Episode 31 – Vasopressors

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The Free Open Access Medical Education (FOAM)

This week we cover posts from the Wessex ICS site, The Bottom Line, which is an excellent source for breakdown of recent and important trials. This site is great for reviews of high impact trials in critical care. We cover their post on a systematic review of peripheral pressor complications and then we delve into a recent prospective trial by Cardenas-Garcia and colleagues that came up at SMACC.

The Bottom Line on the Loubani paper

  • Systematic review of the literature 1946-Jan 2014 (does not include most recent trial)
  • Outcome – local tissue injury or extravasation: 325 separate events, 318/325 peripheral pressors
    • Signal that distal lines are not ideal for running pressors: 204 events (local tissue injury) were distal to the antecubital fossa/popliteal fossa (90% of events)
    • Signal that duration of pressors running peripherally may impact likelihood of adverse event. Increasing number of events were reported at the 6-12 hour mark (n=9) then 12-24 hour (n=18) and then almost all >24 hour

The Cardenas-Garcia Paper

  • Single arm consecutive study of ICU patients
  • ICU fellows and attendings determined if peripheral pressors were warranted and then initiated the following protocol:
    • Vein diameter >4 mm measured with ultrasonography and PIV confirmed with US before pressors started
    • Upper extremity only, contralateral to the blood pressure cuff
    • IV size 20 gauge or 18 gauge
    • No hand, wrist, or antecubital fossa PIV access position
    • Blood return from the PIV access prior to VM administration
    • Assessment of PIV access function q 2h as per nursing protocol
    • Immediate alert by nursing staff to the medical team if line extravasation, with prompt initiation of local treatment
    • 72 hours maximum duration of PIV access use
  • N=734 patients
  • 19/783 peripheral vasopressor administrations with infiltration of site (2%) with no events of local tissue injury

The take home: If a patient needs vasopressors, you can start them through a good, proximal peripheral IV.  Sometimes patient or situation factors delay central lines, this doesn’t mean it needs to delay patient’s therapy.  Know what to do in the event of infiltration (see this EMCrit post).

Core Content
Tintinalli (7e) Chapter 24

Screen Shot 2015-07-25 at 11.14.51 AM

Panchal et al – Phenylephrine bolus dosing in peri-intubation period

Central line technique from Dr. Reuben Strayer – Wire through catheter vs wire through needle

Generously Donated Rosh Review Questions 

1.

Answer. C. Norepinephrine is considered the vasopressor of choice for treatment of septic shock.   Norepinephrine acts primarily as an α-adrenergic agonist, causing vasoconstriction that results in an increase in blood pressure. It also has β-adrenergic properties, which causes an increase in cardiac output and heart rate. The combination of α-adrenergic and β-adrenergic properties benefits patients who have septic shock. Norepinephrine also has a short duration of action, which allows for rapid adjustment of dosing in response to changes in a patient’s hemodynamic status. Dopamine (A) was once widely used in the treatment of septic shock, but studies have shown that it has no advantage over norepinephrine and its use is associated with a higher death rate. Epinephrine (B) has both α-adrenergic and β-adrenergic properties and has a greater affinity for alpha- and beta-receptors than norepinephrine. Its use is associated with a higher rate of cardiac dysrhythmias and a decrease in splanchnic blood flow. Phenylephrine (D) is a pure α-adrenergic agent that causes vasoconstriction and impairment of tissue blood flow throughout the body, most notably in the splanchnic circulation.

FOAMcastini – Dr. Jerome Hoffman on ACEP’s tPA Clinical Policy

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In a prior FOAMcastini, we covered the updated ACEP tPA clinical policy. As residents, we sought perspectives from experts, the FOAMcast brain trust (Drs. Anand Swaminathan, Ken Milne, Ryan Radecki, and David Newman).  We (Jeremy) also interviewed Dr. Jerry Hoffman, faculty at UCLA.

In this interview, Dr. Jerry Hoffman, a public skeptic and author of peer reviewed critiques of tPA provides interesting perspective on more than thrombolysis but on the future of guidelines (referencing this paper) and science in Emergency Medicine.

A few of Dr. Hoffman’s articles on the topic:

Ensuring the integrity of clinical practice guidelines: a tool for protecting patients.

How is more negative evidence being used to support claims of benefit: The curious case of the third international stroke trial (IST-3).

Thrombolysis for stroke: policy should be based on science, and not on politics, money or fear of malpractice.

Stroke thrombolysis: we need new data, not more reviews.

