Emergency And Acute Medicine – Uncomplicated Delivery


Basics And Etiology
Emergency department delivery is uncommon, and the true incidence in the United States is unknown. It occurs more frequently in health care systems where patients have limited or no prenatal care. Most ED deliveries fall into three common scenarios. These include multiparous patients with a history of rapid labor, nulliparous patients who fail to recognize labor symptoms, and patients with limited prenatal care, lack of transportation, or premature labor.


Diagnosis – Signs And Symptoms
True labor is defined by regular uterine contractions occurring at least every five minutes and lasting 30–60 seconds. Significant vaginal bleeding during labor requires immediate evaluation for placenta previa or placental abruption. Patients may report abdominal or pelvic cramping, rupture of membranes that may feel like urinary incontinence, an urge to push or defecate, and bloody show due to loss of the mucous plug.


History
Key historical elements include last menstrual period and estimated gestational age, recent infections, pregnancy history and complications, prior cesarean delivery, and adequacy of prenatal care.


Physical Examination
Signs of imminent delivery include a fully effaced and dilated cervix, approximately 10 cm in a term pregnancy, palpable fetal parts, bulging of the perineum, and widening of the vulvovaginal opening. Fetal position and presenting part should be assessed by abdominal palpation when possible.


Essential Workup
A sterile bimanual pelvic examination is the most important assessment tool to evaluate labor and imminent delivery. Cervical dilation, effacement, and fetal station should be assessed. Patients should not push until full dilation is confirmed. Pelvic examination should be deferred in patients with vaginal bleeding until ultrasound excludes placenta previa. Fetal heart tones should be obtained using Doppler.


Diagnosis Tests And Interpretation
If the patient is in active labor, laboratory evaluation should include complete blood count, blood type, and Rh screen. If an Rh-negative mother delivers an Rh-positive infant, Kleihauer-Betke testing should be performed and Rh immunoglobulin administered within 72 hours. Urinalysis may be obtained if urinary tract infection or preeclampsia is suspected. Imaging is not required for uncomplicated vaginal delivery. Third-trimester vaginal bleeding requires emergent ultrasound to assess for placenta previa or placental abruption. If time allows, ultrasound may assist in determining placental location.


Differential Diagnosis
Consider Braxton Hicks contractions, which are irregular and do not cause cervical dilation or effacement. Other considerations include musculoskeletal low back pain, round ligament pain, ovarian torsion, appendicitis, and nephrolithiasis.


Treatment – Prehospital Care
Patients should be placed in the left lateral recumbent position. Emergency medical services personnel should be properly trained and equipped for obstetric emergencies. Transport of high-risk obstetric patients prior to delivery is associated with lower neonatal morbidity and mortality compared with post-delivery neonatal transport. Air transport is safe when necessary, though supplemental oxygen should be provided to mitigate fetal hypoxia from altitude exposure.


Initial Stabilization And Therapy
A sterile pelvic examination should be performed promptly if there is no vaginal bleeding. Patients in active labor should be transferred to labor and delivery unless birth is imminent. If the cervix is fully dilated and fetal parts are visible at the perineum, preparation for ED delivery is required.


Emergency Department Treatment And Procedures
Notify obstetrics, pediatrics or neonatology, and the neonatal intensive care unit. Prepare for neonatal resuscitation. Position the patient supine or in Sims position, establish IV access with normal saline or D5NS, provide supplemental oxygen, and place the patient in lithotomy position. Assemble an obstetric delivery kit including bulb syringe, sterile clamps, scissors, and umbilical clamp. If time allows, cleanse the perineum with povidone-iodine.


During delivery, guide the fetal head in a controlled manner as crowning occurs. Routine episiotomy is not required but may be performed if uncontrolled tearing occurs. After delivery of the head, suction the nasopharynx and assess for a nuchal cord. If present and loose, reduce it over the head; if tight, double clamp and cut before completing delivery. Apply gentle downward traction to deliver the anterior shoulder, followed by the posterior shoulder and body. Hold the infant at the level of the uterus, suction again, clamp and cut the cord, and initiate warming, drying, and stimulation. Provide oxygen or neonatal resuscitation as indicated.


The placenta typically delivers spontaneously within 20–30 minutes. Monitor closely for postpartum hemorrhage. Uterine massage promotes placental separation and uterine contraction. Avoid traction on the umbilical cord to prevent uterine inversion or cord rupture. If the placenta does not deliver and bleeding is severe, emergent operative management is required. After placental delivery, inspect it for completeness and examine the uterus, vagina, and perineum for lacerations. Persistent bleeding without laceration suggests uterine atony.


Medication Management
Routine medications are not required after uncomplicated delivery. If uterine atony persists despite massage, administer oxytocin intravenously. Continued bleeding may require methylergonovine intramuscularly, followed by carboprost tromethamine if refractory.


Follow-Up And Disposition
All women who deliver in the emergency department should be admitted to labor and delivery or a postpartum unit for monitoring, even if the delivery is uncomplicated. Neonatal consultation and NICU admission are required for infants with respiratory distress, gestational age less than 36 weeks, low birth weight, low Apgar scores, or other complications. Term infants without complications may be admitted to the nursery or remain with the mother in a combined unit. If post-delivery transfer is required, consider separate ambulances for mother and infant.


Key Clinical Lessons And Common Errors
Be prepared for obstetric emergencies such as cord prolapse, shoulder dystocia, and breech delivery. Always remember that after delivery, there are two patients requiring care—the mother and the newborn.

