The Undifferentiated Altered Mental Status — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Robert Chen is an 82-year-old retired engineer who presents with an acute confusional state over four days, on a background of mild vascular dementia, type 2 diabetes on gliclazide and insulin glargine, hypertension, atrial fibrillation on apixaban, and chronic kidney disease stage 3 with a baseline creatinine of 150. He was previously independent and lives alone. ^[1]

His main problems are:

1. Delirium, CAM-positive, multifactorial, superimposed on his vascular dementia.
2. Sepsis from a community-acquired pneumonia and a urinary tract infection — CRP 96, WCC 16.2, fever 38.3.
3. Severe hyponatraemia at 124, requiring controlled correction at no more than 8 to 10 mmol per 24 hours to prevent osmotic demyelination.
4. Acute kidney injury with the creatinine risen from 150 to 195.
5. A chronic subdural haematoma on the left, found on the CT, on apixaban — requiring anticoagulation reversal and neurosurgical consultation.
6. A drug review — withholding the gliclazide for the hypoglycaemia risk in the AKI, the apixaban for the subdural, and the antihypertensives for the hypotension. ^[1]

My immediate priorities are the ABCDE assessment with the GHOST reversible causes checked, the intravenous antibiotic for the pneumonia and the UTI dose-adjusted for the CKD, the controlled correction of the hyponatraemia, the reversal of the apixaban and the neurosurgical consultation for the subdural, the empirical thiamine 500 mg IV, and the non-pharmacological delirium bundle alongside the medical management. I will also, in parallel, involve the family in the care plan and the cognitive-recovery discussion, and I will set up the delirium prevention measures for the ward." ^[1]

Examiner probing questions and model answers

Q1: "Walk me through your assessment of his cognitive function using the CAM." ^[1]

"The CAM is the Confusion Assessment Method, developed by Inouye in 1990, and it is the standard bedside diagnostic tool for delirium. It has four features. Feature 1 is the acute onset and fluctuating course — from the daughter's history, Mr Chen was well four days ago and has become progressively and fluctuatingly confused. Feature 2 is inattention — at the bedside, I test this by asking him to recite the months of the year backwards, and he cannot get beyond September. Feature 3 is disorganised thinking — from the conversation and the disorientation, he is rambling and illogical. Feature 4 is the altered level of consciousness — he is drowsy, with a GCS of 13. The CAM diagnostic algorithm requires Features 1 and 2 plus either 3 or 4; he has all four, so the CAM is positive and the diagnosis of delirium is confirmed ^[1]. The teaching point is that the CAM is quick (under five minutes), validated with a sensitivity of 94 to 100 per cent and a specificity of 90 to 95 per cent, and reproducible across observers — it is tool examiner expects you to name and to use."

Q2: "How do you correct his hyponatraemia, and what is the danger?" ^[1]

"The sodium of 124 is severe and is contributing to the confusion and the drowsiness. The correction must be controlled — no more than 8 to 10 mmol per litre in 24 hours — because over-rapid correction risks osmotic demyelination syndrome, the devastating pontine and extrapontine myelinolysis first described by Sterns in 1986 ^[5]. The risk factors include the severity of the hyponatraemia, the chronicity, the alcohol use, the malnutrition, and the hypokalaemia — and this patient is elderly and possibly nutritionally depleted, which raises his risk.

My approach is to treat the underlying cause — the sepsis, the dehydration, and the SIADH-like state that can accompany the pneumonia — with cautious normal saline, 250 to 500 mL over 4 to 6 hours, and to monitor the sodium every 4 to 6 hours. I do not use hypertonic saline unless he seizes or his conscious level falls precipitously, because the risk of overcorrection is highest in the patient who is rapidly fluid-resuscitated. If the sodium rises faster than 10 mmol in 24 hours, I stop the normal saline, give desmopressin and free water to re-lower it, and consult nephrology. The osmotic demyelination syndrome is irreversible and catastrophic — it produces a quadriparetic, dysarthric, often comatose patient — and it is preventable by the controlled correction rate." ^[1]

Q3: "What is your approach to the chronic subdural on apixaban?" ^[1]

"The subdural is a known complication of the atrophic elderly brain on anticoagulation, and it may be contributing to the confusion, though the sepsis and the hyponatraemia are more likely the primary drivers. My management has four steps. First, I reverse the apixaban — I discuss with haematology, and the options are andexanet alfa or four-factor prothrombin complex concentrate, depending on the severity, the local protocol, and the availability. Second, I consult the neurosurgical team — a small chronic subdural with no mass effect may be managed conservatively with serial imaging, but the decision is the neurosurgeon's, and the threshold for surgical evacuation (burr-hole drainage) is lower if the GCS falls or a focal deficit emerges. Third, I monitor the GCS hourly and repeat the CT if the GCS drops by 2 points or a new focal deficit appears. Fourth, I assess the fall — how did he fall, was fall cause of the subdural or was the confusion and unsteadiness cause of the fall, and I address the underlying contributors and the future fall prevention. ^[1]

