raised intracranial pressure

Raised intracranial pressure in hepatic encephalopathy

Authors: Mukherjee KK, Chhabra R, Khosla VK.

Intracranial hypertension secondary to cerebral edema is the cause of death in 50%-80% of patients with fulminant hepatic failure (FHF). This is rarely seen in chronic hepatic failure. The genesis of cerebral edema in FHF is poorly understood. The grade of encephalopathy and coagulopathy are the most important predictors of outcome in FHF. However, it is important to emphasize that intracranial pressure (ICP) may not reflect clinical course. Decerebrate posturing may be seen with ICP recording of 16 mmHg, while a quarter of the patients may have brain damage without clinical signs of raised ICP. ICP monitoring is therefore vital. The gold standard for ICP monitoring is the intraventricular method. Non-invasive methods like computerized tomography scan and magnetic resonance imaging have poor correlation with ICP. Other methods like transcranial Doppler and jugular venous oximetry measurement of brain metabolites need evaluation. The main indications for ICP monitoring in FHF are (a) patients in grade III or IV encephalopathy and (b) patients undergoing liver transplantation. Generally, patients with an ICP >40 mmHg with cerebral perfusion pressure <50 mmHg for over 2 hours are poor subjects for liver transplant.

Elevated Intracranial Pressure, Low Cerebral Perfusion Pressure, and Impaired Brain Metabolism Correlate with Fatal Outcome after Severe Brain Injury

Authors: Hejčl A, Bolcha M, Procházka J, Hušková E, Sameš M.

BACKGROUND: New brain tissue monitoring techniques (tissue oxymetry, microdialysis) provide direct information about the state of brain oxygenation and brain metabolism in patients with severe traumatic brain injury (TBI). Despite this information being limited to a small region of the brain surrounding the probes, it could be associated with such global parameters as the clinical outcome.

OBJECTIVE: To study the predictive value of monitoring brain oxygenation and metabolism on clinical outcome in patients in the acute phase of severe TBI.

METHODS: An observational study of 20 patients with a severe TBI was undertaken, utilizing intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain tissue oxygenation, and brain metabolism monitoring. We correlated the clinical outcome of the patients with the following parameters: ICP, CPP, brain tissue oxymetry (PbtO (2)), glucose and glycerol levels, and the lactate/pyruvate (LP) ratio. Further, we analyzed the relationship between ICP, CPP, PbtO (2), and the metabolism parameters.

RESULTS: We found a correlation of the mean ICP values (8.73±1.18 in group A vs. 26.32±5.01 mmHg in group B, p <0.005), the mean CPP values (84.82±2.02 in group A vs. 66.62±4.64 mmHg, p<0.005), the LP ratio (37.36±3.44 vs. 199±87.97, p<0.05), and glycerol levels (62.07±12.14 vs. 215±46.52 μmol/l, p<0.05) with the clinical outcome. High ICP correlated with both a high LP ratio (Spearman R=0.61, p<0.05), and elevated glycerol concentrations (Spearman R=0.48, p<0.05). A low CPP correlated with a high LP ratio (Spearman R=-0.57, p<0.05), while a low PbtO (2) correlated with a high LP ratio (Spearman R=-0.49, p<0.05).

CONCLUSIONS: High ICP, low CPP, an elevated mean LP ratio, and high glycerol concentrations in the acute phase predict fatal outcome 6 months after TBI. Further, high ICP, low CPP, and low PbtO (2) correlate with impaired brain metabolism.

Headache caused by raised intracranial pressure and intracranial hypotension

Author: N M Ramadan.

Extremes of intracranial pressure commonly cause headache. Benign intracranial hypertension is a rare syndrome of increased intracranial pressure manifesting as headache, intracranial noises, transient visual obscuration, and palsy of the sixth cranial nerve. Endocrine disorders such as obesity and hypoparathyroidism, hypervitaminosis A, tetracycline use and thyroid replacement are probable causes of benign intracranial hypertension. In the majority of cases, however, it is idiopathic. Benign intracranial hypertension is though to be caused by cerebral edema, high cerebrospinal fluid outflow resistance and high cerebral venous pressure, or a combination of the three. The management of benign intracranial hypertension includes, symptomatic headache relief, removal of offending risk factor(s), and medical or surgical reduction of intracranial pressure. Spontaneous intracranial hypotension is more rare than benign intracranial hypertension. Postural headache (worse in the upright position) is the hallmark of spontaneous intracranial hypotension. Typically, the cerebrospinal fluid pressure is less than 60 mm H2O. Diminished cerebrospinal fluid production, hyperabsorption, and leak are postulated mechanisms of spontaneous intracranial hypotension. Empirical treatment includes bed rest, administration of caffeine, corticosteroids or mineralocorticoids, epidural blood patch, and epidural saline infusion.

Increased intracranial pressure in a case of pediatric multiple sclerosis

Authors: Brice J Williams, Holly J Skinner, Bernard L Maria.

A 15-year-old girl presented to our emergency department with dizziness, anorexia, nausea, and malaise. Clinical examination and magnetic resonance imaging studies showed characteristic features of multiple sclerosis. Surprisingly, a diagnostic lumbar puncture showed significant intracranial hypertension in addition to numerous oligoclonal bands, elevated immunoglobulin G index and immunoglobulin G/albumin ratio in the cerebrospinal fluid. It is proposed that a large burden of active demyelinating disease may cause increased intracranial pressure, thus providing an additional sound rationale for prompt therapeutic administration of intravenous high-dose steroids.

Raised intracranial pressure in acute viral encephalitis

Authors: Gyanendra Kumar a, Jayantee Kalita b and Usha Kant Misra b

There is paucity of data evaluating intracranial pressure (ICP) rise and its management in acute viral encephalitis (AVE). Noteworthy is the current prevalence of unselective and broad utilization of ICP lowering therapies in clinical practice. Trends in current management of ICP in AVE emanate from data extrapolated from results of studies done on cerebral malaria, bacterial meningitis, stroke, and brain trauma patients. In this article we review (1) clinical correlates of raised ICP, (2) pathology, (3) imaging data, (4) monitoring, and, (5) treatment, of raised ICP in AVE. ICP monitoring is a useful adjunct to management of raised ICP in adults, becoming especially important in Herpes encephalitis and encephalitis with status epilepticus. In children it substantially influences clinical management and continuous monitoring of mean blood pressure (MBP) and ICP can aid in early diagnosis and treatment when cerebral perfusion pressure (CPP) falls below critical levels. Current evidence suggests that the pathomechanisms that contribute to the development of raised intracranial pressure vary in viral encephalitides of different etiology, and different forms of cerebral edema result at different times in the course of the illness, thus creating a need for studies to investigate the usefulness of various edema-specific ICP lowering modalities in AVE.

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