Against: And just what is the emperor of stroke wearing?

Thrombolytic therapy for acute ischemic stroke – Tissue plasminogen activator for acute ischemic stroke: Is the CAEP Position Statement too negative?

FOAMcastini – ACEP tPA Clinical Policy

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In a prior FOAMcastini, we covered a draft of an ACEP clinical policy on tPA for acute ischemic stroke.  This came in the wake of years of controversy over the aggressive position taken in the 2012 clinical policy.  In June ACEP released the final version of this policy.

Screen Shot 2015-07-15 at 5.42.07 PM

Per the policy within 3 hours:

  • NNT of 8 for excellent functional outcomes; 95% [CI] 4-31
    • Paucity of patients presenting with mild stroke (NIHSS score 0 to 4)
  • NNH of 17 for symptomatic intracerebral hemorrhage; 95% CI 12-34

While FOAMcast is not an interview style podcast, we felt compelled to get some perspective on Emergency Physicians a little more experienced than ourselves.  Here we interview:

Dr. Ryan Radecki (@emlitofnote), Assistant Professor, University of Texas – Houston

  • See his response to the policy on his blog here

Dr. David Newman (#draftnewman), Associate Professor of Emergency Medicine, Mount Sinai Hospital

Dr. Anand Swaminathan (@EMSwami), Assistant Professor of Emergency Medicine, NYU

Dr. Ken Milne (@thesgem), Chief of Staff at South Huron Hospital

FOAMcastini – SMACC Day 3

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We are bringing you pearls from conferences we attend including SMACC (#smaccUS).  This conference was amazing and we enjoyed meeting everyone.  We look forward to seeing y’all at SMACC in Dublin June 13-16, 2016 and hope you check out the Free Open Access Medical education (FOAM) lectures from SMACC, in podcast form, until then.

Things in medicine aren’t always engineered to help us succeed. Engineering the environment smarter may make care safer. – Kevin Fong

  • Medication vials often look quite similar and in a busy, heated moment this may lead to medication errors.  Check out the EZdrugID project.
EZdrugID

Photo: Dr. Nicholas Chrimes

Analgesia, there’s more to it than medicine – Jeremy Faust

  • Distraction is a good thing.  Doing a painful procedure such as injecting local anesthetic? Distract the patient in tactile fashion by lightly scratching the patient proximal to the procedure. Alternative, music and videos can distract children and adults.
  • Calm music may reduce perception of pain.
  • Take advantage of child life, if you have them [AHRQ]!

The Glasgow Coma Scale is a problem – Mark Wilson (see this blog post)

  • The score doesn’t have intrinsic meaning. A GCS score can be associated with mortality ranging from 20-57%, depending on the individual components [Healey]
  • We’re really bad at assigning correct GCS scores to patients, even when we have cheat sheets [Feldman]
  • The interrater reliability of the GCS is abysmal [Bledsoe, Gill]
  • Describe the patient’s exam!

Shift work is disruptive – Haney Mallemat

  • Microsleep is dangerous, yet fairly common in the over tired provider
  • Replacing traditional night shifts with “casino shifts” may help.  These are often comprised of 2 short shifts from 10p-4a and 4a-10a with the notion that each provider would get sleep during the “anchor period” of the Circadian cycle, 2am-6am.  Small studies have shown this feasible, preferred by many, and perhaps perceived [Croskerry, Dukelow]

FOAMcastini – SMACC Day 2

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We are bringing you pearls from conferences we attend including SMACC (#smaccUS).  The plenary, facilitated by the brilliant Dr. Victoria Brazil, focused on the impaired provider. At SMACC we’ve heard time and time again – we are fallible, we make mistakes.

Dying – Dr. Ashley Shreves

  • What often presume what our patients want without asking them.  When dying patients are asked what they want, it comes down to dignity. 1) Being clean 2) Naming a decision maker and then other top priorities essentially come down to healthcare providers listening [Steinhauser et al]
  • We don’t ask patients about their code statuses appropriately. First, we often spend almost no time doing this.  One study of hospitalists found that code status discussions lasted, on average, one minute. Further, that one minute was spent mostly focused on procedures [Anderson et al]
  • Communicate!

Evidence Based Medicine – The consensus of these cage matches was that evidence isn’t all equal; the existence of data doesn’t necessarily mean it’s good data.

