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La enfermedad pulmonar intersticial difusa (EPID) supone un amplio grupo heterogéneo de enfermedades caracterizadas por hallazgos en su intersticio pulmonar, específicamente relacionados con su engrosamiento, lo cual impacta significativamente en el intercambio gaseoso y la mecánica ventilatoria del paciente. El diagnóstico se genera acorde a la clínica del paciente, el uso de imágenes y la histopatología. El tratamiento guarda relación directa con el patrón pulmonar estructural que presente la EPID. Se presenta el caso clínico de una paciente femenina de 32 años, indígena, quien ingresa por exacerbación de disnea, con antecedente de neumonitis por hipersensibilidad, adicional a otros antecedentes clínicos que guardan relación estrecha con la EPID.
Diffuse interstitial lung disease (ILD) is a large heterogeneous group of diseases characterized by findings in the pulmonary interstitium, specifically changes related to thickening of the interstitium, which significantly impacts the patient's gas exchange and ventilatory mechanics. The diagnosis is generated according to the patient's clinical presentation, imaging and histopathology. The treatment is directly related to the structural pulmonary pattern of ILD. We present the clinical case of a 33-year-old female patient of indigenous ethnicity who is admitted for exacerbation of dyspnea, with a history of hypersensitivity pneumonitis in addition to other clinical antecedents that are closely related to ILD.
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HumanosRESUMO
Objective In the present study, we aimed at determining the correlation between tomographic findings of intracranial hypertension and ultrasound measurement of the optic nerve sheath diameter (ONSD). Methods Observational, descriptive, prospective, cross-sectional pilot study. The present research was performed in a tertiary hospital in Cali, Colombia, from March 2019 to October 2019. Twenty-five patients constituted the intracranial hypertension group, and 25 patients without intracranial hypertension constituted the control group. Ultrasound measurements of the ONSD were assessed using a Sonosite Turbo (SonoSite Inc., Bothell, WA, USA) ultrasound. The computed tomogra phy (CT) images obtained from each patient diagnosed with intracranial hypertension were available in the software of the hospital. The primary outcome was the ultrasound measurement of the ONSD. Results The ONSD values of the right eye of the intracranial hypertension group ranged from 5.2 to 7.6 mm, and the ONSD of the left eye ranged from 5.3 to 7.3 mm. The global ONSD values, obtained from the average between the right and left eye, were recorded between 5.25 and 7.45 mm. Overall, our study indicated that ultrasound measurements of the ONSD were effective in differentiating a group with intracranial hypertension, previously diagnosed by CT scan images, from patients without this condition. According to the ROC curve, the optimal cutoff point for detecting intracranial hypertension was 5.2 mm. Conclusions Ultrasound measurements of the ONSD correlated with the measurements obtained from CT scan images, suggesting that the ultrasound technique can be efficient in identifying patients with intracranial hypertension and valuable in cases when CT scan images are not an available option.
Objetivo No presente estudo, pretendemos determinar a correlação entre os achados tomográficos da hipertensão intracraniana e a medida ultrassonográfica do diâmetro da bainha do nervo óptico (DBNO). Métodos Estudo piloto, observacional, descritivo, prospectivo e transversal. A presente pesquisa foi realizada em um hospital terciário de Cali, na Colômbia, de março de 2019 a outubro de 2019. Vinte e cinco pacientes fizeram parte do grupo de hipertensão intracraniana e 25 pacientes sem hipertensão intracraniana fizeram parte do grupo controle. O ultrassom Sonosite Turbo (SonoSite Inc., Bothell, WA, EUA) foi utilizado para a medição ultrassonográfica do DBNO. As imagens tomográficas computadorizadas obtidas de cada paciente com diagnóstico de hipertensão intracraniana estavam disponíveis no software do Hospital. O resultado primário foi a medida ultrassonográfica do DBNO. Resultados Os valores de DBNO do olho direito do grupo de hipertensão intracraniana foram de 5,2 a 7,6 mm e o DBNO do olho esquerdo foi de 5,3 a 7,3 mm. No que se refere aos valores globais de DBNO obtidos a partir da média entre o olho direito e o olho esquerdo, registrou-se entre 5,25 e 7,45mm. No geral, o presente estudo indicou que as medições ultrassonográficas do DBNO foram eficazes na diferenciação de um grupo com hipertensão intracraniana, previamente diagnosticada por imagens de tomografia computadorizada (TC), de pacientes sem essa condição. De acordo com a curva ROC, o ponto de corte ideal para detectar hipertensão intracraniana foi de 5,2 mm. Conclusões De acordo com nossos achados, as medidas ultrassonográficas do ONSD se correlacionaram com as medidas obtidas nas imagens de TC, sugerindo que a técnica ultrassonográfica pode ser eficiente para identificar pacientes com hipertensão intracraniana e útil nos casos em que as imagens tomográficas não são uma opção disponível.
