A Comfortable Miss Rate? Who Needs an LP after CT?

Clinical Scenario: A middle-aged man with a history of hypertension, diabetes mellitus, obesity, and peripheral vascular disease presents to the ED after an episode of syncope about 30 minutes ago. He is now completely alert and oriented and complains of a severe headache. Your initial workup, including basic labs, EKG, troponin, and non-contrast head CT, is unremarkable, and you prepare to admit him for observation and an inpatient syncope workup. The hospitalist service calls back to request a lumbar puncture to rule out subarachnoid hemorrhage before the patient comes up to the floor. Should you get the LP?

Clinical Question: In patients with a non-diagnostic non-contrast head CT, is a lumbar puncture necessary to completely rule out subarachnoid hemorrhage?

Literature Review:  In medical school, we all learn that head CT alone is not sufficient to rule out a subarachnoid hemorrhage (SAH) in a patient with a sufficiently suspicious history- you also need a lumbar puncture (LP), to evaluate for blood in the CSF or xanthochromia. On standardized tests, no patient with risk factors and a sudden-onset headache gets to escape the LP needle… but is this the right way to go about things in clinical practice?

Most experts and clinical guidelines continue to recommend LP after negative head CT in patients at high risk of SAH. In the 2012 guidelines for the diagnosis and treatment of SAH, the American Heart Association and American Stroke Association recommend that “head CT, if nondiagnostic, should be followed by lumbar puncture (Class I, Level of Evidence: B).”[1] This recommendation is based mainly on older studies demonstrating decline in the sensitivity of head CT over the course of days.

However, newer studies using modern multi-detector CT scanners may have identified a subclass of patients in whom an LP is not required to rule out SAH.  Perry and colleagues performed a multi-center prospective cohort study to assess the sensitivity of modern third-generation CT in ED patients being evaluated for SAH [2]. Patients presenting to 11 Canadian tertiary care referral centers between November 2000 and December 2009 with suspected SAH were prospectively enrolled. Alert (GCS=15) patients over 15 years of age presenting with non-traumatic acute headache or syncope associated with headache were included in the study. Exclusion criteria included the presence of focal neurologic deficits or papilledema, known history of CNS abnormality (such as neoplasm, aneurysm, or shunt), recurrent headaches, and transfer from another center with an established diagnosis of SAH. The gold standard for diagnosis of SAH was subarachnoid blood on non-contrast head CT, any visually identified xanthochromia on CSF analysis, or RBCs in the final tube of CSF collected AND aneurysm identified on CT angiography. A major weakness of the study was that not all patients enrolled had both a head CT and a lumbar puncture. In an attempt to correct for this weakness, all patients who did not have a definitive diagnosis based on neuroimaging OR a negative LP were followed for six months to ascertain their outcomes. By the conclusion of the study, 3,132 patients had been enrolled; of these, 240 had confirmed SAH. For all comers, the sensitivity of head CT was 92.9% (95% CI 89.0%-95.5%) and the negative predictive value was 99.4% (99.1%-99.6%). However, for patients who were scanned within six hours of headache onset, the sensitivity of head CT was 100% (97.0%-100%), and the negative predictive value was 100% (99.5%-100%). Likelihood ratios were not reported; however, using data available in the paper, they were calculated as a negative likelihood ratio of 0.07 (0.05-0.11) for all comers, and an impressive 0.00 (0.00-0.03) for patients scanned within six hours of headache onset. 

The results of this study were later replicated by Backes and colleagues [4]. In this retrospective single-center cohort study, patients presenting to the ED with a history suspicious for SAH between 2005 and 2012 were enrolled. Patients with clinical suspicion of a non-traumatic SAH and a normal level of consciousness (GCS=15) were included. Exclusion criteria included unknown time of symptom onset, focal neurologic deficits on presentation, referral from another hospital with a confirmed diagnosis of SAH, and LP in the month before presentation. At the study site, all patients with suspicion of SAH undergo non-contrast head CT, and all patients with a nondiagnostic head CT undergo LP with CSF analysis at least 12 hours after symptom onset; patient databases were reviewed to generate a study population of 250 patients who met criteria.  In all comers, head CT had a sensitivity of 95.4% (89.5%-98.5%), negative predictive value of 96.6% (92.2%-98.9%), and negative likelihood ratio of 0.05 (0.02-1.11). In patients scanned within 6 hours of symptom onset, sensitivity was 98.5% (92.1%-100%), negative predictive value 98.6% (92.3%-100%), and negative likelihood ratio 0.02 (0.00-0.10). In fact, only one patient with a non-diagnostic head CT had any findings on LP; this was a patient with atypical symptoms who was subsequently found to have a bleeding cervical AVM. The authors conclude that in patients with typical symptoms who present and are scanned within six hours of headache onset, there is no need for an LP after non-diagnostic head CT to rule out SAH. Weaknesses of this study included its small sample size and retrospective design.

There are, of course, many patients who still warrant an LP after non-diagnostic head CT. Patients with an altered level of consciousness or focal neurologic deficits were excluded from the above studies and require more intensive diagnostics. These findings are not generalizable to patients with an unknown time of symptom onset, significant anemia, pediatric patients, or patients who present to community centers that lack 24/7 coverage by experienced neuroradiologists—note that both studies were performed at academic tertiary referral centers. Some experts also raise the possibility that stopping the ED workup after a non-diagnostic head CT might miss minor “sentinel” bleeds [5], citing a 1987 study showing that head CT missed “sentinel” bleeds in 55% of patients, while LP, when performed, was positive in all patients later diagnosed with SAH[6]. However, this study was performed in 1987, prior to the introduction of modern third-generation CT scanners, and any attempt at replication would likely show improved testing characteristics for CT alone.

Clinical Takehome : In alert adult patients with a suspected non-traumatic SAH and no focal neurologic deficits who are scanned within 6 hours of symptom onset, a non-diagnostic head CT is sufficient to exclude SAH in patients with a low to moderate pre-test probability of SAH.

