UMEM Educational Pearls

Category: Pediatrics

Title: Ketamine and RSI for pts p TBI

Keywords: Ketamine, RSI, TBI (PubMed Search)

Posted: 1/18/2008 by Sean Fox, MD (Updated: 10/20/2019)
Click here to contact Sean Fox, MD

Ketamine and RSI for pts p TBI

  • Traditionally, Ketamine has been avoided for patients with traumatic brain injury; however, this may be unwarranted…
    • Early after TBI, ICP is not usually elevated.
    • Early after TBI there is a low blood flow state, and Ketamine can increase cerebral blood flow.
    • As long as there is no obstruction to CSF flow, Ketamine will not increase ICP.
  • Evidence now states that Ketamine can be neuroprotective because it blocks glutamine because of it NMDA antagonist properties.
  • Ketamine also has antiepileptic properties (which improve pediatric TBI outcomes).
  • End result, if a patient has TBI and there is no concern for obstruction to CSF drainage, then Ketamine can be a possible option for RSI.
     

Category: Neurology

Title: Uremic Encephalopathy

Keywords: encephalopathy, neurological, mental status abnormality (PubMed Search)

Posted: 1/17/2008 by Aisha Liferidge, MD (Updated: 10/20/2019)
Click here to contact Aisha Liferidge, MD

  • Neurologic manifestations are often the first, yet most insidious, signs of uremia (i.e. electrolyte abnormalities due to renal insufficiency).
  • Signs and symptoms of uremic encephalopathy range from normal to comatose.  Some specific examples include dysarthria, pruritus, restless legs, mental status abnormality, myoclonic jerks, tetany, seizure, confusion, asterixis.
  • Elevated PTH and calcium levels have been shown to particularly correlate with uremic encephalopathy.
  • Elevated BUN levels tend to correlate with the degree of decreased level of consciousness.
  • Ammonia levels are not typically elevated with uremic encephalopathy unless there is simultaneous liver disease.
  • The treatment is dialysis.

 

http://www.emedicine.com/neuro/topic388.htm


Category: Critical Care

Title: Mean arterial pressure

Keywords: mean arterial pressure (PubMed Search)

Posted: 1/15/2008 by Mike Winters, MD (Updated: 10/20/2019)
Click here to contact Mike Winters, MD

Mean Arterial Pressure

  • Arterial pressure is the input pressure for organ perfusion
  • Mean arterial pressure (MAP) is the best physiologic estimate of perfusion pressure
  • MAP is less subject to measurement variability than SBP and DBP
  • MAP remains relatively constant when measured at different sites throughout the arterial circuit
  • MAP of 60 mmHg is considered the autoregulatory threshold below which perfusion becomes compromised
  • Goal: maintain MAP > 65 mmHg
  • There is no proven value to achieving a MAP higher that 65 mmHg.  In fact, there is some literature to support that if you try and drive the MAP higher, patients do worse

Category: Vascular

Title: How good was that PE Protocol CT you ordered?

Keywords: PE, Pulmonary Embolism (PubMed Search)

Posted: 1/14/2008 by Rob Rogers, MD (Updated: 10/20/2019)
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Optimal pulmonary artery opacification  for detecting pulmonary embolism-how good was the CT you ordered?

The PE literature is pretty clear about one thing: a CT with well-timed opacification of the pulmonary arteries is very sensitive for detecting pulmonary embolism. This means that there needs to be enough contrast in the central pulmonary arteries to be able to detect clot. So how can you be really sure the PE Protocol CT you ordered is adequate? Have you really ruled out PE?

What does this mean for the emergency physician?

  • The pulmonary arteries on CT should be approximately 200 or so Hounsefield units (HU).
  • What this means is that you slide the cursor over the pulmonary arteries and see what their HUs are. On the computer screens at UMMS, Hounsefield units are on the bottom of the screen and change as you roll the cursor over different densities (bone, soft tissue, calcium, etc).
  • If the central pulmonary arteries are a lot less than 200 Hounesfield units (e.g. 100 HU) the scan would be considered suboptimal.

Some predict that in the future WE (the emergency physician) may in fact be held accountable for knowing whether or not a CTPA (CT Pulmonary Angiography) is optimal or not.

