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Acutely Ill Patient > Acute Confusional State > Flashcards

Acute Confusional State Flashcards

1
Q

What is the definition of delirium?

A

An acute, transient and reversible cause of confusion - usually fluctuates in intensity.

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2
Q

What are the four DSM-IV criteria for delirium?

A
  1. Disturbance of consciousness (arousal/ awareness)
  2. Worsening confusion
  3. Acute onset with fluctuating course
  4. Due to a medical condition, substance intoxication, or withdrawal
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3
Q

Key questions to ask in a delirium history?

A

Collateral history:

  • Onset and course of confusion
  • Previous episodes
  • Exclude head injuries
  • Full systems review to establish cause
  • Past medical history and medication history important
  • Conversation with patient is also important
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4
Q

Two types of delirium…

A

Hypoactive: Lethargy, slowness, inattention, excessive sleeping
Hyperactive: Agitation, delusions, hallucinations, wandering, aggression

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5
Q

Causes of delirium…

A 
PINCH ME:
Pain 
Infection
Nutrition 
Constipation 
Hydration
Medication 
Environmental changes
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6
Q

Confusion Assessment Method

A
  1. Acute onset and fluctuating course
    AND
  2. Inattention (easily distracted, difficulty following conversation)
    AND
  3. Disorganised thinking
    OR
  4. Altered level of consciousness (GCS<15, vigilant, hyper-alert)
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7
Q

4-AT Method

A
  1. Alertness (normal=0, mild=0, clearly abnormal =4)
  2. AMT 4 - age,DoB, place, current year (0 mistakes =0, 1 mistake = 2, 2 or more mistakes =2)
  3. Attention - months backwards (7 or more= 0, less than 7 =1, cannot test =2)
    4.Fluctuating course (No=0, Yes=4)
    TOTAL SCORE: 4 or more =possible delirium, 1-3= possible mild cognitive impairment, 0 = delirium unlikely)
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8
Q

Investigations for delirium

A 
Urinalysis and MC&amp;S 
Drug levels (intoxication)
Infection screen: CXR 
Head imaging 
EEG
Specific cultures : blood, CSF, sputum
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9
Q

Management of delirium

A

Conservative:
- Quiet environment with clock to orientate
- Adequate spectacles and hearing aid
- Reassure patient frequently
- Encourage relatives to visit
Medical: (only when pt is danger to themselves/ others)
- Rapid tranquillisation - haloperidol 0.5mg PO (1st line), lorazepam 0.5-1mg PO (2nd line)
*UNDERLYING CAUSE MUST BE ADDRESSED: Remove offending meds, treat infections, correct hypoxia

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10
Q

What is the action of ADH?

A
  • Stimulates thirst

- AQP2 channel insertion to increase renal water reabsorption

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11
Q

What is the normal range for Sodium?

A

133-146 mmol/L

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12
Q

Why is a faster rate of hyponatraemia developing more dangerous?

A

Water will move intracellularly in an attempt to increase the plasma Na+ conc, which will cause cerebral oedema

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13
Q

What are the symptoms of hyponatraemia?

A

<125mmol/L : headache, nausea, vomiting, muscle cramps, lethargy, restlessness, disorientation
<120mmol/L: seizure, coma, brain damage, brainstem herniation

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14
Q

Differential causes for hyponatraemia…

A

Dependent on urinary sodium and patient fluid status:

  • Hypovolaemic + Urine [Na] >20 = high Na loss from kidneys (nephropathy, adrenal insufficiency, diuretics)
  • Hypovolaemic + Urine [Na] <20 = extra-renal sodium loss i.e. diarrhoea, vomiting, GI fistula, burns
  • Normovolaemic + Urine [Na] >20 = SIADH
  • Normovolaemic + Urine [Na] <20 = severe polydipsia, hypothyroidism
  • Hypervolaemic = likely to be fluid overload secondary to organ failure (renal, cardiac, liver)
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15
Q

Treatment of hyponatraemia…

A

Replace sodium and water at the rate they were lost

  • Patient can be given dietary salt/ IV normal saline
  • Oedematous patients should be fluid restricted
  • In emergencies where patient is having seizures - hypertonic 1.8% saline can be used
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16
Q

Why is rapid correction of hyponatraemia dangerous?

