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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The records of all patients undergoing optic nerve sheath decompression for visual failure in chronic raised intracranial pressure performed over a 15 year period have been reviewed. The aim was to study the visual outcome and relation to any shunting procedures. Fourteen patients (20 eyes) were identified in whom follow up information of at least one year was available. Eleven patients had benign intracranial hypertension (idiopathic intracranial hypertension) and three had dural venous sinus occlusive disease. Eight patients had unilateral surgery and six had bilateral surgery. Visual acuity and fields either improved or stabilised in 17 out of 20 eyes and three deteriorated. Of the eight patients undergoing unilateral surgery, the other eye remained stable in seven and deteriorated in one. Four patients required optic nerve sheath decompression despite previous shunting or subtemporal decompression. Five patients required shunts or subtemporal decompression after optic nerve sheath decompression because of persistent headache in three cases and for uncontrolled visual failure in two cases. No patients lost vision as a direct consequence of surgery. It is concluded that optic nerve sheath decompression is a safe and important therapeutic option in the management of chronic raised intracranial pressure complicated by visual loss. Vision can be saved after shunt failure, and in other cases may be maintained without the need for a shunt. Shunts may still be required, however, after optic nerve sheath decompression, especially for persistent headache.
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PMID:Optic nerve sheath decompression for the treatment of visual failure in chronic raised intracranial pressure. 796 27

A 12-year-old girl presented with primary hypothyroidism, secondary pituitary hyperplasia, and intracranial hypertension. Cranial computed tomography revealed a sellar mass with suprasellar extension. She responded to medical treatment. Intracranial hypertension may be associated with primary hypothyroidism prior to thyroxine treatment. Because significant pituitary hyperplasia can be associated with primary hypothyroidism, it is vital to have endocrine investigation prior to consideration of surgical removal of an apparent pituitary tumor.
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PMID:Primary hypothyroidism with intracranial hypertension and pituitary hyperplasia. 802 69

Seven term neonates with encephalopathy resulting from asphyxia and/or intracranial hemorrhage underwent invasive monitoring of intracranial pressure through the epidural or intracerebral space. The average age (in hours) at insertion of the monitor was 27 h in the 3 neonates with asphyxia and 70 h in the 4 neonates with hemorrhage. Intracranial hypertension was noted in 6 neonates. The management of the hypertension included hyperventilation followed by mannitol for pressures that were sustained above 20 mmHg and pentobarbital for pressures above 30 mmHg. The duration of the hypertension varied in 5 neonates from 4 to 72 h, while in the remaining neonates, the pressure remained elevated until death at 70 h. All 4 survivors with intracranial hemorrhage have minimal neuromotor deficits on follow up and 2 survivors with asphyxia have cognitive deficits and are microcephalic. From this small series, it appears that in the management of term neonates with intracranial hemorrhage, monitoring of intracranial pressure should be considered.
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PMID:Feasibility of invasive monitoring of intracranial pressure in term neonates. 804 99

Raised intracranial pressure is the final common path to brain damage and brain death from a variety of intracranial conditions. Since the introduction of continuous monitoring of intracranial pressure into neurosurgical practice, much work has been undertaken which has advanced our knowledge of intracranial pressure and its management. The treatment of raised intracranial pressure should begin as soon as possible. The position of the head and neck should be checked to ensure that there is not an excessive degree of flexion or rotation. The airway should also be checked for obstruction and the patient observed to ensure that he is not making respiratory efforts against the respirator. The body temperature should not be above normal. Blood gases or other parameters of the adequacy of ventilation should be assessed and any abnormalities corrected. The sedation/analgesia regimen should be checked to ensure that it is sufficient and the patient is not experiencing pain. The serum sodium should be checked to ensure that hyponatraemia is not the cause of the intracranial hypertension. If intracranial hypertension persists despite the meticulous applications of these measures, then more specific therapy is required. This essentially reduces to a choice between osmotic agents, hypnotic drugs and drainage of cerebrospinal fluid.
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PMID:[Therapy for high intracranial pressure]. 804 76

The association of intracranial hypertension and arteriovenous malformations is described in two patients. Both patients had the typical clinical features of pseudotumour cerebri and were found to have intracranial arteriovenous malformations on arteriography. The mechanism of raised intracranial pressure in patients with arteriovenous malformations is discussed.
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PMID:Pseudotumour cerebri associated with arteriovenous malformations. 823 11

We present a patient with chronic myeloid leukemia (CML) who had marked bilateral disc swelling as part of his initial presentation. This occurred in the setting of raised intracranial pressure (ICP), with normal cerebrospinal fluid (CSF) composition and cell content, and normal neuroimaging. We discuss the possible mechanisms which could lead to disc swelling in CML and conclude that the raised ICP and subsequent papilloedema in our patient were the result of poor absorption of CSF into the dural venous sinuses. We propose that the very high white cell count (WCC) led to a hyperviscosity state which resulted in poor absorption of CSF and in so doing, created a clinical picture of benign intracranial hypertension (BIH).
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PMID:Benign intracranial hypertension in chronic myeloid leukemia. 826 Jan 57

