3.21.19 Conference Summary

ED Pharmacology: Vasoactive Medications and Aseptic Technique

Dr. Christy McKenzie, PharmD

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  • Vasoactive Receptor Review

    • Alpha-1: vasoconstriction

    • Alpha-2: vasoconstriction

    • Beta-1: increases myocardial force and rate of contraction

    • Beta-2: Peripheral vasodilation and bronchial relaxation

    • Dopamine-1: increases renal blood flow

  • Norepinephrine

    • Agonist

    • Alpha>Beta

    • Increases MAP and SVR

    • First line agent for septic shock

    • Dose Range: 0.01-0.3 mcg/kg/min

      • Add vasopressin at norepinephrine doses between 0.2-0.4 mcg/kg/min

    • Onset of action: rapid (seconds-minutes)

    • Duration: 2-3 min

    • Adverse effects: limb ischemia

    • Typical concentration: 8mg/250mL D5W or NS

  • Epinephrine

    • Combined alpha and beta agonist

    • Considered a second line agent for septic shock

    • Considered first line agent for anaphylaxis

    • Can cause hyperglycemia

    • Onset: immediate (seconds)

    • Duration: ~5 min

    • Typical concentration: 4 mg/250 mL D5W or NS

  • Dopamine

    • Dose related receptor activity

      • <5 mcg/kg/min: dopaminergic

      • 5-10 mcg/kg/min: inotropy (beta-1)

      • >10 mcg/kg/min: vasopressor (alpha-1)

    • Precursor of epinephrine and norepinephrine

    • Adverse effects: tachyarrhythmia

    • Typical concentration: 400mg/250 mL D5W or NS

  • Phenylephrine

    • Pure alpha 1 agonist

    • Case cause reflex bradycardia

    • Caution with history or active severe HTN

    • Adverse effects: decreased CO, worsened peripheral vascular disease

    • Onset of action: seconds

    • Typical concentration: 10mg/250 mL D5W or NS

  • Vasopressin (aka anti-diuretic hormone)

    • Potent vasoconstrictor

    • Adverse effects: sodium and water retention

    • Typical concentration: 40 U/250mL D5W or NS

  • Dobutamine

    • Predominantly Beta-1 agonism, but some beta-2

    • Primarily used in cardiogenic shock

    • Onset: 1-10 min

    • Duration: 10 min

    • Typical concentration: 1000 mg/250 mL D5W

  • Milrinone

    • Phosphodiesterase inhibitor

    • Increases Inotropy and vasodilation

    • Used in cardiogenic shock when dobutamine has failed

    • Adverse effects: hypotension

    • Typical Concentration: 10 mg/200 mL D5W

  • Must remember to always give resuscitation goals when ordering vasoactive medications

    • i.e. MAP>65 mmHg or SBP>90 mmHg or HR >75 BPM

  • Aseptic technique:

    • Always use new sterile syringe and sterile needle

    • Proper hand hygiene

    • Rubber septum should be disinfected EVERY SINGLE TIME with alcohol prior to piercing it

    • Never leave a needle inserted into the septum

    • Single vs multi-dose vials

      • Multi-dose vials typically contain an antimicrobial preservative to help prevent the growth of bacteria, but has no effect on viruses and does not protect against contamination

      • Single dose vials can only be punctured a single time

    • Medication vials should always be discarded whenever sterility is compromised or questionable

    • Never use a normal saline “flush” to prepare medications as this is considered a device and not a medication

  • “Push dose Pressors”

    • Phenylephrine 40mcg/mL premix syringes are stocked in our ED

      • To make this quickly: 10mg/mL phenylephrine vial with 100 mL IVPB NS bag

        • Use aseptic technique

        • Draw up 10 mg of phenylephrine and inject into 100mL IVPB bag

        • Draw back 10mL into syringe and you should have 100mcg/mL phenylephrine

        • THIS IS ONLY GOOD FOR 1 HOUR FROM PREP

        • ALWAYS REMEMBER TO LABEL

        • 40-200 mcg q1-5min based on patient response

        • This is only a temporizing measure

    • Epinephrine push dose

      • Inject 1 mg epinephrine (as 1mg/10mL) with 100 mL IVPB NS

        • Use aseptic technique

        • Inject 0.1mg of epinephrine into 9 mL of NS

        • 5-20 mcg q1-5min based on patient response


EBM: Cardiac Risk Stratification in the ED

Dr. Jake Flinkman, PGY-4

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  • Why do we care?

