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)

Neonatal nonbacterial thrombotic endocarditis (NBTE), a rare disorder yet to be diagnosed antemortem, is described in two infants. The first infant was postmature and suffered from polycythemia and meconium aspiration. The meconium-stained placenta manifested evidence of ischemia and disseminated intravascular coagulation (DIC). The second patient was delivered near term by cesarean section, and hyaline membrane disease developed. The pathogenesis of NBTE may relate to perinatal hypoxia with transient tricuspid insufficiency, polycythemia, and DIC.
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PMID:Neonatal nonbacterial thrombotic endocarditis. 58 32

Infants with platelet counts below 100,000/mm3 should be evaluated for the cause of the thrombocytopenia. A maternal history to determine previous illnesses and particularly thrombocytopenia, drugs taken, and perinatal complications is important, and a maternal platelet count must be obtained. Physical examination of the infant is revealing in the TAR and giant cavernous hemangioma syndromes and may suggest intrauterine infection. A complete blood cell count (CBC) should be done to look for associated anemia and neutropenia or for polycythemia. Red cell morphology may be helpful. A bone marrow examination may be necessary if the etiology is unclear after the initial studies are done. Investigation of the well child will usually find an etiology for the thrombocytopenia. It is important to consider and test for isoimmune thrombocytopenia and intrauterine infection. In the ill infant multiple factors may contribute to a low platelet count, and a single, precise etiology often cannot be established. Thrombocytopenia with or without DIC may be an important indicator of sepsis. Platelet transfusions are helpful if the thrombocytopenia is due to decreased production or intrinsic platelet defects. In disorders with increased platelet destruction, donor platelets may survive long enough to be of some benefit. In ill infants treatment of the underlying problem often results in resolution of the thrombocytopenia. Transfusions should be used for the bleeding child and for the infant with severe thrombocytopenia who is the product of a vaginal delivery. In addition to being therapeutic, platelet transfusions may also assist in diagnosis.
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PMID:Thrombocytopenia in the newborn. 635 31

Hematologic alterations unrelated to neoplastic bone marrow involvement include polycythemia, anemia, leukocytosis, leukopenia, thrombocytosis, thrombocytopenia and coagulopathies. Serum globulin levels may be increased or decreased, depending on the type of neoplasm. Plasma fibrinogen and fibrin degradation product concentrations are usually elevated in cancer patients, whereas cancer patients with DIC have low plasma fibrinogen concentrations. Hypercalcemia can be a sequel of osseous metastases. Neoplasia may cause the nephrotic syndrome in some patients. Effusions should be examined microscopically for signs of malignancy. Elevated serum enzyme levels are not specific in neoplastic disease.
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PMID:Laboratory aspects of cancer. 650 15

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

Cerebellar infarcts have been neglected for a long time and are now shown well by CT and especially MRI. Some infarcts involve the full territory supplied by a cerebellar artery. They are frequently complicated by edema with brain stem compression and supratentorial hydrocephalus, requiring at times emergency surgery, and are often accompanied by other medullary, medial pontine, mesencephalic, thalamic and occipital infarcts. On the other hand, partial territory infarcts are usually confined to the cerebellum and have a benign outcome with total recovery or minimal disability. They are more common than full territory infarcts. However, clinical presentations are similar to those full territory infarcts, differing mainly by the lack of drowsiness or unconsciousness. The main symptoms are vertigo, headache, vomiting, unsteadiness of gait and dysarthria. Signs include ipsilateral limb dysmetria, ipsilateral axial lateropulsion, ataxia and dysarthria. Vertigo is more severe and rotary in posterior inferior cerebellar artery territory infarcts, whereas dysarthria and ataxia are prominent in superior cerebellar artery territory infarcts. A few brain stem signs are sometimes added. In these territorial cerebellar infarcts, cardioembolism is the most common cause. Atherosclerotic occlusion comes next, involving the intracranial part of the vertebral artery and, less frequently, the lower basilar artery, both locations inaccessible to surgery. Other causes are artery to artery embolism from a vertebral artery origin stenosis, or the aortic arch, in situ intracranial branch atherosclerotic occlusion, and vertebral artery dissection. Border zone cerebellar infarcts occur in one third of the cases. They are small cortical or deep infarcts. They have the same symptoms and signs as territorial infarcts except for more frequent postural symptoms occurring over days, weeks or months after the ischemic event. The infarcts mainly have a thromboembolic mechanism, and sometimes have a hemodynamic mechanism: 1) focal cerebellar hypoperfusion due to large artery occlusive disease in more than half the cases, 2) small or end (pial) artery disease due to hypercoagulable state (thrombocythemia, polycythemia, hypereosinophilia, disseminated intravascular coagulation), arteritis or intracranial atheroma, and 3) rarely systemic hypotension due to cardiac arrest.
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PMID:[Cerebellar infarctions and their mechanisms]. 809 Oct 85

