Emergency And Acute Medicine - Ehrlichiosis


Foundational overview
Ehrlichiosis is a tick-transmitted human infection that typically presents as a nonspecific febrile illness. Multiple forms exist, but two predominate in North America. Human monocytic ehrlichiosis was first recognized in 1987 and is transmitted by the lone star tick, Amblyomma americanum, with distribution primarily in the central, southern, and mid-Atlantic United States and expansion into parts of New England. Human granulocytic ehrlichiosis, also known as human granulocytic anaplasmosis, was described in 1994 and is transmitted by Ixodes scapularis, the same vector responsible for Lyme disease. Although all forms are tick borne, they differ in vectors and geographic distribution, with HME and HGE/HGA representing the clinically most relevant pathogens.


Causative organisms and pathogenesis
Ehrlichiosis is caused by obligate intracellular bacteria. Human monocytic ehrlichiosis results from infection with Ehrlichia chaffeensis, whereas human granulocytic ehrlichiosis/anaplasmosis is caused by Anaplasma phagocytophila. Taxonomic classification has evolved with advances in molecular diagnostics. Unlike Rocky Mountain spotted fever, vasculitis is typically absent. A third clinically similar infection caused by Ehrlichia ewingii may occur, also transmitted by the lone star tick. Compared with RMSF, ehrlichiosis more commonly affects adults over 40 years of age.


Clinical manifestations and symptom patterns
The clinical features of HME and HGE/HGA are largely overlapping. Many infected individuals experience asymptomatic seroconversion, and reported cases often represent more severe illness. Coinfection with other tick-borne pathogens from a single bite may complicate the presentation. Approximately one-quarter of pediatric patients develop severe disease.


Historical features
Epidemiologic context is critical. Most cases occur between April and October, with seasonal variability related to climate and geography. Symptoms typically begin 1–2 weeks after a tick bite, with a median onset of 9–10 days. Patients may recall a lone star tick bite more readily than a deer tick bite. Onset is often abrupt and includes fever, chills, headache, myalgias, and malaise. Rash is common in HME but infrequent in HGE/HGA and is often delayed. Severe illness may involve complications such as acute respiratory distress syndrome, renal failure, shock, rhabdomyolysis, gastrointestinal symptoms, central or peripheral nervous system involvement, seizures, or disseminated intravascular coagulation. Immunocompromised patients are at higher risk for severe outcomes.


Physical examination findings
Patients are typically febrile. Rash, when present, may be macular, maculopapular, or petechial and usually involves the trunk while sparing the palms and soles. Lymphadenopathy and hepatosplenomegaly may occur. Neurologic abnormalities can include altered mental status or meningismus, and pulmonary findings such as rales or rhonchi may be evident in patients with respiratory complications. In children, fever, headache, and rash are common, with lymphadenopathy frequently noted.


Essential diagnostic approach
Ehrlichiosis is primarily a clinical diagnosis and should be considered in patients with undifferentiated febrile illness during warm months, particularly with possible tick exposure. The CDC defines the illness as fever accompanied by symptoms such as headache, myalgia, cytopenias, or elevated transaminases, along with confirmatory laboratory evidence.


Laboratory evaluation and interpretation
Common laboratory abnormalities include leukopenia, thrombocytopenia, anemia, and elevated hepatic transaminases, often two to six times normal. Indirect immunofluorescence antibody testing is widely available and highly sensitive when paired acute and convalescent samples are obtained. Peripheral blood smear may reveal morulae, more commonly in HGE/HGA than HME, though sensitivity varies. PCR and culture testing are not routinely available. Lumbar puncture may show lymphocytic pleocytosis and elevated protein. Imaging is guided by complications, including head CT for encephalopathy and chest radiography for respiratory symptoms.


Conditions to distinguish from ehrlichiosis
The differential diagnosis includes other tick-borne illnesses such as Rocky Mountain spotted fever, Lyme disease, and babesiosis, as well as viral syndromes, mononucleosis, thrombotic thrombocytopenic purpura, hematologic malignancies, cholangitis, and pneumonia.


Initial stabilization principles
Standard airway, breathing, and circulation assessment should be performed in all patients.


