Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolism and in vivo kinetics of fibrinogen labelled with radioactive iodine was studied in children with cyanotic congenital heart disease. The patients had a significantly lowered plasma fibrinogen pool, shortened fibrinogen half-life and increased fractional catabolic rate of fibrinogen compared with healthy children. The average plasma fibrinogen and absolute catabolic rate of fibrinogen did not differ from control values. The shortened fibrinogen half-life together with the correcting effect of anticoagulation with heparin indicated that fibrinogen was consumed by chronic disseminated intravascular coagulation. Inhibition of the fibrinolytic system with epsilon-aminocaproic acid in three cyanotic patients had no influence on the fibrinogen half-life in two of them but resulted in its prolongation in one patient.
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PMID:Fibrinogen metabolism in cyanoti congenital heart disease. 61 88

A total of 209 consecutive neonate and infant autopsies were reviewed with special attention to papillary muscle necrosis (PMN) of the heart. Associated major pathological findings were analysed for the evaluation of significant pathological accompaniments of PMN. PMN was found in 52 cases among 171(30.4%) neonates and major pathological accompaniments were bronchopneumonia, hyaline membrane disease, hypoxic neuronal change, sepsis, subarachnoid hemorrhage, disseminated intravascular coagulation (DIC) and acute tubular necrosis, among which hypoxic neuronal change and ATN had a statistically significant higher incidence when compared with the control group. (p < 0.005). PMN was found in 13 cases among 38(34.2%) infants and accompaniments were congenital heart disease, sepsis, bronchopneumonia, DIC and hypoxic neuronal change, all of which showed no difference from the control group in incidence. The results imply that PMN is a kind of organ damage in stressed subjects regardless of age, that it is not a special form of myocardial injury in any specific age group including the newborn period, and is possibly of different pathogenesis and significance.
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PMID:Papillary muscle necrosis in neonates and infants--analysis of 209 autopsies. 129 38

A neuropathologic study in 190 consecutive autopsies of patients with congenital cardiopathy was performed: 116 cases underwent a surgical procedure (S group) and the remaining 74 were non-surgical (NS group). Neuropathologic alterations were observed in 71 cases (41 in the S group and 30 in the NS group). However, most of the 129 cases with a normal examination had died in the first 72 hours either after surgery or the clinical events responsible for the death. Almost all the neuropathologic alterations were hypoxic ischemic. Infarctions, single or multiple, were found in 41 cases (23 in the S and 18 in the NS group). An embolic mechanism could be detected in 12 cases. Diffuse hypoxic changes were present in 17 cases (10 in the S and 7 in the NS group). Hemorrhages were found in 11 (6 in the S and 5 in NS group), 4 of which were related to a disseminated intravascular coagulation. In 17 cases (5 in the NS and 12 in the S group), the picture was of a periventricular leukomalacia. All these cases concerned children under 6 months of age. In 7 cases inflammatory alterations were present (diffuse micro-abscesses in 6 and a frontal lobe abscess in 1). Almost all cases in both groups presented clinical complications, isolated or associated, potentially harmful to the brain, as cardiac arrest, cardiac low output, hypoxemia, and respiratory distress. If was impossible to determine in each case the magnitude of the factor or factors responsible for the correspondent pattern of neuropathologic damage. There was no difference as to the neuropathologic pattern between congenital cardiopathies leading to increased or decreased pulmonary blood flow.
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PMID:[Neurologic changes in congenital heart diseases: a neuropathologic study]. 130 82

Disseminated intravascular coagulation (DIC) and other clotting abnormalities are common in sick newborn infants who have a variety of conditions. To document evidence of DIC at autopsy, immunoperoxidase staining of fibrin-related antigens (FRA) was used to detect intravascular microthrombi in liver, kidney, and lung from 127 newborns. Patients were selected from seven major disease groups: hyaline membrane disease/bronchopulmonary dysplasia, infection, meconium aspiration, necrotizing enterocolitis, congenital heart disease, other congenital anomalies, and extreme prematurity. Staining for FRA in intravascular microthrombi was seen in 40% of cases studied. The liver showed the highest frequency of intravascular microthrombi, located predominantly in the sinusoids. Unlike the adult kidney, the newborn kidney seldom had evidence of intravascular coagulation. Extravascular staining of FRA was observed in the renal distal tubular epithelium in 48 cases, many of which also had evidence of intravascular FRA staining. No significant differences in FRA staining patterns were seen among the disease groups except for cases of extreme prematurity in which all tissues showed minimal staining. Control tissues from SIDS patients also showed minimal FRA staining. Hepatic sinusoidal staining was the only tissue finding that correlated with thrombocytopenia, a clinical indicator of DIC. Despite the use of this immunohistochemical staining method, discrepancies between the clinical and autopsy diagnosis of DIC remain.
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PMID:Immunohistochemical diagnosis of disseminated intravascular coagulation in newborns. 170 Apr 4

