Hippo ERcast September 2021

A Diabetic Patient with Headache and Puffy Eyes

Cerebral venous thrombosis is an uncommon stroke mimic that often presents as persistent headache, vomiting, or papilledema rather than a focal deficit. Acute pericarditis and myopericarditis commonly raise high-sensitivity troponin, but echo remains the key test for immediate risk assessment and disposition. Cerebral venous thrombosis clues High-risk headache pattern: CVT should stay on the list when a young patient has a 5-day global headache with persistent vomiting and a miserable appearance, even with normal vitals and no classic focal deficit. Thrombosis risk factors: Estrogen exposure, diabetes-related comorbidity, and possible autoimmune disease created a hypercoagulable frame that mattered more than the initially bland neurologic exam. We walk through that gestalt in the episode. Periorbital edema clue: Bilateral periorbital puffiness without dependent edema or proteinuria was an atypical finding that signaled this was not a routine migraine, DKA, or simple viral syndrome. Imaging pitfall recognition: Initial CT and MRI language pointed toward possible otomastoiditis, but the neuroradiology overread revealed extensive thrombi in the superior sagittal sinus, right sigmoid sinus, and right internal jugular vein. Best confirmatory imaging: CT venography has about 95% sensitivity and specificity and is a reliable alternative to MRV for suspected CVT, while MRV may perform better when deep venous involvement is a concern. Pericarditis troponin and echo Troponin elevation context: High-sensitivity troponin is often elevated in pericarditis and myopericarditis, so a positive result does not by itself mean an occlusion MI pattern or a poor cardiac prognosis. Older assay literature: Older studies found troponin elevation in roughly 38% to 49% of acute pericarditis cases, and modern high-sensitivity assays likely push that proportion even higher. Echo as key modality: Echocardiography is the most useful immediate test in suspected myopericarditis or pericarditis because it helps separate reassuring presentations from patients who need admission. Generally favorable prognosis: Myopericarditis is usually a good-prognosis disease; in one cohort of 486 patients, more than 90% had a normal ejection fraction and there were no deaths at 36 months. Borderline disposition nuance: A mildly elevated high-sensitivity troponin with a normal echo does not automatically mandate admission if cardiology agrees and follow-up is solid. We get into the discharge nuance in the episode.

Lit Matters #1: Thromboembolic Events After Cardioversion of Acute Atrial Fib/Flutter

Thromboembolic risk after cardioversion for acute atrial fibrillation or flutter is far lower than many clinicians were taught. In acute-onset AF or atrial flutter, 30-day post-cardioversion event rates are under 1%, and the biggest uncertainty is whether low-risk patients benefit from short-course oral anticoagulation at all. Post-cardioversion Stroke Risk in Acute AF Thirty-day event rate: Across more than 14,000 cardioversions, thromboembolic events at 30 days were just 0.42%, reinforcing that acute AF/flutter cardioversion is a low-event pathway rather than a routinely high-risk one. Anticoagulation effect uncertainty: Oral anticoagulation did not show a clear reduction in post-cardioversion thromboembolism in the higher-quality pooled data, largely because event rates were very low in both treated and untreated groups. Risk score signal: The thromboembolic events that did occur clustered in patients with higher baseline stroke risk by CHA2DS2-VASc, while low-risk patients had extremely few events. We get into how that shapes bedside counseling in the episode. Acute onset population: Most included patients had AF or flutter of less than 48 hours' duration, making the data especially relevant to the common ED question of whether recent-onset dysrhythmia can be cardioverted safely. Guideline disagreement: Canadian, American, and European guidance diverges on routine anticoagulation after cardioversion, reflecting how limited the evidence remains despite reassuringly low absolute event rates. Shared decision making: For low-risk patients considering forgoing four weeks of anticoagulation, the conversation hinges on a very small absolute stroke risk balanced against bleeding, cost, and follow-up realities.

Lit Matters #2: Out-of-Hospital Rapid Sequence Intubation with Ketamine

Ketamine does not appear to cause clinically important post-intubation hypotension during rapid sequence intubation when induction dosing is appropriate. In out-of-hospital RSI for traumatic brain injury, the more credible question is not ketamine versus another agent, but fixed dosing versus hemodynamically tailored induction. Ketamine RSI and Hypotension Dosing over drug choice: Post-intubation hypotension after RSI is framed here as a dosing problem more than an agent problem, especially when one pathway allows blood-pressure adjustment and the ketamine pathway uses a fixed 1.5 mg/kg dose. Observational signal limits: The prehospital TBI study found a 5% step-up in hypotension after ketamine rollout, but the interrupted time-series design cannot tell whether the signal came from ketamine itself or from who got it. Granular confounding concern: Paramedics could down-titrate midazolam and fentanyl based on systolic pressure, while ketamine was protocolized at a fixed dose, creating a built-in hemodynamic mismatch that matters more than the label on the syringe. Best comparative evidence: A stronger randomized trial comparing ketamine 2 mg/kg with etomidate 0.3 mg/kg found no meaningful difference in blood pressure or 28-day mortality after RSI. We get into why that trial should outweigh this newer paper in the episode. Prehospital airway context: Overall intubation success was 97.5% in the cohort, but the practical takeaway is not that ketamine is dangerous; it is that induction strategy in field RSI has to match the patient's shock risk.

