Increased Intracranial Pressure ANYPHY The human skull is made up of 22 bones.

Fourteen are associated with the face, and eight with the cranium. The cranium consists of the paired temporal and parietal bones, as well as the frontal bone, sphenoid, ethmoid and occipital bone. Together, the fused cranial bones create the cranial cavity, which encloses and protects the brain. The bones of the cranium average between 2 and 6 mm in thickness in the adult, with the temporal bones usually being the thinnest. Exceptions to this include the newborn, whose fontanels are yet to close. The outsides of the cranial bones are smooth and articulate with the scalp via the pericranium, the deepest layer of the scalp. The inside of the cranium is not as smooth. While the interiors of the superior and lateral sides of the cranial vault are relatively smooth (with the exception of grooves for cranial arteries), the cranial floor has numerous ridges and bony protrusions that can injure the brain if it moves violently within the cranial vault. Recall that countercoup injuries occur opposite from the site of impact in head trauma as the moving brain strikes the opposite wall of the cranium; these injuries are exacerbated by the bony protrusions within the vault. The average volume of the adult cranium is about 1,900 mL, about 80% of which is occupied by the brain.1There are three major divisions of the brain: the cerebrum, cerebellum and brain stem. The cerebrum is divided into two lobes, and each is responsible for specific higher functions, such as consciousness and thought. The cerebellum is responsible for balance and fine-tuned movements. The brain stem is made up of the diencephalon, midbrain and medulla oblongata. The medulla oblongata connects the brain with the spinal cord and is responsible for control of cardiovascular and respiratory function. Through childhood and the prime years of adulthood, the brain takes up most of the space within the cranium. As people age, however, the brain begins to atrophy and shrink. While there is no set timeframe for brain atrophy, it is exacerbated by dementia and Alzheimers and theorized to also be exacerbated by nonuse (sedentary lifestyles). The consequence of this atrophy is that upon brain injury, the brain has an increased space in which to bleed and/or swell, potentially delaying the onset of the symptoms of increasing ICP, which can delay recognition as well. Conversely, this extra space can afford the patient more time for treatment access and in some ways be helpful. The brain and spinal cord are covered by a protective layer of tissue called the meninges. There are three layers: the pia mater, the arachnoid membrane and the dura mater. The pia mater is a thin membrane bound tightly against the brains surface. The arachnoid membrane lies above the pia mater, and between the two is the subarachnoid space, which is filled with cerebrospinal fluid (CSF). Outside the arachnoid membrane is the dura mater, the outermost layer of the meninges. There are two tough, fibrous layers that make up the dura matter. The outer layer is fused to the periosteum of the inside of the cranium, and the inner layer lies over the top of the arachnoid membrane, with a space between them. This inner layer of the dura mater extends deep into the cranial cavities in several areas to form dural folds. These act as

