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[Inflammatory bowel disease and latent thrombocythemia: a novel cause of hepatic vein thrombosis?].

It has been suggested in previous studies, that inflammatory bowel disease can induce hepatic vein thrombosis. However, the main weakness of those studies was the lack of extensive screening of prothrombotic factors. We report an unusual association of severe inflammatory bowel disease, hepatic vein thrombosis and latent platelet proliferation disorder. Early treatment with heparin and cyclosporin administered intravenously induce a remission of intestinal disease and total disappearance of hepatic vein thrombosis. Extensive screening excluded the classical causes of hepatic vein thrombosis, inherited coagulation disorders and latent polycythemia by culture of erythroid progenitors without added erythropoietin. However, using recent bone marrow culture conditions, we observed spontaneous colony formation of megakaryocyte progenitors revealing latent thrombocythemia. In summary, progress in the diagnosis of haemostasis disorders, will probably confirm that one or more additional predisposing prothrombotic factors are needed to the development of hepatic vein thrombosis in inflammatory bowel disease. This hypothesis could explain the scarcity of this complication in inflammatory bowel disease. Moreover, this case-report suggests that administration of heparin at the onset of the thrombosis may induce a complete regression of the thrombus in hepatic veins.

Adult↗

Epidemiology and pathogenesis of venous thrombosis.

Venous thrombi are intravascular deposits composed predominantly of fibrin and red blood cells with a variable platelet and leukocyte component. They frequently arise in large venous sinuses in the calf, in valve cusp pockets either in the deep veins of the calf or thigh or in venous segments that have been exposed to direct trauma. Venous thrombosis can be produced experimentally by a combination of stasis and systemic hypercoagulability or by stasis and endothelial damage. Thrombosis is augmented if the fibrinolytic mechanism is inhibited or defective. A number of clinical conditions and laboratory abnormalities are associated with and predispose to venous thrombosis and, in many of these, it is possible to identify one or more of the thrombogenic factors discussed. Venous thromboembolism (venous thrombosis and pulmonary embolism) is a serious and potentially fatal disorder that usually complicates the course of sick hospitalized patients, but occasionally affects ambulant and otherwise healthy individuals. Screening studies with iodine-125 fibrinogen leg scanning, impedance plethysmography and perfusion lung scanning have shown that the majority of venous thrombi and pulmonary emboli that occur in hospitalized patients are small and asymptomatic, and it is likely that most are clinically insignificant. In bedridden patients, most thrombi commence in the calf and are asymptomatic. When a calf vein thrombus extends into the proximal venous segment, the risk of clinically significant pulmonary embolism increases. Less is known about the incidence and clinical significance in a nonhospital population; although asymptomatic disease occurs, its frequency is unknown. In contrast to the patients with asymptomatic venous thrombosis, symptomatic patients with venous thrombosis usually have large occulsive thrombi localized in their proximal veins.

Blood Circulation↗

Venous valvular reflux in veins not involved at the time of acute deep vein thrombosis.

PURPOSE: The aim of this study was to determine whether, in lower extremities with documented episodes of acute deep venous thrombosis (DVT), incompetence develops in veins that were not the site of thrombosis. METHODS: Patients were monitored with serial duplex ultrasonography at 1 day, 1 week, 1, 3, 6, 9, and 12 months, and then annually after detection of acute DVT. The following venous segments were analyzed: common femoral, greater saphenous, proximal superficial femoral, deep femoral, popliteal, and posterior tibial. The incidence of reflux development in both thrombosed and uninvolved segments was determined. Reflux was categorized as either transient or permanent. RESULTS: A total of 227 limbs in 188 patients were serially studied. Mean follow-up was 19.9 months (range 1 to 88 months). Overall, 403 of the 1423 segments (28.3% +/- 2.3%) developed reflux during the study, of which 118 (29.3% +/- 4.4%) had no prior or concurrent history of thrombosis. Considering only the segments that developed incompetence, the percent without prior thrombosis at each level was as follows: common femoral vein (40.0%), greater saphenous vein (53.1%), deep femoral vein (20.6%), proximal superficial femoral vein (23.9%), popliteal vein (8.9%), and posterior tibial vein (31.9%). Valvular insufficiency developing in segments uninvolved with thrombus was more likely to be transient (40.2%) than was the reflux in thrombosed segments (22.6%). This difference was statistically significant (p < 0.05). CONCLUSIONS: Permanent venous valvular damage can occur in the absence of thrombosis after DVT. Reflux in uninvolved venous segments has a different anatomic distribution and is more likely to be transient than the incompetence associated with thrombosis.

