Phẫu Thuật Bỏng: Tiếp Cận Và Phương Pháp Điều Trị Từ Trung Quốc (Chinese Burn Surgery)

393
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15  Metabolism in Burns

395
Z. Yang, Chinese Burn Surgery, DOI 10.1007/978-94-017-8575-4_16,
© Springer Science+Business Media Dordrecht and People’s Medical Publishing House 2015
16.1
Enteral Nutrition
Shiliang Wang
16.1.1
Early Enteral Nutrition
Enteral nutrition (EN) has followed a long history, and
hyperalimentation has had an epoch-making signifi cance
since the end of the 1960s. From the 1980s, enterogenous
infection and the complications of the catheter, metabolism,
infection, etc., have been raised, and gradually much atten-
tion has been devoted to EN and especially early feeding. We
began to serially study the effect and mechanism of early EN
since 1985.
Overall, more than 700 rats, guinea pigs, rabbits, mini-
pigs, and 200 burns patient were used to compare early
feeding (EF) with delayed feeding (DF). Placing emphasis
on 21 cases of severe burns (32.8 ± 10.9 years, total body
surface area burned (TBSAB) 45 ± 12.6 %, deep burn
29.8 ± 8.9 %) in 200 burn patients. Feeding was started
within PBH 2 (2 h post-burn, in animals) or PBH 12
(patients) in the EF group and after PBH 48 (animal) or
PBH 72 (patient) in the DF group. In addition, we created
three animal models to study the effect and mechanism of
early feeding.
16.1.1.1 Creation of Three Animal Models
to Study Early Feeding (Figs. 16.1 , 16.2 ,
and 16.3 ) [ 1 – 3 ]
1. The model of gastrostomy and neglecting jejunum in burn
rabbit)
The jejunum is cut off 5 cm under the ligament of
Treitz, close to the distal end of the cut jejunum, end-to-
side anastomosis between the upper end and the side
under the distal end 15 cm from the cut jejunum. The
intestine up to 15 cm of anastomotic stoma is the neglect-
ing jejunum; several interrupted sutures are performed
just above the anastomotic stoma to form an artifi cial
valve to prevent food regurgitation into the neglected
jejunum. This model is used to study the effect of early
feeding post-burn on protecting intestinal mucosa and the
mechanism (Fig. 16.1 ).
2. The model of gastrostomy and central vein, portal vein,
and mesenteric vein catheterization in Gui-zhou
mini-pigs).
This model is used to investigate the effect and its
mechanism of early feeding on central and portal vein
blood fl ow, intestinal absorption function, barrier func-
tion of the intestinal mucosa, and hypermetabolism
(Fig. 16.2 ).
3. The model of gastrostomy and central vein, portal vein,
mesenteric vein, iliac vein, and artery catheterization in
Gui-zhou mini-pigs
One the basis of the model (Fig. 16.2 ), this mode is
used to further study the protection effect of early feeding
and glutamine on intestinal structure and function, and
understanding substance metabolic changes of muscle in
the lower extremities (Fig. 16.3 ).
16.1.1.2 Early Feeding Could Lessen Intestinal
Anoxia Injury and Promote Intestine
Resuscitation [ 4 – 22 ]
Early feeding (EF) post-burn could improve portal and
intestinal blood fl ow, lessen intestinal ischemia and reper-
fusion injury, provide better energy metabolism of intesti-
nal mucosa cells, lower depression of mucosa proliferation
and reparation, and maintain the intestinal structure and
function.
1. Early feeding could lessen intestinal ischemia and anoxia
injury (Tables 16.1 , 16.2 , 16.3 , 16.4 , 16.5 , 16.6 , 16.7 ,
16.8 , and 16.9 )
Early feeding could improve portal and intestinal
blood fl ow and lessen intestinal ischemia and reperfu-
sion injury. EF could lower the reduction of portal and
intestinal blood fl ow, decrease plasma malondialdehyde
(MDA), raise plasma superoxide dismutase (SOD),
decrease mitochondrion MDA of intestinal mucosa
Nutrition in Burns
Shiliang Wang and Shilin Deng
16

396
cells, improve the vessel permeability of the intestine in
rats and mini-pigs with third-degree burns covering
30 % of the TBSA.
Blood from the rat aorta (a) and superior mesenteric
vein (v) should be drawn, hemoglobin (Hb) and blood gas
analysis measured, and the oxygen uptake rate (OUR)
calculated according to the following equation.

Oxygen Uptake Rate
SaO
Hba
SvO
Hbv
SaO
Hba
=
´
-
´
(
)
´
2
2
2
/

Changes in rat intestinal vascular permeability were
measured by 99m Tc labeled albumin (Table 16.9 ).
2. Early feeding could improve the energy metabolism of
intestinal mucosa (Tables 16.10 , 16.11 , 16.12 , and 16.13 )
Treitz ligament
15 cm
5 cm
A
B
Treitz ligament
C
Artificial valve
A
C
B
Intestinal clamp
Fig. 16.1 The model of
gastrostomy and neglecting the
jejunum in rabbits with burns
Jugular vein to
central vein
Gastrostomy
Portal vein
catheterization
Inferior-mesentric
vein catheterization
Fig. 16.2 Model of gastrostomy, central vein, portal vein, and inferior
mesenteric vein catheterization in Gui-zhou mini-pigs
Jugular vein to
central vein
Gastrostomy
Portal vein
catheterization
Inferior-mesentric
vein catheterization
Iliac vein
& artery
catheterization
Fig. 16.3 Model of gastrostomy, central vein, portal vein, inferior mes-
enteric vein, iliac vein and artery catheterization in Gui-zhou mini-pigs



16 Nutrition in Burns

397
Table 16.2 Ileum mucosa blood fl ow in rats with third-degree burns covering 30 % of the TBSA (mv, x
s
±
, n = 10)
PB
0
6 h
1 day
3 days
7 days
10 days
EF
144.3 ± 17.3
85.9 ± 11.1**
94.2 ± 11.7**
117.9 ± 11.5**
147.5 ± 10.5
129.8 ± 12.9*
DF
65.4 ± 12.7
62.2 ± 10.3
99.5 ± 9.3
149.1 ± 8.1
114.6 ± 10.6
vs DF* p < 0.05, ** p < 0.01
Table 16.3 Intestinal oxygen uptake rate (OUR) in rats with third-degree burns covering 30 % of the TBSA (%, x
s
±
, n = 8)
PB
0
6 h
1 day
3 days
7 days
10 days
EF
34.8 ± 3.0
24.1 ± 2.7**
20.1 ± 2.1**
29.3 ± 3.1**
33.9 ± 2.2*
29.7 ± 4.5*
DF
21.6 ± 1.9
14.9 ± 1.8
23.4 ± 2.9
31.1 ± 2.0
24.7 ± 2.4
vs DF * p < 0.05, ** p < 0.01
Table 16.1 Portal blood fl ow in mini-pigs with third-degree burns covering 30 % of the total body surface area (TBSA) [ml/(kg·min), x
s
±
,
n = 6]
PB
0
6 h
4 days
7 days
10 days
EF
25.8 ± 5.2
12.6 ± 3.2**
14.1 ± 2.2**
20.6 ± 2.9
24.4 ± 5.1*
DF
25.7 ± 6.1
6.4 ± 2.8
8.8 ± 3.0
17.3 ± 3.1
16.4 ± 3.3
PB post-burn, EF enteral feeding, DF delayed feeding
vs DF * p < 0.05, ** p < 0.01
Table 16.4 Plasma malondialdehyde (MDA) in rats with third-degree burns covering 30 % of the TBSA (nmol/L, x
s
±
, n = 10)
PBH
0
6
12
24
48
72
EF
2.89 ± 0.85
4.34 ± 1.47
7.21 ± 1.21*
4.44 ± 0.91**
4.88 ± 1.15*
4.21 ± 1.10**
DF
4.39 ± 1.27
10.33 ± 1.00
8.24 ± 1.42
6.98 ± 1.60
6.41 ± 1.20
PBH post-burn hours
vs DF * p < 0.05, ** p < 0.01
Table 16.5 Plasma superoxide dismutase (SOD) in rats with third-degree burns covering 30 % of the TBSA (nU/ml, x
s
±
, n = 10)
PBH
0
6
12
24
48
72
EEF
137.27 ± 22.11
50.87 ± 14.33
86.25 ± 12.83*
91.75 ± 15.14**
117.75 ± 21.86*
130.37 ± 16.91*
DDF
59.00 ± 11.04
63.65 ± 11.04
60.87 ± 14.40
84.87 ± 24.65
99.75 ± 17.25
vs DF * p < 0.05, ** p < 0.01
Table 16.6 Changes in chondriosome MDA in intestinal mucosa cells of rats with third-degree burns covering30 % of the TBSA (nmol/g protein,
x
s
±
, n = 6)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
577 ± 71
764 ± 115*
783 ± 102*
745 ± 104*
709 ± 86
697 ± 98
DF
932 ± 165
1,042 ± 177
905 ± 96
743 ± 108
803 ± 112
vs DF * p < 0.05
Table 16.7 Plasma SOD in adults with burns covering 45 % of the TBSA (nU/ml, x
s
±
)
PBD
1
4
8
14
EF ( n = 11)
106.46 ± 11.17
135.70 ± 14.12*
149.37 ± 21.11*
134.42 ± 18.20*
DF ( n = 10)
111.20 ± 21.30
84.20 ± 11.46
96.64 ± 17.14
102.45 ± 19.53
PBD post-burn day
vs DF * p < 0.01
16.1 Enteral Nutrition

