Kidney Week

Abstract: PO1497

A Case of Extreme Alkalosis: A Perfect Combination of Perpetuators

Session Information

• Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
  October 22, 2020 | Location: On-Demand
  Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

• 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

• Valerio, Patrícia, Centro Hospitalar de Setubal EPE, Setubal, Setúbal, Portugal

Patrícia Valerio,

• Ferreira, Hugo, Instituto Portugues de Oncologia do Porto Francisco Gentil EPE, Porto, Porto, Portugal

Hugo Ferreira,

• Chuva, Teresa, Instituto Portugues de Oncologia do Porto Francisco Gentil EPE, Porto, Porto, Portugal

Teresa Chuva,

• Paiva, Ana Maria, Instituto Portugues de Oncologia do Porto Francisco Gentil EPE, Porto, Porto, Portugal

Ana Maria Paiva,

• Neves, Inês, Instituto Portugues de Oncologia do Porto Francisco Gentil EPE, Porto, Porto, Portugal

Inês Neves,

• Faria, Filomena, Instituto Portugues de Oncologia do Porto Francisco Gentil EPE, Porto, Porto, Portugal

Filomena Faria,

• Costa, José Maximino, Instituto Portugues de Oncologia do Porto Francisco Gentil EPE, Porto, Porto, Portugal

José Maximino Costa,

Introduction

Metabolic alkalosis results from retention of alkali excess. Normally, a physiological response leads to hypoventilation with a secondary increase of PaCO₂. The most common cause is H⁺ loss, through kidney or gastrointestinal tract, usually with concurrent loss of Cl^- and K⁺.

Case Description

70 y/o caucasian man was admitted for a scheduled surgery due to a stage II urothelial carcinoma. The immediate postoperative period occurred without complications. The patient presented with abdominal distention and gastric stasis. He remained fasting, with gastric tube draining freely. Surgical team performed an exploratory laparotomy with correction of a small bowl internal hernia. In the postoperative period Nephrology collaboration was requested due to acute kidney injury (AKI), with a creatinine (Cr) of 3,39 mg/dL (baseline 1,5 mg/dL) and urea 89,5 mg/dL.
On examination the patient was prostrate, severely dehydrated and bradypneic, with oxygen supply FiO₂ 28%. He maintained gastric passive drainage for 3 days, around 3 to 3,5 L/day. Blood work showed Cr 4,15 mg/dL, urea 103,9 mg/dL, hypernatremia 147 mEq/L, hypochloremia 78 mEq/L, hypokalemia 3,2 mEq/L, uric acid 16,8 mg/dL, albumin 3,2 g/dL and a total corrected calcium 9,5 mg/dL. Urinalysis revealed a pH of 9,0 and arterial blood gas analysis presented severe metabolic alkalosis (pH 7,63, PaO₂ 90 mm Hg, PaCO₂ 99 mm Hg, bicarbonate 104,1 mmol/L), low ionized calcium 0,86 mmol/L and lactate 1,9 mg/dL.
The patient was immediately admitted in ICU, starting aggressive IV hydration with NaCl 0,9%, IV potassium supplementation and parenteral nutrition.

Discussion

This is an extreme case of metabolic alkalosis where a myriad of contributors gathered in a perfect storm to achieve a bicarbonate concentration above 100 mmol/L, thought to be incompatible with life and, to our knowledge, never reported in the literature. However, the pH value was maintained in life-compatible values by an extreme respiratory compensation which may have saved the patient before treatment initiation.
An approach correcting the cause and, at the same time, the perpetuators are the key factors to successfully treat a metabolic alkalosis. Due to severe AKI and alkalosis, dialysis with low bicarbonate dialysate may be indicated.