Submitted by Kevin Baumgartner, PGY-1
Faculty Reviewed by Brian Cohn

Additional related #FOAMed resources:
LP for subarachnoid hemorrhage: The 700 Club
SGEM #134: on what British docs say about LP    

References: 
1. Connolly et al. “Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guide for healthcare professionals from the American Heart Association/American Stroke Association.” Stroke 2012 Jun; 43(6): 1711-1737 
2. Perry 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 
3. Alan Schwartz. “Diagnostic Test Calculator.” Department of Medical Education, University of Illinois at Chicago. [http://araw.mede.uic.edu/cgi-bin/testcalc.pl] 
4. Backes et al. “Time-dependent characteristics of head computed tomography in patients suspected of nontraumatic subarachnoid hemorrhage.” Stroke 2012 Aug; 43(8):2115-9 
5. Singer RJ, Ogilvy CS, Rodorf G. “Clinical manifestations and diagnosis of aneurysmal subarachnoid hemorrhage.” UpToDate. Literature review complete through September 2015; article last updated September 2013. 
6. Leblanc R. “The minor leak preceding subarachnoid hemorrhage.” J Neurosurg 1987; 66(1):35

Consultant Teachings No. 4: "I'm Dizzy"

 
Clinical Scenario: It’s 3 AM in the ED when a 70 year old male with a history of hypertension comes in complaining of dizziness. You spend 10 minutes trying to get him to describe his dizziness, getting various descriptions of “lightheaded”, “spinning”, “imbalanced”, with him eventually saying “I’m just dizzy doc!!!”. The dizziness was described as sudden onset and had been constant for an hour, but had spontaneously resolved on arrival to the ED. During the episode, he had difficulty standing and stated that it felt like he would fall if he "didn’t hold onto something". He also noted some mild nausea and diaphoresis. Finally, he complained of a headache, though he has a long history of similar headaches. His initial head CT showed no acute process. 

Clinical Question: How do you evaluate a patient with acute dizziness?

Discussion & Literature Review: 
Dizziness and vertigo make up about 4% of chief complaints in the emergency department (ED) [1]. This chief complaint can be caused by pathology in many different body systems, and that pathology can range from benign to acutely life-threatening. For patients presenting to an ED with dizziness, affected systems include otologic/vestibular (32.9%), cardiovascular (21.1%), respiratory (11.5%), and neurologic (11.2%) as the top four diagnostic groups [2].

Dizziness Conundrum: Despite dizziness being a relatively common complaint, it can be very challenging to work up and manage. Traditional teaching on the evaluation of dizziness is to rely heavily on the quality of the dizziness, whether it is “spinning”, “lightheaded” or other similar descriptors [3]. However, this has been shown to be an ineffective means of establishing a differential diagnosis and may lead to dangerous misdiagnosis. Emergency department physicians (including residents) have been specifically studied and found to demonstrate over-reliance on symptom quality leading to subsequent high-risk reasoning [4,5]. There is also evidence that patients with the two most common vestibular disorders (benign paroxysmal positional vertigo (BPPV) and acute peripheral vestibulopathy) are often managed sub-optimally both in terms of diagnostic testing and prescribed treatment in the ED [6]. These studies suggest an opportunity to improve the emergency management of dizzy patients. 

History is Everything In the Dizzy Patient: As in all of medicine, obtaining an accurate and useful history is the single most important step in establishing the diagnosis of a patient with dizziness. The quality of dizziness lacks specificity in ED patients; one study found that patients describe their dizziness in multiple ways if given multiple options, may change their description of the dizziness if asked again only 5-10 minutes after initial questioning, and answer open-ended questions with vague or circular answers [7]. 

As opposed to the quality of symptoms, patients have been found to more reliably answer questions about the timing and triggers of their dizziness. This had led to the formulation of the “timing and triggers” model of history taking in the evaluation of a dizzy patient [8]. The goal of history-taking in this model is to identify the patient as having one of four syndromic patterns of dizziness:

· acute, spontaneous, prolonged (also known as the acute vestibular syndrome) 
· episodic, positional 
· episodic, spontaneous 
· chronic unsteadiness [8]. 

When asking about timing, attempt to clarify whether the dizziness is sudden or gradual onset, episodic or continuous, the duration of symptoms, and the frequency of symptoms. If the symptoms are episodic, clarify how long each episode lasts (seconds, minutes, hours, days) and make sure to ask if they completely return to normal between episodes or if they have constant symptoms with exacerbations. When asking about triggers, it is important to define true triggers as opposed to exacerbating factors. A common exacerbating factor is any form head movement, which generally worsens all forms of acute vestibular dizziness, so does not often help establish a diagnosis. However, if specific movements (i.e. rolling over in bed or changing posture) trigger the dizziness, this can lead to a diagnosis.  

Examination Tools and Tips: On physical examination, general medical and neurologic screening exams are important. Focal abnormalities on these exams may suggest a diagnosis (i.e. unilateral weakness or ataxia may suggest stroke, new cardiac murmur may suggest myocardial infarction or aortic dissection). However, there are specific physical exam maneuvers that can also be performed. The most commonly employed is the Dix-Hallpike maneuver to evaluate for benign paroxysmal positional vertigo (BPPV). This should be employed only if the patient describes episodic dizziness. The Dix-Hallpike maneuver will worsen the already-present spontaneous nystagmus during the acute vestibular syndrome, but this should not be taken as a positive test. The other test an ED provider should be familiar with is the HINTS-Plus exam [9]. This is a three step test of skew deviation, nystagmus, and head impulse testing (video links to a positive head impulse test, which suggests a peripheral etiology) combined with an assessment for unilateral hearing loss. This test is concerning for a central etiology with the presence of skew deviation, direction changing or vertical nystagmus, a negative head impulse test, and/or new unilateral hearing loss. In the evaluation of the acute vestibular syndrome, this bedside test is more accurate in the acute setting than MRI for diagnosing a posterior circulation stroke. Another physical exam pearl is that some patients can suppress nystagmus with visual fixation, so removing fixation can bring out their nystagmus. An easy way to do this is to turn off the lights and use your ophthalmoscope, which will block fixation and give you a magnified view of the eye for easier visualization of the nystagmus.

Summary and differential diagnosis: Once a patient’s complaints have been characterized by history as one of the four syndromic patterns discussed above, the differential diagnosis is much more limited. The physical examination assesses for specific diagnoses, which then guides further workup and treatment.

Source: Newman-Toker, D. E., Symptoms and signs of neuro-otologic disorders, Continuum (Minneap Minn), 2012, 18(5 Neuro-otology):1016-1040.

