Posterior Lateral Maleolus, My Old Friend

Source: See citation below

Pearl:  When applying the Ottawa Ankle Rule, we specifically palpate the posterior maleoli.

Explanation: When reviewing the Ottawa Ankle Rule today during morning report the question came up: why do we specifically palpate the posterior lateral and medial maleoli to assess for bony tenderness? The image above, from the initial derivation study and also reproduced on MDCalc, describes the intended areas of palpation. Looking into the original paper, the authors explain that they chose the posterior aspect of the lateral maleolus in order to avoid confusing ATFL (most common ankle sprain tear) tenderness with bony pain. The posterior lateral maleolus keeps you clear of the ATFL. The posterior medial maleolus appears to have been chosen because it had the best inter-rater reliability on that side. So there you have it.

Source:  Stiell IG, Greenberg GH, McKnight RD, Nair RC, McDowell I, Worthington JR. A study to develop clinical decision rules for the use of radiography in acute ankle injuries. Ann Emerg Med. 1992; 21:384–90.

The 52 in 52 Review: CT Before LP?

Note: Some of the junior residents are unaware of what the 52 in 52 Review is. In brief. The ALIEM blog picked a list of 52 influential papers in EM (we are on version 2 now) to provide a weekly reading topic. The full list is available here.

Article Citation: Hasbun R, Abrahams J, Jekel J, Quagliarello VJ. Computed tomography of the head before lumbar puncture in adults with suspected meningitis. N Engl J Med. 2001 Dec 13;345(24):1727-33. PMID: 11742046

What we already knowMany of us have been taught to perform a CT prior to an LP to reduce the risk of LP-induced herniation. Now certainly this is not the only reason that we perform a CT before an LP. In many cases, meningitis is one among our differential, and may only reach the top of our DDx if the CT head is negative for other pathology. However, even when we have a high suspicion for meningitis we often obtain a CT first to look for evidence of elevated ICP or mass effect. Is this practice necessary?

Why this study is important: This study attempted to identify the relationship between clinical features on presentation and likelihood of findings on CT that would alter our pursuit of LP.

Brief overview of the study: From 1995-1999, adults strongly suspected of having meningitis were prospectively enrolled at Yale-New Haven prior to CT or LP. All included participants had an evaluation including the 11-scale NIH stroke scale and all had an LP. CT performance was up to provider choice. 235 patients received a CT. 66 did not. No patients herniated from CT in either group. 25% of the CTs were abnormal but only 5% showed any evidence of mass effect. Factors associated (with statistical significance) with an RR ~2 or greater of any abnormal CT finding (not only mass effect) included age > 60, recent seizure, immunocompromise, prior CNS disease and any NIH stroke scale finding. Applying these rules to the “low-risk” patients who received CT, 93/96 had completely normal CTs and none had mass effect. Interestingly, the patients who received a CT spent 2 hours longer in the ED and took ~1hr longer to receive empiric antibiotics.

Limitations: My largest concern is that the authors do not report on the percentage of each group (with and w/o “high risk” features) who ultimately had meningitis. If the low risk group is also less likely to have meningitis the results are less helpful because rather than trying to avoid CT before LP we should be finding a way to exclude them from the meningitis pathway. Second, this study took place while the AIDS epidemic remained in full swing and a healthy percentage of patients presented with well progressed opportunistic infections (including one who died of toxo herniation prior to CT). This may not be representative of a typical patient population. Third, we do not know whether there would have been findings on those who did not receive a head CT due to the observational nature of the study. In short, this study suggests that a patient who is an adult under 60, not immunocompromised and with a negative NIH stroke score in whom you have high suspicion for meningitis may not need a CT because their risk of intracranial mass effect is low. However, since so few of our high-suspicion meningitis cases meet those criteria, it is unclear how much CT use this could truly result in. Better, randomized studies are needed.

Esmolol for Refractor VFib

By Jer5150 – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=19669589

Pearl: In cardiac arrest, consider esmolol (500mcg/kg loading dose, then 0-100mcg/kg/min drip) for refractory ventricular fibrillation.

Background: Ventricular fibrillation is one of our two “shockable” rhythms and is supposed to portend a better cardiac arrest outcome. But what if your patient is refractory to standard treatment (defibrillation, amiodarone, lidocaine) either by never exiting v-fib or by returning to v-fib immediately? Aside from dual-synchronous defibrillation, which is not yet a data-driven technique, to we have any other tools in our back pocket?

Explanation: There is some data, retrospective and non-randomized, to support improved outcomes with the infusion of esmolol to patients in refractory v-fib cardiac arrest. Two studies, one at Hennepin County (1) and one in Korea (2) both retrospectively analyzed patients in refractory v-fib arrest (defined as at least 3 shocks in both, amiodarone was also required by Hennepin). At Hennepin, sustained ROSC was 100% better and survival to discharge was 300% better, but no p-values were provided. In the Korean study, 56% in the esmolol group achieved sustained ROSC vs 16% in the non-esmolol group (p 0.007). There are also some pig model studies that support esmolol reducing the rate of v-fib recurrence after treatment (3,4)

Bottom Line: There are no randomized or large studies, but if your patient will not come out of ventricular fibrillation, consider giving esmolol as a bolus (500mcg/mg/kg) followed by an infusion.

(1) Driver BE1Debaty G2Plummer DW3Smith SW3. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillationResuscitation. 2014 Oct;85(10):1337-41. doi: 10.1016/j.resuscitation.2014.06.032. Epub 2014 Jul 14.

(2) Lee YH1Lee KJ2Min YH3Ahn HC4Sohn YD5Lee WW6Oh YT7Cho GC8Seo JY9Shin DH10Park SO11Park SM12. Refractory ventricular fibrillation treated with esmololResuscitation. 2016 Oct;107:150-5

(3) Jingjun L1Yan ZWeijieDongdong ZGuosheng LMingwei B.Effect and mechanism of esmolol given during cardiopulmonary resuscitation in a porcine ventricular fibrillation model.Resuscitation. 2009 Sep;80(9):1052-9.

(4) Wallis DE1Wedel VAScanlon PJEuler DE.Effect of esmolol on the ventricular fibrillation threshold.Pharmacology. 1988;36(1):9-15.