Biomedical subjects
Publications and source records attributed to D Balogh.
In 12 severely burned patients the input of fluid and sodium, as well as sodium concentration in plasma and urine, was studied. The osmolarity in plasma and 24-h urine was measured. The high initial sodium input is noted. Plasma sodium levels stay within the normal range when the amount of sodium given during the further treatment is reduced. The importance of urea production in affecting plasma osmolarity is demonstrated.
A prospective randomized double blind investigation was made in 24 multiple injured patients. All patients were treated with a combined parenteral-enteral nutrition during 7 days. A group of 11 patients received as a continuous infusion over 16 h 60 mg/kg BW carnitine daily. Beside carnitine and acetylcarnitine levels in plasma and urine the following parameters were determinated to evaluate the effect of carnitine: for the metabolism of fatty acids: triglycerides, free fatty acids (FFA), alpha-hydroxy-butyrate for the metabolism of carbohydrates: glucose, insulin and lactate in plasma. Finally for amino acid metabolism: urea, creatinine, cholinesterase and kolloid osmotic pressure in plasma as well as ureanitrogen and alpha-aminonitrogen excretion in urine. In the patients receiving carnitine especially acetyl-carnitine in plasma and acetyl-carnitine excretion in urine increased, proving that the administered carnitine can pass through the mitochondrial membrane. In these patients the plasma level of FFA was markedly lower than in the group without carnitine. Simultaneously the level of the alpha-hydroxybutyrate was elevated, equivalent to an increased oxydation of fatty acids. There was no difference between the two groups in the metabolism of carbohydrates. Administration of carnitine caused a slight increase of the production of urea (PU), catabolism could not be reduced. The excretion of alpha-aminonitrogen in urine augmented after carnitine infusion. Carnitine is an AA itself and so the amount of excreted alpha-amino nitrogen will increase; additionally the reabsorption of AA in the proximal renal tubulus may be inhibited by carnitine.
Third-degree burn management with state-of-the-art surgery and intensive care technique has been available in Innsbruck since 1969. This statistical survey covers the period 1970 to 1982, with follow-ups on a total of 424 burn patients. Dividing the study into two periods, namely 1970-1976 and 1977-1982, permits a critical assessment of progress in burn management. A comparison of our results with those from other prominent burns units shows that the survival rate is considerably lower in Innsbruck, especially in the case of patients with burns of over 60% of body surface area. It is essential that similar burns units should be set up elsewhere in Austria.
Post mortem examinations were carried out on 52 patients who died from major burn injury from 1971-1985. Causes of death were accounted for by pneumonia and sepsis 44.2%, shock syndrome 21.2%, and cardiac failure 19.2%. The relationship between duration of survival and cause of death revealed that if the patient died in the first three days after burn injury it was usually due to "shock", if between the fourth to twentieth day then 34.6% had pneumonia and 30.8% cardiac failure. "Accidental" sepsis (46.1%) was the most frequent cause of death after three weeks. Clinical and pathological diagnosis varies between burns centers and may cause confusion. An international standardization register should be sought to permit comparison of results.
Average iodine serum levels of 2.5 mg/100 ml were obtained in 10 patients with an average burn area of 50% and treated with povidone-iodine. Simultaneous measurements of the thyroid hormones failed to reveal any significant impairment of thyroid function apart from depressed T3 coupled with increased reverse T3. Similar findings were obtained with a control group of 10 multiply-injured patients. If renal function is unimpaired the resorbed iodine is quickly excreted. No clinical signs of iodine intoxication were observed.
A questionnaire was developed to gain information on the medical, social and psychological rehabilitation of 62 burn patients. The questionnaire was answered by each patient and a close relative of their choice. The patients selected were those with burns involving hands and face, or with burns exceeding 30% of the body surface area. The returned questionnaires were analysed with respect to posttraumatic care, the extent of physical reconstruction, changes in personality and social behaviour, occupation, workman's compensation and cause of accident.
