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PubMedDate not supplied

Thrombolytic therapy for prosthetic cardiac valve thrombosis.

During 1992-93 12 patients (5 males, 7 females) with thrombosed prosthetic cardiac valves were treated with streptokinase on 13 occasions (one patient with prosthetic tricuspid valve had two thrombotic episodes). Their age ranged from 14 to 52 years (median 39). Two valves were in aortic position, six in mitral and four in tricuspid position. Eight were Bjork-Shiley prosthesis, three were Medtronic Hall valves and one was a St. Jude Valve. Timing of prosthetic valve thrombosis ranged from 3 months to 12 years after valve replacement surgery. Duration of symptoms due to valve thrombosis ranged from 1-4 months with tricuspid valve thrombosis and 1-14 days with left sided valve thrombosis. Five were in functional class II and four each were in functional class III and class IV. All patients were evaluated by echo Doppler and cine fluoroscopy. Loading dose of streptokinase was 2.5 lakh units in 4 patients and 1 lakh units in 9 patients. Maintenance infusion was at 1000 units/Kg/hour in 11 patients and 1 lakh units/hour in 2 patients. Duration of streptokinase infusion ranged from 3 hr to 38 hr. Thrombolytic therapy was successful (clinical, echo Doppler and fluoroscopy) in 12 out of 13 cases (92%). It was unsuccessful in a patient with valve at tricuspid position in whom infusion had to be stopped after 24 hour due to bleeding gums. One patient developed intracerebral bleed and expired. In conclusion streptokinase therapy is useful for prosthetic cardiac valve thrombosis.

Adolescent↗

PubMed1994

[A rare cause of portal vein thrombosis: closed abdominal trauma].

Abdominal trauma is a rare and poorly documented cause of portal vein thrombosis. We report here the case of a patient in whom portal vein thrombosis was diagnosed one month after an abdominal blunt trauma. Post-traumatic origin of thrombosis was confirmed by the negativity of an exhaustive aetiological investigation. Thrombosis involved portal bifurcation and right and left portal veins, but remained asymptomatic. A particularity of this case was that a total regression of the thrombosis was observed under anticoagulation therapy.

Abdominal Injuries↗

PubMed1994

[Thrombosis and stenosis of central venous access in hemodialysis].

Thrombosis or stenosis of the vessel is an usual complication of the long term catheterization of the veins. In hemodialysis, thrombosis and/or stenosis of the subclavian vein occur in 35% of the patients receiving a subclavian dialysis catheter. This complication is usually asymptomatic but, in some cases, the thrombosis or the stenosis of the subclavian vein leads to a painful oedema of the arm when an arteriovenous fistula is created on the same side. Sometimes, the closure of the fistula is required and a whole arm is excluded for future vascular access. Thrombosis or stenosis of central veins is significantly less frequent (3%) when the jugular veins are used for the insertion of the dialysis catheter. When the thrombosis is acute, spontaneous resolution may occur following catheter removal. When the thrombus does not resolve, anticoagulation with heparin or thrombolytic therapy with or without angioplasty has been used. Surgery with by pass of the subclavian vein may be necessary as a final option in an attempt to salvage a fistula. Taken into account these stenotic or thrombotic complications of dialysis catheters, subclavian route should be abandoned in chronic uremic patients and femoral route should be preferred for a short period access while jugular route could be used for long term temporary vascular access for hemodialysis.

Arm↗

PubMed1994

Gene expression of plasminogen activator inhibitor 1 in transplant kidneys complicated by renal vein thrombosis: a combined study by in-situ hybridization and immunohistochemistry.

In an attempt to understand the pathogenesis of renal vein thrombosis occurring early after renal transplantation, gene expression of plasminogen activator inhibitor-1 (PAI-1) was investigated by an in-situ hybridization technique. The cases examined were six transplant kidneys complicated by renal vein thrombosis, four 'normal' kidneys and five time-matched transplant kidneys not complicated by renal vein thrombosis but showing acute tubular necrosis, infection, or normal histology. The cell types expressing PAI-1 mRNA were also studied by combined in-situ hybridization and immunohistochemical double staining techniques. Our results showed that PAI-1 mRNA was expressed in transplant kidneys complicated by renal vein thrombosis but there was no detectable expression in 'normal' kidneys, nor in time-matched transplant kidneys not complicated by thrombosis. Double staining showed that PAI-1 mRNA was predominantly expressed by capillary endothelial cells, particularly around large- or medium-sized renal arteries and small nerves. Smooth-muscle cells in the wall of major or medium-sized renal arteries also showed positive expression of PAI-1 in three of six thrombosed transplants. However, endothelium in the major renal vein showed relatively little signal. The pattern was different from that in rejection. The possible relevance of these findings is discussed.

