Episode 34 – Tachyarrhythmias

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The Free Open Access Medical Education (FOAM)

The St. Emlyn’s team ran a post on the REVERT trial, which added a new spin to the traditional (and traditionally ineffective) Valsalva maneuver for stable supraventricular tachycardia (SVT). In this post, Dr. Rick Body goes through the trial covering not only the results but also drops pearls on methodology.

  • Randomized 433 patients with SVT to one of the following:
    • “Modified” Valsalva maneuver: patient sitting up performs Valsalva using a syringe to maintain 40 mm Hg for 15 sec and then placed supine with passive leg raise immediately after procedure (see video)
    • “Standard” Valsalva maneuver: patient sitting up performs Valsalva using a syringe to maintain 40 mm Hg for 15 sec while maintaining upright position
  • 43% of the patients in modified Valsalva group versus 17% in the standard technique achieved sinus rhythm at one minute yielding an absolute risk reduction of 26.2% (p<0.001) with a number needed to treat of about 4 (3.8).

Core Content – Supraventricular Tachycardia (SVT) and Ventricular Tachycardia (VT)

Tintinalli (7e) Chapter 22;  Rosen’s Emergency Medicine (8e) Chapter 79

SVT 

Broad term referring to tachycardias originating above the ventricles, including the regular rhythms of sinus tachycardia, AV nodal reentrant tachycardia, AV reentrant tachycardia, and the irregular rhythms of multifocal atrial tachycardia, atrial fibrillation, and some forms of atrial flutter.

Diagnosis: JACC algorithm

Treatment:

  • Unstable patients – electrical cardioversion at 0.5-1 J/kg (100J for an adult) + ABCs!
  • Stable patients-
    • Valsalva maneuver – we like this method of having a patient blow on a syringe. Unfortunately, prior to the REVERT trial, the valsalva maneuver success rate has been documented ~19% [3].
    • Adenosine (0.1mg/kg or 6 mg in adult; 2nd dose 0.2 mg/kg or 12 mg in adult, with occasional dose adjustments) – administration can be tricky because of the drug’s short half life, necessitating proximal administration, elevation of the arm, and a quick saline flush afterwards. You can combine the adenosine IN the flush as detailed in this post, meaning no stopcock.
    • Calcium channel blockers or beta-blockers (verapamil, diltiazem or even metoprolol, esmolol) – Recently the calcium channel blockers have increased in popularity in the FOAM world and these are Rosenalli approved [4,5].

VT

Diagnosis: Typically wide QRS complex (95% with QRS >120 ms) and fast (150-200 beats per minute).

  • SVT with abberency can have a wide complex but this should be treated as VT [4,5] (see this video)
  • Monomorphic – complexes have same morphology
  • Polymorphic – complexes of various morphologies, associated with poor prognosis [4,5]

Treatment:

  • Unstable patients – electrical cardioversion at 0.5-1 J/kg (100J for an adult) + ABCs!
  • Stable patients with monomorphic VT
    • Electrical cardioversion
    • Procainamide – Level B recommendation for first line treatment of monomorphic VT[6].
    • Amiodarone – common in the US but per the AHA guidelines “reasonable in patients with sustained monomorphic VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite procainamide or other agents. (Level of Evidence: C)” [6].
      • Note: Dangerous if prolonged QT [6]
    • Lidocaine – “may be reasonable” [6]
  • Stable patients with polymorphic VT
    • Electrical cardioversion
    • Beta-blockers (particularly if ischemic)
    • Amiodarone
    • Cardiac catheterization if potentially ischemic cause [6]
  • Torsades de Pointes – withdraw offending agent, magnesium sulfate IV if “a few episodes” per the AHA

Generously Donated Rosh Review Questions 

Question 1. A 26-year-old woman presents with dizziness and palpitations. She reports episodes of these symptoms beginning about 1 week ago, which initially only lasted a few minutes. However, for the past two days, she has had about 4 episodes a day which last about 20 minutes each. Her social history is significant for heavy caffeine intake. Her pulse is 166 bpm and her blood pressure is 140/70. Her rhythm strip is seen below. [polldaddy poll=9061960]

Screen Shot 2015-09-05 at 9.52.22 AM

Question 2. A 33-year-old woman with chronic persistent asthma presents with palpitations. Her vital signs are HR 210, BP 118/73, and pulse oxygenation of 97% on room air. An ECG is shown below. [polldaddy poll=9061966]