EEM Rewind: The PECARN Fever Rule

Well-appearing febrile infants 29 to 60 days old can be risk-stratified for serious bacterial infection with three objective tests: urinalysis, absolute neutrophil count, and procalcitonin. PECARN outperforms older fever rules on specificity while maintaining very high sensitivity, but age, exclusions, and biomarker availability matter. PECARN Fever Rule Basics Age window and appearance: PECARN applies only to clinically well infants 29 to 60 days old; the first 3 weeks are a different HSV-heavy risk zone, with age nuances we get into in the episode. Key exclusion criteria: Former prematurity, antibiotics in the prior 48 hours, congenital malformation, chronic illness, and indwelling devices push patients outside the rule before you ever interpret labs. Three objective variables: The rule uses a negative urinalysis, ANC, and procalcitonin rather than subjective clinical impressions, which makes it easier to standardize and embed in the EHR. Performance characteristics: PECARN showed about 98% sensitivity with roughly 60% specificity, meaning many low-risk infants can avoid lumbar puncture, antibiotics, and admission. Procalcitonin requirement: Procalcitonin is not optional in PECARN; if your institution cannot obtain it, you cannot claim the rule has been applied as validated. Clinical Caveats and Practical Use Serious infection prevalence: In the derivation and validation cohort, about 9% had a serious bacterial infection, mostly UTI, with bacteremia and meningitis far less common but still consequential. Positive urinalysis nuance: A positive UA does not carry the same implication across both months of life; in older infants, blood testing and E coli coverage become central, and we walk through that distinction in the chapter. Fever duration debate: A rigid fever-duration cutoff is less reliable than it sounds, especially when onset depends on parent report, and external validation concerns matter when interpreting short-duration fever data. Lumbar puncture limits: PECARN helps identify infants at low risk for invasive bacterial infection, but it does not erase meningitis or HSV from the differential, especially in the youngest babies. Older rules comparison: Compared with Boston, Rochester, and Philadelphia criteria, PECARN and Step-by-Step rely on modern biomarkers and better statistical derivation rather than expert consensus alone.

LEGAL LESSONS: Cellulitis

Cellulitis is common, but the harder problem is deciding when erythema is infection and when it is pseudocellulitis. Initial outpatient treatment still fails in about 1 in 5 cases, while mortality is low enough that well-appearing patients with good return precautions can often go home on oral antibiotics. Cellulitis Diagnosis and Disposition Pseudocellulitis look-alikes: Venous stasis dermatitis, lymphedema, DVT, gout, and contact dermatitis commonly mimic cellulitis, and one admitted cohort found a 30% misdiagnosis rate. Failure to diagnose risk: The bigger medicolegal hazard is missing true infection rather than overtreating pseudocellulitis, because diagnostic error matters when it departs from the standard of care. Outpatient failure rate: Even correctly diagnosed cellulitis has a meaningful early relapse rate, with oral antibiotic treatment failing in roughly 21% of discharged patients. We get into the return-precaution wording in the episode. High-risk failure features: Fever at triage, chronic edema or leg ulcers, prior cellulitis in the same area, and infection at a wound site all raise the odds of outpatient treatment failure. Admission decision frame: IDSA flags systemic signs, altered mental status, hemodynamic instability, deep infection concern, severe immunocompromise, and failed outpatient therapy as reasons to consider IV therapy or admission. Low mortality perspective: Cellulitis mortality is very low, so a well-appearing patient who understands follow-up and return instructions can often be managed safely with oral antibiotics. Medicolegal Lessons From the Case Atypical first presentation: A blanching, ill-defined, non-tender erythematous thigh lesion without fluctuance or crepitus was initially labeled a drug reaction, then returned days later as septic group B strep cellulitis. Margin marking myth: Drawing a line around erythema is common practice, but there is no good evidence that border tracking improves outcomes or safely guides return decisions. Causation versus negligence: A bad outcome months later does not automatically make the index visit malpractice; the key legal question is whether the initial assessment violated an actual standard of care. Discussing expected failure: Because cellulitis treatment failure is common, risk management starts with explicitly warning patients that worsening can happen despite appropriate therapy and requires prompt reassessment. Settlement pressure factors: Venue, community dynamics, and jury risk can drive settlement decisions even when causation feels tenuous. We walk through that courtroom reality in the chapter.