A

Causes intracellular dehydration as water moves out, leading to pontine myelinosis (permanent spastic paraperesis, seizures, coma)

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17
Q

Causes of SIADH…

A
  • Tumours - small cell lung carcinoma
  • Chest disease - TB, pneumonia
  • CNS disorders - pituitary adenomas, infections, head injury
  • Iatrogenesis- chemotherapy agents, MAOIs, phenothiazines, carbamazepine
  • Metabolic disorders - hypothyroidism, porphyria
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18
Q

Treatment of SIADH…

A

Treat the underlying cause with fluid restriction, and increased salt intake
Long term problem=>demeclocycline 600mg OD to induce nephrogenic DI

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19
Q

What are the symptoms of hypernatraemia?

A

[Na]> 145mmol/L = lethargy, thirst, weakness, irritability, confusion
[Na] > 160mmol/L = seizure , coma

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20
Q

Causes of hypernatraemia

A
  • Water loss in excess of sodium loss / sodium excess
  • Fluid loss without replacement e.g. dehydration, burns
  • Diabetes insipidus
  • Osmotic diuresis e.g. hyperglycaemia
  • Primary hyperaldoseronism
  • Iatrogenic- excessive saline use
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21
Q

Differential causes of hypernatraemia

A

High circulating vol= hyperaldosteronism (increased Na)
Low circulating vol= most other states
Hypertonic urine = extra-renal fluid losses, and reduced fluid intake
Hypotonic urine = diabetes insipidus
Isotonic urine = osmotic diuresis

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22
Q

Treatment of hypernatraemia

A
  • Give water orally
  • Give IV 5% dextrose solution
  • Guided by urine output and plasma sodium level
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23
Q

Two types of Diabetes Insipidus

A

Central DI = reduced ADH production so less circulating ADH

Nephrogenic DI = caused by renal resistance to ADH (which is still being produced by the pituitary)

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24
Q

Investigations for DI

A
  • 24 hour measurement of urine volume (>3L /day)
  • Fluid deprivation testing: If patient continues to produce large volumes of urine despite high plasma osmolality, it is likely to be DI
  • IM desmopressin given to distinguish between nephrogenic and central DI- increase in urine osmolality to >800mOsm/kg
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25
Q

Treatment of DI

A
  • Maintain adequate fluid intake
  • ADH analogue desmopressin
  • Need to treat the cause in nephrogenic DI, high-dose desmopressin and thiazide diuretics can be used
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26
Q

Why is ionised free calcium the important component of total circulating calcium?

A

This component regulates the negative feedback mechanism in calcium homeostasis

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27
Q

What is the mechanism of action of PTH?

A
  • PTH secreted in response to low serum calcium or high serum phosphate
  • Increases calcium renal reabsorption
  • Activation of Vit D in kidneys to promote intestinal calcium absorption
  • Activation of osteoclasts which increase calcium release from the bone
  • Decreases renal phosphate reabsorption
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28
Q

Hypercalcaemia - symptoms…

A
  • STONES, BONES, ABDOMINAL MOANS, AND PSYCHIC GROANS
  • Renal sx: polyuria, polydispia
  • Gastro sx: anorexia, vomiting, constipation, abdo pain
  • CNS sx: confusion, lethargy, depression
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29
Q

Causes of hypercalcaemia

A
  • Primary/ tertiary hyperparathyroidism
  • Malignancy: lytic bony metastases, ectopic secretion , multiple myeloma
  • Vit D intoxication
  • Familial hypocalcuric hypercalcaemia (FHH)
  • Sarcoidosis - granulomas produce active Vit D
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30
Q

Investigations for differential causes of hypercalcaemia

A
  • U+Es measurement to assess renal function
  • Phosphate measurement: low phosphate in hyperparathyroidism, phosphate raised in myeloma, vit D excess, bony malignancy, sarcoidosis
  • ALP measurement: ALP raised in bone mets, sarcoidosis, lithium toxicity
  • PTH measurement: PTH increased in parathyroid overactivity
  • Urine calcium measurement: Low conc in FHH
31
Q

Treatment of hypercalcaemia

A
  • Rehydration - 6L 0.9% saline over 24 hrs

- IV bisphosphonate - zoledronate 4mg (prevents osteoclast resorption)

32
Q

Symptoms of hypocalcaemia

A
  • Numbness and tingling
  • Muscle cramps
  • Spasm
  • Seizures
33
Q

Signs of hypocalcaemia

A

Chvostek’s sign: tap facial nerve to get spasm of corner of mouth
Trousseau’s sign: inflate sphygmanometer, causing carpopedal spasm

34
Q

Causes of hypocalcaemia

A
  • Hypoparathyroidism
  • Vit D deficiency
  • Conditions preventing calcium release from bone e.g. sclerotic bony mets, osteomalacia
  • Acute pancreatitis
  • CKD
35
Q

ECG changes in hypocalcaemia…

A

Prolonged QT interval

36
Q

ECG changes in hypercalcaemia…

A

Shortened QT interval

37
Q

Treatment of hypocalcaemia

A

Acute hypocalcaemia: IV calcium gluconate - over 10 mins, then a continuous calcium infusion
Chronic hypocalcaemia: vit D analogues e.g. calcitriol

38
Q

What is the normal reference range for potassium?

