Abstract: SA-PO514
Therapeutic Plasma Exchange Complicated by Hyperchloremic Metabolic Acidosis in a Patient with Myasthenia Gravis and CKD
Session Information
- Acid-Base, Calcium, Potassium, and Magnesium Disorders: Clinical
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Gilleo, Michael, Maine Medical Center, Portland, Maine, United States
- Mahmoud, Hassan, Maine Medical Center, Portland, Maine, United States
Introduction
Therapeutic plasma exchange (TPE) is commonly associated with metabolic derangements such as hypocalcemia and hypomagnesemia. Hyperchloremic metabolic acidosis is a rare complication previously reported in patients undergoing multiple days of consecutive TPE. We present a case of hyperchloremic acidosis in a patient with baseline renal dysfunction undergoing TPE every other day.
Case Description
An 88 year old with CKD 3B was admitted for acute myasthenia gravis with respiratory failure, a category I indication for plasma exchange. They underwent TPE treatment on two consecutive days, followed by another three treatments each separated by 48 hours. Plasma was replaced at 105% fluid balance with 50 g/L albumin in saline solution (3-4L per treatment). Citrate anticoagulation was used for the apheresis circuit.
The patient developed hyperchloremic acidosis following initial TPE treatment (Figure 1). The anion gap was normal. The acidosis persisted throughout the duration of TPE therapy and corrected two days after therapy completion.
Discussion
This case highlights the rare complication of hyperchloremic acidosis during TPE. The acidosis was likely caused by replacement of plasma with large volumes of chloride-containing fluids, with underlying renal dysfunction impairing excretion of excess chloride. Chloride concentrations of 109-145 mmol/L have been reported in albumin solutions, but this measurement was not made for the albumin used in this patient. Citrate toxicity was not a factor, as hepatic function and total-to-ionized calcium ratio were normal.
Hyperchloremic acidosis may result in reduced renal perfusion, increased ventilatory needs, and symptoms such as nausea, vomiting, or myalgias. Providers must be aware of this risk associated with TPE, even when treatment frequency is reduced to every 48 hours. Early recognition may allow for treatment of the acidosis, or changes to replacement fluids used during plasma exchange.
Figure 1: Serum chloride and bicarbonate throughout TPE treatment