Hippo ERcast November 2023

Drugs to Stop “Cold Turkey”: Tramadol

Tramadol is not a benign middle-ground analgesic; it is a weak opioid with serotonergic activity, seizure risk, and highly variable metabolism. In emergency medicine pain management, its benefits are modest while its adverse effects and overdose pitfalls are unusually broad. Why Tramadol Falls Short Questionable analgesic efficacy: Head-to-head trials show tramadol often performs no better than acetaminophen for some acute pain syndromes and can underperform hydrocodone-acetaminophen in musculoskeletal pain. Weak opioid with extra baggage: Tramadol adds serotonin and norepinephrine reuptake effects to modest mu-opioid activity, creating a side-effect profile that is more complex than its analgesic payoff suggests. Unpredictable CYP2D6 metabolism: Its active metabolite depends on CYP2D6, so poor and ultrarapid metabolizers can see either disappointing pain control or outsized toxicity from the same prescribed dose. Not first choice in ED: For acute pain, acetaminophen and ibuprofen are preferred starts, and if an opioid is truly needed, a direct opioid is usually the cleaner choice. We get into the practical prescribing logic in the episode. Major Safety Problems With Tramadol Seizure-provoking potential: Tramadol lowers the seizure threshold enough that one Australian ED study linked it to more than 8% of first-time seizure presentations, a memorable signal against casual use. Serotonergic toxicity risk: Because tramadol inhibits serotonin reuptake, combining it with antidepressants and other serotonergic drugs can precipitate serotonin syndrome rather than simply additive sedation. Hypoglycemia association: Tramadol has been associated with clinically important hypoglycemia, an adverse effect easy to miss when altered mental status or diaphoresis is attributed to pain or opioid exposure alone. Overdose reversal limitations: Tramadol overdose is not a straightforward naloxone story because toxicity can include seizures and non-opioid mechanisms, with management nuances we walk through in the episode. Dependence and withdrawal: Despite early safer-opioid marketing, tramadol can cause addiction and a mixed withdrawal syndrome with both opioid-like and atypical features after regular use.

Post-Intubation Paralysis with Awareness is Unacceptable

Post-intubation awareness is far more common in the ED than many clinicians realize, especially when long-acting paralysis outlasts inadequate sedation. Rocuronium, underdosed induction, and low post-intubation propofol rates are recurring drivers of awareness with paralysis. Preventing Awareness During Paralysis ED awareness signal: Recent ED data put awareness with paralysis around 1 in 20 patients, a stark contrast to classic anesthesia estimates and a reminder that emergency intubation is a different risk environment. Rocuronium risk profile: Long-acting rocuronium is a major setup for awareness when sedation fades before paralysis does, with observational data showing much higher recall rates than in patients not receiving it. DSI over blind RSI: Delayed sequence intubation helps confirm the patient is actually sedated before paralysis, and a recent trial also found less peri-intubation hypoxia with better first-pass success. We get into when that tradeoff makes sense in the episode. Ketamine first choice: Ketamine is favored for induction because it can be titrated to effect and lasts longer than etomidate or propofol, giving useful overlap through the early paralyzed period. Propofol ready now: Post-intubation sedation should not wait for the drip to arrive; for most non-elderly adults, maintaining roughly 100 mcg/kg/min is the headline target while paralysis is still on board. Pressor protects sedation: Have norepinephrine in the room before intubation so hypotension does not force you to stop propofol; turning off sedation during paralysis is the exact failure mode to avoid. Sedation and Comfort After Intubation Amnesia as backup: Benzodiazepines remain useful here for their amnestic effect, even if they are poor primary sedatives, and a small midazolam dose is advocated as added protection against recall. Etomidate mismatch problem: Etomidate is often a bad fit for the unstable patient because the hemodynamically cautious dose may be inadequate for hypnosis, creating a high-risk setup for awareness. Tube pain matters: The endotracheal tube is a major ongoing pain source, and good analgesia can reduce sympathetic stress and sometimes allow lower sedative requirements after paralysis wears off. Push-dose opioid strategy: Intermittent morphine or hydromorphone is preferred over an opioid infusion for tube discomfort in the ED, keeping analgesia practical without committing to another continuous drip. Why not fentanyl: Fentanyl is discouraged for post-intubation tube pain because its short duration makes repeated redosing impractical in real ED workflow. That bedside reasoning is worth hearing in the chapter.

Lit Matters #1: Should We be Doing a Brain CT in patients with ROSC after OHCA?

