<div class="ec-hub-title">Welcome to Critical</div> <div class="ec-hub-intro">A free USMLE Step 2 CK question bank — 214 cases, one best answer per item, immediate feedback, retries, and a sourced debrief for every choice. Built for medical students.</div> <div style="margin:1em 0 1.6em; padding:.9em 1.1em; border-left:3px solid #f59e0b; background:rgba(245,158,11,.06); color:#cbd5e1; font-size:.88rem; line-height:1.55; border-radius:0 4px 4px 0;"><b style="color:#f59e0b;">⚠ Beta — read this before you use it to study.</b><br>Critical is a free, community-audited tool. Every clinical claim carries a source line, and each was checked against a live guideline at the time the case was written. <b>No physician has yet done a formal content review.</b> Some citations are tertiary (StatPearls, AMBOSS, Medscape) and citation drift — a real source attached to a claim it does not quite support — is a real risk that no automated check can rule out. Use Critical as practice, not as your only reference; verify high-stakes points against a primary guideline; and if you spot an error, please report it.</div> [[→ Sepsis — Ix->Sepsis — Ix]] [[→ Acute GI bleed (Sequential — 3 Questions) — Ix->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[→ STEMI — Ix->STEMI — Ix]] [[→ Pulmonary embolism — Ix->Pulmonary embolism — Ix]] [[→ Tension pneumothorax — Dx->Tension pneumothorax — Dx]] [[→ Aortic dissection — Dx->Aortic dissection — Dx]] [[→ Acute appendicitis — Rx->Acute appendicitis — Rx]] [[→ Acute kidney injury — Ix->Acute kidney injury — Ix]] [[→ DKA management — Rx->DKA management — Rx]] [[→ Thyroid storm — Dx->Thyroid storm — Dx]] [[→ Acute chest syndrome — Dx->Acute chest syndrome — Dx]] [[→ Status epilepticus — Opening->Status epilepticus — Opening]] [[→ Stroke — Ix->Stroke — Ix]] [[→ Opioid overdose — Rx->Opioid overdose — Rx]] [[→ Ectopic pregnancy — Dx->Ectopic pregnancy — Dx]] [[→ Eclampsia — Dx->Eclampsia — Dx]] [[→ Compartment syndrome — Ix->Compartment syndrome — Ix]] [[→ Acute gout — Rx->Acute gout — Rx]] [[→ Error disclosure — Opening->Error disclosure — Opening]] [[→ Neonatal jaundice — Rx->Neonatal jaundice — Rx]]<div class="ec-scene">Emergency Department · 21:50</div> A 4-year-old boy weighing 17 kg is lethargic after two days of fever and vomiting. He is mottled with cool peripheries and a capillary refill of four seconds. Temperature is 39.2°C, heart rate 178/min, respiratory rate 36/min, and blood pressure 72/38 mm Hg. He responds only to voice. Intravenous access has just been obtained and you are about to give antibiotics. <span class="ec-prompt">Which is the most appropriate next step in diagnosis?</span> [[Blood cultures before antibiotics->Sepsis — Ix correct]] [[CT of the abdomen->Sepsis — Ix D3]] [[Lumbar puncture->Sepsis — Ix D1]] [[Repeat serum lactate in 2 hours->Sepsis — Ix D2]] [[Serum procalcitonin->Sepsis — Ix D5]] [[Urine culture by bag specimen->Sepsis — Ix D4]]<div class="ec-scene">Emergency Department · 03:15</div> <div class="ec-seq-badge">Sequential Case — Question 1 of 3</div> A 62-year-old man with a history of cirrhosis presents with large-volume hematemesis. He is pale, diaphoretic, and confused. Temperature is 36.4°C (97.5°F), heart rate is 124/min, blood pressure is 78/52 mm Hg, and respirations are 22/min. Hemoglobin is 6.8 g/dL. Which is the most appropriate initial step? [[CT angiography of the abdomen to localize the bleeding source->Acute GI bleed — Q1 E]] [[Emergent upper endoscopy before any resuscitation->Acute GI bleed — Q1 A]] [[Immediate surgical consultation for exploratory laparotomy->Acute GI bleed — Q1 D]] [[Oral proton pump inhibitor and observation->Acute GI bleed — Q1 C]] [[Volume resuscitation with crystalloid and packed RBC transfusion->Acute GI bleed — Q1 Correct]]<div class="ec-scene">Emergency Department · 06:15</div> A 59-year-old man has 50 minutes of crushing central chest pain with diaphoresis. The initial 12-lead ECG shows ST elevation in leads II, III and aVF with reciprocal depression in I and aVL. Temperature is 36.8°C, heart rate 58/min, respiratory rate 16/min, and blood pressure 112/70 mm Hg. Aspirin has been given and the catheterization laboratory has been alerted. <span class="ec-prompt">Which is the most appropriate next step in diagnosis?</span> [[Bedside echocardiography->STEMI — Ix D2]] [[Chest radiography->STEMI — Ix D5]] [[CT coronary angiography->STEMI — Ix D4]] [[Posterior leads V7 to V9->STEMI — Ix D3]] [[Right-sided ECG leads V4R to V6R->STEMI — Ix correct]] [[Serial troponin measurement->STEMI — Ix D1]]<div class="ec-scene">Emergency Department · 17:30</div> A 58-year-old woman has one day of pleuritic chest pain and breathlessness, three weeks after a total knee replacement. Temperature is 37.4°C, heart rate 112/min, respiratory rate 22/min, blood pressure 118/74 mm Hg, and oxygen saturation 91% on room air. There is mild right calf swelling and tenderness. She has no hemoptysis. Chest radiograph is clear and the ECG shows sinus tachycardia. She has no contrast allergy and renal function is normal. Pulmonary embolism is your leading diagnosis. <span class="ec-prompt">Which is the most appropriate next step in diagnosis?</span> [[CT pulmonary angiography->Pulmonary embolism — Ix correct]] [[D-dimer measurement->Pulmonary embolism — Ix d-dimer]] [[Echocardiography->Pulmonary embolism — Ix echocardiography]] [[Lower extremity compression ultrasonography->Pulmonary embolism — Ix lower]] [[Repeat chest radiography in 6 hours->Pulmonary embolism — Ix repeat]] [[Ventilation-perfusion scanning->Pulmonary embolism — Ix ventilation-perfusion]]<div class="ec-scene">Emergency Department · 21:15</div> A 27-year-old man is brought in after a motorcycle crash with severe breathlessness. Temperature is 36.9°C, heart rate 138/min, respiratory rate 34/min, blood pressure 76/48 mm Hg, and oxygen saturation 84% on high-flow oxygen. Breath sounds are absent over the left hemithorax, which is hyperresonant to percussion. The trachea is deviated to the right and the jugular venous pressure is raised. He is becoming agitated. <span class="ec-prompt">Which is the most likely diagnosis?</span> [[Cardiac tamponade->Tension pneumothorax — Dx D2]] [[Flail chest with pulmonary contusion->Tension pneumothorax — Dx D3]] [[Massive hemothorax->Tension pneumothorax — Dx D1]] [[Ruptured thoracic aorta->Tension pneumothorax — Dx D5]] [[Tension pneumothorax->Tension pneumothorax — Dx correct]] [[Traumatic diaphragmatic rupture->Tension pneumothorax — Dx D4]]<div class="ec-scene">Emergency Department · 02:35</div> A 62-year-old man with long-standing hypertension has sudden severe chest pain that he describes as tearing and radiating between his shoulder blades. It was maximal at onset. Systolic pressure differs by nearly 40 mm Hg between arms. A soft early diastolic murmur is heard at the left sternal border. ECG shows left ventricular hypertrophy without ST elevation. Chest radiograph shows a widened mediastinum. <span class="ec-prompt">Which is the most likely diagnosis?</span> [[Acute pericarditis->Aortic dissection — Dx acute]] [[Aortic dissection->Aortic dissection — Dx correct]] [[Esophageal rupture->Aortic dissection — Dx esophageal]] [[ST-elevation myocardial infarction->Aortic dissection — Dx st-elevation]] [[Tension pneumothorax->Aortic dissection — Dx tension]]<div class="ec-scene">Emergency Department · 01:15</div> A 19-year-old man presents with 18 hours of abdominal pain that began periumbilically and migrated to the right lower quadrant. He has anorexia, nausea, and low-grade fever. Temperature is 37.9°C (100.2°F), blood pressure 122/76 mm Hg, and heart rate 94/min. On examination there is focal tenderness at McBurney’s point with guarding. WBC is 14,200/mm³. CT abdomen shows a dilated appendix with periappendiceal fat stranding and no perforation. <span class="ec-prompt">Which is the most appropriate management?</span> [[Intravenous antibiotics alone without surgery->Acute appendicitis — D2]] [[Laparoscopic appendectomy within 24 hours->Acute appendicitis — Correct]] [[Observation with serial abdominal examinations for 1 week->Acute appendicitis — D3]] [[Oral antibiotics and outpatient follow-up->Acute appendicitis — D1]] [[Percutaneous CT-guided drainage->Acute appendicitis — D4]]<div class="ec-scene">Emergency Department · 11:45</div> A 68-year-old woman has four days of vomiting and poor oral intake. She is orthostatic with dry mucous membranes. Creatinine has risen from a baseline of 0.9 to 3.1 mg/dL, with a blood urea nitrogen to creatinine ratio of 28. She takes lisinopril and ibuprofen. Urinalysis shows no protein, no blood and no casts on dipstick. <span class="ec-prompt">Which is the most appropriate next step in diagnosis?</span> [[Renal biopsy for histologic diagnosis->Acute kidney injury — Ix D5]] [[Renal ultrasonography->Acute kidney injury — Ix D1]] [[Repeat FENa after starting a diuretic->Acute kidney injury — Ix D2]] [[Serum and urine protein electrophoresis->Acute kidney injury — Ix D3]] [[Urine microscopy for sediment->Acute kidney injury — Ix correct]]<div class="ec-scene">Emergency Department · 07:20</div> A 22-year-old woman with type 1 diabetes presents with vomiting, diffuse abdominal pain, and Kussmaul respirations. Blood pressure is 94/62 mm Hg and heart rate is 118/min. Glucose is 480 mg/dL, arterial pH 7.12, serum bicarbonate 8 mEq/L, and β-hydroxybutyrate is 5.8 mmol/L. Serum potassium is 4.8 mEq/L. She has received 1 L of normal saline. <span class="ec-prompt">Which is the most appropriate next step in management?</span> [[Aggressive IV fluid resuscitation alone without insulin->DKA management — D2]] [[Continuous IV insulin with potassium and fluid management->DKA management — Correct]] [[Intravenous furosemide 40 mg for osmotic diuresis->DKA management — D1]] [[Intravenous sodium bicarbonate in all DKA patients->DKA management — D4]] [[Subcutaneous long-acting insulin glargine alone->DKA management — D3]]<div class="ec-scene">Emergency Department · 12:15</div> A 38-year-old woman with untreated Graves disease presents two days after an appendectomy with fever, agitation and palpitations. Temperature is 40.2°C, heart rate 168/min and irregularly irregular, respiratory rate 26/min, and blood pressure 148/62 mm Hg. She is tremulous with warm moist skin, a diffusely enlarged thyroid with an audible bruit, and lid lag. She has vomited repeatedly and has diarrhea. She is confused and intermittently combative. <span class="ec-prompt">Which is the most likely diagnosis?</span> [[Alcohol withdrawal->Thyroid storm — Dx alcohol]] [[Malignant hyperthermia->Thyroid storm — Dx malignant]] [[Postoperative sepsis->Thyroid storm — Dx postoperative]] [[Pulmonary embolism->Thyroid storm — Dx pulmonary]] [[Thyroid storm->Thyroid storm — Dx correct]]<div class="ec-scene">Hematology Floor · 05:15</div> A 24-year-old woman with homozygous sickle cell disease was admitted two days ago with a painful vaso-occlusive crisis affecting her back and thighs, treated with opioids and intravenous fluids. Overnight she develops fever, pleuritic chest pain and increasing dyspnea. Oxygen saturation has fallen to 88% on room air from 97% on admission. Chest radiograph now shows a new infiltrate in the left lower zone that was not present on admission. <span class="ec-prompt">Which is the most likely diagnosis?</span> [[Acute chest syndrome->Acute chest syndrome — Dx correct]] [[Fat embolism syndrome->Acute chest syndrome — Dx fat]] [[Hospital-acquired pneumonia->Acute chest syndrome — Dx hospital-acquired]] [[Pulmonary embolism->Acute chest syndrome — Dx pulmonary]] [[Vaso-occlusive crisis alone->Acute chest syndrome — Dx vaso-occlusive]]<div class="ec-scene">Emergency Department · 23:15</div> A 6-year-old girl with known epilepsy is brought in generalized tonic-clonic and still convulsing after eight continuous minutes. Her parents report she missed her evening medication. She weighs 21 kg. Intravenous access has been established and a bedside glucose is normal. <span class="ec-prompt">Convulsive status epilepticus. Which is the most appropriate pharmacotherapy?