Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Coagulopathy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1976

[The clinical significance of deficiency coagulopathy in relationship to consumption coagulopathy (authors' transl)].

A deficiency coagulopathy may lead to a coagulation defect in the presence of massive blood loss which is characterized by a dilution of the coagulation factors especially a dilution of the plasma fibrinogen and the platelets and a dilution of their function. Hemorrhages which are triggered by a coagulation defect (consumption coagulopathy) may be aggravated by the additional loss of coagulation factors. The combination of a coagulation coagulopathy with a deficiency coagulopathy results in a bad prognosis. A case of deficiency coagulopathy and a case of consumption coagulopathy with additional deficiency coagulopathy are reported, the clinical importance and the management of these conditions are discussed.

Adult↗
PubMed1976

[Consumption coagulopathy and acidosis in the diabetic patient (author's transl)].

Four cases of intravascular coagulation associated with a state of acidosis in diabetics were observed in 57 patients with diabetic acidosis and 19 with lactic acidosis, in a series of 112 cases of consumption coagulopathy admitted to a department of medical resuscitation. In three cases the coagulopathy was found only on investigation; in one there were clinical and anatomic signs. The coagulopathy may be found either during the phase of recovery from ketoacidosis, or during the course of severe lactic acidosis, particularly during a recurrence of this form of acidosis. In spite of the unfavorable outcome in 3 of the 4 cases, the abnormal findings of coagulopathy reverted toward normal along with successful metabolic corrections. The factors responsible for consumption coagulopathy are acidosis, collapse, generalised systemic reactions and alterations of platelet function, of coagulation, of the balance between fibrin deposition and lysis and of lipid levels, all characteristic of diabetes. The clinical effects of this coagulopathy seldom become apparent but provide a possible explanation of some of the complications of diabetic ketoacidosis, particularly certain hemorrhagic or thrombotic events, as well as certain visceral complications, especially those affecting renal, pulmonary and cerebral areas.

Adolescent↗
PubMed2026

Coagulopathy in Neonates With Classic Galactosemia: A Life-Threatening Yet Underrecognized Complication.

INTRODUCTION: Classic galactosemia (CG) is a rare metabolic disorder caused by galactose-1-phosphate uridylyltransferase deficiency, leading to toxic metabolite accumulation and life-threatening complications such as failure to thrive, sepsis, and acute liver failure. We hypothesize that coagulopathy is an underrecognized complication of CG and that this gap is reflected by limited documentation in the medical literature. METHODS: A PubMed literature review was conducted to identify articles describing coagulopathy in CG. We filtered for guidelines, meta-analyses, reviews, and systematic reviews. Our article screening followed PRISMA guidelines. RESULTS: Of 49 identified articles, 26/49 (53%) met inclusion criteria. Only 6/49 (12%) explicitly described coagulopathy in CG, and only 1/49 (2%) discussed management. DISCUSSION: These data supports our hypothesis that coagulopathy may be an underrecognized complication of CG by clinicians and identifies a gap in current medical literature. Improved early recognition of coagulopathy in neonates with CG could prevent delays in treatment and improve outcomes.

Humans↗
PubMed1975

[Consumption coagulopathy and isolated platelet deficiency in childhood septicaemia].

In a retrospective study 40 children were selected out of 53 cases of septicaemia with thrombocytopenia. They were divided into two coincidentally equally large groups of patients with consumption coagulopathy on the one side and patients with isolated thrombocytopenia without consumption coagulopathy on the other side. Both groups were of comparable age and sex distribution. Two-thirds of the children were under three months. For the differential diagnosis of both groups the activated partial thromboplastin time, the thrombotest, the factor V plasma concentration, the serum concentration of fibrin (fibrinogen) degradation products as well as control coagulation studies can be considered to have the greatest diagnostic value. The results of the study permit the following conclusions: 1. Platelet deficiency in sepsis does not prove the presence of consumption coagulopathy. 2. Consumption coagulopathy and isolated thrombocytopenia differ statistically significantly according to the bacteria cultured from the blood, the circulatory state and the pH of the blood. 3. The finding of thrombocytopenia in a patient with shock, acidosis and gramnegative septicaemia justify the suspicion of consumption coagulopathy.

Acidosis↗
PubMedDate not supplied

Consumption coagulopathy associated with arterial aneurysms.

Consumption coagulopathy resulting from arterial aneurysm is an uncommon entity. Two patients, one with a femoral artery aneurysm and one with an abdominal aortic aneurysm containing fresh blood clot associated with a coagulopathy are presented. Reasonable preoperative control of the bleeding disorder with appropriate blood products followed by aneurysmectomy is recommended. Except to treat severe bleeding disorders associated with arterial aneurysms, heparin therapy is rarely necessary, as spontaneous reversal of the coagulopathy usually occurs. A high index of suspicion for the presence of an underlying arterial aneurysm as the cause for the consumption coagulopathy is necessary when no other etiology is obvious.