The authors report the clinicopathological findings in six cases of bacterial intracranial aneurysms. All patients received appropriate high-dose antibiotics, and four were treated surgically. One patient with multiple aneurysms of the main trunks died of disseminated intravascular coagulation. Autopsy disclosed no apparent aneurysm or inflammatory cell infiltration, but a partially interrupted internal elastic lamina and thickened intima were disclosed at the angiographical aneurysm sites. These findings suggest that 1) appropriate high-dose antibiotics are effective against inoperable bacterial aneurysms in the main trunks, 2) new aneurysms may be formed in patients with cyanotic congenital heart disease, because bacterial emboli can directly reach the cerebral circulation and reimplant on the fragile arterial walls after vasculitis. Histological examination of aneurysmal walls revealed inflammatory cell infiltration after resolution of clinical endocarditis. This suggests that both appropriate high-dose antibiotic therapy and surgery should be considered in patients with distal bacterial aneurysms.
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PMID:Clinicopathological study of bacterial intracranial aneurysms. 172 79

Coagulation abnormalities with and without haemorrhagic manifestations have been frequently reported in newborn-infants affected by hypoxia. Particularly in postmature-infants and in those ones with acute asphyxia at birth, respiratory distress syndrome (RDS), intra-uterine growth retardation (IUGR) and cyanotic congenital heart disease (CCHD). A reduction of synthesis or a consumption of blood coagulation factors are the main causes of these abnormalities. The anomalies of platelet number and of their function, of haemostasis global tests, of coagulation factors and physiologic inhibitors levels, of fibrinogenesis and fibrinolysis are examined, including authors' studies and a review of literature too. The authors think platelet count, PT, PTT, fibrinogen, factor V and VIII, and PDF determinations are necessary laboratory investigations for newborn-infants with RDS or acute asphyxia for about the first week of life, because of the risk of consumption coagulopathy. In the other hypoxic newborns (IUGR, CCHD, postmature infants) platelets count, PT, PTT and serum PDF determinations could be enough in order to value any coagulation abnormalities presence.
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PMID:[Neonatal hypoxia and hemocoagulative changes]. 269 28

We introduced continuous intravenous infusion of amphotericin-B (AMPH-B) to extremely low birthweight (ELBW) infants (< 1000 g) with or without renal failure as a single agent for treating definite or probable systemic candidiasis. The species of Candida isolated from blood or tracheal aspirate or urine were C. albicans in seven infants, C glabrata in two, C. tropicalis in one and C. parapsilosis in one. The minimal inhibitory concentrations (MIC) of AMPH-B required against these isolates were less than 0.2 micrograms/mL except for that against one strain of C. albicans (0.78 microgram/mL). Serum AMPH-B levels were 0.31-0.78 (0.51 +/- 0.14) micrograms/mL when doses of 0.2-0.55 (0.32 +/- 0.11) mg/kg per day were being administered. The serum level was higher than the MIC of each isolate in all but one infant who died of disseminated intravascular coagulation and Candida pneumonia. Another infant died of congenital heart disease. The other nine infants survived. The serum level showed no correlation with the daily dose. The ratio of the serum level to the daily dose (L/D ratio) showed a significant correlation to serum creatinine (r = 0.787) and the linear regression curve followed the equation: L/D ratio = 0.223 x serum creatinine + 1.11 (P < 0.01). Few adverse effects due to AMPH-B were noted. Our data may give a simple reference to serum AMPH-B levels during continuous intravenous infusion from the dose and the serum creatinine level.
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PMID:Increased level/dose ratio of amphotericin-B in premature infants with renal failure. 835 92

