La muerte clínica: un diagnóstico y un testimonio / Clinical death: A diagnosis and a testimony

La muerte clínica de una persona es la muerte delencéfalo. Hay un consenso bastante generalizado ennuestra medicina occidental sobre los criterios necesariosy el modo de proceder para un correcto diagnósticode “muerte encefálica”. En un caso concreto, cuandoexisten antecedentes razonables de daño cerebral catastróficoy determinados signos clínicos en la exploraciónneurológica, un médico con suficiente experiencia puedellegar a emitir un diagnóstico de muerte clínica.Aceptando que el diagnóstico de muerte es unejercicio de puro juicio práctico, y que como tal nuncapuede dar certidumbre absoluta, debemos asumir quea pesar de la incertidumbre debemos tomar decisionesrazonables y prudentes.Sin embargo, existen opiniones discrepantes queconsideran sería necesario un más alto grado de certezaantes de tomar decisiones.Para tomar decisiones responsables se requiereintentar comprender el concepto de la muerte cerebralcomo un auténtico constructo cultural en el que sonnecesarios conocimientos a cerca de “qué” es lo que sedefine científicamente como muerte; el “cómo” sepuede diagnosticar en la práctica; el “cuándo” se diceque un hombre está clínicamente muerto, y de “cual”es el grado de evidencia que conlleva el diagnóstico

The clinical death of a person is the death of thebrain. There is a fairly general consensus in westernmedicine on the necessary criteria and the mode ofproceeding for a correct diagnosis of “brain death”. Ina specific case, with a reasonable previous record ofcatastrophic brain damage and certain neurologicalexploratory signs, an expert practitioner is able todiagnose clinical death.Accepting that the diagnosis of death is anexercise of diagnostic judgement, in practicalapplication, which cannot as such provide absolutecertainty; we have to accept that, in spite of thisuncertainty, we have to take sensible and prudentdecisions.However, there are dissenting opinions thatbelieve in the need for a higher degree of certaintybefore taking decisionsIt is necessary to try to understand the concept of“brain death” in order to be able to take responsibledecisions. This concept is a real “culturalconstruction”, in which it is necessary to haveknowledge about the scientific definition of death, howdeath can be diagnosed in practice, when it is possibleto say that someone is clinically dead, and what is thedegree of evidence carried by the diagnosis

Fístula pancreaticobronquial como primera manifestación de seudoquistes pancreáticos / Pancreaticobronchial fistula as the first manifestation of pancreatic pseudocysts

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Exagerada respuesta cardiovascular durante la escisión de un hipernefroma / Exaggerated cardiovascular response during excision of a hypernephroma

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¿Qué implicaciones éticas tiene el diagnóstico de muerte encefálica? Retirada de las medidas de soporte y donación de órganos / What ethic implications does brain death have? Withdrawal of support measures and organ donation

Fundamento. Tratar de responder desde una racionalidad ética a la cuestión ¿qué implicaciones éticas tiene el diagnóstico de muerte encefálica para la retirada de las medidas de soporte y donación de órganos? Método. Se utiliza el método principalista para la toma de decisiones clínicas, según el procedimiento descrito por el Prof. D. Gracia que diferencia dos niveles de jerarquización entre los cuatro principios de la bioética. Resultados. Entre las decisiones clínicas que debe tomar el médico intensivista cuando se ha realizado el diagnóstico de muerte encefálica destacan, por sus implicaciones éticas, la posible retirada de las medidas de soporte y la donación de órganos. Ambos fines no son idénticos y para una argumentación racional desde los cuatro principios bioéticos de beneficiencia, autonomía, justicia y no maleficiencia descubren aspectos diferenciales que permiten fundamentar la toma de decisiones de un modo más racional y comprensible. Conclusión. La ponderación resultante del abordaje principalista (deontológico), para cada caso, evita una exclusiva argumentación utilitarista que responda al objetivo del mejor beneficio para el mayor número, con lo cual se pueden asumir mejor los casos diferentes y favorecer, así, el caso particular y la decisión individual de los que intervienen en la relación clínica (AU)

[Estimation of the neurologic demand in a health care area of Madrid, Spain (area 11, University Hospital, 12 of October)]. / Estimación de la demanda neurológica en un área sanitaria de Madrid (area 11, Hospital Universitario 12 de Octubre).

OBJECTIVES: To analyse the demand for neurologic care and the neurological resources in a health district. PATIENTS AND METHODS: Demographic, medical care aspects, neurologic care demands and neurological resources of the health district 11 of Madrid (University Hospital "12 de Octubre"), referred to 1996, were reviewed. RESULTS: The rate of aging (17%) and the consulting rates in the National Health System (86%) versus private care were high in this health district. The neurologic care demands were 17.5-18.1 and 36 consultations respectively per 1,000 inhabitants/year. There were 2 patient-care neurologists and 3.7 neurologic beds per 100,000 inhabitants. CONCLUSIONS: The neurologic care was considered high and with a tendency to increase. The available neurological resources were judged to be insufficient.

[Amyotrophic neuralgia: review of 37 cases]. / Neuralgia amiotrófica: revisión de 37 casos.

