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T4: ICP
Ch. 57: ICP
| Question | Answer |
|---|---|
| What are the 3 essential volume components of the skull? | brain tissue, blood, cerebrospinal fluid (CSF) |
| The intracellular and extracellular fluids of brain tissue make up approximately what percent of volume? | 78% |
| Blood in the arterial, venous, and capillary network makes up what percent of the volume? | 12% |
| The CSF makes up what percent of the volume? | 10% |
| The hydrostatic force measured in the brain CSF compartment. | intracranial pressure (ICP) |
| What maintains the ICP? | Under normal conditions in which intracranial volume remains relatively constant, the balance among the three components (brain tissue, blood, CSF) maintain ICP. |
| What are some factors that influence ICP? | changes in: arterial pressure, venous pressure, intraabdominal and intrathoracic pressure, posture, temperature, and blood gases, particularly CO2 levels |
| What does the Monro-Kellie doctrine state? | The 3 components must remain at a relatively constant volume w/i the closed skull. If the volume of any one of the 3 components increases w/i the cranial vault and the volume from another component is displaced, the total intracranial volume won't change. |
| What is the normal ICP range? | 5-15 mm Hg |
| A sustained pressure greater than what is considered abdnormal and must be treated. | 20 mm Hg |
| According to the Monro-Kellie doctrine, the body ca adapt to volume changes w/i the skull in three different ways to maintain a normal ICP. | Changes in CSF volume; changes in intracranial blood volume; changes in tissue brain volume |
| Compensatory mechanisms can include changes in the CSF volume. How can the CSF volume be changed? | By altering the CSF absorption or production and by displacement of CSF into the spinal subarachnoid space. |
| Changes in intracranial blood volume can occur through what? | The collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation, and changes in venous outflow. |
| How does tissue brain volume compensate? | Through distention of the dura or compression of brain tissue. |
| Initially, an increase in volume produces no increase in ICP as a result of these what? | compensatory mechanisms |
| If volume increase continues, the ICP rises, and ultimately this will occur? | decompensation resulting in compression and ischemia |
| The amount of blood in milliliters passing through 100 g of brain tissue in 1 minute. | cerebral blood flow (CBF) |
| What is the global CBF? | approximately 50 mL/min per 100g of brain tissue |
| Why is maintenance f blood flow to the brain critical? | The brain requires a constant supply of oxygen and glucose. |
| What percent of the body's oxygen does the brain use? | 20% |
| What percent of the body's glucose does the brain use? | 25% |
| The brain has the ability to do what in response to its metabolic needs despite wide fluctuations in systemic arterial pressure. | regulate its own blood flow |
| 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. | autoregulation |
| What is the purpose of autoregulation? | To ensure a consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure within normal limits. |
| Autoregulation is only effective if the mean arterial pressure (MAP) is what? | 70-150 mmHg |
| What happens if the MAP is below 70? | CBF decreases and symptoms of cerebral ischemia, such as syncope and blurred vision occur. |
| What happens if the MAP is above 150? | The vessels are maximally constricted, and further vasoconstricotor response is lost. |
| Autoregulation | Adjusts diameter of blood vessels. Ensures consistent CBF. Is only effective if MAP is b/t 70-150 mm Hg. |
| This is the pressure needed to ensure blood flow to the brain. | cerebral perfusion pressure (CPP) |
| CPP is equal to the MAP minus the ICP | CPP = MAP - ICP |
| What is normal CPP? | 60-100 mm Hg |
| What happens as the CPP decreases? | Autoregulation fails and CBF decreases. |
| A CPP <50 mm Hg is associated with what? | ischemia and neuronal death |
| A CPP <30 mm Hg results in what? | ischemia and is incompatible with life |
| Normally, this maintains an adequate CBF and perfusion pressure primarily by adjusting the diameter of cerebral blood vessels and metabolic factors that affect ICP. | autoregulation |
| It is critical to maintain what when ICP is elevated? | MAP |
| Cerebral vascular resistance, generated by the arterioles within the vascular resistance, links CPP and blood flow as follows by using this equation. | CPP = Flow x Resistance |
| When cerebral vascular resistance is high what occurs? | blood flow to brain tissue is impaired |
| This is a noninvasive technique used in ICUs to monitor changes in cerebrovascular resistance. | Transcranial Doppler |