​Emergency And Acute Medicine – Dementia
Basics And Description
Dementia is a chronic, progressive deterioration in cognition, behavior, or both that is severe enough to interfere with activities of daily living and occurs without impairment of consciousness. It represents a progressive form of organic brain syndrome due to alterations in cortical brain function. More than 50 etiologies exist, with over 60% of cases caused by Alzheimer disease, which is associated with increased neurofibrillary tangles and elevated beta-amyloid plaques. Prevalence rises from approximately 1% at age 60 years to 30–50% by age 85 years. The condition is characterized by a gradual cognitive decline over years, though the course is variable. Rapid decline suggests alternative etiologies or rare rapidly progressive dementias such as prion disease or progressive supranuclear palsy. There is variable hereditary contribution, with increased risk of Alzheimer disease in first-degree relatives. Apolipoprotein ε4 is the only well-established mutation linked to late-onset Alzheimer disease.
Etiology
Primary dementias include cortical types such as Alzheimer disease and frontotemporal dementia, and subcortical types such as Huntington disease, Parkinson disease, and progressive supranuclear palsy. Secondary dementias result from cerebrovascular disease including multi-infarct dementia, toxic, metabolic, or nutritional derangements, prion disorders such as Creutzfeldt–Jakob disease, infectious causes including HIV and syphilis, vasculitic disorders such as systemic lupus erythematosus and thrombotic thrombocytopenic purpura, traumatic causes including chronic subdural hematomas and pugilistic dementia, and structural causes such as normal pressure hydrocephalus and brain masses. Binswanger disease is also included. Approximately 15% of cases are potentially reversible, including normal pressure hydrocephalus, medication effects, intracranial masses, and alcohol-related syndromes. Pseudodementia, often due to depression in elderly patients, can mimic dementia and is suggested by a short duration of symptoms, pinpoint onset, prior psychiatric history, and emphasis on perceived failures.
Diagnosis – Signs And Symptoms
Dementia typically has an insidious onset, often beginning with anxiety, depression, frustration, and increasing forgetfulness. It is frequently preceded by mild cognitive impairment, an intermediate state between normal aging and dementia. Clinical progression is commonly divided into early, moderate, and severe stages. Early disease presents with difficulty concentrating, memory deficits, impaired complex task performance, and social withdrawal. Moderate disease involves major memory impairment and need for assistance with activities of daily living. Severe disease is marked by minimal verbal communication, difficulty eating, and loss of psychomotor skills. Diagnostic criteria require memory impairment plus at least one additional cognitive disturbance such as aphasia, apraxia, agnosia, or executive dysfunction, with deficits causing significant functional decline and not occurring exclusively during delirium.
History
A thorough history must include collateral information from family or caregivers, complete medication review, comorbid conditions, prior similar behaviors, and details regarding onset and progression. Cognitive screening tools such as the Montreal Cognitive Assessment or Short Test of Mental Status may be useful.
Physical Examination
A comprehensive head-to-toe physical examination is required, with special emphasis on a detailed neurologic exam including mental status, cranial nerves, reflexes, motor and sensory function, cerebellar testing, and gait assessment.
Essential Workup
The primary goal is exclusion of acute reversible or exacerbating conditions. The extent of evaluation depends on whether dementia is newly diagnosed, rapidly worsening, or previously established and stable. Clinicians must actively assess for reversible causes.
Diagnosis Tests And Interpretation
Laboratory evaluation for new diagnosis or sudden deterioration includes complete blood count, ESR or CRP, comprehensive metabolic panel, ammonia, urinalysis, toxicology screen, thyroid-stimulating hormone, vitamin B12, syphilis serology, HIV testing, blood cultures if febrile, urine cultures if febrile, and antinuclear antibody testing if systemic lupus erythematosus is suspected. Imaging in these cases may include chest radiograph, noncontrast or contrast-enhanced head CT, EEG if seizures are suspected, and brain MRI or MRA in selected patients. Advanced imaging such as PET is reserved for specialist evaluation. In stable, previously diagnosed dementia, testing may not be required. Lumbar puncture and cerebrospinal fluid analysis are indicated when infection or inflammatory disease is suspected.
Differential Diagnosis
Consider toxic, metabolic, or nutritional abnormalities including narcotics, sedatives, alcohol, heavy metals, dehydration, and electrolyte disorders. Other considerations include pseudodementia, delirium, and normal aging. Delirium should be strongly suspected in febrile patients, especially with urinary tract infection or pneumonia.
Treatment – Prehospital Care
Obtain collateral history from family or caregivers, ensure patient and staff safety, manage agitation, and address comorbid conditions. Treat acute metabolic or toxic disturbances such as hypoglycemia, hypothermia, or hyperthermia.
Initial Stabilization And Therapy
Ensure airway patency, provide supplemental oxygen if hypoxic, stabilize vital signs, and establish IV access as needed. Safety measures are essential in agitated patients.
Emergency Department Treatment And Procedures
Determine whether there is an acute change in mental status and evaluate broadly for reversible causes. Treat hypoglycemia with dextrose, opioid toxicity with naloxone, hypothermia with rewarming, and hyperthermia with antipyretics. Administer IV fluids for dehydration and correct electrolyte abnormalities. Treat infections promptly, with urinary tract infections and pneumonia being common occult sources. Manage seizures with appropriate anticonvulsants. Agitation should be managed with the lowest effective doses of medications, prioritizing safety and minimizing polypharmacy. Treat depression when present.
Medication Management
Cholinesterase inhibitors should be initiated at the lowest dose and include donepezil, rivastigmine, and galantamine, with monitoring for gastrointestinal side effects. Memantine may be considered in patients with poor response to anticholinesterase agents. Antidepressants may be useful but carry risk of oversedation. For agitation, options include haloperidol, risperidone, ziprasidone, lorazepam, or midazolam, always starting at low doses. Naloxone should be used when opioid toxicity is suspected.
Follow-Up And Disposition
Admission is indicated for unstable vital signs, significant comorbid illness requiring parenteral therapy, unclear diagnosis requiring inpatient evaluation, or inadequate home support. Discharge may be considered for patients with stable vital signs, no life-threatening condition identified, secure diagnosis, adequate caregiver support, and reliable follow-up.
Follow-Up Recommendations
Follow-up care should be arranged with primary care, geriatrics, psychiatry, or neurology as appropriate. Social support needs, including transportation and financial assistance, should be addressed.
Key Clinical Lessons And Common Errors
Primary dementia typically follows a slow, steady progression over 5–10 years but may fluctuate due to intercurrent illness. Cholinesterase inhibitors can modestly improve function in Alzheimer disease. Vigilant management of medications, comorbidities, and early treatment of infections improves quality of life and survival. Death most commonly results from infection, cardiovascular disease, or injury.

