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Case 7-09 Electrolytes

Patient ID 41-year-old female

Patient Location Medical Outpatients

Clinical Notes on Request Form

Polyuria and polydipsia. Cause?

Case Details

Early morning spot urine

Osmolality 611 mmol/kg

Additional Information

Other laboratory results taken at the same time:

Serum

Sodium 145 mmol/L (134–146)

Potassium 4.3 mmol/L (3.4–5.0)

Urea 8.5 mmol/L (3.0–8.0)

Creatinine 84 µmol/L (45–90)

Glucose 5.1 mmol/L (3.5–5.4)

Ionised Calcium 1.23 mmol/L (1.12–1.32)

Osmolality 302 mmol/kg (275–295)

Suggested Comment

Suboptimal urine concentration in the setting of raised serum osmolality suggests possible partial diabetes insipidus. Suggest document degree of polyuria and consider fluid deprivation challenge with DDAVP administration to differentiate central from nephrogenic causes. Further endocrine review may be appropriate depending upon findings.

Rationale

Timed urine collection helps document the degree of polyuria, and by definition should be >2.5–3 L/day. The present case shows raised serum osmolality, which makes primary polydipsia less likely. Urine is inadequately concentrated as one would expect a urine osmolality of >750 mmol/kg with this serum osmolality. This suggests (partial) diabetes insipidus, of either central or nephrogenic origin. The former is caused by inadequate antidiuretic hormone (ADH) production while the latter is due to inadequate ADH action on the renal tubules.

Formal fluid deprivation protocol (1) can help to resolve differential diagnosis with lack of further urine concentration following DDAVP in nephrogenic cases. Hypokalaemia, hyperglycaemia and renal impairment have been excluded as causes, although drugs, particularly lithium, may be contributory. Endocrine review with further pituitary studies may be appropriate depending on the findings.

Reference

1. Baylis PH. Investigation of suspected hypothalamic diabetes insipidus. Clin Endocrinol (Oxf) 1995;43:507-10.

|PREFERRED KEY WORDS |LESS RELEVANT KEY WORDS |UNACCEPTABLE KEY WORDS |

|Consistent with dehydration |Serum osmolality raised |Appropriate concentration of urine |

|Consider diabetes insipidus |?Diuretic use |?Osmotic diuresis |

|Suggest water deprivation test ± DDAVP |Suggest urine Na/electrolytes |No evidence of diabetes insipidus |

|Inadequately concentrated urine |Slightly increased urea |Suggest assess patient fluid status |

|?Nephrogenic diabetes insipidus |Suggest 24 h urine collection |Suggest repeat tests |

|?Central diabetes insipidus |Normal serum Na/glu/Ca/K |1°/psychogenic polydipsia |

|Suggest endocrinology consultation |Diabetes mellitus excluded |Suggest thyroid studies |

|?Drug therapy |Suggest ADH |?Salt and water overload |

|?Lithium Rx |No osmolar gap |Assess risk/investigate diabetes mellitus |

| |?Renal disease |Suggest other tests |

| |?Ethanol |Elevated urine osmolality |

| |High normal sodium |Suggest CNS imaging/investigation |

| |Normal kidney function |Suggest urine urea |

| |No evidence 1°/psychogenic polydipsia |?SIADH |

| |Normal biochemical profile |Increased osmolar gap |

| |Suggest urine MC&S |Suggest ACTH, cortisol |

| |Creatinine upper end reference range |?Pregnant |

| |Suggest eGFR |Suggest urine sodium |

| |Consider trial DDAVP |Serum osmolality normal |

| |Renal disease |?Hypoaldosteronism with salt wasting |

| | |Suggest aldosterone:renin ratio |

| | |?Fanconi syndrome |

| | |?Hyperthyroidism |

| | |No comment |

| | |?Hyperalimentation |

| | |Avoid nicotine, alcohol, caffeine |

| | |Suggest urine drug screen |

| | |?Unmeasured solute |

| | |SIADH unlikely |

| | |Suggest abdominal imaging |

| | |No polyuria by urine:serum osmolality |

| | |Normal urea, creatinine |

Case 8-05 Electrolytes

Patient ID 51-year-old male

Patient Location Emergency Department

Clinical Notes on Request Form

Acute confusional state. On risperidone.