| Pressure changes | Compliance is the expandibility of the brain. Impacts effect of volume change on pressure. Compliance = Volume/Pressure |
| What is the concept of the pressure-volume curve? | Can be used to represent the stages of increased ICP. |
| At stage 1 on the pressure-volume curve | There is high compliance. An increase in volume (in brain, tissue, blood, or CSF) does not increase the ICP. |
| At stage 2 on the pressure-volume curve | 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 on the pressure-volume curve | There is significant reduction in compliance. Any small addition of volume causes a great increase in ICP. |
| Entering stage 4 on the pressure-volume curve | The ICP rises to lethal levels with little increase in volume. |
| Stages of increased ICP: Stage 1 | total compensation, with accommodation and autoregulation intact |
| Stages of increased ICP: Stage 2 | decreased compensation; an increase in volume places the patient at risk for increased ICP and secondary injury |
| Stages of increased ICP: Stage 3 | compensatory mechanisms fail; there is loss of autoregulation; clinical manifestations of increased ICP (headache, change in LOC or pupil responsiveness, Cushing's triad) |
| Stages of increased ICP: Stage 4 | Herniation occurs as the brain tissue is forcibly shifted from the compartment of greater pressure to a compartment of lesser pressure. Intense pressure is placed on the brainstem, & if herniation continues to occur, brainstem death is imminent. |
| In stage 3 of increased ICP with a loss of autoregulation what does the body attempt to do? | Attempts to maintain cerebral perfusion by increasing systolic BP. |
| In stage 3 of increased ICP decompensation is imminent. What is the patient's response? | Systolic htn 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. |
| What are some factors that affect cerebral blood vessel tone? | Carbon dioxide, oxygen, hydrogen ion concentration |
| What happens when there is an increase in partial pressure of carbon dioxide in arterial blood (PaCO2)? | Relaxes smooth muscle, dilates cerebral vessels, decreases cerebrovascular resistance, and increase CBF. |
| What happens when there is a decrease in PaCO2? | Constricts cerebral vessels, increases cerebrovascular resistance, and decreases CBF. |
| Cerebral O2 tension less than what results in cerebrovascular dilation. | 50 mm Hg |
| When cerebrovascular dilation occurs it causes what? | Decreases cerebral vascular resistance, increases CBF, and increases O2 tension. |
| With cerebrovascular dilation if O2 tension is not increased what would happen? | Anaerobic metabolism begins resulting in an accumulation of lactic acid. |
| When lactic acid increases what accumulates and what happens to the environment? | hydrogen ions accumulate and the environment becomes more acidic. Within this acidic environment, further vasodilation occurs in a continued attempt to increase blood flow. |
| A severely low partial pressure of O2 in arterial blood (PaO2) and an elevated hydrogen ion concentration (acidosis) are both what? | potent cerebral vasodilators |
| A severely low PaO2 combined with an elevated hydrogen ion concentration (acidosis) may produce what? | A state where autoregulation is lost and compensatory mechanisms fail to meet tissue metabolic demands. |
| Increased ICP is a potentially life-threatening situation that results from an increase in what? | any or all of the three components (brain tissue, blood, CSF) within the skull |
| Elevated ICP is clinically significant because it diminishes this and increases risks of what? | diminishes CPP; increases the risks of ischemia and infarction, and is associated with a poor prognosis |
| What are some common causes of increased ICP? | A mass (hematoma, contusion, abscess, tumor) and cerebral edema (associated with brain tumors, hydrocephalus, head injury, or brain inflammation). |
| What can result from these cerebral insults (mass, cerebral edema)? | Hypercapnia, cerebral acidosis, impaired autoregulation, and systemic hypertension, increase the formation and spread of cerebral edema. |
| Herniation forces the cerebellum and brainstem downward through the what? | foramen magnum |
| If compression of the brainstem is unrelieved what will occur? | Respiratory rest will occur due to compression of the respiratory control center in the medulla. |
| An increased accumulation of fluid in the extravascular spaces of brain tissue. | cerebral edema |
| What can cause cerebral edema? | mass lesions, head injuries, cerebral infection, vascular insult, and toxic or metabolic encephalopathy |
| Regardless of the cause, cerebral edema results in an increase in this which can increase ICP. | tissue volume |
| What factors determine the degree of cerebral edema? | the extent and severity of the original insult |
| What are the 3 types of cerebral edema? | vasogenic, cytotoxic, and interstitial |
