Thalidomide-type malformations and subsequent osteosarcoma.
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Biomedical subjects
Publications and source records attributed to V Avikainen.
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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.
Forty-five patients with multiple injuries treated at an intensive care unit were studied prospectively. The patients were divided into two groups: the severely injured (no mortality) and critically injured (56% mortality). Treatment was started within two hours from the accident in all cases. The following coagulation parameters were measured for eight days: euglobulin lysis time (ELT), thromboelastography (TEG), vecalcification time (RECA), partial thromboplastin time (PTT), factor V, factor VIII, Normotest, Thrombotest, thrombin time, fibrinogen and platelets. Severe coagulation disorders were observed in one-third of the patients 12-48 hours after trauma. The abnormalities were more pronounced in patients who had sustained very severe injuries and arrived in a state of shock. The ELT was shortened 0-6 hours after the accident and accelerated coagulation was indicated simultaneously by decreased PTT, RECA, and r-values as well as by elevated Thrombotest and factor VIII values. The factor V and fibrinogen levels were initially lowered. Low platelet values at 2-4 days, prolonged thrombin and r-times, secondary decrease of fibrinogen FV, FVIII, and low Thrombotest values suggested disseminated intravascular coagulation associated with complications, such as fat embolism and "shock lung" syndromes. General bleeding tendency with high mortality was observed in 16% of the patients.
The role of intravascular coagulation in severely injured patients was studied by the ethanol gelation test (EGT). Increased frequency of positive EGT's was observed following trauma, the highest on the fifth posttraumatic day (25 %). A positive test did not correlate with the quantity of blood received and the severity of the trauma. Patients with higher haematocrit, serum protein and platelet values showed a positive test more frequently.
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.
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