Confusion Flashcards

1
Q

Which syndromes may cause a patient to appear confused?

A
  1. Delirium - acute impairment in cognitive ability alongside impaired consciousness
  2. Dementia - chronic progressive impairment in cognitive ability - with intact consciousness.
  3. Mental impairment
  4. Psychosis - not confused but disorder of perception
  5. Receptive dysphasia - difficulty comprehending questions (e.g. due to damage to Wernicke’s area)
  6. Expressive dysphasia - patient cognitively intact but difficulty verbalising answers (e.g. due to damage to Broca’s area)
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2
Q

With any confused patient, always do ABCDE first. Then how do you conduct a quick screen of confusion?

A
  1. AMTS (Abbreviated Mental Test Score) = 10 questions to check if they’re orientated in time, place and person. <6/10 indicates cognitive impairment. (NB on MMSE, <26/30 indicates cognitive impairment).
  2. If conversational ability impaired, can they follow a 3 step command? Can they name 3 common objects? - these test for receptive and expressive dysphasia
  3. Other symptoms - e.g. pain, UTI etc
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3
Q

How does time course of confusion affect the diagnosis?

A

Acute onset indicates delirium.

Fluctuating course of confusion indicates delirium also.

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4
Q

What are the causes of delirium ? (INVITED MD)

A

Infectious - chest, urinary, sepsis
Neoplastic - brain tumour
Vascular - stroke, MI causing hypo perfusion
Immune - rare conditions,e.g. Hashimoto’s encephalopathy
Trauma - subdural haematoma
Endocrine - thyroid disorders, DKA
Drugs - alcohol, opiates, diuretics/digoxin/thyroid medication
Metabolic - electrolyte imbalances, hypoxia, hypercapnia
Degenerative conditions - they won’t cause delirium but predispose patients to becoming delirious

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5
Q

Which vital signs are important in confused patients?

A
  1. Pulse/resp rate = tachycardia/tachypnoea secondary to infection?
  2. BP = hypotension may indicate hypo perfusion to brain - decreased consciousness. Bradycardia + hypertension (called Cushing’s response) indicates raised ICP
  3. Oxygen saturation - hypoxia affects consciousness
  4. Temperature - fever may suggest underlying infection. Hypothermia common in elderly and may cause confusion
  5. Blood glucose - hypoglycaemia/hyperglycaemia? In T1DM, hyperglycaemia –> DKA? In T2DM, extreme hyperglycaemia —> HHS
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6
Q

What does a “confusion screen” consist of?

A
  1. Septic screen - FBC (WCC - infection. Anaemia - hypoxia). CRP. Blood cultures. Urine analysis - positive leukocytes and nitrites = UTI, positive glucose + ketones = DKA. Urine MC&S. Chest radiograph.
  2. Metabolic screen - ABG (informs re hypercapnia and acid base balance. Uraemia/DKA can cause metabolic acidosis). U&Es - including calcium. TFTs. Liver enzymes (disproportionately raised GGT = alcohol abuse). Thiamine/folate/Vit B12 - indicates malnourishment.
  3. Toxicology screen (if necessary)
  4. ECG - arryhthmias/ischaemia can lead to low output state.
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7
Q

How do you manage someone who is acutely confused? (e.g. with UTI)

A
  1. ABCDE + resuscitation
  2. Antibiotics - to treat UTI. Avoid unnecessary catheters/cannulas
  3. Confusion - conservative measures + must treat any deficiencies (e.g. thiamine).
  4. Sedation if patient is a risk to themselves/others. Sedation done by giving haloperidol (CAREFUL if they have Parkinsons/Lewy body dementia) or Lorazepam (quick acting)
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8
Q

Irreversible damage to what system can thiamine deficiency cause?

A

Cerebral system - Wernicke’s encephalopathy

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9
Q

If someone ha a history of alcoholism and perhaps an extended hospital stay (e.g. 4 days), what is the most likely diagnosis for confusion?

A

Alcohol withdrawal

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10
Q

Alcohol withdrawal requires the immediate prescription of which drug?