Screen Shot 2015-09-05 at 9.53.15 AM

References:

  1. Whinnett ZI, Sohaib SM, Davies DW. Diagnosis and management of supraventricular tachycardia. BMJ (Clinical research ed.). 345:e7769. 2012
  2. Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. The New England journal of medicine. 367(15):1438-48. 2012.
  3. Smith et al. Effectiveness of the Valsalva Manoeuvre for reversion of supraventricular tachycardia. Cochrane Database Syst Rev. 2013 Mar 28;3:CD009502. doi: 10.1002/14651858.CD009502.pub2
  4. ”Cardiac Rhythm Disturbances.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide.  7th ed. pp 136-146.
  5. “Tachyarrhythmias.” Rosen’s Emergency Medicine. 8th ed. Chapter 79.
  6. Zipes DP, Camm AJ, Borggrefe M et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Journal of the American College of Cardiology. 48(5):e247-e346. 2006
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Episode 33 – Hemoptysis

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The Free Open Access Medical Education (FOAM)

Dr. Ryan Radecki of Emergency Medicine Literature of Note reviews Gestational Age D-Dimers covering an article by Murphy and colleagues in BJOG.  

The paper: The authors took blood samples from 760 healthy pregnant patients at one point during their pregnancy. They propose a continuous increase for a normal d-dimer cut off throughout gestation.

  • 1-12 weeks:    n=33, 81% with normal d-dimer
  • 19-21 weeks:  n=53, 32% with normal d-dimer
  • 28-36 weeks: n=8, 6% with normal d-dimer
  • 39-40 weeks: 0, 0% normal d-dimer
  • Postpartum day 2: n=12, 8% with normal d-dimer

Dr. Radecki’s “Take Home:

  • Dr. Kline has advocated for the following d-dimer cut offs in pregnancy: 1st trimester 750 ng/mL, 2nd trimester 1000 ng/mL, and 3rd trimester 1250 ng/mL(based on a standard cut-off of 500 ng/mL) and this may be reasonable but is not rooted in robust evidence.

Interestingly, this post was followed by another post covering an article by Hutchinson et al from Am J Roentgenol showing that of 174 CTPAs initially read as positive, 45 were read as negative by chest radiologist upon blinded retrospective review.  That means 25.9% of this cohort diagnosed with PE apparently had negative CT scans.

Core Content – Hemoptysis

Tintinalli (7e) Chapter 66;  Rosen’s Emergency Medicine (8e) Chapter 24

Etiology: Most common causes are bronchitis (often blood tinged sputum), infection (abscess, pneumonia, tuberculosis), neoplasm (lung cancer).  Other causes include iatrogenic causes (bronchoscopy, biopsy, aspirated foreign body), anticoagulation, and autoimmune diseases such as granulomatous polyangiitis (Wegener’s), lupus, and Goodpasture’s.

Workup:

Hemoptysis Workup

Generously Donated Rosh Review Questions 

Question 1. A 50-year-old man, nonsmoker, presents to the ED with a 2-day history of cough now associated with frank hemoptysis. He denies any constitutional symptoms. Vital signs are BP 125/70, HR 80, RR 16, and pulse oximetry is 98% on room air. On exam, his lung fields are clear; the remainder of the exam is unremarkable. A chest radiograph is performed, which is normal. [polldaddy poll=9039260]

Question 2. A 55-year-old man, smoker, presents to the ED with hemoptysis and dyspnea for 4 weeks. His VS are T 37°C, BP 146/76 mm Hg, HR 85 bpm, RR 20 per minute, and oxygen saturation 96% on RA. His lung exam reveals distant breath sounds on the left side. His chest X-ray is shown below. [polldaddy poll=9039262]

Rosh Review
Rosh Review

Answers

1.C. The patient is hemodynamically stable with a normal chest radiograph, so he does not require ICU admission (A). Patients with massive hemoptysis require ICU admission. The decision to perform a bronchoscopy (B) in this patient will be left up to the pulmonologist. Given the overall clinical picture, urgent bronchoscopy is not required in this case. With massive hemoptysis, an emergent bronchoscopy is indicated. Bronchitis (D) typically presents with the abrupt onset of cough with blood-streaked purulent sputum. The patient in the clinical scenario has persistent frank hemoptysis, which mandates further investigation. In a patient who does not smoke, is under the age of 40, and has a normal chest radiograph and scant hemoptysis, treatment for bronchitis can be initiated with outpatient follow-up.