</span> [[CT head and labs first->Status epilepticus — Workup trap]] [[Give IV levetiracetam->Status epilepticus — Keppra first]] [[IV fosphenytoin as the initial agent->Status epilepticus — Fosphenytoin first trap]] [[IV lorazepam->Status epilepticus — Benzo correct]] [[Rectal diazepam as the initial benzodiazepine->Status epilepticus — Route trap]]<div class="ec-scene">Emergency Department · 08:20</div> A 72-year-old man developed right-sided weakness and difficulty speaking 65 minutes ago; the onset was witnessed by his wife. He takes amlodipine and no anticoagulant. Blood pressure is 168/94 mm Hg, glucose is 106 mg/dL. Examination shows a right facial droop, right arm and leg weakness, and expressive dysphasia. NIH Stroke Scale score is 14. He is within the thrombolysis window. <span class="ec-prompt">Which is the most appropriate next step in diagnosis?</span> [[Carotid duplex ultrasonography->Stroke — Ix carotid]] [[CT angiography of the head and neck->Stroke — Ix ct]] [[Diffusion-weighted MRI of the brain->Stroke — Ix diffusion-weighted]] [[Echocardiography with bubble study->Stroke — Ix echocardiography]] [[Lumbar puncture->Stroke — Ix lumbar]] [[Non-contrast CT of the head->Stroke — Ix correct]]<div class="ec-scene">Emergency Department · 23:55</div> A 31-year-old man is brought in unresponsive with a respiratory rate of 5/min, pinpoint pupils and oxygen saturation of 82%. Bag-valve-mask ventilation has been started with immediate improvement in saturation. Intravenous access is established. Bystanders report he uses heroin regularly and that the substance may have been mixed with fentanyl. <span class="ec-prompt">Which is the most appropriate pharmacotherapy?</span> [[Intramuscular naloxone as the initial route->Opioid overdose — Rx D3]] [[Intubate without naloxone->Opioid overdose — Rx D5]] [[Large single IV naloxone bolus->Opioid overdose — Rx D1]] [[Naloxone infusion instead of bolus->Opioid overdose — Rx D2]] [[Small titrated IV naloxone doses->Opioid overdose — Rx correct]]<div class="ec-scene">Emergency Department · 09:45</div> A 27-year-old woman has one day of increasing right-sided pelvic pain and light vaginal spotting. Her last menstrual period was seven weeks ago. She had chlamydial pelvic infection three years ago. Serum hCG is 2,400 mIU/mL. Transvaginal ultrasonography shows no intrauterine gestational sac, a small amount of free fluid in the pouch of Douglas, and a 2 cm right adnexal mass separate from the ovary. <span class="ec-prompt">Which is the most likely diagnosis?</span> [[Acute appendicitis->Ectopic pregnancy — Dx acute]] [[Ectopic pregnancy->Ectopic pregnancy — Dx correct]] [[Ovarian torsion->Ectopic pregnancy — Dx ovarian]] [[Pelvic inflammatory disease->Ectopic pregnancy — Dx pelvic]] [[Ruptured ovarian corpus luteum cyst->Ectopic pregnancy — Dx ruptured]]<div class="ec-scene">Labor and Delivery · 03:25</div> A 24-year-old primigravida at 34 weeks has a witnessed generalized tonic-clonic seizure lasting 90 seconds. Blood pressure is 172/112 mm Hg with 3+ proteinuria. She had reported headache and visual disturbance the previous day. She has no history of epilepsy, no fever and no neck stiffness. Platelets are 96,000/mm3, aspartate aminotransferase is 88 U/L, and alanine aminotransferase is 76 U/L. <span class="ec-prompt">Which is the most likely diagnosis?</span> [[Amniotic fluid embolism->Eclampsia — Dx D4]] [[Cerebral venous sinus thrombosis->Eclampsia — Dx D2]] [[Eclampsia->Eclampsia — Dx correct]] [[HELLP syndrome without eclampsia->Eclampsia — Dx D1]] [[New-onset idiopathic epilepsy->Eclampsia — Dx D3]]<div class="ec-scene">Emergency Department · 04:05</div> A 24-year-old man had a below-knee cast applied 8 hours ago for a tibial shaft fracture. He now has severe leg pain unrelieved by repeated opioid doses, with agony on passive extension of the toes. The dorsalis pedis pulse is palpable and capillary refill is 2 seconds. Sensation over the first web space is reduced. <span class="ec-prompt">Which is the most appropriate next step in management?</span> [[Arterial duplex ultrasonography->Compartment syndrome — Ix D2]] [[Elevate the limb and reassess in 1 hour->Compartment syndrome — Ix D5]] [[Measure compartment pressures first->Compartment syndrome — Ix D1]] [[Split the cast to skin and reassess->Compartment syndrome — Ix correct]] [[Urgent MRI of the leg->Compartment syndrome — Ix D3]]<div class="ec-scene">Emergency Department · 06:30</div> A 58-year-old man presents with acute severe pain, swelling, and erythema of the first metatarsophalangeal joint that began overnight. Temperature is 37.3°C (99.1°F), blood pressure 142/86 mm Hg, and heart rate 82/min. Arthrocentesis yields cloudy synovial fluid with needle-shaped, negatively birefringent crystals under polarized light. Gram stain is negative. Renal function is normal and he has no peptic ulcer disease. <span class="ec-prompt">Which is the most appropriate treatment for this acute flare?</span> [[An NSAID, colchicine, or a glucocorticoid->Acute gout — Correct]] [[Empiric intravenous antibiotics->Acute gout — D3]] [[Febuxostat 80 mg daily for urate lowering->Acute gout — D5]] [[Initiation of allopurinol during the acute flare without anti-inflammatory coverage->Acute gout — D4]] [[Probenecid for uricosuric therapy->Acute gout — D2]]<div class="ec-scene">Medical Floor · 07:50</div> You realize that an order you wrote overnight delivered ten times the intended insulin dose. The patient became hypoglycemic, was treated with dextrose, and has recovered fully. She is alert and does not know anything went wrong. Your senior suggests that since she is fine, there is no need to raise it. <span class="ec-prompt">Your error caused transient harm. Which is the most appropriate next step in management?</span> [[Disclose but blame a systems failure->Error disclosure — Deflection trap]] [[Disclose to the patient with an apology; file an incident report->Error disclosure — Disclose correct]] [[Document only; don't tell her, since she recovered->Error disclosure — Chart only trap]] [[File the report; let risk management decide on disclosure->Error disclosure — Delegation trap]] [[Say nothing; disclosure only invites litigation->Error disclosure — Silence trap]]<div class="ec-scene">Newborn Nursery · 08:00</div> A full-term, otherwise healthy 3-day-old infant appears visibly jaundiced. Temperature is 37.0°C (98.6°F), heart rate 148/min, and respiratory rate 42/min. Total serum bilirubin is 19.8 mg/dL, which plots above the phototherapy threshold on the Bhutani nomogram for this age. The direct bilirubin is 0.4 mg/dL. The infant is breastfeeding well and has no signs of hemolysis. <span class="ec-prompt">Which is the most appropriate next step?</span> [[Discontinue breastfeeding permanently->Neonatal jaundice — D2]] [[Immediate exchange transfusion->Neonatal jaundice — D1]] [[Intensive phototherapy->Neonatal jaundice — Correct]] [[Observe without treatment for 72 hours->Neonatal jaundice — D3]] [[Phenobarbital->Neonatal jaundice — D4]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Blood cultures drawn now, immediately before the first antibiotic dose.</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment — and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div> [[Next case->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Imaging has a role once a surgical source is suspected and the child is stabilized. Taking a shocked 4-year-old to the scanner before resuscitation is where these patients deteriorate. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment — and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis — Ix]] [[Next case->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Cerebrospinal fluid is valuable and meningitis is plausible with fever, vomiting and lethargy. He is in shock with a capillary refill of four seconds, and lumbar puncture is deferred in hemodynamic instability — antibiotics and resuscitation come first. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment — and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis — Ix]] [[Next case->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Serial lactate is genuinely part of sepsis management and is used to assess response, so this is a real step. It is a monitoring parameter for later, not the sample that must be obtained in the next thirty seconds. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment — and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis — Ix]] [[Next case->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Procalcitonin can support antibiotic decisions in some settings and has a role in de-escalation. Withholding antibiotics in septic shock pending a biomarker is indefensible. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment — and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis — Ix]] [[Next case->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Urine is a common source in this age group and should be sampled, but a bag specimen is frequently contaminated and unreliable — catheter or suprapubic sampling is used. It does not take priority over blood cultures and antibiotics. <div class="ec-teach"><div class="th">What the findings point to</div> Cultures obtained before antibiotics substantially raise the yield, and a single dose can sterilize them within an hour. Drawing them takes seconds through access that is already in place, so it does not delay treatment — and if obtaining cultures would delay antibiotics, the antibiotics go first. <div class="ec-src"><b>Source:</b> Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med 2020;21(2):e52-e106.</div></div></div> [[Try this question again->Sepsis — Ix]] [[Next case->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">\u2715 Not the best answer.</div> The correct answer is Volume resuscitation with crystalloid and packed RBC transfusion. In acute upper GI hemorrhage with hemodynamic instability (tachycardia, hypotension, altered mental status) and severe anemia (Hgb 6.8), the immediate priority is hemodynamic resuscitation — IV crystalloid and packed RBC transfusion to restore circulating volume and oxygen-carrying capacity. Endoscopy is essential but should follow initial stabilization. Oral PPI is insufficient for active hemorrhage. Surgery is premature before endoscopic assessment. CT angiography delays resuscitation without changing the immediate management. <div class="ec-src">Laine L, et al. ACG Clinical Guideline: upper gastrointestinal and ulcer bleeding. Am J Gastroenterol 2021;116(5):899-917. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013;368(1):11-21.</div></div> [[Try this question again->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Next question \u2192->Acute GI bleed — Q2]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">\u2715 Not the best answer.</div> The correct answer is Volume resuscitation with crystalloid and packed RBC transfusion. In acute upper GI hemorrhage with hemodynamic instability (tachycardia, hypotension, altered mental status) and severe anemia (Hgb 6.8), the immediate priority is hemodynamic resuscitation — IV crystalloid and packed RBC transfusion to restore circulating volume and oxygen-carrying capacity. Endoscopy is essential but should follow initial stabilization. Oral PPI is insufficient for active hemorrhage. Surgery is premature before endoscopic assessment. CT angiography delays resuscitation without changing the immediate management. <div class="ec-src">Laine L, et al. ACG Clinical Guideline: upper gastrointestinal and ulcer bleeding. Am J Gastroenterol 2021;116(5):899-917. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013;368(1):11-21.</div></div> [[Try this question again->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Next question \u2192->Acute GI bleed — Q2]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">\u2715 Not the best answer.</div> The correct answer is Volume resuscitation with crystalloid and packed RBC transfusion. In acute upper GI hemorrhage with hemodynamic instability (tachycardia, hypotension, altered mental status) and severe anemia (Hgb 6.8), the immediate priority is hemodynamic resuscitation — IV crystalloid and packed RBC transfusion to restore circulating volume and oxygen-carrying capacity. Endoscopy is essential but should follow initial stabilization. Oral PPI is insufficient for active hemorrhage. Surgery is premature before endoscopic assessment. CT angiography delays resuscitation without changing the immediate management. <div class="ec-src">Laine L, et al. ACG Clinical Guideline: upper gastrointestinal and ulcer bleeding. Am J Gastroenterol 2021;116(5):899-917. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013;368(1):11-21.</div></div> [[Try this question again->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Next question \u2192->Acute GI bleed — Q2]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">\u2715 Not the best answer.