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The incidence of non-traumatic subarachnoid hemorrhage (SAH) is 9 cases per 100,000 person-years, and it mainly affects relatively young patients with the highest productivity in life
.
The biphasic course of SAH patients begins at an early stage, which is a direct result of blood extravasation into the subarachnoid space (early brain injury, EBI, the first 72 hours, affecting 30% of patients), followed by the second stage, 20-30% Of patients have a higher risk of exacerbation (delayed cerebral ischemia, DCI), which peaks in the second week
.
Cerebral infarction caused by DCI is one of the most important factors for the long-term morbidity of survivors
.
Yimaitong compiles and organizes, please do not reprint without authorization
.
How to diagnose delayed cerebral ischemia and symptomatic vasospasm? 1.
Clinical diagnosis DCI is diagnosed by reliable neurological examination of the patient's clinical deterioration
.
In 2010, DCI was defined as "the occurrence of a new focal defect (hemiparesis, aphasia, apraxia, hemianopia or neglect) or a decrease in Glasgow coma score of at least 2 points and a duration of more than 1 hour
.
It is important to exclude secondary Other causes of neurological deterioration make DCI a diagnosis of exclusion
.
These factors include fever, infectious complications, hydrocephalus, seizures, respiratory failure, or electrolyte disturbances
.
The uniform definition of DCI promotes the relationship between the clinical environment and the trial.
Comparability
.
For patients who cannot undergo proper neurological examination, the diagnosis of DCI or related large vasospasm is challenging and the definition is not clear
.
It is very important to distinguish between delayed cerebral ischemia and delayed cerebral infarction (defined as irreversible lesions found on neuroimaging)
.
Symptomatic vasospasm refers to the clinical deterioration in the presence of vasospasm, while DCI is caused by a variety of reasons
.
2.
Neurological monitoring methods There are several monitoring techniques that can help detect DCI or related vasospasm
.
In the case of limited information on neurological examinations, these monitoring techniques are particularly important for patients who require sedation
.
However, the arousal test can overcome this limitation.
It can lead to an increase in ICP and a significant decrease in cerebral oxygenation, so it should not be performed in patients with a high risk of ICP
.
➤Transcranial Doppler Ultrasound and Transcranial Color Coded Duplex Ultrasound Bedside Transcranial Doppler Ultrasound (TCD) and Color Coded Duplex Ultrasound (TCCS) are widely used as screening methods to detect large vasospasm.
They It is cost-effective, easy to use, non-invasive, widely available, and allows dynamic monitoring through repeated measurements
.
The observer's dependence on predicting DCI and low specificity limit the accuracy of this method
.
A Lindegaard ratio greater than 3 (defined as the flow rate ratio between the middle cerebral artery and the distal end of the ipsilateral internal carotid artery, MCA/ICA) should be used to distinguish between vasospasm and congestion
.
Importantly, blood flow speed may be affected by hemoglobin levels (Hb), patient temperature, blood pressure (in the case of self-regulation disorders), pH and PaCO2 levels
.
➤Cerebral blood flow Cerebral blood flow (CBF) can be quantified by thermal diffusion flow meter or imaging methods (perfusion computed tomography (CTP), MR perfusion, PET)
.
CTP is used more and more, and by reducing cerebral perfusion to detect impending ischemia, it has the advantage of finding salvable brain tissue before irreversible brain damage occurs
.
➤Cerebral oxygenation measures cerebral perfusion pressure (CPP) and intracranial pressure in patients with low-grade SAH, and additionally monitors brain tissue oxygen partial pressure (PbtO2) to detect cerebral ischemia with high time resolution
.
➤Continuous EEG Continuous EEG (cEEG) is another option for detecting and predicting changes in DCI
.
The most commonly described quantitative EEG results for predictable DCI include a decrease in the alpha/delta ratio and a decrease in alpha variability
.
Changes in EEG may precede clinical deterioration by several hours
.
In addition, through the use of cEEG, it is feasible to exclude nonconvulsive status epilepticus that may cause clinical deterioration that may confuse the diagnosis of DCI
.
➤Cortical diffusion depolarization/ischemia Diffusion depolarizations (SDs) are self-propagating waves in gray matter at a speed of 2–5mm/min
.
SDs can appear in clusters or in isolation, and are still monitored by invasive subdural strip electrodes
.
In patients with brain injury, SDs are associated with reverse neurovascular coupling and vasoconstriction, leading to hypoperfusion, hypoxia and metabolic disorders in the brain, all of which may lead to DCI
.
➤Pupillary measurement The pupil measurement tool used to assess pupil reactivity is increasingly used in patients with brain injury
.