Submitted by Alex Dietz, Neurology PGY-4
Faculty Reviewed by Peter Panagos
Everyday EBM Editor: Maia Dorsett, PGY-4

References
[1] Saber Tehrani, A. S., Coughlan, D., Hsieh, Y. H., Mantokoudis, G., Korley, F. K., Kerber, K. A., Frick, K. D., et al., Rising annual costs of dizziness presentations to U.S. emergency departments, Acad Emerg Med, 2013, 20(7):689-696.
[2] Newman-Toker, D. E., Hsieh, Y. H., Camargo, C. A., Pelletier, A. J., Butchy, G. T. and Edlow, J. A., Spectrum of dizziness visits to US emergency departments: cross-sectional analysis from a nationally representative sample, Mayo Clin Proc, 2008, 83(7):765-775.
[3] Kerber, K. A. and Newman-Toker, D. E., Misdiagnosing Dizzy Patients: Common Pitfalls in Clinical Practice, Neurol Clin, 2015, 33(3):565-575.
[4] Newman-Toker, D. E., Charted records of dizzy patients suggest emergency physicians emphasize symptom quality in diagnostic assessment, Ann Emerg Med, 2007, 50(2):204-205.
[5] Stanton, V. A., Hsieh, Y. H., Camargo, C. A., Edlow, J. A., Lovett, P. B., Lovett, P., Goldstein, J. N., et al., Overreliance on symptom quality in diagnosing dizziness: results of a multicenter survey of emergency physicians, Mayo Clin Proc, 2007, 82(11):1319-1328.
[6] Newman-Toker, D. E., Camargo, C. A., Hsieh, Y. H., Pelletier, A. J. and Edlow, J. A., Disconnect between charted vestibular diagnoses and emergency department management decisions: a cross-sectional analysis from a nationally representative sample, Acad Emerg Med, 2009, 16(10):970-977.
[7]Newman-Toker, D. E., Cannon, L. M., Stofferahn, M. E., Rothman, R. E., Hsieh, Y. H. and Zee, D. S., Imprecision in patient reports of dizziness symptom quality: a cross-sectional study conducted in an acute care setting, Mayo Clin Proc, 2007, 82(11):1329-1340.
[8] Newman-Toker, D. E., Symptoms and signs of neuro-otologic disorders, Continuum (Minneap Minn), 2012, 18(5 Neuro-otology):1016-1040.
[9] Saber Tehrani, A. S., Kattah, J. C., Mantokoudis, G., Pula, J. H., Nair, D., Blitz, A., Ying, S., et al., Small strokes causing severe vertigo: frequency of false-negative MRIs and nonlacunar mechanisms, Neurology, 2014, 83(2):169-173.
 
Title Image source: wikipedia.

If There's a Delay, Consider TXA: On Anti-fibrinolytic Therapy for Management of Aneurysmal Subarachnoid Hemorrhage

Clinical Scenario: While working in a community emergency department you see a middle aged otherwise healthy female who developed a thunderclap headache two hours ago while lifting weights.  She is very nauseated, has intermittent vomiting, but is able to respond to your questions. An emergent Head CT shows subarachnoid hemorrhage involving the suprasellar, interpeduncular, and ambient cisterns with associated ventriculomegaly.  You call the neurosurgeon at the closest tertiary care hospital and he asks whether you considered giving tranexamic acid (TXA) prior to transport.

 
Clinical question: Does TXA improve outcomes for patients with spontaneous subarachnoid hemorrhage? Does it increase the risk for thrombotic event/stroke? 

Literature Review: 
In people who suffer from aneurysmal subarachnoid hemorrhage, rebleeding is a cause of significant death and disability, peaking in incidence 24 hrs from the initial presenting event [1].   More than a third of rebleeding events occur within 3 hrs and more than half within 6 hrs [2].  It is thought that part of the mechanism of rebleeding is dissolution of the clot at the site of the aneurysm.  While securing the aneurysm via coiling or clipping is the standard of care to prevent rebleeding, in instances where there is an delay of care is unavoidable, it was been postulated that anti-fibrinolytic therapy, which may mitigate this process, may decrease the incidence of rebleeding.

One form of anti-fibrinolytic therapy is TXA, a synthetic analog of the amino acid lysine that works as a hemostatic agent by binding to the lysine binding sites on plasminogen, thereby competitively inhibiting its conversion to plasmin and subsequently fibrin degradation.  Existing studies suggest that TXA decreases bleeding in menorrhagia and cardiopulmonary bypass, as well as to improves mortality in trauma patients dying of massive hemorrhage [3,4,5,6].  Does this hemostatic benefit apply to spontaneous subarachnoid hemorrhage?

A large number of studies regarding anti-fibrinolytic therapy for aneurysmal subarachnoid hemorrhage have been published.    These were assessed in a 2013 Cochrane meta-analysis aimed at addressing the overall clinical effects of such therapies on rates of rebleeding and overall morbidity/mortality in aneurysmal SAH [7].  This was prompted in part because of concern that even if antifibrinolytics decreased risk of rebleeding, this would be offset by an increased risk of cerebral ischemia, which tends to develop between 4-14 days after initial SAH.  The Cochrane review included only randomized trials that compared antifibrinolytic to placebo vs. control and assessed subsequent outcomes on an intention to treat basis.   Their systematic review included 10 studies [with a pooled patient sample of 1904 who received TXA, 597 placebo, and 348 control].  Nine of these studies used TXA as the antifibrinolytic agent and one used epsilon-amino-caproic acid (39 patients).  These studies were extremely heterogeneous in their anti-fibrinolytic treatment regimens.  One study treated for less than 72 hrs (before onset of potential cerebral ischemia) [8] and others treated up to six weeks (through peak time of cerebral ischemia).  Two of the studies concurrently treated patients with therapy (such as nimodipine) to reduce the risk of cerebral ischemia [8,9].  Their analysis found that that TXA did not affect the overall morbidity (risk of poor outcome was RR 1.02; 95% 0.91-1.15) or mortality (death from all causes RR 1.00; 95% CI 0.85-1.18). Administration of TXA did decrease the risk of rebleeding (RR 0.65, 95% CI 0.44 to 0.97; 78 per 1000 people), but this was offset by the increased the risk of cerebral ischemia (RR 1.41, 95% CI 1.04 to 1.91; 83 per 1000 people). 

There was was considerable heterogeneity between the older studies and the newer studies, which may be attributed to newer studies using specific treatments to prevent the risk of cerebral ischemia. 

While this overall analysis suggests that TXA may not significantly benefit long term outcome in aSAH, the majority of the studies administered the drug for a prolonged period time of > 10 days, at which point definitive aneurysmal treatment via endovascular or surgical intervention should be achieved.  One study examined short term  (mean of 15.3 +/- 16 hrs) use of an anti-fibrinolytic therapy (E-Aminocaproic acid - EACA) on risk of rebleeding, mortality and favorable neurologic outcome at 3 months [10].  They prospectively studied 248 patients with aSAH.  Patients were not randomized, but the two groups were similar with regard to baseline characteristics predictive of rebleeding risk and neurologic outcome, including anticoagulation and Hunt-Hess grade (with the exception of blood pressure which was not assessed).  The authors compared the outcomes of 73 patients who received EACA with those of 175 patients who did not.  They found that there was a significant decrease in rebleeding in EACA-treated patients (2.7% vs. 11.4%), as well as a general trend towards favorable neurologic outcome in those who received anti-fibrinolytic therapy.  While we will continue to await randomized, placebo-controlled trials to determine if (and which) antifibrinolytic therapy improves outcome for patients with aSAH, the AHA/ASA guidelines have incorporated anti-fibrinolytic therapy into the recommendations for medical measures to prevent rebleeding [2]:

Current AHA/ASA Guidelines for Medical Management to Prevent Rebleed in Aneurysmal SAH (Ref 2)

  Take home: TXA may reduce the risk of rebleeding in aneurysmal subarachnoid hemorrhage, but current evidence does not strongly support a benefit regarding survival or morbidity.   In studies using prolonged anti-fibrinolytic therapy, the benefit conferred by decreased risk of rebleed was offset by increase in cerebral ischemia.  However, more recent trials of short-term antifibrinolytic therapy have had promising, but far from definitive results.  Current AHA/ASA guidelines encourage its use for patients who will have a delay in aneurysm obliteration.

