Chapter 42: Nursing Care of Patients with Intracranial Disorders (Medical-Surgical Nursing, LeMone & Burke, 6th ed.) PDF

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Detailed lecture notes for Ch. 42 (N253, Guta/Wilson)...

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Chapter 42: Nursing Care of Patients with Intracranial Disorders Medical-Surgical Nursing (LeMone & Burke, 6th ed.) Altered level of consciousness * - Consciousness: a condition in which the individual is aware of self and environment and is able to respond appropriately to stimuli - Cognition: complex process involving all mental activities controlled by the cerebral hemispheres, including thought processes, memory, perception, problem solving, emotion - Arousal and cognition (components of consciousness) are dependent on normal physiologic functions and connections between the arousal mechanism of the reticular formation and cognitive functions of the cerebral hemisphere - RAS – diffuse system of neurons in the thalamus and the upper brainstem responsible for arousal or alertness o RAS reacts to the discomfort caused by a full bladder by waking the person in the middle of night o Once awake, frontal cortex alerts the person that bladder is full - Major Causes o AEIOU o TIPSS  Alcoh  Tumor ol  Injury  Epilep  Psychiatric sy  Stroke  Insulin  Sepsis  Opium  Uremi a Progression of Deteriorating Brain Function LOC Pupillary response Oculomotor response Brisk and equal; Eyes move as Alert, oriented to pupils regular head turns Caloric time, place, and testing (ear person irrigation) produces nystagmus Small and reactive Responds to Roving eye movements; doll’s verbal stimuli; eyes positive, with decreased gaze fixed straight concentration; ahead; eye agitation, confusion, deviation away lethargy; from cold caloric disorientated stimulus and Requires toward warm continuous stimulus stimulation to rouse

Reflexive positioning to pain stimulus

Pupils fixed (nonreactive) in mid position

Caloric testing produces nystagmus

Motor response

Breathing pattern

Purposeful movement; responds to commands

Regular pattern with normal rate and depth

Purposeful movement in response to pain stimulus

Yawning, sighing respirations

Decorticate posturing with upper extremity flexion

Cheyne-Stokes respiration with crescendodecrescendo pattern in rate and depth followed by period of apnea Central neurogenic hyperventilation with rapid, regular and deep respirations; apneustic breathing with prolonged

Decerebrate posturing with adduction and rigid extension of upper and lower extremities

No response to stimuli

Pupils fixed in midpositio n

No spontaneous eye movement or nystagmus

Extension of upper extremities with flexion of lower extremities; flaccidity

inspiration and pauses at full inspiration and following expiration Cluster or ataxic breathing with irregular pattern and depth of respirations; gasping respirations or apnea

Terms Used to Describe Level of Consciousness Terms Characteristics of Patients Full consciousness Alert; oriented to time, place, person; comprehends spoken and written words Confusion Unable to think rapidly and clearly; easily bewildered, with poor memory and short attention span; misinterprets stimuli; judgement is impaired Disorientation Not aware of or not oriented to time, place, or person Obtundation Lethargic, somnolent; responsive to verbal or tactile stimuli but quickly drifts back to sleep Stupor Generally unresponsive; may be briefly aroused by vigorous, repeated or painful stimuli; may shrink away from or grab at the source of stimuli Semicomatose Dose not move spontaneously; unresponsive to stimuli, although vigorous or painful stimuli may result in stirring, moaning, or withdrawal from the stimuli, without actual arousal Coma Unarousable; will not stir or moan in response to any stimulus; may exhibit nonpurposeful response (slight movement) of area stimulated but makes no attempt to withdraw Deep Coma Completely unarousable and unresponsive to any kind of stimulus, including pain; absence of brainstem reflexes; corneal, papillary, and pharyngeal reflexes; and tendon and plantar reflexes