Emergency And Acute Medicine – Dental Trauma


Basic Overview
Primary teeth erupt between 6 and 10 months of age and eruption is usually complete by 30 months. Eruption is bilaterally symmetric, with a total of 20 primary teeth. Permanent teeth begin erupting at approximately 6 years of age and total 32 teeth, including 4 central incisors, 4 lateral incisors, 4 canines, 8 premolars, and 12 molars. Teeth are commonly numbered from 1 to 32, beginning with the upper right third molar and ending with the lower right third molar, though anatomical description of the involved tooth is often clearer in clinical practice.
The most frequently injured teeth are the maxillary central incisors, followed by maxillary lateral incisors and mandibular incisors.


Tooth Fractures
Crown fractures are classified as uncomplicated when only enamel or enamel and dentin are involved, and complicated when the neurovascular pulp is exposed. The Ellis classification system is commonly used.
Ellis class I fractures involve only enamel, appear chalky white, and are painless to temperature, air, and percussion.
Ellis class II fractures involve enamel and dentin, appear ivory or pale yellow compared with enamel, and may be sensitive to heat, cold, or air but are not typically tender.
Ellis class III fractures involve enamel, dentin, and pulp and represent a true dental emergency. Pulp exposure appears pink or red with possible frank bleeding or a pink blush after wiping the surface. These injuries may be exquisitely painful or paradoxically desensitized due to neurovascular disruption.


Luxation Injuries
Luxation injuries involve the supporting structures of the tooth, including the periodontal ligament and alveolar bone.
Concussed teeth are neither loose nor displaced but are sensitive to chewing or percussion.
Subluxed teeth are loose but not displaced, with bleeding from the gingival sulcus and sensitivity to chewing or percussion due to periodontal ligament damage.
Intrusion occurs when the tooth is driven into the socket with compression of the periodontal ligament and fracture of the alveolar socket.
Avulsion refers to complete displacement of the tooth from the alveolar ridge with severing of the periodontal ligament.
Extrusion is partial axial displacement of the tooth from the socket.
Lateral luxation involves nonaxial displacement of the tooth and is often associated with alveolar socket fracture.
Alveolar bone fractures affect tooth-bearing portions of the maxilla or mandible and present with painful bite, malocclusion, and en bloc tooth mobility.


Etiology And Risk Factors
Nearly half of all children sustain a dental injury. Peak incidence occurs in toddlers from falls and possible abuse, in school-aged children from falls and bicycle or playground injuries, and in adolescents from sports, altercations, and motor vehicle collisions. Mouth guard use significantly reduces sports-related dental trauma. Other causes include assault, domestic violence, motor vehicle and bicycle accidents, laryngoscopy, and child abuse, which is frequently associated with orofacial injury.
Predisposing anatomic factors include an anterior overbite greater than 4 mm, which increases risk two- to threefold, incompetent upper lip, mouth breathing, physical disabilities, and fixed orthodontic appliances.


Clinical Presentation
Patients may report tooth mobility, avulsion, laxity, malocclusion, or trismus. Pain may worsen with chewing, drinking, temperature extremes, or palpation, suggesting pulp exposure or periodontal ligament injury. Mechanism of injury should be carefully assessed, as significant force may indicate associated facial or jaw fractures. The exact time of injury is important for prognosis, especially with avulsions.


Physical Examination
All teeth should be examined for trauma and fracture. Fractured teeth must be dried and inspected for pulp exposure. Percussion and mobility testing should be performed. Occlusion and midface stability should be assessed, and all missing teeth accounted for, as fragments may be aspirated, swallowed, embedded in soft tissue, or impacted in the alveolus. The oral cavity should be inspected for associated soft tissue or bony injury. Mandibular fracture should be suspected if the patient cannot open the mouth more than 5 cm or has a positive tongue blade bite test. Associated injuries to salivary glands, ducts, blood vessels, and mental or infraorbital nerves should be considered.


Evaluation And Imaging
A thorough physical examination is essential. Dental radiographs are useful for complicated fractures. Panoramic imaging is indicated for foreign bodies or displaced teeth. CT is recommended when malocclusion, trismus, or alveolar or mandibular fracture is suspected. Chest radiography is indicated if teeth or fragments are missing; teeth visualized below the diaphragm do not require removal. Bronchoscopy is indicated for aspirated teeth.


Prehospital Management
Only permanent teeth should be reimplanted. Avulsed permanent teeth should be gently rinsed with cold running water and reimplanted immediately if possible. Each minute out of the socket reduces viability by approximately 1%, with best outcomes if reimplantation occurs within 5–15 minutes. Viability is poor after more than one hour.
If immediate reimplantation is not possible, the tooth should be stored in an appropriate medium, preferably Hanks balanced salt solution, cold milk, or saliva. Tap water and dry storage must be avoided.


Emergency Department Management
Ensure airway patency and control bleeding with gauze. Account for all teeth and fragments. Reimplant avulsed permanent teeth immediately. Occlusion is the best guide to proper positioning. Splinting should be done before laceration repair when needed.
Tetanus prophylaxis should be considered for dirty wounds, deep lacerations, avulsions, intrusion injuries, and fractures. Antibiotics are indicated for open alveolar fractures, secondary infection, or patients at risk for subacute bacterial endocarditis.


Injury-Specific Management
Ellis class I fractures require no emergency treatment other than smoothing sharp edges and dental referral for cosmetic repair.
Ellis class II fractures require coverage of exposed dentin with calcium hydroxide or a similar barrier, followed by dental foil; cyanoacrylate tissue adhesive may be used if no barrier is available. A liquid diet, pain control, and dental follow-up within 48 hours are recommended.
Ellis class III fractures require immediate dental or endodontic referral. If unavailable, cover the pulp as above, control bleeding, and provide pain management.
Concussed teeth require no splinting and a soft diet.
Subluxed teeth may require splinting if excessively loose and a soft diet for one week.
Extruded teeth should be repositioned with gentle pressure and splinted for two weeks.
Lateral luxation often requires forceful repositioning, sometimes with local anesthesia, followed by splinting for up to four weeks.
Intruded teeth should not be manipulated and require dental follow-up within 24 hours.
Avulsed permanent teeth should be handled only by the crown, gently rinsed, reimplanted, and splinted as needed. Primary teeth should never be reimplanted.
Alveolar fractures require oral surgery or dental consultation for reduction and fixation.


