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

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.
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PMID:[The internal environment and intracranial hypertension]. 975 May 95

Three children (two girls aged 7 and 9 years, and one boy aged 4 years) with diuretic resistant oedema in steroid resistant nephrotic syndrome were treated with a combination of intravenous mannitol and frusemide. All three responded with loss of oedema of 10% to 30% of body weight over one week. There were no complications of hypertension or hypovolaemia. Mannitol-frusemide combination is a safe, inexpensive, and effective treatment for diuretic resistant oedema. Its use in other conditions and in developing countries (where the availability and purity of 20% albumin is limited) needs to be explored.
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PMID:Mannitol and frusemide in the treatment of diuretic resistant oedema in nephrotic syndrome. 1032 39

We had performed indirect revascularization surgery, mainly EMS, for cases with moyamoya disease, because EMS can revascularize a large area including the territory of anterior cerebral artery. However, in our initial cases, we found that three sides in two cases had post-operative ischemic complications. These cases suggested that intracranial hypertension due to pressure exerted by swelling caused by edema in the myoflap after EMS was one of the reasons for these infarctions. For the prevention of intracranial hypertension due to the edema in the myoflap, when we did EDAMS with dural pedicle insertion, we put into practice the new ideas about shaving the boneflaps to half of their original thickness, and prescribed 20% Mannitol after surgery. We tried these new ideas concerning treatment on four sides in three cases with moyamoya disease, and we were able to get good outcomes without any new neurological deficits.
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PMID:[New ideas for indirect revascularization surgery for moyamoya disease]. 1056 41

Limitation of secondary insults after severe head injury is a permanent concern during the early phase of head trauma management. The objectives are to maintain mean arterial pressure between 80 and 100 mmHg, to avoid hypoxaemia, and to maintain arterial PCO2 near to 35 mmHg. Volume loading can be necessary to improve arterial pressure, and is carried out with isotonic critalloid (NaCl 9/1000) or colloids, with the exclusion of all hypotonic solutions (Ringer lactate or glucose). The use of catecholamines is reserved for patients with unstable haemodynamics despite an adequate volume loading. The rapid sequence induction is recommended for endotracheal intubation and is followed by continuous analgesia-sedation to keep patient-ventilator dysynchrony, but without compromising haemodynamic objectives. Mannitol is used in case of life-threatening intracranial hypertension. Conversely, specific treatment of intracranial hypertension, especially hypocapnia, is not recommended. Initial diagnostic procedures include cerebral tomodensitometry (TDM). However, TDM may be delayed in case of haemorrhage, which requires a rapid treatment. Intrahospital transport for additional explorations risks secondary insults, and thus requires close monitoring to detect and treat in due time all adverse events. This monitoring includes invasive arterial blood pressure assessment, use of continuous capnography and repeated arterial blood gas measurements. The usefulness of transcranial Doppler for initial management of head-trauma patients needs further evaluation.
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PMID:[Management of severe head-injured patients in the first 24 hours. Resuscitation and initial diagnostic strategy]. 1083 16

Intracranial and systemic mechanisms of the secondary brain lesion are the targets of specific therapy for the head-injured patient. Recommendations for good clinical practice have recently defined the role of the main therapeutic measures. There is no indication for corticosteroids in head injury. Mannitol is the first-choice therapy for increased intracranial pressure, and barbiturates are still considered as a rescue therapy in case of refractory intracranial hypertension. The place of hypothermia remains to be defined. Although controversial, optimized hyperventilation, induced systemic hypertension and vasoconstrictive therapy are optimally used under multimodal monitoring. New therapeutic perspectives, aimed at controlling biochemical disorders at a cellular level, are under investigation, but are still inconclusive at the present time.
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PMID:[Management of severely head-injured patients during the first 24 hours. Which specific therapeutics?]. 1083 22

There are two "class 1" studies, and one "class 2" study, and a large body of "Class 3" data, which can be used to support mannitol. The evidence supporting use of mannitol for ICP control is sufficiently strong to warrant guideline status. Mannitol is effective in reducing ICP, and its use is recommended as a guideline in the management of traumatic intracranial hypertension. Serum osmolalities >320 mOsm and hypovolemia should be avoided. There is some data to suggest that bolus administration is preferable to continuous infusion.
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PMID:The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Use of mannitol. 1093 95

