[Anesthetic management for thoracoscopic repair of type I esophageal atresia with continuous-flow single-lung ventilation]. / Manejo anestésico en la corrección toracoscópica de atresia de esófago tipo I con ventilación unipulmonar con modalidad de flujo continuo.

We describe a continuous flow mode of ventilation for repair of type I esophageal atresia in an infant. This type of atresia is defined by distal stenosis of the esophagus with a proximal blind pouch and no connection to the tracheobronchial tree. In traditional repair procedures the surgical approach is by thoracotomy, but newer videoassisted thoracoscopic techniques have introduced novel challenges to ventilatory mechanics in these low-weight infants. The literature contains little discussion of the anesthetic management or respiratory mechanics of these patients. Trying to maintain adequate tidal volume and oxygenation while thoracoscopic maneuvers take place increases the risk of barotrauma. Single-lung ventilation with a continuous flow respirator was effective in the case we report.

Manejo anestésico en la corrección toracoscópica de atresia de esófago tipo I con ventilación unipulmonar con modalidad de flujo continuo / Anesthetic management for thoracoscopic repair of type I esophageal atresia with continuous flow ventilation of a single lung

Describimos el modo de ventilación con flujo continuo para la reparación de un caso de atresia de esófago tipo I en un lactante. Este tipo de atresia se caracteriza por estenosis esofágica distal, con bolsón proximal sin fístula en el árbol bronquial. Las técnicas clásicas quirúrgicas realizan la reparación por toracotomía, pero la nueva introducción de técnicas videotoracoscópicas para este tipo de cirugía establece un nuevo reto en la mecánica ventilatoria de estos lactantes de bajo peso. La literatura es escasa en el manejo anestésico y de la mecánica ventilatoria de estos pacientes. Intentar mantener un adecuado volumen de ventilación, junto con una adecuada oxigenación añadido a la toracoscopia aumenta el riesgo de barotrauma. Con ventilación unipulmonar y con modalidad de flujo continuo se consiguió ventilar a este paciente eficazmente

We describe a continuous flow mode of ventilation for repair of type I esophageal atresia in an infant. This type of atresia is defined by distal stenosis of the esophagus with a proximal blind pouch and no connection to the tracheobronchial tree. In traditional repair procedures the surgical approach is by thoracotomy, but newer videoassisted thoracoscopic techniques have introduced novel challenges to ventilatory mechanics in these low-weight infants. The literature contains little discussion of the anesthetic management or respiratory mechanics of these patients. Trying to maintain adequate tidal volume and oxygenation while thoracoscopic maneuvers take place increases the risk of barotrauma. Single-lung ventilation with a continuous flow respirator was effective in the case we report

Central pontine myelinolysis induced by hypophosphatemia following Wernicke's encephalopathy.

A 62-year-old woman, after a resection and ileostomy for multiple perforations of the terminal ileum and prolonged postoperative parenteral nutrition, developed thiamine deficiency with clinical and magnetic resonance imaging features of Wernicke's disease. Later on the patient developed central pontine myelinolysis. For this condition, a pathogenetic role of a transient hypophosphatemia was suggested by both laboratory data and course of the disease.

Anaesthetic management in a case of a type IV laryngotracheo-oesophageal cleft.

We report the case of a newborn baby with a type IV laryngotracheo-oesophageal cleft and the anaesthetic management during the rigid bronchoscopy that was performed at 5 days of age. After anaesthetic induction with sevoflurane and atropine, the child was maintained with sevoflurane 2-2.5% and remifentanil at an infusion rate of 0.5 microg.kg(-1).min(-1). Ventilation was managed through the lateral port of the bronchoscope. The patient breathed sevoflurane and oxygen/N2O spontaneously via a Jackson-Rees circuit. To prevent the stomach from filling up with anaesthetic gases, a Foley catheter was placed orally into the stomach. The Foley balloon was inflated and retracted until it sealed the gastro-oesophageal junction. Tracheal intubation was performed after bronchoscopy to allow suture of the stomach into two chambers. Oxygenation was adequate with no air leakage, with spontaneous ventilation. The Foley catheter was removed afterwards and the patient awakened. We review the literature on different ways of managing the airway in these cases and protecting it from gastric aspiration during ventilation.

