Internal Medicine

A

• Acute Gout Flare — NSAIDs, Colchicine, Corticosteroids, and When to Start ULT

  Treat acute gout with NSAIDs, colchicine, or corticosteroids (intra-articular or systemic). Exclude septic arthritis when uncertain. Start urate-lowering therapy after flares are controlled in patients with tophi, frequent flares, or CKD; provide flare prophylaxis during ULT initiation.
• Acute Kidney Injury — KDIGO Staging, Prerenal vs Intrinsic vs Postrenal, and Nephrotoxins

  AKI is an abrupt decline in kidney function. Identify prerenal, intrinsic, and postrenal causes using history, exam, labs, and ultrasound; stage using KDIGO criteria; stop nephrotoxins; optimize hemodynamics; and involve nephrology for refractory complications or RRT indications.
• Acute Pyelonephritis — Risk Stratification, Imaging Indications, and Antibiotic Therapy

  Fever, flank pain, and CVA tenderness with pyuria/bacteriuria. Outpatient therapy for uncomplicated cases; admit if severe, pregnant, septic, or unable to tolerate PO. Obtain imaging if obstruction suspected or no improvement by 48–72 hours.
• Adult Asthma Exacerbation — SABA, Systemic Steroids, Magnesium, and Disposition

  Treat acute asthma with repeated inhaled short-acting beta-agonists (± ipratropium for severe), early systemic corticosteroids, and adjunct IV magnesium for severe exacerbations; provide oxygen to maintain SpO₂ 93–95%. Consider epinephrine and noninvasive ventilation/intubation if impending failure.
• Alcohol Withdrawal - Inpatient Benzodiazepine and Phenobarbital Algorithm

  Use symptom triggered benzodiazepines when possible; give thiamine before glucose, consider phenobarbital adjunct or loading in severe cases, and escalate monitoring for refractory agitation.

C

• Chronic Hyponatremia - Safe Correction Limits and Desmopressin Clamp

  Chronic hyponatremia becomes dangerous when serum sodium is corrected faster than the brain can readapt, producing osmotic demyelination syndrome. Treatment therefore balances relief of severe cerebral edema against strict correction limits. High-risk patients should generally remain within an 8 mmol/L rise in any 24-hour period. Desmopressin and electrolyte-free water can prevent or reverse overcorrection when a sudden water diuresis causes sodium to rise unexpectedly.
• Clostridioides difficile Infection - Severity Assessment and Treatment

  Clostridioides difficile infection is diagnosed when compatible diarrhea or ileus is accompanied by appropriate microbiologic evidence. Treatment depends on severity, recurrence history, and fulminant features. Fidaxomicin is preferred for many initial and recurrent nonfulminant episodes when available, with oral vancomycin an acceptable alternative. Fulminant disease requires high-dose enteral vancomycin, IV metronidazole, aggressive supportive care, and early surgical consultation.
• Clostridioides difficile Infection — Severity Stratification, Fidaxomicin/Vancomycin, and FMT

  Suspect CDI with new-onset diarrhea after antibiotics or hospitalization. Use toxin immunoassay and NAAT algorithm. Treat initial episodes with fidaxomicin (preferred) or vancomycin; use vancomycin taper or fidaxomicin for recurrences; consider FMT after multiple recurrences.
• Community-Acquired Cellulitis — MRSA Considerations, Lymphatic Care, and Source Control

  Erythema, warmth, and tenderness of skin/subcutaneous tissue. Differentiate purulent vs nonpurulent cellulitis; drain abscesses and choose antibiotics considering MRSA risk. Address risk factors (tinea pedis, edema, venous stasis) to prevent recurrence.

D

• Deep Vein Thrombosis — Wells Score, Compression Ultrasound, and Anticoagulation

  Evaluate suspected DVT using Wells score and D-dimer in low probability cases. Confirm with compression ultrasonography. Start anticoagulation with DOACs or LMWH/warfarin; determine duration based on provoked vs unprovoked events and bleeding risk.
• Diabetic Foot Osteomyelitis — Probe-to-Bone, MRI, Debridement, and Targeted Antibiotics

  Suspect osteomyelitis in chronic or deep diabetic foot ulcers, especially with positive probe-to-bone test. Confirm with MRI and bone culture when feasible. Combine surgical debridement/revascularization with prolonged targeted antibiotics and offloading for limb salvage.

H

• Heparin-Induced Thrombocytopenia — 4T Score, PF4 Testing, and Non-Heparin Anticoagulation

  Suspect HIT with platelet fall 5–10 days after heparin exposure or sooner with prior exposure. Stop all heparin immediately, estimate probability with the 4T score, send PF4 ELISA and functional assay, and start a non-heparin anticoagulant while awaiting results in intermediate/high probability.
• Hypernatremia — Volume Repletion, Free Water Deficit, and Correction Limits

  Hypernatremia reflects hypertonicity, usually from water deficit. Restore intravascular volume with isotonic fluids first, then replace free water based on deficit and ongoing losses, limiting correction to ≤10–12 mEq/L/day (≤8 in high-risk) to avoid cerebral edema.
• Hyperosmolar Hyperglycemic State — Cautious Fluids, Insulin, and Electrolyte Strategy

  HHS features profound hyperglycemia, hyperosmolality, and minimal ketosis. Begin cautious isotonic fluids, correct potassium, then start insulin at lower rates than DKA; avoid rapid osmotic shifts. Search for precipitants (infection, MI, stroke, medications).

