Current Practices of Triple-H Prophylaxis and Therapy in Patients with Subarachnoid Hemorrhage

Meyer, Rachel; Deem, Steven; Yanez, N. David; Souter, Michael J.; Lam, Arthur M.; Treggiari, Miriam M.

doi:10.1007/s12028-010-9437-z

Cited by 77 publications

(51 citation statements)

References 16 publications

(11 reference statements)

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“…It is possible that the effect of norepinephrine on CBF is more predictable than the effect of dopamine. Phenylephrine is equally used as norepinephrine [49], without solid evidence for superiority of one agent over the other. AVP may be considered in patients who failed to respond to other vasopressor agents.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic Management of Subarachnoid Hemorrhage

Treggiari

2011

Neurocrit Care

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Hemodynamic augmentation therapy is considered standard treatment to help prevent and treat vasospasm and delayed cerebral ischemia. Standard triple-H therapy combines volume expansion (hypervolemia), blood pressure augmentation (hypertension), and hemodilution. An electronic literature search was conducted of English-language papers published between 2000 and October 2010 that focused on hemodynamic augmentation therapies in patients with subarachnoid hemorrhage. Among the eligible reports identified, 11 addressed volume expansion, 10 blood pressure management, 4 inotropic therapy, and 12 hemodynamic augmentation in patients with unsecured aneurysms. While hypovolemia should be avoided, hypervolemia did not appear to confer additional benefits over normovolemic therapy, with an excess of side effects occurring in patients treated with hypervolemic targets. Overall, hypertension was associated with higher cerebral blood flow, regardless of volume status (normo- or hypervolemia), with neurological symptom reversal seen in two-thirds of treated patients. Limited data were available for evaluating inotropic agents or hemodynamic augmentation in patients with additional unsecured aneurysms. In the context of sparse data, no incremental risk of aneurysmal rupture has been reported with the induction of hemodynamic augmentation.

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Section: Discussionmentioning

confidence: 99%

Hemodynamic Management of Subarachnoid Hemorrhage

Treggiari

2011

Neurocrit Care

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“…Two recent surveys of predominant strategies and practices for patients with aneurysmal subarachnoid hemorrhages have been published. One revealed that up to 60% of respondents used HHH therapy prophylactically (Sakowitz et al, 2006), whereas the second found that nearly 30% of respondents actively used the practice (Meyer et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…In spite of this, it is practiced 30% to 60% of the time (Meyer et al, 2011;Sakowitz et al, 2006). Inducing hemodilution aims to maximize oxygen delivery across the stenosis of vasospastic vessels by decreasing viscosity.…”

Section: Introductionmentioning

confidence: 99%

A Computational Simulation of the Effect of Hemodilution on Oxygen Transport in Middle Cerebral Artery Vasospasm

Chittiboina

Guthikonda

Wollblad³

et al. 2011

J Cereb Blood Flow Metab

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Cerebral vasospasm after aneurysmal subarachnoid hemorrhage is a potentially severe sequel. The induction of hypertension, hypervolemia, and hemodilution is advocated for vasospasm, but it is unclear whether hemodilution confers any benefit. A finite element model of oxygen transport in the proximal middle cerebral artery (MCA) was used to evaluate the complex relationship among hematocrit, viscosity, oxygen content, and blood flow in the setting of vasospasm. A single-phase non-Newtonian finite element model based on three-dimensional incompressible Navier-Stokes equations was constructed of the M1 segment. The model was solved at vessel stenoses ranging from 0% to 90% and hematocrit from 0.2 to 0.6. A small area of poststenotic recirculation was seen with mild (30%) stenosis. Poststenotic eddy formation was noted with more severe (60% to 90%) stenosis. Volumetric flow was inversely related to hematocrit at mild stenosis (0% to 30%). With near-complete stenosis (90%), a paradoxical increase in flow was seen with increasing hematocrit. Oxygen transport across the segment was related to hematocrit at all levels of stenosis with increasing oxygen transport despite a reduction in blood flow, suggesting that with clinically significant vasospasm in the MCA, hemodilution does not improve oxygen transport, but to the contrary, that ischemia may be worsened.

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“…In the absence of controlled comparative studies, the choice between PE and NE is often arbitrary and primarily dependent upon the preference of the treating clinician. A survey of Neurocritical Care Society members showed that 48% of providers primarily used PE, while 39% used NE [9]. However, theoretical and practical differences, which could be significant, exist.…”

Section: Introductionmentioning

confidence: 99%

Comparison of Initial Vasopressors Used for Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage

Roy¹,

McCullough²,

Dhar³

et al. 2017

Cerebrovasc Dis

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Background: The main reason for morbidity after aneurysmal subarachnoid hemorrhage (aSAH) is delayed cerebral ischemia (DCI). The mainstay of medical therapy for treating DCI is induced hypertension with vasopressors to restore cerebral perfusion. Both phenylephrine (PE) and norepinephrine (NE) are commonly used for induced hypertension, but the impact of the initial choice of vasopressor on the efficacy, adverse effects, or outcome after hemodynamic therapy for DCI is unknown. Methods: Sixty-three patients with aSAH between January 2012 and October 2014, who developed DCI (defined as new focal deficit or decline in Glasgow Coma Score) and in which PE (n = 45) or NE (n = 18) treatment was initiated were evaluated in this retrospective study. Baseline characteristics, adverse effects, the need to change or add vasopressors, the response to therapy, the need for endovascular therapy, new infarct development, discharge disposition, and 3 months modified Rankin score were all compared between pressor groups. Results: Baseline characteristics (e.g., Hunt Hess and Fisher grades) were similar. There were no differences in the overall rate of complications including arrhythmia, pulmonary edema, or kidney injury. However, those initiated on PE were more likely to be changed to an alternate vasopressor (64 vs. 33%, p = 0.016), mostly for bradycardia or failure to reach therapeutic targets. Patients initially treated with PE were less likely to respond neurologically (71 vs. 94%, p = 0.01) or to be discharged to home or acute rehabilitation facilities (73 vs. 94%, p = 0.02) and were more likely to have a delayed infarct on imaging (62 vs. 33%, p = 0.04). Conclusions: Our study suggests that patients with DCI after aSAH initiated on PE are more likely to require treatment change to another vasopressor and are at greater risk for poor clinical outcomes compared to patients started on NE. Larger comparative studies are warranted.

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Current Practices of Triple-H Prophylaxis and Therapy in Patients with Subarachnoid Hemorrhage

Cited by 77 publications

References 16 publications

Hemodynamic Management of Subarachnoid Hemorrhage

Hemodynamic Management of Subarachnoid Hemorrhage

A Computational Simulation of the Effect of Hemodilution on Oxygen Transport in Middle Cerebral Artery Vasospasm

Comparison of Initial Vasopressors Used for Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage

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