Grand Rounds Summary 12.21.16

/

Mortality and Morbidity Conference with Dr. Jon McKean

Transfusion Related Lung Injury (TRALI)

  • Acute onset of symptoms of acute lung injury (ALI) within 6h of blood transfusion
  • PaO2/FiO2 <300 mm Hg, or worsening of P/F ratio
  • Bilateral infiltrative changes on CXR
  • No signs of hydrostatic pulmonary edema

Suspect TRALI: 

  • ALI happening within 6h of blood transfusion
  • No preexisting ALI
  • Clear temporal association for an alternative risk factor for ALI

2 Hit Hypothesis: 1st hit is pre-disposing factor (liver disease, infection) and then 2nd hit is the inflammatory factors in the blood products themselves

Risk of TRALI: FFP>PRBC; older product>newer product

Treatment: Stop transfusion, support through ALI

Aspiration Pneumonitis

Mortality in TBI after acute period: respiratory compromise is a common cause of mortality in TBI patients

Selective Attention: make sure to continue to look at the whole picture even when only looking for a certain abnormality 

Pulmonary Embolism

Patients who have missed PEs are more likely to have something else that would cause SOB, such as COPD (OR 4.3) or Asthma (OR 3.4). 

Ambulatory vital signs as prediction of PE: increased HR >10 or SpO2 that drops >2% on a 3 min walk test is extremely sensitive but very non-specific for PE.

EKG predictors of hemodynamic collapse with PE:

  • HR >100
  • S1Q3T3
  • RBBB
  • Inverted T waves in V2 & V3
  • ST Elevation in aVR

PE in first time syncope patients: Recent NEJM publication showing 17% prevalence of PE in patients admitted for syncope in Italy. Take in the context of patient population who was admitted for syncope, not necessarily our every day syncope patient population.

TCA Overdose

Toxicity: 

  • Sodium Channel Blockage
    • Sodium Bicarb
  • Alpha blockade
    • Fluids (norepinephrine & epinephrine) and pressors
  • GABA antagonism
    • Benzos
  • Anticholinergic
    • No physostigmine (caused asystole in case reports)

QT prolongation: with a toxic TCA level the OR is 4.94 for QT prolongation to a level above the line on a QT interval nomogram which raises concern for Torsades 

Intralipid Emulsion (ILE) Treatment: Data is sparse, however may be a place for use in patients with cardiac arrest or shock from certain overdoses (local anesthetics, many antidepressants, and antipsychotics). 

Platelets in ICH

Retrospective Review of 9 papers on giving platelets for ICH on anitplatelet agents: nothing reached statistical significance

PATCH Trial Inclusion Criteria

  • Age +18
  • Supratentorial, non-traumatic ICH
  • GCS 8-15
  • Timeline parameters (within 6h of LKNT)
  • Had to be on anti-platelet agents in the previous 7 days

PATCH Trial Exclusion criteria:

  • If it is likely to be is or a SDH/epidural
  • Caused by aneurysm or AVM
  • Plan for surgery
  • Intraventricular bleeding of significant extent
  • Imminent Death

Patch Trial Conclusions: worse outcomes, increase AE, and increase in mortality in those who received platelets

R1 Clinical Diagnostics: Renal Panel with Dr. Owens'

Before reading the summary, please check out Dr. Owens' asynchronous piece on the basics of the Basic Metabolic Panel.  

Case #1: Hyponatremia secondary to diluting formula in a 3 week old female presenting with seizures.

1cc/kg of 3% NaCl flushed with NS, up to 3 doses repeated q1min until the baby stops seizing. Rough rule of thumb: 1cc/kg of 3% will raise it sodium 1meq

Initial management: 3-4 ml/k/h of 3% saline, once mental status normalizes then can use normal saline to correct at a rate of 0.5meq/hr for a max increase of 12 meq/24h

Case #2: Hypercalcemia in SLC with EKG changes (biphasic T waves in anterior leads, shortened QRS)

Initially use NS to resuscitate, and calcitonin initially, then bisphosphonates to correct more long term. Can use cancer related hypercalcemia specific antibody in conjunction with oncology. 