2. B. Although bronchitis (A) is the most common cause of hemoptysis (responsible for 15%-30% of cases), patients present with cough as the dominant symptom and have abnormal lung exams and normal chest x-rays. The cough may be productive of sputum. The diagnosis of pneumonia (C) requires focal findings on physical exam or infiltrates on radiographic imaging and is typically accompanied by a fever. Patients with lung cancer are at increased risk for pulmonary embolism (D). This patient’s Wells score is 2 (one point each for hemoptysis and malignancy), which makes the likelihood of PE 16% in an ED population. Given the lung mass seen on chest x-ray, lung cancer is more likely than PE.

References:

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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.[polldaddy poll=8996471]

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.

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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

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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]
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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. [polldaddy poll=8935230]

2. [polldaddy poll=8936552]

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

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Episode 29 – Hyperglycemia

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The Free Open Access Medical Education (FOAM)

We review a post on Pediatric DKA from Dr. Anton Helman’s Emergency Medicine Cases.

 Pearls from this episode:

  • Fluids come first in DKA but you may not need as much as you think. They recommend only using fluid boluses, and even then a baby bolus of 5-10 cc/kg, in the hypotensive decompensated patients, coupled with frequent re-assessments.  Other patients can get up to twice maintenance of 0.9% NaCl.
  • No insulin bolus for pediatric patients, ever.
  • Cerebral edema is the most dreaded complication of DKA and seems to be associated with severe presentations, young children (<5), or DKA as the presentation of diabetes.  Treatment related factors such as administration of an insulin bolus or sodium bicarbonate may also contribute. The role of fluids (particularly over-aggressive fluids) is less clear [1-3].
  • Management of cerebral edema: ABCs, Elevate head of the bed 30 degrees, Mannitol 0.5-1g/kg IV over 20min AND/OR hypertonic (3%) NaCl 5-10cc/kg IV over 30min

The Bread and Butter

We cover hyperglycemia including diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). We do this based on  osen’s Emergency Medicine, Chapter 126 (8th ed) and Tintinalli, Chapter 222 (7th ed). But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

 Diabetic Ketoacidosis

Diagnosis – glucose >250 mg/dL, pH <7.3, bicarbonate <18, anion gap >10

Workup – evaluate electrolytes (particularly potassium) and potential triggers for DKA.

Treatment – fluid resuscitation is initial intervention as these patients are typically 4-6 L down.  In adults we hold insulin treatment until we know the patient’s serum potassium, as these patient’s are depleted secondary to osmotic diuresis.  Further, the patient’s serum potassium may be falsely elevated by acidosis.  Insulin may be started once the potassium is >3.5 (with potassium replacement if <5.3).  We do not bolus pediatric patients but the ADA guidelines and Rosenalli state we do not need the insulin bolus in adults either [4-6].  The use of subcutaneous insulin in DKA is popular amongst pediatric patients and growing in popularity in adults [7,8].

Screen Shot 2015-06-02 at 11.19.08 AM

Hyperosmolar Hyperglycemic State (HHS)

Diagnosis – elevated serum glucose (often >600 mg/dL), serum osmolar >315-320 mOsm/kg. Patient’s may have a concomitant acidosis or ketosis, but this is often less profound than in DKA.

Workup – ascertain why the patient ended up in HHS – whether it was a mobility issue or polypharmacy (diuretic, lithium, etc). Check osmolality and for DKA.

Treatment – these patients are often severely dehydrated (>8 Liters). Start with volume resuscitation and add an insulin infusion (0.1 units/kg/hr).