  • The Randomized Control Trial (RCT) has problems – Drs. Paul Young and Simon Finfer
    • Beware the Fragility Index – small effects in RCTs
    • Caution with Base Rate Neglect – we jump to inappropriate conclusions.  For example, pretend you have tested positive for a typically fatal disease.  The test is accurate 95% of the time.  Most people would conclude that there was a 95% chance they have the disease – a death sentence. Yet, one would need to know the prevalence of the disease in the general population to determine the actual likelihood that the test was correct.  If the prevalence of the disease is 1 in 1000, the likelihood that you actually have the disease based on this test is <2%.
  • We should read the primary literature, but we can’t read all of it. Use FOAM (judiciously) – Drs. Rory Spiegel and Ken Milne
    • Due to the volume of literature, we have to make some decisions on what to read (Systematic reviews? Meta-analyses? RCTs? Case Reports?)

Impact Apnea

  • Severe traumatic brain injury can cause apnea which leads to a spiral of hypoxia (and thus cell death) and hypercapnea (with cerebral vasodilation causing cerebral edema) which can result in poor neurologic outcome.
  • The key?  Resuscitate these patients as a hypoxic arrest. These are patients that need an airway and need oxygen.

FOAMcastini – SMACC Day 1

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We are bringing you pearls from conferences we attend including SMACC (#smaccUS).  The overarching theme to Day 1 at SMACC?  Use your team- to keep you in check and for feedback.  Our cases and errors are opportunities for reflection. Dr. Cliff Reid reminded us to follow up our patients and outcomes and learn from it all, without letting our egos get in the way.   Dr. Simon Carley (St. Emlyn’s) gave a powerful talk on learning from mistakes later in the day; you will definitely want to listen to these when they come out.

The sub theme?  Experts don’t need algorithms and tests. But the novices? That’s another story.

TraumaWeingart.  We won’t delve into his thoughts on ATLS here (hint: ATLS isn’t for experts).

  • Ignore the first automated blood pressure, it’s probably wrong.  Get a manual blood pressure.
  • Giving 3 units of blood in one hour? Prepare for massive transfusion, that means FFP, platelets, everything
  • If you go down the massive transfusion pathways, give an ampule of calcium every 4-6 units of plasma to combat the transfusion induced hypocalcemia from citrate.
  • The Shock Index (HR/SBP), isn’t as exciting as we once thought. It may be a guide, but not reliably so.

Pain – Strayer

  • Analgesia doesn’t = opiates.  Think about local analgesia.
  • Pain as the “5th vital sign” – probably more harmful than helpful [Gussow]
  • In fact, in 2009, there were

Polypharmacy – Juurlink

  • Trimethoprim/sulfamethoxazole and ace-inhibitors/angiotensin receptor blockers, used in combination can lead to hyperkalemia and, in some cases, death [Juurlink et al]
  • Acetaminophen, at just 2 grams/day, can elevate the INR in patients on warfarin [Pinson]. Acetaminophen is still probably the analgesic of choice, but something to be aware of

Sepsis 

  • Lactate is not a measure of tissue hypoxia/anaerobic metabolism [Marik et al]
  • Too much fluid is not a good thing = iatrogenic salt water drowning [Marik et al]
  • Patients may need vasopressors.  If they do, don’t delay based on central access.  Vasopressors are ok through good peripheral lines for a day or so. [Loubani et al, Mayo et al] However, we should probably place the lines when we’re safely able.
    • Of note, this does require strict protocols. Ex: Mayo study had stringent inclusion criteria
Mayo et al

Mayo et al

 

Episode 30 – Thyroid

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The Free Open Access Medical Education (FOAM)

This week we cover Dr. Scott Weingart’s EMCrit episode on Thyroid Storm

Diagnosis: Hyperthyroid, Fever, Altered Mental Status, Sympathetic Surge, Precipitating Event

Treatment (PPID – PTU, propranolol, iodine, dexamethasone or MIEH – methimazole, iodine, esmolol, hydrocortisone):

  • Supportive care – IV fluids, identify trigger (infection, DKA, trauma, etc)
  • Block production of thyroid hormone: Methimazole or Propothiouracil (PTU)
  • Block thyroid hormone release: Iodine (wait 60 min after giving methimazole or PTU)
  • Calm the sympathetic surge: beta-blockade (propranolol – also inhibits conversion of T4 to the more active T3, metoprolol or esmolol)
  • Block conversion of T4 to T3 and prevent adrenal insufficiency: steroids (dexamethasone, hydrocortisone)

From Rosh Review

Core Content
Rosen’s Emergency Medicine (8e) Chapter 128, Tintinalli (7e) Chapter 223

Thyroid disorders exist on a spectrum from myxedema coma to thyroid storm, with a large area in between.

