2.21.19 Conference Summary

Morbidity & Mortality - Dr. Andrew Schaub


Case #1

Middle-aged male presented to the ED for fever. Also c/o cough, sob, myalgias. Tachycardic. EKG showing nonspecific ST/T changes (no prior EKG for comparison). Labs notable for troponin of 12, elevated inflammatory markers. Normal cardiac POCUS. Admitted for myocarditis. Infectious workup significant for coxsackie B virus. Diagnosis supported by cardiac MRI. Improved and was discharged a few days later.



  • Inflammation of heart muscle with lymphocytic infiltatration

  • Causes - most commonly idiopathic vs viral (coxsackie); also other infections, vasculitides, immunologic process, toxins/drugs

  • Clinical features: fever, myalgias, tachycardia disproportionate to clinical assessment

    • May have component of pericarditis with pericardial effusion

    • Wide range of presentations (mild URI symptoms to fulminant cardiogenic shock)

  • Diagnosis

    • Typical symptoms + fever + troponin elevation

    • Cardiac MRI can be useful adjunct

    • Endomyocardial biopsy is gold standard (usually only performed to evaluate for non-infectious causes)

  • Treatment

    • Supportive - fever control and fluid resuscitation as needed

    • Severe cases that result in dilated cardiomyopathy and cardiogenic shock, requiring pressors or mechanical circulatory support

  • Prognosis

    • Highly variable, depends on etiology

    • CK-MB is helpful predictor

    • Pediatric cases have poorer prognosis regardless of cause

    • Myocarditis-related cardiomyopathy does not usually result in chronic cardiomyopathy

Case #2

30s yo M presented for shortness of breath, billed as ‘asthma exacerbation.’ Went into PEA arrest with ROSC x2. Started on epi drip. TTM initiated. CT PE study showing massive PE. Initially heparinized then received tPA. Reduced cardiac function on echo. IVC filter placed. Hypercoagulable workup unremarkable. Cardiac function normalized on repeat echo. Patient discharged from the hospital four days later without oxygen requirement, neurologically intact, on rivaroxiban.


Massive PE

  • Acute PE with sustained hypotension for at least 15 min or pulselessnes or profound bradycardia with signs/symptoms of shock

  • All-cause mortality 64.8% when associated with CPR

  • Quickly leads to acute right heart strain as the right heart has poor compensatory mechanisms. This, in turn, leads to decreased LV preload.

  • Way to prevent/improve RV failure 

    • Optimize preload - use POCUS, be judicious with fluids; less of an option in large PE (large mechanical obstruction)

    • Increase afterload – to decrease DBP + increase CPP; norepi (or epi), avoid phenylephrine (inc pulm pressure)

    • Increase contractility – dobutamine, epi, or milrinone

    • Reduce PVR – TPA, nitric oxide, ECMO; consider systemic TPA early in crashing PE patients

    • Respiratory support – avoid hypoxia/hypercapnia as this will worsen PVR; optimize hemodynamic status prior to intubation

  • Treatment

    • Systemic thrombolysis indicated if persistent hypotension/shock or in suspected or confirmed PE in arrest

      • Contraindications to fibrinolytic therapy include: prior ICH, known structural cerebral vascular lesion or neoplasm, AVM, ischemic CVA within 3 months, suspected aortic dissection, active bleeding

    • Adjunctive therapy: suction embolectomy, surgical embolectomy, catheter directed thrombolysis (decreases amount of tPA)

    • Role of IVC filter unclear; consider if recurrent PE despite anticoagulation or if anticoagulation contraindicated

Case #3

30yo M presented for abdominal pain. Labs suggestive of acute pancreatitis with severely elevated triglycerides >2500. Received pain control and fluids. Diagnosed with acute pancreatitis and discharged home. Returned later that day with persistent pain. Biliary ultrasound showing fluid around pancreas. Admitted to the floor. A few hours later he was transferred to the MICU, started on insulin drip. Within 8 hrs, TG improved to 300s. Pt discharged 4 days later.


Hypertriglyceride-induced acute pancreatitis

  • Accounts for approximately 1-4% of pancreatitis (relatively rare compared to gallstones and EtOH, the two most common causes)

  • Tends to be more painful than other etiologies

  • TG levels almost always >1000mg/dL

  • Insulin drips are the preferred treatment (highly effective in both diabetics and non-diabetics) — 0.1 u/kg/hr

    • Insulin stimulates TG removal from blood

  • Plasmapheresis also highly effective but costly and higher risk

Case #4

20yo F presented to the ED for nausea and acute on somewhat chronic abdominal pain. Labs notable for mild leukocytosis and UTI. Negative urine preg. Received fluids, toradol, and antiemetics, symptoms improved and she was discharged. Returned to the ED the next day with nearly identical course. Discharged home and returned to the ED later that day. TVUS showing IUP. Had trichomonas. Quantitative HCG elevated. Discharged home and returned a 4th time, several hours later. Ultimately admitted to OB for hyperemesis. At this point she was treated for trichomonas, UTI, fluids, antiemetics.


