Could some aviation deep vein thrombosis be a form of decompression sickness?

Aviation deep vein thrombosis is a challenge poorly understood in modern aviation. The aim of the present project was to determine if cabin decompression might favor formation of vascular bubbles in commercial air travelers. Thirty commercial flights were taken. Cabin pressure was noted at take-off and at every minute following, until the pressure stabilized. These time–pressure profiles were imported into the statistics program R and analyzed using the package SCUBA. Greatest pressure differentials between tissues and cabin pressures were estimated for 20, 40, 60, 80 and 120 min half-time compartments. Time to decompress ranged from 11 to 47 min. The greatest drop in cabin pressure was from 1022 to 776 mBar, equivalent to a saturated diver ascending from 2.46 msw depth. Mean pressure drop in flights >2 h duration was 193 mBar, while mean pressure drop in flights <2 h was 165 mBar. The greatest drop in pressure over 1 min was 28 mBar. Over 30 commercial flights it was found that the drop in cabin pressure was commensurate with that found to cause bubbles in man. Both the US Navy and the Royal Navy mandate far slower decompression from states of saturation, being 1.7 and 1.9 mBar/min respectively. The median overall rate of decompression found in this study was 8.5 mBar/min, five times the rate prescribed for USN saturation divers. The tissues associated with hypobaric bubble formation are likely slower than those associated with bounce diving, with 60 min a potentially useful index.     

Loco-regional thrombolysis for deep vein thrombosis: fact or fiction? A study of hemostatic parameters.

Loco-regional thrombolysis for deep-vein thrombosis (DVT) has been claimed to be equally effective and safe compared with systemic thrombolysis. It is not known whether a loco-regional thrombolytic effect exists and of what it might consist. To investigate this issue, we studied eight patients with DVT undergoing loco-regional thrombolysis with 20 mg alteplase infused over 4 h in a dorsal foot-vein of the affected leg, while the leg was kept tightly bandaged; alteplase infusions were repeated every 24 h, the number of therapy cycles (TC) was seven, and full-dose heparin was given. For coagulation analyses, 'loco-regional' blood samples were taken from a vein of the affected leg and 'systemic' samples were taken from an antecubital vein. After a median number of six TC, good partial reperfusion was achieved in 4/8 patients, moderate partial reperfusion in 2/8, major bleedings occurred in 2/8, and minor bleedings in 1/8 patients. During the first TC, recombinant tissue-type plasminogen activator (rtPA) activity and antigen, as well as FgDPs and d-dimers, were elevated significantly loco-regionally over systemic values, and a complete breakdown of plasmin-inhibitor activity occurred with only a slight systemic reduction; no other differences were found. During successive TC, differences in rtPA-activity and -antigen levels decreased, and no significant differences were found for all other parameters. Thus, a local fibrinolytic effect was demonstrable during loco-regional thrombolysis for DVT; the magnitude of this effect diminished during successive TC, giving rise to the hypothesis that the fibrinolytic efficacy may be decreased due to growing, antifibrinolytic activity. The preserved, loco-regional plasmin-inhibitor activities during the later TC, in contrast to the complete breakdown during the first TC, suggest that part of the enhanced antifibrinolytic activity is due to loco-regionally increased plasmin-inhibitor activity. The ultimate goal of loco-regional thrombolysis, the induction of local fibrinolysis without systemic effects, has not, however, been achieved.     

Angina pectoris in a patient with protein C deficiency and deep vein thrombosis: Thrombus versus myxoma?

A 55‐year‐old Caucasian man with history of hypertension, diabetes mellitus, protein C deficiency, and deep vein thrombosis presented with typical angina. Both computed tomography and transesophageal echocardiography identified a mobile mass in left atrium but could not differentiate between thrombus and myxoma. A cardiac catheterization with coronary angiography demonstrated tumor neovascularization, suggestive of myxoma. Pathology examination after mass resection confirmed the diagnosis. Patients with myxoma could present with obstructive, embolic, or constitutional symptoms. However, typical angina has never been reported as the primary manifestation. Although being helpful, various noninvasive imaging modalities, including magnetic resonance image, often have limitations to help making a definitive diagnosis, before surgery decision, especially under hypercoagulable condition. In contrast, cardiac catheterization can help not only in differentiation diagnosis but also in detecting possible intracoronary embolization from myxoma. In patients with myxoma complicated with hypercoagulable disorders, anticoagulation will play essential role in long‐term care. © 2011 Wiley Periodicals, Inc.     

Portal vein thrombosis: What is new?