Hyperthyroidism – too much thyroid hormones only from the thyroid gland

Thyrotoxicosis –  too much thyroid hormone from any cause (i.e. taking too much thyroid supplement)

Thyroid Storm – see above. Thyrotoxicosis with  increased adrenergic hyperactivity or abnormal response to the thyroid hormones by the peripheral tissues

Myxedema coma – These patients are the opposite of thyroid storm, all the systems are depressed (they are essentially hypo-everything).  The diagnosis is clinical but these patients will have significantly elevated TSH with low T3/T4.

  • Altered mental status
  • Hypothermic, <35.5°C (95.9°F)
  • Hypotensive
  • Bradycardic
  • Hyponatremic
  • Hypoglycemic

Treatment

  • Intravenous levothyroxine (T4) although endocrine may recommend that some patients get intravenous T3
  • Supportive care – passive rewarming, dextrose, intravenous fluids
  • Steroids
  • Identify underlying cause

Generously Donated Rosh Review Questions 

1. A 28-year-old woman with no past medical history presents to the emergency department with acute dyspnea. Physical exam reveals tachycardia, warm extremities, wide-pulse pressure, bounding pulses, a systolic flow murmur, exophthalmos and a neck mass. 

2. 

Answers

1. This patient most likely has high-output heart failure secondary to thyrotoxicosis. High output heart failure occurs when cardiac output is elevated in patients with reduced systemic vascular resistance. Examples include thyrotoxicosis, anemia, pregnancy, beriberi and Paget’s disease. Patients with high output heart failure usually have normal pump function, but it is not adequate to meet the high metabolic demands. In high output heart failure the heart rate is typically elevated, the pulse is usually bounding and the pulse pressure wide. Pistol-shot sounds may be auscultated over the femoral arteries, which is referred to as Traube’s sign. Subungual capillary pulsations, often referred to as Quincke’s pulse, may be also be present. Although these findings may be seen in other cardiac conditions, such as aortic regurgitation or patent ductus arteriosus, in the absence of those conditions, these signs are highly suggestive of elevated left ventricular stroke volume due to a hyperdynamic state. Patients with chronic high output also may develop signs and symptoms classically associated with the more common low-output heart failure; specifically, they may develop pulmonary or systemic venous congestion or both, while maintaining the above normal cardiac output.

Low output heart failure (C) is often secondary to ischemic heart disease, hypertension, dilated cardiomyopathy, valvular and pericardial disease or arrhythmia. It can cause dyspnea but is not associated with symptoms of a hyperdyanmic state. Aortic regurgitation (A) is classically associated with bounding pulses, a wide pulse pressure and subungual capillary pulsations; however, aortic regurgitation is less likely in a young woman with no past cardiac history. Additionally, this woman has exophthalmos and a goiter on exam, which support the diagnosis of thyrotoxicosis. Methamphetamine intoxication (D) usually presents with agitation, tachycardia, and psychosis; however, it is not associated with a hyperdynamic state, exophthalmos or a goiter.

2.  Hyperthyroidism is a condition in which there is overproduction and increased circulation of thyroid hormone. Hyperthyroidism has a variety of causes and variable presentation. Increased circulating thyroid hormone causes a hypermetabolic state and increases beta-adrenergic activity. Initially, patients may have vague constitutional symptoms. As the disease progresses, clinical manifestations may become more organ-specific. Thyrotoxicosis or thyroid storm represents the most severe manifestation of the disease. Thyroid storm is life threatening and characterized by hyperadrenergic activity. Patients present with vital sign abnormalities including tachypnea, tachycardia, hyperthermia and hypertension. ECG may show atrial dysrhythmias like atrial flutter and fibrillation or simple sinus tachycardia. High-output cardiac failure is common as well. Physical features include goiter, opthalmopathy and tremors. Patients will also have increased reflexes and altered mental status. Thyroid storm treatment involves suppression of thyroid hormone synthesis and secretion, prevention of peripheral conversion from T4 to T3 and blocking the peripheral adrenergic stimulation. Blocking the peripheral effects of thyroid hormone is best accomplished with a beta-blocker and propranolol is preferred as it also decreases conversion of T4 to T3.

Lithium (A) is a cause of hypothyroidism. In hyperthyroidism, TSH is depressed (C). Weight gain (D) is common in hypothyroidism.

Theme Music:  Flippen performed by The Punch Brothers, used with permission