Cognitive disorders theme – ppt download anoxia fetal

1 cognitive disorders theme

Fahad alosaimi MD psychiatry psychosomatic medicine consultant assistant professer KSU

2 case study abdullah is a 72-year-old male. He was brought to the emergency department by his son for vomiting, new onset urinary incontinence, confusion, and incoherent speech for the past 2 days. The patient was disoriented and could see people climbing trees outside the window. He had difficulty sustaining attention, and his level of consciousness waxed and waned. He had been talking about his deceased wife. Patient was also trying to pull out his intravenous access line. Past history included diabetes mellitus, hyperlipidemia, osteoarthritis, and stroke.

3 case study on examination, the patient was drowsy and falling asleep while practitioners were talking to him.Anoxia fetal patient was not cooperative with the physical examination and with a formal mental status examination. Limited examination of the abdomen indicated that it was flat and soft with normal bowel sounds. The patient moves all 4 limbs and plantar is bilateral flexor. Laboratory test results revealed elevated BUN and creatinine levels, and the urine analysis was positive for urinary tract infection. CT scan of the head showed cortical atrophy plus an old infarct. The patient’s family physician had recently prescribed tylenol with codeine for the patient’s severe knee pain 5 days earlier.

4 A- analysis of symptoms, MSE and psychopathology especially perception; differential diagnosis discussion (including drug intoxication and withdrawal): analyze the symptoms (presented and expected) in this case and signs, including mood, thoughts, cognition, perception and physical aspects discuss other elements related to the case includes possible etiological reasons discuss the initial possible diagnosis of this case and different types of such clinical presentation

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5 neurocognitive disorders

Disruption in one or more of the cognitive domains, and are also frequently complicated by behavioral symptoms. Neurocognitive disorders exemplify the complex interface between neurology, medicine, and psychiatry in (DSM-5), neurocognitive disorders are: delirium major neurocognitive disorder (dementia) mild neurocognitive disorder major or mild neurocognitive disorder due to: alzheimer’s disease frontotemporal lewy bodies vascular traumatic brain injury substance/medication-induced HIV infection prion disease parkinson’s disease huntington’s disease another medical condition multiple etiologies unspecified

6 delirium acute onset of fluctuating cognitive impairment (global)and a disturbance of consciousness.Anoxia fetal delirium is a syndrome, not a disease, and it has many causes, all of which result in a similar pattern of signs and symptoms. Delirium is acute brain failure. A common disorder: hospitalized medically ill % hospitalized elderly % postoperative patients up to 50% near-death terminal patients up to 80% 10 to 30 percent of medically ill inpatients 30 percent of patients in intensive care units 40 to 50 percent of patients who are recovering from surgery for hip fractures underrecognized and undertreated !!

7 reversal of sleep-wake pattern.

Classically, delirium has a sudden onset (hours or days) A brief and fluctuating course rapid improvement when the causative factor is identified and eliminated abnormalities of mood, perception, and behavior are common psychiatric symptoms.Anoxia fetal reversal of sleep-wake pattern. Tremor, asterixis, nystagmus, incoordination, and urinary incontinence are common

8 delirium has bad prognosis

May progress to stupor, coma, seizures or death, particularly if untreated. Increased risk for postoperative complications, longer postoperative recuperation, longer hospital stays, long-term disability. Elderly patients 22-76% chance of dying during that hospitalization several studies suggest that up to 25% of all patients with delirium die within 6 months

9 risk factors extremes of age number of medications taken

Preexisting brain damage (e.G., dementia, cerebrovascular disease, tumor) history of delirium alcohol dependence diabetes cancer sensory impairment malnutrition

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10 causes: “I WATCH DEATH”

I nfections W ithdrawal A cute metabolic T rauma C NS pathology H ypoxia D eficiencies E ndocrinopathies A cute vascular T oxins or drugs H eavy metals 44% estimated to have 2 or more etiologies this mnemonic worked for me, so I’ll pass it on to you. I watch death is a catchy little phrase that always reminds you of the grave nature of delirium. I nfections W ithdrawal A cute metabolic T rauma C NS pathology H ypoxia D eficiencies E ndocrinopathies A cute vascular T oxins or drugs H eavy metals I will give examples on the next few slides.

11 “I WATCH DEATH” infections: encephalitis, meningitis, sepsis

Withdrawal: ETOH, sedative-hypnotics, barbiturates acute metabolic: acid-base, electrolytes, liver or renal failure trauma: brain injury, burns the most common infections would be those affecting the brain like encephalitis and meningitis, but any systemic infection can certainly cause delirium.Anoxia fetal as mentioned previously, withdrawal from drugs is one of the 4 major contributors to delirium. Alcohol, sedatives and barbiturates are the most common. Any acute metabolic change can account for altered mental status: altered acid-base status. Electrolyte imbalance, and particularly liver or renal impairment. The most likely traumatic contributors are burns and brain injury.

