Mild TBI and head CT Courtesy of: Annals
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Mild TBI and head CT Courtesy of: Annals
Possible future management of PE?
Drug-induced nystagmus
@PharmERToxGuy: Common drug causes of nystagmus: Phenytoin, carbamazepine, VPA, lamotrigine, topiramate, EtOH, lithium, dextromethorphan, PCP, ketamine, LSD
Phenobarbital dosing
Ovarian torsion primer
Atrial Fibrillation/Atrial Flutter with Rapid Ventricular Response (RVR)
Differential Diagnosis for Rapid, Narrow Complex, Irregular Rhythm:
- Atrial Fibrillation with RVR
- Atrial Flutter with variable conduction
- Multifocal Atrial Tachycardia
Treatment:
Synchronized cardioversion for patients with myocardial ischemia, symptomatic hypotension, angina, acute heart failure, pre-excitation (WPW) with hemodynamic instability.
Start with 120-200J biphasic
Start with 200J monophasic
Escalate energy levels with subsequent shocks as needed
Diltiazem:
- 10 mg to 25 mg IV push (0.25 mg/kg dose over 2 minutes)
- May repeat dose in 15 minutes if needed
- 20 mg to 25 mg IV push for repeat dose (0.35 mg/kg)
- Continuous infusion of 5mg to 15 mg/hr titrated for maintenance
OR
Metoprolol:
- 2.5 mg to 5 mg IV bolus over 2 minutes
- May repeat dose every 5 minutes up to 15 mg total
- Consider oral beta blockers for maintenance
OR
Esmolol:
- 0.5 mg/kg bolus infused over one minute with 50mcg/kg per minute infusion maintenance
- If inadequate response after 5 minutes: may repeat bolus of 0.5mg/kg and increase infusion to 100mcg/kg per minute
- If inadequate response after 5 minutes: may repeat bolus of 0.5mg/kg and increase infusion to 150 mcg/kg per minute (maximum dose of 300 mcg/kg per minute)
OR
Digoxin: Consider digoxin in patients with advanced heart failure or hypotension or in whom inadequate rate control is achieved with above medications
- 250 mcg every 2 hours given IV or orally
- Total combined loading dose is typically 750 mcg to 1 mg (maximum is 1.5mg)
Consider
Amiodarone: Amiodarone may be less likely to cause systemic hypotension than calcium channel blockers or beta-blockers
- Consider amiodarone in patients in whom above therapies are ineffective or contraindicated
- Load with 150 mg over 10 minutes – may repeat load if necessary
- Maintenance of 1 mg/min for 6 hours then 0.5mg/min
- Do not exceed 2.2 g in 24 hours
Magnesium: consider magnesium sulfate 2 g IV over 15 minutes
- additional doses of 2-4 g IV may be given
- caution in renal failure also monitor for magnesium toxicity, hypotension in higher doses
PEARLS
- Atrial flutter may only require 50 J – 100J initially
- If cardioversion is needed and it is impossible to synchronize because the rhythm is too irregular then use defibrillation dose (high energy, unsynchronized)
- Atrial fibrillation with pre-excitation should be considered with wide-complex irregular rhythm; avoid - AV nodal blocking agents which can cause paradoxical increase in ventricular rate
- IV calcium channel blockers and beta-blockers may cause transient hypotension
- Use caution in patients with severe or decompensated heart failure when giving negative inotropes (especially calcium channel blockers)
- Amiodarone is a rhythm control agent that may chemically convert to sinus rhythm and should be used with caution in patients in whom thromboembolic events are a risk
- There is limited data to suggest magnesium may help with rate control in atrial fibrillation
- Start heparin bolus and infusion in patients requiring emergent cardioversion with A-fib and A-flutter >48 hours
- Consider procainamide or ibutilide for rapid A-fib with pre-excitation not requiring emergent cardioversion
RUSH in Cardiac Arrest
RUSH in Cardiac Arrest
References:
Atkinson, P R T, D J McAuley, R J Kendall, O Abeyakoon, C G Reid, J Connolly, and D Lewis. “Abdominal and Cardiac Evaluation with Sonography in Shock (ACES): An Approach by Emergency Physicians for the Use of Ultrasound in Patients with Undifferentiated Hypotension.” Emergency medicine journal : EMJ 26, no. 2 (2009): doi:10.1136/emj.2007.056242.
Blaivas, M, and J C Fox. “Outcome in Cardiac Arrest Patients Found to Have Cardiac Standstill on the Bedside Emergency Department Echocardiogram.” Academic emergency medicine : official journal of the Society for Academic Emergency Medicine 8, no. 6 (2001): 616-21.