Case Details

Plasma

Sodium 108 mmol/L (136–146)

Potassium 4.1 mmol/L (3.5–5.5)

Creatinine 80 µmol/L (50–110)

Urea 2.0 mmol/L (2.7–7.8)

Osmolality 227 mmol/kg (280–300)

Urine

Sodium 12 mmol/L

Potassium 8 mmol/L

Osmolality 70 mmol/kg

Suggested Comment

Severe hyponatraemia and a hypo-osmotic plasma with appropriately dilute urine and no evidence of salt wasting. This pattern is in keeping with primary (psychogenic) polydipsia with water intoxication. While risperidone is not necessarily the cause of the polydipsia, an alternative atypical antipsychotic may be more effective in improving psychogenic polydipsia.

Rationale

Hyponatraemia is classified based on hydration status and plasma osmolality. The kidney’s response allows assessment of whether the cause is renal salt wasting. In this instance renal sodium loss is close to the 20 mmol/L used to rule-in salt wasting. The urine is appropriately almost maximally dilute, and is not suggestive of SIADH or dehydration (1). The results are most consistent with polydipsia, most commonly due to psychiatric illness and frequently affecting chronic schizophrenic patients.

While antipsychotics are a well-recognised cause of hyponatraemia (secondary to SIADH), the literature surrounding their effects on polydipsia is controversial. ‘Typical’ antipsychotics have been associated with aggravating polydipsia, while atypical antipsychotics have been reported to be useful in treating these patients (2). Risperidone has not been shown to be clearly effective in this group. At least one case in the literature cites risperidone as the likely cause (3).

References

1. Burtis CA, Ashwood ER, Bruns DE (eds). Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 4th Edition. St Louis: Elsevier Saunders; 2006. pp. 1751-53.

2. Bersani G, Pesaresi L, Orlandi V, et al. Atypical antipsychotics and polydipsia: a cause or a treatment? Hum Psychopharmacol 2007;22:103-7.

3. Kar N, Sharma PS, Tolar P, et al. Polydipsia and risperidone. Aust N Z J Psychiatry 2002;36:268-70.

|PREFERRED KEY WORDS |LESS RELEVANT KEY WORDS |UNACCEPTABLE KEY WORDS |

|Severe hyponatraemia |Low plasma osmolality |?SIADH |

|Low urine osmolality |Hyponatraemia |Suggest water deprivation test |

|Low urine sodium |?Other drugs |?Adrenal insufficiency |

|Consistent with polydipsia |Confusion due to hyponatraemia |?Hypothyroidism |

|?Psychogenic polydipsia |?Extra-renal loss |Suggest cortisol / synacthen stimulation test |

|Suggests water intoxication |Suggest thyroid function tests |?Cardiac/liver failure |

|Secondary water intoxication |Due to risperidone |?Renal loss |

|Acute water overload |Low plasma urea |?Hyperglycaemia |

|?Polydipsia |Action required |Urine not maximally dilute |

|?Due to risperidone |Patient history required |Suggest ADH |

|Urine appropriately dilute |Cerebral oedema risk |?Alcoholism |

|Not suggestive of SIADH |Suggest fluid restriction |?Disease causing oedema |

|Evaluate total body water |Suggest glucose |?Diabetes insipidus |

|Dilutional hyponatraemia |Monitor results |Check pituitary function |

|Suggest withdrawal risperidone |Suggest liver function tests |Suggest serum/urine myoglobin |

