Question of the Week # 228

228 )  A 70-year-old white man  with type 2 diabetes mellitus and hypertension is evaluated in the emergency room for lacy purplish discoloration of the lower extremities that developed few hours ago. He reports diffuse bodyaches and low grade fever. He denies chest pain or shortness of breath. His past medical history is significant for coronary artery disease for which he underwent cardiac catheterization with percutaneous coronary intervention one week ago.  He has a history of chronic atrial fibrillation for which he is on 5mg coumadin daily. His most recent INR has been therapeutic at 2.5. Physical examination reveals lacy purplish pattern on bilateral lower extremities shown in the image below.

The site of cardiac catheterization in the femoral area is clean and healing with out any tenderness or erythema. Neurological examination is normal. Laboratory studies reveal a creatinine of 4.2mg% as opposed to his baseline creatinine of 1.8mg% one week ago. Hemoglobin and platelet count are within normal limits. WBC count is 12.6k/µl with neutrophils 70%, bands of 2% , eosinophils 18% and lymphocytes 10%. Which of the following is the most likely diagnosis?

A)  Toxic shock syndrome

B)  Atheroembolism

C)  Contrast Nephropathy

D)  Anti-Phospholipid antibody syndrome

E)  Cryoglobulinemia

8 Responses

  1. b

  2. answer is B

  3. The answer D- This is called Livedo Reticularis and could be seen in patients with APS or Lupus.

  4. ans B.
    The diagnosis of cholesterol embolism must be considered in patients older than 50 years who have atherosclerotic disease presenting with multisystem dysfunction after undergoing an invasive vascular procedure or receiving an anticoagulant or thrombolytic agent within the past several months. All patients with the classic triad of livedo reticularis, acute renal failure, and eosinophilia should be evaluated for cholesterol embolism, including a funduscopic examination.
    medscape.

  5. B……
    Cholesterol embolism syndrome, shown below, should be suspected in a patient who develops worsening renal function, hypertension, distal ischemia, or acute multisystem dysfunction after an invasive arterial procedure. Atheroemboli may also occur spontaneously. The protean manifestations of this syndrome make the diagnosis challenging. As the population ages, the incidence of cholesterol embolism syndrome will increase

    Key components of cholesterol embolism syndrome include the following:

    Proximal, large caliber arterial plaque


    Plaque rupture with embolization of debris


    Mechanical occlusion of small arteries


    Intense foreign body inflammation


    End organ damage from mechanical obstruction


    Inflammatory vascular changes

    Any organ system, with the exception of the lungs, may be directly affected. Cholesterol embolism syndrome has 2 mechanisms of action.

    In the first, cholesterol crystals spontaneously break off from severely atherosclerotic plaques and shower into downstream organs, occluding arterioles 100-200 micrometers in diameter. The crystals induce an inflammatory body reaction and adventitial fibrosis, which eventually obliterate the vessel lumen. Local vasospastic mediators compound tissue ischemia and produce progressive, irreversible organ damage.

    With the second mechanism, larger cholesterol plaques break off and occlude larger arteries, causing tissue infarction with acute organ dysfunction. This can occur after local trauma to the atherosclerotic plaque, such as that caused by angiography or aortic trauma, or it can occur after destabilization of the protective clot overlying the plaque, which can occur as a result of anticoagulation.

    Cholesterol crystal embolization occurs from the arterial system, and crystals are trapped in the arterioles where they either immediately occlude the vessels or induce an intense inflammatory response that leads to tissue ischemia. Crystals do not travel to the lungs; however, inflammatory mediators released by ischemic tissue may result in acute lung injury.

    The mortality rate of severe cholesterol embolism is 90% at 3 months.

    Mild cases with renal dysfunction with or without skin findings had a mortality of 16%.

    The diagnosis of cholesterol embolism must be considered in patients older than 50 years who have atherosclerotic disease presenting with multisystem dysfunction after undergoing an invasive vascular procedure or receiving an anticoagulant or thrombolytic agent within the past several months. All patients with the classic triad of livedo reticularis, acute renal failure, and eosinophilia should be evaluated for cholesterol embolism, including a funduscopic examination.

    • •Eosinophilia strongly suggests atheroembolization and is present in as many as 80% of patients with cholesterol embolism syndrome.

  6. bbb

  7. B:)

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