Emergency department management
Empiric antimicrobial therapy should be initiated promptly when ehrlichiosis is suspected. Doxycycline is the treatment of choice for adults and children, including those under 9 years of age, as short courses have not been shown to cause clinically significant tooth discoloration. Therapy should continue for at least three days after fever resolution, with a minimum total course of seven days; longer treatment is required for severe disease. Rifampin may be used in pregnant patients, those with doxycycline allergy, or mildly affected young children. Coverage for other potential coinfections should be considered.


Medication considerations
Doxycycline is administered at 100 mg IV or orally every 12 hours in adults. Pediatric dosing is weight based, up to adult maximums. Despite typical age-related contraindications, doxycycline remains the drug of choice for severe pediatric disease. Rifampin is an alternative in selected populations. In pregnancy, rifampin is preferred, though doxycycline may be considered in life-threatening illness.


Disposition and follow-up planning
Hospital admission is recommended for patients with severe disease, significant comorbidities, immunosuppression, or inability to tolerate oral therapy. The case fatality rate for HME may reach 3%. Patients with mild illness who appear clinically stable may be discharged with close follow-up, as symptoms usually resolve within one to two weeks, though rare long-term neurologic sequelae have been reported.


Referral considerations
Specialty consultation is indicated for patients with severe or complicated disease.


Key clinical insights and common errors
Ehrlichiosis is a potentially fatal but treatable tick-borne illness that is frequently diagnosed clinically. Failure to consider it in patients with nonspecific febrile illness during tick season is a common error. Early initiation of doxycycline significantly improves outcomes and should not be delayed pending confirmatory testing. Coinfection with other tick-borne pathogens should always be considered, particularly in endemic regions.

Emergency And Acute Medicine – Diaper Rash


Basics
Description Very common dermatologic disorder of infancy. Most frequent in the first month of life and again between 12–24 months. In adult incontinent patients, incidence ranges from 5.7% to more than 42% and increases with age. Diaper rash is most often a primary irritant or contact dermatitis in which disruption of the outer skin layers leads to inflammation, impairment of normal skin microflora, and loss of barrier function. Excess moisture promotes microbial overgrowth. Secondary fungal or bacterial infection may result in more severe disease. Also referred to as irritant diaper dermatitis.


Etiology
Irritants Moisture from prolonged overhydration due to infrequent diaper changes, poorly absorbent or cloth diapers, and urinary or fecal incontinence in adults. Friction from diaper rubbing or loose-fitting diapers. Chemical irritation from prolonged exposure to stool enzymes, urine, scented wipes, soaps, diaper materials, or adhesives.
Infection Candida albicans is isolated in up to 80% of infants, particularly after systemic antibiotic use. Bacterial infection is usually secondary and commonly involves Staphylococcus aureus, Streptococcus, or Escherichia coli, with occasional Peptostreptococcus and Bacteroides. Other etiologies include seborrheic diaper dermatitis and atopic (contact) diaper dermatitis. Risk factors include oral thrush, multiple prior episodes, prolonged diaper use, and diarrhea.


Diagnosis
Diagnosis is typically clinical and based on the appearance and distribution of the rash.


Signs And Symptoms
History The child may cry during diaper changes or wiping and may appear irritable.
Physical exam Irritant dermatitis presents as beefy-red confluent patches with sharp borders at the diaper edges, usually sparing skin folds. Candidal dermatitis appears as a well-demarcated erythematous rash with satellite pustules or papules and commonly involves skin folds. Bacterial infection may cause superficial erosions with yellow crusting or bullae. Seborrheic diaper dermatitis presents with erythematous plaques and greasy yellow or gray scale and is often associated with scalp involvement. Atopic diaper dermatitis resembles irritant dermatitis but includes lesions on other areas such as the face. Variants include Jacquet erosive dermatitis with ulcers or erosions, psoriasiform dermatitis with silvery scale and spared folds, and granuloma gluteale infantum characterized by violaceous papules or nodules that resolve over weeks to months and may scar.


Essential Workup
Assess diaper-changing practices and urinary and fecal habits. Examine other body areas for associated rashes. Consider child abuse or neglect by evaluating hygiene and looking for burns or other trauma.


Diagnosis Tests And Interpretation
Laboratory testing is usually unnecessary. Bacterial cultures are reserved for complicated cases. Skin scrapings with potassium hydroxide preparation or culture may help distinguish candidal infection from atypical seborrheic dermatitis by identifying budding yeast or pseudohyphae.