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Pathophysiology o Arousal and Cognition  Reticular formation is a mas of nerve cells and fibers that make up the core of the brainstem, extending from medulla to the mid brain  System of reticular neurons within the RAS passes steady streams of impulses through thalamic relays in order to stimulate the cerebral cortex into wakefulness  Interactions of bodies sensory tract with RAS neurons helps control the strength of the rousing effect on the cerebrum  RAS Destruction  Impairs individual’s ability to maintain wakefulness and arousal  Stroke is most common cause of destruction  MS, tumors, abscesses, and head injury also damage RAS  Edema, ischemia, tumors, IICP, hematomas, hemorrhage, or aneurysm can compress brainstem which also suppresses function of RAS  Can still assess LOC if RAS is damaged however, impairment in arousal may make it impossible to assess cognitive function  Function of cerebral hemisphere depends on continuous blood flow with unimpeded supplies of O2 and glucose. Processes that disrupt blood flow can lead to impaired arousal and cognition.  Bilateral hemispheric lesions (global ischemia) and metabolic disorders (hypoglycemia) are most common cause of ALOC r/t cerebral dysfunction of the hemispheres  Localized masses that cause direct/indirect pressure on the opposite hemisphere or brainstem can also affect LOC  Patient who has damage to cerebral hemisphere, but intact RAS has sleep-wake cycles and may rouse in response to stimuli… but they are still not said to be alert b/c cognition is impaired  If cerebral blood flow is impaired or the patient becomes hypoxic or hypoglycemic, cerebral metabolism is impaired and consciousness declines rapidly  Severe hypoxia → ischemia  Ischemia may be focal (stroke) or global (cardiac arrest or hypovolemic shock)  Those at risk are those with poorly controlled diabetes and those with cardiac or respiratory failure  Other metabolic alterations that affect LOC are… fluid and electrolyte imbalances (hyponatremia), hyperosmolality, and acid-base alterations (hypercapnia (elevated arterial CO2)  Accumulated waste products and toxins from liver or renal failure can also affect LOC  Drugs that suppress the CNS (alcohol, analgesics, anesthetics) suppress metabolic activities in the RAS and cerebral hemispheres  Glutamate (main excitatory neurotransmitter in the brain) may accumulate during prolonged ischemia leading to toxicity and cell death  Seizure activity with abnormal electrical discharges from the brain affect LOC  Consciousness after the seizure returns when the metabolic balance of the neuron is restored  As impairment of brain function progresses, higher intensity stimuli are required to elicit a response  Patient may become more difficult to rouse, or may be agitated and confused when awakened  Orientation to time is lost first then place and person  Vigorous shaking may be needed to maintain wakefulness as LOC decreases  Eventually pt does not respond even with painful stimuli o Patterns of Respirations  Normal respiration: rhythmic pattern is maintained by neural centers in the pons and medulla that respond to changes in arterial levels of oxygen (PaO2) and carbon dioxide (PaCO2)  RAS or cerebral hemisphere damaged → neural control of these centers are lost and lower brainstem centers regulate breathing pattern by responding only to changes in PaCO2 resulting in irregular patterns

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 Initial manifestations of deteriorating brain function = yawning and sighing  Diencephalon: Cheyne-Stokes respirations (alternating periods of deep, rapid breathing followed by periods of apnea)  Midbrain: neurogenic hyperventilation (may exceed 40 breaths/min), the result of uninhibited stimulation of the respiratory centers  Pons: apneustic respirations, characterized by sighing on midinspiration or prolonged inhalation and exhalation; results from excessive stimulation of the respiratory centers  Medulla: ataxia/apneic respirations (totally uncoordinated and irregular), probably as a result of the loss of responsiveness to CO2 o Pupillary and oculomotor responses  Area of brainstem that controls arousal is adjacent to the area that controls the pupils  If lesions or process affecting neurologic function is localized, effects may initially be seen in the ipsilateral pupil (the pupil on the same side of the lesion)  With generalized or systemic processes, pupils are affected equally  If pupils are small and equally reactive, metabolic processes affecting LOC may be present  With compression of cranial nerve VIII at the midbrain, the pupils may become oval or eccentric (off center)  As level of functional impairment progresses, the pupils become fixed (unresponsive to light) and dilated this is known as blown pupils  In deteriorating LOC and coma, spontaneous eye movement is lost and reflexive ocular movements are altered  Doll’s-eye movements → reflexive movements of the eyes in the opposite direction of head rotation (indicator of brain stem function)