restraints for the brain, holding it in position within the cranium. Examples of these dural folds include the falx cerebri and the tentorium cerebelli (Figure 1). The falx cerebri separates the two hemispheres of the brain from one another, and the tentorium cerebelli separates the cerebellum and brain stem from the cerebrum. The brain is suspended in cerebrospinal fluid, which is produced in the choroid plexus located in the ventricles of the brain. CSF passes from the ventricles into the subarachnoid space of the meninges that covers the brain and spinal cord. In addition to cushioning the brain and protecting it from trauma, CSF also serves as a transport system for waste products, nutrients, chemical messengers and gases such as carbon dioxide and oxygen. The brain requires a constant and significant supply of oxygen and glucose to function properly. Accordingly, it has a rich vascular supply and receives about 15% of total cardiac output. Additionally, the brain is responsible for 20% of the bodys total oxygen demand. 2 The paired carotid and vertebral arteries (which fuse to form the basilar artery) ensure a constant flow of blood to the brain, or cerebral blood flow (CBF). Cerebral blood flow is controlled by a process termed autoregulation, in which the volume of the cerebral vasculature is tightly controlled to allow just enough blood to ensure adequate cerebral perfusion. This is important because too little blood flow fails to meet the brains oxygen and glucose demands, while too much can actually cause a rise in ICP. To support autoregulation, the cerebral vasculature is extremely sensitive to the concentration of carbon dioxide in the blood (partial pressure, or pCO 2). Increased pCO2 (hypercapnia) results in vasodilation and increased CBF, and decreased pCO2(hypocapnia) results in vasoconstriction of the cerebral vasculature and decreased CBF. The normal pCO2 is 3545 mmHg. The vascular response to changes in pCO2 is nearly linear between values of 2060 mmHg, and results in a change in the diameter of cerebral blood vessels by 2%3%.2,3 Adequate CBF also depends on the cerebral perfusion pressure (CPP), the pressure of the blood flowing into the brain. CPP is unique because it is not related to blood pressure alone. Rather, it depends on the relationship between the mean arterial pressure (MAP) and intracranial pressure (Table 2). Normal MAP is between 70110 mmHg. Normal ICP is between 715 mmHg, or about 10 mmHg. This means there is always some intracranial pressure. An adequate CPP is at least 70 mmHg. When cerebral perfusion pressure drops below 70 mmHg for sustained periods, cerebral hypoxia and ischemia occur. Under normal physiologic conditions, autoregulation ensures CPP is kept between 7090 mmHg, which is enough to ensure adequate cerebral blood flow. Autoregulation occurs primarily via control of the cerebral vasculature. Pathophysiology Intracranial pressure (ICP) is the pressure in the skull that results from the volume of three essential components: cerebrospinal fluid (CSF), intracranial blood volume and central nervous system tissue. The normal intracranial pressure is between 5-15 mmHg. This is slightly lower than the mean systemic arterial pressure but considerably higher than venous pressure. The intact cranium is essentially inexpandable containing about 1400 grams of central nervous system (CNS) or brain tissue, 75 ml of blood and about 75 ml of cerebrospinal fluid (CSF). These three components of the cranial vault maintain a state of equilibrium. Their pressure and

volume determine the condition of balance. According to Monro-Kellie hypothesis, any increase in one of these elements must be balanced or compensated by a proportional constriction either or both of the other two components such as decreasing the volume of cerebral blood flow, shifting CSF flow (into the spinal canal) or increasing CSF absorption. Absence of these compensatory changes results to increased intracranial pressure. Once ICP reaches around25 mmHg marked elevation in intracranial pressure will be noted. CSF is formed from the blood by the choroid plexuses, which are hanging at the roof of the brains ventricles. From the point where it is produced, it flows through the aqueduct of Sylvius to the fourth ventricles. Three apertures (opening) are found in the fourth ventricle which serves as passageway going to the subarachnoid spaces in the brain and spinal cord. These openings are Foramina of Magendie (median aperture) and two Foramina of Luschka (lateral apertures). A presence of tumor in choroid plexus may cause an overproduction of CSF. If the passageway of CSF is obstructed or brain tissue damage during surgery occurs, elevated ICP is inevitable. Normally, a change in CSF and blood volume occurs. For instance, during exhalation a temporary rise in intrathoracic pressure occurs. This impairs cerebral venous drainage and thereby reabsorption of CSF. An increase in ICP might likely occur, unless the blood will be expelled or the brain tissue will shrink (compensatory mechanism). If no compensation will occur, based on Monro-Kellie hypothesis, a slight increase in intracranial pressure will take place. The same process occurs during Valsalva maneuver (forcible exhalation against a closed glottis), sneezing, coughing and straining at stool. This is the main reason why people with increase ICP and at risk for cerebral hemorrhage are instructed to avoid these instances. Presence of carbon dioxide can also increase ICP. Carbon dioxide is a potent vasodilator that dilates aretrioles (including those in the chorionic plexus in the brain) which elevates cerebral blood volume and ICP. Risk Factors

Severe head injury Subdural hematoma A hematoma or localized swelling filled with blood that occurs in the dura matter and the arachnoid membrane of the brain. Hydrocephalus Abnormal accumulation of fluid in cerebral ventricles Brain tumor Brain hemorrhage Bleeding in the brain Meningitis Inflammation of the meninges (membrane that covers the brain) due to bacterial or viral infection.

