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Acutely Ill Patient > Acute Confusional State > Flashcards

Acute Confusional State Flashcards

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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
Treatment of DI
- Maintain adequate fluid intake - ADH analogue desmopressin - Need to treat the cause in nephrogenic DI, high-dose desmopressin and thiazide diuretics can be used
26
Why is ionised free calcium the important component of total circulating calcium?
This component regulates the negative feedback mechanism in calcium homeostasis
27
What is the mechanism of action of PTH?
* 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
28
Hypercalcaemia - symptoms...
* STONES, BONES, ABDOMINAL MOANS, AND PSYCHIC GROANS - Renal sx: polyuria, polydispia - Gastro sx: anorexia, vomiting, constipation, abdo pain - CNS sx: confusion, lethargy, depression
29
Causes of hypercalcaemia
- Primary/ tertiary hyperparathyroidism - Malignancy: lytic bony metastases, ectopic secretion , multiple myeloma - Vit D intoxication - Familial hypocalcuric hypercalcaemia (FHH) - Sarcoidosis - granulomas produce active Vit D
30
Investigations for differential causes of hypercalcaemia
- 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
Treatment of hypercalcaemia
* Rehydration - 6L 0.9% saline over 24 hrs | - IV bisphosphonate - zoledronate 4mg (prevents osteoclast resorption)
32
Symptoms of hypocalcaemia
- Numbness and tingling - Muscle cramps - Spasm - Seizures
33
Signs of hypocalcaemia
Chvostek's sign: tap facial nerve to get spasm of corner of mouth Trousseau's sign: inflate sphygmanometer, causing carpopedal spasm
34
Causes of hypocalcaemia
- Hypoparathyroidism - Vit D deficiency - Conditions preventing calcium release from bone e.g. sclerotic bony mets, osteomalacia - Acute pancreatitis - CKD
35
ECG changes in hypocalcaemia...
Prolonged QT interval
36
ECG changes in hypercalcaemia...
Shortened QT interval
37
Treatment of hypocalcaemia
Acute hypocalcaemia: IV calcium gluconate - over 10 mins, then a continuous calcium infusion Chronic hypocalcaemia: vit D analogues e.g. calcitriol
38
What is the normal reference range for potassium?
3.5-5.3 mmol/L
39
Main causes of hyperkalaemia
- Renal: AKI, CKD, Addison's disease, medications (ACEi, AT2 blockers) - Increased circulation of potassium: tumour lysis, rhabdomyolisis - DKA (shift from intracellular to extracellular)
40
Why does high [K+] cause cardiac dysrhythmias?
Raised extracellular [K] causes reduced conc. gradient, therefore sodium -potassium channel becomes dysfunctional
41
ECG changes in hyperkalaemia...
- Tented T waves - Flattened P waves - Prolonged PR interval - Widening of QRS complexes
42
Treatment of hyperkalaemia
- 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
Causes of hypokalaemia
- GI loss: diarrhoea, vomiting - Renal loss: thiazide diuretics - Salbutomol overdose - Decreased intake: TPN, malnutrition - Burns
44
Symptoms of hypokalaemia
- Alkalosis - Shallow respirations - Irritability - Confusion - Weakness - Arrhythmias - Lethargy - Thready pulse
45
ECG changes in hypokalaemia
- Flat T waves - ST depression - Prominent U waves
46
Treatment of hypokalaemia
- Mild- moderate: oral potassium replacement e.g. bananas, avocados, KCl - Severe: pt admission - oral potassium, KCl slow infusion in normal saline
47
Potential complications of alcohol intoxication
- Acute gastritis (nausea, vomiting, abdo pain and GI bleeding) - Respiratory depression - Hypoglycaemia - Alcoholic ketoacidosis - Accidental injuries
48
Important investigations in alcohol intoxication
- Blood alcohol level - U+Es, glucose, amylase, lactate, ammonia - ABG
49
Management of alcohol intoxication:
- A-E assessment - Nurse in recovery position - Need admission for IV rehydration
50
What is the process of substance dependence developing?
1. Experimental use 2. Social use 3. Casual use - more regular 4. Compulsive use - problematic
51
Describe the states of change model...
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
What is the CAGE questionnaire
- 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
Recommended alcohol intake in the UK...
14 units per week for both men AND women
54
Key features of dependence syndrome
- 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
Signs of chronic liver disease...
- Asterixis - Clubbing - Dupurtene's contracture - Palmar erythema - Spider naevi - Gynaecomastia - Jaundice - Splenomegaly
56
Investigations for alcohol consumption
- 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
Management of alcohol dependence
- 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
Medical management of alcohol dependence
- 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
What occurs within 6-24 hrs of alcohol withdrawal?
Insomnia, tremor, anxiety, GI upset, headache, diaphoresis (excessive sweating), palpitations, anorexia
60
What occurs within 24-72 hrs of alcohol withdrawal?
Withdrawal seizures
61
What occurs after 72 hrs of alcohol withdrawal?
Delirium Tremens : hallucinations, disorientation, tachycardia, hypertension, fever, agitation
62
What is the triad of features present in Delirium Tremens?
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
How long can delirium tremens last?
Usually lasts 3-5 days
64
How do deaths occur from delirium tremens?
- Arrhythmias - Infection - Fits - Cardiovascular collapse
65
Medical management of alcohol withdrawal...
- 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
What is in Pabrinex?
- B vitamins (thiamine B1, riboflavin B2, pyridoxine B6) - Vitamin C - Vitamin E - Nicotinic acid - Folate
67
What is alcoholic ketoacidosis?
- 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
What causes Wernicke's Korsakoff
- Thiamine deficiency leads to haemorrhages in floor of third ventricle, mammillary bodies, brain stem, thalamic nuclei
69
Presentation of Wernicke's encephalopathy...
- Acute confusional state - Nystagmus - Ophthalmoplegia - Ataxia - Polyneuropathy
70
Presentation of Korsakoff's psychosis...
- 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
Different causes of hypothermia...
- 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
Presentation of hypothermia...
- Apathy - Amnesia - Ataxia - Dysarthria - Reduced BP - Arrhythmias (VF can be provoked from movement) - Respiratory depression - Muscular rigidity - Coma
73
ECG changes seen in hypothermia...
- J waves (small upwards deflection after QRS complex) - Prolongation of QRS - ST abnormalities
74
Management of hypothermia...
- 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

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