| This type of cerebral edema is the most common, occurs mainly in the white matter, and is characterized by fluid leaks from intravascular to extravascular space. | vasogenic cerebral edema |
| What can cause an increase in the permeability of the blood-brain barrier and produce an increase in the extracellular (ECF) volume? | brain tumors, abscesses, and ingested toxins |
| What influences the speed and extent of the spread of the edema fluid? | systemic BP, the site of the brain injury, and the extent of the blood-brain barrier defect |
| What are the symptoms of vasogenic cerebral edema? | Range from headache to disturbances in consciousness, including coma 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 what? | coma and death |
| This edema results from disruption of the integrity of the cell membranes. | cytotoxic cerebral edema |
| What causes cytotoxic cerebral edema? | develops from destructive lesions or trauma to brain tissue |
| What can result from cytotoxic cerebral edema? | cerebral hypoxia or anoxia and SIADH secretion |
| What occurs with cytotoxic cerebral edema? | The blood-brain barrier remains intact with cerebral edema occurring as a result of a fluid and protein shift from the extracellular space directly into the cells, with susequent swelling and loss of cellular function. |
| What causes interstitial cerebral edema? | Usually result of hydrocephalus but it can be due to excess CSF production, obstruction of flow, or an inability to reabsorb the CSF. |
| What is hydrocephalus? | A build up of fluid in the brain and is manifested by ventricular enlargement. |
| How is hydrocephalus treated? | Usually consists of a ventriculostomy or ventriculoperitoneal shunt. |
| CM of increased ICP | change in LOC; change in vital signs; ocular signs; decrease in motor function; headache; vomiting; |
| This is the most sensitive & reliable indicator of the patient's neurologic status and are a result of impaired CBF, which deprives the cells of the cerebral cortex & the reticular activating system (RAS) of oxygen. | level of consciousness |
| Manifestations of this 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). | Cushing's triad |
| What is cranial nerve (CN) III? | the oculomotor nerve |
| Compression of CN III results in what? | 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. |
| A change in LOC may be dramatic, as in ____, or subtle such as? | coma; flattening of affect, change in orientation, or decrease in level of attention |
| When a patient is in a coma the patient does not do what? | Respond to painful stimuli; corneal & pupillary reflexes are absent; cannot swallow or cough; is incontinent of urine and feces; the EEG pattern demonstrates suppressed or absent neuronal activity. |
| Changes in vital signs are caused by what? | pressure on the thalamus, hypothalamus, pons, and medulla |
| Some changes in vital signs include? | Cushings triad (systolic htn w/a widening pulse pressure, bradycardia w/a full & bounding pulse, & irregular respirations), and a change in body temperature b/c increased ICP affects the hypothalamus |
| What are some ocular signs of increased ICP? | Compression of CN III which 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, & ptosis of the eyelid. |
| Ocular signs can be the result of what? | A shifting of the brain from the midline, compressing the trunk of CN III & paralyzing the muscles controlling pupillary size & shape. |
| This is a neurologic emergency that indicates herniation of the brain. | a fixed, unilateral, dilated pupil |
| What other cranial nerves may also be affected by increased ICP? | the optic nerve (CN II), trochlear (CN IV), and abducens (CN VI) |
| What are some signs of dysfunction of CN II, IV, & VI? | blurred vision, diplopia, and changes in extraocular eye movements |
| This may initially manifest as sluggish but equal pupil response. | central herniation |
| This may cause a dilated unilateral pupil. | uncal herniation |
| This is an edematous optic disc seen on retinal examination. | papilledema |
| As the ICP continues to rise, the patient manifests changes in motor ability such as? | A contralateral (opposite side of mass lesion) hemiparesis or hemiplegia, depending on the location of the source of the increased ICP. |
| If painful stimuli are used to elicit a motor response, the patient may do what? | localize to the stimuli or withdraw from it |
| Noxious stimuli may also elicit what? | decorticate (flexor) or decerebrate (extensor) posturing |
| This 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. | decorticate posture |
| This may indicate a more serious damage and results from disruption of motor fibers in the midbrain and brainstem. The arms are stiffly extended, adducted, & hyperpronated. There is also hyperextension of the legs w/plantar flexion of the feet. | decerebrate posture |
