[Status epilepticus following propofol anesthesia].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Lahdensuu.
Explore the source record for details and available documents.
The role of endogenous catecholamines in various clinical shock and stress states is reviewed; the effects, especially on the peripheral circulation, of catecholamine secretion are the same independent of the cause. Risks of using sympathomimetic agents in the treatment of shock are evaluated. A prolonged noradrenaline activity is to be expected in surgical stress states, e.g. multiple injuries, fat embolism syndrome, burns and infections; therapeutic approaches to minimize the sympathoadrenal activity are outlined.
In 45 patients with multiple injuries due to trauma, admitted consecutively to our clinic, the following enzyme activities were studied, beginning at the onset of treatment: SDH, GPT, GLDH, and acid phosphatase. The mean levels of SDH rose in all patients between 2 and 24 h after trauma. The mean values of GPT were above normal between 2 and 48 h after trauma; this rise was more pronounced and statistically significant in those patients who eventually died of trauma than in the less severely injured ones. Twenty-four hours after trauma, the levels of GLDH were 16 times higher in the first group of patients than in the less severely injured group. These results lead us to the conclusion that through serum level measurements of these enzymes particularly of GPT it is possible to evaluate the degree of tissue damage and the general state of this group of patients.
Plasma catecholamine levels were studied in 45 severely injured patients for 8 days after the trauma. Sixteen of the patients were classified as critically injured and 29 as seriously injured. The total plasma catecholamine values of the whole group immediately after the injury were almost twice as high as the eighth day reference values and remained significantly higher than these values for 6 hours after the trauma. On admission both the plasma adrenaline and noradrenaline levels were elevated. The plasma adrenaline levels on admission correlated with the blood volume replacement which was required within the first 6 hours. The plasma noradrenaline levels in the critically injured group were significantly higher throughout the observation period than in the seriously injured group. A corresponding difference was observed in the plasma adrenaline concentrations only during the first 12 hours. The results showed that strong stimulation of the sympathetic nervous system occurs in severely injured patients. Factors stimulating the sympathetic nervous system apparently included hypovolaemia, tissue hypoxia, acidosis and the pain produced by the trauma and therapeutic measures.
During eight post-traumatic days, the blood loss and severity of trauma were correlated with the blood levels of lactate, creatinine and catecholamines in 45 patients with multiple blunt injuries. During two days these biochemical indicators correlated with the extent of thoracoabdominal, pelvic and cerebral injuries. In the critically injured patients all three parameters were elevated throughout the observation period. No correlations were observed between plasma catecholamines and lower limb injuries, which seems to make the importance of catecholamines for predicting the onset of fat embolism syndrome less useful.
Forty-five patients with severe blunt injuries were examined during eight posttraumatic days. At random, 14 patients were given three doses of methylprednisolone intravenously; 10 mg/kg at 8-hour intervals. Fat embolism syndrome was diagnosed in 13/45 patients, only one of whom had received corticosteroid (p = 0.03). Shock, acidosis and elevated plasma catecholamines showed no correlation with the occurrence of fat embolism syndrome. Platelet counts immediately after trauma were significantly lower in the fat embolism patients than in the other trauma patients, indicative of early platelet aggregation. Prophylactically administered methylprednisolone in pharmacological doses appeared to inhibit the emergence of fat embolism syndrome.
Explore the source record for details and available documents.
The effect of phenoxybenzamine and dopamine on the respiratory and metabolic changes in experimental traumatic shock was examined in 45 rabbits. Phenoxybenzamine caused a more effective release of the peripheral vasoconstriction than dopamine. The effect of these drugs without similar restoration of blood volume was unfavourable. This should be borne in mind when the use of these drugs is meditated in clinical work.
Different opinions seem to exist as to the use of analgesies in the treatment of trauma patients. For this reason we investigated experimentally the effect of pethidine in traumatic shock. Pethidine was administrated to eight of sixteen anaesthetized rabbits with lower limb injuries. The effect of pethidine was unfavourable. This was due to the effect of the drug on circulation and not on respiration.
The effects of methylprednisolone in connexion with a standardized trauma was studied on 30 rabbits. The treatment with glucocorticoid accentuated the hemodilution due to the trauma. Intensified lactacidosis was also demonstrated.