Survey Monkey Feb 2019

Supporting Studies

  1. Perry JJ et al. Sensitivity of Computed Tomography Performed Within Six Hours of Onset of Headache for Diagnosis of Subarachnoid Haemorrhage: Prospective Cohort Study. BMJ 2011; 343: d4277. PMID: 21768192
  2. Backes D et al. Time-Dependent Test Characteristics of Head Computed Tomography in Patients Suspected of Nontraumatic Subarachnoid Hemorrhage. Stroke 2012; 43(8): 2115 – 9. PMID: 22821609
  3. Blok KM et al. CT Within 6 Hours of Headache Onset to Rule Out Subarachnoid Hemorrhage in NonAcademic Hospitals. Neurology 2015; 84(19): 1927 – 32. PMID: 25862794

From REBELEM

Discussion:

  • Between the three studies reviewed ZERO cases of aneurysmal SAH were missed if a patient had a head CT performed within 6 hours of headache onset, a normal mental status, and no focal neurologic deficits.
  • Multiple cases of perimesencephalic bleeding were missed and undiagnosed, but none of the patients had a poor outcome (i.e. death). It turns out that 1 in 20 patients can actually have an aneurysmal perimencephalic bleed.
  • Doing LPs is not a benign procedure. It can be uncomfortable; can have complications such as post LP headaches, subdural hematomas, or even cerebral venous sinus thrombosis. LPs can also cause false positive results leading to more down stream testing.
  • So in a patient with a negative head CT within 6 hours the chances of having an aneurysmal SAH is <1%. Adding an LP is a balance between catching the rare SAH vs the complications of the lumbar puncture as well as the complications of false positive tests (i.e. additional downstream testing, surgical intervention etc).
  • In the Blok trial, there are a lot of assumptions made with the group of patients who had + bilirubin on LP especially the group found to have an aneurysm. In the study the authors stated that aneurysm rupture was unlikely because of the following:
    • Trace of bilirubin, but no RBCs in CSF
    • Pituitary Apoplexy was diagnosed with CT and MRI
    • Marginally elevated bilirubin excess, but proof of absence of bilirubin with regular spectrophotometry and RBC count in CSF of 5×106/L
    • CSF Leiden method suggested presence of bilirubin, but inspection of the absorption spa turn proved absence of bilirubin
    • RBC count in CSF <100×106/L
    • Marginally elevated bilirubin excess, but proof of absence of bilirubin with regular spectrophotometry
  • There was a 4th study performed by Sayer et al [4] looking at the rate of SAH diagnosis via an LP after a negative non-contrast head CT, which they defined as spectrophotometric detection of bilirubin, not by CSF RBC count or xanthochromia. There were 2,248 patients who met inclusion criteria with only 92 (4.8%) of LPs being positive. All patients with a positive LP underwent CTA or MRA with only 8 aneurysms and one carotid cavernous fistula diagnosed.  In other words 9/2248 (0.47%) of all patients receiving LPs after negative head CT were found to have a vascular abnormality. There was however no data provided on the timing to CT or LP in this study.
  • Finally, not all headaches are SAH only. Certainly other life threatening etiologies exist such as meningitis/encephalitis and an LP is the gold standard test in making this diagnosis.

Clinical Take Home Point: In patients with a history consistent with SAH, normal mental status, no focal neurologic deficits, and a negative head CT performed within 6 hours, a shared decision strategy should be used as this is not a 100% sensitive strategy, but should also be balanced with the risk of complications such as post LP headache and false positive testing.

From EMRAP circa Rob:
Outpatient treatment (in younger, less severe cases), options include

  • A macrolide alone such as azithromycin, clarithromycin, or erythromycin (level I recommendation from the IDSA)
  • Doxycycline – has a level III recommendation for outpatient treatment of pneumonia from the IDSA
  • For patients with comorbidities or immune compromise:
    • Macrolide + a beta-lactam [high dose amoxicillin (1g TID) or amoxicillin-clavulanate (2g BID)]
      • An alternative to macrolides is doxycycline
      • An alternative to a beta-lactam is a 3rd generation cephalosporin
    • Monotherapy with fluoroquinolones is another option
      • Keep in mind that alternatives to fluoroquinolones should be considered due to concerns about side effects (notably, tendinopathy and neuropsychiatric effects) and bacterial resistance, which develops more quickly in the community with this class of drugs
 
I think Azithro vs Doxy is fine either way, but what I’ll do differently after reading this is to add on Amox 1g TID for patients with comorbidities.
Also worth mentioning renally dosing quinolones. Probably worth asking our pharmacist for the Rx dosing. 

From Peay via a reference article:
Each 10-ms increase in QTc contributes approximately a 5% to 7% exponential increase in risk for TdP in these patients.3,4 Therefore, a patient with a QTc of 540 ms has a 63% to 97% higher risk of developing TdP than a patient with a QTc of 440 ms. There is no threshold of QTc prolongation at which TdP is certain to occur. Data from congenital LQTS studies5,6 indicate that a QTc >500 ms is associated with a 2- to 3-fold higher risk for TdP. Likewise, case reports and small series of patients with drug-induced TdP show similar increased risk when the threshold of QTc >500 ms is exceeded.7–9
Table 2. Risk Factors for Torsade de Pointes in Hospitalized Patients

Clinically recognizable risk factors61–65
    QTc >500 ms71–74
        LQT2-type repolarization: notching, long Tpeak–Tend11,12
    Use of QT-prolonging drugs75–77
        Concurrent use of more than 1 QT-prolonging drug78–80
        Rapid infusion by intravenous route59
    Heart disease64,73,75,76
        Congestive heart failure39
        Myocardial infarction39,73
    Advanced age75,77,86
    Female sex64,72,73,75–77,79,81–85
    Hypokalemia46,74,87–90
    Hypomagnesemia89,91–94
    Hypocalcemia95,96
    Treatment with diuretics72,74,97
    Impaired hepatic drug metabolism (hepatic dysfunction or drug-drug interactions)76,79
    Bradycardia65,87
        Sinus bradycardia, heart block, incomplete heart block with pauses98,99
        Premature complexes leading to short-long-short cycles65,72
    Multiple clinically recognizable risk factors64,65,76,79,84
Clinically silent risk factors
    Occult (latent) congenital LQTS23,64
    Genetic polymorphisms (reduced repolarization reserve)26,27,31,66–69
However the total risk is low and hard to quantify there is not a lot of data for our setting and related to this question.  Especially as we don’t often continue the haldol for a prolonged period of time.
I attached and interesting article form the ED setting that looked at a qt monitoring system and the take away from the article I got is that prolonged QT was associated with an increased risk of mortality, but they didn’t find it due to Torsades and it may be a marker of sicker of sick patients.
My overall take away: Below 500 and a single dose in the ed you are probably fine.  Consider correcting the K  if below 3.5.  Be careful with prolonged use and dosing amount. Many studies show that people with prolonged QT have an increased risk of death overall but Torsades is not necessarily the cause.   It is not clear if changing meds decreases these risks.  However people with at prolonged QT may die for many other reasons and the finger may get pointed at you!