Management of Patients with Neurologic Dysfunction Chap 61

1. Management of Patients with Neurologic Dysfunction Chap 61

2. Altered Level Of Consciousness: • Unresponsive to and unaware of environmental stimuli (momentary to several hours) • Coma:clinical state of uncon. In which the patient is unaware of self or environment for prolonged period (days, to months, even years) • Akinetic mutism:is a stat of unresponsiveness to the environment in which the pt make no movements or sound but sometimes opens the eyes. • Persistent vegitative state:pt is wakeful but devoid of conscious content, without cognitive of affective mental function

3. Clinical Manifestations: • Behavioral changes : Restlessness, or increasing anxiety • Changes in Pupillary reaction: become sluggish • Eye opening • Verbal Response • Motor response

4. Altered LOC (cont...) • Causes: neurlogic (head injury, stroke), toxicology, or metabolic (hepatic and renal failure, Diabetic ketoacidosis) • Assessment and diagnostic findings: CT, MRI, EEG, blood glucose, electrolyte, serum ammonia, BUN, osmolarity, Ca level, PT, serum ketones. Pupillary light reflex is presented a toxic or metabolic cause is suspected • Complications: respiratory failure, pneumonia, pressure ulcer, and aspiration • Medical management: Maintain patent airway, establish IV line, NGT for nutritional support, and monitoring V/S

5. Increased Intracranial pressure (ICP): • The cranium contain:1400g brain tissue,75ml CSFand 75ml Blood ( these value always in state of equilibrium) • Monro-Kellie hypothesis:An increase in anyone of these component causes in changes in the volume of the others by displacing or shifting of CSF, increase absorption of CSF, or decreasing cerberal blood flow volume. Without such changes, ICP will begin to rise.

6. ICP cont… • Minor CSF volume and blood volume changes occur when there are changes in the intra-thoracic pressure ( coughing, sneezing, straining), posture, and blood pressure, and fluctuation in the arterial blood gases level • Normal ICP is 10 to 20 mm Hg

7. Pathophysiology: • Increased ICP is a syndrome due to alteration of the relation between intracranial volume and pressure. • Causes: head injury (most common), brain tumors, Subarachnoid hemorrhage, and toxic and viral encephalopathy. • Increased ICP affects cerebral perfusion…… produce distortion, and shifts brain tissue.

8. Effect of Increased ICP on Brain Tissue: I. Decreased Cerebral blood flow: • Cause ischemia, leading to cell death (irreversible damage), if complete ischemia lasts for 3-5 min. which can lead to further Brain Edema • In early ischemia, vasomotor center stimulated, causing Increasing in systemic BP ( to maintain cerebral blood flow), Bradycardia (slow bounding pulse), and respiratory irregularities. • Increased PaCO2 cause cerebral vasodilation, leading to increase cerebral blood flow and increased ICP • Decreased venouse outflow may also increase cerebral blood volume, thus raising ICP

9. II.Cerebral edema: • Or swelling defined as abnormal accumulation of water or fluid in the Intracellular or extracellular spaces or both, associated with an increase in brain tissue volume thus increasing ICP. Certain tumors may lead to excessive production of ADH, resulting in fluid retention. Small tumors may create a great increase in ICP. • Mechanisms of compensation: I. Decrease the production and flow of CSF. II. Autoregulation: • the ability of the brain to change the diameter of its blood vessels automatically to maintain a constant cerebral blood flow during alteration in systemic blood pressure.

10. Cerebral Response to increased ICP • Compenstion made to maintain cerebral blood flow and prevent tissue damage • Brain can maintain a steady cerebral perfusion pressure (CPP) when the arterial BP is 50-150 mmHg and ICP less than 40 mmHg • Cerebral perfusion pressure (CPP)=mean arterial pressure - ICP =70 to 100 mm Hg • CPP less than 50 cause irreversible neurologic dysfunction due to decrease cerebral perfusion, cerebral ischemia and the resulting is Cushing’s response

11. Cushing’s response: • Stimulation of Vasomotor center • Leads to rise arterial pressure to overcome the increased ICP • Sympathetic stimulation which leads to rising of arterial blood pressure by: A. Rising in systolic blood pressure B. widening of the pulse pressure C. Cardiac slowing: decrease heart rate • Cushing’s triad: bradycardia, hypertension, bradypnea. Indicates a potentially terminal event and requires emergent intervention ( failure of Autoregulation). • Herniation of the brain stem and occlusion of the cerebral blood flow occure (ischemia, infarction and brain death) if therapeutic intervention is not initiated.

