IICP

Decorticate and Decerebrate

, Decorticate response. Flexion of arms, wrists, and fingers with adduction in upper extremities. Extension, internal rotation, and plantar flexion in lower extremities. B, Decerebrate response. All four extremities in rigid extension, with hyperpronation of forearms and plantar flexion of feet. C, Decorticate response on right side of body and decerebrate response on left side of body. D, Opisthotonic posturing.

Leveling a vnetriculostomy

A, Leveling a ventriculostomy. B, CSF is drained into a drainage system. •In this system, the transducer is external. •It is important to make sure that the transducer of the ventriculostomy is level to the foramen of Monro (interventricular foramen) and that the ventriculostomy system is at the ideal height. •A reference point for this foramen is the tragus of the ear. When the patient is repositioned, the system needs to be re-zeroed.

A patient with a head injury has an arterial BP of 92/50 (64) mm Hg and ICP of 18 mm Hg. The nurse uses the assessments to calculate the cerebral perfusion pressure (CPP). How should the nurse interpret the results? a.The CPP is so low that brain death is imminent. b.The CPP is low, and the BP should be increased. c.The CPP is high, and the ICP should be reduced. d.The CPP is adequate for normal cerebral blood flow.

Answer: B Rationale: The cerebral perfusion pressure (CPP) is the pressure needed to ensure blood flow to the brain. CPP is equal to the MAP minus the ICP (CPP = MAP - ICP). MAP = DBP + 1/3 (SBP-DBP) = 50 + 1/3 (92-50) = 64 mm HgCPP = MAP - ICP = 46 mm HgNormal CPP is 60 to 100 mm Hg. CPP <50 mm Hg is associated with ischemia and neuronal death. A CPP <30 mm Hg results in ischemia and is incompatible with life. It is critical to maintain MAP when ICP is elevated. A patient with a head injury may require a higher blood pressure, increasing MAP and CPP, to increase perfusion to the brain and prevent further tissue damage. memorize how to calculate map and cpp: on test

Herniation

NOTE A, Normal relationships of intracranial structures. B, Shift of intracranial structures. •Compression of the brainstem and cranial nerves may be fatal. •Herniation forces the cerebellum and brainstem downward through the foramen magnum. •If compression of the brainstem is unrelieved, respiratory arrest will occur due to compression of the respiratory control center in the medulla. know about bushings triad: on test

components of brain: % of fluid volume --intracellular and extracellular fluid of the brain tissue --blood in arterial, venous, and capillary networks --CSF

NOTE •The intracellular and extracellular fluids of brain tissue make up approximately 78% of this volume. •Blood in the arterial, venous, and capillary network makes up 12% of the volume, and the remaining 10% is the volume of the CSF. •Intracranial pressure (ICP) is the hydrostatic force measured in the brain CSF compartment. •Under normal conditions in which intracranial volume remains relatively constant, the balance among the three components (brain tissue, blood, CSF) maintains the ICP.

Progression of increased intracranial pressure

NOTES •Cerebral edema distorts brain tissue, further increasing the ICP, and leads to even more tissue hypoxia and acidosis. This figure illustrates the progression of increased ICP. •It is critical to maintain CBF to preserve tissue and thus minimize secondary injury. Sustained increases in ICP result in brainstem compression and herniation of the brain from one compartment to another. •Displacement and herniation of brain tissue can cause a potentially reversible process to become irreversible. Ischemia and edema are further increased, compounding the preexisting problem.

Potential Placements of ICP --monitoring devices

NOTES •Patients with conditions known to elevate ICP usually undergo ICP monitoring in an ICU, except those with irreversible problems or advanced neurologic disease. •Multiple methods and devices are available to monitor ICP in various sites. •This graphic shows a coronal section of brain showing potential sites for placement of ICP monitoring devices.

LICOX Catheter

The LICOX brain tissue O2 system involves insertion of a catheter. B, The system measures O2 in the brain (PbtO2), brain tissue temperature, and intracranial pressure. NOTES Visual of the LICOX brain tissue oxygen system. •Catheter inserted through an intracranial bolt (A). •The system measures oxygen in the brain (PbtO2), brain tissue temperature, and intracranial pressure (ICP) (B).

Cerebral Blood Flow --autoregulation fnx (2) •only effective if:

—Autoregulation •Adjusts diameter of blood vessels •Ensures consistent CBF •Only effective if mean arterial pressure (MAP) 70 to 150 mm Hg --MAP is very important NOTES •The brain has the ability to regulate its own blood flow in response to its metabolic needs despite wide fluctuations in systemic arterial pressure. •Autoregulation is the automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintain a constant blood flow during changes in arterial blood pressure (BP). •The purpose of autoregulation is to ensure a consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure within normal limits. •The lower limit of systemic arterial pressure at which autoregulation is effective in a normotensive person is a mean arterial pressure (MAP) of 70 mm Hg. •Below this, CBF decreases, and symptoms of cerebral ischemia, such as syncope and blurred vision, occur. •The upper limit of systemic arterial pressure at which autoregulation is effective is a MAP of 150 mm Hg. •When this pressure is exceeded, the vessels are maximally constricted, and further vasoconstrictor response is lost.

Cerebral Blood Flow --cerebral perfusion pressure (calculation) --normal= --what level is associated w/ ischemia & neuronal death? --what to know about cerebral vascular resistance

—Cerebral perfusion pressure (CPP) •The cerebral perfusion pressure (CPP) is the pressure needed to ensure blood flow to the brain. •CPP = MAP - ICP •Normal is 60 to 100 mm Hg •<50 mm Hg is associated with ischemia and neuronal death •As the CPP decreases, autoregulation fails, and CBF decreases. •A CPP less than 30 mm Hg results in ischemia and is incompatible with life. •Normally, autoregulation maintains an adequate CBF and perfusion pressure primarily by adjusting the diameter of cerebral blood vessels and metabolic factors that affect ICP. It is critical to maintain MAP when ICP is elevated. —Effect of cerebral vascular resistance •CPP = Flow x Resistance NOTES •The cerebral perfusion pressure (CPP) is the pressure needed to ensure blood flow to the brain. •CPP is equal to the MAP minus the ICP (CPP = MAP - ICP). •This formula is clinically useful, although it does not consider the effect of cerebral vascular resistance. Cerebral vascular resistance, generated by the arterioles within the cranium, links CPP and blood flow as follows: CPP = Flow x Resistance. •When cerebral vascular resistance is high, blood flow to brain tissue is impaired. •Transcranial Doppler is a noninvasive technique used in ICUs to monitor changes in cerebrovascular resistance.

