Introduction: We present a case where there was a delay in the diagnosis of severe metabolic acidosis in a patient with an orthotopic neobladder. There are a growing number of patients with orthotopic neobladders and a wider range of clinicians are encountering these patients. A delay in the diagnosis can lead to significant morbidity but if identified early it can be easily treated.
Presentation Of Case: A 59-year old patient with a recent neobladder augmentation cystoplasty was admitted under the medical team with a metabolic acidosis which was incorrectly presumed to be secondary to urosepsis. His condition rapidly deteriorated until a surgical review identified hyperchloremic metabolic acidosis secondary to neobladder augmentation. The patient required admission to the intensive care unit where he was treated with intravenous alkalising therapy which produced rapid metabolic improvement. Following a full recovery, he underwent neo-bladder excision and ileal conduit formation.
Discussion: Hyperchloraemic metabolic acidosis develops due to the bowel segment absorbing urinary constituents including ammonium, hydrogen ions and chloride in exchange for sodium and bicarbonate. It can be diagnosed by careful interpretation of the arterial blood gas and calculation of the anion gap. This hyperchloraemic metabolic acidosis can be corrected with alkalizing agents combined with catheterisation.
Conclusion: Hyperchloremic metabolic acidosis is a well-established complication of urinary diversion. Patient with orthotopic neobladder with high residual urine and large capacity are at even higher risk of metabolic acidosis. This information should be clearly documented in the post-operative discharge documentation to ensure early recognition by non-specialists.
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http://dx.doi.org/10.1016/j.ijscr.2015.03.039 | DOI Listing |
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Department of Adult Critical Care, Guy's and St Thomas' NHS Foundation Trust, King's Health Partners, London SE1 9RT, UK.
Extracorporeal carbon dioxide removal (ECCOR) is an emerging technique designed to reduce carbon dioxide (CO) levels in venous blood while enabling lung-protective ventilation or alleviating the work of breathing. Unlike high-flow extracorporeal membrane oxygenation (ECMO), ECCOR operates at lower blood flows (0.4-1.
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Division of Endocrinology & Metabolism, McGill University Health Centre, Montréal, Quebec, Canada.
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Center for Outcomess Research and Department of Anesthesiology, UTHealth, Houston, TX, United States of America. Electronic address:
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