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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 50-year-old Japanese female with chronic renal failure who had been on continuous ambulatory peritoneal dialysis developed fulminant systemic cutaneous necrosis that began as painful livedo reticularis-like skin lesions on her thighs. Because of disseminated vascular calcification within the muscular layer of her lower limbs, we eventually diagnosed her with calciphylaxis. The skin necrosis progressed rapidly, and she died of sepsis and pneumonia on the 53rd hospital day. In addition to her long-lasting severe hyperparathyroidism and extremely elevated serum phosphorus and calcium levels, mechanical, frictional stimulation inflicted on the local skin and administration of corticosteroids were suspected to have precipitated the calciphylaxis. Our lack of awareness of this disease in its early stages resulted in our missing the chance to do a parathyroidectomy that might have changed the course. It is important to know the clinical features of this rare disease in order to make a diagnosis as early as possible.
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PMID:Fulminant and relentless cutaneous necrosis with excruciating pain caused by calciphylaxis developing in a patient undergoing peritoneal dialysis. 1128 Apr 61

Calciphylaxis is a rare and life-threatening condition of progressive cutaneous necrosis secondary to small and medium-sized vessel calcification. It is seen almost exclusively in patients with end-stage renal disease and secondary hyperparathyroidism. We experienced a case of 67-year-old man with calciphylaxis that manifested with characteristic skin lesions, pathologic findings, and laboratory changes. His skin lesions began as painful erythematous patches and subsequently progressed to necrotic ulcers with eschars on the distal aspect of the extremities. Pathologically, calcification was found in small and medium-sized blood vessels in the deep dermis and subcutaneous tissue. His serum calcium was 9.5 mg/dL, phosphorus was 7.8 mg/dL, and nPTH was 99.9 pg/mL. The patient had been treated with surgical debridement and other supportive treatment. However, he eventually underwent an amputation below the right knee and died from sepsis.
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PMID:Calciphylaxis in a patient with end-stage renal disease. 1143 66

Hypophosphatemia in critically ill and postoperative (p.o.) patients is a multifactorial event, and is also related to severity of illness. This study was conducted to assess pathophysiologic correlates of hypophosphatemia and the simultaneous relationship with clinical events after hepatectomy. A total of 333 measurements were obtained in 59 patients: these were performed preoperatively and at p.o. days 1, 3, and 7 in all patients, and subsequently, until recovery or death, only in those with complications. Measurements included plasma phosphate together with a large number of additional blood chemistries, taking into account primary and associated diseases, events associated with the operation, doses of parenteral substrates, occurrence of sepsis or other p.o. complications, outcome, and a consistent set of complementary variables. Plasma phosphate decreased at p.o. days 1 and 3 (P < 0.001) and retumed to a level close to baseline at p.o. day 7. Regression analysis showed that phosphate was related simultaneously to patient age (inversely), levels of creatinine and potassium (directly), and dose of parenteral amino acids (inversely; P < 0.001 for all). Independently of covariation with these variables, there was a decrement in phosphate at p.o. days 1 and 3 that was related specifically to p.o. condition; this decrement had a general component common to all patients, an additional component related to duration of previous hepatic ischemia at surgery, and a further component predictive of the subsequent development of complications (in most cases, sepsis). Plasma phosphate at p.o. day 1 was related inversely to APACHE II score (r2 = 0.4, P < 0.001), and levels lower than 1.5 mg/dL were associated with an almost 4-fold increase in the rate of complications compared with cases with higher phosphate (P < 0.001). The best single variable bridging early evidence of hypophosphatemia to subsequent development of complications was plasma cholesterol, which fell significantly from p.o. day 3 onward in patients with complications compared with those recovering normally (P < 0.01), and in nonsurvivors compared with survivors (P < 0.01). Hypophosphatemia may anticipate clinical evidence of complications by reflecting an early stronger acute-phase response, with shift of phosphate from intra- to extravascular space, or true phosphorus deficiency, which may favor development of complications by impairing high-energy substrate availability for host defense and other cell functions.
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PMID:Pathophysiologic and clinical correlates of hypophosphatemia and the relationship with sepsis and outcome in postoperative patients after hepatectomy. 1216 71

