Neumoencéfalo, otitis media y meningitis a neumococo / Pneumocephalus, middle otitis and meningococcic meningitis

La meningitis bacteriana es una enfermedad con alta morbi-mortalidad, el germen prevalente es el Strep pneumoniae y constituye la complicación intracraneal más frecuente de la otitis media aguda en el adulto. La TAC de cerebro es de indicación habitual ante su sospecha, previa a la realización de la punción lumbar, y en el 13 por ciento de los casos, los hallazgos son compatibles con una disrupción de la barrera dural, de la que el neumoencéfaloi (NE) es una de las consecuencias. Se presenta un paciente con meningitis bacteriana aguda por neumococo, otitis media y NE, sin traumatismo, malformación, tumor o cirugía previa

Neumoencéfalo, otitis media y meningitis a neumococo / Pneumocephalus, middle otitis and meningococcic meningitis

La meningitis bacteriana es una enfermedad con alta morbi-mortalidad, el germen prevalente es el Strep pneumoniae y constituye la complicación intracraneal más frecuente de la otitis media aguda en el adulto. La TAC de cerebro es de indicación habitual ante su sospecha, previa a la realización de la punción lumbar, y en el 13 por ciento de los casos, los hallazgos son compatibles con una disrupción de la barrera dural, de la que el neumoencéfaloi (NE) es una de las consecuencias. Se presenta un paciente con meningitis bacteriana aguda por neumococo, otitis media y NE, sin traumatismo, malformación, tumor o cirugía previa(AU)

[Platypnea-orthodeoxia syndrome, atrial septal aneurysm and right hemidiaphragmatic elevation with a right-to-left shunt through a patent foramen ovale]. / Sindrome platipnea-ortodeoxia por foramen oval permeable, aneurisma del septum interauricular y paralisis del hemidiafragma derecho.

Platypnea-orthodeoxia is an uncommon syndrome of dyspnea and hypoxemia induced by upright position, which is subsequently relieved by recumbency. The case reported involved a 75-year-old man with a seven days history of dyspnea in the upright position. The chest radiograph and CT scan demonstrated an elevated right hemidiaphragm. A surface echocardiogram with saline solution showed a patent foramen ovale (PFO) and atrial septal aneurysm. A pulmonary arteriogram was performed showing no evidence of pulmonary embolism and normal pulmonary arterial pressures. Later, he also developed dyspnea in the supine position and a transesophageal echocardiogram with contrast demonstrated a large right to left shunt through a PFO. The closure by a catheter-deployed double-umbrella device caused an immediate improvement in the patient's oxygenation.

[Platypnea-orthodeoxia syndrome]. / Sindrome platipnea-ortodeoxia.

Platypnea-orthodeoxia is an uncommon syndrome of dyspnea and hypoxemia induced by upright posture, which is subsequently relieved by recumbency. Traditionally, this condition has been reported in association with pulmonary, hepatic and cardiac diseases, but the mechanism is different in each situation. In presence of an atrial septal defect, a right to left cardiac shunt resulting as a consequence of redirection of the inferior vena cava flow towards the atrial septum and results in postural hypoxemia. In pulmonary shunts, as in hepatopulmonary syndrome and a-v pulmonary fistulas, the mechanism of hypoxemia is related to the preferential circulation to basal areas of both lungs in the upright position. On the other hand, lung diseases affecting basal areas and increasing the alveolar pressure are related to the development of parenchimal pulmonary shunts with hypoxemia during postural changes, since the dead space, the functional shunt and the hypoxic vascular pulmonary constriction are affected. The autonomic neuropathy may attenuate normal sympathetic vasoconstrictor responses during postural changes, resulting in ventilation-perfusion mismatching and hypoxemia. Clinical and therapeutic aspects of this sindrome are provided.

Sindrome platipnea-ortodeoxia por foramen oval permeable, aneurisma del septum interauricular y paralisis del hemidiafragma derecho. / [Platypnea-orthodeoxia syndrome, atrial septal aneurysm and right hemidiaphragmatic elevation with a right-to-left shunt through a patent foramen ovale]

Platypnea-orthodeoxia is an uncommon syndrome of dyspnea and hypoxemia induced by upright position, which is subsequently relieved by recumbency. The case reported involved a 75-year-old man with a seven days history of dyspnea in the upright position. The chest radiograph and CT scan demonstrated an elevated right hemidiaphragm. A surface echocardiogram with saline solution showed a patent foramen ovale (PFO) and atrial septal aneurysm. A pulmonary arteriogram was performed showing no evidence of pulmonary embolism and normal pulmonary arterial pressures. Later, he also developed dyspnea in the supine position and a transesophageal echocardiogram with contrast demonstrated a large right to left shunt through a PFO. The closure by a catheter-deployed double-umbrella device caused an immediate improvement in the patients oxygenation.