A

Chlordiazepoxide (using CIWA scale as a guide).

Also prescribe thiamine to prevent irreversible brain damage

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11
Q

What are the most common reasons why postoperative patients may be confused?

A
  1. Hypoxia - e.g. anaemia from blood loss, opiate induced depressed respiratory rate, PE, etc
  2. Opiates may directly affect their mental state
  3. Electrolyte derangement - e.g. due to intra/postop fluid replacement, renal failure due to hypoperfusion
  4. Infection
  5. Sleep loss
  6. Alcohol withdrawal
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12
Q

In patients with bipolar disorder, what may cause confusion?

A

Lithium toxicity

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13
Q

What may indicate an acute renal impairment (e.g. dehydration)?

A

Raised urea with normal creatinine

as urea normally reabsorbed in PCT, whereas creatinine isn’t

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14
Q

What would be results indicative of meningococcal meningitis?

A

High WCC (mainly neutrophils), gram positive intracellular diplococci, high protein, CSF:blood glucose ration <0.5)

May/may not also present with neck stiffness etc

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15
Q

In patients suspected to be hyponatraemic, what must you rule out and how do you do this?

A

Pseudohyponatraemia

Do this by checking serum osmolality - high or normal indicates pseudohyponatraemia (because Na is dominant ion determining osmolarity).

i.e. low sodium would give low osmolality, so if the serum osmolality is normal/high we know that it is not low sodium

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16
Q

What signs may indicate hypervolaemia?

What conditions may hypervolaemic hyponatraemia suggest?

A

Raised JVP, peripheral/pulmonary oedema

Hypervolaemic hyponatraemia may indicate CCF, hepatic failure, nephrotic syndrome

17
Q

What is nephrotic syndrome?

A

Condition whereby you pass too much protein in your urine

18
Q

What signs would a hypovolaemic (dehydrated) patient have?

How does hypovolaemia result in hyponatraemia

A

Low urine output, tachycardia, low BP, dry mucous membranes, decreased skin turgor

Hypovolaemia stimulates secretion of ADH - which retains fluid in body - hence sodium levels are diluted

19
Q

To distinguish the site of sodium loss in hyponatraemic hypovolaemia, urine sodium is measured. How can we tell if the problem is renal or extra renal from the results?

A

Urine sodium <220mM = kidneys are normal. They are responding normally to drop in circulating volume by concentrating the urine. Thus the sodium loss is extra renal e.g. gut (vomiting/diarrhoea), skin (sweating/burns) or pancreatitis/small bowel obstruction

Urine sodium >220mM = kidneys abnormally concentrating the urine and salt is being lost in this manner. Causes include diuretics, renal failure, mineralocorticoid insufficiency (Addisons disease)

20
Q

If patients are euvolaemic, measure urine osmolality. What diagnoses may the results of the urine osmolality point towards?

A

High urine osmolarity (>500mmol/kg) = SIADH (NB other criteria must be met before diagnosing SIADH)

Fluid overload (psychogenic polydipsia / iatrogenic) - acute 
Severe hypothyroidism (rare) may also cause hyponatraemia
21
Q

What other sign may indicate Addisons disease except high urine sodium?

A

High potassium and low sodium in biochemistry.

Because in adrenal insufficiency, failure of Na/K exchange in DCT, due to lack of aldosterone synthesis.

22
Q

How does one confirm Addisons disease?

A

SynACTHen test = Addisons will show no increase in cortisol after stimulation with ACTH

23
Q

How is hypovolaemic hyponatraemia managed?

A

Slow infusion of normal saline - correcting Na too quickly may cause central pontine myelinolysis and death.

So infuse Na every 2-4 hours and try to increase his Na by <2mM/hour and no more than 10mM/day.

24
Q

To treat hypoglycaemia, what do you do?

A

Give a sweet drink/glucose tablet.

If unconscious, could give dextrose gel rubbed into mouth or glucose IV or glucagon IM

Seizures/coma may occur in hypoglycaemia.