Aged↗
PubMed1977

Trousseau's syndrome and other manifestations of chronic disseminated coagulopathy in patients with neoplasms: clinical, pathophysiologic, and therapeutic features.

Analysis of 182 patients with chronic disseminated intravascular coagulopathy and malignancy shows common features. Migratory thrombophlebitis occurred in 96 patients while at least a single episode of thrombophlebitis was noted in 113. Seventy-five of the patients bled and 45 had arterial emboli in various organs. Twelve patients had the triad of thrombophlebitis, hemorrhage, and arterial emboli, often sequentially. Hematologic data showed derangements associated with intravascular coagulation, the most prominent of which were hypofibrinogenemia and thrombocytopenia. Other abnormalities included prolonged prothrombin time, increased fibrinogen-fibrin degradation products, decreased levels of factors V and VIII, cryofibrinogenemia, and microangiopathic hemolytic anemia. Forty-one patients had lesions of non-bacterial thrombotic endocarditis at autopsy; 31 of these had arterial emboli during life. None of the lesions were infected. Mitral and aortic valves were most frequently involved. No single mechanism that causes the disseminated intravascular coagulopathy has been identified. However, cell products--secretions and enzymes--and the cells themselves have been proposed as the procoagulant(s) responsible for the syndrome. In addition to treatment of the underlying neoplasm, symptomatic disseminated intravascular coagulopathy should be controlled. Heparin is the drug of choice for treatment of this problem, very little benefit having been observed with warfarin therapy. Long-term use of anticoagulants is potentially feasible for control of chronic disseminated intravascular coagulopathy, but without effective control of the underlying tumor ultimately will be unsuccessful.

Adult↗
PubMed1976

Consumptive coagulopathy in severe preeclampsia.

Our experience with consumptive coagulopathy associated with preeclampsia at North Carolina Baptist Hospital is presented. All cases of recognized consumptive coagulopathy on the obstetric service from 1969 to 1975 are reviewed and the associated obstetric entities given. Two cases of consumptive coagulopathy complicating severe preeclampsia are presented. Consumptive coagulopathy occurred in 9.1% of eclamptic patients and in 2.6% of severe preeclamptic patients. No previous incidence figures were found in the literature.

Adolescent↗
PubMedDate not supplied

Coagulopathy following experimental cerebral ischemia.

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.

Animals↗
PubMed1975

[Therapy of consumption coagulopathy and hyperfibrinolysis with urokinase in a case of acute promyelocytic leukemia].

A case report is presented of a 20 year old patient with an acute promyelocytic leukemia. The presenting symptom was a macrohematuria caused by a consumption coagulopathy. Consumption coagulopathy has only been observed in acute promyelocytic leukemia in contrast to other coagulopathies in acute leukemia. The clotting disorder was successfully treated by administration of urokinase.

Acute Disease↗
PubMed1975

Hemangioma-thrombocytopenia syndrome; a disseminated intravascular coagulopathy.

A patient who had multiple hemangiomas and for whom results of coagulation studies were consistent with hemangioma-thrombocytopenia (Kasabach-Merritt) syndrome and a microangiopathic hemolytic process was asymptomatic prior to surgical removal of a lipoma. Postoperatively, she developed bleeding secondary to a disseminated intravascular coagulopathy. Her bleeding was controlled by anticoagulation therapy. A review of the literature provides evidence suggesting that the hemangioma-thrombocytopenia syndrome is due to a disseminated intravascular coagulopathy initiated within the hemangioma. Surgical trauma may precipitate exacerbations of the coagulopathy in these patients and all unnecessary surgical procedures should be avoided.

Disseminated Intravascular Coagulation↗
PubMed1978

A case of giant cavernous hemangioma of the liver complicated by intravascular coagulopathy.

A case of liver hemangioma complicated by intravascular coagulopathy is presented because of the rarity of the association. Hemangioma of the liver was suspected by palpation of the liver tumor, scintigraphy and x-ray examination, and confirmed by selective hepatic arteriography in combination with exploratory laparotomy. Intravascular coagulopathy was established by demonstrating secondary fibrinolysis and consumption of platelets and coagulation factors. Unconjugated hyperbilirubinemia due to micro-angiopathic hemolytic anemia was also present. The clinical course of the clotting abnormalities was basically a chronic one with an occasional acute or subacute defibrination process associated with further enlargement of the hepatic tumor. These provide sufficient evidence that the intravascular coagulopathy was closely related with the hemangioma in the liver. Neither ligation of a presumed nutritional artery of the hemangioma nor radiation therapy caused any demonstrable reduction in the tumor size.

Adult↗
PubMed1979

Severe coagulopathy following insertion of the LeVeen shunt: a potentially fatal complication.

