findings, with chest radiography used to assess for aspiration and head CT considered for possible trauma.
Management is primarily supportive, with attention to airway protection, breathing, and circulation. Hypotension is treated with intravenous fluids and vasopressors if needed. There is no specific antidote, and treatment with ethanol or fomepizole is contraindicated. Activated charcoal may be considered if coingestants are suspected. Skin and eye exposures require copious irrigation. Hemodialysis effectively removes isopropanol and acetone and is reserved for patients with refractory hypotension, severe toxicity, or serum levels greater than 400 mg/dL.
Patients with moderate to severe toxicity, including altered mental status or hypotension, require hospital admission. Asymptomatic or mildly intoxicated patients may be observed for 2 to 4 hours and discharged if symptoms resolve. Referral for alcohol detoxification or psychiatric evaluation is recommended for intentional ingestions.
Supportive care remains the cornerstone of treatment, and a key pitfall is inappropriate use of ethanol or fomepizole, which should be avoided in isopropanol poisoning.

Infectious Diseases and Microbiology: Ear Pain
Basics
Description
Otalgia denotes pain originating in or perceived in the ear. Evaluation should consider patient age and associated symptoms such as sore throat, fever, headache, visual changes, and symptom duration. A systematic ear examination is essential, beginning with the auricle and external auditory meatus, followed by inspection of the auditory canal and tympanic membrane to guide the differential diagnosis. A complete head and neck examination may uncover lymphadenopathy, pharyngeal or nasal inflammation, thyroid disease, or dental and oral pathology. Cerumen can obstruct visualization of the tympanic membrane and should be gently removed when necessary. Any exudate within the auditory canal should be cultured. Pain elicited by movement of the pinna suggests otitis externa, foreign body, or impacted cerumen. Perichondritis, an infectious process of the outer ear cartilage, must be differentiated from relapsing polychondritis, a noninfectious rheumatologic condition.
Epidemiology
Approximately half of ear pain cases are referred from non-otologic sources. Acute otitis externa, commonly termed swimmer’s ear, occurs more frequently during summer months. Recurrent acute otitis media affects about one-fifth of children. Head and neck malignancies typically occur after age 50 but may present earlier, even without classic risk factors; several forms of nasopharyngeal carcinoma are associated with Epstein–Barr virus infection. Auricular cellulitis often follows minor trauma. Perichondritis usually develops after burns, trauma, or upper-ear piercings and is most commonly caused by Pseudomonas aeruginosa or Staphylococcus aureus. Chronic otitis externa often results from repeated minor trauma such as scratching or cotton swab use, and chronic middle-ear drainage may be mistaken for this condition. Malignant otitis externa is a destructive infection of the external canal and skull base.
Etiology
Ear pain is frequently referred because the ear receives sensory innervation from cranial nerves V, VII, VIII, IX, and X. Referred otalgia may arise from dental disease, gingival abscesses, nasopharyngeal or laryngeal inflammation or tumors, sinusitis, temporomandibular joint disorders, tonsillitis, tongue lesions, cervical spine disease, neural irritation such as trigeminal neuralgia or acoustic neuroma, gastroesophageal reflux in infants, thyroiditis, lateral sinus thrombosis, posterior fossa inflammation, or medication effects. Primary ear pathology causing otalgia includes acute or chronic otitis media, tympanic membrane rupture, anterior canal wall fracture, mastoiditis, Ménière disease, and eustachian tube dysfunction. Malignant otitis externa is almost always due to Pseudomonas aeruginosa. Otalgia may also accompany migraine, atypical facial pain, and herpes simplex infection of cranial nerves V, VII, or IX. Herpes zoster affecting the external auditory canal may produce ipsilateral facial paralysis, known as Ramsay Hunt syndrome, from involvement of the geniculate ganglion. Facial nerve palsy may also occur with Lyme disease. Neoplasms of the infratemporal fossa may present solely with ear pain. Acute otitis externa is most often caused by Pseudomonas aeruginosa, Staphylococcus aureus, or streptococcal species, with swimming and canal trauma as major risk factors.
