[Alcoholic ketoacidosis and reversible neurological complications due to hypophosphataemia]. / Cetoacidosis alcohólica y complicaciones neurológicas reversibles de la hipofosfatemia.

A 57-year-old man with chronic alcoholism was admitted to our hospital due to disturbance of consciousness and polyradiculitis. Laboratory examination revealed metabolic acidosis, hypokalemia and hypophosphataemia. Alcoholic ketoacidosis is a common disorder in alcoholic patients. All patients present with a history of heavy alcohol misuse, preceding a bout of particularly excesive intake, which had been terminated by nausea, vomiting and abdominal pain. The most important laboratory results are: normal or low glucose level, metabolic acidosis with a raised anion GAP, low or absent blood alcohol level and urinary ketones. The greatest threats to patients are: hypovolemia, hypokaliemia, hypoglucemia and acidosis. Alcohol abuse may result in a wide range of electrolyte and acid-base disorders including hypophosphataemia, hypomagnesemia, hypocalcemia, hypokalemia, metabolic acidosis and respiratory alkalosis. Disturbance of consciousness in alcoholic patients is observed in several disorders, such drunkenness, Wernicke encephalopathy, alcohol withdrawal syndrome, central pontine myelinolysis, hepatic encephalopathy, hypoglucemia and electrolyte disorders.

Cetoacidosis alcohólica y complicaciones neurológicas reversibles de la hipofosfatemia / Alcoholic ketoacidosis and reversible neurological complications due to hypophosphataemia

Un paciente varón de 57 años alcohólico ingresó en nuestro hospital por alteración del nivel de conciencia y polirradiculitis. En el estudio analítico aparecía acidosis metabólica, hipopotasemia e hipofosfatemia. La cetoacidosis alcohólica es frecuente en estos pacientes. Todos ellos se presentan con una historia de abuso del alcohol, con cese del consumo los días previos por la aparición de náuseas, vómitos y dolor abdominal. Los datos básicos de laboratorio son: glucemia normal o baja, acidosis metabólica con anión GAP elevado, ausencia de alcohol en sangre y cetonuria. Los mayores peligros son la hipovolemia, hipopotasemia, hipoglucemia y acidosis. El abuso del alcohol puede provocar un amplio rango de trastornos electrolíticos y del equilibrio ácido-base, incluyendo hipofosfatemia, hipomagnesemia, hipocalcemia, hipopotasemia, acidosis metabólica y alcalosis respiratoria. El deterioro del nivel de conciencia puede observarse en relación con intoxicación etílica aguda, encefalopatía de Wernicke, síndrome de abstinencia, mielinolisis central pontina, encefalopatía hepática, hipoglucemia y trastornos electrolíticos (AU)

A 57-year-old man with chronic alcoholism was admitted to our hospital due to disturbance of consciousness and polyradiculitis. Laboratory examination revealed metabolic acidosis, hypokalemia and hypophosphataemia. Alcoholic ketoacidosis is a common disorder in alcoholic patients. All patients present with a history of heavy alcohol misuse, preceding a bout of particularly excesive intake, which had been terminated by nausea, vomiting and abdominal pain. The most important laboratory results are: normal or low glucose level, metabolic acidosis with a raised anion GAP, low or absent blood alcohol level and urinary ketones. The greatest threats to patients are: hypovolemia, hypokaliemia, hypoglucemia and acidosis. Alcohol abuse may result in a wide range of electrolyte and acid-base disorders including hypophosphataemia, hypomagnesemia, hypocalcemia, hypokalemia, metabolic acidosis and respiratory alkalosis. Disturbance of consciousness in alcoholic patients is observed in several disorders, such drunkenness, Wernicke encephalopathy, alcohol withdrawal syndrome, central pontine myelinolysis, hepatic encephalopathy, hypoglucemia and electrolyte disorders (AU)

[Wilkie syndrome: report of a case]. / Síndrome de Wilkie: a propósito de un caso.

