REBEL Cast

By Salim R. Rezaie, MDMedicine Health & Fitness

REBEL Cast episodes

September 27, 2023REBEL Core Cast 109.0 – Na Channel Blocker Poisoning
Take Home Points:
In the context of poisoning, a “wide QRS” is anything greater than 100 milliseconds.
A newly “wide QRS”, especially with hemodynamic instability, should prompt consideration of sodium channel blockade and not ventricular tachycardia. Treatment is guided by administration of sodium-bicarbonate.
Recall that the resultant alkalemia driven by sodium-bicarbonate will shift potassium intracellularly. As a result, if a bicarbonate infusion is started, potassium should
simultaneously be given as to avoid life-threatening hypokalemia.
REBEL Core Cast 109.0 – Na Channel Blocker Poisoning
Click here for Direct Download of the Podcast
Definition and Physiology
Standard definition of a wide QRS is anything > 120 msec (3 small boxes on the ECG)
In the context of poisoning, a “wide QRS” is anything greater than 100 milliseconds. (Boehnert 1985).
Authors evaluated the relationship between QRS duration and negative clinical events in patients with confirmed tricyclic anti-depressant (TCA) poisoning.
If QRS >100 msec = 33% chance of seizures
If QRS >160 msec = 50% of ventricular dysrhythmias
Often extrapolated to other sodium channel blocking agents: diphenhydramine, loperamide, cocaine, lamotrigine, Type 1A/1C Anti-Dysrhythmics.
Clinical Manifestations
The right bundle is more susceptible to sodium-channel blockade than the left bundle and as a result, rightward manifestations will appear on the ECG: right axis deviation, terminal R wave in aVR, and a widened QRS complex.
With severe toxicity, the ECG can mimic ventricular tachycardia and clinically, the patient may decompensate hemodynamically (ie. tachycardia and hypotension)
Management
Critically ill patients will be hemodynamically unstable and present with a “wide complex tachycardia.” While ACLS will recommend shocking these patients, as with everything else in medicine, clinical context is essential.
If pre-test probability is high for poisoning, this is sodium channel blockade until proven otherwise. These patients need sodium-bicarbonate and not electricity.
Dosing: 1-2 mEq/kg bolus
If there is a response, initiate an infusion: 150 mEq in 1L of D5W at maintenance
Severely poisoned patients, may require multiple boluses of sodium-bicarbonate until the QRS narrows. (Mohan 2021)
Recall that the subsequently alkalemia will shift potassium intracellular. As a result, it is essential to replete potassium simultaneously.
References
Boehnert MT, Lovejoy FH Jr. Value of the QRS duration versus the serum drug level in predicting seizures and ventricular arrhythmias after an acute overdose of tricyclic antidepressants. N Engl J Med. 1985 Aug 22;313(8):474-9. doi: 10.1056/NEJM198508223130804. PMID: 4022081.
Mohan S, Backus T, Furlano E, Howland MA, Smith SW, Su MK. A Case of Massive Diphenhydramine and Naproxen Overdose. J Emerg Med. 2021 Sep;61(3):259-264. doi: 10.1016/j.jemermed.2021.04.020. Epub 2021 Jun 17. PMID: 34148773.
Post Created By: Sanjay Mohan MD
Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)
The post REBEL Core Cast 109.0 – Na Channel Blocker Poisoning appeared first on REBEL EM - Emergency Medicine Blog.
11 min
September 13, 2023REBEL Core Cast 108.0 – Angioedema
Take Home Points:
Airway management is paramount; expect a challenging intubation and consider controlling the airway early if there is apparent airway compromise.
Understanding the cause of angioedema (mast cell vs. bradykinin mediated) helps dictate directed management.
Urticaria and pruritus = MAST CELL mediated, which is treated like a standard allergic reaction.
REBEL Core Cast 108.0 – Angioedema
Click here for Direct Download of the Podcast
Angioedema:
A transient, localized, non-pitting distention of the skin (subcutaneous layer) or the respiratory and gastrointestinal tracts (submucosal layer)
Inflammatory mediators cause vascular permeability, allowing fluid to diffuse into the interstitium
Effects areas with loose connective tissue, like the oropharynx, extremities, and genitalia
Epidemiology:
0.1 to 0.3% of people who take NSAIDs (Nzeako 2010).