</div> The correct answer is Volume resuscitation with crystalloid and packed RBC transfusion. In acute upper GI hemorrhage with hemodynamic instability (tachycardia, hypotension, altered mental status) and severe anemia (Hgb 6.8), the immediate priority is hemodynamic resuscitation — IV crystalloid and packed RBC transfusion to restore circulating volume and oxygen-carrying capacity. Endoscopy is essential but should follow initial stabilization. Oral PPI is insufficient for active hemorrhage. Surgery is premature before endoscopic assessment. CT angiography delays resuscitation without changing the immediate management. <div class="ec-src">Laine L, et al. ACG Clinical Guideline: upper gastrointestinal and ulcer bleeding. Am J Gastroenterol 2021;116(5):899-917. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013;368(1):11-21.</div></div> [[Try this question again->Acute GI bleed (Sequential — 3 Questions) — Ix]] [[Next question \u2192->Acute GI bleed — Q2]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">\u2713 Volume resuscitation with crystalloid and packed RBC transfusion.</div> In acute upper GI hemorrhage with hemodynamic instability (tachycardia, hypotension, altered mental status) and severe anemia (Hgb 6.8), the immediate priority is hemodynamic resuscitation — IV crystalloid and packed RBC transfusion to restore circulating volume and oxygen-carrying capacity. Endoscopy is essential but should follow initial stabilization. Oral PPI is insufficient for active hemorrhage. Surgery is premature before endoscopic assessment. CT angiography delays resuscitation without changing the immediate management. <div class="ec-src">Laine L, et al. ACG Clinical Guideline: upper gastrointestinal and ulcer bleeding. Am J Gastroenterol 2021;116(5):899-917. Villanueva C, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med 2013;368(1):11-21.</div></div> [[Next question \u2192->Acute GI bleed — Q2]] [[Start another case->Hub]]<div class="ec-seq-badge">Sequential Case — Question 2 of 3</div> After resuscitation, blood pressure improves to 102/64 mm Hg and heart rate decreases to 98/min. Octreotide infusion is started. Upper endoscopy is performed and reveals three columns of large esophageal varices with active spurting from one varix. Which endoscopic intervention is most appropriate? [[Application of hemostatic clips to the varix->Acute GI bleed — Q2 C]] [[Argon plasma coagulation of all three columns->Acute GI bleed — Q2 D]] [[Endoscopic sclerotherapy with ethanolamine oleate as first-line->Acute GI bleed — Q2 E]] [[Endoscopic variceal band ligation->Acute GI bleed — Q2 Correct]] [[Epinephrine injection into the varix->Acute GI bleed — Q2 B]]<div class="ec-seq-badge">Sequential Case — Question 3 of 3</div> Band ligation is successfully performed. Forty-eight hours later, the patient has another episode of large-volume hematemesis with recurrent hemodynamic instability. Repeat endoscopy shows rebleeding from the variceal site despite banding. Which is the most appropriate next step? [[Balloon tamponade as definitive long-term therapy->Acute GI bleed — Q3 D]] [[Initiation of oral propranolol for portal pressure reduction->Acute GI bleed — Q3 C]] [[Placement of a transjugular intrahepatic portosystemic shunt (TIPS)->Acute GI bleed — Q3 Correct]] [[Repeat band ligation a third time->Acute GI bleed — Q3 A]] [[Watchful waiting with continued octreotide alone->Acute GI bleed — Q3 E]]<div class="ec-verdict bad"><div class="ec-vhead bad">\u2715 Not the best answer.</div> The correct answer is Endoscopic variceal band ligation. Endoscopic variceal band ligation (EVL) is the recommended first-line endoscopic treatment for acute esophageal variceal hemorrhage (Baveno VII consensus, AASLD guidelines). It has superior efficacy and fewer complications compared to endoscopic sclerotherapy. Epinephrine injection and hemostatic clips are used for non-variceal bleeding (peptic ulcers). Argon plasma coagulation is used for vascular ectasias and is not appropriate for variceal bleeding. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Tsao G, et al. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management (AASLD). Hepatology 2017;65(1):310-335.</div></div> [[Try this question again->Acute GI bleed — Q2]] [[Next question \u2192->Acute GI bleed — Q3]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">\u2715 Not the best answer.</div> The correct answer is Endoscopic variceal band ligation. Endoscopic variceal band ligation (EVL) is the recommended first-line endoscopic treatment for acute esophageal variceal hemorrhage (Baveno VII consensus, AASLD guidelines). It has superior efficacy and fewer complications compared to endoscopic sclerotherapy. Epinephrine injection and hemostatic clips are used for non-variceal bleeding (peptic ulcers). Argon plasma coagulation is used for vascular ectasias and is not appropriate for variceal bleeding. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Tsao G, et al. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management (AASLD). Hepatology 2017;65(1):310-335.</div></div> [[Try this question again->Acute GI bleed — Q2]] [[Next question \u2192->Acute GI bleed — Q3]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">\u2715 Not the best answer.</div> The correct answer is Endoscopic variceal band ligation. Endoscopic variceal band ligation (EVL) is the recommended first-line endoscopic treatment for acute esophageal variceal hemorrhage (Baveno VII consensus, AASLD guidelines). It has superior efficacy and fewer complications compared to endoscopic sclerotherapy. Epinephrine injection and hemostatic clips are used for non-variceal bleeding (peptic ulcers). Argon plasma coagulation is used for vascular ectasias and is not appropriate for variceal bleeding. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Tsao G, et al. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management (AASLD). Hepatology 2017;65(1):310-335.</div></div> [[Try this question again->Acute GI bleed — Q2]] [[Next question \u2192->Acute GI bleed — Q3]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">\u2713 Endoscopic variceal band ligation.</div> Endoscopic variceal band ligation (EVL) is the recommended first-line endoscopic treatment for acute esophageal variceal hemorrhage (Baveno VII consensus, AASLD guidelines). It has superior efficacy and fewer complications compared to endoscopic sclerotherapy. Epinephrine injection and hemostatic clips are used for non-variceal bleeding (peptic ulcers). Argon plasma coagulation is used for vascular ectasias and is not appropriate for variceal bleeding. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Tsao G, et al. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management (AASLD). Hepatology 2017;65(1):310-335.</div></div> [[Next question \u2192->Acute GI bleed — Q3]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">\u2715 Not the best answer.</div> The correct answer is Endoscopic variceal band ligation. Endoscopic variceal band ligation (EVL) is the recommended first-line endoscopic treatment for acute esophageal variceal hemorrhage (Baveno VII consensus, AASLD guidelines). It has superior efficacy and fewer complications compared to endoscopic sclerotherapy. Epinephrine injection and hemostatic clips are used for non-variceal bleeding (peptic ulcers). Argon plasma coagulation is used for vascular ectasias and is not appropriate for variceal bleeding. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Tsao G, et al. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management (AASLD). Hepatology 2017;65(1):310-335.</div></div> [[Try this question again->Acute GI bleed — Q2]] [[Next question \u2192->Acute GI bleed — Q3]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad"> Not the best answer.</div> The correct answer is Placement of a transjugular intrahepatic portosystemic shunt (TIPS). When variceal bleeding is refractory to endoscopic therapy (defined as failure to control bleeding or early rebleeding despite two endoscopic attempts), salvage TIPS is indicated (Baveno VII). Balloon tamponade (Sengstaken-Blakemore or Minnesota tube) is a temporizing bridge to TIPS, not definitive therapy. Propranolol is for secondary prophylaxis, not acute rebleeding. Watchful waiting with octreotide alone is inadequate for refractory hemorrhage. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Pagán JC, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med 2010;362(25):2370-2379.</div></div> [[Try this question again->Acute GI bleed — Q3]] [[Next case ->STEMI — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad"> Not the best answer.</div> The correct answer is Placement of a transjugular intrahepatic portosystemic shunt (TIPS). When variceal bleeding is refractory to endoscopic therapy (defined as failure to control bleeding or early rebleeding despite two endoscopic attempts), salvage TIPS is indicated (Baveno VII). Balloon tamponade (Sengstaken-Blakemore or Minnesota tube) is a temporizing bridge to TIPS, not definitive therapy. Propranolol is for secondary prophylaxis, not acute rebleeding. Watchful waiting with octreotide alone is inadequate for refractory hemorrhage. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Pagán JC, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med 2010;362(25):2370-2379.</div></div> [[Try this question again->Acute GI bleed — Q3]] [[Next case ->STEMI — Ix]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good"> Placement of a transjugular intrahepatic portosystemic shunt (TIPS).</div> When variceal bleeding is refractory to endoscopic therapy (defined as failure to control bleeding or early rebleeding despite two endoscopic attempts), salvage TIPS is indicated (Baveno VII). Balloon tamponade (Sengstaken-Blakemore or Minnesota tube) is a temporizing bridge to TIPS, not definitive therapy. Propranolol is for secondary prophylaxis, not acute rebleeding. Watchful waiting with octreotide alone is inadequate for refractory hemorrhage. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Pagán JC, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med 2010;362(25):2370-2379.</div></div> [[Next case ->STEMI — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad"> Not the best answer.</div> The correct answer is Placement of a transjugular intrahepatic portosystemic shunt (TIPS). When variceal bleeding is refractory to endoscopic therapy (defined as failure to control bleeding or early rebleeding despite two endoscopic attempts), salvage TIPS is indicated (Baveno VII). Balloon tamponade (Sengstaken-Blakemore or Minnesota tube) is a temporizing bridge to TIPS, not definitive therapy. Propranolol is for secondary prophylaxis, not acute rebleeding. Watchful waiting with octreotide alone is inadequate for refractory hemorrhage. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Pagán JC, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med 2010;362(25):2370-2379.</div></div> [[Try this question again->Acute GI bleed — Q3]] [[Next case ->STEMI — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad"> Not the best answer.</div> The correct answer is Placement of a transjugular intrahepatic portosystemic shunt (TIPS). When variceal bleeding is refractory to endoscopic therapy (defined as failure to control bleeding or early rebleeding despite two endoscopic attempts), salvage TIPS is indicated (Baveno VII). Balloon tamponade (Sengstaken-Blakemore or Minnesota tube) is a temporizing bridge to TIPS, not definitive therapy. Propranolol is for secondary prophylaxis, not acute rebleeding. Watchful waiting with octreotide alone is inadequate for refractory hemorrhage. <div class="ec-src">de Franchis R, et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-974. Garcia-Pagán JC, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med 2010;362(25):2370-2379.</div></div> [[Try this question again->Acute GI bleed — Q3]] [[Next case ->STEMI — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Echocardiography is useful when the ECG is equivocal or to look for mechanical complications and alternative diagnoses such as dissection. The ECG here is diagnostic, so it adds delay rather than information. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI — Ix]] [[Next case →->Tension pneumothorax — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A film may be obtained if dissection is genuinely suspected, but routine radiography delays reperfusion without changing the decision. