Name:
A 63-Year-Old with a Skin Lesion
Description:
A 63-Year-Old with a Skin Lesion
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T00H05M24S
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Upload Date:
2022-02-28T00:00:00.0000000
Transcript:
Language: EN.
Segment:0 .
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CATHY: Hi, welcome to Harrison's Podclass, where we discuss important concepts in internal medicine. I'm Cathy Handy.
CHARLIE: And I'm Charlie Wiener,
CHARLIE: and we're coming to you from the Johns Hopkins School of Medicine. Episode 28: A 63-Year-Old with a Skin Lesion. So, here's the question: a 63-year-old woman with chronic kidney disease is maintained on daily peritoneal dialysis. Her past medical history is notable for hypertension and atrial fibrillation. Her medications include losartan and warfarin. Two days ago, she noticed a small painful nodule on her abdomen that has progressed to involve skin necrosis and ulceration of the abdominal wall.
CHARLIE: Okay, Cathy, what do you think so far of this?
CATHY: Painful skin nodules with necrosis and ulceration in someone who is on dialysis, makes me think of calciphylaxis. This is also called calcific uremic arteriolopathy and it is seen almost exclusive in patients who are on dialysis. But the other disorder to think of in a patient on warfarin therapy is warfarin-induced skin necrosis, but that is seen during initial warfarin administration because you get protein C deficiency which causes a transient hypercoagulable state and that in turn leads to the vascular occlusion and tissue infarction which produces the ulceration.
CHARLIE: But with the painful skin nodule, don't you have to think of infectious causes also?
CATHY: Yeah, absolutely, and if the patient were neutropenic, a necrotic nodule that you could see would be ecthyma gangrenosum and that's due to pseudomonas, or a disseminated fungal infection. But we don't have any information that this patient is neutropenic and it sounds like there have been no recent changes in medication, so I would go with calciphylaxis as the most likely cause, given the information that we have.
CHARLIE: What's the pathophysiologic mechanism of calciphylaxis?
CATHY: So, what you see pathologically is that there is evidence of vascular occlusion in association with extensive vascular and soft tissue calcification. A patient will first get livedo reticularis and then that advances to patches of ischemic necrosis. You typically find it on the legs, thighs, abdomen, and breasts and a skin biopsy can be used for diagnosis if you're not sure based on the clinical presentation.
CHARLIE: So, this question asks, all the following statements regarding her condition are true except: option A says, oral calcium supplementation may be a risk factor; option B says, pathologically, there is vascular occlusion; option C says, pseudomonas co-infection is typical; option D says, severe hyperparathyroidism may not be present; and E says, warfarin is a risk factor for the development of the lesion.
CATHY: So, let's start with A. That's true. Oral calcium supplementation is considered a risk factor and as is warfarin. So, E is also true. Other risk factors for calciphylaxis would include hyperphosphatemia, obesity, diabetes, hypercoagulable states, and also hypoalbuminemia, inflammatory and autoimmune diseases, and recurrent skin trauma. It is more commonly found in females compared to males, and the incidence is increasing, although it is not really clear why that's the case.
CHARLIE: Tell me more about the warfarin. Why is that ought to be a risk factor?
CATHY: With regards to warfarin since the patient here is on it, it's commonly used in hemodialysis patients and one of the effects of warfarin therapy is to decrease the vitamin K-dependent regeneration of matrix GLA protein. This latter protein is important in preventing vascular calcification. So, warfarin treatment is considered a risk factor for calciphylaxis and if a patient develops this syndrome while on warfarin, this medication should be discontinued and you can replace it with alternative forms of anticoagulation.
CHARLIE: Okay. So, that rules out two of the choices. And you also mentioned previously that pathologically there is vascular occlusion, so, we can rule out option B as well. What about C and D?
CATHY: So, D is true. Severe hyperparathyroidism is not always present. Originally, it was ascribed to severe abnormalities in calcium and phosphorus control in dialysis patients, and that's usually associated with advanced hyperparathyroidism. However, more recently, calciphylaxis has been seen with increasing frequency, in the absence of severe hyperparathyroidism. The exact reason for this isn't clear.
CHARLIE: Okay. So, C is a false statement. Pseudomonas co-infection, in fact, is not typical in patients with calciphylaxis, right?
CATHY: Yeah, I'm not aware of any literature supporting bacterial infection as typically co-occurring with calciphylaxis. And as I mentioned before, if the patient were neutropenic, then ecthyma gangrenosum may be in the differential, but that's not the case here.
CHARLIE: Okay. So, what would you do to help this patient?
CATHY: First, you start off with supportive care that would include, for me, local wound care and you can treat with hyperbaric oxygen if it's very severe, and then intravenous thiosulfate is also used. And, as I mentioned before, in this patient I would change the anticoagulation and stop the warfarin.
CHARLIE: Okay. So, the teaching point, in this case, is that calciphylaxis is most commonly seen in patients with advanced kidney disease, although it is not always, and is caused by vascular occlusion in association with extensive vascular necrosis and soft tissue calcification. Warfarin and calcium supplementation are risk factors for its development and patients-- taking care of patients on renal dialysis should be aware of this complication of dialysis, both hemodialysis and peritoneal dialysis.
CATHY: And to read more about this, you can check out the Harrison's chapter on Chronic Kidney Disease and Disorders of the Kidney and Urinary Tract. ♪ (music) ♪