0.1 to 0.7% patients that take ACE inhibitors (but 20-30% of all angioedema presentations to the Emergency Department)
3 times more common in Black Americans (Kostis 2005)
0.01 to 0.002% of general population exhibit some form of hereditary angioedema (Zuraw 2008)
Mechanism and Pathophysiology:
Mast Cell Mediated
Bradykinin Mediated
Other
IgE Dependent
ACE-Inhibitor
Infectious
IgE Independent
Hereditary Angioedema
Iatrogenic
NSAIDs
Acquired C1 Inhibitor Deficiency
Idiopathic
Mast Cell (granulocyte) Mediated
Mast cell activation (by IgE crosslinking or directly) leads to the generation of mediators (histamine, heparin, leukotriene and prostaglandin D2), which increases vascular permeability.
Features
Urticaria and pruritis
Rapid onset (1-2 hours)
IgE Dependent (Type I Hypersensitivity) Reactions
An allergen cross-links two or more IgE molecules on mast cells or basophils and initiates a signal cascade leading to degranulation.
Pro-inflammatory mediators then act on the mucosa and cause angioedema. These chemicals can recruit other cells, like eosinophils, and may lead to anaphylaxis.
IgE Independent Reactions
Mast cells are activated directly by certain medications (i.e. meperedine, radiocontrast agents)
Release inflammatory mediators and lead to angioedema.
NSAIDs hinder the formation of prostaglandins within mast cells and other leukocytes. This can cause an abundance of leukotrienes and other pro-inflammatory mediators and precipitate angioedema (Nzeako 2010).
Bradykinin Mediated
Plasma globulins called kininogens release bradykinin and cause vascular permeability.
Features
Absence of urticaria and pruritus
Insidious onset (24-36 hours)
ACE Inhibitors
Inhibition of ACE hinders the degradation of bradykinin and can lead to idiosyncratic angioedema.
Typically involves the mouth, larynx, pharynx, and subglottic tissue (Kostis 2005).
Hereditary Angioedema (presents in childhood) and Acquired C1 Inhibitor Deficiency (adulthood)
Both involve abnormalities in the level or function of the C1 inhibitor.
Without the C1 inhibitor, the plasma-kallikrein-kinin system produces more bradykinin.
Both conditions can range in severity from benign to life threatening (Wilkerson 2012).
Other Etiologies
In pediatrics, illnesses like the common cold, Streptococcus pyogenes (GAS) pharyngitis, and urinary tract infections can cause isolated angioedema (without urticaria).
Iatrogenic agents like calcium channel blockers, fibrinolytic agents, estrogens, and herbal supplements
Idiopathic
Differential:
Anaphylaxis
Erysipelas or cellulitis
Contact dermatitis
Superior vena cava syndrome
Hypothyroidism
Peritonsillar abscess
Autoimmune disease
Parasitic Infection
Presentation:
Asymmetrical
Does not regularly involve gravitationally dependent areas
Frequently painless
Non blistering, non desquamating
Hives, pruritus, bronchospasm or flushing = mast cell release (histaminergic)
Abdominal pain, nausea, vomiting
Hoarse voice
Stridor
Drooling, difficulty swallowing
Throat tightness
Inability to phonate high pitched “E” sound
Management:
Basics- ABCs, IV, O2, Cardiac Monitor
Anatomically challenging airway
Edema of the anterior tongue, base of the tongue, or larynx significantly increases the likelihood of intubation or tracheostomy. Stable patients with isolated anterior tongue edema should undergo fiberoptic laryngoscopy in the ED (McCormick 2011)
Avoid unnecessary airway manipulation (can exacerbate edema)
Edema may obscure the neck anatomy
Airway Management
Early intubation often indicated as swelling may progress and supraglottic rescue devices may be ineffective
Consider awake intubation
Double setup with standard intubation equipment and surgical airway tools for possible failed orotracheal airway