Clinical Manifestations --vision ??

—Compression of oculomotor nerve •Unilateral pupil dilation •Sluggish or no response to light •Inability to move eye upward •Eyelid ptosis (drooping lid) NOTES •Ocular Signs •Compression of cranial nerve (CN) III, the oculomotor nerve, results in dilation of the pupil on the same side (ipsilateral) as the mass lesion, sluggish or no response to light, inability to move the eye upward and adduct, and ptosis of the eyelid. •These signs can be the result of a shifting of the brain from the midline, compressing the trunk of CN III and paralyzing the muscles controlling pupillary size and shape. In this situation, a fixed, unilateral, dilated pupil is considered a neurologic emergency that indicates herniation of the brain. •Other cranial nerves may also be affected, such as the optic (CN II), trochlear (CN IV), and abducens (CN VI) nerves. Signs of dysfunction of these cranial nerves include blurred vision, diplopia, and changes in extraocular eye movements. •Central herniation may initially manifest as sluggish but equal pupil response. •Uncal herniation may cause a dilated unilateral pupil. •Papilledema (an edematous optic disc seen on retinal examination) is also noted and is a nonspecific sign associated with persistent increases in ICP.

Drug therapy --corticosteroids

—Corticosteroids (not trauma) •Vasogenic edema (tumors and abcesses) •Monitor fluid intake, serum sodium and glucose levels •Concurrent antacids, H2 receptor blockers, proton pump inhibitors NOTES •Corticosteroids (e.g., dexamethasone [Decadron]) are used to treat vasogenic edema surrounding tumors and abscesses. •However, these drugs are not recommended for traumatic brain injury. •Corticosteroids stabilize the cell membrane and inhibit the synthesis of prostaglandins, thus preventing the formation of proinflammatory mediators. Corticosteroids also improve neuronal function by improving CBF and restoring autoregulation. •Complications associated with the use of corticosteroids include hyperglycemia, increased incidence of infections, and gastrointestinal (GI) bleeding. •Regularly monitor fluid intake and sodium and glucose levels. •Perform blood glucose monitoring at least every 6 hours for any patient receiving corticosteroids until hyperglycemia is ruled out as a concern. •Patients receiving corticosteroids should concurrently be given antacids or histamine (H2)-receptor blockers (e.g., cimetidine [Tagamet], ranitidine [Zantac]) or proton pump inhibitors (e.g., omeprazole [Prilosec], pantoprazole [Protonix, Protonix IV]) to prevent GI ulcers and bleeding.

Nursing assessment --cranial nerves

—Cranial nerves •Eye movements •Corneal reflex •Oculocephalic reflex (doll's eye reflex) •Oculovestibular (caloric stimulation) NOTES •Evaluation of other cranial nerves can be included in the neurologic assessment. •Eye movements controlled by cranial nerves III, IV, and VI can be examined in the patient who is awake and able to follow commands and can be used to assess the function of the brainstem. •Testing the corneal reflex gives information about the functioning of cranial nerves V and VII. If this reflex is absent, initiate routine eye care to prevent corneal abrasion. •Eye movements of the uncooperative or unconscious patient can be elicited by reflex with the use of head movements (oculocephalic) and caloric stimulation (oculovestibular). To test the oculocephalic reflex (doll's-eye reflex), turn the patient's head briskly to the left or right while holding the eyelids open. A normal response is movement of the eyes across the midline in the direction opposite that of the turning. Next, quickly flex and then extend the neck. Eye movement should be opposite to the direction of head movement—up when the neck is flexed and down when it is extended. Abnormal responses can help locate the intracranial lesion. This test should not be attempted if a cervical spine problem is suspected

Cerebral edema --cytotoxic cerebral edema

—Cytotoxic cerebral edema •Disruption of cell membrane integrity •Secondary to destructive lesions or trauma to brain tissue •Fluid shift from extracellular to intracellular NOTES•Cytotoxic cerebral edema results from disruption of the integrity of the cell membranes. •Cytotoxic cerebral edema develops from destructive lesions or trauma to brain tissue resulting in cerebral hypoxia or anoxia and syndrome of inappropriate antidiuretic hormone (SIADH) secretion. •In this type of edema, the blood-brain barrier remains intact. Cerebral edema occurrs as a result of a fluid and protein shift from the extracellular space directly into the cells, with subsequent swelling and loss of cellular function.

Cerebral Blood Flow --definition of cerebral blood flow --maintenance of blood flow --what % of body o2 does brain use?

—Definition •Amount of blood in mL passing through 100 g of brain tissue in 1 minute •About 50 mL/min per 100 g of brain tissue NOTES •Cerebral blood flow (CBF) is the amount of blood in milliliters passing through 100 g of brain tissue in 1 minute. •The global CBF is approximately 50 mL/min per 100 g of brain tissue. •The maintenance of blood flow to the brain is critical because the brain requires a constant supply of oxygen and glucose. The brain uses 20% of the body's oxygen and 25% of its glucose.

Evaluation

—Expected Outcomes •Maintain ICP and CPP within normal parameters •No serious increases in ICP during or following care activities •No complications of immobility NOTES The expected outcomes are that the patient with increased ICP will •Maintain intracranial pressure and cerebral perfusion within normal parameters. •Experience no serious increases in intracranial pressure during or following care activities. •Experience no complications of immobility.

Cerebral Blood Flow --factors affecting cerebral blood vessel tone (3)

—Factors affecting cerebral blood vessel tone •CO2 •An increase in the partial pressure of carbon dioxide in arterial blood (PaCO2) relaxes smooth muscle, dilates cerebral vessels, decreases cerebrovascular resistance, and increases CBF. A decrease in PaCO2 constricts cerebral vessels, increases cerebrovascular resistance, and decreases CBF. •O2 •Cerebral O2 tension less than 50 mm Hg results in cerebrovascular dilation. This dilation decreases cerebral vascular resistance, increases CBF, and increases O2 tension. However, if O2 tension is not increased, anaerobic metabolism begins, resulting in an accumulation of lactic acid. •Hydrogen ion concentration •As lactic acid increases and hydrogen ions accumulate, the environment becomes more acidic. Within this acidic environment, further vasodilation occurs in a continued attempt to increase blood flow. NOTES •Carbon dioxide, oxygen, and hydrogen ion concentration affect cerebral blood vessel tone. •The combination of a severely low partial pressure of oxygen in arterial blood (PaO2) and an elevated hydrogen ion concentration (acidosis), which are both potent cerebral vasodilators, may produce a state where autoregulation is lost and compensatory mechanisms fail to meet tissue metabolic demands.

