I wanted to plug two excellent issues of EMPractice that had relevance to today’s conference — one on ED evaluation of vision change and one on musculoskeletal imaging. If you want to see more on knee arthocentesis, the NEJM has a nice video.

The following teaching points were adapted from Reueben’s M+M recap and subsequent emails:

Thanks to Dr. Fawaz for his expertly-presented case of the patient with multiple myeloma and anemia who complained of generalized and lower extremity weakness, back pain, and falls. This patient was seen a several times in the ED and admitted twice before the diagnosis of compressive spinal cord metastasis was made.

Key teaching points:

*New back pain in a cancer patient is cord compression until proven otherwise. The threshold to push forward with MRI on these patients should be low.

*Cord compression should also be considered in the cancer patient with new ataxia, lower extremity weakness, bowel/bladder dysfunction, and falls.

*Pain often precedes neurological symptoms, sometimes by months.

*The gait exam is often the most important part of the neurological exam.

*When imaging for cancer-related cord compression, consider including the entire spine, as metastasis at multiple sites is common.

*Negative plain films are not reassuring in the context of possible cord compression.

An excellent summary. I would only add some nuance to the first point — the threshold for MRI should be low, perhaps as low as your threshold for ordering a two sets and stress — both MI and SCC are disastrous if missed, yet we seem more reluctant to pull the trigger on MRI for SCC rule-out.

Peter also wanted to highlight a memorable article about ED evaluation of vertigo, in a neurology journal. The take home point, however, about ambulating your patients, is valuable.

Finally, Braden emphasized Dan’s point that cord compression isn’t always from the lumbar spine, and that 60% are due to the thoracic spine. “Patients may complain of upper arm weakness greater than leg weakness (check triceps extension strength!). These signs are sometimes subtle and patients have vague ‘weakness’ complaints but physical exam can sometimes lower your threshold for imaging (and make you look really smart in front of your consultants if you pick it up).”

We recently saw a patient with active malignancy present with typical symptoms of hypercalcemia. Though the GEMM was resulted shortly after presentation and demonstrated a very high ionized calcium (more than twice the upper limit of normal and qualifies as hypercalcemic crisis), the diagnosis was not made for some time.

Consider the following diagnoses in patients with malignancies who present with unexplained symptoms.

1. Malignant pericardial effusion. Have a low threshold to perform point-of-care ultrasound to evaluate for an effusion.

2. Spinal cord compression. Back pain, lower extremity weakness, urinary retention, fecal incontinence.

3. Hypercalemia. Lethargy, confusion, generalized weakness.

4. Tumor lysis syndrome. Hematologic malignancy s/p chemotherapy with renal failure and electrolyte disturbances.

5. Neutropenic fever. Definition is a single temperature ? 101 (38.3) or fever of 100.4 (38.0) lasting longer than 1 hour in patient with ANC < 500. ANC = WBC * (%PMNs + %bands).

6.  SVC syndrome. Dyspnea, hoarseness, cough, facial and upper extremity swelling with distended neck and chest wall veins, facial edema and plethora.

7. Intracranial metastases. Seizure, altered mentation, neurologic symptoms or signs.

8. Hyperviscosity syndrome. Multiple myeloma / Waldenstrom’s / Leukemia blast crisis / Polycythemia patient with visual changes, mental status changes or neurologic symptoms, bleeding diathesis, or CHF.

I began the hour with a quick look at a fifth paper (Chang and Gallagher, Annals of EM 2006, Vol. 48 No 2), previously covered in this blog, about a RCT of patient’s reduction in pain after hydromorphone (dilaudid) vs. morphine. It served as a good introduction to pain assessment tools and I liked the author’s candid writing about factors in physician ordering beyond need — such as perceived price or just the psychological barrier to ordering 10mg of morphine over 1 mg or 2 mg of dilaudid. I also had to point out how great it was to see acknowledgment in print of our practice reality — the mode for initial pain score in this study was 10/10. A good read if you have the time.

I also recommended as background reading the section on Pain Assessment Tools, page 8-11 in the July 2006 edition of EMPractice by Curtis & Morrell.  The sections on pathophysiology of pain and ED pain epidemiology was also recommended.

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Thanks also to Dr. Constantine for his wonderful M+M presentation yesterday. The following M+M tips are adapted from Dr. Strayer’s followup email:

Key teaching points from this case of infective endocarditis:

* Do not convey undue diagnostic certainty to patients. In patients without definitive evidence of a specific diagnosis, consider that their symptoms, instead of reflecting a benign disease, could be the early symptoms of a more serious disease that hasn’t declared itself yet, and advise accordingly.

* Be careful about assigning specific diagnoses when lack of definitive evidence of these diagnoses exists. Gastritis, gastroenteritis, reflux, dyspepsia, heartburn, constipation, costochondritis, migraine, influenza, muscle spasm, sprain, strain, and anxiety are examples of diagnoses that should be assigned cautiously.  Symptom-based diagnoses such as chest pain, abdominal pain, headache, cough, and knee pain, while less satisfying to patients, usually better reflect the degree of diagnostic certainty we are able to generate in an emergency visit.