 

Generously Donated Rosh Review Questions 

1. A 43-year-old man presents with altered mental status. His vital signs are HR 113, BP 143/63, T 98.9°F and blood glucose of 750 mg/dl. During your evaluation he has a brief generalized tonic-clonic seizure. [polldaddy poll=8904849]

Answers

1. This patient presents with signs and symptoms consistent with hyperglycemic hyperosmolar state (HHS) and intravenous fluids should be given aggressively early in management. HHS is a syndrome characterized by dehydration, hyperglycemia, hyperosmolarity and altered mental status. Patients may present with confusion, lethargy, seizures, focal neurologic deficits or frank coma. Pathophysiologically, decreased insulin (or insulin action) leads to gluconeogenesis and increased circulating glucose levels. This in turn draws fluid from the intracellular space into the intravascular space. The resultant osmotic diuresis leads to profound intravascular dehydration, electrolyte abnormalities and hyperosmolarity. Typically, patients will have a blood glucose >600 mg/dl and an osmolarity >350 mOsm/L. Blood urea nitrogen and creatinine are usually elevated. Initial management focuses on supportive care and aggressive fluid resuscitation. Patients with HHS are estimated to be 5-10 liters behind. In addition to fluid administration, electrolyte repletion is paramount.

2. A 45-year-old man presents with altered mental status. On arrival, his finger stick is 35 mg/dL. He is given dextrose leading to the return of a normal mental status. On history, he reports he may have accidentally taken extra medication. Which of the following medications requires prolonged observation in the hospital?

  • Glipizide
  • Metformin
  • Novolog
  • Sitagliptin

In most adults, symptomatic hypoglycemia occurs when glucose levels reach 40 to 50 mg/dL. Glipizide is a sulfonyurea oral hypoglycemic drug. This class of medication is associated with hypoglycemic episodes through their action as an insulin secretagogue. In a sulfonylurea overdose, patients should be observed for 24 hours. When the etiology is unclear, laboratory testing including renal function is indicated. In situations without large ingestions, patients may be discharged if no additional episodes of hypoglycemia occur after an observation period. In cases of severe, prolonged or recurrent episodes of hypoglycemia from sulfonylureas, additional therapy with octreotide as an inhibitor of insulin release is indicated.

References:

  1. Glaser NS, Wootton-Gorges SL, Buonocore MH, et al. Subclinical cerebral edema in children with diabetic ketoacidosis randomized to 2 different rehydration protocols. Pediatrics. 2013;131(1):e73–80. doi:10.1542/peds.2012-1049.
  2. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001;344(4):264–9. doi:10.1056/NEJM200101253440404.
  3. Lawrence SE, Cummings E a, Gaboury I, Daneman D. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr. 2005;146(5):688–92. doi:10.1016/j.jpeds.2004.12.041.
  4. Diabetic Emergencies : New Strategies For An Old Disease.
  5. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32(7):1335–43. doi:10.2337/dc09-9032.
  6. Goyal N, Miller JB, Sankey SS, Mossallam U. Utility of initial bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med. 2010;38(4):422–7. doi:10.1016/j.jemermed.2007.11.033.
  7. Umpierrez GE, Cuervo R, Karabell A, Latif K, Freire AX, Kitabchi AE. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Diabetes Care. 2004;27(8):1873–8. Available at: http://www.ncbi.nlm.nih.gov/pubmed/15277410. Accessed July 17, 2014.
  8. Umpierrez GE, Latif K, Stoever J, et al. Efficacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of patients with diabetic ketoacidosis. Am J Med. 2004;117(5):291–6. doi:10.1016/j.amjmed.2004.05.010.
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Episode 26 – The Spinal Cord

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The Free Open Access Medical Education (FOAM)

In January 2015, ACEP recommended against the use of long backboards by EMS, “Backboards should not be used as a therapeutic intervention or as a precautionary measure either inside or outside the hospital or for inter-facility transfers.”

We review the use of longboards and cervical collars for spinal immobilization using posts by Thomas D of ScanCrit (Curse of the Cervical Collar, Cervical Collar RIP,  Cervical Collars Slashed From Guidelines), a post by Dr. Minh Le Cong from PHARM, and this Medest118 post.

The bottom line:

  • The benefits of devices to aid in spinal immobilization such as cervical collars and long backboards are controversial.  Guidelines and protocols are continuing to recommend judicious use of these devices.  Examples include:
    • Clearing collars in obtunded blunt trauma patients with negative high quality CT [EAST]
    • Selective application of cervical collars [ILCOR]
    • No backboards and selective pre-hospital immobilizaiton [ACEP]

The Bread and Butter

We differentiate between spinal shock and neurogenic shock, cover the incomplete cord syndromes (anterior cord, central cord, Brown-Sequard Syndrome), and fly through some of the cover using Tintinalli (7e) Chapter 255; Rosen’s (8e) Chapter 43, 106  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Spinal shock – Reduced reflexes following think of this as a stunning of the spinal cord.