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI — Ix]] [[Next case →->Tension pneumothorax — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This has a role in stable chest pain to exclude coronary disease. It has no place in an evolving ST-elevation infarction, where invasive angiography is both diagnostic and therapeutic. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI — Ix]] [[Next case →->Tension pneumothorax — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Posterior leads are genuinely valuable and are the right addition when there is ST depression in V1 to V3 suggesting posterior involvement, so this is the strongest wrong answer. His reciprocal changes are in I and aVL, which points to right ventricular rather than posterior extension. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI — Ix]] [[Next case →->Tension pneumothorax — Dx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Right-sided ECG leads V4R to V6R.</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div> [[Next case →->Tension pneumothorax — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Troponin confirms myocardial injury but is often normal in the first hours, and ST elevation with this history is already an indication for immediate reperfusion. Waiting for a biomarker is the classic way to lose myocardium. <div class="ec-teach"><div class="th">What the findings point to</div> Inferior infarction involves the right coronary artery in most cases, and right ventricular infarction accompanies it in a substantial minority. Identifying it changes management immediately: these patients are preload-dependent, so nitrates and diuretics can cause profound hypotension, and they need fluid loading instead. Right-sided leads take under a minute and must not delay reperfusion. <div class="ec-src"><b>Source:</b> Rao SV, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Circulation 2025;151(13):e771-e862.</div></div></div> [[Try this question again->STEMI — Ix]] [[Next case →->Tension pneumothorax — Dx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ CT pulmonary angiography.</div> She has a high pretest probability — recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing you were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div> [[Next case →->Aortic dissection — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ D-dimer measurement is not the next step.</div> This is the answer at low or intermediate probability, and it is the most tempting option here. D-dimer earns its place by ruling out disease when the pretest probability is low enough — through PERC, Wells, or a YEARS approach with age-adjusted or 1000 ng/mL thresholds. She meets two YEARS criteria and has a high clinical probability, so the test cannot exclude the diagnosis and only delays imaging. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability — recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing you were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism — Ix]] [[Next case →->Aortic dissection — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Echocardiography is not the next step.</div> Bedside echocardiography is valuable in the hemodynamically unstable patient, where right ventricular strain can justify treatment when the patient is too unwell for the scanner. She is normotensive, so she can be imaged definitively. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability — recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing you were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism — Ix]] [[Next case →->Aortic dissection — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Lower extremity compression ultrasonography is not the next step.</div> A positive leg ultrasound in this setting would justify anticoagulation without further imaging, so this is a legitimate strategy — particularly in pregnancy or renal failure. A negative result does not exclude pulmonary embolism, and she has neither contraindication to computed tomography. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability — recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing you were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism — Ix]] [[Next case →->Aortic dissection — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Repeat chest radiography in 6 hours is not the next step.</div> Plain radiography cannot diagnose or exclude embolism. Its role is to identify alternative causes, and it has already done that by being clear. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability — recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing you were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism — Ix]] [[Next case →->Aortic dissection — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ventilation-perfusion scanning is not the next step.</div> This is the alternative when iodinated contrast is contraindicated — severe allergy, renal impairment — or in pregnancy where breast radiation matters. Neither applies, and it is less specific and more often non-diagnostic in a patient with any pre-existing lung disease. <div class="ec-teach"><div class="th">What to do instead</div> She has a high pretest probability — recent major orthopedic surgery, signs of deep venous thrombosis, tachycardia, hypoxemia, and pulmonary embolism as the most likely diagnosis. At high probability, imaging is the next step: a negative D-dimer does not lower the post-test probability enough to be safe, and a positive one changes nothing you were not already going to do. With normal renal function and no contrast allergy, CT pulmonary angiography is the test of choice. <div class="ec-src"><b>Source:</b> 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults. Circulation 2026;153:e977-e1051; van der Hulle T, et al. Lancet 2017 (YEARS).</div></div></div> [[Try this question again->Pulmonary embolism — Ix]] [[Next case →->Aortic dissection — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Tamponade gives obstructive shock with raised venous pressure and can follow penetrating trauma, so it belongs on the list. Breath sounds are equal and the chest is not hyperresonant, and the trachea is central. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical — this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax — Dx]] [[Next case →->Pulmonary embolism — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This causes respiratory distress and hypoxemia after blunt trauma, with paradoxical chest wall movement. It does not produce tracheal deviation or a hyperresonant hemithorax. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical — this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax — Dx]] [[Next case →->Pulmonary embolism — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This also gives unilateral absent breath sounds and shock after trauma, so it is the closest alternative. The hemithorax is dull to percussion rather than hyperresonant, and the venous pressure is typically low from blood loss rather than raised. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical — this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax — Dx]] [[Next case →->Pulmonary embolism — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Aortic injury after deceleration causes shock and a widened mediastinum on imaging, but with equal breath sounds and no hyperresonance or tracheal deviation. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical — this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax — Dx]] [[Next case →->Pulmonary embolism — Ix]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Tension pneumothorax.</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical — this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div> [[Next case →->Pulmonary embolism — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Herniated bowel can reduce breath sounds on the left and shift the mediastinum, which makes this a genuine consideration in left-sided blunt trauma. It develops less abruptly and gives bowel sounds in the chest with a dull or mixed percussion note. <div class="ec-teach"><div class="th">What the findings point to</div> Obstructive shock with absent breath sounds and hyperresonance on one side, contralateral tracheal deviation and raised venous pressure after trauma. Rising intrapleural pressure displaces the mediastinum and obstructs venous return, so the shock is mechanical — this is a clinical diagnosis and imaging must not precede decompression. <div class="ec-src"><b>Source:</b> ATLS Advanced Trauma Life Support, 10th ed.</div></div></div> [[Try this question again->Tension pneumothorax — Dx]] [[Next case →->Pulmonary embolism — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Acute pericarditis does not fit.</div> Pericarditis gives pleuritic pain that eases on sitting forward, a friction rub, and widespread concave ST elevation with PR depression. It does not produce an interarm pressure difference or a widened mediastinum. <div class="ec-teach"><div class="th">What the findings actually point to</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div></div> [[Try this question again->Aortic dissection — Dx]] [[Next case →->Acute kidney injury — Ix]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Aortic dissection.</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div> [[Next case →->Acute kidney injury — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Esophageal rupture does not fit.</div> Boerhaave syndrome follows forceful vomiting and gives pain with subcutaneous emphysema and often a pleural effusion. There is no vomiting history here, and it does not cause aortic regurgitation or unequal arm pressures. <div class="ec-teach"><div class="th">What the findings actually point to</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div></div> [[Try this question again->Aortic dissection — Dx]] [[Next case →->Acute kidney injury — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ ST-elevation myocardial infarction does not fit.</div> Infarction is the most important thing to distinguish this from, because anticoagulating or lysing a dissection is catastrophic. His ECG shows no ST elevation, and neither the interarm difference nor the widened mediastinum belongs to infarction — though a dissection extending into the right coronary ostium can produce inferior changes. <div class="ec-teach"><div class="th">What the findings actually point to</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div></div> [[Try this question again->Aortic dissection — Dx]] [[Next case →->Acute kidney injury — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Tension pneumothorax does not fit.</div> This causes acute dyspnea with absent breath sounds, tracheal deviation and hemodynamic collapse. His breath sounds and trachea are not described as abnormal, and it does not cause an interarm gradient. <div class="ec-teach"><div class="th">What the findings actually point to</div> Sudden maximal-at-onset tearing pain radiating to the back, an interarm systolic difference, a new diastolic murmur from aortic regurgitation, and a widened mediastinum are the classic combination. Pain that is worst at the very first moment points to a vascular catastrophe rather than to an evolving one. <div class="ec-src"><b>Source:</b> Isselbacher EM, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease. Circulation 2022;146(24):e334-e482.</div></div></div> [[Try this question again->Aortic dissection — Dx]] [[Next case →->Acute kidney injury — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Antibiotics alone have a 25–40% recurrence rate.</div> The CODA trial and others have shown that antibiotic treatment of uncomplicated appendicitis is feasible but carries a substantial recurrence risk. Appendectomy remains the guideline-recommended definitive treatment, particularly in a young, healthy patient with a clear CT diagnosis. <div class="ec-teach"><div class="th">What to do instead</div> Acute uncomplicated appendicitis in a young adult with CT confirmation is a surgical indication. Laparoscopic appendectomy remains the standard of care and is associated with low complication rates, rapid recovery, and definitive treatment. While recent trials have explored antibiotic-first strategies for uncomplicated appendicitis, appendectomy remains the guideline-recommended definitive treatment, particularly given the 25–40% recurrence rate with antibiotic-only management. <div class="ec-src"><b>Source:</b> Di Saverio S, et al. Diagnosis and Treatment of Acute Appendicitis: 2020 Update of the WSES Jerusalem Guidelines. World J Emerg Surg 2020;15(1):27.