Parkinson’s Disease Case Study: Muhammad Ali Adult Med-Surg II 04/05/10 Allen, S., Daniels, M., Masih, L., Nirala, K., Swartz, E.
Feb 25, 2016
Parkinsons Disease
Parkinsons DiseaseCase Study:Muhammad AliAdult Med-Surg II04/05/10Allen, S., Daniels, M., Masih, L., Nirala, K., Swartz, E.
Case Study: Muhammad Ali
Patient: Muhammad Ali(born Cassius M. Clay)Male, 68 y/o, retired American boxerAdmission: 03/27/2010Hx: Parkinsons Disease (PD) (1992).Falls, tremors, mild dementia, and dysphagia secondary to PD.
(http://en.wikipedia.org/wiki/Muhammad_Ali)What is Parkinsons Disease (PD)
A slowly progressing neurologic movement disorder that leads to disability. Degenerative or idiopathic form is the most common.Secondary form usually linked to a known or suspected cause.
Muhammed Ali Parkinsons Center Movement Disorders Clinic., Parkinsons disease. http://maprc.com.
IncidenceFourth most common neurologic disorder.1% of persons age 65 and older2% of persons age 85 and olderAffects men more frequently than women. Usually first appears in fifth decade of life.Can occur as early as 30 years of age.
(Smeltzer, S.C., Barle, B.G., Hinkle, J.L, & Cheever, K.H. ,2008)
DiagnosisCriteria for diagnosis of PDGroup A: Features characteristics of PD:Resting tremor Bradykinesia Rigidity Asymmetric onset
Gelb (1999), Advisory Council of the National Institute of Neurological Disorders and Stroke, US National Institutes of Health.DiagnosisCriteria for diagnosis of PDGroup B: Features suggestive of alternative diagnosesFeatures unusual early in the clinical course Prominent postural instability in the first 3 years after symptom onset Freezing phenomena in the first 3 years Hallucinations unrelated to medications in the first 3 years Dementia preceding motor symptoms or in the first year
DiagnosisGROUP B (cont.):Supranuclear gaze palsy (other than restriction of upward gaze) or slowing of vertical saccades Severe, symptomatic dysautonomia unrelated to medications Documentation of a condition known to produce Parkinsonism and plausibly connected to the patients symptoms.
DiagnosisCriteria for POSSIBLE diagnosis of Parkinsons diseaseAt least 2 of the 4 features in Group A are present; at least 1 of these is tremor or bradykinesia And either: none of the features in Group B is present or symptoms have been present for less than 3 years, and none of the features in Group B is present to date And either: substantial and sustained response to levodopa or a dopamine agonist has been documented or patient has not had an adequate trial of levodopa or dopamine agonist
DiagnosisCriteria for probable diagnosis of Parkinsons diseaseAt least 3 of the 4 features in Group A are present And none of the features in Group B is present (note: symptom duration of at least 3 years is needed to meet this requirement)And substantial and sustained response to levodopa or a dopamine agonist has been documented
DiagnosisCriteria for definite diagnosis of PD:All criteria for possible PD are met, and Histopathological confirmation (autopsy):Substantial nerve cell depletion with gliosis in substantia nigra At least one Lewy body in substantia nigra or in locus coeruleus.No pathological evidence for other diseases that produce Parkinsonism (eg progressive supranuclear palsy, multiple system atrophy, corticalbasal ganglionic degeneration).
DiagnosisBasal Ganglia
Diagnosis
The basal ganglia includes the caudate nucleus, putamen, globus pallidus, subthalamic nucleus, and substantia nigra.DiagnosisGliosis: A process leading to scars in the central nervous system(CNS) that involves CNS production of a dense fibrous network of neuroglia (supporting cells) in areas of damage. Gliosis is a prominent feature of many diseases
Lewy BodiesLewy bodies: Abnormal aggregates of protein that develop inside the nerve cells in PD.PathophysiologyAssociated with loss of dopamine nerve cells in the substantia nigra in the basal ganglia of the brain.Loss of dopamine causes imbalance of neurotransmitters, which affects voluntary movement.Clinical symptoms do not appear until 60% of dopamine neurons are lost and dopamine level is decreased by 80%.Cellular degeneration impairs control of semiautomatic functions and coordinated movements.
