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Skin Necrosis: An Unusual Complication of Hyperphosphatemia During Total Parenteral Nutrition Therapy
Author(s) -
Janigan David T.,
Perey Bernard,
Marrie Thomas J.,
Chiasson Patrick M.,
Hirsch David
Publication year - 1997
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/014860719702100150
Subject(s) - hyperphosphatemia , parenteral nutrition , complication , medicine , necrosis , intensive care medicine , culprit , surgery , kidney disease , myocardial infarction
Background:. Hyperphosphatemia complicated by calcification of subcutaneous arteries and skin infarcts are very rarely reported in the absence of chronic renal failure (CRF). We describe identical lesions in an obese woman with sepsis. Hyperphosphatemia resulted from an unintended excess of phosphate in her total parenteral nutrition (TPN) formulations. She did not have CRF or hyperparathyroidism. Methods: The patient's records during 37 weeks of hospitalization 12 years ago and, subsequently, her outpatient records were reviewed. Results: During a 7‐week period, the total elemental phosphorus infused daily, as divalent phosphate, ranged from 1.8 to 4.2 g, median 3.1, over triple the normal daily requirement. This excess was unintended. This occurred before the current practice of pharmacist‐monitoring of TPN formulations, and possibly resulted from misinterpretation of a revised formulation sheet, newly introduced to the nursing units at the start of that period. Serum phosphorus increased to 3.02 mmol/L (normal 0.76 to 1.46 mmol/L). She developed calcification of subcutaneous arteries, which was complicated by widespread infarcts of the anatomically related skin and subcutis, apparently the result of hypoperfusion of these vessels during an episode of septic shock. The infarcts were heralded by unusual, blotchy skin discolorations. Conclusions: This report, illustrating a startling cutaneous complication associated with apparent misinterpretation of TPN formulations, demonstrates a pathogenetic relationship between hyperphosphatemia, calcification of subcutaneous arteries, and necrosis of the skin and subcutis in the absence of CRF and hyperparathyroidism and introduces a new differential diagnosis for unusual skin lesions appearing during TPN therapy. ( Journal of Parenteral and Enteral Nutrition 21: 050–052, 1997)