    • 6 million patient ED visits/year, chest pain is the #2 complaint

    • Close to 50% of chest pain complaints are admitted

    • 35% of ACS admissions don’t have ACS

  • Background on chest pain risk stratification scores

    • Classically, clinical gestalt, EKG, and troponin were primary drivers used to stratify patients

    • Significant inconsistency and over-admissions

      • ACI-TIPI, Vancouver Chest Pain Rule, EDACS, North American Chest Pain Rule, and GRACE were historical stratification systems used but some were overly complicated and varied widely in their use

  • HEART score (2008)

    • 5 components

      • History

      • ECG

      • Age

      • Risk factors

      • Troponin

    • Scores range 0-10 with scores >4 typically requiring admission at least for provocative testing

    • MACE <2%

    • The data:

      • Can the HEART score rule out ACS in the ED?

        • The HEART score can indeed reliably r/o ACS with a MACE<2%

      • MACE 30 days-6 weeks when using HEART score?

        • MACE is similar

      • HEART pathway

        • HEART score + serial troponin increases sensitivity to r/o ACS and decreases MACE in 30 days to <1%

      • Comparison of nine coronary risk scores in evaluating patients presenting to the hospital with chest pain?

        • HEART, TIMI, and GRACE scores were all included

        • Endpoint was not MACE

        • The North American Chest Pain Rule maximized yield of low risk patients with lowest miss rate for ischemic chest pain

        • HEART score was second best

      • HEART score in the setting of the HEART pathway demonstrates a high sensitivity for identifying patients with low risk chest pain

      • HEART pathway RCT completed in June 2018

        • 0% of patient categorized as low risk and discharged home had MACE

  • How long is a cardiac catheterization/Stress test valid for?

    • Catheterization

      • ? 3 years (no consensus yet)

      • Depends on the story

      • Does a ruptured thrombus change the validity?

    • Stress test

      • ? 1 year (again, there is no consensus based on the present literature to date)

      • Depends on the story

  • Areas for further research?

    • Larger sample size prospective randomized trials

    • Gestalt vs scores

    • Should we include HEART scores in chart of non-cardiac chest pain

    • High sensitivity troponin with HEART pathway and delta troponin

Supertrack Series: Atraumatic Low Back Pain

Dr. Alex Votruba, PGY-1

  • Epidemiology

    • #1 cause of disability in the U.S.

    • 3% of all ED visits

  • Risk Factors

    • Smoking, obesity, age, female gender, low educational attainment, history of anxiety/depression

  • Differential Diagnoses

    • Non-specific (most common diagnosis): sprain/strain, mechanical back pain, lumbago

    • Specific (readily identifiable on imaging or lab work): vertebral compression fracture, radiculopathy, spinal stenosis, spinal cord compression, metastatic cancer, spinal epidural abscess, epidural hematoma, vertebral osteomyelitis, GERD, AAA, nephrolithiasis, etc.

  • History and Physical

    • Look for red flags

      • Age <18 or >50 yo

      • Fever, rigors, weight loss

      • Hx of cancer, IVDU, immunocompromised states, anticoagulation, or coagulopathy

      • Pain >4-8 weeks, unresponsive to previous therapies, associated neurologic symptoms

    • Perform DT reflexes, straight leg raise test, clonus, consider rectal exam, strength testing, sensation testing

  • Labs and Imaging

    • Most patients presenting with acute low back pain do not require lab testing or imaging

    • Lab testing is indicated when suspecting:

      • Infection

      • Tumor/malignancy

      • Rheumatologic disease

    • Imaging

      • X-rays: fracture

      • CT: vertebral fracture, facet joints, or posterior elements of spine

      • CT myelogram

        • Useful when MRI is not available and visualization of cord is necessary

      • MRI: infection, neoplasm, or cord compression

  • Treatment

    • Conservative therapy initially

      • Continue daily activity, acetaminophen (+- NSAIDs)

    • Adjunctive therapy

      • Muscle relaxant such as diazepam and methocarbamol are options

      • Manipulative therapy

    • Corticosteroids have no role in acute nonspecific LBP

EM/Trauma: Traumatic Brain Injury

Dr. Alan Hoffer, Neurosurgery

  • Glasgow Coma Scale (scores range from 3-15)

    • Motor score is most helpful prognosticator in TBI

    • As cortices are destroyed, midbrain and lower brainstem reflexes take over, resulting in decorticate or decerebrate posturing, and finally flaccidity

  • CT head w/o contrast is initial imaging modality of choice

  • Skull fractures depressed more than 1 skull thickness, comminution, and open fractures are all indications for operative repair

