Use this section to build teaching modules, quick conference topics, and procedural lessons.
- Airway management
- Resident performance feedback
- Case-based pearls
Use this section to build teaching modules, quick conference topics, and procedural lessons.
increasing prevalence due to SGLT2 inhibitors (empagliflozin, canagliflozin, dapagliflozin) other risk factors: vomiting, partially treated DKA (insulin), poor PO intake, ketosis/keto diet challenge is in the diagnosis: will have normal glucose, probably didn’t order BOHB off the bat anion gap of unexplained etiology; acidosis (though could have concomitant metabolic alkalosis from vomiting; may have normal pH with acidosis and alkalosis) treatment nearly identical, though start glucose drip earlier generally glucose <250, start glucose ...
acidosis (blood gas), correct underlying/bicarb gtt? hypothyroidism (TSH, FT4); levothyroxine (myxedema coma- 300-500mcg + hydrocortisone) anaphylaxis (history/exam): epinephrine, methylene blue, ECMO adrenal insufficiency (clinical, cortisol, hypoNa + hyperK): hydrocort 100-200mg hypocalcemia (iCa, long QTc): calcium gluconate 2-3g occult bleed (clinical; retroperitoneal/GIB/ectopic): transfuse, reverse AC, surgery/IR toxicologic (clinical; BB, CCB, TCA): by etiology alternate cause to shock (obstructive, DVT)
brain teaser: two case where VT/F arrest should not be treated with epi - hydrocarbon toxicity and electrical or thyroid storm (instead give lido; beta sympathetic surge) Sudden sniffing death syndrome: sniffer startled during use, goes into VT, dies gasoline, lighter fluid, lamp oil, petrol, paint thinners Huffing: smelling a soaked rag Bagging: sprayed/poured into bag and inhaled Sniffing: directly inhaled pulmonary toxicity: can get ARDS, aspiration risk (low viscosity, low surface tension) ...
concrete experience: delivering patient care reflective observation: staffing patient, on-shift teaching abstract conceptualisation: reading at home, feedback and reflection active experimentation: trying a new approach next time
Why EM? 15% of complications occur at presentation (85% in hospital) MECHANICAL RV infarct Hypotension, JVD, clear lungs Treatment: decrease RV afterload IV fluids, if they can handle it Flolan (epoprostenol): PGI2/prostacyclin; direct pulmonary vasodilator; not available at MAMC Entresto (sacubitril-valsartan): neprilysin inhibitor/ARB Hydralazine: smooth muscle relaxation Inhaled nitric oxide? Papillary muscle rupture Do you hear a murmur? NOT reliably: murmur requires difference in flow; in acute MR from pap rupture, flow equalizes across LA/LV ...
study on low-dose droperidol in the ED 68 pts, median dose 1.875 (0.625-2.5mg) mostly given for headache mean QTc change 30msec (SD 15), 4% had change >60msec 18% had QTc >500 no arrhythmia or death 13% had restlessness/anxiety Hernández-Rodríguez L, Bellolio F, Cabrera D, et al. Prospective real-time evaluation of the QTc interval variation after low-dose droperidol among emergency department patients. Am J Emerg Med. 2022 Feb;52:212-219.
pericarditis causes viral: HIV, coxsackie, echovirus, bacterial, chlamydia, mycoplasma, syphilis) idiopathic radiation malignant (lung, breast, Hodgkin, mesothelioma) hemorrhagic (from malignancy, bleeding diathesis) toxin (procainamide, phenytoin, minoxidil, doxo/daunorubicin) iatrogenic (post-MI, post-pericardiotomy) uremic, OHSS, collagen vascular disease, hypothyroidism diagnosis (2+/4) 1: history (pericarditic chest pain) 2: exam (friction rub) 3: ECG (diffuse STE, PR depression) 4: imaging (US with new/worsening PCE) disposition admit for fever, instability/tamponade, immunosuppressed, on anticoagulants, not improving with treatment, myocarditis ...
serotonergic medications SSRIs, MAOIs trazodone, TCAs, lithium, valproate cocaine, ecstacy, meth, linezolid, carbamazepine, ondansetron, dextromethorphan, fentanyl, tramadol, flexeril ginseng, st johns wort, yohimbine, nutmeg clinical features AMS, hyperactive autonomic instability: hyperthermia, tachycardia, hypertension, diaphoresis GI upset clonus- ocular, lower extremities tremor, seizures hyperreactive vs rigid (NMS) differential sepsis (infection) thyroid storm (clonus; TSH) NMS (rigidity) sympathomimetic (clonus) anticholinergic toxicity malignant hyperthermia (are you standing in an OR) hunter criteria spontaneous clonus ...
Subtypes Cavernous sinus thrombosis (often complication of local infection- paranasal or sinus; V1/2 and III, IV, VI, internal carotid in cavernous sinus) Risk factors Hypercoagulable states cancer (leukemia, adenocarcinoma) pregnancy, including up to 6wk postpartum OCP use, obesity polycythemia vera sickle cell disease factor V Leiden, protein C/S deficiency, hyperhomocysteinemia Behcet disease COVID vaccines? 1 in 1mil for J&J, 1/100k for AZ Local infection AOM sinusitis cellulitis odontogenic infections mastoiditis tumor/abscess compressing venous sinus Clinical features headache (74-92%), usually progressive over hours/days; severe, aching, throbbing throughout coughing, bending over, head movement worsens headache (positional- red flag) seizures (35-50%), often focal convulsions papilledema (28-45%), vomiting focal neuro deficit (often hours-days after headache) superior sagital sinus: motor deficits (hemiparesis) left transverse sinus: aphasia, confusion cavernous sinus: ocular pain, oculomotor palsy, proptosis deep venous: drowsiness/stupor from thalamic dysfunction/hydrocephalus dizziness encephalopathy/AMS Workup MRI and MR venogram study of choice CT venogram reasonable alternative empty delta sign: dense triangle in superior sagittal sinus vs dense delta sign on NCCTH: hyperattenuation (thrombus) in posterior sinus vein sign: see thrombus in the vein, usu after two weeks labs poor; d-dimer not a reliable test evaluate for coagulopathy Treatment anticoag with heparin or LWMH; lower dose (3-5k U) than VTE oral anticoagulation for 3-6 months (warfarin) cavernous sinus thrombosis seizure prophylaxis if p/w seizure admit with neuro checks, watch for increased ICP (intravascular thrombolytics) possible nsgy intervention (hemicrani) if decompensating
conductive: cerumen, external ear, middle ear, ossicular chain sensorineural: inner ear, cochlea, auditory nerve most common cause: presbycusis history med changes family history of hearing loss trauma scuba/flying (barotrauma) high vs low pitch loss prior ear surgeries qtip use exam ABCs ear exam- EAC, impaction, mass neuro exam, CNs Weber: put TF on forehead — louder in affected ear: conductive loss — louder in unaffected ear: sensorineural Rinne: vibrating TF on mastoid behind ear, then when not heard, place at EAC — AC > BC (can still hear at the EAC) normal ...