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PubMed1999

Thrombosis of bileaflet tricuspid valve prosthesis: clinical spectrum and the role of nonsurgical treatment.

BACKGROUND: Thrombosis of a mechanical tricuspid valve prosthesis is a potentially hazardous event. This study aimed to explore the incidence and the clinical presentation of tricuspid valve thrombosis occurring in bileaflet valves and to evaluate the diagnostic and the therapeutic approach. METHODS AND RESULTS: Tricuspid valve thrombosis was sought in 22 late survivors with the CarboMedics valve in a follow-up period of 36.0 +/- 20.8 months. Limited leaflet motion and/or a visible thrombus were considered diagnostic of valve thrombosis. Eight episodes of tricuspid valve thrombosis were diagnosed among 5 patients (12.1 episodes per 100 patient-years). Anticoagulation was inadequate in 3 patients and fair in 2. Florid right heart failure occurred in 3 episodes. Common physical findings included increased jugular venous pulse (5 patients), diastolic tricuspid murmur (4 patients), and peripheral edema (4 patients). The diagnosis was suspected in all clinically and by transthoracic echocardiography and confirmed by fluoroscopy and/or transesophageal echocardiography. In 4 patients, both leaflets were involved. No thrombi were visualized. Three patients received thrombolytic therapy in 4 episodes (complete success in 3, partial success in 1) without hemorrhagic or embolic complications. One patient responded to aggressive anticoagulant therapy. One patient required an emergent repeat surgery. In 1 patient, valve thrombosis recurred thrice. CONCLUSIONS: In patients with fair or poor anticoagulation, a bileaflet valve in the tricuspid position is associated with a high incidence of valve thrombosis. Hinge entrapment requires only a small amount of thrombotic material. Valve thrombosis may be asymptomatic. Involvement of both leaflets is usually required to produce symptoms. A nonsurgical approach (thrombolysis or intensified anticoagulation) is usually successful. Patients should be instructed about heralding signs of valve thrombosis.

Adult↗
PubMed1994

The antiphospholipid and thrombosis syndromes.

Anticardiolipin antibodies and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The commonest thrombotic events associated with anticardiolipin antibodies are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). The relative frequency of anticardiolipin antibodies in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through IV) should be defined if possible because this may dictate both type and duration of immediate and long-term anticoagulant therapy. In contrast to those with anticardiolipin antibodies, patients with primary lupus anticoagulant thrombosis syndrome usually suffer venous thrombosis. Because the aPTT is unreliable in patients with lupus anticoagulant (prolonged in only about 40% to 50% of patients) and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests (ELISA for anticardiolipin antibody and the dRVVT for lupus anticoagulant) should be immediately ordered when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events.

Antibodies, Anticardiolipin↗
PubMed2003

Eversion thromboendovenectomy for organized portal vein thrombosis encountered during liver transplantation.

INTRODUCTION: Due to the technical experience acquired in the field of liver transplantation portal vein thrombosis is no longer considered a contraindication for transplantation. Nevertheless, the results obtained in patients with portal vein thrombosis are at times suboptimal, and there is no consensus on the appropriate surgical technique. PATIENTS AND METHODS: Among the 455 liver transplants performed between May 1988 and December 2001, 32 (7%) presented with portal vein thrombosis. Twenty (62%) were type Ib, seven (22%) type II/III, and five (16%) type IV. Twenty-two were men (69%), with a mean age of 50 years (range: 30-70 years); the thrombosis in all cases developed in a cirrhotic liver. The surgical method in all cases consisted of an eversion thromboendovenectomy under direct visual guidance, with occlusion of the portal flow using a Fogarty balloon. RESULTS: Among the 32 cases undergoing thrombectomy, 31 (96%) were successful with a failure in a case of type IV thrombosis, which was resolved by portal arterialization. Of the 31 successful cases, only one with type IV thrombosis rethrombosed. The 5-year survival rate of the patients in the series was 69%. Only two patients died from causes related to the thrombosis, both showing type IV thrombosis. CONCLUSION: The ideal treatment for portal thrombosis during liver transplantation depends on its extension and on the experience of the surgeon. In our experience, eversion thromboendovenectomy resolves most thromboses (types I, II, and III), but management of type IV, which occasionally can be treated with this technique, may require more complex procedures such as bypass, portal arterialization or cavoportal hemitransposition.