Acute Disease↗

The molecular genetics of familial venous thrombosis.

This study of naturally occurring mutations predisposing to venous thrombosis has led to a number of important advances in our understanding of protein structure and function relationships and the molecular basis of gene mutation. It has also potentiated the accurate and reliable presymptomatic and antenatal detection of predisposing gene lesions. Perhaps the major challenge facing us is the probabilistic nature of thromboembolism; only a certain proportion of patients with recognized gene defects predisposing to thrombosis will actually suffer from thrombotic episodes. Environmental insults of various kinds, and perhaps epistatic effects resulting from the influence of other loci, are likely to be contributory factors and will help to determine whether a thrombotic event occurs in individuals already compromised by a defect in a gene whose malfunction is known to predispose to thrombosis. Since molecular genetic techniques allow us to dissect the allelioheterogeneity of the different deficiency states by characterizing the wide spectrum of gene mutations giving rise to thrombosis, it may eventually prove possible to relate specific gene lesions to the probability of thromboembolism as well as to the severity and frequency of thrombotic episodes. The multifactorial nature of thrombosis demands a multidisciplinary approach to the analysis of its causation, early detection, treatment and prevention. The application of the new and powerful techniques of molecular genetics promises to make a substantial contribution to all aspects of thrombosis research.

Afibrinogenemia↗

Utility of intra-access pressure monitoring in detecting and correcting venous outlet stenoses prior to thrombosis.

Vascular access thrombosis is a major problem for hemodialysis patients. Over 7.75 years, we performed intra-access venous pressure monitoring at zero dialyzer blood flow (VP0), correlated VP0 with access anatomy angiographically, and examined the effect of two levels of stenosis, 50% and > 65% luminal diameter reduction (% D) as selection criteria for referral and elective angioplasty or surgical revision upon access outcomes. Summary receiver outcome curves for absolute intra-access pressure (VP0) and intra-access pressure normalized for systemic pressure (VP0/systolic BP) were constructed to evaluate sensitivity and specificity and compared to recirculation and duplex color-flow Doppler. Access outcomes included thrombosis, revision, replacement, and angioplasty rates that were normalized per 100 patient years (100 pt-yrs). During the 7.75 year long study period totaling 832 patient-access years of risk, the percentage of prosthetic bridge grafts increased from 65% to 80%. SROC showed better sensitivity for normalized (VP0/systolic BP) than absolute intra-access pressure (VP0) in grafts. Recirculation had poor predictive power in prosthetic bridge grafts compared to VP0. Predictive power of recirculation was superior to VP0 in native arteriovenous fistulae. The angioplasty rate correlated inversely with the degree of luminal reduction used as selection criterion for referral for angioplasty or surgical revision. A strong inverse relationship between thrombosis rate and the angioplasty rate (R2 = 0.99) but not between thrombosis rate and the number of angiograms performed (R2 = 0.39) was noted. A consistent, yet evolving, intensive graft maintenance protocol produced a 70% decrease in the thrombosis rate, a 79% decrease in the access replacement rate, and an increase in the average age of patent usable vascular accesses from 1.97 to 2.98 years that was associated with a 13-fold increase in the angioplasty rate. We conclude that vascular access monitoring with VP0/systolic BP provides excellent selection criteria for angiographic referral. Intervention for stenotic lesions > 50% D using angioplasty or surgical revision markedly reduces thrombosis and access replacement rates.

