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PubMed2006

Noncirrhotic portal vein thrombosis exhibits neuropsychological and MR changes consistent with minimal hepatic encephalopathy.

Hepatic encephalopathy can arise from portal-systemic shunting in the absence of intrinsic liver disease. However, there are few descriptions of this form of encephalopathy. Portal vein thrombosis is an infrequent disease that causes portal-systemic shunting. Episodic hepatic encephalopathy has been described in patients with portal vein thrombosis, but it is not known if these patients develop minimal hepatic encephalopathy. We designed a study to investigate the neurological consequences of portal vein thrombosis in patients without cirrhosis and no clinical signs of encephalopathy. For this purpose, 10 patients underwent neuropsychological tests, an oral glutamine challenge test, and brain magnetic resonance (MR) imaging. The results were compared with those obtained in 10 healthy controls. Patients with portal vein thrombosis exhibited abnormalities in the results of neuropsychological tests, oral glutamine challenge test, and MR similar to those described in hepatic encephalopathy associated with cirrhosis. MR spectroscopy revealed a decrease in myo-inositol and an increase in glutamine. The increase in glutamine correlated with an increase in ammonia following the oral glutamine challenge test, signs of increased brain water (decrease in magnetization transfer ratio), and impairment of attention tests. In conclusion, patients with noncirrhotic portal vein thrombosis develop subclinical neurological abnormalities compatible with minimal hepatic encephalopathy. These disturbances, which include signs of increase in brain water and a compensatory osmotic response (decrease in brain myo-inositol), appear to be secondary to brain exposure to ammonia induced by portal-systemic shunting.

Administration, Oral↗
PubMed2002

Arterial thrombosis in a gynecologic oncology patient: evaluation and management.

BACKGROUND: Arterial thrombosis is an extremely rare complication in gynecologic oncology with only two cases previously reported in the literature. Presentation, evaluation, and treatment varied considerably in all previous reports of arterial thrombosis associated with any malignancy. CASE: We report a case of discontinuous arterial thrombosis in the upper extremity of a patient with fallopian tube cancer. Her initial evaluation, done in the acute setting of the thrombosis, revealed multiple thrombophilia abnormalities, including an elevated Factor VIII, and a borderline positive lupus anticoagulant. Follow-up studies over 2 years showed resolution of all coagulation abnormalities, thus indicating no genetic propensity for thrombosis. CONCLUSION: This case highlights the need for appropriate timing of the initial laboratory studies and follow-up so that patients can be managed appropriately.

Arm↗
PubMed2002

Arterial blood flow and microcirculatory changes in a rat groin flap after thrombosis induced by electrical stimulation of the artery.

An experimental model of acute arterial thrombosis was developed in a rat groin flap model. Electrical stimulation was delivered to the flap artery while measuring blood flow in the artery and in the flap microcirculation using a laser Doppler system. Electrical stimulation produced an occlusive thrombosis in 10 rats within 68.1 +/- 19.26 (mean +/- SE) min. Thrombosis formation produced a rapid decrease of the LDF readings in the artery (90%) and in the flap (70%), the decrease being fairly parallel. Following the spontaneous thrombolysis, the artery perfusion recovered to baseline level but the flap blood flow only recovered by 10-20%. During electrical stimulation there was no change of the systemic blood pressure. The dynamic course of thrombus formation was documented on a videotape recorder through a microscope-mounted video camera and monitored on a television screen. Segments of the artery were obtained during and at the end of the experiments. The histological examination revealed arterial thrombosis composed of red blood cells, fibrin, and white blood cells, without any significant architectural and endothelial changes in the vessel walls. The study suggests that this model using electric vessel stimulation is effective for inducing arterial thrombosis and provides a simple method for recording the dynamic course of thrombus formation.

Animals↗
PubMed1993

Diagnosis of cardiac thrombosis in patients with atrial fibrillation in the absence of macroscopically visible thrombi.

Cardiac thrombosis due to atrial fibrillation (AF) has been recognized as the most common cause of cerebral embolism. However, sometimes no macroscopic thrombus is found at autopsy in the heart of a victim of this type of cerebral embolism. We investigated morphological changes in the left atrial endocardium of 31 patients (including 21 cases with AF) who had died of cerebral embolism. "Rough endocardium" (RE) seen macroscopically provided evidence for the existence of atrial thrombosis. The RE that appeared in AF cases was due to a granular and wrinkled appearance of the endocardium associated with oedematous and fibrous thickening. Fibrin-thread deposits were also always distinguishable. Mural thrombi and oedema with neutrophil infiltration in the subendocardium could be seen under the microscope. Small areas of endothelial denudation and thrombotic aggregations were commonly observed by scanning electron microscopy (SEM). These SEM lesions were significantly more frequent in cases with AF than in controls (P < 0.001). The diagnostic success rate for atrial thrombosis among cases with AF increased from 33.3% to 81% when thrombi proven by histological investigation of the areas with RE were added. Left atrial RE may be an anatomically relevant finding for the existence of atrial thrombosis with AF, when the thrombosis cannot be detected upon gross observation at autopsy.

