[Neuroprotector therapy of patients with decompensated diabetes mellitus type 1].

The influence of actovegin and reamberin on diabetic ketoacidotic crises has been studied on a group of 128 patients with severe diabetic ketoacidosis on the background of diabetes mellitus type 1 with disorders ranging from consciousness to coma or precoma states. Patients of group 1 received standard intensive therapy of diabetic ketoacidosis. In group 2, an intensive therapy for neuroprotection by actovegin was added. In group 3, patients received reamberin on the background of standard therapy. In group 4, the neuroprotective therapy using actovegin and reamberin was combined. The mental status was estimated upon recovery from coma, on 5th and 28th days from the beginning of treatment, by taking into consideration cognitive functions such as attention, memory, mentality. The results showed that the use of neuroprotective drugs, including the combination of actovegin and reamberin, allowed to the restore the compensatory-adaptive reaction of patients to ketoacidotic crisis, accelerate the restoration of consciousness within 19.2 +/- 3.8 h, restore the cognitive functions with exceeding norm for patients with diabetes mellitus in compensation stage and maintain their high level on 28th day after crisis.

Curso de atualização em emergências médicas: aula 17: emergência em diabéticos / Course of updating in medical emergencies: class 17: emergency in diabetics

A cetoacidose diabética e o estado hiperosmolar hiperglicêmico não cetótico são complicações hiperglicêmicas agudas do diabetes mellitus e representam um desafio para o clínico que trabalha no terreno das emergências médicas. A cetoacidose diabética pode ser a manifestação inicial ou resultar de intercorrências havidas em pacientes com diabetes tipo 1. Além disso, pode se instalar em pacientes diabéticos tipo 2 submeticos a situações de extrema gravidade, tais como sepse. O coma hiperosmolar hiperglicêmico não cetótico costuma acometer portadores de diabetes tipo 2. Tais complicações trazem risco à vida do paciente diabético, com elevada taxa de mortalidade. Estas e outras emergências diabéticas são abordadas no presente artigo, com ênfase em diagnóstico e tratamento.

Diabetic ketoacidosis and nonketotic hyperosmolar hyperglycemic syndrome are challenging metabolic complications of diabetes mellitus, especially in the setting of the emergency department. Diabetic ketoacidosis can be the first clinical manifestation of type 1 diabetes or result of intercurrent events in someone already diagnosed with type 1 diabetes. Nonketotic hyperosmolar hyperglycemic coma is more frequently associated with type 2 diabetes. Both complications are lefe-threatening and the mortality rate is high. Management of this and other acute complications of diabetes are discussed, emphasizing diagnosis and treatment.

Profound hypokalemia in diabetic ketoacidosis: a therapeutic challenge.

OBJECTIVE: To describe profound hypokalemia in a comatose patient with diabetic ketoacidosis. METHODS: We present a case report, review the mechanisms for the occurrence of hypokalemia in diabetic ketoacidosis, and discuss its management in the setting of hyperglycemia and hyperosmolality. RESULTS: A 22-year-old woman with a history of type 1 diabetes mellitus was admitted in a comatose state. Laboratory tests revealed a blood glucose level of 747 mg/dL, serum potassium of 1.9 mEq/L, pH of 6.8, and calculated effective serum osmolality of 320 mOsm/kg. She was intubated and resuscitated with intravenously administered fluids. Intravenous administration of vasopressors was necessary for stabilization of the blood pressure. Intravenous infusion of insulin was initiated to control the hyperglycemia, and repletion of total body potassium stores was undertaken. A total of 660 mEq of potassium was administered intravenously during the first 12.5 hours. Despite such aggressive initial repletion of potassium, the patient required 40 to 80 mEq of potassium daily for the next 8 days to increase the serum potassium concentration to normal. CONCLUSION: Profound hypokalemia, an uncommon initial manifestation in patients with diabetic ketoacidosis, is indicative of severe total body potassium deficiency. Under such circumstances, aggressive potassium repletion in a comatose patient must be undertaken during correction of other metabolic abnormalities, including hyperglycemia and hyperosmolality. Intravenously administered insulin should be withheld until the serum potassium concentration is (3)3.3 mEq/L.

[Mechanisms of acute respiratory insufficiency in patients with hyperglycemic coma]. / O mekhanizmakh ostroi dykhatel'noi nedostatochnosti u bol'nykh s giperglikemicheskimimi komami.

Basic parameters of pulmonary gas exchange, central and pulmonary hemodynamics, and colloid osmotic pressure were investigated in 31 patients in diabetic hyperglycemic coma over the course of intensive care. Pulmonary gas exchange disorders were observed in all patients in the presence of increased shunting of the blood in the lungs and disorders of transcapillary liquid exchange. On the other hand, we failed to obtain data indicative of an increase in the volume of extravascular water in the lungs. However, it does not rule out the possibility of iatrogenic disorders of gas exchange during noncontrolled rehydration.

