[Parenteral nutrition at home].
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Biomedical subjects
Publications and source records attributed to M E Koller.
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The incidence of postdural puncture headache after spinal anaesthesia with two types of 26- and 29-gauge needles was investigated in 149 patients less than 30 years old. Ten patients, (6.7%), six men and four women, developed typical symptoms of postdural puncture headache, while six (4.0%) developed headache of other origin. There were no headaches in the 29-gauge group. Spinal anaesthesia in four patients (8%) was impossible to perform with the 29-gauge needle. By using the latter, spinal anaesthesia can be given to young adults with little risk of postdural puncture headache.
Reports of midazolam interaction with vecuronium in animals prompted us to compare midazolam (0.25 mg kg-1) with thiopentone (5 mg kg-1) for possible interactions with vecuronium in patients, when used for induction of anaesthesia. After the administration of either of the two induction agents, the patients received vecuronium 0.1 mg kg-1. The onset time, duration of action and 25-75% recovery index of the neuromuscular blockade were recorded by measuring the force of thumb adduction evoked by ulnar nerve stimulation. We found no differences between patients receiving either midazolam or thiopentone in their response to vecuronium. In three of the ten patients receiving midazolam, the injection of this drug produced a 8-29% reduction of the initial twitch height.
Dose-duration relationships for vecuronium were determined and the duration of action produced by vecuronium 0.3 mg kg-1 shown to equal that of pancuronium 0.1 mg kg-1. Using these doses, the neuromuscular blocking properties and cardiovascular effects of the two drugs were compared. With large dose administration of vecuronium (0.3 mg kg-1), both the onset time (mean 81 s) and the 25-75% recovery index (mean 13.9 min) were about one-half those associated with pancuronium (mean 168.5 s and 29.3 min, respectively). The duration of action until 25% recovery was similar with both drugs. There was no evidence of cardiovascular instability with the large dose of vecuronium. Heart rate, however, was significantly slower (range 89.7-94.2% of control) 2-20 min after the injection of vecuronium. Vecuronium 0.3 mg kg-1 may have more favourable neuromuscular blocking effects than pancuronium 0.1 mg kg-1 and may be preferable to pancuronium when prolonged neuromuscular blockade is required.
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A patient with severe arterial hypoxemia in adult respiratory distress syndrome (ARDS) secondary to a fractured femur is reported. A marked discrepancy between the clinical condition and laboratory findings was observed. At one point, PaO2 was below 4 kPa (30 mm Hg) on F1O2 0.21 without signs of tissue hypoxia. This patient illustrates beneficial effects of a leftward shift of the oxyhemoglobin dissociation curve.
The effects of spinal cord transection and acidosis on succinylcholine (SCC)-induced hyperkalemia were studied in Sprague-Dawley rats. The effectiveness of pretreatment with subparalyzing doses ("self-taming") of SCC or with the cholinesterase inhibitor hexafluorenium bromide in preventing hyperkalemia was also studied. The increase in plasma potassium after administration of SCC (1 mg/kg) was found to be significantly increased 10 days after spinal cord transection. This potassium increase could not be prevented by pretreatment with either hexafluorenium (0.3 mg/kg) or subparalyzing doses (0.15 mg/kg) of SCC. Respiratory acidosis caused an increase in plasma K+ in both normal and in spinal cord transected rats. Acidosis had a synergistic effect on succinylcholine-induced hyperkalemia. These findings support the clinical practice of not using succinylcholine in patients at risk of having a pathological sensitivity to SCC. Furthermore, SCC may be especially dangerous when administered to patients who are acidotic.
The hemodynamic effects of changes in PaCO2 during intermittent positive pressure ventilation (IPPV) were studied in nine dogs with acute cardiac tamponade. During steady state light thiopental anesthesia, measurements were performed during hypocarbia (24.0 +/- 2.6), normocarbia (40.4 +/- 2.4), and hypercarbia (56.8 +/- 3.1 mm Hg; mean +/- SD). The study was carried out at a standardized level of cardiac tamponade that gave a 60% reduction in cardiac output (CO) at normocarbia. Changes in airway pressure were avoided by adding CO2 to the inspiratory gas to obtain the desired PaCO2. Hypercarbia increased pericardial pressure 2-4 mm Hg and significantly decreased CO. During hypocarbia CO increased as pericardial pressure decreased 3-6 mm Hg. These findings are the reverse of changes seen when tamponade is not present. The changes in pericardial pressure most likely influence myocardial tone and cardiac volume and, thus, CO. The results suggest that patients with cardiac tamponade requiring general anesthesia should not breathe spontaneously if there is any danger of respiratory depression and hypercarbia.