Sindrome platipnea-ortodeoxia. / [Platypnea-orthodeoxia syndrome]

Platypnea-orthodeoxia is an uncommon syndrome of dyspnea and hypoxemia induced by upright posture, which is subsequently relieved by recumbency. Traditionally, this condition has been reported in association with pulmonary, hepatic and cardiac diseases, but the mechanism is different in each situation. In presence of an atrial septal defect, a right to left cardiac shunt resulting as a consequence of redirection of the inferior vena cava flow towards the atrial septum and results in postural hypoxemia. In pulmonary shunts, as in hepatopulmonary syndrome and a-v pulmonary fistulas, the mechanism of hypoxemia is related to the preferential circulation to basal areas of both lungs in the upright position. On the other hand, lung diseases affecting basal areas and increasing the alveolar pressure are related to the development of parenchimal pulmonary shunts with hypoxemia during postural changes, since the dead space, the functional shunt and the hypoxic vascular pulmonary constriction are affected. The autonomic neuropathy may attenuate normal sympathetic vasoconstrictor responses during postural changes, resulting in ventilation-perfusion mismatching and hypoxemia. Clinical and therapeutic aspects of this sindrome are provided.

[Acute cardiovascular beriberi (shoshin-beriberi)]. / Beriberi cardiovascular agudo (shoshin-beriberi).

Beriberi (BB), thiamine deficiency, has been described in the Asian literature in the 17th century and is characterized by peripheral neuropathy and muscle weakness, also called "dry" beriberi (BB) to differentiate it from "wet" BB, with essentially cardiovascular manifestations. Wet can be either "classic" wet BB in which signs and symptoms of right-sided heart failure with normal or high cardiac output are the presenting features or the "shoshin" BB variant with severe biventricular failure and metabolic acidosis, which must be treated early to prevent the rapid development of low cardiac output failure and sudden death. In this case, we report a 58 year old alcoholic woman who developed dyspnea, oliguria, edema, cardiac failure with high output, metabolic acidosis, renal tubular dysfunction and serum lactate level of 5.6 mEq/L. Neurological examination revealed peripheral neuropathy in the lower legs and cognitive alteration. She was treated with a loading dose of 100 mg of intravenous thyamine and responded with a marked increase in urine output, correction of acidosis, reduction in pulmonary-capillary wedge pressure and a change of the hemodynamic pattern. We conclude that shoshin-BB is uncommonly encountered but not widely recognized. In lactic acidosis and/or hyperdynamic circulation without any other apparent etiology in patients with possible vitamin B1 deficiency, the diagnosis of BB must be considered and thiamine should be administered.

Beriberi cardiovascular agudo (shoshin-beriberi) / Acute cardiovascular beriberi (shoshin-beriberi)

Beriberi (BB), thiamine deficiency, has been described in the Asian literature in the 17th century and is characterized by peripheral neuropathy and muscle weakness, also called "dry" beriberi (BB) to differentiate it from "wet" BB, with essentially cardiovascular manifestations. Wet can be either "classic" wet BB in which signs and symptoms of right-sided heart failure with normal or high cardiac output are the presenting features or the "shoshin" BB variant with severe biventricular failure and metabolic acidosis, which must be treated early to prevent the rapid development of low cardiac output failure and sudden death. In this case, we report a 58 year old alcoholic woman who developed dyspnea, oliguria, edema, cardiac failure with high output, metabolic acidosis, renal tubular dysfunction and serum lactate level of 5.6 mEq/L. Neurological examination revealed peripheral neuropathy in the lower legs and cognitive alteration. She was treated with a loading dose of 100 mg of intravenous thyamine and responded with a marked increase in urine output, correction of acidosis, reduction in pulmonary-capillary wedge pressure and a change of the hemodynamic pattern. We conclude that shoshin-BB is uncommonly encountered but not widely recognized. In lactic acidosis and/or hyperdynamic circulation without any other apparent etiology in patients with possible vitamin B1 deficiency, the diagnosis of BB must be considered and thiamine should be administered