Angiography↗

A simple clinical model for the diagnosis of deep-vein thrombosis combined with impedance plethysmography: potential for an improvement in the diagnostic process.

OBJECTIVES: We recently demonstrated the utility of a clinical model combined with ultrasonography to assist the diagnostic approach in patients with suspected deep-vein thrombosis (DVT). In this study we also sought to demonstrate that the model is useful with impedance plethysmography, a less accurate and less utilized diagnostic test. The original clinical model is slightly cumbersome to use; thus at the completion of the study we attempted to develop a simpler scoring system with a goal of maintaining accuracy. DESIGN: An open, nonrandomized, multicentre trial. SETTING: Three centres, two in Canada, and one in Italy. SUBJECTS: Ambulatory patients with suspected deep-vein thrombosis. INTERVENTIONS: All patients were assessed clinically to determine the probability for deep-vein thrombosis prior to performing impedance plethysmography and venography. We compared the accuracy of impedance plethysmography between the three pretest probability categories of high, moderate and low. All of the above were performed and interpreted by independent observers. When the study was completed, we revised the clinical model by first performing a simple regression analysis then a multiple logistic regression analysis; a scoring system was devised using the latter. RESULTS: Impedance plethysmography is significantly more sensitive and less specific for all DVT in patients with high pretest probability for deep-vein thrombosis (P = 0.001). The post- test probability (positive predictive value) for deep-vein thrombosis with an abnormal impedance plethysmography result was significantly different (P = 0.0001) between the three pretest probability categories. Multiple regression analysis has provided a new model with only nine variables and a simple scoring system. The retrospective application of the revised clinical model, which is simpler to use, suggests it will provide similar results as the original clinical model when combined with impedance plethysmography. The combination of impedance plethysmography and the clinical model suggests patients are likely to have false positive results if they have a low or moderate pretest probability for deep-vein thrombosis and false negative results if the pretest probability is high. The combination of a low pretest probability and a normal impedance plethysmography result may exclude the need for serial testing, and represented more than 50% of our patient population. CONCLUSIONS: The use of the clinical model in conjunction with impedance plethysmography would decrease the number of false positive and negative diagnoses and could markedly decrease the need for serial impedance plethysmography. Combining the clinical model with impedance plethysmography could overcome the fact that impedance plethysmography is clearly less accurate than venous ultrasound imaging. The use of the revised clinical model may increase acceptability and utility, but prospective testing is required before widespread use.

Diagnosis, Differential↗

[Acute venous thrombosis: localization, extent and aetiology with special consideration of paraneoplasia].

Among 279 consecutive patients (average age 53.8 years) with acute venous thrombosis, "complete" or "nearly complete" search for neoplasm was undertaken in 93 (average 60.6 years), "not complete" search in 186 (average 50.1 years). Subsequently the patients were followed regularly for possible malignant tumour (average follow-up period 36.9 months). In the group as a whole the following causes of thrombosis were identified: contraceptives 9.3%; post-operative 9%; malignant tumour diagnosed immediately or within 12 months 5.8%; traumatic 5%; immobilization 3.2%; post-partum 2.9%; diverse other causes 8.2%; unknown 59.5%. Neoplasm was found in 12.9% of 93 somewhat older "completely" examined patients. Taking into account age, 7.8% of all patients over 50 years developed thrombosis in association with neoplasm. In 6 of 16 patients with malignant tumour the venous thrombosis followed a particular course. Extensive thromboses in several bouts predominated. In 48.4% there were three-bout thromboses, in a further 27.4% four-bout thromboses involving also the pelvic vein. Isolated lower-leg venous thrombosis occurred in 9.2%, while the remaining one or multiple-bout thromboses occurred only in a few. Massive pelvic and leg vein thrombosis occurred in 43% of patients with malignant neoplasm, much more frequently than in those without neoplasm.

Acute Disease↗

A comparison of subcutaneous low-molecular-weight heparin with warfarin sodium for prophylaxis against deep-vein thrombosis after hip or knee implantation.