Acute Care

—Fluid and electrolyte balance •Monitor IV fluids •Daily electrolytes •Monitor for DI or SIADH --DI: peeing a lot --SIADH: —Monitor and minimize increases in ICP NOTES •Fluid and electrolyte disturbances can have an adverse effect on ICP. •Closely monitor IV fluids with the use of an accurate IV infusion control device or pump. •Intake and output, with insensible losses and daily weights taken into account, are important parameters in the assessment of fluid balance. •Electrolyte determinations should be made daily, and any abnormal values should be discussed with the HCP. It is especially important to monitor serum glucose, sodium, potassium, magnesium, and osmolality. •Monitor urinary output to detect problems related to diabetes insipidus and syndrome of inappropriate antidiuretic hormone (SIADH). Diabetes insipidus is caused by a decrease in antidiuretic hormone (ADH). It results in increased urinary output and hypernatremia. The usual treatment of diabetes insipidus is fluid replacement, vasopressin (Pitressin), or desmopressin acetate (DDAVP) (see Chapter 49). If not treated, severe dehydration will occur. SIADH is caused by an excess secretion of ADH. SIADH results in decreased urinary output and dilutional hyponatremia. It may result in cerebral edema, changes in LOC, seizures, and coma. •ICP monitoring is used in combination with other physiologic parameters to guide the care of the patient and assess the patient's response to treatment. Valsalva maneuver, coughing, sneezing, suctioning, hypoxemia, and arousal from sleep are factors that can increase ICP. Be alert to these factors and attempt to minimize them.

Measurement of ICP --indications

—Guides clinical care —Indications •Glasgow Coma Scale of ≤8 •Abnormal CT scans or MRI NOTES •ICP monitoring is used to guide clinical care when the patient is at risk for or has elevations in ICP. •It may be used in patients with a variety of neurologic insults, including hemorrhage, stroke, tumor, infection, or traumatic brain injury. •ICP should be monitored in patients admitted with a Glasgow Coma Scale (GCS) score of less than or equal to 8 and an abnormal CT scan or MRI (hematomas, contusion, edema). These results indicate that the patient may have bleeding, contusion, edema, or other problems.

Clinical Manifestations--s/s 2

—Headache •Often continuous •Worse in the morning --"worse headache iv've ever had" : believe them —Vomiting (projectile): s/s of IICP •Not preceded by nausea •Projectile NOTES •Although the brain itself is insensitive to pain, compression of other intracranial structures, such as arteries, veins, and cranial nerves, can cause a headache. •A nocturnal headache and/or headache in the morning is cause for concern and may indicate a tumor or other space occupying lesion that is causing increased ICP. •Straining, agitation, or movement may accentuate the pain. •Vomiting, usually not preceded by nausea, is often a nonspecific sign of increased ICP. •This is called unexpected vomiting and is related to pressure changes in the cranium. •Projectile vomiting may also occur and is related to increased ICP.

Complications 2

—Inadequate cerebral perfusion —Cerebral herniation (dont need to know all of these, just know there are differ kinds) •Tentorial herniation (downward towards brainstem) •Uncal herniation (lateral and downward) •Cingulate herniation (displacement of brain tissue) NOTES •The major complications of uncontrolled increased ICP are inadequate cerebral perfusion and cerebral herniation. •To better understand cerebral herniation, two important structures in the brain must be described. The falx cerebri is a thin wall of dura that folds down between the cortex, separating the two cerebral hemispheres. The tentorium cerebelli is a rigid fold of dura that separates the cerebral hemispheres from the cerebellum. It is called the tentorium (meaning tent) because it forms a tentlike cover over the cerebellum. •Tentorial herniation (central herniation) occurs when a mass lesion in the cerebrum forces the brain to herniate downward through the opening created by the brainstem. •Uncal herniation occurs with lateral and downward herniation. •Cingulate herniation occurs with lateral displacement of brain tissue beneath the falx cerebri.

Cerebral Edema --interstitial cerebral edema

—Interstitial cerebral edema •Usually result of hydrocephalus •Excess CSP production, obstruction of flow, or inability to reabsorb •Treat with ventriculostomy or shunt NOTES •Interstitial cerebral edema is usually a result of hydrocephalus. •Hydrocephalus is a build-up of fluid in the brain and is manifested by ventricular enlargement. •It can be due to excess CSF production, obstruction of flow, or an inability to reabsorb the CSF. •Hydrocephalus treatment usually consists of a ventriculostomy or ventriculoperitoneal shunt.

Acute Care --interventions to optimize ICP and CPP

—Interventions to optimize ICP and CPP •HOB elevated appropriately •Prevent extreme neck flexion •Turn slowly •Avoid coughing, straining, Valsalva •Avoid hip flexion (increase intra-abdominal pressure, and ICP) NOTES •Maintain the patient with increased ICP in the head-up position. The head should be maintained in a midline position, avoiding extreme neck flexion. This position can cause venous obstruction and contribute to elevated ICP. •Adjust the body position to decrease the ICP and to improve the CPP. •Elevation of the head of the bed promotes drainage from the head and decreases the vascular congestion that can produce cerebral edema. However, raising the head of the bed above 30 degrees may decrease the CPP by lowering systemic BP. •Careful evaluation of the effects of elevation of the head of the bed on both the ICP and CPP is required. Position the bed so that it lowers the ICP while optimizing the CPP and other indices of cerebral oxygenation. •Take care to turn the patient with slow, gentle movements because rapid changes in position may increase the ICP. •Prevent discomfort in turning and positioning the patient because pain or agitation also increases pressure. •Increased intrathoracic pressure contributes to increased ICP by impeding the venous return. Thus coughing, straining, and the Valsalva maneuver should be avoided. •Avoid extreme hip flexion to decrease the risk of raising the intra-abdominal pressure, which increases ICP.