  • Epidural hematoma

    • Rupture of middle meningeal artery

    • Lentiform shape

    • Typically better prognosis than SDH (if intervention performed quickly)

  • Subdural hematoma

    • Tearing of bridging veins

    • Prognosis is worse than EDH because of inflammatory response of blood directly on brain tissue as well as more commonly occurring in elderly age

    • Chronic SDH can present in a number of different ways such as seizure, difficulty walking, headaches, hemiparesis, aphasia, or lethargy

  • Subarachnoid hemorrhage

    • Trauma is the #1 cause

      • Blood will collect along the convexities with coup-countercoup pattern

    • Ruptured aneurysm is the #2 cause

      • Blood will be located in the deep cistern and if present, necessitates CT angiography to eval for vessel integrity/rupture

  • Diffuse axonal injury

    • Often poor prognosis as central nervous axons do not regenerate

    • Seen in rapid acceleration-deceleration injuries

  • Management of intracranial hypertension

    • Intracranial hypertension occurs as a result of a complex cascade of physiological processes including opening of blood brain barrier, cytotoxic chemical entrance in neurons, free radial damage, etc.

    • Cerebral perfusion pressure: MAP - intracranial pressure (ICP)

      • Increased intracranial pressure can be caused by increased parenchymal volume or space occupying lesion

      • Normal ICPs + CPP 60-70 mmHg are best therapy to improve outcome in traumatic brain injuries

      • If autoregulation is not intact, vascular engorgement will occur and worsen clinical status so ICP management is more important

      • If autoregulation is intact, CPP is most important so vasopressor therapy is mainstay

    • Avoiding hypoxia or hypercarbia is paramount to increasing chances of meaningful outcome s/p TBI, as a single episode of either can be detrimental

    • Managing ICP:

      • 1st tier: elevate HOB, correct hypotension and hypoxia, and hyperthermia, sedation

      • 2nd tier: osmotic therapy, CSF drainage, neuromuscular blockade

      • 3rd tier: barbiturate coma

      • Last resort: hemicraniectomy

        • Allows for extra space to accommodate further swelling and relax pressure on the midbrain

      • Avoid hyperthermia at all costs as increased temperature increases inflammatory cascade and worsens TBI outcomes

      • Therapeutic hypothermia may be beneficial, but literature is unclear

      • Don’t use corticosteroids as this worsens outcomes

Toxicology Series: Lithium Toxicity

Dr. Laura Throckmorton, PGY1

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  • Lithium was first used in the late 1800s as a treatment for bipolar disorder

  • Pharmacology

    • GI absorption ~100% with immediate release 1-2 hours; levels peak 4-6 hours after ingestion

    • Eliminated 80% renally

      • Decreased clearance can be caused dehydration, diuretics, or co-ingestion with other nephrotoxic medications

  • Toxic dose: >25g (i.e. 83x 300mg tablets) so toxicity is much more common in chronic users

  • Acute toxicity symptoms: primarily GI with N/V/D and abdominal pain

  • Chronic toxicity symptoms primary neurologic

    • Confusion, tremors, lethargy, ataxia, seizures, numbness, tingling, and weakness

    • EKG changes with T wave flattening or inversions

    • Nephrogenic diabetes insipidus (DI)

      • Lithium accumulates in principal cells of the collecting duct and interferes with the action of ADH

    • Causes: result of concentrating deficit of the kidneys -> dilute urine, chronic dehydration, NSAIDs co-ingestion, ACE-i

  • Differential diagnosis: serotonin syndrome, NMS, benzo/ETOH withdrawal, meningitis, stroke, ICH, seizures, myxedematous coma

  • Work-up

    • Lithium level, CBC, BMP, POC blood glucose, TSH, pregnancy test, EKG (VBG, ASA, APAP level if concerning for co-ingestion)

  • Lithium level

    • Therapeutic range: 0.8-1.2 mEq/L

    • Levels most helpful in chronic toxicity

      • 1.5-2.5: mild symptoms with tremors, slurred speech, fatigue

      • 2.5-3.5: lethargy, coarse tremors, clonus

      • >3.5: severe lethargy, clonus, seizures, airway compromise

  • Treatment

    • IV hydration with isotonic saline @ 2x maintenance rate for 2-3L

    • Check Na levels Q 4-6H if suspecting Li-induced DI

      • Hypernatremia can increase neurotoxicity of Li toxicity so need to avoid this

    • Polyethylene glycol via NG tube with whole bowel irrigation

      • Recommended if awake, asymptomatic, within 2-4 hours of ingestion, or >10-15 sustained released tablets