Neurogenic shock –  This is loss of sympathetic innervation from injury to the cervical or thoracic spine, typically from a cervical or upper thoracic spinal cord injury, resulting in bradycardia and hypotension.

  • Warm, peripherally vasodilated , and hypotensive  from loss of sympathetic arterial tone with a relative bradycardia from unopposed parasympathetic (vagal) tone
  • Typically presents within 30 minutes, can last 6 weeks
  • Diagnose only after excluding other sources of shock
  • Treatment: crystalloid, vasopressors

Incomplete Cord Syndromes

 Better prognosis than complete cord syndromes. Means there is some sensory or motor preserved distal to lesion (i.e. rectal tone or perineal sensation)

Anterior Cord Syndrome 

  • Complete loss of motor, pain, and temperature below but retain posterior columns (position and vibration)
  • Flexion injury or decreased perfusion (aortic surgery or injury)
  • Paralysis and hypalgesia below the level of injury with preservation of posterior column (position and vibration)

Central Cord Syndrome

  • Sensory and motor deficit, often associated with hyperextension injuries (think whiplash)
  • Affects arms>legs
  • Think MUDE (pronounced muddy): Motor, Upper, Distal, Extension (injury)

Brown-Sequard Syndrome

  • Classically associated with a stab wound
  • Loss of motor function and position and vibration on ipsilateral side with contralateral loss of pain and temperature (fibers cross)

 Reflex Review

C4 Spontaneous breathing: “3-4-5 keep the diaphragm alive”
C5 Shoulder shrug
C6 Flexion at elbow:  think flexing your elbow up to drink before…
C7 Extension at elbow: …extending it to set a drink down.
C8-T1 Flexion of fingers
T1-T12 Intercostal and abdominal muscles
L1-L2 Flexion at hip
L3 Adduction at hip
L4 Abduction at hip
L5 Dorsiflexion of foot
S1-S2 Plantar flexion of foot
S2-S4 Rectal sphincter tone: “2-3-4 keeps your junk off the floor”

Generously Donated Rosh Review Questions 

Question 1. A patient arrives to the ED 15 minutes after being involved in a MVC. He is conscious, and there is no obvious trauma. He is immobilized on a long spine board with a cervical collar in place. His BP is 60/40 mm Hg and HR is 60 bpm. His skin is warm.

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Question 2. [polldaddy poll=8776250]

Answers

1.  A. Loss of deep tendon reflexes is expected. Neurogenic shock occurs after an injury to the spinal cord. Sympathetic outflow is disrupted resulting in unopposed vagal tone. The major clinical signs are hypotension and bradycardia. Patients are generally hypotensive with warm, dry skin because the loss of sympathetic tone impairs the ability to redirect blood flow from the periphery to the core circulation. The most commonly affected area is the cervical region, followed by the thoracolumbar junction, the thoracic region, and the lumbar region. The anatomic level of the injury to the spinal cord impacts the likelihood and severity of neurogenic shock. Injuries above the T1 level have the capability of disrupting the spinal cord tracts that control the entire sympathetic system leading to the loss of deep tendon reflexes.Neurogenic shock must be differentiated from “spinal” shock, which refers to neuropraxia (B) associated with incomplete spinal cord injuries. This state is transient (C) and resolves in 1 to 3 weeks. Alpha-1 vasopressors (e.g., phenylephrine), in addition to dopamine, norepinephrine, and epinephrine (D), should be used to maintain blood pressure and ensure organ perfusion.

2. C.  In the anterior spinal cord syndrome, just the posterior columns are preserved and so patients lose all pain and temperature sensation as well as motor function. Most cases of anterior cord syndrome follow aortic surgery, but it has also been reported in the setting of hypotension, infection, vasospasm, or anterior spinal artery ischemia or infarct. In trauma, typically hyperflexion of the cervical spine causes the injury to the spinal cord.

Loss of all motor and sensory function (B) occurs with a complete transection of the spinal cord. Most commonly this occurs after a significant trauma. Isolated motor function loss (A) is not a classic syndrome and would result from a small area of injury on the cord just involving the corticospinal tract. Upper greater than lower motor weakness occurs (D) with a central cord syndrome. Sensory involvement is variable although burning dysesthesias in the upper extremities may occur. Most commonly the syndrome occurs after a fall or motor vehicle accident.