398
Compared with DF, ATP, ADP, energy charge
(ATP+1/2ADP)/(ATP+ADP+AMP), respiratory control
rate (RCR, ST3/ST4), and the ratio of phosphorus to oxy-
gen (P/O) were all increased and AMP decreased in the
jejunal and ileal mucosa of the EF group in rats with third
degree burns covering 30 % of the TBSA.
3. Early feeding could promote proliferation and reparation
of intestinal mucosa
EF could lessen depression of intestine mucosa prolif-
eration and repair after burn injury, reducing the drop in
the intestinal mucosa incorporation rate of 3 H thymidine
( 3 HTIR), the incorporation rate of 3 H uridine, ( 3 HUIR),
the incorporation rate of 3 H leucine ( 3 HLIR), proliferating
index (PI, S+G 2 +M), and intestine mucosa DNA, RNA,
protein (Tables 16.14 , 16.15 , 16.16 , 16.17 , 16.18 , 16.19 ,
16.20 , 16.21 , 16.22 , 16.23 , and 16.24 ).
4. Early feeding maintains intestinal structure and function
Early feeding may decrease the fall in intestinal
mucosa thickness, wet weight, villus height, and trans-
membrane electric potential difference (TEPD, refl ecting
the integrality of the intestinal mucosal barrier), improv-
ing the intestine’s absorptive function, reducing the drop
in blood gastrin and motilin (Tables 16.25 , 16.26 , 16.27 ,
16.28 , 16.29 , 16.30 , 16.31 , and 16.32 ).
Table 16.8 Plasma MDA in adults with burns covering 45 % of the TBSA (nmol/ml, x
s
±
)
PBD
1
4
8
14
EF ( n = 11)
7.88 ± 0.93
6.52 ± 1.43**
7.60 ± 1.32*
6.42 ± 0.86*
DF ( n = 10)
7.68 ± 1.18
11.30 ± 2.28
9.88 ± 2.31
9.08 ± 2.94
vs DF * p < 0.05, ** p < 0.01
Table 16.9 Changes in intestinal vascular permeability in rats with third-degree burns covering 30 % of the TBSA (% of normal value, x
s
±
,
n = 8)
PBH
0
6
12
24
48
72
EF
100
330.8 ± 55.7
197.1 ± 35.4*
182.3 ± 41.5*
133.8 ± 25.5*
134.2 ± 27.1
DF
374.3 ± 78.2
304.0 ± 30.5
218.2 ± 27.9
180.8 ± 29.7
161.8 ± 29.1
vs DF * p < 0.01
Table 16.10 Changes in jejunal mucosa energy charge in rats with third-degree burns covering 30 % of the TBSA ( x
s
±
, n = 6)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
0.84 ± 0.02
0.66 ± 0.03
0.64 ± 0.03*
0.66 ± 0.03*
0.75 ± 0.04*
0.68 ± 0.03*
DF
0.63 ± 0.04
0.55 ± 0.04
0.58 ± 0.04
0.65 ± 0.05
0.60 ± 0.04
vs DF * p < 0.01
Table 16.11 Changes in ileal mucosa energy charge in rats with third-degree burns covering 30 % of the TBSA ( x
s
±
, n = 6)
PB
0
6 h
12 h
3 days
7 days
10 days
EF
0.83 ± 0.02
0.64 ± 0.04
0.60 ± 0.03*
0.65 ± 0.03*
0.74 ± 0.04*
0.60 ± 0.05*
DF
0.61 ± 0.04
0.53 ± 0.03
0.57 ± 0.02
0.65 ± 0.03
0.55 ± 0.03
vs DF * p < 0.01
Table 16.12 Changes in intestinal mucosa chondriosome respiratory control rate (RCR) in rats with third-degree burns covering 30 % of the
TBSA x
s
±
(
)
PB ( n )
0 (6)
6 h (5)
12 h (6)
3 days (6)
7 days (6)
10 days (5)
EF
4.21 ± 0.29
3.17 ± 0.23
3.15 ± 0.21*
3.68 ± 0.25*
3.81 ± 0.28*
3.37 ± 0.31**
DF
3.02 ± 0.17
2.88 ± 0.13
3.29 ± 0.21
3.43 ± 0.24
2.77 ± 0.20
vs DF * p < 0.05, ** p < 0.01
Table 16.13 Changes in intestinal mucosa chondriosome P/O in rats with third-degree burns covering 30 % of the TBSA x
s
±
(
)
PB ( n )
0 (6)
6 h (5)
12 h (6)
3 days (6)
7 days (6)
10 days (5)
EF
2.52 ± 0.22
2.03 ± 0.24
2.07 ± 0.12*
2.19 ± 0.23*
2.24 ± 0.21
2.14 ± 0.26*
DF
1.88 ± 0.22
1.83 ± 0.14
1.91 ± 0.17
2.18 ± 0.19
1.79 ± 0.12
vs DF * p < 0.05
16 Nutrition in Burns

399
Table 16.14 Changes in Jejunal mucosa 3 HTIR in rats with third-degree burns covering 30 % of the TBSA (dpm/cm × 10 3 , x
s
±
, n = 6)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
3.14 ± 0.27
2.60 ± 0.25
2.38 ± 0.23*
2.62 ± 0.23*
2.95 ± 0.29**
2.61 ± 0.27**
DF
2.54 ± 0.23
1.97 ± 0.27
2.21 ± 0.26
2.42 ± 0.26
1.98 ± 0.22
vs DF * p < 0.05, ** p < 0.01
Table 16.15 Changes in ileal mucosa 3 H thymidine ( 3 HTIR) in rats with third-degree burns covering 30 % of the TBSA (dpm/cm × 10 3 , x
s
±
,
n = 6)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
2.67 ± 0.27
2.17 ± 0.22
1.94 ± 0.22*
2.12 ± 0.21**
2.38 ± 0.24*
1.85 ± 0.26*
DF
2.10 ± 0.20
1.54 ± 0.25
1.69 ± 0.22
2.04 ± 0.19
1.46 ± 0.19
vs DF * p < 0.05, ** p < 0.01
Table 16.16 Changes in Jejunal mucosa 3 H uridine ( 3 HUIR) in rats with third-degree burns covering 30 % of the TBSA (dpm/cm × 10 3 , x
s
±
,
n = 6)
PB
0
24 h
7 days
EF
2.235 ± 0.247
1.691 ± 0.260*
2.158 ± 0.273*
DF
1.272 ± 0.253
1.849 ± 0.227
vs DF * p < 0.05
Table 16.17 Changes in ileal mucosa 3 HUIR in rats with third-degree burns covering 30 % of the TBSA (dpm/cm × 10 3 , x
s
±
, n = 6)
PB
0
24 h
7 days
EF
1.923 ± 0.213
1.311 ± 0.191*
1.728 ± 0.204*
DF
1.039 ± 0.168
1.427 ± 0.162
vs DF * p < 0.05
Table 16.18 Changes in jejunal mucosa 3 HLIR in rats with third-degree burns covering 30 % of the TBSA (dpm/cm × 10 3 , x
s
±
, n = 6)
PB
0
24 h
7 days
EF
1.307 ± 0.169
0.884 ± 0.161*
1.222 ± 0.132**
DF
0.686 ± 0.138
0.877 ± 0.139
vs DF * p < 0.05, ** p < 0.01
Table 16.19 Changes in ileal mucosa 3 HLIR in rats with third-degree burns covering 30 % of the TBSA (dpm/cm × 10 3 , x
s
±
, n = 6)
PB
0
24 h
7 days
EF
1.117 ± 0.148
0.697 ± 0.128*
0.981 ± 0.102*
DF
0.547 ± 0.121
0.720 ± 0.114
vs DF * p < 0.05
Table 16.20 Changes of intestinal mucosa proliferating index (PI) in rats with third-degree burns covering 30 % of the TBSA ( x
s
±
, n = 4)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
37.59 ± 2.81
29.73 ± 3.47
25.01 ± 3.59
31.58 ± 2.92**
36.61 ± 3.53*
32.47 ± 2.81*
DF
31.03 ± 3.06
20.70 ± 3.52
23.30 ± 3.19
30.44 ± 2.58
24.88 ± 3.76
vs DF * p < 0.05, ** p < 0.01
Table 16.21 Changes in jejunal mucosa DNA in rats with third-degree burns covering 30 % of the TBSA (μg/cm, x
s
±
, n = 6)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
118.17 ± 8.70
111.83 ± 8.61
83.33 ± 7.71
101.82 ± 7.57**
106.15 ± 9.49*
97.65 ± 8.41**
DF
108.50 ± 10.45
76.50 ± 7.50
88.67 ± 6.06
92.00 ± 6.78
80.99 ± 6.96
vs DF * p < 0.05, ** p < 0.01
16.1 Enteral Nutrition

