Study of the efficiency and workflow of femtosecond laser-assisted cataract surgery in a Spanish public hospital.

BACKGROUND: To assess the time-efficiency of a designated operating room (OR) workflow in the introduction of femtosecond laser-assisted cataract surgery (FLACS, LenSx, Alcon®). The study was carried out in a public hospital a with high-volume of procedures. METHODS: We performed this prospective, controlled, surgical intervention study in the ophthalmology department of a Spanish tertiary referral public hospital. A total of 167 eyes were enrolled, including 62 eyes undergoing conventional phacoemulsification surgery. In phase I, patients were assigned either to FLACS-I (n=63) or conventional phacoemulsification surgery (n=62). One surgeon operated the femtosecond laser, and another completed the procedure, while a third performed conventional phacoemulsification. In the second phase (FLACS-II), all the surgeries were FLACS (n=42). One surgeon performed the FLACS procedure, and two different surgeons completed the surgeries in separate ORs. Surgical and turnover times of all the patients were recorded. RESULTS: Preparation time was statistically significantly lower in FLACS-I and FLACS-II (P<0.001), whereas the duration of the cataract procedure per se was higher in FLACS-II compared to conventional phacoemulsification (P=0.03). Phacoemulsification energy was higher in FLACS-II compared to FLACS-I (P=0.01), whereas laser-related surgical time was lower (P=0.001). Surgical complications and total surgical time showed no statistically significant differences between any of the three groups. CONCLUSIONS: This study suggests a time-efficient and suitable workflow model for FLACS, considering the specific requirements and restrictions of a fully booked public hospital. Even so, we have shown that the FLACS procedure does not take longer than conventional phacoemulsification when following a detailed plan for OR workflow. In addition, our data reflect an improvement in FLACS surgical times with ongoing experience. TRIAL REGISTRATION: NCT03931629 (retrospectively registered).

Focal EEG abnormalities and focal ictal semiology in generalized epilepsy.

In clinical practice, the diagnosis of focal vs generalized epilepsy dictates the management of the patient. The distinction between generalized and focal epilepsy is at times imperfect and some epilepsies have features that fall in between these two extremes. An example is the occurrence of focal interictal and focal ictal abnormalities in generalized epilepsies. As a part of the special issue on "The epileptogenic zone in pediatric epilepsy surgery", this focused narrative review will discuss different focal abnormalities seen in generalized epilepsy. An overlap of focal and generalized epileptiform abnormalities may support a continuum between focal and generalized epilepsy. When evaluating patients in the "gray zone", other factors such as ictal semiology, neuroimaging, genetic testing and functional deficits may need to be considered to reach an accurate diagnosis. Being aware of possible occurrence of focal clinical and EEG features in generalized epilepsy will help clinicians select more preferred AED (s), avoiding potential iatrogenic side effects and inappropriate consideration for epilepsy surgery.

Functional neuroanatomy of the insular lobe.

The insula is the fifth lobe of the brain and it is the least known. Hidden under the temporal, frontal and parietal opercula, as well as under dense arterial and venous vessels, its accessibility is particularly restricted. Functional data on this region in humans, therefore, are scarce and the existing evidence makes conclusions on its functional and somatotopic organization difficult. 5 patients with intractable epilepsy underwent an invasive presurgical evaluation with implantation of diagnostic invasive-depth electrodes, including insular electrodes that were inserted using a mesiocaudodorsal to laterorostroventral approach. Altogether 113 contacts were found to be in the insula and were stimulated with alternating currents during preoperative monitoring. Different viscerosensitive and somatosensory phenomena were elicited by stimulation of these electrodes. A relatively high density of electrode contacts enabled us to delineate several functionally distinct areas within the insula. We found somatosensory symptoms to be restricted to the posterior insula and a subgroup of warmth or painful sensations in the dorsal posterior insula. Viscerosensory symptoms were elicited by more anterior electrode contacts with a subgroup of gustatory symptoms occurring after stimulation of electrode contacts in the central part of the insula. The anterior insula did not show reproducible responses to stimulation. In line with previous studies, we found evidence for somato- and viscerosensory cortex in the insula. In addition, our results suggest that there is a predominantly posterior and central distribution of these functions in the insular lobe.

[Nomogram for ocular hypertension progression risk based on the ocular hypertension treatment study]. / Nomograma de riesgo de progreso de hipertensión ocular basado en el ocular hypertension treatment study.