The aim of this pilot study was to evaluate the incidence of hypophosphatemia and its association with clinical outcome in fulminant hepatic failure (FHF). Patients with FHF referred for orthotopic liver transplantation (OLT) between January, 1991 and May, 2002 were identified. FHF was defined as the development of coagulopathy and encephalopathy within 8 weeks of onset of jaundice. Demographic and laboratory data, including serum phosphate, calcium, magnesium, creatinine, and PT/INR were obtained from medical records. Clinical outcomes (death, OLT, or hepatic recovery) and associated morbidities (renal failure, bleeding, and sepsis) also were noted. Thirty-eight patients, 8 men and 30 women, aged 34 +/- 4 years, were included in the study. Hypophosphatemia (< 2.5 mg/dL) developed in 33 of 38 (87%) patients within 10 days of referral. Twelve patients (32%) died, 14 patients (37%) underwent OLT, and 12 patients (32%) recovered. The mean nadir serum phosphorus level was significantly lower in those who recovered compared with those who either died or required OLT (1.18 +/- 0.54 versus 1.79 +/- 1.00 mg/dL; P =.02). A trend toward lower mean serum phosphorus level also was noted in those who recovered compared with those who died (1.18 +/- 0.54 versus 1.96 +/- 1.35 mg/dL; P =.09). Serum phosphorus levels > 2.5 mg/dL was a predictor of mortality, and when used alone, was equivalent to the King's College Criteria. In conclusion, hypophosphatemia occurred frequently in patients with FHF. Lower serum phosphorus levels were observed in patients who recovered as compared with those who died or required OLT, and may be associated with recovery of hepatic function. The greater decline in serum phosphorus level in those who recover hepatic function may represent cellular use of phosphorus during hepatocyte regeneration.
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PMID:Serum phosphorus levels predict clinical outcome in fulminant hepatic failure. 1475 96

Calcific uremic arteriolopathy (calciphylaxis) is one of the more devastating complications that can develop in patients with chronic renal failure. This disorder is associated with calcium-phosphorus deposition in the subcutaneous arterial vessels and presents as a progressive ischemic necrosis of the skin resulting in large subcutaneous ulcerations with eschar formation. Mortality rates are substantially greater in chronic renal failure patients with calciphylaxis, and the major cause of death is infection and sepsis. We have developed a treatment strategy that employs a combination of therapies, which is based on reducing the known risk factors for the development of calciphylaxis as well as utilization of a number of treatment modalities that have been proven successful in the treatment of this disorder.
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PMID:A strategy for the treatment of calcific uremic arteriolopathy (calciphylaxis) employing a combination of therapies. 1283 80

Acute renal failure is a common occurrence in sepsis, but is rarely reported in meningococcemia. We present a young child diagnosed with fulminant meningococcemia who had several poor prognostic factors, including hypotension, thrombocytopenia, purpura fulminans, seizures, the absence of meningitis with meningococcemia, and acute renal failure, which was successfully treated with peritoneal dialysis. Peritoneal dialysis was started on the 5th day because the patient had been anuric for 48 h. At that time, analysis showed that the child was both hypokalemic and hypophosphatemic. His serum blood urea nitrogen was 61 mg/dl, creatinine 2.75 mg/dl, potassium 2.8 mEq/l, and phosphorus 0.7 mg/dl. Urine output began on the 12th day post admission and normalization of serum creatinine was achieved on the 26th day. In conclusion, renal failure is an important complication of meningococcemia and, to be effective, sometimes long-term peritoneal dialysis is required. Profound metabolic abnormalities, such as hypokalemia and hypophosphatemia, may occur paradoxically in the presence of oliguria.
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PMID:Fulminant meningococcemia and acute renal failure in a 3-year-old boy. 1549 Feb 48

