% vol = 15 number = 3 prevlink = 120 nextlink = 132 titolo = "ASSESSMENT OF THE ROLE OF ARTIFICIAL NUTRITION IN THE MANAGEMENT OF CRITICALLY ILL BURN PATIENTS" volromano = "XV" data_pubblicazione = "September 2002" header titolo %>
SUMMARY. This study considering the effects of artificial nutrition in burn patients was carried out in 15 females and 25 males admitted to a burns unit in Egypt between January 2000 and January 2001. The burn surface was 25-50% and the patients’ age ranged from 15 to 50 yr. All the patients received standard resuscitation measures during the first 48 h. On day 3, the patients were divided into two groups. One group received ordinary enteral nutrition plus artificial nutrition through a peripheral vein, while the other control group received only enteral nutrition. Each group was considered with regard to anthropometric measurements and laboratory analyses. The group receiving artificial nutrition was found to have excellent results, compared with the other group that received only enteral nutrition - body weight was maintained or slightly increased, while in the other group body weight markedly decreased. There was an increase in S. proteins, S. albumin, and S. transferrin in the first group. It is concluded that artificial nutrition can play an important role in the management of critically ill burn patients, in addition to the oral route, improving patient immunity and healing capacity, reducing the infection rate, and decreasing hospital stay.
Extensively burned patients make up a subgroup of critical patients in whom the nutri-metabolic support is of maximum importance, owing to the fact that thermal injury induces a hypermetabolic response that is prolonged until wound coverage, in the form of negative nitrogen loss, malnutrition, and immunological deficiency, thus predisposing the patient to frequent infection, poor wound healing, and increased mortality.
Thermal injury also induces the release of counter-regulatory hormones and other mediators that favour protein catabolism - mainly muscular lipolysis and gluconeogenesis as well as alteration of thermoregulation, raising the equilibrium point.
Full nutritional support has become of great importance in the management of these patients in order to reduce complications and facilitate wound closure and the patient’s recovery. Enteral feeding is the route of choice as it is the cheapest, safest, and most physiological way and its use prevents the onset of certain complications (bacterial translocation, Curling ulcer). Enteral feeding may not however cover all a burn patient’s nutritional needs and parenteral nutrition should be associated to it.
In pre-Christian Egypt, Herodotus administered a nutrient enema. In the 16th century the surgeon and physiologist Hunter was the first to introduce a hollow flexible tube into the stomach for nutritional purposes. In 1656 a physician demonstrated infusion therapy in a dog - he infused wine into the animal until it got drunk. In 1712 W. Courten administered fat infusion therapy. At the end of the 19th century Lodrer recommended a combination of glucose and saline infusion.
In 1937 Elman introduced amino acid infusion therapy in man.
In 1945 Murlin and Richie intravenously injected fat emulsion in a dog. The injection was however accompanied by serious complications.
In 1961 Wretlind succeeded in developing a metabolizable and safe intravenous fat emulsion for clinical use.
This study was carried out in 40 burn patients admitted to the burns unit in Assiut University Hospital, Egypt, between January 2000 and January 2001. The burn surface ranged from 25 to 50% and the patients’ age from 15 to 50 yr (mean age, 31.5 yr); there were 15 females and 25 males (Table I).
<% createTable "Table I "," Hospital Stay","; Cases no. 20;Control cases no. 20@;Age range (yr) (mean ± SD);32.53 ± 11.65 (15-50);32.80 ± 10.30 (18-50)@;Female Male;7 (35%) 13 (65%);8 (40%) 12 (60%)@;Hospital stay (days); 31.33 ± 6.40;49.73 ± 13.79 p = 0.001","",4,300,true %>Each patient received standard resuscitation measures during the first 48 h (fluid resuscitation with the Parkland formula, painkiller i.v., and broad-spectrum antibiotics).