Submitted by Melissa Kroll, PGY-3
Edited by Maia Dorsett, PGY-4
Faculty Reviewed by Peter Panagos  


References
1.Guo, L. M., Zhou, H. Y., Xu, J. W., Wang, Y., Qiu, Y. M., & Jiang, J. Y. (2011). Risk factors related to aneurysmal rebleeding. World neurosurgery, 76(3), 292-298.
2. Connolly, E. S., Rabinstein, A. A., Carhuapoma, J. R., Derdeyn, C. P., Dion, J., Higashida, R. T., ... & Vespa, P. (2012). Guidelines for the management of aneurysmal subarachnoid hemorrhage a guideline for healthcare professionals from the American heart association/American stroke association. Stroke, 43(6), 1711-1737.
3. Jimenez, J. J., Iribarren, J. L., Lorente, L., Rodriguez, J. M., Hernandez, D., Nassar, I., ... & Mora, M. L. (2007). Tranexamic acid attenuates inflammatory response in cardiopulmonary bypass surgery through blockade of fibrinolysis: a case control study followed by a randomized double-blind controlled trial. Crit Care, 11(6), R117.
4. Lethaby, A., Farquhar, C., & Cooke, I. (2000). Antifibrinolytics for heavy menstrual bleeding (Cochrane Review). The Cochrane Library, (4).
5. Williams-Johnson, J. A., McDonald, A. H., Strachan, G. G., & Williams, E. W. (2010). Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2) A randomised, placebo-controlled trial. The West Indian medical journal, 59(6), 612-624.
6. Morrison, J. J., Dubose, J. J., Rasmussen, T. E., & Midwinter, M. J. (2012). Military application of tranexamic acid in trauma emergency resuscitation (MATTERs) study. Archives of surgery, 147(2), 113-119.
7.Baharoglu, M. I., Germans, M. R., Rinkel, G. J., Algra, A., Vermeulen, M., van Gijn, J., & Roos, Y. B. (2013). Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage. The Cochrane Library.
8.Hillman, J., Fridriksson, S., Nilsson, O., Yu, Z., Säveland, H., & Jakobsson, K. E. (2002). Immediate administration of tranexamic acid and reduced incidence of early rebleeding after aneurysmal subarachnoid hemorrhage: a prospective randomized study. Journal of neurosurgery, 97(4), 771-778.
9.Roos, Y. B. W. E. M., & STAR Study Group. (2000). Antifibrinolytic treatment in subarachnoid hemorrhage A randomized placebo-controlled trial. Neurology, 54(1), 77-77.
10. Starke, R. M., Kim, G. H., Fernandez, A., Komotar, R. J., Hickman, Z. L., Otten, M. L., ... & Connolly, E. S. (2008). Impact of a protocol for acute antifibrinolytic therapy on aneurysm rebleeding after subarachnoid hemorrhage. Stroke, 39(9), 2617-2621.

An Imperfect Science: Diagnosis of CSF Shunt Malfunction

Clinical scenario: Your patient is a 20 yo male with a history of VP shunt placement as a child for obstructive hydrocephalus. He was brought to the emergency department by his family because of decreased responsiveness over the past day. On arrival to the emergency department, he has aniscoria (L greater than R), no verbal response, and withdraws his extremities symmetrically. An emergent non-contrast head CT shows no change in ventricular size from prior CT scan one year prior and a VP shunt series demonstrates no evidence of fracture of the shunt line. Clearly, something is critically wrong with the patient, but is it his VP shunt to blame?

Clinical question: What is the spectrum of shunt complications? What is the sensitivity of clinical exam and various imaging modalities in detecting shunt malfunction?

Literature Review: There are multiple forms of CSF shunts, the most common of which is the Ventriculo-Peritoneal shunt (as opposed to ventriculo-atrial & ventriculo-pleural) which shunts CSF into the peritoneal cavity. A CSF shunt is composed of a proximal catheter, reservoir, valve and distal catheter [1]. The proximal catheter starts in the frontal horn of the lateral ventricle and exits through a burr hole to connect to the reservoir which is located in the subcutaneous tissue (this is what is accessed when neurosurgery taps a shunt). Flow from the reservoir to the distal catheter is regulated by a one way valve. Programmable shunts allow for the setting of a specific pressure above which fluid drains through a valve. This is sometimes adjusted in one direction or another for VP shunt patients who experience headaches, lightheadedness or other symptoms related to the pressure when their evaluation is negative for obstruction, infection etc. For VP shunts, the distal catheter is then tunneled into the peritoneum

Image Source: Cancer Research UK / Wikimedia Commons

As an emergency physician, one must be familiar with the presentation and diagnosis of shunt complications because they are relatively common; incidence of VP shunt failure is close to 40% at one year and 50% at two years from initial shunt placement, at least in the pediatric population where it has been most actively studied[2]. There are multiple types of shunt malfunctions leading to increased intracranial pressure, including but not limited to:

1. Mechanical Obstruction - Most proximally, the catheter can be obstructed by blood, debris or in-growth of the choroid plexus. The catheter position within the lateral ventricle can also migrate. Kinking or fracture along the catheter track at any point will also lead to shunt failure, as will distal obstruction which can occur when the catheter adheres to the omentum or erodes into intra-abdominal organs.

2. Infection - This often presents with shunt failure, and occurs most commonly within 6 months of placement due to intraoperative contamination with skin flora. The overall incidence of shunt infection is common (8-10%).

3. Ventricular Loculations - Loculations within the ventricle can create non-communicating pockets of CSF that are not drained by the VP shunt. If these grow, they can cause symptoms of hydrocephalus.

At least in very young children, depressed level of consciousness, nausea/vomiting, headache, irritability, and fluid tracking along the shunt site are highly predictive of shunt malfunction (see positive LR below). However, none of these clinical signs and symptoms are adequately sensitive to rule out shunt malfunction in their absence [2,3]. Some signs like abdominal pain/peritonitis are less commonly seen, but more highly predictive of shunt infection.