Portal vein thrombosis (PVT) is one of the most common vascular disorders of the liver with significant morbidity and mortality. Large cohort studies have reported a global prevalence of 1%, but in some risk groups it can be up to 26%. Causes of PVT are cirrhosis, hepatobiliary malignancy, abdominal infectious or inflammatory diseases, and myeloproliferative disorders. Most patients with PVT have a general risk factor. The natural history of PVT results in portal hypertension leading to splenomegaly and the formation of portosystemic collateral blood vessels and esophageal, gastric, duodenal, and jejunal varices. Diagnosis of PVT is made by imaging, mainly Doppler ultrasonography. According to its time of development, localization, pathophysiology, and evolution, PVT should be classified in every patient. Some clinical features such as cirrhosis, hepatocellular carcinoma, and hepatic transplantation are areas of special interest and are discussed in this review. The goal of treatment of acute PVT is to reconstruct the blocked veins. Endoscopic variceal ligation is safe and highly effective in patients with variceal bleeding caused by chronic PVT. In conclusion, PVT is the most common cause of vascular disease of the liver and its prevalence has being increasing, especially among patients with an underlying liver disease. All patients should be investigated for thrombophilic conditions, and in those with cirrhosis, anticoagulation prophylaxis should be considered.     

Should symptomatic,isolated distal deep vein thrombosis be treated with anticoagulation?

BACKGROUND:

During the past two decades, the diagnosis of deep venous thrombosis (DVT) has made considerable progress. The term distal or calf vein thrombosis includes thrombosis in infrapopliteal veins, including the posterior tibial, peroneal, anterior tibial and muscular calf veins. The necessity of treating of distal DVT is debatable.

OBJECTIVE:

To determine whether treatment of isolated, distal DVT with anticoagulation versus no treatment affects patient outcome.

METHODS:

All patients discharged with a diagnosis of distal DVT from Tan Tock Seng Hospital, Singapore, between January 1, 2006, and December 31, 2007, were identified by the medical records office of the hospital. Compression of the intraluminal thrombus by duplex scan was used to diagnose distal DVT. Excluded were patients who either had both distal and proximal DVT, or had distal DVT along with pulmonary embolism (PE) at presentation.Complete resolution of distal DVT on repeat duplex scan was used to measure the primary outcome. Repeat follow-up scans were performed at two weeks, one month, three months and six months, or on subsequent follow-up until the distal DVT had resolved completely.Secondary outcome measures were complete improvement of symptoms, progression of thrombosis, or PE or death during the follow-up period.The study included 68 patients with distal DVT; however, 17 patients with PE, two of whom had proximal DVT (in the iliac and common femoral veins) at the first presentation along with distal DVT, were excluded from the study. In total, 51 patients were included for analysis. The follow-up scan was available in 35 patients; therefore, the primary analysis was performed in 35 patients (47 incidences of distal DVT). However, the secondary analysis was available in all 51 patients.Of the 35 patients available for follow-up scans, 17 patients (25 incidences of distal DVT) received anticoagulation and 18 patients (22 incidences of distal DVT) received no anticoagulation.Of the 17 patients who were treated with anticoagulation, nine patients (13 incidences of distal DVT) received enoxaparin at a dose of 1 mg/kg twice a day for two weeks and eight patients (12 incidences of distal DVT) received warfarin for a period of three months with initial overlap of enoxaparin 1 mg/kg twice a day for three to five days. Once the prothrombin time international normalized ratio of a patient on warfarin was between 2 and 3, enoxaparin was discontinued. The 18 patients who did not receive anticoagulation received follow-up with regular duplex scan.

RESULTS:

There were no statistically significant differences among the groups in the resolution of distal DVT or symptom improvement with or without treatment. In the group that received no treatment, one death occurred. Proximal extension and PE were not recorded in any of the patients.

CONCLUSION:

Distal DVT may not require treatment with anticoagulation. If leg symptoms worsen, or if there is an extension of distal DVT on the follow-up scan, treatment with anticoagulation is recommended.     

F9 Malm?, factor IX and deep vein thrombosis

Background

We recently reported the association between the Malmö sequence variant in F9 (rs6048) and deep vein thrombosis.

Design and Methods

We aimed to study whether the association between F9 Malmö and deep vein thrombosis is explained by linkage disequilibrium with nearby single-nucleotide polymorphisms, and whether the association is explained biologically by F9 Malmö affecting factor IX antigen levels or activation of factor IX. We investigated the association of F9 Malmö and 28 nearby single-nucleotide polymorphisms with deep vein thrombosis in men from two case-control studies, LETS (n=380) and MEGA (n=1,469). We assessed the association of F9 Malmö with factor IX antigen level in male control subjects from LETS (n=191) and two subsets of MEGA (n=823 and n=484) and the association with endogenous thrombin potential in LETS control men. We studied the association between F9 Malmö and factor IX activation peptide in 1,199 healthy middle-aged men from the NPHS-II cohort.

Results

In the combined LETS and MEGA studies, the odds ratio (95% confidence interval) for the G allele of F9 Malmö, compared with the A allele, was 0.80 (0.69–0.93). One single-nucleotide polymorphism in F9, rs422187, was strongly linked to F9 Malmö (r²=0.94) and was similarly associated with deep vein thrombosis. No other single-nucleotide polymorphism or haplotype tested was more strongly associated. Factor IX antigen level, factor IX activation peptide levels and endogenous thrombin potential did not differ between F9 Malmö genotypes.

Conclusions

The F9 Malmö sequence variant was the most strongly associated with deep vein thrombosis among common single-nucleotide polymorphisms in the region. However, the biological mechanism by which F9 Malmö affects risk remains unknown.