Adult↗

PubMed1994

Effect of human IgG antiphospholipid antibodies on an in vivo thrombosis model in mice.

High levels of IgG antiphospholipid antibodies (aPL) have been associated with clinical thrombosis. It is uncertain however whether these antibodies play a direct role in thrombosis or are merely epiphenomena. To investigate whether antiphospholipid antibodies might play a role in thrombosis, we utilized a novel mouse model in which the dynamics of in vivo thrombosis can be studied. CD1 mice (26-30 g) were passively immunized with 25 mg of human IgG from a patient with the Antiphospholipid Syndrome (IgG-APS) (n = 17), IgG from normal pooled sera (IgG-NHS) (n = 9), or saline solution (n = 12), followed by 40 mg of the same preparations at 48 h. At 72 h, levels of human aPL antibodies, detected using the anticardiolipin ELISA test (aCL ELISA test), in mice immunized with IgG-APS, were 50-100 GPL units. Each animal was anesthetized, femoral vein minimally mobilized and subjected to a standardized "pinch" injury to induce thrombosis. The vessel was transilluminated using acrylic optical fibers connected to a light source, and clot formation and dissolution were visualized by a standard surgical microscope equipped with a video camera, video recorder, and computer assisted analysis system. Results showed that average clot size was significantly larger in mice immunized with IgG-APS compared to those treated with saline (p < 0.037). In addition, the thrombus persisted longer in a significantly higher number of mice immunized with IgG-APS (10/17) compared to mice immunized with IgG-NHS (1/9) or saline (2/12) (p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

A comparative study of heparin responses in arterial and venous thromboembolism using molecular markers for thrombosis.

BACKGROUND: Compared with the therapy of venous thromboembolism, there is little consensus regarding guidelines for heparin anticoagulation of patients with arterial thrombosis. This study aimed to identify the quantitative differences in the activation of the coagulation cascade and platelets in these two syndromes and to characterize their specific biological responses to heparin therapy. METHODS AND RESULTS: Eighteen patients receiving intravenous heparin to treat venous (n = 9) or arterial (n = 9) thromboembolism were prospectively studied for an average of 4 days each. Clinical responses to treatment, activated partial thromboplastin time (aPTT), and molecular markers for thrombosis were measured regularly. Although both groups received equivalent doses of heparin (approximately 1100 units/h), the resulting aPTTs and plasma heparin activity were significantly lower in the arterial patients (P < .05 and P < .01, respectively). The plasma levels of beta-thromboglobulin (a marker for platelet activation and granule release) were significantly higher in the arterial patients (109 +/- 9.5 versus 79 +/- 7.1 ng/mL, mean +/- SEM, P < .05). In vivo fibrin formation, as evidenced by plasma levels of fibrinopeptide A, was less effectively suppressed in the patients with arterial versus venous thrombosis (18.5 +/- 3.2 versus 10.4 +/- 2 ng/mL, P < .05). Prothrombin fragments 1 + 2, a marker for prothrombinase complex activity, was nearly normal in both heparinized groups. CONCLUSIONS: The anticoagulant response to heparin is blunted in patients with arterial thrombosis, at least in part by the antagonistic actions of increased platelet activation. Comparing arterial with venous thrombosis, higher doses of heparin on the average may be required to achieve comparable aPTTs, plasma heparin activity, and comparable suppression of fibrin formation.

Aged↗

PubMed1976

[Disorders of haemostasis in patients undergoing maintenance haemodialysis, with special reference to recurrent arteriovenous fistula thrombosis. Effects of dipyridamole (author's transl)].

Platelet functions and blood coagulation have been regularly investigated in 31 patients undergoing maintenance haemodialysis for 5 months to 6 years. Fifteen of them suffered from at least two arteriovenous fistula thrombosis during the year prior the first examination. Eleven patients, including eight with recurrent thrombosis, received 300-400 mg per day dipyridamole during 1 month to 2 years. Some abnormalities are commonly observed in the whole studied population: lowering of platelet adhesiveness, defective aggregation in the presence of both collagen and ADP 5. 10-5 M; increased level of factor V and mainly factor VIII. Mean platelet factor 3 activity was in the normal range with variations from one case to another. The only unusual feature observed in patients with recurrent thrombosis was an increase of platelet aggregation induced by ADP 0.5. 10-6 M. Neither spontaneous aggregation nor significant abnormality of plasminogen level and plasma antithrombin activity were observed. Under dipyridamole therapy, correction of platelet hyperaggregability was observed in all patients and improvement of platelet adhesiveness in half the studied cases (despite the unchanged anaemia). The treatment significantly decreased the frequency of arteriovnous fistule thrombosis in the six patients observed during two consecutive years, the first one without and the second under treatment: the total number of thrombosis was 18 during the first and 3 in the second period.