LR, Sensitivity, & Specificity for clinical signs and symptoms associated with shunt failure in two large pediatric studies

In addition to overall clinical exam and picture, radiographic imaging plays a central role in the emergency department evaluation of VP shunt malfunction.

CT scans are the most commonly used imaging modality to evaluate for shunt malfunction. While enlarged ventricles (when compared with prior imaging studies) are the canonical feature of shunt obstruction, other CT findings correlated with increased intracranial pressure include effacement of the cortical sulci, loss of the basal cisterns and periventricular edema due to transependymal CSF absorption [4]. Based on multiple retrospective pediatric studies using surgical shunt revision as a "gold standard", CT has a sensitivity for shunt malfunction of anywhere between 53% to 92% [4,5; see Table below]. In one small retrospective study of 174 adults evaluated for shunt malfunction with both shunt series and head CT, head CT had a sensitivity of only 52%, a specificity of 78% and negative predictive value of 88% for shunt malfunction [6]. This study only included patients who had had shunt series performed, so it may have underestimated the sensitivity of CT by excluding patients who were evaluated with CT alone. While this is a wide range of estimations for sensitivity, the important point is that a negative head CT does not completely rule out a shunt malfunction.

Shunt series radiographs are used to identify mechanical shunt defects such as shunt discontinuity or kinking. Studies in both children [4,7] and adults [6] support the conclusion that although the yield and sensitivity of radiographic shunt series is very low (see Table below), it is not zero. Shunt series rarely (~ 1-2%) detect abnormalities not identified on initial CT that prompt surgical revision. Therefore, shunt series are still indicated in the evaluation of potential shunt malfunction.

Table 2 from Boyle and Nigrovic, 2015. Reference 4.

In some cases, more commonly in pediatric institutions, MRI protocols have been instituted to reduce cranial radiation in children [4,8,9]. This has been made possible in part due to advances in MRI technology that have allowed for development of "ultra-fast" or Rapid MRI protocols that can acquire images in a span of ~ 1-4 minutes. Rapid Cranial MRI has been studied in comparison to CT for detection of ventricular shunt malfunction in the pediatric population, and appears to be comparable at least with respect to specificity and accuracy [8]. When considering using MRI in place of CT, the provider should be aware that some VP shunts have a programmable shunt valves that can be affected by the magnetic force of the MRI machine and may need to be readjusted after the exam. For this reason, it is common practice to obtain coned-down radiographs of a small indicator usually located near the proximal portion of the distal catheter to identify the setting prior to MR and then again after MR. If the programmed setting has changed, the neurosurgeon can use a magnet to reprogram the setting. The radiologist uses an indicator that looks like a clockface to determine the settings. 

Image source: http://www.ajnr.org

Take home Points: Malfunction and infection are common complications of CSF shunts. No single clinical exam finding or image study is sufficient to rule out shunt malfunction, and clinical management should take into account patient history, overall clinical picture, diagnostic data and neurological assessment.
 
Submitted by Maia Dorsett @maiadorsett
Faculty Reviewed by Peter Panagos and Richard Griffey
 
References: 
1. Wallace, A. N., McConathy, J., Menias, C. O., Bhalla, S., & Wippold, F. J. (2014). Imaging Evaluation of CSF Shunts. American Journal of Roentgenology, 202(1), 38-53.
2.Garton, H. J., Kestle, J. R., & Drake, J. M. (2001). Predicting shunt failure on the basis of clinical symptoms and signs in children. Journal of neurosurgery, 94(2), 202-210.
3. Piatt Jr, J. H., & Garton, H. J. (2008). Clinical diagnosis of ventriculoperitoneal shunt failure among children with hydrocephalus. Pediatric emergency care, 24(4), 201-210.
4. Boyle, T. P., & Nigrovic, L. E. (2015). Radiographic Evaluation of Pediatric Cerebrospinal Fluid Shunt Malfunction in the Emergency Setting. Pediatric emergency care, 31(6), 435-440.
5.Lehnert, B. E., Rahbar, H., Relyea-Chew, A., Lewis, D. H., Richardson, M. L., & Fink, J. R. (2011). Detection of ventricular shunt malfunction in the ED: relative utility of radiography, CT, and nuclear imaging. Emergency radiology, 18(4), 299-305.
6. Griffey, R. T., Ledbetter, S., & Khorasani, R. (2007). Yield and utility of radiographic “shunt series” in the evaluation of ventriculo-peritoneal shunt malfunction in adult emergency patients. Emergency radiology, 13(6), 307-311.
7. Desai, K. R., Babb, J. S., & Amodio, J. B. (2007). The utility of the plain radiograph “shunt series” in the evaluation of suspected ventriculoperitoneal shunt failure in pediatric patients. Pediatric radiology, 37(5), 452-456.
8.Boyle, T. P., Paldino, M. J., Kimia, A. A., Fitz, B. M., Madsen, J. R., Monuteaux, M. C., & Nigrovic, L. E. (2014). Comparison of rapid cranial MRI to CT for ventricular shunt malfunction. Pediatrics, 134(1), e47-e54.
9. Koral, K., Blackburn, T., Bailey, A. A., Koral, K. M., & Anderson, J. (2012). Strengthening the argument for rapid brain MR imaging: estimation of reduction in lifetime attributable risk of developing fatal cancer in children with shunted hydrocephalus by instituting a rapid brain MR imaging protocol in lieu of head CT. American Journal of Neuroradiology, 33(10), 1851-1854.10.

Consultant Teachings No. 1: Acute Neuromuscular Respiratory Failure

Clinical Scenario: You are working in EM 2. It’s 3 AM and a 32 year old woman is roomed with the chief complaint of shortness of breath. She has been getting progressively more short of breath for the past 2 days. She’s also noticed that she just can’t keep her eyes open, though her right eyelid droops more than her left. You notice her head is falling forward. When you question her about that, she says she has had trouble holding it up for 4 days. Your general exam is normal, with no wheezing and normal heart sounds. Her neuro exam shows weakness on eye closure, neck flexion, and neck extension. She has no weakness anywhere else.

Clinical Question: How should acute neuromuscular respiratory failure be evaluated and managed?