BACKGROUND: Deep-vein thrombosis is a potentially life-threatening complication of total hip or knee replacement. There are few data on the effectiveness and safety of warfarin as compared with low-molecular-weight heparin as prophylaxis against this problem. METHODS: We therefore performed a randomized, double-blind trial in 1436 patients to evaluate the effectiveness and safety of low-molecular-weight heparin (given subcutaneously once daily) as compared with adjusted-dose warfarin to prevent venous thrombosis after hip or knee replacement. Treatment with the drugs was started postoperatively. The primary end point was deep-vein thrombosis as detected by contrast venography (performed a mean of 9.4 days after surgery in each group). RESULTS: Among the 1207 patients with interpretable venograms, 231 of 617 patients (37.4 percent) in the warfarin group and 185 of 590 patients (31.4 percent) in the low-molecular-weight-heparin group had deep-vein thrombosis (P = 0.03). The reduction in risk with low-molecular-weight heparin as compared with warfarin was 16 percent, and the absolute difference in the incidence of venous thrombosis was 6 percent in favor of low-molecular-weight heparin (95 percent confidence interval, 0.8 to 11.4 percent). The incidence of major bleeding was 1.2 percent (9 of 721 patients) in the warfarin group and 2.8 percent (20 of 715 patients) in the low-molecular-weight-heparin group (P = 0.04), and the absolute difference was 1.5 percent in favor of warfarin (95 percent confidence interval, 0.1 to 3.0 percent). CONCLUSIONS: Our data demonstrate that the small reduction in the incidence of venous thrombosis with low-molecular-weight heparin, as compared with warfarin, was offset by an increase in bleeding complications. Although the use of low-molecular-weight heparin is simpler, because it is administered subcutaneously without the need for monitoring, it may be more costly than warfarin. Warfarin is inexpensive, but the overall cost of its use is increased by the need to monitor the intensity of anticoagulation. At this time it is unclear which of these approaches is the most cost effective.

Administration, Oral↗

The inherited basis of venous thrombosis.

Venous thrombosis represents a manifestation of disordered hemostatic balance. The classical presentation is of pain and swelling of the lower limb, although clinical history and examination are notoriously misleading in reaching a diagnosis. A number of acquired predispositions have been associated with a tendency to thrombosis, such as immobilisation, surgery, malignancy and certain types of oral contraception, but in at least half of the instances no predisposition can be identified. A variety of genetic risk factors have also been identified. Mutations within the genes for antithrombin, protein C and protein S are associated with a venous thromboembolic phenotype. The commonest thrombophilic predisposition however is a variant of coagulation factor V, factor V Leiden, which results from a single amino acid substitution rendering the factor V molecule resistant to activated protein C. Factor V Leiden is present in approximately 5% of individuals of European origin, and is found in up to 40% of those with confirmed venous thrombosis. Increasingly it is recognised that venous thrombosis should be considered a polygenic disorder, with interactions between the various single gene defects which predispose to thrombosis, as well as normal genetic variation between individuals in the levels of both procoagulant and anticoagulant proteins, all determining which individuals will express the phenotype of venous thrombosis.

Antithrombin III↗

Limitation of central vein thrombosis in total parenteral nutrition by continuous infusion of low-dose heparin.

The use of continuous, low-dose heparin in total parenteral nutrition (TPN) formulas to limit central venous thrombosis was retrospectively evaluated. Seven of 129 patients (5.4%) developed central vein thrombosis when TPN solutions provided less than 6,000 units (usually 1,000 units/liter) heparin per day. In the subsequent period when heparin was increased to 6,000 units per day, 10 of 858 (less than 1.2%) patients developed a TPN-related thrombosis (P less than 0.0005). The incidence of antithrombin III (AT III) deficiency in a subset of high-risk patients scheduled to receive TPN was 51% (23 of 55). Twelve of the 23 had clinical evidence of thrombosis, whereas only 3 of 22 patients with normal AT III levels did (P less than 0.01) A major contributing factor to the development of thrombosis in TPN appears to be depression in antithrombin III levels, which is commonly found in patients who require this therapy. Low-dose heparin appears to reduce the incidence of thrombosis with TPN when provided continuously in sufficient amounts.