Wilkie syndrome is an unusual form of high gastrointestinal obstruction resulting from compression of the duodenum between the abdominal aorta and the superior mesenteric artery (SMA). The conditions that cause this syndrome can be classified into five categories: severe wasting diseases, severe injuries, diseases, deformity or trauma to the spine, dietary disorders and posoperative state. The symptoms include nausea, vomiting, distention postprandrial, epigastric pain and weight loss. Barium meal and arteriography were used as diagnostic tools, now CT-angiography is being used and shown higher diagnostic sensitivity. The diagnostic criteria are: dilated duodenum, compression of the duodenum by the SMA and aortomesenteric angle <20 degrees. Patients with acute syndrome often respond to conservative treatment (decompression, correction of dehydration and electrolyte imbalance and nutrition support). Most of the patients with chronic syndrome require surgical intervention. Duodenojejunostomy is the most effective surgical option, with a success rate of 90%.

Síndrome de Wilkie: a propósito de un caso / Wilkie syndrome: report of a case

El Síndrome de Wilkie es una causa poco frecuente de obstrucción intestinal alta, resultante de la compresión del duodeno entre la aorta abdominal y la arteria mesentérica superior (AMS). Sus causas se pueden clasificar en cinco grupos: síndromes consuntivos, trastornos de la alimentación, postoperatorio, trauma severo y deformidades, enfermedades o traumatismos de la columna vertebral. Los síntomas incluyen náuseas, vómitos, pérdida ponderal, saciedad precoz, distensión abdominal y dolor epigástrico. Historicamente el estudio con bario y la arteriografía eran las pruebas diagnósticas utilizadas; más recientemente el angioTAC ha demostrado mayor sensibilidad. Los criterios diagnósticos son: duodeno dilatado, compresión duodenal por la AMS y ángulo aortomesentérico menor de 20 grados. Los pacientes con un cuadro agudo suelen responder al tratamiento conservador (descompresión, corrección de las alteraciones hidroelectrolíticas, apoyo nutricional); sin embargo aquellos con cuadros crónicos habitualmente requieren ser intervenidos. La duodenoyeyunostomía es el procedimiento de elección(tasa de éxito superior al 90%) (AU)

Wilkie syndrome is an unusual form of high gastrointestinal obstruction resulting from compression of the duodenum between the abdominal aorta and the superior mesenteric artery (SMA). The conditions that cause this syndrome can be classified into five categories: severe wasting diseases, severe injuries, diseases, deformity or trauma to the spine, dietary disorders and posoperativestate. The symptoms include nausea, vomiting, distention postprandrial, epigastric pain and weight loss. Bariummeal and arteriography were used as diagnostic tools, now CT-angiography is being used and shown higherdiagnostic sensitivity. The diagnostic criteria are: dilated duodenum, compression of the duodenum by the SMA and aortomesenteric angle <20 degrees. Patients with acute syndrome often respond to conservative treatment(decompression, correction of dehydration and electrolyte imbalance and nutrition support). Most of the patients with chronic syndrome require surgical intervention. Duodenojejunostomy is the most effective surgical option, with a success rate of 90% (AU)

Fístula linfática cervical: manejo conservador / Neck chylous fistula: conservative treatment

La fístula quilosa, por daño del conducto torácico, aparece en el 1-2,5% de los pacientes sometidos a disección cervical. Las complicaciones asociadas incluyen desnutrición, compromiso inmune, formación de fístulas y necrosis cutánea con exposición carotídea, e incluso ruptura. De la literatura actual no se puede deducir ningún algoritmo de tratamiento definitivo, pero parece existir un consenso en realizar un manejo conservador de la mayoría de los casos. El manejo médico se basa en la teoría de que si se disminuye el flujo de quilo se permitirá el cierre espontáneo de la fístula, e incluye: drenaje conectado a vacío, reposo, vendaje compresivo (en discusión),intervención nutricional y uso de análogos de somatostatina. El manejo nutricional implica el uso de dietas bajas en grasa suplementadas con Triglicéridos de Cadena Media (MCT), Nutrición Enteral con TCM o Nutrición Parenteral total (NPT) (AU)

