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Home , Subarachnoid hemorrhage, Vasospasm

Neurocrit Care DOI 10.1007/s12028-011-9589-5

REVIEW

Hemodynamic Management of

Miriam M. Treggiari • Participants in the International Multi-disciplinary Consensus Conference on the Critical Care Management of Subarachnoid Hemorrhage

Ó Springer Science+Business Media, LLC 2011

Abstract Hemodynamic augmentation therapy is con- the context of sparse data, no incremental risk of aneu- sidered standard treatment to help prevent and treat rysmal rupture has been reported with the induction of and delayed cerebral . Standard triple- hemodynamic augmentation. H therapy combines volume expansion (), augmentation (), and hemodi- Keywords Hemodilution Á Hypertension Á lution. An electronic literature search was conducted of Hypervolemia Á Inotropic Á Volume expansion English-language papers published between 2000 and October 2010 that focused on hemodynamic augmentation therapies in patients with subarachnoid hemorrhage. Introduction Among the eligible reports identified, 11 addressed volume expansion, 10 blood pressure management, 4 inotropic Delayed cerebral ischemia (DCI) is an important cause of therapy, and 12 hemodynamic augmentation in patients secondary neuronal after aneurysmal subarachnoid with unsecured . While hypovolemia should be hemorrhage (SAH). Hemodynamic augmentation is the avoided, hypervolemia did not appear to confer additional mainstay of medical management among patients with benefits over normovolemic therapy, with an excess of side vasospasm. The natural history of circulating blood volume effects occurring in patients treated with hypervolemic after SAH is characterized by a reduction in blood volume targets. Overall, hypertension was associated with higher in patients undergoing surgery within 72 h of hemorrhage cerebral blood flow, regardless of volume status (normo- or [1]. Volume expansion and blood pressure manipulation hypervolemia), with neurological symptom reversal seen in can play an important role in maintaining cerebral blood two-thirds of treated patients. Limited data were available flow, particularly in setting of impaired autoregulation. In for evaluating inotropic agents or hemodynamic augmen- the experimental setting, as well as, following traumatic tation in patients with additional unsecured aneurysms. In injury, norepinephrine has been shown to be more predictable in maintaining cerebral perfusion pressure compared with dopamine [2, 3]. In patients with intact Participants in the International Multi-disciplinary Consensus autoregulation, dopamine has been shown to increase intra- Conference: Michael N. Diringer, Thomas P. Bleck, Nicolas Bruder, cranial pressure and cerebral blood flow, while no effect was E. Sander Connolly, Jr., Giuseppe Citerio, Daryl Gress, Daniel seen on cerebral with norepinephrine or Hanggi, J. Claude Hemphill, III, MAS, Brian Hoh, Giuseppe Lanzino, epinephrine [4]. However, it is unknown if data observed in Peter Le Roux, David Menon, Alejandro Rabinstein, Erich Schmutzhard, Lori Shutter, Nino Stocchetti, Jose Suarez, Miriam these settings extrapolate to the situation of ischemia in the Treggiari, MY Tseng, Mervyn Vergouwen, Paul Vespa, Stephan context of cerebral vasospasm, where there is likely to be at Wolf, and Gregory J. Zipfel. least regional impairment of autoregulation. In addition, enhancing cardiac performance in the context of hemody- & M. M. Treggiari ( ) namic augmentation after SAH might also be considered as a Department of Anesthesiology and Pain Medicine, University of Washington, Box 359724 Seattle, WA, USA strategy to reduce DCI. Hemodynamic management is e-mail: [email protected] often dubbed triple-H therapy, combining hypervolemia 123 Neurocrit Care from volume expansion, hypertension with blood pressure Summary of the Literature augmentation, and hemodilution through optimizing blood viscosity and oxygen-carrying ability. A total of 35 papers were included in this review, with most Although hemodynamic management is standard prac- papers addressing volume expansion therapy and blood tice in patients with SAH, limited data are available to pressure management. The only randomized trials included evaluate both the efficacy and safety of the different were two that focused on prophylactic hypervolemia [6, 7]. components of triple-H therapy for preventing or reducing vasospasm and DCI [5]. This review was designed to Volume Expansion Therapy evaluate available evidence for hemodynamic augmenta- tion after SAH by evaluating data for the treatment of A total