Diagnosis
Clinical Manifestations
Auricular cellulitis presents with a swollen, erythematous, warm, mildly tender ear. Perichondritis causes marked swelling, redness, heat, and severe tenderness of the pinna with relative sparing of the lobule. Chronic otitis externa more commonly causes itching than pain. Nasopharyngeal carcinoma may be asymptomatic early but often produces unilateral serous otitis media from eustachian tube obstruction, nasal blockage, or epistaxis, and advanced disease may cause cranial nerve palsies, especially involving nerves III, IV, VI, and VII. Malignant otitis externa typically affects elderly patients with diabetes or individuals with HIV and presents with severe otalgia, otorrhea, possible hearing loss, tender pinna, trismus from temporomandibular involvement, and sometimes cranial nerve palsies, most often of nerve VII. Fever and weight loss are uncommon. Examination reveals canal edema, erythema, purulent discharge, debris, and granulation tissue. Vesicular lesions in the external canal suggest herpes zoster and warrant evaluation for facial nerve palsy. Hearing loss with abnormal tympanic membrane findings indicates serous or bacterial otitis media or cholesteatoma. Nasal polyps, marked septal deviation, or nasopharyngeal tumors may be associated with otitis media.
Physical Examination
Findings such as an erythematous canal with discharge, preauricular lymphadenopathy, and pain on tragal or pinna manipulation suggest otitis externa. Fever, irritability in children, and a bulging or erythematous tympanic membrane with loss of the cone of light indicate otitis media, sometimes with canal pus if perforation is present. Altered mental status or meningeal signs such as headache and neck stiffness indicate possible central nervous system involvement and require urgent management.
Diagnostic Tests and Interpretation
Laboratory Studies
Peripheral leukocytosis is uncommon in malignant otitis externa, whereas erythrocyte sedimentation rate is typically elevated. Cerebrospinal fluid analysis may occasionally show pleocytosis and increased protein.
Imaging
Dental pathology can be assessed with panoramic radiography. In malignant otitis externa, CT of the temporal bone or mastoid often demonstrates bony erosion and new bone formation, while MRI more accurately defines soft-tissue extension and skull-base involvement.
Treatment
Medications
Acute otitis externa is managed with careful canal cleaning and topical therapy using antiseptics or antibiotic drops such as polymyxin–neomycin, along with counseling on ear hygiene and water avoidance. Malignant otitis externa requires urgent otolaryngology consultation and prolonged antipseudomonal therapy with agents such as cefepime, ceftazidime, carbapenems, or fluoroquinolones, typically for at least three to four weeks and longer if bone involvement is present. Auricular cellulitis is treated with warm compresses and intravenous antibiotics targeting staphylococci and streptococci. Severe perichondritis requires extended antibiotic therapy, often with agents such as piperacillin–tazobactam or nafcillin combined with ciprofloxacin, and may benefit from incision and drainage. Ramsay Hunt syndrome is treated with acyclovir and corticosteroids, and early therapy improves facial nerve outcomes; ophthalmologic evaluation is recommended to assess ocular involvement.
Ongoing Care and Follow-Up
Referral to an otolaryngologist is advised when ear pain persists despite appropriate initial evaluation and management.
Complications
Otitis media can lead to mastoiditis, epidural abscess, dural venous sinus thrombosis, meningitis, or brain abscess. Malignant otitis externa may extend to the cavernous sinus or contralateral petrous apex, and although meningitis and brain abscess are uncommon, they are serious potential sequelae.

