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What's new in subarachnoid hemorrhage.

Smith M, Citerio G - Intensive Care Med (2014)

View Article: PubMed Central - PubMed

Affiliation: Neurocritical Care Unit, The National Hospital for Neurology and Neurosurgery, University College London Hospitals, Queen Square, London, WC1N 3BG, UK, martin.smith@uclh.nhs.uk.

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The importance of treatment in high-volume centres by a multidisciplinary team cannot be over-emphasised... Endovascular coiling of intracranial aneurysms represents a major advance in the treatment of SAH and allows minimally invasive and effective treatment... DCI can occur in the absence of vasospasm and vice versa, and brain ischemia often involves more than one vascular territory... Other mechanisms contributing to DCI include distal vascular dysautoregulation, micro-thrombi, direct neurotoxic effects, inflammation and cortical spreading depolarizations (SDs)... A combination of hypervolemia, hemodilution and hypertension (triple H therapy) has historically been the mainstay of treatment to prevent and treat DCI, but the focus of cardiovascular management after SAH is now on a single H—hypertension... Prophylactic hypervolemia is not effective in increasing CBF or improving neurological outcome, and there is some evidence of harm from overly aggressive filling... Intracranial hypertension and lack of ICP response to medical therapy appear to be associated with DCI and poor clinical outcome after SAH, and ICP and CPP monitoring have a role in guiding therapy... Multimodal cerebral monitoring, including brain tissue oxygen tension, TCD, cerebral microdialysis and electrophysiological monitoring in addition to ICP, allows individualized therapy with the aim of preventing or minimizing secondary ischemic injury... Figure 1 shows a practical approach to monitoring-guided management of DCI after SAH... Using surface electroencephalography (EEG), seizures are recorded in around 8 % of patients after SAH but invasive EEG monitoring identifies seizure activity in almost 40 %... Continuous EEG monitoring is the only reliable way to detect subclinical seizures, and it may also predict DCI many hours in advance of clinical symptoms... Actual seizures must be treated aggressively but universal prophylaxis remains controversial... Three days of treatment offers similar seizure prevention and better outcome than longer-term therapy... Phenytoin has been associated with cognitive effects and poor outcome and, although of equal efficacy in controlling seizures, levetiracetam is often chosen for the management of early-onset seizures because of its more favourable side-effect profile.

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Monitoring-guided management of delayed cerebral ischemia after subarachnoid haemorrhage. The figure shows a practical approach to monitoring-guided management of DCI after subarachnoid hemorrhage. The starting point is a frequent neurological evaluation and daily TCD, with clinically significant changes defined as new focal deficit or altered consciousness and TCD mean flow velocity >120 cm/s, increase >50 cm/s in 24 h, and/or a Lindegaard index (MCA/ICA blood flow velocity ratio) >6. If the neurological examination or TCD indicates a worsening state, a reasonable approach is to search for a potential reversible cause with a CT scan, CT angiography and perfusion CT. If angiographic vasospasm is present and CBF is reduced and/or MTT increased, a trial of stepwise-induced hypertension is recommended. If this strategy reverses DCI, close monitoring with maintenance of the higher blood pressure for 2–3 days is recommended. If hypertension alone does not reverse DCI, advanced neuromonitoring and further imaging prior to interventional radiological treatment should be considered in salvageable patients. CBF cerebral blood flow, CT computerized tomography, DCI delayed cerebral ischemia, DSA digital subtraction angiography, ICA internal carotid artery, MCA middle cerebral artery, MTT mean transmit time, ptO2 brain tissue oxygen tension, rCBF regional cerebral blood flow, TCD transcranial Doppler ultrasonography, VS vasospasm
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Fig1: Monitoring-guided management of delayed cerebral ischemia after subarachnoid haemorrhage. The figure shows a practical approach to monitoring-guided management of DCI after subarachnoid hemorrhage. The starting point is a frequent neurological evaluation and daily TCD, with clinically significant changes defined as new focal deficit or altered consciousness and TCD mean flow velocity >120 cm/s, increase >50 cm/s in 24 h, and/or a Lindegaard index (MCA/ICA blood flow velocity ratio) >6. If the neurological examination or TCD indicates a worsening state, a reasonable approach is to search for a potential reversible cause with a CT scan, CT angiography and perfusion CT. If angiographic vasospasm is present and CBF is reduced and/or MTT increased, a trial of stepwise-induced hypertension is recommended. If this strategy reverses DCI, close monitoring with maintenance of the higher blood pressure for 2–3 days is recommended. If hypertension alone does not reverse DCI, advanced neuromonitoring and further imaging prior to interventional radiological treatment should be considered in salvageable patients. CBF cerebral blood flow, CT computerized tomography, DCI delayed cerebral ischemia, DSA digital subtraction angiography, ICA internal carotid artery, MCA middle cerebral artery, MTT mean transmit time, ptO2 brain tissue oxygen tension, rCBF regional cerebral blood flow, TCD transcranial Doppler ultrasonography, VS vasospasm