Adult↗
PubMed2002

Frequency and correlates of coronary stent thrombosis in the modern era: analysis of a single center registry.

OBJECTIVES: The study examined the frequency, correlates, and outcome of patients with stent thrombosis within 30 days of stent placement. BACKGROUND: Patients in trials evaluating stents or dual antiplatelet therapy to prevent coronary stent thrombosis have generally had narrow inclusion criteria; the extent to which stent thrombosis rates in such trials represent current practice, particularly with the availability of newer stents, is unclear. METHODS: We performed a retrospective analysis of the Mayo Clinic Percutaneous Coronary Intervention database and identified all patients who received at least one coronary stent and dual antiplatelet therapy (aspirin and ticlopidine or clopidogrel for two to four weeks). RESULTS: Four thousand five hundred nine patients underwent successful coronary stent implantation and were treated with dual antiplatelet therapy between July 1, 1994, and April 30, 2000. Stent thrombosis occurred in 23 patients (0.51%; 95% confidence interval 0.32%, 0.76%) within 30 days of stent placement. Multivariate analysis using bootstrap model selection to avoid over-fitting the model indicated that only the number of stents placed was an independent correlate of stent thrombosis (odds ratio 1.80, p < 0.001). The frequency of death and frequency of nonfatal myocardial infarction (MI) among the 23 patients with stent thrombosis were 48% and 39%, respectively. CONCLUSIONS: Stent thrombosis is even more rare in the current era than in earlier trials. Number of stents placed was an independent correlate of stent thrombosis. Most patients who suffer stent thrombosis either die or suffer MI.

Aged↗
PubMed2005

Analysis of prothrombotic mutations and polymorphisms in children who developed thrombosis in the perioperative period of congenital cardiac surgery.

In this study, we investigated some of the prothrombothic mutations and polymorphisms in 15 children with congenital cardiac malformations who developed severe thrombosis in the perioperative period following surgical repair. The mutations and polymorphisms included in the study were Factor V Leiden, prothrombin G20210A, methylentetrahydrofolate reductase C677T, endothelial nitric oxide synthase intron 4 VNTR, alpha-fibrinogen Thr312Ala, Factor XIII Val34Leu, and insertion or deletion of angiotensin 1 converting enzyme. Compared to the healthy Turkish subjects, our patients had a similar rate of mutation of Factor V Leiden, Factor XIII Val34Leu, and endothelial nitric oxide synthase a/b polymorphisms, but higher frequency of the prothrombotic angiotensin 1 converting enzyme deletion/deletion genotype, and lower frequency of the antithrombotic alpha fibrinogen Thr/Thr genotype. None of the patients exhibited mutations involving prothrombin G20210A or methylentetrahydrofolate reductase C677T. The results of our study suggest that, in addition to prothrombotic mutations such as Factor V Leiden, single-nucleotide polymorphisms should be considered in all children with congenital cardiac malformations who develop thrombosis. Malformations of the heart are the most common of all serious lesions that are present at birth, with an incidence of 4 to 8 cases per 1,000 live births. If needed, corrective surgery is usually the optimal treatment for these anomalies, but perioperative morbidity and mortality still remain high due to several factors. Arterial or venous thrombosis, or both varieties of thrombosis, is among these factors. Prior to surgery, the most frequent time at which these children develop thrombosis is during cardiac catheterization. Postoperative thrombosis in this group of patients is a more complex disorder, which can affect both small and large vessels, and is associated with a high morbidity and mortality. Recent studies indicate that both point mutations and single-nucleotide polymorphisms of genes that encode proteins involved in the coagulative and anticoagulative cascades are important risk factors for development of thrombosis. Patients with these risk factors are most likely to develop thrombosis when triggering elements, such as placement of catheters, prolonged immobilization, or surgery, are also present. In this study, we investigated some of the above-mentioned mutations and polymorphisms in children who developed thrombosis in the perioperative period after correction of congenital cardiac malformations.