INTRODUCTION: A practical nomogram has been designed in order to present the results obtained from the Ocular Hypertension Study (Gordon et al. Arch Ophthalmol 2002; 120: 714-720), where the relation between intraocular pressure (IOP) and corneal thickness becomes apparent, involving the risk of evolution from ocular hypertension into glaucoma within a 6 year period. MATERIAL AND METHODS: We used a multiple logarithmic regression for the nine parameters shown in figure 1 of the above mentioned paper. RESULTS: A correlation coefficient of 0.91 (p<0.001) permits to establish the following equation: Probability of evolution (%) = 13539.5 x (1.1385IOP) x (0.9818(CORNEAL THICKNESS)). This implies that a variation of 10 microns on corneal thickness leads to an IOP's modification of 1.5 mmHg in the same sense. From these data, we designed the nomogram included in this paper. CONCLUSIONS: IOP and pachymetry together allow an estimation of the risk of evolution from ocular hypertension into glaucoma in a graphical practical way. From this indirect estimation, the influence of corneal thickness on IOP's measure seems to be much higher than previously estimated.

Nomograma de riesgo de progreso de hipertensión ocular basado en el Ocular Hypertension Treatmetn Study / Nomogram for ocular hypertension progression risk based on the Ocular Hypertension Treatment study

Introducción: Se ha construido un nomograma práctico para representar los resultados del Ocular Hipertensión Study (Gordon et al. Arch Ophthalmol 2002;120: 714-720) que relacionan la presión intraocular y el espesor corneal con el riesgo de evolucionar de hipertensión ocular a glaucoma en un plazo de 6 años.Material y Métodos: Se ha aplicado una regresión logarítmica múltiple a los 9 datos mostrados en la figura 1 del trabajo señalado anteriormente.Resultados: Un coeficiente de correlación de 0,91 (p<0,001) permite definir la siguiente ecuación:Probabilidad de evolución (%) = 13539,5 x (1,1385 PIO) x (0,9818 espesor corneal)Esto significa que una variación de 10 micras en el espesor corneal equivale a una variación de 1,5 mmHg en el mismo sentido de la presión intraocular. Con estos datos se ha construido un nomograma que se incluye en el trabajo.Conclusiones: La PIO y la paquimetría permiten estimar el riesgo de evolución de hipertensión ocular a glaucoma de una manera gráfica práctica. Estimada de esta manera indirecta, la influencia del espesor corneal sobre la medida de la presión intraocular parece muy superior a la que se había estimado hasta el momento

Introduction: A practical nomogram has been designed in order to present the results obtained from the Ocular Hypertension Study (Gordon et al. Arch Ophthalmol 2002; 120: 714-720), where the relation between intraocular pressure (IOP) and corneal thickness becomes apparent, involving the risk of evolution from ocular hypertension into glaucoma within a 6 year period.Material and Methods: We used a multiple logarithmic regression for the nine parameters shown in figure 1 of the above mentioned paper.Results: A correlation coefficient of 0.91 (p<0.001) permits to establish the following equation:Probability of evolution (%) = 13539.5 x (1.1385 IOP) x (0.9818 CORNEAL THICKNESS)This implies that a variation of 10 microns on corneal thickness leads to an IOP’s modification of 1.5 mmHg in the same sense. From these data, we designed the nomogram included in this paper.Conclusions: IOP and pachymetry together allow an estimation of the risk of evolution from ocular hypertension into glaucoma in a graphical practical way. From this indirect estimation, the influence of corneal thickness on IOP’s measure seems to be much higher than previously estimated

Anemia hemolítica autoinmune secundaria a infección por citomegalovirus / Autoinmune hemolytic anemia secondary to cytomegalovirus infection

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Glucose-6-phosphate dehydrogenase mutations and haplotypes in Mexican Mestizos.

