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.
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 obesewoman 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 elementalphosphorus 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.
Authors: Sagar U Nigwekar; Daniela Kroshinsky; Rosalynn M Nazarian; Jeremy Goverman; Rajeev Malhotra; Vicki Ann Jackson; Mihir M Kamdar; David J R Steele; Ravi I Thadhani Journal: Am J Kidney Dis Date: 2015-05-07 Impact factor: 8.860