CME INDIA Case Presentation by Dr Mritunjay Kumar Singh, Nephrologist, Physician, Gaya.

CME INDIA Case Study

ECG done in medical emergency is shown below:

Quadriparesis case ECG

CME INDIA Discussion:

Dr Bipin Sinha, DM, Card, Delhi: Hypokalaemia, QU waves with QU prolongation in V4 clearly Small T wave on the ascending limb of SU segment.

Dr Sangita Kamath, TMH, Jamshedpur:

  • Suggestive of severe hypokalaemia.
  • Also, check for serum magnesium levels.
  • It is hypokalaemia quadriparesis.
  • To be rxed with IV K & Mg.
  • Cause of hypokalaemia to be evaluated.

Dr Bhanu Pratap Singh, Physician, Siwan, Bihar: Apart from serum k, serum calcium and thyroid function to be assessed. Low T prominent u with QT prolongation without even slight ST depression needs hypocalcaemia to r/o apart from hypokalaemia.

Dr V P Youmash, Assistant Professor, KAPV Medical College, Trichy:

  • 50/min, sinus rhythm, normal axis, PR interval borderline 0.20 sec, T wave almost flattened, prominent U waves, so its QU interval interpreted as prolonged QTc…possibly it’s hypokalaemia paralysis.
  • Any previous similar episodes point to the possibility of hypokalaemia periodic paralysis.
  • Patient needs urgent serum electrolytes-Na, K, Ca, Mg, thyroid function tests, urine potassium-ABG.
  • Patient needs potassium supplementation in the form of oral or iv potassium depending on hemodynamic status and paralytic ileus.
  • Every alternative beat is not arising from SA node, Bradycardia + Prominent U wave + PR interval 0.20 sec. As suggested electrolyte abnormalities, to be ruled out Thyroid assessment to be done.

 Dr D P Khaitan, Consultant Physician, Gaya: The findings to me on this ECG:

  • Heart rate =50 /mt, with regular sinus rhythm = Sinus Bradycardia
  • A slight prolongation of P R interval / border line= 0.20-0.22″= mild 1st degree AV block
  • QU interval prolongation with a tendency to merge with T wave with somewhat flattened T over frontal and anterolateral leads
  • Remarkable point is-the terminal s over the frontal leads and anterolateral leads is somewhat widened with r’ in V1 as well. This might indicate some delay over the RBBB

Conclusion:

These findings are highly suggestive of Hypokalaemia. By seeing so young age of the patient with the history of LMN type of Quadriparesis and other vitals within normal, I would say this quadriparesis is possibly due to Hypokalaemia.

Hypokalaemia periodic paralysis should be excluded by the family history – because this might be an autosomal dominant in nature. A rare disorder mainly observed in younger generation.

This might also be due to associated thyrotoxicosis as hypokalaemia periodic paralysis. I would like to have his thyroid profile as well to exclude this condition. – an interesting case.

Dr Raju Sharma, Physician, Jamshedpur: Do you need to wait for Magnesium levels before correction?

Dr Mritunjay Kumar Singh, Gaya: Yes, hypomagnesemia can lead to hypokalaemia which is refractory to treatment. Serum potassium was 1.7mg/dl He came to my OPD.  He showed signs of improvement after IV potassium in day care. I have advised him to go for serum magnesium and thyroid profile but not done so far.

Quadriparesis case report

Dr S K Goenka, Begusarai: Excessive glucose can also aggravate hypokalaemia.

Dr Mritunjay, Gaya: Yes, but he is normoglycemic and it happens early morning before he consumed any carbohydrate rich meal.

CME INDIA Leaning Points:

  • The ECG can also provide early indication of a low potassium level.
  • Hypokalaemia is defined as a potassium level less than 3.5
  • ECG changes generally do not occur until the level goes below 2.7.
  • Low potassium levels can cause myocardial arrhythmias and significant ectopy.
  • ECG changes can include increased amplitude and width of P wave, T wave flattening and inversion, prominent U waves and apparent long QT intervals due to merging of the T and U wave. The U-wave is a deflection following the T wave. Hypokalaemia causes enlarged and prominent T waves on the ECG.
  • Potassium levels that are critically low (<1.7) can lead to torsade’s de pointes.
  • Hypokalaemia can occur secondary to medications (common culprits include hydrochlorothiazide and furosemide), gastrointestinal loss, overzealous treatment for hyperkalaemia or shifting of potassium into the cell.
  • Hypomagnesemia is often times associated with hypokalaemia; thus, it is important to check a magnesium level in any patient who presents with arrhythmia.
  • Severe hypokalaemia with EKG changes should be treated emergently with repletion with intravenous potassium chloride to a K of 4-4.5.
  • The magnesium level should be repleted as well to a level greater than 2.
  • Hypokalaemia paralysis is an important and reversible cause of acute flaccid paralysis.
  • Periodic paralysis was the most common form of hypokalaemia paralysis in some study.
  • dRTA may be the most common secondary cause of hypokalaemia paralysis followed by Gitelman syndrome.
  • Patients with non-periodic paralysis present with more urinary potassium loss, a higher potassium requirement, and longer recovery time. (http://www.indianjnephrol.org/text.asp?2018/28/5/365/236563)


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