Measurements of the concentrations of pituitary, thyroid and gonadal hormones have been made under both basal conditions and after adequate stimulation using a combined arginine TRH-LHRH stimulation test in 10 patients with deep burns covering between 30 and 70 per cent of the body surface during the first 20 days after injury. The most remarkable changes were found in the pituitary-gonadal system with testosterone concentrations significantly decreased at all times during the periods of study. Stimulation with LHRH resulted in a prompt response of FSH and LH during the first 10 days after burning whereas between 10 and 20 days after injury the basal concentrations for both hormones were significantly lower and showed a delayed response to stimulation. During the period of early fluid therapy large amounts of glucose without additional insulin were given, resulting in elevated blood glucose and high plasma insulin levels. It is concluded that normal pancreatic insulin production is sufficient to avoid excessive hyperglycaemia even during the period soon after burning. Compared with the findings in control patients the HGH levels in burned patients were not significantly different at any time during the periods of study.
Plasma amino acids were measured in 10 severely burned patients during 4 weeks and were compared with plasma amino acids of 12 multiple injured patients measured in the first and second week after the accident. There is only little difference between the amino acid pattern of the two groups. The total amount of plasma amino acids was in the normal range in both groups. In burned patients the high ornithine level was striking, especially in the 1st week (140 mumol/l +/- 46). During all 4 weeks glutamatic acid in burned patients was three to four times of the normal. The levels of asparagic acid were significantly higher in burned patients than in multiple injured patients and reached the highest value in the 2nd week (21,5 mumol/l +/- 8). The branched-chain amino acids decreased to low normal values in the 3rd and 4th week after an elevation in the 2nd week. Citrullin levels (mean 6-12 mumol/l) of both groups were below the normal range, as well as cystin levels (mean 5-36 mumol/l). A possible connection to the increased production of urea is pointed out and the consequence for the nutrition of burned patients is discussed.
Urinary amino acids were measured in 10 severely burned patients weekly during 4 weeks after burning. For control the same measurements have been made in 12 multiple injured patients during the first two weeks after the accident. In burned patients the renal loss of free amino acids was up to 3 g/24 h +/- 1 in the first week, together with a high excreation of sodium (450 mmol/24 h +/- 73) in the first week. Urinary output of ornithin (highest value in the 2nd week: 1093 +/- 525% of normal) and lysin (highest value in the 2nd week: 1093 +/- 525% of normal) and Lysin (highest value in the 1st week: 654 +/- 166% of normal) was increased and caused an augmented loss of cystin (645 +/- 133% of normal in the first week) and 742 +/- 64% of normal in the second week. In the first and second week after burning the excretion of valin was up to 12 times the normal. Methionine-excretion staid high (5 times the normal) during all 4 weeks. The mean rate of 3-methylhistidine output in urine (80 +/- 38 mg/24 h) was elevated from the second until fourth week, suggesting muscle protein breakdown. In the control group urinary excretion of glutamin and asparagin (1st week: 608 +/- 97% of normal), threonin (2nd week: 693 +/- 240% of normal), serin (2nd week: 517 +/- 232% of normal) and histidin (1st week: 358 +/- 115% of normal) was high. Only urinary citrullin, isoleucin, prolin and taurin were not elevated in both groups during all 4 weeks.
The influence of anaesthesia and operation on plasma catecholamine level (Group A) and on the production of urea (PU) (Group B) was investigated in two groups of severely burned patients. Plasma catecholamine levels increased at every operation. The increase of noradrenaline however was always higher than that of adrenaline. The elevation of NA in operations performed during the first week was significantly higher than in all later operations. The production of urea (PU) was chosen as a parameter of protein catabolism. The PU was measured on the day before the operation, on the operation day and on the 1st, 2nd and 3rd postoperative day. The highest mean values of the PU could be found on the 2nd and 3rd postoperative day, but the increase was less than expected. There was no difference in plasma catecholamine levels in PU between the different methods of anesthesia. The advantages and disadvantages of the methods of anaesthesia studied are discussed.
In 58 patients with extensive deep dermal burns the consequences of intubation, tracheotomy and central venous catheter in respect to pneumonia and bacteriaemia were studied. The sputum of tracheotomized patients showed twice as many pathogenic bacteria as the sputum of patients with prolonged intubation. From 93 subclavian catheters under bacteriological control 16 (17%) showed pathogenic bacteria on the tip. An identity between the bacille found in the blood stream and on the catheter tip was only found in 21%. From this study it seems conclusively that prolonged intubation is generally preverable to tracheostomy in severely burned patients and that the venous catheter can not be the most frequent cause of bacteriaemia.