INTRODUCTION: Amyotrophic neuralgia is characterized by pain of acute or subacute onset, accompanied by weakness and occasionally by atrophy of the brachial muscles, of unknown origin. We present our experience over the past 20 years. PATIENTS AND METHODS: We made a retrospective review of 37 patients with the above diagnosis, following the criteria of other series of such cases published in the literature. RESULTS: Twenty four of the patients were men and thirteen were women. The average age was 38 (11 to 71). A relevant clinical history was recorded in 9 cases; infection (5), surgery (4), remote trauma (3) and vaccination (1). There was a painful onset of the condition in 32 patients; objective weakness of the superior brachial plexus (30), inferior (5) or both (2). Atrophy was present in 23 and hypoaesthesia in 13. Two patients had fasciculations and 9 had hyperreflexia. In all patients electromyographic studies showed a neurogenic pattern of denervation of the muscles clinically affected. The severity of the condition was divided into mild (18), moderate (16) and intense (3). Prognosis was good in 24 and sequelae remained in 11. There were 2 bilateral cases and 2 relapses but no familial cases. CONCLUSIONS: There was a ratio of men/women of 1.8:1 and onset usually when the patient was in his forties. Mild infection, surgery, remote trauma and vaccination were the commonest clinical factors. Onset was painful in 85%. Muscular weakness was predominantly in the superior brachial plexus (85%), followed by atrophy in 62%. There was hypoaesthesia in a third of the patients. Most cases were mild (50%) and made a complete recovery (70%). Our findings are similar to those described in most series in the literature.

[Hypothyroid myopathy. Clinico-pathologic study of 20 cases]. / Miopatía hipotiroidea. Estudio clínico-patológico de 20 casos.

20 patients afflicted with primary hypothyroidism were studied in order to evaluate the association of clinical or sub-clinical myopathy, detected by neurophysiological (electromyography) (EMG) or neuropathological methods (muscular biopsy with enzymatic study). 70% of the patients had muscular weakness (moderate in 30% and severe in 40%) of the scapular and pelvic muscles. 60% of the patients had muscular cramps. There was no myodema nor muscular atrophy or hypertrophy. Seric CPK was high in 70% of the cases. EMG was myopathic in 65%. All cases with weakness registered EMG alterations. The histological findings were import findings were important. The enzymatic techniques showed alterations of the fiber subtypes in 90% of the cases. The type I fibers had sarcolemmal and mitochondrial accumules in 85% and 70% had areas without oxidative activity, similar to "core". In this study, we did not find any correlation between the evolution time of hypothyroidism, hormonal levels, CPK increase, and muscular weakness. The EMG was myopathic in cases with severe weakness, however, in patients with moderate weakness it could also prove abnormal. There was no correlation between the electric myopathic pattern, CPK levels and thyroid hormones.

[Thyroid myopathy. Effect of treatment with thyroid hormones]. / Miopatía tiroidea. Efecto del tratamiento con hormonas tiroideas.

We studied 20 patients afflicted with primary hypothyroidism and treated with thyroid hormone replacements, with the aim of evaluating the clinical, biochemical, EMG and anatomo-pathological effects. Cramps, as well as subjective and objective proximal muscular weakness, disappeared. Seric CPK was normalized in all cases after 1-8 weeks of treatment. EMG myopathic patterns faded away in all cases. Anatomopathological changes took longer to observe; 5 cases with new biopsy showed an isolate atrophy of type II fibers, one of them after 18 months in treatment; type I fibers had mitochondrial accumula without change compared to the initial biopsy. There was a clear tendency for the destroyed fibers to become normalized and for the structures similar to the "core" to vanish.

Myotonic dystrophy associated with thyroid disease.

Two patients with hereditary, clinical, electromyographical and histological data typical of myotonic dystrophy are discussed. In both there was a thyroid disorder. The first patient had primary hypothyroidism, and the second a non-toxic multinodular goiter which necessitated total thyroidectomy. The EMG findings and the muscle histopathology of both patients are commented on and compared with the changes described in hypothyroidism. The disease processes in both patients are also discussed in relation to the muscle and metabolic changes described in myotonic dystrophy. The coexistence of these two diseases is not explicable in the light of present knowledge on the basis of a known genetic predisposition. Only two similar cases of myotonic dystrophy and hypothyroidism have been reported.

Mitochondrial functions in five cases of human neuromuscular disorders.

We determined the respiration, respiratory control, and Pi:O ratios with different substrates in mitochondria isolated from five cases of human neuromuscular disorders (two cases of central core disease, two cases of neuropathy of Dejerine-Sottas, and one case of Kugelberg-Welander's disease) and compared them with normal human muscle. In all the myopathies studied, a severe derangement of the respiratory control with variable derangement of oxidative phosphorylation was found. This supports the idea that a group of neuromyopathies shares the same biochemical lesion as the so-called mitochondrial myopathies, forming with them a group of myopathies which may be related through a similar biochemical lesion of varying degree. Alternatively, disturbance of mitochondrial functions in a number of myopathies could be considered as a non-specific finding.