Causes
Cause is unknown, may be linked to:GeneticsAtherosclerosisExcessive oxygen free radicals Viral infectionsHead traumaChronic use of antipsychotic medicationsEnvironmental exposures.
CausesHead traumaConsidered a risk factor for PD since past episodes are reported more frequently by individuals with PD than by others in the population. Recent studies suggest no true relationship between severe head injury and PD.
Causes GeneticsSomeone with PD is more likely to have relatives who also have PD.Inheritance of PD is usually complex and not due to a single gene defect.
Pharmacological TherapyAntiparkinsonian medicationsAnticholinergicsAntiviral therapyDopamine AgonistsMonoamine oxidase inhibitorsCatechol-O-methyltransferase (COMT) inhibitorsAntidepressantsAntihistaminesSmeltzer, et al (2008)
Pharmacologic TherapyAntiparkinsonian medications:Increase striatal dopaminergic activityReduce excessive influence of excitatory cholinergic neuronsRestore balance between dopaminergic and cholinergic activitiesOrAct on neurotransmitter pathways other than the dopaminergic pathway.
Antiparkinsonian MedicationsLarodopa (Levodopa) Most effective treatmentConverted to dopamine in basal ganglia, producing symptom relief.Benefits wane over several yearsAdverse effects with long-term use - confusion, hallucinations, depression, sleep alterationsProtein, Vitamin B6 may decrease effectivenessDeglin, J. and Vallerand, A. (2009)
Antiparkinsonian MedicationsSinemet (carbidopa)Usually administered with levodopa Prevents breakdown of levodopa; reduces adverse effects of levodopaLong-term use can cause:DyskinesiaOn-off syndrome (acute episodes of near- immobility followed by sudden return of mobility)Neuroleptic malignant syndrome (medical emergency)Deglin (2009)
Anticholinergics
CogentinControl tremor may be used in combination with levodopa. Counteracts action of acetylcholine. Side effects poorly tolerated in the elderly (blurred vision, flushing, rash, constipation, urinary retention, acute confusion)Monitor for urinary retention in patients with enlarged prostateContraindicated in patients with narrow-angle glaucoma
Deglin (2009)
Dopamine Agonists
Parlodel and PermaxMay postpone the need for carbidopa or levodopa therapy.May be used after carbidopa or levodopa lose effectiveness. Monitor for adverse reactions:N/V, diarrheaLightheadedness, hypotensionImpotencePsychiatric effects
Smeltzer, et al (2008)Other Pharmacological TherapyMonoamine Oxidase InhibitorsEldepry - inhibits dopamine breakdownSelegiline - Used with dopamine agonist to delay carbidopa or levodopa therapyCatechol-O-methyltransferase (COMT) InhibitorsComtan and TasmarIncrease duration of action of carbidopa or levodopaReduce motor fluctuations in patients with Parkinsons
Smeltzer, et al (2008)
Other Pharmacological TherapyAntiviral TherapySymmetrelUsed in early stages of diseaseReduces rigidity, tremor, bradykinesia, postural changesLow incidence of side effects
AntihistaminesBenadryl, Banflex, Neo-SynephrineMild central anticholinergic and sedative effectsMay reduce tremors.
Smeltzer, et al (2008)
AssessmentClinical diagnosis based on:Patients historyPresence of two of the four cardinal manifestations: Tremors; pill-rolling tremor of the handsMuscle rigidityBradykinesia (abnormal slow movement)Stooping, forward posture
Smeltzer, et al (2008)
AssessmentObserve the degree of disability and functional changes that occur throughout the day, such as response to medication.Assess nutritional status.Assess for mood swings, depression, and cognitive impairments.