​Emergency And Acute Medicine – Knee Dislocation
Basics Description
Knee dislocation is defined by displacement of the tibia relative to the distal femur and represents a true orthopedic emergency because of the high risk of vascular and neurologic injury. Anterior dislocation is the most common type, accounting for approximately 60% of cases, and typically results from hyperextension. Rupture of the posterior capsule may occur at 30° of hyperextension, with disruption of the posterior cruciate ligament and potential popliteal artery injury at greater degrees. Posterior dislocation usually results from a direct blow to the anterior tibia with the knee flexed, such as a dashboard injury. Medial and lateral dislocations occur from varus or valgus stress, respectively, and are associated with multiligamentous injuries.
Popliteal artery injury occurs in up to 35% of knee dislocations and is the most limb-threatening complication. Anterior dislocations commonly cause traction-related intimal injury with delayed thrombosis, whereas posterior dislocations are more likely to cause direct arterial transection and immediate thrombosis. Peroneal nerve injury is less common but clinically significant and often accompanies arterial injury, particularly in medial or rotational dislocations.
Etiology
Knee dislocations typically result from high-energy mechanisms such as motor vehicle collisions, auto–pedestrian trauma, or athletic injuries, most commonly football.
Diagnosis Signs And Symptoms
Patients may present with a grossly deformed or unstable knee, though spontaneous reduction can mask deformity. Absence of distal pulses or signs of ischemia such as pallor, paresthesia, pain, paralysis, or poikilothermia raise immediate concern for popliteal artery injury. Neurologic deficits may include decreased sensation in the first web space or inability to dorsiflex the foot. A careful history of the mechanism of injury and repeated neurovascular examinations are essential.
Essential Workup
Evaluation requires a detailed history and thorough physical examination with emphasis on vascular and neurologic status. Distal pulses should be assessed by palpation and Doppler, capillary refill documented, and ankle–brachial index calculated. Neurologic examination should assess peroneal nerve function. Repeat examinations are mandatory, especially after reduction.
Diagnosis Tests And Interpretation
AP and lateral knee radiographs are required to confirm alignment and exclude associated fractures. MRI within one week is useful for defining ligamentous injury. An ABI ≥0.9 suggests low likelihood of major arterial injury, but abnormal findings warrant further evaluation. Vascular ultrasound or arteriography should be considered when pulses are diminished, ischemic symptoms persist, or peroneal nerve injury is present.
Differential Diagnosis
Conditions to consider include tibial plateau fracture, supracondylar femoral fracture, and ligamentous or tendinous avulsion injuries.
Treatment Pre Hospital
Initial management focuses on airway, breathing, and circulation. Distal pulses and motor function must be documented. The knee should be splinted in slight flexion to minimize popliteal artery tension.
Initial Stabilization Therapy
Address ABCs, particularly in polytrauma patients. Hypotension should be corrected, as it may obscure vascular compromise. Immediate closed reduction is indicated for any evidence of limb ischemia, with early orthopedic and vascular consultation.
Ed Treatment Procedures
Closed reduction is performed using longitudinal traction with gentle realignment, avoiding pressure in the popliteal fossa. The knee is immobilized in 15–20° of flexion. Neurovascular status must be reassessed immediately after reduction and monitored frequently. IV analgesia should be provided, and surgical consultation obtained for open injuries, vascular compromise, or irreducible dislocations.
Medication
IV narcotic analgesia is first-line. Oral medications should be avoided due to the high likelihood of operative intervention.
Follow-Up Disposition
All patients with knee dislocation require admission for observation and management of potential vascular injury. Discharge from the ED is not appropriate.
Follow-Up Recommendations
Orthopedic follow-up is required for staged ligamentous repair, typically delayed until swelling subsides. Vascular surgery follow-up is necessary if popliteal artery injury is identified.
Pearls And Pitfalls
Failure to restore popliteal artery flow within 6–8 hours carries an amputation risk approaching 90%. Peroneal nerve injury has a poor prognosis for recovery. Delayed compartment syndrome may occur and requires vigilant monitoring.

Emergency and Acute Medicine – Kawasaki disease
Kawasaki disease is an acute, self-limited inflammatory illness involving multiple organ systems and is the leading cause of acquired heart disease in children in developed countries. It is a medium-vessel vasculitis with particular predilection for the coronary arteries. Acute cardiac complications include myocarditis, pericarditis, and coronary artery aneurysms, which may later progress to stenosis or thrombosis; giant aneurysms carry a risk of rupture. The disease progresses through three stages: an acute phase lasting 1–2 weeks characterized by fever and systemic inflammation; a subacute phase extending to approximately 4 weeks marked by desquamation, thrombocytosis, and the highest risk of sudden death from coronary involvement; and a convalescent phase lasting 6–8 weeks during which symptoms resolve and inflammatory markers normalize.

