How would you treat both PE and acute stroke?
A 72-year-old patient, independent for basic activities of daily living, with cardiovascular risk factors, type 2 diabetes, COPD, and dyslipidemia. His relatives found him on the floor of his home with a decreased level of consciousness, unresponsive to stimuli.
Five days earlier, he had consulted the emergency department for chronic pain in both upper limbs with paresthesia and decreased strength that had worsened in the last 48 h. A diagnosis of acute chronic arterial ischemia had been made and treatment with acetylsalicylic acid and pentoxifylline was prescribed.
For his current symptoms, investigations show acute ischemic stroke with massive PE.
What would be your therapeutic approach and in which order?
For your information, these were the other investigation results -
Blood tests: hemogram with chronic polyglobulia. Coagulation screen without alterations. Elevated D-dimer. Antiplatelet factor IV antibody: negative.
Cranial CT: loss of differentiation of gray substance-white substance with a blurring of furrows and hypodensity at the level of the vascular territory of the left PCA.
Angio-CT: thrombosis at the level of the left subclavian artery, stop at the level of left PCA, repletion defects extending to the level of the left vertebral artery, and subocclusive thrombus at the level of the basilar artery are identified. Repletion defect in pulmonary arteries, compatible with massive pulmonary thromboembolism.
Perfusion: an area of penumbra is observed at the level of the vascular territory of the left PCA.
Aortic thrombosis on chemotherapy - duration of anticoagulation
I have an update on my previous case (https://www.g-med.com/page/view-post?id=198754) - the 55 year old patient with colon cancer on his third cycle of capecitabine and oxaliplatin chemotherapy, who presented with chest discomfort and dyspnoea. An aortic thrombosis was found on CT incidentally.
After consultation, we decided to initiate low-molecular-weight heparin therapy and temporarily suspended his chemotherapy. We have also tested for hypercoagulable disorder but have not found evidence of any. Another CT coronary angiography of the chest shows no indication of embolic complications.
What is the ideal duration of anticoagulation therapy for a patient diagnosed with aortic thrombosis and cancer?
Aortic thrombosis on chemotherapy
A patient aged 55 with stage III colon cancer presents with chest discomfort and dyspnoea. He is currently on day 13 of cycle 3 of capecitabine and oxaliplatin chemotherapy. There was an incidental discovery of aortic thrombosis affecting the descending thoracic aorta made through a CT scan. Subsequent investigations did not indicate any indications of aortic dissection, and CT angiography of the chest did not reveal any proof of pulmonary embolism. He did not have any prior medical records indicating the presence of coronary artery disease or hypercoagulable conditions.
Are there any special considerations in managing aortic thrombosis in a patient receiving chemotherapy? How should we change his chemotherapy management?
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Fully agree with Dr. Luca Puccetti. His management is exactly mine and this is how I would act in every suspected case of DVT, Deep venous THROMBOSIS, Wells score respected. No doubt, D-dimers can be elevated by various processes, for example, by a tumor event - but even then heparin would be correct: Heparin counteracts metastasis of most tumors. I also use Doppler and sonography - but heparin ensures immediate safety and my statistics justify this approach. Addendum: Three weeks ago one of my patients developed DVT - D-Dimers extremely high - 87 years old, lean and on APIXABAN, Factor Xa-Inhibitor, because of AF. So Heparin was not an option there. His DVT subsided significantly under temporary doubling of APIXABAN-Administration for about ten days - kidney compliant - and stomach protected by PPI Pantoprazole.
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Very good question. Thank you. Patients with IgM paraproteinemia are at increased risk of thrombosis, both arterial and venous. In this patient, the anemia is compensation for the hyperviscosity, mediated by the systemic vascular resistance response (SVRR). Once the response is complete and anemia develops, the risk of thrombosis is reduced because whole blood viscosity (as compared to serum viscsoity) approaches normal. However, if hydration is not maintained for some reason, hyperviscosity may ensue and thrombosis can develop. I would recommend that the patient be diligent about hydration and not start an anticoagulant. .
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Viscosity testing must be ordered separately. Plasma and serum are the most common specimens. Elevated blood viscosity can be caused by inflammation and dehydration. Suspect hyperviscsoity in patients with thrombosis or extremely high erythrocyte sedimentation rates, Hyperviscosity can also cause viscual or hearing loss. Because elevated blood viscosity reduces blood flow,to all organs, hyperviscosity can cause reduced function of any organ, particualrly the brain or heart. I have seen hyperviscosity cause altered level of consciousness and arrhythmia.
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