Adult↗

Thrombosis in inflammatory bowel disease: clinical setting, procoagulant profile and factor V Leiden.

Patients with inflammatory bowel disease have an increased frequency of thromboembolism, and microvascular thrombosis has been proposed as a contributory pathogenic factor. The mechanism of enhanced procoagulant activity is not understood. We examined the clinical setting of thromboembolic events in 52 patients with Crohn's disease or ulcerative colitis, and assessed the procoagulant laboratory profile, including Factor V Leiden, in a subset of 20 patients to identify procoagulant risk factors. Patients who developed thrombosis tended to be young; 60% of thrombotic events occurred in patients under 50 years. Multiple thromboembolic episodes occurred in 13% and unusual sites of thrombosis (e.g. intracardiac, cerebral, inominate veins) in 11%. No risk factor was identifiable in 52% of cases and two-thirds of thromboses occurred in an out-patient setting. The mortality rate was 8%. Evidence for inflammatory disease activity was found in only 45% of patients with ulcerative colitis at the time of the thromboembolic event, in contrast to 89% of those with Crohn's disease. Assays for specific coagulation defects were negative in all cases tested (protein S, C were normal in 17/17; anti-thrombin III, anti-phospholipid antibodies and activated protein C resistance were negative in 20/20, and only 1/20 patients was found to be heterozygous for Factor V leiden. Thrombosis in inflammatory bowel disease is important because it occurs in a young population, often in unusual sites, and has a high mortality. The development of thrombosis is related to active inflammatory disease in most patients with Crohn's disease but apparently not in those with ulcerative colitis. Since approximately half of the patients had no other identifiable risk factor, there remains a substantial group of patients with IBD who develop thrombosis for unknown reasons.

Acute Disease↗

Low prevalence of thrombophilic coagulation defects in patients with deep vein thrombosis of the upper limbs.

While many studies have demonstrated the pathogenetic role of inherited deficiency of natural clotting inhibitors in patients in the development of deep vein thrombosis of lower limbs, no data are available on the prevalence of these abnormalities in patients with upper vein thrombosis. In this study, antithrombin III, protein C, protein S, plasminogen, resistance to activated protein C and factor V Leiden mutation were assayed in 27 consecutive patients with thrombosis of upper extremities. Only two patients (7.4%) showed a congenital defect (one patient with deficiency of protein C, confirmed by family study, and one patient with factor V Leiden mutation). Anticardiolipin antibodies were also measured and four patients (14.8%) had increased levels, confirmed on a subsequent occasion 3 months later. Eighteen out of 27 (67%) had a predisposing or triggering factor, thus emphasizing the role of physical stress in the development of upper vein thrombosis. At variance with what is observed in deep vein thrombosis of the lower limbs, inherited clotting abnormalities seem to be rarely responsible for upper vein thrombosis, whereas anticardiolipin antibodies and cancer are implicated in a significant proportion of cases.

Adolescent↗

Increased risk of venous thrombosis in carriers of natural anticoagulant deficiencies. Results of the family studies of the Spanish Multicenter Study on Thrombophilia (EMET study).