Since 1995 a Group of Italian Neurointensivists and Neurosurgeons belonging to the Italian Societies of Neurosurgery (SINch) and Anesthesia & Intensive Care (SIAARTI) has produced some recommendations for treatment of adults with severe head trauma. They have been published in 3 parts: Part I (Initial assessment, Evaluation and pre-hospital treatment, Criteria for hospital admission, Systemic and cerebral monitoring), Part II (Medical treatment) and Part III (Surgical treatment criteria). These recommendations reflect a multidisciplinary consent and are mostly based on expert opinion. The main aim is to provide a practical reference for all those dealing with severe head injuries from first-aid to intensive care units, setting out the minimal goals of management to be reached throughout the Country. These recommendations need a continuous critical review and updating. Medical treatment is aimed at preventing or minimizing secondary brain damage following acute brain injury, provided that surgical masses have been promptly identified and removed. In order to assure cerebral perfusion, systemic hemodynamics and respiratory exchanges should be normal. Volemia is crucial, and mean arterial pressure should remain above 90 mmHg. Good general intensive care, including gastroprotection, water-electrolyte balance, infection control, nutrition and physiotherapy, is assumed as the basis for brain-oriented therapy. Intracranial hypertension requires an approach based on various steps. First, factors that can directly rise intracranial pressure (ICP) such as venous outflow obstruction, fever, pain etc. should be checked and corrected. Second, Mannitol, CSF withdrawal, sedation and moderate hyperventilation should be applied. This can be done by targeting specific problems with specific treatment (which is possible when the cause of ICP rise is known) or in a step-wise approach, by using less aggressive interventions before than more aggressive ones, with a higher risk of complications. Third, extreme treatment, such as barbiturates, should be reserved to cases with refractory intracranial hypertension. The main goal of ICP treatment is not simply ICP reduction, but the maintenance of adequate cerebral perfusion pressure.
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PMID:Guidelines for the treatment of adults with severe head trauma (part II). Criteria for medical treatment. 1096 91

Acute bacterial meningitis (ABM) in children is associated with a high rate of acute complications and mortality, particularly in the developing countries. Most of the deaths occur during first 48 hours of hospitalization. Coma, raised intracranial pressure (ICP), seizures, shock have been identified as significant predictors of death and morbidity. This article reviews issues in critical care with reference to our experience of managing 88 children with ABM in PICU. Attention should first be directed toward basic ABCs of life-support. Children with Glasgow Coma Scale (GSC) score < 8 need intubation and supplemental oxygen. Antibiotics should be started, even without LP (contraindicated if focal neuro-deficit, papilledema, or signs of raised ICP). Raised ICP is present in most of patients; GCS < 8 and high blood pressure are good guides. Mannitol (0.25 gm/Kg) should be used in such patients. If there are signs of (impending) herniation short-term hyperventilation is recommended; prolonged hyperventilation (> 1 hour) must be avoided. Any evidence of poor perfusion, hypovolemia and/or hypotension needs aggressive treatment with normal saline boluses and inotropes, if necessary, to maintain normal blood pressure. Empiric fluid restriction is not justified. Seizures may be controlled with intravenous diazepam or lorazepam. Refractory status epilepticus may be treated with continuous diazepam (0.01-0.06) mg/kg/min) or midazolam infusion. Ventilatory support may be needed early for associated pneumonia, poor respiratory effort and/or coma, and occasionally to reduce work of breathing in shock. Provision of critical care to children with ABM may reduce the mortality significantly as experienced by us.
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PMID:Bacterial meningitis in children: critical care needs. 1156 52

Mannitol overuse-induced acute renal failure (ARF) has rarely been described. We report four cases, all male, between the ages of 20 and 42 years, who developed acute renal failure (3 anuric, 1 nonoliguric) after receiving mannitol 1,172 +/- 439 g (mean +/- SD) during a time period of 58 +/- 28 h. The infusion rate was 0.25 +/- 0.02 g/kg/h. The onset of acute renal failure was detected 48 +/- 22 h after infusion. In 2 of the 3 cases in which urinary cytology was evaluated, the presence of vacuole-containing renal tubular cells was observed. All patients had hyponatremia (120 +/- 11 mEq/l), and hyperosmolality (osmolar gap 70 +/- 11 mosm/kg water). No other factors could be pointed to as causing acute renal failure. In the 3 anuric cases in which hemodialysis was performed, immediate recovery of diuresis was observed. Two patients recovered renal function on the fifth and sixth days, and 2 died due to endocranial hypertension - one of them while recovering - on the fourth and sixth days. In the present report, mannitol-induced ARF occurred at clustered doses of 0.25 mg/kg/h.
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PMID:Acute renal failure following massive mannitol infusion. 1238 62

Increased intracranial pressure (ICP) in patients with acute liver failure (ALF) remains a major cause of morbidity and mortality. Conventional methods of ammonia reduction such as the use of lactulose do not improve outcome, and metabolic substrates such as L-ornithine L aspartate may offer more promise. Mannitol remains the mainstay of therapy. An important role for cerebral hyperemia in the pathogenesis of increased ICP has led to a reevaluation of established therapies such as hyperventilation, N-acetylcysteine, thiopentone sodium, and propofol. Recent studies have focused on the role of systemic inflammatory response in the pathogenesis of increased ICP and support the use of antibiotics prophylactically. Moderate hypothermia reduces ICP in patients with uncontrolled intracranial hypertension and prevents increases in ICP during orthotopic liver transplantation (OLT). Advances in understanding the pathophysiological basis of intracranial hypertension in ALF have outstripped appropriate testing of the newly generated ideas in appropriate clinical trials, and more effort should be mounted at a national level to organize the appropriate multicenter studies required.
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PMID:Intracranial hypertension in acute liver failure: pathophysiological basis of rational management. 1452 80


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