AssessmentAsk patient if they ever experience:Leg or arm stiffnessIrregular jerking of your arms or legsFeeling frozen to a spot and unable to moveExcessive saliva production or droolingGrimacing, facial contortions, or chewing movementsDifficulty performing specific activitiesAssessmentObserve patient for:Dysphonia - soft, slurred, low-pitched, and quiet speechDysphagia - swallowing deficits Drooling, poor head control, coughingBradykinesia (slowness of movement)Tremors (pill-rolling movements)WeaknessStooping, forward postureMuscle rigidityLoss of facial expression (flat effect)Autonomic symptoms (orthostatic hypotension, flushing, and diaphoresis).
AssessmentAssess for medication-related S/S:Adverse reactionsSide effectsFood-drug interactionsDrug-drug interactionsEffectiveness of medications
Deglin (2009)Nursing DiagnosesRisk for aspiration r/t swallowing deficits.Risk for falls r/t impaired balance and tremors.Constipation r/t medication and reduced activity.Impaired mobility r/t muscle rigidity and weakness.Imbalanced nutrition - less than body requirements, r/t chewing and swallowing deficits.Self-care deficits r/t tremor and motor disturbance.Impaired verbal communication r/t dysphonia Ineffective coping r/t depression, secondary to disease progression.
Ackley, B. J. & Ladwig, G. B., (2006).
PlanningImprove functional mobilityImplement an exercise program that will increase muscle strength, improve coordination and dexterity, reduce muscular rigidity, and prevent contractures that occur when muscles are not used.Examples: walking with care, riding a stationary bike, swimmingPT/OT referral
Ackley (2006)
PlanningAchieve adequate bowel eliminationEncourage increase fluid intakeFollow a regular time patternStool softener (avoid laxatives b/c they may cause bowel obstruction)Eat balanced diet with plenty of fruits, vegetables, and whole grains b/c of their high fiber contentPlanningAttain and maintain acceptable nutritional statusSupplemental feedings to increase caloric intakeConsult dieticianIn later stage of disease, a nasogastric tube or percutaneous endoscopic gastroscopy may be needed to maintain adequate nutritionPlanningAchieve effective communicationSpeech therapy referralUse of electronic amplifier if difficulty hearing patientOther referrals/consultsCase managerHome healthSocial workerInterventionsEnhance SwallowingEnsure patient is in upright position during mealtime.Provide semisolid diet with thick liquids; avoid thin liquids.Teach patient to think through the swallowing sequence with eat bite.Teach patient to chew first on one side of the mouth and then the other. Teach patient to hold head upright and make conscious effort to swallow to control saliva buildup.
Smeltzer et al (2008)InterventionsImprove Bowel EliminationEncourage moderate fiber intake.Provide adequate fluids.Encourage and assist with regular, daily exercise.Provide raised toilet seat.Allow pt sufficient time for toileting.Avoid psyllium (can cause bowel obstruction).
InterventionsImprove MobilityEncourage and assist with daily exerciseImproves muscle strength, coordination and dexterity; can delay progression of the disease.Reduces muscular rigidity; prevents contractures.Walking, riding stationary bicycle, swimming, and gardening can help maintain joint mobility.
InterventionsImprove MobilityStretching (stretchholdrelax) and range-of-motion exercises promote joint flexibility.Postural exercises - counter the tendency of the head and neck to be drawn forward and down. Special walking techniques - compensate for balance issues caused by arm rigidity.InterventionsImprove NutritionMonitor daily weight during inpatient stay.Request swallowing and nutrition consults.Identify patients food likes and dislikes- provide food the patient enjoys. Provide supplemental feedings.Encourage daily exercise to stimulate appetite.Provide adaptive equipment for meals (non-tip cup, raised utensils, warming tray).