References:

(1) Kline-Carolinas Medical Center (2) Journal of Thrombosis and Hemostasis 2007 (3) AJR 2006,2007


Category: Cardiology

Title: ST depression and atrial fibrillation

Keywords: atrial fibrillation, ST-segment depression (PubMed Search)

Posted: 1/13/2008 by Amal Mattu, MD (Updated: 10/20/2019)
Click here to contact Amal Mattu, MD

Transient ST-segment depression during rapid atrial fibrillation is of uncertain clinical significance (much as is true for ST segment depression in SVTs). A recent study indicates that ST-segment depression in rapid AFib is not consistently associated with positive stress testing or occlusions on cardiac catheterization.

On the other hand, if the ST-segment depression persists after the rate is controlled, then there should be greater concern.

[Androoulakis A. J Am Coll Cardiol 2007;50:1909-1911.]

 

 


Category: Infectious Disease

Title: Ludwig's Angina

Keywords: Ludwig, Angina (PubMed Search)

Posted: 1/13/2008 by Michael Bond, MD (Updated: 10/20/2019)
Click here to contact Michael Bond, MD

 Ludwig’s Angina:

Ludwig’s angina is most commonly a polymicrobial disease of mixed aerobic / anaerobic bacterial origin. Dental disease is the most common cause of Ludwig’s angina.

Diagnosis is usually made after obtaining a CT scan of the Neck and upper chest. 

Once the diagnosis is made, treatment should consist of broad spectrum antibiotics and surgical evaluation by ENT or Oral Surgery for possible I&D. Aggressive management of the patient’s airway is a must, and the patient should be intubated early in the course of the illness if there is any sign of airway compromise. Nasal intubation may be preferred by ENT/Oral Surgery.

Typical Antibiotics include a Penicillin with clindamycin or metronidazole.

Ludwig’s Angina Trivia:

  • Initially described in 1836 by the German physician Wilhelm Frederick von Ludwig.
  • It was called angina, which finds its origin from the Greek word, anchone, which means strangulation.  The term, angina was used to connote throat pain and infection as angina originates from the Greek word, anchone, that means strangulation.
  • It is believed that Elizabeth I of England died of Ludwig's angina in 1603.
 

Category: Pediatrics

Title: Newly Diagnosed ITP in Children

Keywords: ITP, Leukemia, Steroids, IVIG, Anti-Rh(d), Bone Marrow Aspiration (PubMed Search)

Posted: 1/11/2008 by Sean Fox, MD (Updated: 10/20/2019)
Click here to contact Sean Fox, MD

Pediatric ITP – Bone Marrow Aspiration

 

  • ITP is an acquired disorder characterized by:
    • thrombocytopenia (platelet < 150)
    • a purpuric rash
    • normal bone marrow
    • the absence of signs of other identifiable causes of thrombocytopenia.

 

  • Therapeutic options include Steroids, IVIG, and Ant-Rh(d)
    • For patients with new Diagnosis, consultation with a hematologist is warranted:
    • Despite the growing number of studies that state there is a low probability of newly diagnosed leukemia presenting as isolated thrombocytopenia, the risk exists.
    • Bone Marrow Bx is the Gold Standard prior to starting steroids currently.
    • Steroids may partially treat a leukemia.
    • Can avoid Bone Marrow Bx if you use IVIG (which needs to be given in consultation with Hematology)
       

Category: Neurology

Title: Recurrent Stroke and Post-TIA Stroke Risks

Keywords: stroke, tia, prevention, recurrent (PubMed Search)

Posted: 1/10/2008 by Aisha Liferidge, MD (Updated: 10/20/2019)
Click here to contact Aisha Liferidge, MD

  • Of the 700,000 annual strokes in the U.S., 200,000 are recurrent.
  • Risk of recurrent stroke is reported to be:

              -->  11.5% at 1 week

              -->  6-15% at 1 month

              -->  18.5% at 3 months

  • Risk of stroke following TIA is reported to be:

              -->  8% at 1 week

              -->  11.5% at 1 month

              -->  17.3% at 3 months

  • Due to the significant risk of stroke recurrence and new stroke after TIA, many of which lead to permanent disability, death, and health care costs, it is imperative that due diligence be given to proactively and thoroughly working stroke/TIA patients up in a timely fashion after the initial event. 
  • Secondary prevention, such as smoking cessation, weight management, alcohol consumption moderation, tight glucose control, and anti-platelet therapy, should also be encouraged.

