Bocio endotorácico como causa infrecuente de síndrome de vena cava superior / Endothoracic goitre as an uncommon cause of superior vena cava syndrome

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Contribution of magnetic resonance imaging to prenatal differential diagnosis of renal tumors: report of two cases and review of the literature.

Enlargement of a kidney on prenatal imaging is usually due to hydronephrosis or cystic renal disease, and much less often results from solid tumors such as mesoblastic nephroma, Wilms' tumor, nephroblastomatosis, renal sarcoma, and angiomyolipoma. All can be diagnosed by ultrasound. Magnetic resonance imaging is useful not only in confirming the presence of a renal mass, but also in the evaluation of the contralateral kidney for subtle abnormalities. We present one case each of Wilms' tumor and mesoblastic nephroma, both detected on antenatal ultrasound and further studied with fetal magnetic resonance imaging.

[Sagittal sinus thrombosis as a rare cause of postpartum headache: a case report]. / Trombosis del seno sagital cerebral: causa infrecuente de cefalea del postparto: a propósito de un caso.

Postpartum cerebral vein thrombosis is a very rare entity (3-4 cases per million). Clinical manifestations vary, though persistent headache is almost always reported, meaning that differential diagnosis should be performed to rule out other causes of postpartum headache. Recognized risk factors for this disease are the prothrombotic state of pregnancy (third trimester), excess weight, and thrombophilia Accidental dural puncture, protein C and S deficiencies, factor V Leiden mutation, antiphospholipid syndrome, and the use of oral contraceptives have also been implicated. The diagnostic test of choice is magnetic resonance imaging, as it is convenient and harmless, though transcranial Doppler ultrasound can also be used. Pulmonary angiography is the gold-standard test. The treatment of choice is anticoagulant therapy with heparin (a treatment that is controversial, however, due to the high risk of rebleeding), followed by long-term treatment with antivitamin K drugs. We report a case of thrombosis of the upper longitudinal sinus associated with persistent postpartum headache and a history of a failed attempt at epidural puncture for analgesia during labor. The case posed interesting diagnostic questions.

Trombosis del seno sagital cerebral: causa infrecuentede cefalea del postparto: a propósito de un caso / Sagittal sinus thrombosis as a rare cause of postpartum headache: a case report

Las trombosis venosas cerebrales del postparto sonuna entidad muy poco frecuente (3-4 casos por millón).Sus manifestaciones clínicas son variadas, siendo la cefaleapersistente casi una constante, lo que implica hacerun diagnóstico diferencial con otras causas de cefaleadurante el puerperio. Los factores predisponentes reconocidosde ésta patología son el estado protrombótico delembarazo (tercer trimestre), el sobrepeso y la existenciade trombofilias. Además se han implicado en su producciónla punción dural accidental, la existencia de deficienciasde proteína C y S, Factor V Leiden, el síndromeantifosfolípido e ingesta de anticonceptivos orales. Laprueba diagnóstica de elección es por su comodidad einocuidad la resonancia magnética, aunque puede utilizarsetambién la ecografía Doppler transcraneal. Laarteriografía es la prueba de referencia. El tratamientode elección es la anticoagulación con heparina (controvertidopor el riesgo elevado de nuevo sangrado), seguidade fármacos antivitamina K durante largos periodos.Describimos un caso de trombosis de seno longitudinalsuperior en el contexto de una cefalea persistente duranteel puerperio con el antecedente de intento fallido depunción epidural para analgesia de trabajo de parto quesupuso un interesante dilema diagnóstico (AU)

Postpartum cerebral vein thrombosis is a very rareentity (3-4 cases per million). Clinical manifestationsvary, though persistent headache is almost alwaysreported, meaning that differential diagnosis should beperformed to rule out other causes of postpartumheadache. Recognized risk factors for this disease are theprothrombotic state of pregnancy (third trimester),excess weight, and thrombophilia Accidental duralpuncture, protein C and S deficiencies, factor V Leidenmutation, antiphospholipid syndrome, and the use of oralcontraceptives have also been implicated. The diagnostictest of choice is magnetic resonance imaging, as it isconvenient and harmless, though transcranial Dopplerultrasound can also be used. Pulmonary angiography isthe gold-standard test. The treatment of choice isanticoagulant therapy with heparin (a treatment that iscontroversial, however, due to the high risk ofrebleeding), followed by long-term treatment withantivitamin K drugs. We report a case of thrombosis ofthe upper longitudinal sinus associated with persistentpostpartum headache and a history of a failed attempt atepidural puncture for analgesia during labor. The caseposed interesting diagnostic questions (AU)

Acquired renal cysts after pediatric liver transplantation: association with cyclosporine and renal dysfunction.

ACKD has been observed in children on dialysis and with chronic renal insufficiency. In one report, ACKD was observed in 30% of pediatric liver transplant recipients after 10 yr. We retrospectively reviewed all renal imaging and measurements of GFR of 235 childhood liver transplant recipients with no known risk for renal cyst formation, no evidence of renal cyst(s) at the time of transplantation and renal imaging at least one yr post-transplant. Twenty-six patients (11%) developed one or more cyst(s). Mean GFR was significantly lower in patients with renal cyst(s). Two (1.4%) of the 146 patients treated with tacrolimus and 24 (27%) of the 89 patients treated with CsA acquired renal cyst(s) (p < 0.001). CsA-treated patients had significantly lower GFR. Multivariate analysis identified CsA as the only independent variable associated with ACKD. These results confirm that ACKD can be a late complication of pediatric liver transplantation. Those at most risk are at least 10-yr post-liver transplantation, have been treated with CsA and have impaired renal function. We speculate that ACKD in these patients is the result of calcineurin inhibitor nephrotoxicity. Whether patients with ACKD will be prone to develop solid renal tumors is unknown.