</div></div></div> [[Try this question again->Acute appendicitis — Rx]] [[Next case →->Thyroid storm — Dx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Appendectomy.</div> Acute uncomplicated appendicitis in a young adult with CT confirmation is a surgical indication. Laparoscopic appendectomy remains the standard of care and is associated with low complication rates, rapid recovery, and definitive treatment. While recent trials have explored antibiotic-first strategies for uncomplicated appendicitis, appendectomy remains the guideline-recommended definitive treatment, particularly given the 25–40% recurrence rate with antibiotic-only management. <div class="ec-src"><b>Source:</b> Di Saverio S, et al. Diagnosis and Treatment of Acute Appendicitis: 2020 Update of the WSES Jerusalem Guidelines. World J Emerg Surg 2020;15(1):27.</div></div> [[Next case →->Thyroid storm — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Prolonged observation risks complications.</div> A week of observation for confirmed appendicitis risks progression to perforation, abscess, and peritonitis. <div class="ec-teach"><div class="th">What to do instead</div> Acute uncomplicated appendicitis in a young adult with CT confirmation is a surgical indication. Laparoscopic appendectomy remains the standard of care and is associated with low complication rates, rapid recovery, and definitive treatment. While recent trials have explored antibiotic-first strategies for uncomplicated appendicitis, appendectomy remains the guideline-recommended definitive treatment, particularly given the 25–40% recurrence rate with antibiotic-only management. <div class="ec-src"><b>Source:</b> Di Saverio S, et al. Diagnosis and Treatment of Acute Appendicitis: 2020 Update of the WSES Jerusalem Guidelines. World J Emerg Surg 2020;15(1):27.</div></div></div> [[Try this question again->Acute appendicitis — Rx]] [[Next case →->Thyroid storm — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Antibiotics alone have a 25–40% recurrence rate.</div> The CODA trial and others have shown that antibiotic treatment of uncomplicated appendicitis is feasible but carries a substantial recurrence risk. Appendectomy remains the guideline-recommended definitive treatment, particularly in a young, healthy patient with a clear CT diagnosis. <div class="ec-teach"><div class="th">What to do instead</div> Acute uncomplicated appendicitis in a young adult with CT confirmation is a surgical indication. Laparoscopic appendectomy remains the standard of care and is associated with low complication rates, rapid recovery, and definitive treatment. While recent trials have explored antibiotic-first strategies for uncomplicated appendicitis, appendectomy remains the guideline-recommended definitive treatment, particularly given the 25–40% recurrence rate with antibiotic-only management. <div class="ec-src"><b>Source:</b> Di Saverio S, et al. Diagnosis and Treatment of Acute Appendicitis: 2020 Update of the WSES Jerusalem Guidelines. World J Emerg Surg 2020;15(1):27.</div></div></div> [[Try this question again->Acute appendicitis — Rx]] [[Next case →->Thyroid storm — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Percutaneous drainage is for complicated appendicitis.</div> CT-guided drainage is used for appendiceal abscess in patients who are poor surgical candidates or as a temporizing measure. In uncomplicated appendicitis confirmed by CT, appendectomy is the definitive treatment. <div class="ec-teach"><div class="th">What to do instead</div> Acute uncomplicated appendicitis in a young adult with CT confirmation is a surgical indication. Laparoscopic appendectomy remains the standard of care and is associated with low complication rates, rapid recovery, and definitive treatment. While recent trials have explored antibiotic-first strategies for uncomplicated appendicitis, appendectomy remains the guideline-recommended definitive treatment, particularly given the 25–40% recurrence rate with antibiotic-only management. <div class="ec-src"><b>Source:</b> Di Saverio S, et al. Diagnosis and Treatment of Acute Appendicitis: 2020 Update of the WSES Jerusalem Guidelines. World J Emerg Surg 2020;15(1):27.</div></div></div> [[Try this question again->Acute appendicitis — Rx]] [[Next case →->Thyroid storm — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Biopsy is reserved for unexplained acute kidney injury after non-invasive evaluation, or where glomerular or interstitial disease is suspected. The cause here is apparent from the history. <div class="ec-teach"><div class="th">What the findings point to</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside — bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div></div> [[Try this question again->Acute kidney injury — Ix]] [[Next case →->DKA management — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Excluding obstruction is part of any acute kidney injury workup and this should be done — but her history, orthostasis, fractional sodium excretion of 0.4% and urea-to-creatinine ratio of 28 all point to a prerenal cause, and imaging must not delay fluid resuscitation. <div class="ec-teach"><div class="th">What the findings point to</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside — bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div></div> [[Try this question again->Acute kidney injury — Ix]] [[Next case →->DKA management — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Fractional sodium excretion is unreliable once a diuretic has been given — the fractional excretion of urea is used instead in that situation. Deliberately confounding your own test is the error. <div class="ec-teach"><div class="th">What the findings point to</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside — bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div></div> [[Try this question again->Acute kidney injury — Ix]] [[Next case →->DKA management — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This screens for myeloma-related kidney disease and is appropriate when the cause is unexplained, particularly with anemia, hypercalcemia or bone pain. It is not the immediate question in a woman with four days of vomiting. <div class="ec-teach"><div class="th">What the findings point to</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside — bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div></div> [[Try this question again->Acute kidney injury — Ix]] [[Next case →->DKA management — Rx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Urine microscopy for sediment.</div> Sediment examination is the test that distinguishes prerenal azotemia from established acute tubular necrosis at the bedside — bland sediment with hyaline casts supports a prerenal state that will reverse with volume, whereas muddy brown granular casts indicate tubular injury that will not. That distinction determines whether fluid alone is the treatment. <div class="ec-src"><b>Source:</b> KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012;2(1):1-138.</div></div> [[Next case →->DKA management — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fluids alone do not stop ketogenesis.</div> Volume resuscitation is critical in DKA and modestly reduces glucose through dilution and improved renal clearance. However, without insulin, lipolysis and hepatic ketogenesis continue unchecked. Insulin is the only agent that directly suppresses the ketogenic pathway. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis — the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient’s potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div></div> [[Try this question again->DKA management — Rx]] [[Next case →->Acute appendicitis — Rx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Intravenous insulin infusion with concurrent fluid and electrolyte management.</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis — the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient’s potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div> [[Next case →->Acute appendicitis — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Furosemide worsens dehydration.</div> DKA patients are profoundly volume-depleted from osmotic diuresis. Furosemide would worsen dehydration and electrolyte losses. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis — the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient’s potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div></div> [[Try this question again->DKA management — Rx]] [[Next case →->Acute appendicitis — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Bicarbonate is not routinely indicated.</div> Sodium bicarbonate is considered only in severe acidosis with pH below 7.0. Routine use can worsen intracellular acidosis, cause hypokalemia, and delay ketone clearance. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis — the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient’s potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div></div> [[Try this question again->DKA management — Rx]] [[Next case →->Acute appendicitis — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Subcutaneous long-acting insulin is not the acute treatment.</div> The acute management of DKA requires a continuous intravenous insulin infusion for precise dose titration. Long-acting insulin is transitioned to once the anion gap closes and the patient can eat. <div class="ec-teach"><div class="th">What to do instead</div> Insulin is the only treatment that directly suppresses lipolysis and hepatic ketogenesis — the pathophysiologic engine of DKA. However, insulin cannot be given safely without addressing the potassium: insulin drives potassium intracellularly, and hypokalemia kills before acidosis does. With this patient’s potassium at 4.8 mEq/L, insulin can be started immediately with potassium replacement running concurrently. If potassium were below 3.5 mEq/L, insulin would be withheld and potassium repleted (about 10 mEq/h) until it rises above that threshold. Aggressive isotonic fluid resuscitation corrects dehydration and improves renal perfusion. <div class="ec-src"><b>Source:</b> Umpierrez GE, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (ADA/EASD/AACE/JBDS/DTS). Diabetes Care 2024;47(8):1257-1275; ADA Standards of Care 2026.</div></div></div> [[Try this question again->DKA management — Rx]] [[Next case →->Acute appendicitis — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Alcohol withdrawal does not fit.</div> Withdrawal gives tremor, agitation, fever, tachycardia and diaphoresis and would be a reasonable postoperative thought. It does not produce a goiter with a bruit, lid lag, or atrial fibrillation with a wide pulse pressure, and there is no drinking history. <div class="ec-teach"><div class="th">What the findings actually point to</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant — recent surgery — is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div></div> [[Try this question again->Thyroid storm — Dx]] [[Next case →->Status epilepticus — Opening]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Malignant hyperthermia does not fit.</div> This would be the fear after recent anesthesia, so the timing invites it. It presents during or within hours of the anesthetic with masseter spasm, generalized rigidity and a rapidly rising end-tidal carbon dioxide — not two days later with a goiter. <div class="ec-teach"><div class="th">What the findings actually point to</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant — recent surgery — is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div></div> [[Try this question again->Thyroid storm — Dx]] [[Next case →->Status epilepticus — Opening]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Postoperative sepsis does not fit.</div> Infection is the other major postoperative cause of fever, tachycardia and confusion, and is also a recognized precipitant of storm. It does not explain the goiter, the bruit, the lid lag or the wide pulse pressure, though it should still be sought and treated. <div class="ec-teach"><div class="th">What the findings actually point to</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant — recent surgery — is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div></div> [[Try this question again->Thyroid storm — Dx]] [[Next case →->Status epilepticus — Opening]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pulmonary embolism does not fit.