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Table of Contents
CASE REPORT
Year : 2020  |  Volume : 17  |  Issue : 2  |  Page : 108-110

Refractory hypokalemia – An exigent concern: Case series and review of literature


Department of Critical Care Medicine, Apollo Hospitals, Navi Mumbai, Maharashtra, India

Date of Submission15-Mar-2020
Date of Acceptance25-Apr-2020
Date of Web Publication18-Jun-2020

Correspondence Address:
Gunadhar Padhi
Flat No. D 1703, Sai Mannat CHS Plot No. A B1 B6 Sector 34, Kharghar, Navi Mumbai - 410 210, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/am.am_14_20

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  Abstract 


Potassium is a major intracellular cation affecting tonicity and regulating intracellular processes such as protein/glycogen synthesis and carbohydrate metabolism and partially responsible for maintaining the potential difference across the membrane, particularly in excitable tissues such as nerve and muscle. Of all the electrolytes, a rapid change in potassium concentration is life-threatening. Hypokalemia is a common electrolyte disturbance, especially in hospitalized patients. Severe hypokalemia is life-threatening and requires urgent medical attention. It may trigger dangerous arrhythmias such as ventricular fibrillation and tachycardia, leading to cardiac arrest. It leads to neuromuscular weakness prolonging weaning in mechanically ventilated patients and also contributes to paralytic ileus. The body maintains serum potassium concentration within very narrow limits through tightly regulated feedback and feedforward systems. Understanding the physiology of potassium homeostasis and diverse etiologies of hypokalemia spanning from error in sample collection, endocrine abnormalities, renal tubular acidosis, and many more may guide toward the appropriate treatment of hypokalemia.

Keywords: Electrolytes, hypokalemia, potassium


How to cite this article:
Padhi G, Chandsha MA. Refractory hypokalemia – An exigent concern: Case series and review of literature. Apollo Med 2020;17:108-10

How to cite this URL:
Padhi G, Chandsha MA. Refractory hypokalemia – An exigent concern: Case series and review of literature. Apollo Med [serial online] 2020 [cited 2020 Jul 8];17:108-10. Available from: http://www.apollomedicine.org/text.asp?2020/17/2/108/287078




  Introduction Top


Patients with hypokalemia are frequently encountered, and its refractoriness to regular supplementation is exasperating. Potassium is a major intracellular cation, and the body maintains its concentration within very narrow limits. Potassium is partially responsible for maintaining the potential difference across the membrane, particularly in excitable tissues such as nerve and muscle, and it catalyzes enzyme activities, as well as cell division and growth, and participates in acid–base regulation.

Hypokalemia reflects either total body potassium depletion or redistribution from extracellular to intracellular fluid. Discerning the underlying physiologic mechanisms of hypokalemia and stepwise approach is important to establish a diagnosis as well as to make appropriate therapeutic decisions.


  Case Reports Top


Case 1

A 55-year-old female, known hypertensive, presented with complaints of breathlessness, sweating, and giddiness. Heart rate was 120/min and blood pressure (BP) – 180/90 mmHg. Initial laboratory values are as follows: white blood cell (WBC) – 12,600, platelets – 185,000, Rutherford backscattering spectroscopy (RBS) – 575 mg, Na + –128 meq/L, K + – 2.6 meq/L, urea –5 mg/dl, creatinine – 0.4, arterial blood gas (ABG) K + –4.3 meq/L, and repeat K + –2.8 meq/L.

Case 2

A 43-year-old male, hypertensive, presented with complaints of repeated episodes of lethargy and sweating. On examination, he is tachycardic with mild breathlessness. ABG pH was 7.56, PCO2–43 mmHg, PO2–213 mmHg, HCO3–28 meq/L, Na –134 meq/L, K + –3.2 meq/L, urine output –1.5 L/day, urinary potassium –20 meq/L, correction started, repeated samples of potassium came low.

Case 3

A 57-year-old male, diabetic, chronic alcoholic, presented with complaints of generalized weakness. Persistent serum K + was <4 meq/L. He was hemodynamically stable.

Case 4

A 34-year-old male presented with complaints of generalized weakness, occasional pain abdomen, and easy fatigability. He was hemodynamically stable. RBS was 160 mg, ABG pH –7.32, PCO2–32 mmHg, HCO3–17 meq/L, Na + –143 meq/L, K + –2.9 meq/L, and urinary potassium –34 meq/L.

Case 5

A 44–year-old male, postoperative day 5, ileal resection and anastomosis done for perforation. He was hemodynamically stable. He was started on nasogastric feed. Laboratory investigations showed Hb of 9.8, WBC –10,500, creatinine – 1.1, blood urea nitrogen – 26 mg/dl, Na + –135 meq/L, K + – 2.8 meq/L (repeated samples – low), and PO4–1.8 meq/L.


