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In the management of severe pediatric brain injury, attention has previously been paid to brain edema, ICP elevation and low cerebral perfusion pressure (CPP). However, in the acute stage within 3-6 hours after trauma, brain hypoxia and hyperglycemia associated with diffuse brain injury are often observed. We have pointed out brain thermo-pooling (elevation of brain tissue temperature) and brain hypoxia caused by defective release of oxygen from hemoglobin (due to decrease in red blood cell enzyme (DPG)) as a new mechanism of brain injury. To treat these pathologic changes, we have developed a brain hypothermia treatment, the major purpose of which is to prevent brain hypoxia, brain thermo-pooling, neurohormonal changes causing cytokine encephalopathy, and a selective, radical-mediated damage of the dopamine A10 nervous system. The brain tissue temperature is initially adjusted to 35 degrees C with adequate cerebral oxygenation, followed by brain hypothermia at 34 degrees C for 1 weeks to prevent brain hypoxia, free radical reactions, brain edema and ICP elevation. What is most difficult in the pediatric brain hypothermia treatment is to maintain metabolic balance in the injured brain tissue and pulmonary infections associated with an immune crisis. When a rapid elevation of serum glucose is noted it is critical to lower the value because glucose quickly penetrates the blood-brain barrier and increases pyruvate and lactate by inhibiting the TCA cycle metabolism. Thus, hyperglycemia during brain hypothermia treatment is one of the major target of management. Another problem is immune crisis associated with secondary pulmonary infections. To prevent them, early enteral nutrition and replacement of L-arginine were most useful, as well as preconditioning for rewarming as follows: serum albumin > 3.0 g/dl; lymphocyte > 1500/mm3; T-H (CD4) lymphocytes > 55%; serum glucose, 120-140 mg/dl; vitamin A > 50 mg/dl; Hb > 12 g/dl and 2,3 DPG, 10-15 mumol/gHb; O2 ER, 23-25% and AT-III, > 100%. The clinical benefit of this therapy is still controversial.
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PMID:[Brain hypothermia treatment for the management of severe pediatric brain injury]. 1072 86

Intracerebral contusions can lead to regional ischemia caused by extensive release of excitotoxic aminoacids leading to increased cytotoxic brain edema and raised intracranial pressure. rCBF measurements might provide further information about the risk of ischemia within and around contusions. Therefore, the aim of the presented study was to compare the intra- and perilesional rCBF of hemorrhagic, non-hemorrhagic and mixed intracerebral contusions. In 44 patients, 60 stable Xenon-enhanced CT CBF-studies were performed (EtCO2 30 +/- 4 mmHg SD), initially 29 hours (39 studies) and subsequent 95 hours after injury (21 studies). All lesions were classified according to localization and lesion type using CT/MRI scans. The rCBF was calculated within and 1-cm adjacent to each lesion in CT-isodens brain. The rCBF within all contusions (n = 100) of 29 +/- 11 ml/100 g/min was significantly lower (p < 0.0001, Mann-Whitney U) compared to perilesional rCBF of 44 +/- 12 ml/100 g/min and intra/perilesional correlation was 0.4 (p < 0.0005). Hemorrhagic contusions showed an intra/perilesional rCBF of 31 +/- 11/44 +/- 13 ml/100 g/min (p < 0.005), non-hemorrhagic contusions 35 +/- 13/46 +/- 10 ml/100 g/min (p < 0.01). rCBF in mixed contusions (25 +/- 9/44 +/- 12 ml/100 g/min, p < 0.0001) was significantly lower compared to hemorrhagic and non-hemorrhagic contusions (p < 0.02). Intracontusional rCBF is significantly reduced to 29 +/- 11 ml/100 g/min but reduced below ischemic levels of 18 ml/100 g/min in only 16% of all contusions. Perilesional CBF in CT normal appearing brain closed to contusions is not critically reduced. Further differentiation of contusions demonstrates significantly lower rCBF in mixed contusions (defined by both hyper- and hypodense areas in the CT-scan) compared to hemorrhagic and non-hemorrhagic contusions. Mixed contusions may evolve from hemorrhagic contusions with secondary increased perilesional cytotoxic brain edema leading to reduced cerebral blood flow and altered brain metabolism. Therefore, the treatment of ICP might be individually modified by the measurement of intra- and pericontusional cerebral blood.
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PMID:rCBF in hemorrhagic, non-hemorrhagic and mixed contusions after severe head injury and its effect on perilesional cerebral blood flow. 1145 9

