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      Enfermedad ateroembólica y hemorragia pulmonar Translated title: Atheroembolic disease and pulmonary haemorrhage

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          Abstract

          El síndrome de embolismo de colesterol se produce por la liberación de cristales de colesterol de placas ateroscleróticas ulceradas de grandes arterias. Puede afectar múltiples órganos simulando enfermedades sistémicas como las vasculítis, y debe ser incluido en el diagnóstico diferencial de los síndromes neumo-renales. El diagnóstico de embolismo de colesterol debería contemplarse en pacientes de edad, con enfermedad aterosclerótica previa, que desarrollan fallo renal o deterioro de una insuficiencia renal previa, y en los que aparecen hallazgos clínicos sugestivos de embolismos de colesterol periféricos, asociado a factores precipitantes, sin necesidad de demostración histológica. Este síndrome se ha asociado tradicionalmente a una alta morbi-mortalidad, aunque en recientes series se sugiere que un manejo agresivo con medidas de soporte, evitando factores precipitantes y el uso de corticoides a bajas dosis pueden proporcionar una mejoría en su pronóstico.

          Translated abstract

          The cholesterol embolism syndrome is a multisystemic disease resulting from cholesterol crystal emboli deriving from ulcerous atherosclerotic plaques of the aorta or large arteries. Cholesterol crystal embolization can affect multiple organ, including the skin, kidney, brain, eyes, gastrointestinal tract and extremities, and mimic other systemic diseases like vasculitis. Cholesterol crystal embolization of lungs has been described and should be included in the differential diagnostic of pulmonary-renal syndromes. The diagnosis of cholesterol embolism should be considered in elderly patients with pre-existing atherosclerotic disease who develop renal failure and clinical features of peripheral cholesterol crystal embolization in association with precipitanting event, without the need for histological demostration of cholesterol clefts. This syndrome is associated with high morbidity and mortality but recents reports suggest that an aggresive therapeutic management with patient-tailored supportive measures, avoids precipitating factors, and the use of corticosteroids may be associated with a favorable clinical outcome.

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          Most cited references43

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          Cholesterol crystal embolization: a review of 221 cases in the English literature.

          Cholesterol crystal embolization (CCE) frequently presents with nonspecific manifestations that mimic other systemic diseases. The authors reviewed 221 cases of histologically proven CCE in the English literature to define the clinical, laboratory, and pathologic characteristics of this disorder. CCE affected predominantly elderly males (mean age sixty-six) with a frequent history of hypertension (61%), atherosclerotic cardiovascular disease (44%), renal failure (34%), and aortic aneurysms (25%) at presentation. At least one possible predisposing factor was present in 31% and included operative and radiological vascular procedures and the use of anticoagulants. Cutaneous findings (34%) and renal failure (50%) were two of the most common clinical findings throughout the course of CCE. The nonspecific signs and symptoms included: fever (7%), weight loss (7%), myalgias (4%), and headache (3%). Premortem diagnoses were established in 31% of patients most commonly by biopsy of the muscle, skin, and kidney. Mortality was high (81%) and was most commonly due to multifactorial, cardiac, and renal etiologies. The authors conclude that CCE should be strongly considered in elderly patients with atherosclerotic vascular disease who have the onset of renal insufficiency and cutaneous manifestations. CCE may be confirmed by a skin or muscle biopsy.
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            Supportive treatment improves survival in multivisceral cholesterol crystal embolism.

