Janigan D T, Perey B, Marrie T J, Chiasson P M, Hirsch D
Department of Pathology, Dalhousie University, Halifax, Nova Scotia.
JPEN J Parenter Enteral Nutr. 1997 Jan-Feb;21(1):50-2. doi: 10.1177/014860719702100150.
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.
The patient's records during 37 weeks of hospitalization 12 years ago and, subsequently, her outpatient records were reviewed.
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.
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.
在无慢性肾衰竭（CRF）的情况下，高磷血症并发皮下动脉钙化和皮肤梗死的病例鲜有报道。我们描述了一名患有败血症的肥胖女性出现的相同病变。高磷血症是由于她的全胃肠外营养（TPN）配方中意外过量的磷酸盐所致。她没有CRF或甲状旁腺功能亢进。
回顾了该患者12年前住院37周期间的病历以及随后的门诊病历。
在7周的时间里，每天输注的二价磷酸盐形式的总元素磷为1.8至4.2克，中位数为3.1克，超过正常每日需求量的三倍多。这种过量是意外发生的。这发生在目前药剂师监测TPN配方的做法之前，可能是由于对当时护理单元新引入的修订配方表的误解所致。血清磷升至3.02 mmol/L（正常范围为0.76至1.46 mmol/L）。她出现了皮下动脉钙化，并伴有与之相关的皮肤和皮下组织广泛梗死，这显然是败血症休克发作期间这些血管灌注不足的结果。梗死之前有异常的斑片状皮肤变色。
本报告说明了与TPN配方明显误解相关的一种惊人的皮肤并发症，证明了在无CRF和甲状旁腺功能亢进的情况下，高磷血症、皮下动脉钙化与皮肤和皮下组织坏死之间的发病机制关系，并为TPN治疗期间出现的异常皮肤病变引入了一种新的鉴别诊断方法。