| Although the brain itself is insensitive to pain, compression of other intracranial structures, such as the walls of arteries and veins and the cranial nerves, can produce what? | headache |
| With increased ICP, the headache is often continuous but worse in the morning. What may accentuate the pain? | straining, agitation, or movement |
| This is often a nonspecific sign of increased ICP. | unexpected vomiting, usually not preceded by nausea; or projectile vomiting |
| What causes unexpected vomiting with increased ICP? | pressure changes in the cranium |
| What are the major complication of uncontrolled increased ICP? | inadequate cerebral perfusion and cerebral herniation |
| This is a thin wall of dura that folds down b/t the cortex, separating the two cerebral hemispheres. | falx cerebri |
| This is a rigid fold of dura that seperates the cerebral hemispheres from the cerebellum. It forms a tentlike cover over the cerebellum. | tentorium cerebelli |
| This occurs when a mass lesion in the cerebrum forces the brain to herniate downward through the opening created by the brainstem. | tentorial herniate (central herniation) |
| This occurs with lateral and downward herniation. | uncal herniation |
| This occurs with lateral displacement of brain tissue beneath the falx cerebri. | cingulate herniation |
| What diagnostic studies can identify the cause of increased ICP? | CT scan, MRI, PET, EEG, cerebral angiography, ICP and brain tissue oxygenation measurement (LICOX catheter), doppler and evoked potential studies, NO lumbar puncture |
| Why is a lumbar puncture not performed when increased ICP is suspected? | Cerebral herniation could occur from the sudden release of the pressure in the skull from the area above the lumbar puncture. |
| Some places use this to detect life-threatening intracranial bleeding. | a hand held Infrascanner |
| How does the Infrascanner work? | It 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. |
| This is used to guide clinical care when the patient is at risk for or has elevations in ICP. | ICP monitoring |
| ICP should be monitored in patients with an abnormal CT scan or MRI (hematomas, contusion, edema) and a Glasgow Coma Scale (GCS) score of what? | less than or equal to 8 |
| This is the "gold standard" for monitoring ICP, in which a specialized catheter is inserted into the lateral ventricle and coupled to an external transducer. | ventriculostomy |
| What are the functions of the ventriculostomy? | The pressure within the ventricles, facilitates removal and/or sampling of CSF, and allows for intraventricular drug administration. |
| When the ventriculostomy is in place this can be done when ICP exceeds the upper pressure parameter set by the physician. | CSF can be drained |
| Intermittent drainage with a ventriculostomy involves doing what? | Opening the three-way stopcock to allow CSF to flow into the drainage bag for brief periods (30-120 secs) until the pressure is below the upper pressure parameters. |
| When leveling a ventriculostomy it is important to make sure that the transducer of the ventriculostomy is level to what? | The foramen of Monro (interventricular foramen) and that the ventriculostomy system is at the ideal height. |
| Where is a reference point for the Monro (interventricular) foramen? | the tragus of the ear |
| With a ventriculostomy when the patient is repositioned what should be done? | the system needs to be re-zeroed |
| This uses a sensor transducer located within the catheter tip. The sensor tip is placed within the ventricle or the brain tissue and provides a direct measurement of brain pressure. | fiberoptic catheter |
| This is another method of monitoring ICP. It is placed just through the skull between the arachnoid membrane and the cerebral cortex. It does not allow for CSF drainage but is ideal for patients w/mild or moderate head injury. | subarachnoid bolt or screw |
| What method of monitoring ICP can easily be converted into a ventriculostomy if the patient decompensates? | the subarachnoid bolt or screw |
| What are some factors that contribute to the development of infection with ICP monitoring? | ICP monitoring more than 5 days, use of a ventriculostomy, the presence of a CSF leak, and a concurrent systemic infection |
| What are some important interventions for monitoring infections with ICP monitoring? | Routing assessment of the insertion site, the use of aseptic technique, and monitoring the CSF for a change in drainage color or clarity. |
| ICP should be measures as a? | mean pressure |
| If a CSF drainage device is in place, what must be done to ensure an accurate reading? | the drain must be closed for at least 6 minutes |
| ICP monitoring can be used to continuously measure ICP. The ICP tracing show what? | Shows normal, elevated, and plateau waves that should be recorded. |
