phenprocoumon and Chronic-Disease

A cardiac pacemaker was to be implanted in a 74-year-old man, known for many years to have cardiac arrhythmias. Lown type IVb, because of the onset of severe bradycardic episodes. After appropriate preoperative preparation the patient's anticoagulant medication was changed over 5 days from phenprocoumon (Marcumar) to heparin. The procedure and the immediate postoperative period were without complication. But two days later he had to be admitted to the intensive care unit because of cardiac failure and bleeding into the operation site.. One week after starting heparin the platelet count had fallen from 154 x 10(9)/l preoperatively to 92 x 10(9)/l. Haemoglobin concentration was 8.9 g/dl, haematocrit 26.7%. The Quick value of 51%, partial thromboplastin time of 54.1 s, thrombin time of 17.6 s and plasma antithrombin level of 61% provided no further diagnostic pointers. An HIPA test and a PF4/heparin immunoassay, performed as heparin-induced type II thrombocytopenia was suspected, subsequently confirmed the diagnosis.. After the cardiac status had stabilized the operative wound was explored, but no bleeding site found. Other causes having been excluded (liver failure, disseminated intravascular coagulopathy, septicemia, dilution thrombocytopenia), heparin was discontinued 2 days later. Recombinant hirudin infusion, 0.025 mg/kg per hour, was begun. After 4 days the platelet count had improved, the other clotting parameters were stable within the therapeutic anticoagulant range and the diffuse bleeding had stopped.. When changing from phenprocoumon to heparin preoperatively one must be aware of the rare risk of acquired heparin-induced thrombocytopenia. Intravenous recombinant hirudin proved to be a safe treatment until oral anticoagulation had been established, quickly normalizing the platelet count.

Topics: Aged; Anticoagulants; Bradycardia; Chronic Disease; Heparin; Humans; Male; Pacemaker, Artificial; Phenprocoumon; Postoperative Hemorrhage; Preoperative Care; Thrombocytopenia

The coincidence of coagulatopathy and chronic subdural haematoma (CSH) requires correction of coagulation to facilitate surgery. We investigated the correlation between coagulopathy and outcome in CSH patients.. We analysed past medical history, surgical treatment and coagulation parameters of 114 patients.. Coagulation disorders were found in 42%. Preoperative treatment with prothrombin complex concentrate was necessary in 14%. A significant difference (P < 0.05) of the preoperative level of platelets was found between recurrent CSH and non-recurrent group. Totally, we had to perform re-operations in 17.5%. Eighty-one patients presented with Glasgow coma scale (GCS) > or = 13. After surgery GCS was > or = 13 in n = 92. There was an improvement of GCS in 46 cases, 61 patients maintained GCS score levels. Outcome was significantly worse in the alcoholic group (P < 0.001), and in the recurrent group (P < 0.05). In patients with substitution of coagulation factors, outcome was worse in the group with post-operative substitution only (P < 0.05).. In CSH, the coagulation parameters and a subtle correction of coagulation are of special interest, regarding the worse outcome in patients with recurrent CSH and in those requiring post-operative substitution.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Alcoholism; Anticoagulants; Blood Coagulation Disorders; Blood Coagulation Factors; Blood Coagulation Tests; Chronic Disease; Craniotomy; Factor XIII Deficiency; Female; Glasgow Coma Scale; Hematoma, Subdural; Humans; Male; Middle Aged; Phenprocoumon; Platelet Count; Postoperative Hemorrhage; Preoperative Care; Recurrence; Reoperation; Survival Rate; Tomography, X-Ray Computed; Treatment Outcome

In portal vein thrombosis, various hypercoagulable conditions and inherited or acquired thrombophilias have already been described as predisposing factors. In a 33-year-old man admitted to a hospital with upper abdominal pain, a partial portal vein and upper mesenteric vein thrombosis, respectively, and a complete splenic vein thrombosis were diagnosed. Further diagnostic procedures showed no evidence for local precipitating factors or any underlying infectious, paraneoplastic or inflammatory disease. Thrombophilia screening demonstrated elevated factor VIII levels (206 %) and von Willebrand factor levels (> 440 %). An acute-phase reaction was excluded. Oral anticoagulant therapy with phenprocoumon was started. Factor VIII and von Willebrand factor were reproducibly elevated to high activity levels over a period of 12 months in absence of acute or chronic inflammatory reaction. Increased levels of factor VIII and von Willebrand factor may play a pathogenetic role in the development of portal, splenic, and mesenteric thrombosis.