In a screening for glucose-6-phosphate dehydrogenase (G-6-PD) deficiency in 1985 unrelated male subjects from the general population (Groups A and B) belonging to four states of the Pacific coast, 21 G-6-PD-deficient subjects were detected. Screening for mutations at the G-6-PD gene by PCR-restriction enzyme in these 21 G-6-PD-deficient subjects as well as in 14 G-6-PD-deficient patients with hemolytic anemia belonging to several states of Mexico showed two common G-6-PD variants: G-6-PD A-(202A/376G) (19 cases) and G-6-PD A-(376G/968C) (9 cases). In 7 individuals the mutations responsible for the enzyme deficiency remain to be determined. Furthermore, four silent polymorphic sites at the G-6-PD gene (PvuII, PstI, 1311, and NlaIII) were investigated in the 28 individuals with G-6-PD A- variants and in 137 G-6-PD normal subjects. As expected, only 10 different haplotypes were observed. To date, in our project aiming to determine the molecular basis of G-6-PD deficiency in Mexico, 60 unrelated G-6-PD-deficient Mexican males-25 in previous studies and 35 in the present work-have been studied. More than 75% of these individuals are from states of the Pacific coast (Sinaloa, Nayarit, Jalisco, Michoacán, Guerrero, Oaxaca, and Chiapas). The results show that although G-6-PD deficiency is heterogeneous at the DNA level in Mexico, only three polymorphic variants have been observed: G-6-PD A-(202A/376G) (36 cases), G-6-PD A-(376G/968C) (13 cases), and G-6-PD Seattle(844C) (2 cases). G-6-PD A- variants are relatively distributed homogeneously and both variants explain 82% of the overall prevalence of G-6-PD deficiency. The variant G-6-PD A-(202A/376G) represents 73% of the G-6-PD A- alleles. Our data also show that the variant G-6-PD A-(376G/968C)-which has been observed in Mexico in the context of two different haplotypes-is more common than previously supposed. The three polymorphic variants that we observed in Mexico are on the same haplotypes as found in subjects from Africa, the Canary Islands, and Spain.

Molecular genetics of glucose-6-phosphate dehydrogenase deficiency in Mexico.

Several studies carried out between 1965 and 1985 showed that G-6-PD deficiency in Mexico is heterogeneous at the biochemical level and that the G-6-PD A- phenotype is relatively common. We have now investigated the molecular basis of G-6-PD deficiency in Mexico. Up-to-date 60 chromosomes with G6PD mutations have been studied, 16 in previous studies and 44 in the present work. Molecular analysis of DNA from G-6-PD deficient Mexican mestizos and their relatives show that G-6-PD A- genotypes are relatively common but also that in Mexico G-6-PD deficiency is heterogeneous at the DNA level. Thus, five different genotypes have been observed: G-6-PD A-(202A/376G) (41 chromosomes), G-6-PD A-(376G/968C) (14 chromosomes), G-6-PD Seattle844C (3 chromosomes), G-6-PD "Mexico City"680A (1 chromosome) and G-6-PD Guadalajara1159T (1 chromosome). The G-6-PD A-(202A/376G), G-6-PD A-(376G/968C) and G-6-PD Seattle844C mutations in Mexico are on the same Pvu II/ Pst I/ 1311 / Nla III haplotypes as found in individuals from Africa, Spain and the Canary Islands. Consequently, these mutations were probably imported to Mexico through African slaves and/or the Spanish immigrants during and after the colonization.

[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. / Envenenamiento mortal causado por el aceite de epazote, Chenopodium graveolens.

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.

Successful treatment of transverse myelitis in a child with systemic lupus erythematosus.

We describe a 13-year-old female patient with systemic lupus erythematosus (SLE) who presented with acute transverse myelitis (ATM) in the course of SLE. IgG and IgM anticardiolipin antibodies (aCL) were positive at moderate titers. Magnetic resonance imaging (MRI) of the thoracic spine demonstrated decreased signal intensity and diffuse edema of the spinal cord from T2 to T6 on T1-weighted images. Dramatic clinical improvement of the neurologic impairment was noted a few days after high dose intravenous (IV) methylprednisolone (MP) and cyclophosphamide (Cy). Herein we further emphasize the benefit of IV MP and Cy in ATM and the relationship between ATM and antiphospholipid antibodies (aPLA) in SLE.

Tratamiento oral de la leishmaniasis americana en el Ecuador: primer reporte / Oral processing of the American leishmaniasis in Ecuador first report

Evalua la acción antileishmaniásica que podría tener la mefloquina que normalmente se usa como droga antimalárica con gran efectividad para la curación de todas sus formas. Desde 1994, 120 pacientes con leishmaniasis cutánea han sido tratados y curados con la administración oral de mefloquina, siguiendo un protocolo, con la dosis de 125 mg después del desayuno y merienda durante 10 días para los adultos, y una dosis total de 40-50 mg/kg. para los niños, en tomas de 62,5 mg cada 12 horas, con las comidas. En casos severos se repite el tratamiento después de un período de 7-10 días a partir de la última toma. El porcentaje de cicatrización después del tratamiento fue del 100xciento con un tiempo promedio de 27,1 días para las lesiones pequeñas (hasta 1 cm) y de 35,5 días para las lesiones medianas y grandes (de 1.2 a 2.5 cm y de 2.6 en adelante, respectivamente). El tiempo de seguimiento mínimo de 1 año ha sido alcanzado ya por 40 de los pacientes tratados y curados con mefloquina quienes constituyen en primer grupo que presentamos a manera de informe preliminar. Inicialmente se utilizó un grupo control de 18 pacientes quienes recibieron placebo, sin haber ninguno de ellos cicatrizado sus lesiones durante 6 meses de observación. Con esta referencia no se han utilizado nuevamente grupos de control, ya que usualmente los pacientes vienen de sitios lejanos realizando gastos superfluos sin resultados positivos...