Child, Preschool↗
PubMed1994

Exogenous nitric oxide prevents endotoxin-induced glomerular thrombosis in rats.

Nitric oxide (NO) synthesized from L-arginine is an endogenous vasodilator and inhibitor of platelet adhesion and aggregation. Gram-negative lipopolysaccharide (LPS) can induce NO synthesis, which may mediate the pathophysiologic effects of endotoxemia. In addition, our previous studies suggested that LPS-induced NO may protect against thrombosis in rats. In the present study, male Sprague-Dawley rats given LPS (0.1 mg/kg) i.p. increased their urinary excretion of NO2 + NO3 (stable end-products of NO) by 4.3-fold. Rats given 10 micrograms/kg/hr i.v. of nitroglycerin (GTN), an exogenous NO donor, showed a similar increase. L-NAME, an inhibitor of NO synthesis, abrogated the increase in urinary NO2 + NO3 in LPS-treated rats but not in rats given GTN. Glomerular thrombosis developed in rats given LPS + L-NAME (thrombosis score = 3.02 +/- 0.4), while those given LPS + L-NAME + GTN were largely protected (thrombosis score = 1.37 +/- 0.5, P < 0.05). Atrial natriuretic peptide (ANP), an NO-independent vasodilator, neither increased urinary NO2 + NO3 nor prevented glomerular thrombosis (thrombosis score = 2.68 +/- 0.5, NS). Hydralazine, another vasodilator without effects on NO or platelets, also failed to prevent glomerular thrombosis in rats given LPS + L-NAME. We conclude that in endotoxemia, the antithrombogenic properties of endogenously synthesized NO are important in preventing alomerular thrombosis. The exogenously NO donor, GTN, can substitute for the antithrombogenic effect of endogenous NO. Clinically, administration of NO synthesis inhibitors to treat endotoxic shock may need to be combined with concomitant administration of exogenous NO donors to prevent microvascular thrombosis.

Animals↗
PubMed1997

Predictive measures of vascular access thrombosis: a prospective study.

Malfunction of permanent vascular accesses remains a cause of frequent and costly morbidity in patients receiving chronic hemodialysis (CHD). Several recommendations for routine monitoring of these permanent vascular accesses for incipient failure have been proposed. In this study, multiple indicators of incipient vascular access dysfunction, including "venous" and "arterial" pressures at serial blood flows (200 ml/min, 300 ml/min, and 400 ml/min), percent urea recirculation, Doppler ultrasound, and access blood flow by ultrasound dilution technique were simultaneously evaluated in a total of 220 vascular accesses in 170 chronic hemodialysis patients in two separate study periods (6 months apart). The rate of thrombosis was determined within the subsequent 12 weeks of each study period to assess the short-term predictive power of access thrombosis. During the period of follow-up, there were 34 thrombotic events in 172 polytetrafluoroethylene (PTFE) grafts and only one thrombotic event in 48 arterio-venous fistulas (AVF). Therefore, the statistical analysis was limited to the PTFE grafts. When grafts with thromboses were compared to those without thrombosis by univariate analysis, access blood flow measured either by ultrasound dilution technique (875 +/- 426 ml/min with thrombosis vs. 1193 +/- 677 ml/min without thrombosis, P = 0.001) or by Doppler ultrasound (762 +/- 420 ml/min with thrombosis vs. 1171 +/- 657 ml/min without thrombosis, P = 0.001) were significantly different in the two groups. There was good correlation (r = 0.79, P = 0.0001) between the blood flows determined by both techniques. The grade of stenosis determined by ultrasound was also a statistically significant predictor (P = 0.02). "Venous" and "arterial" pressures were numerically similar and were not statistically different between the accesses that did and those that did not thrombose. When multivariate analysis was used, there was a significantly increased risk of thrombosis only with decreasing access blood flow determined by ultrasound dilution techniques after adjusting for other confounding variables. When the average blood flow of all grafts (1134 ml/min) is considered as the reference access blood flow (relative risk of 1.0), the relative risk of a PTFE thrombotic event within the subsequent 12 weeks was 1.23 at a blood flow 950 ml/min, 1.67 at a blood flow of 650 ml/min and to 2.39 at a blood flow of 300 ml/min. In summary, access blood flow measured by either Dilution or Doppler is a reliable indicator of subsequent short-term thrombosis risk. Other proposed methods of evaluating access dysfunction were not useful in our patients. If simple to use, cost-effective devices to measure dialysis access blood flow become readily available, the measurement of access blood flow will likely become the method of choice for screening of PTFE vascular access dysfunction in hemodialysis patients.

