Herniation, brain

An estimated oral dose of 260 mg endosulfan/kg caused severe seizures in a 43-year-old man, and brain death from cerebral herniation and massive cerebral edema occurred within 4 days of exposure (Boereboom et al. 1998) there were no signs of myocardial infarction and only slight congestion of the heart, but pulmonary congestion and atelectasis were evident at autopsy. 

Brain metastases are among the most feared complications of cancer and generally carry a poor prognosis. One serious consequence of brain metastases is elevated intracranial pressure, which can rapidly lead to fatal intracranial herniation and death. Rapid identification of the signs and symptoms of brain metastases is critical to improve long-term outcome and avoid mortality. 

Mannitol is an agent that may be used in patients with I impending cerebral herniation. Mannitol is an osmotic diuretic that shifts brain osmolarity from the brain to the blood. Doses of 100 g (1-2 g/kg) as an intravenous bolus should be used. Repeated doses typically are not recommended because mannitol may diffuse into damaged brain tissue, leading to rebound increased ICP.21... 

If uncontrolled, hyponatremia may cause increased intracranial pressure, brain herniation and death 595... 

The presence of blood in the brain parenchyma causes damage to surrounding tissue through a mass effect and the neurotoxicity of blood components and their degradation products. Compression of tissue surrounding hematomas may lead to secondary ischemia. Much of the early mortality of hemorrhagic stroke is due to an abrupt increase in intracranial pressure that can lead to herniation and death. 

The use of acetazolamide in the presence of unrecognized cerebral edema due to fat embolism, with sudden normalization of brain C02, as occurred in this patient when her previous state of hypocapnia was no longer sustained by ventilatory effort, resulted in cerebral acidosis, vasodilatation, and a further increase in intracranial pressure. This proved catastrophic and led to brainstem herniation and brain death. Acetazolamide should be avoided if at all possible in patients with bony and traumatic brain injuries, particularly during weaning from mechanical ventilation, since it can precipitate coning in patients with raised intracranial pressure. 

Lumbar puncture is considered mandatory in patients with suspected bacterial meningitis but the procedure can be hazardous with a risk of brain herniation in patients with raised intracranial pressure, and imaging with computed tomography or MRI is recommended for selected patients to detect brain shift. Patients who are in an immunocompromised state, have new-onset seizures, moderate-to-severe impairment of consciousness or signs that are suspicious of space-occupying lesions (e.g. papilloedema - oedema of the optic disk) should undergo neuroimaging prior to lumbar puncture. 

Cerebral edema not only increases local hydrostatic pressure and compromises blood flow further but also causes mass effect, brain shift and eventually brain herniation (Fig. 5.1). Death in the first week after cerebral infarction is often a result of these mass effects. 

Fig. 5.1. Brain CT images showing a large hypodense (arrows) edematous cerebral infarct in the distribution of the middle cerebral artery, with midline shift. Such large infarcts cause herniation of the cingulate gyrus under the falx cerebri of the ispsilateral uncus under the tentorium to compress the oculomotor nerve, posterior cerebral artery and brainstem and of the contralateral cerebral peduncle to cause ipsilateral hemiparesis.

The hematoma continues to expand after stroke onset, frequently causing further deterioration (Brott et al. 1997 Leira et al. 2004). Some brainstem hemorrhages evolve subacutely, particularly those caused by a vascular malformation (O Laoire et al. 1982 Howard 1986). Any large hematoma may cause brain shift, transtentorial herniation, brainstem compression and raised intracranial pressure. Hematomas in the posterior fossa are particularly likely to cause obstructive hydrocephalus. Rupture into the ventricles or on to the surface of the brain is common, causing blood to appear in the subarachnoid space. 

Peri-infarct edema reduces local cerebral blood flow and causes brain shift and herniation, the last being the most common neurological cause of death. This complication is a common explanation for worsening over the first few days and can often be detected by CT scan. Intravenous mannitol may reduce the deficit for a while but is unlikely to have a major impact on outcome. Recently, surgical decompression using hemicraniectomy has been shown to improve survival, with satisfactory functional outcome in many patients (Ch. 21). 

Cerebral edema occurs in response to a wide variety of insults, including ischemia, hypoxia, infection, and noninfectious inflammation. Shifts in brain water, which is the basis of the cellular swelling, are due to osmotic forces, and result in increases in intra- and extracellular spaces. A reasonable amount of tissue swelling can be tolerated in most parts of the body, however, the restrictions imposed by the rigid tentorium and bony skull cause life-threatening herniation with relatively small increases in the brain compartments. Two early anatomists, Monroe (1733-1817) and Kellie (1758-1829), recognized that increased intracranial pressure due to swelling in the cerebrospinal fluid (CSF), blood, or brain tissue compartments could increase intracranial pressure the concept of limited expansion capacity of the intracranial contents is called the Monroe-Kellie doctrine. 

The consequences of brain edema depend on the amount of tissue involved, the effect by intracranial pressure, and the threat of herniation. Small lesions such as limited edema around a metastatic lesion or an early abscess may have little clinical... 

In a few rare instances, lumbar puncture cannot be performed, because the amount of swelling within the skull is so great that the intracranial pressure (pressure within the skull) is extremely high. This pressure is always measured immediately upon insertion of the LP needle. If it is found to be very high, no fluid is withdrawn, because withdrawal of fluid could cause herniation of the brain stem. Herniation of the brain stem occurs when the part of the brain connecting to the spinal cord is thrust through the opening at the base of the skull into the spinal canal. Such herniation will cause com-... 

Liver transplantation is the method of choice in all patients with acute liver failure whose spontaneous survival rate without a transplant is <20%, taking into account all the parameters. Criteria proposed by King s College or Clichy provide a useful basis for assessment. The crucial factor, however, remains the choice of the appropriate time for carrying out the transplantation (i.) the possibility of eliminating decompensation by means of regeneration should be exploited (2.) delayed indications should not result in complications which would prevent a transplantation from being carried out (e. g. brain-stem herniation, sepsis). 

In five patients cerebral herniation followed cisplatin therapy (94). However, all had evidence of an intracerebral tumor with mass effect and the herniation of the brain was thought to be multifactorial rather than directly attributable to cisplatin. 

Glasscock III ME, Dickins JR, Jackson CG, et al. Surgical management of brain tissue herniation into the middle ear and mastoid. Laryngoscope. 1979 89(11) 1743-1754. 

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