</div> Embolism after abdominal surgery gives dyspnea, pleuritic pain, tachycardia and hypoxemia, and can cause atrial fibrillation. It does not cause a temperature of 40°C with diarrhea and a thyroid bruit. <div class="ec-teach"><div class="th">What the findings actually point to</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant — recent surgery — is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div></div> [[Try this question again->Thyroid storm — Dx]] [[Next case →->Status epilepticus — Opening]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Thyroid storm.</div> Decompensated thyrotoxicosis with hyperpyrexia, atrial fibrillation with a wide pulse pressure, gastrointestinal upset and central nervous system dysfunction, in a patient with untreated Graves disease and a clear precipitant — recent surgery — is thyroid storm. The goiter with a bruit and lid lag anchor the underlying diagnosis. <div class="ec-src"><b>Source:</b> Ross DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism. Thyroid 2016;26(10):1343-1421; Burch HB, Wartofsky L. Endocrinol Metab Clin North Am 1993 (diagnostic criteria).</div></div> [[Next case →->Status epilepticus — Opening]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Acute chest syndrome.</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to three days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div> [[Next case →->Stroke — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Fat embolism syndrome does not fit.</div> Marrow fat embolism does complicate sickle crisis and can look similar, so it is a genuine consideration. It typically gives a petechial rash, marked neurologic change and thrombocytopenia, and is far less common than acute chest syndrome. <div class="ec-teach"><div class="th">What the findings actually point to</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to three days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div></div> [[Try this question again->Acute chest syndrome — Dx]] [[Next case →->Stroke — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Hospital-acquired pneumonia does not fit.</div> Infection is a frequent trigger of acute chest syndrome rather than a competing diagnosis, and the two are treated together. Labeling it pneumonia alone risks omitting transfusion and the specific management this syndrome requires. <div class="ec-teach"><div class="th">What the findings actually point to</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to three days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div></div> [[Try this question again->Acute chest syndrome — Dx]] [[Next case →->Stroke — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pulmonary embolism does not fit.</div> Embolism gives pleuritic pain, dyspnea and hypoxemia and is more common in sickle cell disease, but it does not typically cause fever with a new alveolar infiltrate on plain radiograph. <div class="ec-teach"><div class="th">What the findings actually point to</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to three days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div></div> [[Try this question again->Acute chest syndrome — Dx]] [[Next case →->Stroke — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Vaso-occlusive crisis alone does not fit.</div> Her crisis is ongoing, and chest pain can be part of it. What changes the diagnosis is the new radiographic infiltrate with fever and falling saturation — chest pain in sickle disease is never assumed to be crisis alone once the film changes. <div class="ec-teach"><div class="th">What the findings actually point to</div> A new pulmonary infiltrate with fever and respiratory symptoms in a patient with sickle cell disease is acute chest syndrome by definition. It characteristically appears two to three days into an admission for a painful crisis, as opioid-related hypoventilation and splinting from back and rib pain promote atelectasis and local sickling. <div class="ec-src"><b>Source:</b> American Society of Hematology 2020 Guidelines for Sickle Cell Disease: Transfusion Support. Blood Adv 2020;4(2):327; NHLBI Evidence-Based Management of Sickle Cell Disease, 2014.</div></div></div> [[Try this question again->Acute chest syndrome — Dx]] [[Next case →->Stroke — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ The seizure won't wait for the scanner.</div> You send an actively seizing patient for imaging before treating. Prolonged convulsions cause progressive neuronal injury — the drug comes first, the workup follows once the seizure is controlled (glucose is already checked and normal). <div class="ec-teach"><div class="th">Why not this</div> Active status epilepticus is treated immediately with a benzodiazepine. Imaging and further labs follow seizure control; the one lab you need up front — glucose — is already normal here. <div class="ec-src"><b>Source:</b> Standard status epilepticus algorithms; Kapur J, et al. (ESETT). N Engl J Med 2019.</div></div></div> [[Try this question again->Status epilepticus — Opening]] [[Next case →->Acute chest syndrome — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Second-line drug in the first-line slot.</div> Levetiracetam is a genuine status epilepticus drug and it will appear later in this algorithm - but it is slower to abort a seizure than a benzodiazepine. The brain keeps seizing while it loads. <div class="ec-teach"><div class="th">The order matters</div> Benzodiazepines are first-line for convulsive status epilepticus. Levetiracetam, fosphenytoin and valproate are second-line, used after an adequate benzodiazepine dose fails. <div class="ec-src"><b>Source:</b> Kapur J, et al. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT). N Engl J Med 2019;381(22):2103-2113.</div></div></div> [[Try this question again->Status epilepticus — Opening]] [[Next case →->Acute chest syndrome — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Right family, wrong order.</div> Fosphenytoin is a real status-epilepticus drug — but it's second-line. It takes time to load and won't abort the seizure as fast as a benzodiazepine. Meanwhile the brain keeps seizing. <div class="ec-teach"><div class="th">Where this breaks down</div> Second-line antiseizure medications (fosphenytoin, levetiracetam, valproate) come after a benzodiazepine, not before. The benzodiazepine is the first move. <div class="ec-src"><b>Source:</b> Kapur J, et al. (ESETT). N Engl J Med 2019.</div></div></div> [[Try this question again->Status epilepticus — Opening]] [[Next case →->Acute chest syndrome — Dx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Benzodiazepine first.</div> IV lorazepam goes in at an adequate weight-based dose. Benzodiazepines are the established first-line abortive for status epilepticus, and adequate dosing is what actually stops the seizure. <div class="ec-teach"><div class="th">Why a benzodiazepine</div> Benzodiazepines (IV lorazepam, or IM midazolam if no IV) are first-line for convulsive status epilepticus. Under-dosing is a common error and is especially common in children, where the weight-based calculation invites hesitancy — give the full dose. If intravenous access had not been available, intramuscular midazolam, or the buccal or rectal route, is effective. The ESETT trial enrolled children as well as adults and found levetiracetam, fosphenytoin and valproate equivalent as second-line agents. <br><br><b>Then:</b> After an adequate benzodiazepine, the second-line options — levetiracetam, fosphenytoin, and valproate — showed no significant difference in seizure cessation or safety in a major randomized trial. Any of the three is a reasonable choice. <div class="ec-src"><b>Source:</b> Kapur J, et al. Randomized Trial of Three Anticonvulsant Medications for Status Epilepticus (ESETT). N Engl J Med 2019;381(22):2103-2113.</div></div></div> <b>Seizure aborted → admitted for monitoring.</b> [[Next case →->Acute chest syndrome — Dx]] [[Start another case->Hub]] [[Restart this case->Status epilepticus — Opening]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Right drug class, and a route chosen for the wrong reason.</div> Rectal diazepam is a genuine and valuable option in children — it is what parents use at home and what is given when there is no intravenous access. Here access is already established. Choosing a less reliable route when a reliable one is in place delays the effective dose, and being a child is not by itself a reason to avoid the intravenous route. <div class="ec-teach"><div class="th">Why this is wrong</div> Give an intravenous benzodiazepine at the full weight-based dose. Reserve intramuscular midazolam, or the buccal or rectal route, for when intravenous access is unavailable — in that situation they are first-line rather than second-best. <div class="ec-src"><b>Source:</b> Glauser T, et al. Evidence-Based Guideline: Treatment of Convulsive Status Epilepticus. Epilepsy Curr 2016;16(1):48-61.</div></div></div> [[Try this question again->Status epilepticus — Opening]] [[Next case →->Acute chest syndrome — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Carotid duplex ultrasonography is not the next step.</div> This informs secondary prevention and the timing of endarterectomy. It has no role in the hyperacute decision. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct — an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke — Ix]] [[Next case →->Opioid overdose — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ CT angiography of the head and neck is not the next step.</div> Vessel imaging identifies a large-vessel occlusion and is essential for selecting thrombectomy candidates, so it is a genuine and important part of modern stroke care — often performed in the same sitting. It does not replace the non-contrast study, because the decision it informs comes after hemorrhage has been excluded. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct — an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke — Ix]] [[Next case →->Opioid overdose — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Diffusion-weighted MRI of the brain is not the next step.</div> MRI is far more sensitive for early ischemia and is the better test for posterior circulation and for wake-up strokes where mismatch imaging guides treatment. It is slower and less available, and taking a thrombolysis candidate to MRI first costs viable brain. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct — an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke — Ix]] [[Next case →->Opioid overdose — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Echocardiography with bubble study is not the next step.</div> This looks for a cardioembolic or paradoxical source and belongs to the workup after stabilization, particularly in a younger patient. It does not affect what happens in the next hour. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct — an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke — Ix]] [[Next case →->Opioid overdose — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Lumbar puncture is not the next step.</div> This is reserved for suspected subarachnoid hemorrhage with a negative computed tomography, in a patient with thunderclap headache. It is not part of an ischemic stroke pathway and would be dangerous before imaging. <div class="ec-teach"><div class="th">What to do instead</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct — an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div></div> [[Try this question again->Stroke — Ix]] [[Next case →->Opioid overdose — Rx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Non-contrast CT of the head.</div> The single question that has to be answered before thrombolysis is whether this is hemorrhagic. Non-contrast computed tomography answers it in minutes and is available everywhere, which is why it is the immediate study in every acute stroke pathway. It need not show the infarct — an early ischemic stroke often looks normal, and that is an acceptable result. <div class="ec-src"><b>Source:</b> Powers WJ, et al. AHA/ASA Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2019;50(12):e344-e418.