Preoperative fibre and postoperative ileus.
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Biomedical subjects
Publications and source records attributed to D Radrizzani.
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In a 3 year period (1975-77) 50 patients have been admitted to the I.C.U. of Polyclinic Hospital of Milan for poisoning from mushrooms of Amanita genus. In 47 cases the diagnosis was confirmed "a posteriori" by serum or urinary detection of amtoxins and/or by clinical evidence of typical liver injury. Besides the symptomatologic support, the therapeutic treatment included combined removal procedures, such as peritoneal dialysis, plasmapheresis, forced diuresis. The detection by radioimmunoassay of amatoxins [6] in the serum and in the urine of these patients proves that this therapeutic treatment can be effective within about 36 hours from ingestion time. The intensive medical care and the removal approach yielded as the whole favourable results in our patients (overall mortality was 6 patients, i.e. 12,7%). It should moreover be emphasized that of the 35 patients, who had been treated with early removal techniques, 12 with ascertained amanita poisoning, had neither clinical nor biochemical evidence of hepatic damage; 14 had a moderate liver damage; 9 experienced a severe liver failure and hepatic coma occurred in 4 of the latter. These poor results can be ascribed to the severity of the poisoning as well as to a peculiar kinetic of amatoxins in each subject.
Echocardiography is a non invasive technique particularly useful to assess both hemodynamics and left ventricular performances; different methods have been proposed to evaluate echocardiographically the cardiac output. The aim of this work is to suggest a new method (planimetry of the area enclosed by echoes from the mitral valve) stating its advantages and limits and to test three already known methods (cubes method, method of Lalani and Lee, method of Rasmussen and coll.) comparing them to thermodilution. In 24 patients admitted in our Coronary Care Unit for acute myocardial infarction 30 measurements have been performed simultaneously with echocardiography and thermodilution. Statistical analysis (correlation coefficient with the method of the square minimums and Student's 't') of the results has shown that the cubes method is unprecise (P = NS) and unbiased (d = 0.97 +/- 15.46); Lalani-Lee method is unprecise (P = NS) and biased (d = 9.64 +/- 21.36) by a systematic underestimate error concealed by the poor precision; Rasmussen and coll. method is precise (P < 0.01) but biased (d = --3.03 +/- 5.5), the systematic mistake being entirely due to the group of patients with abnormal hemodynamics. Our method is precise (P < 0.01) and unbiased (d = --0.04 +/- 9.62) in patients both with normal and abnormal hemodynamics. Therefore this method offers the following advantages: 1) it is unbiased, even in the presence of abnormal left ventricular performance; 2) it is sufficiently precise, having a correlation coefficient with thermodilution of r = 0.80; 3) it measures directly the amount of flow due to the atrial systole; 4) the measurement is rapid and hardly biased by the reader.
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Traumatized critically ill patients with either a moderate or severe catabolic response were studied. Patients were randomly allocated to receive an intravenous solution which was either protein-free or contained protein and hypertonic glucose. The overall energy intake in both groups was equivalent to each patient's daily requirement. In both the moderately catabolic and severely catabolic patients the urinary nitrogen loss with the protein-free solution was negatively correlated to the energy intake/energy need ratio (p less than 0.01, moderate catabolism; p less than 0.001, severe catabolism). The ratio of energy intake/energy need was correlated with the nitrogen loss. From the resultant straight line, the obligatory nitrogen loss was determined for those patients receiving the protein containing solution (test diet). The net protein utilization was subsequently calculated using this value of the obligatory nitrogen loss. The net protein utilization was inversely correlated with the severity of trauma. It was significantly (p less than 0.005) greater in the patients with a moderate catabolic response. In the acute postinjury phase, the net protein utilization of infused amino acids was similar to that for protein fed orally to normal healthy subjects.