| |Central pontine myelinolysis risk with rapid |?Patient non-compliance |

| |correction |?Increased sodium loss |

| |Risk of death |Sodium depletion unlikely |

| |Check results repeated |Suggest renal function tests |

| |Patient likely requires hypertonic saline |?Pseudohyponatraemia |

| |Renal function tests normal |?Low salt intake |

| |Check protein/lipids |?Renal failure |

| |Risk rhabdomyolysis during treatment |?Reset osmostat |

| |Low plasma sodium | |

| |?Patient on fluid replacement | |

| |Suggest drug screen | |

| |Contact Pathologist | |

| |?Beer potomania | |

Case 8-09 Electrolytes

Patient ID 78-year-old man

Patient Location Nursing Home

Clinical Notes on Request Form

Demented, percutaneous endoscopic gastrostomy (PEG) fed

Case Details

Sodium 169 mmol/L (135–145)

Potassium 3.6 mmol/L (3.5–5.0)

Chloride 121 mmol/L (98–107)

Bicarbonate 37 mmol/L (21–32)

Urea 18.0 mmol/L (2.0–8.5)

Creatinine 90 µmol/L (60–110)

Suggested Comment

Profound hypernatraemia with raised urea/creatinine ratio is suggestive of marked dehydration. Suggest urgent review of clinical volume status and fluid balance.

Rationale

Marked hypernatraemia with elevated urea to creatinine ratio is consistent with dehydration, specifically water depletion. Percutaneous endoscopic gastrostomy (PEG) feeding tubes are increasingly used for patients who cannot maintain adequate nutrition with oral intake. They include patients with neurological disorders, other conditions where swallowing is impaired, or there is obstruction of the upper gastrointestinal tract.

Artificial feeding may cause metabolic problems, including deficiencies or excess of fluid, electrolytes, vitamins and trace elements. Hypernatraemia is usually due to inadequate water intake. Loss of water in excess of sodium may also be contributory. It may develop rapidly in patients who are unable to experience or communicate their thirst, and especially in institutionalised subjects, who are reliant on caregivers to maintain their fluid intake.

Reference

1. Gault MH, Dixon ME, Doyle M, et al. Hypernatremia, azotemia, and dehydration due to high-protein tube feeding. Ann Intern Med 1968;68:778-91.

|PREFERRED KEY WORDS |LESS RELEVANT KEY WORDS |UNACCEPTABLE KEY WORDS |

|Consistent with marked dehydration |Elevated urea |?Drip arm |

|Marked hypernatraemia |Hypernatraemia |?Renal failure |

|?Inadequate water intake |Elevated bicarbonate |?Catabolism |

|?Hypovolaemic hypernatraemia |Suggest urine/plasma osmolality |?Cushing’s disease |

|Increased urea/creatinine ratio |Elevated chloride |Suggest occult blood |

|?Dehydration |?Metabolic alkalosis |No comment |

|Water/hypotonic fluid depletion |?Diarrhoea/stomal loss |Suggest cortisol/aldosterone |