Hipertensión pulmonar en cirugía cardíaca pediátrica / Pulmonary hypertension in pediatric heart surgery

Las cardiopatías congénitas pueden disminuir o aumentar el flujo sanguíneo pulmonar (FSP), la resistencia vascular pulmonar (RVP) y la presión de la arteria pulmonar (PAP). La PAP es el producto de la RVP por el volumen por minuto pulmonar (Qp); por ello, la hipertensión pulmonar (HTP) puede deberse al aumento aislado de la RVP, del Qp o de ambos factores. Siendo el lecho vascular pulmonar un sistema de baja presión con alto flujo, todo aumento de la resistencia generará HTP. El valor normal de la RVP es de 2 unidades Woods (mmHg - l-1 - min-1). El aumento de la PAP se debe a lesiones hipóxicas del endotelio, que provocan una liberación de enzimas proteolíticas que alteran el equilibrio de los metabolitos del ácido araquidónico, reguladores del tono vasomotor pulmonar. La hipoxia y la acidosis provocan una intensa vasoconstricción pulmonar (reflejo vasoconstrictor hipóxico).El aumento de la RVP se debe a una combinación de procesos de vasoconstricción y remodelación con hipertrofia de la arteria pulmonar. Las lesiones anatomopatológicas están relacionadas con la hipertrofia del endotelio, la transformación de fibroblastos a miocitos y la disminución de la relación alveoloarteriolar con la formación de neovasos.La HTP puede ser primaria o secundaria a otra enfermedad. La HTP primaria es una enfermedad genética y poco frecuente; las secundarias más frecuentes en pediatría son debidas a persistencia de la anatomía neonatal (HTP del neonato), a las cardiopatías con shunt de izquierda a derecha (CIV, DAP, etc.), a las enfermedades del parénquima pulmonar (virosis intersticial, mucovisidosis) y a postoperatorios de cirugía cardíaca. Todas las cardiopatías congénitas son capaces de producir HTP si no son tratadas de forma temprana. La sintomatología clínica de la HTP es sumamente inespecífica: disnea, fatiga, síncopes, intolerancia al ejercicio, precordalgia, cianosis y edemas, y los mejores métodos para el diagnóstico y el pronóstico son la ecocardiografía y el cateterismo cardíaco con fármacos vasodilatadores.Al realizar una anestesia en estos pacientes se debe utilizar técnicas y fármacos que no alteren la RVP. Los pacientes con HTP son sensibles a los cambios en la ventilación pulmonar, a las alteraciones del gasto cardíaco y a los agentes anestésicos. El tratamiento de la hipertensión pulmonar en el intra y el postoperatorio en pediatría se basa en el uso de una concentración de oxígeno inspirada elevada (100 por ciento), una buena sedación y el uso de vasodilatadores (prostaglandinas I2, óxido nítrico, nitroprusiato de sodio y milrinona) solos o asociados (AU)

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[Pulmonary hypertension in pediatric heart surgery]. / Hipertensión pulmonar en cirugía cardíaca pediátrica.

Congenital heart disease can increase or decrease pulmonary blood flow, pulmonary vascular resistance (PVR) or pulmonary artery pressure (PAP). PAP is the product of PVR and pulmonary minute volume (Qp), such that pulmonary hypertension (PHT) may develop as a result of an increase in either PVR or Qp or both. Given that the pulmonary vascular bed is a low pressure system with high flow, any increase in resistance would generate PHT. The normal value of PVR is 2 Woods units (mm Hg/l/min). Increased PAP is due to hypoxic lesions of the endothelium, which release proteolytic enzymes that alter the balance of metabolites of arachidonic acid, regulators of pulmonary vasomotor tone. Hypoxia and acidosis cause intense pulmonary vasoconstriction (hypoxic vasoconstrictor reflex). An increase of PVR is due to a combination of vasoconstrictive processes and remodeling, with hypertrophy of the pulmonary artery. Structural lesions are related to hypertrophy of the endothelium, the transformation of fibroblasts to myocytes and the decrease of the alveolar/arteriolar ratio with the formation of new vessels.PHT may be primary or secondary to another disease. Primary PHT is a rare genetic disease. The most common secondary forms of PHT in pediatrics are due to persistence of neonatal anatomy (neonatal PHT), to heart diseases with left-right shunt (CIV, DAP, etc.), to diseases of the pulmonary parenchyma (interstitial viral infection, mucoviscidosis), and complications of heart surgery. All congenital heart diseases can lead to PHT if not treated promptly. Clinical signs of PHT are highly non-specific: dyspnea, fatigue, syncopes, exercise intolerance, precordialgia, cyanosis and edema. The best approaches to diagnosis and prognosis are echocardiography and cardiac catheterization with vasodilators. Anesthetics that do not alter PVR should be used in such patients, who are sensitive to changes in pulmonary ventilation, to changes in cardiac output and to anesthetics. The treatment of PHT during intra and postoperative pediatric surgery is based on the use of high inspirated oxygen concentration (100%), an adequate sedation and the use of vasodilators (prostaglandin I2, nitric oxide, sodium nitroprusiate and milrinone).

