Open Resources and Online MSc from the University of Edinburgh and RCPE

Hypomagnesaemia in a young man

April 15, 2012 — Eleri Williams

A 24 year old nursing student is admitted to hospital. He complains of muscle cramps that have been getting progressively worse since they started six weeks ago. He also complains of increasing weakness over the last few days. He is normally fit and well, and takes no regular medication, prescribed or otherwise. He is a non-smoker and drinks around 10 units of alcohol a week. He denies any illicit drug use.

He is seen on the medical assessment unit. Examination reveals global weakness. Pulse is 68 bpm, with a blood pressure of 115/70 mmHg.

 

Initial investigations reveal the following:

Na 138 mmol/L

K 2.3 mmol/L

Bicarbonate 34 mmol/L

Creatinine 80 micromol/L (0.9mg/dL)

Calcium 2.4mmol/L (9.6 mg/dL)

Phosphate 0.8 mmol/L (2.48 mg/dL)

He is treated with potassium and you see him on the ward round the following day. You suggest checking his magnesium level which is low at 0.4 mmol/L (0.9 mg/dL).

  • What is the differential diagnosis of hypomagnesaemia?
  • How will you proceed with your investigations in this man?

More information later in the week for our students.

Show the answer

Many thanks to our Programme Director, Professor Neil Turner for this case. We had an interesting discussion in the classroom.

We discussed the differential diagnosis of hypomagnesaemia, and stressed that it rarely occurs as an isolated biochemical abnormality. This patient’s urinary magnesium levels were measured, which confirmed ongoing renal losses in the face of hypomagnesaemia.

So, hypokalaemia, hypomagnesaemia, a modest alkalosis and a clinical picture of weakness and fatigue would all fit with Gitelman’s syndome. It is an autosomal recessive condition where there is a loss-of-function mutation in the sodium-chloride co-transporter (NCCT) of the distal convoluted tubule. This is where thiazide diuretics act, so it is no coincidence that over treatment with thiazides can lead to a similar picture. Several of you mentioned this, and it is important to remember especially given his occupation. Though you would perhaps see less marked hypomagnesaemia. The diagnosis of Gitelman’s would need to be confirmed with genetic testing.

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A fall

March 26, 2012 — Eleri Williams

A 72 year old woman is seen in the emergency department following a fall. She has lived alone since her husband died six months ago, and she is normally fit and well. She had been tending to her garden when she slipped. She sustained a pre-tibial laceration, requiring treatment with adhesive strips. She is about to be sent home with her daughter, when the results of some routine blood tests are noted. These reveal a Na of 125 mmol/L, K 4.9 mmol/L, urea 4.5 mmol/L and creatinine of 65 micromol/L. Full blood count is normal. Liver biochemistry is normal. She is referred to the medical admissions unit, where you see her.

  • How will you approach the investigation of this woman’s hyponatraemia?

Further clinical information in a couple of days for our students.

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A 54 year old hypertensive woman

February 19, 2012 — Eleri Williams

A 54 year old woman is found to be hypertensive following an annual work medical assessment. Her blood pressure is 170/95mmHg. She was not hypertensive when reviewed the previous year. She is otherwise fit and well, and practices yoga regularly. She has never smoked and drinks only occasional alcohol. She takes no prescribed medication, and denies any over the counter medication use.

 

As part of the assessment she has some further tests, the results of which are as follows:

Na 140mmol/L

K 2.7mmol/L

Urea 4.1mmol/L

Creatinine 63μmol/L (0.7mg/dL)

Calcium (corrected) 2.4mmol/L (9.6mg/dL)

Liver function tests normal

Thyroid function tests normal

An ECG demonstrates prominent U waves.

  • What is the differential diagnosis of her hypokalaemia?
  • How would you like to further investigate this woman to establish the cause of her hypertension and hypokalaemia?

MSc students have a think about what you would do and put your thoughts up in the discussion board.

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A confused 83 year old woman

October 2, 2011 — Eleri Williams

An 83 year old woman presents to the medical assessment unit, having been found in a confused state by a neighbour. She lives alone, and is normally independent. The neighbour had last seen her tending to her garden 5 days previously, when she had been well.

No history is available from the patient. A recent prescription from her GP is found in her handbag, which shows that she is on regular aspirin 75mg daily, bendroflumethiazide 2.5mg daily and furosemide 40mg daily.

Initial examination reveals her to be afebrile. She is dehydrated with a BP of 110/65. Respiratory and GI examinations are normal. She is confused and disorientated, but otherwise neurological examination is normal.