Aim of the current study was to investigate the influence of intracranial hypertension on the resolution of vasogenic brain edema following intracerebral hemorrhage. An intracerebral hematoma was induced by 500 microliters of blood injected into the left frontal lobe of rabbits (n = 25). Na(+)-fluorescein (MW376) and Texas-Red-albumin (MW67.000) were administered intravenously as edema markers. By using a closed cranial window for superfusion of the brain surface and a ventriculo-cisternal perfusion the clearance of both fluorescence markers was measured in the CSF-effluates up to 8 hours using spectrophotometry. ICP was adjusted between 2-6 mmHg (low pressure, n = 10), 8-12 mmHg (moderate pressure, n = 10) or 14-20 mmHg (high pressure, n = 5). In all groups Na(+)-fluorescein started to accumulate at 60 min after induction of the hematoma in the subarachnoid space, while at 90 min in the ventricular system. In the low intracranial pressure group Na(+)-fluorescein (mean +/- SEM) in the ventricular system amounted to 1.47 +/- 0.42 nmol as compared to 1.34 +/- 0.41 nmol in the moderate, or 0.38 +/- 0.11 nmol in the high intracranial pressure group. In the subarachnoid space the marker reached 1.96 +/- 0.57 nmol, 4.15 +/- 1.28 nmol, or 0.96 +/- 0.32 nmol, respectively. In conclusion, the data demonstrate that vasogenic edema induced by an intracerebral hematoma is cleared into both CSF compartments, albeit with delay into the ventricular system. Edema resorption occurred earlier and to a higher extent into the subarachnoid space as compared to the ventricular system. Further, edema resorption is influenced by the actual intracranial pressure, with marked inhibition by a high intracranial pressure.
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PMID:Intracranial hypertension influences the resolution of vasogenic brain edema following intracerebral hemorrhage. 1145 77

Of all the possible clinical factors affecting the outcome of patients suffering acute subdural hematomas (SDH), timing of surgical evacuation is certainly the most debated. The purpose of this study was to develop an experimental model able to reproduce the clinical behavior of post-traumatic SDH as observed in head injured patients. We present a novel model of SDH combined with diffuse brain injury (DBI), and investigate the effects of early and delayed surgical evacuation. Following Impact Acceleration DBI, adult Sprague-Dawley rats were given a 400 microliters SDH. Hematoma was then evacuated at one (rapid evacuation) or four hours (delayed evacuation) post-injury. Physiological parameters were measured for 5 hours, followed by the assessment of brain water content. In this experimental model, there is strong evidence that trauma acts synergistically with SDH enhancing brain edema formation and increasing ICP. In absence of secondary insult, rapid evacuation of traumatic SDH limits exposure to high ICP, reduces brain edema and is beneficial.
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PMID:Diffuse brain injury complicated by acute subdural hematoma in the rodents: the effect of early or delayed surgical evacuation. 1216 16

Idiopathic intracranial hypertension (IDICH) and idiopathic normal pressure hydrocephalus (IDNPH) are disorders of the circulation of the cerebrospinal fluid (CSF) with opposite diagnostic features, obscure etiology but the same treatment: CSF drainage. In both diseases a large quantity of CSF exists: equilibrated by the brain edema in IdICH with high ICP and not equilibrated by brain pressure, and the ventricles are enlarged in IdNPH. The same anatomical structure involved in both diseases is the ventricular wall and this represents a true barrier, a glial-ependymal barrier and it acts as a barrier only in connection with the difference between the pressures. The spontaneous course of both diseases suggests that an open glial-ependymal barrier protects the brain parenchyma.
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PMID:Idiopathic intracranial hypertension and idiopathic normal pressure hydrocephalus: diseases with opposite pathogenesis? 1459 81

The term hydrostatic brain edema results from unfavorable hydrtostatic pressure gradiernts between blood vessels and brain tissue. Arterial hypertension combined with decompressive craniectomy produces extensive brain edema in the arterial boundary zone of the decompressive area. The increased hydrostatic pressure gradient enhances tissue damage and causes the biphasic opening of the blood-brain barrier (BBB). The hydrostatic pressure alone is capable of causing the initial BBB opening and this induced edema results in derangement of cerebral microcirculation and metabolism. With morphological opening and metabolic damage of the vascular wall, the second BBB opening is elicited by the amplified hydrostatic pressure gradient, which is similar to that in vasogenic edema. In the clinical aspect, the beneficial effect of decompressive craniectomy in the treatment of uncontrollable ICP and brain edema remains controversial. External decompression may have adverse effects on severe brain edema and swelling. In this regards, control of driving force for the formation of brain edema could be the treatment of choice as an initial step. In addition, recent reports provided by MR imaging indicated new information on the pathophysiological features of the patients with acute hypertension. In the patients with hypertension due to reversible posterior leucoencephalopathy (RPL) syndrome, MR images show reversible signal abnormalities in the bilateral occipital lobes, suggesting hydrostatic brain edema.
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PMID:Hydrostatic brain edema: basic mechanisms and clinical aspect. 1475 96