Out-of-hospital cardiac arrest with ROSC is usually cardiac in origin, and routine brain CT rarely changes management when no clear neurologic cause is apparent. Post-arrest imaging still matters when the etiology is unclear, especially when intracranial hemorrhage or another occult neurologic trigger would redirect care. Brain CT After OHCA ROSC Predominantly cardiac etiology: Most OHCA cases are driven by cardiac causes, so a routine head CT after ROSC has a relatively low yield unless the history, exam, or arrest context points toward a neurologic trigger. Clinically significant CT yield: In this prospective cohort, clinically significant brain CT findings appeared in 12% of scanned patients, with acute ischemia more common than hemorrhage, mass, edema, or herniation. Normal scan frequency: Nearly half of post-ROSC head CTs were normal, a useful reminder that universal imaging consumes substantial resources in a population already difficult to move and stabilize. Management change definition: The study counted pathology as significant only when it changed treatment, but that endpoint is inherently subjective and leaves room for wide physician-level variation in what action follows a finding. Outcome implications: Patients with acute intracranial pathology after OHCA had poor outcomes, and mortality was similar between groups, which complicates the assumption that finding an abnormality necessarily improves prognosis. Selective imaging strategy: A reasonable approach is to reserve brain CT for patients without a clear arrest cause or with neurologic red flags, and we get into that post-ROSC decision tension in the episode.

Top Trauma Pearls From the Recent Literature

Not every traumatic pneumothorax on positive-pressure ventilation needs a chest tube. Recent trauma literature also supports 14 Fr drainage for hemothorax and targeted antibiotic prophylaxis for tube thoracostomy, especially after penetrating injury. Chest Tube Decisions in Trauma Occult pneumothorax observation: Occult pneumothorax in a stable, mechanically ventilated trauma patient can often be watched rather than drained, especially when extubation is expected within 4 days. Low tension progression rate: Progression to tension physiology was uncommon in the pooled data, and most observed patients never needed any intervention. We get into the selection nuances in the episode. Rescue tube strategy: Patients initially observed and later needing tube thoracostomy had fewer overall complications than those getting an upfront prophylactic chest tube. Small-bore hemothorax drainage: Traumatic hemothorax can be managed with a 14 Fr percutaneous catheter, with failure rates comparable to traditional 28-32 Fr chest tubes. Pain and satisfaction advantage: Smaller percutaneous tubes were associated with less pain and better patient-reported satisfaction, a meaningful bedside advantage when drainage efficacy is equivalent. Antibiotics for Tube Thoracostomy Penetrating trauma benefit: Prophylactic antibiotics reduce empyema after chest tube placement, with the clearest benefit seen in penetrating trauma. Skin flora coverage: The microbiology signal is skin flora, making a first-generation cephalosporin a practical first-line choice for prophylaxis. Procedure-timed dosing: Best-supported prophylaxis starts at the time of tube insertion and continues briefly afterward rather than becoming a prolonged antibiotic course. Focused outcome effect: The observed benefit is lower empyema rates, without a clear pooled reduction in pneumonia or mortality. We walk through what that means in the chapter.

High Risk, Low Prevalence: BRASH Syndrome

BRASH syndrome is a synergistic spiral of bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia. The clue is disproportionate bradycardia with only mild to moderate potassium elevation, often after dehydration, sepsis, or a medication change in an older patient with kidney disease. Recognizing BRASH Syndrome Five-part vicious cycle: BRASH is not just hyperkalemia plus bradycardia; it is a self-amplifying loop of bradycardia, renal failure, AV nodal blocker exposure, shock, and hyperkalemia that requires treating every limb of the syndrome. Disproportionate bradycardia clue: Severe bradycardia can appear when potassium is only 5-7 mEq/L, far earlier than the classic hyperkalemia picture, and that mismatch is the bedside clue we emphasize in the episode. Atypical EKG pattern: The ECG finding is often mainly bradycardia rather than the full textbook progression of peaked T waves and QRS widening, so a relatively bland tracing should not reassure you. High-risk medication stack: AV nodal blockers are central, especially atenolol, nadolol, and labetalol, while ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs, trimethoprim, digoxin, tacrolimus, and cyclosporine raise the risk. Typical clinical trigger: The syndrome is often unmasked by dehydration, GI illness, sepsis-related hypotension, or a recent dose increase or new nephrotoxic medication in an older patient with baseline renal vulnerability. Initial Management Priorities Treat the whole syndrome: Management has four parallel targets: volume status, bradycardia, hyperkalemia, and the precipitating cause, because fixing only one piece often leaves the cycle running. Volume status first pass: Volume management is nuanced because these patients may be oliguric and overloaded; history, exam, and POCUS are key to finding euvolemia, and we walk through that bedside approach in the chapter. Calcium as first move: Calcium is the first-line stabilizer for the bradycardic hyperkalemic patient, and repeat dosing is often needed when the initial response is incomplete. Epinephrine over atropine: Epinephrine is the preferred pressor for unstable BRASH because it raises heart rate and shifts potassium intracellularly, whereas atropine is usually not helpful in this physiology. Dialysis and mimics: If medical therapy fails, dialysis may be required; persistent instability should also prompt reconsideration of beta-blocker, calcium-channel blocker, or digoxin toxicity and adrenal insufficiency.