Underlying diseases, complications, clinical findings, and laboratory findings were evaluated in 158 cases of septicaemia admitted to Jikei University Hospital from 1975 to 1994, in order to conjectured factors that prescribe for the prognosis. 50% of the patients had underlying diseases. Malignancy including leukaemia (31 cases, 39.2%) was the most common underlying disease, followed by low birth weight infant (17 cases, 21.5%), aplastic anemia (9 case, 11.4%), and congenital heart disease (7 cases, 8.9%). The death rate for patients with underlying disease (27.8%) was significantly greater than the mortality for normal patients with septicaemia (8.9%) (p < 0.05). Meningitis (24.7%) was the most common complication, followed by DIC (19.6%), shock (15.2%), and pneumonia (10.8%). The mortality rate of septicaemia complicated by shock was 66.7% (p < 0.01), and that complicated by DIC was 45.2% (p < 0.01). The mortality rate for patients with the clinical findings of respiratory distress, cough, abdominal distention, cyanosis, splenomegaly, or peripheral coldness was more than 40% and significantly greater (p < 0.01). Mortality rate in patients with granulocyte counts of < 4.000/mm3, platelet counts of < 5 x 10(4)/ mm3, total protein of < 5.0 g/dl, or ESR of < 20 mm/hr were significantly greater (p < 0.01) than those in patients with normal laboratory findings. Coincidence rate of blood and stool cultures was 57.9% for E. coli, and 28.6% for Klebsiella sp., and that of blood and throat cultures was more than 30% for Pseudomonas sp., Haemophilus influenzae, and Staphylococcus aureus. In the study of antimicrobial susceptibility for microorganisms isolated, the number of drug resistant S. aureus had increased in the last 10 years.
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PMID:[Study on septicaemia in infants and children in the past 20 years. Part 2. An analysis of factors that prescribe for the prognosis]. 889 May 45

From March 1993 to February 1993, 36 patients with chronic renal failure underwent cardiac surgery with intraoperative hemodialysis (HD). We examined and compared the medium term results of those patients cased upon the time periods of operation and types of heart disease. With respect to the time periods of operation, the 1st term (n = 12) was between March 1985 and February 1989, and the 2nd term (n = 24) was between March 1989 and February 1993. Concerning types of disease, Group A was comprised of 24 patients with ischemic heart disease, and Group B was comprised of 12 patients with valvular or congenital heart disease. Only one early death was observed in the 1st term (8.3%: LOS). As for late death, 5 cases were observed in the 1st term (45.3%), and 2 cases were observed in the 2nd term (8.3%). The actuarial survival rate (post 3 years) was 72.7% in the 1st term and 91.3% in the 2nd term. In each case, the survival rate of the 2nd term was significantly better than the that of the 1st term (p < 0.025). When compared cased upon the types of disease, the actuarial survival rate (post 6 years) was 84.6% in Group A, and 45.5% in Group B, respectively. This difference was statistically significant (p < 0.05). Causes of late death were cerebral hemorrhage in 5 cases, sudden and unknown in one and DIC in the remaining one patient. There were many postoperative complications in this series in addition to the above stated fatal ones. The majority of them, however, were successfully treated, if early diagnosis of them was obtained. During the perioperative period through the long-term period, incidents of fatal hemorrhage among patients on chronic dialysis were reduced by 1) strict management of hypertension; 2) HD without use of Heparin; and 3) with respect to patients who required Warfarin after valve replacement, through the careful anti-coagulant therapy which maintained the thrombo-test (TT) value at precise levels.
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PMID:[Cardiac surgery in patients on chronic hemodialysis]. 891 Oct 41

Haemophilus parainfluenzae, a human commensal, is an infrequent cause of serious disease. A case of endocarditis caused by this organism in a five year old boy with complex congenital heart disease is reported. The course of this disease was very aggressive, leading to heart failure, disseminated intravascular coagulation and multiorgan failure in spite of appropriate antibiotics and surgical intervention. The difficulties in the detection and identification of H parainfluenzae using conventional culture based technology, and the potential role of molecular techniques, are highlighted.
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PMID:Endocarditis caused by Haemophilus parainfluenzae identified by 16S ribosomal RNA sequencing. 905 63


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