USE OF HEMODIALYSIS FOR THE CORRECTION OF EXTREME METABOLIC ALKALOSIS

Introduction:

Metabolic alkalosis is a generalized acid-base disorder, especially in hospitalized patients. It is characterized by primary elevation of serum bicarbonate and arterial pH, together with a compensatory increase in PCO2 as a consequence of adaptive hypoventilation. The pathogenesis of metabolic alkalosis involves a loss of fixed acid or a net accumulation of bicarbonate in the extracellular fluid. Acid loss may occur through the gastrointestinal tract or the kidney, while sources of excess alkali may be oral or parenteral alkali intake. Severe metabolic alkalosis in critically ill patients (arterial blood pH of 7.55 or higher) is associated with a significantly increased mortality rate and cardiovascular events.

Methods:

Report of clinical case

Results:

A 77-year-old woman with a history of arterial hypertension with a clinical picture of progressive edema in the lower extremities for one month, with a weight gain of 20 kg. Laboratory tests revealed proteinuria of 23.8 g in 24 h, creatinine of 0.7 mg/dL, albumin of 2 g/dL. Given the condition compatible with nephrotic syndrome, a renal biopsy was performed without incident. While awaiting the biopsy result, home care with furosemide 40 mg every 12 hours and metolazone 2.5 mg every 12 hours was indicated. Seven days later, the patient consulted the emergency room for a condition characterized by weight loss of 10 kg, general malaise and impaired consciousness with drowsiness and lethargy. The emergency room evaluation revealed metabolic alkalosis (MA) with pH 7.84, Phosphorus 1,63 mg/dL and Potassium 1,9 mEq/L. It was decided to admit the patient to a monitored intensive care unit, intravenous potassium and phosphorus supplementation, and central venous catheter placement to perform intermittent hemodialysis (IHD). After a 4-hour IHD session, 0.9% saline solution and suspension of diuretics, the patient's progress was favorable with improvement of metabolic alkalosis within 24 hours of admission, clinically with gradual improvement of consciousness impairment. Subsequently, a renal biopsy result was obtained, which concluded minimal change disease. The study of paraneoplastic syndrome with CT of the chest, abdomen and pelvis concluded a 2.8 cm mediastinic mass, with a biopsy compatible with thymoma, and a thymectomy was performed. After 9 days from hospital admission, the patient was discharged, with improvement of the internal environment disorder and subsequently with improvement of the nephrotic syndrome.

Conclusions:

Management of severe MA begins with the etiological diagnosis of MA, continuing with the removal of the causative agent and the correction of the perpetuators of alkalosis (hyperaldosteronism, chloride deficiency, hypokalemia and decreased glomerular filtration rate). Generally, the first step will be volume supplementation with 0.9% NaCl solution. However, when alkalosis puts the patient's life at risk, as in our case, there are 2 alternatives for prompt correction; One is to add an acid to the internal medium to lower the pH; and the other option is the removal of excess bicarbonate through the use of renal replacement therapy.

I have no potential conflict of interest to disclose.

I did not use generative AI and AI-assisted technologies in the writing process.