Hemorrhagic Tendency Following Massive Transfusions at Surgery

2015 ◽  
pp. 78-78
Author(s):  
Mario Stefanini
Keyword(s):  
Hemorrhagic Tendency

scholarly journals Congenital Vascular Defect Associated with Platelet Abnormality and Antihemophilic Factor Deficiency

Blood ◽  
1960 ◽  
Vol 15 (6) ◽  
pp. 807-829 ◽  
Author(s):  
GIOVANNI RACCUGLIA ◽  
JAMES V. NEEL ◽  
Ruth T. Davidson ◽  
Mary Jane Ussery
Keyword(s):  
Bleeding Time ◽  
A Priori ◽  
Dominant Gene ◽  
Hemorrhagic Diathesis ◽  
Prolonged Bleeding ◽  
Prolonged Bleeding Time ◽  
Factor Deficiency ◽  
Hemorrhagic Tendency ◽  
Vascular Defect ◽  
Antihemophilic Factor

Abstract 1. A kindred of 311 individuals, many members of which are affected by a hemorrhagic diathesis, has been described. 2. The variability in the manifestations of this diathesis is extreme. In its fullest expression the disease is characterized by a prolonged bleeding time with evidence of a morphologic defect in the platelets, and a deficiency in antihemophilic globulin. Some possibly affected individuals exhibit only a prolonged bleeding time, while, on the other hand, the clinically most severely affected individual, with AHF levels on several occasions of 5 to 10 per cent, has not been observed by us to have a prolonged bleeding time, although his platelets are morphologically abnormal. 3. Genetic analysis suggests that the hemorrhagic tendency is determined by a single dominant gene of variable penetrance and expressivity. 4. No satisfactory explanation can be developed on the basis of these studies for the association between platelet abnormality and AHF deficiency. More specifically, it is impossible to conclude whether the platelet defect is precursor to the AHF deficiency, or whether—as on a priori grounds seems less likely—this is an example of true genetic pleiotropy. 5. The terminologic chaos which afflicts the literature on hemorrhagic diatheses characterized by a prolonged bleeding time is discussed in the light of the findings in this one large kindred, and suggestions are advanced for minimizing confusion based on terminology alone.

RUPTURE OF THE SPLEEN IN AN ERYTHROBLASTOTIC INFANT

PEDIATRICS ◽  
1949 ◽  
Vol 4 (3) ◽  
pp. 296-300
Author(s):  
EUGENE L. SLOTKOWSKI ◽  
ALBERT M. HAND
Keyword(s):  
Blood Volume ◽  
Extramedullary Hematopoiesis ◽  
Abdominal Pressure ◽  
Precipitating Factors ◽  
Birth Process ◽  
Splenic Parenchyma ◽  
Hemorrhagic Tendency ◽  
Rupture Of The Spleen

Rupture of the spleen is reported in an erythroblastotic infant who died during an exsanguination-replacement transfusion. The changes in the spleen incident to erythroblastosis fetalis render this organ more vulnerable to trauma and rupture. The predisposing and precipitating factors include extramedullary hematopoiesis in the splenic parenchyma, increased phagocytosis, weakening of the capsule and trabeculae, increased intra-abdominal pressure during the birth process, congestive splenomegaly, hemorrhagic tendency, displacement of the spleen and the increased blood volume during a transfusion.

THE VITAMIN K DEFICIENCY IN INFANCY IN JAPAN -- THE SECOND NATIONWIDE SURVEY

1987 ◽  
Author(s):  
T Nagao ◽  
Y Hanawa ◽  
K Sawada ◽  
I Tsukimoto ◽  
I Ikeda ◽  
...  
Keyword(s):  
Vitamin K ◽  
Nationwide Survey ◽  
Near Miss ◽  
Screening Tests ◽  
Hemorrhagic Disease ◽  
Vitamin K Deficiency ◽  
K Deficiency ◽  
Hemorrhagic Tendency ◽  
Bile Duct Atresia ◽  
Nation Wide Survey

