Risk factors and outcomes for nosocomial infection after prosthetic vascular grafts.

OBJECTIVE: The objective of this study was to determine risk factors for nosocomial infections (NIs) and predictors of mortality in patients with prosthetic vascular grafts (PVGs). METHODS: This was a prospective cohort study of all consecutive patients who underwent PVG of the abdominal aorta with or without iliac-femoral involvement and peripheral PVG from April 2008 to August 2009 at a university hospital. Patients younger than 15 years and those with severe immunodeficiency were excluded. The follow-up period was until 3 years after surgery or until death. RESULTS: There were 261 patients included; 230 (88.12%) were male, and the mean age was 67.57 (standard deviation, 10.82) years. The reason for operation was aortic aneurysm in 49 (18.77%) patients or lower limb arteriopathy in 212 (81.23%) patients. NIs occurred in 71 (27.20%) patients. Of these, 42 were surgical site infections (SSIs), of which 61.9% occurred in the lower extremities (14 superficial, 10 deep, and 2 PVG infections) and 38.1% in the abdomen (7 superficial, 7 deep, and 2 PVG infections); 15 were respiratory tract infections; and 15 were urinary tract infections. Active lower extremity skin and soft tissue infection (SSTI) at the time of surgery was a significant predictor of NI for both types of PVG (abdominal aortic PVG: adjusted odds ratio [OR], 12.6; 95% confidence interval [CI], 1.15-138.19; peripheral PVG: adjusted OR, 2.43; 95% CI, 1.08-5.47). Other independent predictors of NI were mechanical ventilation (adjusted OR, 55.96; 95% CI, 3.9-802.39) for abdominal aortic PVG and low hemoglobin levels on admission (adjusted OR, 0.84; 95% CI, 0.71-0.99) and emergent surgery (adjusted OR, 4.39; 95% CI, 1.51-12.74) for peripheral PVG. The in-hospital mortality rate was 1.92%. The probability of surviving the first month was 0.96, and significant predictors of mortality were active lower extremity SSTI (adjusted risk ratio [RR], 12.07; 95% CI, 1.04-154.75), high postsurgical glucose levels (adjusted RR, 1.02; 95% CI, 1.00-1.04), and noninfectious surgical complications (adjusted RR, 19.38; 95% CI, 2.25-167.29). The long-term mortality rate was 11.88%. The probability of surviving at 12, 24, and 36 months was 0.94, 0.92, and 0.87, respectively. Variables significantly associated with long-term death were older age (adjusted RR, 1.08; 95% CI, 1.01-1.15), high values of creatinine on discharge (adjusted RR, 1.91; 95% CI, 1.08-3.38), and an SSI with the highest adjusted RR (6.35; 95% CI, 1.87-21.53). CONCLUSIONS: SSI was the primary NI. The risk of NI depended primarily on the presence of a lower extremity SSTI at the time of surgery, whereas mortality was determined by age, surgical complications during the operation, and SSI. These findings suggest that in those cases in which surgery is reasonably delayed, surgery should be deferred until the lower extremity SSTIs are resolved.

Mutilating Purpura Fulminans in an Adult with Meningococcal Sepsis.

We report a dramatic case of meningococcal sepsis manifesting as purpura fulminans in an elderly diabetic woman. Hemodynamic instability and severe bilateral cutaneous lesions involving her hands and feet developed rapidly. Specific antibiotic therapy and the administration of inotropic and vasopressor drugs were initiated. The severity and extension of the cutaneous lesions (attributed to purpura fulminans) worsened because of the need for vasoconstrictors for the treatment of septic shock. Bilateral transmetatarsal and metacarpal amputations were required to stabilize the patient.

BMP-7 attenuates left ventricular remodelling under pressure overload and facilitates reverse remodelling and functional recovery.