Medications
Analgesics include acetaminophen with codeine or oxycodone, with pediatric weight-based dosing. Antibiotics include penicillin V or clindamycin for penicillin-allergic patients. Tetanus prophylaxis should be administered when indicated. Total daily acetaminophen dose must not exceed 4 g.


Disposition And Follow-Up
Admission is indicated for associated injuries, suspected abuse, or lack of a safe environment. Stable patients without additional traumatic injuries may be discharged.
Immediate dental referral is required for Ellis class III injuries and for loose, displaced, or missing teeth. Patients with avulsions or Ellis class II and III fractures should see a dentist within 24 hours.


Key Clinical Insights And Common Errors
Avulsed teeth must never be stored dry or in tap water. Occlusion is the most reliable guide to correct repositioning. Patients should be counseled regarding risks of tooth resorption, discoloration, tooth loss, and the potential need for future root canal therapy.

Emergency And Acute Medicine – Depression


Basic Overview
Major depression is defined by a depressed mood with associated signs and symptoms lasting longer than two weeks. It is associated with significant morbidity and mortality, including a substantial risk of suicide, and frequently coexists with other medical illnesses.


Etiology And Risk Factors
Depression is a biologic illness associated with dysregulation of multiple neurotransmitter systems, including serotonin, norepinephrine, and dopamine. Contributing factors include genetic predisposition, medical illness, medication effects, and psychosocial stressors. Episodes may follow adverse life events, trauma, loss of important relationships, or changes in life roles. Depression is more prevalent in women, although men are more likely to die by suicide.


Clinical Features
Diagnosis requires five or more symptoms present for at least two weeks, with either depressed mood or loss of interest or pleasure being mandatory. Symptoms include depressed mood, diminished interest or pleasure, appetite or weight change, sleep disturbance, fatigue, impaired concentration, feelings of worthlessness or guilt, psychomotor agitation or retardation, and recurrent thoughts of death or suicide. Depression may present with anxious agitation or social withdrawal and is often accompanied by somatic complaints such as weakness, malaise, weight loss, headache, or back pain. Subtypes include psychotic, melancholic, catatonic, atypical, postpartum, and seasonal depression.


History And Examination
Assessment should include symptom time course, acuity, psychosocial stressors, past medical and psychiatric history, medication and substance use, family history, and social and occupational functioning. A focused safety assessment is essential, evaluating suicide risk, risk of harm to others, and ability to care for oneself. Collateral information from family or outpatient providers is often crucial. Physical examination includes vital signs, a focused neurologic exam, cognitive assessment, and a full mental status examination. Cultural and language barriers should be addressed with interpreters when needed.


Special Populations
In children and adolescents, depression may present as changes in school performance, sleep, social withdrawal, or somatic complaints, and diagnosis may be challenging. Bipolar disorder must be excluded, as treatment differs and antidepressants may precipitate mania.


Evaluation
Initial evaluation relies on history and physical examination, with attention to coexisting psychiatric disorders, substance use, and medical causes. Safety assessment is mandatory. First-line laboratory studies include CBC, basic chemistries, renal function, glucose, calcium, liver function tests, urinalysis, serum and urine toxicology screens, thyroid function tests, and vitamin B12 and folate levels. Additional tests, such as HIV testing, RPR, inflammatory markers, or autoimmune studies, are guided by clinical suspicion. Brain imaging is reserved for atypical presentations or focal neurologic findings, with MRI preferred over CT when available.


Differential Diagnosis
Psychiatric conditions include dysthymia, adjustment disorder, bipolar disorder, anxiety disorders, psychotic disorders, personality disorders, eating disorders, and substance-induced mood disorders. Medical conditions that may mimic or cause depression include endocrine disorders, neurologic diseases, infections, nutritional deficiencies, electrolyte disturbances, chronic organ failure, obstructive sleep apnea, chronic pain syndromes, and medication effects.


Emergency Management
Initial management focuses on patient and staff safety, assessment of suicide and violence risk, and identification of underlying medical contributors. One-to-one observation and suicide precautions are indicated when risk is high. Medical causes such as hypoglycemia, infection, electrolyte abnormalities, or intoxication should be treated promptly. Empathic listening, reassurance, and education that depression is treatable are essential components of care.


Pharmacologic Treatment
Antidepressant therapy may be initiated in selected patients with a clear diagnosis and reliable follow-up, recognizing that symptom improvement typically takes weeks. First-line agents include SSRIs, SNRIs, bupropion, and mirtazapine, chosen based on side-effect profile, comorbidities, cost, and patient factors. Tricyclic antidepressants and monoamine oxidase inhibitors are second-line options due to higher risk profiles and should be used cautiously. Low-dose benzodiazepines or antipsychotics may be used short term for agitation, insomnia, or psychosis. Elderly patients require lower starting doses and careful monitoring for orthostasis and drug interactions. In children and adolescents, antidepressants carry an FDA black box warning for increased suicidal ideation. In pregnancy and lactation, risks and benefits must be weighed carefully, ideally with specialist input. Electroconvulsive therapy may be considered for severe, psychotic, catatonic, or treatment-resistant depression.


Disposition
Admission is indicated for patients with suicidal ideation or high suicide risk, psychotic features, severe functional impairment, unreliable social support, or need for involuntary commitment. Patients with low suicide risk, adequate support, and reliable follow-up may be discharged.


Follow-Up And Referral
Outpatient mental health follow-up should be arranged, typically within one to two weeks for patients with significant symptoms or those started on medication. More stable patients may follow up less urgently. Coordination with primary care, psychiatry, and social services is often necessary.


Key Clinical Insights And Common Errors
Depression carries significant morbidity and risk of self-harm. Always assess suicide risk and consider medical and psychiatric conditions that can mimic or exacerbate depression. Awareness of local involuntary commitment criteria and careful coordination of follow-up care are essential to safe management.

Emergency And Acute Medicine – Dermatomyositis And Polymyositis


Basic Description
Dermatomyositis and polymyositis are systemic inflammatory myopathies and represent the most common group of acquired, potentially treatable causes of skeletal muscle weakness. Both conditions are characterized by progressive, symmetrical muscle weakness developing over weeks to months. Respiratory insufficiency may occur due to respiratory muscle involvement, and aspiration pneumonia can result from weak cough, pharyngeal muscle dysfunction, and esophageal dysmotility. Cardiac involvement may include myocarditis, conduction abnormalities, cardiomyopathy, and congestive heart failure. Arthralgias commonly affect the hands, wrists, knees, and shoulders. Ocular muscles are spared, although facial weakness may appear in advanced disease.