400
Table 16.22 Changes in ileal mucosa DNA in rats with third-degree burns covering 30 % of the TBSA (μg/cm, x
s
±
, n = 6)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
105.73 ± 8.83
95.23 ± 6.83
72.53 ± 6.22
82.87 ± 8.08
92.17 ± 8.45**
81.38 ± 8.17*
DF
96.68 ± 9.84
65.35 ± 7.01
73.18 ± 7.12
76.78 ± 8.45
69.58 ± 8.17
vs DF * p < 0.05, ** p < 0.01
Table 16.23 Changes of jejunal mucosa protein in rats with third-degree burns covering 30 % of the TBSA (mg/cm, x
s
±
, n = 6)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
4.19 ± 0.36
3.98 ± 0.21
3.24 ± 0.21*
3.47 ± 0.25*
3.66 ± 0.31**
3.39 ± 0.19*
DF
3.86 ± 0.19
2.96 ± 0.15
3.09 ± 0.28
3.19 ± 0.20
3.11 ± 0.17
vs DF * p < 0.05, ** p < 0.01
Table 16.24 Changes in ileal mucosa protein in rats with third-degree burns covering 30 % of the TBSA (mg/cm, x
s
±
, n = 6)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
3.35 ± 0.31
3.08 ± 0.22
2.27 ± 0.20
2.71 ± 0.21*
2.86 ± 0.16**
2.48 ± 0.18
DF
3.04 ± 0.21
2.16 ± 0.24
2.39 ± 0.19
2.42 ± 0.27
2.12 ± 0.35
vs DF * p < 0.05, ** p < 0.01
Table 16.27 Ileal mucosa transmembrane electric potential difference (TEPD) in rats with third-degree burns covering 30 % of the TBSA (mv,
x
s
±
, n = 10)
PB
0
6 h
24 h
3 days
7 days
10 days
EF
13.07 ± 1.44
6.08 ± 1.14
6.83 ± 0.88*
8.98 ± 1.39**
11.76 ± 1.23*
8.24 ± 0.89*
DF
5.85 ± 1.13
5.60 ± 1.17
7.28 ± 0.90
10.41 ± 1.01
6.65 ± 1.53
vs DF * p < 0.05, ** p < 0.01
Table 16.28 Changes in serum gastrin in adults with burns covering 45 % of the TBSA (ng/L, x
s
±
)
PBD
1
4
8
14
EF ( n = 11)
59.99 ± 7.84
68.99 ± 6.44**
75.39 ± 9.48**
68.41 ± 8.04**
DF ( n = 10)
63.01 ± 8.40
43.99 ± 7.94
50.00 ± 9.11
51.89 ± 7.11
vs DF ** p < 0.01
Table 16.25 Changes in PBD
10 intestinal mucosa in mini-pigs
with third-degree burns covering
30 % of the TBSA (mg/cm,
x
s
±
, n = 6)
Preburn jejunum
PBD 10 jejunum
Preburn ileum
PBD 10 ileum
EF
684 ± 20
793 ± 83*
427 ± 70
448 ± 34*
DF
627 ± 74
324 ± 31
vs DF * p < 0.05
Table 16.26 Changes in PBD
5 jejunal mucosa thickness ( MT )
and villus height ( VH ) in rats
with third-degree burns covering
30 % of the TBSA (μm, x
s
±
)
Normal MT
PBD 5 MT
Normal VH
PBD 5 VH
EF
2.618 ± 0.437
2.604 ± 0.259**
1.608 ± 0.344
1.576 ± 0.129**
DF
1.986 ± 0.319
1.154 ± 0.155
vs DF ** p < 0.01
Table 16.29 Changes in plasma
motilin in adults with burns
covering 45 % of the TBSA
(ng/L, x
s
±
)
PBD
1
4
8
14
EF ( n = 11)
419.45 ± 72.29
598.18 ± 85.76**
665.27 ± 98.39**
500.64 ± 79.08
DF ( n = 10)
433.20 ± 77.86
373.3 ± 82.5
454.60 ± 87.68
507.30 ± 78.50
vs DF ** p < 0.01
16 Nutrition in Burns

401
16.1.1.3 EF Could Decrease the Level of
Hormone and Infl ammatory Mediator,
and Reduce Intestinal Endotoxin
Translocation [ 23 – 27 ]
Early feeding could decrease the level of blood glucagon,
cortisol, and urine catecholamine, reduce the level of tumor
necrosis factor (TNF), interleukin-8 (IL-8), etc. infl amma-
tory mediators, raise the blood insulin, modulate activated
Kupffer cells (KFs), and lower the endotoxin level of the por-
tal and central vein.
1. Early feeding could decrease the level of hormone and
infl ammatory mediator (Tables 16.33 , 16.34 , 16.35 ,
16.36 , 16.37 , 16.38 , 16.39 , 16.40 , 16.41 , 16.42 , and
16.43 )
2. Early feeding decreases the level of blood endotoxin
( Tables 16.44 , 16.45 , and 16.46 )
3. EF Could Modulate Activated KCs
Table 16.32 Absorption
changes of 18 types of amino
acid amount in mini-pigs with
third-degree burns covering 30 %
of the TBSA (mmol/kg·min,
x
s
±
, n = 6)
PBD
0
4
7
EF
79.61 ± 7.89
43.71 ± 12.75**
66.50 ± 8.69
DF
77.01 ± 21.51
16.26 ± 6.24
61.10 ± 17.44
vs DF ** p < 0.01
Table 16.30 Changes in PB
min 15–60 glucose absorption in
mini-pigs with third-degree burns
covering 30 % of the TBSA
(μmol/(kg·min), x
s
±
, n = 6)
PBD
0
4
7
10
EF
141.25 ± 20.64
78.68 ± 8.48**
119.93 ± 19.62*
128.10 ± 23.51**
DF
134.26 ± 33.20
48.28 ± 16.41
102.99 ± 19.84
94.84 ± 18.87
vs DF * p < 0.05, ** p < 0.01
Table 16.31 Changes in PB
min 15–60 lipid absorption in
mini-pigs with third-degree burns
covering 30 % of the TBSA
(mg/kg·min, x
s
±
, n = 6)
PBD
0
4
7
10
EF
42.01 ± 7.66
29.62 ± 5.94**
38.95 ± 6.83
41.06 ± 10.29**
DF
38.68 ± 8.02
13.93 ± 5.27
33.46 ± 5.59
28.76 ± 7.52
vs DF ** p < 0.01
Table 16.33 Changes in plasma
cortisol in rats with third-degree
burns covering 30 % of the
TBSA (nmol/L, x
s
±
)
PBD ( n )
0 (15)
1 (45)
3 (45)
5 (45)
EF
120.06 ± 25.39
184.09 ± 46.37*
205.07 ± 73.14*
118.40 ± 34.78*
DF
311.20 ± 38.64
426.97 ± 62.38
235.98 ± 64.03
vs DF * p < 0.05
Table 16.34 Changes in portal
plasma glucagon in mini-pigs
with third-degree burns covering
30 % of the TBSA (pmol/L,
x
s
±
, n = 6)
PBD
0
1
4
7
10
EF
21.35 ± 8.22
22.25 ± 11.87
22.44 ± 10.55*
19.32 ± 7.92
31.09 ± 8.33**
DF
20.77 ± 11.03
43.36 ± 24.39
54.15 ± 24.76
30.13 ± 13.72
47.77 ± 24.25
vs DF * p < 0.05, ** p < 0.01
Table 16.35 Changes in plasma
cortisol of the central vein in
mini-pigs with third-degree burns
covering 30 % of the TBSA
(μg/L, x
s
±
, n = 6)
PBD
0
1
4
7
10
EF
53.13 ± 17.26
50.15 ± 17.06*
51.85 ± 10.62**
67.95 ± 29.61
99.82 ± 39.33*
DF
61.38 ± 20.98
25.90 ± 6.70
162.68 ± 37.42
58.63 ± 14.52
156.18 ± 32.49
vs DF * p < 0.05, ** p < 0.01
Table 16.36 Changes in portal
serum insulin in mini-pigs with
third-degree burns covering 30 %
of the TBSA (mU/L, x
s
±
, n = 6)
PBD
0
1
4
7
10
EF
12.32 ± 5.92
9.30 ± 4.05
13.01 ± 2.98*
14.27 ± 2.55*
18.59 ± 2.67
DF
10.99 ± 2.95
5.01 ± 2.19
6.20 ± 2.11
8.40 ± 3.01
15.96 ± 4.82
vs DF * p < 0.05
Table 16.37 Changes in serum glucagon in adults with burns covering 45 % of the TBSA (ng/L, x
s
±
)
PBD
1
4
8
14
EF ( n = 11)
130.18 ± 20.22
139.09 ± 21.98**
158.64 ± 17.77**
157.18 ± 19.23
DF ( n = 10)
134.00 ± 23.28
206.20 ± 24.04
207.50 ± 19.05
158.30 ± 12.12
vs DF ** p < 0.01
16.1 Enteral Nutrition