Aged↗
PubMed2002

The risk of thrombosis in essential thrombocythemia and polycythemia vera.

Thrombotic events are present in 20% to 50% of patients with polycythemia vera (PV) and essential thrombocythemia (ET) at diagnosis and involve major vessels and the microcirculation. Establishing the precise risk of thrombosis in ET and PV is difficult. However, estimates may be obtained from retrospective and prospective studies, and some risk factors have been defined. In ET, increasing age and previous thrombosis emerge as major factors. The level of the platelet count per se does not correlate with thrombotic incidence. However, there is substantial evidence that adequate control of the platelet count reduces the frequency of thrombosis. While aspirin is usually effective at relieving vasomotor and microvascular occlusive symptoms or signs, there is only limited evidence that its use reduces the risk of larger vessel thrombosis. Other suggested risk factors include apparent clonal hematopoiesis in younger patients, hypercholesterolemia, and cigarette smoking. In PV, the overall impression is that the incidence of thrombosis is greater than in ET. As in ET, increasing age and previous thrombosis are significant risk factors. In addition, adequate reduction of the hematocrit reduces the incidence of thrombosis. Identifying the risk associated with thrombocytosis in PV is confounded by the overall myeloproliferation usually found in these patients and the fact that the thrombocytosis is not usually as marked as in ET. However, by analogy with ET, one could argue that the risk associated with the thrombocytosis in ET is equally applicable to PV. In support of this, there is overwhelming evidence that patients treated with adequate myelosuppression with complete normalization of their blood counts have the lowest thrombotic incidence. Essential thrombocythemia and PV patients presenting with thrombosis should be investigated for other congenital or acquired prothrombotic conditions. Establishment of the presence of one or the other of these may alter the long-term management of these patients with the use of either aspirin or anticoagulation in addition to cytoreduction. Thrombotic risk has emerged as a major factor in stratifying patients with myeloproliferative disease. While some clear thrombotic risk factors have been defined, there is a need to identify further additive risk factors in patients considered to be at low risk of thrombosis.

Humans↗
PubMed1999

[Deep vein thrombosis following total arthroplasty hip replacement. Ultrasonographic screening in the rehabilitation phase].