Adult↗
PubMed1990

[Surgical therapy of acute and embolizing deep venous thrombosis--indication, technical principle, results].

Between 1977 and 1986, 185 patients with deep venous thrombosis (117 with acute occlusive and 68 with embolizing deep venous thrombosis) underwent venous thrombectomy with arterio-venous fistula. The early patency rate was 96%, and the perioperative mortality rate, 3.8%. Of the 157 patients in whom extremities were involved, 147 were examined 12-118 months postoperatively (mean 43 +/- 23 months) clinically, by Doppler ultrasound and by light reflexion rheography (LRR). In 49% of the patients, various kinds of swelling or oedema of the involved extremities were present. There were no hemodynamical disturbances in 53% (LRR-examination); competent venous valves were found in 44%. According to the severity of symptoms and hemodynamical findings, postthrombotic syndrome was absent in 47%, mild in 20%, moderate in 28%, and severe in 5% (7 patients, 4 with venous ulcers). Six of the 7 patients with severe postthrombotic syndrome belonged to the group operated for embolizing thrombosis, where no selection of cases was performed. The best long-term results were achieved in patients operated for acute occlusive thrombosis of the iliac and iliofemoral veins. Venous thrombectomy with av fistula can achieve sufficient early and long-term results in the treatment of deep venous thrombosis, provided strict selection of patients and a meticulous technique are practised.

Adolescent↗
PubMed1986

Influence of serotonin, serotonin antagonists, some vasoactive substances and temperature on carrageenin-induced tail thrombosis in rats and mice.

Tail thrombosis (infarction) induced by injection of kappa-carrageenin (0.88 or 1.76 mg/kg i.v.) is increased by i.v. or i.p. serotonin (1-2 mg/kg) but is decreased by cyproheptadine and ketanserin (minimal effective dose less than 1 mg/kg) as well as by preceding serotonin depletion by comp. 48/80 or reserpine. The effect of exogenous serotonin is antagonized by ketanserin and cyproheptadine, respect. In the anaphylactoid reaction induced by dextran, only weak thrombosis increasing effects were seen, apparently, because of vasodilation in this reaction. Application of heat to the tail weakly decreased tail thrombosis, application of cold strikingly increased it. Vasodilating substances (nicotinate, 3-hydroxymethylpyridine, trapidil, dipyridamole, iloprost) as well as the thromboxane antagonist BM 13,177 were without significant effect on tail thrombosis, even if vasodilating substances were applicated in form of ointments on the tail. The participation of endogenous serotonin in carrageenin-induced tail thrombosis has further to be substantiated.

Animals↗
PubMed1991

Intraoperative ultrasonography for location of proximal limit of inferior vena caval thrombosis.

Appropriate surgical management of inferior vena caval thrombosis is dependent on the proximal limit of the thrombus. Cavograms, computed tomography, or magnetic resonance imaging all have their shortcomings in locating this limit. Intraoperative ultrasonography has allowed us to determine the exact proximal limit of vena caval thrombosis in two patients, one with suprarenal thrombosis, the other with infrarenal thrombosis. In the first patient, caval interruption and clearance of the inferior vena cava was greatly enhanced by the use of this method. Intraoperative sonography is useful in the surgical treatment of thrombosis of the inferior vena cava.

Adult↗
PubMed2003

Neonatal thrombosis.

Neonatal thrombosis is a serious event that can cause mortality or result in severe morbidity and disability. The most important risk factor for the development of thrombosis during the neonatal period is the presence of an indwelling central line and consequently the vessels involved tend to be those most frequently used for catheterization. Other documented risk factors for the development of neonatal thrombosis include asphyxia, septicemia, dehydration, maternal diabetes and cardiac disease. Main laboratory findings for the diagnosis of hypercoagulable states, include shortened aPTT, decreased levels of inhibitors (AT III, Protein C and Protein S), increased resistance to activated protein C, defective fibrinolysis (basal and after stimuli), increased levels of clotting factors (fibrinogen, factor VII, factor VIII, etc.), increased and/or hyperactive platelets, increased whole blood and/or plasma viscosity, Antiphospholipid antibodies and presence of prothrombotic molecular defects like FV Leiden, P20210 and MTHFR. Approximately 4% and 2% respectively of Caucasians are heterozygous for these gene defects. Their causative role in neonatal thrombosis is unknown but they may have a contributory role in the pathogenesis of thrombosis in neonates.

