The Undifferentiated Altered Mental Status — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Robert Chen, 82 years old, retired engineer. ^[1]

Presenting complaint: Acute confusional state over four days, found by his daughter at his home this morning, confused and dishevelled. He was well and independent when she last visited four days ago. ^[1]

Past history: Mild vascular dementia (MMSE 24 six months ago; the daughter confirms he was previously independent with his finances, cooking, and self-care), type 2 diabetes (gliclazide 80 mg twice daily, insulin glargine 22 units nocte; last HbA1c 58 mmol/mol), hypertension (perindopril 5 mg daily, amlodipine 10 mg daily), atrial fibrillation (apixaban 5 mg twice daily; CHA2DS2-VASc score 4), chronic kidney disease stage 3 (baseline creatinine 150 micromol/L, attributed to hypertensive and ischaemic nephropathy), and a prior cholecystectomy 12 years ago. He lives alone in his own home, mobilises independently with a stick, and his daughter visits weekly. He has no formal advance care directive. ^[1]

Examination findings (trainee elicits):

• GCS 13 (E3 V4 M6). Disoriented in time (thinks it is March; it is July) and place (cannot name the hospital). Inattentive — cannot recite the months of the year backwards. Intermittently drowsy.
• Temperature 38.3, respiratory rate 22, SpO2 94 per cent on room air, heart rate 96 in atrial fibrillation, blood pressure 104/64, capillary refill 3 seconds.
• Pupils equal and reactive (3 mm). No focal motor deficit. No neck stiffness. No asterixis. No papilloedema on fundoscopy.
• Chest: reduced air entry and crackles at the right base.
• Abdomen: soft, non-tender. No palpable bladder.
• Skin: no rash, no cellulitis, no pressure ulcer. ^[1]

Investigations (available results):

• Finger-prick glucose: 6.2 mmol/L.
• Sodium 124, potassium 4.8, creatinine 195 (up from baseline 150), urea 14.2, calcium 2.35 (corrected), magnesium 0.85, TSH 3.2.
• CRP 96, WCC 16.2 (neutrophils 13.8), Hb 128, platelets 245, INR 1.1.
• Lactate 2.4.
• LFTs: bilirubin 14, ALT 28, ALP 95, albumin 32.
• Chest X-ray: right lower lobe consolidation.
• Urine dipstick: positive for nitrites and leucocytes.
• CT head (non-contrast): mild cerebral atrophy consistent with age and the known vascular dementia; a small chronic subdural haematoma on the left (hypodense, approximately 7 mm thick, no midline shift, no mass effect). ^[1]

Drug chart on admission: gliclazide 80 mg twice daily, insulin glargine 22 units nocte, perindopril 5 mg daily, amlodipine 10 mg daily, apixaban 5 mg twice daily, atorvastatin 40 mg nocte, metformin (held by the GP three months ago due to the CKD). ^[1]

Candidate's structured presentation (model)

Opening statement (SASPOP): ^[1]

"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 — sepsis, hyponatraemia, AKI, chronic subdural — superimposed on the 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.
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.
6. A drug review — withholding the gliclazide, the apixaban, and the antihypertensives. ^[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 with serial monitoring, 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." ^[1]

Management plan: ^[1]

