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DISTURBANCES OF THE NERVOUS SYSTEM (Series 1) By Franklin C. Barberan R.N. 2nd Place Board Topnotcher
DISTURBANCE # 1: INCREASED INTRACRANIAL PRESSURE NORMALLY; The cranium vault contains: 1,450 grams of brain tissue 75 ml blood 75 ml CSF K! The MONRO-KELLIE HYPOTHESIS An increase in any of the above components results to increased ICP Cerebral ischemia Shifting of brain tissues & Herniations
ETIOLOGY Increased PaCO2
cerebral vasodilation Increased blood flow Increased ICP
Cerebral Edema (secondary to tumor, fluid shifts, hyponatremia) Secondary effect of : head injury brain tumors subarachnoid hemorrhages viral encephalitis
CLINICAL MANIFESTATIONS K! There are two stages of cerebral adjustment. 1. Compensation- the brain and its components alter their volume 2. Decompensation ability of the brain to adjust becomes ineffective changes in mental status. o K! LETHARGY is the earliest sign of increasing ICP. o Slowing of speech o Delayed response to verbal suggestions Abnormal motor response o Decortication - Internal rotation and flexion of upper extremities - Plantar flexion of lower extremities - K! occurs with damage to cerebral hemispheres o Decerebration - extension and outward rotation of upper extremities - plantar flexion of lower extremities o Flaccidity - flaccid extremities - absent reflexes - jaw sags, tongue flaccid 1
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NURSING ALERT! Cushings response (or Cushings reflex) is seen when cerebral blood flow
decreases. Watch out for the Cushings Triad: bradycardia, hypertension, and bradypnea a grave signs . It leads to brain stem herniation. (Notes by: by Franklin C. Barberan- Health Ambassadors Nursing Review)
MANAGEMENT MONITORING ICP Purpose:
1. To identify increased pressure. 2. To quantify the degree of elevation. 3. To initiate appropriate treatment. 4. To provide access to CSF for sampling and drainage. 5. To evaluate the effectiveness of treatment. HOW IS THE PRESSURE MONITORED: Through insertion of: 1. Intraventricular catheter (ventriculostomy), 2. Subarachnoid bolt. 3. An epidural or subdural catheter, or a 4. Fiberoptic transducer-tipped catheter placed in the subdural space or the ventricle to monitor ICP
INTERVENTIONS: K! GOAL: Decrease cerebral edema Lower the volume of the CSF Decrease blood volume
DECREASING CEREBRAL EDEMA 1. Osmotic diuretics (mannitol) may be given to dehydrate the brain tissue and reduce cerebral edema. They act by drawing water across intact membranes, thereby reducing the volume of brain and extracellular fluid. An indwelling urinary catheter is usually inserted to monitor urinary output and to manage the resulting diuresis. When a patient is receiving osmotic diuretics. 2. Fluid restriction- limiting overall fluid intake leads to dehydration and hemoconcentration, drawing fluid across the osmotic gradient and decreasing cerebral edema. 3. Decreasing metabolic rate and body temperature. decrease cerebral edema, reduce the oxygen and metabolic requirements of the brain, and protect the brain from continued ischemia. REDUCING CSF AND INTRACRANIAL BLOOD VOLUME 1. CSF drainage is frequently performed because the removal of CSF with a ventriculostomy drain may dramatically reduce ICP and restore cerebral perfusion pressure. Risk: Excessive drainage may result in collapse of the ventricles. 2. Hyperventilation, which results in vasoconstriction, has been used for many years in patients with increased ICP. Hyperventilation is indicated in patients whose ICP is unresponsive to conventional therapies, but it should be used judiciously. CONTROLLING FEVER Preventing a temperature elevation is critical because fever increases cerebral metabolism and the rate at which cerebral edema forms. Monitor closely, and the patient is observed for shivering, which should be avoided because it increases ICP (Sund-Levander & Wahren, 2000). MAINTAINING OXYGENATION Arterial blood gases must be monitored to ensure that systemic oxygenation remains optimal. Hemoglobin saturation can also be optimized to provide oxygen more efficiently at the cellular level. REDUCING METABOLIC DEMANDS Cellular metabolic demands may be reduced through the administration of high doses of barbiturates when the patient is unresponsive to conventional treatment. The mechanism how barbiturates decrease ICP is uncertain. TRENDS IN NEUROLOGIC MONITORING One controversial trend in cerebral monitoring is the ongoing measurement of venous oxygen saturation in the jugular bulb (SjO2). The invasive nature of this type of monitoring and current limitations in technology mandate caution in its use. More study is needed before SjO2 monitoring can be considered a valid and reliable tool for the management of cerebral ischemia (Clay, 2000).
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NURSING PROCESS: DELIVERED DURING CLASSROOM LECTURES INTENSIVE FOCUS
1. Osmotic diuretics Mannitol Corticosteroids (dexamethasone) Helps reduce edema around the brain tumor 2. CSF drainage 3. Hyperventilation- leads to respiratory alkalosis that consequently produces cerebral vasoconstriction (short term control) 4. Control of fever. K! Prevent shivering (Rationale: Shivering causes increased intracranial pressure). To control shivering : Chlorpromazine (Thorazine) is given. 5. Reducing metabolic demands. K! paralyzing agents are given( muscle relaxants); Pancuronium (Pavulon) Barbiturates
COMPLICATIONS OF INCREASED ICP: The following complications are explained on letures. 1. Brain stem herniation. 2. Diabetes insipidus (due to decreased antidiuretic hormone) 3. Syndrome of Inappropriate antidiuretic hormone (SIADH)
DISTURBANCE #2: TRANSIENT ISCHEMIC ATTACKS (TIAs)
DEFINITION: Temporary episodes of neurologic deficits characterized by loss of motor, sensory, and visual function, lasting for a few seconds or minutes but not more than 24 hours. K! TIAs serves as a warning of impending CVA or stroke. K! No permanent brain damage yet. ETIOLOGY: Temporary impairment of blood flow t regions of the brain and maybe due to: Atherosclerosis Obstruction by an embolus Decreased cerebral perfusion pressure MANIFESTATION: K! The classic symptom is AMAUROSIS FUGAX (fleeting blindness) sudden painless loss of vision of one eye, or dimming or graying of vision of one eye vertigo diplopia alterations in consciousness numbness/ weakness of either hand or leg difficulty of speaking or understanding of speech N! a bruit may be heard on the carotid artery Diminished pulsations on the neck
suggests retinal detachment
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DIAGNOSTIC EVALUATION: Carotid phonoangiography- auscultation, direct visualization, and photographic recording of carotid bruits. Oculoplethysmography- measures pulsations in blood flow through ophthalmic artery. Carotid angiography visualize intracranial and cervical vessels Digital subtraction angiography. MANAGEMENT: 1. Platelet deaggregators. Ex. Aspirin 2. Anticoagulant therapy. Ex. Warfarin sodium 3. Management of hypertension and hyperglycemia 4. Cessation of smoking. Surgical management: K! Carotid endarterectomy - removal of atherosclerotic plaque or Thrombus Post Operative care: Maintain adequate blood pressure. N! Hypotension is avoided. (Rationale: to prevent cerebral ischemia). N! Hypertension should be avoided. (Rationale: Might lead to cerebral hemorrhage, edema, disruption of arterial reconstruction). K! To control hypertension: Give Sodium nitroprusside as ordered.
TOPNOTCHERS FOCUS: DELIVERED DURING CLASSROOM LECTURES INTENSIVE FOCUS
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