so this is a complicated case: . 83 Male. presented to BHH on 26/07 following an unwitnessed fall. Discharged against med advice on the same day and represented on 28/07 after another unwitnessed fall. Attempting to go to the toilet and landed on his left side. . PMH: Cognitive impairment, Angina pectoris, Osteoarthritis,Depression,Type 2 Diabetes Mellitus,Chronic Kidney Disease Stage 3 ,supracondylar fracture 2025BHH Issues : 1. Left NOF Fracture- Left DHS 29/6/20262. Post Op-Hyperactive Delirium 3. Postural hypotension- improving SOL Issues :1. IV Zol given on 10/072. Hypernatraemia - started on IV fluids Urine Na <20, plasma osmolality 331, urine osmolality 664 ( dehydration picture )3. Hypocalcemia: Recieved Iv Ca gluconate on 17/07 & 22/07 D/W Endocrine 22/7: For maintenance 100ml 10% Ca gluconate ( given 22/7)4. Ongoing worsening delirium and agitation, dehydration, reduced oral intake, difficult cannulation and blood sampling Urine MSU -ve 15/07, blood cs (-)ve, Ct head Nil acute HAP/ ?UTI: ON IV Abx, Abx escalated to IV Taz . patient sodium is 156 still after giving IV dextrose and dex saline, hb 79, K 3.1. what might be the cause ???

Reading File
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Searching the Web

persistent hypernatraemia IV dextrose elderly post-op delirium causes inadequate correction

Finding Sources
Finding Sources
Searching PubMed

hypernatraemia elderly hospitalised persistent correction

Reading File
Reading Web Page

https://pmc.ncbi.nlm.nih.gov/articles/PMC12275548

Now I have enough to give a thorough, structured clinical analysis. Here is the full breakdown:

Why Na+ Remains 156 Despite IV Dextrose/Dex-Saline - and the Full Electrolyte Picture


1. Persistent Hypernatraemia (Na 156) - Reasons for Failure to Correct

This is the central question. Hypernatraemia reflects a total body free-water deficit relative to solute, and the reason it is not correcting is almost certainly multi-factorial in this patient:

A. Ongoing losses exceed replacement rate

This is the most common reason - and the PMC review on hypernatraemia in older patients specifically states that in most cases hypernatraemia is under-corrected and prolonged due to suboptimal fluid management. His losses include:
  • Insensible losses from fever/infection - he is on IV Tazocin for HAP/?UTI. Pyrexia dramatically increases insensible losses (roughly +10% per 1°C above 37°C). These are often not accounted for in fluid prescriptions.
  • Respiratory losses - particularly relevant if he is tachypnoeic from pneumonia.
  • Reduced oral intake - he has delirium, agitation, and difficult IV access. If oral fluids are not being reliably consumed, and IV fluids are running behind or being interrupted due to cannula issues, the deficit is not being replaced.

B. Free-water deficit calculation almost certainly underestimates the true deficit

The standard formula: Free water deficit = 0.6 × body weight × ([Na/140] - 1)
For an ~65-70 kg man with Na 156:
  • Deficit ≈ 0.6 × 67 × (156/140 - 1) = ~4.6 L just as the static deficit
But this does not include ongoing daily losses (urine ~1000 mL, stool 250 mL, insensible 600-900 mL/day baseline, more if febrile). If only the static deficit is being replaced without accounting for ongoing losses, sodium will not drop.

C. Type and rate of IV fluids

  • 5% Dextrose (D5W) delivers free water but raises blood glucose - and this patient has Type 2 Diabetes. Hyperglycaemia causes an osmotic diuresis, which drives further free-water loss and perpetuates hypernatraemia. The glucose in dextrose is metabolised, leaving free water, but if he is hyperglycaemic, glucose is acting as an osmotic diuretic.
  • Dex-saline (0.18% NaCl / 4% Dextrose) is a hypotonic solution but still delivers some sodium. If large volumes are used, the sodium load can slow correction.
  • If either is running too slowly (e.g. short IV access, infiltration, nursing holds for agitation), it will not correct.

D. Diabetes insipidus (nephrogenic or central) - less likely but worth considering

His plasma osmolality is 331 and urine osmolality is 664. A urine osmolality of 664 with this degree of hypernatraemia shows the kidneys are concentrating appropriately - this effectively rules out central or nephrogenic DI as a cause. The kidneys are trying hard to conserve water. The problem is intake/external losses, not renal wasting.

E. Post-zoledronate considerations

IV Zoledronate (given 10/07) causes an acute-phase reaction with fever in ~15-20% of patients (particularly first dose), lasting 1-3 days but sometimes longer. This contributes to:
  • Pyrexia and sweating - increased insensible losses
  • Anorexia and reduced oral intake
  • Contributes to his hypocalcaemia (zoledronate inhibits osteoclasts, reducing calcium release from bone; this is the expected mechanism - hence the repeated IV calcium gluconate)

F. CKD Stage 3

Impaired concentrating and diluting capacity means the kidney is less able to handle large water loads rapidly. Paradoxically, it also means less flexible response to replacement fluids.