Lit Matters #2: Should We do Head-to-Pelvis CT in OHCA?

Post-ROSC whole-body CT can uncover a time-critical cause of out-of-hospital cardiac arrest when the etiology is unclear, but the yield is far from universal. Early head-to-pelvis imaging appears safe in selected stable patients and is most compelling as a targeted rather than automatic post-arrest strategy. Whole-Body CT After OHCA Targeted post-ROSC imaging: Whole-body CT is most useful after ROSC when out-of-hospital cardiac arrest has no obvious cause, especially for occult intracranial hemorrhage, pulmonary embolism, pneumonia, or abdominal catastrophe. Selective rather than routine use: The pragmatic takeaway is not to scan every post-arrest patient; hemodynamic instability and an obvious cath-lab pathway still trump a protocolized head-to-pelvis CT. We get into that bedside triage in the episode. Meaningful diagnostic yield: Early sudden-death CT identified the etiology of arrest only by imaging in 13% of cases, a modest number that still matters when the diagnosis is immediately management-changing. Time-critical findings detected: Among patients with urgent diagnoses, whole-body CT captured nearly all of them and missed only one, supporting its value as a screen for immediately actionable pathology. Safety signal in selected patients: Contrast exposure did not appear to trigger major downstream harm in this cohort; AKI was common after arrest, but only one patient ultimately required CRRT. Study design caveats: This was a 104-patient observational cohort with exclusions for unstable patients and those needing emergent catheterization, so the results support feasibility more than a universal protocol.

2022 Guideline Update: Lower GI Bleeds

Acute lower GI bleeding is risk-stratification and hemodynamics first, not a reflex colonoscopy problem. The updated ACG guidance clarifies who can go home, when CTA changes management, and how to handle transfusion, anticoagulant reversal, and antithrombotic restart decisions. Lower GI Bleed Guideline Pearls Oakland score triage: The Oakland Score helps identify low-risk lower GI bleed patients for possible discharge and gives a quantitative footing for admission decisions when the bedside picture is less obvious. Restrictive transfusion threshold: Hemoglobin under 7 g/dL is the headline transfusion trigger, but hypotension or ongoing bleeding still calls for immediate IV fluid resuscitation while the rest of the picture comes together. Selective anticoagulant reversal: Anticoagulant reversal is reserved for life-threatening bleeding or markedly supratherapeutic warfarin effect, with 4-factor PCC preferred over FFP for faster INR correction. CTA over routine CT: CT angiography of the abdomen and pelvis is the preferred study for significant or ongoing hematochezia because active extravasation can directly route the patient to IR. We get into that consultant-facing workflow in the episode. No rush to colonoscopy: Inpatient colonoscopy is still recommended for most admitted patients, but emergent scope has not shown better rebleeding or mortality outcomes than a routine inpatient approach. Antithrombotic restart decisions: After bleeding control, anticoagulation should usually be resumed because it lowers thromboembolism and mortality, while aspirin and non-aspirin antiplatelet decisions depend on the indication for use.

What’s New in Bronchiolitis

Bronchiolitis is a clinical diagnosis in children under 2, and routine chest radiographs, labs, and respiratory viral panels usually add little. Supportive care drives outcomes, while steroids and routine beta-agonists do not; lung ultrasound and emerging bronchiolitis endotypes may refine bedside decisions. Diagnosis and Natural History Clinical diagnosis first: Bronchiolitis is diagnosed from history and exam, not testing, with classic fever, rhinorrhea, cough, crackles, wheeze, or apnea in a child younger than 2 years. Testing usually unnecessary: Chest radiographs, routine labs, and respiratory viral panels generally do not improve management and often add noise to a straightforward bronchiolitis presentation. Lung ultrasound clues: Adjacent B-lines, hyperechoic areas, and air bronchograms on lung ultrasound track with more severe disease and can help separate bronchiolitis from reactive airway disease. We get into the bedside distinction in the episode. Expected illness timeline: Symptoms typically peak on illness days 3 to 5, improve over 1 to 2 weeks, and are resolved in roughly 90% of children by 2 to 3 weeks. Escalation warning signs: If impending respiratory failure is a concern, a blood gas can reveal CO2 retention and respiratory acidosis before the child declares themselves clinically. Management and Disposition Supportive care essentials: Nasal suction, hydration, and oxygen remain the core therapies, with suction especially useful before checking saturations and before feeds. Oxygen target strategy: Use the lowest oxygen flow that maintains a pulse oximetry above 92%, escalating support only when simple oxygen no longer corrects hypoxemia. Noninvasive respiratory support: High-flow nasal oxygen at 1 to 2 L/kg is a common next step, while CPAP around 7 cm H2O is reserved for more severe bronchiolitis. Therapies to avoid: Steroids, racemic epinephrine, antibiotics, and chest physiotherapy are not recommended routine treatments for bronchiolitis. Beta-agonist controversy: AAP guidance recommends against even a trial of inhaled beta-agonists, though emerging endotype data suggest a subset with atopic or reactive-airway features may differ. We cover that nuance in the chapter. Admission risk factors: Hypoxemia, dehydration, increased work of breathing, young age under 2 months, and comorbidities like prematurity, congenital heart disease, or immunodeficiency all push toward admission.