402
Table 16.38 Changes in plasma
cortisol in adults with burns
covering 45 % of the TBSA
(nmol/L, x
s
±
)
PBD
1
4
8
14
EF ( n = 11)
1,258.4 ± 357.0
987.0 ± 258.9**
858.3 ± 230.6**
1,201.6 ± 286.0
DF ( n = 10)
1,207.8 ± 263.0
1,572.0 ± 260.7
1,401.1 ± 347.7
1,401.1 ± 221.0
vs DF ** p < 0.01
Table 16.41 Changes in central vein tumor necrosis factor (TNF) in mini-pigs with third-degree burns covering 30 % of the TBSA (μg/L,
x
s
±
, n = 6)
Pre-burn
PBH 4
PBH 6
PBH 12
PBD 1
PBD 2
PBD 3
PBD 4
PBD 5
PBD 7
PBD 10
EF 1.14 ± 0.16 1.19* ± 0.12 1.42* ± 0.13 1.18* ± 0.15 1.02* ± 0.08 1.22* ± 0.11 1.21** ± 0.17 1.14** ± 0.09 1.22 ± 0.12 1.28* ± 0.10 1.35** ± 0.18
DF 1.11 ± 0.15 1.45 ± 0.16
1.59 ± 0.21 1.50 ± 0.14
1.26 ± 0.16 1.48 ± 0.15
1.59 ± 0.13
1.52 ± 0.23
1.34 ± 0.27 1.53 ± 0.17 1.59 ± 0.17
vs DF * p < 0.05, ** p < 0.01
Table 16.39 Changes in urine
catecholamine in adults with
burns covering 45 % of the
TBSA (nmol/L, x
s
±
)
PBD
1
4
8
14
EF ( n = 11)
2,881.8 ± 375.9
1,694.9 ± 269.8**
1,574.2 ± 407.2**
1,347.0 ± 301.7**
DF ( n = 10)
2,876.5 ± 379.1
2,872.0 ± 322.1
2,559.5 ± 345.5
1,864.8 ± 328.7
vs DF ** p < 0.01
Table 16.40 Changes in serum
insulin in adults with burns
covering 45 % of the TBSA
(mU/L, x
s
±
)
PBD
1
4
8
14
EF ( n = 11)
22.38 ± 4.38
36.65 ± 5.69**
40.95 ± 6.91**
32.98 ± 6.38*
DF ( n = 10)
21.90 ± 5.74
21.92 ± 4.93
24.28 ± 5.22
28.61 ± 7.51
vs DF * p < 0.05, ** p < 0.01
PBD
1
4
8
14
EF ( n = 11)
1.875 ± 0.179
2.410 ± 0.028**
2.617 ± 0.176**
2.608 ± 0.193**
DF ( n = 10)
1.946 ± 0.204
3.162 ± 0.165
3.729 ± 0.356
3.360 ± 0.241
vs DF * * p < 0.01
Table 16.42 Changes in plasma
TNF in adults with burns
covering 45 % of the TBSA
(μg/L, s)
PBD
1
4
8
14
EF ( n = 11)
1.43 ± 0.60
1.60 ± 0.73**
1.99 ± 0.96*
1.77 ± 1.04
DF ( n = 10)
1.39 ± 0.74
3.14 ± 1.24
3.05 ± 1.30
2.68 ± 1.38
vs DF * p < 0.05, ** p < 0.01
Table 16.43 Changes in plasma
interleukin-8 (IL-8) in adults
with burns covering 45 % of the
TBSA (μg/L, x
s
±
)
Table 16.45 Changes in portal endotoxin in mini-pigs with third-degree burns covering 30 % of the TBSA (EU/L, x
s
±
, n = 6)
Preburn
PBH 4
PBH 6
PBH 12
PBD 1
PBD 2
PBD 3
PBD 4
PBD 5
PBD 7
PBD 10
EF 257.0 ± 28.7 420.2** ± 44.7 455.7** ± 20.2 231.8** ± 27.9 475.3** ± 24.1 279.0** ± 19.0 365.5** ± 15.4 260.0** ± 9.8 275.8** ± 27.1 266.5** ± 14.5 329.0 ± 16.7
DF 230.2 ± 23.5 591.3 ± 28.4
928.7 ± 40.7
436.0 ± 52.1
975.7 ± 48.3
543.5 ± 41.4
591.8 ± 19.8
637.2 ± 27.7
356.8 ± 22.9
318.7 ± 19.9
399.8 ± 13.5
vs DF * p < 0.05, ** p < 0.01
PBD ( n )
0 (15)
1 (45)
3 (45)
5 (45)
EF
120 ± 24
296 ± 50**
362 ± 80**
398 ± 99**
DF
626 ± 139
1,232 ± 384
1,201 ± 264
vs DF ** p < 0.01
Table 16.44 Changes in plasma
endotoxin in rats with third-
degree burns covering 30 % of
the TBSA (endotoxin units,
EU/L, x
s
±
)
PBD
1
4
8
14
EF ( n = 11)
308 ± 63
546 ± 118**
495 ± 150**
449 ± 133
DF ( n = 10)
321 ± 101
756 ± 113
754 ± 130
533 ± 164
vs DF ** p < 0.01
Table 16.46 Changes in plasma
endotoxin in adults with burns
covering 45 % of the TBSA
(EU/L, x
s
±
)
16 Nutrition in Burns

403
The count of liver KCs in every rat with a burn cov-
ering 30 % of the TBSA (5.124 ± 0.650) × 10 7 , was
329.7 % of normal rat (4.50 ± 0.93)pg/10 6 . The normal
values of TNF and PGE 2 in cultured 12-h KC superna-
tant were (4.50 ± 0.93) pg/10 6 cells and (261 ± 21)
pg/10 6 cells respectively. There are 311.8 %, 904.2 %,
513.3 % of normal TNF values and 226 %, 329.9 %,
203.4 % of normal PGE 2 on PBD 1, 3, and 5 respec-
tively (vs normal TNF and PGE 2 , p all < 0.01;
Tables 16.47 and 16.48 )
Twelve hours before the rat was killed, India ink was
injected (diluting it 14 times with 1 % gelatin) 1 ml/g body
weight into the coccygeal vein of normal rats and those with
third-degree burns covering 30 % of the TBSA. The count
(No/100×) of normal rat KCs phagocytosing ink particles
was 64.80 ± 8.87, and the burn rat KCs phagocytosing ink
particles were 236.4, 308.6, and 270.9 % of normal on PBD
1, 3, 5 respectively. The area of the normal rat KC phagocy-
tosing ink particles (μm 2 /100×) was 0.852 ± 0.291, the KC
phagocytizing ink particle areas were 619.2, 801.9, and
635.2 % of normal on PBD 1, 3, 5 respectively (vs normal
KC phagocytizing ink particle and area, p all <0.01;
Tables 16.49 and 16.50 ).
16.1.1.4 EF Could Decrease Hypermetabolism
After Burn Injury [ 16 , 19 , 21 , 28 , 29 ]
1. EF could decrease the analysis of skeletal muscle
Early feeding could reduce the decreasing nitrogen
content of gastrocnemius muscle in burn rat, lower the
releasing tyrosine amount of soleus muscle in scalding
rat, modulate the activation of 20S proteasome in skeletal
muscle post-burn (Tables 16.51 , 16.52 , and 16.53 ).
PBD
0
1
3
5
EF
4.50 ± 0.93
5.56 ± 1.21**
28.78 ± 3.31**
14.24 ± 3.74**
DF
14.03 ± 4.91
40.59 ± 5.30
23.10 ± 3.40
vs DF ** p < 0.01
Table 16.47 TNF content of
cultured 12 h Kupffer cell (KC)
supernatant in rats with
third-degree burns covering 30 %
of the TBSA (pg/10 6 cells,
x
s
±
, n = 15)
PBD
0
1
3
5
EF
261 ± 21
415 ± 36**
670 ± 4**
391 ± 29**
DF
590 ± 115
861 ± 111
531 ± 97
vs DF ** p < 0.01
Table 16.48 Prostaglandin E2
(PGE 2 ) content of cultured 12 h
KC supernatant in rats with
third-degree burns covering 30 %
of the TBSA (pg/10 6 cells,
x
s
±
, n = 15)
PBD
0
1
3
5
EF
64.80 ± 8.87
102.00 ± 18.85*
132.40 ± 20.89**
121.20 ± 16.15**
DF
153.20 ± 42.75
200.00 ± 62.96
175.60 ± 54.42
vs DF * p < 0.05, vs DF ** p < 0.01
Table 16.49 The count of KC
phagocytizing ink particles in
rats with burns covering 30 % of
the TBSA (no./100×, x
s
±
,
n = 15)
PBD
0
1
3
5
EF
0.852 ± 0.291
1.866 ± 0.242**
3.402 ± 1.277**
3.150 ± 0.589**
DF
5.276 ± 0.791
6.832 ± 1.193
5.412 ± 0.572
vs DF ** p < 0.01
Table 16.50 The area of KC
phagocytizing ink particles in
rats with third-degree burns
covering 30 % of the TBSA
(μm 2 /100×, x
s
±
, n = 15)
Table 16.51 The nitrogen content of gastrocnemius muscle (both
sides) in rats with third-degree burns covering 30 % of the TBSA
(mg, x
s
±
, n = 15)
Normal control
PBD 5
EF
37.00 ± 0.09
29.90 ± 0.04*
DF
20.10 ± 0.04
vs DF * p < 0.05
Table 16.52 Releasing content of tyrosine in soleus muscle of rats
with third-degree burns covering 37 % of the TBSA (nmol/g wet tissue.
2 h, x
s
±
, n = 7)
Normal control
PBD 5
EF
260.38 ± 19.69
314.70 ± 25.90**
DF
348.34 ± 12.14
vs DF ** p < 0.01
16.1 Enteral Nutrition