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FOAMcastini – Kappa

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Reading papers is hugely important but learning how to read medical literature is an entirely different realm and many of us have statsphobia.

The Free Open Access Medical Education (FOAM)

Kappa – It’s Greek To Me

The Bread and Butter

Kappa – a coefficient indicating the degree of inter-rater reliability.  How reliability are people getting the same result for a certain test or evaluation?

  • For example, you would want two people looking at the same chest x-ray to agree on the presence or absence of an infiltrate. Sometimes, chance comes into play and kappa tries to account for this.  Similarly, clinical decision aids are often comprised of various historical and physical features.  It would be nice if different clinicians evaluating the same patient would turn up the same results (thereby yielding the decision aid consistent and reliable).

To see how to calculate kappa, check this out.

The value of kappa ranges from -1 (perfect disagreement that is not due to chance) to +1 (perfect agreement that IS due to chance).  A value of 0 means than any agreement is entirely due to chance [1-2].

kappa

People debate over what a “good” kappa is.  Some say 0.6,  some say 0.5 [1-2]. In the PECARN decision aid, for example, the authors only included variables with a kappa of 0.5 [3-4].

Limitations:

  • Prevalence – if prevalence is high, chance agreement is also high.  Kappa takes into account the prevalence index; however, raters may also be predisposed to not diagnose a rare condition, so that the prevalence index provides only an indirect indication of true prevalence, altered by rater behavior [6].
  • The raters – agreement may vary based on rater skill, experience, or education.  For example, when PECARN variables were looked at between nurses and physicians, the overall kappa for “low risk” by PECARN was 0.32, below the acceptable threshold as this number suggests much of the agreement may be due to chance [6].
  • Kappa is based on the assumption that ratings are independent (ie a rater does not know the category assigned by a prior rater).

References
1. Viera AJ, Garrett JM. Understanding interobserver agreement: the kappa statistic. Fam Med. 2005;37:(5)360-3.

2. McGinn T, Wyer PC, Newman TB, et al. Tips for teachers of evidence-based medicine: 3. Understanding and calculating kappa. CMAJ. 2004;171 (11)

3.Kuppermann N, Holmes JF, Dayan PS, et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374:(9696)1160-70. [pubmed]

4. Gorelick MH, Atabaki SM, Hoyle J, et al. Interobserver agreement in assessment of clinical variables in children with blunt head trauma. Acad Emerg Med. 2008;15:(9)812-8.

5. Nigrovic LE, Schonfeld D, Dayan PS, Fitz BM, Mitchell SR, Kuppermann N. Nurse and Physician Agreement in the Assessment of Minor Blunt Head Trauma. Pediatrics. 2013.

6. de Vet HC, Mokkink LB, Terwee CB, Hoekstra OS, Knol DL.  Clinicians are right not to like Cohen’s κ 2013;346:f2125

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Episode 24 – Mild Traumatic Brain Injury/Concussion

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The Free Open Access Medical Education (FOAM)

We cover the Taming the SRU podcast, “Ketamine Cagematch” (iTunes), a debate between Dr. Minh Le Cong and Dr. Chris Zammit.

Dogma persists that ketamine may increase intracranial pressure, which would be bad in traumatic brain injury (TBI) given the fixed space in the cranial vault.  These are largely from Yet, these patients often need sedation, for agitation or intubation, and drops in blood pressure are also deleterious (see EMCrit on neuroprotective intubation).

PRO (Le Cong): The literature doesn’t show clinically significant deleterious outcomes from ketamine use in the head injured patient.  Review in Annals on ketamine and ICP.  Deleterious effects of apnea may result from other sedative agents.

CON (Zammit): Studies showing that ketamine does not increase ICP confounded by the presence of other sedatives on board.  As a result, there may still be a risk to using ketamine in these patients.

The Bread and Butter

We cover key points on concussion and mild TBI from Tintinalli 254 but to be honest, Rosenalli is lacking on this topic so we’ve turned to the ACEP clinical policy, AAN guidelines, Ontario Pediatric Guidelines, and the  AAP guidelines on the topic.  But, don’t just take our word for it.  Go enrich your fundamental understanding yourself.

Mild TBI and concussion are often referred to interchangeably and the definition varies [1-3].  Unfortunately, concussion is often thought of only in the sports population and not all-comers to the Emergency Department (ED) so patients may not receive proper .