            Disseminated cholesterol crystal embolism (CCE) is a devastating complication of atherosclerosis that is often considered beyond therapeutic resources. We designed and implemented a treatment protocol based on an analysis of the main causes of death in disseminated CCE with renal involvement. From 1985 to 1996, we applied this protocol in 67 consecutive atherosclerotic patients admitted to our renal intensive care unit for acute renal failure (serum creatinine level, 6 +/- 2.5 mg/dL) accompanied by signs and symptoms of CCE. The other principal clinical features in these patients were cardiac failure with pulmonary edema (61%), gastrointestinal ischemia (33%), cutaneous ischemia (90%), and retinal cholesterol embolism (22%). Disseminated CCE followed one or several precipitating factors, including angiographic procedure(s) (85%), anticoagulant treatment (76%), and cardiovascular surgery (33%). Our treatment schedule systematically addressed the identified causes of death in these patients. (1) To avoid CCE recurrence, any form of anticoagulant treatment was withdrawn, and aortic catheterization and surgery were proscribed. (2) To treat or prevent cardiac failure, a high-dose vasodilator regimen was instituted, including angiotensin-converting enzyme (ACE) inhibitors. In case of cardiac failure refractory to vasodilators, loop diuretics were added and, if necessary, overhydration was corrected by ultrafiltration/hemodialysis (11 patients). (3) To avoid cachexia, severe metabolic disorders were treated by hemodialysis (41 patients), and special attention was given to providing enteral or parenteral nutritional support. Patients with declining general status and laboratory evidence of inflammation, as well as those with new episodes of CCE, were treated with corticosteroids. Statistical analysis found a significant correlation between the requirement for hemodialysis and previous anticoagulation, degree of renal insufficiency, and severity of cardiac failure. Conversely, there was no correlation between requirement for hemodialysis and ACE inhibitor treatment or presence of atherosclerotic renal artery stenosis/thrombosis. The inhospital mortality rate was 16%. There were no clinical or laboratory elements found on admission that were predictive of inhospital mortality. Among survivors, 32% had to remain on maintenance hemodialysis therapy for irreversible chronic renal failure. Including initial hospitalization, the 1-year survival rate was 87%, which compares favorably with reports in the literature indicating a first-year mortality rate of 64% to 81%. Overall follow-up was 19 +/- 20 months, ranging from 1 to 74 months. The 4-year survival rate was 52%. We conclude that an intensive-care, specific-treatment schedule reduces mortality in multivisceral cholesterol embolism.
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              Atheroembolic renal failure after invasive procedures. Natural history based on 52 histologically proven cases.

              Atheromatous plaque material containing cholesterol crystals may dislodge and cause distal ischemia. To characterize atheroembolic renal failure, we retrospectively evaluated all patients at the Massachusetts General Hospital from 1981 to 1990 with both renal failure and histologically proven atheroembolism after angiography or cardiovascular surgery. Over the 10-year period, 52 patients were identified. They tended to be elderly men with a history of hypertension (81%), coronary artery disease (73%), peripheral vascular disease (69%), and current smoking (50%). Within 30 days of their procedure, only 50% of patients had cutaneous signs of atheroembolism, and 14% had documented blood eosinophilia. Urinalysis was often abnormal. Hemodynamically unstable patients died shortly after their procedure, yet renal function in the remainder continued to decline over 3 to 8 weeks. Patients who received dialysis had a higher baseline serum creatinine than those who did not (168 +/- 44 mumol/L versus 133 +/- 18 mumol/L, p = 0.02), with dialysis starting a median of 29 days after the procedure. Patients with renal failure due to atheroembolism alone, as opposed to multiple renal insults, were more likely to recover renal function (24% versus 3%, p = 0.03) and had a lower risk of death during the 6 months after their procedure (log-rank p = 0.002). Renal failure due to procedure-induced AE is characterized by a decline in renal function over 3 to 8 weeks. This time course is not consistent with most other iatrogenic causes of renal failure, such as radiocontrast or nephrotoxic medications, which present earlier and often resolve within 2 to 3 weeks after appropriate intervention.(ABSTRACT TRUNCATED AT 250 WORDS)
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                ami
                Anales de Medicina Interna
                An. Med. Interna (Madrid)
                Arán Ediciones, S. L. (, , Spain )
                0212-7199
                May 2004
                : 21
                : 5
                : 31-34
                Affiliations
                [03] Sevilla orgnameHospital Virgen Macarena orgdiv1Servicio de Medicina Interna
                [01] orgnameHospital Universitario Son Dureta orgdiv1Servicio de Nefrología
                [04] Palma de Mallorca orgnameHospital Universitario Son Dureta orgdiv1Servicio de Anatomía Patológica
                [02] orgnameHospital Universitario Son Dureta orgdiv1Servicio de Cuidados Intensivos
                Article
                S0212-71992004000500006
                10.4321/s0212-71992004000500006
                e3f52f65-f82e-4183-9ea5-ab55f0074eef

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                Embolización de cristales de colesterol,Atheroembolic disease,Cholestherol crystal embolization

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