UNLABELLED: Deep vein thrombosis requires intensive therapy--either the patients require hospitalisation or their rehabilitation scheme must be adjusted and medical treatment applied. The total number of patients with deep vein thrombosis undetected before admission to rehabilitation facilities is unknown. AIM: Study parameters: 1. The occurrence of undetected deep vein thrombosis upon admittance to a rehabilitation facility. 2. The value of sonography in diagnosing, localising and determining the extent of deep vein thrombosis and 3. the influence of prophylactic antithrombotic treatment applied in the surgical hospital, as well as during the intermittent outpatient phase before admittance to the rehabilitation centre, on the occurrence of deep vein thrombosis. METHODS: 305 patients were examined between Nov. 95 and Dec. 96. The first check was carried out on the day of admission (on the 26th postoperative day, on average). The second check was done on the day of discharge from the rehabilitation centre. RESULTS: Deep vein thrombosis was found in 30 patients (10%). In 27 cases the thrombosis was located in the thigh, in one case it was found in the contralateral leg. 18 of these patients had been discharged from the surgical hospital on the 22nd postoperative day, for an average time of 7 days of outpatient care, before being admitted to the rehabilitation centre. 11 of these patients had not received any prophylactic antithrombotic treatment. One patient developed deep vein thrombosis of the thigh during the rehabilitation phase despite of prophylactic treatment. CONCLUSION: Postoperative sonographic screening of all patients undergoing hip surgery is a useful method to detect deep vein thrombosis. Prophylactic postoperative antithrombotic treatment in the rehabilitation phase is mandatory.

Aged↗
PubMed2000

[Sonographic diagnosis of thrombosis of the calf muscle veins and the risk of pulmonary embolism].

AIM: To determine the frequency of deep vein thrombosis in the veins of the calf muscles. The risk of embolism in relation to the localisation of thrombosis was also evaluated. METHOD: 357 consecutive patients submitted for colour Doppler sonography of the lower extremities were prospectively examined for deep vein thrombosis (DVT). Both axial and muscular calf veins were investigated. 184 of these patients underwent additional investigation for pulmonary embolism. RESULTS: Diagnosis of DVT was made by means of colour Doppler sonography in 179 patients. Soleal veins (n = 88), peroneal veins (n = 84), the popliteal vein (n = 69), and the superficial femoral vein (n = 53) were the most common sites of thrombosis. Thrombosis of the gastrocnemial veins (n = 49) occurred less frequently. 85 patients (47% of all patients having DVT) showed isolated calf vein thrombosis, in 45 patients (25%) the gastrocnemial and/or soleal veins were the only site of thrombosis. 60% of patients with symptomatic DVT also had pulmonary embolism. The embolic frequency for isolated calf vein thrombosis and muscular calf vein thrombosis was 48% and 50%, respectively. CONCLUSION: The veins of the calf muscles are a common site of acute DVT and a source of pulmonary embolism. They should always be investigated in patients with suspected DVT of the calf, and in patients with pulmonary embolism.

Adolescent↗
PubMed2003

Venous and arterial thrombosis during oral contraceptive use: risks and risk factors.

Since the introduction of oral contraceptives, their use has been associated with an increased risk of both venous and arterial thrombosis. Pulmonary embolism, myocardial infarction, and stroke are serious disorders with a considerable risk of mortality. Because worldwide over 100 million women use oral contraceptives, issues of drug safety are of great importance. The risk of venous thrombosis during low-dose oral contraceptive use is three- to sixfold increased compared with that of nonusers. The association is not only attributed to the estrogen component of the pill: the risk is twice as high for desogestrel and gestodene (third generation) containing oral contraceptives as for levonorgestrel (second generation) containing oral contraceptives. The risk of venous thrombosis is highest in the first year of use and in women with genetic or acquired risk factors for thrombosis. Both venous or arterial thrombosis are unrelated to duration of use or past use of combined oral contraceptives. The risk of myocardial infarction and stroke during low-dose oral contraceptive use is two- to fivefold increased relative to that of nonusers. The risk of arterial thrombosis induced by oral contraceptive use is more pronounced in smokers and women with hypertension, diabetes, and hypercholesterolemia. All types of thrombosis have strongly age-dependent incidences, and therefore in absolute figures the risks and effects of risk factors increase with age. The lowering of the estrogen dose in combined oral contraceptives from 50 microg to 20-30 microg in the last decade did not clearly reduce the risk of venous thrombosis, myocardial infarction, stroke, or peripheral arterial disease. For stroke and peripheral arterial disease no difference in risk was found between second and third generation oral contraceptives. For myocardial infarction study results are conflicting, and a small benefit of third- over second-generation oral contraceptives cannot be ruled out. However, this is unlikely to counterbalance the adverse effect of third generation contraceptives on venous thrombosis.