Definition: Essentially, any alteration in mental status following head injury. Per the CDC:  Head injury from blunt trauma or acceleration/deceleration with GCS 14-15 PLUS

  • observed or self-reported transient confusion, disorientation, or impaired consciousness
  • Amnesia around the time of injury
  • Signs of other neurologic or neuropsychological dysfunction
  • Any loss of consciousness (LOC) less than 30 minutes (!) [3]

For more on how reliable LOC is in these patients, see this post.

Causes: Falls and motor vehicle collisions are the most common causes in adults, whereas sports are the more common in kids.

  • The effects on the brain are largely a result of “secondary injury,” consistent of alterations in ion-channel, metabolic pathways, and electrochemical imbalances.  These are more functional than structural.

Symptoms: There’s a good bit of overlap with migraine, more significant head trauma, and symptoms that may be confused for behavioral issues in younger populations.

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Testing: Not all head injuries require imaging.  Certainly, patients with focal neurologic findings warrant imaging; yet, in other cases, validated decision aids exist to help determine which patients may or may not need imaging.  In adults, we like the Canadian CT Head tool , although the ACEP clinical policy uses the New Orleans Criteria.  For a solid review of the two, check out this SGEM episode.  In children, consider the use of the PECARN decision aid. Otherwise, a good neurologic exam and observation should suffice.

Something to consider – patients often believe that a “normal” CT scan of the head means that they don’t have a concussion.  As a result, they may not take concussion precautions seriously.  In this case, imaging may provide false reassurance.

There’s increased attention on biomarkers like GFAP, total tau, and S-100B but these are not ready for prime time and are not incredibly specific [3].  Further, standardized assessment tools such as SCAT3 and ACE may be useful, but are used predominantly on-site for sports related incidents.

Treatment

  • Education – this is one of the biggest areas in which ED providers may make a difference. Give patients or family members precautions for concussion, even if the injury or mechanism seems relatively mild.  Studies show that a majority of pediatric patients do not follow up as instructed after a concussion [4].  Perhaps communication of the the potential gravity of concussion and long-term implications may improve follow up.
  • Rest – This the is the mainstay of initial treatment for most mild TBI [1-3, 5].  It’s unclear how strict this rest needs to be, but a recent study in the pediatric literature found no benefit to strict rest versus standard instructions (1-2 days rest + graduated return) [6].
  • Graduated return to activity – after a period of rest, it’s recommended to slowly resume activities, spending at least 24 hours at each level of increased activity.  If an individual gets symptomatic, they should return to the level of activity at which they were asymptomatic (see the Zurich protocol).
  • Return to play – clearing people from the ED is NOT a good idea.  For those on the sidelines, a player should be removed from activity for the day after a suspected concussion.

Why do we care in the ED?

  • Quality of Life – Concussive symptoms can be quite disabling.  Giving patients a name for their symptoms, resources, and education may help them understand the process of recovery and available resources.
  • Second Impact Syndrome – A second head injury in a patient symptomatic from a concussion may experience diffuse cerebral edema, possibly from loss of cerebral autoregulation.* [2]
  • Post Concussion Syndrome (PCS) – a subset of the concussion population will have persistence of symptoms which, if they persist > 1 week to 3 months after the injury, is deemed PCS. *  This is thought to be more prevalent in individuals with a history of depression, anxiety, or migraines and in those with more severe ED presentations [2].
  • Bouncebacks – Patients may present to the ED with symptoms of concussion but may not give a history of significant trauma.  Remember that concussion may occur after a seemingly minor bump to the head and elderly may need extra support with activities of daily living or may bounce back with a more life threatening injury.
  • Lack of follow up.  While some may follow up with concussion specialists, the majority of our patient population lacks the ability for meaningful or specialist follow up.  We can’t assume that someone else is going to guide our patients through concussion recovery or that when we write “follow  up with _____” that it will happen.  Our care may be it, make it good.

*The literature on these is sparse and complicated by variable definitions, information, and standardized reporting.