| This might not occur until ICP elevation is pronounced and sustained. | neurologic deterioration |
| What can cause inaccurate ICP readings? | CSF leaks,; obstruction in catheter/kinks in tubing; differences in height of bolt/transducer; incorrect height of drainage system; bubbles/air in tubing |
| A mean increase in pressure or an abnormal waveform configuartion is indicative of what? What should you do immediately? | ICP elevation; report it to the HCP |
| What can control ICP by removing CSF? | ventricular catheter |
| When will the doctor order a specific level to initiate drainage? | 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, what happens to relieve the pressure inside the cranial vault. | The ventriculostomy system is opened by turning a stopcock and allowing the drainage of CSF. |
| What are the two option for CSF drainage? | intermittent and continuous |
| If intermittent drainage is ordered, what should be done/ | Open the ventriculostomy system at the indicated ICP and allow CSF to drain for 2-3 mins. Then the stopcock is closed to return the ventriculostomy to a closed system. |
| If continuous ICP drainage is ordered, what should be done? | Careful monitoring of the volume of CSF drained is essential, keeping in mid that normal CSF production is about 20-30 ml/hr w/a total CSF volume of 90-150 ml w/i the ventricles & subarachnoid space. |
| What is imperative during dressing changes or sampling of CSF to prevent infection? | strict aseptic technique |
| What are some complications with the ventriculostomy drainage system? | ventricular collapse, infection, herniation or subdural hematoma formation from rapid decompression |
| What devices are used to measure cerebral oxygenation and assess perfusion? | LICOX catheter and jugular venous bulb catheter |
| This measures brain oxygenation (PbtO2) and temperature and is placed in healthy white brain matter. | LICOX catheter |
| What is another advantage of the LICOX catheter? | It is able to measure brain temperature. |
| This is placed in the internal jugular vein and positioned so that the catheter tip is located in the jugular bulb. It measures jugular venous oxygen saturation (SjvO2), which indicates total venous brain tissue extraction of oxygen. | jugular venous bulb catheter |
| What is used to verify placement of the jugular venous bulb catheter? | x-ray |
| What is the normal SjvO2 range? | 55-75% |
| What does a SjvO2 of less than 50% mean? | impaired cerebral oxygenation |
| What are the goals of collaborative care with increased ICP? | treat underlying cause; adequate oxygenation; surgery |
| The underlying cause of increased ICP is usually what? | 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 what is being maintained? | adequate oxygenation to support brain function |
| With increased ICP, what guides the oxygen therapy? | arterial blood gas (ABG) analysis |
| The goal is to maintain the PaO2 at greater than or equal to what? And to keep PaCO2 in the normal range of what? | 100 mm Hg; 35-45 mm Hg |
| What may be necessary to maintain adequate ventilation? | an endotracheal tube or tracheostomy |
| If increased ICP is caused by a mass lesion (tumor, hematoma) what is the best treatment? | surgical removal of the mass |
| In aggressive situations this may be performed to reduce ICP and prevent herniation. | craniectomy (removal of part of skull) |
| This is an osmotic diuretic given IV to decrease ICP. | mannitol (Osmitrol) 25% |
| Mannitol decreases the ICP in two ways. What are they? | plasma expansion and osmotic effect |
| Mannitol has an immediate plasma-expanding effect that reduces this and increases what? | hematocrit & blood viscosity; increases CBF & cerebral oxygen delivery |
| Mannitol creates a vascular osmotic gradient that causes fluid to move where? The ICP is reduced by a decrease in what? | Fluid moves from the tissues into the blood vessels thereby decreasing total brain fluid content. |
| What IV solution can be given to manage increased ICP? | hypertonic saline |
| Hypertonic solutions produce massive movement of water out of where and into what? | edematous swollen brain cells; into the blood vessels |
| When using a hypertonic solution what requires frequent monitoring? | BP and serum sodium levels as intravascular fluid volume excess can occur |
| What drugs are used to treat vasogenic edema surrounding tumors and abscesses but are NOT recommended for head-injured patients? | corticosteroids such as dexamethasone (Decadron) |
| What is the function of corticosteroids for increased ICP? | Stabilizes the cell membrane and inhibit the synthesis of prostaglandins, thus preventing the formation of proinflammatory mediators. Also improve neuronal function by improving CBF & restoring autoregulation. |
