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Brain Injury 2

Brain Injury 2

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Published by: seigelystic on Sep 14, 2012
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Increased Intracranial Pressure (ICP).
 
The brain is enclosed in the rigid confines of the skull, or cranium, making it particularly susceptibleto increases in ICP. Increased ICP is a common pathway for brain injury from different types of insults and agents. Excessive ICP obstruct cerebral blood flow, destroy brain cells, displace braintissue as in herniation, and otherwise damage delicate brain structures.The cranial cavity contains blood (approximately 10%), brain tissue (approximately 80%), and CSF(approximately 10%) in the rigid confines of a nonexpendable skull. Each of these volumescontributes to the ICP, which normally is maintained within a range of 0 to 15 mm Hg whenmeasured in the lateral ventricles. The volumes of each of these components can vary slightlywithout causing marked changes in ICP. This is because small increases in the volume of thecomponent can be compensated for a decrease in the volume of one or both of the other twocomponents. This association is called the
Monro-Kellie hypothesis.
Normal fluctuation in ICP occurwith respiratory movements and activities of daily living such as straining, coughing, and sneezing.Abnormal variation in intracranial volume with subsequent changes in ICP can be caused by avolume change in any of the three intracranial components. For example, an increase in tissuevolume can result from a brain tumor, brain edema, or bleeding into brain tissue. An increase inblood volume develops when there is vasodilation of cerebral vessels or obstruction of venousoutflow. Excess production, decrease absorption, or obstructed circulation of CSF affords thepotential for an increase in the CSF component. When the change in volume is caused by a braintumor, it tends to occur slowly and usually is localized to the immediate area, whereas the increaseresulting from head injury usually develops rapidly.According to the modified Monro-Kellie hypothesis, reciprocal compensation occurs among thethree intracranial compartments. Of the three intracranial volumes, tissue volume is relativelyrestricted in its ability to udergo change; CSF and blood volume are best able to compensate forchanges in ICP. Initial increases in ICP are buffered by a translocation of CSF to the spinalsubarachnoid space and increased reabsorption of CSF. The compensatory ability of the bloodcompartment is limited by a small amount of blood that is in the cerebral circulation. The cerebralblood vessels contain less than 10% of the intracranial volume, most of which is contained in thelow-pressure venous system. As the volume-buffering capacity of this compartment becomesexhausted, venous pressure increases, and cerebral blood volume and ICP rise. Also, cerebral bloodflow is highly controlled by autoregulatory mechanisms, which affects its compensatory capacity.Conditions such as ischemia and elevated partial pressure of carbon dioxide (PCO2) in the bloodproduce a compensatory vasodilation of the cerebral blood vessels. A decrease in PCO2 has theopposite effect; for this reason, hyperventilation, which results in a decrease in PCO2 levels, is somesused in the treatment of ICP.
BRAIN INJURY: INCREASED INTRACRANIAL PRESSURE AND HERNIATIONMEDICALVILLAGE.BLOGSPOT.COM SPECIAL MEDICAL REPORT PART 2 
 
Cerebral Compliance and the Impact of Intracranial Pressure. The impact of increases in blood, braintissue, or CSF volumes on ICP varies among individuals and depends on the amount of increase thatoccurs, the effectiveness of compensatory mechanisms, and the compliance of brain tissue.Compliance represents the ratio of change in volume to the resulting change in pressure(compliance = change in volume / change in pressure). The effects of intracranial volume changes(horizontal axis) on ICP changes (vertical axis are depicted in Figure 1.3. The shape of the curvedemonstrates effects of intracranial volume changes on ICP. The ICP remains constrant from point ato point B when volume is added to the intracranial space. Because the compensatory mechanismare adequate, compliance is high in this area of the curve, and there is little change in ICP. Frompoints B to C, thecompensatory mechanismsbecomes less efficient;compliance decreases andICP begins to rise. At pointsC to D, the compensatorymechanisms have beenexceeded such that evensmall changes in volumeproduce large changes inICP.Impact of IntracranialPressure on CerebralPerfusion.The cerebralperfusion pressure (CPP),which represents thedifference between themean arterial blood pressure(MAB) and the ICP(CPP = MABP
 –
ICP), is thepressure perfusing the brain.CPP is determined by thepressure gradient betweenthe internal carotid arteryand subarachnoid veins. TheMABP and ICP aremonitored frequently in persons with brain conditions that increase ICP and impair brain perfusion.Normal CPP ranges from 70 to 100 mmHg. Brain ischemia develops at levels below 40 mmHg. Whenthe pressure in the cranial cavity approaches or exceeds the MABP, tissue perfusion becomesinadequate, cellular hypoxia results, and if the pressure is maintained, neuronal death may occur.The highly specialized cortical neurons are the most sensitive to oxygen deficit; a decrease in thelevel of consciousness is one of the earliest and most reliable signs of increased ICP. The continuedcellular hypoxia leads to general neurologic deterioration; the level of consciousness maydeteriorate from alertness through confusion, lethargy, obtundation, stupor, and coma.
 
One of the late reflexes seen with a marked increase in ICP is the CNS ischemic response, whichtriggered by ischemia of the vasomotor center in the brain stem. Neurons in the vasomotor centerrespond directly to ischemia by producing a marked increase in MABP, sometimes to levels as highas 270 mmHg, accompanied by a widening of the pulse pressure and reflex slowing of the heart rate.These three signs, sometimes called the Cushing reflex, are important but late indicators of increased ICP. The ischemic reflex is a last-ditch effort by the nervous system to maintain cerebralcirculation. The Cushing reflex seldom is seen in modern clinical settings since the advent of ICPmonitoring.
Brain Herniation
The brain is protected by the nonexpendable skull and supporting septa, the falx cerebri and thetentorium cerebelli, that divide the intracranial cavity into fossae or compartments that normallyprotect against excessive movement. The falx cerebri is a sickle shaped septum that separates thetwo hemispheres. The tentorium cerebelli divides the cranial cavity into anterior and posteriorfossae (Fig. 1.4A). this inflexible dual sheath extends posteriorly from the bony petrous ridges andthe anterior to the clinoid process, sloping downward and outward from its medial edge to attachlaterally to the occipital bone. Extending posteriorly into the center of the tentorium is a largesemicircular opening called the incisures or tentorial notch. The temporal lobe rests on the tentorialincisura, and the midbrain occupies the anterior portion of the tentorial notch. The cerebellum isclosely opposed to the dorsum of the midbrain and fills the posterior part of the notch. Otherimportant anatomic associations exists among the anterior cerebral, internal carotid, and posteriorcommunication, and posterior and superior cerebellar arteries, and the incisures (see Fig. 1.4.B). Theoculomotor nerve (cranial nerve III) emerges from the mediolateral surfaces of each peduncle justcaudal to the tentorium.Brain herniation represents a displacement of brain tissue under the falx cerebri or through thetentorial notch or incisures of the tentorium cerebelli. It occurs when an elevated ICP in one of braincomparments causes displacement of the cerebral tissue toward an area of lower ICP. The differenttypes of herniation syndromes are based on the area of the brain that has herniated and thestructure under which it has been pushed. (see Figure 1.4C). they commonly are divided into twobroad categories, supratentorial and infratentorial, based on whether they are located above orbelow the tentorium.

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