1. ABCDE and the GHOST check. Glucose 6.2 (normal). Oxygen — give 2 L via nasal speculum to target 94 to 98 per cent. Sodium 124 — controlled correction as below. Thiamine — 500 mg IV empirically. Hypotension — cautious fluid, treat the sepsis.
2. Sepsis management. Blood cultures, urine MC&S, commence ceftriaxone 1 g IV daily plus azithromycin 500 mg orally daily for three days, per the local CAP guideline. Paracetamol 1 g for the fever. Cautious normal saline (250 to 500 mL, reassess) given the CKD and the hyponatraemia. Hourly urine output — catheterise if not already (and remove as soon as possible).
3. Hyponatraemia correction. The sodium of 124 is severe. Controlled correction at no more than 8 to 10 mmol per 24 hours. Treat the underlying cause (the sepsis, the dehydration) with cautious normal saline. Check the sodium every 4 to 6 hours. No hypertonic saline unless he seizes or his GCS falls precipitously.
4. Subdural management. Reverse the apixaban (discuss with haematology — andexanet alfa or PCC). Neurosurgical consultation. Hourly GCS monitoring. Repeat the CT if the GCS drops or a focal deficit emerges.
5. Drug review. Withhold the gliclazide (hypoglycaemia risk in the AKI; manage with a variable-rate insulin infusion). Withhold the apixaban (subdural). Withhold the perindopril and amlodipine (hypotension). Continue the insulin glargine at a reduced dose, with hourly glucose monitoring. Continue the atorvastatin.
6. Non-pharmacological delirium bundle. Orientation cues (clock, calendar, board with the date). Glasses and hearing aids. Family presence (the daughter is here). Sleep protection. Early mobilisation. Minimise lines and catheters. Consistent communication and reorientation. ^[1]

Communication and shared decision-making: Explain to the daughter that her father has become confused because of a combination of medical problems — a chest and urine infection, a low sodium level, and a small bleed on the surface of the brain — and that the confusion is a symptom of these illnesses, not a progression of his dementia. Explain that the treatment is the treatment of these causes, that the confusion will usually improve as the causes are corrected, but that the full recovery may take days to weeks and may be incomplete given his underlying dementia. Ask her about his prior wishes, his baseline function, and what he would want if the treatment is not working. Document the discussion and the plan. Involve the family in the care — their presence is part of the treatment. ^[1]

Examiner discussion questions

Q1: "How do you distinguish the delirium from the underlying dementia, and why does it matter?" ^[1]

"I cannot fully distinguish the two at the bedside in the acute presentation — they overlap, and the delirium is the foreground. What I can do is establish the baseline from the collateral history (the daughter's account of his function four days ago, the MMSE of 24 from six months ago), diagnose the acute change as a delirium by the CAM, and commit to the workup and the treatment of the precipitants. The delirium will resolve as the precipitants are treated, and the residual cognitive impairment at that point will be the underlying dementia. The reason it matters is that the management diverges: delirium is treated by finding and reversing the precipitants (an active, urgent, medical process), while dementia is managed with cognitive support, cholinesterase inhibitors in selected cases, and advance care planning (a longitudinal, supportive process). The registrar who attributes the acute confusion to the dementia without diagnosing and treating the delirium has failed the patient — the dementia is the predisposing factor, not the explanation for the acute change." ^[1]

Q2: "Walk me through your hyponatraemia correction strategy and the danger of over-rapid correction." ^[1]

"The sodium of 124 is severe and is contributing to the confusion. 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. This was first described by Sterns in 1986, who reported eight patients who developed a neurological syndrome with central pontine myelinolysis following the rapid correction of severe chronic hyponatraemia ^[5]. The pathophysiology: when the serum sodium is corrected rapidly, the brain — which has adapted to the chronic hypo-osmolar state by extruding osmolytes — cannot re-accumulate the osmolytes fast enough, and the rapid rise in serum osmolality draws water out of the brain cells, causing the demyelination. The risk factors include the severity and chronicity of the hyponatraemia, the alcohol use, the malnutrition, the hypokalaemia, and the advanced age.

My approach is the treatment of the underlying cause with cautious normal saline and the serial monitoring of the sodium every 4 to 6 hours. 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. I do not use hypertonic saline unless he seizes or his conscious level falls precipitously. The osmotic demyelination syndrome is irreversible — it produces a quadriparetic, dysarthric, often comatose patient — and it is preventable by the controlled correction rate." ^[1]

Q3: "What is the multifactorial model of delirium, and how does it apply to this patient?" ^[1]

"The multifactorial model, described by Inouye in her 2006 NEJM review, frames delirium as the result of the interaction between a vulnerable patient (the predisposing factors) and an acute insult (the precipitating factors) ^[2]. The predisposing factors lower the threshold for the delirium, and the precipitating factors push the patient over that threshold. The implication is that delirium is rarely caused by a single factor — there are usually several — and the management must address all of them.