Disseminated Intravascular Coagulation↗
PubMedDate not supplied

Assessing thrombosis risk in patients with idiopathic, diabetic, and postsurgical gastroparesis.

Patients with severe gastrointestinal motility disorders are often found to have intravenous access clots or deep venous thrombosis. It has previously been reported that many patients who have intravenous access thrombosis have concomitant thrombotic risk factors. In this study, the goal was to determine the underlying prevalence of hypercoagulable risk in a series of patients with documented gastroparesis. Investigators studied 62 consecutive patients (52 female; mean age, 42 y) who had symptoms of gastroparesis. All patients were evaluated for placement of a gastric neural stimulation device, or they had had one placed previously. Patients underwent a hematologic interview and standardized coagulation measures of thrombotic risk. Laboratory studies measured acquired elevations of Factor VII, Factor VIII, fibrinogen, lupus anticoagulant panel, antiphospholipid antibody panel, homocysteine (in the setting of kidney disease), and activated protein resistance. Investigators also measured congenital factors: Factor VIII (with C-reactive protein levels), antithrombin III, protein C, protein S (total and free), Factor II mutation, Factor V Leiden, methylenetetrahydrofolate reductase, and homocysteine. Fifty-five patients (89%) were found to have detectable hypercoagulable risk factors. Twenty-five of the 62 patients (40%) had a documented history of abnormal clotting, including deep venous thrombosis, intravenous access thrombosis, and pulmonary embolism. All patients with a previous history of thrombosis had detectable clotting abnormalities. Of 56 patients, 40 (71%) had hypercoagulability and did not have diabetes (P=.036), and 20 (36%) had hypercoagulability and no known history of infection. However, this value was not statistically significant when infection and hypercoagulability were compared (P=.408). A high prevalence of acquired and congenital hypercoagulable defects has been observed in patients with gastroparesis, which may predispose them to arterial and venous clots. This unique finding warrants consideration of coagulation evaluation in patients with severe gastroparesis, especially when these patients are placed in high-risk thrombophilic situations, such as hospitalization, prolonged intravenous access, and surgery.

Adult↗
PubMed1985

Postpartum renal vein thrombosis.

Renal vein thrombosis in adults is usually a complication of the nephrotic syndrome. Rarely, it has been reported in nonnephrotic women postpartum. The thrombosis may be a complication of the hypercoagulable state associated with both the nephrotic syndrome and pregnancy. Two postpartum patients with renal vein thrombosis and no prior history of renal disease are reported here. Neither patient had heavy proteinuria. In both cases, pyelonephritis was suspected clinically and the diagnosis of renal vein thrombosis was first suggested and confirmed by radiologic examination. Renal vein thrombosis should be considered in women presenting postpartum with flank pain.

Angiography↗
PubMedDate not supplied

The incidence of postoperative venous thrombosis among patients with ulcerative colitis.

BACKGROUND: Patients with Ulcerative Colitis (UC) have inherent prothrombotic tendencies. It is unknown whether this necessitates the use of additional perioperative anti-thrombotic prophylaxis when such patients require major surgery. METHODS: The postoperative courses of 79 patients with UC undergoing 180 major abdominal and pelvic operations were examined for clinical and radiological evidence of venous thrombosis. Eighteen patients with Familial Adenomatous Polyposis (FAP) having surgery (35 operations) of similar magnitude were also studied. Standard anti-thrombosis prophylaxis was utilised in all patients. RESULTS: Nine patients with UC were clinically suspected of developing postoperative venous thrombosis, but only three (3.8%) had their diagnosis confirmed radiologically (all had a pulmonary embolus). Therefore, the overall postoperative thrombosis rate, on an intention to treat basis, was 1.7% (3/180). No patient with FAP developed significant venous thrombosis. CONCLUSION: Standard perioperative antithrombotic modalities are sufficient to maintain any potential increase in postoperative thrombotic risk at an acceptable level in patients with UC undergoing operative intervention.

Adolescent↗
PubMed1999

Role of genetic prothrombotic risk factors in childhood caval vein thrombosis.