  Discussion Top


Case 1

Drip arm sample can lead to spuriously low potassium. Here, potassium levels in the ABG sample are normal compared to venous sample, which are persistently low due to dilution by the drip. A 3-min interval is recommended when drawing blood proximal to a shut-off infusion. Longer intervals may be advisable for analytes present in the infused substance.[1]

Case 2

Mineralocorticoid excess is characterized by hypertension, hypokalemia, low renin, and hypoaldosteronism. It results due to deficiency of 11β-hydroxysteroid dehydrogenase. The hormonal diagnosis of the disorder is made by the increased ratio of urine-free cortisol to cortisone. Addition of spironolactone results in a decrease in BP, a rise in serum potassium, and a gradual increase in plasma renin activity.[2] Bartter syndrome is a rare inherited disease characterized by a defect in the thick ascending limb of the loop of Henle autosomal recessive renal tubular disorders characterized by hypokalemia, hypochloremia, metabolic alkalosis, and hyperreninemia with normal BP.[3]

Case 3

Refractory hypokalemia associated with hypomagnesemia and intravenous magnesium therapy reverses the hypokalemia. Magnesium deficiency impairs Na-K-ATPase, which would decrease cellular uptake of K +. A decrease in cellular uptake of K +, if it occurs along with increased urinary or gastrointestinal excretion, would lead to K + wasting and hypokalemia. Little K + is excreted by the gastrointestinal tract normally; therefore, hypokalemia in magnesium deficiency is likely associated with enhanced renal K + excretion. Hypomagnesemia may coexist with hypokalemia, hypocalcemia, and hypophosphatemia.[4] Persons with chronic alcohol use disorder are prone to a variety of acid–base disturbances and some with mixed disturbances. Hypomagnesemia occurs in almost one-third of patients with chronic alcohol use disorder.[5]

Case 4

Renal tubular acidosis (RTA) Type 1 and 2 is characterized by hypokalemia and metabolic acidosis. Distal RTA, also known as Type 1 RTA or classic RTA, is a complex entity characterized by an inability to acidify the urine, a process that occurs in the distal parts of the nephron, including the connecting tubule and the collecting duct. It can lead to marked acidbase abnormalities, including hyperchloremic metabolic acidosis and severe hypokalemia. The pathogenesis of renal potassium wasting and hypokalemia in classic RTA remains uncertain. The prevailing theory is that K +-Na + exchange is stimulated due to an inability of the distal tubule to establish a normal steep lumen-peritubular H + gradient. According to this hypothesis, the gradient restriction of renal proton secretion reduces the rate of H +-Na + exchange; K +-Na + exchange increases reciprocally, and urinary loss of sodium results in sodium depletion and secondary hypoaldosteronism. This hypothesis is based on the observation that correction of acidosis with alkali therapy can lead to decrease in urinary excretion of potassium concomitant with correction of hypokalemia.[6]

In RTA Type 2 (proximal RTA), there are hypokalemia and increased urinary potassium wasting due to an increased rate of urine flow to the distal nephron due to distal delivery of bicarbonate ions and also activation of the renin–angiotensin–aldosterone system from the mild hypovolemia induced by bicarbonate loss in urine, leading to increased collecting duct sodium reabsorption and potassium excretion. Administration of alkali in these patients increases bicarbonate wasting in urine and can worsen hypokalemia unless potassium is replaced simultaneously.

Case 5

Refeeding syndrome can be defined as the potentially fatal shifts in fluids and electrolytes that may occur in malnourished patients receiving artificial refeeding (whether enterally or parenterally).[7] The hallmark biochemical feature of refeeding syndrome is hypophosphatemia. However, the syndrome is complex and may also feature abnormal sodium and fluid balance; changes in glucose, protein, and fat metabolism; thiamine deficiency; hypokalemia; and hypomagnesemia.[8]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
van Vonderen MG, Voerman BJ, Hensgens BE. Effect of intravenous infusions on laboratory results in blood specimens drawn proximal to the insertion site of an intravenous canula. Neth J Med 1998;53:224-7.  Back to cited text no. 1
    
2.
Al-Harbi T, Al-Shaikh A. Apparent mineralocorticoid excess syndrome: Report of one family with three affected children. J Pediatr Endocrinol Metab 2012;25:1083-8.  Back to cited text no. 2
    
3.
Prakash L, Shyam M, Meena MS. Classical Bartter syndrome – A case report. Indian J Med Spec 2015;6:116-8.  Back to cited text no. 3
    
4.
Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol 2007;18:2649-52.  Back to cited text no. 4
    
5.
Elisaf M, Bairaktari EK, Siamopoulos KC. Hypomagnesemia in alcoholic patients. Alcohol Clin Exp Res 1998;22:134.  Back to cited text no. 5
    
6.
Muto S, Asano Y, Okazaki H, Kano S. Renal potassium wasting in distal renal tubular acidosis: Role of aldosterone. Intern Med 1992;31:1047-51.  Back to cited text no. 6
    
7.
Solomon SM. The refeeding syndrome: A review. JPEN J Parenter Enter Nutr 1990;14:90-7.  Back to cited text no. 7
    
8.
Crook MA, Hally V, Panteli JV. The importance of the refeeding syndrome. Nutrition 2001;17:632-7.  Back to cited text no. 8
    




 

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