Encephalitis or cephalitis Inflammation of the brain Aneurysm Localized dilation of a blood vessel Status epilepticus Rapid and successive attacks of epilepsy Stroke Rupture or a blood vessel in the brain

Hydrocephalus is due to a problem with the flow of cerebrospinal fluid (CSF), the liquid that surrounds the brain and spinal cord. The fluid brings nutrients to the brain, takes away waste from the brain, and acts as a cushion. Encephalitis is irritation and swelling (inflammation) of the brain, usually due to infections. Aneurysms in the brain occur when there is a weakened area in the wall of a blood vessel. An aneurysm may be present from birth (congenital) or it may develop later in life. (For example, after a blood vessel is injured.) Subarachnoid hemorrhage due to rupture of a cerebral aneurysm occurs in approximately 1015 out of 10,000 people. Subarachnoid hemorrhage due to rupture of a cerebral aneurysm is most common in persons age 20 to 60. It is slightly more common in women than men. Meningitis is swelling and irritation (inflammation) of the membranes covering the brain and spinal cord. This inflammation causes changes in the cerebrospinal fluid (CSF) that surrounds the brain and spinal cord. A stroke happens when blood flow to a part of the brain is interrupted because a blood vessel in the brain is blocked or bursts open. If blood flow is stopped for longer than a few seconds, the brain cannot get blood and oxygen. Brain cells can die, causing permanent damage. There are two major types of stroke: ischemic stroke and hemorrhagic stroke.

Clinical Manifestations

Infants: Drowsiness Separated sutures on the skull Bulging of the soft spot on top of the head (bulging fontanelle) Vomiting Older children and adults: Behavior changes Decreased consciousness Headache Lethargy Neurological symptoms, including weakness, numbness, eye movement problems, and double vision Seizures Vomiting Medical Management Osmotic Diuretics 1. Mannitol a. MOA: reduces the water content of the brain due to the establishment of an osmotic gradient between the brain and the intravascular compartment. Mannitol is a large moleculeand will not cross the BBB. b. Dose: Initial dose -- 0.5 to 1.0 gram/kg IV over 10-20 minutes. Maximum effect is seen in 20 minutes and duration of action is 4 hours. Repeat doses of 0.25 to 0.5 gm/kg Q 4-6 hours are frequently used. c. an administration set with a 0.22 micron filter must be used. d. available IV as 20% solution (100 gm in 500 ml of D5W) e. must be kept warm or will precipitate f. Adverse Effects: CHF, pulmonary edema, kidney failure g. Monitoring: serum and urine osmolarity, serum and urine electrolytes 2. Glycerol a. MOA: reduces CSF production along with osmotic effects b. Dose: 0.5 to 1.0 gm/kg Q 4-6 hours; do not exceed 0.2-1.0 gm/kg/hour c. give IV as a 10-20% solution in 0.45% or 0.9% saline over several hours (3-5 hours) d. Side Effects: rate-related; reduced with slow infusion b. Loop Diuretics-Furosemide, Ethacrynic Acid