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 Oculocephalic reflex → the eyes move upward with passive flexion of the neck and downward with passive neck extension. As brain function deteriorates, this reflex is lost and the eyes fail to turn together and eventually remain fixed in the midposition as the head is turned o Motor Responses  Motor responses are the most accurate identifier of changes in mental status  In altered LOC, motor responses to stimuli range from an appropriate response to a command (squeeze my hand) to flaccidity  As function declines, movements become more generalized and less purposeful  Decorticate posturing may occur  With further decline, decerebrate posture is seen  Without intervention, the patient eventually becomes flaccid, w/ little or no motor response to stimuli o Coma States and Brain death  Persistent Vegetative State  Permanent condition of complete unawareness of self and the environment and loss of all cognitive fxn  Usually the result of severe brain trauma or global ischemia, this condition results from death of the cerebral hemispheres with continued function of the brainstem and cerebellum  Homeostatic regulation function of the brain continues, but ability to respond meaningfully to the environment is lost  Patient has sleep-wake cycles and retains the ability to chew, swallow, and cough, but cannot interact with the environment  Eyes may wander back and forth but cannot track an object or person  In a minimally conscious state, patient is aware of the environment and can follow simple commands  Diagnosis of PVS requires that the condition be present at 1 month after acute brain injury and present for at least 1 month in degenerative/metabolic disorders or developmental malformations  Prevents difficult ethical, moral, and legal issues  Locked-in Syndrome  Patient is alert and fully aware of the environment and has intact cognitive abilities, but is unable to communicate through speech or movements b/c of blocked efferent pathways from the brain  Motor paralysis affects all voluntary muscles, although the upper cranial nerves (I-IV) may remain intact, allowing the pt to communicate through eye movements and blinking  Patient is locked inside a paralyzed body while remaining fully conscious of self and environment  Cause: infarction or hemorrhage of the pons that disrupts outgoing nerve tracts but spares the RAS o Can also be caused as a result of corticospinal tracts between the midbrain & pons are interrupted o Disorders of lower motor neurons or muscles such as poliomyelitis, MG, or ALS

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Diagnostics

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Brain when there is no evidence of cerebral or brainstem fxn for an extended period Death (6-24hr) in a pt who has a normal body temp and is not affected by depressant  The cessa drug or alcohol poisoning  Generally recognized criteria: tion and o Unresponsive coma w/absent motor and reflexes o No spontaneous resp (apnea) irrev ersib o Absent ocular responses to head turning and caloric stimulation (putting ility cold water in the ear to test the occulovestibular reflex and watch to see if of all eyes move to irrigated side then back to the middle) brain o Flat ECG and no cerebral blood circulation present on angiography (if fxn performed) inclu o Persistent of these manifestations for 30mins to 1 hour and for 6 hours ding after onset of coma and apnea the stem  Apnea in the comatose patient is determined by the apnea test  Oc  Ventilator is removed while maintaining oxygenation by tracheal cannula and cu allowing PCO2 to increase to 60mmHg or higher. This level of CO2 is high rs enough to stimulate respirations if the brainstem is functional. o Tests used to evaluate possible metabolic, toxic, or drug-induced disorders include radiologic and lab tests o CT and MRI: done to detect neurologic damage due to hemorrhage, tumor, cyst, edema, MI, or brain atrophy o Radioisotope brain scans: may be done to identify abnormal lesions in brain and evaluate cerebral blood flow o Cerebral angiography: can identify lesions such as aneurysms, occluded vessels, or tumors, and may also be used to determine cessation of cerebral blood flow and brain death o Transcranial Doppler: can assess cerebral blood flow o Lumbar puncture with CSF analysis: to detect possible infection like meningitis o EEG: to evaluate electrical activity of the brain o Blood glucose: measured when coma is of unknown origin and hypoglycemia is suspected or possible  BG < 40-50 mg/dL = cerebral function declines rapidly o Serum electrolytes: sodium, potassium, bicarbonate, chloride, calcium – measured to assess for metabolic disturbances and guide IV therapy  Hyponatremia ( 320 mOsm/kg H2O) = cellular dehydration of brain

