UMEM Educational Pearls

Physical Examination finding in inferior vena cava thrombosis

Consider IVC thrombosis if you ever see vertically oriented, dilated abdominal wall veins, or dilated veins on the back. As opposed to abdominal wall veins that radiate out from the umbilicus in patients with cirrhosis-known as caput medusae.

Etiologies include hepatic tumors abutting the IVC, renal cell tumors, open abdominal surgery, catheter related, IVC filter-related.

The ACC/AHA just recently published a "Focused Update" of their guidelines for management of ST-elevation MI. Amongst the changes:

Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI who receive thrombolytics.

Clopidogrel 300-600 mg orally should be added to aspirin in patients that are going for PCI for STEMI. This is listed as a Class I intervention, although the level of evidence is rated "C." In other words, it is judged to be definitely helpful though based on not-so-robust evidence (you figure that one out!).

Glycoprotein receptor antagonists can also be added (Class IIa, level of evidence B).

[I personally believe there is better evidence for the GP2B3A inhibitors than for clopidogrel, but there is a general push for more and more guideline writers to support clopidogrel. The number of writers for these ACC/AHA guidelines who have affiliations with the drug companies, including the ones that manufacture clopidogrel (Plavix), is tremendous; the list of disclosures is listed at the back of the document. Nevertheless, people tend to want to follow guidelines, and the boards will test you on this stuff so it is worth knowing.]

[Also for the record, if I have a STEMI, here's what I want: 162 mg ASA (not 325 mg), unfractionated heparin (not enoxaparin), abciximab/ReoPro (not eptifibitide/Integrilin) in the cath lab (not in the ER), and quick PCI; if I can't get the PCI within 60 minutes (not 90, but 60 minutes!), give me either tenectaplase or retaplase (not tPA) + 162 mg ASA + UFH; if I have a lot of pain that is not responding to NTG, give me dilaudid or fentanyl (not morphine)...and some Bailey's on ice; add oral BBs, ACEIs, and a statin at the 24 hour mark, NOT any earlier (early BBs only if I have Bailey's-resistant hypertension). Thanks.]

Amal

 

We have seen this lovely  bug infect our patients and have to instutitue therapy. But do you know what is the first line drug and which one has now become second line due to its toxicity? Here is the short list:

First Line Therapy: Permethrin (Nix) - least toxic, only causes local irritation

Second Line Therapy: Crotamiton (Eurax) - again local irritation

Third LIne Therapy: Lindane - SEIZURES if you leave it on too long or put on too much. Children were particularly susceptible and relatively contraindicated.

Metacarpal Neck Fractures (i.e.: Boxer’s Fracture if 5^th Metacarpal)

Depending on the MCP joint involved a certain amount of angulation is permissible before it adversely affects normal function.

• 2^nd and 3^rd Metacarpal fractures < 10۫ angulation ideally these should be perfectly aligned.
• 4^th Metacarpal fracture <20۫ angulation allowed
• 5^th Metacarpal fracture <30۫ angulation. 
  • Studies have shown that even 30۫ angulation will decrease normal function by 20%.  
  • Normal excursion of the 5^th MCP is 15۫ to 25۫.
• No amount of rotation deformity should be allowed.

Tissue adhesives:

Cyanocrylate Tissue Adhesive is an excellent product to use when repairing linear lacerations.

A few things to remember:

The wound needs to be irrigated as you would any other wound prior to closure.

Gravity works.  Consider where the product may drip to before you apply it (Eyes, Ears, Nose, etc).  

Use Surgi-Lube (or other petroleum product) to create a barrier to limit the flow of the cyanocrylate.

For long lacerations, you may use steri-strips to help approximate edges before applying the tissue adhesive.

What to do if the glue gets out of control and drips onto the eyelids... may also apply to Krazy-Glue:

Use copious irrigation and then Mineral Oil (not acetone or alcohol - which won't go well in the eyes).

Often there will be an associated corneal abrasion... treat it as other corneal abrasion.

Here is a list of drugs that can cause hyperkalemia either at therapeutic levels or in overdose:

Amiloride, ACEI, Beta Blockers, Cardiac Glycosides, FLuoride

Heparin, NSAIDS, Penicillin (the Pen VK formulation), Spironolactone

Succinycholine and triamterene

• Dihydroergotamine (DHE) is an older medication approved for the treatment of intractable migraine and cluster headaches.  Many of our Neurology colleagues still use this drug and its administration could start while the patient is 
  in the ED.
  
• Intranasal forms have become popular (i.e. Migranal).  Intramuscular and subcutaneous administration are also possible.
  
• The typical intravenous dose is 0.25 to 1 mg IV push over 2-3 minutes q 6 hours for 24 to 72 hours.
  