The objective pupil variables (size, contraction speed, latency, and expansion speed) are standardized, and the neurological pupil index (NPi) range is 0-5, and at least 3 values are considered normal
.
In a study of 56 SAH patients, 70% of the abnormal decrease in NPi was related to DCI that occurred more than 8 hours before clinical deterioration
.
Pupil measurement can be used as a supplement to other monitoring equipment, and the change of NPi may have a particularly important significance in improving the speed of TCD for early diagnosis of DCI
.
➤Cerebral angiography Angiography is still the gold standard for detecting cerebral vasospasm
.
The definition of severe vasospasm is more than 70% stenosis of the lumen
.
Vasospasm after subarachnoid hemorrhage most commonly affects the anterior cerebral artery (ACA) and the middle cerebral artery (MCA)
.
Treatment intervention ➤ Preventive treatment So far, there is no specific treatment strategy to effectively prevent DCI
.
Nimodipine is the only drug intervention to improve the prognosis of SAH patients and is recommended as a preventive treatment
.
Both intravenous and oral preparations are available in Europe, but intravenous nimodipine has not yet been approved by the U.
S.
Food and Drug Administration (FDA)
.
Nimodipine is a dihydropyridine calcium channel antagonist that blocks the flow of extracellular calcium ions through voltage-gated calcium channels
.
The neuroprotective mechanism is inferred by inhibiting SDs, reducing microthromboembolism, reducing vasospasm and enhancing fibrinolytic activity
.
➤General interventions The basic interventions for the treatment of all SAH patients are aimed at minimizing secondary brain injury, DCI, and improving functional outcomes
.
The principles of DCI management include optimizing cerebral blood flow, glucose delivery, and cerebral oxygenation
.
Fever is associated with a higher incidence of DCI.
Under the guidance of vigilant assessment of fluid balance and arterial blood pressure monitoring, all patients should maintain normal blood volume
.
In the case of hyponatremia [secondary to cerebral salt wasting syndrome (CSWS) or syndrome of inappropriate antidiuretic hormone secretion (SIADH)] and hypernatremia caused by diabetes insipidus or iatrogenic osmotic therapy, correct Abnormal natriemia is important
.
In SAH patients, strict glycemic control of intensive insulin therapy can lead to a higher rate of metabolic distress, lower brain glucose levels, and a worse prognosis
.
Currently, it is recommended to prevent hypoglycemia and aim for a more relaxed systemic blood glucose range (130-180mg/dl)
.
Blood pressure should be continuously monitored, and the use of multi-mode neuromonitoring can achieve individualized blood pressure management for unconscious patients
.
Under normal circumstances, it is recommended to keep the PaCO2 level between 35 and 45mmHg, and it can be individually adjusted through multi-mode neuromonitoring to achieve personalized treatment
.
The intensive care management of SAH patients advocates avoiding hypoxemia (PaO2<60mmHg) or hyperoxemia (>150mmHg)
.
➤Symptomatic interventions (applicable to patients with delayed cerebral ischemia) ①Permissive hypertension and hemodynamic enhancement are the most common interventions in DCI patients to improve cerebral perfusion, although there is no randomized study yet Prove its efficacy
.
Patients with hypovolemia can use vasopressors or fluids to gradually increase blood pressure levels, and it is possible to increase cerebral blood flow and improve microcirculation
.
Goal-directed therapy using transpulmonary thermodilution systems for fluid management may have a positive impact on DCI
.
In a randomized, controlled, single-center study in Germany, 108 SAH patients of all severity levels were assigned to receive goal-directed hemodynamic therapy (GDHT) or standard clinical treatment
.
The incidence of DCI in GDHT patients (13%) was significantly lower than that of patients based on standard clinical treatment (32%)
.
②Intra-arterial calcium channel antagonists If the neurological deficit caused by cerebral vasospasm does not contribute to induced hypertension, intra-arterial calcium channel antagonists (nimodipin, verapamil or nicardipine) can relieve the brain Vasospasm
.
However, in the guide, time and intensity are not fixed, and the effect may be short-lived
.
Summary Based on the complex pathophysiology of DCI, clinicians should devote themselves to multi-modal diagnostic methods, including clinical examination, multi-modal neural monitoring, and advanced imaging technology to detect high-risk patients and prevent cerebral infarction
.
More active interventions require a programmatic approach to obtain evidence beyond case reports and single-center experience
.
Yimaitong compiled from: Rass V, Helbok R.
How to diagnose delayed cerebral ischaemia and symptomatic vasospasm and prevent cerebral infarction in patients with subarachnoid haemorrhage.
Curr Opin Crit Care.