UNLABELLED: Childhood caval vein thrombosis has a high incidence especially in the first year of life. Besides deficiencies of protein C, protein S, antithrombin and plasminogen, the factor (F) V G1691A mutation, the prothrombin (PT) G20210A variant, the methylenetetrahydro-folate reductase (MTHFR) TT677 genotype, or increased lipoprotein (Lp) (a) > 30 mg/dl have emerged as important prothrombotic risk factors in childhood vascular accidents. 27 consecutive childhood patients with inferior caval vein thrombosis and 100 healthy age-matched controls were investigated for the presence of these prothrombotic risk factors with respect to the first thrombotic onset. In 19 out of 27, patients thrombosis occurred during infancy; the remaining vascular accidents were diagnosed during puberty. In 13 out of the 19 infants, vascular occlusion occurred spontaneously, five times associated with renal venous thrombosis. 68.4% of patients in the first year of life (n = 13) showed at least one prothrombotic risk factor. The FV mutation (heterozygous n = 4, homozygous n = 1). Lp (a) > 30 mg/dl and kringle 4 repeats < 28 (n = 4), MTH FR TT677 with mild hyperhomocysteinaemia (> 95th age-dependent percentile, i.e. 8.5 micromol/l: n = 3) and antithrombin deficiency type II (n = 1) were diagnosed with an overall odds ratio/95% confidence interval of 9.2/3.1-27.4. In the adolescent group, genetic risk factors were found in 50% of patients investigated (FV mutation (n = 1), PT variant (n = 3); odds ratio/95% confidence interval: 4.2/0.97-18.6). CONCLUSION: Data presented here suggest that genetic prothrombotic risk factors play an important role in childhood caval vein thrombosis. Remarkably, during puberty and adolescence the predominant defect diagnosed was the PT G20210A variant, whereas the FV G1691A mutation had a higher incidence during infancy.

Adolescent↗
PubMed2002

Diffusion-weighted magnetic resonance imaging of dural sinus thrombosis.

Magnetic resonance imaging (MRI) is useful to diagnose dural sinus thrombosis. However, the representative appearance of dural sinus thrombosis on diffusion-weighted MRI has not been established. This study was aimed at determining whether cytotoxic or vasogenic edema is more predominant in the affected cerebral parenchyma and assessing the time courses and prognosis of dural sinus thrombosis lesion. The studies on sixteen patients with dural sinus thrombosis who underwent diffusion-weighted MRI were retrospectively reviewed. The diagnosis was confirmed by digital subtraction angiography in 11 patients and magnetic resonance angiography in five patients. Diffusion-weighted images with echo-planar imaging were obtained using two or three b values, with the highest b value of up to 1,000 s/mm(2). A region of interest was placed on an area of abnormal signal intensity to calculate apparent diffusion coefficients (ADCs). Nine of the 16 patients had lesions with an increased ADC, whereas, three of these nine patients also had lesions with a decreased ADC. Among 11 patients who underwent initial MRI within 7 days of their last episode, eight had lesions with an increased ADC, of whom three had lesions mixed with both decreased and increased ADC areas. Follow-up studies of these three patients revealed the development of hemorrhagic infarction in two and subcortical hemorrhage in one. Vasogenic edema develops more predominantly and earlier in dural sinus thrombosis, though cytotoxic edema was also associated with the pathological changes in the early phase. Decrease of ADC value is presumed to reflect severe pathological conditions and indicate possible future development of infarction or hemorrhage.

Adult↗
PubMed2004

Gadolinium-enhanced magnetic resonance angiography in neonates and infants suspected of caval or aortic thrombosis.

BACKGROUND: Gadolinium-enhanced magnetic resonance angiography (MRA)is a well-established technique in older children and adults. No studies have focused on its use in neonates and small infants. OBJECTIVE: Our objective was to study the use of gadolinium-enhanced MRA in neonates and infants suspected of caval or aortic thrombosis. MATERIALS AND METHODS: Gadolinium-enhanced MR angiography was performed on seven neonates and small infants for the evaluation of caval or aortic thrombosis. Gadolinium-DTPA at a dose of 0.3 mmol/kg (minimum dose 1 ml) was injected using a power injector (0.2 ml/s). Contrast-enhanced MRA was performed using a 3-D, fast, radiofrequency spoiled gradient-echo sequence (TR/TE: 4.8/1.1, flip angle 45 degrees , matrix 256 x 128, slice thickness 2.6 mm interpolated to 1.3 mm, FOV variable, NEX=1.0). RESULTS: Diagnostic-quality angiograms were obtained in all seven neonates. Superior vena cava thrombosis was identified in two neonates, and abdominal aortic thrombosis was present in one neonate. CONCLUSION: It is practical to perform gadolinium-enhanced MRA in neonates weighing as little as 600 g for the detection of caval or aortic thrombosis.