AIMS: TGF-ß regulates tissue fibrosis: TGF-ß promotes fibrosis, whereas bone morphogenetic protein (BMP)-7 is antifibrotic. To demonstrate that (i) left ventricular (LV) remodelling after pressure overload is associated with disequilibrium in the signalling mediated by these cytokines, and (ii) BMP-7 exerts beneficial effects on LV remodelling and reverse remodelling. METHODS AND RESULTS: We studied patients with aortic stenosis (AS) and mice subjected to transverse aortic constriction (TAC) and TAC release (de-TAC). LV morphology and function were assessed by echocardiography. LV biopsies were analysed by qPCR, immunoblotting, and histology. Pressure overload reduced BMP-7 and pSmad1/5/8 and increased TGF-ß and pSmad2/3 in AS patients and TAC mice. BMP-7 correlated inversely with collagen, fibronectin, and ß-MHC expressions, and with hypertrophy and diastolic dysfunction, and directly with the systolic function. Multiple linear regression disclosed BMP-7 and TGF-ß as hypertrophy predictors, negative and positive, respectively. BMP-7 prevented TGF-ß-elicited hypertrophic program in cardiomyocytes, and Col1A1 promoter activity in NIH-3T3 fibroblasts. The treatment of TAC mice with rBMP-7 attenuated the development of structural damage and dysfunction, and halted ongoing remodelling. The reverse remodelling after pressure overload release was facilitated by rBMP-7, and hampered by disrupting BMP-7 function using a neutralizing antibody or genetic deletion. CONCLUSION: The disequilibrium between BMP-7 and TGF-ß signals plays a relevant role in the LV remodelling response to haemodynamic stress in TAC mice and AS patients. Our observations may provide new important insights aimed at developing novel therapies designed to prevent, halt, or reverse LV pathological remodelling in pressure overload cardiomyopathy.

Successful retrieval of an irretrievable jugular tesio catheter using a fogarty arterial embolectomy catheter.

Long life expectancy and wide development of therapies have increased the number of patients under artificial treatment for lost kidney function or dialysis. Different options for vascular access are suitable for receiving this therapy. The use of tunneled catheters has consequently increased complications related to its use. A difficult retrieval of catheters caused by a hard fibrin sheath along its trajectory is a common drawback. Herein, we report a woman with suspicion of hemodialysis catheter infection and an irretrievable Tesio catheter. A novel technique using a Fogarty arterial catheter allowed a successful retrieval and avoided an aggressive management.

Cardiac papillary fibroelastoma: retrospective clinicopathologic study of 17 tumors with resection at a single institution and literature review.

Cardiac papillary fibroelastomas (PFEs), which are mainly found in the valves, are rare benign tumors that can cause embolism. Single-center surgical experience in the treatment of this tumor is uncommon. All patients surgically treated for this neoplasm at our institution from January 1995 to October 2012 (15 patients with 17 lesions) were queried for clinical and pathologic characteristics, and the literature was reviewed. The mean age of detection was 55.8±11.48 years. Twenty percent of the patients were male. The tumor was an incidental finding in 60%. Symptoms directly related to PFEs occurred in 40% of patients. The most common clinical presentation in symptomatic cases was embolism (40%), mostly transient ischemic attack or stroke. Cardiac valves were predominantly involved (76.5%); the most commonly valve affected was the aortic valve (29.4%), followed by the mitral valve (17.6%). Concurrent valvular disease was observed in 41.7% of patients. The mean size of tumors was 11.4±7.9mm (range 2-25mm). In 86.7% of the patients, the tumor was solitary. The mitral valve was the most common origin of tumor systemic embolism. Fronds core could be the end stage of hypermature elastic fibers, which grows in apposition to young fibers. Simple surgical excision or valvular reconstruction was accomplished in most patients (58.3%). PFE is usually small, appears singly, and can cause potentially serious complications. Symptomatic and left side tumors should undergo surgical excision with valve-spare surgery when possible. Surgical removal of PFE is safe, efficacious, and definitive.

Divertículo de Kommerell y arteria subclavia derecha aberrante / Kommerell diverticulum and aberrant right subclavian artery

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