Cardiology Expert Advises on Coumadin Overdose

Oral anticoagulation is considered in these patients based on their overall risk factors for stroke most commonly summarized by the CHADS-VASc score, though other risk factors should also be taken into account. Not all patients meet indications for the initiation of anticoagulation and a proportion of those meeting these indications do not qualify as a high bleeding risk. The risk of stroke should be weighed against the risk of bleeding, which is more difficult to quantify. There are several scoring systems available to assess the risk of bleeding (eg HAS-BLED score) but these are less commonly used. A patient’s likelihood of compliance with drug administration and monitoring should also be considered as should their consumption of foods or medications known to interact with Coumadin metabolism. If a patient is deemed to be a Coumadin candidate (i.e., meets indications and does not exhibit evidence of contraindications) Coumadin may be started. Ideally, the patient should be educated regarding the risks of bleeding with Coumadin, the need for compliance with drug administration and monitoring, and the potential for drug or dietary interactions. I encourage the use of a formalized Coumadin clinic or in office system. Regarding the initial dosing of Coumadin, there are two typical regimens. The one I use involves starting at 5 mg daily. However, many practitioners begin at 10 mg daily for the first few days and then lower the dose. There is data to support the use of either regimen, though there is controversy regarding which regimen is best. Furthermore, there are multiple approaches to the frequency of INR monitoring during the initiation phase of Coumadin therapy. I will typically test the INR 2 to 4 days after initiation of Coumadin and every 3 to 5 days thereafter until the INR level has been therapeutic for at least 2 consecutive checks. I do not routinely prescribe daily monitoring of outpatients as it is of limited utility and places a significant burden on patients and their families. Attached to this email please find several references. You will note that there is variation in the recommended frequency of monitoring. In regards to the possibility of a Coumadin overdose, mechanisms whereby pulmonary function may be affected include but are not limited to intra pulmonary hemorrhage, hemorrhagic pleural effusion leading to compression of the lungs, hematoma formation leading to compression of intra or extra thoracic airways. The likelihood of death from acute pulmonary hemorrhage varies depending on multiple other factors. Coumadin overdose could contribute to loss of pulmonary function and death through several mechanisms. A few of these mechanisms of death include, but are not limited to, death though exsanguination (if intra-abdominal, retroperitoneal, alimentary, or external), brain injury (if intracerebral), cardiac tamponade (if pericardial) or asphyxiation (if intra-pulmonary).