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[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

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

[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

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

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

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

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

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

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

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

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

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

Case report: intestinal bypass and severe coagulopathy.

A 29-year-old woman, two years post-ileojejunal bypass, developed a serious coagulopathy. Studies utilizing heparin, epsilon-aminocaproic acid, and plasma, in vivo, indicated that the coagulation abnormalities were multiple in origin. Correction of most of the abnormalities permitted revision of bypass which led rapidly to total permanent correction of the coagulopathy.

Adult

Consumption coagulopathy and microangiopathic hemolytic anemia with an axillo-femoral graft.

Consumption coagulopathy and microangiopathic hemolytic anemia occurred as a complication of insertion of an axillofemoral, preclotted dacron graft. Treatment with heparin followed by dipyridamole and aspirin normalized the hematologic and coagulation abnormalities over a two month period. The mechanism of consumption coagulopathy associated with prosthetic grafts is discussed and a possible role for treatment with antiplatelet agents is suggested.

Aged

Heparin-induced coagulopathy.

Intravenous heparin, at doses of 3.0 U./gm of body weight, produced an intravascular coagulopathy in rats which was manifested by intestinal tract hemorrhage, a reduction in plasma fibrinogen concentration, a rise in fibrinogen-fibrin degradation products, and the absence of a rise in platelet count noted in the control animals. This coagulopathy could not be produced by conventional anticoagulant doses of heparin or the injection of large doses of heparin in the presence of protamine sulfate. Specific studies excluded hypoxemia, metabolic acidosis, and endotoxemia as possible etiologic factors. The coagulation abnormalities observed in this study differ from those produced by injection of other polyanionic substances but their precise pathogenesis is still uncertain.

Animals

[Aetiopathology and forms of obstetric coagulopathies (author's transl)].

An account is given of the pathological mechanism of coagulopathies resulting from excessive loss of blood, exhaustive consumption of coagulation factors or hyperfibrinolysis. While there is no unambiguous differentiation between various forms of coagulopathies in obstetrics, major characteristics should be well understood for therapeutic decision-making. The early high-accuracy laboratory test, therefore, is imperative.

Blood Coagulation Disorders

[Microangiopathic hemolytic anemia and consumption coagulopathy with metastasizing gastric carcinoma (author's transl)].

Microangiopathic hemolytic anemias (MHA) are frequently at the root of metastasizing gastric carcinoma. If the characteristic fragmented erythrocytes ("schistocytes") are found to be increased in the blood smear, this can be taken as a pointer to gastric neoplasm. Consumption coagulopathy frequently intensifies the clinical symptoms. A report of a 51-year-old woman with gastric carcinoma, MHA and consumption coagulopathy is given in whom the determination of numerous schistocytes in the peripheral blood was of decisive significance for the diagnosis.

Adenocarcinoma

[The development of coagulopathy in missed abortion (author's transl)].

A case of fetal death is demonstrated, where a primary hyperfibrinolysis induced a bleeding tendency after curettage. Writings on the subject give differing opinions on the pathogenesis of coagulopathy in the case of fetal demise (= dead fetus syndrome). It is shown that the coagulopathy is caused most frequently by a combination of disseminated intravascular coagulation (DIC) and subsequent hyperfibrinolysis. In sporadic cases, however, one of both pathogenetic mechanisms can occur isolated.

Abortion, Missed