404
2. Early feeding could decrease the resting energy expenditure
(REE) and urinary nitrogen output in adults with burns cov-
ering 45 % of the TBSA and rats with third- degree burn cov-
ering 30 % of the TBSA (Tables 16.54 , 16.55 , and 16.56 )
Early feeding could decrease the average value of the
REE in burn mini-pigs on PBD 4, 7, 10, which was
13.6 %, and reduce the average value of REE on PBD 7
and 10, which was 24.3 %.
Early feeding could decrease the mean value of REE in
an adult with a burn on PBD 4, 8, and 14, which was
17.7 %.
The average value of urinary nitrogen on PBD 1–14 is
20.4 ± 4.2 g/day in the EF group, and 25.8 ± 5.4 g/day in
the DF group, EF vs DF p < 0.02.
Mochizuki and Alexander advance the viewpoint that
EF could reduce hyper-metabolism. Since 1984, this has
been the cause of controversy. The mechanism of hyper-
metabolism post-burn is not yet completely clear, and the
source of hypermetabolism was seen from two rough
aspects. One is secondary to increased evaporative heat
loss through the burn wound; the other is the result of
internal organ variation. We found that one of the impor-
tant causes of internal organ change is the intestinal injury
of ischemia and anoxia during the early phase post-burn.
According to the experimental animal and clinical data
mentioned above, the reason why EF could reduce hyper-
metabolism is that EF could resuscitate the intestine’s
“covert compensated shock,” thus lessening the intestinal
injury of ischemia and anoxia, reducing the translocation
of intestinal endotoxin, decreasing the level of hormone
and infl ammatory mediator, lowering the metabolic rate,
and decreasing muscle decomposition. Therefore, the key
point of EF reducing hypermetabolism is not “nutrition” or
“lowering evaporative heat loss through the burn wound”
but “resuscitation” of the intestine. Moreover, if the
application of EF is inappropriate, it could be more disad-
vantageous than advantageous.
16.2
Parenteral Nutrition
Shilin Deng
16.2.1
Development and Advancement
of Parenteral Nutritional Support
of Burn Injury in China [ 30 – 35 ]
Parenteral nutritional support of burn injury in China began
to develop with the improvement of the amino acid pharma-
ceutical industry. Before the 1980s compound amino acid
infusion, lipid emulsion, trace elements, and gastrointestinal
nutrient preparation were all dependent on importation. At
that time, the nitrogen source of intravenous nutrition was
protein hydrolysate, whose use was restricted owing to obvi-
ous side effects and high osmotic pressure. Up to the 1980s,
with the economic development in China, the Chinese amino
acid pharmaceutical industry was rising and began to pro-
duce domestic-made amino acid crystal compound injec-
tions. The author fi rst published an article about the
application of F-11 crystal amino acid-sorbitol compound
injection made at the Tianjin amino acid pharmaceutical
company on parenteral nutritional (PN) support in Tianjin
Medical Journal in 1981. From then on, a series of relevant
reports were published, such as Guo et al. reporting on the
application of parenteral hyperalimentation and prevention
of its complications in burns patients ( Medical Journal of
Chinese People’s Liberation Army , 1982), Deng Shilin
Normal control
PBD5
EF
123.97 ± 16.87
315.61 ± 51.05*
DF
409.15 ± 40.27
Data of Tables 16.52 and 16.53 are from the Department of Biochemistry, the Third Military Medical
University
vs DF * p < 0.05
Table 16.53 The activation of
20S proteasome in soleus muscle
of rats with third-degree burns
covering 37 % of the TBSA
(cpm/100 μg protein·2 h, x
s
±
,
n = 6)
PBD
0
1
4
7
10
EF
17.00 ± 2.69
12.57 ± 1.78
17.96 ± 5.93
18.25 ± 2.40**
27.76 ± 2.90*
DF
16.80 ± 2.78
10.74 ± 2.48
13.28 ± 3.54
27.18 ± 4.27
33.57 ± 3.62
vs DF * p < 0.05, ** p < 0.01
Table 16.54 Changes in resting
energy expenditure (REE) in
mini-pigs with third-degree burns
covering 30 % of the TBSA
(kcal/kg·day, x
s
±
, n = 6)
PBD
Normal ( n = 8)
PBD1
PBD4
PBD8
PBD14
EF ( n = 11)
38.4 ± 3.9
47.8 ± 5.4
50.0 ± 7.9*
53.8 ± 9.2**
60.3 ± 9.1**
DF ( n = 10)
47.0 ± 4.2
62.1 ± 9.7
66.7 ± 6.8
70.7 ± 10.1
vs DF * p < 0.05, ** p < 0.01
Table 16.55 Changes in REE in
adults with burns covering 45 %
of the TBSA (kcal·m −2 ·h −1 , x
s
±
)
16 Nutrition in Burns

405
Table 16.56 Changes in 24 h urinary nitrogen in adults with burns covering 45 % of the TBSA (g/day, x
s
±
)
PBD
1
2
3
4
5
6
7
8
9
10
11
12
13
14
EF ( n = 11)
12.8 ± 2.6 13.1 ± 4.2 16.4 ± 5.8 18.9 ± 7.7 21.5 ± 9.3 25.0 ± 7.8 25.2* ± 9.1 25.5 ± 9.4 20.2** ± 7.4 18.2** ± 4.4 22.6 ± 8.8 22.5** ± 7.2 23.9** ± 6.9 20.4** ± 6.6
DF ( n = 10) 13.1 ± 4.2 16.1 ± 6.3 21.7 ± 6.6 22.0 ± 5.6 24.4 ± 6.8 28.7 ± 5.5 30.2 ± 6.3
31.0 ± 6.9 25.2 ± 9.3
28.4 ± 8.3
28.5 ± 6.1 28.8 ± 6.7
30.2 ± 4.9
33.5 ± 9.2
vs DF * p < 0.05, ** p < 0.01
16.2 Parenteral Nutrition

406
describing the application of crystalline amino acid made in
China in intravenous nutritional treatment for burns patients
( Chinese Journal of Surgery , 1983), You Zhongyi outlined
changes in nitrogen balance and amino acids in blood after
amino acid mixed liquor treatment in burns patients
(Proceedings of the First Assembly of the Burn Research
Congress between Chinese and Americans, 1985), Zhang
Xiaojun and Xu Huizhen published an article on 14 amino
acid injection-800 in burns treatment ( Chinese Journal of
New Drugs and Clinical Remedies , 1985), Wang Qifang
studied the application of compound amino acid injection in
severe burns patients ( Chinese Journal of Surgery , 1985),
Dong Zhilin reported on delayed hypersensitivity and levels
of serum transferrin in burns patients and their clinical sig-
nifi cance ( Chinese Journal of Surgery , 1986), Deng Shilin
described the experience of PN treatment in 31 severe burns
patients ( Chinese Journal of Plastic Surgery and Burns ,
1987). In the 1980s articles on the nutrition of burns were
published in Tianjin, Shanghai, and Beijing, and Chongqing
evaluated the early amino acid preparations comprising 11,
14, or 17 amino acids made in the domestic amino acid phar-
maceutical industry, proved their clinical effects, and they
were safe because of the containment of all the essential
amino acids and proper ratios of essential amino acids/total
nitrogen and essential amino acids/total amino acids.
In the 1990s with the clinical need for and development of
intravenous nutrition preparations, the low-chlorine and phos-
phorus-containing compound amino acid infusion, which can
relieve hyperchloremia and supply phosphorus, and high
branched chain amino acid injection, which was adapted to the
hypermetabolic reaction of trauma and burn, were produced
for clinical application. In the basic area of nutrition of burn
metabolism, some institutes (the Institute for Burn Research
of The Third Military Medical University in Chongqing, the
Institute for Nutrition and Health of the Academy of Military
Medical Sciences, the Institute for Burn Research of the 304
Hospital of PLA in Beijing, the Institute for Burn Research of
Ruijin Hospital in Shanghai, and the Institute for Burn
Research of Tianjin) introduced the adult calorie supply for-
mula of Chinese people, and the new concepts of hyperme-
tabolism molecule in a slow ascending period and an
intestinally originating hypermetabolism in a rapid ascending
period, investigated the degradation pathway of protein metab-
olism, analyzed the mechanisms, effects, and safety concerns
of nutriments such as vitamins, trace elements, special nutri-
ments, arginine, glutamine, and recombinant human growth
hormone on the nutrition of burn metabolism, and proposed
the operation rules and treatment guidelines in accordance
with the Chinese conditions. These studies enhanced greatly
the effects of nutrition of burn metabolism on the treatment of
large-area burns. In the aspect of academic exchange, domes-
tic burn nutrition experts actively joined domestic and interna-
tional academic conferences of nutrition, surgery, and critical
diseases, reported their research achievements, exchanged dif-
ferent academic viewpoints, visited other domestic or foreign
researchers, and made great contributions to the development
of domestic clinical nutriology and the joint track with foreign
clinical nutriology.
The Clinical Nutriology of Chinese Surgery, established
in 1990, performed a great number of basic and clinical stud-
ies on PN/EN support and fi rst formulated the parenteral and
EN operational guidelines (draft) in 2004. The Parenteral
and Enteral Nutriological Association of the Chinese
Medical Association, established in 2005, promoted the
guiding role of evidence-based medicine in clinical nutriol-
ogy, performed the nutritional status screening of surgical
patients in the form of multiple centers and large samples
over the whole country, and is now formulating the guide-
lines and operational rules of indications for parenteral and
EN support. Domestic clinical nutriology experts, led by the
Chinese Medical Association, are also formulating guide-
lines and operational rules for burns nutrition support. These
guidelines standardize parenteral and EN support, direct the
treatment of and research into burns nutrition, develop
domestic parenteral and EN support from the present non-
treatment status to evidence-based medicine, and integrate
the nutritional support into comprehensive burns treatment
to provide greater benefi t for burns patients.
16.2.2
Determination of Energy
Consumption and Nutritional
Support Requirements of Burns
Patients [ 36 – 39 ]
Reasonable nutritional supply is the main purpose of PN
support of burns. To achieve this purpose we fi rst need to
understand precisely the energy consumption after a burn,
also called REE, and provide energy requirements on the
basis of REE. However, because of the complications and
variations of the energy metabolism of burns patients, REE
is usually predicted by a formula. With the application of an
indirect calorimeter, formula-predicted REE has been found
to be signifi cantly different from the actual data. Therefore,
the indirect calorimeter should be applied widely to measure
the REE of burns patients in China and provide reasonable
nutritional supply for clinical nutritional support.
16.2.2.1 Analysis of the Reasons
for the Changes in Burn Energy
Consumption
1. The Tianjin Burn Institute performed a study of 45 burns
patients during the period 1994–1997. Of these patients,
34 were male, 11 were female, aged 18–63, and the burn
areas were 20–93 % of the TBSA. All patients were
burned by fl ames and had been healthy before injury.
16 Nutrition in Burns