Measurement of Cerebral Oxygenation and Perfusion --LICOX catheter

—LICOX catheter •Measures brain oxygenation (PbtO2) and temperature •Placed in healthy white brain matter —Jugular venous bulb catheter •Measures jugular venous oxygen saturation (SjvO2) NOTES •Technology is available to measure cerebral oxygenation and assess perfusion. Three intracranial devices used in ICU care settings are the LICOX catheter, Neurovent catheter, and jugular venous bulb catheter. •The LICOX and Neurovent catheters are placed in viable (healthy) white matter of the brain. These catheters can measure brain oxygenation and temperature. These systems provide continuous monitoring of the pressure of oxygen in brain tissue (PbtO2). The normal range for PbtO2 is 20 to 40 mm Hg. A lower than normal PbtO2 level is indicative of ischemia. These catheters can also measure brain temperature. A cooler brain temperature (96.8° F [36° C]) may produce better outcomes. •The jugular venous, which measures global oxygen extraction, is also used in some institutions. The jugular venous bulb catheter is placed in the internal jugular vein and positioned so that the catheter tip is located in the jugular bulb. •Placement is verified by an x-ray. •This catheter provides a measurement of jugular venous oxygen saturation (SjvO2), which indicates total venous brain tissue extraction of oxygen. •This is a measure of cerebral oxygen supply and demand. The normal SjvO2 range is 55% to 75%. Values less than 50% demonstrate impaired cerebral oxygenation. • In addition to measuring ICP and brain oxygenation, many clinicians are now looking at multimodality monitoring in traumatic brain injury and intracranial hypertension. This technology includes brain microdialysis (measurement of small molecules), continuous EEG, and blood flow monitoring.

Increased ICP --what three component = life-threatening w/ increased ICP

—Life-threatening —Increase in any of three components •Brain tissue •Blood •CSF —↑ Cerebral edema NOTES •Increased ICP is a potentially life-threatening situation that results from an increase in any or all of the three components (brain tissue, blood, CSF) within the skull. •Elevated ICP is clinically significant because it diminishes CPP, increases risks of brain ischemia and infarction, and is associated with a poor prognosis. •Increased ICP can be caused by changes in any of the three components. •Common causes of increased ICP include a mass (e.g., hematoma, contusion, abscess, tumor) and cerebral edema (associated with brain tumors, hydrocephalus, head injury, or brain inflammation). These cerebral insults, which may result in hypercapnia, cerebral acidosis, impaired autoregulation, and systemic hypertension, increase the formation and spread of cerebral edema.

Regulation and Maintenance --monro-kellie doctrine --normal ICP, elevated level =

—Monro-Kellie doctrine the three components must remain at a relatively constant volume within the closed skull structure •If one component increases, another must decrease to maintain ICP •This hypothesis is only applicable in situations in which the skull is closed. •The hypothesis is not valid in persons with displaced skull fractures or hemicranectomy. —Normal ICP 5 to 15 mm Hg •Elevated if >20 mm Hg sustained NOTES •ICP can be measured in the ventricles, subarachnoid space, subdural space, epidural space, or brain tissue using a pressure transducer. •Normal intracranial ICP ranges from 5 to 15 mm Hg. A sustained pressure greater than 20 mm Hg is considered abnormal and must be treated.

Nursing Assessment --motor strength --motor response

—Motor strength •Squeeze hands •Pronator drift test •Raise foot off bed or bend knees —Motor response •Spontaneous or to pain —Vital signs NOTES •Test motor strength by asking the awake and cooperative patient to squeeze your hands to compare strength in the hands. The pronator drift test is an excellent measure of strength in the upper extremities. The patient raises the arms in front of the body with the palmar surface facing upward and eyes closed. If there is any weakness in the upper extremity, the palmar surface turns downward, and the arm drifts down. This would indicate a problem in the opposite motor cortex. Asking the patient to raise the foot from the bed or to bend the knees up in bed is a good assessment of lower extremity strength. Test all four extremities for strength and evaluate for any asymmetry in strength or movement. •Assess the motor response of the unconscious or uncooperative patient by observation of spontaneous movement. If no spontaneous movement is possible, apply a pain stimulus to the patient and note the response. Resistance to movement during passive range-of-motion exercises is another measure of strength. Do not include hand squeezing as part of the assessment of motor movement in the unconscious or uncooperative patient, as this is a reflex action and can provide a misrepresentation of the patient's status. •Also record the vital signs, including BP, pulse, respiratory rate, and temperature. Be aware of Cushing's triad because this indicates severely increased ICP. Besides recording respiratory rate, also note the respiratory pattern.

Regulation and Maintenance --normal compensatory adaptations 3 --ability to compensate

—Normal compensatory adaptations •Changes in CSF volume The CSF volume can be changed by altering CSF absorption or production and by displacement of CSF into the spinal subarachnoid space. •Changes in intracranial blood volume changes in intracranial blood volume can occur through the collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation, and changes in venous outflow. •Changes in tissue brain volume tissue brain volume compensates through distention of the dura or compression of brain tissue. —Ability to compensate is limited •If volume increase continues, ICP rises → decompensation NOTES •Initially an increase in volume produces no increase in ICP as a result of these compensatory mechanisms. However, the ability to compensate for changes in volume is limited. As the volume increase continues, the ICP rises, and decompensation ultimately occurs, resulting in compression and ischemia.

Nutritional Therapy

—Nutritional Therapy •Hypermetabolic and hypercatabolic state ↑ need for glucose •Enteral or parenteral nutrition •Early feeding (within 3 days of injury) •Keep patient normovolemic •IV 0.9% NaCl preferred over D5W or 0.45% NaCl (cerebral edema) NOTES •Regardless of their state of consciousness, patients must have their nutritional needs met. Because malnutrition promotes continued cerebral edema, maintenance of optimal nutrition is imperative. •The patient with increased ICP is in a hypermetabolic and hypercatabolic state that increases the need for glucose to provide the necessary fuel for metabolism of the injured brain. •If the patient cannot maintain an adequate oral intake, other means of meeting the nutritional requirements, such as enteral feedings or parenteral nutrition, should be initiated. •Early feeding following brain injury may improve outcomes. Nutritional replacement should begin within 3 days after injury to reach full nutritional replacement within 7 days after injury. •Patients should also be kept in a normovolemic fluid state. •Continuously evaluate patients based on clinical factors such as urine output, insensible fluid loss, serum and urine osmolality, and serum electrolytes. •IV 0.9% sodium chloride is the preferred solution for administration of piggyback medications. If 5% dextrose in water or 0.45% sodium chloride is used, serum osmolarity decreases, and an increase in cerebral edema may occur.

Clinical manifestations --other cranial nerves

—Other cranial nerves •Diploplia, blurred vision, EOM changes NOTES •Ocular Signs •Other cranial nerves may also be affected, such as the optic (CN II), trochlear (CN IV), and abducens (CN VI) nerves. Signs of dysfunction of these cranial nerves include blurred vision, diplopia, and changes in extraocular eye movements. •Central herniation may initially manifest as sluggish but equal pupil response. •Uncal herniation may cause a dilated unilateral pupil. •Papilledema (an edematous optic disc seen on retinal examination) is also noted and is a nonspecific sign associated with persistent increases in ICP.