Lit Matters #3: Glasgow Blatchford Score for UGIB

The Glasgow Blatchford Score helps risk-stratify suspected upper GI bleeding before endoscopy. In non-variceal UGIB, a GBS of 0-2 identifies a very low-risk group for rebleeding and short-term mortality, while possible variceal bleeding remains a separate, higher-risk problem. Glasgow Blatchford Score in UGIB Low-risk non-variceal group: In suspected non-variceal upper GI bleeding, a Glasgow Blatchford Score of 0-2 identified patients with extremely low short-term risk and essentially no 30-day mortality in this cohort. Rebleeding signal: Thirty-day rebleeding was rare in the low-risk non-variceal group, around 2%, supporting selective outpatient management rather than routine admission for every suspected bleed. Variceal bleed exception: Possible variceal bleeding is different: mortality and rebleeding were much higher, and the score was not used to label these patients low risk. We get into that separation in the episode. History limitation: Cirrhosis history alone is an unreliable shortcut for excluding variceal hemorrhage, since many variceal bleeds present without a known cirrhosis diagnosis. Practice-changing threshold: The key bedside move is recognizing that GBS 0-2 may be low enough for discharge planning in the right non-variceal patient, a threshold supported by this study and multiple guidelines.

Resuscitative Thoracotomy

Resuscitative thoracotomy is a time-critical salvage procedure for traumatic arrest, but patient selection and coordinated damage-control resuscitation matter more than bravado. In traumatic arrest, repeated eFAST, rapid blood delivery, and clear signs-of-life criteria can be the difference between futility and neurologically intact survival. Traumatic Arrest Decision-Making Neurologically intact survival: The goal is not transient ROSC but neurologically intact survivability, which sharpens decisions around who should undergo resuscitative thoracotomy and who should not. Mechanism-specific survival odds: Penetrating trauma with signs of life has the best outcomes, with neuro-intact survival reported up to 16.5%, while blunt-trauma thoracotomy remains low yield but not universally futile at 2.4%. Signs of life window: Elapsed arrest time and signs of life drive candidacy, with penetrating and blunt trauma following different time windows under Western Trauma Association guidance. We walk through that prearrival decision frame in the episode. Clearly futile scenarios: A gunshot wound to the head is a classic nonstarter, and prolonged blunt traumatic arrest without signs of life rarely justifies exposing the team to the risks of thoracotomy. REBOA versus thoracotomy: REBOA is better suited to peri-arrest non-thoracic hemorrhage such as abdominal or pelvic bleeding, while thoracotomy remains the rescue move for thoracic causes and cross-clamping physiology. Team Execution and Bedside Pearls Repeated eFAST reassessment: Tamponade can declare itself during the resuscitation, so a repeat eFAST after decompensation may reveal a new pericardial effusion that changes the destination from ED procedure to immediate OR. Dual-shock recognition: Traumatic arrest may involve both hemorrhagic and cardiogenic shock, and the winning move is treating both in parallel with blood, airway control, and rapid identification of obstructive physiology. Role-defined team flow: Successful thoracotomy care is choreography: one clinician at the airway, one committed to the left chest, another handling right chest decompression, and multiple lines dedicated to fast blood delivery. Pacing as bridge maneuver: In profound traumatic bradycardia, transcutaneous pacing can temporarily restore rate and pressure long enough to reach the OR, as in this case before epicardial pacing achieved capture. That bridge strategy is worth hearing in the episode. Post-thoracotomy priorities: After ROSC, the next move is definitive hemorrhage control in the OR; arterial lines, ventilator optimization, and ongoing transfusion help, but should not slow operative transfer. Open-chest VT management: If ventricular tachycardia develops with an open chest, use internal paddles at 30 joules and make sure the team already knows where that equipment is and how to operate it. Safety, Systems, and Preparation Prearrival surgeon-ED huddle: Before the patient arrives, the ED physician and trauma surgeon should align on mechanism, downtime, age, and likely trajectory so the thoracotomy decision is joint and fast. Small-team contingency planning: If staffing is thin, one experienced proceduralist may need to own the thoracotomy while a second clinician manages supraglottic airway, right-sided decompression, and delegation of blood resuscitation. Provider injury exposure: Thoracotomy carries real risk to the team from rib injury, sharps, and blood exposure, and that risk rises sharply in systems that perform the procedure infrequently. Blunt-trauma exposure calculus: Bloodborne pathogen prevalence is not trivial in blunt trauma, with reported rates including HCV 12.3% and HIV 3.7%, which reinforces the need to avoid futile thoracotomy. Prevention over heroics: The best resuscitative thoracotomy is often the one avoided by early recognition of traumatic decompensation, aggressive blood-first resuscitation, and rapid movement to definitive hemorrhage control.