12 “I WATCH DEATH” CNS pathology: hemorrhage, seizures, stroke, tumor (don’t forget metastases) hypoxia: CO poisoning, hypoxia, pulmonary or cardiac failure, anemia deficiencies: thiamine, niacin, B12 endocrinopathies: hyper- or hypo- adrenocortisolism, hyper- or hypoglycemia direct CNS damage causes delirium, specifically, hemorrhage, seizures, stroke, and tumor.Anoxia fetal it’s good to think about brain mets in any cancer patient who appears delirious. Anything that can reduce the supply of blood (ie. Oxygen) to the brain counts: so CO, hypoxia from pulm or cardiac origins, and anemia- acute blood loss, usually. Vitamin deficiencies- usually thiamine, niacin, or B12. (worry about alcoholics) endocrinopathies: too much or too little cortisol or glucose. DKA is classic for delirium.

13 “I WATCH DEATH” acute vascular: hypertensive encephalopthy and shock

Toxins or drugs: pesticides, solvents, medications, (many!) drugs of abuse anticholinergics, narcotic analgesics, sedatives (BDZ) heavy metals: lead, manganese, mercury vascular causes include hypertensive encephalopathy and shock.Anoxia fetal toxins cover anything from pesticides and solvents, to prescription meds. Any textbook will provide a list of at least 100 potential offenders. I want you to remember three major classes that are the most common culprits: anticholinergics- like phenergan, benadryl, tricyclics, narcotic analgesics- like demerol, morphine,and sedatives- like ativan and valium.These account for the majority of troublemakers.The next slide will show possible drugs of abuse that can cause delirium. Rarely, heavy metal exposure will be the cause.

14 life threatening causes of delirium(WHHHIMP)

Wernicke’s encephalopathy hypoxia hypoglycemia hypertensive encephalopathy intracerebral hemorrhage meningitis/encephalitis poisoning

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15 DSM-5 diagnostic criteria for delirium

A) A disturbance in attention (reduced ability to focus, sustain and shift attention) and awareness (reduced orientation to the environment). B) the disturbance develops over a short period of time (usually hours to days) and tends to fluctuate in severity during the course of the day. C) an additional disturbance in cognition ( e.G. Memory deficit, disorientation, language, visuospatial ability) or perception. D) the changes in criteria A C are not better explained for by a preexisting, established or evolving neurocognitive disorder or not in the context of coma. E) there is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by the direct physiological consequences of another medical condition or substance

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16 clinical features prodrome (restlessness ,anxiety, sleep disturbance)

Fluctuating course attentional deficits arousal /psychomotor disturbance impaired cognition sleep-wake disturbance altered perceptions affective disturbances these are the core clinical features of delirium. I will go through each one separately. Prodrome fluctuating course attentional deficits arousal disturbances disturbances in normal arousal are key features of DELERIUM. Hyperactive (agitated, hyperalert) hypoactive (lethargic, hypoalert) mixed it is important to note that patients don’t have to be slowed down, or unresponsive, in order to have delirium. And the fluctuation in the level of alertness is often a key diagnostic feature.Anoxia fetal psychomotor abnormalities sleep-wake disturbance impaired cognition altered perceptions emotional disturbances


18 workup history interview- also with family, if available

Physical, cognitive, and neurological exam vital signs, fluid status review of medical record anesthesia and medication record review – temporal correlation? The most important part of the workup for delirium is to have the suspicion. As with most other diagnoses, the answer can often be found in the history and interview. Speaking with family members to see if the new behavior is a change from baseline is a huge help. Physical, cognitive, and neurological exams should be performed, to include vital signs and fluid status. Perhaps the most important piece of investigative work is the review of medical and anesthesia records.Anoxia fetal this will often point to an event that precipitated the worsened mental status.

19 mini-mental state exam

Tests orientation, short-term memory, attention, concentration, constructional ability 30 points is perfect score 7 days): symptoms peak severity at 36 hours 90% of AW seizures most cases self-limited  stage I symptoms “delirium tremens” protracted withdrawal

47 delirium tremens features: course : complications : delirium.

Gross tremor . Autonomic disturbances . Dehydration and elecrolyte disturbances.. Marked insomnia. Course : peaks on third or fourth day, lasts for 3 – 5 days, worsens at night, and followed by a period of prolonged deep sleep, complications : seizures. Chest infection, aspiration.Anoxia fetal violent behaviour. Coma. Death; mortality rate: 5-15%. Why ? It may be precipitated by infections, fluctuating consciousness, disorientation, agitation, hallucinations, illusions, delusions. From which the person awakes with no symptoms and has amnesia for the period of delirium. Death; mortality rate: 5-15%. Why ? Volume depletion. * cardiac arrhythmias. * electrolyte imbalance. * infections. * suicide.