of 282 unique references were identified during the patients with SAH using volume expansion therapy, initial PubMed and Embase search that addressed volume induced hypertension, inotropic agents, and hemodynamic expansion, with 52 identified in the secondary search and augmentation. from reference lists. A total of 11 studies were selected for review of volume expansion therapy data, including 2 randomized trials of prophylactic hypervolemia, although these did not specifically address treatment of established Methods vasospasm [6–16]. The first randomized controlled trial of prophylactic An electronic literature search was conducted by searching normovolemia versus hypervolemia found that hypervole- PubMed for data from the National Center for Biotech- mia did not increase blood volume or cerebral blood flow nology Information at the US National Library of Medicine (CBF) compared with normovolemia [6]. Likewise, there and Embase. An initial search was performed to identify were no differences in several other outcome measures English-language articles published between 2000 and including symptomatic vasospasm (20% in both groups), October 2010 using the key word ‘‘hemodynamics’’ and need for hypertensive hypervolemic therapy (17% vs. at least one of the following additional key words: ‘‘sub- 15%), (17% vs. 10%), or complications com- arachnoid hemorrhage/drug therapy,’’ ‘‘subarachnoid paring the hypervolemia versus the normovolemia group, hemorrhage/surgery,’’ or ‘‘subarachnoid hemorrhage/ther- respectively. In contrast, an observational study of induced apy.’’ Titles and abstracts were reviewed to identify hypervolemic hemodilution in patients with documented candidate articles that addressed volume expansion ther- vasospasm found increased cardiac output, blood pressure apy, blood pressure management, inotropic agents, and and filling pressure, blood volume, and CBF after the ini- hemodynamic augmentation in patients with unsecured tiation of therapy [8]. In this study, the hemodynamic aneurysms. Secondary searches were performed to identify management called for more aggressive targets, including additional appropriate articles for each topic, using the daily fluid administration of 4–5 L, hematocrit target key word ‘‘subarachnoid hemorrhage’’ plus additional >29%, use of desmopressin to ensure positive fluid bal- terms: ‘‘hemodynamics,’’ ‘‘hemodilution,’’ ‘‘hypervole- ance, and systolic blood pressure >120 mm Hg. mia,’’ ‘‘hypervolemic,’’ ‘‘euvolemia,’’ or ‘‘euvolemic’’ for Egge et al. [7] conducted an open-label, randomized volume status; ‘‘blood pressure,’’ ‘‘agent,’’ ‘‘target,’’ controlled trial of 32 patients with SAH (Hunt & Hess ‘‘hemodynamics,’’ or ‘‘hemodilution’’ for blood pressure grades I–III) who were treated within 72 h of with management; ‘‘hemodynamics,’’ ‘‘hemodilution,’’ ‘‘inotro- normovolemia or triple H (hypervolemia, increase in mean pic,’’ or ‘‘hyperdynamic’’ for inotropic therapy; and arterial pressure by 20 mm Hg, and hematocrit 30–35%) ‘‘hemodynamics,’’ ‘‘hemodilution,’’ ‘‘unruptured aneu- for approximately 12 days. Several early and late endpoints rysm,’’ or ‘‘unsecured ’’ for hemodynamic aug- were measured. The occurrence of symptomatic vasospasm mentation in patients with unsecured aneurysms. (32% normovolemia vs. 25% triple H), transcranial Titles and abstracts of candidate articles were evaluated Doppler vasospasm (62% in both groups), and poor for possible inclusion. Citations were included if they were Glasgow Outcome Scale (GOS) at 1 year (13% normo- original data from studies that addressed treatment in volemia vs. 19% triple H) were not different between humans. Papers were excluded if they were reviews or the two groups. However, triple H was associated with commentaries, letters, case reports, duplicate data from higher rate of complications and higher cost, compared other studies, or not relevant to the topic of interest. with normovolemia. Additional references were sought by reviewing references In a prospective observational study, Muench et al. [9] lists from retrieved papers, recent review articles, and suggested that hypertension was associated with an systematic reviews for appropriate articles that might have increase in relative CBF and brain tissue oxygenation, been missed. irrespective of volume status (i.e., euvolemia vs. 123 Neurocrit Care hypervolemia and hemodilution, on days 1, 3, and 7 after . These data need to be interpreted in the bleed). The brain oxygenation data are consistent with the context of a number of additional concomitant treat- the findings from Raabe et al. [10] who