Several studies have demonstrated a higher risk of thrombosis in carriers of anticoagulant deficiencies than in non-deficient individuals from families with thrombophilia. The prevalences in Spain were established in a multicenter study (the EMET study) and all the deficient individuals were invited to recruit all available family members to be screened for the same deficiency in order to establish the risk of thrombosis in deficient individuals. Five-hundred-and-eighty-three individuals from 114 families with natural anticoagulant deficiencies were analysed. Propositi and relatives with a history of thrombosis were asked about the localization and the age at the first episode and whether or not it was spontaneous. Three families with antithrombin deficiency, 35 with protein C, 60 with protein S, four with plasminogen, four with heparin cofactor II, seven with combined deficiencies and one family with dysfibrinogenemia were included in the analysis. The risk of thrombosis was increased for individuals deficient in antithrombin (adjusted odds ratio 21.23; 95% confidence interval 5.71-78.94), protein C (adjusted odds ratio 12.62; 95% confidence interval 4.75-33.51), protein S type I (adjusted odds ratio 19.95; 95% confidence interval 7.40-53.82), protein S type III (adjusted odds ratio 8.11; 95% confidence interval 2.66-21.99) or in protein C plus protein S (adjusted odds ratio 8.99; 95% confidence interval 2.79-28.93), but not for those deficient in plasminogen or heparin cofactor II. The thrombosis-free survival was shortened for deficient individuals in antithrombin (median 30 years), protein C (median 46 years), protein S type-I (median 48 years), protein S type III (median 61 years) and combined protein C and S (median 40 years). In conclusion, individuals carrying anticoagulant deficiencies have an increased risk of thrombosis, especially those with antithrombin, protein C or type I protein S deficiencies.

Adult↗

Procainamide-induced lupus anticoagulants and thrombosis.

The specific factors predisposing to thrombosis in patients with LAs have not been resolved. With extensive cross-reactivity, and several proposed sites of action, LAs and their effects may be heterogeneous. While the risk of thrombosis with phenothiazine-induced LAs is probably low, the incidence of thrombosis in association with procainamide-induced LAs is uncertain. Procainamide is a commonly used antiarrhythmic drug associated with the induction of autoantibodies, and occasionally with a lupus-like syndrome. Serologic and coagulation profile monitoring may be required to detect patients in whom LAs develop since these individuals may be at increased risk for thrombosis. Monitoring may be especially important in patients who are receiving procainamide and who have atherosclerosis and cardiac disease, since they may be at increased risk for thrombosis of coronary and other arteries. Future prospective studies are needed to investigate whether the development of lupus anticoagulants during procainamide therapy increases the risk of thrombosis.

Aged↗

Incidence of deep vein thrombosis in major adult spinal surgery.

Deep vein thrombosis and pulmonary embolus are well known complications of lengthy orthopaedic procedures. Historically spine surgery has been associated with few thrombotic complications. Recent widespread use of instrumentation in adult cases led to concern regarding the incidence of deep vein thrombosis and pulmonary embolus. Forty-one patients underwent posterior spinal procedures using either pedicular or segmental instrumentation. One day before discharge all patients underwent noninvasive testing using color duplex Doppler imaging to rule out deep vein thrombosis. Six patients were noted to have tests results compatible with deep vein thrombosis. The incidence of deep vein thrombosis during this study (14%) reveals a group of patients who would have been discharged with ongoing thrombosis and potential pulmonary embolism.

Adult↗

John Hageman's factor and deep-vein thrombosis: Leiden thrombophilia Study.

Because the relationship between factor XII deficiency and venous thrombosis is unclear and study results seem contradictory, we undertook a population-based case-control study. Among 350 unselected patients younger than 70 years, with a first, objectively confirmed, episode of deep-vein thrombosis and without underlying malignant disease we detected a 6% frequency (21/350 patients) of factor XII deficiency (activity level < 57%). Among 350 healthy control subjects, matched for age and sex, the frequency was 5% (18 subjects). Thus there is no increase in prevalence of factor XII deficiency among thrombosis patients and no increase in thrombosis risk for subjects with low factor XII levels (matched odds ratio 1.2 (95% CI 0.6-2.4)). In addition, there was no relation between strata of factor XII levels and thrombosis risk. In conclusion, we do not consider factor XII to be a determinant of deep-vein thrombosis.

Adolescent↗

Red blood cell aggregability in patients with a history of leg vein thrombosis: influence of post-thrombotic treatment.