Arterial Occlusive Diseases↗
PubMed2004

The association of antibodies to cardiolipin, beta 2-glycoprotein I, prothrombin, and oxidized low-density lipoprotein with thrombosis in 292 patients with familial and sporadic systemic lupus erythematosus.

OBJECTIVE: To determine the prevalence of antibodies to phospholipid-binding plasma proteins (aPL) and to oxidized low-density lipoprotein (OX-LDL), and to study the association of these antibodies with thrombosis and coronary heart disease (CHD) in patients with systemic lupus erythematosus (SLE). METHODS: Clinical data and sera from 89 Finnish patients with familial and 203 with sporadic SLE were available for the study. Enzyme-linked immunosorbent assays (ELISA) were used for antibody determination. RESULTS: The occurrence of thrombosis in our SLE patients was 13.7% (40/292) and of clinically diagnosed CHD was 1.4% (4/292). All antibody assays, except IgM-aCL, were significantly associated with thrombosis. IgG-aCL alone or in combination with anti beta 2-GPI or with anti OX-LDL were reasonably sensitive (38%, 48%, and 58%, respectively) and specific (87%, 80% and 72%, respectively) for a history of thrombosis. A high risk of arterial thrombosis (TIA or stroke) was associated with positivity of IgG-aCL, anti beta 2-GPI, and anti-prothrombin. Venous thrombosis was significantly associated with all other assays except IgM-aCL and anti-prothrombin. No test correlated with CHD, but the number of affected patients was small. There were three multiplex SLE families with two patients having a history of thrombosis: no consistent pattern of aPL or anti OX-LDL was found in these patients. CONCLUSION: IgG-aCL alone or in combination with anti beta 2-GPI or anti OX-LDL are sensitive and specific tests for detecting SLE patients at increased risk of thrombosis. The aetiopathogenesis of thrombosis in familial SLE appears to be multifactorial.

Adult↗
PubMed1997

Plasma levels of thrombomodulin and lipoprotein (a) in patients with cerebral thrombosis.

To evaluate the clinical implications of soluble thrombomodulin and lipoprotein (a) [Lp(a)] in patients with cerebral thrombosis, these parameters were measured in the plasma of 28 patients with cerebral thrombosis within 3 days of onset, 36 with cerebral thrombosis more than 1 month after onset, six with cerebral hemorrhage more than 3 months after onset and 37 healthy volunteers. In the patients with chronic-phase cerebral thrombosis, the thrombomodulin and Lp(a) levels were significantly higher and the total cholesterol level was significantly lower than in the normal group, while the patients with acute-phase cerebral thrombosis had significantly lower total cholesterol levels. The plasma level of Lp(a) in acute-phase cerebral thrombosis, but not that of thrombomodulin, was significantly higher in thromboses located in the cortex area and in patients with recurrent attacks than in the normal controls. There were no significant differences in thrombomodulin, Lp(a) or total cholesterol levels between the chronic-phase cerebral hemorrhage and normal groups. These findings support the hypothesis that Lp(a) plays a part as a risk factor in cerebral thrombosis, especially in patients with a cortex area thrombosis and in patients with a recurrent attack. The high levels of thrombomodulin in the chronic-phase cerebral thrombosis group suggests the presence of continuous endothelial cell damage.

Adult↗
PubMed2000

Epidemiology of thrombosis in HIV-infected individuals. The Adult/Adolescent Spectrum of HIV Disease Project.