• DHE use is contraindicated in the following patients: 
  
  >    Patients concurrently on a protease inhibitor or macrolide antibiotic because of increased risk of life- threatening peripheral ischemia (**Black Box Warning**) 
  >    Patients with a hypersensitivity to ergot alkaloids 
  >    Patients with increased risk of developing vasospastic events 
  >    Patients who are concurrently taking vasoconstrictors 
  >    Patients who are pregnant or nursing 
  >    Patients with hemiplegic or basilar migraines
  
• Monitor for the following potential adverse reactions, which are typically related to vasoconstriction/spasm
  and warrant immediate abortion of the drug’s administration: 
  
  >    Myocardial infarction (check ECG's)
  >    Arrhythmia (place on cardiac monitor)
  >    Stroke (regular neuro. checks)
  >    Hypertension (check often) 
  >    Ischemia (monitor for clinical signs/symptoms) 
  
  
  
  
  -- Diener HC, Kaube H, Limmroth V. A practical guide to the management and prevention of migraine. Drugs. 1998;56(5):811-824.
  -- Fisher M, Gosy EJ, Heary B, Shaw D. Dihydroergotamine nasal spray for relief of refractory headache: A retrospective chart review. Curr Med Res Opin. 2007;23(4):751-755.
  -- http://www.aetna.com/cpb/medical/data/400_499/0462.html
  -- http://www.rxlist.com/cgi/generic/dihyergmes.htm
  
   

Invasive Arterial Pressure Monitoring - Complications

In critically ill patients with hemodynamic instability we often place arterial catheters to continuously monitor mean arterial pressure.  Since we frequently use the radial artery for cannulation, it is important to know the complications associated with these catheters.  Scheer et al performed, perhaps, the largest review of complications of peripheral arterial catheters.  The results:

• Radial arterial catheters
  • 19,617 cannulations reviewed
  • temporary occlusions - 19.7%
  • hematoma - 14.4%
  • serious ischemic damage - 0.09%
  • pseudoaneurysm - 0.09%
  • sepsis - 0.13%

Pearl: Although permanent ischemic damage is rare, when placing a radial artery catheter use the non-dominant hand.

Scheer BV, Perel A, Pfeiffer UJ. Clinical review: Complications and risk factors of peripheral arterial catheters used for haemodynamic monitoring in anaesthesia and intensive care medicine. Crit Care 2002;6:198-204.

Fenoldopam Pearls

Intravenous Fenoldopam has been shown in recent years to be a very effective antihypertensive medication. Studies have compared it to Nitroprusside (Nipride), the older generation "gold standard" antihypertensive, and have found to be just as effective.

• Think of Fenoldopam as Nipride without the toxicity....taste great, less filling
• Works by peripheral dopamine agonism
• Increases renal blood flow and induces a natriuresis (patient pees sodium)-so works well in our chronic kidney disease and ESRD patients
• Easy to titrate and very well tolerated
• Contraindication in patients with glaucoma-The drug elevates IOP.

Journal of Hypertension 2007

Recent literature (Collins, et al, Ann Emerg Med, Jan 2008; and Cotter, et al, Am Heart J, Jan 2008) confirms something that we've been talking about for YEARS....more than 50% of patients presenting with acute cardiogenic pulmonary edema are not fluid overloaded, but rather have fluid mis-distributed into the lungs. Management should focus on fluid re-distribution rather than diuresis. Use of diuretics in these patients is associated with worsening renal function, which is a significant predictor of in-hospital mortality.

The best patients to use diuretics on are patients with slow progression of dyspnea, lower extremity edema, and weight gain over days-weeks. In the absence of a history of this slow progression, don't go crazy with the diuretics!

Migraines and Pregnancy

• Typically headache frequency will increase during the first 2 to 3 months of pregnancy
• 70% of women report significant improvement in headaches during their second and third trimester.
• Most migraine medication should NOT be given to pregnant woman.  Verify prior to prescribing.
  • Class X/D drugs include
    • Cafergot (ergotamine)
    • Depakote
    • Dihydroergotamine (DHE)
  • Class C drugs include
    • Imitrex
    • Zomig
    • Midrin
    • Relapex
• Some headache centers will prophalax pregnant woman with Vitamin B2 and Magnesium.

Pediatric Back Pain

• Back Pain in PrePubertal Children is rare and often due to serious underlying disorder
  • Infection (diskitis or osteomyelitis)
  • Malignancy
    • Osteoma, Osteoblastoma
    • Histiocytosis X
    • Lymphoma, Leukemia
    • Ewing Sarcoma
    • Neuroblastoma, Spinal Cord Glioma
• Back Pain in adolescent children is more likely to be due to muscular skeletal injury (as with adults)
  • Classified as chronic back pain (greater than 4 weeks duration) in up to 13%

• Red Flags for Serious Underlying Disorders
  • <4yrs of age
  • Back Pain causing functional disability (child not willing to play)
  • Fever
  • Neurologic Abnormality (get the child undressed and do a good neuro exam).
     

• 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