CME INDIA Case Presentation by Dr Mritunjay Kumar Singh, Nephrologist, Physician, Gaya.
CME INDIA Case Study
ECG done in medical emergency is shown below:
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.
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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In Hypokalemic periodic paralysis we should always do thyroid profile to rule out thyrotoxicosis,because symptoms of thyrotoxicosis is subtle in thoes patients…I have came across one patient who have recurrent Hypokalemic paralysis when we did thyroid profile he came out to be a case of thyrotoxicosis,once he was put on antithyroid medication,he never had any episods of paralysis….