Topics: Adult; Chronic Disease; Diagnosis, Differential; Factor VIII; Humans; Magnetic Resonance Angiography; Male; Mesenteric Vascular Occlusion; Mesenteric Veins; Phenprocoumon; Portal Vein; Thrombophilia; Thrombosis; von Willebrand Factor

A 39-year-old woman complained of dyspnoea and increasing abdominal pressure sensation. A Greenfield filter had been implanted into her inferior vena cava (IVC) 4 years previously because of pulmonary embolism from a deep vein thrombosis after a hysterectomy with abscess formation. Physical examination revealed neck vein congestion, jaundiced sclerae, a tense abdominal wall, ascites and a soft machinery murmur in the paraumbilical region.. Transaminase activities were slightly raised (GOT 38 U/I, GPT 20 U/I), but total bilirubin and direct bilirubin were markedly elevated (2.9 mg/dl and 1.1 mg/dl, respectively). There was no evidence of cholestasis or decreased liver synthesis. Ultrasound showed marked dilatation of the IVC and hepatic veins, and echocardiography revealed right ventricular enlargement with grade II tricuspid regurgitation. Calculated pulmonary arterial systolic pressure averaged 50 mmHG. Colour-coded Doppler sonography demonstrated an aorto-caval shunt at the level of the filter in the IVC and penetration of a filter strut into the aortic lumen.. After removing the ascitic fluid by fluid and sodium restriction, and administration of an aldosterone antagonist and a loop diuretic, the A-V fistula was closed surgically and the filter removed. Three months after operation she was put on phenprocoumon (Quick value 20-30%). At the latest outpatient examination, 6 months after the operation, she was free of symptoms.. As filter implantation in the IVC may produce severe complications, indications for it need to be demonstrated by further studies of its efficacy.

Topics: Adult; Anticoagulants; Aorta, Abdominal; Aortic Diseases; Arteriovenous Fistula; Chronic Disease; Echocardiography; Female; Follow-Up Studies; Heart Failure; Humans; Phenprocoumon; Time Factors; Ultrasonography, Doppler, Color; Vena Cava Filters; Vena Cava, Inferior

Topics: Age Factors; Aged; Anticoagulants; Aspirin; Atrial Fibrillation; Chronic Disease; Heparin; Humans; Middle Aged; Phenprocoumon; Platelet Aggregation Inhibitors

Topics: 4-Hydroxycoumarins; Anticoagulants; Chronic Disease; Female; Hematoma; Humans; Laryngeal Diseases; Middle Aged; Penicillin G Benzathine; Pharyngeal Diseases; Phenprocoumon; Thrombophlebitis; Tonsillitis

A case of primary vascular pulmonary hypertension (PVPH) in a 53-year old woman (160 cm, 90 kg) is reported. She first complained of symptoms of breathlessness on exertion 2-3 months after completion of three courses of fenfluramine (Ponderax). The courses began in October 1977 and ended in May 1978. Despite persisting symptoms no relevant clinical findings were obtained. The patient was admitted to this hospital after complaining of short syncopal attacks on exertion, in November 1981. Typical signs of PVPH were now demonstrable, with a resting pulmonary pressure of 98/45 mm Hg. Clinical findings showed a similarity to those obtained in patients suffering from aminorex-induced PVPH, although fenfluramine shows some biological differences to aminorex. A causality between the development of PVPH and fenfluramine intake is probable on the basis of the patient's history, but it cannot be proven.

Topics: Chronic Disease; Female; Fenfluramine; Humans; Hypertension, Pulmonary; Middle Aged; Nifedipine; Obesity; Phenprocoumon; Syncope