Mentions: Increased ICP is common after SAH, particularly early after the ictus and in comatose patients [12]. The indications for ICP monitoring are often inter-related with the need to treat obstructive hydrocephalus, so a ventricular catheter is the optimal ICP monitor, being both a diagnostic and therapeutic modality. Intracranial hypertension and lack of ICP response to medical therapy appear to be associated with DCI and poor clinical outcome after SAH, and ICP and CPP monitoring have a role in guiding therapy. Multimodal cerebral monitoring, including brain tissue oxygen tension, TCD, cerebral microdialysis and electrophysiological monitoring in addition to ICP, allows individualized therapy with the aim of preventing or minimizing secondary ischemic injury [13]. Monitoring allows early detection of DCI and identifies end points for cardiovascular augmentation in its management. Changes in brain tissue oxygenation and biochemistry may identify impending or actual cerebral hypoxia/ischemia before changes in other monitoring modalities or clinical status, but it remains to be determined whether interventions directed towards normalization of these variables affects outcome. Data from small studies investigating the efficacy of multimodal neuromonitoring-guided treatment after SAH have been encouraging, but outcome data are lacking [12]. Figure 1 shows a practical approach to monitoring-guided management of DCI after SAH.Fig. 1


What's new in subarachnoid hemorrhage.

Smith M, Citerio G - Intensive Care Med (2014)

Monitoring-guided management of delayed cerebral ischemia after subarachnoid haemorrhage. The figure shows a practical approach to monitoring-guided management of DCI after subarachnoid hemorrhage. The starting point is a frequent neurological evaluation and daily TCD, with clinically significant changes defined as new focal deficit or altered consciousness and TCD mean flow velocity >120 cm/s, increase >50 cm/s in 24 h, and/or a Lindegaard index (MCA/ICA blood flow velocity ratio) >6. If the neurological examination or TCD indicates a worsening state, a reasonable approach is to search for a potential reversible cause with a CT scan, CT angiography and perfusion CT. If angiographic vasospasm is present and CBF is reduced and/or MTT increased, a trial of stepwise-induced hypertension is recommended. If this strategy reverses DCI, close monitoring with maintenance of the higher blood pressure for 2–3 days is recommended. If hypertension alone does not reverse DCI, advanced neuromonitoring and further imaging prior to interventional radiological treatment should be considered in salvageable patients. CBF cerebral blood flow, CT computerized tomography, DCI delayed cerebral ischemia, DSA digital subtraction angiography, ICA internal carotid artery, MCA middle cerebral artery, MTT mean transmit time, ptO2 brain tissue oxygen tension, rCBF regional cerebral blood flow, TCD transcranial Doppler ultrasonography, VS vasospasm
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4264958&req=5