G. Delirium impairs voluntary fluid intake

His worsening delirium means he cannot self-regulate thirst and voluntarily drink. This patient is entirely dependent on staff-administered fluids. Any gaps in IV access = gaps in fluid replacement.

2. Anaemia - Hb 79

This is a significant drop. Multiple causes are stacking here:
CauseMechanism
Surgical blood loss - Left DHS (29/06)Expected post-operative anaemia; may not have been fully corrected
Anaemia of chronic inflammationActive infection (HAP/?UTI), ongoing inflammatory state suppresses erythropoiesis
CKD Stage 3Reduced erythropoietin production (EPO-relative deficiency)
ZoledronateCan rarely cause bone marrow suppression; more importantly, it triggers acute-phase reaction which worsens anaemia of inflammation
NutritionalReduced oral intake = iron, B12, folate deficiency contribution
Repeated blood samplingDifficult blood sampling as documented - phlebotomy anaemia is real in frail elderly
HaemodilutionIV fluid resuscitation can dilute Hb
Pre-existingOsteoarthritis, depression, CKD, diabetes - multiple chronic disease burden
Anaemia also worsens delirium (reduced oxygen delivery to brain), which closes the loop on his clinical deterioration.

3. Hypokalaemia - K 3.1

Several concurrent causes:
CauseMechanism
Poor oral intakePotassium is predominantly dietary; he is not eating/drinking adequately
IV Piperacillin-Tazobactam (Tazocin)Piperacillin is a non-reabsorbable anion - it acts at the distal nephron to increase urinary potassium wasting (similar mechanism to high-dose penicillins). This is a well-recognised cause of hypokalaemia
Furosemide or other diuretics (check his drug chart - common in elderly with postural hypotension)Loop diuretics cause kaliuresis
Secondary hyperaldosteronism from dehydration/hypovolaemiaVolume depletion activates RAAS - aldosterone drives Na reabsorption at the expense of K excretion
AlkalosisAny metabolic alkalosis shifts K intracellularly
Ongoing fluids without K supplementationD5W and dex-saline contain no potassium
Critical point: Hypokalaemia worsens delirium, causes muscle weakness (increasing fall risk and aspiration risk), and in the context of Hb 79, contributes to cardiovascular instability.

4. The Vicious Cycle This Patient Is In

Delirium + agitation
        ↓
Poor oral intake + difficult IV access
        ↓
Ongoing free-water deficit not replaced
        ↓
Persistent hypernatraemia → worsens delirium
        ↓
Infection (HAP/?UTI) → pyrexia → more insensible losses
        ↓
Hypokalaemia (Tazocin + poor intake + RAAS activation)
        ↓
Further muscle weakness, delirium, cardiac risk

5. Practical Actions to Address This

  1. Recalculate free-water deficit properly and add ongoing losses (especially insensible if febrile). Target correction at 10-12 mmol/L per 24 hours (not faster). Use this PMC correction guide as a framework.
  2. Monitor Na every 6-12 hours - daily bloods are insufficient when Na is 156 and not responding.
  3. Secure IV access - PICC line or midline if peripheral cannulas keep failing. Without reliable access, fluids cannot be delivered.
  4. Account for hyperglycaemia - if blood glucose is elevated, D5W will worsen osmotic diuresis. Consider 0.45% NaCl (half-normal saline) as an alternative, or tight glycaemic control alongside D5W.
  5. Potassium replacement - add KCl 20-40 mmol/L to maintenance fluids. Recheck K 4-6 hourly. Target K >3.5.
  6. Treat pyrexia actively (paracetamol regularly) to reduce insensible losses.
  7. Consider NG tube if oral intake remains minimal - allows free-water delivery, medications, and nutrition without IV access dependency.
  8. Anaemia - check iron studies, B12, folate. Consider transfusion if symptomatic (Hb 79 in context of angina and delirium is clinically significant) - discuss with haematology/cardiology. A threshold of 80 g/L is often used in surgical patients with cardiovascular disease.
  9. Review all medications - ensure no agents contributing to K loss, and consider dose adjustment for CKD.
  10. Delirium care - non-pharmacological bundle: orientation aids, adequate lighting, familiar faces, sleep-wake cycle preservation. Pharmacological management only as last resort.

Bottom line: The persistent Na 156 is most likely explained by ongoing losses (insensible from fever, respiratory, GI) exceeding the rate of IV replacement, compounded by hyperglycaemia-driven osmotic diuresis from D5W, interrupted IV access, and inadequate volume of free-water administered. The Hb 79 is multifactorial (post-op, CKD, inflammation, nutrition). The K 3.1 is driven by Tazocin-related renal K wasting, poor intake, and RAAS activation from volume depletion. All three derangements are feeding his delirium and are interconnected.
This is a shared conversation. Sign in to Orris to start your own chat.