THE 3 D’S DEMENTIA, DELIRIUM, DEPRESSION Ida Shepherd 1.

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THE 3 D’SDEMENTIA, DELIRIUM,

DEPRESSIONIda Shepherd

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LEARNING OUTCOMESDistinguish between the functions of the left & right brain as well as the lobe functions.

Define and discuss the differences between DDD.

Identify the causes of DDD.

Identify & define the behavioural & psychological Sx of dementia.

Identify the diagnostic interventions that aid diagnosis in dementia & delirium.

List medications useful in the Tx of DDD

Identify the Risk Factors for depression in the elderly.

Identify & discuss the clinical manifestations of depression in the elderly.

Discuss what Cognitive Behavioural Therapy is.

Identify & explain de-escalation strategies for personal & patient safety.

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o Right Brain- the intuitive/creative half-ARTISTICPassion / musical Intuition Imaginative &

philosophicalArt & music

o Left Brain-the rational half-ACADEMICAnalyticLogicThoughtScience & mathComprehension &

knowledge

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CRITICAL THINKINGMr K is a 75 year old retired engineer seen in the emergency room with his wife of 50 years who reports that her husband is confused, agitated, and has been seeing and hearing things that were not there. A major nursing intervention in caring for Mr K must include which of the following?

A. Assess duration of symptoms

B. Inquire about his current and over-the-counter medications, including if new medications hav3e been added recently

C. Inquire about substance abuse/dependence history

D. All of the above

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DEMENTIA

• Multiple causes of dementia

• Is a syndrome associated with a range of diseases characterised by the progressive impairment of brain functions, which include loss of memory, cognitive skills, orientation, attention, language, judgment and reasoning, and personality.

• Manifestations can be mild – moderate – severe• See Table 56-6 “Causes of Dementia” Lewis Chapter 56.

• All dementias share a common symptom presentation but are differentiated based on etiology.

• The disorder may be progressive or static, permanent or reversible.

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ALZHEIMER’S DISEASE

FIRST DESCRIBED BY ALOIS ALZHEIMER IN 1907

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ALZHEIMER’S DISEASE IS THE DEGENERATION OF THE CEREBRAL CORTEX OF THE BRAIN RESULTING IN A CORTICAL DEMENTIA. IT IS CHARACTERIZED BY MULTIPLE IMPAIRMENTS IN COGNITIVE FUNCTION WITHOUT IMPAIRMENT OF CONSCIOUSNESS.” - DSM4

PathologyAlzheimer’s disease is the most common cause of dementia accounting for

more than 60% of diagnoses.

The pathology of Alzheimer’s disease includes diffuse, progressive atrophy of the cortex (resulting in smaller brain size) (& also in the parietal & temporal lobes), & with a loss of neurons, there is ventricular enlargement with a concomitant appearance of neuritic senile plaques ( secretion of amyloid β protein & degenerating axonal & dendritic nerve terminals) and neuro-fibrillary tangles (masses of non-functioning neurons composed of tau protein).

The number of plaques and tangles correlates to the severity of the dementia.

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DEMENTIA WITH LEWY BODIES(DLB)

A neurodegenerative disease assoc with the formation & accumulation of round α-synuclein protein lumps called Lewy bodies inside affected neurons. They interfere with the actions of acetylcholine & dopamine.

Risk Factors: >60 yrs, male, family hx of DLB or a carrier of the apolipoprotein E46K allele.

May be the 2nd most prevalent type of dementia after AD.

Dx is challenging because some of the symptoms of DLB resemble those of AD or PD. Early course resembles AD, later course looks like PD.

DLB has distinct symptoms: behavioural problems, fluctuations in cognition, movement symptoms, extreme sensitivity to antipsychotics, sleep problems, & V/S changes

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LEWY BODY DEMENTIAhttp://www.youtube.com/watch?v=O1UJZRkpZ5w&feature=related

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CLINICAL MANIFESTATIONS

Depending on the cause of the dementia, symptoms can be insidious and gradual or more abrupt.

Neurological degeneration is gradual and progressive

Vascular dementia takes a stepwise deterioration.

