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Query: UMLS:C0268318 (ICP)
 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

If good anesthesia is to be provided to the patient undergoing surgery for an expanding intracranial lesion, certain principles should be borne in mind. These principles include: 1. Careful preoperative assessment of the patient 2. Awareness of abnormal intracranial dynamics in the presence of an intracranial mass lesion 3. The importance of a smooth induction of anesthesia 4. Adequate depth of anesthesia and complete muscle paralysis before laryngoscopy and intubation 5. The choice of a maintenance technique that does not increase ICP and allows adequate CPP. Failure to adhere to these principles may lead to sudden increases in intracranial pressure, decreased cerebral perfusion pressure, and regional ischemia. In the closed skull, internal herniation of brain tissue through the tentorial notch or the foramen magnum may occur. External brain herniation, with increased bleeding and rupture of cerebral cortex, may occur after the dura mater has been opened if these anesthetic parameters are not controlled. Neuroanesthesia, therefore, plays an important role in the reduction of morbidity and mortality in the surgery of intracranial lesions of all types, including neoplasms - not only in the operating room, but also in the pre- and postoperative care of the neurosurgical patient.
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PMID:Anesthesia for intracranial surgery with particular reference to surgery for neoplasms. 77 21

The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
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PMID:The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction. 159 96

The ICP monitoring is currently used in the treatment of the head injured patients in order to avoid dangerous increases of the pressure and critical reduction of cerebral perfusion pressure (CPP). The cerebral blood flow is dependent on the CPP and is kept constant, under normal circumstances, by autoregulation. When autoregulation is impaired or overwhelmed oxygen delivery becomes uncoupled to the metabolic needs of cerebral tissue: in such a condition the rate of oxygen extraction changes and the artero-jugular difference for O2 (AVDO2) reflects this change. The AVDO2 can be used as an estimate of the CBF and can detect a situation of hyperemia (low AVDO2) or ischemia (high AVDO2). In 224 comatose head injured patients the ICP was measured using ventricular or subarachnoid catheters: the CPP was continuously assessed and the outcome was evaluated six months after the trauma. In 45 patients the AVDO2 was studied and the data were corrected for a PaCO2 of 40 mmHg and investigated. The severity of the ICP is decisive for the prognosis and, accordingly, the number of times the CPP is below 60 mmHg plays a major role in the outcome. The mortality rate was 21% for the patients without ICP greater than 20 mmHg and 54% for the patients with severe increases in ICP. The mean values of AVDO2 were low, ranging around 4.6 vol%; only 4 patients showed some temporary evidence of ischemia, as assessed by an AVDO2 greater than 8 vol%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arterio-jugular difference of oxygen and intracranial pressure in comatose, head injured patients. II. Clinical correlations]. 175 72

Barbiturates reduce cerebral activity which again reduce the cerebral metabolic rate probably by activating chloride channels and potentiating GABA's effects on these channels. Protection of the brain against hypoxia might theoretically occur by this mechanism, by vasoconstriction or by inhibiting calcium or glutamate. The barbiturates appear to have a positive effect in head-injury patients with high ICP uncontrollable by conventional therapy (in one study 5% of patients with a GCS < or = 7), and in animal studies of regional ischemia. No effect has been established in complete cerebral ischemia (cardiac arrest). The barbiturates have a depressant effect on the cardiovascular and respiratory systems, and the patients require intensive care. Thus there are some indications in the literature that the barbiturate treatment itself causes complications, and it is possible that this might cancel a potential beneficial effect in some patients. Clinically, the barbiturates are effective anticonvulsants, can be used in an attempt to control an elevated ICP uncontrollable by conventional means, and during transient ischemic episodes in the operating room with adequate monitoring and support systems already in place.
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PMID:Barbiturates in neuroanesthesia and neuro-intensive care. 184 34