Nursing Planning

—Overall Goals •Maintain a patent airway •ICP within normal limits •Normal fluid and electrolyte balance •Prevent complications secondary to immobility and decreased LOC NOTE The overall goals for the patient with increased ICP are to (1) maintain a patent airway; (2) have ICP within normal limits; (3) have normal fluid, electrolyte, and nutritional balance, and (4) prevent complications secondary to immobility and decreased LOC.

Acute Care --pain and anxiety management

—Pain and anxiety management •Opioids •Propofol (Diprivan) •Dexmedetomidine (Precedex) •Neuromuscular blocking agents •Benzodiazepines --pts are truly scared and anxious NOTES •Pain, anxiety, and fear from the primary injury, therapeutic procedures, or noxious stimuli can increase ICP and BP, thus complicating the management and recovery of the brain-injured patient. •The appropriate choice or combination of sedatives, paralytics, and analgesics for symptom management presents a challenge to the ICU team. Administration of these agents may alter the neurologic state, thus masking true neurologic changes. It may be necessary to temporarily suspend drug therapy to appropriately assess neurologic status. The choice, dose, and combination of agents may vary depending on the patient's history, neurologic state, and overall clinical presentation. •Opioids, such as morphine sulfate and fentanyl (Sublimaze), are rapid-onset analgesics with minimal effect on CBF or oxygen metabolism. •The IV anesthetic sedative propofol (Diprivan) is used in the management of anxiety and agitation in the ICU because of its rapid onset and short half-life. An accurate neurologic assessment can be performed very soon after turning off the infusion of propofol. •Dexmedetomidine (Precedex), an alpha-2 adrenergic agonist, is used for continuous IV sedation of intubated and mechanically ventilated patients in the ICU setting for up to 24 hours. When using continuous IV sedatives, be aware of the side effects of these drugs, especially hypotension, as this can result in a lower CPP value. •Nondepolarizing neuromuscular blocking agents (e.g., vecuronium [Norcuron], cisatracurium besylate [Nimbex]) are useful for achieving complete ventilatory control in the treatment of refractory intracranial hypertension. Because these agents paralyze muscles without blocking pain or noxious stimuli, they are used in combination with sedatives, analgesics, or benzodiazepines. •Benzodiazepines, although useful for sedation, are usually avoided in the management of the patient with increased ICP because of the hypotensive effect and long half-life, unless they are used as an adjunct to neuromuscular blocking agents.

Cerebral Blood Flow --pressure changes: compliance

—Pressure changes •Compliance is the expandability of brain •Impacts effect of volume change on pressure •Compliance = Volume/Pressure NOTES •The relationship of pressure to volume is depicted in the pressure-volume curve (see figure next slide). •The curve is affected by the brain's compliance. •Compliance is the expandability of the brain. •It is represented as the volume increase for each unit increase in pressure. •With low compliance, small changes in volume result in greater increases in pressure. •Compliance = Volume/Pressure

Acute Care

—Respiratory function •Maintain patent airway •Elevate head of bed 30 degrees •Suctioning needs •Minimize abdominal distention •Monitor ABGs •Maintain ventilatory support NOTES •Maintenance of a patent airway is critical in the patient with increased ICP and is a primary nursing responsibility. As the LOC decreases, the patient is at an increased risk of airway obstruction from the tongue dropping back and occluding the airway or from accumulation of secretion. •In general, any patient with a GCS less than or equal to 8 or an altered LOC who is unable to maintain a patent airway or effective ventilation needs intubation and mechanical ventilation. •Prevent hypoxia and hypercapnia in order to minimize secondary injury. Proper positioning of the head is important. Elevation of the head of the bed to 30 degrees enhances respiratory exchange and aids in decreasing cerebral edema. •Remove accumulated secretions by suctioning as needed. An oral airway facilitates breathing and provides an easier suctioning route in the comatose patient. •Suctioning and coughing will cause transient decreases in the PaO2 and increases in the ICP. •Keep suctioning to a minimum and less than 10 seconds in duration, with administration of 100% oxygen before and after to prevent decreases in the PaO2. •To avoid cumulative increases in the ICP with suctioning, limit suctioning to two passes per suction procedure, if possible. •Try to prevent abdominal distention as it can interfere with respiratory function. Insertion of a nasogastric tube to aspirate the stomach contents can prevent distention, vomiting, and possible aspiration. However, in patients with facial and skull fractures, a nasogastric tube is contraindicated unless a basal skull fracture has been ruled out, and oral insertion of a gastric tube is preferred. •ABGs should be measured and evaluated regularly. Frequently monitor the ABG values and take measures to maintain the levels within prescribed or acceptable parameters. The appropriate ventilatory support can be ordered on the basis of the PaO2 and PaCO2 values.

Cerebral Blood Flow --stages of increased ICP 4

—Stages of increased ICP •Stage 1: Total compensation •Stage 2: ↓ Compensation; risk for ↑ICP •Stage 3: Failing compensation; clinical manifestations of ↑ ICP (Cushing's triad) •Stage 4: Herniation imminent → death NOTES •At stage 1 the brain is in total compensation, with accommodation and autoregulation intact. •At stage 2, the compliance is beginning to decrease, and an increase in volume places the patient at risk of increased ICP and secondary injury. •At stage 3, compensatory mechanisms fail, there is a loss of autoregulation, and the patient will exhibit manifestations of increased ICP (e.g., headache, changes in level of consciousness or pupil responsiveness). •With a loss of autoregulation, there is an attempt to maintain cerebral perfusion by the body's attempt to increase systolic BP. •However, decompensation is imminent. The patient's response is characterized by systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and altered respirations. This is known as Cushing's triad and is a neurologic emergency. •As the patient enters stage 4, herniation occurs as the brain tissue is forcibly shifted from the compartment of greater pressure to a compartment of lesser pressure. In this situation, intense pressure is placed on the brainstem, and if herniation continues to occur, brainstem death is imminent.

Interprofessional Care

—Treat underlying cause —Adequate oxygenation •PaO2 > 100 mm Hg •PaCO2 35-45 mm Hg •Intubation •Mechanical ventilation —Surgery NOTES •The goals of interprofessional care are to (1) identify and treat the underlying cause of increased ICP and (2) support brain function. The earlier the condition is recognized and treated, the better the patient outcome. A careful history is an important diagnostic aid that can direct the search for the underlying cause. The underlying cause of increased ICP is usually an increase of blood (hemorrhage), brain tissue (tumor or edema), or CSF (hydrocephalus) in the brain. •For any patient with increased ICP it is important to ensure that adequate oxygenation is being maintained to support brain function and prevent secondary injury. •Arterial blood gas (ABG) analysis guides the oxygen therapy. The goal is to maintain the PaO2 at greater than or equal to 100 mm Hg and to keep PaCO2 in normal range at 35 to 45 mm Hg. •An endotracheal tube or tracheostomy may be necessary to maintain adequate ventilation. •It may be necessary to maintain the patient on a mechanical ventilator to ensure adequate oxygenation. •If increased ICP is caused by a mass lesion (e.g., tumor, hematoma), surgical removal of the mass is the best treatment (see the sections on brain tumors and cranial surgery later in this chapter). In aggressive situations, a craniectomy (removal of part of skull) may be performed to reduce ICP and prevent herniation.