OBJECTIVE: To describe the incidence of clinically recognized thrombosis and associated factors among individuals infected with HIV. DESIGN: A longitudinal medical record review. SETTING: Over 100 medical clinics in nine US cities. PATIENTS: A total of 42 935 individuals aged 13 years or older with HIV infection, observed for an average of 2.4 years. MAIN OUTCOME MEASURES: The incidence of thrombosis among HIV-infected individuals; adjusted odds ratios for factors associated with thrombosis. RESULTS: The incidence of thrombosis among HIV-infected individuals was 2.6/1000 person-years (PY). Factors significantly associated with thrombosis included: age of 45 or more years (adjusted odds ratio [AOR], 1.9; 95% confidence interval [CI], 1.4-2.7); a diagnosis of cytomegalovirus disease or retinitis (AOR, 1.9; CI, 1.2-2.9), or other AIDS-defining opportunistic illness (AOR, 1.5; CI, 1.1-2.2); hospitalization (AOR, 3.3; CI, 2.5-4.4); and the prescription of megestrol acetate (AOR, 2.0; CI 1.3-2.9) or indinavir (AOR, 2.4; CI 1.4-4.3). The prescription of other protease inhibitors, sex, race, and mode of HIV exposure were not associated with thrombosis. CONCLUSION: Among HIV-infected individuals, clinically detected thrombosis is more common in those who have opportunistic illnesses, for whom megestrol acetate or indinavir have been prescribed, who have been hospitalized, and who are aged 45 years or older. Physicians should be aware of the risks of thrombosis in order to promote the early identification and appropriate treatment or prophylaxis. Further study is needed to characterize the association between indinavir and thrombosis.

Adolescent↗
PubMed1986

Septic thrombosis of the dural venous sinuses.

From 1940 to 1984, 19 cases of septic dural-sinus thrombosis have been diagnosed at the Massachusetts General Hospital, and some 136 cases have been reported from other institutions. Septic thrombosis most frequently involves the cavernous sinuses (96 cases). Facial or sphenoid air sinus infection often precede cavernous-sinus disease. In addition to the classical signs of proptosis, chemosis, and oculomotor paralysis, isolated sixth-nerve palsy and hypo- or hyperesthesia of the fifth nerve may be found. The major pathogens associated with cavernous-sinus infection include Staphylococcus aureus, other gram-positive organisms, and anaerobes. Septic lateral-sinus thrombosis (64 cases) is almost exclusively a complication of otitis media and/or mastoid infection. Organisms causing this infection include Proteus species, Escherichia coli, S. aureus, and anaerobes. Septic thrombosis of the superior sagittal sinus (23 cases) most frequently accompanies bacterial meningitis or air sinus infection. Causative organisms include Streptococcus pneumoniae, S. aureus, other streptococci, and Klebsiella species. Because septic dural-sinus thrombosis is rare, this disease is frequently misdiagnosed. Evaluation should include lumbar puncture, air sinus films, and computed tomographic scan with contrast. Other helpful diagnostic tests may include carotid angiography, and dynamic brain scan. Orbital venography is the most definitive study in cases of chronic cavernous-sinus thrombosis. Therapy should include intravenous antibiotics and early surgical drainage of purulent exudate in the air sinuses or mastoid regions. Retrospective analysis suggests that treatment with heparin may reduce mortality in carefully selected cases of septic cavernous-sinus thrombosis. Anticoagulation is not recommended in other forms of septic dural-sinus thrombosis. Mortality in the antibiotic-era remains high, particularly in patients with septic thrombosis of the cavernous (30%) and superior sagittal (78%) sinuses.

Adolescent↗
PubMed2000

Deep venous thrombosis after posterior spinal surgery.

