Background. Pulmonary artery perforation is a rare but often fatal complication of the pulmonary artery catheter occurring in cardiovascular operations and at catheterization facilities. We used our experience and a review of the literature to formulate diagnostic and management strategies.
Methods. During a 13-year period, 12 patients with pulmonary artery perforations were treated in a center that performed an average of 860 open-heart procedures per year. Clinical presentation varied from minor hemoptysis to major airway hemorrhage, hypoxia, exsanguination, and cardiac arrest. Airway bleeding occurred shortly after weaning from cardiopulmonary bypass in 5 patients or postoperatively after wedging the catheter in 6. One patient developed a hemothorax and had a cardiac arrest. Treatment included assurance of gas exchange, endobronchial lavage, isolation of the bleeding bronchus and control of hemorrhage by conservative therapy, pulmonary resection, pulmonary artery repair, and arterial embolization.
Results. Five of the 12 patients died (42%). Recurrent hemorrhage occurred in 40% of patients (2 of 5) treated conservatively compared with none of the patients (0 of 7) having surgical treatment. Forty three percent of patients (3 of 7) treated surgically died; 20% of patients (1 of 5) treated conservatively died. One patient succumbed without treatment.
Conclusions. Pulmonary artery perforation is a rare and often fatal complication of pulmonary artery catheterization. This was apparent with patients who had airway hemorrhages as a result of weaning from cardiopulmonary bypass or after balloon inflation. Recurrent and fatal hemorrhage was frequent in patients treated by conservative therapy alone. Surgical intervention was effective in control of hemorrhage but did not reduce the number of deaths. Treatment remains highly individualized. It is advisable to be cautious in inserting Swan-Ganz catheters and to avoid their use unless absolutely necessary. 相似文献
BACKGROUND/PURPOSE: Fluorescence of Skh-1 hairless mouse and calf skin acid-soluble type I collagens are envelopes of several bands putatively due to tyrosine (excitation/emission peak at 275/300 nm), dihydroxyphenylalanine (dopa; 280/325 nm), tyrosine aggregate (285/360 nm), dityrosine 325/400 nm), and advanced glycation end (AGE) product (370/450 nm), respectively. As these fluorophores can be markers of pathological conditions, we wish to present further evidence for or against these assignments. METHODS: We analysed intact type I mouse collagens and AGE by conventional fluorescence spectroscopy, synchronous spectroscopy, high-performance liquid chromatography (HPLC), and borate quenching. RESULTS: The relative amount of each fluorophore depends on the collagen sample. Acid- or enzyme-hydrolysis results in loss of fluorescence intensity at 350-400 nm, and enhanced emission 400-500 nm which could be reproduced by controlled dopa oxidation. Borate buffer quenches fluorescence at lambda>400 nm from intact collagens, dityrosine, dopa, and oxidized dopa but does not quench tyrosine or AGE fluorescence. CONCLUSION: Collagen fluorescence depends on its source and previous history. The data indicate that collagen fluorescence is derived from tyrosine, dopa, interacting tyrosine residues, covalent dityrosine, and dopa oxidation product(s), but not AGE. 相似文献
Although the overall incidence is low, bleeding complications in dermatologic surgery can occur and be the source of significant patient morbidity. In this article, we summarize the key aspects of preoperative assessment of patients at risk for bleeding. A review of current issues and literature regarding safe continuation of anticoagulant and antiplatelet medications in dermatologic surgery patients is also presented. In addition, principles for management of bleeding events, should they occur, are also highlighted. 相似文献
An 80-year-old man presented with a 50-year history of asymptomatic, subcutaneous masses on the arms, trunk, and legs. His father and maternal grandmother had had similar lesions. Histopathologic examination showed a benign angiolipoma; the same diagnosis has been made on several previous biopsy specimens. This patient's history and physical examination support the diagnosis of familial angiolipomatosis, which is a benign, autosomal-dominant condition that may be regarded as a subtype of familial multiple lipomatosis (FML) or as a distinct entity. Management of this condition may include liposuction or surgery to reduce the tumor burden. 相似文献