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The use of total parenteral nutrition after acute injury, either surgical or accidental, is widely accepted for its important benefits, although it is not yet completely understood whether a reduction of body protein catabolism can be effectively achieved. We applied total parenteral nutrition to 14 critically ill patients after either trauma or major surgery. Their daily nitrogen balance, urinary 3-methylhistidine and creatinine excretion, and molar 3-methylhistidine/creatinine ratio, during initial 24-hr fasting period, were respectively -0.19 +/- 0.01 (SEM) g kg-1, 5.46 +/- 0.47 mumol kg-1, 27 +/- 4 mg kg-1, and 0.030 +/- 0.005. Daily nonprotein calorie intake of 31.11 +/- 0.58 kcal kg-1, as glucose, and administration of nitrogen 0.350 +/- 0.004 g kg-1, as 10% crystalline L-aminoacids solution, and insulin 1 IU every 5.03 +/- 0.14 g of glucose, resulted in progressive decline of urinary 3-methylhistidine (4.21 +/- 0.43 mumol kg-1, p less than 0.001), creatinine (22 +/- 2 mg kg-1, NS), and their molar ratio (0.022 +/- 0.002, NS). Mean nitrogen balance resulted in 0.032 +/- 0.008 g kg-1. Since urinary 3-methylhistidine role as a marker of protein catabolism is well established, its decrease under total parenteral nutrition together with greatly improved nitrogen balance, demonstrates that our treatment can effectively quench protein catabolism, meanwhile enhancing protein synthesis.
In patients with trauma or sepsis, carnitine is known to be produced to a greater extent; deficient production could impair the energy management that is required in such patients. To clarify the requirements of carnitine after injury, we studied carnitine elimination (in 10 critically ill injured patients) both during fasting and early parenteral nutrition. Increased carnitine (mainly, free) output after injury (9.36 +/- 1.63 mumol/kg p less than 0.02 vs reference) was negatively related to nitrogen balance (p less than 0.05) and positively to 3-methyl-histidine output (p less than 0.01), acting as a market of body mass catabolism. The output of both total and free carnitine progressively decreased (p less than 0.01) throughout the course of total parenteral nutrition. In conclusion, our data definitively suggest that carnitine loss after injury reflects body cell mass wastage and does not necessarily mean an increased need.
BACKGROUND: Throughout the world, the cost of critical care medicine is increasing more than the overall health care cost. Thus, a higher attention to improve the efficiency of the use of ICU resources is indispensable. The objective of this study was the development of a simple and reliable tool for the evaluation of the appropriateness of ICU utilization. METHODS DESIGN: A repeated cross-sectional data collection was performed twice a week, during a 61-day study period. SETTING: Twenty-three Italian general ICUs. PATIENTS: All patients present in the 23 ICUs on the 17 index days. INTERVENTIONS: On each index day, patients were checked for receiving ventilation/CPAP, pulmonary arterial pressure monitoring, intracranial pressure monitoring, vaso-active drug infusion and hemodialysis-ultrafiltration. Simultaneously, each ICU bed was assessed for its technical and personnel facilities in order to estimate the deliverable level of care. RESULTS: A total of 1250 patients were studied, for a total number of 7533 patient-days. The overall occupancy rate per ICU was 83.8% (-range: 54.4% to 96.1%). The high-level occupancy rate (rate of patients requiring high level of care and actually occupying high-facility beds) was 69.4% (range: 25.0% to 149.0%), while the corresponding low-level occupancy rate was 101.1% (range: 31.3% to 329.4%). CONCLUSIONS: Our model clearly showed up a certain degree of inappropriateness in the use of ICU resources. Most of the ICUs (69.6%) used a very large proportion of their high-facility beds for patients who did not need high-level care. Being very simple, our method could represent a useful tool for continuous evaluation of the appropriateness of resource utilization in the ICU.