A

3.5-5.3 mmol/L

39
Q

Main causes of hyperkalaemia

A
  • Renal: AKI, CKD, Addison’s disease, medications (ACEi, AT2 blockers)
  • Increased circulation of potassium: tumour lysis, rhabdomyolisis
  • DKA (shift from intracellular to extracellular)
40
Q

Why does high [K+] cause cardiac dysrhythmias?

A

Raised extracellular [K] causes reduced conc. gradient, therefore sodium -potassium channel becomes dysfunctional

41
Q

ECG changes in hyperkalaemia…

A
  • Tented T waves
  • Flattened P waves
  • Prolonged PR interval
  • Widening of QRS complexes
42
Q

Treatment of hyperkalaemia

A
  • 10ml 10% calcium gluconate - cardioprotective as it stabilises the myocardium
  • 10-15 units of insulin in 50ml 50% glucose
  • Nebulised salbutomol
  • IV sodium bicarbonate
  • Removal of excess potassium: restrict potassium intake, stopping potassium sparing diuretics, stop digoxin, give calcium resonium
43
Q

Causes of hypokalaemia

A
  • GI loss: diarrhoea, vomiting
  • Renal loss: thiazide diuretics
  • Salbutomol overdose
  • Decreased intake: TPN, malnutrition
  • Burns
44
Q

Symptoms of hypokalaemia

A
  • Alkalosis
  • Shallow respirations
  • Irritability
  • Confusion
  • Weakness
  • Arrhythmias
  • Lethargy
  • Thready pulse
45
Q

ECG changes in hypokalaemia

A
  • Flat T waves
  • ST depression
  • Prominent U waves
46
Q

Treatment of hypokalaemia

A
  • Mild- moderate: oral potassium replacement e.g. bananas, avocados, KCl
  • Severe: pt admission - oral potassium, KCl slow infusion in normal saline
47
Q

Potential complications of alcohol intoxication

A
  • Acute gastritis (nausea, vomiting, abdo pain and GI bleeding)
  • Respiratory depression
  • Hypoglycaemia
  • Alcoholic ketoacidosis
  • Accidental injuries
48
Q

Important investigations in alcohol intoxication

A
  • Blood alcohol level
  • U+Es, glucose, amylase, lactate, ammonia
  • ABG
49
Q

Management of alcohol intoxication:

A
  • A-E assessment
  • Nurse in recovery position
  • Need admission for IV rehydration
50
Q

What is the process of substance dependence developing?

A
  1. Experimental use
  2. Social use
  3. Casual use - more regular
  4. Compulsive use - problematic
51
Q

Describe the states of change model…

A
  1. Pre-contemplation: user did not recognise problems
  2. Contemplation: user accepts there is a problem, begins to weigh up positive and negative aspects of coninued drug use
  3. Decision making: user decides whether to continue
  4. Action: user attempts change
  5. Maintenance: positive life changes must be maintained
  6. Relapse: return to previous behaviour - but gain useful strategies on how to overcome
52
Q

What is the CAGE questionnaire

A
  • Cutting down - ever thought about cutting down?
  • Annoyed - feeling annoyed when people ask about habits
  • Guilty - feel of guilt after drinking?
  • Eye opener - need a drink first thing in the morning
53
Q

Recommended alcohol intake in the UK…

A

14 units per week for both men AND women

54
Q

Key features of dependence syndrome

A
  • Salience: change in life priorities
  • Tolerance: pt drinking more alcohol for same effect
  • Impaired control of consumption
  • Compulsion: very difficult for patient to resist
  • Withdrawal syndrome: user learns to anticipate and avoid withdrawals
  • Continued use despite harmful effects
  • Reinstatement of previous pattern of drug use
55
Q

Signs of chronic liver disease…

A
  • Asterixis
  • Clubbing
  • Dupurtene’s contracture
  • Palmar erythema
  • Spider naevi
  • Gynaecomastia
  • Jaundice
  • Splenomegaly
56
Q

Investigations for alcohol consumption

A
  • Breath/ blood alcohol levels
  • FBC- MCV can be raised in alcoholism
  • LFTs: Gamma-GT raised in alcohol abuse, AST:ALT >2
  • Clotting screen
  • U+Es
  • Fasting glucose (as chronic pancreatitis can cause diabetes)
57
Q