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BPSD - BEHAVIOURAL & PSYCHOLOGICAL SYMPTOMS OF DEMENTIA

BehaviouraloAggressionoWanderingoSleep disturbanceoShadowingoIntrusivenessoDisinhibitionoSocial withdrawaloPsycho-motor agitationoResistiveness

PsychologicaloDelusionsoHallucinationsoParanoiaoDepressionoAnxietyoMisidentificationoMisinterpretationoCatastrophic reactionsoAdjustment problems

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ABBEY PAIN SCALE

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ALZHEIMER’S DISEASE

Diagnostic Primarily based on exclusion MRI & PET scans to identify

hippocampal atrophy CT or MRI may show brain atrophy,

enlarged ventricles in late stages (not definitive)

FBC, ECG, glucose, creatinine, urea, Vit B1-B6 & B12 levels, TFT, LFT

Neuropsychological testing, clock drawing and MMSE

Treatment Donepezil(acetylcholinesterase inhibitor) Galantamine(cholinomimetic) Rivastigmine(brain selective cholinesterase inhibitor) Risperidone(antipsychotic-neuroleptic) Nefazodone(anti-depressant) Memantine(noncompetitive N-methyl-D-aspartate [NMDA] antagonist

Gingko Biloba

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PHARMACOLOGICAL INTERVENTIONS:THERE IS NO KNOWN DRUG TREATMENT THAT CAN REVERSE THE COURSE OF ALZHEIMER’S DISEASE.

Cholinesterase inhibitorso Initial brief improvement in cognitive ability

o Can help with behavioral and psychological symptoms

o Slows the progression of cognitive and non-cognitive loss

o Blocks cholinesterase which is an enzyme responsible for bkdwn of aceytylcholine

Antipsychotics – typical vs atypical Can help reduce BPSD Can cause cognitive impairment, sedation, and falls Multiple side-effects Same meds as in delirium

inhibitors

Benzodiazepines Anxiolytic effect Help with agitation and aggression Help reestablish sleep/wake cycle Cause motor & cognitive impairment Addiction & withdrawal Falls Paradoxical effects

AntidepressantsSSRIs help reduce distress and treat

SSRIs help reduce distress and treat depression

Occasionally help reduce BPSD

Can cause delirium

Fluoxetine, sertraline, CITALOPRAM (SSRI)

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DELIRIUM AKA ACUTE CONFUSIONAL STATE

A transient, organic mental syndrome characterized by reduced level of consciousness, reduced ability to maintain attention, perceptual disturbances, and memory impairment (DSM4-TR in Meiner, 2006).

Delirium has a sudden onset, a usually brief, fluctuating course, and a rapid improvement once the causative factor is identified and treated.

Shows poor concentration, language disturbance, clouding of consciousness, misperceptions, illusions, or hallucinations, disorientation to PPT, memory problems, incr or decr physical activity, impaired judgment

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POTENTIAL CAUSES OF DELIRIUM...

Absence of time and place cues

Change in environmentChronic illness (CHF)DehydrationElectrolyte imbalancesHospitalisation (ICU)Hypercarbia/capniaSensory deprivationSensory overloadStressTrauma

HyperthermiaHypoglycaemiaHypothermiaHypoxiaImmobilisationInfectionLiver diseaseMeds: sedative hypnotics, narcotics, benzosMetabolic disordersPain (untreated)Renal disease

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DELIRIUM CONTINUED...

Can manifest as: hypoactivity or hyperactivity, and can be mixed at different times of the day.

Delirium will usually develop over 2-3 days

Diagnosis:

Med Hx

Physical exam

Medication scrutiny

MMSE

FBC, lytes, urea, creatinine, ECG, u/a, LFT, TFT’s, SP02, and if suspected - drug &/or ETOH levels, Ca, B12, ESR, CRP, glucose

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DEPRESSION Common disorder throughout the lifespan

Most commonly diagnosed mental disorder in NZ & Australia

OA ‘s – diagnosis in relation to isolation, loss of partner, medical diagnoses that may require regular medical input e.g. MI or CA or functional/cognitive impairment

Increases the risk of suicide – very elderly most at risk of taking their own life

Australia has the highest rate for suicides among men in the 85+ age group compared to NZ where adults aged 65+ had the lowest suicide rate

A very uneven gender distribution as depression is about twice as common in women than in men. The reasons not entirely clear, but are thought to be partly biological, partly psychological, and partly sociocultural.