You receive a call from the biochemistry lab an hour later with the following blood results:

 

  • Na 137 mmol/L
  • K 4.6 mmol/L
  • Creatinine 291 μmol/L (3.3 mg/dL)
  • Ca (corrected) 3.3 mmol/L (13.3 mg/dL)
  • Bicarbonate 34 mmol/L

The patient has one other biochemistry result on the hospital computer system from 6 months previously: all investigations were normal at this time.

  • What is your immediate management plan?
  • What is the differential diagnosis, and how would you proceed with your investigations?

MSc students, please add your comments to the class discussion board.

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A 22 year old woman with hyperkalaemia

September 25, 2011 — Neil Turner

A 22 year old woman presents with severe nausea and vomiting.  She denies any obvious cause or previous illness and has no other symptoms.

She is alert and responsive but vomits repeatedly.  She is well-perfused with blood pressure 135/75, but an irregular pulse at 90/min.  Temperature is 36.8C, respiratory rate 15/minute and oxygen saturation 97%.  Examination of skin, cardiovascular and respiratory systems and the abdomen are normal.

ECG strips taken (1) on admission (2) at 3h and (3) at 12h are shown.  Click on the image to enlarge.

She has a normal blood count but serum K is 7.4 mmol/l.  Other results show Na 135 mmol/l, Urea 2.5, HCO3 27, Creatinine 45 micromol/l (0.5 mg/dl).

The admitting physicians administer insulin and dextrose.  Subsequently the patient becomes bradycardic and atropine is administered.

  • Have the attending doctors taken all the right immediate steps so far?
  • What are the major possibilities to explain this presentation?
  • Are there any additional tests that might be useful?
  • Is there any specific additional therapy to recommend?

Think carefully about your answers before clicking below for more info …

A bit more info?

Follow-up info: Potassium improved quite quickly so that by the time of the 2nd ECG strip K was 6; and by the third, 4.4.

Further background: she attended hospital alone.  The patient is an overseas student from Taiwan in her third year of study in the UK. She is living in a shared house with other third year students.

Does this influence your thinking?

Think hard again before clicking through to find out what happened …

Show the answer?

Our students discussion was fascinating and in over 70 posts covered all aspects of hyperkalaemia.  Not much support for the periodic paralyses – she wasn’t paralysed.  Her glucose was indeed normal.  No renal failure.  Normal blood pressure against Addison’s.  All these are important points.  Many reached the correct conclusion:

The triad of vomiting, hyperkalaemia and heart block strongly suggests cardiac glycoside toxicity.  This was later confirmed by serum digoxin level.

The absence of classic features of hyperkalaemia on the ECG is repeatedly mentioned in the literature, but apparently not much in the textbooks. The AV nodal blockade may be followed by ventricular arrhythmias, as it was in her (not shown – in fact these ECG strips are from a relevant case with permission). She was therefore given anti-digoxin Fab fragments and recovered quite quickly.

The patient did not have any obvious access to digoxin, so how was she poisoned? Her flatmates reported that she had brought back traditional Chinese medicines, and these seemed to have been used – but they had disposed of them as they feared that she or they would get into trouble. She never admitted to taking them or explained why but was not thought to have had suicidal intent.

There are several reports in the literature of both deliberate ingestion of toads, usually with therapeutic intent, and toxicity from Chinese medicines containing toad venom. An identical syndrome is caused by taking the seeds (or other parts, but usually seeds) of yellow oleander. This is a common mode of attempted suicide in Sri Lanka but is prevalent elsewhere too.

Traditional teaching is that you should not give calcium in digoxin toxicity. One of the admitting doctors made the diagnosis quickly and this is why no calcium was given.  Although clinical studies have failed to prove negative consequences from calcium administration, many recommendations avoid it, and suggest focusing on Mg instead.

So the full answer is toad poisoning – but as this is the same as cardiac glycoside toxicity in every respect, you are right if you chose that!

So my additional tests were Mg, and digoxin level

Additional therapy: if Fab frags affordable where you are, give them if the cardiac and clinical picture are poor. Otherwise, ventricular pacing for bradycardia is recommended and could reduce risk of lethal ventricular arrhythmia which is the main killer.

Anything else?  Activated charcoal is a universal recommendation if ingestion was recent.  In poisoning associated with vomiting, the use of activated charcoal has been described as ‘decorative’, but the possibility of reducing absorption without any known risks must be worthwhile.  As cardiac glycosides undergo some entero-hepatic recirculation, you might expect repeated doses to increase excretion.  A trial in yellow oleander poisoning in Sri Lanka did find this, but a later larger study didn’t confirm it.

Thanks to Oxford University Press for permission to use images from Cheng et al (2006), Nephrol Dial Transplant 21:3320-3.

 

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