Adenosine Diphosphate↗

PubMed1993

[Hereditary protein S deficiency and familial thrombosis. A review with description of a Danish family with protein S deficiency].

Protein S is approximately 69,000 Da polypeptide that acts as a co-factor in conjunction with activated protein C, in the natural anticoagulant system of protein C which irreversibly cleaves activated coagulation factors Va and VIIIa on the cell surface. Although synthesis of protein S takes place in several tissues, the hepatic production of protein S is presumably the most important. It has been established that heterozygous deficiency of protein S may be found in families with increased tendency to thrombosis (thrombophilia). The protein S gene, located on chromosome No. 3, consists of a translated gene, denoted PS alpha, and homologous untranslated region, designated PS beta. In inherited protein S deficiency deletions in PS alpha and PS beta have been detected. The present report deals with a Danish family with highly increased tendency to thrombosis, the propositus of which is a male who developed a large deep-vein thrombosis at the age of 18 months. In this family, nine cases with a plasma level of total protein S close to 50% of normal were identified, six of which had experienced one or more incidents of thrombosis in the past. We recommend that young patients who develop spontaneous arterial or venous thrombosis should be tested for the presence of inherited abnormalities of natural anticoagulants like antithrombin-III and proteins S and C.

Adolescent↗

PubMed1993

[Early thrombosis of the portal vein after orthoptic liver transplantation. A case report].

We report on a case of early portal vein thrombosis occurring after liver transplantation in a patient with alcoholic cirrhosis. Although this complication is usually accompanied by acute graft failure and/or gastroesophageal bleeding, in this patient the portal thrombosis occurred with the appearance of general dropsy and encephalopathy, serum protein deficiency and a slight rise in liver function test values. Echo-Doppler and arteriography showed portal thrombosis, arterial hyperflow and the persistence of a large spontaneous spleno-renal shunt, identified before the transplant had taken place. Endoscopy did not reveal gastroesophageal varices. Since there was no sign of serious ischemic damage or of a serious deterioration of liver function, the patient was treated non-operatively. Some particular hemodynamic aspects implicated in the appearance of portal thrombosis in our case are discussed. However, the authors consider that spontaneous portal-systemic shunt, in the presence of advanced cirrhosis, inverted portal flow, without gastroesophageal varices, can be considered as a surgical total diverting shunt and should be taken as a risk for portal thrombosis after transplantation.

Diabetes Mellitus, Type 1↗

PubMed1993

[Superior sagittal sinus thrombosis in paroxysmal nocturnal hemoglobinuria--an autopsied case].

A 43-year-old Japanese man was admitted to our hospital because of acute occipital headache and drowsiness. He had been diagnosed as paroxysmal nocturnal hemoglobinuria (PNH) with acute renal failure for 2 months prior to the admission. He had abdominal pain and fever of unknown origin for 2 weeks. On admission neurological examination revealed mild disturbance of consciousness, right papilledema and minimal nuchal rigidity. The urinalysis was normal and blood hemoglobin was 8.3 g/dl. Mild hemolysis was suspected because of decreased level of the serum haptoglobin. The magnetic resonance imaging (MRI) of the brain demonstrated the complete occlusion of the superior sagittal sinus by fresh thrombus and the cerebral hemorrhage in the right parieto-occipital subcortex. No other cause for cerebral sinus thrombosis was detected. The patient was treated medically using anti-edema agents, but on the twentieth hospital day he died because of brain herniation. The postmortem examination disclosed thrombosis in the superior sagittal sinus and transverse sinus on both side. There was a massive hematoma in the right parieto-occipital subcortex. The spleen and kidney also contained multiple venous thromboses. Twelve cases of cerebral sinus thrombosis with PNH have been reported in the literatures. Although cerebral sinus thrombosis is a common complication with PNH in Caucasian, but is rare in Asian including Japanese. This may probably depend upon a racial difference. To our knowledge, this is the first report of a patient with cerebral sinus thrombosis with PNH in Japan.

Adult↗

PubMed1993

[Venous thrombosis after closed head injury: a report of two cases presenting as intracranial hypertension].