407
(a) Grouping: the patients were divided into five
groups according to burn area: 9 patients in the
group with 21–30 % of the TBSA, 13 patients of
the group with 31–40 % of the TBSA, 9 patients of
the group with 41–50 % of the TBSA, 6 patients
of the group with 51–70 % of the TBSA, and
8 patients of the group with >71% of the TBSA.
(b) Time of measurement: REE was measured consecu-
tively immediately after the patients had been admit-
ted to hospital. Seven days later, the measurement
was being carried out at regular intervals until wound
healing or hospital discharge.
(c) Conditions of measurement: measurement was per-
formed using a metabolic cart (Medical Graphics, St.
Paul, MN, USA) 2 h after breakfast, 1–2 h after intra-
venous infusion of nutrition, and 30–60 min after rest-
ing. Before measurement the environmental parameters
such as room temperature, humidity, and atmospheric
pressure were inputted into the instrument to calibrate
the capacity and O 2 and CO 2 detectors, and then the
measurement could be carried out. The measurement
fi nished when a stable z curve was displayed for 5 min
on the computer screen. The time was adjusted for
critical patients or patients assisted by a respirator.
(d) Statistical analysis: ANOVA and t test were used, and
the data were shown as mean±standard deviation. q
test was used for paired analysis when p value was
less then 0.05.
2. Results:
(a) The time of the peak level of REE: of 45 burns
patients, 3 patients reached the peak level of REE
within 3 days, 12 patients within 5 days, 8 patients
within 6 days, 7 patients within 7 days, and 6 patients
within 9 days. 73.3 % of the TBSA of patients reached
the peak REE within 5–9 days after the burn, and the
mean value was 6.7 days.
(b) The changes in REE: each group had a similar trend
of energy changes after a burn. In the early stage after
a burn the REE increased but did not reach a peak,
and later the REE continued to rise and gradually
descended until reaching a peak. A larger burn area
suggested higher REE (Fig. 16.4 ).
(c) There was a positive correlation between the burn
area and the REE (Fig. 16.5 ).
(d) Energy expenditure (EE) at the burn shock stage was
signifi cantly higher than the value predicted, but it
did not reach the peak, which was much higher
(Table 16.57 ).
(e) Variation of EE: the variation of EE at each post-burn
time point was higher than the value predicted; the
early variations were higher than the later ones, and
variations in patients with a large burn area were
higher than those of patients with a small burn area
(Table 16.58 ).
(f) The relation between the EE and the burn area: the
EE increased slightly when the burn area covered
more than 10 % of the TBSA, but statistical analysis
showed no signifi cant difference. EE increased
500
400
300
200
REE[kj(kcal)/m2-h]
100
0
3
5
7
9
Days
11
13
21
28
>71 %
51–70 %
41–50 %
31–40 %
21–30 %
Fig. 16.4 Changes in resting energy expenditure (REE)
18,300
16,300
14,300
12,300
10,300
8,300
6,300
4,300
2,300
REE(kj/d)
300
0
20
40
60
Burn area (%)
80
100
Fig. 16.5 Relation between the burn area and the REE
Table 16.57 Comparison among predicted energy expenditure (EE),
EE in the shock stage, and EE at peak value (kJ/day, x
s
±
)
Predicted EE
EE in the shock stage
EE at peak value
6,350.73 ± 701.36
10,269.96 ± 2,881.77* 11,443.78 ± 3,295.32 △
vs predicted EE ** p < 0.01, vs EE in shock stage △ p < 0.05
Burn area (%
TBSA± SD)
Predicted
variation
PBD
3
5
7
9
13
20
25
83.00 ± 6.56
3.35
30.00
31.34
25.97
19.62
18.36
11.90
11.59
59.38 ± 6.92
5.12
33.78
22.95
22.67
16.38
16.78
15.35
20.14
43.42 ± 1.90
4.34
17.17
31.71
13.97
13.30
13.17
15.94
36.00 ± 3.16
5.78
28.04
21.54
23.79
17.26
18.24
17.48
16.71
24.33 ± 3.94
3.39
17.76
18.47
14.34
14.00
13.21
15.32
Table 16.58 Post-burn variation
of EE in burns patients


16.2 Parenteral Nutrition

408
signifi cantly when the burn area was more than 30 %
of the TBSA (Table 16.59 ).
(g) For patients of the middle burn area and a similar
total burn size and deep burn size, the EE of patients
with inhalation injury was higher than that of those
without inhalation injury; statistical analysis showed
no signifi cant difference ( p > 0.05; Table 16.60 ).
(h) EE did not change signifi cantly before and after sur-
gical excision when the burn size was less than 40 %
of the TBSA, but showed a signifi cant difference
when the burn size was more than 40 % of the TBSA
(Table 16.61 ).
(i) In all patients the burn sizes in women were clearly
larger than those of men, but EE values of women
were similar to or lower than those of men at each
time point (Table 16.62 ).
3. Conclusion:
(a) Characteristics of variations in EE: the high metabo-
lism post-burn is the organism’s reaction to stress sta-
tus and varies with the degree of burn and post-burn
time. EE increases immediately after the burn occurs,
ascends gradually in the early burn stage, but did not
reach the peak. The time in which EE reaches the
peak is usually 5–9 days with a mean of 6.7 days,
which is a skewed distribution and suggests that EE
might reach a peak about 1 week after the burn.
Therefore, nutritional support should be provided
after the shock stage in order to suppress the degrada-
tion of protein and fat. EE is compared among
patients of similar age, weight, and height, and the
result indicates that EE is directly correlated with
burn size. In addition, post-burn EE varies with time.
EE increases as post-burn time increases before
reaching a peak. Then, EE descends as post-burn
time increases, and the degree of decline is relevant to
the burn size. The EE of a patient with burns covering
<30 % of the TBSA decreases rapidly to a low level
after reaching the peak, while the EE of a patient with
burns covering >70 % of the TBSA remains at a high
level after reaching a peak. However, the EE of none
of groups recovers to the pre-burn level when the
wounds are healed. Milner et al. performed a long-
term monitoring of post-burn EE, and they found that
100–150 days were needed for the EE of patients
with burns covering 20–40 % of the TBSA to recover
to normal and 250 days were needed for patients with
burns covering >75 % of the TBSA to do so.
Therefore, the recovery of post-burn EE is a long
process.
(b) Factors related to the variation in EE: variation in
post-burn EE is considerable and not is stable as pre-
dicted. In addition to individual differences, there are
many factors related to variation in post-burn
EE. The analysis of peak EE in 45 burns patients
Table 16.59 Relation between EE post-burn and different deep burn area (kJ·m −2 ·h −1 , x
s
±
)
Deep burn area (TBSA)
Patient no.
Burn area (% TBSA± SD)
EE at time of half wound healing
0
6
33.00 ± 13.16
226.35 ± 30.59
1~
8
36.75 ± 11.28
226.31 ± 42.28
11~
7
37.28 ± 9.28
240.45 ± 46.53
31~
9
39.11 ± 9.12
280.54 ± 59.71
Note: ** p < 0.01
Table 16.60 Energy expenditure in burns patients with and without inhalation injury (IHIJ)
Groups
Case no.
Burn area (% TBSA±SD)
Deep burn area (% TBSA±SD) EE (kJ·(m 2 ) −1 ·h −1 , x
s
±
)
With IHIJ
5
36.80 ± 6.46
33.40 ± 5.27
288.69 ± 70.96
Without IHIJ
5
37.80 ± 6.34
29.40 ± 8.17
267.57 ± 44.64
Table 16.62 Changes in EE in burns patients of different genders (kJ/m 2 ·h)
Gender
TBSA (%)
Case no.
PBD
3
5
7
9
13
15
20
25
Male
35.96
24
224.09
256.81
258.15
255.22
245.94
250.20
229.79
215.14
Female
48.27
11
212.63
243.80
255.98
219.66*
210.12*
224.72
216.65
213.38
vs male * p < 0.05
Table 16.61 Mean EE in
different burn sizes before and
1 week after surgical excision
(kJ/day, x
s
±
)
Burn area (% TBSA)
Before surgical excision
After surgical excision
>40
11,035.55 ± 1,307.40
9,670.52 ± 1,943.55**
<40
10,295.82 ± 3,100.43
9,718.13 ± 2,027.65
Compare between before and after surgical excision ** p < 0.01
16 Nutrition in Burns