1. MOA: inhibit sodium and chloride resbsorption in the loop of Henle resulting in contraction of the blood volume which may mobilize cerebral edema 2. usually administered with mannitol to increase the therapeutic effect 3. Dose: 0.5 to 1.0 mg/kg prn 4. Side Effects: hypokalemia, dehydration, hypotension, glucose intolerance c. Corticosteroids 1. only proven to be effective in reducing cerebral edema associated with brain tumors; role in traumatic cerebral edema is uncertain 2. MOA: exact mechanism unknown; may decrease CSF production and stablize brain cell membranes 3. Dose: dexamethasone most commonly used; 10 mg IV/IM followed by 4 mg IV/IM Q 6 hrs 4. Side Effects: hyperglycemia, GI bleeding, increased infection risk d. Barbiturate Coma 1. used when patients are refractory to conventional therapy 2. thiopental and pentobarbital are most frequently used; effect on outcome not clear 3. MOA a. decrease cerebral metabolism and oxygen requirements; increase cerebral vascular resistance b. leads to a decrease in cerebral blood flow and in blood volume, therefore a decreased ICP c. may protect or allow the brain cells to withstand a decreased CPP 4. Dosing a. Pentobarbital 1. Loading Dose: 10-15 mg/kg IV over one hour 2. Maintenance Dose: 2-3 mg/kg/hour; give by IV infusion as IV push has caused vascular thrombosis b. Thiopental

1. Loading Dose: 20-30 mg/kg over 30-60 minutes 2. Maintenance Dose: 2-3 mg/kg/hour 5. Administration a. these agents have a very alkaline pH b. do not mix with other agents or infuse into the same line due to incompatibilities 6. Side Effects a. hypotension b. hypothermia c. decreased GI muscle tone 7. Monitoring a. b. c. d. e. ICP: goal<15 mmHg MAP: goal is between 90-120 mmHg CPP: goal is between 50-60 mmHg ABG's, ventilator settings EEG; may see an isoelectric EEG in which the ECG tracing is recorded due to lack of electrical activity in the brain f. temperature g. "therapeutic serum concentration" of barbiturates: 25-40 mcg/ml h. patient is comatose, pupils are small and nonreactive, and exhibits no response to verbal stimuli i. no voluntary respirations

Nursing interventions o Achieve cerebral tissue perfusion o l Elevate HOB 30-45 degrees with head in neutral position o l Cervical collar if needed to keep head neutral o l Avoid extreme hip flexion o l Avoid Valsalva maneuvers ask client to exhale when being moved or turned o l Avoid isometric exercises that increase SBP o l Preoxygenate and hyperventilate prior to suctioning o Achieve cerebral tissue perfusion o Space nursing interventions o l Avoid emotional distress and frequent arousal from sleep o l Note abdominal distension o l Avoid high levels of PEEP o Achieve airway clearance o l Suction to maintain patent airway

o l Hyperoxygenation for suctioning o l Nasal drainage may indicate dural tear; suctioning of nares contraindicated o l Auscultate lung fields o l No close mouth coughing o l Elevate HOB o Attain normal respiratory pattern o Attain fluid balance o l Monitor skin turgor, mucous membranes, serum and urine osmolality o l Monitor IVF carefully o l Observe for CHF and pulmonary edema if giving Mannitol o l Good oral hygiene, monitor VS, monitor I&O Attain normal urine and bowel elimination o l Test urine for specific gravity and glucose o l Indwelling catheter o l Monitor UOP every 2-4 hours; output of > 200 ml/hr over two consecutive hours may = diabetes insipidus o l Monitor bowel sounds; abd. Distension o l Test stools for occult blood Hyperventilation o l PaCO2 ranged from 25-30 mm Hg Temperature control o l Prevent hyper- or hypothermia B/P control o l High range normal essential for adequate perfusion pressure; too high may increase ICP; sedation and antihypertensives Seizure control Monitor for complications o l Brain herniation o l Cushings stress ulcer o l Diabetes insipidus Severe polyuria followed by polydipsia UOP more than 9 L/day and urine osmolality of < 100 mOsm/kg after dehydration or water restriction test require ADH replacement (desmopressin/DDAVP) Monitor for complications o l Syndrome of Inappropriate Secretion of ADH (SIADH) o High levels of ADH that result in oliguria in the absence of normal physiologic stimuli for its release o Pituitary surgery, ectopic tumors that secrete ADH