D-dimer assays have been previously hypothesized to be useful for many disease entities including pulmonary embolism, disseminated intravascular coagulation (DIC) and subarachnoid hemorrhage (sampled from the CSF). Now, D-dimer is being considered for the evaluation of possible aortic dissection. 10 in 100,000 Americans will experience an aortic dissection annually with 38% being misdiagnosed initially. Clearly, we need help making this diagnosis. However, is D-dimer the right tool?
The current database includes approximately 10 original articles using D-dimer assays to “rule out” aortic dissections. These articles suggest sensitivities near 100%. Unfortunately, sensitivities can be misleading. A good screening test should provide nearly 100% sensitivity to avoid missing any subjects with the disease. Unfortunately, relying on sensitivities alone results in many false positives. In particular, in ruling out a disease entity, we should be most concerned with negative predictive value, related to specificities. There are several limitations to the available data. The studies are largely based on case series, without any prospective trials. Thus, patients with known dissection were studied. The D-dimer sensitivities were likely skewed to the positive from selection bias, as patients with dissection were predominantly selected. Furthermore, imaging had already been performed in most patients, which indicates a higher pre-test probability for the patients selected. Additionally, the European Heart Journal review lowered their threshold for positive result.
Finally, due to small sample sizes, the confidence intervals associated with these sensitivities were fairly wide.
So, what about specificity. Unfortunately, the data isn’t much better. “Healthy, normal controls,” “chronic dissection,” and patients with “known PE or AMI” were specifically selected. This sample is hardly representative of any population, let alone the kind of patients who present to the ED.
In short, there is no convincing evidence supporting the use of D-dimer to rule out aortic dissection.
D-dimer as the sole screening test for acute aortic dissection: a review of the literature. Ann Emerg. Med. 2008;52:339-43.
European Heart Journal review. Eur Heart J. 2007;28:3067-75
In reference to Arrhythmias by Mel Herbert, EMRAP Sept. 2008
Adenosine vs. Verapamil
Why choose adenosine when it makes patients feel terrible? There are reasonable alternatives in the appropriate circumstances. Calcium channel blockers, such as Verapamil (consider administering calcium if hypotensive) or Diltiazem.
With wide complex rhythms, possibly atrial flutter, temporarily slowing the rhythm with adenosine for identification may be helpful. Adenosine is a great drug to drop in the “Dumb Doctor Box.”
You can safely use it at 3 AM, or whenever your brain is tired, regardless of the QRS width. Adenosine is a strong consideration, with comparison to Verapamil in patients at risk for cardiovascular collapse such as in cardiomyopathy.
The only people who do not need sedation are dead, or near dead & unresponsive SVT/Afib/VT with hypotension need cardioversion ASAP. But, that does not mean without sedation.
-Propofol 20mg q30 sec g rarely get hypotensive!
Propofol: 2-3mg/kg. Thiopental literature shows required dose of sedation exponentially decreases as cerebral perfusion decreases, therefore no hypotension w/small boluses & perfect titration
-Fentanyl 1mcg/kg g sleeping within 2 minutes, pain free!
-Propofol only g groan and arms flexing at chest
-Fentanyl then Propofol (20-40mg)g no arm flinging, less response to shock
Other options: short acting agent
-Sufentanil – sedation + analgesia, rapid on & off
-Brevital 20mg q 30sec g sedated within 1-2 doses
If you cardiovert them, their hypotension goes away
In continuation of CSF in Meningitis, Nate Kupperman, EMRAP Nov. 2008
Pretreatment with antibiotics
Which is more important: Timely antibiotic administration before LP or avoiding potential alteration of the CSF by doing so?
Well, here is your answer. It is always of critical importance to treat suspected meningitis when you consider the diagnosis, as opposed to when the diagnosis is made.
Many, particularly pediatricians, have argued that pre-treatment with antibiotics prior to LP alters the CSF results and may reduce the diagnostic yield from an LP performed subsequent to delivery of antimicrobials. So, how do antibiotics impact CSF analysis? CSF cultures may be falsely negative. The most likely organisms to be effected are meningococcus, with sterilization occurring as early as two hours post administration and pneumococcus at four hours. Of particular importance is that CSF WBC and neutrophil counts are unaltered, while glucose and protein are likely to be impacted. For the emergency physician, the WBCs are arguably the most important CSF parameter in the analysis for meningitis. Glucose and protein rarely have an impact. Thus, their alterations are inconsequential. Although CSF culture sterilization may occur, if the LP is performed in a timely manner, this phenomenon is substantially limited as well. Pre-treatment with antibiotics, prior to LP, is an acceptable practice. Also, an interesting pearl from Nate: no screening tests adequately distinguish bacterial from viral (aseptic) meningitis. Err on the side of treatment for bacterial meningitis.
Necrotizing fasciitis is a rare but devastating disease. Early consideration and recognition of this disease are key. Although any patient could develop necrotizing fasciitis, those with diabetes mellitus, alcoholism, chronic medical conditions, a history of intravenous drug abuse and those with recent surgical wounds are at greatest risk. Those with “spider bites” often discovered to be community acquired MRSA (not due to a spider bite after all) are at risk as well. However, they will experience a more indulent course (Harbor-UCLA. N Eng J Med. 2005;352:1445-53). These patients may present in one of two ways. First is the classic presentation of POOP, pain out of proportion to exam. These patients are in agony, as their pain is intractable, despite generous doses of narcotic analgesics. The second is “La belle indifference.” Despite the grotesque appearance of the limb, they will seem somewhat indifferent to it.
On physical examination, they will often be tachycardic and hypotensive. The effected area will be edematous, malodorous, crepitant with decreased sensation. They may exhibit hemorrhagic bullae. Necrosis is a very late finding.
Diagnostics may be helpful. Leukocytosis, hyponatremia and an elevated lactate are often present. Plain radiographs may reveal subcutaneous gas. However, MRI and CT, respectively, are more sensitive. The mainstay of treatment is surgical debridement. When considering this diagnosis, the first step should be to call the surgeon. Supportive care, goal directed sepsis (Manny Rivers Protocol (N Engl J Med. 2001;345:1368-77) and borad-spectrum antimicrobials are also critical to the effective management of necrotizing fasciitis. Antimicrobial coverage should include gram negatives, positives, MRSA and anaerobes. Clindamycin may used to cover gram positive organisms and provide anaerobic coverage. Vancomycin should be used if Clindamycin resistant MRSA is suspected. Efficacy has been described for IV immunoglobulin for toxic shock syndrome from group A Streptococcus. The closer to the torso this infection is, the more vigilant you must be. Patients who experience sepsis from necrotizing fasciitis on the torso, have a grave prognosis.