How do you screen for central venous sinus thrombosis?
Hello, I would like to ask if anyone uses Hounsfield units and Hb/Htc ratio to screen for or diagnose central venous sinus thrombosis. I work in the emergency setting, and a MR venogram is not always available to us. I have read several studies where HU values are used alongisde Hb/Hct values, but I have not seen this being done in real life. Can someone advise? Many thanks
Patient with DVT and PE has adrenal hemorrhage and then DVT again..
I have another question and update regarding the 45 year old man with recent DVT and PE, who was on apixiban. He then had an acute adrenal hemorrhage, which prompted us to stop his anticoagulation. This was the previous post: https://www.g-med.com/page/view-post?id=207443
Now he has presented with a right lower extremity DVT. The antiphospholipid syndrome panel, which was requested earlier, indicatesthe presence of lupus anticoagulant. His anti-nuclear antibody titer was 1 : 40, and the anti-double stranded DNA antibody test was negative. Laboratory workup for other causes of thrombosis was negative. I would be happy to hear your considerations regarding future anticoagulation, especially because of previous hemorrhage.
VTE events and adrenal hemorrhage
Hello colleagues, any ideas for this case? A 45 year old male patient without significant past medical history presented with a seemingly unprovoked left lower leg deep vein thrombosis and pulmonary embolism. He was discharged on apixaban.
Three days later, he was readmitted with bilateral flank pain. Abdominal CT showed bilateral adrenal gland edema and enlargement concerning for adrenal hemorrhage. He is hemodynamically stable.
Further tests revealed a reduced morning cortisol (1.5 μg/dL) and an elevated morning ACTH. Plasma DHEA was reduced. Aldosterone, epinephrine, and norepinephrine were undetectable and renin activity was normal. We have started steroids.
What plan would you suggest for this patient? Do you think the adrenal hemorrhage related to apixiban or is there an underlying pathogy that could explain DVT/PE and hemorrhage?
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Hello!
Perhaps D-dimer can give a little help.
The sinus thrombosis is one of the most disguised illnesses.
Best regards!
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Hello Andrew, our everyday experience tells us how difficult it is to diagnose CVS on MR: you need a lot of experience to avoid disapointments... Non contrast CT is the work-horse for this pathology, especially in the early time-window (first days or hours after initial clinical symptoms when MR is so difficult to read for junior radiologists or in the middle of the night...), but be sure to check and COMPARE (and measure if necessary) the density of superior sinus, straight sinus, lateral sinuses. Sagittal and coronal reformats can be a great help (providing you have access to 1mm non-contrast CT). If ALL sinuses are dense, confront with hematocrit. Otherwise be highly suspicious of CVT, and compare the anomalous sinuses with the same post IV-contrast. Deep venous thrombosis (straight sinus and internal cerebral veins) can be challenging and misleading before a hemorrhage occurs... Hope this is helpful!
Best regards,
Marc BINTNER, Neuroradiologist
Reunion island
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In 30 years and having placed many thousands of ports (the word 'Port a Cath' was a trade name of a device from the US not used as far as I am aware for decades) I have seen many develop a fibrin sheath which is managed with small dose of local strptokinase.
Vessel thrombosis is rarer and in practice many of my colleagues get worried when arm oedema occurs but again I have never seen a case of embolism and it always resolves on line removal even in a few cases where the patient has been travelling and clearly had thrombosis for months
What is clear is inserting a new system even in the other arm rapidly leads to similar fibrin / thrombosis issues.
I also suspect a degree of thrombosis is almost universal but in most cases not symptomatic and not identified.
In summary I try never to remove these systems. Peer pressure and patient fear sometimes forces my hand and then I resist a new system for at least six weeks.
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Leukocyte Glucose Index, Arteriovenous Fistula Failure Linked in ESKD
MONDAY, April 22, 2024 (HealthDay News) -- For patients with end-stage kidney disease (ESKD), a high preoperative leukocyte glucose index (LGI) is associated with arteriovenous fistula (AVF) failure, according to a study published online April 1 in the Journal of Clinical Medicine.
Adrian Vasile Muresan, Ph.D., from the George Emil Palade University of Medicine, Pharmacy, Science and Technology of Targu Mures in Romania, and colleagues examined the impact of LGI on long-term primary patency of AVF following initiation of dialysis in 158 patients with ESKD. AVF failure, defined as the impossibility of performing chronic dialysis due to severe restenosis or AVF thrombosis, was examined as the primary end point.
The researchers found that the prevalence rates of atrial fibrillation and diabetes were higher in patients with AVF failure, and they had a higher LGI value. In a receiver operating characteristic analysis, the strongest association with the outcome was seen for LGI, with an area under the curve of 0.729 and an optimal cutoff of 0.95 (sensitivity and specificity of 72.4 and 68 percent, respectively). Patients in the highest versus the lowest tertile of LGI had a significantly higher incidence of AVF failure in Kaplan-Meier survival analyses. The risk for AVF failure during follow-up was significantly higher for patients with higher baseline LGI values (hazard ratio, 1.48); the association was independent of age and sex, cardiovascular risk factors, and preoperative vascular mapping determinations (hazard ratios, 1.65, 1.63, and 3.49, respectively).
"LGI can be used as a potential biomarker to identify patients from risk groups that require more careful monitoring of AVF in order to improve the management and care of patients with ESKD," the authors write.
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