Rat liver mitochondria accumulate protoporphyrin IX from the suspending medium into the inner membrane in parallel with the magnitude of the transmembrane K+ gradient (K+in/K+out). Only protoporphyrin IX taken up in parallel with the transmembrane K+ gradient is available for haem synthesis. Coproporphyrins (isomers I and III) are not taken up by the mitochondria. The results support the suggestion by Elder & Evans [(1978) Biochem. J. 172, 345-347] that the prophyrin to be taken up by the inner mitochondrial membrane belongs to the protoporphyrin(ogen) IX series. Protoporphyrin IX at concentrations above 15 nmol/mg of protein has detrimental effects on the structural and functional integrity of the mitochondria. The relevance of these effects to the hepatic lesion in erythropoietic protoporphyria is discussed.
The clinical and radiological features of a dominant bone disorder found in six members of the same family are described. The bone disorder was mainly characterized by endosteal cortical thickening of long tubular bones and bowing of the weight-bearing ones. The clinical symptoms were waddling gait, muscle weakness and leg pains, and there was a tendency to fractures. All affected individuals had icthyosis of slight or moderate degree.
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Thirty children with acute lymphoblastic leukemia were monitored with serial serum ferritin determinations for up to 17 months. In children with acute lymphoblastic leukemia before initiation of therapy, or in relapse, the mean serum ferritin concentration was 636 microgram/l. In children who went into primary remission. the mean serum ferritin concentration fell from 265 microgram/l prior to start of treatment, to 161 microgram/l after 3 months of treatment. Five patients relapsed. Their serum ferritin levels prior to the relapses ranged from 7 to 135 microgram/l. At the time of relapse a further increase in serum ferritin was found in only 2 of the children. Thus, whereas high serum ferritin levels may signal disease activity in acute lymphoblastic leukemia, a normal serum ferritin level does not exlude disease activity or impending relapse.
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1. The uptake of deuteroporphyrin by isolated rat liver mitochondria proceeds by two different mechanisms, a passive binding, and a mechanism sensitive to CCCP plus valinomycin, with different pH, temperature and time dependencies. 2. The CCCP plus valinomycin-sensitive uptake of deuteroporphyrin parallels the transmembrane potassium gradient ([K+in]/[K+out]). 3. Only that deuteroporphyrin taken up in parallel to the transmembrane potassium gradient is accessible to ferrochelatase. 4. The uptake of deuteroporphyrin at high concentrations is followed by series of damaging effects on the mitochondria: uncoupling, dissipation of the mitochondrial energy potential, increased ion permeability and leakage of endogenous potassium. 5. The detrimental effects of porphyrins at high concentrations on mitochondrial structure might explain the apparently unrelated metabolic aberrations characteristic of certain porphyric diseases.
Free erythrocyte protoporphyrin (FEP) and serum ferritin have been determined in 57 healthy children and in 25 children with varying degrees of iron deficiency. FEP was found to be inversely correlated to the concentration of hemoglobin (r = -0.80) as well as to serum ferritin (r=-0.64). Elevated FEP was found in children with hemoglobin less than 12.5 g/dl, or serum ferritin less than 8 microgram/l. In a group of apparently hematologically normal children between the age of 10--14 years (hemoglobin greater than 12.5 g/dl), a 2-month-trial of iron medication resulted in an increase in hemoglobin and ferritin, and a decrease in FEP, indicating suboptimal supply of iron for hemoglobin synthesis before iron medication. In a patient with iron deficiency (FEP 15.3 mumole/l, hemoglobin 5.2 g/dl), iron therapy was followed by a rapid fall in FEP before any changes in hemoglobin, serum iron transferrin saturation and ferritin could be detected. The rapid fall in FEP during start of treatment in iron deficiency makes FEP a sensitive biochemical parameter on iron homeostasis in iron deficiency anemia.