On day 3, the patients were divided into two groups. The first group (20 cases) received ordinary enteral nutrition plus artificial nutrition through a peripheral vein in the form of 4 ampoules of concentrated glucose (25%) on glucose (5%)+, 10 units of crystalline insulin every 8 h, amino acid in the form of amino sterile every 12 h, and fat in the form of intralipid every 12 h, according to a standard caloric requirement formula (Currie formula). The twenty patients in the second, control group received only enteral nutrition according to standard caloric requirements (Figs. 1, 2).
<% immagine "Fig. 1","gr0000001.jpg","Patent receiving artificial nutrition.",230 %> | <% immagine "Fig. 2","gr0000002.jpg","Artificial nutritional kit.",230 %> |
Each group was considered with regard to the following parameters:
This study was carried out in 40 burn patients divided into two groups (20 per group). We made the following findings (Table II):
<% createTable "Table II "," Descriptive cases and control and significance between the two groups",";Variable;Cases;Control;p@;Age (yr);32.53 ± 11.65;32.80 ± 10.30;0.948 n.s.@;Sugar 1;5.16 ± 2.14;4.98 ± 1.52;0.793 n.s.@;Sugar 2;5.15 ± 1.61;5.37 ± 1.20;0.667 n.s.@;Sugar 3;5.19 ± 1.01;5.66 ± 1.06;0.229 n.s.@§1,4§Proteins:@;Total protein 1;41.87 ± 9.51;63.47 ± 6.95;0.000 ***@;Total proteins 2;61.73 ± 8.12;56.40 ± 5.80;0.048 *@;Total protein 3;83.26 ± 4.79;52.33 ± 5.62;0.000 ***@;Albumin 1;28.07 ± 5.713;35.80 ± 4.66;0.000 ***@;Albumin 2;39.80 ± 3.57;32.66 ± 4.58;0.000 ***@;Albumin 3;48.33 ± 3.49;30.60 ± 2.55;0.000 ***@;Transf. 1;171.27 ± 28.43;175.33 ± 25.61;0.684 n.s.@;Transf. 2;261.26 ± 51.05;174.0 ± 15.02;0.000 @;Transf. 3;374.66 ± 13.02;169.33 ± 28.42;0.000 ***@§1,4§Liver function:@;SGOT 1;23.46 ± 3.68;25.20 ± 3.72;0,145833333@;SGOT 2;32.20 ± 6.74;27.67 ± 5.08;0.047 *@;SGOT 3;32.40 ± 4.42;28.73 ± 3.01;0.013 *@;SGPT 1;23.66 ± 3.84;26.46 ± 4.38;0.074 n.s.@;SGPT 2;31.86 ± 4.37;29.73 ± 3.89;0.170 n.s.@;SGPT 3;31.60 ± 3.16;29.67 ± 3.59;0.129 n.s.@;Bilirubin 1;4.48 ± 1.57;4.35 ± 1.07;0.788 n.s.@;Bilirubin 2;8.46 ± 2.41;5.53 ± 1.04;0.000 ***@;Bilirubin 3;8.61 ± 4.05;6.53 ± 1.55;0.074 n.s.@;ALP 1;198.0 ± 55.31;107.66 ± 3.74;0.000 ***@;ALP 2;191.40 ± 36;114.53 ± 43.56;0.000 ***@;ALP 3;178.93 ± 3.44;120.8 ± 44.57;0.000 ***@§1,4§Total lipids@;1;156.33 ± 9.86;106.0 ± 4.54;0.000 ***@;Cholesterol 2;183.67 ± 22.55;105.66 ± 31.5;0.000 ***@;Cholesterol 3;193.93 ± 34.7;116.33 ± 33.88;0.000 ***@;Triglycerides 1;67.53 ± 12.24;62.80 ± 6.00;0.190 n.s.