Literature Review:
Neuromuscular respiratory failure is relatively rare but constitutes a medical emergency with significant morbidity and mortality, particularly with delays in recognition. The most common causes are acute inflammatory demyelinating polyneuropathy (e.g. Guillain-Barre syndrome, GBS) myasthenia gravis (MG), motor neuron disease (e.g. amyotrophic lateral sclerosis, ALS) and some forms of myopathy. A study in Northern Ireland found the causes of acute respiratory failure due to neuromuscular conditions were GBS (62%), MG (18%), ALS (9%), then a variety of other conditions (2, 3). Early recognition of these conditions by history and physical exam, combined with specific bedside testing, can help appropriately triage and manage these patients. GBS has an incidence of 1-4 per 100,000 and represents the most common cause of acute paralysis. It is also often missed early in the disease, with patient’s requiring an average of 2 ED visits before diagnosis [1]. GBS can progress from symptom onset to respiratory failure in 48 hours, so early identification is important. The mechanism of respiratory failure is loss of activity of the diaphragm and accessory muscles of respiration, and can often be complicated by aspiration due to craniobulbar weakness. The diaphragm is innervated by the phrenic nerve, derived from the C3-5 nerve roots (remember: “C3, 4, and 5 keep you alive”).

The initial evaluation should begin with a careful history, including the time from symptom onset to ED presentation. When taking the history, it is important to ask specifically about:

1) Drooping eyes (ptosis)

2) Double vision (diplopia)

3) Change in speech (breathy or nasal)

4) Difficulty swallowing including nasal regurgitation (food/liquid coming out the nose)

5) Fatigue with chewing

6) Head drop (inability to support their head)

All of these can be findings of bulbar and high cervical spine pathology, and can be warning signs for impending respiratory failure. The history should also include characterization of weakness in other places (i.e. leg or arm weakness), sensory symptoms (ascending numbness or paresthesias) and autonomic symptoms (new-onset orthostatic symptoms, bowel or bladder retention/incontinence, changes in sexual functioning).

On physical exam, after doing a routine medical exam, specifically test:

1) Eye movements (looking for impairment of extraocular musculature)

2) Eye closure strength

3) Mouth closure strength

4) Tongue strength and palate elevation

5) Assess for a weak cough

6) Neck flexion and extension strength

7) Breath count (ask the patient to count up at a rate of one number per second after taking a full breath. This is a crude estimate of vital capacity, with each number being ~100 ml.)

Numbers 1-5 detect craniobulbar weakness. Neck flexion and extension are well correlated with diaphragmatic strength. Neck flexion weakness correlates with impaired respiratory function, while neck extension weakness should be considered a warning sign of impending respiratory failure.

Laboratory testing: History and exam should guide testing, but a full set of screening labs is generally appropriate (CBC, BMP, HFP). Other bloodwork that can be obtained include CK, TSH, and ESR [4].

Respiratory therapy should measure forced vital capacity (FVC) and negative inspiratory force (NIF). FVC < 20 ml/kg (~ 1- 1.5L) or NIF < -30 cm H20 are warning signs for impending respiratory failure [5].  It is important to discuss the effort provided and the quality of the lip seal with the respiratory therapist that performs the testing.

If there is evidence of severe diaphragmatic weakness (very weak neck extension or low NIF/FVC), it is reasonable to check an ABG or VBG for hypercapnea and a respiratory acidosis, consistent with inadequate ventilation.

If there are signs of impending respiratory failure, it is important to determine if non-invasive ventilation (e.g. BiPAP) or intubation and mechanical ventilation is most appropriate. This is a decision that should be made with the consulting neurologist and with the admitting ICU. However, if the objective findings (NIF/FVC and ABG) or trajectory (rapid deterioration) are poor, it is reasonable to electively intubate in the ED instead of an emergent intubation in the ICU.  Concurrent craniobulbar weakness and/or a weak cough are relative contraindications for use of non-invasive ventilation given the increased risk of aspiration.


Intubation in patients with neuromuscular weakness carries special risks.   In myasthenia gravis, due to a complex interaction between the number of ACh receptors at the neuromuscular junction, antibodies inhibiting those receptors, and the effects of treatment such as plasmapheresis and enzyme inhibitors, neuromuscular blockade can have unpredictable effects.

Image source: http://jama.jamanetwork.com/article.aspx?articleid=200737

Myasthenia patients have net loss of AChR at the neuromuscular junction (see Figure), making these patients relatively resistant to succinylcholine.  However, in cases where myasthenic crisis is treated with plasmapharesis, which also incidentally rcmoves the enzymes required for breakdown of paralytic agents, patients can have very  prolonged neuromuscular blockade.  While the effect of succinylcholine can go either way, patients with myasthenia gravis can be extremely sensitive to nondepolarizing blockade (one study found that the effective dose of vecuronium in MG was 1/5 that in controls) [6,7].

 In addition to the unpredictable effects of neuromuscular agents, patients with neuromuscular weakness is general are at higher risk of developing critical illness myopathy following exposure to paralytics. Avoidance of any paralytic is the goal when intubating a patient with MG, so consider using topical lidocaine with a sedative such as propofol [8]. Patients with GBS often develop significant autonomic dysfunction, with concomitant extreme swings in blood pressure and heart rate [9]. Autonomic dysfunction can be exacerbated during intubation. It is important to avoid treating these swings in blood pressure and/or heart rate unless there is evidence of end organ damage. Treating these rapid swings places the patient at a high risk of iatrogenic injury when their blood pressure or heart rate spontaneously rebounds and this rebound is exaggerated by the medications provided.

Clinical Take home:1) Have a high index of suspicion for neurologic causes of respiratory failure.
2) Check craniobulbar and neck flexion/extension strength in patients in whom you suspect neuromuscular pathology.
3) Check NIF/FVC and an ABG on any patient with a suspected neuromuscular condition and dyspnea.
4) Intubate with a reduced dose of non-depolarizing agent or preferably no paralytics at all
5) Expect heart rate and blood pressure swings, especially during intubation. Don’t treat them unless there is end-organ damage, as they are likely to spontaneously resolve.

Submitted by Alex Dietz, Neurology PGY-3
Additional Review by Jennifer Griffith
Faculty Reviewed by Robert C. Bucelli (Neurology)

Everyday EBM Editor: Maia Dorsett

References:
[1]Noto A, Marcolini E. Select topics in neurocritical care. Emerg Med Clin North Am 2014;32:927-938.
[2]Carr AS, Hoeritzauer AI, Kee R, et al. Acute neuromuscular respiratory failure: a population-based study of aetiology and outcome in Northern Ireland. Postgrad Med J 2014;90:201-204.
[3]Pfeffer G, Povitz M, Gibson GJ, Chinnery PF. Diagnosis of muscle diseases presenting with early respiratory failure. J Neurol 2014.
[4]Flower O, Bowles C, Wijdicks E, Weingart SD, Smith WS. Emergency neurological life support: acute non-traumatic weakness. Neurocrit Care 2012;17 Suppl 1:S79-95.
[5]Lawn ND, Fletcher DD, Henderson RD, Wolter TD, Wijdicks EF. Anticipating mechanical ventilation in Guillain-Barré syndrome. Arch Neurol 2001;58:893-898.
[6] Roppolo, L. P., & Walters, K. (2004). Airway management in neurological emergencies. Neurocritical care, 1(4), 405-414.
[7]Martyn JA, White DA, Gronert GA, Jaffe RS, Ward JM. Up-and-down regulation of skeletal muscle acetylcholine receptors. Effects on neuromuscular blockers. Anesthesiology 1992;76:822-843.
[8]Della Rocca G, Coccia C, Diana L, et al. Propofol or sevoflurane anesthesia without muscle relaxants allow the early extubation of myasthenic patients. Can J Anaesth 2003;50:547-552.
[9]Rabinstein AA, Wijdicks EF. Warning signs of imminent respiratory failure in neurological patients. Semin Neurol 2003;23:97-104.