Management of alcohol dependence

A
  • Need to treat initial withdrawal first with detoxification
  • Encourage abstinence through pscyhological interventions (motivational interviewing, CBT, relapse prevention, AA)
  • Patients <40 y/o and with minimal dependence should normally opt for controlled drinking rather than abstinence
58
Q

Medical management of alcohol dependence

A
  • Disulfiram- inhibits ALDH causing build up of acetylaldehyde causing sx such as flushing, headache, nausea, vomiting
  • Acomprostate - enhances GABA transmission which reduces cravings
  • Naltrexone - opioid antagonist which decreases pleasurable effects of drinking
59
Q

What occurs within 6-24 hrs of alcohol withdrawal?

A

Insomnia, tremor, anxiety, GI upset, headache, diaphoresis (excessive sweating), palpitations, anorexia

60
Q

What occurs within 24-72 hrs of alcohol withdrawal?

A

Withdrawal seizures

61
Q

What occurs after 72 hrs of alcohol withdrawal?

A

Delirium Tremens : hallucinations, disorientation, tachycardia, hypertension, fever, agitation

62
Q

What is the triad of features present in Delirium Tremens?

A
  1. Delirium - fluctuating acute confusional state, with clouding of consciousness and disorientation in time and space
  2. Hallucinatory experiences - vivid, chaotic and bizarre, mainly visual
  3. Tremor
63
Q

How long can delirium tremens last?

A

Usually lasts 3-5 days

64
Q

How do deaths occur from delirium tremens?

A
  • Arrhythmias
  • Infection
  • Fits
  • Cardiovascular collapse
65
Q

Medical management of alcohol withdrawal…

A
  • Chlordiazepoxide (20-30mg QDS reduced over 5-7 days) or diazepam (especially in withdrawal seizures)
  • 500mg IV Pabrinex TDS for 3 days , then switched to oral thiamine 100mg TDS and vit B co-strong
66
Q

What is in Pabrinex?

A
  • B vitamins (thiamine B1, riboflavin B2, pyridoxine B6)
  • Vitamin C
  • Vitamin E
  • Nicotinic acid
  • Folate
67
Q

What is alcoholic ketoacidosis?

A
  • When an alcoholic stops drinking, and they vomit repeatedly, without eating
  • Occurs from fatty acid breakdown, leading to ketone production that causes the ketoacidosis
  • Presents 1-2 days after last binge
68
Q

What causes Wernicke’s Korsakoff

A
  • Thiamine deficiency leads to haemorrhages in floor of third ventricle, mammillary bodies, brain stem, thalamic nuclei
69
Q

Presentation of Wernicke’s encephalopathy…

A
  • Acute confusional state
  • Nystagmus
  • Ophthalmoplegia
  • Ataxia
  • Polyneuropathy
70
Q

Presentation of Korsakoff’s psychosis…

A
  • Amnesic state with profound retrograde and anterograde amnesia with other intellectual abilities maintained
  • Patients tend to fill gaps in memory by confabulating
  • Typically develops after Wernicke’s encephalopathy
  • Some patients develop both concurrently to give Wernicke’s Korsakoff syndrome
71
Q

Different causes of hypothermia…

A
  • Primary hypothermia: environmental exposure, not underlying medical condition e.g. hill walking, water immersion, poor housing, drugs, alcohol
  • Secondary hypothermia: decreased heat production (hypothyroidism, hypoadrenalism, malnutrition) , increased heat loss (vasodilation, burns, erythroderma), impaired thermoregulation (CNS trauma, stroke, sepsis, pancreatitis)
72
Q

Presentation of hypothermia…

A
  • Apathy
  • Amnesia
  • Ataxia
  • Dysarthria
  • Reduced BP
  • Arrhythmias (VF can be provoked from movement)
  • Respiratory depression
  • Muscular rigidity
  • Coma
73
Q

ECG changes seen in hypothermia…

A
  • J waves (small upwards deflection after QRS complex)
  • Prolongation of QRS
  • ST abnormalities
74
Q

Management of hypothermia…

A
  • Treat in a warm room >21 C
  • Passive rewarming in mild hypothermia (T>32)= wrap in warm blankets and polythene sheets
  • Active rewarming= water bath is useful for immersion hypothermia
  • Core rewarming= airway warming with warm, humidified O2 , peritoneal lavage - warm saline runs through peritoneum
  • Be careful not to warm too quickly (target = 0.5-2C/ hr) in case of peripheral vasodilation leading to shock

Acutely Ill Patient (16 decks)

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