409
demonstrates that the increase in EE correlated
weakly with burn size, and there are some other fac-
tors, such as area of deep burn, inspiration jury, and
surgical excision, that infl uence post-burn EE. The
actual measurement of EE indicates that under the
condition of the same burn size a higher EE occurs in
patients who have a larger area of deep burn, espe-
cially in those who have burns covering >30 % of the
TBSA, and under the condition of a medium burn
size, there is no difference in EE between patients
with and without inspiration jury, which probably
results from the fact that the increase in EE is not
unlimited. Surgical excision is an important treat-
ment for patients with deep burn, and its aim varies
with different burn size. For patients with a small or
medium burn size, the main purpose of surgical exci-
sion is to recover function and appearance, while for
those with a large burn area, the aim is to save their
lives. Large areas of necrotic tissue are removed by
surgical excision and skin grafting is used at the
same time to cover the wounds; thus, infection and
other complications may be prevented.
The research showed that post-burn EE is clearly
decreased ( p < 0.01). The change mainly took place in
burns patient whose burn area exceeded 40 % of the
TBSA, and it illustrated that the purpose of eschar
excision and skin grafting operations was not only to
heal raw surfaces in the early stages, but also effec-
tively regulated high-energy metabolism post-burn.
This research also explained that the mechanism of
eschar excision and skin grafting operations in the
early stages could increase the healing rate consider-
ably in patients with severe burns and could be
speared in patients with a large burn area all the over
China for several decades. In addition, the body’s
reaction to trauma and sexuality also obviously
affected post-burn EE. EE varies tremendously in dif-
ferent individuals with the same burn area. The ear-
lier in the post-burn period, the greater the extent of
variation. The larger the burn area, the greater the
extent of variation. This showed that the body was
gravely injured in the early stages after a burn, espe-
cially in patients with severe burns. The body’s reac-
tion to trauma was considerable. The internal
environment in the body achieved a new balance as
the post-burn time increased, and the extent of varia-
tion of EE was lower. The author also detected that
EE showed tremendous changes in patients of differ-
ent sexes. Post-burn EE was considerably lower in
women than in men. The gender of the patient should
be taken into consideration when calculating the req-
uisite amount of EE, and it could avoid inappropriate
nutrition in treatment.
16.2.2.2 Application of Indirect Calorimetry
Instruments in the Measurement
of Energy Consumption of Burns
Patients
Forty-fi ve burns patients were divided into three groups at
the Tianjian Burn Institute, and provided 1.0 REE, 1.2 REE,
and 1.5 REE for nutritional support, and their metabolic hor-
mone level was detected regularly. The change in blood ami-
nogram showed that the 1.2 REE group was more rational
for EN and parenteral alimentation treatment than the 1.0
REE group and the 1.5 REE group. The principle of energy
metabolism measurement by an indirect calorimetric metab-
olism machine was the law of conservation of energy and
geometric proportion law of chemical reaction.
After measuring the amounts of oxygen consumption,
urine total nitrogen, and carbon dioxide generated within a
period of time, we can work out the energy consumption,
nonprotein respiratory quotient (NPRQ), and the oxida-
tion rate of three nutritional substrates in this period on the
basis of the Weir formula. REE = [(3.9 × VO 2 ) + (1.1 × VCO
2 )] × 1.44 − (2.8 × UUN). The NPRQ is the complete oxida-
tion index of nutrient substances, and can provide further
energy. Mathematical expression is carbon dioxide in units
of time (VCO 2 , L/min) divided by oxygen capacity (VO 2 , L/
min). NPRQ of 0.7 indicates fat oxidization in the organism.
NPRQ of 1.0 indicates glucose oxidization in the organism.
If NPRQ is 0.85, fat and glucose oxidization constitute 50 %
each. NPRQ can indicate the proportion of nutrient sub-
stance utilization or the condition of mixed energy oxidation.
Energy consumption measurement by computer control of
indirect calorimetric appearance has been utilized in China
since the 1980s, and in contrast to predicting by formula it
can continuously monitor and detect changes in the patient’s
condition. It can illustrate the effect of nutritional support
and deposit function. We have been continuously measur-
ing oxidation rates of REE, NPRQ, glucose, fat, and protein
in patients with serious burns using a CCM Metabolic Cart
since 1990. An indirect calorimetric metabolism machine is
accurate, reproducible, has no traumatic occlusion and dis-
placement ability, and it is a sensitive index for assessing
REE under the condition of stress hypermetabolism.
16.2.3
Operational Rules of Parenteral
Nutritional Support in Burns [ 35 , 37 ,
39 – 41 ]
16.2.3.1 Indications for and Choice of Parenteral
Nutritional Support in Burns
1. Indications:
(a) Patients with burns covering >20–30 % of the TBSA
and vigorous metabolism whose requirements cannot
be satisfi ed by EN support.
16.2 Parenteral Nutrition

410
(b) Patients with severe oral and gastrointestinal chemi-
cal burns.
(c) Patients with severe inspiration injury, or tracheal
cannula or respirator users.
(d) Patients with severe burns of the anterior cervicalis or
mental region who cannot chew and swallow.
(e) Patients who cannot or refuse to take food for other
reasons such as suicide or crime.
(f) Patients with severe burn complications:
(i) Digestive system complications such as stress
ulcer, alimentary tract hemorrhage, gastric
retention, enteroplegia, and intestinal failure.
(ii) Sepsis or multiple organ dysfunction syndrome.
(iii) Disturbance of consciousness.
2. Choice:
(a) We should correctly understand the damage caused to
the gastrointestinal organs by a burn. In the early and
middle stages of a burn, the gastrointestinal functions
are impaired by internal milieu disorder and organ
damage, which are caused by stress, fear, pain, fever,
trauma, infl ammation, surgical excision, and anes-
thesia. Therefore, gastrointestinal motility is often
depressed during the early and middle stages after
a burn, and gastrointestinal paralysis is clinically
found several hours afterward. Experiments demon-
strate that in the early stage in patients with a burn
the gastric emptying time is prolonged, intestinal
peristalsis is reduced, and the colon drive is delayed;
thus, patients show loss of appetite, abdominal dis-
tension, and even slight gastric paralysis, enterople-
gia, or stress ulcer and gastrointestinal dysfunction.
Accordingly, patients fi nd it hard to take food through
the mouth during the infection or shock stage and
need to be feed via PN support, which is complemen-
tary to EN support.
Parenteral nutritional support is often used for
patients with large burns and provides 50–75 % of
total calories. Only a minority of patients need com-
plete PN support. PN support can be used in different
stages in different patients and should be adopted
when they have recovered from shock and they are
hemodynamically stable. The course of treatment of
PN support is basically identical to that of catabo-
lism, and after 1–1.5 months of use, especially after
gastrointestinal function recovery, PN support should
be stopped and EN support adopted.
(b) We should abide by the medical and ethical princi-
ples when using PN support. The question of how PN
support should be chosen should be taken seriously,
because of the complex operations, the large number
of medicine and fl uids, the high costs, and the poten-
tial complications. Thus, the following rules should
be obeyed:
(i) It should bring advantages to patients

(ii) There should be no disadvantages

(iii) Patients should make independent decisions
(iv) It should be impartial for every patient.
The following points should be given attention:
(i) Parenteral nutrition support should be used
when the patients cannot or refuse to take food
or cannot get enough energy via oral feeding.

(ii) PN support should be used when the patients
suffer from malnutrition or are at risk of
malnutrition.

(iii) For severe burns patients PN support is prohib-
ited when fl uid resuscitation as an anti-shock
cure is on- going, and can only be used when the
blood volume, hemodynamics, tissue oxygen-
ation, and internal environment are stable and
guaranteed.
16.2.3.2 Ingredients and Preparations
of Injection Solution Used
in Parenteral Nutritional Support
1. Ingredients of injection solution used in parenteral nutri-
tional support
The nutrients of parenteral nutrition (PN) solution
should meet the needs of metabolism and provide enough
energy and anabolism substrates to synthesize proteins.
Owing to the different conditions and stages of each
patient the ingredients of the PN solution should be deter-
mined according to the status of the patient in order to
achieve nutritional support. In principle, the ingredients
and proportions of the nutritional solution are established
on the basis of the nutritional needs and metabolism of the
patients. The Parenteral and Enteral Nutritional
Operational Guidelines (draft), formulated in 2004 by the
Clinical Nutriology of the Chinese Surgery Association,
introduced the requirement doses of energy and protein
for surgical patients (Table 16.63 ) and daily recommenda-
tion doses of the nutrients of PN (Table 16.64 ). The
European Society of Parenteral and Enteral Nutrition
(ESPEN) formulated the requirements of the nutrients for
PN in the Textbook of Continuing Education in 2002
(Table 16.65 ).
The Tianjin Burn Institute has been studying the ingre-
dients of PN solution since the 1980s, which has good
effects and safety at clinical application. The ingredients
are listed below:
The ingredients above are prepared as a total nutrient
admixture (TNA). According to recent studies, for
patients with large burns PN support can be used under
the principle of “permission for under-feeding, which will
bring more advantages for the metabolism. In the calories
the fat emulsion should be less than 30 % of the total
energy, because an excessive intake of fat emulsion has
16 Nutrition in Burns