Hypertensive Encephalopathy

A middle age woman with  a history of chronic kidney disease and hypertension presents with chest pain and altered mental status. Paramedics note that she is having decreased responsiveness, moaning to questions, and stating only that she has pain everywhere.  Her blood pressure is 230/165 on arrival.  She is alert and oriented only to self with an otherwise nonfocal neurologic exam.  Head CT is negative for intracranial hemorrhage.  As you work through your differential, you wonder how should the diagnosis of hypertensive encephalopathy be made?  How should it be managed in the emergency department and what is the prognosis for patients who have a hypertensive crisis like this patient?

Literature Review:
In a patient with altered mental status in the setting of severe hypertension (systolic >180 or diastolic >120), a hypertensive emergency needs to be on the differential, which is defined by signs of acute end-organ damage in the setting of severe hypertension.  Examples of end-organ damage include altered mental status, pulmonary edema, elevated troponins, and acute kidney injury.  Approximately 1-2% of people with HTN will have an episode of hypertensive encephalopathy in their lifetime, which may manifest as headache, nausea, vomiting, and confusion [1].

There is little evidence in the management of a hypertensive emergency; differences in medicine choices appear mostly based on symptoms of the crisis.  Initial management of hypertensive encephalopathy is to rule out other causes for encephalopathy (ischemic stroke accounts for 25% of all hypertensive encephalopathy cases), other considerations are intracranial bleed (SAH, IPH), posterior reversible encephalopathy syndrome (PRES) or even carotid or vertebral-basilar dissection. After ruling out other causes focus should be on treating the blood pressure with a IV anti-hypertensive that can be quickly titrated, such as nicardipine or nitroprusside [2].  Blood pressure should be lowered approximately 10-20% in the emergency department, and should not be lowered more than 25% in the first day due to the risk of ischemia from dropping pressures below the brain's autoregulatory range.  Keep in mind that the diagnosis of hypertensive encephalopathy is a diagnosis of exclusion and is only confirmed retrospectively with resolution of symptoms after treating the blood pressure [3]. 

Prognosis for hypertensive emergencies is variable.  In 2009 Katz et al. looked at 1,568 patients presenting with SBP >180 or DBP >110 or those with SAH and SBP >140 to evaluate practice patterns, mortality, and complications. Over 50% required more than one anti-hypertensive for blood pressure control. In-hospital mortality in this group was 6.9%, with 90 day mortality of 11%.  59% had acute worsening of end organ damage during the hospitalization. Hypertension has a high health burden, as 37% of the patients analyzed were re-admitted with-in 90 days, of which over 25% were due to repeat “severe hypertension” [4].  Of course, patients do much better if they can take their blood pressure medicines consistently, and this was demonstrated as far back as 1958 where an old study by Dustan showed that without any anti-hypertensive treatment, the survival at 1 year for those admitted for hypertensive encephalopathy was 10-20%.  However, with adherent treatment, 5 year survival rates were 70% [5].


Take-home Points:

Hypertensive encephalopathy is a diagnosis of exclusion, retroactively diagnosed after symptoms resolve with lowering blood pressure. BP should only be lowered 10-20% in the ED. Patients with HTN encephalopathy have an in hospital mortality between 6-11% at 90 days. Mortality reduction is related to long term compliance with antihypertensives. 

References
1.  Vaughan C, Delanty N. Hypertensive emergencies. Lancet. 2000;356:411–7.
2.  Price RS, Kasner SE. Hypertension and hypertensive encephalopathy. Handb Clin Neurol. 2014;119:161-7.
3.  Manning L, Robinson TG, Anderson CS. Control of blood pressure in hypertensive neurological emergencies. Curr Hypertens Rep. 2014 Jun;16(6):436.
4.  Katz JN, et al. Practice patterns, outcomes, and end-organ dysfunction for patients with acute severe hypertension: the Studying the Treatment of Acute hyperTension (STAT) registry.  Am Heart J. 2009 Oct;158(4):599-606.
5.  Dustan HP, Schneckloth RE, Corcoran AC, Page IH. The effectiveness of long-term treatment of malignant hypertension. Circulation. 1958 Oct;18(4 Part 1):644-51.

Submitted by Melissa Kroll, PGY-2
Edited by Philip Chan, PGY-2 & Louis Jamtgaard, PGY3 @lgaard
Faculty reviewed by Joan Noelker

EKG Challenge #8 Case Conclusion - The Way to the Heart is through the BRAIN

A middle-aged female is brought in by EMS yelling and thrashing on a stretcher.  Per report, she was found unresponsive next to the couch by her daughter.  She was given 2mg of IM Narcan and woke up a bit and has been agitated ever since.  You just begin your assessment and order some labs before you are pulled away to two Level I traumas and an impending respiratory arrest.  As you head back to the patient's room to complete your assessment, you receive a "critical value" phone call from the chemistry lab.  You are told that your patient has a troponin of 0.65.

After thinking to yourself, "Oh S--- I didn't expect that, not even 100% sure why I ordered it", you realize that you have not yet seen the EKG.  It's not in the chart, so you hurry to her room to find a nurse and security wrestling with  half-naked agitated patient who is trying to stand up on the stretcher and grab on to the light fixture above.  You call your attending and he agrees "that THIS" (turning to the wrestling match) "is not going to work."  You decide to intubate her to facilitate your greatly expanded workup for altered mental status.  Post intubation, you get this EKG:

When you first look at the EKG nothing in particular really jumps out at you.   There are some T wave inversions in I and avL,  as well as a biphasic T wave in V2. Sure that there is something more, you decide to take a moment and go through it systematically.  When you get to examining the intervals, everything on the surface looks fine, but you remember reading on Steve Smith's ECG blog that calculating the QT interval can be tricky (especially for computers) and decide to calculate it yourself:

To calculate the QT interval, you start by drawing a line along the maximum slope of the T wave  and marking where it intersects the isoelectric line.  The distance from the preceding Q wave to this intersection point is the  QT interval :

To calculate the corrected QT (QTc), you  use Barrett's formula and divide the QT interval in milliseconds by the square-root of the preceding RR interval (in seconds).   In the case of our patient, the QTc is 525 ms, prolonged by any standard.