    • Indications for hemodialysis

      • Li >2.5 + comorbid conditions that preclude aggressive IV hydration (i.e. CHF(

      • Li >4 + renal impairment

      • Li >5

      • Decreased level of consciousness or seizure, regardless of level

  • Disposition

    • Treat/observe for minimum of 6 hours

    • Symptomatic: admit

  • Always remember

    • Symptoms of acute toxicity may not correlate with lithium levels

    • Symptoms of chronic toxicity correlate more closely with lithium levels

Procedural Essentials in EM: Emergency Pacing

Dr. Colin McCloskey

  • Always remember, before considering emergency pacing

    • Treat the underlying cause

    • If trans-cutaneously pacing, be actively preparing for trans-venous pacing

    • Know your supplies

  • Indications for pacing

    • Any unstable bradyarrhythmia, i.e.

      • BB toxicity

      • Mobitz Type II with hypotension or complete heart block

  • “Respect the Vector”

    • Anterior-Posterior has greater chances of sustained capture

    • Larger chest wall sizes will require higher mAMP to obtain capture

  • 50-100 mAMP is typical dose necessary for transcutaneous pacing capture

    • Skeletal muscle twitching will begin around 10 mAMP, but don’t assume skeletal muscle twitching = cardiac muscle twitching

  • Sedation is usually necessary

    • Consider using sedative medicine that has less hemodynamic effects, i.e. ketamine

  • Pepare for TVP

    • Just a 6 Fr central line, always use a condom, ventricular pacing 80 BPM with 20 mAMP and walk down, look for STEMI pattern on telemetry, mechanical capture should be confirmed after electrical capture

    • Relative contraindications: mechanical tricuspid valve

    • Distances to remember

      • 20 cm: distance to right atrium, then inflate balloon

      • 30-40 cm: look for capture

    • Pitfalls:

      • Coiling in right atrium -> consider rotating 180 degrees

      • Failure to capture -> consider correcting underlying etiology or look to ensure appropriate placement of pacer wire in RV

    • Once capture occurs, lower mAMP to lowest threshold required for capture and increase by 1.5x or 2x (i.e. 5 mAMP threshold for capture, increase to 7.5 or 10 mAMP for final settings

History of Emergency Medicine

Dr. Louis Horwitz

  • June 1961, Dr. Mills staffed the emergency room at Alexandria Virginia Hospital

    • First full time group to provide exclusive care in the ED

  • 1972: first EM residency at University of Cincinnati

  • 1976: American board of emergency medicine (ABEM) was incorporated on Sept 21

  • 1979 Sept 21: emergency medicine recognized as an official speciality

  • ACEP founded on Aug 16, 1968 by 8 physicians in Lansing, Michigan

    • First president was John Wiegenstein

    • First ACEP assembly was in Nov 1969 in Denver, CO and cost $50 to attend

  • AMA initially resisted the idea of recognizing emergency medicine as a specialty as they felt there was no unique body of knowledge for EM, no research base, and too many specialties already in existence at the time

  • 1970: Dr. Bruce Janiak was the first EM resident

  • ABEM was established in 1976 and in 1979, EM became 23rd medical specialty

  • The “Grandfather clause” allowed practicing emergency physicians who had accumulated enough clinical practice to continue practicing with board accreditation

  • Judith Tintinallli: wrote first EM textbook

  • Procedures and treatments no longer used:

    • Trans-thoracic pacer

    • Neosynephrine IV for SVT (looking for reflex bradycardia)

    • MAST pants (increased mortality)

    • Peritoneal lavage for trauma (CTs and FAST have replaced this)

    • Ewald gastric tube for stomach evaluation

    • Meat tenderizer for esophageal food FBs

    • Microfiche poison control

    • Blind naso-tracheal intubation

    • Procardia SL for “HTN urgencies” (increases stroke risk)

    • “DPT” (demerol/phenergan/thorazine) for pediatric sedation

    • Schiotz tonometer for ocular pressure

    • Physostigmine as part of the “wake-up” cocktail (glucose, narcan, and physo)

    • Intracoronary TPA for MIs

    • Calcium and bicarb as first line per the ACLS protocol for Vfib, asystole, and PEA (EMD, i.e. electro-mechanical dissociation)

    • C spine “shoot thru” with lateral and swimmer’s views

    • Bretylium used for Vfib (only drug ever shown to chemically convert Vfib, including hypothermic Vfib)