@;Triglycerides 2;117.00 ± 58.94;81.00 ± 21.39;0.034 *@;Triglycerides 3;163.33 ± 66.08;96.66 ± 24.39;0.001 **@;LDL 1;63.20 ± 8.88;40.33 ± 5.16;0.000 ***@;LDL 2;81.33 ± 19.86;52.40 ± 10.06;0.000 ***@;LDL 3;98.40 ± 19.97;62.20 ± 14.34;0.000 ***@;HDL 1;46.06 ± 20.92;67.73 ± 3.39;0.000 ***@;HDL 2;64.33 ± 15.9;74.33 ± 8.42;0.040 *@;HDL 3;94.33 ± 29.39;85.33 ± 12.45;0.284 n.s.@§1,4§Blood picture:@;HB 1;10.26 ± 0.8967;10.233 ± 2.865;0.973 n.s.@;HB 2;10.686 ± 1.09;9.966 ± 0.855;0.049 *@;HB 3;11.426 ± 0.535;9.50 ± 0.6268;0.000 ***@;RBC 1;3.28 ± 0.2366;3.306 ± 0.2017;0.742 n.s.@;RBC 2;3.646 ± 0.614;3.353 ± 0.1885;0.088 n.s.@;RBC 3;4.0467 ± 0.5235;3.3933 ± 0.2549;0.000 ***@;WBC 1;4.433 ± 0.403;4.2667 ± 0.235;0.177 n.s.@;WBC 2;6.253 ± 1.458;4.45 ± 0.485;0.000 ***@;WBC 3;5.88 ± 1.05;4.67 ± 0.650;0.001 **@;Plt 1;162.00 ± 24.698;29.60 ± 2.52;0.000 ***@;Plt 2;238.667 ± 49.94;31.40 ± 2.72;0.000 ***@;Plt 3;234.133 ± 58.619;32.00 ± 2.53;0.000 ***@;Ht 1;30.40 ± 2.87;29.60 ± 2.529;0.425 n.s.@;Ht 2;32.33 ± 2.79;31.4 ± 2.72;0.362 n.s.@;Ht 3;33.466 ± 4.7339;32.00 ± 2.535;0.099 n.s.@§1,4§Kidney function:@;Urea 1;3.153 ± 0.778;3.5133 ± 1.019;0.286 n.s.@;Urea 2;3.693 ± 1.132;4.00 ± 1.13;0.464 n.s.@;Urea 3;4.40 ± 1.58;4.76 ± 1.45;0.521 n.s.@;Creat. 1;44.26 ± 5.035;43.60 ± 3.50;0.677 n.s.@;Creat. 2;55.60 ± 10.554;53.133 ± 5.034;0.426 n.s.@;Creat. 3;60.333 ± 9.34;60.20 ± 10.29;0.971 n.s.","n.s.=non significantWe also performed a paired T test between the variables in each group and made the following findings (Table III):
<% createTable "Table III "," Paried t-test for comparison betweeen variables in each group",";Variable;Cases;Control@;Sugar 1 - sugar 2;0.961 n.s.;0.040 *@;Sugar 1 - sugar 3;0.947 n.s.;0.023 *@;Sugar 2 - sugar 3;0.903 n.s.;0.081 n.s.@;T. prt 1 - t. prt 2;0.000 ***;0.003 **@;T. prt 1 - t. prt 3;0.000 ***;0.01 *@;T. prt 2 - t. prt 3;0.000 ***;0.026 *@;Albumin 1 - Albumin 2;0.000 ***;0.034 *@;Albumin 1 - Albumin 3;0.000 ***;0.002 **@;Albumin 1 - Albumin 2;0.000 ***;0.025 *@;Transf. 1 - transf. 2;0.000 ***;0.844 n.s.@;Transf. 1 - transf. 3;0.000 ***;0.592 n.s.@;Transf. 2 - transf. 3;0.000 ***;0.572 n.s.@;SGOT1 - SGOT2;0.000 ***;0.122 n.s.@;SGOT1 - SGOT3;0.000 ***;0.026 *@;SGOT2 - SGOT3;0.912 n.s.;0.382 n.s.@;SGPT1 - SGPT2;0.000 ***;0.011 *@;SGOT1 - SGOT3;0.000 ***;0.024 *@;SGOT2 - SGOT3;0.844 n.s.;0.937 n.s.@;Bilirubin 1 - Bilirubin 3;0.000 ***;0.000 ***@;Bilirubin 2 - Bilirubin 3;0.813 n.s.;0.001 **@;ALP1 - ALP2;0.693 n.s.;0.410 n.s.@;ALP1 - ALP3;0.292 n.s.;0.137 n.s.@;ALP2 - ALP3;0.348 n.s.;0.020 *@;Cholest. 1 - Cholest. 2;0.001 **;0.962 n.s.@;Cholest. 1 - Cholest. 3;0.001 **;0.307 n.s.@;Cholest. 2 - Cholest. 3;0.216 n.s.;0.060 n.s.@;Tryg. 1 - Tryg. 2;0.002 **;0.004 **@;Tryg. 1 - Tryg, 3;0.000 ***;0.000 ***@;Tryg. 2 - Tryg. 3;0.004 **;0.015 *@;LDL1 - LDL2;0.002 **;0.000 ***@;LDL1 - LDL3;0.000 ***;0.000 ***@;LDL2 - LDL3;0.009 **;0.001 **@;HDL1 - HDL2;0.008 **;0.010 *@;HDL1 - HDL3;0.000 ***;0.000 ***@;HDL2 - HDL3;0.001 **;0.003 **@;HB1 - HB2;0.071 n.s.;0.695 n.s.