Recombinant human granulocyte-macrophage colony-stimulating factor ameliorates zidovudine-induced neutropenia in patients with acquired immunodeficiency syndrome (AIDS)/AIDS-related complex.

To evaluate the effect of recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF) on patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) who were intolerant to zidovudine because of neutropenia, we performed a randomized, open-label study in which patients were assigned to one of two groups. Zidovudine was discontinued in group A patients before instituting GM-CSF treatment and was restarted in a graduated fashion over 4 weeks. Group B patients continued on full-dose (1,200 mg/d) zidovudine therapy while beginning GM-CSF therapy. A total of 17 patients were entered, eight in group A and nine in group B. Five of eight patients in group A and seven of nine in group B had a history of Pneumocystis carinii pneumonia (PCP). All were homosexual males, except one female in group A who was the sex partner of a bisexual male with AIDS. All patients had neutropenia (absolute neutrophil count [ANC] less than 1,000/microL) while taking full-dose zidovudine. The mean CD4 (+/- SD) lymphocyte level was 37 (+/- 29)/microL and 39 (+/- 44)/microL in groups A and B, respectively. After randomization, patients were begun on subcutaneous GM-CSF at a dose of 1.0 microgram/kg/d. Patients in group A received 2 weeks of daily GM-CSF, at which time zidovudine was restarted if the ANC was greater than 1,000/microL; if the ANC was less than 1,000/microL, the dose of GM-CSF was increased to 3.0 micrograms/kg, and at 2-week intervals either zidovudine was restarted or the dose of GM-CSF was increased to 5 micrograms/kg and then 10 micrograms/kg, to maintain the ANC greater than 1,000/microL. Group B patients received full-dose zidovudine concurrently with GM-CSF administration. The dose of GM-CSF was increased every 2 weeks if necessary to keep the ANC greater than 1,000/microL while maintaining full-dose zidovudine therapy. Patients in each group showed an increase in total white blood cell (WBC) count. Neutrophils and eosinophils were responsible for the majority of this increase. Patients in group A had a more rapid increase in WBC than those in group B; however, by week 8, the WBC in each group was essentially equal. Viral replication as measured by human immunodeficiency virus (HIV) p24 antigen (Ag) was decreased in four patients in each group, increased in one patient in each group, and remained unchanged in the remainder. The ability to culture virus from peripheral blood mononuclear cells was not changed by the regimen. The major toxicities of the regimen were fever and malaise.(ABSTRACT TRUNCATED AT 400 WORDS)

[Clinical considerations and EEG-CT correlations in lacunar infarcts]. / Considerazioni cliniche e correlazioni EEG-TC negli infarti lacunari.

56 cases of lacunar stroke were reviewed retrospectively. The patients showed a clinic picture which could be classified within nine of the lacunar syndromes recognized by Fisher. The localization of the lacunes was considered with respect to the clinical symptoms and the characteristics of the EEG and the TC and their different correlations were examined. The EEGrafic patterns of the lacunar strokes with normal TC were compared with those showing an altered one. Our study suggests that the absence of EEGrafic alterations may be a useful characteristic for the diagnosis of lacunar stroke, even when TC is normal. No significant correlations were found between the alterations of the EEG and the dimensions and/or localizations of the lacunes, as well as between the type of EEG (localized-wide-spread) and the size (large-small) of the lacunar infarcts.