InterventionsPromote Self-Care ActivitiesEncourage, teach, and support the patient during ADLs.Overbed frame with a trapeze can provide assistance in pulling up without help. Allow sufficient time to self-dress, eat, and perform personal hygiene.Encourage pt to wear clothing without buttons, zippers, or snaps; slip-on, non-skid shoes.Encourage use of assistive devices.Wissman (2007)
InterventionsImprove CommunicationTeach the patient to:Face the listenerExaggerate enunciation of wordsSpeak in short sentencesTake a few deep breaths before speaking. Provide a sign board/marker boardRequest speech therapy consult
InterventionsSupport Coping AbilitiesVisit with patient daily to reduce social isolation/Refer to support groups, community resources and Internet resources:
Discharge PlanningEnsures that the patient leaves the hospital in a timely manner with the necessary resources.Begins at admission.Nurse provides information about to the patient and caregivers r/t the disease and self-care.
Potter, P.A. & Perry, A., (2008).
Discharge PlanningNurse provides information about:Medication instructions; potential food-drug interactionsActivity restrictionsRehabilitation techniques/adaptationAccess to available community resourcesGuidance on when and how to obtain follow-up carePatient/family responsibilities in patients careDischarge PlanningMultidisciplinary process that may involve:Speech-Language Therapy (SLT)- Swallowing and speech needs.PT consult Walking/balance issues; assistive equipment needsOT ADL teaching/adaptive equipment needsCase Manager Coordination of discharge planningSocial Worker Financial, caregiver, and home environment needs.Dietitian - Nutritional/dietary educationHome Health In-home careEvaluationStrives toward improved mobilityRange-of-motion exercise to all joints three times dailyMassage and stretch muscles to reduce stiffnessWalks with wide base of support; exaggerates arm swinging when walkingAvoid staying in one position for prolonged periodsRest without a pillow and lie prone frequently to deter flexed postureAckley (2007)
EvaluationProgresses toward self-careAllows time for self-care activitiesExplore the use of assistive devicesEvaluation SafetyExamine the home environment for risks of injuryModify the environment to improve lighting and remove hazardsConsider installing devices such as raised toilet seats and grab barsChange position slowly if orthostatic hypotension develops
Smeltzer et al (2008)
EvaluationMaintains adequate nutrition and bowel functionTakes time when eatingSmall frequent meals if fatigue is a problem during mealsSwallow without aspiration and practice taking small bitesConsumes adequate fluid Increase intake of fiberReports regular pattern of bowel function
EvaluationAchieves a method of communicationExercise the voice regularly by singing or reading aloudAttempt to project the voice and alter volume and pitchConsult a speech therapist if vocal problems are severe
EvaluationCopes with effects of Parkinsons diseaseSets realistic goalsDemonstrates persistence in meaningful activitiesVerbalizes feelings of appropriate person
ReferencesAckley, B. J. & Ladwig, G. B., (2006). Nursing diagnosis handbook: an evidence-based guide to planning care. St. Louis: Mosby Elsevier.American Parkinson's Disease Association. (n.d). Basic information about Parkinsons disease. Retrieved March 31, 2010, from www.apdaparkinson.org.Deglin, J. and Vallerand, A. (2009). Daviss Drug Guide for Nurses. (20th ed.). Philadelphia: F.A. Davis Company.Muhammad Ali Parkinsons Center Movement Disorders Clinic. (n.d.). Parkinsons disease. Retrieved March 31, 2010, from http://maprc.com.Potter, P.A. & Perry, A., (2008). Fundamentals of nursing (7th ed.). St. Louis: Mosby Elsevier.Smeltzer, S.C., Barle, B.G., Hinkle, J.L, & Cheever, K.H., (2008). Brunner & Suddarths textbook of medical-surgical nursing (11th ed.). Philadelphia: Lippincott Williams & Willams.Wissmann, J., (2007). Adult medical-surgical nursing RN edition (7.1 ed.). Olathe, KS: Assessment Technologies Institute.