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

The properties of Althesin (anticonvulsant activity, depression of oxygen consumption, lowering of ICP, rapid excretion) led us to use this steroid combination to treat 11 patients in status epilepticus resistant to the standard drugs (benzodiazepines and barbiturates). The administration of Althesin by slow intravenous injection was ineffective in 2 of the 3 patients thus treated. The doses used (2--10 ml) were probably too small. One only administration of a 10% solution of Althesin in 10% fructose by intravenous drip (the rate was calculated so as to obtain the burst suppression stage at the EEG) stopped status epilepticus in 7 of the 9 patients thus treated. In this group the doses used varied from 25 to 50 ml. The 2 patients in whom it was necessary to repeat Althesin administration and combine it with other drugs had both been operated on for severe brain injuries involving marked cerebral edema. In spite of the very small number of cases, the definitive arrest of status epilepticus obtained in 8 out of 11 patients first treated with other drugs is encouraging: Althesin probably may be regarded as an adjunct in the treatment of status epilepticus.
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PMID:The use of althesin in drug-resistent status epilepticus. 47 37

Patients undergoing anesthesia soon after head trauma are at great risk for further neural damage during the anesthetic, especially if the head injury is severe or the anesthetic technique is suboptimal. Secondary complications of the anesthetic that are often lethal include hypoventilation, increases in ICP, airway obstruction, and brain-stem herniation. Anesthetic management of patients with head injury must include intravenous induction with barbiturates or narcotics, smooth endotracheal intubation, controlled ventilation with oxygen, and minimal amounts of inhalational agents. It is important to position the patient so that jugular veins are not occluded, in about 10 degrees head up position, and to avoid inducing patient coughing and straining. Recovery from anesthesia should be quiet and rapid, with the maintenance of a clear airway and the use of as little depressant medication post-operatively as possible. Oxygen should be provided.
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PMID:Anesthesia for patients with head trauma. 158 13

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

Changes of oxygen metabolism were observed in 8 experimental dogs and in 9 patients with head injury. Each dog harbored a bag in the epidural space, and was injected normal saline. The ICP was raised to 13.3 kPa and to 20.0 kPa respectively. Arterial oxygenation declined and mixed venous oxygenation went up when the ICP was raised to the given level and maintained for 30 minutes. The oxygen extraction rate decreased from 25.00 +/- 5.40% to 21.50 +/- 4.60% (P less than 0.01) at the ICP level of 20 kPa. Tissue hypoxia was observed in all patients. Although PaO was higher than inspiring air when patients inhaled 50% oxygen. Tissue hypoxia was not improved. The results suggest that the patients head injury is complicated by not only hypoxemia but decrease of oxygen extraction in tissue and organs. We consider that the alteration is responsible for multiple organs failure injury.
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PMID:[Changes in oxygen extraction rate after craniocerebral injury]. 187 4

The authors determined the effect of propofol on cerebral blood flow, intracranial pressure, and cerebral arteriovenous oxygen content difference in severely brain-injured patients during orthopedic treatment of fractures of the extremities. The Glasgow Coma Scale score was 6 or 7 at the time of the study. Data were collected in the operating room before and during (5 and 15 min) administration of propofol (2 mg/kg iv bolus immediately followed by a 150 micrograms.kg-1.min-1 infusion) before surgical stimulation. Propofol was infused during 41.4 +/- 7.3 min. After operation, the last set of measurements was made 15 min after propofol was stopped. The study was performed on 10 adults (age range, 15-40 yr) whose lungs were mechanically ventilated (air/O2) and who were sedated (phenoperidine, 1 mg/h), and was conducted using a radial artery cannula; a 7.5-Fr, thermodilution, flow-directed, pulmonary artery catheter; an intraventricular catheter; and a catheter in the jugular venous bulb. The 133xenon intra-internal carotid artery injection technique was used to determine regional cerebral blood flow (rCBF). Anesthetic blood concentration of propofol (3-5 micrograms/ml) was associated with decreases in cerebral perfusion pressure (CPP; from 82 +/- 14 to 59 +/- 7 mmHg; P less than 0.001), rCBF (from 35 +/- 6 to 26 +/- 5 ml.100 g-1.min-1; P less than 0.001), and intracranial pressure (ICP; from 11.3 +/- 2.6 to 9.2 +/- 2.5 mmHg; P less than 0.001). Cerebrovascular resistance and cerebral arteriovenous oxygen content difference were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of propofol on cerebral hemodynamics and metabolism in patients with brain trauma. 211 15

Ischemic cerebral edema frequently develops after aneurysm surgery and may lead to severe intracranial hypertension. Of prime importance are reducing the level of ICP and preserving oligemic areas from becoming infarcted. Besides correction of factors known to worsen intracranial hypertension, several therapeutics may be of value: external CSF drainage, perfusion of mannitol, induced arterial hypertension and use of anesthetic agents with cerebral vasoconstricting capability. Hyperventilation is not recommended. Arterial hypotension and hypovolemia certainly contribute to aggravate cerebral ischemia and must be corrected. Cerebral ischemia may be reduced by two specific approaches: by improving cerebral oxygen transport in ischemic areas using arterial hypertension and calcium blockers rather than hemodilution or hypervolemia; by reducing cerebral metabolic rates with heavy anesthesia under the cover of a complete cardiovascular monitoring. In view of the large heterogenicity in cerebral lesions and physiopathological stages, a therapeutical trial appears suitable in each individual case. Criteria allowing to know if any therapeutic, used alone or in association, is beneficial include increase in blood flow in ischemic areas, reduction of ICP level and normalizing of indices like CSF or venous jugular blood lactate.
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PMID:[Treatment of ischemic cerebral edema with intracranial hypertension after neurosurgery of intracranial aneurysms]. 212 75