Cerebral Edema --vasogenic

—Vasogenic cerebral edema •Most common type •Occurs mainly in white matter •Fluid leaks from intravascular to extravascular space •Variety of causes •Continuum of symptoms → coma NOTES •Vasogenic cerebral edema, the most common type of edema, occurs mainly in the white matter and is characterized by leakage of large molecules from the capillaries into the surrounding extracellular space. •This results in an osmotic gradient that favors the flow of fluid from the intravascular to the extravascular space. •A variety of insults, such as brain tumors, abscesses, and ingested toxins, may cause an increase in the permeability of the blood-brain barrier and produce an increase in the extracellular fluid volume. The speed and extent of the spread of the edema fluid are influenced by the systemic BP, site of the brain injury, and extent of the blood-brain barrier defect. •This edema may produce a continuum of symptoms ranging from headache to disturbances in consciousness, including coma (profound state of unconsciousness) and focal neurologic deficits. •It is important to recognize that although a headache may seem to be a benign symptom, in cases of cerebral edema, it can quickly progress to coma and death. Therefore you must be vigilant in your assessment skills.

Measurement of ICP --ventriculostomy

—Ventriculostomy •Gold Standard for monitoring ICP •Catheter inserted into lateral ventricle •Coupled with an external transducer NOTES•The "gold standard" for monitoring ICP is the ventriculostomy, in which a specialized catheter is inserted into the lateral ventricle and coupled to an external transducer (Figs. 56-7 and 56-8). •This technique directly measures the pressure within the ventricles, facilitates removal and/or sampling of CSF, and allows for intraventricular drug administration.

Clinical Manifestations

—↓ In motor function •Hemiparesis/hemiplegia •Decerebrate posturing (extensor) —Indicates more serious damage •Decorticate posturing (flexor) NOTES •As the ICP continues to rise, the patient manifests changes in motor ability. •A contralateral (opposite side of the mass lesion) hemiparesis or hemiplegia may develop, depending on the location of the source of the increased ICP. •If painful stimuli are used to elicit a motor response, the patient may localize to the stimuli or withdraw from it. •Noxious stimuli may also elicit decorticate (flexor) or decerebrate (extensor) posturing (Fig. 56-5). Decorticate posture consists of internal rotation and adduction of the arms with flexion of the elbows, wrists, and fingers as a result of interruption of voluntary motor tracts in the cerebral cortex. Extension of the legs may also be seen. A decerebrate posture may indicate more serious damage and results from disruption of motor fibers in the midbrain and brainstem. In this position, the arms are stiffly extended, adducted, and hyperpronated. There is also hyperextension of the legs with plantar flexion of the feet. •{See next slide for figure.}

Drug Therapy Cont.

•Antiseizure medications •Antipyretics •Sedatives •Analgesics •Barbiturates NOTES •Metabolic demands such as fever (greater than 38°C), agitation/shivering, pain, and seizures can also increase ICP. The health care team should plan to reduce these metabolic demands in order to lower the ICP in the at-risk patient. Monitor patients for seizure activity. They may need to be placed on prophylactic antiseizure medication. •Fever should be well-controlled in order to maintain a temperature of 36° to 37°C by using antipyretics (e.g., acetaminophen), cool baths, cooling blankets, ice packs, or intravascular cooling devices as necessary without causing the patient to shiver or shake. Shivering should be avoided as this increases the metabolic workload on the brain, and sedatives may be needed or a different type of cooling method selected. •Manage pain while being careful not to oversedate or medicate. Finally, the patient should remain in a quiet and calm environment with minimal noise and interruptions. Observe the patient for signs of agitation, irritation, or frustration. Also teach the caregiver and family about decreasing stimulation. Coordinate with the interprofessional team to minimize procedures that may produce agitation. •Drug therapy for reducing cerebral metabolism may be an effective strategy to control ICP. Reducing the metabolic rate decreases the CBF and therefore the ICP. High doses of barbiturates (e.g., pentobarbital [Nembutal], thiopental [Pentothal]) are used in patients with increased ICP refractory to other treatments. Barbiturates decrease cerebral metabolism, causing a decrease in ICP as well as a reduction in cerebral edema.

ventriculostomy in place

•CSF can be drained via a ventriculostomy when ICP exceeds the upper pressure parameter set by the physician. Intermittent drainage involves opening the three-way stopcock to allow CSF to flow into the drainage bag for brief periods (30 to 120 seconds) until the pressure is below the upper pressure parameters. ICP, Intracranial pressure.

Diagnostic Studies

•CT scan / MRI / PET •EEG •Cerebral angiography •ICP and brain tissue oxygenation measurement (LICOX catheter) •Doppler and evoked potential studies •NO lumbar puncture (cerebral herniation) on test --The reason for this is that cerebral herniation could occur from the sudden release of the pressure in the skull from the area above the lumbar puncture. NOTES •Diagnostic studies can be used to identify the cause of increased ICP. •Computed tomography (CT) and magnetic resonance imaging (MRI) are used to differentiate the many conditions that can cause increased ICP and to assess the effect of treatment. •Positron emission tomography (PET) is also used to diagnose the cause of increased ICP. •Additional tests include EEG, cerebral angiography, ICP measurement, brain tissue oxygenation measurement via the LICOX catheter (described later), transcranial Doppler studies, and evoked potential studies. •In general, a lumbar puncture is not performed when increased ICP is suspected. The reason for this is that cerebral herniation could occur from the sudden release of the pressure in the skull from the area above the lumbar puncture. •In some institutions a hand-held near-infrared scanner (Infrascanner) is used to detect life-threatening intracranial bleeding. The scanner directs a wavelength of light that can penetrate tissue and bone. Blood from intracranial hematomas absorbs the light differently than other areas of the brain.