Injury to the thoracic duct, leading to chyle leak, occursin 1-2,5% of patients who undergo neck dissection. Associated complications include malnutrition, immunecompromise, fistula formation and carotid blowout. No definitive treatment algorithm can be deduced from the current literature, but on last reviews, there is an agreementon the conservative management. Medical managementis based on that decreasing chyle flow will allow for spontaneous closure of the chyle leak. Conservative treatment includes: closed vacuum drainage, bed-rest,nutrition modification and synthetic somatostatin analog. Nutrition modification involves a low-fat diet supplemented with medium-chain triglycerides (MCT),enteral nutrition with high percentage of MCT or parenteral nutrition (AU)

[Neck chylous fistula: conservative treatment]. / Fístula linfática cervical: manejo conservador.

Injury to the thoracic duct, leading to chyle leak, occurs in 1-2,5% of patients who undergo neck dissection. Associated complications include malnutrition, immune compromise, fistula formation and carotid blowout. No definitive treatment algorithm can be deduced from the current literature, but on last reviews, there is an agreement on the conservative management. Medical management is based on that decreasing chyle flow will allow for spontaneous closure of the chyle leak. Conservative treatment includes: closed vacuum drainage, bed-rest, nutrition modification and synthetic somatostatin analog. Nutrition modification involves a low-fat diet supplemented with medium-chain triglycerides (MCT), enteral nutrition with high percentage of MCT or parenteral nutrition.

Refeeding syndrome.

Refeeding syndrome is a complex syndrome that occurs as a result of reintroducing nutrition (oral, enteral or parenteral) to patients who are starved or malnourished. Patients can develop fluid-balance abnormalities, electrolyte disorders (hypophosphataemia, hypokalaemia and hypomagnesaemia), abnormal glucose metabolism and certain vitamin deficiencies. Refeeding syndrome encompasses abnormalities affecting multiple organ systems, including neurological, pulmonary, cardiac, neuromuscular and haematological functions. Pathogenic mechanisms involved in the refeeding syndrome and clinical manifestations have been reviewed. We provide suggestions for the prevention and treatment of refeeding syndrome. The most important steps are to identify patients at risk, reintroduce nutrition cautiously and correct electrolyte and vitamin deficiencies properly.

Síndrome de realimentación / Refeeding syndrome

El síndrome de realimentación (SR) es un cuadro clínico complejo que ocurre como consecuencia de la reintroducción de la nutrición (oral, enteral o parenteral) en pacientes malnutridos. Los pacientes presentan trastornos en el balance de fl uidos, anomalías electrolíticas —como hipofosfatemia, hipopotasemia e hipomagnesemia— alteraciones en el metabolismo hidrocarbonado y déficits vitamínicos. Esto se traduce en la aparición de complicaciones neurológicas, respiratorias, cardíacas, neuromusculares y hematológicas. En este artículo se han revisado la patogenia y las características clínicas del SR, haciendo alguna sugerencia para su prevención y tratamiento. Lo más importante en la prevención del SR es identificar a los pacientes en riesgo, instaurar el soporte nutricional de forma prudente y realizar una corrección adecuada de los déficits de electrolitos y vitaminas (AU)

Refeeding syndrome is a complex syndrome that occurs as a result of reintroducing nutrition (oral, enteral or parenteral) to patients who are starved or malnourished. Patients can develop fluid-balance abnormalities, electrolyte disorders (hypophosphataemia, hypokalaemia and hypomagnesaemia), abnormal glucose metabolism and certain vitamin defi ciencies. Refeeding syndrome encompasses abnormalities affecting multiple organ systems, including neurological, pulmonary, cardiac, neuromuscular and haematological functions. Pathogenic mechanisms involved in the refeeding syndrome and clinical manifestations have been reviewed. We provide suggestions for the prevention and treatment of refeeding syndrome. The most important steps are to identify patients at risk, reintroduce nutrition cautiously and correct electrolyte and vitamin defi ciencies properly (AU)

Long-term improvement of metabolic control without increased risk of hypoglycaemia by intensive insulin regimens in type 1 diabetes patients treated in a regular clinical setting.