Beriberi cardiovascular agudo (shoshin-beriberi) / Acute cardiovascular beriberi (shoshin-beriberi)

Beriberi (BB), thiamine deficiency, has been described in the Asian literature in the 17th century and is characterized by peripheral neuropathy and muscle weakness, also called "dry" beriberi (BB) to differentiate it from "wet" BB, with essentially cardiovascular manifestations. Wet can be either "classic" wet BB in which signs and symptoms of right-sided heart failure with normal or high cardiac output are the presenting features or the "shoshin" BB variant with severe biventricular failure and metabolic acidosis, which must be treated early to prevent the rapid development of low cardiac output failure and sudden death. In this case, we report a 58 year old alcoholic woman who developed dyspnea, oliguria, edema, cardiac failure with high output, metabolic acidosis, renal tubular dysfunction and serum lactate level of 5.6 mEq/L. Neurological examination revealed peripheral neuropathy in the lower legs and cognitive alteration. She was treated with a loading dose of 100 mg of intravenous thyamine and responded with a marked increase in urine output, correction of acidosis, reduction in pulmonary-capillary wedge pressure and a change of the hemodynamic pattern. We conclude that shoshin-BB is uncommonly encountered but not widely recognized. In lactic acidosis and/or hyperdynamic circulation without any other apparent etiology in patients with possible vitamin B1 deficiency, the diagnosis of BB must be considered and thiamine should be administered (AU)

Beriberi cardiovascular agudo (shoshin-beriberi). / [Acute cardiovascular beriberi (shoshin-beriberi)]

Beriberi (BB), thiamine deficiency, has been described in the Asian literature in the 17th century and is characterized by peripheral neuropathy and muscle weakness, also called [quot ]dry[quot ] beriberi (BB) to differentiate it from [quot ]wet[quot ] BB, with essentially cardiovascular manifestations. Wet can be either [quot ]classic[quot ] wet BB in which signs and symptoms of right-sided heart failure with normal or high cardiac output are the presenting features or the [quot ]shoshin[quot ] BB variant with severe biventricular failure and metabolic acidosis, which must be treated early to prevent the rapid development of low cardiac output failure and sudden death. In this case, we report a 58 year old alcoholic woman who developed dyspnea, oliguria, edema, cardiac failure with high output, metabolic acidosis, renal tubular dysfunction and serum lactate level of 5.6 mEq/L. Neurological examination revealed peripheral neuropathy in the lower legs and cognitive alteration. She was treated with a loading dose of 100 mg of intravenous thyamine and responded with a marked increase in urine output, correction of acidosis, reduction in pulmonary-capillary wedge pressure and a change of the hemodynamic pattern. We conclude that shoshin-BB is uncommonly encountered but not widely recognized. In lactic acidosis and/or hyperdynamic circulation without any other apparent etiology in patients with possible vitamin B1 deficiency, the diagnosis of BB must be considered and thiamine should be administered.

Perdida cerebral de sal: medio siglo de un síndrome no bien definido / Cerebral salt wasting: half a century of a largely undefined syndrome

Peters made the original description of the cerebral salt wasting syndrome (CSWS) in 1950 in three patients with hyponatremia that he assumed to be secondary to natriuresis of cerebral mechanism. Few years later, Schwartz describe the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in two patients with bronchial carcinoma, with characteristics similar to CSWS. Wijdicks gave clinical entity to CSWS when referring that it is the prevalent cause of hyponatremia in patients with subarachnoid hemorrhage, and stressed the risk of secondary cerebral infarction if restrictive plans of water and salt were used as a consequence of a miss diagnosis. However, CSWS has been recently questioned because of its atypical characteristics, not shared by other saline wasting syndromes. The volume status of patients with hyponatremia and natriuresis determines whether the cause of this disorder is SIADH or CSWS. Nevertheless the evidence are contradictory, the vasopressin level can be recognized only in relation to the tonicity of body fluids, and the natriuresis is a common final pathway for both syndromes. In this literature review, some issues of CSWS that are associated or opposed with SIADH and other saline wasting syndrome are discussed. We conclude that the reports that sustain CSWS are insufficient in their methodology and interpretation of the results. The absence of strict metabolic studies has been negatively replaced by the original information casually quoted, and the strength of tradition. Thereafter, the paradigm generates unfounded ethical dilemmas which render difficult any further investigations with appropriate controls.