Can’t intubate, cant ventilate event necessitates surgical airway
Do not rely on external anatomy for cricothyroidotomy as edema will obscure landmarks (Hessert 2013)
Plan for a large vertical incision in the midline of the neck
Directed Treatment
Mast cell mediated (histaminergic) angioedema
Epinephrine 300 to 500 mcg IM
H1 antihistamines
Diphenhydramine 25-50 mg PO/IM/IV
Cetirizine 5-10 mg PO
H2 antihistamines
Ranitidine 50 – 150 mg PO/IV
Glucocorticoids: Methylprednisolone 1-2mg/kg per day x 2 days
Bradykinin mediated angioedema
Unlikely to respond to epinephrine, antihistamines, or glucocorticoids
Hereditary Angioedema and C1 esterase deficiencies (Wilkerson 2012)
Replace C1 inhibitor with Berinert 20units/kg IV (harvested from pooled human plasma)
Antagonize kallikrein with Ecallantide 30mg IM
Antagonize bradykinin b2 receptor with Icatibant 30mg SQ
Replace ACE with 2 units FFP (2nd line)
ACE inhibitor related angioedema
Discontinue ACE Inhibitor
Secure airway, supportive care
Icatibant
A single randomized controlled trial comparing Icatibant with prednisone and antihistamines demonstrated more rapid improvement of symptoms with Icatibant (Bas 2015)
CAMEO: phase III, double blind, placebo controlled trial showed no benefit.
Fresh Frozen Plasma (FFP)
Case reports and case series have shown a benefit from FFP (Wilkerson 2012, Hassen 2013)
However, FFP also contains bradykinin and high molecular weight kininogen which may exacerbate angioedema
Tranexamic Acid (TXA)
TXA inhibits the conversion of plasminogen to plasmin which, in theory, could reduce bradykinin production.
Low quality evidence (case reports and case series) have hinted at benefit but are mixed.
There is no high-quality evidence to support its use and no safety data.
Take Home Points:
Airway management is paramount; expect a challenging intubation and consider controlling the airway early if there is apparent airway compromise.
Understanding the cause of angioedema (mast cell vs. bradykinin mediated) helps dictate directed management.
Urticaria and pruritus = MAST CELL mediated, which is treated like a standard allergic reaction.
Read More
EMCrit: Podcast 145 – Awake Intubation Lecture from SMACC
ERCast: Angioedema
References:
Baş M et al. A randomized trial of icatibant in ACE-inhibitor-induced angioedema. N Engl J Med. 2015; 372(5):418-25. PMID 25629740
Hassen GW et al. Fresh frozen plasma for progressive and refractory angiotensin-converting enzyme inhibitor-induced angioedema. J Emerg Med 2013; 44 (4): 764-772. PMID: 23114109
Hessert MJ and Bennett BL. Optimizing Emergent Surgical Cricothyrotomy for Austere Environments. Wilderness and Environmental Medicine. 2013;24:53-66. PMID 23062323
Kostis JB et al. Incidence and characteristics of angioedema associated with enalapril. Arch Intern Med. 2005;165(14):1637-1642. PMID 16043683
McCormick M et al. Site involvement as a predictor of airway intervention in angioedema. Laryngoscope. 2011;121:262–266. PMID 21271571
Morgan PB. Hereditary angioedema—therapies old and new. N Engl J Med. 2010;363(27):2673. PMID 20818894
Nzeako UC. Diagnosis and management of angioedema with abdominal involvement: A gastroenterology perspective. World J Gastroenterol, 2010;16(39):4913-4921. PMID 20954277
Sinnert R et al. Randomized Trial of Icatibant for Angiotensin- Converting Enzyme InhibitoreInduced Upper Airway Angioedema (CAMEO Study). J Allergy Clin Immune Tract 2017; 5(5): 1402-9. PMID: 28552382
Wilkerson RG. Angioedema in the Emergency Department: An Evidence Based Review. Emergency Medicine Practice. EBMedicine.net. 2012; 14(11).
Zuraw et al. An overview of angioedema: Clinical features, diagnosis, and management. In: UptoDate, Feldweg AM (ed.) UpToDate, Waltham, MA.