Reversible aggregation of red blood cells (RBC) plays an important role in determining blood flow properties, and it is this aggregation which increases blood viscosity at low shear rates. The structure and sites of venous thrombi, as well as the fact that stasis is a major predisposing factor in venous thrombosis, suggest a strong association between vein thrombosis, slow blood flow and increased blood viscosity. RBC aggregation and disaggregation were measured (SEFAM erythroaggregameter, France) in 54 patients with a history of unexplained leg vein thrombosis. Results were compared to those of controls classified according to age. Increased RBC aggregability was observed in 41% of the patients, and the mean values indicated a significant elevation of RBC aggregability in patients when compared with controls (P < 0.05). Subgroups were compared to study the influence of thrombus recurrence and thrombosis type (deep versus superficial vein thrombosis) on the aggregation parameters. No significant difference was found between these subgroups. The use of compression stockings and veinotropic drugs tended to reduce the abnormalities in RBC aggregability (P < 0.05). An increase in RBC aggregability and in the shear resistance of RBC aggregates, by predisposing to circulatory stasis, is likely to contribute to the evolution and complications of leg vein thrombosis.

Adult↗

Cerebral Venous Thrombosis - a new diagnosis in travel medicine.

Dr. Pfausler and colleagues report in this issue of Journal of Travel Medicine a series of patients with an interesting and potentially fatal neurovascular disorder; they raise the question, is this condition more frequent in travelers? Over a period of 18 months, Dr. Pfausler and colleagues identified five of fifteen consecutive patients presenting with occlusion of the cerebral veins who had been traveling on long distance flights. Some of these patients also had a history of diarrhea, and exposure to heat or dehydration associated with their air travel. It is important to note that their air travel experience was also associated with other precipitating factors in several of the cases. One patient had been mountaineering at high altitude and also had donated plasma. Another had severe diarrhea. A third patient was taking oral contraceptives. Whereas more than a coincidental link appears to be related to air travel, some of the authors' statements implying causality should be qualified in the absence of a larger, more formal, epidemiologic analysis. How might air travel lead to cerebral venous thrombosis? In clinical practice, thrombosis of the cerebral veins most commonly occurs after trauma or infection of the head and neck. However, thrombosis is also seen in conditions of heightened coagulability or viscosity. One could conjecture that prolonged air travel in a cabin, pressurized to the equivalent of high altitude, might lead to compensatory hemoconcentration and heightened blood viscosity, which could be aggravated further by other conditions such as diarrhea or oral contraceptive use. A critical point made by the authors is that the clinical presentation of cerebral venous thrombosis differs from that of conventional stroke. Patients with venous occlusion often present with headache and behavioral abnormalities, which often lead to a mistaken diagnosis of psychogenic illness before seizures or signs of increased intracranial pressure become obvious. Neurologists are trained to have a high index of suspicion for this condition in patients with trauma, infection, or in the peri-partal period. If the observations of Pfausler et al are confirmed, we should add prolonged air travel to the list of predisposing conditions. Cerebral venous thrombosis is a very treatable type of stroke. Major morbidity is due to increased intracranial pressure, which can be relieved by steroids or dehydrating agents. Treatment of underlying infection or hypercoagulability is critical. In the past, most patients were given anticoagulants, despite the risk of hemorrhage into a venous infarct. If the major draining veins of the brain are affected - in particular, the sagittal sinus - a malignant form of increasing intracranial pressure with high morbidity ensues. Recently, direct infusion of thrombolytic agents in the venous sinuses through a retrograde placed catheter has been used in patients with this condition. Cerebral venous thrombosis can be diagnosed readily with magnetic resonance imaging and angiography, which have largely replaced conventional angiography in suspected cases. The development of thrombolytic therapy for acute occlusive stroke and the demonstration of its efficacy and relative safety in carefully selected patients1 have focused attention on the need for ultra-fast recognition and treatment of cerebrovascular disease. As stroke enters the era of emergency therapy, all health professionals, including those who care for air travelers, should be aware of the various presentations of stroke syndromes and the need for urgent therapy.

Journal Article↗