</div></div> [[Next case →->Opioid overdose — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> The intramuscular route is appropriate in the community and when no access is available, so it is not wrong in principle. He already has intravenous access, which allows titration and onset within a minute or two. <div class="ec-teach"><div class="th">What to give instead</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and — in a patient who cannot protect his airway — aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> ACMT/AACT position statement on naloxone dosing in the out-of-hospital setting.</div></div></div> [[Try this question again->Opioid overdose — Rx]] [[Next case →->Ectopic pregnancy — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> Intubation is appropriate if he fails to respond, and airway support is already working by bag-valve-mask. Intubating a reversible poisoning without trying the antidote commits him to ventilation and an intensive care bed unnecessarily. <div class="ec-teach"><div class="th">What to give instead</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and — in a patient who cannot protect his airway — aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> ACMT/AACT position statement on naloxone dosing in the out-of-hospital setting.</div></div></div> [[Try this question again->Opioid overdose — Rx]] [[Next case →->Ectopic pregnancy — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> Right antidote, wrong dose. A full reversal bolus in a dependent patient precipitates acute withdrawal with vomiting and combativeness, and the risk of aspiration in someone already obtunded is exactly what you are trying to avoid. <div class="ec-teach"><div class="th">What to give instead</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and — in a patient who cannot protect his airway — aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> ACMT/AACT position statement on naloxone dosing in the out-of-hospital setting.</div></div></div> [[Try this question again->Opioid overdose — Rx]] [[Next case →->Ectopic pregnancy — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best choice.</div> An infusion is genuinely required for long-acting opioids such as methadone, or where sedation recurs — and it may well follow here given possible fentanyl. It takes time to reach effect while he is not breathing, so it supplements rather than replaces initial titrated dosing. <div class="ec-teach"><div class="th">What to give instead</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and — in a patient who cannot protect his airway — aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> ACMT/AACT position statement on naloxone dosing in the out-of-hospital setting.</div></div></div> [[Try this question again->Opioid overdose — Rx]] [[Next case →->Ectopic pregnancy — Dx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Naloxone in small titrated intravenous doses aimed at restoring adequate ventilation.</div> The endpoint is adequate respiration, not full alertness. Small titrated doses in an opioid-dependent patient reverse the respiratory depression while avoiding precipitated withdrawal, which causes vomiting, agitation and — in a patient who cannot protect his airway — aspiration. Larger or repeated doses may be needed with fentanyl analogues. <div class="ec-src"><b>Source:</b> ACMT/AACT position statement on naloxone dosing in the out-of-hospital setting.</div></div> [[Next case →->Ectopic pregnancy — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Acute appendicitis does not fit.</div> Appendicitis gives periumbilical pain migrating to the right iliac fossa with anorexia and localized peritonism. It does not explain the amenorrhea, the positive hCG, or an adnexal mass separate from the ovary. <div class="ec-teach"><div class="th">What the findings actually point to</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy — Dx]] [[Next case →->Error disclosure — Opening]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Ectopic pregnancy.</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div> [[Next case →->Error disclosure — Opening]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ovarian torsion does not fit.</div> Torsion gives sudden severe unilateral pain with vomiting and an enlarged edematous ovary. Here the mass is separate from the ovary and the positive hCG with an empty uterus is the finding that decides it. <div class="ec-teach"><div class="th">What the findings actually point to</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy — Dx]] [[Next case →->Error disclosure — Opening]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Pelvic inflammatory disease does not fit.</div> Her history of chlamydia makes this tempting. Pelvic infection gives bilateral pain with cervical motion tenderness and discharge, and it does not produce an empty uterus with a positive hCG above the discriminatory level. <div class="ec-teach"><div class="th">What the findings actually point to</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy — Dx]] [[Next case →->Error disclosure — Opening]]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Ruptured ovarian corpus luteum cyst does not fit.</div> A ruptured cyst gives sudden unilateral pain with free fluid and can occur in early pregnancy, so it is a real consideration. It does not produce a discrete adnexal mass separate from the ovary, and an intrauterine sac should be visible at this hCG. <div class="ec-teach"><div class="th">What the findings actually point to</div> An hCG above the discriminatory threshold with no intrauterine sac, an adnexal mass separate from the ovary, and free fluid is ectopic pregnancy. Prior chlamydial infection with tubal damage is among the strongest risk factors. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin No. 193: Tubal Ectopic Pregnancy. Obstet Gynecol 2018;131(3):e91-e103.</div></div></div> [[Try this question again->Ectopic pregnancy — Dx]] [[Next case →->Error disclosure — Opening]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> This causes sudden cardiorespiratory collapse with coagulopathy, typically during labor or immediately postpartum, and seizure can occur. She is hemodynamically stable and not in labor. <div class="ec-teach"><div class="th">What the findings point to</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin on gestational hypertension and preeclampsia.</div></div></div> [[Try this question again->Eclampsia — Dx]] [[Next case →->Compartment syndrome — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pregnancy and the puerperium are prothrombotic and this causes headache and seizure, so it stays on the list — particularly if she fails to improve. It does not explain the hypertension with proteinuria and the HELLP laboratory pattern. <div class="ec-teach"><div class="th">What the findings point to</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin on gestational hypertension and preeclampsia.</div></div></div> [[Try this question again->Eclampsia — Dx]] [[Next case →->Compartment syndrome — Ix]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Eclampsia.</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin on gestational hypertension and preeclampsia.</div></div> [[Next case →->Compartment syndrome — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Her platelets and transaminases do meet the pattern, so this is genuinely present — but HELLP does not itself cause seizures. Naming it alone omits the event that has just occurred and the magnesium she needs. <div class="ec-teach"><div class="th">What the findings point to</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin on gestational hypertension and preeclampsia.</div></div></div> [[Try this question again->Eclampsia — Dx]] [[Next case →->Compartment syndrome — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A first seizure in pregnancy is eclampsia until excluded. Diagnosing epilepsy here would omit magnesium and delivery planning in a woman with severe-range hypertension and proteinuria. <div class="ec-teach"><div class="th">What the findings point to</div> A new generalized seizure in pregnancy beyond 20 weeks with hypertension and proteinuria, preceded by headache and visual symptoms, is eclampsia. The thrombocytopenia and raised transaminases indicate HELLP overlapping with it, which is common and worsens the prognosis for both. <div class="ec-src"><b>Source:</b> ACOG Practice Bulletin on gestational hypertension and preeclampsia.</div></div></div> [[Try this question again->Eclampsia — Dx]] [[Next case →->Compartment syndrome — Ix]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> A palpable pulse does not exclude compartment syndrome — compartment pressure rises well above venous but below arterial pressure, so pulses are typically present until very late. Documenting flow would falsely reassure. <div class="ec-teach"><div class="th">What the findings point to</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction — splitting the cast and underlying padding down to skin substantially lowers compartment pressure — while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome — Ix]] [[Next case →->Acute gout — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Elevation is intuitive and it is harmful here: raising the limb lowers arterial inflow pressure and reduces perfusion of an already ischemic compartment. Keep the limb at heart level. <div class="ec-teach"><div class="th">What the findings point to</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction — splitting the cast and underlying padding down to skin substantially lowers compartment pressure — while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome — Ix]] [[Next case →->Acute gout — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> Pressure measurement is valuable where the picture is equivocal or the patient cannot report pain — obtunded, anesthetized, or very young. His examination is unequivocal, delta pressure is more reliable than an absolute threshold, and splitting the cast costs seconds and is itself therapeutic. <div class="ec-teach"><div class="th">What the findings point to</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction — splitting the cast and underlying padding down to skin substantially lowers compartment pressure — while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome — Ix]] [[Next case →->Acute gout — Rx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Split the cast to skin and reassess immediately.</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction — splitting the cast and underlying padding down to skin substantially lowers compartment pressure — while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div> [[Next case →->Acute gout — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Not the best answer.</div> MRI cannot diagnose compartment syndrome, takes the patient away from the department, and delays decompression in a condition where muscle necrosis begins within hours. <div class="ec-teach"><div class="th">What the findings point to</div> Pain out of proportion, unrelieved by opioids, with pain on passive stretch and early sensory loss in the deep peroneal distribution is acute compartment syndrome. The first intervention is to remove the circumferential constriction — splitting the cast and underlying padding down to skin substantially lowers compartment pressure — while orthopedics is called for fasciotomy. <div class="ec-src"><b>Source:</b> McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures: the pressure threshold for decompression. J Bone Joint Surg Br 1996;78(1):99-104.</div></div></div> [[Try this question again->Compartment syndrome — Ix]] [[Next case →->Acute gout — Rx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ An NSAID, colchicine, or a glucocorticoid.</div> Acute gout is treated with anti-inflammatory therapy to terminate the flare. NSAIDs (indomethacin, naproxen), colchicine (most effective within 36 hours of onset), and glucocorticoids (oral, IM, or intra-articular) are all first-line options. The choice depends on comorbidities: NSAIDs are avoided in CKD and peptic ulcer disease; colchicine requires dose adjustment in renal impairment. Urate-lowering therapy (allopurinol, febuxostat) is for chronic management and should not be initiated during an acute flare without concurrent anti-inflammatory prophylaxis, as sudden urate changes can prolong or worsen the attack. <div class="ec-src"><b>Source:</b> FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care Res 2020;72(6):744-760.</div></div> [[Next case →->Neonatal jaundice — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ This is crystal arthritis, not septic arthritis.