Zuraw BL. Clinical practice. Hereditary angioedema. N Engl J Med. 2008;359(10):1027-1036.
PMID 18768946
Post Created By: Anand Swaminathan MD, MPH (Twitter @EMSwami)
Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)
The post REBEL Core Cast 108.0 – Angioedema appeared first on REBEL EM - Emergency Medicine Blog.
11 min
August 30, 2023REBEL Core Cast 107.0 – Vertebral Osteomyelitis
Take Home Points
Clinical presentation is very nonspecific; evaluate all patients presenting with back pain for infectious risk factors.
Baseline labs should not guide diagnosis, but may assist in later management.
MRI is key to diagnosis, obtain this imaging in all patients who raise clinical suspicion
Patients with hemodynamic instability and neurologic compromise warrant empiric antibiotics. The initiation of empiric antibiotics in hemodynamically stable, neurologically intact patients should be done on a case-by-case basis.
REBEL Core Cast 107.0 – Vertebral Osteomyelitis
Click here for Direct Download of the Podcast
Definition
Inflammation of the vertebrae due to a pyogenic, fungal or mycobacterial organism.
Classified as either acute (days), subacute (weeks) or chronic (months)
Spondylodiscitis: a term encompassing osteomyelitis, spondylitis and discitis. Often used interchangeably with osteomyelitis.
Epidemiology
1 to 2.4 cases per 100,000 people (Zimmerli 2010)
More common in males with M:F of 3:1
Rate is also increasing due to increased number of spinal procedures
Typically affects adults, with most cases occurring in patients over 50 years old.
Pathogenesis
Infection occurs by three routes:
Hematogenous spread – secondary to infections of the GU, skin, soft tissue and respiratory system, indwelling catheters or endocarditis
Due to the bifurcated structure of the arterial supply, generally presents as infection of 2 contiguous vertebrae and the intervertebral disc
Direct inoculation during trauma or spinal surgery
Spread from adjacent soft tissue infection
Organism
Most cases in the United States are pyogenic.
Most common organism is Staph Aureus (36-67% of cases) (Boody 2015).
Other pathogens include: E. Coli, Pseudomonas Aeruginosa and Group B and G hemolytic Strep
Other pathogens to consider:
Fungal – blastomycosis, coccidiomycosis, histoplasmosis, aspergillosis
Brucellosis
Mycobacterial
Location: lumbar (48%) most common, followed by thoracic (35%) and cervical (6.5%)
History and Physical
Symptoms
Back pain – often described as dull, may be present for weeks to months
Neurologic symptoms (paresthesias, weakness or radiculopathy) present in approximately one-third of patients
Most patients lack systemic symptoms
Exam
Tenderness over affected vertebrae
Paraspinal tenderness or spams may be present which may mislead the clinician towards a musculoskeletal diagnoses
Risk Factors:
Diabetes Mellitus (most common)
Immunosuppression: HIV, Malignancy, chronic steroids or immunosuppressant medication use
Spinal fracture, trauma or recent procedure
Substance Abuse: Alcoholism and IVDU
Presence of an indwelling vascular device
Elderly
Diagnosis
Labs
Leukocytosis and Neutrophilia are poorly sensitive and highly non-specific (Gouliouris 2010). The degree of elevation does not predict disease severity.
ESR and CRP are sensitive, yet not specific.
CRP concentration rise and fall quicker than ESR, often used to guide treatment
Blood Cultures – an important element in management and treatment
Blood culture positivity often decides whether a patient will require a bone biopsy.
Cultured specimen narrows antibiotic coverage
Urinalysis/Urine Culture –UTI is a frequent missed source of bacteremia (especially in diabetic patients).
Imaging
Gadolinium enhanced MRI – modality of choice, highly sensitive and specific (Mylona 2009).
Although MRI with and without contrast is preferred, a non-contrast MRI can evaluate for inflammatory processes.
If a patient requires premedication or has renal failure, obtain the non-contrast MRI first. A contrast MRI can be done later to delineate subtle findings.
