J Mocco, Carlton S. Prickett, Ricardo J. Komotar, E. Sander Connolly and Stephan A. Mayer
✓In an attempt to elucidate the pathophysiology and clinical significance of global cerebral edema (GCE) following aneurysmal subarachnoid hemorrhage (SAH), the authors explored potential mechanisms and reviewed findings associated with this phenomenon. Admission computed tomography (CT) scans show GCE in up to 20% of patients experiencing aneurysmal SAH. This edema is likely to have been initiated by transient global ischemia, as indicated by an association between ictal loss of consciousness and the development of edema. A further cascade of events, including a rise in intracranial pressure and compromise of the blood–brain barrier, are also likely contributors. Clinically, GCE on CT after aneurysmal SAH is predictive of a poor outcome. Further investigation is needed to gain a full understanding of edema development following SAH, with the hope that the knowledge can be used to influence treatment positively and improve outcome.
William J. Mack, Ryan G. King, Andrew F. Ducruet, Kurt Kreiter, J Mocco, Ahmed Maghoub, Stephan Mayer and E. Sander Connolly Jr.
Elevated intracranial pressure (ICP) is an important consequence of aneurysmal subarachnoid hemorrhage (SAH) that often results in decreased cerebral perfusion and secondary clinical decline. No definitive guidelines exist regarding methods and techniques for ICP management following aneurysm rupture. The authors describe monitoring practices and outcome data in 621 patients with aneurysmal SAH admitted to their neurological intensive care unit during an 8-year period (1996–2003).
A fiberoptic catheter tip probe or external ventricular drain (EVD) was used to record ICP values. The percentage of monitored patients varied, as expected, according to admission Hunt and Hess grade (p < 0.0001). Intracranial pressure monitoring devices were used in 27 (10%) of 264 Grade I to II patients, 72 (38%) of 189 Grade III patients, and 134 (80%) of 168 Grade IV to V patients. There was a strong propensity to favor transduced ventricular drains over parenchymal fiberoptic bolts, with the former used in 221 (95%) of 233 cases. This tendency was particularly strong in the poor-grade cohort, in which EVDs were placed in 99% of monitored individuals. The rates of cerebrospinal fluid infection in patients in whom ICP probes (0%) and ventricular drains (12%) were placed accorded with those in the literature.
Following aneurysmal SAH, ICP monitoring prevalence and techniques differ with respect to admission Hunt and Hess grade and are associated with the patient's functional status at discharge.
Stephan A. Mayer, Gregory K. Yim, Stephen T. Onesti, Timothy Lynch, Phyllis L. Faust and Karen Marder
✓ Neurosarcoidosis without systemic involvement is rare and difficult to diagnose. The case of a 27-year-old man with a 6-week history of headache, mental status changes, and polyradiculopathy attributable to hypoglycorrheic lymphocytic meningitis is presented. Extensive testing for occult systemic sarcoidosis was negative. The presence of noncaseating granulomatous inflammation was established by open brain biopsy, and the patient improved clinically with oral steroid therapy. In individuals with undiagnosed chronic meningitis, brain biopsy may be necessary to rule out isolated neurosarcoidosis.
Shouri Lahiri, Mani Nezhad, Konrad H. Schlick, Brenda Rinsky, Axel Rosengart, Stephan A. Mayer and Patrick D. Lyden
Intravenous nicardipine is commonly used for blood pressure reduction in patients with acute stroke. However, few studies have described its effects on cerebrovascular hemodynamics as measured by transcranial Doppler (TCD) waveform analysis and pulsatility index (PI). In this study, the authors report examples of a consistent but paradoxical finding associated with nicardipine that suggests intracranial vasoconstriction, contrary to what is expected from a vasodilator.
The data presented are from a convenience sample of patients who underwent TCD monitoring before, after, or during nicardipine administration. In each case, TCD waveform morphologies and PIs were compared.
The TCD waveforms during nicardipine infusion are characterized by a prominent systolic peak and dicrotic notch. Systolic deceleration was more pronounced and PIs were significantly elevated in patients who were on nicardipine (p < 0.001). This finding was not evident when patients were not on nicardipine.