Perdida cerebral de sal: medio siglo de un síndrome no bien definido / Cerebral salt wasting: half a century of a largely undefined syndrome

Peters made the original description of the cerebral salt wasting syndrome (CSWS) in 1950 in three patients with hyponatremia that he assumed to be secondary to natriuresis of cerebral mechanism. Few years later, Schwartz describe the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in two patients with bronchial carcinoma, with characteristics similar to CSWS. Wijdicks gave clinical entity to CSWS when referring that it is the prevalent cause of hyponatremia in patients with subarachnoid hemorrhage, and stressed the risk of secondary cerebral infarction if restrictive plans of water and salt were used as a consequence of a miss diagnosis. However, CSWS has been recently questioned because of its atypical characteristics, not shared by other saline wasting syndromes. The volume status of patients with hyponatremia and natriuresis determines whether the cause of this disorder is SIADH or CSWS. Nevertheless the evidence are contradictory, the vasopressin level can be recognized only in relation to the tonicity of body fluids, and the natriuresis is a common final pathway for both syndromes. In this literature review, some issues of CSWS that are associated or opposed with SIADH and other saline wasting syndrome are discussed. We conclude that the reports that sustain CSWS are insufficient in their methodology and interpretation of the results. The absence of strict metabolic studies has been negatively replaced by the original information casually quoted, and the strength of tradition. Thereafter, the paradigm generates unfounded ethical dilemmas which render difficult any further investigations with appropriate controls. (Au)

El factor edad en terapia intensiva / The factor age in intensive care

Se estudió la incidencia del factor edad en la sobrevida temprana y alejada en un área de Terapia Intensiva en función al costo-beneficio y/o los conceptos ético-morales. Se tomó una muestra retrospectiva de 521 pacientes con edades superiores, a los 50 años, estableciéndose cinco grupos etarios de acuerdo a las décadas evaluadas. En ellos se consideró el sexo, edad, días de estada, mortalidad en Terapia Intensiva y la sobrevida hasta las 36 semanas de su ingreso a la Unidad. Los resultados fueron tratados estadísticamente mediante la aplicación del X2. Ellos demostraron que el sexo masculino padece enfermedades críticas a edad más temprana que el femenino (p<0.001); que la edad en sí misma, no es un factor que origine un mayor promedio de días de estada; que la mortalidad en Terapia Intensiva fue para el grupo A (51-60 años) del 22.8 por ciento, aumentando progresivamente para alcanzar en el grupo E (>90 años) el 62.5 por ciento (p<0.001); que la misma se incrementó a las 36 semanas de su ingreso a un 36.9 por ciento y 84.4 por ciento respectivamente (p<0.001). Se discuten los resultados en función del costo-beneficio y conceptos ético-morales, concluyéndose que el tema requiere la confección de una norma que considere la asistencia de los pacientes con edad superior a los 80 años en áreas de complejidad adecuada, en donde se contemple más el aspecto humano, reservando su internación en Terapia Intensiva solamente en circunstancias justificadas

El factor edad en terapia intensiva / The factor age in intensive care

Se estudió la incidencia del factor edad en la sobrevida temprana y alejada en un área de Terapia Intensiva en función al costo-beneficio y/o los conceptos ético-morales. Se tomó una muestra retrospectiva de 521 pacientes con edades superiores, a los 50 años, estableciéndose cinco grupos etarios de acuerdo a las décadas evaluadas. En ellos se consideró el sexo, edad, días de estada, mortalidad en Terapia Intensiva y la sobrevida hasta las 36 semanas de su ingreso a la Unidad. Los resultados fueron tratados estadísticamente mediante la aplicación del X2. Ellos demostraron que el sexo masculino padece enfermedades críticas a edad más temprana que el femenino (p<0.001); que la edad en sí misma, no es un factor que origine un mayor promedio de días de estada; que la mortalidad en Terapia Intensiva fue para el grupo A (51-60 años) del 22.8 por ciento, aumentando progresivamente para alcanzar en el grupo E (>90 años) el 62.5 por ciento (p<0.001); que la misma se incrementó a las 36 semanas de su ingreso a un 36.9 por ciento y 84.4 por ciento respectivamente (p<0.001). Se discuten los resultados en función del costo-beneficio y conceptos ético-morales, concluyéndose que el tema requiere la confección de una norma que considere la asistencia de los pacientes con edad superior a los 80 años en áreas de complejidad adecuada, en donde se contemple más el aspecto humano, reservando su internación en Terapia Intensiva solamente en circunstancias justificadas (AU)