 

 

Thom, et al.  AHA Statistics Committee and StrokeStatistics Subcommittee.  Heart Disease and Stroke Statistics-2006 Update.  Circulation 2006; 113:e85-151.

Sacco, et al.  Predictors of Mortality and Recurrence after Hospitalized Cerebral Infarction in an Urban Community:  the Northern Manhattan Stroke Study.  Neurology 1994;44:626-34.

Coull, et al.  Population Based Study of Early Risk of Stroke after Transient Ischaemic Attack or Minor Stroke:  Implications for Public Education and Organisation of Services.  BMJ 2004;328:326.

 

 


Category: Toxicology

Title: Bisphosphonates - A Recent FDA Warning

Keywords: bisphosphonates (PubMed Search)

Posted: 1/10/2008 by Fermin Barrueto, MD (Updated: 10/20/2019)
Click here to contact Fermin Barrueto, MD

With the aging population, bisphosphonate use will continue to increase. They promote bone growth by inhibiting osteoclast action and resorption of bone. Unfortunately, they have their side effects and the FDA has sent out a recent warning that affects us all:

  • [Posted 01/07/2008] FDA informed healthcare professionals and patients of the possibility of severe and sometimes incapacitating bone, joint, and/or muscle (musculoskeletal) pain in patients taking bisphosphonates.

If a patient presents with severe bone/joint pain, check the med list to see if they are on a bisphosphonate - they may not be faking the pain. This can occur days, weeks or even years after initiation of dose


Category: Critical Care

Title: Pulmonary Hypertension Pearls

Keywords: pulmonary hypertension, hypotension, calcium channel blockers (PubMed Search)

Posted: 1/8/2008 by Mike Winters, MD (Updated: 10/20/2019)
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Pulmonary Hypertension Pearls

We are beginning to see more and more patients with pulmonary hypertension (PAH),  many of whom are on continuous IV infusions of new medications.  With that in mind, here are a few pearls:

  • The most common causes of rapid deterioration in patients with PAH are: catheter occlusion/pump malfunction, pneumonia, indwelling catheter infection, RV ischemia, PE, and GI bleeding
  • Hypotension is usually due to worsening RV failure and less likely to hypovolemia
  • If a catheter occlusion or pump failure is found, the drug should be restarted as soon as possible through an alternative access (including peripheral)
  • Calcium channel blockers, a prior treatment for PAH, are no longer indicated and should not be given

Category: Vascular

Title: Risk Factors for Pulmonary Embolism

Keywords: Pulmonary Embolism (PubMed Search)

Posted: 1/7/2008 by Rob Rogers, MD (Updated: 10/20/2019)
Click here to contact Rob Rogers, MD

 

Risk Factors for Pulmonary Embolism

  • Remember that as many as 20-25% of patients with proven VTE (DVT and PE) will not have identifiable risk factors at the the time you evaluate them.
  • 6 hours of flight (or car ride) with the knees flexed at about 90 degrees is considered by many to be a risk factor.
  • Inflammatory bowel disease (Crohns and Ulcerative Colitis) are hypercoagulable disorders and have been linked to VTE.

Can you imagine one of  our patients saying"Dr. Abaraham, I have what is known in the hematology community as a Factor 5 Leiden mutation"?


Category: Cardiology

Title: cardiology literature update

Keywords: aVR, electrocardiography, prehospital, pulmonary edema, CPAP, noninvasive ventilation (PubMed Search)

Posted: 1/7/2008 by Amal Mattu, MD (Updated: 10/20/2019)
Click here to contact Amal Mattu, MD

 