This study was carried out to clarify the changes of pulse pressure of the intracranial pressure pulse wave in ischaemic brain oedema. Intracranial pressure and PP were measured in two groups of anaesthetized dogs; 1) increased volume of cerebrospinal fluid by cisternal saline injection (control group), 2) brain oedema caused by focal ischaemia (oedema group). Ischaemia was induced by 2 hours of occlusion of the anterior, middle cerebral and internal carotid arteries. The canine focal ischaemic model showed consistent ischaemic damage in the caudate nucleus and produced brain oedema successfully. PP increased linearly with rising ICP to 35 mm Hg, and PP in the oedema group was significantly smaller than that in the control group at the same ICP value. The slopes of the regression equation of ICP and PP were significantly different between the oedema and control group (oedema: 0.057 +/- 0.029, control: 0.106 +/- 0.009), mean +/- SD, P less than 0.005). These results suggest that PP is easily affected by ischaemic brain oedema, which indicates increase of the brain tissue in the cranium. We conclude that PP is affected even at the same ICP value when intracranial components have altered.
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PMID:Changes in epidural pulse pressure in brain oedema following experimental focal ischaemia. 208 49

CPP reflects perfusion problems related to increased ICP or inadequate MAP. CPP is a most helpful and practical management tool. The relationship of CBF and CPP depends on cerebral vascular resistance (flow equals pressure divided by resistance). At present, we do not have a practical method to measure vascular resistance or CBV. A close relationship between an increase in CBV and increase in ICP exists. However, the relationship between CBF and ICP is more complex. Whereas CBV is strongly dependent on vasodilation and venous return, CBF is influenced by CPP, vascular resistance, viscosity changes, and focally or diffusely increased ICP. For instance, in hypotensive shock one finds a low CBF with an elevated CBV (and ICP) from vasodilation related to hypercapnia, anoxia, or acidosis. Nevertheless, about two thirds of patients with increased ICP after head injury have increased CBF (hyperemia) and increased CBV. This frequent hyperemia is one rationale for the wide usage of hyperventilation to treat increased ICP. It must be recognized that a group of patients may have ischemia caused by excessive hyperventilation therapy for increased ICP. The PaCO2 must not be allowed to decrease to 20 mmHg or lower, but in some patients a PaCO2 level of 21 to 25 may be predisposing to ischemia. Strong consideration is thus given to monitoring CBF and cerebral oxygen metabolism (arteriovenous oxygen content difference [AVDO2], CMRO2) in states of coma and increased ICP. In such patients, continuous infusion of mannitol may result in improved CBF, and hyperventilation therapy can be less aggressive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonsurgical management of increased intracranial pressure. 270 May 10

Monitoring modalities unique to the neurologic intensive care unit include intracranial pressure monitors and neuroelectrophysiologic monitors. Each modality fullfills criteria for accuracy, responsivity during clinical change, and stability over time for trend analysis. Intracranial pressure monitoring may be accomplished by any of three approaches--ventricular catheter, subarachnoid bolt, or epidural pressure transducer. Intracranial pressure control has proved beneficial in at least three different illnesses--acute closed head injury, acute noncommunicating hydrocephalus, and Reye's syndrome. Other illnesses, such as cerebral hemorrhage, near drowning, meningitis, encephalitis, and cerebral mass lesions, are often associated with ICP elevations. Neuroelectrophysiologic monitoring encompassing electroencephalography (EEG), signal-processed EEG, and evoked potentials has proved to be most beneficial to the intensive care setting. Evoked potentials are most useful for monitoring patients in drug-induced coma or muscle paralysis in whom a clinical neurologic examination is unreliable. Focal neurologic deficits, incipient brainstem ischemia, and possibly brain death can be deduced from multimodality-evoked potentials (brainstem auditory and somatosensory). Evoked potential apparatus can be used to record sequential stimuli and trend changes. Signal-processed EEG apparatus (compressed spectral array and cerebral function monitor) are used to assess global or regional EEG activity for longer periods of time. Interpretation of signal-processed EEG recording requires some experience with this technique, but it is much easier to interpret than a standard 16-lead EEG. These monitors are useful in evaluating some forms of abnormal EEG activity and in monitoring gross changes in global or regional electrical activity. Currently available technology offers dynamic insight into the management of acute neurologic illnesses. The technology in evoked potential and signal processed EEG monitoring will eventually reduce the size and complexity of the instrumentation, making its application routine. Intracranial pressure monitoring is already routine in many intensive care units, although its use is occasionally sporadic. We believe that application of appropriate neurologic monitors improves therapy and outcome in neurologically injured and ill patients.
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PMID:Neurologic intensive care unit monitoring. 391 79