Etiology And Pathophysiology
The exact cause is unknown, but autoimmune mechanisms are central. There is a female predominance, with an incidence of approximately 1 per 100,000. Associations include HLA-B8 and HLA-DR3. Polymyositis may be linked to viral, bacterial, or parasitic infections, and both conditions coexist with collagen vascular diseases in about 20% of cases. In dermatomyositis, humoral immune mechanisms cause microangiopathy leading to muscle ischemia. In polymyositis, T-cell–mediated cytotoxicity predominates, with CD8 T cells and macrophages destroying non-necrotic muscle fibers expressing class I MHC. Complement deposition is an early lesion, followed by inflammation, ischemia, microinfarction, necrosis, and muscle fiber destruction.


Pediatric Considerations
Dermatomyositis occurs in both children and adults, whereas polymyositis is rare in children. Juvenile dermatomyositis primarily affects skin and skeletal muscle and may include vasculitis, calcinosis cutis, and lipodystrophy. Coxsackievirus infection has been associated with the juvenile form.


Clinical Presentation
Polymyositis presents with muscle pain and proximal muscle weakness without rash. Dermatomyositis presents with characteristic skin findings in addition to muscle pain and weakness. Constitutional symptoms include weight loss, fever, anorexia, morning stiffness, myalgias, and arthralgias. Patients commonly report fatigue during routine activities such as brushing hair, climbing stairs, reaching overhead, or rising from a chair. Dysphagia, dyspnea, and cough may be present. Weakness primarily involves proximal limb and girdle muscles early and may progress distally later.


Physical Examination Findings
General findings include fatigue, fever, weight loss, dysphagia, and progressive symmetrical proximal muscle weakness. Dermatomyositis skin findings include heliotrope rash with eyelid edema, Gottron papules over extensor joint surfaces, a V-shaped or shawl rash over the back and shoulders, periungual telangiectasias with abnormal cuticles, and “mechanic’s hands” with hyperkeratotic fissuring of the fingers.


Essential Emergency Assessment
Assessment should prioritize airway protection and evaluation for aspiration, respiratory compromise, and cardiac involvement.


Diagnostic Evaluation
Serum muscle enzymes are typically elevated, especially creatine phosphokinase, with possible elevation of aldolase. Diagnostic criteria include symmetrical proximal muscle weakness, elevated muscle enzymes, electromyographic evidence of myopathy, and muscle biopsy demonstrating inflammatory changes, with characteristic rash required for dermatomyositis. Newer criteria incorporate autoantibodies such as anti–Jo-1, anti–SRP, and anti–Mi-2. Chest radiography may show interstitial lung disease, aspiration pneumonia, or cardiomyopathy. EMG supports but does not confirm diagnosis. MRI is increasingly used to localize inflamed muscle for biopsy. Muscle biopsy remains definitive, showing endomysial inflammation in polymyositis and perivascular inflammation with B-cell predominance in dermatomyositis. Pulmonary function testing helps monitor interstitial lung disease.


Differential Diagnosis
Consider collagen vascular diseases, muscular dystrophies, spinal muscular atrophy, myasthenia gravis, amyotrophic lateral sclerosis, poliomyelitis, Guillain–Barré syndrome, endocrine disorders, Cushing syndrome, drug-induced myopathies, infections, electrolyte abnormalities, vasculitis, paraneoplastic syndromes, and hypereosinophilic myalgia.


Emergency Management
Initial care focuses on airway, breathing, and circulation, with head-of-bed elevation and early airway protection if needed. Mechanical ventilation may be required in severe respiratory weakness. Nasogastric suction can reduce aspiration risk. High-dose corticosteroids are the cornerstone of therapy to suppress inflammation and improve strength, avoiding agents known to cause steroid-induced myopathy. Treatment response should be judged by clinical improvement rather than enzyme levels alone. Immunosuppressive agents such as methotrexate or azathioprine may be added if steroid response is inadequate. Other therapies including IVIG, plasmapheresis, or cyclosporine are used selectively under specialist guidance.


Medication Therapy
First-line therapy is prednisone 60 mg daily orally, or weight-based dosing in children, with intravenous methylprednisolone pulses for severe disease. Second-line agents include methotrexate, azathioprine, IVIG, plasmapheresis, or cyclosporine as determined by rheumatology.


Disposition And Follow-Up
Admission is indicated for respiratory insufficiency, aspiration pneumonia, profound weakness, ineffective cough, pharyngeal dysfunction, or congestive heart failure. Stable patients without aspiration risk who can tolerate oral therapy may be managed as outpatients. Early rheumatology consultation is recommended. Because dermatomyositis carries an increased malignancy risk, ongoing cancer surveillance with regular examinations and screening studies is advised.


Key Clinical Insights
Diagnosis is primarily clinical and supported by laboratory testing and biopsy. Most patients improve with treatment, many achieving sustained functional recovery, though residual weakness may persist in up to one-third. Relapses can occur at any time despite prior successful therapy.

Emergency And Acute Medicine – Diabetes Insipidus


Overview And Definition
Diabetes insipidus is a disorder characterized by excretion of abnormally large volumes of dilute urine due to impaired action of arginine vasopressin. Polyuria is typically defined as urine output exceeding 3 liters in 24 hours and is often accompanied by excessive thirst and fluid intake. Two major forms exist: central diabetes insipidus, caused by deficient synthesis or release of vasopressin, and nephrogenic diabetes insipidus, caused by renal resistance to vasopressin. Familial cases occur in both forms, with some nephrogenic cases inherited in an X-linked recessive pattern.


Causes And Risk Factors
Central diabetes insipidus results from disruption of the hypothalamic–pituitary axis and is most common between 10 and 20 years of age. Causes include head trauma, neurosurgery, pituitary or hypothalamic tumors such as craniopharyngioma or germinoma, metastatic disease, granulomatous disorders, congenital CNS anomalies, CNS infections, pregnancy-related pituitary injury, idiopathic autoimmune processes, Wolfram syndrome, and ethanol use. Nephrogenic diabetes insipidus arises from intrinsic renal pathology or impaired tubular response to vasopressin and may be due to congenital renal disorders, obstructive uropathy, polycystic kidney disease, systemic diseases such as sickle cell disease or amyloidosis, medications such as lithium, amphotericin, aminoglycosides, and demeclocycline, or electrolyte disturbances including hypercalcemia and hypokalemia.


