Therapeutic Plasma Exchange Complicated by Hyperchloremic Metabolic Acidosis in a Patient with Myasthenia Gravis and CKD

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

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Journal
Journal of the American Society of Nephrology
Published
2024-10-01
DOI
https://doi.org/10.1681/asn.202445hb562b
Primary Topic
Intensive Care Unit Cognitive Disorders
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article
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article

Therapeutic Plasma Exchange Complicated by Hyperchloremic Metabolic Acidosis in a Patient with Myasthenia Gravis and CKD

Hassan Mahmoud, Michael Gilleo
Journal of the American Society of Nephrology
Intensive Care Unit Cognitive Disorders
article

Therapeutic Plasma Exchange Complicated by Hyperchloremic Metabolic Acidosis in a Patient with Myasthenia Gravis and CKD

Hassan Mahmoud, Michael Gilleo
article en

Abstract

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

Journal of the American Society of NephrologyVol. 35(10S)
Maine Medical Center (US)
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Openalex Percentile: Top 76%
Intensive Care Unit Cognitive Disorders
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Therapeutic Plasma Exchange Complicated by Hyperchloremic Metabolic Acidosis in a Patient with Myasthenia Gravis and CKD — Hassan Mahmoud, Michael Gilleo · Journal of the American Society of Nephrology (2024) | TGRS Research Map | TGRS