* Unless a patient is discharged without a period of observation or diagnostic studies, the chart should include a follow-up note, documenting the evolution of care and justifying discharge.

* Abnormal vital signs should either be normalized, explained, or a plan for addressing them included in the chart.

* Infective endocarditis may present with a variety of signs and symptoms. Consider the diagnosis in patients who have risk factors (intravenous drug use, abnormal heart valves) or suggestive findings (prolonged course of fevers and malaise, new murmur).

Jim has graciously agreed to let me load his first “Screen Sim” program online — you can download the whole zipped folder onto your computer here (see me if you need help). I just tried it and am thrilled to have my own little window with Jim speaking to me about stroke. Hopefully more simulators are on the way.

Also, thanks to Chris Strother for pointing me to some screen-simulators hosted at trauma.org. They’re called Moulages, a word that’s amazingly appropriate.

If you enjoyed the debate on dobutamine in sepsis, between our own Dr. Weingart and the MICU’s Dr. Kalb, you can relive the magic by downloading the audio (mp3 format).

Alternatively, Shawn has transcribed the key points, below (and thrown in some of his own thoughts, at the end): (more…)

Mieka’s case report and talk on Sgarbossa’s criteria for AMI in LBBB provided a great overview of this controversial topic. The criteria are below, and I’m reprinting the findings from an EM meta-analysis in last month’s Annals (Tabas et al, Volume 52, Issue 4, October 2008, Pages 329-336,  PMID: 18342992): (more…)

Corticosteroids have been shown to decrease mortality in the treatment of adults with bacterial meningitis — particularly pneumococcal meningitis — but the data on children are less clear. Although steroid therapy reduces hearing loss in Hib meningitis, vaccination has made Hib (and pneumococcus) much less prevalent in developed nations, and it is unclear whether steroids lower mortality in children with meningitis. This is the question a group of CHoP researchers set out to settle. However, much like the earlier literature, this paper failed to show any benefit from corticosteroid therapy.

The theoretical mechanism for steroid therapy is plausible enough — antibiotics lead to bacteriolysis, which leads to inflammation and cerebral edema. Corticosteroids control this response, but could also lead to decreased CSF penetration of antibiotics; GIB and other direct adverse effects could also result. Finally, there is the fear that steroids would mask a secondary fever if antibiotics failed.

The researchers’ methodology had its strengths and weaknesses. They used a retrospective cohort (children <18 years with bacterial meningitis), as a prospective double-blinded RCT would be difficult due to the relatively low prevalence of meningitis, and the risk associated with randomizing very sick children to treatment groups. The cohort was obtained from the Pediatric Health Information System (PHIS), a network of 27 tertiary care children’s hospitals in 18 states and DC, providing a strong multicenter patient and provider base.

However, study participants were identified through ICD-9 primary discharge code of meningitis, which can be problematic and was likely too narrow. It is conceivable that a large subset of meningitis patients are primarily coded as “fever,” “sepsis,” etc. Also, does this exclude patients who died during admission, a presumably important subset?

Furthermore, the while the usage of corticosteroids in adults has been shown to work, it is administered either 20 minutes prior to antibiotics, or with the first dose. The AAP’s current recommendation for children is similar, if the provider decides to give steroids.

However, in this paper, patients were given steroids at any point within the first 24 hours of hospitalization. As the authors used a fairly advanced statistical analysis (propensity scores), which required both a PhD and a very dense “Methods” section. The first analysis showed no difference when adjusted for propensity scores, except that the sickest patients were much more likely to have been given steroids, and the least sick were much less likely. Resultantly, they repeated the analysis, excluding the sickest and healthiest quintiles. The end result was again an insignificant difference, both in hospital length of stay and in mortality.

The main outcome measures: mortality rates of 6% (15/248) for the corticosteroid group, and 4% (102/2532); a relative risk of 1.5, but the confidence interval “crosses unity” (0.89-2.54). Very nice graphs also demonstrate that mortality and LOS follow essentially the same curves. Therefore, either there is no true difference in outcome, or the sample size (117 deaths among 2780 patients) was too small to demonstrate a difference.

Also thanks to Evelyn, whose Senior Lecture on US-guided regional anesthesia generated interest. Some of her links for futher information, anatomic diagrams, and sono screencaptures  are below:

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Some points I thought bear repeating, or that I want to expand upon:

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And a group of researchers at the Integrated Soft Tissue Infection Services (ISIS) Clinic at San Francisco General Hospital attempted to answer it with a randomized, double-blind, placebo-controlled trial (Editor’s note: This Journal Club recap, written by guest-blogger Jennifer, covers a paper by Rajendran et al. in Antimicrobial Agents and Chemotherapy, Nov. 2007; pdf and background articles here). Patients who met rather broad inclusion criteria (including febrile and immune deficient patients) were treated with incision and drainage, and then randomized to receive either cephalexin or placebo.

The results? There was no significant difference between the “treatment” arm of the study and the “placebo” arm of the study.

Although the study design seems reasonable, several holes in the investigators’ plan were brought up at this month’s Journal Club.
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As for my senior lecture, there were many topics I didn’t get to include — so let me just point you to a few excellent articles and some practical tips:
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