Measurement of ICP --

•Can control ICP by removing CSF (with ventricular catheter) •Intermittent or continuous drainage •Careful monitoring of volume of CSF drained is essential •Prevent infection and other complications NOTES •With the ventricular catheter, it is possible to control ICP by removing CSF. •The HCP -will typically order a specific level to initiate drainage (e.g., if ICP is greater than 20 mm Hg) as well as the frequency of drainage (intermittent or continuously). •When the ICP is above the indicated level, the ventriculostomy system is opened by turning a stopcock and allowing the drainage of CSF, thus relieving the pressure inside the cranial vault . •There are two options for CSF drainage: intermittent and continuous. If intermittent drainage is ordered, open the ventriculostomy system at the indicated ICP and allow CSF to drain for 2 to 3 minutes. Then the stopcock is closed to return the ventriculostomy to a closed system. If continuous ICP drainage is ordered, carefully monitor the volume of CSF drained is essential. keep in mind that normal CSF production is about 20 to 30 mL/hr, with a total CSF volume of about 150 mL within the ventricles and subarachnoid space. •It is also recommended that a sign be posted above the patient's bed to notify anyone before turning, moving, or suctioning the patient to prevent the removal of too much CSF, which can result in other complications. •Strict aseptic technique during dressing changes or sampling of CSF is imperative to prevent infection. The system must remain intact to ensure that the ICP readings are accurate because treatment is initiated based on the pressures. •Complications of this type of drainage system include ventricular collapse, infection, and herniation or subdural hematoma formation from rapid decompression. •Infection is a serious complication with ICP monitoring. Factors that contribute to the development of infection include ICP monitoring more than 5 days, use of a ventriculostomy, a CSF leak, and a concurrent systemic infection. Routinely assess the insertion site, use aseptic technique, and monitor the CSF for a change in drainage color or clarity.

Cerebral Edema Clinical Manifestations --LOC, vitals, sensory

•Change in level of consciousness •Change in vital signs —Cushing's triad (late sign of increase ICP) •Ocular signs --cranial nerve 3 compression NOTES •The patient's state of consciousness is defined by the patient's clinical responses and pattern of brain activity •Level of consciousness is the most sensitive and reliable indicator of the patient's neurologic status. Changes in LOC are a result of impaired CBF, which causes oxygen deprivation to the cells of the cerebral cortex and reticular activating system (RAS). •Manifestations such as Cushing's triad may be present but often do not appear until ICP has been increased for some time or is suddenly markedly increased (e.g., head trauma). •Compression of cranial nerve (CN) III, the oculomotor nerve, results in dilation of the pupil on the same side as or ipsilateral to the mass lesion, sluggish or no response to light, inability to move the eye upward, and ptosis of the eyelid.

Clinical Manifestations --LOC --cushing's triad 4 s/s

•Change in level of consciousness —Flattening of affect → coma •Change in vital signs —Cushing's triad (increased systolic pressure with widened pulse pressure, bradycardia, irregular decreased respirations) - Emergency (brainstem compression) —Change in body temperature (hypothalmus) NOTES•Changes in LOC are a result of impaired CBF, which causes oxygen deprivation to the cells of the cerebral cortex and reticular activating system (RAS). •A change in consciousness may be dramatic (as in coma) or subtle (such as a flattening of affect, change in orientation, or decrease in level of attention). •In the deepest state of unconsciousness (i.e., coma), the patient does not respond to painful stimuli. Corneal and pupillary reflexes are absent. The patient cannot swallow or cough and is incontinent of urine and feces. The EEG pattern demonstrates suppressed or absent neuronal activity. •Changes in vital signs are caused by increasing pressure on the thalamus, hypothalamus, pons, and medulla. •Manifestations such as Cushing's triad (systolic hypertension with a widening pulse pressure, bradycardia with a full and bounding pulse, and irregular respirations) may be present but often do not appear until ICP has been increased for some time or is suddenly and markedly increased (e.g., head trauma). •Always recognize Cushing's triad as a medical emergency as this is a sign of brainstem compression and impending death. A change in body temperature may also occur because increased ICP affects the hypothalamus

Pupillary Check for Size and Response

•Compare the pupils with one another for size, shape, movement, and reactivity. •If the oculomotor nerve (CN III) is compressed, the pupil on the affected side (ipsilateral) becomes larger until it fully dilates. If ICP continues to increase, both pupils dilate. •Test pupillary reaction with a penlight. The normal reaction is brisk constriction when the light is shone directly into the eye. Also note a consensual response (a slight constriction in the opposite pupil) at the same time. A sluggish reaction can indicate early pressure on CN III (oculomotor nerve). •A fixed pupil unresponsive to light stimulus usually indicates increased ICP. However, it is important to note that there are other causes of a fixed pupil, including direct injury to CN III, previous eye surgery, administration of atropine, and use of mydriatic eye drops. •In some hospitals, clinicians are using a handheld device (pupillometer) to measure the pupil reactivity and size. The device removes any subjectivity from the pupil evaluation.

Nursing Diagnoses

•Decreased intracranial adaptive capacity •Risk for ineffective cerebral tissue perfusion •Risk for disuse syndrome --not using arms and legs NOTES Nursing diagnoses for the patient with increased ICP include, but are not limited to, the following: • Decreased intracranial adaptive capacity related to decreased cerebral perfusion or increased ICP • Risk for ineffective cerebral tissue perfusion related to reduction of venous and/or arterial blood flow and cerebral edema • Risk for disuse syndrome related to altered level of consciousness, immobility, and altered nutritional intake

Interprofessional Care --drug therapy

•Drug Therapy —Mannitol (Osmitrol) •Plasma expansion •Osmotic effect (tissue to blood vessels) •Monitor fluid and electrolyte status —Hypertonic saline •Moves water out of cells and into blood •Monitor BP and serum sodium levels NOTES Drug therapy plays an important part in the management of increased ICP. •Mannitol (Osmitrol) (25%) is an osmotic diuretic given IV. •Mannitol acts to decrease the ICP in two ways: plasma expansion and osmotic effect. •An immediate plasma-expanding effect reduces the hematocrit and blood viscosity, thereby increasing CBF and cerebral oxygen delivery. • A vascular osmotic gradient is created by mannitol. Thus fluid moves from the tissues into the blood vessels. Therefore the ICP is reduced by a decrease in the total brain fluid content. •Monitor fluid and electrolyte status when osmotic diuretics are used. •Hypertonic saline is another drug treatment used to manage increased ICP. •It produces massive movement of water out of edematous swollen brain cells and into blood vessels. •Hypertonic solution requires frequent monitoring of BP and serum sodium levels as intravascular fluid volume excess can occur. •Hypertonic saline has been shown to be just as effective as mannitol when treating increased ICP, and both are often used concurrently when caring for severely brain-injured patients.