Although sinus thrombosis occurs owing to various causes, sinus thrombosis after closed head injury is rarely reported. The authors encountered 2 cases with sinus thrombosis in whom intracranial hypertension occurred after closed head injury. In case 1, left abducens and oculomotor palsy developed as a false localizing sign, together with symptoms of intracranial hypertension 10 days after head injury. Using angiography, we made a diagnosis of stenosis of the superior sagittal sinus. Since the symptoms were aggravated under conservative treatment, V-P shunt was performed, but impaired vision was not improved. In case 2, symptoms of intracranial hypertension occurred 10 days after head injury. We performed magnetic resonance angiography (MRA) and made a diagnosis of stenosis of the bilateral transverse sinuses. The symptoms improved under conservative treatment. The use of conventional angiography has been the most reliable for a diagnosis of sinus thrombosis, but MRA will become useful from now on. For diagnosis, it is important to suspect sinus thrombosis after closed head injury. Surgical decompression is required for patients in whom symptoms are aggravated under conservative treatment.

Child↗

PubMed1993

Successful thrombectomy for thrombosis of the right side of the heart after the Fontan operation. Report of two cases and review of the literature.

We performed operative thrombectomy for the treatment of cardiac thrombosis on the right side of the heart in two patients; thrombosis occurred after a total cavopulmonary connection (modified Fontan operation). In the first case, thrombosis occurred approximately 6 months postoperatively, and the thrombus was evacuated without cardiopulmonary bypass. In the second case, an emergency open atrial thrombectomy and revision of the stenotic inferior cavopulmonary anastomosis was performed on the tenth postoperative day. Review of the literature identified 12 previously reported cases that were similar. In these 12 cases 6 patients died, 5 of them early after diagnosis and institution of treatment. We believe that appropriate management should include thrombectomy and revision if a surgically remediable cause of the thrombosis is identified; otherwise, thrombolytic therapy should be initiated. The use of heparin and then sodium warfarin (Coumadin) has also been successful. Risk of thrombosis of the right side of the heart after the Fontan repair may be minimized by the use of prophylactic anticoagulation in high-risk patients soon after the Fontan operation.

Emergencies↗

PubMed1993

[Renal venous thrombosis in neonates].

The authors present an account on a neonate with dextro-lateral renal venous thrombosis. They focus attention on the diagnostic and therapeutic procedure and compare it with available data from the literature. Contrary to data in the literature, they did not observe in the acute stage of renal venous thrombosis signs of disseminated intravascular coagulation in peripheral blood. It did not prove possible to elucidate the action of any of the factors leading to the development of renal venous thrombosis. After evidence of permanent functional loss of the right kidney nephrectomy was performed. Histopathological examination provided evidence of obliterating thrombosis of the renal veins with partial recanalization and calcifications. The authors emphasize the necessity of early diagnosis of renal venous thrombosis and adequate treatment based on the revealed findings.

Female↗

PubMed1995

The factor V Leiden mutation which predisposes to thrombosis is not common in patients with antiphospholipid syndrome.

Antiphospholipid syndrome is associated with venous, arterial, and placental thrombosis, possibly through autoantibody impairment of phospholipid-dependent protein C activation. Recently, a missense mutation in the factor V gene (1691 G-->A) has been identified that results in an abnormal factor V product (1). This mutation, known as the Leiden mutation, causes an amino acid substitution of glutamine for arginine at position 506 in the factor V molecule and renders the protein resistant to proteolytic inactivation by activated protein C and thus predisposes to thrombosis (2, 3). We hypothesized that some individuals with antiphospholipid syndrome may also carry the Leiden mutation, and thus have a "second hit" predisposition to thrombosis. To test this hypothesis, allele-specific hybridization and allele-specific restriction analysis were used to test for the Leiden mutation in thirty women with the antiphospholipid syndrome, 10 of whom had a history of thrombosis. None of the women were heterozygous or homozygous for the factor V mutation. We conclude that the presence of the factor V Leiden mutation is not a prerequisite for the thrombotic events in patients with antiphospholipid syndrome, due to the occurrence of thrombosis seen in patients lacking the factor V mutation.

Alleles↗

PubMedDate not supplied

Cerebral venous thrombosis in children.

From May 1984 to April 1995, a total of 16 patients (12 females, 4 males) with cerebral venous thrombosis, diagnosed by computed tomography (CT), conventional cerebral angiography, magnetic resonance imaging (MRI) or magnetic resonance angiography (MRA), were reviewed retrospectively. The age ranged from 1 month to 16 years of age (average: 2.5 years) with 8 below 1 year of age. The presenting symptoms for infants were mental change (75%) and seizure (100%), mainly generalized (63%) in character. Associated illness was mainly closed head injury, diarrhea or dehydration. All infants had mild to severe motor handicap in a 1 to 10 year follow-up. In contrast, older children frequently presented with headache (37%) or consciousness change (50%), and were more frequently associated with sepsis or local infections. Four (50%) of them recovered completely, but two died and two were finally in a vegetative state. For the four patients with poor prognosis, all had severe initial insults and widespread sinus thrombosis. MRI and MRA are better than CT for the diagnosis of cerebral venous thrombosis. It was concluded that prognosis for venous thrombosis cases in infants is worse than in older children, but this also depends on the severity of initial insults. For infants who present with intractable seizures, cerebral venous thrombosis should be taken into account when the seizures are difficult to control.

