UMEM Educational Pearls

• Transient Neurological Attack (TNA) = attacks of sudden onset consisting of focal or non-focal neurological deficit, lasting no longer than 24 hours.
• Examples of TNA include TIA (when the deficit is focal), global amnesia, acute confusion, and syncope without a known cause.
• Patients who experience non-focal TNA are at higher risk for major vascular diseases and dementia than those without TNA.

Bos, et al.  "Incidence and Prognosis of Transient Neurologcial Attacks, " JAMA, pgs. 2877-85.  Dec. 26,  2007.

Johnston.  "Transient Neurological Attack:  A Useful Concept?," JAMA, pgs. 2912-13.  Dec. 26, 2007

Pitfalls in pulse oximetry in the critically ill

• Pulse oximeters are calibrated by manufacturers using data collected from healthy volunteers
• In general, pulse oximeters are accurate  within +/- 2% for sats > 70%
• In the critically ill, however, the accuracy of pulse oximetry diminishes when sats drop below 90%
• Also, there may be a significant lag time between a hypoxic event and the actual display of the event - most commonly seen in low flow states, hypotension, mild hypothermia, and when using vasoactive medications
• Prolonged lag times are more common with finger probes
• Pitfall - pulse oximetry does not provide any assessment regarding ventilation (P_aCO₂) or acid-base status (pH) - it is simply an estimate of arterial oxgyen saturation
• Pearl: anemia does not affect the accuracy of pulse oximetry

Pulmonary CTA Sensitivity and PIOPED II

The publication of PIOPED II has led some to doubt the sensitivity of pulmonary CTA for pulmonary embolism. This study reported an overall sensitivity of 83% which could be increased to nearly 90% with the addition of CTV (CT Venography). 83% is a horrible sensitivity. So, why should you care?

• This study used 16 detector CTs...not the 64+ head scanners we are now using. This study, like many others, suffers from the explosion of CT technology. As soon as a study is published, the technology the study used becomes outdated. Most studies now look at OUTCOME...i.e., what % of patients with a negative CT who do not receive anticoagulation develop a PE at 30, 60, 90 days? Current literature shows that the chances of VTE at 90 days for patients with negative CTAs is less than 2%.
• Bottom line, don't be too discouraged by the PIOPED II study.  In addition, many of the authors of the study actually advocate for CTA/CTV to rule out PE. This is a tremendous amount of radiation and has NOT been validated as a "standard" approach to ruling out PE.
• Lastly, it is generally a good idea to try to limit the use of CT scans (yes, that is what I said) by using a d-dimer/pretest probability or PERC/clinical gestalt approach. This is a defensible strategy.

Aspirin is the only NSAID that should be used in the acute treatment and also the in-hospital management of patients with STEMI or NSTEMI/unstable angina, even if the patient is chronically managed on other NSAIDs. The use of any of the non-ASA NSAIDS, both nonselective as well as COX-2 selective agents, in these patients is associated with increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture. Their use should be discontinued immediately at the time of admission.

So you are getting sued.  Here are some tips to handle your Deposition:

• Don’t bring any documents
• You may charge an expert witness fee if you are not a party and the deposing attorney asks your opinion, rather than just asking you to testify about facts.
• Say “yes” or “no,” rather than making gestures.
• Absolute honesty is the best policy.
• Listen carefully and only answer what is asked.  Don’t try to educate the deposing attorney.
• Don’t argue or interrupt
• Nothing is “authoritative.”
• Pause before answering
• Avoid saying “always” or “never.”
• Be brief.  Long-winded answers will get you in trouble.
• Rather than guessing exactly what you did, its okay to testify what you do “as a matter of habit.”
• Don’t exaggerate, over-emphasize, or speak in absolute terms.
• Don’t answer the same question twice.
• Don’t let the plaintiff attorney refer to you as an employee if you are an independent contractor.
• Don’t agree with the inane statement “if it wasn’t documented it wasn’t done.”

Courtesy of Larry Weiss, MD, JD

Disclaimer: This information does not constitute legal advice, is general in nature, and because individual circumstances differ it should not be interpreted as legal advice.The speaker provides this information only for Continuing Medical Education purposes.

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.
   

• 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

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

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

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.]

 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.

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)
     

• 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.

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

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

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"?

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.

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.

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.