The aim of this study was to evaluate the kinetics of arterial plasma amino acid profile during the first 48 h of clinical TPN in order to assess the time necessary to reach the steady-state condition during infusion. Each patient was treated with one of three different amino acid solutions yielding, in the same nitrogen intake, different intakes of individual amino acids. We found four different kinetics for the administered amino acids: an increase of plasma levels immediately after the start of the TPN with no variations during the steady period; the same trend with the steady-state obtained after 6-24 h of TPN infusion; no influence at all; a decrease of fasting plasma levels with the steady-state attained variably during the study period. Each given amino acid showed a different trend partly depending on the supply, suggesting that the steady-state was reached sooner for most amino acids, when the supply was larger. With lower intakes, plasma levels were unaffected or decreased. We conclude that in critically ill patients at least 24 h are needed to obtain stable arterial plasma amino acid concentration during TPN with adequate intakes of amino acid. Knowledge offers the possibility for a quick and accurate assessment of the adequacy of a given preparation (tailored for critically ill patients), it reduces the time span of the study and, as a consequence, the influence of varied metabolic conditions.
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Blood stored in acid-citrate-dextrose (ACD) shows a progressive decrease in 2,3-diphosphoglycerate (DPG) content. Since the decrease in DPG increases hemoglobin oxygen affinity, which in turn may reduce tissue and venous PO2 and peripheral oxygen delivery, many efforts have been made to preserve or restore DPG levels in stored blood. An in vivo rejuvenating technique, employing fructose-1,6-diphosphate (FDP) at a mean dosage of 1 mmol kg-1 day-1 of phosphate, to increase the DPG circulating level in multi-transfused patients is proposed. Eighteen patients, who received at least one-third of their estimated blood volume (3990 +/- 480 (SEM) ml of ACD stored blood) in blood transfusion, were treated: nine with inorganic phosphate, and nine with FDP. Basal DPG was very low in both groups: 12.61 +/- 1.34 (SEM) and 10.42 +/- 0.98 (SEM) mumol g-1, respectively (normal value is 14.5 mumol g-1, at pH 7.40). However, DPG values increased significantly and promptly in patients receiving FDP, whereas in cases of inorganic phosphate administration, it was not significantly raised over the basal value until the third day. Phosphatemia remained normal and constant with FDP, but it rose significantly on the third day of treatment with inorganic phosphate. FDP appears to consistently and rapidly increase DPG levels after transfusion with blood stored in ACD, and to be particularly safe.
AIM: We evaluated muscle-visceral interorgan flux of substrates in 8 critically ill patients in the flow phase after injury. SETTING: This study was conducted on critically ill patients admitted in ICU. PATIENTS: 8 patients were studied immediately after injury. RESULTS: We measured leg flux for oxygen, amino acids, glucose, lactate pyruvate, keton bodies, free fatty acids (FFA), free and total carnitine, and whole body oxygen consumption, nitrogen (N) balance and 3-methyl hystidine (3MEH) excretion during fasting and the second day of metabolic treatment (10.7 +/- 0.06 g x N x m-2 e 1035.5 +/- 3.9 kcal x m-2 x die). During fast the leg shows a net release of N, pyruvate, FFA and free carnitine while glucose, lactate and keton bodies fluxes are not different from zero. The energy balance of the leg is markedly negative (substrate for 79 kcal x m-2 burned for leg energy requirement and 347 kcal x m-2 released as a such). Assuming the body muscle tissue 4.5 times the leg tissue and knowing whole body energy balance, we were able to assess that the non muscular (visceral) part of the body resulted in a consistently positive energy balance. The metabolic treatment is able to match the energy expenditure and the substrate efflux of the leg (and the whole body muscle tissue). In fact the efflux of amino acids and FFA is reduced pyruvate blunted while glucose is remarkably taken up (the uptake of the whole muscle tissue accounted for 72% of the daily load). At the same time, the treatment blunts leg free carnitine and reduces body 3MEH output. Moreover, the caloric balance of the non muscular part of the body remains positive even if the qualiquantitative uptake of substrates is different from fasting. CONCLUSION: Substrates for energy requirements of visceral tissue came from muscular tissue. The metabolic treatment is able to modulate this process.