2021;27(2):103-114.
doi:10.
1097 /MCC.
0000000000000798
.
The biphasic course of SAH patients begins at an early stage, which is a direct result of blood extravasation into the subarachnoid space (early brain injury, EBI, the first 72 hours, affecting 30% of patients), followed by the second stage, 20-30% Of patients have a higher risk of exacerbation (delayed cerebral ischemia, DCI), which peaks in the second week
.
Cerebral infarction caused by DCI is one of the most important factors for the long-term morbidity of survivors
.
Yimaitong compiles and organizes, please do not reprint without authorization
.
How to diagnose delayed cerebral ischemia and symptomatic vasospasm? 1.
Clinical diagnosis DCI is diagnosed by reliable neurological examination of the patient's clinical deterioration
.
In 2010, DCI was defined as "the occurrence of a new focal defect (hemiparesis, aphasia, apraxia, hemianopia or neglect) or a decrease in Glasgow coma score of at least 2 points and a duration of more than 1 hour
.
It is important to exclude secondary Other causes of neurological deterioration make DCI a diagnosis of exclusion
.
These factors include fever, infectious complications, hydrocephalus, seizures, respiratory failure, or electrolyte disturbances
.
The uniform definition of DCI promotes the relationship between the clinical environment and the trial.
Comparability
.
For patients who cannot undergo proper neurological examination, the diagnosis of DCI or related large vasospasm is challenging and the definition is not clear
.
It is very important to distinguish between delayed cerebral ischemia and delayed cerebral infarction (defined as irreversible lesions found on neuroimaging)
.
Symptomatic vasospasm refers to the clinical deterioration in the presence of vasospasm, while DCI is caused by a variety of reasons
.
2.
Neurological monitoring methods There are several monitoring techniques that can help detect DCI or related vasospasm
.
In the case of limited information on neurological examinations, these monitoring techniques are particularly important for patients who require sedation
.
However, the arousal test can overcome this limitation.
It can lead to an increase in ICP and a significant decrease in cerebral oxygenation, so it should not be performed in patients with a high risk of ICP
.
➤Transcranial Doppler Ultrasound and Transcranial Color Coded Duplex Ultrasound Bedside Transcranial Doppler Ultrasound (TCD) and Color Coded Duplex Ultrasound (TCCS) are widely used as screening methods to detect large vasospasm.
They It is cost-effective, easy to use, non-invasive, widely available, and allows dynamic monitoring through repeated measurements
.
The observer's dependence on predicting DCI and low specificity limit the accuracy of this method
.
A Lindegaard ratio greater than 3 (defined as the flow rate ratio between the middle cerebral artery and the distal end of the ipsilateral internal carotid artery, MCA/ICA) should be used to distinguish between vasospasm and congestion
.
Importantly, blood flow speed may be affected by hemoglobin levels (Hb), patient temperature, blood pressure (in the case of self-regulation disorders), pH and PaCO2 levels
.
➤Cerebral blood flow Cerebral blood flow (CBF) can be quantified by thermal diffusion flow meter or imaging methods (perfusion computed tomography (CTP), MR perfusion, PET)
.
CTP is used more and more, and by reducing cerebral perfusion to detect impending ischemia, it has the advantage of finding salvable brain tissue before irreversible brain damage occurs
.
➤Cerebral oxygenation measures cerebral perfusion pressure (CPP) and intracranial pressure in patients with low-grade SAH, and additionally monitors brain tissue oxygen partial pressure (PbtO2) to detect cerebral ischemia with high time resolution
.
➤Continuous EEG Continuous EEG (cEEG) is another option for detecting and predicting changes in DCI
.
The most commonly described quantitative EEG results for predictable DCI include a decrease in the alpha/delta ratio and a decrease in alpha variability
.
Changes in EEG may precede clinical deterioration by several hours
.
In addition, through the use of cEEG, it is feasible to exclude nonconvulsive status epilepticus that may cause clinical deterioration that may confuse the diagnosis of DCI
.
➤Cortical diffusion depolarization/ischemia Diffusion depolarizations (SDs) are self-propagating waves in gray matter at a speed of 2–5mm/min
.
SDs can appear in clusters or in isolation, and are still monitored by invasive subdural strip electrodes
.
In patients with brain injury, SDs are associated with reverse neurovascular coupling and vasoconstriction, leading to hypoperfusion, hypoxia and metabolic disorders in the brain, all of which may lead to DCI
.
➤Pupillary measurement The pupil measurement tool used to assess pupil reactivity is increasingly used in patients with brain injury
.