Four patients who underwent insertion of the LeVeen shunt for treatment of medically intractable hepatic ascites had coagulation changes. Peritoneo-venous shunting was associated with a mild coagulopathy in two patients, simulating disseminated intravascular coagulation or primary fibrinolysis. The coagulopathy was severe in two patients and life-threatening in one of these. Postoperative coagulopathy may be detected by careful monitoring of coagulation indices and the risk of its development parallels the severity of liver disease.

Adult↗
PubMed1978

Consumptive coagulopathy. A complication of therapy of solid tumors in childhood.

The association of consumptive coagulopathy and malignancy is thought to be rare in pediatrics. In one patient with Ewing's sarcoma and in two with rhabdomyosarcoma consumptive coagulopathy developed in the presence of either diffuse metastatic disease or an extensive primary tumor. The coagulopathy was a major clinical problem, developing within five days of the onset of chemotherapy. Resolution coincided with the clinical response of the tumor.

Adolescent↗
PubMed1976

[Acute consumption coagulopathies. 120 cases].

Consumption coagulopathy is frequently observed in a resuscitation department. 120 cases of various etiologies are reviewed: complications of pregnancy (61 cases), infections (23 cases) or various stresses: acute hemolysis, shock, severe hepatic failure, intoxications, acidosis, heat-stroke... Consumption coagulopathy is intricated with the general stress which induces it, and with the visceral lesions induced by the stress and which can be aggravated by the consumption coagulopathy. The state of shock is observed in 76% of the cases, the haemorrhagic syndrome in 73%. Acute hemolysis and the clinical signs evocative of disseminated intravascular coagulation (cutaneous signs) are more rare. Following the initial manifestations, visceral complications may develop: renal, hepatic, respiratory, neurological, digestive. The evolution of the biology must be carefully studied. The diagnosis is made on both clinical and biological data. Etiological and pathophysiological treatment should be carried out. In our series, controlled and adapted heparin therapy was given systematically.

Disseminated Intravascular Coagulation↗
PubMed1978

Acute promyelocytic leukemia. Management of the coagulopathy during daunorubicin-prednisone remission induction.

Seven adults with acute promyelocytic leukemia (APL) and disseminated intravascular coagulation were treated for remission induction with daunorubicin hydrochloride and prednisone. In all patients the coagulopathy was managed with continuous-infusion heparin sodium and vigorous transfusion with platelets, cryoprecipitate, and fresh frozen plasma. Five patients survived induction; they all achieved complete remission (CR). Median duration of CR was 27 + months; two patients presently survive in their initial CR at 28 and 48 months. Recognition of APL as a distinct type of acute leukemia and prompt initiation of treatment aimed at rapid cytoreduction and control of the coagulopathy has resulted in a prolonged disease-free survival for the majority of patients.

Adolescent↗
PubMed1976

Chronic consumption coagulopathy accompanying abdominal aortic aneurysm.

Each of two patients harboring a stable abdominal aortic aneurysm manifested severe recurrent bleeding consequent to chronic consumption coagulopathy (CCC). Both underwent successful aneurysmectomy, but in only one patient did bleeding cease and depressed clotting factors return to normal activity. In the other patient, subsequent observations suggested that his coagulopathy actually resulted from occult pancreatic carcinoma. We propose here criteria for establishing stable aneurysm as the cause of CCC and demonstrate the efficacy of heparin in reversing the coagulation defect prior to surgical intervention. These cases also illustrate that the discovery of CCC accompanying stable aneurysm may signal the presence of another underlying disorder.

Aged↗
PubMed1976

Acute coagulopathy following infusion of prothrombin complex concentrate.

An acute coagulopathy developed in a 49 year old woman with severe liver disease after she received an infusion of prothrombin complex concentrate. The concentrate used in the infusion was subsequently studied by observing the effect of the concentrate on the partial thromboplastin times of various plasmas. The evidence suggests that activated coagulation factors, including activated factor X, were present in the concentrate, and probably played a role in initiating the acute change in the patient's coagulation status. Mechanisms whereby liver disease predisposes toward the development of such a coagulopathy are discussed. It would appear that prothrombin complex concentrates should be used in patients with liver disease only with utmost caution.

Alcoholism↗
PubMed1977

Coagulopathy with midtrimester induced abortion: association with hyperosmolar urea administration.

Coagulation changes, usually subclinical, have been reported in association with the induction of midtrimester abortion by the administration of intra-amniotic hypertonic sodium chloride, hyperosmolar urea, hyperosmolar urea plus prostaglandin F2alpha, and hyperosmolar ura or hypertonic glucose plus prostaglandin E2. In addition, clinically significant coagulopathy has been described in association with the administration of hypertonic sodium chloride. This study details a three-year experience involving 3,034 cases of midtrimester elective abortion and describes six cases of coagulopathy in association with the administration of hypertonic sodium chloride and two cases in association with the administration of hyperosmolar urea. The significance of these findings and etiologic considerations are discussed.

Abortifacient Agents↗