 Generously Donated Rosh Review Questions (scroll for answers)

Question 1. A 33-year-old man with no past medical history presents with a headache 3 days after a closed head injury. The patient states that he stood up from kneeling and hit the top of his head on a wood cabinet. There was no loss of consciousness or seizure activity. In addition to the headache, he complains of difficulty concentrating at work and dizziness. His physical examination is unremarkable.[polldaddy poll=8663736]

Question 2. A 42-year-old man is brought to the ED after he tripped and fell while he and his wife were on a walk. His wife notes that she saw him hit his head on the pavement and that he did not respond to her for 45 seconds. When he started to respond, she says that he was very confused. In the ED, his vital signs are BP 135/75, HR 88, RR 14, and oxygen saturation 98% on room air. On exam, you note some minor lacerations on the patient’s upper extremities, face, and scalp and his GCS is 15. As the wife recounts what happened, the patient does not recall any of the events and continuously asks to repeat what happened to him. A CT scan of the brain is normal. The patient is diagnosed with a concussion and is ready to be discharged from the ED. [polldaddy poll=8663741]

References

1. Tavender EJ, Bosch M, Green S, et al. Quality and consistency of guidelines for the management of mild traumatic brain injury in the emergency department. Acad Emerg Med. 2011;18:(8)880-9. [pubmed]

2. Haydel M.  Management Of Mild Traumatic Brain Injury In The Emergency Department. Emergency Medicine Practice.  September 2012 Volume 14, Number 9

3. Jagoda AS, Bazarian JJ, Bruns JJ, et al. Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Ann Emerg Med. 2008;52:(6)714-48. [pubmed]

4.Hwang V, Trickey AW, Lormel C, et al. Are pediatric concussion patients compliant with discharge instructions? J Trauma Acute Care Surg. 2014;77(1):117–22; discussion 122.

5. Brown NJ, Mannix RC, O’Brien MJ, Gostine D, Collins MW, Meehan WP. Effect of cognitive activity level on duration of post-concussion symptoms. Pediatrics. 2014;133(2):e299–304.

6.Thomas DG, Apps JN, Hoffmann RG, McCrea M, Hammeke T. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics. 2015;135:(2)213-23. [pubmed]

Answers

 1.  D.  The patient presents with minor head trauma and complaints consistent with a concussion and should have neurology follow up arranged. A concussion is a minor TBI that is often seen in MVCs and collision sports (football, hockey). It is typically caused by a rotational injury or an acceleration-deceleration injury. Patients will present with a number of non-specific symptoms including headaches, dizziness, confusion, amnesia, difficulty concentrating, and blurry vision but do not have focal neurologic findings. Despite the absence of severe intracranial injury, patients can have chronic and debilitating symptoms from concussions. Neurology referral is recommended, as patients should have functional testing and tracking of their symptoms for resolution. It is vital to counsel patients to avoid contact sports or activities that increased the risk of recurrent injury as these patients are at risk for more severe injury with second impact.In the absence of focal neurologic findings, absence of antiplatelet or anticoagulant use and minor trauma, imaging is not needed (A, B, C).

2. Cerebral concussions are clinically characterized by headaches, confusion, dizziness, and amnesia for the event. Concussions are characterized by a transient loss of consciousness that occurs immediately following blunt, nonprenetrating head trauma, caused by impairment of the reticular activating system. Concussions present without focal neurologic deficits, and CT and MRI show no acute abnormalities. Although not commonly performed for concussions, functional imaging, such a PET scan, may show changes in blood flow and glucose uptake. It is critical to inform the patient and his or her family of the second impact syndrome (SIS), which occurs when a patient suffers a second concussion after being symptom-free from the first. Although SIS is more common in sports based injuries, especially among teenagers, the risk of serious sequelae following a second concussion is immense. Due to neurochemical and autoregulatory changes that may still be present, a second concussion soon after a first generally produces a rapid neurologic decline that proves fatal. Patients should be told to avoid activities that could cause falls or trauma for at least 1 week after the patient is completely asymptomatic from the first concussion. Most patients with a concussion can be discharged from the emergency department and advised to follow-up with a primary care physician within 1 week (B). Although some patients have only transient symptoms from a concussion, others may experience persistent symptoms termed postconcussive syndrome (PCS).  PCS symptoms most often include headache as well as memory, sensory, sleep, and concentration disturbances. It is important to consider PCS in all patients with a concussion, but a primary care physician is generally able to care for these patients. It is unnecessary to obtain an MRI (C).  Although patients should avoid trauma and falls for at least 1 week after being completely asymptomatic after the first concussion, a change insleeping position (D) is unnecessary.

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