Pregnancy-Related Considerations
Transient diabetes insipidus may occur during the second trimester due to increased circulating vasopressinase, leading to reduced vasopressin activity. Symptoms usually resolve within weeks after delivery. Desmopressin is effective because it is resistant to vasopressinase. Sheehan syndrome is another pregnancy-related cause of central diabetes insipidus.


Clinical Features And Presentation
Patients commonly report marked polyuria, sometimes producing 16–24 liters of urine daily, along with intense polydipsia, often preferring cold fluids. Additional features may include medication exposure or symptoms suggestive of hypothalamic or pituitary tumors such as headache, visual changes, growth abnormalities, obesity, temperature dysregulation, sleep disturbance, or behavioral changes. Physical examination may reveal dehydration, cachexia, head trauma signs, visual field deficits, or seizures.


Pediatric Presentation
In children, polyuria and polydipsia may go unrecognized until dehydration develops. Neonates may present at birth and are at risk for severe hypernatremia and permanent neurologic injury if untreated. Infants may show irritability, poor feeding, weight loss, constipation, growth failure, recurrent fever, or abnormal behavior. Older children may present with enuresis or difficulty with toilet training.


Essential Emergency Evaluation
In the emergency setting, the diagnosis is largely clinical, supported by hypernatremia with copious dilute urine output. A careful history of fluid intake, voiding frequency, medication use, and physical findings is essential.


Diagnostic Studies And Interpretation
Urinalysis typically shows low specific gravity. Serum and urine osmolality reveal elevated serum osmolality with inappropriately low urine osmolality. Electrolyte testing may demonstrate hypernatremia, hypercalcemia, or hypokalemia. Renal function tests and glucose help exclude other causes of polyuria. Serum and urine vasopressin levels are not required in the emergency department. Imaging such as CT or chest radiography may be indicated for trauma or malignancy evaluation, while MRI of the pituitary axis is usually performed outpatient. Water deprivation testing is not recommended in the emergency setting because of safety concerns, especially in hypotensive patients and children.


Differential Diagnosis
Alternative considerations include inadequate access to free water, excessive insensible losses, primary sodium excess, psychogenic polydipsia, diuretic use, osmotic diuresis, resolving acute renal failure, and uncontrolled diabetes mellitus.


Initial And Emergency Management
Initial care focuses on airway, breathing, and circulation, with attention to possible head trauma. Hypotension should be treated with isotonic saline. Because intravascular volume represents a small fraction of total water deficit, careful correction is required. Central diabetes insipidus is treated with desmopressin, administered intranasally, orally, intravenously, or subcutaneously in divided doses. Caution is required in postoperative patients due to risk of cerebral edema. Nephrogenic diabetes insipidus is managed by treating the underlying cause, discontinuing offending medications, correcting electrolyte abnormalities, implementing dietary sodium restriction, and using thiazide diuretics, often with amiloride. NSAIDs such as indomethacin may reduce urine output. Parenteral free-water replacement is reserved for symptomatic hypernatremia when oral intake is not possible.


Medication Therapy
Common agents include desmopressin in various formulations, thiazide diuretics, amiloride, and in selected cases chlorpropamide or clofibrate for partial central disease. Aqueous vasopressin has limited use due to short half-life and adverse effects.


Disposition And Follow-Up
Admission is indicated for altered mental status, seizures, severe dehydration, significant electrolyte abnormalities, associated trauma, or need for diagnostic testing under observation. Patients with a known diagnosis, stable electrolytes, and adequate hydration may be discharged with close follow-up. Referral to endocrinology or nephrology depends on the underlying etiology.


Key Clinical Insights And Pitfalls
Always consider diabetes insipidus in patients with unexplained polyuria and low urine osmolality. Central diabetes insipidus typically responds to desmopressin, whereas nephrogenic diabetes insipidus does not and requires management of renal resistance and contributing factors.

Emergency and Acute Medicine - Juvenile Diabetes Mellitus


Basics
Description Decrease in effective circulating insulin. Increase in counter regulatory hormones including glucagon, catecholamines, cortisol, and growth hormone. Hyperglycemia owing to: Decreased peripheral glucose utilization. Increased hepatic gluconeogenesis. Hyperosmolality and osmotic diuresis due to hyperglycemia. Ketoacidosis produced by increased lipolysis, with ketone body (β-hydroxybutyrate, acetoacetate) production, causes ketonemia and metabolic acidosis, which is augmented with lactic acidosis from poor tissue perfusion. Potassium deficit: Intracellular shifts into extracellular space owing to hydrogen ion exchange. Loss from osmotic diuresis.


Etiology
Mechanism: Immune-mediated pancreatic islet β-cell destruction. The overall incidence has been increased worldwide by 2–5% over the past 20 yr. Precipitating events leading to diabetic ketoacidosis (DKA): Infection, often minor acute illness such as virus, group A streptococcal pharyngitis, or UTI. Stress. Endocrine: Pregnancy, puberty, hyperthyroidism. Psychiatric disorders, including eating disorders. Medication noncompliance, inappropriate interruption of insulin pump therapy, or treatment error. Risk factors for cerebral edema: Attenuated rise in measured serum sodium during DKA therapy (unrelated to the volume or sodium content of IV fluid or rate of change in serum glucose). Bicarbonate treatment for acidosis correction. Hypocapnia. Increased serum urea nitrogen. No association with degree of hyperglycemia. Demographic factors that have been associated with an increased risk of cerebral edema include younger age, longer duration of symptoms, and new onset diabetes mellitus. These factors are also associated with increased risk of severe DKA.