Epidemiologically, 80% of cases occur in children younger than 4 years, with a peak incidence between 1 and 2 years of age. The disease is rare in infants younger than 3 months, though adult cases have been reported. Males are affected more often than females, and children of Asian descent have the highest incidence, suggesting a genetic predisposition. Delayed diagnosis, prolonged fever, male sex, extremes of age, elevated inflammatory markers, anemia, hypoalbuminemia, and abnormal initial echocardiography increase the risk of coronary artery aneurysm formation. Approximately 10–15% of patients are resistant to standard therapy.
The etiology remains unknown, but the disease is thought to represent an abnormal immune response to an infectious trigger in genetically susceptible individuals. Seasonal clustering and epidemic patterns support this hypothesis, with increased incidence in winter and early spring.

Diagnosis is clinical. Classic Kawasaki disease is defined by fever lasting at least 5 days in combination with four of five features: bilateral nonexudative conjunctival injection, oral mucosal changes (such as strawberry tongue or cracked lips), polymorphous rash, extremity changes (erythema, edema, or desquamation), and cervical lymphadenopathy greater than 1.5 cm. Incomplete or atypical Kawasaki disease should be suspected in children with prolonged fever and fewer criteria accompanied by elevated ESR or CRP and supportive laboratory findings such as anemia, hypoalbuminemia, elevated ALT, leukocytosis, thrombocytosis after day 7, or sterile pyuria.

Clinical presentation typically includes abrupt onset of high, spiking fever persisting longer than 5 days. Children often appear irritable and ill. Ocular findings include conjunctivitis without exudate and photophobia. Oral findings include erythema, fissured lips, and strawberry tongue. Skin findings are variable and usually involve the trunk, while extremity changes include painful edema and erythema followed later by desquamation of the fingers and toes. Gastrointestinal symptoms such as vomiting, diarrhea, abdominal pain, and gallbladder hydrops may occur. Cardiac manifestations include myocarditis, pericarditis, heart failure, and, later, coronary artery aneurysms.

Evaluation requires a high index of suspicion in any febrile child with rash. Laboratory findings typically include elevated ESR and CRP, leukocytosis with left shift, normocytic anemia, thrombocytosis in the subacute phase, sterile pyuria, and mild transaminase elevation. Blood, urine, CSF, and throat cultures are negative. Echocardiography is essential to assess coronary artery involvement and should be performed at diagnosis, at 2–3 weeks, and again at 6–8 weeks. ECG may be indicated if myocardial involvement is suspected.

The differential diagnosis includes viral illnesses such as adenovirus, measles, Epstein–Barr virus, and influenza; bacterial infections such as scarlet fever, staphylococcal scalded skin syndrome, and rickettsial disease; immune-mediated conditions including Stevens–Johnson syndrome and serum sickness; and other vasculitides or connective tissue diseases.

Management focuses on early treatment to prevent cardiac complications. All patients meeting diagnostic criteria should be admitted. Initial therapy consists of intravenous immunoglobulin and high-dose aspirin, ideally within the first 10 days of illness, which reduces the incidence of coronary artery aneurysms from approximately 20–25% to 2–4%. Cardiology consultation is required, and myocardial infarction is treated similarly to adults if it occurs.

First-line treatment includes IVIG at 2 g/kg administered over 10–12 hours, with repeat dosing for persistent or recrudescent fever. High-dose aspirin is given during the acute phase for anti-inflammatory effect, followed by low-dose aspirin for antiplatelet therapy during the convalescent period. Patients who fail two doses of IVIG may require corticosteroids or other immunomodulatory therapies such as infliximab or cyclosporine.

All patients diagnosed with Kawasaki disease require hospitalization, while nontoxic children who do not meet diagnostic criteria may be discharged with close follow-up. Long-term cardiology follow-up is mandatory for monitoring coronary artery involvement.
​
Early recognition and treatment are critical, as prompt IVIG and aspirin therapy prevent coronary aneurysm formation in the vast majority of patients. Kawasaki disease should be strongly considered in children with persistent fever and repeated emergency visits, and incomplete presentations must not be overlooked.