The teaching point: the elderly patient on a DOAC with new or worsening confusion gets a CT head — the subdural may be chronic and asymptomatic at presentation, but the risk of expansion in the anticoagulated patient is significant, and the early identification and the coagulation reversal are the interventions that prevent the deterioration." ^[1]

Q4: "What is your drug review, and which drugs do you withhold?" ^[1]

"The drug chart is the highest-yield document in the unexplained delirium. In Mr Chen, I withhold the gliclazide — he has an acute kidney injury with the creatinine risen from 150 to 195, and the sulfonylurea persists for hours with a high risk of prolonged refractory hypoglycaemia; I manage the glucose with a variable-rate intravenous insulin infusion and hourly monitoring. I withhold the apixaban — for the subdural and the fall risk. I withhold the antihypertensives — his blood pressure is 104 over 64, which is low for a baseline hypertensive, and the antihypertensives will worsen the hypotension, the cerebral hypoperfusion, and the confusion. I continue the insulin glargine but adjust the dose for the AKI and the reduced intake. And I review every other drug for the dose adjustment the renal failure requires — the antibiotics, the analgesia, and any other renally-cleared agent. ^[1]

The teaching point: the acute confused patient on multiple medications is the patient most at risk of the drug-induced delirium and the drug-drug interactions, and the drug chart is the document that most often holds the answer to the cause. Review every drug, every dose, and every recent change." ^[1]

Q5: "How do you decide whether to sedate him, and with what?" ^[1]

"The principle is that the treatment of delirium is the treatment of the underlying cause, and the symptomatic sedation is the last resort, not the first step. At present, Mr Chen is confused but not dangerously agitated — he is drowsy rather than combative — so my primary management is the non-pharmacological delirium bundle (orientation cues, glasses and hearing aids, family presence, sleep protection, early mobilisation, minimisation of lines and catheters) alongside the medical treatment of the precipitants. ^[1]

If his agitation were to endanger him (pulling at lines, falling out of bed) or the delivery of essential care (refusing the antibiotic or the fluids), then I would use low-dose haloperidol — 0.25 to 0.5 mg orally or intramuscularly in the elderly, repeated and titrated. I check the ECG and the QTc first, because haloperidol prolongs the QT and can precipitate torsades de pointes. I avoid haloperidol in Parkinson disease and Lewy body dementia — the dopamine blockade worsens the motor symptoms. ^[1]

I avoid benzodiazepines in delirium — they worsen the confusion, prolong the course, and cause respiratory depression — except in two specific situations: alcohol or benzodiazepine withdrawal (first-line) and severe serotonin syndrome or catatonia (adjunctive). Mr Chen is not in withdrawal, so benzodiazepines are not indicated. The teaching point: the registrar who reaches for the midazolam for the agitated delirious elderly patient has made a serious error — the correct agent is haloperidol, at a low dose, titrated, with the ECG monitored." ^[1]

Q6: "What is the prognosis of delirium in the elderly, and how do you discuss this with the family?" ^[1]

"The prognosis is nuanced. The acute episode usually resolves over days to weeks if the precipitants are treated, but the full cognitive recovery may take months, and a proportion of elderly patients do not return to their baseline — the delirium has unmasked or accelerated the underlying neurodegenerative process. Delirium in the elderly is associated with prolonged hospital stay, increased institutionalisation, increased mortality, and an increased risk of subsequent dementia ^[2].

I discuss this honestly and hopefully with the family. I explain that Mr Chen has an acute medical illness — the infection, the sodium disturbance, and the subdural — that has caused the confusion, and that the confusion is a symptom of the illness, not the illness itself. I explain that the treatment is the treatment of the causes, and that the confusion will usually improve as the causes are corrected. I am honest about the uncertainty — that the full recovery may take weeks, that his underlying dementia means the recovery may be incomplete, and that some patients do not return to their previous level of function. I frame the care positively — the active treatment of the reversible causes, the delirium bundle to support his brain, the family's presence as a therapeutic intervention, and the plan for the cognitive reassessment at discharge and at follow-up. I ask the family about his prior wishes, his baseline function, and his values, and I incorporate these into the care plan. The conversation is ongoing, not a one-off." ^[1]