Findings include: enhancement (hypointense on T1 and hyperintense on T2) of vertebral endplates and adjacent disc space (Image 1)
CT Scan with IV contrast – use only of MRI contraindicated
Inferior in evaluation of disc spaces and neural tissues
Less sensitive than MRI and may be falsely negative in early disease
Used primarily by surgeons for biopsy of spine
Findings include loss of end plate definition and narrowing of disc space (Image 2)
Previously used CT Myelogram now out of favor due to potential for intradural spread of infection.
Plain Radiographs – often done to evaluate other causes (masses, fracture) however not recommended for diagnosis
Poorly sensitive and findings typically present in advanced disease (10-14 days after onset), once significant bone demineralization has already occurred
Radionuclide studies – (including: Tech 99m Bone scan, Gallium -67)
Sensitive but not specific, long acquisition time and difficult to obtain in the emergent setting
Management
Pathogen directed therapy – Antibiotics tailored towards cultured organism
Given the dependence on blood culture results to guide therapy, current recommendations (IDSA 2015 Guidelines) suggest holding empiric antibiotics in medically stable patients (non-septic, hemodynamically stable, neurologically intact) until cultures grow out.
Note: this is a weak recommendation based on low quality evidence and patients should be managed on a case by case basis in conjunction with the inpatient treatment team
Empiric coverage:
Vancomycin 15-20 mg/kg/dose every 8-12 hrs
PLUS
3rd Generation Cephalosporin: Cefotaxime (2 g IV every 6 hrs), Ceftriaxone (1 to 2 g IV daily) or Ceftazidime (1 to 2 g IV every 8 -12 hrs)
OR
Cefepime 2 g IV every 12 hours
Duration: 6 weeks (occasionally 12 weeks if advanced disease) of IV antibiotics followed by 1-2 months of oral antibiotics
Surgical Consult – although most patients are successfully treated with antibiotics alone, some may require surgical intervention if there is concern for vertebral instability or spinal cord compromise.
Indications for surgical intervention include: associated abscess formation, spinal cord compression, progression of disease despite antimicrobial treatment
Obtain consult (Neurosurgery or Orthopedics) early, since patients may require bone biopsy for detection of organism
Take Home Points
Clinical presentation is very nonspecific; evaluate all patients presenting with back pain for infectious risk factors.
Baseline labs should not guide diagnosis, but may assist in later management.
MRI is key to diagnosis, obtain this imaging in all patients who raise clinical suspicion
Patients with hemodynamic instability and neurologic compromise warrant empiric antibiotics. The initiation of empiric antibiotics in hemodynamically stable, neurologically intact patients should be done on a case-by-case basis.
Graphics
Image 1: http://www.mghradrounds.org/clientuploads/nov_dec_2006/figure2.jpg
Image 2: http://www.thelancet.com/cms/attachment/2000991969/2003662063/gr3.jpg
References
Berbari EF, Kanj SS, et al. Executive Summary: 2015 Infectious Disease Society of America (IDSA) Clinical Practice Guidelines for the Diagnosis and Treatment of Native Vertebral Osteomyelitis in Adults. Clin Infect Dis 2015 Sept 15;61(6):859-63. PMID: 26316526
Boody B, et al. Vertebral Osteomyelitis and Spinal Epidural Abscess: An Evidence-based Review. J Spinal Disord Tech. 2015 Jul;28(6):E316-27 PMID: 26079841
Chowdhury V, Gupta A, Khandelwal N. Diagnostic Radiology: Musculoskeletal and Breast Imaging. 3rd ed. New Delhi: JP Brothers Medical Ltd; 2012
Della-Guistina, D. Evaluation and Treatment of Acute Back Pain in the Emergency Department. Orthopedic Emergencies 2015 May; 33(2) 311-26. PMID: 25892724
Gouliouris T, et al. Spondylodiscitis: update on diagnosis and management. J Antimicrob Chemother. 2010 Nov;65 Suppl 3:iii 11-24 PMID: 20876624
Mylona E, et al. Pyogenic Vertebral Osteomyelitis: A Systematic Review of Clinical Characteristics. Semin Arthritis Rheum. 2009 Aug; 39(1):10-7. PMID: 18550153
Pruitt CR, Perron AD. Specific Disorders of the Spine. In: Sherman SC eds. Simon’s Emergency Orthopedics. 7th ed. New York, NY: McGraw-Hill; 2014
Winters ME, Kluetz P et al. Back Pain Emergencies. Med Clin North Am, 2006 May;90(3):505-23. PMID: 16473102
Zimmerli W. Vertebral Osteomyelitis. N Engl J Med 2010 Mar; 362(11)1022-9. PMID: 20237348
Post Created By: Anand Swaminathan MD, MPH (Twitter @EMSwami)
Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)
The post REBEL Core Cast 107.0 – Vertebral Osteomyelitis appeared first on REBEL EM - Emergency Medicine Blog.