Previous studies have suggested that only a small proportion (< 15%) of comatose head-injured patients whose initial computerized tomography (CT) scan was normal or did not show a mass lesion, midline shift, or abnormal basal cisterns develop intracranial hypertension. The aim of the present study was to re-examine this finding against a background of more intensive monitoring and data acquisition. Eight severely head-injured patients with a Glasgow Coma Scale score of 8 or less, whose admission CT scan did not show a mass lesion, midline shift, or effaced basal cisterns, underwent minute-to-minute recordings of arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) derived from blood pressure minus ICP. Intracranial hypertension (ICP > or = 20 mm Hg lasting longer than 5 minutes) was recorded in seven of the eight patients; in five cases the rise was pronounced in terms of both magnitude (ICP > or = 30 mm Hg) and duration. Reduced CPP (< or = 60 mm Hg lasting longer than 5 minutes) was recorded in five patients. Severely head-injured (comatose) patients whose initial CT scan is normal or does not show a mass lesion, midline shift, or abnormal cisterns nevertheless remain at substantial risk of developing significant secondary cerebral insults due to elevated ICP and reduced CPP. The authors recommend continuous ICP and blood pressure monitoring with derivation of CPP in all comatose head-injured patients.
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PMID:Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography. 808 May 31

During the past decade the management of clients with severe head injuries has been influenced by the use of hyperventilation. Increased intracranial pressure (I.C.P.) is the major cause of death following head injury and outcome has been linked to the ability of the practitioner to control intracranial hypertension. Hyperventilation is one method that is frequently employed to control increases in I.C.P. There is no doubt that hyperventilation effectively reduces intracranial pressure, but controversy surrounds the influence that this procedure may inflict upon the cerebral hemodynamic reserve (C.H.R.). The literature indicates that in spite of normal cerebral perfusion pressure, associated with raised I.C.P., that C.H.R. may be compromised. This paper will examine the controversy that surrounds the use of hyperventilation in the client with severe head injury.
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PMID:Hyperventilation in head injury does it do more harm than good? 827 95

This review has been written at an unfortunate time. Novel questions are being asked of the old therapies and there is an abundance of new strategies both to lower ICP and protect the brain against cerebral ischaemia. In the United Kingdom, the problem is to ensure that appropriate patients continue to be referred to centres where clinical trials of high quality can be undertaken. One of the success stories of the past decade has been the decline in the number of road accidents as a result of seat belt legislation, improvements in car design and the drink/driving laws. Hence, fortunately there are fewer patients with head injuries to treat and it is even more important that patients are appropriately referred if studies to assess efficacy of the new strategies are not to be thwarted. The nihilistic concept that intensive investigation with ICP monitoring for patients with diffuse head injury or brain swelling following evacuation of a haematoma or a contusion has no proven beneficial effect on outcome, requires revision. A cocktail of therapies may be required that can be created only when patients are monitored in sufficient detail to reveal the mechanisms underlying their individual ICP problem. Ethical problems may arise over how aggressively therapy for intracranial hypertension should be pursued and for how long. There has always been the concern that cranial decompression or prolonged barbiturate coma may preserve patients but with unacceptably severe disability. Some patients may be salvaged from herniating with massive cerebral infarction with the use of osmotherapy but is the outcome acceptable? Similar considerations apply to some children with metabolic encephalopathies. Where such considerations have been scrutinised in patients with severe head injury, the whole spectrum of outcomes appears to be shifted so that the number of severe disabilities and persistent vegetative states are not increased. However, it is important to be sensitive to such issues based on experience of the particular cause of raised intracranial pressure in a given age group.
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PMID:Management of raised intracranial pressure. 835 99

Intracranial hypertension following traumatic brain injury is associated with considerable morbidity and mortality. Hemorrhagic hypovolemia commonly coexists with head injury in this population of patients. Therapy directed at correcting hypovolemic shock includes vigorous volume expansion with crystalloid solutions. It is hypothesized that, following traumatic brain injury, cerebrovascular dysfunction results in rapid loss of brain compliance, resulting in increased sensitivity to cerebrovascular venous pressure. Increased central venous pressure (CVP) occurring with vigorous crystalloid resuscitation may therefore contribute to the loss of brain compliance and the development of intracranial hypertension. The authors tested this hypothesis in miniature swine subjected to traumatic brain injury, hemorrhage, and resuscitation. Elevated CVP following resuscitation from hemorrhage to a high CVP significantly worsened intracranial hypertension in animals with concurrent traumatic brain injury, as compared to animals subjected to traumatic brain injury alone (mean +/- standard error of the mean: 33.0 +/- 2.0 vs. 20.0 +/- 2.0 mm Hg, p < 0.05) or to animals subjected to the combination of traumatic brain injury, hemorrhage, and resuscitation to a low CVP (33.0 +/- 2.0 vs. 24.0 +/- 2.0 mm Hg, p < 0.05). These data support the hypothesis that reduction in brain compliance can occur secondary to elevation of CVP following resuscitation from hemorrhagic shock. This may worsen intracranial hypertension in patients with traumatic brain injury and hemorrhagic shock.
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PMID:Traumatic brain injury, hemorrhagic shock, and fluid resuscitation: effects on intracranial pressure and brain compliance. 796 34


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