Breitkreutz, Raoul, Susanna Price, Holger V Steiger, Florian H Seeger, Hendrik Ilper, Hanns Ackermann, Marcus Rudolph, and others. “Focused Echocardiographic Evaluation in Life Support and Peri-Resuscitation of Emergency Patients: A Prospective Trial.” Resuscitation 81, no. 11 (2010): doi:10.1016/j.resuscitation.2010.07.013.
Hernandez, C, K Shuler, H Hannan, C Sonyika, A Likourezos, and J Marshall. “C.A.U.S.E.: Cardiac Arrest Ultra-Sound Exam–A Better Approach to Managing Patients in Primary Non-Arrhythmogenic Cardiac Arrest.” Resuscitation 76, no. 2 (2008): 198-206.
Jones, A E, V S Tayal, D M Sullivan, and J A Kline. “Randomized, Controlled Trial of Immediate Versus Delayed Goal-Directed Ultrasound to Identify the Cause of Nontraumatic Hypotension in Emergency Department Patients*.” Critical care medicine 32, no. 8 (2004): doi:10.1097/01.CCM.0000133017.34137.82.
Lichtenstein, Daniel A, and Gilbert A Mezière. “Relevance of Lung Ultrasound in the Diagnosis of Acute Respiratory Failure: The BLUE Protocol.” Chest 134, no. 1 (2008): doi:10.1378/chest.07-2800.
Rose, J S, A E Bair, D Mandavia, and D J Kinser. “The UHP Ultrasound Protocol: A Novel Ultrasound Approach to the Empiric Evaluation of the Undifferentiated Hypotensive Patient.” The American journal of emergency medicine 19, no. 4 (2001): 299-302.
Salen, Philip, Larry Melniker, Carolyn Chooljian, John S Rose, Janet Alteveer, James Reed, and Michael Heller. “Does the Presence or Absence of Sonographically Identified Cardiac Activity Predict Resuscitation Outcomes of Cardiac Arrest Patients?” The American journal of emergency medicine 23, no. 4 (2005): 459-62.
Weingart, Scott, Daniel Duque and Bret Nelson. “The RUSH Exam – Rapid Ultrasound for Shock / Hypotension.” http://www.webcitation.org/5vyzOaPYU (accessed January 9, 2011).
Courtesy of: SinaiEMUS
Hypertensive Emergencies
Definition: Severe hypertension (SBP >160, DBP>110) associated with end-organ dysfunction as manifested by, but not limited to, intracerebral hemorrhage, retinopathy, acute renal failure, pulmonary edema, myocardial ischemia, infarction, dissection.
Treatment:
Nitroprusside:
- Initial dose: 0.25 – 0.5 mg/kg/min, increase by same increment every 2-3 minutes until desired effect
- Maximum dose: 8-10 mg/kg/min (not for longer than 10 minutes)
- Will cause tachyphylaxis, avoid in renal failure
Nitroglycerin
- Initial dose: 10mcg/min, increase by 5-10 mcg/min every 5-10 minutes
- Maximum dose: 200 mg/min
Clevidipine
- Initial dose: 1mg/hour, double rate every 90 seconds until close to goal, then increase rate every 5-10 minutes as needed
- Maximum dose: 21 mg/hour
Nicardipine
- Initial dose: 5mg/hour, increase by 2.5mg/hour every 5-15 minutes
- Maximum dose: 15mg/hour
- May cause tachycardia, local phlebitis
Fenoldopam
- Initial dose: 0.1 mcg/kg/min, increase by 0.05 – 0.1 mcg/kg/min every 15 minutes
- Maximum dose: 1.6 mcg/kg/min
- Caution in glaucoma
Labetalol
- Bolus dose: 20mg IV, double dose at 10-minute intervals to max of 80mg
- Continous: 2-10mg/min, if titrating, increase by 1mg/min every 10 minutes
- Not to exceed maximum dose of 300mg.
- IV b:a ratio is 7:1
Esmolol
- Bolus dose: 500m/kg
- Continous dose: 25 – 300 mg/kg/min
- Titration: Increase by 50mg/kg.min every 4 minutes
- Bolus with every rate increase
Enalapril
- Initial dose: 1.25mg.
- Maximum dose: 5mg every 6 hours
- Avoid in renal failure
Pearls:
- Consider placement of an arterial line for more precise monitoring.
- Set an initial goal to reduce MAP by 20%.
- Do not exceed a MAP reduction >25% in 24 hours.
- Volume depletion is common; administration of a diuretic in conjunction with an anti-hypertensive agent can lead to a precipitous drop in BP.
- Be wary of over-zealous correction, as this can lead to organ hypo-perfusion.
References:
- Marik PE, Rivera R. Hypertensive emergencies: an update. Curr Opin Crit Care 2011; 17:569-80.
- Flanigan, J., & Vitberg, D. (2006). Hypertensive emergency and severe hypertension: What to treat, who to treat and how to treat. Medical Clinics of North America, 90, 439–451.
