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)

Coagulation and fibrinolysis studies were performed on 64 newborns; 16 premature infants with hyaline membrane disease (HMD), 17 newborns with other forms of respiratory distress syndrome (RDS) (8 of them were premature), 31 healthy newborns (11 of them were premature). All the babies were studied once in the first 48 hours of life. There was no significant difference between sick and healthy babies for 5 parameters; platelet count, factor VIII, fibrinogen, fibrin(ogen) degradation products, euglobulin lysis time. Factor II, VII and X were low in all infants, and premature infants had significantly lower levels compared to full term newborns. Factor V, plasminogen, alpha 2 macroglobulin (alpha 2M) and antithrombin III (AT III) levels were significantly lower in sick infants. Except for AT III, these deficiencies were not related to prematurity. No significant difference was found between HMD and other RDS. Of the 33 sick infants, 5 developed laboratory findings consistent with disseminated intravascular coagulation (DIC). The results indicate that the coagulation and fibrinolytic abnormalities reported are not specific to HMD.
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PMID:Haemostatic disorders and respiratory distress in the newborn. 7 54

In 70 newborns with respiratory distress syndrome (RDS) and in roughly the same number of eutrophic mature newborns the total antiplasmin, progressive antithrombin and alpha 2-macroglobulin was determined, the latter in an enzymatical as well as immunochemical way. In healthy mature newborns the progressive antithrombin was somewhat below the level of adults, alpha 2-macroglobulin was above it in both methods and total antiplasmin within it. All parameters of protease inhibitory capacity were significantly lowered in newborns with RDS. Smaller values could be found in patients with bleedings and in those who died later on. Even in those patients with a birth weight under 2,000 g there was a tendency to lower values which can only be partially due to the specificity of development of inhibitors. Progressive antithrombin, total antiplasmin and alpha 2-macroglobulin determined enzymatically are correlated in newborns with RDS jointly and with numerous other parameters of the coagulation system. These relations point to the fact that all components are included in the same consumption process, viz. in the process of disseminated intravascular coagulation. Alpha 2-macroglobulin values determined immunochemically do not correlate with coagulation parameters determined enzymatically as well as with other parameters. They lay partially above or below those determined enzymatically. This behaviour can only be explained by a partial enzyme complex binding of alpha 2-macroglobulin in newborns with RDS.
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PMID:[The protease inhibitor potential in newborns with respiratory distress syndrome]. 8 94

Two cases of fatal heat stroke, concerning a 20 year-old soldier and a 44 year-old psychiatric patient, treated with neuroleptics, are reported. The clinical picture, starting suddenly with coma and hyperthermia, was quite identical for both. Secondarily, while hyperthermia decreases and the conscience improved partially, an hemorrhagic syndrome similar to a consumption coagulopathy, acute renal insufficiency and acute hepatic failure appear. Death occurred after aggravated neurological disorders and respiratory distress. The anatomical lesions spread on all the viscera include tubular nephritis, and hepatic centro-lobular necrosis and an interstitial and alveolar oedema with hemorrhages and hyaline membranes in the lungs.
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PMID:[Heat stroke and disseminated intravascular coagulation. Apropos of 2 cases]. 21 8

Coagulation studies were done on 78 consecutive cases of obstructive jaundice with or without biliary tract infection. Among 26 cases with biliary tract infection 20 cases showed no bleeding tendency but remarkable hypercoagulability with decreased fibrinolytic activity. Other six cases developed diffuse bleeding tendency in addition to the signs of hypotension and multiorgan dysfunction such as oliguria, respiratory distress and mental confusion. Most showed marked coagulation defects characterized by thrombocytopenia, decreased fibrinogen, antithrombin III and plasminogen levels and narrowing of maximal amplitude in thrombelastogram as well as the increase of fibrin degradation products and positive soluble fibrin monomer complexes. All except one died and three cases were autopsied. In two cases postmortem examination revealed multiple fibrin thrombi in lungs and other organs. A cause of the development of bleeding tendency in obstructive jaundice presently observed may likely to be due to the occurrence of disseminated intravascular coagulation (DIC), i.e. hypercoagulability caused by the biliary tract infection is responsible.
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PMID:Occurrence of disseminated intravascular coagulation (DIC) in obstructive jaundice and its relation to biliary tract infection. 32 28