| What are some complications associated with the use of corticosteroids? | hyperglycemia, increased incidence of infections, and gastrointestinal (GI) bleeding |
| What should be monitored with corticosteroid use? | fluid intake, sodium and glucose levels |
| Perform blood glucose monitoring at least every 6 hours for any patient receiving corticosteroids until what is ruled out? | hyperglycemia |
| Patients receiving corticosteroids should concurrently be given this to prevent what? | antacids or histamine (H2)-receptor blockers such as cimetidine (Tagamet), ranitidine (Zantac), or PPIs such as omeprazole (Prilosec), pantoprazole (Protonix) to prevent GI ulcers & bleeding. |
| What are some drugs used for patients with increased ICP? | Mannitol, hypertonic saline, corticosteroids w/PPIs, antacids, or H2 receptor blockers; antiseizure meds; antipyretics; sedatives; analgesics; and barbiturates |
| What are some metabolic demands that can increase ICP? | fever, agitation/sivering, pain, and seizures |
| Fever should be well-controlled in order to maintain a temperature of 36-37 C by using what? | antipyretics (acetaminophen), cool baths, cooling blankets, ice packs, or intravascular cooling devices |
| Manage pain but do not? | oversedate |
| What type of environment should a patient with ICP have? | Quiet and calm environment with minimal noise and interruptions. Observe pt for signs of agitation, irritation, or frustration. Teach family about decreasing stimulation & minimize procedures that may produce agitation. |
| High doses of this are used in patients with increased ICP refractory to other treatments. It decreases cerebral metabolism, causing a decrease in ICP as well as a reduction in cerebral edema. | barbiturates such as pentobarbital (Nembutal), thiopental (Pentothal) |
| Patients with increased ICP are in what type of state and require an increase need for glucose to provide the necessary fuel for metabolism of the injured brain. | hypermetabolic and hypercatabolic state |
| If the patient cannot maintain an adequate oral intake what should be done? | enteral feedings or parenteral nutrition should be initiated |
| When should nutritional replacement begin? | Within 3 days after injury to reach full nutritional replacement within 7 days after injury. |
| What is the preferred solution for admnistration of piggyback medications for increased ICP? | 0.9% NaCl |
| What happens if 5% dextrose in water or 0.45% NaCl is used to administer piggyback medications? | serum osmolarity decreases and an increase in cerebral edema may occur |
| How should you assess the LOC in a patient with increased ICP? | Glasgow Coma Scale |
| What are the 3 indicators of response in the GCS? | 1) opening of the eyes; 2) the best verbal response, 3) the best motor response |
| What is the highest GCS score a patient can get? | 15 for a fully alert person |
| What is the lowest possible GCS score a patient can get? | 3 |
| A GCS score of less than or equal to 8 is generally indicative of what? | coma |
| When checking the pupils of a patient with increased ICP what should you check for? | Compare with one another for size, shape, movement, and reactivity. |
| What happens to the pupils 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. |
| The normal pupillary reaction is brisk constriction when the light is shone directly into the eye. What does a sluggish reaction indicate? | early pressure on CN III (oculomotor nerve) |
| What does a fixed pupil unresponsive to light stimulus indicate? | increased ICP |
| A fixed pupil can also be caused by what? | direct injury to CN III, previous eye surgery, administration of atropine, and use of mydriatic eyedrops |
| Eye movements controlled by what cranial nerves 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? | CN III, IV, VI |
| Testing the corneal reflex gives information about the functioning of what cranial nerves? | CN V, VII |
| If the corneal reflex is absent what should be initiated? | Routine eye care to prevent corneal abrasion. |
| How can you test eye movements of the uncooperative or unconscious patient? | With the use of head movement (oculocephalic) and caloric stimulation (oculovestibular). |
| How do you test the oculocephalic reflex (doll's-eye reflex)? | Turn the patient's head briskly to the left or right while holding eyelids open. Next, quickly flex and then extend the neck. Eye mvmt should be opposite to the direction of head mvmt. |
| Abnormal responses while testing the oculocephalic reflex can help to locate what? | the intracranial lesion |
| The oculocephalic reflex should not be attempted if what is suspected? | cervical spine problem |
| How do you test motor strength with an awake and copperative patient? | Have pt squeeze your hands to compare strength in the hands. The palmar drift test measures strength in upper extremities. Ask pt to raise the foot from the bed or bend the knees up to assess lower extremity strength. |
