UMEM Educational Pearls

 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.

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

• 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.

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)

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

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.

Fraud (PATH audits)    (PATH = physicians at teaching hospitals)

• As a general rule, faculty may not bill Medicare for the work of residents.
• Faculty may bill for their own work, and may repeat a resident examination if necessary.
• To appropriately bill under PATH audit guidelines, faculty may make reference to a resident’s history, may simply document the variance between their exam and the resident’s exam, and should document medical decision making.
• Faculty may bill for a procedure if:
  • faculty performs the procedure
  • faculty was present for the entire procedure
  • faculty was present for the key portion of the procedure
  • faculty actively assisted the resident in performance of the procedure.

So for the residents, a lot of attendings will want to be present when you do a procedure, not because they think you will need their assistance, but because, procedures are a large revenue stream that can be lost if the attending is not present.

Thanks to 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.

Pediatric Leukemia/Lymphoma Presentation in the ED

• Pts most commonly present with c/o pallor or decreased activity
• Physical Exam commonly demonstrates pallor, splenomegaly, fever, hepatomegaly, lymphadenopathy, and ecchymoses/petechiae.
• CBC’s and peripheral smears are realiably abnormal
• Patients with solid tumor more commonly present with symptoms related to tumor location (ie Abd pain, Headache, etc.)

Jaffe D, Fleisher G, Grosflam J. Detection of cancer in the pediatric emergency department. Pediatr Emerg Care. 1985 Mar;1(1):11-5.

                                      Phenytoin po      Phenytoin IV       Fosphenytoin

Time to therapeutic       6.4 hrs                  1.7 hrs                 1.3 hrs

Adverse Events              0.69/pt                   1.86/pt                 1.87/pt

Also to take into account  is that the adverse events with IV phenytoin include soft-tissue necrosis if there is extravasation of infusion. The cardiotoxicity seen with phenytoin and fosphenytoin is largely due to the propylene glycol diluent and thus not seen with oral loading or even in oral overdosing.

You decide, at least you have the data to properly evaluate the risk:benefit ratio.

• Less than 10% of sarcoidosis cases affect only the nervous system.
• In such cases, granulomas form within nervous tissue and usually only occurs when there is significant systemic involvement.
• Most sarcoid exacerbations affecting the nervous system are not recurrent. 
• Manifestations of neurosarcoidosis include:
  • 1)  Mononeuropathy - Cranial nerve dysfunction most common     (Heerfordt  syndrome = uveitis, fever, parotid gland inflammation, and facial nerve palsy).
  • 2)  Peripheral neuropathy - Sensation and/or motor dyusfunction
  • 3)  Central Nervous System -  Hypothalamus/pituitary gland, cerebral cortex, cerebellum, spinal cord (rare)

The PERC Rules revisted

How can I rule out PE without ANY testing, you ask? Do I have to get a d-dimer on that low risk patient?

Do these things keep you up at night like they do me?

Consider using the PERC rule (Pulmonary Embolism Rule Out Criteria)

This set of rules was mentioned in an earlier pearl, but there are now 3 large studies (and one on the way) that validate the use of these rules.

So, if you have a patient who is LOW risk for PE but you would like to document something in the chart that proves you thought about the diagnosis and clinically ruled it out:

If the patient is LOW risk for PE by your clinical gestalt and if the answer to ALL of the following questions is YES, then the patient is considered PERC negative:

• Age < 50 years
• Pulse < 100 bpm
• SpO2 > 95%
• No unilateral leg swelling
• No hemoptysis
• No recent trauma or surgery
• No prior PE or DVT
• No hormone use

PERC negative + Low Risk clinical gestalt = PE ruled out

Caution!

• Most people are comfortable with: LOW risk + negative d-dimer = PE ruled out but use of the PERC rules has not gained wide acceptance yet. Experts in this area predict this will change.
• Clinical gestalt must be used and the patient must be LOW risk for PE
• The PERC rule is not intended for use in moderate risk patients or in patients without an alternative diagnosis.
• The rule is really only intended to avoid testing in the patient you were really not thinking about PE in the first place. Some experts agree that writing "PERC negative" in the chart is defensible.

Jeff Kline, PERC rule. Journal of Thrombosis and Hemostasis. 2007/2008