Neuropatía óptica isquémica no arterítica como lesión de órgano diana en la hipertensión arterial / Non-arteritic ischaemic optic neuropathy as a target organ lesion in arterial hypertension

Varón de 39 años, de raza negra que consultó por pérdida de visión súbita e indolora del ojo derecho en el contexto de una crisis hipertensiva. Antecedente de hipertensión arterial esencial, sin control domiciliario por falta de adherencia terapéutica y con afectación de órganos diana: infarto lacunar, retinopatía hipertensiva grado IV e hipertrofia concéntrica del ventrículo izquierdo. La función renal era normal, sin albuminuria. El cuadro clínico se etiquetó de neuropatía óptica isquémica no arterítica tras descartarse enfermedad vascular, traumática, infecciosa o autoinmune. Presentó una discreta mejoría del déficit visual con el control de la presión arterial. Dados los antecedentes y las pruebas complementarias, se concluyó que la neuropatía óptica isquémica fue debida a malignización de su hipertensión arterial. (AU)

A 39-year-old black male who consulted with sudden and painless loss of vision in his right eye in the context of a hypertensive crisis. A history of essential arterial hypertension uncontrolled at home due to lack of therapeutic adherence and with target organ involvement: lacunar infarct, grade IV hypertensive retinopathy and left ventricular concentric hypertrophy. Renal function was normal, without albuminuria. The clinical picture was classified as non-arteritic ischaemic optic neuropathy after ruling out vascular, traumatic, infectious and autoimmune disease. The patient presented discrete improvement of the visual deficit with the control of blood pressure. From his history and complementary tests, it was concluded that the ischaemic optic neuropathy was due to malignization of his arterial hypertension. (AU)

Hipertensión arterial por hiperactividad simpática tras traumatismo craneoencefálico grave / Hypertension due to sympathetic hyperactivity after severe head injury

Presentamos el caso de un paciente de 34 años que sufre un traumatismo craneoencefálico grave con afectación cerebral severa. Evoluciona de manera tórpida precisando varias reintervenciones por sangrado y herniación de masa encefálica. Nos interconsultan desde Neurocirugía por irregular control de cifras de presión arterial a pesar de tratamiento con calcioantagonistas. El paciente asocia diaforesis, taquipnea y taquicardia, junto a fiebre de alto grado de forma persistente sin evidencia microbiológica. Analítica con función renal normal, sin proteinuria y sin datos de hipertrofia de ventrículo izquierdo que sugieran hipertensión arterial previa. Esto nos hace plantearnos como primera posibilidad diagnóstica un síndrome de hiperactividad simpática debido al daño neurológico severo. Se inicia terapia antihipertensiva orientada a esta sospecha, entre los que se incluyen betabloqueantes no cardioselectivos, alfa-2-agonistas, benzodiacepinas y agonistas de los receptores GABA. Así se consigue mejorar la labilidad de las cifras de presión arterial, lo que apoya el diagnóstico

We present the case of a 34-year-old patient with severe head trauma and severe brain involvement. The patient deteriorated progressively and required several reinterventions for bleeding and brain herniation. We were consulted by neurosurgery due to irregular blood pressure control despite treatment with calcium antagonists. The patient had associated diaphoresis, tachypnoea and tachycardia, together with persistent high-grade fever with no microbiological evidence. Laboratory tests showed normal kidney function, with no proteinuria and no signs of left ventricular hypertrophy to suggest previous arterial hypertension. This led us to consider sympathetic hyperactivity syndrome as a first possible diagnosis due to severe neurological damage. In line with this suspicion, antihypertensive therapy was initiated which included non-cardioselective beta-blockers, alpha-2 agonists, benzodiazepines and GABA receptor agonists. Thus, we were able to improve the labile blood pressure levels, which supports the diagnosis

[Non-arteritic ischaemic optic neuropathy as a target organ lesion in arterial hypertension]. / Neuropatía óptica isquémica no arterítica como lesión de órgano diana en la hipertensión arterial.

A 39-year-old black male who consulted with sudden and painless loss of vision in his right eye in the context of a hypertensive crisis. A history of essential arterial hypertension uncontrolled at home due to lack of therapeutic adherence and with target organ involvement: lacunar infarct, grade IV hypertensive retinopathy and left ventricular concentric hypertrophy. Renal function was normal, without albuminuria. The clinical picture was classified as non-arteritic ischaemic optic neuropathy after ruling out vascular, traumatic, infectious and autoimmune disease. The patient presented discrete improvement of the visual deficit with the control of blood pressure. From his history and complementary tests, it was concluded that the ischaemic optic neuropathy was due to malignization of his arterial hypertension.

[HYpertension due to sympathetic hyperactivity after severe head injury]. / Hipertensión arterial por hiperactividad simpática tras traumatismo craneoencefálico grave.

We present the case of a 34-year-old patient with severe head trauma and severe brain involvement. The patient deteriorated progressively and required several reinterventions for bleeding and brain herniation. We were consulted by neurosurgery due to irregular blood pressure control despite treatment with calcium antagonists. The patient had associated diaphoresis, tachypnoea and tachycardia, together with persistent high-grade fever with no microbiological evidence. Laboratory tests showed normal kidney function, with no proteinuria and no signs of left ventricular hypertrophy to suggest previous arterial hypertension. This led us to consider sympathetic hyperactivity syndrome as a first possible diagnosis due to severe neurological damage. In line with this suspicion, antihypertensive therapy was initiated which included non-cardioselective beta-blockers, alpha-2 agonists, benzodiazepines and GABA receptor agonists. Thus, we were able to improve the labile blood pressure levels, which supports the diagnosis.

Visceral Leishmaniasis in Renal Transplant Recipients: Report of 2 Cases.

Visceral leishmaniasis is a disease caused by the protozoan Leishmania and is transmitted by Lutzomyia longipalpis (sand fly). It is an endemic parasitic infection in numerous areas around the Mediterranean basin. Though immunocompetent patients may not develop the disease, in transplant recipients the use of corticoids and intensified immunosuppressants to prevent graft rejection may accelerate the disease, causing severe damage to the liver, spleen, and hematopoietic system. We report 2 cases of visceral leishmaniasis with an atypical presentation in transplant recipients. The first patient, who had a kidney transplant, was treated successfully with liposomal amphotericin B, and the second patient, a combined kidney-pancreas transplant recipient, suffered a relapse 3 years after treatment. Visceral leishmaniasis should be considered in the differential diagnosis of pancytopenia or unexplained fever occurring after organ transplantation in patients living in endemic areas or returning from endemic countries.