A 60-year-old Japanese woman was admitted to our hospital because of fatigue, weight loss and abdominal distension. Myelofibrosis was diagnosed, based on anemia, huge hepatosplenomegaly, leukoerythroblastosis and bone marrow fibrosis. Following treatment with ranimustine, anemia and splenomegaly improved. Seven months after initial therapy of ranimustine, however, polycythemia (RBC 7.39 x 10(6)/microliter; Hb 19.1 g/dl, Ht 65.9%) developed gradually, then RBC decreased to normal level following venesection (total 1,200 ml). After 32 months, blastic transformation occurred. The blasts were negative for myeloperoxidase. By flow cytometric analysis, the cells were positive for CD2, CD13, CD33 and HLA DR. Thus, AML (M0) was diagnosed. Despite of treatment with multicytotoxic agents, she died of DIC 36 months after the initial diagnosis of myelofibrosis. The progression from myelofibrosis to polycythemia is rare and only 15 cases have been reported so far. In addition, although a chromosomal abnormality, 46, XX, t(3; 12) (q25; p11), was present at the time of first diagnosis of myelofibrosis, the development of an additional abnormality, del(11) (q-), might be related to the transformation to AML.
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PMID:[A case of myelofibrosis that developed polycythemia vera following treatment with ranimustine and then acute myelogenous leukemia (M0)]. 882 83

A 32-year-old Japanese man was hospitalized for evaluation of unconsciousness. He was diagnosed as having primary pulmonary hypertension (PPH) with severe systemic hypertension, Raynaud's phenomenon and relative polycythemia. Hemostatic studies revealed increased coagulation and decreased fibrinolysis, similar to findings of chronic disseminated intravascular coagulation (DIC). Although activation of coagulation and systemic hypertension were improved after treatment with phlebotomy and administration of nifedipine, enerapril and warfarin, pulmonary hypertension was unchanged, suggesting that irreversible change had already occurred in the pulmonary arteries. Those complications could modify the process of pulmonary hypertension by inducing a hyperviscosity state.
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PMID:Primary pulmonary hypertension with severe systemic hypertension, Raynaud's phenomenon and relative polycythemia. 1157 54

The dramatic advances that have taken place in recent years in the care of sick and premature infants also have been matched by a similar increase in the use of blood transfusion therapy. Haematological features indicate that a newborn has a blood volume of 85-125 ml/kg the foetal haemoglobin is 60-85% and average Hb in full term infant is 18 gm/dl. By 2-3 months it falls to 11-12 g/dl the main cause of anemia are iron poor diet, weaning diets recurrent or chronic infections and hemolytic episodes in malarious areas. The red cells transfusions are usually top up transfusions, exchange transfusions, partial exchange transfusions. Top up- are for investigational losses and correction of mild degrees of anemias, upto to 5-15 ml/kg. They comprise 90% of all neonatal transfusions and are used in low birth babies in special care units for a maximum of 9-10 episodes. The walk in donor programs once popular are not much in vogue. The threshold for transfusion is 8-10 g/dl Hb for upto 5 weeks. Exchange transfusions are done for correction of anemia, removal of bilirubin, removal of antibodies and replacement of red cells. Ideally plasma reduced red cells that are not older than 5 days are used. It is prepared by removal of 120 ml of standard whole blood donation. The advantage of fresh cells is that hyperkalemia is avoided and good post transfusion survival acceptable red cell oxygen affinity. However it has to be screened for sickle cell disease and G6PD deficiency. Indications for exchange transfusion are kernicterus, neonatal hemolysis, G6PD deficiency, ARDS, neonatal sepsis, DIC and neonatal isoimmune thrombocytopaenia. Complications include over transfusion, perforation of major vessels, hypocalcaemia, citrate toxicity, hypothermia, hypoglycaemia, thrombocytopenia, necrotizing enterocolitis, GVHD, bacterial, viral infections. Partial exchange transfusions are done for symptomatic anemia, where Hb<10 g/dl, it is indicated in polycythemia and hyperviscosity syndromes. Exchange volume = Blood volume x (observed Hct-Desired HCt) divided observed Hct. Points to consider-there is weak expression of ABO antigens so particular care while grouping. Transfusing volumes should be 2-5 ml/kg/hour in paediatric bags of 50-100 ml with infusion devices. Platelet transfusion are indicated in neonatal throbocytopaenia, thrombocytopaenia due to sepsis, DIC, bacterial pathogens, CMV, TORCHS, Obstetric conditions such as pre eclampsia, intrauterine death abruption placenta birth injury hypoxia schock neonatal iso immune thrombocytopaenia and maternal ITP. Administration 1 RDE/pack per 2.5 kg single dose of fresh platelets less than 24hrs which contains 55 x 10(9) cells. This also contributes fresh plasma so is useful for coagulation defects also, though there is a risk of CMV and GVHD due to leucocyte contamination. Granulocyte concentrate; Gravity leucopheresis-1:8 ratio of 60 ml of 6% HES made to stand for 1hr.
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PMID:Component therapy. 1451 88