I

• Inpatient Delirium - Prevention and Management Bundle

  Prevent and treat delirium with multicomponent non pharmacologic measures, regular screening, and judicious medication use while correcting underlying precipitants.
• Inpatient Glycemic Control - Basal Bolus Insulin Protocol

  Inpatient glycemic management should prevent both clinically important hyperglycemia and hypoglycemia while adapting insulin to nutrition, illness severity, renal function, and prior therapy. For most noncritically ill hospitalized adults, the 2026 ADA Standards recommend a glucose target of 100 to 180 mg/dL. Basal plus correction insulin is preferred with poor intake, while basal-prandial-correction therapy is preferred when nutritional intake is reliable; prolonged correction-only treatment is discouraged
• Iron Deficiency Anemia - Intravenous Iron Selection and Dosing

  Intravenous iron rapidly replaces iron stores when oral iron is ineffective, poorly tolerated, too slow, or poorly absorbed. Selection among ferric carboxymaltose, ferric derisomaltose, ferumoxytol, iron sucrose, and low-molecular-weight iron dextran depends on required elemental iron dose, number of visits, kidney disease, infusion setting, cost, and adverse-effect profile. The underlying cause of iron deficiency must be identified rather than treating the ferritin alone.
• Iron Deficiency Anemia — Evaluation, Oral/IV Iron Dosing, and Transfusion Strategy

  Microcytic anemia with low ferritin and high transferrin indicates iron deficiency. Identify source of blood loss (GI, gynecologic), dose oral iron using alternate-day schedules for better absorption, use IV iron when intolerance or malabsorption, and transfuse based on symptoms and thresholds.

L

• Lower Gastrointestinal Bleeding — Resuscitation, Colonoscopy Timing, and IR Options

  Hematochezia often from diverticulosis, angiodysplasia, or hemorrhoids. Resuscitate with restrictive transfusion, exclude brisk upper source when indicated, perform colonoscopy within 24 hours after prep; use CT angiography and IR embolization for ongoing massive bleeding.

M

• Myxedema Coma — IV Thyroxine, Hydrocortisone, and Gentle Rewarming

  Severe decompensated hypothyroidism with hypothermia, bradycardia, hypotension, and altered mental status. Give IV levothyroxine (± liothyronine), administer stress-dose steroids until adrenal insufficiency excluded, correct precipitating factors, and provide slow rewarming and ventilatory support.

P

• Periprocedural Anticoagulation - DOAC and Warfarin Interruption and Bridging

  Periprocedural anticoagulation management balances procedure bleeding risk against the patient's risk of thrombosis during interruption. Most patients taking DOACs require a short drug hold without heparin bridging. Most patients with atrial fibrillation receiving warfarin also should not be bridged. Timing depends on the anticoagulant, renal function, procedure bleeding risk, and whether neuraxial anesthesia or another especially high-risk procedure is planned.
• Positive Blood Cultures without Source - Inpatient Evaluation and Follow Up

  A positive blood culture without an obvious source requires rapid distinction among true bloodstream infection, catheter-related infection, endovascular infection, and contamination. Interpretation depends on the organism, number of positive sets, time to positivity, host factors, prosthetic material, and clinical syndrome. Staphylococcus aureus, Candida species, and many gram-negative organisms should generally be treated as clinically significant until proven otherwise, while a single bottle with common s

R

• Refeeding Syndrome - Prevention and Electrolyte Protocol

  Refeeding syndrome is a potentially fatal shift in phosphate, potassium, magnesium, fluid, and thiamine metabolism after nutrition is restarted in a severely undernourished patient. Prevention requires identifying high-risk patients before feeding, checking and replacing electrolytes, giving thiamine, initiating calories cautiously, and advancing nutrition while monitoring closely. New arrhythmia, weakness, edema, respiratory failure, delirium, or falling phosphate after feeding should prompt immediate reas

S

• Severe Alcohol Withdrawal (Delirium Tremens) — Benzodiazepines, Phenobarbital Pathway, and Thiamine

  Autonomic hyperactivity, agitation, hallucinations, and seizures peak at 48–72 hours after cessation. Use symptom-triggered or front-loaded benzodiazepines; consider adjunct phenobarbital or dexmedetomidine/propofol in ICU. Give high-dose IV thiamine before glucose to prevent Wernicke's.
• Severe Hyponatremia — Symptom-Driven 3% Saline, DDAVP Clamp, and Safe Correction

  Manage severe or symptomatic hyponatremia with hypertonic saline boluses and a desmopressin ('DDAVP') clamp to prevent overly rapid correction. Identify etiology (hypovolemic, euvolemic/SIADH, hypervolemic) and treat the cause while monitoring sodium correction limits to prevent osmotic demyelination.

V

• VTE Prophylaxis for Medical Inpatients - Risk Stratification and Dosing

  Venous thromboembolism prevention in hospitalized medical patients begins with individualized assessment of VTE risk, bleeding risk, mobility, renal function, and contraindications. Acutely ill patients at sufficient VTE risk generally receive pharmacologic prophylaxis with low-molecular-weight heparin, low-dose unfractionated heparin, or fondaparinux when bleeding risk is acceptable. Mechanical prophylaxis is reserved mainly for patients in whom anticoagulant prophylaxis is inappropriate.