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Hypoosmolality (< 250 mOsm/kg H2O) = cerebral edema and swelling → impairing consciousness o ABGs: to evaluate arterial oxygen and carbon dioxide levels as well as acid-base balance  Hypoxemia is frequent cause of ALOC  Increased CO2 are also toxic to brain and can induce coma o Liver function tests (bilirubin, AST, ALT, LDH, albumin, ammonia): to evaluate hepatic function  High ammonia = hepatic failure interfering with cerebral metabolism and neurotransmitters → ALOC o Toxicology screening: to determine if altered LOC is the result of acute drug or ETOH toxicity Increased Intracranial Pressure: sustained elevated pressure (greater than 10 mmHg) within the cranial cavity - Normally skull is filled to capacity with the brain (80%), CSF (8%), and blood (12%) - Normal ICP is from 5 – 10 mmHg measured with pressure transducer while pt is laying with HOB at 30 - Increased intracranial pressure (IICP) or intracranial hypertension is sustained pressure above 10mmHg o Can lead to tissue ischemia and damage to neural tissue o Most often caused by cerebral edema, head trauma, tumors, abscesses, stoke, inflammation and hemorrhage - ICP refers to the pressure of the CSF within the CNS, closely related to brain perfusion - Cerebral Perfusion Pressure (CPP) is the difference between the systemic blood pressure (MAP) minus the ICP o CPP=MAP-ICP (Normal range: 70-90mmHg) - GOAL: To keep ICP within normal range (0-15 mmHg/cm H2O) - ICP = sustained > 10 mmHg within cranial cavity - Pathophysiology o The brain requires a constant supply of O2 and glucose to meet its metabolic needs  15-20% of cardiac output goes to the braininterruption of blood flow leads to ischemia and disruption of cerebral metabolism o Pressure and chemical auto regulation are compensatory mechanisms in which cerebral arterioles change diameter to maintain cerebral blood flow when ICP increases  Increased arterial pressure leads to vasoconstriction & when arterial pressure is low, there is relaxation and vasodilation  Fall in PaCO2 causes cerebral vasoconstriction o Displacement of CSF to the spinal subarachnoid space and increased CSF absorption are early compensatory mechanisms  Relationship between intracranial components and ICP is called compliance o Intracranial hypertension is long term IICP and is potentially life threatening - Cerebral Edema: increase in the volume of brain tissue due to abnormal accumulation of fluid o Vasogenic edema = extracellular edema of the white matter from an increase in the capillary permeability of cerebral vessels, local edema occurs around brain tumors and globally around cerebral trauma and meningitis o Cytotoxic edema = increase in fluid in neurons, glia, and endothelial cells due to failure of Na and K pump accumulation of water and sodium in the cells. Both white and gray matter can be involved. Usually associated with event causing anoxia or hypoxia, such as cardiac arrest. Also hyponatremia or syndrome of inappropriate secretion of ADH - Hydrocephalus: syndrome in which abnormal overproduction, circulation, or reabsorption of CSF occurs o Noncommunicating hydrocephalus occurs when CSF drainage from ventricular system is obstructed due to mass, tumor, inflammation o Communicating hydrocephalus occurs when CSF is not effectively reabsorbed, can be secondary to subarachnoid hemorrhage or scarring from infection - Brain Herniation o Can result from untreated IICP o Displacement of brain tissue from its normal compartment under dural folds of the falx celebri or through the tentorial notch or incisura of the tentorium cerebelli  Cingulate herniation occurs when cingulate gyrus is under falx cerebri, local blood supply and cerebral tissue are compressed, resulting in ischemia and further increases ICP  Central or transtentorial herniation is downward displacement of brain structures, including cerebral hemispheres, basal ganglia, diencephalon, and midbrain through the tentorial incisura  S/S: neurologic signs, decreased LOC progressing to coma, Cheyne-Stokes

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respirations progressing to hyperventilation, pupils from small and reactive to midsize and fixed, may demonstrate unilateral decorticate posturing Uncal or lateral transtentoial herniation occurs when lateral mass displaces the cerebral tissue centrally, forcing the medial aspect of the temporal lobe under the edge of the tentorial incisura. Oculomotor nerve (III) becomes entrapped and may cause ipsilateral pupillary dilation  S/S: ALOC, motor deficits on same side as herniation, decreased sensation, respiratory changes, abnormal positioning and eventual respiratory arrest Infratentorial herniation results from increased pressure within infratentorial compartment. Downward displacement compresses medulla, including its center for vital control  S/S: coma, alteration in resp, fixed pupils, decorticate or decerebate posturing, resp or cardiac arrest

Manifestations o Level of Consciousness: personality changes, irritability, memory and judgement impaired, speech changes, decreased LOCeventual coma and unresponsiveness o Motor Responses: weakness on contralateral side in early IICP, as it continues- hemiplegia, abnormal motor response such as decorticate or decrebrate posturing o Vision and Pupils: altered vision is early manifestation- blurred vision, decreased visual acuity, diplopia o Vitals: CNS ischemic response is a late sign of IICP. Neuronal ischemia causes increase in mean arterial pressure with increase in systolic BP and increased pulse pressure.

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Cushing’s Response = ↑ systolic BP, widening pulse pressure (ex. 280/55), bradycardia–  In response to try and maintain cerebral perfusion pressure  Cushing’s Triad = loss of compensatory mechanism and brain stem failure –  Late sign indicated by HTN, bradycardia, and respiratory abnormalities o Other: headache, papilledema, vomiting (projectile) Diagnostics o CT scan or MRI – initial test used to identify possible causes of IICP (such as space-occupying lesions or hydrocephalus) and to evaluate therapeutic options o Serum osmolality: indicator of hydration status in the patient with IICP – (Normal: 280-300) o ABGs: to assess pH and levels of oxygen and carbon dioxide Mechanical Ventilation o Pts are usually on vent to maintain partial pressure of O2 and CO2, pre...