8 min
August 16, 2023 REBEL Core Cast 106.0 – Nerve Block Basics
Take Home Points REBEL Core Cast 106.0 – Nerve Block Basics Click here for Direct Download of the Podcast Resources REBEL EM: Local Anesthetic Systemic Toxicity Sono in Staten Blog: https://www.statenislandem.com/sono-in-staten Core Ultrasound: https://www.coreultrasound.com/ POCUS Atlas: https://www.thepocusatlas.com/ Highland Ultrasound: http://highlandultrasound.com/ Post Created By: Billy Caputo MD Post Peer Reviewed By: Anand Swaminathan MD, MPH (Twitter ... Read more
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27 min
August 07, 2023 REBEL Cast Ep122 – Delayed vs Rapid Sequence Intubation in Agitated Trauma Patients
Background: Getting a definitive airway in a critically ill trauma patient can be a stressful situation. The potential for soiled airways, cervical spine injuries, maxillofacial injuries and head injuries combined with agitation/delirium, altered mental status and hypoxemia can make securing a definitive airway both an anatomic and physiologic challenge. Traditional RSI entails preoxygenation followed by ... Read more
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20 min
July 31, 2023 REBEL Cast Ep121: The Battle of the Blades – Video Laryngoscopy vs. Direct Laryngoscopy
Background: The ongoing debate between video laryngoscopy (VL) and direct laryngoscopy (DL) has ignited intense debate within the emergency medicine and critical care communities. A recent pragmatic, randomized, multicenter trial (The DEVICE Trial) compared the two techniques to determine if VL outperformed DL in first-pass success (FPS). In this blog post, we explore the study’s ... Read more
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27 min
July 26, 2023 REBEL Core Cast 105.0 – Methylxanthine Toxicity
Take Home Points Methylxanthines are a drug class that includes caffeine, theophylline, and theobromine. The three main mechanisms that account for the clinical presentation of methylxanthine toxicity are: catecholamine release, adenosine antagonism, and phosphodiesterase inhibition. Beta agonism will lead to hyperlactatemia, hypokalemia, hyperglycemia, and tachycardia. Adenosine antagonism may lead to seizures and/or supraventricular tachycardia that ... Read more
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10 min
July 17, 2023 REBEL Cast Ep120: Etomidate vs Ketamine for RSI in the ED?
Background: Standard rapid sequence intubation (RSI) in the emergency department involves administration of an induction agent and a neuroblocking agent in quick succession. RSI inherently carries with it risks of complications such as post-intubation hypotension and cardiac arrest in the most extreme cases. It is possible that the induction agent used could play an important ... Read more
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18 min
July 05, 2023 REBEL Core Cast 104.0 – Subtle ECGs in Acute Coronary Occlusion
Take Home Points Provider assessment of how the patient looks is extremely important. If it looks and feels like a STEMI clinically, get serial ECGs and consult Cardiology immediately. POCUS has been a phenomenal tool in the management and early diagnosis of a lot of abnormal ECG and chest pain presentations. Isolated elevation in aVR ... Read more
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34 min
June 29, 2023 REBEL Cast Ep119: A Discussion with Scott Weingart on the CT FIRST Trial
Back on June 1st, 2023, Swami wrote a blog post on REBEL EM titled, The CT FIRST Trial, Should We Pan-CT After ROSC?. This stemmed a lot of discussion in the background between Swami, myself, and Scott. We felt it was worthwhile to record this as a podcast to better flush out some nuanced points. ... Read more
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34 min