Aorta, Abdominal↗
PubMed2001

Cerebral venous thrombosis in childhood.

This was a retrospective study to determine different etiologies of cerebral venous thrombosis (CVT) in childhood and to correlate extent and location of thrombosis with the etiology and the age of the child as well as the final outcome. In addition, the radiologic approach is discussed. This was a retrospective analysis of 19 children with CVT. The children were examined by contrast-enhanced dynamic CT. Radiologic findings were correlated with the etiology of CVT. Cerebral venous thrombosis is not as infrequent in children as has been thought. Cerebral venous thrombosis in children can occur due to trauma (n=9), infections (n=7), or coagulation disorders (n=3). Extent and location of thrombosis, as well as complications, final outcome, and therapy, depend on the etiology. Computed tomography remains a valuable primary imaging modality in the diagnosis of CVT in the acutely injured or diseased child.

Child↗
PubMed2004

Uncommon cause of sinus thrombosis following closed mild head injury in a child.

OBJECT: Sinus thrombosis following a closed mild head injury is rare. A case of dural sinus thrombosis following a mild closed head injury due to an uncommon cause is reported. METHODS: A 7-year-old child presented with GCS 15 after a road traffic accident. CT revealed an occipital fracture. Ten days later the child developed signs of increased intracranial pressure. An MR venogram at this time revealed thrombosis of the transverse sinus with hypoplasia of the contralateral transverse and sigmoid sinuses. The patient's anitiphospholipid antibody titres were elevated. The patient was treated with anticoagulants and improved. CONCLUSIONS: The role of inherited and acquired procoagulant factors in the aetiology of sinus thrombosis is increasingly being recognized. When a patient presents with sinus thrombosis after a closed mild head injury, it is necessary to investigate for the presence of risk factors for thrombophilia as it has implications for the long-term management of the patient.

Child↗
PubMed1998

Increased rate of factor V Leiden mutation in patients with cerebral venous thrombosis.

We investigated the association between cerebral venous thrombosis and hereditary resistance to activated protein C (APC) in 12 consecutive German patients with non-fatal cerebral venous thrombosis and in 187 controls without a history of thrombotic disorder. Three patients (25%) had a mutation in the factor V Leiden gene against only one subject in the control group. This difference was significant (P < 0.05), with an odds ratio of 11.7 (1.5-87; 95% confidence interval). Two patients carrying the mutation had additional common risk factors for thrombosis, and 2 had a positive family history of thromboembolism. We conclude that inherited APC resistance by a mutation in factor V Leiden is an important risk factor in non-fatal cerebral venous thrombosis. We recommend testing for APC resistance and, if abnormal for factor V Leiden mutation in patients with cerebral venous thrombosis.

Adult↗
PubMed1998

Venous transcranial Doppler in acute dural sinus thrombosis.

The value of conventional transcranial Doppler ultrasound in the diagnosis and monitoring of cerebral vein thrombosis is unclear. Previous studies have suggested the usefulness of this method in two cases with superior sagittal sinus thrombosis that showed increased velocities of deep cerebral veins. The purpose of the present study was to evaluate the deep intracranial venous circulation in patients with that pathology. Venous transcranial Doppler ultrasound was performed with a range-gated 2 MHz transducer in 17 healthy volunteers and in six cases of proven acute superior sagittal sinus thrombosis. Peak systolic, end diastolic and mean blood flow velocities were measured in the basal vein of Rosenthal (BVR) and deep middle cerebral vein (DMCV) through a posterior temporal window. In 16 controls and in one patient, the straight sinus was also studied through an occipital approach. Sex distribution and mean age of controls and patients were similar. Mean blood flow velocities in controls were as follows (mean, SD): DMCV, 10.4, 1.4 cm/s; BVR, 11.3, 1.8 cm/s; straight sinus, 29.5, 9.9 cm/s. Three of the patients with superior sagittal sinus thrombosis showed increased velocities either in the DMCV, the BVR or the straight sinus. One patient showed slightly increased velocities in the BVR, and the other two showed normal venous velocity values. This study confirms the usefulness of conventional transcranial Doppler ultrasound in detecting superior sagittal sinus thrombosis. However, a normal examination does not exclude this diagnosis.

Adult↗