Case #3: Hyperkalemia in CHF on spironolactone

EKG progression: Classically: peaked T waves-->loss of P waves-->widened QRS-->sin wave

EKG Mimics: TCA overdose, bundle branch blocks, wide complex rhythms

No data for: kayaxelate  (bowel necrosis and doesn't work) or bicarb in patients without acidosis

Use calcium, insulin + D50 then albuterol for synergistic effects

Case #4: Hyperchloremia, negative anion gap, rash and headaches--> Bromide toxicity

Still in some soda, need to drink a lot to get toxicity

Machine can't tell the difference between Bromide and Chloride, so you can still give NS because their chloride is usually normal. Can use chloride as a rough monitor for levels but does not directly correlate with bromide levels.

Consider hemodialysis to remove the bromine. 

Clinicopathologic conference with Drs. Summers & Betz

Case: Middle aged female with TKA 4 months previous with recurrent septic arthritis of the artificial joint with recent exchange of the hardware, on antibiotics PO (rifampin) & APAP at home presents with fever to 103.3, diffuse myalgias, swelling around the knee and mild abdominal pain. Has normal WBC with leukopenia

Diagnosis: Drug induced Hepatitis

1/10,000 presentations to the ED will be drug induced hepatitis

Consider non-traditional medications: 20% of people are on non-vitamin supplement, 70% of people don't tell healthcare providers about these supplements. 

APAP being the most common

Stages of acute APAP:

<24h non specific

24-72h: RUQ pain and LFTS

72-96h: Maximal hepatotoxicity

5-7days: If alive, can start to see recovery

Chronic ingestion APAP: Toxic at 7.5g/24h without risk factors; toxic at 4g/24h with risk factors

R2 Case Follow-up with Dr. McKee

Case: Middle aged male patient on prednisone with multiple presentations for n/v, then possible seizure at home. He gets admitted for steroid withdrawal syndrome then continues to decline. Found to have multiple strokes on MRI, continues to decline and eventually on HD 12 he gets an LP diagnosing him with cryptococcal meningitis. 

Steroid Withdrawal Syndrome (not adrenal crisis)

  • As soon as 1 day after abrupt cessation 
  • seen with doses >20mg for >21 days
  • Etiology
    • Suppression of HPA axis
    • Suppress synthesis of prostaglandins from FA

Cryptococcal Meningitis

  • 1 million cases per year globally
    • Africa>>SE Asia
  • Most in HIV/AIDs patients
  • Presenting symptoms: HA malaise>>meningismus 
  • High level of suspicion in CD4 <100
  • High level of suspicion in solid organ transplant >3y out
  • In non-HIV, non-solid organ transplant patients
    • 90 day mortality 27%
    • Do worse because their intact immune response increases their ICP
  • Dx: CSF Antigen has replaced the India Ink Stain
  • Treatment: Antifungals
    • In immune compromised patients, reversing their immunosuppression can help but watch for Immune reconstitution inflammatory syndrome (IRIS)

Intractable nausea/vomiting: Can't miss diagnoses

  • CNS Changes: Increased CSF (Mass, hemorrhage, meningitis, abscess, pseudotumor, hydrocephalus), Vestibular disorders (central or peripheral) 
  • Vision Changes: acute angle closure (glaucoma) 
  • Abdominal Pain: pancreatitis
  • Pelvic GU: ovarian or testicular torsion
  • Toxicologic

 

Levy Cup Pre-season with Drs. Boyer and Winders

The Levy Cup is the UC EM annual simulation day where resident teams battle it out for a spot on a trophy, and immortality. This year we are counting points early with a series of trivia games throughout the year. Here were some clinical pearls from this week's answers:

Arrythmogenic Right Ventricular Dysplasia: 2nd most common cause of sudden cardiac death in the young

  • Episilon Wave: specific
  • T wave inversions in V2-V4: sensitive

American Trypanosomiasis: can cause an acute cardiomyopathy causing complete heart block

Sub-aortic stenosis: maintenance medication is B-blockers 

Congenital short QT syndrome: peaked T waves with short QT interval (<360ms), 1/3 show up as sudden cardiac death

Posterior Reversible Encephalopathy Syndrome: most common presenting complaint is seizure

Wernicke's Encephalopathy: MRI abnormality at the mammillary bodies