Urine Pregnancy Tests

  • POC urine pregnancy tests used in the ED have similar reliability and sensitivity as home pregnancy tests

    • Tests rely on preformed antibodies to detect beta-HCG

    • Most tests detect HCG with nearly 100% sentivitity within 9-10 days of implantation

  • False negatives

    • Most commonly a result of test being done before there is sufficient levels of HCG to produce a positive result

    • Other causes:

      • Operator error (requires waiting a sufficient amount of time to show a positive result)

      • Assay’s antibody may not recognize certain variants

      • Unusually high concentrations of the core fragment of HCG which can occur in later stages of pregnancy

      ***dilution is key to an accurate test

  • Bottom line: obtain quantitative HCG or other testing if clinically concerning

EM/Trauma: Intracerebral Hemorrhage - Dr. Wei Xiong, Neurointensivist

  • Risk factors: hypertension, older age, alcohol abuse

  • More commonly seen in African Americans, Asians

  • Etiology

    • Hypertensive vasculopathy most common

      • Small vessels more prone to damage resulting in rupture

      • Correlates with higher blood pressures and age

    • Vascular malformations - includes aneurysms; can cause ICH or SAH

    • Cerebral amyloid angiopathy

      • Associated with dementia

      • Amyloid protein deposition in smaller vessels leads to micro bleeds over time

      • Presents with lobar hemorrhages (grey-white junctions)

      • Diagnosed with MRI

      • Hemorrhagic transformation

    • Others: dural sinus thrombosis, anticoagulation use, neoplasm, septic emboli, drugs, vasculitis, moya moya

  • Clinical presentation

    • Stroke-like symptoms

    • Abrupt onset with gradual worsening of symptoms

    • Initial bleeding is painless but headache can develop from increased ICP or meningeal irritation

  • Locations

    • Putamen most common —> lobar, thalamus, cerebellum, pons

  • Scoring systems

    • ICH Score - measures severity and predicts mortality (vs NIHSS which quantifies neurologic deficits)

    • FUNC Score - functional outcome risk stratification scale; useful for goals of care

  • Imaging

    • CT is best modality for acute imaging of blood in the brain

    • Volume estimated by measuring width x height x depth/2

    • MRI useful to evaluate underlying lesion and age of blood

    • Gradient echo: blood of any age = dark spots

  • BP Management in ICH

    • Overarching goal: balance lowering risk of hematoma expansion vs decreasing CPP in setting of raised ICP

    • AHA/ASA 2007 Guidelines

      • Goal SBP < 180 mmHg or MAP < 130 mmHg and CPP > 60-80mmHg

    • INTERACT2 Trial (2013) — looked at lowering SBP below 140 (vs standard <180)

      • Targeting SBP < 140 is safe and probably beneficial

    • ATACH 2 Trial - 2016

      • SBP 110-139 vs SBP 140-179

      • No difference in outcome (death or disability) between the two groups but more renal adverse events in the intensive treatment group

    • UHCMC protocol: Goal SBP < 160 mmHg with option to target <140 mmHg based on patient characteristics and clinical judgment (such as AVM)

  • Reversal of anticoagulation

    • Heparin - protamine sulfate

    • Warfarin - PCC (4-factor)

      • Pros: rapid administration, high concentration in small volumes, few adverse reactions

      • Cons: very expensive

    • DOAC reversal

      • Idarucizumab (Praxbind) -dabigatran reversal; one-time dose

      • Adnexanet (Andexxa) - rivaroxaban, apixaban, edoxaban reversal; low dose vs high dose, effective, but also very expensive

  • Resuming anticoagulation

    • Risk of recurrent ICH is dependent on location

    • AHA/ASA 2015 Guidelines

      • Lobar ICH - never resume AC

      • Non-lobar - consider resuming if strong indications but wait at least 4 weeks (aspirin can be restarted in a few days)

  • Intraventricular Hemorrhage

    • High mortality (51% vs 20%)

    • CLEAR III Trial

      • Intraventricular tPA vs placebo

      • No difference in primary endpoint (functional status) but 10% absolute risk reduction in mortality in the tPA group

  • Surgical Evacuation

    • Cerebellar hemorrhage > 3cm diameter should undergo surgical decompression

    • Large brainstem hemorrhages unlikely to benefit from surgical intervention

    • Supratentorial hemorrhage

      • STICH I, II Trial

        • Early surgery vs initial conservative treatment in patients with spontaneous supratentorial ICH —> No significant difference in outcomes

      • MISTIE II & III Trial

        • Minimally invasive stereotactic tPA administration vs conservative treatment —> no improvement in outcomes, modest improvement in mortality

      • MISTIE-ICES (in progress)

        • Comparing endoscopic surgery (ICES) or minimally invasive surgery + clot lysis with rt-PA (MISTIE) for ICH

      • AHA/ASA 2015 Guidelines: Early hematoma evacuation not clearly beneficial compared with hematoma evacuation when patients deteriorate (but may be considered life-saving intervention in the deteriorating patients)