STUDY DESIGN: A prospective clinical study using venography to evaluate deep venous thrombosis after posterior spinal surgery. OBJECTIVES: To demonstrate the prevalence of deep venous thrombosis after posterior spinal surgery with no prophylaxis. SUMMARY OF BACKGROUND DATA: There have been few studies about the occurrence of deep venous thrombosis after spinal surgery in which venography was used for screening. METHODS: Of the enrolled 134 patients undergoing posterior spinal surgery, 110 (82.1%) were examined with complete surveillance for deep venous thrombosis by venography. There were 64 males and 46 females. The average age at operation was 59.0 years (range, 14-86 years). The levels of the operation were cervical in 54, thoracic in 7, and lumbar in 49. All procedures were performed with patients under general anesthesia. Neither mechanical methods nor anticoagulation medications were used for prophylaxis against thromboembolism. Bilateral ascending venography was performed within 14 days after surgery. RESULTS: There were no patients with clinical signs of deep venous thrombosis and pulmonary embolism. However, 17 patients (15.5%) showed venographic evidence of deep venous thrombosis, of whom 16 had distal thrombi, and only one had a proximal thrombus. Deep venous thrombosis was venographically evident in 3 (5.6%) of 54 patients who underwent cervical procedures, and it was evident in 13 (26.5%) of 49 patients who underwent lumbar procedures. This difference was statistical significant (chi2 test, P = 0.003). Statistical comparison between patients who did and did not have deep venous thrombosis showed that age was statistically significant (Mann-Whitney test; P < 0.05). CONCLUSIONS: The prevalence of deep venous thrombosis after posterior spinal surgery is higher than generally recognized. Therefore, further study is necessary to clarify the appropriate method for screening and the effect of prophylaxis against thromboembolism after spinal surgery.

Adolescent↗
PubMedDate not supplied

Outcome of noncatheter-related thrombosis in children: influence of underlying or coexisting factors.

PURPOSE: To determine the hereditary and nonhereditary risk factors contributing to the development of noncatheter-related thrombosis in children. PATIENTS AND METHODS: Ninety-five children with noncatheter-related thrombosis from a single center were analyzed for clinical manifestations and outcome during a period of 3.5 years. Patients with thrombosis were evaluated for congenital and acquired risk factors, and patients were screened for factor V Leiden, prothrombin 20210A mutations, protein C, protein S, antithrombin III deficiencies, and antiphospholipid antibodies. RESULTS: Twelve patients (12.5%) died of thrombosis that was associated with a nonmalignant underlying disorder, and 19 patients (20%) had significant complications, including amputation of extremities, epilepsy, hemiplegia, portal hypertension, recurrence of deep vein thrombosis, and postphlebitic syndrome. Two common mutations (factor V Leiden and prothrombin 20210A) were found in 32.5% of the patients with thrombosis. The most frequent underlying disorder was infection (68%). Ninety-three patients (98%) had one or more risk factors. CONCLUSIONS: The coexistence of an underlying disorder and the presence of predisposing factors such as infection and the factor V Leiden mutation may cause high rates of death and complications in children with noncatheter-related thrombosis. The results of this study indicate that the underlying disorder and the site of thrombosis determine the rates of death and complications in children with thrombosis.

Adolescent↗
PubMed2005

Zebrafish: a tool to study hemostasis and thrombosis.

PURPOSE OF REVIEW: In the past eight years our laboratory has developed the zebrafish model to study hemostasis and thrombosis. The purpose of this review is to explore current developments involving the zebrafish model in the study of hemostasis and thrombosis because the time is now ripe to apply this model to identify novel players that participate in hemostasis and thrombosis. RECENT FINDINGS: In the past twelve months, three papers appeared in the hemostasis and thrombosis area using the zebrafish model. The first one is a review article that summarizes establishment of the zebrafish model to study hemostasis and thrombosis. The second study is a methodological paper describing assays for measuring hemostasis and thrombosis by inducing vascular occlusion in zebrafish larvae. The third paper describes a knockdown of prothrombin in zebrafish, which recapitulates knockout studies in mouse, and marks the beginning of studies in the hemostasis and thrombosis area by this new knockdown technology. In addition to the above papers, there is one abstract that describes kinetics of thrombocyte and thrombocyte-microparticle recruitment in laser-induced arterial thrombus formation in zebrafish. SUMMARY: With the above advances, the zebrafish model has now matured to the point that it can address more important questions in the hemostasis and thrombosis area using genetic approaches. This review therefore summarizes the issues described in the above papers along with thoughts about future progress of the zebrafish model as a tool to study hemostasis and thrombosis.

Animals↗