Secondary Insults in Subarachnoid Hemorrhage

Ryttlefors, Mats; Howells, Tim; Nilsson, Pelle; Ronne-Engström, Elisabeth; Enblad, Per

doi:10.1227/01.neu.0000298898.38979.e3

Cited by 81 publications

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“…PTD ICP15 , PTD ICP20 , PTD ICP25 and PTD ICP30 ) as defined by different predefined ICP threshold (15,20,25 and 30 mmHg). Values are expressed as relative frequencies (%) for categorical variables and medians (ranges) for continuous factors.…”

Section: Supplemental Table II Univariate Logistic Regression Analysmentioning

confidence: 99%

“…15 Univariate analysis demonstrated that HICP increased the risk of clinical deterioration without significant effect on functional outcome. The burden of HICP has recently been more precisely characterized in traumatic brain injury (TBI) using a method that accounts for the cumulative extent and duration of HICP episodes, namely the ICP pressure-time dose (PTD ICP ).…”

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confidence: 99%

“…Monitored data, including intraparenchymal ICP, were digitally recorded minute-by-minute in the first 7 days. PTD ICP (mm Hg h) was computed using 4 predefined thresholds (15,20, 25, and 30 mm Hg). Outcome was assessed through Extended Glasgow Outcome Scale at hospital discharge and at 6 months.…”

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High-Resolution Intracranial Pressure Burden and Outcome in Subarachnoid Hemorrhage

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Even though intracranial hypertension is common after aSAH, only a limited number of studies have assessed the course of ICP and its effects on outcome.10-14 Heuer 10 described the relative frequency of this condition in aSAH; 54% had HICP, including a significant proportion (48.7%) with a good clinical grade compared with the 63.6% who were with a poor grade on admission. HICP was associated with poor outcome, particularly where it did not respond to treatment. In a small microdialysis study, HICP was associated with severely deranged cerebral metabolism, namely a pathological increase in lactate/pyruvate ratio and glutamate and glycerol, probably reflecting secondary brain injury.11 Recently, Zoerle 12 demonstrated that >80% of aSAH patients suffered at least one episode of HICP in the first week, with the highest mean ICP exceeding 20 mm Hg in 36%. The burden of HICP peaked 3 days after subarachnoid hemorrhage and declined after day Background and Purpose-Intracranial pressure (ICP) control is a therapeutic target in patients with aneurysmal subarachnoid hemorrhage, although only a limited number of studies assessed its course and effect on outcome. Pressuretime dose (PTD ICP ) is a method to quantify the burden and the time spent above a defined threshold of ICP. PTD ICP or its relationship with outcome has never been evaluated in aneurysmal subarachnoid hemorrhage. Methods-Analysis of data prospectively collected from aneurysmal subarachnoid hemorrhage patients admitted toNeurointensive Care Unit. Monitored data, including intraparenchymal ICP, were digitally recorded minute-by-minute in the first 7 days. PTD ICP (mm Hg h) was computed using 4 predefined thresholds (15,20, 25, and 30 mm Hg). Outcome was assessed through Extended Glasgow Outcome Scale at hospital discharge and at 6 months. Results-Fifty-five patients were enrolled. Forty-two patients (76%) presented with a poor clinical grade. Overall, mortality was 17% at hospital discharge and 34% at 6 months. Half of patients required extensive therapy to control high ICP during day 1. Median ICP was 10 mm Hg (4-75), whereas median PTD ICP15 , PTD ICP20 , PTD ICP25 , PTD ICP30 were, respectively, 13, 4, 2, and 1 mm Hg h. We observed an association between mortality at hospital discharge and higher level of PTD ICP using 20, 25, and 30 mm Hg as thresholds and between exposure to a moderate-level PTD ICP30 and unfavorable long-term outcome. Conclusions-PTD ICP may better define one of the insults that the brain suffers after aneurysmal rupture, and exposure to moderate PTD ICP30 was significant prognostic factor of 6-month unfavorable outcome.

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Section: Supplemental Table II Univariate Logistic Regression Analysmentioning

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High-Resolution Intracranial Pressure Burden and Outcome in Subarachnoid Hemorrhage

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“…All SAH patients were managed according to a standardized protocol based on intensive physiological monitoring and aggressive therapy of any derangement to avoid or minimize secondary brain injury (4). All unconscious patients and patients with clinical and radiological signs of intracranial hypertension received a ventriculostomy.…”

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confidence: 99%

“…Positron emission tomography (PET) studies have shown that subarachnoid hemorrhage (SAH) causes both global and focal hemodynamic and metabolic disturbances in the brain early after aneurysm rupture (1), which makes the brain vulnerability for secondary insults (2–4). Secondary ischemic brain injury may be caused by cerebral vasospasm and also by various other secondary insults, e.g., high intracranial pressure (ICP), hypotension, hypoxemia, and seizures.…”

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Monitoring of Cerebral Blood Flow and Metabolism Bedside in Patients with Subarachnoid Hemorrhage â€“ A Xenon-CT and Microdialysis Study

et al. 2014

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Cerebral ischemia is the leading cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). Although 70% of the patients show angiographic vasospasm only 30% develop symptomatic vasospasm defined as delayed cerebral ischemia (DCI). Early detection and management of reversible ischemia is of critical importance in patients with SAH. Using a bedside Xenon enhanced computerized tomography (Xenon-CT) scanner makes it possible to measure quantitative regional Cerebral blood flow (CBF) bedside in the neurointensive care setting and intracerebral microdialysis (MD) is a method that offers the possibility to monitor the metabolic state of the brain continuously. Here, we present results from nine SAH patients with both MD monitoring and bedside Xenon-CT measurements. CBF measurements were performed within the first 72 h following bleeding. Six out of nine patients developed DCI at a later stage. Five out of six patients who developed DCI had initial global CBF below 26 ml/100 g/min whereas one had 53 ml/100 g/min. The three patients who did not develop clinical vasospasm all had initial global CBF above 27 ml/100 g/min. High lactate/pyruvate (L/P) ratio was associated with lower CBF values in the area surrounding the catheter. Five out of nine patients had L/P ratio ≥25 and four of these patients had CBF ≤ 22 ml/100 g/min. These preliminary results suggest that patients with initially low global CBF on Xenon-CT may be more likely to develop DCI. Initially low global CBF was accompanied with metabolic disturbances determined by the MD. Most importantly, pathological findings on the Xenon-CT and MD could be observed before any clinical signs of DCI. Combining bedside Xenon-CT and MD was found to be useful and feasible. Further studies are needed to evaluate if DCI can be detected before any other signs of DCI to prevent progress to infarction.

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Subarachnoid Hemorrhage

Herrera¹,

Puppo²

2015

Neurointensive Care

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Secondary Insults in Subarachnoid Hemorrhage

Abstract: Elevated ICP not responding to treatment is predictive of clinical deterioration, whereas high CPP decreases the risk of clinical deterioration. It may be beneficial to not lower spontaneous high CPP in patients with subarachnoid hemorrhage.

Cited by 81 publications

References 27 publications

High-Resolution Intracranial Pressure Burden and Outcome in Subarachnoid Hemorrhage

High-Resolution Intracranial Pressure Burden and Outcome in Subarachnoid Hemorrhage

Monitoring of Cerebral Blood Flow and Metabolism Bedside in Patients with Subarachnoid Hemorrhage â€“ A Xenon-CT and Microdialysis Study

Subarachnoid Hemorrhage

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