UTI workup for febrile kids
Courtesy of myemergencymedicineblog.
Reference: Singh, R. and Carpenter, C. "Does This Child Have a Urinary Tract Infection?" Annals of Emergency Medicine. May 2009.
Sterile arterial lines?
Still placing a-line's in non-sterile fashion?
Maybe we shouldn't.
"Conclusions: The risks of colonization and catheter-related infection did not differ between arterial catheters and central venous catheters, indicating that arterial catheter use should receive the same precautions as central venous catheter use. The daily risk was constant over time for central venous catheter after the fifth catheter day but increased significantly over time after the seventh day for arterial catheters."
Reference: Crit Care Med 2010; 38:1030–1035
Screening for Hypertensive Emergency with UA
Hate having to send a BMP just to see if your hypertensive patient has signs of end organ dysfunction?
Maybe you don't have to....
"We have found that the urine dipstick is a highly sensitive screening test for acute SCr elevation in patients presenting to the ED with severe hypertension. The presence of any amount of blood or at least 1+ protein by dipstick was relatively nonspecific but perfectly sensitive in detecting patients with elevated SCr"
Reference:
Karras, D. J., Heilpern, K. L., Riley, L. J., Hughes, L. and Gaughan, J. P. (2002), Urine Dipstick as a Screening Test for Serum Creatinine Elevation in Emergency Department Patients with Severe Hypertension. Academic Emergency Medicine, 9: 27–34. doi: 10.1197/aemj.9.1.27
Sgarbossa Criteria
Rule of appropriate discordance:
In LBBB with out STEMI the major terminal portion of QRS and initial upsloping portion of the ST/T segment should lie on opposite sides of isoelectric baseline = "discordance"
Sgarbossa Criteria for MI in presence of LBBB
ST-segment elevation ≥1 mm concordant with (in the same direction as) a predominantly positive QRS complex in at least one lead. (5 pt.)
ST ↓ ≥ 1mm in leads V1, V2 or V3 (3 pt).
ST ↑ ≥ 5mm discordant (in the opposite direction from) a predominantly negative QRS complex. (1 pt.) This 3rd criteria has not been shown to be useful.
Ref: Sgarbossa NEJM 334:8 481-7 Feb 1996
CD4 count estimation
In conclusion, when faced with a patient in an acute setting who has HIV or HIV risk factors, and a recent CD4 count is unavailable, a physician may obtain a CBC with differential. The ALC can be easily calculated by multiplying the WBC×lymphocyte percentage. In a population with a relatively high prevalence of low CD4 counts, an ALC less than 1,000 cells/mm3 was 91% predictive in identifying patients with CD4 counts less than 200 cells/mm3 , and those patients could be presumed to be more susceptible to opportunistic infections. An ALC greater than 2,000 cells/mm3 was 95% predictive in identifying CD4 counts greater than 200 cells/mm3 ; therefore patients with ALCs greater than 2,000 cells/mm3 can be presumed to be less susceptible to opportunistic infections. This surrogate marker can then be combined with other clinical information to determine a patient's risk for opportunistic infection.
Ref: Annals of Emergency Medicine - Volume 32, Issue 3 (September 1998)
Aortic Dissection
The mortality rate for patients with untreated proximal aortic dissections has been reported to increase by 1–3% per hour. Ref: JEM, 1/11, pg. 62 courtesy of emedhome
Cannabinoid Hyperemesis Syndrome
Essential for diagnosis: Long-term cannabis use Major features: Severe cyclic nausea and vomiting Resolution with cannabis cessation Relief of symptoms with hot showers or baths Abdominal pain, epigastric or periumbilical Weekly use of marijuana Supportive features: Age less than 50 y Weight loss of > 5 kg Morning predominance of symptoms Normal bowel habits Negative laboratory, radiographic, and endoscopic test results Ref: Cannabinoid Hyperemesis: A Case Series of 98 Patients. Simonetto DA et al. Mayo Clin Proc 2012;87:114-119. Courtesy of TPR
Crack eye
“Crack eye” refers to corneal injury associated with the use of crack cocaine. The smoke emanating form crack cocaine may be directly damaging to the corneal epithelium that may be enhanced by the anesthetic properties of cocaine that can result in a decreased blink rate. The cited reference points out “devitalization of the corneal nerves decreases the corneal epithelial integrity, leading to neurotrophic keratopathy”. In addition, cocaine smoke can be very irritating and thus users may repeatedly rub their eyes causing infectious complications often due to Staphylococcus aureus and streptococcal species. Fungal infections have been implicated in some cases Ref: Miller AD and Sherman SC. Crack eye. 2009 J Emerg Med, 37(1):75–76 courtesy of AACT