Parkinson’s Disease Case Study: Muhammad Ali Adult Med-Surg II 04/05/10 Allen, S., Daniels, M.,...

Parkinson’s DiseaseCase Study:Muhammad AliAdult Med-Surg II

04/05/10

Allen, 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 boxer

Admission: 03/27/2010Hx: Parkinson’s Disease (PD)

(1992).◦ Falls, tremors, mild dementia,

and dysphagia secondary to PD.

(http://en.wikipedia.org/wiki/Muhammad_Ali)

What is Parkinson’s 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 Parkinson’s Center Movement Disorders Clinic., Parkinson’s 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)

Diagnosis

Criteria 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 diagnoses◦Features 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

Diagnosis

GROUP 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 patient’s symptoms.

DiagnosisCriteria for POSSIBLE diagnosis of Parkinson’s

disease At 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

Parkinson’s 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, cortical–basal ganglionic degeneration).

Diagnosis

Basal Ganglia

Diagnosis

The basal ganglia includes the caudate nucleus, putamen, globus pallidus, subthalamic nucleus, and substantia nigra.

Diagnosis

Gliosis: 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 Bodies

Lewy 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 trauma

◦Considered 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 Genetics

◦Someone 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 alterations

Protein, Vitamin B6 may decrease effectiveness

Deglin, 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:

◦Dyskinesia◦On-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 prostate

Contraindicated 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, diarrhea◦Lightheadedness, hypotension◦ Impotence◦Psychiatric effects

Smeltzer, et al (2008)

Other Pharmacological TherapyMonoamine Oxidase InhibitorsEldepry - inhibits dopamine breakdownSelegiline - Used with dopamine agonist to

delay carbidopa or levodopa therapy Catechol-O-methyltransferase (COMT) InhibitorsComtan and TasmarIncrease duration of action of carbidopa or

levodopaReduce motor fluctuations in patients with

Parkinson’s

Smeltzer, et al (2008)

Other Pharmacological TherapyAntiviral TherapySymmetrel

◦ Used in early stages of disease◦ Reduces rigidity, tremor, bradykinesia, postural

changes◦ Low incidence of side effects

AntihistaminesBenadryl, Banflex, Neo-Synephrine

◦ Mild central anticholinergic and sedative effects◦ May reduce tremors.

Smeltzer, et al (2008)

AssessmentClinical diagnosis based on:

◦Patient’s history◦Presence of two of the four cardinal

manifestations: Tremors; pill-rolling tremor of the hands Muscle rigidity Bradykinesia (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 activities

AssessmentObserve patient for: Dysphonia - soft, slurred, low-pitched, and quiet

speech Dysphagia - swallowing deficits Drooling, poor head control, coughing Bradykinesia (slowness of movement) Tremors (pill-rolling movements) Weakness Stooping, forward posture Muscle rigidity Loss of facial expression (“flat” effect) Autonomic symptoms (orthostatic hypotension,

flushing, and diaphoresis).

Assessment

Assess 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 mobility

◦Implement 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, swimming

◦PT/OT referral

Ackley (2006)

PlanningAchieve adequate bowel

elimination◦Encourage increase fluid intake◦Follow a regular time pattern◦Stool 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 content

PlanningAttain and maintain acceptable

nutritional status◦Supplemental feedings to increase

caloric intake◦Consult dietician◦In later stage of disease, a

nasogastric tube or percutaneous endoscopic gastroscopy may be needed to maintain adequate nutrition

PlanningAchieve effective communication

◦Speech therapy referral◦Use of electronic amplifier if difficulty

hearing patientOther referrals/consults

◦Case manager◦Home health◦Social worker

InterventionsEnhance 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)

Interventions

Improve 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).

Interventions

Improve MobilityEncourage and assist with daily

exercise◦Improves 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.

Interventions

Improve MobilityStretching (stretch–hold–relax)

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 patient’s 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)

Interventions

Improve CommunicationTeach the patient to:

◦Face the listener◦Exaggerate enunciation of words◦Speak in short sentences◦Take a few deep breaths before

speaking. Provide a sign board/marker

boardRequest speech therapy consult

Interventions

Support 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

patient’s care

Discharge 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 care

EvaluationStrives 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 posture Ackley (2007)

Evaluation

Progresses toward self-careAllows time for self-care activitiesExplore the use of assistive

devices

Evaluation 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

Evaluation

Achieves a method of communication

Exercise the voice regularly by singing or reading aloud

Attempt to project the voice and alter volume and pitch

Consult a speech therapist if vocal problems are severe

Evaluation

Copes with effects of Parkinson’s disease

Sets 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 Parkinson’s disease. Retrieved March 31, 2010, from www.apdaparkinson.org.

Deglin, J. and Vallerand, A. (2009). Davis’s Drug Guide for Nurses. (20th ed.). Philadelphia: F.A. Davis Company.

Muhammad Ali Parkinson’s Center Movement Disorders Clinic. (n.d.). Parkinson’s 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 & Suddarth’s 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.