12. Clinical manifestations: • Changes in the level of consciousness ( review terms and stages of altered level of consciousness) • Abnormal respiratory and vasomotor responses. • Restlessness, confusion, drawsness • Decortication (adduction and flexion of upper extremities, internal rotation of lower extremities and planter flexion of the feet), decerebration (extension and outward rotation of the upper extremities and planter flexion of the feet), or falcidity • At the end fixed dilated pupils and respiratory impairment which alarm death is near.

13. Assessment and diagnostic findings: • to check the cause of Increased ICP • Cerebral angiography, CT-scan, MRI, or position emission tomography (PET), Transcranial doppler • Lumber puncture is avoided.

14. Complications: • Brain stem herniation, • diabetes insipidus: due to decreased secretion of ADH which leads to polyurea. The patient needs fluid and electrolyte replacement and vasopresine administration • syndrome of inappropriate antidiuretic hormone (SIADH): (increase secretion of ADH)which leads to fluid retention (fluid overload).phenytoin used to decrease ADH secretion, or Lithium to increase free water loss

15. Management: • Monitoring ICP: to identify increased pressure early, quantify the degree of abnormality, initiate appropriate treatment, provide access to CSF for sampling and drainage and to evaluate the effectiveness of the treatment. • Can be monitored by: intraventricular catheter, subarachnoid (screw) bolt, an epidural or subdural catheter, or fiberoptic transducer-tipped catheter place in the brain tissue or the ventricle. • Changes of ICP are indicated by waves of high pressure and normal pressure

16. Cont….. • Decrease cerebral edema: • Osmotic diuretics (mannitol), • corticosteriods ( dexamethasone) if the increased ICP due to brain tumor. • Fluid restriction • Lowering body temperature to reduce metabolic rate 3. Maintain cerebral perfusion: improvement of cardiac output.

17. Cont… Management 4. Reducing CSF and Intracranial blood volume: hyperventilation is used to decrease the concentration of CO2 thus vasoconstriction to decrease blood volume ( PaCO2 should be maintained between 30-35 mm Hg to prevent hypoxia, ischemia, and accumulation of cerebral lactate levels) 5. Controlling Fever: fever increases cerebral metabolic and the rate at which cerebral edema forms. Avoid shivering, which increase the ICP • Reducing metabolic demands: high doses of Barbiturates, muscle relaxants (Vecuronium bromide) • Maintaing Oxygenation

18. Intracranial Surgery: • A craniotomy involves opening the skull surgically to gain access to intracranial structure ( supratentorial, infratentorial, and transsphenoidal approach). Preoperative Evaluation: CT, MRI, Cerebral angiography, and transcranial Doppler flow studies. Complications: Increased ICP, infection, and neurologic deficit.

19. Preoperative Management: • Anticonvulsant therapy to prevent postoperative seizures • Steroids to decrease cerebral edema • Fluid may be restricted • Hyperosmotic agent and diuretics may be given immediately before and sometimes during surgery • Insert folly catheter • Central line may administered for fluid administration and central venous pressure monitoring after surgery • Antibiotics and diazepam • Preparation the site of the surgery

20. Postoperative Management: • Reducing cerebral edema • Relieving pain and Seizures • Monitoring ICP Nursing Management: • Evaluating the level of consciousness and responsiveness to stimuli and identify any neurologic deficit. • Patient and family education • Preparation for surgery: Psychological support • Postoperative: assessment and routine nursing care

21. Headache or Cephalgia • Symptoms rather than disease and may indicate organic disease. • Primary headache: no identified cause such as migraine and cluster headache • Secondary headache: due to organic cause such as tumor or aneurysm Assessment and diagnostic findings: • detailed history, physical examination of head and neck and complete neurologic examination , headache may be a symptom of endocrine, hematologic, gastrointestinal, infection, renal, cardiovascular, and psychiatric disease • Medication history: antihypertensive, anti-inflamatory • Stress

22. Migraine: • Periodic and recurrent attacks of sever headache. • Vascular disturbances more commonly in women and has strong familial tendency. Incidence highest in adults 20-35 years Pathophysiology: varying degrees of cortical ischemia followed by vasodilation. • Abnormal metabolism of Serotonin ( Vasoactive neurotransmitter). Rise in plasma seratonin, dilate the extracranial carotid artery and constrict the intracranial carotid artery. This process is followed by a fall in plasma seratonin (vasodilation) and a pulsating, throbbing pain. • Headache can be triggered by menstrual cycle, bright light, stress, depression, sleep deprivation, fatigue, over use of certain medication such as oral contraceptive, and some milk product.