Diagnosis
Signs and symptoms Polydipsia. Polyuria (may have good urine output despite dehydration). Nocturia. Polyphagia. Malaise, weight loss. DKA: Initial presentation in 20-40% of patients. Often associated with tachypnea (Kussmaul respiration), tachycardia, orthostatic BP changes. Nausea. Vomiting. Abdominal pain, often resolving with reduction in ketosis/acidosis. Hyperpnea. Fruity breath secondary to ketones. Rapid onset of DKA can occur within 7-8 hr with the use of insulin pump therapy if there is an infusion set or insulin delivery malfunction. This is due secondary to lack of long acting insulin to provide a safety net (more commonly seen in female >10 yr of age). Findings with more advanced disease: Dehydration, drowsiness, altered mental status, and ultimately, late stage coma and shock. Cerebral edema: The incidence ranges from 0.87–1.1%. Cerebral edema accounts for 57–87% of all DKA deaths. It typically occurs 4–12 hr after treatment is initiated, but can be presenting (subclinical) before treatment has started. Headache. Change in neurologic status, such as drowsiness, irritability, or specific neurologic deficit, such as pupillary responses or cranial nerve palsies. Inappropriate slowing in pulse rate. Increase in BP. Hyperglycemic hyperosmolar nonketotic coma: Glucose level of 800–1,200 mg/dL. Rare in children; more common in adults.


Essential workup
For DKA: The International Society for Pediatric and Adolescent Diabetes (ISPAD) defines DKA as blood bicarbonate level <15 mmol /> or venous pH <7.3 and hyperglycemia (>200 mg/dL) with related ketonemia or ketonuria. DKA classification: Mild DKA: Venous pH <7.2–7.3 or hco3 <10–15 mmol />. Moderate DKA: Venous pH <7.1–7.2 or hco3 <5–10 mmol />. Severe DKA: Venous pH <7.1 or hco3 <5 mmol />. Hourly vital signs and neurologic checks. Frequent blood chemistries. ECG monitoring (in severe DKA) to assess T-waves for evidence of hyperkalemia or hypokalemia. Accurate fluid input and output. Consider urinary catheterization in patients with impaired level of consciousness.


Diagnosis tests & interpretation
Lab For DKA: Glucose, serum: Hyperglycemia. Urinalysis: Glycosuria. Ketonuria. Exclude UTI. Blood chemistries every 2–4 hr until acidosis has resolved (more frequent as clinically indicated in the more severe cases). Electrolytes and venous pH. Anion gap metabolic acidosis: Potassium—high or normal (artifactual owing to extracellular shift). Serum potassium rises 0.5 mEqL for each 0.1 decrease in pH. Sodium—low or normal (may be artifactual owing to hyperglycemia). Corrected Na (mEq/L) = [measured serum Na (mEqL) + plasma glucose (mg/dL) – 100] × 0.016. Bicarbonate—low. Calculation: Na – (Cl + HCO3). Serum ketones—elevated. β-hydroxybutyrate (BHOB) is a quantitative test that is available to replace the classic nitroprusside test for serum ketones. Serum osmolality. CBC: WBC often elevated owing to stress or infection. Calcium. Phosphate. Cultures as indicated: Group A streptococcal pharyngeal swab, urine, etc. Pregnancy test if indicated. ECG if potassium markedly abnormal. Imaging: CXR if any suggestion of pneumonia. Head CT if there are concerns about cerebral edema.


Differential diagnosis
Infection (may precipitate): UTI. Gastroenteritis. Appendicitis. Sepsis. Ingestion (salicylates, alcohols, glycols). Diabetes insipidus.


Treatment
Pre hospital For DKA: ABCs. Airway protection. Establish IV access and initiate fluid therapy.
Initial stabilization/therapy For DKA: Oxygen. Cardiac monitor. IV access and volume resuscitation.
Ed treatment/procedures For DKA: Fluid replacement: Assume fluid deficit of 10% of body weight. Initial volume expansion with 10-20 mL/kg of 0.9% NaCl or lactated Ringer; may repeat to achieve hemodynamic stability. Correct 50% of fluid deficit over 1st 8 hr, remainder over 24-48 hr. Do not give >3 L/m2 over 1st 24 hr. Begin IV insulin infusion after ketoacidosis confirmed: Initial rate of continuous infusion (regular insulin) 0.1 U/kg/h IV. Adjust rate to drop serum glucose 50–100 mg/dL/h. Add dextrose to infusion fluid when serum glucose <300 mg />L. Change to SC insulin when no longer significantly acidotic and able to eat. Some clinicians prefer IM route, commonly initially using regular insulin at a dose of 0.1–0.2 U/kg/h. Replace potassium and phosphate losses: Verify adequate urine output. Add to fluids as K-acetate (or KCl if acetate not available) and K3PO4 in equal amounts. Large doses of K+ may be necessary; guide therapy by frequent monitoring of K+. Monitor serum sodium: Risk for cerebral edema if Na+ fails to rise as glucose falls. Bicarbonate therapy: Not recommended in most cases since generally it does not alter outcome and it increases risk for cerebral edema with its use. Use it with caution in patients with severe acidosis (pH <6.9) in whom peripheral vasodilation and decreased cardiac contractility may further impair tissue perfusion potentially life-threatening hyperkalemia. cerebral edema: treat edema as soon the condition is suspected due to its high mortality morbidity rates: 21–25% 10–26%, respectively. decrease fluid administration rate. mannitol (0.25–1 g />g over 20 min): No large studies to date demonstrate definitive beneficial or detrimental effects. Consider its use in patients with signs of cerebral edema before impeding respiratory failure. Dose can be repeated in 2 hr if there is no initial response. Endotracheal intubation and ventilation: Avoid aggressive hyperventilation since it has been associated with poor outcome in DKA-related cerebral edema (similar to that found in head trauma).


Medication
Insulin drip: Start regular insulin 0.1 U/kg/h IV (some clinicians prefer the IM dosing and route). Mannitol: 0.25–1 g/kg IV.


Follow-up disposition
Admission criteria For DKA: ICU: Altered mental status. Shock or cardiac dysrhythmia. Initial glucose >700 mg/dL. Initial pH <7. risk factors for cerebral edema (age <5 yr, prolonged symptoms, high bun). inpatient unit: stable new-onset diabetic patients requiring intensive education. with ketoacidosis not meeting requirements icu care. compliance concerns or other social issues. discharge criteria known who respond well to therapy normalization of glucose, ph, and ketosis. tolerating oral fluids. reliable parents. follow-up within 24 hr including appropriate issues referral critically ill. persistent abnormal mental status. poorly controlled diabetes.< />pan>


Follow-up recommendations
Close follow-up with the primary care physician is important even after the resolution of DKA to ensure appropriate management of the patient’s diabetes to prevent further occurrence of DKA. Many children with diabetes are followed at comprehensive diabetes centers in collaboration with primary care physician.