The aims of this study were to estimate the occurrence of hypophosphatemia and to identify potential risk factors and outcome measures associated with this disturbance in children admitted to a pediatric intensive care unit. Data concerning 42 children admitted consecutively to 1 pediatric intensive care unit over a 1-year period were examined. Serum phosphorus levels were measured on the third day of admission, where levels below 3.8 mg/dL were considered indicative of hypophosphatemia. Hypophosphatemia was found in 32 children (76%), and there was a significant association between this disturbance and malnutrition (P = .04). Of the potential risk factors such as sepsis, diuretic/steroid therapy, starvation (over 3 days), and Pediatric Index of Mortality, none discriminated for hypophosphatemia. There were no associations between hypophosphatemia and mortality, length of stay in the pediatric intensive care unit, or time on mechanical lung ventilation. Hypophosphatemia was a common finding in critically ill children and was associated with malnutrition.
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PMID:Hypophosphatemia in children hospitalized within an intensive care unit. 1685 58

Calcific uremic arteriolopathy (CUA) is a rare but serious complication of end-stage renal disease presenting as painful cutaneous lesions and progressing to non-healing ulcers and gangrene. This syndrome is associated with calcium and phosphorus deposits within small arteries of the skin. The pathognomonic lesion is vascular calcification with intimal arterial hypertrophy and superimposed small-vessel thrombosis. The condition is being increasingly recognized and reported as a contributing factor to death in dialysis patients, with secondary infection and sepsis as the major cause of mortality. No standard treatment has been established for this syndrome. We present the therapeutic approach employed in two patients, which successfully resulted in healing of the lesions, using a combination of measures to control the factors potentially related to development of CUA and hyperbaric oxygen therapy.
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PMID:Management of calcific uremic arteriolopathy (calciphylaxis) with a combination of treatments, including hyperbaric oxygen therapy. 1879 71

Acute kidney injury (AKI) is a serious condition that affects many ICU patients. The most common causes of AKI in ICU are severe sepsis and septic shock. The mortality of AKI in septic critically ill patients remains high despite of our increasing ability to support vital organs. This is partly due to our poor understanding of the pathogenesis of sepsis-induced renal dysfunction. However, new concepts are emerging to explain the pathogenesis of septic AKI, which challenge previously held dogma. Throughout the past half century, septic AKI has essentially been considered secondary to kidney ischemia. However, recent models of experimental sepsis have challenged this notion by demonstrating that, in experimental states, which simulate the hemodynamic picture most typically seen in man (e.g. hyperdynamic sepsis) renal blood flow, actually increases as renal vascular resistance decreases. These experimental observations provide proof of concept that septic AKI can occur in the setting of renal hyperemia and that ischemia is not necessary for loss of glomerular filtration rate (GFR) to occur. They also suggest that similar hemodynamic event may occur in man. In addition, preliminary studies in septic sheep show that, when ATP is measured using an implanted phosphorus coil and magnetic resonance technology, renal bioenergetics are preserved in the setting of advanced septic shock. While these findings need to be confirmed, they challenge established paradigms and offer a new conceptual framework of reference for further investigation and intervention in man.
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PMID:Septic acute kidney injury: new concepts. 1880 75

A 52-year-old woman was admitted with complaints of nonhealing skin ulcers. The laboratory assessment showed a calcium level of 13.2 mg/dL (normal 8.4-10.2 mg/dL), albumin 2 g/dL (normal 3.5-4.8 g/dL), corrected calcium 14.8 mg/dL, phosphorus 1.4 mg/dL (normal 2.4-4.7 mg/dL), creatinine 0.7 mg/dL (normal 0.5-1.2 mg/dL), parathyroid hormone 893.3 pg/mL (normal 11.1-79.5 pg/mL). A technetium-sestamibi scan showed a left inferior parathyroid adenoma. The patient underwent a parathyroidectomy. Pathology showed a parathyroid adenoma. Despite treatment of her skin wounds with broad spectrum antibiotics and local wound care, the patient died of overwhelming sepsis. Calciphylaxis is a rare but serious disorder that leads to skin and soft tissue necrosis and requires prompt diagnosis and management.
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PMID:Calciphylaxis in primary hyperparathyroidism: a case report and brief review. 1920 21


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