23. Clinical manifestations: • The headache often start early morning • Prodome phase: symptoms occur hours to days before a migraine headache ( depression, irritability, feeling cold, food craving, anorexia, changes in activity level, increased urination, diarrhea or constipation • Aura phase: last less than one hour: visual disturbances (light flashes and bright spots, numbness and tingling of the lips, face, or hands, mild confusion, slight weakness, drowsiness, and dizziness.

24. Cont… • Headache phase: a vasodilation and a decline in seratonin levels occur, throbbing headach (unilateral) intensive for several hours, associated with photophobia, nausia, and vomiting (4-72 hours) • Recovery phase: the pain gradually subsides, muscle contraction in the neck and scalp, muscle ache, exhaustion, and mood changes. During this phase, pt may sleep for extended periods

25. Prevention: • Avoid specific triggers that are known to initiate the headache syndrome. • Medication therapy: Propranolol ( inderal) the mostly wide used medication, calcium antagonists ( Verapamil HCL), Methysegide (Sansert) block the effect of seratonin, Anticonvulsants, antidepressent, barbiturates, tranquilizer. • Avoid vasodilators, alcohol, nitrites, and histamines • Medical management: • Symptomatic: • And preventive • Nursing management: • Administer medication to relieve pain • Comfort measures (quite dark environment and elevation of the head of the bed 30 degree

26. Chap 62 Management of patients with Cerebrovascular Disorders

27. Cerebrovascular Disorders • Functional abnormality of the CNS that occurs when the blood supply is disrupted • Stroke is the primary cerebrovascular disorder and the third leading cause of death in the U.S. • Stroke is the leading cause of serious long-term disability in the U.S. • Direct and indirect costs of stroke are $53.6 billion

28. Prevention • Nonmodifiable risk factors • Age (over 55), male gender, African American race • Modifiable risk factors: see Chart 62-1 • Hypertension: the primary risk factor • Cardiovascular disease • Elevated cholesterol or elevated hematocrit • Obesity • Diabetes • Oral contraceptive use • Smoking and drug and alcohol abuse

29. Stroke • “Brain attack” • Sudden loss of function resulting from a disruption of the blood supply to a part of the brain • Types of stroke: see Table 62-1 • Ischemic (80% to 85%) • Hemorrhagic (15% to 20%)

30. Ischemic Stroke • Disruption of the blood supply due to an obstruction, usually a thrombus or embolism, that causes infarction of brain tissue • Types • Large artery thrombosis • Small penetrating artery thrombosis • Cardiogenic embolism • Cryptogenic (unknown cause • Other such as cocain use, coagulopathies, migraine…

31. Manifestations of Ischemic Stroke • Symptoms depend upon the location and size of the affected area • Numbness or weakness of face, arm, or leg, especially on one side • Confusion or change in mental status • Trouble speaking or understanding speech • Difficulty in walking, dizziness, or loss of balance or coordination • Sudden, severe headache • Perceptual disturbances • See Tables 62-2and62-3

32. Cerebrovascular Terms • Hemiplegia • Hemiparesis • Dysarthria: difficulty in speaking (muscle paralysis) • Aphasia: expressive aphasia, receptive aphasia • Hemianopsia: Loss of half visual field • Apraxia: inability to perform previously learened actions.

33. Transient Ischemic Attack (TIA) • Temporary neurologic deficit resulting from a temporary impairment of blood flow • “Warning of an impending stroke” • Diagnostic work-up is required to treat and prevent irreversible deficits

34. Assessment and diagnostic findings: • CT, MRI, EEG, carotid ultrasound, cerebral angiography • Prevention: alter the risk factors, administration of anticoagulants • Complications: Cerebral hypoxia, decreased cerebral blood flow, extension of the affected area

35. Preventive Treatment and Secondary Prevention • Health maintenance measures including a healthy diet, exercise, and the prevention and treatment of periodontal disease • Carotid endarterectomy • Anticoagulant therapy • Antiplatelet therapy: aspirin, dipyridamole (Persantine), clopidogrel (Plavix), and ticlopidine (Ticlid) • Statins • Antihypertensive medications