In Mr Chen, the predisposing factors are his age (82), his baseline vascular dementia (the reduced cognitive reserve), his CKD, and his polypharmacy. The precipitating factors are the pneumonia, the UTI, the severe hyponatraemia, the AKI, and the chronic subdural. The delirium is the product of all of these interacting, and the management must address each one. The corollary is that delirium is preventable in a large proportion of cases through the targeting of the modifiable predisposing and precipitating factors — this is the basis of the delirium prevention bundles (the HELP program and the NICE CG103 recommendations), which address orientation, hydration, sleep, sensory aids, mobility, and medication review in every elderly hospitalised patient." ^[1]

Q4: "How do you manage the chronic subdural on apixaban?" ^[1]

"The chronic 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 (a recombinant modified factor Xa that decoys the apixaban) or four-factor prothrombin complex concentrate. The choice depends on the severity, the local protocol, and the availability. Second, I consult the neurosurgical team — a small chronic subdural (7 mm, no mass effect) may be managed conservatively with serial imaging, but the decision is the neurosurgeon's. Third, I monitor the GCS hourly and repeat the CT if the GCS drops by 2 points or a new focal deficit emerges. Fourth, I assess the fall and the future risk — was fall cause of the subdural, or was the confusion and unsteadiness cause of the fall? I address the underlying contributors (the sepsis, the hyponatraemia, the polypharmacy) and the fall prevention. The teaching point: the elderly patient on a DOAC with new or worsening confusion gets a CT head, and the finding of a subdural mandates the coagulation reversal and the neurosurgical consultation, not the assumption that it is incidental." ^[1]

Q5: "He is on gliclazide and insulin. How do you manage his diabetes during this admission?" ^[1]

"He has an acute kidney injury with the creatinine risen from 150 to 195, and the gliclazide (a sulfonylurea) carries a high risk of prolonged, refractory hypoglycaemia in the AKI — the drug persists for hours and the renal clearance is reduced. I withhold the gliclazide immediately and manage the glucose with a variable-rate intravenous insulin infusion, checking the glucose hourly and titrating the rate to a target of 6 to 10 mmol/L. I continue the insulin glargine at a reduced dose (the basal insulin provides the background, and the variable-rate infusion covers the prandial component), but I reduce it by 20 to 30 per cent given the AKI and the reduced intake. I monitor the glucose closely — hourly while on the infusion, two-hourly when stable — and I transition back to the subcutaneous regimen once the AKI is resolving and the glucose is stable. ^[1]

The teaching point: the sulfonylurea in the AKI is one of the highest-risk drug continuations in the confused elderly patient — the hypoglycaemia is prolonged, refractory, and may require an octreotide infusion if the dextrose alone does not control it. The registrar who continues the gliclazide in the AKI has not recognised the renal clearance and the accumulation risk." ^[1]

Q6: "What is the single most important lesson from this case for a registrar managing the acutely confused elderly patient?" ^[1]

"The single most important lesson is that the acute confusion is a medical symptom with a medical cause, and the workup must be systematic and exhaustive — the DIMTOP mnemonic ensures no category is missed, and the CAM diagnostic algorithm confirms the delirium and frames it as a multifactorial process. The registrar who labels the confusion as 'just dementia' or 'just old age' without working the precipitants has failed the patient. ^[1]

The second lesson is the integration: the ABCDE resuscitation, the GHOST reversible-cause check, the DIMTOP differential, the tiered investigation ladder, and the non-pharmacological delirium bundle are not separate tasks but a single coordinated response. The registrar who treats the sodium but not the sepsis, or who treats the sepsis but not the subdural, or who treats the medical causes but not the delirium itself (with the orientation, the sensory aids, the family presence, and the sleep protection) has not completed the management. ^[1]

The third lesson is the communication: the confused patient frightens the family, and the honest, hopeful explanation — that the confusion is a symptom of a treatable medical illness, that the treatment is the treatment of the causes, and that the family's presence is part of the treatment — is one of the most important interventions the registrar can make." ^[1]