Using DSM-IV’s criteria for ‘major depressive disorder’an average person has about a one in seven (15 percent) chance of developing depression in the course of his or her lifetime

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DEPRESSION CONT’D..........

MANIFESTATIONS Fatigue

Constipation

Psychomotor retardation

Depressed mood

Loss of interest

Decreased Energy

Failing to pay attention to pre-existing conditions

Decreased Libido or pleasure

Changes in appetite

Decreased Weight

Sleep patterns

Agitation

Anxiety

Crying

Increased somatic complaints

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DEPRESSION CONT’D…

Risk assessment & suicide prevention

High rates of substance abuse being noticed in the OA population

Treatment is effective when there is a combination of psychological and medicinal therapies.

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TREATMENT: Cognitive Behaviour Therapy & Interpersonal Psychotherapy

Drugs:

TCA’s (Tricyclic antidepressants) amitryptyline, imipramine, chlomipramine, nortriptyline.

MAOI’s: (Monoamine Oxidase inhibitors) Isocarboxzid (Marplan), Phenelzine (Nardil)

SSRI’s: (Selective Serotonin Receptive Inhibitors) Fluoxetine (Prozac) Sertraline, Fluvoxamine, Paroxetine

SNRI’s: (Serotonin and norepinephine reuptake inhibitors) Venalfaxine (Effexor XR), Duloxetine (Cymbalta), Desvenlafaxine (Pristia)

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A CASE STUDY:

An 86-year-old man has just been admitted with dehydration. He is not a good historian because of acute confusion. However, his family indicates that he is an active, independent man who recently participated in the Senior Olympics. The nurse instructs him not to get out of bed by himself because he is old and frail. He has to void and calls for the nurse, but he cannot wait, so he walks to the bathroom and falls. To protect him from further falls, he is put in a vest restraint. He already has a reddened area over his sacrum. He then needs to void again but cannot, so he wets the bed. The patient is now restrained and has an incontinent brief in place.

Symptoms of depression and loss of appetite soon become evident. A feeding tube is inserted. The confusion gradually becomes more apparent; the patient pulls at his various tubes, prompting the nurse to apply wrist restraints. The patient's whole life has become a hospital bed. The cognitive impairments and the ever-changing environment prompt yelling out (from fear and anger). A chemical restraint is then applied in the form of a medication to reduce the agitation

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DE-ESCALATION – SOME BASICS…

If you choose not to speak (up), see (what’s happening) or hear (what’s occurring), then all hell can break loose!!

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HOW TO STAY CALM IN STRESSFUL SITUATIONS

Breathing

o as you initiate the event take a deep breath

consciously control your breathing

Self Talk

o Unconscious automatic thoughts generate emotions, emotions stimulate behaviour and physical responses, so . . . what we do is a result of what we feel and what we feel is a result of what we think

Body Language & Voice

o Relax – clench and unclench your fists

o check your body language

o check your voice

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DE-ESCALATION STRATEGIESSAFETY – KEEP YOURSELF SAFE, THEN OTHERS, THEN THE PERSONIntervene early Be courteous

Inform others Express concern

Know your exits Acknowledge feelings

Know when to get help Avoid being judgmental

Stay calm Be willing to listen

Monitor your voice Provide reassurance

Monitor your body language Give the person a way out with dignity

Use open gestures Use humor

Remember KISS Be kind

Be assertive Permit verbal venting

Offer choice Set reasonable limits

Use open ended questions Use self talk

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REFERENCES

Brown, D., & Edwards, H. (2008). Lewis’s medical-surgical nursing: Assessment and management of clinical problems. Sydney: Mosby Elsevier.

Meiner, S. E., & Lueckenotte, A. G. (2006).Gerontologic nursing (3rd ed.). St Louis: Mosby Elsevier.

Nay, R., & Garratt, S. (2009). Older people: Issues and innovations in care. (3rd ed.). Sydney: Churchill Livingstone Elsevier.

http://www.healthline.com/health/depression/medication-list