36. Medical Management: I. Thrombolytic therapy : should be administer within 3 hours of stroke attack • t-PA (tissue plasminogen activator: is an example. Stimulate firbinolysis of the atherosclerotic lesion • Pt preparation for t-PA: • Definitive Diagnosis of ischemia • Pt meeting the criteria for the t-PA (Chart 62-3- p 1893) • Preparation of the dose (0.9 mg/kg, the maximum dose is 90 mg), 10% of the dose given over one min the remaining dose is administered over one hour via an infusion pump, the line then infused with 20 ml normal saline

37. Cont… • Pt care post t-PA: admit the pt to ICU, Cont. cardiac monitoring, V/S every 15 min for the first 2 hrs, every 30 min for the next 6 hrs, then every hrs for the next 16 hrs, systolic BP should maintained less than 180mmHg, and diastolic BP less than 100 mmHg, start airway management. • Side effects of t-PA: is Bleeding

38. Therapy for pt with ischemic stroke not receiving t-PA: • Maintain of pt airway, and administer of supplemental O2 • Administer of Anticoagulant agent • Maintain a cerebral hemodynamics, Decrease ICP if occur (mannitole, maintain PaCO2 within 30-35 mmHg, and avoiding hypoxia, elevation of the head of the bed • Carotid endarterectomy: it is the removal of an atherosclerotic plaque or thrombus from the carotid artery to prevent stroke in the pt with occlusive disease of the extracranial cerebral ateries. • Neurological assessment • Therapy For Complications: maintaining cardiac output within the normal range of 4-8L/min to improve cerebral perfusion and oxygenation to prevent hypoxia and ischemia, maintenance of airway and administer supplemental O2

39. Carotid Endarterectomy

40. Nursing Process—Assessing the Patient Recovering From an Ischemic Stroke • Acute phase • Ongoing/frequent monitoring of all systems including vital signs and neurologic assessment: LOC and motor, speech, and eye symptoms • Monitor for potential complications including musculoskeletal problems, swallowing difficulties, respiratory problems, and signs and symptoms of increased ICP and meningeal irritation • After the stroke is complete • Focus on patient function; self-care ability, coping, and teaching needs to facilitate rehabilitation

41. Nursing Process—Diagnosis of the Patient Recovering From an Ischemic Stroke • Impaired physical mobility • Acute pain • Self-care deficits • Disturbed sensory perception • Impaired swallowing • Urinary incontinence

42. Nursing Process—Diagnosis of the Patient Recovering From an Ischemic Stroke (cont.) • Disturbed thought processes • Impaired verbal communication • Risk for impaired skin integrity • Interrupted family processes • Sexual dysfunction

43. Collaborative Problems/Potential Complications • Decreased cerebral blood flow • Inadequate oxygen delivery to brain • Pneumonia

44. Nursing Process—Planning Patient Recovery After an Ischemic Stroke • Major goals include: • Improved mobility • Avoidance of shoulder pain • Achievement of self-care • Relief of sensory and perceptual deprivation • Prevention of aspiration • Continence of bowel and bladder

45. Nursing Process—Planning Patient Recovery After an Ischemic Stroke (cont.) • Major goals include (cont): • Improved thought processes • Achievement of a form of communication • Maintenance of skin integrity • Restoration of family functioning • Improved sexual function • Absence of complications

46. Interventions • Focus on the whole person • Provide interventions to prevent complications and to promote rehabilitation • Provide support and encouragement • Listen to the patient

47. Improving Mobility and Preventing Joint Deformities • Turn and position the patient in correct alignment every 2 hours • Use splints • Practice passive or active ROM 4 to 5 times day • Position hands and fingers • Prevent flexion contractures • Prevent shoulder abduction • Do not lift by flaccid shoulder • Implement measures to prevent and treat shoulder problems

48. Positioning to Prevent Shoulder Abduction

49. Prone Positioning to Help Prevent Hip Flexion

50. Improving Mobility and Preventing Joint Deformities • Perform passive or active ROM 4 to 5 times day • Encourage patient to exercise unaffected side • Establish regular exercise routine • Use quadriceps setting and gluteal exercises • Assist patient out of bed as soon as possible: assess and help patient achieve balance and move slowly • Implement ambulation training