While you are running through your differential for altered mental status + positive troponin + prolonged QT, the patient is taken get a head  CT.  You go with her and recognize the subarachnoid hemorrhage star of death as it appears on the screen of the CT tech in front of you:

Neurosurgery emergently places a ventriculostomy drain and the patient is admitted to the Neuro ICU.   When you go home after your shift, your brain is buzzing, making sleep impossible.  You've heard the term "neurocardiogenic" injury before and decide to look into this interesting brain-heart connection.

Neurocardiogenic injury is a term used to describe the diverse number of cardiac abnormalities associated with central nervous system disease[1].  Patients with neurovascular emergencies (most notably SAH) can develop subendocardial myocyte damage, global or regional left ventricular systolic dysfunction (incidence of 10-28% in SAH), low-grade troponin elevation (20-40% of patients with SAH), and a diverse number of EKG abnormalities linked to the development of life-threatening cardiac arrythmmias.  Significantly, these occur even in the absence of underlying cardiac disease.  Multiple theories have been proposed for the mechanism of neurocardiogenic injury, the most popular of which postulates that a "catecholamine-surge" leads to myocardial damage.  Others postulate that a wide-spread inflammatory state, such as seen in septic shock -induced myocardial dysfunction, is responsible.  Interestingly, the degree of cardiac injury as measured by troponin level (>0.3 ng/mL) correlates with SAH severity (in terms of Hunt/Hess grading) [2].

With respect to EKG findings specifically, EKG abnormalities are common in the acute phase of neurovascular disorders.  They occur in 60-70% of patients in ICH, 40-70% of patients with SAH, and 15-40% of patients with ischemic stroke [1].  The most common EKG abnormality is QT prolongation, as seen in our patient. QT prolongation may precede sudden death from ventricular arrythmmias among patients with SAH [3].  Other EKG abnormalities in acute stroke include -

1.  Wide, deep and bizarre appearing T wave inversions - The most striking EKG manifestation of CNS disorders are bizarre-appearing, deep and widely splayed T waves usually in the precordial leads [4,6].  Some form of T wave abnormality, including both flattening and inversions, is seen in approximately 15% patients with ischemic stroke and 55% of patients with SAH [1]. While we typically associate T wave inversions with acute myocardial ischemia, the EKG changes can occur even patients with normal coronaries [5].

 EKG from patient with an acute L PCA ischemic stroke. Note marked QT prolongation and bizarre-appearing T wave inversions in V2-V5

2.  U waves - In the original case series by Burch (1954) describing EKG abnormalities in stroke, it was observed that a subset of tracings had U waves even in the absence of hypokalemia [4].  Subsequent studies have found new U waves in 13% - 15% of patients with acute ischemic stroke and SAH [1].  In a subset of these cases, it is possible that some of the prolonged QT observed is actually a form of T-U fusion.

Figure from 4 from Burch (1954) demonstrating U waves in a patient with intracerebral hemorrhage

3.  ST elevation - Some form of ST segment change occurs in approximately 20-30% of patients with stroke.  A small subset of these patients will also have ST elevation (see example below).  While ST elevation can be seen with neurocardiogenic injury, it is still important to consider dissection in patients with cerebral ischemia and ST elevation on their EKG.

EKG from 76 yo male with SAH who subsequently underwent cardiac cath with clean coronaries (Source: Reference 6)

While the EKG changes are interesting,  do they have any clinical significance or prognostic value?  This remains unclear.  Cardiac dysfunction and EKG abnormalities due to neurocardiogenic injury are usually transient, normalizing over days 3-8 post-injury (at least for SAH)[1].  One small retrospective study of only 58 patients attempted to examine whether EKG status was predictive of all cause mortality in SAH [7].  While it was found to correlate strongly with severity of SAH, no independent predictive value was found (see table below).  The EKG, therefore, in addition to the clinical exam, may be an indirect marker of SAH severity associated with increased all-cause mortality.

For the most part, the EKG changes themselves do not require specific treatment, but clinical investigation should include evaluating for other potential causes (i.e. electrolyte abnormalities or true coronary ischemia).  Patients with these changes should have continuous cardiovascular monitoring during the acute period because of the risk of serious arrythmmia.  Despite risk of arrythmmia, these patients benefit from specialized neurocritical care, and belong in a NeuroICU instead of a cardiac care unit.

Submitted by Maia Dorsett (@maiadorsett), PGY-3
Faculty reviewed by Peter Panagos and Douglas Char

Take home points:  Troponin elevation + EKG changes does not automatically point to primary cardiac pathology and can occur even in the absence of underlying cardiac disease.  Remember to consider central nervous system pathology in a patient with altered mental status + EKG changes or elevated troponin.  Because EKG changes can have important clinical effects (such as predisposition to life-threatening arrythmmias), the EKG is an important component of the clinical work-up for CNS disorders. And as always, drug-induced altered mental status should be a diagnosis of exclusion because sometimes people use heroin to treat the worst headache of their life.

References:
1. Kopelnik, A., & Zaroff, J. G. (2006). Neurocardiogenic injury in neurovascular disorders. Critical care clinics, 22(4), 733-752.
2. Hravnak, M., Frangiskakis, J. M., Crago, E. A., Chang, Y., Tanabe, M., Gorcsan, J., & Horowitz, M. B. (2009). Elevated cardiac troponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarachnoid hemorrhage. Stroke, 40(11), 3478-3484.
3.Oppenheimer, S. M., Cechetto, D. F., & Hachinski, V. C. (1990). Cerebrogenic cardiac arrhythmias: cerebral electrocardiographic influences and their role in sudden death. Archives of Neurology, 47(5), 513-519.
4.Burch, G. E., Meyers, R., & Abildskov, J. A. (1954). A new electrocardiographic pattern observed in cerebrovascular accidents. Circulation, 9(5), 719-723.
5.Cropp, G. J., & Manning, G. W. (1960). Electrocardiographic changes simulating myocardial ischemia and infarction associated with spontaneous intracranial hemorrhage. Circulation, 22(1), 25-38.
6. Catanzaro, J. N., Meraj, P. M., Zheng, S., Bloom, G., Roethel, M., & Makaryus, A. N. (2008). Electrocardiographic T-wave changes underlying acute cardiac and cerebral events. The American journal of emergency medicine, 26(6), 716-720.
7. Zaroff, J. G., Rordorf, G. A., Newell, J. B., Ogilvy, C. S., & Levinson, J. R. (1999). Cardiac outcome in patients with subarachnoid hemorrhage and electrocardiographic abnormalities. Neurosurgery, 44(1), 34-39.