48 treatment of delirium tremens

The best treatment is prevention supportive thiamine the mainstay treatments are benzodiazepines. Avoid antipsychotics. The conscious patient: observation, with protective and supportive approach in case of agitation, hyperactivity or risk of violence: restrain the patient and give antipsychotic drugs (e.G.Anoxia fetal haloperidor or droperidol 5 – 10 mg im) sedatives are better avoided because they may potentiate depressant effects of alcohol on the central nervous system. Wait for the alcohol to be metabolized. The unconscious patient: hospitalization is required: protection of the airways, vital signs monitoring, prevention of further loss of body heat, correction of hypovolemia, and forced diuresis with maximal alkalinization of the urine. In extreme situation haemadialysis is necessary maintaining abstinence: disulfiram – blockade of aldehydedehydrogenase  cummulation of acetaldehyde – nausea, flushing, tachycardia, hyperventilation, panic… aim: to make alcohol consumption unpleasant and intolerable naloxone – reduces alcohol-induced reward.Anoxia fetal acamprosate – anti-craving effects . The drugs used to alleviate the acute abstinence syndrome: benzodiazepines, clonidine (inhibits exaggerated neurotransmitter release) and propranolol (blocks excessive sympathetic activity). To explore the reasons for drinking, alternative ways are worked out. For instance, instead of using alcohol in social situations to reduced anxiety, learn anxiety management and assertiveness techniques. Provision of information about the hazards of alcohol group therapy: about 7-12 patients and a staff member in a specialist unit attend regular meetings. It provides an opportunity for frank feedback from other members of the group concerning the problems that the patient faces and to work out better ways of coping with their problems.Anoxia fetal alcoholics anonymous (AA) is a voluntary supportive self-help organization of persons with alcohol-related problems. Members attend group meetings (1-2 / week) and obtain support from one another. The meetings involve repeated emotional confession of each person’s problems. The organization works on the firm belief that total abstinence is the aim.

49 treatment of alcohol withdrawal delirium tremens (1st approach)

50 treatment of alcohol withdrawal delirium tremens(2nd approach)

51 case management discussion including ability to give consent and take decision: (considering the case above) discuss about the acute use of antipsychotics and benzodiazepine discuss about dementia treatments, indication, side effects, etc discuss about ability to give consent and take decision

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52 delirium vs dementia features delirium dementia onset acute insidious

Course fluctuating progressive duration days to weeks months to years consciousness altered clear attention impaired normal, except in severe dementia psychomotor changes increased or decreased often normal reversibility usually rarely

53 treatment the first step in the treatment of dementia is verification of the diagnosis. Preventive measures are important supportive and educational psychotherapy any areas of intact functioning should be maximized by helping patients identify activities in which successful functioning is possible caregivers

54 pharmacotherapy primary treatments:

Cholinesterase inhibitors : donepezil (aricept), rivastigmine (exelon), galantamine (remiryl), and tacrine NMDA glutamate receptors antagonist: memeantine drugs with high anticholinergic activity benzodiazepines should be avoided.Anoxia fetal

55 management of agitation/aggression in demented patients

56 capacity vs. Competency

Clinical vs. Legal term that denotes the ability to make rational and reasonably well informed decisions by a particular patient (vs. Person) in their treatment and/ or life decision/s capacity is a clinical determination that addresses the integrity of mental functions. Competency is a legal determination that addresses societal interest in restricting a person’s right to make decisions or do acts because of incapacity.

57 valid informed consent

Permission voluntary given by a competent person without any elements of force, deceit, coercion after explanation and disclosure of purpose and details of procedure or treatment risks, benefits and available alternative treatment/s the right to withdrawal consent verbally or in written forms at anytime

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58 exceptions life threatening situation

Patient who waive their rights to disclose and consent (do not want to be informed) instances where “ disclosure’ may be harmful to the patient “ therapeutic privileges”

59 rules of capacity being mentally ill doesn’t in itself imply a loss of capacity or competency. Having capacity or being competent should be presumed until proven otherwise.

60 pragmatic approach to address capacity

61 steps in mental capacity assessment

General perspective or specific (psychiatric hospitalization, ECT) find out the best language of communication determine if patient has adequate information on which to base a decision MMSE: attention, concentration, memory inform the patient about the nature of the disorder, AND the risk and benefit of the PROPOSED treatment, and of ALTERNATIVE treatments or of NO treatment B.Anoxia fetal repeat information number of times and in different ways. Let the patient paraphrase or restate the understanding. Evaluate nature of questions that patient asks regarding treatment plan periodical reassessment of capacity ( if any change in clinical conditions or, mental status such as in delirium or any modifications in treatment plan) C. If patient has “severe deficit” in understanding information- no capacity to make informed consent or make decision arrange a process for “ a substitute decision maker” alternate decision maker/ health care proxy vs. Health care surrogate/ living will and advanced directives proxy order spouse, adult children, parents, young siblings, adult relatives, friend/s if non of the above, then it is a legal process.Anoxia fetal emergency temporary guardian if situation is emergency. Then the court determine that pt being incompetent, then a “ legal guardian” is designated who takes decision for the patient in the area specified by the court.