Questionnaires were sent to 1,218 hospitals with more than 200 beds, in order to know the incidence of hemorrhagic disease due to vitamin K deficiency in infancy beyond 2 weeks after birth, during 4 and a half years, i.e. from January 1981 to June 1985. Out of the 534 cases reported, 407 had no obvious reasons for vitamin K deficiency: "idiopathic vitamin K deficiency in infancy". Other 68 cases had bleedingepisodes due to vitamin K deficiency associated with hepatobiliary lesions (e.g.congenital bile duct atresia), chronic diarrhea, long term antibiotic therapy and so on: "secondary vitamin K deficiencyin infancy". The third group consisting of 59 cases was so called "near miss" type, in which hemorrhagic tendency was discovered at the time of mass screening tests for vitamin K deficiency or by chance withoutany clinical hemorrhage. In the idiopatic group, 345 cases (84.8%) developed their bleeding episodes between 21 and 59 days of age, and 368 cases (90.4%) were wholly breast-fed. Intracranial hemorrhage was seen in 338 cases (83.0%) of this group. In most cases of this series (97.3%),no vitamin K was supplemented after birth. Administration of vitamin K is an urgent routine procedure during the first one or two months of life for all newbornbabies, although the incidence of the idiopathic vitamin K deficiency in infancyhas not decreased significantly comparedto the results of the first nation-wide survey (Jan. 1978 - Dec. 1980). This study was sponsored by the Ministry of Health and Welfare of Japan.

scholarly journals THROMBOCYTOPENIC PURPURA COMPLICATING GOLD THERAPY FOR RHEUMATOID ARTHRITIS

Blood ◽  
1948 ◽  
Vol 3 (10) ◽  
pp. 1105-1111 ◽  
Author(s):  
STACY R. METTIER ◽  
ALICE Mc BRIDE ◽  
JONAH LI
Keyword(s):  
Rheumatoid Arthritis ◽  
Blood Platelets ◽  
Spontaneous Remission ◽  
Gold Salt ◽  
Gold Therapy ◽  
Thrombocytopenic Purpura ◽  
Fourth Patient ◽  
Dramatic Rise ◽  
Hemorrhagic Tendency

Abstract Of 160 patients treated with gold salt therapy, four developed thrombocytopenia with mild purpuric manifestations. In three patients there was a spontaneous remission and the hemorrhagic tendency disappeared in about one week’s time. In the fourth patient there was a second occurrence of thrombocytopenia which persisted over a period of four months, and finally failed to respond to transfusions. Splenectomy was followed by a dramatic rise in the blood platelets and recovery of the patient.

scholarly journals THE ONE-STAGE PROTHROMBIN CONSUMPTION TEST

Blood ◽  
1950 ◽  
Vol 5 (10) ◽  
pp. 964-972 ◽  
Author(s):  
MARIO STEFANINI ◽  
WILLIAM H. CROSBY
Keyword(s):  
Polycythemia Vera ◽  
Thrombocytopenic Purpura ◽  
One Stage ◽  
Hemorrhagic Tendency ◽  
The One

Abstract 1. The results of the one-stage prothrombin consumption test, performed in a group of patients with various abnormalities of the hemostatic mechanism, are reported. It appears that the test accurately identifies those conditions such as hemophilia and thrombocytopenic purpura which involve a deficiency of available thromboplastin. Other conditions examined in which a hemorrhagic tendency may develop (hypoprothrombinemia, polycythemia vera, pseudohemophilia) showed a normal consumption of prothrombin. In the hypoprothrombinemia due to dicumarol therapy, the limited amount of available prothrombin appears to have been well utilized during the process of coagulation. 2. It appears that correction of the results obtained for accelerator activity of serum is hardly ever necessary, since this effect is not of such magnitude as to modify the results of the prothrombin consumption test to any extent. A formula for such correction is given.

ABNORMALITIES OF CYTOPLASMIC [Ca++] IN PLATELETS FROM UREMIC PATIENTS STUDIED WITH AEQU0RIN AND INDO-1

1987 ◽  
Author(s):  
J A Ware ◽  
B A Clark ◽  
M Smith ◽  
E W Salzman
Keyword(s):  
Normal Donor ◽  
Ionophore A23187 ◽  
Platelet Surface ◽  
Surface Receptors ◽  
Prolonged Bleeding ◽  
Prolonged Bleeding Time ◽  
Hemorrhagic Tendency ◽  
Uremic Patients ◽  
Plasma Factors