The objective pupil variables (size, contraction speed, latency, and expansion speed) are standardized, and the neurological pupil index (NPi) range is 0-5, and at least 3 values are considered normal
.
In a study of 56 SAH patients, 70% of the abnormal decrease in NPi was related to DCI that occurred more than 8 hours before clinical deterioration
.
Pupil measurement can be used as a supplement to other monitoring equipment, and the change of NPi may have a particularly important significance in improving the speed of TCD for early diagnosis of DCI
.
➤Cerebral angiography Angiography is still the gold standard for detecting cerebral vasospasm
.
The definition of severe vasospasm is more than 70% stenosis of the lumen
.
Vasospasm after subarachnoid hemorrhage most commonly affects the anterior cerebral artery (ACA) and the middle cerebral artery (MCA)
.
Treatment intervention ➤ Preventive treatment So far, there is no specific treatment strategy to effectively prevent DCI
.
Nimodipine is the only drug intervention to improve the prognosis of SAH patients and is recommended as a preventive treatment
.
Both intravenous and oral preparations are available in Europe, but intravenous nimodipine has not yet been approved by the U.
S.
Food and Drug Administration (FDA)
.
Nimodipine is a dihydropyridine calcium channel antagonist that blocks the flow of extracellular calcium ions through voltage-gated calcium channels
.
The neuroprotective mechanism is inferred by inhibiting SDs, reducing microthromboembolism, reducing vasospasm and enhancing fibrinolytic activity
.
➤General interventions The basic interventions for the treatment of all SAH patients are aimed at minimizing secondary brain injury, DCI, and improving functional outcomes
.
The principles of DCI management include optimizing cerebral blood flow, glucose delivery, and cerebral oxygenation
.
Fever is associated with a higher incidence of DCI.
Under the guidance of vigilant assessment of fluid balance and arterial blood pressure monitoring, all patients should maintain normal blood volume
.
In the case of hyponatremia [secondary to cerebral salt wasting syndrome (CSWS) or syndrome of inappropriate antidiuretic hormone secretion (SIADH)] and hypernatremia caused by diabetes insipidus or iatrogenic osmotic therapy, correct Abnormal natriemia is important
.
In SAH patients, strict glycemic control of intensive insulin therapy can lead to a higher rate of metabolic distress, lower brain glucose levels, and a worse prognosis
.
Currently, it is recommended to prevent hypoglycemia and aim for a more relaxed systemic blood glucose range (130-180mg/dl)
.
Blood pressure should be continuously monitored, and the use of multi-mode neuromonitoring can achieve individualized blood pressure management for unconscious patients
.
Under normal circumstances, it is recommended to keep the PaCO2 level between 35 and 45mmHg, and it can be individually adjusted through multi-mode neuromonitoring to achieve personalized treatment
.
The intensive care management of SAH patients advocates avoiding hypoxemia (PaO2<60mmHg) or hyperoxemia (>150mmHg)
.
➤Symptomatic interventions (applicable to patients with delayed cerebral ischemia) ①Permissive hypertension and hemodynamic enhancement are the most common interventions in DCI patients to improve cerebral perfusion, although there is no randomized study yet Prove its efficacy
.
Patients with hypovolemia can use vasopressors or fluids to gradually increase blood pressure levels, and it is possible to increase cerebral blood flow and improve microcirculation
.
Goal-directed therapy using transpulmonary thermodilution systems for fluid management may have a positive impact on DCI
.
In a randomized, controlled, single-center study in Germany, 108 SAH patients of all severity levels were assigned to receive goal-directed hemodynamic therapy (GDHT) or standard clinical treatment
.
The incidence of DCI in GDHT patients (13%) was significantly lower than that of patients based on standard clinical treatment (32%)
.
②Intra-arterial calcium channel antagonists If the neurological deficit caused by cerebral vasospasm does not contribute to induced hypertension, intra-arterial calcium channel antagonists (nimodipin, verapamil or nicardipine) can relieve the brain Vasospasm
.
However, in the guide, time and intensity are not fixed, and the effect may be short-lived
.
Summary Based on the complex pathophysiology of DCI, clinicians should devote themselves to multi-modal diagnostic methods, including clinical examination, multi-modal neural monitoring, and advanced imaging technology to detect high-risk patients and prevent cerebral infarction
.
More active interventions require a programmatic approach to obtain evidence beyond case reports and single-center experience
.
Yimaitong compiled from: Rass V, Helbok R.
How to diagnose delayed cerebral ischaemia and symptomatic vasospasm and prevent cerebral infarction in patients with subarachnoid haemorrhage.
Curr Opin Crit Care.
2021;27(2):103-114.
doi:10.
1097 /MCC.
0000000000000798