RESUMO
ABSTRACT Introduction: Topiramate is a drug used to treat various types of epilepsy and as prophylaxis in cases of migrainous headache. One of its mechanisms of action is the inhibition of carbonic anhydrase in the kidney that triggers the excretion of alkaline urine resulting in metabolic acidosis. Case presentation: 17-year-old female patient from Mexico City who regularly uses topiramate, quetiapine and sertraline for the management of depressive disorder. She developed normal anion gap metabolic acidosis secondary to topiramate intake. As a result, she required invasive ventilatory support due to reduced consciousness and respiratory distress. Adequate response to management with laxatives and bicarbonate was achieved, with full renal and neurological recovery. Discussion: Metabolic acidosis is the most common acid-base disorder observed in clinical practice. The difference between measurable cations and anions, known as anion gap, helps to classify the severity of acidosis. Bicarbonate losses or renal tubular disorders generate normal anion gap acidosis as opposed to acidosis resulting from an overproduction of endogenous acid or renal failure, which causes high anion gap. Topiramate is a little known cause of normal anion gap metabolic acidosis; by inhibiting carbonic anhydrase, it causes mixed renal tubular acidosis or type 3 acidosis, as a consequence of the inability to secrete hydrogen ions in the collecting tubule, and a limitation of bicarbonate reabsorption in the proximal tubule. Conclusion: Topiramate, either in therapeutic doses or in overdose, can lead to normal anion gap metabolic acidosis due to the inhibition of carbonic anhydrase in the kidneys. It is usually reversible after starting bicarbonate.
RESUMEN Introducción. El topiramato es un medicamento que se usa en el tratamiento de varios tipos de epilepsia y como profilaxis en casos de cefalea migrañosa. Entre sus mecanismos de acción, la inhibición de la anhidrasa carbónica en el riñón desencadena la excreción de orina alcalina ocasionando acidosis metabólica. Presentación del caso. Paciente femenino de 17 años procedente de la Ciudad de México con antecedente de consumo de topiramato, quetiapina y sertralina para manejo de síndrome depresivo, quien desarrolla acidosis metabólica de anión restante normal secundaria a ingesta de topiramato. La joven requiere soporte ventilatorio invasivo por deterioro del estado de conciencia y síndrome de dificultad respiratoria y presenta adecuada respuesta a manejo con catártico y bicarbonato sin compromiso renal y sin secuelas neurológicas. Discusión. La acidosis metabólica es la alteración ácido base más frecuente en la práctica clínica. La diferencia entre cationes y aniones medibles, conocida como anión restante o brecha aniónica, permite clasificar este tipo de acidosis. Las pérdidas de bicarbonato o trastornos de la función tubular renal generan acidosis de anión restante normal; por el contrario, la acidosis causada por sobreproducción de ácido endógeno o por insuficiencia renal genera anión restante elevado. El topiramato es una causa poco conocida de acidosis metabólica con anión restante normal; al inhibir la anhidrasa carbónica, se ocasiona una acidosis tubular renal mixta o tipo 3 debido a una in capacidad de secreción de hidrogeniones en el túbulo colector y una limitación en la reabsorción del bicarbonato en el túbulo proximal. Conclusión. El topiramato en dosis terapéutica o en sobredosis puede generar acidosis metabólica de anión restante normal debido a la inhibición de la anhidrasa carbónica a nivel renal. Se trata de un cuadro reversible en el cual el manejo con bicarbonato ha mostrado buenos resultados clínicos.