@;HB1 - HB3;0.000 ***;0.300 n.s.@;HB2 - HB3;0.009 **;0.005 **@;RBC1 - RBC2;0.019 *;0.582 n.s.@;RBC1 - RBC3;0.000 ***;0.372 n.s.@;RBC2 - RBC3;0.016 *;0.472 n.s.@;WBC1 - WBC2;0.000 ***;0.170 n.s.@;WBC1 - WBC3;0.000 ***;0.013 *@;WBC2 - WBC3;0.265 n.s.;0.050 n.s.@;Plt 1 - Plt 2;0.000 ***;0.019 *@;Plt 1 - Plt 3;0.000 ***;0.026 *@;Plt 2 - Plt 3;0.000 ***;0.454 n.s.@;Ht 1 - Ht 2;0.136 n.s.;0.019 *@;Ht 1 - Ht 3;0.082 n.s.;0.026 *@;Ht 2 - Ht 3;0.443 n.s.;0.454 n.s.@;Urea 1 - Urea 2;0.044 *;0.064 n.s.@;Urea 1 - Urea 3;0.004 **;0.001 **@;Urea 2 - Urea 3;0.062 n.s.;0.002 **@;Creat. 1 - Creat. 2;0.002 **;0.000 ***@;Creat. 1 - Creat. 3;0.000 ***;0.000 **@;Creat. 2 - Creat. 3;0.043 *;0.002 **@;Na 1 - Na 2;0.002 **;0.000 ***@;Na 1 - Na 3;0.001 **;0.000 ***@;Na 2 - Na 3;0.808 n.s.;0.821 n.s.@;K 1 - K2;0.018 *;0.001 **@;K 1 - K3;0.000 ***;0.002 **@;K 2 - K3;0.026 *;0.133 n.s.@;Weight 1 - weight 2;0.001 **;0.027 *@;Weight 1 - weight 3;0.000 ***;0.001 **@;Weight 2 - weight 3;0.000 ***;0.005 **","n.s. = non significant<% immagine "Fig. 5","gr0000005.jpg","Comparison between haemoglobin in cases and controls.",230 %> | <% immagine "Fig. 6","gr0000006.jpg","Comparison between body weight in cases and controls.",230 %> |
<% immagine "Fig. 7","gr0000007.jpg","Comparison between S. cholesterol in cases and controls.",230 %> | <% immagine "Fig. 8","gr0000008.jpg","Comparison between S. triglycerides in cases and controls.",230 %> |
<% immagine "Fig. 9","gr0000009.jpg","Comparison between LDL in cases and controls.",230 %> | <% immagine "Fig. 10","gr0000010.jpg","Comparison between HDL in cases and controls.",230 %> |
<% immagine "Fig. 11","gr0000011.jpg","Comparison between SGOT in cases and controls.",230 %> | <% immagine "Fig. 12","gr0000012.jpg","Comparison between SGPT in cases and controls.",230 %> |
<% immagine "Fig. 13","gr0000013.jpg","Comparison between bilirubin in cases and controls.",230 %> | <% immagine "Fig. 14","gr0000014.jpg","Comparison between ALP in cases and controls.",230 %> |
Burn injury results in profound metabolic abnormalities perpetuated by an exaggerated stress response to injury. Hypermetabolism and marked catabolism with rapid erosion of lean body mass become evident shortly after injury, and much of the mortality and morbidity related to major burns can be attributed to this process, which increases infection risk, decreases the healing rate, and alters cell function.4 Early and continued nutritional support play a major and important role in the management of seriously burned patients.