Differential Diagnosis
Includes child abuse or neglect, impetigo, scabies, herpes simplex, varicella, congenital syphilis, psoriasis, atopic dermatitis, seborrheic dermatitis, papular urticaria, bullous pemphigoid, epidermolysis bullosa, acrodermatitis enteropathica, acrodermatitis enteropathica–like eruption, and Langerhans cell histiocytosis.


Treatment
Emergency department treatment and procedures Management focuses on reducing moisture, minimizing contact with urine and feces, and treating infection when present. Cleanse gently with water and cotton balls; avoid wipes, talcum powder, harsh soaps, and alcohol. Change diapers frequently, allow air drying, and keep the area uncovered when possible. Use highly absorbent disposable diapers and avoid cloth diapers during active dermatitis.
Barrier creams Zinc oxide, petroleum, or lanolin applied after each diaper change and continued after resolution to prevent recurrence. Apply over antifungal medication if Candida is present.
Corticosteroids Low-potency topical hydrocortisone (≤1%) for short courses in moderate to severe inflammation; discontinue after 3–5 days.
Antifungals Nystatin, clotrimazole, miconazole, or ciclopirox applied after diaper changes and continued for 1–2 days after clearing. Consider oral antifungal therapy in refractory cases or with concurrent oral candidiasis.
Antibacterials Topical mupirocin if bacterial infection is suspected; systemic antibiotics are rarely required.


Medication
Ciclopirox 0.77% cream, gel, or suspension applied topically twice daily after diaper changes. Clotrimazole 1% cream applied twice daily after diaper changes. Hydrocortisone 0.5–1% cream applied twice daily. Miconazole 2% cream applied twice daily after diaper changes. Miconazole nitrate 0.25% ointment applied after diaper changes and bathing. Mupirocin 2% ointment or cream applied 3–5 times daily after diaper changes in infants older than 3 months. Nystatin 100,000 U/g cream, powder, or ointment applied twice daily after diaper changes.


Follow-Up Disposition
Admission criteria Evidence of child abuse or neglect or signs of sepsis.

Emergency and Acute Medicine - Dialysis Complications


Basics
Description Dialysis complications may be vascular access related, nonvascular access related, or peritoneal. Vascular access complications include infection and bleeding. Nonvascular complications include hypotension and electrolyte disturbances such as hyperkalemia. Peritoneal complications most commonly involve abdominal pain and infection.


Etiology
Vascular access related complications include infections, which are a major cause of morbidity and mortality in dialysis patients and are most often caused by Staphylococcus aureus. These infections may present with localized signs, systemic sepsis, or minimal findings. Thrombosis or stenosis of access sites often presents with loss of bruit or thrill and requires urgent intervention to prevent access loss. Bleeding from access sites can be life-threatening and may be associated with aneurysm formation.


Nonvascular access related complications include hypotension, the most common complication of hemodialysis. This may occur during or after dialysis due to acute intravascular volume depletion, myocardial ischemia, sepsis, dysrhythmias, hypoxia, or cardiac tamponade unmasked by volume shifts. Hemorrhage may result from anticoagulation or platelet dysfunction related to renal failure. Shortness of breath may be caused by volume overload, tamponade, pericardial effusion, pulmonary embolism, air embolism, hemorrhage, or anaphylaxis. Chest pain may be ischemic due to high prevalence of atherosclerotic disease or pleuritic from pericarditis or pulmonary embolism. Neurologic dysfunction may occur due to disequilibrium syndrome caused by rapid decreases in serum osmolality during dialysis.


Peritoneal complications include peritonitis from contamination during exchanges, most commonly due to Staphylococcus aureus or Staphylococcus epidermidis. Perforated viscus presents with severe abdominal pain, fever, feculent effluent, or focal tenderness. Fibrinous catheter blockage may occur secondary to infection or inflammation.


Diagnosis
Signs and symptoms Vascular access complications present with bleeding from puncture sites, loss of bruit or thrill, local infection, fever, distal neurologic deficits, or enlarging masses near access sites. Nonvascular complications include hypotension, palpitations, syncope, chest pain, dyspnea, hemorrhage, and neurologic symptoms such as headache, malaise, seizures, or coma. Peritoneal complications present with abdominal pain, cloudy effluent, nausea, vomiting, or inflammation at the Tenckhoff catheter site.


