CME INDIA Case Presentation by Dr Varun Kumar, DM Card., Orchid Medical Centre, Ranchi.

CME INDIA Case Study:

(Inputs from CSI-Jharkhand)

Dr Varun Kumar, DM Card., Ranchi: 51 yr. old male presented with acute onset flaccid quadriparesis… he is a known hypertensive & on Olmesartan 40 mg & amlodipine 5 mg….admitted under neurologist & referred to me just for hypertension. What is the diagnosis?

CME INDIA Discussion:

Dr Arun Sarkar, Ranchi: Hypokalemic Periodic Palsy.

Dr Rajkumar, Ranchi: Same here. See his serum potassium level and if it reverts with potassium replacement, it will stamp the diagnosis. Also, see thyroid function, as close association with hyperthyroidism.

Dr Varun Kumar, DM Card., Ranchi: In ECG, there is QT prolongation with QTc of 662 ms with merger of T & U waves, suggestive of hypokalaemia. T3, T4, TSH-Normal.

Dr Molio, Margaon, Goa: Prolonged QTU interval, ST depression. T and U wave fusion suggestive of hypokalaemia

Dr Gita Arora, MD Medicine, Bharatpur, Rajasthan: Cause of hypokalaemia in this case?

Dr Prashant Waichal Akola Mahar: Symptomatic treatment. Rule out other infections.

Dr V P Youmash, Assistant Professor, KAPV Medical College, Trichy: 75/min, sinus rhythm, normal axis, PR interval high normal 0.20 secs, diffuse ST sagging, prominent U waves, U wave getting over P wave. ECG wise definite hypokalaemia. With the clinical presentation of SHT/acute onset flaccid quadriparesis, the diagnosis is HYPOKALEMIC PARALYSIS, cause for hypokalaemia has to be evaluated.

1. History of any preceding fever, diarrhoea, vomiting prior to limb weakness.
2. Any previous history of similar episodes in past -especially if onset of first episode before 25 yrs., possible HPP due to calcium channel mutation, HPP is diagnosis of exclusion.
3. Drug history of salbutamol inhalers, loop diuretics, etc which cause hypokalaemia.
4. Renal/adrenal causes, syndromes like bartter, liddle, gitelman, Sjogren’s have to be ruled out.
5. Patient needs basic RFT, Serum electrolytes-sodium, potassium, ca, Mg, urine potassium, ABG.

I have also many a times misdiagnosed as hypokalaemia periodic paralysis in cases of hypokalaemia paralysis. But all hypokalaemia paralysis needs detailed evaluation and the cause has to be found out which might have specific treatment other than potassium correction, and it may also prevent further episodes. Hypokalaemia periodic paralysis is always a diagnosis of exclusion of all other causes.

Dr Premchand Singh, Imphal: RTA with hypokalaemia should also come for D/D.

Dr Vivek Gupta, Surat: Prolonged qt interval with st t changes. Yes. Hypokalemia.

Dr Harishkesh, Ranchi: Hypokalaemia palsy. What probably is being read as T Wave …. Is actually the prominent U wave which is a common accompaniment of Severe hypokalaemia. And hence grossly exaggerated QTc. Workup should include looking for probable type 1 RTA.

Dr Sunendra Kumar, DM Neuro, Ranchi: First do ABG. Many questions will be answered.

Dr Varun Kumar, DM Card., Ranchi: This is the ABG of the patient.

This is his blood levels of different hormones which are in normal range except low ACTH.

Dr Arun Sarkar, Ranchi: Actually, I have suspension of secondary HTN due to Adrenal adenoma. This type of patient’s presents with hypokalaemia & hypertension. CT abdomen can to prove it. Sample collection from suprarenal veins a difficult task, needs expert hands in super speciality centres.

Dr Varun Kumar, DM Card., Ranchi: Not always a sampling from suprarenal veins is needed…. we can take a sample of blood at 8 am & send for testing for Renin, Aldosterone & ARR…. if not non-confirmatory then we can do Captopril challenge test, saline stimulation test, or suprarenal vein sampling. I was highly suspicious for Conn’s syndrome in this patient so ordered for CT abdomen & it revealed adrenal adenoma.

Dr Varun Kumar, DM Card., Ranchi: I started Spironolactone & tapered off Olmesartan & amlodipine. At the time of discharge patient has BP of 110/70 without any other antihypertensive & normal K+. I advised him for surgical removal of adenoma.

Dr Arun Sarkar, Ranchi: Potassium is in an intracellular domain. Only less than 2% of total potassium is extracellular. So, it is really difficult to get an idea of deficiency of total potassium pull in the body, especially intracellular depot. We can’t check it practically.  But ECG can But ECG can reflect trans- membrane gradient of K+. And some idea of intracellular K+ depletion. Secondary HTN with similar ECG and even with sustained mild hypokalaemia should be suspicious of chronic Adrenaline pouring. This is the catch point.

CME INDIA Take Home Message:

(by Dr Varun Kumar, DM, Card.)

• The main catch in the case was from ABG, where you could see metabolic alkalosis, severe hypokalaemia & hypernatremia.
• This was one of the very rare presentation of Conn’s syndrome.
• Patient has secondary hypokalaemia periodic paralysis which recovered after correction of K+.
• We must be aware of the differential diagnosis of any disease; this patient’s adrenal adenoma might have gone undetected if we were not correlated his full medical profile.
• Periodic paralysis presents in young age & presentation after 50 yrs. of age suggested we must look for secondary causes.

CME INDIA Learning Points:

• Do consider possibility of primary aldosteronism if you get patients with spontaneous or unprovoked hypokalaemia, especially if the patient is also hypertensive.
• Primary aldosteronism now is considered one of the more common causes of secondary hypertension 
• Aldosterone, by inducing renal reabsorption of sodium at the distal convoluted tubule, enhances secretion of potassium and hydrogen ions, causing hypernatremia, hypokalaemia, and alkalosis.
• Metabolic alkalosis is diagnosed by measuring serum electrolytes and arterial blood gases. If the etiology of metabolic alkalosis is not clear from the clinical history and physical examination, including drug use and the presence of hypertension, then a urine chloride ion concentration can be obtained.
• Calculation of the serum anion gap may also help to differentiate between primary metabolic alkalosis and metabolic compensation for respiratory acidosis.
• Recognizing such condition is critical because primary aldosteronism–associated HTN can often be cured (or at least optimally controlled) with the proper surgical or medical intervention.
• The diagnosis is generally 3-tiered, involving an initial screening, a confirmation of the diagnosis, and a determination of the specific subtype of primary aldosteronism.
• Prevalence of aldosteronism due to bilateral idiopathic adrenal hyperplasia (IAH; sometimes also abbreviated as BAH) is higher than had previously been believed.
• Clinically, the distinction between the 2 major causes of primary aldosteronism is vital because the treatment of choice for each is markedly different.
• While the treatment of choice for aldosteronomas is surgical extirpation, the treatment of choice for IAH is medical therapy with aldosterone antagonists. (Inputs: Medscape).

CME INDIA Tail Piece:

• Dr Conn initially described Primary hyperaldosteronism.
• It is due to excessive secretion of aldosterone by the zona glomerulosa of the adrenal gland. Excess of aldosterone binding to its receptor in the principal cells will increase the expression of ENaC and potassium channels on the luminal side of those cells.
• It will dramatically increase sodium absorption and potassium excretion in the tubule.
• The excess of sodium absorption will leave a negatively charged lumen.
• This will augment potassium trapping in the lumen as well as protons leading to hypokalaemia and metabolic alkalosis.

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