reported that, while ments, including no head of bed elevation and moderate and aggressive hypertension improved brain tis- administration of blood products, dextran, fludrocortisone, sue oxygen pressure values, hypervolemia was unlikely to atropine, pitressin, and digoxin. In a case series of four change brain tissue oxygenation and was associated with patients (3 postoperative) with SAH who had clinical a higher occurrence of complications (e.g., pulmonary symptoms, dopamine in a dose ranging from 9 to 46 mcg/ edema, , congestive , and cerebral kg/min was accompanied by an increase in blood pressure edema). Ekelund et al. conducted a small trial of isovo- in a range from 160 to 200 mm Hg and associated with lemic and hypervolemic hemodilution with cerebral symptom improvement [18]. In a cohort study of 20 hemodynamic measures collected at baseline and after the patients with SAH evaluated with serial CBF measure- fluid and hematocrit manipulation. In the presence of ments, eight patients developed symptomatic vasospasm hemodilution, there were no substantial differences in CBF [19]. CBF increase in response to blood pressure aug- or volume of ischemic brain between isovolemia and mentation (mean arterial pressure increase by 20 mm Hg) hypervolemia [11]. However, the administration of a saline with dopamine depended on the underlying degree of bolus (15 mL/kg/1 h) in patients with normovolemia at vasospasm (or underlying reduction in CBF). CBF baseline and new symptoms of vasospasm produced an increased up to 37% in patients with symptomatic vaso- increase in CBF, specifically in areas with low baseline spasm versus a 9% change in patients without evidence of flow [12]. clinical vasospasm. In a retrospective series of 13 patients A study investigating the effect of volume expansion who received dopamine in a range from 6.4 to 20 mcg/kg/ using 5% albumin (500 mL in 30 min) suggested a min to increase mean arterial pressure by 10–15 mm Hg, reduction in CBF following albumin administration in Darby et al. [20] observed that the effect of dopamine on patients with vasospasm during the first 2 weeks after CBF was unpredictable. Overall, there was no effect of SAH, with no changes after the second week and in dopamine on CBF with exception of a subgroup of terri- patients without vasospasm [13]. It should be noted that in tories that were ischemic but not infarcted; however, this study, patients had normal baseline CBF. Other studies dopamine was also associated with reduced CBF in some do suggest a beneficial effect of albumin when used as fluid non-ischemic territories. The results of this study need to for volume expansion in patients with SAH [14]. Finally, be interpreted with caution as some patients were on there is some suggestion that in patients with poor-grade dopamine at baseline and multiple measures were taken SAH, 23.5% hypertonic saline solution decreases intra- without accounting for intraclass correlation. Finally, a cranial pressure and increases cerebral perfusion pressure, series of eight patients was treated with baseline dopamine velocities, and CBF [15, 16]. infusion (up to 30 mcg/kg/min) to achieve a target systolic blood pressure of 180 mm Hg for the onset of delayed Blood Pressure Management ischemia [21]. CBF decreased by approximately 7 mL/ 100 g/min with dopamine withdrawal. A greater than 25% A total of 57 citations were identified through the primary CBF reduction was accompanied by a clinically significant search that addressed blood pressure management, with 7 deterioration in four of eight patients. The only unselected additional papers identified. Among these, a total of 10 cohort study reporting clinical outcomes of normovolemic papers were selected, with no randomized trials of induced induced hypertension (systolic blood pressure increase by hypertension identified [17–26]. 50–60 mm Hg, target 180–200 mm Hg) with dopamine Kassell et al. [17] reported one of the first large series of and dobutamine observed beneficial effects [22]. Induced symptomatic patients treated with volume expansion and hypertension resulted in reduction of induced hypertension. In this series, systolic blood pressure of vasospasm in 54% of the patients, with 20% of patients was increased up to 240 mm Hg in patients with secured experiencing hemorrhagic complications, in addition to aneurysms and up to 160 mm Hg in patients with unse- , arrhythmia, and . cured aneurysms using preferentially dopamine, central Kosnik and Hunt reported a selected series of seven venous pressure was maintained >10 mm Hg, heart rate patients whose treatment for ischemic symptoms with between 80 and 120/min, hematocrit >40%, and urine norepinephrine and transfusion resulted in favorable output <200 mL/h. Two-thirds of patients experienced recovery [23]. The therapeutic level of systolic blood symptom reversal, 16% had no changes, and 10% contin- pressure ranged between 140 and 190 mm Hg, approxi- ued to deteriorate. Several serious complications were mately 20–60 mm Hg higher than symptomatic baseline, observed including pulmonary edema, hyponatremia, with an endpoint of producing ‘‘unmistakable clinical aneurysmal rebleeding, coagulopathy, hemothorax, and improvement.’’ 123 Neurocrit Care