Adolescent↗

PubMed1996

Increased incidence of renal allograft thrombosis after continuous ambulatory peritoneal dialysis.

Allograft thrombosis occurred in 44 cases (4.8%) among 915 consecutive cadaveric renal transplantations performed in a single center over a 13-year period. Multiple logistic regression analysis of risk factors revealed that continuous ambulatory peritoneal dialysis (CAPD) was the only independent variable associated with renal allograft thrombosis. When CAPD was used for prior renal replacement therapy graft thrombosis occurred in 7.3% (22/303), whereas hemodialysis was associated with 3.6% (22/612) of graft thromboses (p < 0.02). No differences in transplant characteristics, including hemodynamics, hematological parameters, immunosuppressive therapy, graft anatomy and preservation, were observed between the cases with graft thrombosis and a matched control group (n = 88). CAPD treatment appears to be a risk factor in the development of renal allograft thrombosis that requires further perioperative coagulation studies in order to design an effective prophylaxis.

Adult↗

PubMed1996

[Thrombosis from mechanical valve prostheses in the Reunion island].

Between October 1991 and January 1995, 10 patients presented 14 episodes of thrombosis of mechanical valve prosthesis, 11 obstructive, 3 nonobstructive. In two cases, the thrombosis was recurrent (one after thrombolysis, one after surgical thrombectomy). In another two cases, the thrombosis was a recurrence (on a valve already surgically replaced because of thrombosis). Anticoagulant therapy had been ineffective in 9 cases; protein S deficiency was diagnosed in one case. Transoesophageal echography allowed diagnoses in all cases. Thrombolysis was the treatment of first intention in 9 cases (completed by a second course of thrombolysis in one case and by valvular replacement in two cases. The other patients were managed by immediate valve replacement in two cases, thrombectomy in one case, long-term parenteral anticoagulation in two cases (one of which was followed by valve replacement). Transoesophageal echography showed improved valve motion. Incomplete thrombus dissolution was observed in 50% of cases. Thrombolytic therapy was complicated by cerebrovascular accidents in two patients, one of which was fatal. One patient had regressive hemiplegia, one patient had a local hematoma. The authors conclude that thrombosis is a serious complication of valve replacement and usually occurs in patients inadequately anticoagulated. Thrombolysis may enable some patients to avoid reoperation but its risks limits its use to those patients thought to be unacceptable surgical risks. An apparently high frequency of this complication durind this period has led to the initiation of a study to determine the predisposing factors and to put preventive measures into action.

Adult↗

PubMed1996

Lupus anticoagulant and thromboembolism: evaluation of fibrinogen, natural inhibitors and molecular markers of thrombosis.

It has been speculated that an impairment in anticoagulant pathways (protein C (PC), protein S (PS), resistance to activated protein C (APC)), may contribute to the thrombotic tendency in lupus anticoagulant (LA) patients. Increased plasma levels of fibrinogen are predictive for arterial thrombosis and increased molecular markers of thrombosis are indicative for activation of the clotting cascade. We investigated 25 patients (20 women) with LA. All patients were stratified according to their thromboembolic history and women according to their history of fetal loss. Eighteen patients had a history of venous or arterial thrombosis, or both. Seven of 16 women with at least one pregnancy had a history of fetal loss. The interrelation among the levels of fibrinogen, PC and PS, and resistance to APC, thrombin-antithrombin III complexes (TAT), prothrombin fragment F1 + 2, D-dimer and the history of thrombotic events and obstetric complications in patients with LA were evaluated. LA patients with a history of venous or arterial thrombosis had a significantly higher fibrinogen level than LA patients without (mean 366 versus 304 mg/dl; P = 0.018). Among 16 women a slightly lower mean TAT level in women with fetal loss was found (2.4 versus 4.3 ng/ml; P = 0.02). No other statistically significant difference in the remaining parameters was yielded in both analyzed subgroups. The results of the study suggest an association between increased fibrinogen levels and the history of venous or arterial thrombosis, or both, in patients with LA. In the other investigated parameters, no relationship to the thrombotic or obstetric history was found.

Adult↗