Pearls and pitfalls
Mortality from DKA is predominately related to the occurrence of cerebral edema. Therefore, early and appropriate treatment is of most importance in managing children with DKA. In children, avoid using an insulin bolus since it increase the risk of cerebral edema. Recently, some data suggest that starting insulin drip at 0.05 U/kg/h may reduce the risk for rapid fluid shifts and theoretically for cerebral edema.

Emergency and Acute Medicine - Diabetic Ketoacidosis


Basics
Description Diabetic ketoacidosis (DKA) results from absolute or relative insulin deficiency with excess counterregulatory hormones (catecholamines, glucagon, growth hormone, cortisol). This leads to dehydration from osmotic hyperglycemic diuresis and reduced oral intake, anion gap metabolic acidosis, ketone formation from unrestrained lipolysis and ketogenesis, hyperglycemia from increased gluconeogenesis and glycogenolysis, and significant electrolyte disturbances including hypokalemia, hypo- or hypernatremia, and hypophosphatemia.


Etiology
Medication noncompliance is the most common cause. New-onset diabetes mellitus (type 1 or type 2) is a frequent presentation. Underlying medical illness increases counterregulatory hormones and insulin resistance, including infection, myocardial infarction, gastrointestinal bleeding, and central nervous system events. Pregnancy contributes through relative insulin deficiency. Medications such as protease inhibitors and atypical antipsychotics (e.g., olanzapine, clozapine) and alcohol abuse are additional contributors.


Diagnosis
Signs and symptoms Patients often report polyuria, polydipsia, weakness, abdominal pain, nausea, vomiting, chest pain, febrile illness, and medication noncompliance. Altered mental status may be present. Physical examination commonly reveals tachycardia, hypotension from dehydration or sepsis, tachypnea with hyperpnea, Kussmaul respirations, dehydration with poor skin turgor and dry mucous membranes, ketone odor on the breath, and diffuse abdominal tenderness. Temperature abnormalities may reflect infection.


Essential workup
Diagnostic criteria include venous pH <7.3, serum bicarbonate <15 meq />, hyperglycemia >250 mg/dL, and ketonemia or ketonuria. Initial evaluation requires bedside glucose testing, venous blood gas, serum electrolytes, BUN and creatinine, urine dipstick for ketones, and assessment for a precipitating cause.


Diagnosis tests & interpretation
Lab Serum glucose confirms hyperglycemia. Electrolytes show an increased anion gap metabolic acidosis [Na − (Cl + HCO₃)] >12. Serum sodium may be falsely low due to hyperglycemia and should be corrected by adding 1.6 mEq/L for every 100 mg/dL glucose above 100 mg/dL. Potassium is often normal or elevated initially due to extracellular shift, despite a total body deficit of 3-5 mEq/kg; levels fall rapidly with insulin and fluids. Bicarbonate is typically markedly reduced. BUN and creatinine reflect prerenal azotemia from dehydration. Serum ketones must be present; β-hydroxybutyrate predominates and may be underestimated by nitroprusside testing. Urine ketone dip testing is highly sensitive, and point-of-care β-hydroxybutyrate testing can aid early diagnosis. CBC often shows stress leukocytosis. Serum osmolality may be elevated (>320 mOsm/L). Imaging includes chest radiography for suspected pneumonia, ECG to assess ischemia or potassium abnormalities, and head CT if altered mental status is unexplained.


Differential diagnosis
Other causes of anion gap metabolic acidosis include alcoholic ketoacidosis, lactic acidosis, toxic ingestions (salicylates, methanol, ethylene glycol), uremia, starvation or sepsis, and hyperglycemic hyperosmolar nonketotic syndrome.


Treatment
Pre hospital Early fluid resuscitation is often initiated; total prehospital volume should be documented to guide ongoing therapy.
Initial stabilization/therapy Address airway, breathing, and circulation, particularly in patients with altered mental status. Administer supplemental oxygen as needed and give an initial bolus of 0.9% normal saline for hypotension or tachycardia.
Ed treatment/procedures Continuous cardiac monitoring and pulse oximetry are required for unstable patients. Fluid therapy assumes a total deficit of approximately 100 mL/kg. Administer 1–2 L of 0.9% normal saline in the first hour. Continue isotonic saline if corrected sodium is low, or switch to 0.45% saline if corrected sodium is normal or high. Replace the remaining deficit gradually over 24–36 hours to avoid rapid osmolar shifts. Insulin therapy is initiated with continuous IV regular insulin at 0.1 U/kg/h after confirmation of DKA and adequate potassium levels, titrated to close the anion gap rather than normalize glucose alone. Add dextrose-containing fluids when serum glucose falls below 250–300 mg/dL. Potassium replacement is essential once urine output is established and serum potassium is <5.5 meq />; insulin should be delayed if potassium is <3.5 meq />. Bicarbonate therapy is generally avoided and reserved only for severe acidosis (pH <6.9) with cardiovascular compromise. phosphate and magnesium replacement are not routine but may be required in severe deficiencies. the underlying precipitating cause must identified treated.< />pan>


Medication
Regular insulin infusion at 0.1 U/kg/h IV. Potassium chloride supplementation as indicated. Dextrose-containing IV fluids once glucose levels decline. Magnesium sulfate or phosphate replacement when clinically necessary.


Follow-up disposition
Admission criteria ICU admission is required for severe DKA with pH <7.0, altered mental status, hemodynamic instability, serious comorbid illness, or extremes of age. moderate dka may be managed in a monitored unit, while mild cases without complications observed.< />pan>
Discharge criteria Resolution of anion gap acidosis, tolerance of oral intake, stable vital signs, no ongoing precipitating illness, and reliable follow-up with clear insulin instructions.


Pearls and pitfalls
Insulin infusion should not be reduced or stopped solely because glucose normalizes; it must continue until acidosis and anion gap resolve. Failure to aggressively monitor and replace potassium is a common and dangerous error.