In a series of 5 symptomatic patients treated with Twenty-two (40%) responded to the PA -directed phenylephrine for clinical deterioration, an average therapy, while 23 patients who failed PA-guided hyper- increase in CBF by 12 mL/100 g/min was observed 1 h volemia were started on dobutamine, with symptom after induction of hypertension to a mean arterial pressure reversal in 78% of the patients [29]. ranging from 112 to 173 mm Hg [24]. The individual data The use of intra-arterial combined with intravenous suggest a low baseline CBF and small absolute changes in milrinone has been investigated in three studies. However, CBF, even after increasing the mean arterial pressure to none of these studies focused on the systemic hemody- 173 mm Hg (systolic 240 mm Hg). One of the five patients namic effects, rather on the endovascular results [30, 31, deteriorated and died with inability to obtain CBF mea- 33]. Milrinone was associated with a greater than 50% surements. These changes are consistent with data reported increase in the caliber of the vessel, but also with a con- in the prophylactic setting by Origitano et al. [27]. In this siderable proportion of vasospasm recurrence. Systemic study evaluating a prophylactic approach, systolic blood requiring initiation or increase in vasopressors pressure was increased postclipping with dopamine to was consistently observed. 150–175 mm Hg, resulting in an average increase in CBF It should be noted that in patients with traumatic brain by 7.5 mL/100 g/min (20–30% change from baseline). injury and impaired autoregulation, CBF does not seem to In a safety study of phenylephrine to induce hyperten- be related to cardiac output, irrespective of degree of dis- sion with an increase in mean arterial pressure by 20% and ruption of autoregulation [34]. In general, because it is up to 35% in patients who developed delayed ischemic important to maintain adequate cardiac output in the deficits, phenylephrine appeared to have a favorable safety management of patients with vasospasm following SAH, profile and was not associated with heightened risk of case reports have been published on the use of levosim- cardiac complications [25]. Using an approach of inducing endan [35], discontinuation of dobutamine in situations of aggressive therapy only after the onset of symptoms, neu- left ventricular outflow tract obstruction [36], and insertion rological improvement was observed in 88% of patients. of intra-aortic balloon pump counterpulsation [37, 38] with Arginine vasopressin (AVP) has been considered as a the intent of maximizing cardiac function in situations of supplementary vasopressor in patients with inadequate ventricular failure. response to triple-H therapy [26]. The effect of AVP was examined in a convenience sample of 22 consecutive Hemodynamic Augmentation in the Presence patients treated with AVP due to phenylephrine failure to of Unsecured Aneurysms achieve hemodynamic targets of mean arterial pressure >100 mm Hg for triple-H prophylaxis or >110 mm Hg Seventeen candidate studies were identified, with 12 for triple-H treatment, compared with an historic untreated selected as pertinent, but only 4 studies reporting the control. AVP afforded reduction of phenylephrine dose occurrence of rebleeding in the presence of induced without affecting sodium, , or the hypertension [17, 22, 39, 40]. Not unexpectedly, there were hemodynamic profile, except for an increase in peripheral no controlled trials evaluating the risk of rupture of unse- vascular resistances. However, no clinical endpoints or cured aneurysm. There were no phase III or phase IV trials measures of cerebral blood flow were reported. investigating the optimal blood pressure targets, and therefore, safety data regarding the risk of unsecured Inotropic Agents aneurysm rupture and rebleeding are to a large extent lacking. Nine candidate articles were identified, with four selected Rebleeding or hemorrhagic