Recent Articles from the Cardiology Literature
 
Electrocardiographic Prediction of Acute Left Main Coronary Artery Occlusion
Rostoff P, Piwowarska W, Gackowski A, et al. Amer J Emerg Med 2007;25:852-855.
            This isn’t new news to anyone that’s been attending advanced ECG workshops (e.g. FHC!) or keeping up with some of the ECG literature, but just one more publication on the utility of lead aVR, the lead I refer to as the “forgotten 12th lead” or the “Rodney Dangerfield lead.” The authors wrote this brief report in response to an article we published in November 2006 pertaining to lead aVR.1 In that article, we discussed that ST-segment elevation (STE) in lead aVR in patients with acute cardiac ischemia has been found to be highly specific for acute occlusion of the left main coronary artery (LMCA). Why should we worry more about ACS with LMCA involvement vs. any other ACS case? Very simple...the literature indicates that when a patient has ACS involving the LMCA, they carry a 70% risk of developing cardiogenic shock or dying, and the only treatment that has been demonstrated to improve outcomes in patients with LMCA occlusion is rapid PCI (or often they will need CABG). No medical therapies have been found to reliably improve the prognosis, including thrombolytics. This is not just applicable to patients with STEMI…it also applies if the patient has an ST-depression ACS.
            The authors performed an analysis of published data and report that STE in lead aVR during ACS is 77.6% sensitive, 82.6% specific, and 81.5% accurate for LMCA occlusion. These authors don’t specifically comment on what degree of STE is required (0.5 mm? 1.0 mm?), but in our evaluation of the literature there are three patterns that appear to predict LMCA occlusion: (1) STE in lead aVR which is greater in magnitude than the STE in lead V1; (2) STE in lead aVR with simultaneous STE in lead aVL; or (3) STE in lead aVR > 1.5 mm. Also, it is important to bear in mind that these findings only apply when there is evidence of ischemia or infarction in other leads as well, so this is really not applicable to non-ACS patients. For example, some patients with SVT will develop STE in lead aVR, and this is not clinically predictive of LMCA disease.
            For anyone wondering why STE occurs in lead aVR, apparently it’s not completely clear. The authors cite one theory that “it is caused by transmural ischemia of the basal part of the interventricular septum, where the injury’s current is directed toward the right shoulder” thus producing STE in lead aVR. Sounds good to me. The bottom line is this: when a patient has evidence of ischemia or infarction on the ECG, take a special look at lead aVR. If there is STE there, the first thing you need to do is to get on the phone and find a cardiologist that will take the patient for PCI. And if you have to transfer the patient and have a choice of where to send the patient, opt for a center that also has cardiac surgeons available for CABG. They will often be needed.
 
1. Williamson K, Mattu A, Plautz CU, et al. Electrocardiographic applications of lead aVR. Am J Emerg Med 2006;24:864-874.
 
 
A Randomized Study of Out-of-Hospital Continuous Positive Airway Pressure for Acute Cardiogenic Pulmonary Oedema: Physiological and Clinical Effects
Plaisance P, Pirracchio R, Berton C, et al. Eur Heart J 2007;28:2895-2901.
            Over the past couple of years in this series we’ve reviewed articles demonstrating the utility of non-invasive ventilation (NIV) in the early management of cardiogenic pulmonary edema (CPE). Various studies have demonstrated that NIV is associated with decreased intubation rates, ICU utilization and length of stay, decreased hospital costs, and even decreased mortality. One key, though, is that NIV must be used early in the course of treatment. Logically, one would then assume that application of NIV by prehospital care providers would be very beneficial. Plaisance and colleagues evaluated this assumption in the Paris EMS system. They conducted a randomized, prospective study in which they compared in various combinations early CPAP (during the first 15 minutes), late CPAP (between 30-45 minutes of treatment), medical treatment alone (the loop diuretic bumetanide; NTG added if SBP > 100 mm Hg à 400 mcg SL followed by infusion at 1 mg/hr [pretty low!]; and nicardipine infusion was added for afterload reduction if SBP remained > 160 or DBP > 90 mm Hg despite NTG), and combinations of medical treatment with early or late CPAP for patients with CPE. The primary endpoints they were evaluating was the effect of early CPAP on a dyspnea clinical score and on ABGs after 45 minutes; and the secondary endpoints were the effects of early CPAP on tracheal intubation rates, need for inotropic support, and in-hospital mortality. CPAP pressures were 7.5 cm H2O. 124 patients were enrolled.
            The researchers found that patients receiving early CPAP had greater improvements than patients receiving either medical treatment alone or medical treatment plus late CPAP in terms of dyspnea scores, PO2 levels, and tracheal intubation rates; and patients with early CPAP also had a trend towards lower in-hospital mortality (P=0.05, nearly statistically significant). Additionally, fewer patients in the early CPAP group needed inotropic support. Overall, the efficacy of CPAP was so significant that the authors did not observe any clear benefit of adding medical treatment if CPAP was applied early, whereas the addition of late CPAP to medical treatment was associated with significant improvements.
            There are two major takeaway points here. First, NIV appears to be the best early therapy for CPE. Second, NIV works best when it is applied early. This study demonstrated that even a short 15 minute delay was associated with significant effects on patient outcomes. The authors suggest that the delay in initiation of NIV in patients with CPE might be equated to the delay in aggressive resuscitation of patients with septic shock in terms of outcomes. This paper certainly makes a strong argument for pushing for more prehospital systems to include NIV in their CPE protocols!
           