Raging Hormones: Navigating Thyroid Storm

Thyroid storm is a clinical diagnosis marked by rapidly progressive thyrotoxicosis, adrenergic excess, and end-organ dysfunction. In the ED it commonly masquerades as sepsis, myocarditis, toxidrome, or serotonin syndrome, and treatment should start on suspicion rather than waiting for labs. Recognizing Thyroid Storm Early Sepsis mimic pattern: Think thyroid storm when a presumed sepsis or myocarditis patient has risk factors, rapid deterioration, and poor response to usual therapy; that mismatch is a major bedside clue. High-risk patient profile: Known hyperthyroidism, family history of thyroid disease, recent neck surgery, radioiodine exposure, or a new drug such as amiodarone meaningfully raise pretest probability. Rapid multisystem presentation: Tachycardia, agitation, GI upset, and signs of heart failure developing quickly after a viral illness fit the syndrome better than isolated uncomplicated thyrotoxicosis. Clinical diagnosis first: No rapid test rules thyroid storm in or out in real time, so ED diagnosis is clinical and therapy should begin before confirmatory data return. We get into that decision threshold in the episode. Thyroid lab interpretation: Low TSH plus a very high free T4 supports thyroid storm, but an isolated suppressed TSH is not diagnostic and should not anchor the workup. Acute Management of Thyroid Storm Supportive care priorities: Initial stabilization still matters: IV fluids, antipyretics, antibiotics when infection is possible, and close glucose monitoring address the common physiologic crashes around the storm. Hormone synthesis blockade: Thionamides stop new hormone synthesis, with methimazole and PTU as the key agents; PTU carries a U.S. black box warning for liver injury. Release blockade timing: Iodine is used after a thionamide to shut down thyroid hormone release, while lithium or potassium perchlorate are alternatives when iodine cannot be used. We walk through the sequence in the chapter. Adrenergic symptom control: Beta blockers blunt the systemic effects of free T3, with propranolol a classic choice and esmolol useful when acute heart failure is entering the picture. Steroid adjunct role: Glucocorticoids reduce peripheral conversion of T4 to T3, and hydrocortisone 100 mg IV is a common first dose when thyroid storm overlaps with a sepsis-style presentation. Refractory rescue options: Plasmapheresis and emergent thyroidectomy are the major salvage strategies for refractory thyroid storm or for patients who cannot take a thionamide.

Lit Matters #3: Does a Pan Scan Yield More Diagnostic Accuracy in OHCA?

Whole-body CT after return of spontaneous circulation can find occult causes of out-of-hospital cardiac arrest faster, but faster diagnosis does not necessarily improve survival. In post-ROSC OHCA care, the practical question is not whether imaging matters, but which patients benefit from protocolized head-to-pelvis CT versus a selective, exam-driven approach. Post-ROSC CT Imaging After OHCA Faster diagnosis, same survival: Protocolized head-to-pelvis CT shortened time to identified cause from 14 hours to 3 hours, yet survival to discharge stayed essentially unchanged between groups. Diagnostic yield signal: Finding a clear post-arrest cause in more than 10% of patients is clinically meaningful, especially when the differential includes hemorrhage, PE, aortic disease, or other noncoronary pathology. Selective imaging reality: Even standard care was not no-imaging care: 84% of patients underwent some imaging, with selective CT head doing much of the work in usual post-ROSC evaluation. Protocolized pan scan limits: A universal sudden-death CT pathway improved speed and diagnostic accuracy, but neurologically intact survival did not improve and actually numerically favored standard care. Bedside-first imaging strategy: Noncontrast head CT, targeted physical exam, and hypotension-focused POCUS remain the practical first pass before escalating to chest angiography or coronary CT in selected patients. We walk through that sequencing in the episode. Not ready for all comers: The take-home is that routine pan scan after OHCA with ROSC is not ready for primetime; imaging should be tailored with ICU input, local resources, and the suspected arrest mechanism.