During the last decade several studies of cerebral blood flow (CBF) and metabolism in the acute phase of head injury have been published. It is the aim of this review to describe the dynamic changes in CBF, cerebral metabolic rate of oxygen (CMRO2), cerebral autoregulation (CA), and reactivity to PaCO2 and barbiturate (metabolic reactivity) in the acute phase after severe head injury and to discuss the therapeutical consequences with reference to prolonged artificial hyperventilation, hypothermia, barbiturate sedation, and mannitol therapy. On the basis of present knowledge concerning cerebral circulation and its regulation, the author reviews the literature concerning methodology for experimental and clinical CBF measurements and regulation of CBF and cerebral oxygen uptake. Emphasis is placed on studies of the effect of body temperature (hypothermia) as a therapeutic tool in the control of cerebral metabolism, blood flow, and intracranial pressure. Although hypothermia significantly reduces cerebral metabolism and blood flow, the effect of hypothermia on cerebral blood flow, metabolism, ICP, and outcome after acute head injury has never been investigated in clinically controlled studies. Experimental and clinical studies concerning sensitivity of CBF for changes in PaCO2 are reviewed. The normal CO2 reactivity defined as absolute (delta CBF/delta PaCO2) and relative (% change CBF/delta PaCO2) or delta in CBF/PaCO2 mm Hg are mentioned. In awake normocapnic man the relative CO2 reactivity averages 4%/mm Hg and the absolute CO2 reactivity 2ml/mm Hg. Uncontrolled prospective studies show a therapeutic effect of artificially prolonged hyperventilation on outcome. Only one preliminary controlled study indicates that the outcome is poorer and recovery prolonged. Nevertheless, in the acute phase of HI, artificial hyperventilation is used routinely for control of intracranial hypertension and during the intensive care management of the patients. The steal and inverse steal phenomena are reviewed. Although of considerable theoretical interest these phenomena are without clinical significance in patients with head injury, unless clinical CBF measurements are performed. The frequency of the inverse steal phenomenon in studies of rCBF with a 16-channel Cerebrograph (intraarterial approach) is found to be about 10%. During prolonged hyperventilation experimental studies and clinical studies of apoplexy show an adaptation of CBF and CSF-pH and bicarbonate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cerebral blood flow in acute head injury. The regulation of cerebral blood flow and metabolism during the acute phase of head injury, and its significance for therapy. 227 29

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

Cross-brain oxygen extraction may be altered by coma, hyperventilation, hypothermia, or barbiturates, and has been demonstrated in adults and more recently in children to be related to functional neurologic recovery after a variety of brain injuries. However, measurement of cross-brain oxygen extraction in children is currently not a part of routine clinical care, partly because there have been no published attempts relating the technique of jugular venous bulb (JVB) catheterization and its complication in children. We catheterized the JVB to measure cerebral venous oxygen content and calculate cross-brain oxygen extraction in 26 deeply comatose neonates and children ranging in age from a few hours to 14 yr. Bedside catheterization using the Seldinger technique was successful in 25 children, with standard venous cutdown necessary in the remaining child. All JVB catheterizations were performed with parental consent and during continuous monitoring of the intracranial (ICP) or fontanelle, as well as arterial, pressure. ICP was not significantly altered by the cannulation procedure in any of the children studied, although the cannulation occurred early in the child's course when ICP was well controlled. Inadvertent carotid artery puncture with bleeding controlled by local pressure occurred in four children, and catheter malposition was confirmed on lateral skull xray in two others. Jugular venous bulb catheters remained in place for 2 to 7 days (average 3) and malfunction or obstruction of the catheter did not occur. Organisms were grown from three of 26 catheter tips submitted for culture, with peripheral blood cultures also positive for the same organisms in two of these.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Jugular venous bulb catheterization in infants and children. 231 61

In order to investigate the usefulness of atracurium for neurosurgical anesthesia, we studied its impact on intracranial pressure (subarachnoid bolt) mean arterial pressure (radial artery catheter) and cerebral perfusion pressure (mean arterial pressure-intracranial pressure) in 20 patients undergoing elective craniotomy for brain tumor excision. General anesthesia was induced with thiopental, 4 mg/kg intravenously, and maintained with 70 percent nitrous oxide in oxygen. Ventilation was controlled by face mask, with end-tidal CO2 held constant. Once intracranial pressure and mean arterial pressure had stabilized, the response to atracurium, 0.5 mg/kg intravenously, was continuously recorded for 5 min in 10 patients. An additional 10 patients received no atracurium and served as matched controls. Thiopental caused reductions in ICP in both groups of patients. Comparing the responses of the patients who received atracurium with those who did not, we found that atracurium had no significant effect on intracranial pressure, mean arterial pressure or cerebral perfusion pressure. Based on these data we conclude that atracurium appears to be preferable to the other available neuromuscular blocking agents that have been evaluated for neurosurgical anesthesia.
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PMID:Intracranial pressure after atracurium in neurosurgical patients. 293 38


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