Structural organization of the human sorbitol dehydrogenase gene (SORD).

The primary structure of human sorbitol dehydrogenase (SORD) was determined by cDNA and genomic cloning. The nucleotide sequence of the mRNA covers 2471 bp including an open reading frame that yields a protein of 356 amino acid residues. The gene structure of SORD spans approximately 30 kb divided into 9 exons and 8 introns. The gene was localized to chromosome 15q21.1 by in situ hybridization. Two transcription initiation sites were detected. Three Sp1 sites and a repetitive sequence (CAAA)5 were observed in the 5' noncoding region; no classical TATAA or CCAAT elements were found. The related alcohol dehydrogenases and zeta-crystallin have the same gene organization split by 8 introns, but no splice points coincide between SORD and these gene types. The deduced amino acid sequence of the SORD structure differs at a few positions from the directly determined protein sequence, suggesting allelic forms of the enzyme. High levels of SORD transcripts were observed in lens and kidney, as judged from Northern blot analysis.

Molecular heterogeneity of G-6-PD deficiency in Mexico.

DNA samples from seven G-6-PD deficient Mexican mestizo patients were analyzed. Three different G-6-PD genotypes were observed: G-6-PD A-202A/376G (three patients), G-6-PD A-376G/968C (three patients) and G-6-PD Seattle844C. The present results, along with previous reports, suggest not only G-6-PD A-genotypes are relatively common but also G-6-PD deficiency seems to be heterogeneous at DNA level in Mexico.

Membrane-bound sorbitol dehydrogenase in human red blood cells. Studies in normal subjects and in enzyme-deficient subjects with congenital cataracts.

Membrane-bound and soluble forms of erythrocyte sorbitol dehydrogenase (SORD) activity are compared in normal individuals. Both isoenzymes showed similar properties. In a family with red cell SORD deficiency and congenital cataracts, Km values for sorbitol and NAD+ as well as the effect of the enzymatic deficiency on sorbitol accumulation in red cells incubated in high-glucose or high-fructose media were determined. In SORD-deficient patients, the enzymatic deficiency was observed in both crude haemolysate and SORD-M preparations with sorbitol, galactitol, xylitol or ribitol as substrates. The mutation responsible for SORD deficiency did not modify the Km for sorbitol and NAD+. Finally, SORD deficiency produced a significant increase of sorbitol accumulation in red cells incubated in high-concentration glucose media and a significant decrease when the cells were incubated in high-concentration fructose media.

New glucose-6-phosphate dehydrogenase mutations from various ethnic groups.

Seven new mutations that produce glucose 6 phosphate dehydrogenase (G6PD) deficiency are described. Three are in variants that were biochemically characterized and described previously, while four were found in samples that had not been characterized biochemically. Several of the mutations affect the amino acids that are mutated in other G6PD variants. As had been noted previously, variants that are associated with nonspherocytic anemia are located either near the glucose 6 phosphate or the NADP binding sites. Variants more distant from these sites are not associated with chronic hemolysis.

Effects of G-6-PD deficiency, experimentally induced or genetically transmitted, on the sorbitol pathway activity. In vitro and in vivo studies.

Aldose reductase catalyzes the NADPH-linked reduction of hexoses to their respective sugar-alcohols, which are involved in the pathogenesis of "sugar-cataracts". In the lenses, the reaction catalyzed by G-6-PD is the source of NADPH supply blocking sugar-alcohol formation and consequently prevents or delays the onset of "sugar-cataracts". We have investigated the effect of G-6-PD deficiency, either experimentally induced or genetically transmitted, on the sorbitol accumulation in whole cells incubated in high glucose media and on the "sugar-cataracts" formation in a galactosemic rat model. We also screened 31 Negro male adults with diabetes mellitus for red cell G-6-PD deficiency. G-6-PD deficiency produced a significant inhibition on sorbitol accumulation in rat lenses and human red cells incubated in 50 mM glucose. In the galactosemic rat model G-6-PD deficiency experimentally induced with acetaminophen delayed the development of cataracts. Finally, two diabetic individuals were G-6-PD deficient and did not show cataracts whereas cataracts were identified in six other diabetic patients.