AIM: To evaluate if intensive insulin regimen with multiple daily injections (MDI) is successful for treating type 1 diabetes patients over a long period of time in a regular clinical setting. METHOD: This is a prospective, observational seven-year study. Fifty-nine (35 male) type 1 diabetic patients with bad metabolic control (HbA1c> or =9%), aged 31.9 years, range 18-47 were included in the present study. All of them had had at least 5 years of diabetes duration after diagnosis and showed negative responses of serum C-peptide to a standard breakfast. The main control variables are: Metabolic control measured by serum HbA1c values (values < 6.2 % was the treatment objective) and the frequency of hypoglycaemic episodes (episodes/patient-month). RESULTS: Significant decreases in mean+/-SD HbA1c values in this group of patients were observed from the first year of follow-up, with the mean values being: 7.5+/-1.5%, 7.2+/-1.8%, 7.6+/-1.6%, 7.1+/-1.7%, 7+/-1.4, 6.6+/-1.6% and 6.8+/-1.4% for the first, second, third, fourth, fifth, sixth and seventh years of follow-up respectively. Sixteen %, 27.5%, 15.7%, 33.3%, 28.6%, 42% and 33% of the patients reached the treatment objective (HbA1c values<6.2%) for each year of follow-up. Throughout the study period the rate of severe hypoglycaemia (episodes/patient-year) was 0.32+/-0.2 which was not significantly different compared with the value of 0.28+/-0.1 observed the year before the study began. Similarly frequencies of mild/moderate hypoglycaemia episodes (episodes/patient-month) varies between 16.5+/-4 and 21.7+/-5, which are not significantly different from the value of 17.7+/-6 observed the year before the study began. CONCLUSION: Long-term improvement in metabolic control was observed in this group of type 1 diabetes patients with previous bad control, during treatment in a regular clinical setting. A considerable percentage of type 1 diabetic patients with MDI reached the treatment objective in every year of follow-up. Furthermore improvement in metabolic control is not associated with significantly increased frequency of hypoglycaemia episodes.

Hiperprolactinemia tumoral y obesidad / Tumoral hyperprolactinemia and obesity

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The role of diabetes duration, pubertal development and metabolic control in growth in children with type 1 diabetes mellitus.

OBJECTIVE: To investigate whether pubertal development, duration of type 1 diabetes mellitus (DM1), or metabolic control play some role in the anomalies in growth observed in diabetic children. PATIENTS: We conducted a prospective evaluation of 83 patients (37 female, 46 male) who were followed from the onset of DM1 at the prepubertal stage until they reached final height. All patients were treated with a conventional regimen of insulin. METHODS: Height SDS, weight SDS, BMI SDS, duration of DM1 in years, and values of HbA1c were the study variables. RESULTS: In prepubertal (P1) girls (data for the initial vs the intermediate evaluations): weight SDS was -0.14 +/- 0.19 vs 0.11 +/- 0.20, p = ns; BMI SDS -0.25 +/- 0.15 vs 0.01 +/- 0.13, p = ns. In postpubertal (P3) girls, weight SDS was 0.49 +/- 0.2 vs 1.2 +/- 0.32, p <0.01; BMI SDS 0.09 +/- 0.16 vs 1.03 +/- 0.24, p <0.01, whereas in P1 boys, height SDS was 0.16 +/- 0.30 vs -0.20 +/- 0.27, p <0.05; and in P3 boys: 0.09 +/- 0.21 vs -0.28 +/- 0.26, p <0.05. Thus pubertal development influenced changes observed in girls with DM1, but did not do so in boys. The anomalies described in children with DM1 were observed from the third year of DM1 duration in both girls and boys. We did not observe any correlation between HbA1c values with height SDS, weight SDS or BMI SDS. CONCLUSIONS: The anomalies in growth observed in girls with DM1 are related to pubertal development, but this is not the case in boys. Alterations in children with DM1 were found from the third year of DM1 duration. Furthermore, the present data also indicate that the degree of metabolic control observed in our patients treated with modern but conventional regimen did not play a major role in the anomalies observed.