transformation has been for inclusion [28–31]. There were no randomized trials of reported in early studies of triple-H therapy where systolic hyperdynamic therapy. blood pressure had been allowed to raise up to 160 or Experimental evidence in monkeys suggests that local 200 mm Hg in the presence of unsecured ruptured aneu- CBF in ischemic brain regions varies directly with cardiac rysms [17, 22]. More recent studies in small patient cohorts output, with no effect on normally autoregulated brain [32]. where the ruptured aneurysm has been repaired but other Indeed, enhancing cardiac output with dobutamine pro- unprotected aneurysms persist do not suggest increased risk duced an increase in CBF comparable to the effect of blood of rebleeding [39]. In a cohort of 112 patients managed pressure augmentation afforded by phenylephrine (43% with a current therapeutic approach, 40 patients required increase with dobutamine vs. 75% increase with phenyl- blood pressure augmentation in a systolic range between ephrine) in patients with vasospasm [28]. Reversal of approximately 160–200 mm Hg and had unsecured un- ischemic symptoms was observed in a study of 55 patients ruptured aneurysms averaging 4.5 mm in diameter. No who were unresponsive to fluid therapy and were man- bleeding events were observed under hypertensive therapy. aged with pulmonary (PA) guided hypervolemia. Likewise, in a series of 25 patients who were treated 123 Neurocrit Care endovascularly with Guglielmo detachable coils, systemic measured CBF with a pre-post intervention approach are heparin, and induced hypertension up to a range of systolic consistent in reporting various degree of improvement in blood pressure of 195–250 mm Hg, there were no instances CBF (approximately by 10 mL/100 g/min) with induced of rebleeding or rupture, even in the presence of partial hypertension in areas of ischemia. However, only territo- aneurysm obliteration [40]. Hashimoto and colleagues ries subject to ischemia are likely to have beneficial reported the risk of rebleeding of vertebrobasilar dissecting modification in cerebral hemodynamic profile. aneurysms managed with conservative treatment and did There are no studies comparing the effect of different not observe re-ruptures over a 20-month period [41]. agents on CBF and clinical outcomes in the setting of Because large, population-based studies estimating the delayed ischemic deficits. It is possible that the effect of rupture risk and critical blood pressure augmentation norepinephrine on CBF is more predictable than the effect thresholds are to a large extent lacking and because of dopamine. Phenylephrine is equally used as norepi- hypertension (>160/95 mm Hg) is a risk factor for fatal nephrine [49], without solid evidence for superiority of one aneurysm rupture [42–44], caution should be used when agent over the other. AVP may be considered in patients establishing blood pressure targets. It seems reasonable to who failed to respond to other vasopressor agents. allow modified blood pressure parameters after weighing There are insufficient data to support the enhancement particular circumstances, e.g., aneurysm size, location, of cardiac output to supra-physiologic values; however, aspect ratio, morphology, blood flow characteristics, and optimization of cardiac function should be considered in surrounding vasculature, in patients with unruptured, patients with evidence of ventricular dysfunction that unsecured aneurysms [45–48]. compromises the patient hemodynamic profile. Dobuta- mine should be considered the preferred agent. Reporting of other modalities for cardiac performance optimization, Conclusions including intravenous milrinone or intra-aortic balloon pump counterpulsation to increase cardiac performance The rationale of volume expansion to prevent or treat and cerebral blood flow, is only anecdotal. cerebral ischemia is that, by increasing cardiac filling There is some concern that risk of rebleeding of unse- pressure and optimizing venous return function, there will cured unruptured aneurysms might be increased with be an increase in cardiac output that will elevate blood induced hypertension. However, the few studies reported to pressure and CBF. Volume expansion is also thought to date have not found such a relationship. Other risk factors improve CBF independent of perfusion pressure by for aneurysm rupture should be taken into account when improving blood rheology conditions, especially in the establishing the blood pressure augmentation goals in microcirculation. 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