Measurement of ICP

•Evaluate changes with patient condition •Inaccurate readings caused by —CSF leaks —Obstruction in catheter/ kinks in tubing —Differences in height of bolt/transducer —Incorrect height of drainage system —Bubbles/air in tubing NOTES •It is important to consider the rate at which changes occur and the patient's clinical condition. •Neurologic deterioration might not occur until ICP elevation is pronounced and sustained. •Immediately report to the HCP any ICP elevation, either as a mean increase in pressure or as an abnormal waveform configuration. •Inaccurate ICP readings can be caused by CSF leaks around the monitoring device, obstruction of the intraventricular catheter or bolt (from tissue or blood clot), kinks in the tubing, difference between the height of the bolt and the transducer, and incorrect height of the drainage system relative to the patient's reference point. Bubbles or air in the tubing can also dampen the waveform.

Intracranial Pressure --factors that influence ICP 6

•Factors that influence ICP •Arterial pressure: HTN •Venous pressure •Intraabdominal and intrathoracic pressure •Posture: bending over •Temperature: •Blood gases (CO2 levels) NOTES •Factors that influence ICP under normal circumstances are changes in (1) arterial pressure, (2) venous pressure, (3) intraabdominal and intrathoracic pressure, (4) posture, (5) temperature, and (6) blood gases, particularly CO2 levels. •The degree to which these factors increase or decrease the ICP depends on the brain's ability to adapt to changes.

Acute Care

•Minimize complications of immobility •Protection from self-injury —Judicious use of restraints; sedatives —Seizure precautions —Quiet, nonstimulating environment •Psychologic considerations NOTES •Provide the physical care to minimize complications of immobility, such as atelectasis and contractures. •The patient with increased ICP and a decreased LOC needs protection from self-injury. Confusion, agitation, and the possibility of seizures increase the risk for injury. •Use restraints judiciously in the agitated patient. If restraints are absolutely necessary to keep the patient from removing tubes or falling out of bed, they should be secure enough to be effective, and observe the skin area under the restraints regularly for irritation. Agitation may increase with the use of restraints, which indicates the need for other measures to protect the patient from injury. • Light sedation with agents such as midazolam (Versed) or lorazepam (Ativan) may be needed. Having a family member stay with the patient may have a calming effect. •For the patient with seizures or the patient at risk for such activity, institute seizure precautions. These include padded side rails, an airway at the bedside, suction readily available, accurate and timely administration of antiseizure drugs, and close observation. The use of prophylactic antiseizure drugs has been controversial as their use may not decrease seizures. •The patient can benefit from a quiet, nonstimulating environment. Always use a calm, reassuring approach. Touch and talk to the patient, even one who is in a coma. •In addition to carefully planned physical care, also be aware of the psychologic well-being of patients and their families. Anxiety over the diagnosis and the prognosis can be distressing to the patient, the caregiver and family, and the nursing staff. Your competent and assured manner in performing care is reassuring to everyone involved. Short, simple explanations are appropriate and allow the patient and the caregiver to acquire the amount of information they desire. There is a need for support, information, and education of both patients and families. Assess the family members' desire and need to assist in providing care for the patient and allow for their participation as appropriate. Encourage interprofessional management of the patient (social work, chaplain, etc.) and involve the family in decision making as much as possible.

Measurement of ICP

•Prevent and monitor for infection •Measure as mean pressure •Waveform should be recorded —Normal, elevated, and plateau waves NOTES •Infection is a serious complication with ICP monitoring. •Factors that contribute to the development of infection include ICP monitoring more than 5 days, use of a ventriculostomy, a CSF leak, and a concurrent systemic infection. •Routinely assess the insertion site, use aseptic technique, and monitor the CSF for a change in drainage color or clarity. •ICP should be measured as a mean pressure. •If a CSF drainage device is in place, the drain must be closed for at least 6 minutes to ensure an accurate reading. •Intracranial pressure monitoring can be used to continuously measure ICP. The ICP tracing shows normal, elevated, and plateau waves. •Record the waveform strip along with other pressure monitoring waveforms.

Intracranial Pressure --components of skull (3)

•Skull has three essential components: 1.Brain tissue (pancheyma) 2.Blood 3.Cerebrospinal fluid (CSF) NOTES •Understanding the dynamics associated with ICP is important in caring for patients with many different neurologic problems. •The skull is an enclosed space with three essential volume components: brain tissue, blood, and cerebrospinal fluid (CSF).

Nursing Assessment

•Subjective data •Level of consciousness (LOC) •Glasgow Coma Scale —Eye opening —Best verbal response —Best motor response NOTES •Subjective data about the patient with increased ICP can be obtained from the patient, caregiver, or family who are familiar with the patient. •Describe the LOC by noting the specific behaviors observed. •Assess the LOC using the Glasgow Coma Scale. •The Glasgow Coma Scale (GCS) is a quick, practical, and standardized system for assessing the LOC. •The three areas assessed in the GCS are the patient's ability to (1) speak, (2) obey commands, and (3) open the eyes when a verbal or painful stimulus is applied. •Specific behaviors observed as responses to the testing stimulus are given a numeric value. Your responsibility is to elicit the best response on each of the scales: the higher the scores, the higher the level of brain functioning. The subscale scores are particularly important if a patient is untestable in one area. For example, severe periorbital edema may make eye opening impossible. •The total GCS score is the sum of the numeric values assigned to each of the three areas evaluated. The highest GCS score is 15 for a fully alert person, and the lowest possible score is 3. A GCS score of less than or equal to 8 is generally indicative of coma, and mechanical ventilation should be considered. Plot the data on a graph, which can be used to determine whether the patient is stable, improving, or deteriorating. •The GCS offers several advantages in the assessment of the unconscious patient. It allows different health care professionals to arrive at the same conclusion regarding the patient's status and can be used to discriminate between different or changing states. •Although the GCS is the gold standard assessment tool for LOC, other scales - such as the Full Outline of Unresponsiveness (FOUR) scale are also used in the clinical setting.

Cerebral Edema --characteristics

•↑ Extravascular fluid in brain •Variety of causes •Three types of cerebral edema 1.Vasogenic 2.Cytotoxic 3.Interstitial NOTES •Cerebral edema is defined as an increased accumulation of fluid in the extravascular spaces of brain tissue. •There are a variety of causes, including mass lesions, head injuries, cerebral infection, vascular insult, and toxic or metabolic encephalopathy. •Regardless of the cause, cerebral edema results in an increase in tissue volume that can increase ICP. •The extent and severity of the original insult are factors that determine the degree of cerebral edema. •There are three types of cerebral edema: vasogenic, cytotoxic, and interstitial. More than one type may occur in the same patient.