The newborn infant, particularly when premature, has a haemostatic mechanism which may not be entirely capable of withstanding the onslaughts of trauma, infection, asphyxia or other complications of the neonatal period. He is at risk of local or diffuse haemorrhage, which may at times be serious or even life-threatening. The cause of haemorrhage during the newborn period can generally be ascertained by a careful history and brief physical examination directed toward recognition of any predisposing factors or underlying diseases. Screening laboratory tests can usually be correctly interpreted as long as certain laboratory artifacts and physiological peculiarities of the neonatal coagulation mechanism are kept in mind. Diagnosis of and therapy for vitamin K deficiency and haemophilia in the healthy-appearing neonate is generally carried out with little difficulty. The seriously ill neonate with bacterial sepsis, respiratory distress syndrome, or extreme immaturity presents greater problems, for laboratory tests may be more difficult to obtain and interpret and underlying conditions may be untreatable. DIC occurs commonly in such neonates, and transfusion therapy, with or without heparin, is often unsuccessful. A persistent dilemma are those neonates with fatal intravascular haemorrhage, in whom definable haemostatic abnormalities are few and transfusion therapy is futile.
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PMID:Neonatal coagulation: normal physiology and pathophysiology. 35 Apr 67

Serial quantitative immunoelectrophoretic (IE) measurements of antithrombin III heparin cofactor (AT III) were made in groups of well and sick newborn infants classified by gestational age. Collection methods (venous vs. capillary) did not influence the results; serum IE measurements were comparable to AT III activity by a clotting method. AT III is gestational age-dependent, increasing from 28.7% of normal adult values at 28--32 weeks to 50.9% at 37--40 weeks, and shows a gradual increase to term infant levels (57.4%) by 3--4 weeks of age. Infants with the respiratory distress syndrome (RDS) show lower levels of AT III in the 33--36 week group, 22% vs. 44% and in the 37--40 week group, 33.6% vs. 50.9%, then prematures without RDS. Infants of 28--32 week gestational age had only slight differences, RDS = 24%, non-RDS = 28.7%. The lowest levels of AT III were seen in patients with RDS complicated by disseminated intravascular coagulation and those with necrotizing enterocolitis. Crossed IE on representative infants displayed a consistent pattern which was identical to adult controls except for appropriate decreases in the amplitude of the peaks. The thrombotic complications seen in the sick preterm infant may be related to the low levels of AT III.
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PMID:Immunologic studies of antithrombin III heparin cofactor in the newborn. 70 91

In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.
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PMID:Coagulopathy following experimental cerebral ischemia. 84 91

Of 164 consecutive newborns seen in consultations, three babies had either a preretinal or a vitreous hemorrhage, a rare occurrence. Two of these babies had a mild form of disseminated intravascular coagulation. The hemorrhages cleared within a few months after birth. Each of the three babies was premature, had a respiratory distress syndrome, and was born to a primiparous mother. The possibility of a coagulation defect causing intraocular hemorrhage in newborns should be considered along with the tranditional mechanical theories.
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PMID:Vitreous hemorrhages and disseminated intravascular coagulation in the newborn. 94 72

Haemostasis in the new-born is a product of various factors which are both qualitative and quantitative. The only factors that compare in levels and quality with those in the adult are factors V, VIII and XIII. They are alterations in the semi-analytical tests for coagulation except in the Stypven time. In contrast with this deficit shown up in haemostasis by global tests coagulation is normal and in truth there is hypercoagulability. Using Laurell's method of immunoelectrophoresis for levels of alpha 2 M high levels of this are shown contrasting with progressively lowered antithrombitic action. These paradoxes no doubt arise from the fact that neonatal haemostasis is analysed using standardised techniques and reactions which were developed for adult haemostasis, from which it is certainly as different as from those of other animals. Neonatal haemostasis is perfectly balanced in normal conditions. Important changes occur however in respiratory distress where there is a drop in factor V and soluble complexes appear, bringing about rough shapes suggestive of the subclinical syndrome of defibrination. This situation will be further developed in a forthcoming article.
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PMID:[Peculiarities of hemostasis in the term newborn infant]. 102 58

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


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