This study characterized the health risks due to the consumption of mycotoxin-contaminated foods and assessed the consumer awareness level of mycotoxins in households in two north-central Nigerian states during the harvest and storage seasons of 2018. Twenty-six mycotoxins and 121 other microbial and plant metabolites were quantified by LC-MS/MS in 250 samples of cereals, nuts and legumes. Aflatoxins were detected in all food types (cowpea, maize, peanut and sorghum) except in millet. Aflatoxin B1 was the most prevalent mycotoxin in peanut (64%) and rice (57%), while fumonisin B1 occurred most in maize (93%) and beauvericin in sorghum (71%). The total aflatoxin concentration was highest in peanut (max: 8422 µg/kg; mean: 1281 µg/kg) and rice (max: 955 µg/kg; mean: 94 µg/kg), whereas the totals of the B-type fumonisins and citrinin were highest in maize (max: 68,204 µg/kg; mean: 2988 µg/kg) and sorghum (max: 1335 µg/kg; mean: 186 µg/kg), respectively. Citrinin levels also reached 51,195 µg/kg (mean: 2343 µg/kg) in maize. Aflatoxin and citrinin concentrations in maize were significantly (p < 0.05) higher during storage than at harvest. The estimated chronic exposures to aflatoxins, citrinin and fumonisins were high, resulting in as much as 247 new liver cancer cases/year/100,000 population and risks of nephrotoxicity and esophageal cancer, respectively. Children who consumed the foods were the most vulnerable. Mycotoxin co-occurrence was evident, which could increase the health risk of the outcomes. Awareness of mycotoxin issues was generally low among the households. 相似文献
Hereditary non-polyposis colorectal cancer is a cancer predisposition syndrome known to be caused by heterozygous germline
mutations in DNA mismatch repair genes (MMR) most commonly hMLH1, hMSH2, hMSH6. Heterozygous mutations in one of these genes confer an increased risk, mainly for colon and endometrial cancer. Recently,
several publications identified that biallelic mutations in the MMR genes are associated with a more severe phenotype, including
childhood malignancies and signs of neurofibromatosis type I (NF1). We report on a non-consanguineous Ashkenazi Jewish family
with two affected siblings with features of NF1, colon cancer and astrocytoma at age 13 and 14. Their mother developed endometrial
cancer at age 54. Their father had leukoplakia of the vocal cords with a family history of pancreatic cancer. Molecular and
pathology studies were done on the tumor tissue and on genomic DNA of family members. Tumor testing demonstrated a high degree
of microsatellite instability (MSI analysis), expression of MLH1 and absence of expression of both MSH2 and MSH6 proteins. A biallelic c.1906G > C (p.A636P) mutation
in the hMSH2 gene was detected in the blood of one affected child. Parental genetic testing showed that each parent was heterozygote for
the mutation. The c.1906G > C mutation is a founder mutation in the Ashkenazi Jewish population. To our knowledge this is
the first report of homozygosity for this founder mutation.
H. Toledano and Y. Goldberg contributed equally to the paper. 相似文献
Objective With 2.3 million breast cancer survivors in the US today, identification of modifiable factors associated with breast cancer
recurrence and survival is increasingly important. Only recently new studies have been designed to examine the impact of lifestyle
factors on prognosis, including Pathways, a prospective study of women with breast cancer in Kaiser Permanente Northern California
(KPNC).
Methods Pathways aims to examine the effect on recurrence and survival of (1) lifestyle factors such as diet, physical activity, quality
of life, and use of alternative therapies and (2) molecular factors such as genetic polymorphisms involved in metabolism of
chemotherapeutic agents. Eligibility includes any woman diagnosed with invasive breast cancer within KPNC, no previous diagnosis
of other invasive cancer, age 21 years or older, and ability to speak English, Spanish, Cantonese, or Mandarin. Newly diagnosed
patients are identified daily from electronic pathology records and are enrolled within two months of diagnosis. An extensive
baseline interview is conducted, blood and saliva samples are collected, and body measurements are taken. Women are followed
for lifestyle updates, treatment, and outcomes by self-report and query of KPNC databases.
Results Recruitment began in 9 January, 2006, and as of 16 January, 2008, 1,539 women have been enrolled along with collection of
1,323 blood samples (86%) and 1,398 saliva samples (91%).
Conclusions The Pathways Study will become a rich resource to examine behavioral and molecular factors and breast cancer prognosis. 相似文献