| How do you assess the motor response of the unconscious or uncooperative patient? | by observation of spontaneous movement or apply a pain stimulus to the patient and note the response |
| What are the overall goals for the patient with increased ICP? | Maintain a patent airway; have ICP w/i normal limits; have normal fluid, electrolye, and nutritional balance; and prevent complications secondary to immobility and decreased LOC |
| What are some nursing interventions to maintain respiratory function in a patient with increased ICP? | Elevate HOB 30 degrees; suctioning; minimize abdominal distention (NG tube); monitor ABGs; maintain ventilatory support |
| As the LOC decreases, the patient is at an increased risk of airway obstruction from what? | The tongue dropping back and occluding the airway or from accumulation of secretions. |
| 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 what? | intubation and mechanical ventilation |
| To prevent hypoxia and hypercapnia in order to minimize secondary injury the HOB should be elevated to 30 degrees to enhance what? | respiratory exchange and aid in decreasing cerebral edema |
| You should remove accumulated secretions by suctioning as needed but suctioning and coughing will cause what? | Transient decreases in the PaO2 and increases in the ICP. Keep suctioning to a minimum and less than 10 seconds in duration. |
| What should you do to prevent decreases in the PaO2 while suctioning? | administration of 100% oxygen before and after suctioning |
| When suctioning what should you do to avoid cumulative increases in the ICP? | Limit suctioning to two passes per suction procedure, if possible. |
| Abdominal distention can interfere with respiratory function. Insertion of what can help prevent distention, vomiting, and possible aspiration. | nasogastric tube (NG tube) |
| An NG tube is contraindicated in patients with what? | facial and skull fractures |
| Pain, anxiety, and fear from the primary injury, therapeutic procedures, or noxious stimuli can cause what? | Increased ICP and BP, thus complicating the management and recovery of the brain-injured patient. |
| Why does administration of sedatives, paralytics, and analgesics or a combination of these present a challenge to the ICU team? | May alter the neurologic state, thus masking true neurologic changes. It may be necessary to temporarily suspend drug therapy to appropriately assess neurologic status. |
| These drugs are rapid-onset analgesics with minimal effect on CBF or oxygen metabolism. | opioids such as morphine sulfate and fentanyl (Sublimaze) |
| This IV anesthetic sedative is used to manage anxiety and agitation in the ICU b/c of its rapid onset and short half-life? | propofol (Diprivan) |
| What is a side effect of propofol? | hypotension |
| This 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. | dexmedetomidine (Precedex) |
| Nondepolarizing neuromuscular blocking agents such as these are useful for achieving complete ventilatory control in the treatment of refractory intracranial hypertension. | vecuronium (Norcuron), cisatracurium besylate (Nimbex) |
| Because these nondepolarizing neuromuscular blocking agents paralyze muscles w/o blocking pain or noxious stimuli, they are used in combination with what? | sedatives, analgesics, or benzodiazepines |
| Benzodiazepines, although useful for sedation, are usually avoided in the management of the patient with increased ICP because? | B/c of the hypotensive effect and long half-life, unless they are used as an adjunct to neuromuscular blocking agents. |
| You should monitor urinary output to detect problems related to what? | Diabetes insipidus (DI) and Syndrom of inappropriate antidiuretic hormone (SIADH) |
| This is caused by a decrease in antidiuretic hormone (ADH). | DI |
| What results from DI? | Increased urinary output and hypernatremia. |
| What is the usual treatment of DI? | fluid replacement, vasopressin (Pitressin), or desmopressin acetate (DDAVP) |
| If DI is not treated what will occur? | dehydration |
| This is caused by an excess secretion of ADH? | SIADH |
| What results from SIADH? | Decreased urinary output and dilutional hyponatremia. It may result in cerebral edema, changes in LOC, seizures, and coma. |
| What are some interventions to optimize ICP and CPP? | HOB elevated appropriately; prevent extreme neck flexion; turn slowly; avoid coughing, straining, Valsalva; avoid hip flexion |
| Equation for CPP | CPP = MAP - ICP |
| Equation for MAP | MAP = DBP + 1/3 (SBP-DBP) = 50 + 1/3(92-50) = 64 mm Hg |
| What is normal CPP? | 60-100 mm Hg |
| A CPP <30 mm Hg results in what? | ischemia and is incompatible with life |
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eblanc1
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