This study provides the first evidence of paradoxical intracranial vasoconstriction associated with intravenous nicardipine. In the authors' experience, this finding is consistently encountered in the vast majority of patients who are treated with intravenous nicardipine, and is contradictory to what is expected from a vasodilator. Future studies are needed to confirm this finding in larger populations and diverse clinical settings and to examine mechanisms that explain this phenomenon.
Grace H. Kim, David K. Hahn, Christopher P. Kellner, Ricardo J. Komotar, Robert Starke, Matthew C. Garrett, Jiang Yao, Justin Cleveland, Stephan A. Mayer and E. Sander Connolly Jr.
Heparin-induced thrombocytopenia Type II (HIT II) is a serious complication that occurs in 0.2–3% of patients treated with heparin and is associated with a high risk of thrombotic events. One center recently reported an incidence of HIT II of 15% in a population of patients with aneurysmal subarachnoid hemorrhage (aSAH). Because these patients are typically exposed to heparin during angiography, controversy exists regarding whether prophylaxis with enoxaparin rather than heparin affords any reduction in the risk of developing HIT II. In this study, the authors investigated the effect of heparin compared with enoxaparin on the incidence of HIT II in patients with aSAH.
The authors reviewed the medical records of 300 patients treated for aSAH who received thromboprophylaxis with either heparin or enoxaparin, and identified patients who developed HIT II. The incidences of HIT II in the 2 treatment groups were then compared.
One hundred sixty-six patients with aSAH were treated with heparin, and 134 patients were treated with enoxaparin. Sixteen (5.3%) of 300 patients met the diagnostic criteria for HIT II. Of those treated with heparin, 8 (4.8%) of 166 developed HIT II, compared with 8 (6%) of 134 treated with enoxaparin (difference not significant).
The authors report a lower incidence of HIT II in patients with aSAH than has previously been reported. The data also suggest that patients with aSAH who receive heparin are at no greater risk of developing HIT II than those who receive enoxaparin. This finding challenges the merit of choosing enoxaparin rather than heparin for thromboprophylaxis in patients with a SAH.
J Mocco, William J. Mack, Grace H. Kim, Alan P. Lozier, Ilya Laufer, Kurt T. Kreiter, Robert R. Sciacca, Robert A. Solomon, Stephan A. Mayer and E. Sander Connolly Jr.
Object. Proinflammatory adhesion molecule expression has been demonstrated to be elevated in patients with aneurysmal subarachnoid hemorrhage (SAH). Recent studies have shown that elevations in soluble intercellular adhesion molecule—1 (ICAM-1) may be predictive of poor outcome in patients with good grade (Hunt and Hess Grades 1–2) aneurysmal SAH at delayed time points that correspond with the risk period for cerebral vasospasm. In addition, ICAM-1 is upregulated in experimental models of vasospasm. Unfortunately, the relationship of adhesion molecule expression to human vasospasm remains unclear. The authors hypothesized that the delayed elevation of soluble ICAM-1 in patients with aneurysmal SAH is associated with the development of cerebral vasospasm.
Methods. Eighty-nine patients with aneurysmal SAH were prospectively enrolled in a study and stratified according to the presence or absence of vasospasm, as evidenced by daily monitoring of transcranial Doppler (TCD) velocities (presence, > 200 cm/second; absence, ≤ 120 cm/second). Levels of soluble ICAM-1 were determined using enzyme-linked immunosorbent assay every other day for 12 days post-SAH. An analysis of covariance model was used to evaluate trends in soluble ICAM-1 levels from 2 days prior to 6 days after the occurrence of documented vasospasm. Two groups of patients, matched for admission admission Hunt and Hess grade, were compared: nine patients with TCD velocities greater than 200 cm/second and nine patients with TCD velocities less than 120 cm/second. From among the patients with TCD velocities greater than 200 cm/second six patients with angiographically documented vasospasm were selected. Patients with TCD velocities less than 120 cm/second and matched admission Hunt and Hess grades but without angiographically documented vasospasm were selected. Patients with TCD-demonstrated vasospasm showed a significant mean rate of rise (p < 0.01) in soluble ICAM-1 levels during the perivasospasm period, but admission Hunt and Hess grade—matched control patients did not (p = not significant [NS]). There was a significant difference between these groups' rates of soluble ICAM increase (p < 0.01). Patients with both TCD- and angiographically demonstrated vasospasm likewise showed a highly significant mean rate of increase in soluble ICAM-1 levels during the perivasospasm period (p < 0.01), whereas admission Hunt and Hess grade—matched controls did not (p = NS). The difference beween these groups' rates of increase was highly significant (p < 0.001).