Fig1: Monitoring-guided management of delayed cerebral ischemia after subarachnoid haemorrhage. The figure shows a practical approach to monitoring-guided management of DCI after subarachnoid hemorrhage. The starting point is a frequent neurological evaluation and daily TCD, with clinically significant changes defined as new focal deficit or altered consciousness and TCD mean flow velocity >120 cm/s, increase >50 cm/s in 24 h, and/or a Lindegaard index (MCA/ICA blood flow velocity ratio) >6. If the neurological examination or TCD indicates a worsening state, a reasonable approach is to search for a potential reversible cause with a CT scan, CT angiography and perfusion CT. If angiographic vasospasm is present and CBF is reduced and/or MTT increased, a trial of stepwise-induced hypertension is recommended. If this strategy reverses DCI, close monitoring with maintenance of the higher blood pressure for 2–3 days is recommended. If hypertension alone does not reverse DCI, advanced neuromonitoring and further imaging prior to interventional radiological treatment should be considered in salvageable patients. CBF cerebral blood flow, CT computerized tomography, DCI delayed cerebral ischemia, DSA digital subtraction angiography, ICA internal carotid artery, MCA middle cerebral artery, MTT mean transmit time, ptO2 brain tissue oxygen tension, rCBF regional cerebral blood flow, TCD transcranial Doppler ultrasonography, VS vasospasm
Mentions: Increased ICP is common after SAH, particularly early after the ictus and in comatose patients [12]. The indications for ICP monitoring are often inter-related with the need to treat obstructive hydrocephalus, so a ventricular catheter is the optimal ICP monitor, being both a diagnostic and therapeutic modality. Intracranial hypertension and lack of ICP response to medical therapy appear to be associated with DCI and poor clinical outcome after SAH, and ICP and CPP monitoring have a role in guiding therapy. Multimodal cerebral monitoring, including brain tissue oxygen tension, TCD, cerebral microdialysis and electrophysiological monitoring in addition to ICP, allows individualized therapy with the aim of preventing or minimizing secondary ischemic injury [13]. Monitoring allows early detection of DCI and identifies end points for cardiovascular augmentation in its management. Changes in brain tissue oxygenation and biochemistry may identify impending or actual cerebral hypoxia/ischemia before changes in other monitoring modalities or clinical status, but it remains to be determined whether interventions directed towards normalization of these variables affects outcome. Data from small studies investigating the efficacy of multimodal neuromonitoring-guided treatment after SAH have been encouraging, but outcome data are lacking [12]. Figure 1 shows a practical approach to monitoring-guided management of DCI after SAH.Fig. 1

View Article: PubMed Central - PubMed

Affiliation: Neurocritical Care Unit, The National Hospital for Neurology and Neurosurgery, University College London Hospitals, Queen Square, London, WC1N 3BG, UK, martin.smith@uclh.nhs.uk.

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

The importance of treatment in high-volume centres by a multidisciplinary team cannot be over-emphasised... Endovascular coiling of intracranial aneurysms represents a major advance in the treatment of SAH and allows minimally invasive and effective treatment... DCI can occur in the absence of vasospasm and vice versa, and brain ischemia often involves more than one vascular territory... Other mechanisms contributing to DCI include distal vascular dysautoregulation, micro-thrombi, direct neurotoxic effects, inflammation and cortical spreading depolarizations (SDs)... A combination of hypervolemia, hemodilution and hypertension (triple H therapy) has historically been the mainstay of treatment to prevent and treat DCI, but the focus of cardiovascular management after SAH is now on a single H—hypertension... Prophylactic hypervolemia is not effective in increasing CBF or improving neurological outcome, and there is some evidence of harm from overly aggressive filling... Intracranial hypertension and lack of ICP response to medical therapy appear to be associated with DCI and poor clinical outcome after SAH, and ICP and CPP monitoring have a role in guiding therapy... Multimodal cerebral monitoring, including brain tissue oxygen tension, TCD, cerebral microdialysis and electrophysiological monitoring in addition to ICP, allows individualized therapy with the aim of preventing or minimizing secondary ischemic injury... Figure 1 shows a practical approach to monitoring-guided management of DCI after SAH... Using surface electroencephalography (EEG), seizures are recorded in around 8 % of patients after SAH but invasive EEG monitoring identifies seizure activity in almost 40 %... Continuous EEG monitoring is the only reliable way to detect subclinical seizures, and it may also predict DCI many hours in advance of clinical symptoms... Actual seizures must be treated aggressively but universal prophylaxis remains controversial... Three days of treatment offers similar seizure prevention and better outcome than longer-term therapy... Phenytoin has been associated with cognitive effects and poor outcome and, although of equal efficacy in controlling seizures, levetiracetam is often chosen for the management of early-onset seizures because of its more favourable side-effect profile.

Show MeSH
Related in: MedlinePlus