polyuria and loss of appetite

Polyuria and Loss of Appetite

Try out this endocrine case and test your clinical knowledge. The answers are at the bottom.

Questions

A 31-year-old man presents to his GP complaining about how often he needs togo to the toilet. He mentions that he is always waking up in the night to urinate and that he feels a lot more tired these days.His wife has also noticed that he’s lost his appetite and barely touches his food.

PMHx:

Nil

DHx:

Nil

Allergies:

NKDA

Observations:

SpO2: 99% RA
Temperature: 37.4
BP: 210/132
HR: 93
RR: 21
POC BM: Undetectable
Ketones: +ve on dipstick

Examination:

Cardiovascular and abdominal examination are unremarkable.

Q1: What should the GP do next?

The patient is manage appropriately and undergoes further investigations, as shown below:

 

TestResultReference Range
FBC154135 – 180 g/l
MCV9280-100
WCC7.34-11 x 109/l
Plts287150 – 400 x 109/l
Urea6.02 – 7 mmol/l
Creatinine11255 – 120 umol/l
Na+150135-145 mmol/l
K+2.63.5 – 5 mmol/l
Random Cortisol3282119 – 618 nmol/l
ACTH72810-50 pg/mL
pH7.497.35 – 7.45
HCO33122-29 mmol/l
PaO2 (corrected for FiO2)11.610-13.3 kPa
PaCO26.84.7-6 kPa
Lactate0.50.5 – 1 mmol/l
Glucose27.34 – 7 mmol/l
Ketones0.2< 0.6 mmol/l

Q2: Comment on the blood results. What are the differential diagnoses for this condition?

Q3: What is the most useful next investigation in determining the underlying cause for this condition?

 The on-call consultant requests a full body CT, which is reported by the duty radiologist:  

CT Head: Cortices appear normal. Appropriately sized lateral and fourth ventricles. Minor choroid plexus calcification in third ventricle.Homogenous lesion extending superiorly in the suprasellar space. No chiasmatic involvement. No occult intracranial haemmorhages or midline shift. No evidence of mass effect. Venous sinuses appear within appropriate limits.

CT CAP: NAD. No evidence of pulmonary lesions or consolidation.Abdominal viscera appear grossly normal. Faeces in sigmoid colon observed. Full bladder–approx. 800 ml residual volume.

Q4: What is the likely diagnosis? What further management steps would be appropriate?

Answers

Reveal the Answers

Answer to Question 1

There are several concerning features in this presentation:

1) Very high BP

2) Undetectable glucose reading on background of diabetes-type symptoms

3) Presence of some ketones on urinalysis.

The key takeaway point here is that this patient is clearly too unstable to be managed in the community and needs to go to hospital urgently. With regards to the blood pressure, the GP could check for end-organ damage e.g. fundoscopy + urine dipstick for proteinurea in his surgery but more advanced tests in the workup for severe hypertension e.g. urinary protein. Albumin: Creatinine testing (assessing renal failure)+/-metanephrines and aldosterone testing (testing for a phaeochromocytoma/Conn’s syndrome)+/-CXRsand NT-proBNP (heart failure) would need to be performed in a secondary care setting.

The undetectable glucose reading is extremely concerning, as it could indicate a BM that is either too high or too low. In this case, it is likely to be the former, however an accurate BM measurement is required (usually through a blood gas, but these often cannot be performed in a GP surgery). The final feature is the presence of ketonuria. Alongside this gentleman’s symptoms and age, this could well be an initial presentation of uncontrolled T1DM progressing into DKA. The absence of formal ketone readings and the lack of severe ketonuria (++ or more on dipstick) indicates he is not in DKA currently; however, he could easily progress into this and needs to be managed in a secondary care setting. Equally, the ketonuria could be explained by the gentleman’s lack of appetite.

Answer to Question 2

There are several key points in the blood tests that can be explored:

  • Hypernatremia + hypokalemia – when these are paired it almost always signifies an endocrine disturbance, usually an excess of aldosterone (Conn’s) or overproduction of corticosteroids which have mineralocorticoid action at high doses. Aldosterone acts to promote K+ excretion and sodium (+water) retention in the renal tubules, thus high plasma levels of corticosteroids/aldosterone leads to this clinical picture alongside hypertension
  • Increased cortisol + ACTH – this signifies that the increase in cortisol is being driven by something that is increasing ACTH, as if it was a primary disorder of cortisol production/exogenous steroid usage the ACTH would be suppressed due to negative feedback
  • Metabolic alkalosis – this is secondary to the hypokalemia, as K+ is excreted alongside protons in the renal tubules and as such hypokalemia usually results in metabolic alkalosis (some exceptions apply e.g. diarrhoea leads to potassium AND bicarbonate loss leading to an acidosis). There is some evidence of respiratory compensation, indicating this may be an acute on chronic picture, however it is not enough to compensate.
  • Hyperglycemia – this is now evident with a formal gas reading and the absence of significant ketoacidosis rules out DKA. The hyperglycemia can be explained by the increased cortisol, as this is known to stimulate glucose synthesis and production.

Answer to Question 3

With a raised ACTH induced Cushing’s syndrome, the most important next test is a paired low and high dexamethasone suppression test. The idea behind this is that in Cushing’s disease, usually caused by a pituitary adenoma, the cells retain some functional negative feedback and thus high doses of dexamethasone can ‘suppress’ the adenoma’s ACTH production and temporarily reduce the overall cortisol output of the adrenal glands. In contrast, ectopic ACTH producing cells e.g. small cell lung cancer/renal clear cell cancers do not have any negative feedback sensitivity and as such there is no change in cortisol levels with administration of high doses of dexamethasone.

Answer to Question 4

The CTCAP rules out an ectopic ACTH producing lung or renal cancer. The CT head is more interesting, as it shows a suprasellar mass near the optic chiasm. The pituitary gland sits in the sella turcica, and as such this would be in keeping with a pituitary mass, likely an ACTH producing pituitary adenoma. This may eventually lead to visual disturbance (bitemporal heminopias/quadrantinopias if the chiasm is involved).

The next step would be to assess the lesion in more detail with an MRI of the pituitary fossa, and to consider surgical management options including transsphenoidal hypophysectomies. The hypertension can be managed acutely with IV labetalol.

 

Dr Amol Joshi
University of Cambridge

About The Author

This clinical case is written by Dr Amol Joshi who has an interest in writing medical puzzles.

Disclaimer

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