|Check hydration status |?Vomiting |?Compensated respiratory acidosis |

|Review feed composition |Consider urine sodium |Suggest CK |

|Suggest fluid replacement |?Diabetes insipidus |?Rhabdomyolysis |

|?Insufficient water in PEG feed |Suggest urine electrolytes | |

|Suggest IV fluid replacement |Suggest glucose estimation | |

|Urgent treatment required |?Increased salt intake | |

|Check urine volume |?Diuresis | |

| |?Pre-renal renal failure | |

| |Suggest clinical review | |

| |Suggest blood gas analysis | |

| |Consistent with tube feeding syndrome | |

| |Low normal potassium level | |

| |?Skin/respiratory water loss | |

| |?Secondary hyperaldosteronism | |

| |Excessive salt intake is rare | |

| |?Hyperaldosteronism | |

| |Suggest repeat urea and electrolytes | |

| |Haemoconcentration | |

| |?Head injury | |

| |?Potassium depletion | |

| |Monitor results during fluid treatment | |

| |?Diuretic therapy | |

| |Exclude hypertonic fluid therapy | |

| |?Gastrointestinal bleed | |

| |?Loss of thirst reflect | |

| |Risk coma/death | |

| |?Meningitis/meningoencephalitis | |

| |?Creatinine low due to muscle mass | |

| |Suggest urine creatinine | |

| |?Malnourished | |

| |?Saline-responsive metabolic alkalosis | |

| |Artefact unlikely | |

| |Suggest review fluid management | |

| |?Mineralocorticoid Rx | |

Case 9-07 Electrolytes

Patient ID 55-year-old male

Patient Location General Practice

Clinical Notes on Request Form

Increased blood pressure

Case Details

Sodium 146 mmol/L (135–145)

Potassium 3.6 mmol/L (3.5–5.0)

Chloride 106 mmol/L (96–109)

Bicarbonate 29 mmol/L (23–32)

Urea 5.1 mmol/L (3.5–7.5)

Creatinine 100 µmol/L (40–120)

Cholesterol 5.8 mmol/L (3.9–5.5)

Triglyceride 1.4 mmol/L (0.6–2.0)

Suggested Comment

In the setting of borderline hypokalaemia and high-normal bicarbonate, consider possible secondary causes of hypertension. Measurement of renin and aldosterone might be helpful and further investigations of mineralocorticoid excess, if clinically indicated. Suggest repeat full fasting lipid profile and evaluate in context of absolute cardiovascular risk status.

Rationale

Borderline hypokalaemia and high-normal bicarbonate in the setting of hypertension should prompt review for secondary causes such as diuretic therapy. Renin and aldosterone would be appropriate to investigate possible mineralocorticoid excess. This should be considered in patients with blood pressures of >160 mmHg (systolic and >100 mmHg (diastolic), drug-resistant hypertension, hypertension with: spontaneous hypokalaemia or diuretic-induced hypokalaemia, adrenal incidentaloma, family history of early-onset hypertension or cerebrovascular accident at a young age (20 x2 = microalbuminuria |

| |ACR borderline |AER 10 mIU/L, symptomatic for hypothyroidism, positive TPO antibodies, or evidence of atherosclerotic cardiovascular disease, heart failure, or risk factors associated with these diseases. Guidelines for subclinical hypothyroidism generally suggest assessment of TPO antibody and yearly monitoring.

Reference

1. Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: co-sponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract 2012;18:988-1028.

|PREFERRED KEY WORDS |LESS RELEVANT KEY WORDS |UNACCEPTABLE KEY WORDS |

|Normal thyroid function tests |TSH high normal |Suggest clinical exam |

|Previous results borderline |Risk developing hypothyroidism |Non-steady state thyroid function tests |

|Suggest monitor thyroid function tests |?Subclinical hypothyroidism |Aim lower cholesterol target |

|Suggest anti-TPO Abs |Normal lipids and glucose |Suggest T4 replacement |

| |No comment |Suggest FT3 |

| |?Thyroiditis |T4 replacement effective |

| |Subclinical hypothyroidism unlikely |?Drug-induced TSH |

| |?Transient hypothyroidism |Repeat glucose and lipids |

| |Borderline low thyroid function tests |?Suboptimal replacement |

| |?Previous non-thyroidal illness |?Age-related |

| |Assess cardiovascular disease risk |Suggest lipids and cardiac markers |

| |Normal fasting glucose |?Reference range of 1st results |

| |?Diurnal variation effect |Suggest thyrotropin releasing hormone stimulation |

| |History noted |test |

| |Results similar to previous |Assay CV checked |

| |No treatment required |Consider T4 replacement |

| |?Non-thyroidal illness | |

| |?Goitre | |

| |?Clinical history | |

| |Previous results - ? other causes | |

| |No further action | |

| |Transient compensated hypothyroid | |

| |No clinical risk TSH ................
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