The hypothesis that gut- or wound-derived bacterial translocation is one of the major triggers of the hypermetabolic response has attracted attention recently. The first goal of nutritional support is thus to prevent nutritional deficiency, while the second is to provide correct nutrition and prevent injury-related adverse complications (bacterial translocation and Curling’s ulcer).5 In large burns, patients may not receive full nutritional support through the enteral route. This may be due to several reasons, such as anorexia or facial burn oedema, and nutrition has to be supplemented by an artificial route.
In this study we found an excellent result in the first group compared with the second group with regard to the following:
Liver function and total lipids showed a slight increase in the first group in contrast to the second group, but remained within normal values.
There was good healing power and preparation for grafts in the first group compared with the second but graft take was equal in the two groups.
In this study no major complications developed during parenteral nutrition except in three patients who developed local thrombophlebitis - this rapidly responded to local anti-inflammatory ointment.
Our results were matched with those of Pascal et al.,7 who gave parenteral ornithine ketoglutarate to burn patients and compared the results with those of patients receiving only enteral nutrition.
We also compared our results with those of Bhava and Bavdekard8 in India, who assessed the role of parenteral nutrition in the management of critically ill burn patients
On the basis of the above results we conclude that artificial nutrition can have an important role in the management of critically ill burn patients, in addition to the oral route, improving patient immunity and healing capacity, reducing the infection rate, and decreasing hospital stay.
Artificial nutrition should be performed with meticulous monitoring and changing of the i.v. catheter every 48 h; in order to obviate metabolic disturbances, the patient should be closely monitored as regards liver function, total lipids, and kidney function.
RESUME. Cette étude considère les effets de la nutrition artificielle dans 40 patients (15 femelles et 25 mâles) hospitalisés dans une unité des brûlures en Egypte dans la période janvier 2000-janvier 2001. L’extension des brûlures variait entre 25 et 50% et l’âge des patients entre 15 et 50 ans. Tous les patients recevaient le traitement standard pour la réanimation pendant les premières 48 h. Le jour 3, les patients ont été divisés en deux groupes. Un groupe a reçu la nutrition normale entérale supplémentée avec la nutrition artificielle à travers une veine périphérique, tandis que l’autre groupe témoin a reçu seulement la nutrition entérale. Tous les deux groupes ont été étudiés pour ce qui concerne les aspects anthropométriques et les analyses de laboratoire. Le groupe qui recevait la nutrition artificielle montrait des résultats excellents par rapport à l’autre groupe qui recevait seulement la nutrition entérale - le poids corporel se maintenait constant ou légèrement augmenté, tandis que dans l’autre groupe il se réduisait en manière marquée. Dans le groupe qui recevait la nutrition artificielle, les Auteurs ont observé une augmentation dans la protéine, l’albumine et la transferrine sérique. Ils concluent que la nutrition artificielle, outre la voie orale, peut jouer un rôle important dans la gestion des patients brûlés en phase critique, en améliorant l’immunité des patients et leur capacité de guérir, réduisant le taux d’infection et diminuant la durée de l’hospitalisation.