Essential workup
A thorough physical examination is essential, including complete vital signs with auscultated blood pressure, pulse oximetry, and temperature. Evaluate for occult infection, volume overload, pulmonary findings, and cardiac abnormalities such as murmurs or pericardial rubs. Obtain ECG to assess for electrolyte disturbances or ischemia. Perform blood cultures, wound cultures, and peritoneal fluid analysis when infection is suspected. CBC and coagulation studies are required for bleeding. Chest radiograph, arterial blood gas, and cardiac enzymes are indicated for chest pain or dyspnea. Neurologic symptoms warrant brain imaging to exclude intracranial hemorrhage.


Diagnosis tests and interpretation
Lab studies include glucose, electrolytes, BUN, creatinine, and CBC. Imaging includes ECG for suspected hyperkalemia, pericarditis, effusion, or tamponade. Ultrasound of vascular access evaluates thrombosis or stenosis. Echocardiography assesses pericardial effusion or tamponade. CT angiography may be required for suspected pulmonary embolism, with careful coordination regarding contrast load and dialysis planning.


Differential diagnosis
Hypotension may be due to sepsis, cardiogenic shock, myocardial infarction, tamponade, dysrhythmias, electrolyte abnormalities, embolism, hypovolemia, or autonomic dysfunction. Neurologic symptoms may result from stroke, disequilibrium syndrome, metabolic derangements, hypoxemia, intracranial bleeding, infection, or uremia. Peritoneal symptoms require differentiation from hernia incarceration, perforated viscus, appendicitis, or cholecystitis.


Treatment
Pre hospital Avoid IV access and blood pressure measurement in limbs with functioning arteriovenous fistulas or grafts. Administer IV fluids cautiously and minimize volume. Use high-dose furosemide for pulmonary edema in anuric patients when appropriate.


Initial stabilization and therapy
Assess airway, breathing, and circulation. Control vascular access bleeding with firm pressure without fully occluding flow, document thrill afterward, and use hemostatic agents if needed. Treat hypotension by identifying the cause and administering fluids or vasopressors as indicated. Manage dyspnea with preload and afterload reduction and arrange urgent dialysis. Treat hyperkalemia with calcium, insulin with glucose, bicarbonate when appropriate, and cardiac monitoring, followed by dialysis. Address neurologic complications with glucose checks, naloxone, thiamine, and seizure control.


Emergency department treatment and procedures
Initiate empiric antistaphylococcal antibiotics for suspected access infections. Consult vascular surgery urgently for clotted access. Control hemorrhage and correct coagulopathies with fluids and blood products. Manage electrolyte disturbances and volume overload with medications and dialysis. Perform emergent pericardiocentesis for tamponade in unstable patients. Treat acute myocardial infarction according to standard protocols when appropriate. Manage peritonitis with IV or intraperitoneal antibiotics and obtain surgical consultation for suspected perforation.


Medication
Commonly used medications include calcium gluconate for cardioprotection in hyperkalemia, insulin with dextrose, sodium bicarbonate, loop diuretics, nitrates, ACE inhibitors, vasopressors, antistaphylococcal antibiotics, and intraperitoneal antibiotics for peritonitis.


Follow-up disposition
Admission criteria ICU admission is required for severe hyperkalemia, pulmonary edema, persistent hypotension, uncontrolled seizures, acute myocardial infarction, stroke, tamponade, sepsis, or severe peritonitis. General admission is indicated for fever, vomiting, nonsevere peritonitis, or inability to self-manage peritoneal dialysis.
Discharge criteria Patients with mild access-site infections, successful hemostasis, or select same-day thrombectomy procedures may be discharged with close follow-up.


Follow-up recommendations
Most dialysis patients require close follow-up with their nephrologist for ongoing management.


Pearls and pitfalls
Always consider hyperkalemia in dialysis patients. Cardiac tamponade may present atypically. Infections often have subtle presentations yet carry high mortality. Early vascular surgery consultation is critical for clotted or ruptured access sites.

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.

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 – 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 – 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 – 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.