Uremic patients have a hemorrhagic tendency, often with prolonged bleeding times and abnormalities of platelet function in vitro. Whether these defects result from plasma factors, abnormalities in platelet surface receptors, or intracellular mediators is unknown. Accordingly, blood was obtained from 16 patients with severe uremia (BUN >90), and platelets were washed, loaded with aequorin or indo-1, gel-filtered, and resuspended in either plasma or buffer. Of the 16 patients, 4 had template bleeding times greater than 12 minutes, but platelet aggregation in plasma was not consistently impaired. However, the rise in cytoplasmic [Ca++] in response to the Ca++-ionophore A23187 or ADP in aequorin-loaded platelets from the 4 patients with long bleeding times was much lower than in uremic patients with normal bleejljLng times or in normal volunteers. The reduced [Ca++] response was associated with decreased aggregation of gel-filtered platelets in buffer. Prolonged bleeding time was less consistently correlated with decreased responses to epinephrine or arachidonate. Suspending washed aequorin-loaded uremic platelets in normal plasma for 10-20 min did not reverse the decreased agonist-induced rise in [Ca++]; platelets from a normal donor resuspended in uremic pla^iya responded normally. The agonist-induced rise in [Ca++] shown by indo-1 was not abnormal in patients with prolonged bleeding times; however, uremic patients generally had higher indo-l-indicated basal platelet cytoplasmic [Ca++] than normal. We conclude that the hemorrhagic tendency in some patients with uremia (|s associated with abnormal intracellular platelet [Ca++] regulation marked by elevated resting [Ca++] and a decreased rise in cytoplasmic [Ca++] in response to certain agonists; this latter abnormality appears to be correlated with prolonged bleeding times.

Protection Of Endotoxin Induced Disseminated Intravascular Coagulation In Rats By Gabexate Mesilate

1981 ◽  
Author(s):  
T Yoshikawa ◽  
Y Furukawa ◽  
M Murakami ◽  
S Takemura ◽  
M Kondo
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Femoral Vein ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Gabexate Mesilate ◽  
Intravascular Coagulation ◽  
Wistar Strain ◽  
Potent Inhibitory Effect ◽  
Strong Inhibitory Effect ◽  
Hemorrhagic Tendency

Gabexate mesilate[ methane sulfonic acid salt of ethyl-p- (6-guanidino hexanoyloxy) benzoate : FOY ] has recently been developed in Japan, and has been known to have potent inhibitory effects on trypsin, kallikrein, plasmin, thrombin and C1-esterase. Advantage of clinical use of this agent is that FOY has smaller molecular weight than aproti- nin so that production of antibody against FOY is hardly observed. In the present investigation, effect of FOY on disseminated intravascular coagulation (DIC) was examined using experimental animal models, in comparison with that of heparin.Female rats of Wistar strain (8-weeks) were infused with l00mg/kg of bacterial endotoxin (Lipopolysaccharide B; E. coli; 055, Difco) continuously for 4 hours through femoral vein. Blood samples were serially taken from abdominal artery using catheter and examined for plasma fibrinogen, FDP, platelet counts, prothrombin time and partial thromboplastin time. After the experiment, kidneys were removed to examine the deposition of fibrin to glomeruli.Different concentrations of FOY were intraperitoneally injected to the rats prior to the infusion of endotoxin, and it was found that the administration of 10 mg/kg of FOY showed the most potent inhibitory effect on the development of DIC, either hematologically or histologically. In comparison, heparin showed a strong inhibitory effect on DIC over a dosage of 5 U/kg.It is concluded that, although inhibitory effect of FOY was less significant than heparin, FOY might be valuable agent for the treatment of DIC especially when heparin is difficult to use in such cases as severe hemorrhagic tendency.

scholarly journals Platelet Dysfunction in Glycogen Storage Disease Type I

Blood ◽  
1973 ◽  
Vol 41 (2) ◽  
pp. 235-247 ◽  
Author(s):  
Emily E. Czapek ◽  
Daniel Deykin ◽  
Edwin W. Salzman
Keyword(s):  
Glycogen Storage Disease ◽  
Platelet Function ◽  
Storage Disease ◽  
Glycogen Storage Disease Type ◽  
Glycogen Storage ◽  
Disease Type ◽  
Severe Bleeding ◽  
Type I ◽  
Prolonged Bleeding Time ◽  
Hemorrhagic Tendency

Abstract A hemorrhagic tendency has been observed in patients with glycogen storage disease Type I (GSD-I). We have studied the hemostatic mechanism in six patients with GSD-I who have mild to severe bleeding tendencies. All exhibited abnormalities of platelet function (decreased prothrombin consumption, abnormal aggregation reactions, prolonged bleeding time, and low platelet adhesiveness). The degree of dysfunction correlated with the patients’ general clinical condition: when patients were acidotic and severely lipemic, platelet function was strikingly impaired. Two patients received a course of continuous intravenous alimentation. As their general metabolic state approached normal, abnormal platelet function was corrected. We found normal platelets to contain no glucose-6-phosphatase. There was no consistent increase in platelet glycogen levels in patients with GSD-I. These data indicate that the bleeding disorder in GSD-I is an acquired defect rather than a primary platelet abnormality.

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