Vasospasm after clipping of an acute ruptured aneurysm plays an important role in its prognosis. An effective therapy for vasospasm has not been established. We had attempted to remove the subarachnoid clot, which probably caused vasospasm, by ventriculo-cisternal irrigation and had not so good results (A: a group without decompression). Therefore, we have performed a therapy combined ventriculo-cisternal irrigation with external decompression (B: a group with decompression). We wish to report the efficacy of external decompression for an acute ruptured aneurysm. Evaluation of the outcome is due to Table 2. 55% of A group and 80% of B group have a better grade than "fair". Furthermore, a significant difference lies between A and B group associated with symptomatic vasospasm (brain ischemia caused by vasospasm). Namely, A group has all poor or dead cases but B group has 80% of the cases better than "fair". We concluded that relieving ICP by external decompression could suppress the aggravation of the post operative symptomatic vasospasm.
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PMID:[Combined therapy of ventriculo-cisternal irrigation with external decompression in acute ruptured aneurysm]. 647 46

There is a type of cerebral lesion, which kills neuronal cells at a later stage (greater than 48 hrs) post CA, while the systemic circulation is functioning normally. Although this lesion is probably dependent on multiple factors (----multiple therapies), a keyfactor in the pathogenesis is the loss of autoregulation and "finetuning" of the cerebral bloodflow according to local tissue metabolic needs. Although beneficial effect of almost none of the following therapies has been documented in randomised clinical studies, the following suggestions are made: a) In the CA-CPR phase: efficient respiratory care and external cardiac compressions (ECC), especially during bicarbonate administration; consider open chest CPR early, especially in cases of long arrest time and ineffective ECC. The socalled new CPR does not improve neurological outcome. b) In the post CPR phase: The non-autoregulated brain (cfr. focal ischemia) is kept preferentially at pCO2 values 25-30 mmHg, pO2 values greater than 100 mmHg, and normotension. Some form of stress, seizure and hyperthermia control prevents further imbalance metabolism/bloodflow. Relative dehydration, oncotic balance, steroids, early control of sepsis and uremia, early CT scan and measurement/control of ICP. All the above is currently grouped under "standard neuro-intensive therapy". Some other therapies, presently suggested by animal research are not very obvious, need first randomised clinical studies and are not suggested at this stage for clinical use: barbiturate coma, diphantoine, streptokinase, multifaceted therapy including hemodilution-brainflushing, Ca++ influx blocking drugs (lidoflazine). One such "innovative" therapy, barbiturate coma, has already been proven to be relatively ineffective (BRCT I) (Acta anaesth. belg., 1984, 25, suppl., 219-226).
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PMID:Brain protection in the immediate post-resuscitation phase. 651 33

Therapy for acute ischemic stroke includes general and specific measures. General management such as respiratory and cardiac care, fluid and electrolyte management, blood pressure control, and treatment of increased ICP is the basis of all stroke treatment. Specific treatment is directed to recanalization of the occluded vessel, control of life-threatening brain edema, and protection of neuronal tissue against the toxic effects of ischemia. Although controlled studies are still lacking, application of the proposed general interventions provides a high-quality standard in patients with acute stroke. Among specific therapies, medical thrombolysis has demonstrated instances of significant and sustained neurologic improvement. Several multicenter trials are underway to confirm these preliminary results. In addition to thrombolysis, cell-protecting drugs hold promise for the future. Presumably, a combination of thrombolytic and cell-protecting agents will be the treatment of choice in early stroke in the future.
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PMID:Neurocritical care for acute ischemic stroke. 747 17


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