Análisis de los egresos hospitalarios por cetoacidosis y coma diabético / Analysis of hospital outputs due to ketoacidosis and diabetic coma

Es una revisión retrospectiva de los egresos y defunciones que ocurrieron en las unidades hospitalarias del Instituto Mexicano del Seguro Social de 1980 a 1993. Los diagnósticos de egreso y defunción fueron codificados de acuerdo con la lista tabular de la Clasificación Internacional de Enfermedades. Se consideraron el número de casos, egresos y defunciones por grupo de edad y sexo. Se calcularon tasas específicas por 1,000 egresos y por 100 defunciones hospitalarias. La tendencia fue calculada a través del análisis de regresión por mínimos cuadrados. Los resultados del análisis mostraron que la cetoacidosis representó el 3.02 y 6.47 por ciento del total de egresos y defunciones por diabetes y el 1.07 y 5.60 por ciento respectivamente en coma diabético. La tendencia de ambas afecciones mostró una reducción no significativa durante el periodo analizado. Los pacientes menores de 24 años de edad fueron el grupo predominante en los egresos por cetoacidosis y coma, pero en mortalidad los grupos de 25 a 34 años, y menores de 1 año y de 35 a 44 años en cetoacidosis y coma fueron los más representativos. En ambos grupos hubo un predominio en el sexo femenino (56 por ciento). El análisis del promedio de días de estancia hospitalaria no mostró cambios significativos durante este tiempo, aunque los casos de muerte en ambas enfermedades mostraron los promedios más bajos. Estos hallazgos indican que las complicaciones agudas no representan un problema mayor en la casuística de la diabetes mellitus, aunque un mejor control podría disminuir su frecuencia. Finalmente se hacen algunas consideraciones sobre los resultados del estudio y se toman en cuenta algunos puntos importantes en la fisiopatología, complicaciones y posibles causas de muerte

Increased GABA release in the human brain cortex as a potential pathogenetic basis of hyperosmolar diabetic coma.

Human cerebral cortical slices preincubated with [3H]GABA, [3H]noradrenaline, or 5-[3H]hydroxytryptamine and superfused with Krebs solution or Mg(2+)-free Krebs solution were used to investigate the influence of increased D-glucose concentrations on the release of these [3H]-neurotransmitters evoked by high K+ content or NMDA receptor activation, respectively. An increase in level of D-glucose (normal content, 11.1 mM) by 32, 60, and/or 100 mM (a range characteristic for hyperosmolar diabetic coma) increased the [3H]GABA release and inhibited the [3H]noradrenaline release evoked by both methods of stimulation. The K(+)-induced 5-[3H]hydroxytryptamine release was also inhibited by high D-glucose content. Blockade of GABAB receptors by p-(3-aminopropyl)-p-diethoxymethylphosphinic acid (CGP 35348) attenuated the inhibitory effect of high D-glucose content on the K(+)-evoked release of [3H]noradrenaline and 5-[3H]hydroxytryptamine, suggesting that the effect on monoamine release is, at least to a major part, the result of the increased GABA release and, as a consequence, of an increased GABA concentration at inhibitory GABAB receptors. The membrane-impermeable sorbitol mimicked the increasing effect of D-glucose on [3H]GABA release and its inhibitory effect on 5-[3H]hydroxytryptamine release. However, dimethyl sulfoxide, which is known to permeate rapidly through biological membranes, had no effect at concentrations equiosmolar to D-glucose. It is concluded that a reduction in brain cell volume caused by increased extracellular, compared with cytoplasmic, osmolarity is crucial for the changes in neuronal function observed at high D-glucose and sorbitol content.(ABSTRACT TRUNCATED AT 250 WORDS)

[The reactivity of the mesenteric arterioles to adrenaline in metabolic coma]. / Reaktivnost' arteriol bryzheiki k adrenalinu pri metabolicheskoi kome.

The reactivity of mesoappendix arterioles to applicated epinephrine application was investigated in 2 models of metabolic coma, hypoglycemic and acetonemic. Hypoglycemic coma (HC) was induced by insulin injection (20 IE/kg) i. m. to rats fasting for 18 hours. Acetonemic coma (AC) was induced by i. v. acetone injection (5.5 mmol). The sensitivity of arterioles to applicated epinephrine did not change in HC and increased twofold in AC vs. the control values (p < 0.01). The reaction of arterioles to injection of double threshold dose of epinephrine in HC developed sooner and the degree of vasoconstriction was 41% higher than in controls. In AC the reaction developed two times sooner and the degree of arterioles constriction was 1.5 times higher vs. the control (p < 0.01).

[Critical illness polyneuropathy: clinical aspects and long-term outcome]. / Critical Illness Polyneuropathie: Klinik und Langzeitergebnisse.

Patients treated in intensive care units may develop a primary axonal form of polyneuropathy complicating sepsis and multiple organ failure more frequently than previously assumed. This critical illness polyneuropathy causes difficulty in weaning patients from the ventilator and delays further recovery and mobilisation. Over a period of two years we have treated five patients with flaccid tetra- or paraparesis. Recovery of motor function was largely satisfactory, but a long rehabilitation process was necessary. If attention were paid to detecting this disease in the early stages of intensive care neurorehabilitation might be facilitated. Hence, electrophysiological tests should be performed as soon as possible. The clinical outcome was markedly influenced by long-lasting neuropsychological disturbances in three of the five patients as well as by other complications such as joint contractures.