Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, December 17, 2012

Warfarin-induced calciphylaxis in a chronic hypercalcemic patient

I'm sure your doctor warned you about this side effect.
http://www.ijdvl.com/article.asp?issn=0378-6323;year=2013;volume=79;issue=1;spage=135;epage=135;aulast=Huang



Calciphylaxis most commonly occurs in patients with end-stage renal disease under dialysis. Warfarin is a risk factor for calciphylaxis in uremic patients, but is rarely known to induce calciphylaxis in non-uremic patients. We report herein a warfarin-induced calciphylaxis in a patient with chronic hypercalcemia.

A 19-year-old male patient with history of persistent hypercalcemia of unknown cause and chronic renal insufficiency for 1 year presented himself with extensive painful necrotic ulcer over bilateral legs for 4 months [Figure 1]. Review of history showed that he received bilateral iliac vein stenting for the iliac vein compression syndrome. He then received warfarin after the stent implantation. One month after warfarin treatment, he developed progressive painful ulceration on bilateral legs within 1 week. The results of laboratory examination indicated elevated serum creatinine (2.1 mg/dL), calcium (12.9 mg/dL), normal phosphate (4 mg/dL) and decreased intact parathyroid hormone (6.32 ng/L). The findings of urine analysis were mild proteinuria and hematuria. Renal sonography was found to have bilateral renal stones and right hydronephrosis. The titre values of antinuclear antibody, rheumatoid factor, antineutrophil cytoplasmic antibody, antiphospholipid antibody and cryoglobulin were all negative. The result of immunoelectrophoresis showed no monoclonal gammopathy. As shown in [Figure 2], the specimen picture of skin biopsy presented subcutaneous calcium deposits with diffuse panniculitis and fat necrosis. [Figure 3] shows calcification within the media of small- and medium-sized arterioles, with extensive intimal hyperplasia and fibrosis. We suspected a warfarin-induced calciphylaxis and shifted it to aspirin. The ulcerations were managed by local wound care, and gradually healed with residual scars within 5 months. At that time, all our survey for hypercalcemia only revealed a high 1,25 (OH) vitamin D3 (67 pg/mL), and no etiology of hypervitaminosis D could be identified. Patient's hypercalcemia was persistent and we educated him not to take warfarin anymore.





Figure 1: Widespread necrotic ulcerations over the right leg

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