Conclusions. These data suggest a role for ICAM-1 in the pathophysiology of cerebral vasospasm or its ischemic sequelae. As this relationship is further elucidated, adhesion molecules such as ICAM-1 may provide novel therapeutic targets in the prevention of vasospasm or its ischemic consequences.
William J. Mack, J Mocco, Daniel J. Hoh, Judy Huang, Tanvir F. Choudhri, Kurt T. Kreiter, Alan Lozier, Marcello Opperman, Alexander Poisik, Joshua Yorgason, Robert A. Solomon, Stephan A. Mayer and E. Sander Connolly Jr.
Object. Although upregulated adhesion molecule expression has been demonstrated in experimental models of subarachnoid hemorrhage (SAH) and in the cerebrospinal fluid of patients with aneurysmal SAH, the clinical significance of these proinflammatory findings remains unclear. The authors hypothesize that 1) serum levels of soluble intercellular adhesion molecule-1 (ICAM-1) are increased in all patients with aneurysmal SAH shortly after the hemorrhagic event, and 2) elevated soluble ICAM-1 values are associated with poor patient outcome, even when controlling for the severity of the initial hemorrhagic insult.
Methods. One hundred one patients were prospectively enrolled and stratified according to their admission Hunt and Hess grade and functional status at discharge (modified Rankin Scale [mRS] score). Soluble ICAM-1 levels were determined every other day for 12 days post-SAH by using the enzyme-linked immunosorbent assay. Early soluble ICAM-1 levels (post-SAH Days 2–4) were increased compared with levels in control patients without SAH (p < 0.05). Patients with aneurysmal SAH who had a poor outcome (mRS Grades 4–6) had significantly higher soluble ICAM-1 levels over the first 2 weeks post-SAH compared with patients who had a good outcome (mRS Grades 0–3, p < 0.01). This association with outcome was predicted by late increases (Day 6, p = 0.07; Days 8–12, p < 0.05) rather than early increases (p = not significant) and was best seen in patients with Hunt and Hess Grades I and II, in whom only those with poor outcomes demonstrated delayed ICAM-1 elevations (p < 0.05).
Conclusions. These data demonstrate a correlation between soluble ICAM-1 levels and functional outcome following aneurysmal SAH that appears to be, at least in part, independent of the initial hemorrhage.
Alexander G. Chartrain, Ahmed J. Awad, Christopher A. Sarkiss, Rui Feng, Yangbo Liu, J Mocco, Joshua B. Bederson, Stephan A. Mayer, Neha S. Dangayach and Errol Gordon
Patients who have experienced subarachnoid hemorrhage (SAH) often receive care in the setting of the ICU. However, SAH patients may not all require extended ICU admission. The authors established a protocol on January 1, 2015, to transfer select, low-risk patients to a step-down unit (SDU) to streamline care for SAH patients. This study describes the results of the implemented protocol.
In this retrospective chart review, patients presenting with SAH between January 2011 and September 2016 were reviewed for inclusion. The control group consisted of patients admitted prior to establishment of the SDU transfer protocol, while the intervention group consisted of patients admitted afterward.
Of the patients in the intervention group, 79.2% (57/72) were transferred to the SDU during their admission. Of these transferred patients, 29.8% (17/57) required return to the neurosurgical ICU (NSICU). There were no instances of morbidity or mortality directly related to care in the SDU. Patients in the intervention group had a mean reduced NSICU length of stay, by 1.95 days, which trended toward significance, and a longer average hospitalization, by 2.7 days, which also trended toward significance. In-hospital mortality and 90-day readmission rate were not statistically different between the groups. In addition, early transfer timing prior to 7 days was associated with neither a higher return rate to the NSICU nor higher 90-day readmission rate.
In this retrospective study, the authors demonstrated that the transfer protocol was safe, feasible, and effective in reducing the ICU length of stay and was independent of transfer timing. Confirmation of these results is needed in a large, multicenter study.