Category: Cardiology

Title: ASA in ACS

Keywords: aspirin, acute coronary syndromes (PubMed Search)

Posted: 1/7/2008 by Amal Mattu, MD (Updated: 10/20/2019)
Click here to contact Amal Mattu, MD

In the setting of an ACS, the minimum dose of ASA that should be given is 162 mg. Chewing provides antiplatelet effects slightly faster than simply swallowing, though the difference is probably not clinically significant. Enteric coated aspirin, however, clearly takes longer to work and should therefore be avoided in patients with ACS.

A dose of 325 mg does not appear to provide any further benefit beyond the 162 mg dose, though there might be a slightly higher bleeding rate. Despite that the 2005 PCI guidelines recommend a dose of 325 mg as the initial dose for patients with ACS if they are not chronically taking ASA. Otherwise, 162 mg is sufficient.


Category: Orthopedics

Title: Knee Injuries

Keywords: Knee Injury, ACL, dislocation (PubMed Search)

Posted: 1/5/2008 by Michael Bond, MD (Updated: 10/20/2019)
Click here to contact Michael Bond, MD

Some quick facts about Knee Injuries:

 

  • The most common cause of acute traumatic hemarthrosis of the knee is an anterior cruciate ligament tear.
    • Most patients with an ACL injury will give a history of immediate pain, disability, knee swelling and audible pop.
  • The most common ligament injuried in the knee is the medial collateral ligament.
  • Patella dislocations
    • Usually lateral dislocations and often spontaneous reduce.
    • Hyperextend the knee to make the reduction easier.
  • Dislocation of the knee:
    • Anterior is the most common and usually secondary to hyperextension
    • Popliteal artery injury is commonly seen and must be looked for.  Easy bedside test is Ankle Brachial Indexs.

 


Category: Pediatrics

Title: RSV Rapid testing use

Keywords: RSV, Apnea, Congenital Heart Disease, Chronic Lung Disease, Prematurity, Rapid testing (PubMed Search)

Posted: 1/4/2008 by Sean Fox, MD (Updated: 10/20/2019)
Click here to contact Sean Fox, MD

Bronchiolitis: Use of RSV rapid testing

 

  • Firstly, know that the sensitivity of the test is ~60% (leaving 40% that have the disease testing falsely negative)
  • Secondly, in whom will the result impact your decision?
    • High-risk patient populations (at risk of decompensation or apnea)
      • Premature (especially <34 wks GA)
      • Infants < 2months of age
      • Chronic Lung Disease
      • Congenital Heart Disease
    • Infants undergoing sepsis evaluations
      • The incidence of concominant serious bacterial infection and RSV is low (<1%)
         

Purcell K, Fergie J. Concominant serious bacterial infections in 2396 infans and children hospitalized with respiratory syncytial virus lower respiratory tract infections. Arch pediatr adolesce med. 2002; 156: 322-324.