</div> The negatively birefringent crystals and negative Gram stain confirm gout. Antibiotics treat septic arthritis, which would show organisms on Gram stain or culture. <div class="ec-teach"><div class="th">What to do instead</div> Acute gout is treated with anti-inflammatory therapy to terminate the flare. NSAIDs (indomethacin, naproxen), colchicine (most effective within 36 hours of onset), and glucocorticoids (oral, IM, or intra-articular) are all first-line options. The choice depends on comorbidities: NSAIDs are avoided in CKD and peptic ulcer disease; colchicine requires dose adjustment in renal impairment. Urate-lowering therapy (allopurinol, febuxostat) is for chronic management and should not be initiated during an acute flare without concurrent anti-inflammatory prophylaxis, as sudden urate changes can prolong or worsen the attack. <div class="ec-src"><b>Source:</b> FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care Res 2020;72(6):744-760.</div></div></div> [[Try this question again->Acute gout — Rx]] [[Next case →->Neonatal jaundice — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Probenecid is for chronic management, not acute flares.</div> Probenecid enhances renal uric acid excretion for long-term urate lowering. It does not treat the acute inflammatory response of a gout flare and, like other urate-lowering agents, should not be started during an acute attack without anti-inflammatory coverage. <div class="ec-teach"><div class="th">What to do instead</div> Acute gout is treated with anti-inflammatory therapy to terminate the flare. NSAIDs (indomethacin, naproxen), colchicine (most effective within 36 hours of onset), and glucocorticoids (oral, IM, or intra-articular) are all first-line options. The choice depends on comorbidities: NSAIDs are avoided in CKD and peptic ulcer disease; colchicine requires dose adjustment in renal impairment. Urate-lowering therapy (allopurinol, febuxostat) is for chronic management and should not be initiated during an acute flare without concurrent anti-inflammatory prophylaxis, as sudden urate changes can prolong or worsen the attack. <div class="ec-src"><b>Source:</b> FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care Res 2020;72(6):744-760.</div></div></div> [[Try this question again->Acute gout — Rx]] [[Next case →->Neonatal jaundice — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Starting allopurinol during a flare can worsen it.</div> Initiating urate-lowering therapy during an acute flare without anti-inflammatory prophylaxis can destabilize urate crystals and prolong the attack. Start anti-inflammatory treatment first. <div class="ec-teach"><div class="th">What to do instead</div> Acute gout is treated with anti-inflammatory therapy to terminate the flare. NSAIDs (indomethacin, naproxen), colchicine (most effective within 36 hours of onset), and glucocorticoids (oral, IM, or intra-articular) are all first-line options. The choice depends on comorbidities: NSAIDs are avoided in CKD and peptic ulcer disease; colchicine requires dose adjustment in renal impairment. Urate-lowering therapy (allopurinol, febuxostat) is for chronic management and should not be initiated during an acute flare without concurrent anti-inflammatory prophylaxis, as sudden urate changes can prolong or worsen the attack. <div class="ec-src"><b>Source:</b> FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care Res 2020;72(6):744-760.</div></div></div> [[Try this question again->Acute gout — Rx]] [[Next case →->Neonatal jaundice — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Probenecid is for chronic management, not acute flares.</div> Probenecid enhances renal uric acid excretion for long-term urate lowering. It does not treat the acute inflammatory response of a gout flare and, like other urate-lowering agents, should not be started during an acute attack without anti-inflammatory coverage. <div class="ec-teach"><div class="th">What to do instead</div> Acute gout is treated with anti-inflammatory therapy to terminate the flare. NSAIDs (indomethacin, naproxen), colchicine (most effective within 36 hours of onset), and glucocorticoids (oral, IM, or intra-articular) are all first-line options. The choice depends on comorbidities: NSAIDs are avoided in CKD and peptic ulcer disease; colchicine requires dose adjustment in renal impairment. Urate-lowering therapy (allopurinol, febuxostat) is for chronic management and should not be initiated during an acute flare without concurrent anti-inflammatory prophylaxis, as sudden urate changes can prolong or worsen the attack. <div class="ec-src"><b>Source:</b> FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for Management of Gout. Arthritis Care Res 2020;72(6):744-760.</div></div></div> [[Try this question again->Acute gout — Rx]] [[Next case →->Neonatal jaundice — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ The systems analysis is correct and it is not what she is owed in the room.</div> Most medication errors do have systems causes, and the incident report exists to find them — so the framing is not false. Deploying it during the disclosure converts an apology into an explanation of why no one is at fault, which patients experience as evasion and which is associated with more litigation rather than less. <div class="ec-teach"><div class="th">Why this is wrong</div> Disclose what happened, express regret plainly, explain the consequences and what will be done to prevent recurrence, and answer her questions. File the incident report in parallel; systems analysis belongs to the investigation, not to the conversation with the patient. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics Opinion 8.6; National Quality Forum Safe Practice 4 (disclosure).</div></div></div> [[Try this question again->Error disclosure — Opening]] [[Next case →->Eclampsia — Dx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Disclose promptly, factually, with an apology.</div> You tell her what happened, what harm it caused, that you are sorry it happened, what you did about it, and how it will be prevented. You file an incident report so the system can be examined. <div class="ec-teach"><div class="th">The elements of disclosure</div> Adverse events are disclosed promptly and contain four things: the <b>facts</b> of what happened, an assessment of <b>harm</b>, an <b>apology</b> for the event, and the <b>next steps</b> including prevention. Disclose the event; do not speculate about blame before the facts are established. Patients have a right to know what happened to them, and the event is separately reported through the incident system so the underlying process can be fixed. Concern about litigation is not an ethical justification for withholding disclosure. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics (disclosure of errors to patients); AHRQ Patient Safety Network (communication and disclosure).</div></div></div> <b>Disclosed and reported.</b> [[Next case →->Eclampsia — Dx]] [[Start another case->Hub]] [[Restart this case->Error disclosure — Opening]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Documentation is not disclosure.</div> Writing it in a record she will probably never read satisfies the paperwork and not the obligation. She experienced an adverse event caused by her care and has a right to be told directly. <div class="ec-teach"><div class="th">Where this breaks down</div> Disclosure is a conversation with the patient. Documentation and incident reporting are additional to that conversation, not a substitute for it. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics (error disclosure).</div></div></div> [[Try this question again->Error disclosure — Opening]] [[Next case →->Eclampsia — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ You have handed off the part that was yours.</div> The incident report is right and necessary — it is how the system learns. But it is a parallel process, not a substitute for the conversation. Routing the disclosure decision to risk management reframes a duty you owe the patient as an institutional risk calculation, and in practice it is how disclosures quietly do not happen. <div class="ec-teach"><div class="th">Why this is wrong</div> Reporting and disclosure are separate obligations that run in parallel. Institutions should support disclosure — coaching, a second clinician present, help with wording — but the decision to disclose harm that reached the patient is not discretionary and is not risk management's to make. Harm occurred here; transient harm is still harm. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics Opinion 8.6; Joint Commission standard RI.01.02.01; National Quality Forum Safe Practice 4 (disclosure).</div></div></div> [[Try this question again->Error disclosure — Opening]] [[Next case →->Eclampsia — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Concealment for your own protection.</div> "She is fine, why upset her" reframes an obligation to the patient as a favor to her. The reasoning protects you, not her — and if she learns of it later, the concealment does far more damage than the error did. <div class="ec-teach"><div class="th">Why not this</div> Patients are entitled to know about errors in their care, including those causing only transient harm. Fear of litigation does not justify non-disclosure. <div class="ec-src"><b>Source:</b> AMA Code of Medical Ethics (disclosure of errors to patients).</div></div></div> [[Try this question again->Error disclosure — Opening]] [[Next case →->Eclampsia — Dx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Breastfeeding should continue.</div> Breast-milk jaundice is benign and self-limited. Discontinuing breastfeeding permanently deprives the infant of the established benefits of human milk and is not recommended. <div class="ec-teach"><div class="th">What to do instead</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued — supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Neonatal jaundice — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Exchange transfusion is for higher levels.</div> Exchange transfusion is reserved for bilirubin approaching or exceeding the exchange transfusion threshold (typically 25–30 mg/dL for term infants without risk factors), or when intensive phototherapy fails to produce an adequate rate of decline. <div class="ec-teach"><div class="th">What to do instead</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued — supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Neonatal jaundice — Rx]] [[Start another case->Hub]]<div class="ec-verdict good"><div class="ec-vhead good">✓ Intensive phototherapy.</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued — supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div> [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Observation risks kernicterus.</div> At 19.8 mg/dL above the phototherapy threshold, untreated hyperbilirubinemia can progress to bilirubin encephalopathy (kernicterus), causing permanent neurologic damage. <div class="ec-teach"><div class="th">What to do instead</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued — supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Neonatal jaundice — Rx]] [[Start another case->Hub]]<div class="ec-verdict bad"><div class="ec-vhead bad">✕ Phenobarbital is not standard treatment.</div> While phenobarbital can induce hepatic glucuronidation enzymes, it is not first-line therapy for neonatal jaundice. Phototherapy is more effective and has a more favorable risk profile in neonates. <div class="ec-teach"><div class="th">What to do instead</div> When the total serum bilirubin exceeds the phototherapy threshold on the gestational-age- and hour-specific nomogram, intensive phototherapy is the first-line treatment. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without hepatic conjugation. Exchange transfusion is reserved for bilirubin levels approaching or exceeding the exchange threshold, or when phototherapy fails. Breastfeeding should be continued — supplementation may be offered to improve hydration and enteral output, but permanent discontinuation is not recommended. <div class="ec-src"><b>Source:</b> AAP Subcommittee on Hyperbilirubinemia. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation: Clinical Practice Guideline Revision. Pediatrics 2022;150(3):e2022058859.</div></div></div> [[Try this question again->Neonatal jaundice — Rx]] [[Start another case->Hub]]