Aquaporin-4 (AQP4) is the major water channel in the brain, expressed predominantly in astroglial cell membranes. Initial studies in AQP4-deficient mice showed reduced cellular brain edema following water intoxication and ischemic stroke. We hypothesized that AQP4 deletion would have the opposite effect (increased brain swelling) in vasogenic (noncellular) edema because of impaired removal of excess brain water through glial limitans and ependymal barriers. In support of this hypothesis, we found higher intracranial pressure (ICP, 52+/-6 vs. 26+/-3 cm H2O) and brain water content (81.2+/-0.1 vs. 80.4+/-0.1%) in AQP4-deficient mice after continuous intraparenchymal fluid infusion. In a freeze-injury model of vasogenic brain edema, AQP4-deficient mice had remarkably worse clinical outcome, higher ICP (22+/-4 vs. 9+/-1 cm H2O), and greater brain water content (80.9+/-0.1 vs. 79.4+/-0.1%). In a brain tumor edema model involving stereotactic implantation of melanoma cells, tumor growth was comparable in wild-type and AQP4-deficient mice. However, AQP4-deficient mice had higher ICP (39+/-4 vs. 19+/-5 cm H2O at seven days postimplantation) and corresponding accelerated neurological deterioration. Thus, AQP4-mediated transcellular water movement is crucial for fluid clearance in vasogenic brain edema, suggesting AQP4 activation and/or up-regulation as a novel therapeutic option in vasogenic brain edema.
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PMID:Aquaporin-4 facilitates reabsorption of excess fluid in vasogenic brain edema. 1520 68

In patients with brain edema the pathophysiology of the different forms of edema have to be considered to ensure the prompt, sensible and consistent use of the limited treatment modalities available. Brain edema may be classified into cytotoxic and vasogenic edema, these two types often coexist in one patient. Head elevation, hyperventilation, osmotic therapy and reduction of brain metabolism by sedation or hypothermia should be used closely monitoring ICP and blood pressure. In the future considering the autoregulatory capacity of the individual patient will possibly lead to a more effective action of the treatment modalities described. Further research will open new perspectives how aquaporines are involved in the genesis and mobilisation of brain edema.
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PMID:[Conservative treatment of brain edema--which way is leading to Rome?]. 1895 23

Acute subdural hematoma (ASDH) patients presenting in a severe condition tend to have poor outcomes due to the significant brain edema required to maintain the ICP at less than 20-25 mmHg. This study compared the surgical outcomes of 16 critically ill patients with ASDH who underwent hematoma irrigation with trephination therapy (HITT) based on their initial ICP values. The initial mean GCS score upon admission was four. A unilateral dilated pupil was seen in one and bilateral dilated pupils were seen in seven patients. The co-existence of a brain contusion was seen in seven patients, brain swelling was noted in six patients, and both basal cistern effacement and a midline shift greater than 5 mm were observed in all patients. The mean initial ICP value was 45 mmHg (range: 3 to 85 mmHg). Ten patients (62.5%) underwent a rapid external decompression to evacuate the hematoma. By using the Glasgow Outcome Scale upon discharge a score of good recovery (GR) was assigned to two (12.5 %), moderate disability (MD) to four (25.0 %), vegetative state (VS) to two (12.5 %), and death (D) to eight (50.0 %) patients. All six patients who showed an initial ICP greater than 60 mmHg died despite intensive care. Eight patients who showed an initial ICP less than 40 mmHg had a favorable outcome, but two patients deteriorated due to a traumatic cerebrovascular disorder. It seems that the initial ICP monitoring with HITT for ASDH patients in critical condition may be an important factor for predicting both surgical outcome and clinical course.
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PMID:Significance of monitoring the initial intracranial pressure on hematoma irrigation with trephination therapy for acute subdural hematomas in critical conditions. 1981 60

We report a 57-year old female patient with a rapid and dramatic dynamic of whole brain edema caused by tuberculous meningitis. After initiation of tuberculostatic medication, general condition of the patient worsened and finally she was intubated due to a progredient loss of consciousness and respiratory insufficiency. Repeated cerebral computer tomography (CCT) revealed a global brain edema with slit ventricles and a dramatic progress of generalized brain swelling. Highly interesting, a rapid expanded regime of brain pressure monitoring and treatment according to a neurosurgical intensive standard ICP/CPP management protocol, which was complemented by the tuberculostatic therapy and high dose steroid application, dramatically improved the general conditions, so that the patient is now in a general condition which corresponds that before the occurrence of tuberculous meningitis. Thus, it is mandatory in situations with a rapid progressive brain swelling caused by bacterial meningitis to consider an intensified cerebral monitoring and stratified treatment protocol in order to avoid the devasting effects of a long lasting increase in intracranical pressure.
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PMID:Invasive pressure monitoring saves from tuberculous meningitis with fulminant generalized brain edema. 2211 Apr 66


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