Neonatal renal vein thrombosis (RVT) is associated with potentially serious morbidities. Almost 80% of cases of RVT present within the first postnatal month. The most common risk factors for RVT are birth asphyxia/ in utero fetal distress, being the infant of a diabetic mother, volume contraction and coagulation abnormalities. Thrombus formation may be initiated by vascular injury, diminished vascular flow, increased blood viscosity, hyperosmolality or underlying thrombophilia. The classic triad of RVT includes gross hematuria, flank mass (unilateral or bilateral enlargement of kidneys) and thrombocytopenia. Laboratory tests may reveal hematuria, proteinuria, polycythemia, hemolytic anemia, thrombocytopenia and possibly acute kidney injury. The etiology for a hypercoagulable state should be investigated. Renal ultrasound with Doppler may show increased size of the affected kidney, increased echogenicity and loss of corticomedullary differentiation. Renal venography remains the gold standard for the diagnosis of RVT. Other causes of renal enlargement must be considered. Supportive treatment includes correction of fluid and electrolyte disturbances and treatment of infection and underlying pathophysiologic abnormalities. Use of unfractionated heparin (UFH) or low molecular weight heparin (LMWH) should be considered if there is evidence of disseminated intravascular coagulation. Conventional anticoagulants may attenuate hypercoagulability and decrease the risk for thrombus progression and embolism. Surgery is rarely indicated unless there is bilateral involvement with involvement of the IVC. RVT carries the risk of hypertension and chronic kidney disease.
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PMID:Renal venous thrombosis in neonates. 2508 63

To investigate the incidence and high-risk factors of fetal growth restriction (FGR) in Mainland China and determine the adverse effects of this condition on fetal-neonatal health. This study was a retrospective chart review. We investigated the incidence rate of FGR using a retrospective analysis of clinical data obtained from mothers and newborns from 7 hospitals in Mainland China from January 1 to December 31, 2011. The short-term outcomes of FGR were analyzed based on data obtained from the neonatal intensive-care unit (NICU) of Bayi Children's Hospital. The long-term outcomes of FGR were determined after a follow-up study of 125 cases of FGR in children at 18 months. The physical development index, mental development index (MDI), and psychomotor development index (PDI) were compared between FGR patients and controls. The incidence of FGR was 8.77%. The incidence of FGR was significantly higher in females than in males (9.80% vs 7.84%, P < 0.05). The incidence of FGR in preterm infants was higher than that in full-term infants (16.43% vs 7.87%, P < 0.01). Chronic hypertension, abnormal amniotic fluid, and umbilical cord abnormalities were independent factors of FGR. A significantly higher incidence of complications, including hypoglycemia, asphyxia, hypoxic-ischemic encephalopathy, gastrointestinal bleeding, congenital malformations, polycythemia, lung hemorrhage, apnea, congenital heart disease, and disseminated intravascular coagulation, was observed in FGR patients than in controls. The FGR prolonged the duration of the hospital stay and markedly increased hospitalization expenses (P < 0.05). Children with FGR showed catch-up growth, which reached the level of the control group after 1.5 years, but these individuals still had lower MDI and PDI scores. The incidence rate of FGR in Mainland China was 8.77%. It has a significantly adverse effect on fetal-neonatal health and cognitive development.
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PMID:The incidence rate, high-risk factors, and short- and long-term adverse outcomes of fetal growth restriction: a report from Mainland China. 2550 Oct 78


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