The change in serum lactate level was investigated in 20 patients undergoing reconstruction of the aortic bifurcation. This group of patients was compared with 16 patients undergoing abdominal surgery. There was a remarkable increase of serum lactate in course of the operation in both groups. After the aortic graft serum lactate level was specially elevated (24,96 mg/100 ml +/- 9,71) due to aortic gross-clamping. Simultaneously occurred a decrease in pH and base excess from 7,43 (+/- 0,03) to 7,34 (+/- 0,05) and from -2,2 mmol/1 (+/- 2,5) to -5,7 mmol/l (+/- 1,6). We mentioned the risk of lactic acidosis in vascular surgery caused by fluid therapy with fructose, sorbitol, xylitol and with electrolyte solutions containing lactate.
The Urea production (PU) of three severe burned patients is presented as an example for calculating protein loss. Burn injuries are accompanied by an extensive catabolism more then any other disease, operation or trauma. The operative stress caused a further increase of PU. The highest values are measured in electric burns. Alimentation is considered as an important therapeutic mean to diminish catabolism. Urea production rate is presented as a simple method to control protein loss and can be done in every hospital.
A case of periodic paralysis is reported that had to be treated by mechanical ventilation. Symptoms and course of this attack are demonstrated and it is shown how diagnosis was reached. Provocative factors of periodic hypokaliemic paralysis are discussed and their importance in anaesthesia is emphasised.
Changes of plasma catecholamines during surgery performed in the presence of a combined electrical stimulation analgesia were studied in 11 patients undergoing open heart surgery and in 5 patients undergoing abdominal operations. Stimulation was applied through 2 needles attached subcutaneously to each ear. In 8 of the 11 patients undergoing open heart surgery an up to 20 fold increase in the level of adrenaline in plasma was observed intraoperatively indicating a massive activation of the adrenal medulla. Adrenaline remained elevated also in the postoperative period. The level of noradrenaline did not increase either during the intra- or during the postoperative period. In contrast no changes in adrenaline or noradrenaline could be demonstrated in the remaining 3 patients in whom the concentration of the catecholamines was in the lower normal range. In 5 patients with abdominal surgery noradrenaline was elevated additionally to the increase of adrenaline in the intra- and postoperative period. The increase in the activity of the sympathetic nervous system was associated in these patients with an increase in heart rate and systolic as well as diastolic blood pressure. On the basis of these results the use of a combined electrical stimulation analgesia for abdominal surgery in patients at risk and for open heart surgery is questioned.
The influence of neuroleptanalgesia and halothane-N2O-anaesthesia on the activity of the sympathetic nervous system was studied continuously in the intra- and postoperative period in 2 groups of 10 patients undergoing abdominal operations. In the neuroleptanalgesia-group the noradrenaline level in plasma rose continuously during the course of the operation and this increase was highly significant. The adrenaline level in plasma increased as well, however this increase did not depend on the duration of the operation. In the halothane-N2O-group only a small increase of both adrenaline and noradrenaline in plasma could be demonstrated intraoperatively. One hour after the end of the operation the plasma levels of adrenaline and noradrenaline were elevated in both groups. The noradrenaline level was even higher after neuroleptanalgesia. Four hours after the end of surgery the levels of adrenaline and noradrenaline started to decrease, but were still above the preanaesthetic level. The increase of the concentration of catecholamines in plasma indicating an activation of the sympathetic nervous system was not associated with a corresponding increase in heart rate and blood pressure intra- as well as postoperatively in either group. Only in the neuroleptanalgesia-group was there a small, but insignificant increase of the systolic and diastolic pressure postoperatively.
Five cases of non-biguanide-induced lactic acidoses are reported. The key role of the liver and kidneys in lactate metabolism is stressed. The patients at risk are enumerated and the particular stress in connexion with surgical procedures and the dangers of fructose infusions are pointed out. The coagulation disturbances due to lactic acidosis are discussed. The different operative procedures and their effectiveness are discussed.
Hereditary fructose intolerance (HFI) was diagnosed in a 61 year-old male patient on account of liver dysfunction followed by prolonged shock immediately after the administration of a fructose and lactose infusion postoperatively. The diagnosis of HFI was based on an increased value of fructose, hypoglycaemia, lactic acidosis and diminution of the phosphate level in combination with the typical family history. The patient's children showed a normal reaction to fructose administration. The therapy included glucose, insulin and heparin administration, balance of acidosis and partial exchange of blood, which resulted in improvement in the glucose level, coagulation factors and acidosis, but could not prevent further liver damage and uraemia with a fatal outcome.