Category: Toxicology

Title: Levetiracetam (Keppra)

Keywords: anticonvulsant, status epilepticus, keppra (PubMed Search)

Posted: 1/3/2008 by Fermin Barrueto, MD (Updated: 10/20/2019)
Click here to contact Fermin Barrueto, MD

Levetiracetam

  • A new anticonvulsant that is 100% renally eliminated
  • Does not require therapeutic drug monitoring like phenytoin
  • The IV form does not cause skin necrosis or have cardiotoxicity like phenytoin
  • Is being investigated in benzodiazepine-refracory status epilepticus (1)
  • Fairly safe drug even in overdose (Barrueto et al ;) )

 

Knake et al. Intravenous levetriacetam in thetreatment of benzodiazepine-refractory status epilepticus. J Neurol Neurosurg Psychiatry 2007 Sept 26; Epub


Category: Neurology

Title: Carotid Artery Dissection and Stroke

Keywords: carotid artery dissection, stroke (PubMed Search)

Posted: 1/3/2008 by Aisha Liferidge, MD (Updated: 10/20/2019)
Click here to contact Aisha Liferidge, MD

  • Consider cervical artery dissection as the source of stroke in patients younger than age 40.
  • About 20% of such strokes are due to carotid artery or vertebral artery dissections.
  • Of these, internal carotid artery dissections are the most common.
  • These patients often present with a triad of neck and head pain, Horner's syndrome, and pulsatile tinnitus.
  • MRI/MRA is the best non-invasive diagnostic modality for arterial dissection.  Angiography may needed for confirmation.

 

Selim M, Caplan LR. Carotid Artery Dissection.  Current Treatment Options Cardiovascular Medicine.  2004; 6:  249-253.

Stapf C, Elkind MS, Mohr JP.  Carotid Artery Dissection.  Annual Review Medicine.  2000; 51:  329-47.

Schievink W. Spontatneous Dissection of the Carotid and Vertebral arteries.  NEJM.  2001; 344:  898-906.


Category: Critical Care

Title: Adrenal Insufficiency in the Critically Ill

Keywords: adrenal insufficiency, hypotension, glucocorticoids, hydrocortisone (PubMed Search)

Posted: 1/1/2008 by Mike Winters, MD (Updated: 10/20/2019)
Click here to contact Mike Winters, MD

Adrenal Insufficiency in the Critically Ill

  • Adrenal insufficiency (AI) is estimated to occur in up to 30% of critically ill patients
  • The most common causes of AI in the critically ill are SIRS and sepsis
  • In most cases of critically ill patients, AI is functional (i.e relative) - the adrenal response is insufficient to respond to the degree of stress
  • Diagnostic clues include hyponatremia, hyperkalemia, hypoglycemia (rare), and hemodynamic instability despite IVFs and vasopressors
  • Although still controversial, most feel that AI is present in critically ill patients with either a basal cortisol < 15 mcg/dl, an increase in < 9 mcg/dl after ACTH stimulation, or a random cortisol < 25 mcg/dl
  • IV hydrocortisone, methylprednisolone, and dexamethasone are the 3 glucocorticoids most commonly administered
  • Hydrocortisone is usually the preferred agent because it is the synthetic equivalent of cortisol (and has both glucocorticoid and mineralocorticoid activity)

Category: Vascular

Title: Lytics for catheter occlusion

Keywords: catheter, lytics (PubMed Search)

Posted: 12/31/2007 by Rob Rogers, MD (Updated: 10/20/2019)
Click here to contact Rob Rogers, MD

Thrombolytic infusion for occluded central venous catheters

For patients with long-term indwelling central venous catheters (dialysis catheters, Hickmans, etc) who develop catheter occlusion, consider infusion of thrombolytic therapy for catheter salvage.

How do you do it, you ask?

  • Infuse 2 mg of tPA through the affected port
  • Can also use Urokinase if this is all you have

This treatment is very safe and is well tolerated.

Journal of Vascular Access, 2006


Category: Cardiology

Title: adenosine and WCTs

Keywords: adenosine, ventricular tachycardia (PubMed Search)

Posted: 12/30/2007 by Amal Mattu, MD (Updated: 10/20/2019)
Click here to contact Amal Mattu, MD

Adenosine should be used with great caution in patients with wide complex tachycardia for two major reasons:
1. Adenosine should never be used as  diagnostic maneuver to decide whether someone has ventricular tachycardia vs. SVT. Adenosine is well-reported to convert certain types of VT.
2. If the WCT is irregular, this may be atrial fibrillation with WPW, in which case adenosine is well-known to produce ventricular fibrillation.