411
adverse effects on the metabolism and increases suscepti-
bility to infection. The long-chain/medium-chain triglyc-
eride (LCT/MCT) compound emulsion or ω-3 fi sh fat
emulsion injection is recommended for use in patients.
(a) Proteins and amino acids: 2.0–3.0 g/(kg·day)
(b) Energy: 25–30 kcal/(kg·day)
(c) Ratio of nitrogen to calories: 1:100–150
(d) Fat emulsion/total calories: ≤30 %
(e) Ratio of insulin to glucose: 1:5 mg
(f) Maximum input quantity of glucose: 5 mg/(kg·day)
(g) Supply of electrolytes according to the measurement
of blood biochemistry
(h) Supply of water-soluble and fat-soluble vitamins and
trace elements for patients with long-term PN
2. The regular preparations of compound amino acid injec-
tion used in China:
(a) Pharmacological effects of compound amino acids
injection:
(i) Providing essential amino acids: the common
compound amino acid injections contain eight
essential amino acids and prevent the lack of
essential amino acids.
(ii) Adjusting the nitrogen balance: some diseases
result in high catabolism, protein degradation
exceeding synthesis, which causes negative
nitrogen balance. If there is enough energy the
compound amino acid injection provides a nitro-
gen source for protein synthesis so that a posi-
tive nitrogen balance can be reached.
(iii) Synthesizing proteins and promoting wound
healing.
(iv) Regulating immune and releasing infl ammatory
mediators: injection of common compound
amino acids contains not only essential and non-
essential amino acids but also other condition-
ally essential amino acids such as glutamine,
arginine, and taurine, which are the precursors
of protein synthesis and regulation of immune
and infl ammatory mediators. These condition-
ally essential amino acids, in addition to ω-3
fatty acid and dietary fi ber, are called anti-
infl ammatory immune nutrients.
(b) The preparations of compound amino acids injection
usually used in China
Two types of compound amino acid injection are
clinically used: one is a balanced amino acid prepara-
tion, also called nutritional amino acid preparation,
containing most amino acids in plasma whose pro-
portions are similar to free plasma amino acids; the
other is an unbalanced amino acid preparation, also
called disease-adaptable amino acid preparation,
adding essential amino acids according to the metab-
olism of the plasma amino acids in the status of cer-
tain diseases.
(i) Balanced amino acids
According to Clinical Guide to the Chinese
Pharmacopoeia, the balanced amino acid injection
for adults is divided into six types: 18AA, 18AA-I,
18AA-II, 18AA-III, 18AA-IV, and 18AA-V, all
containing 18 types of amino acid. The main dif-
ferences are the different types of non-essential
amino acids and different total quantity of amino
Table 16.63 Energy and protein requirement of surgical patients
Patient condition
Energy kcal/(kg·day)
Protein g/(kg·day)
NPC:N
Normal or medium malnutrition
(stress at a low level)
20–25
0.6–1.0
150:1
Stress at a middle level
25–30
1.0–1.5
120:1
Hypermetabolism, stress
30–35
1.5–2.0
90–120:1
Burn
35–40
2.0–2.5
90–120:1
NPC :N ratio of nonprotein calories to nitrogen
Table 16.64 Daily recommended amount of parenteral alimentation
Energy: 20–30 kcal/(kg·day)
Water: 1–1.5 ml · kcal −1 · kg −1 · day −1
Glucose: 2–4 g/(kg·day)
Fat: 1–1.5 g/(kg·day)
Nitrogen: 0.1–0.25 g/(kg·day)
Amino acids: 0.6–1.5 g/(kg·day)
Electrolyte: daily requirement of parenteral alimentation in adults
Sodium: 80–100 mmol
Potassium: 60–150 mmol
Chlorine: 80–100 mmol
Calcium: 5–10 mmol
Magnesium: 8–12 mmol
Phosphorus: 10–30 mmol
Fat-soluble vitamin
A 2,500 IU
D 100 IU
E 10 mg
K 1 10 mg
Water-soluble vitamin
B 1 3 mg
B 2 3.6 mg
B 6 4 mg
B 12 5 μg
Pantothenic acid 15 mg
Niacinamide 40 mg
Acidum folicum 400 μg
C 100 mg
Microelement
Copper 0.3 mg
Iodine 131 μg
Zinc 3.2 mg
Selenium 30–60 μg
Molybdenum 19 μg
Manganese 0.2–0.3 mg
Chrome 10–20 μg
Iron 1.2 mg
16.2 Parenteral Nutrition

412
Table 16.65 Routine dosage of parenteral alimentation
Nitrogen
(g)
Glucose
(g)
Fat (g)
Calories (kcal) Na (mmol)
K (mmol)
Ca
(mmol) Mg (mmol)
P (mmol)
Microelement
Vitamin
Volume (ml)
Surrounding
8–10
200–250 50–70
1,300–1,700
80
50
5
8
10–12
Basal amount
Basal amount
2,500–3,000
Typical
10–14
250–300 50–100 1,500–2,200
100
60–80
5
8
12–16
Basal amount
Basal amount
2,250–3,000
Medium stress 12–16
250–300 50–100 1,500–2,200
100–120
75–100
5
10
10–20
Basal amount
Basal amount
2,500–3,000
Heavy stress
12–18
250–300 50–100 1,500–2,200
100–120
80–100
6
10
10–20
Basal amount,
zinc, selenium
Basal amount, B 1 2,500–3,500
Renal failure
6–12
250–300 50–70
1,500–1,900
Individuation Individuation 6
Individuation Individuation Individuation
Add amount
Individuation
Liver failure
4–10
200–250 25–60
1,200–1,700
80
40–60
6
Individuation 10–16
Individuation
Basal amount
2,000–3,000
Infection
10–16
150–250 50–70
1,300–1,900
100
60–100
5
6–8
10–20
Iindividuation
Add amount, B 1
2,500–3,000
Dystrophy
8–16
150–250 50–70
1,200–1,800
50–70
80–100
6
10–16
20–40
Basal amount, zinc,
selenium, copper
Add amount
2,000–2,500
Heart failure
10–12
150–250 50–70
1,200–1,700
50–70
80–100
6
10–12
15–25
Basal amount, zinc,
selenium
Add amount, B 1
2,000–2,250
MODS
10–14
150–300 50–80
1,200–2,000
100–120
60–100
6
6–8
10–20
Individuation, zinc,
selenium
Basal amount, B 1 2,000–3,500
Diabetes
10–14
200–250 50–70
1,300–1,700
100
80
6
8–10
15–40
Basal amount
Basal amount
2,500–3,000
Fat intolerance 10–14
300–400 0–20
1,500–1,600
100
80
6
8–10
10–20
Basal amount
Basal amount
2,500–3,000
Short–bowel
syndrome
7–14
200–350 20–100 1,000–2,400
50–250
50
9
10
10
Basal amount, zinc,
copper
Add amount
1,500–2,500
Prescription recommends of # renal failure or * liver failure
* Recommend amino acids solution, include glutamine or add to glutamine, ** intensively recommend
Supplying calories, nitrogen, electrolytes on the basis of patients’ needs or supernumerary lost
Add insulin if needed
Basal dose of vitamin: one of Soluvit and one of Addamel
Basal dose of microelement: one of Addamel
Add Zn, Cu, and Se if needed
Add vitamin B 1 according to actual condition
Note: guarantee stability of nutrient solution before application all of the individual prescriptions
MODS multiple organ dysfunction syndrome
16 Nutrition in Burns

413
acids per unit volume. The ingredients, specifi ca-
tions, dosage forms, and characteristics are shown
in Tables 16.66 and 16.67 .
The indications for balanced amino acid
injection include: malnutrition caused by
frequent vomiting or fasting in the perioperative
period; high catabolism caused by a large burn
size, severe trauma, and infection; hypoprotein-
emia caused by excessive protein consumption
or protein synthesis disorder; digestive system
Table 16.66 The compositions of six balanced type amino acid injections (g/1,000 ml)
Preparation
Amino acid
compound
injection
(18AA)
Amino acid
compound
injection
(18AA-I)
Amino acid compound
injection (18AA-II)
Amino acid compound
injection (18AA-III)
Amino acid
compound
injection
(18AA-IV)
Amino acid
compound
injection
(18AA-V)
Composition and index
5 %
12 %
5 %
8.5 %
11.4 %
L-cysteine
0.145
1.00
0.48
0.44
L-phenylalanine
5.33
12.80
5.5
3.5
5.9
7.9
9.35
3.11
2.83
L-alanine
2.00
4.80
3.0
7.2
12.2
16.3
6.20
2.07
1.88
L-methionine
2.25
5.40
1.9
2.5
4.2
5.7
3.50
1.17
1.06
L-proline
1.00
2.40
8.1
2.9
5.0
6.8
3.30
1.10
1.00
L-glutamic acid
0.75
1.80
9.0
2.5
4.2
5.7
6.50
2.17
1.97
L-cystine
0.10
0.24
0.2
0.2
0.2
L-arginine
5.00
12.00
3.3
4.9
8.4
11.2
7.90
2.63
2.89
L-lysine
4.30
10.32
4.9
5.5
9.5
12.7
8.80
4.13
3.33
L-tyrosine
0.25
0.60
0.5
0.2
0.2
0.3
0.35
0.116
0.11
L-leucine
4.90
11.76
5.3
3.4
5.9
7.9
12.50
4.17
3.79
L-aspartic acid
2.50
6.00
4.1
1.5
2.5
3.3
3.80
1.27
1.15
L-tryptophane
0.90
2.16
1.0
0.85
1.4
1.9
1.30
0.52
0.39
L-serine
1.00
2.40
7.5
1.9
3.4
4.5
2.20
0.73
0.67
L-threonine
2.50
6.00
3.0
2.5
4.2
5.7
6.50
2.17
1.98
L-valine
3.60
8.64
4.3
3.2
5.5
7.3
4.50
1.50
1.36
L-isoleucine
3.52
8.45
3.9
2.5
4.2
5.7
5.6
1.87
1.70
L-histidine
2.50
6.00
2.4
3.0
5.0
6.8
6.00
2.00
2.46
Glycine
7.60
18.24
2.1
3.5
5.9
7.9
10.70
3.57
3.24
Aminoethylsulfonic acid
Calcium chloride
0.368
Potassium chloride
0.375
Magnesium sulfate
0.37
Sodium hydroxide
2.0
Potassium hydroxide
0.84
Antioxidant
Yes
Yes
Yes
0.03
0.03
0.03
Yes
Yes
Sodium pyrosulfi te
0.3
0.3
0.3
0.3
Sodium bisulfate
0.5
0.5
D-glucitol
50.0
50.0
Xylitol
75
Glucose-H 2 O
1.3 ml
2.5 ml
2.75 ml
Glacial acetic acid
50
85
114
103.60
Total amino acid
100.00 (10 %)
Free amino acid
1.09
Essential amino acid and
non-essential amino acid
Nitrogen
7.9
14
18
1.52 %
Electrolyte concentration
Na+ ≤5 mEq/L,
Cl− = 0, K+ =0,
CH3COO-: 60 mEq/L
Total energy
0.88
(210)
1.46
(350)
1.92
(460)
pH
5.6
5.6
5.6
5.2~6.8
Osmotic pressure
450
810
1,130
3
16.2 Parenteral Nutrition

414
diseases such as severe enteritis and alimentary
tract hemorrhage.
The contraindications are severe azotemia,
hepatic encephalopathy, hepatic insuffi ciency,
renal failure, amino acid metabolism disorder,
and allergy to the preparation.
The adverse reactions of balanced amino
acid injection include: nausea, vomiting, dys-
pnea, palpitations, chill, fever, headache, or
facial fl ush probably caused by rapid infusion;
thrombophlebitis caused by single-bottle infu-
sion via a peripheral vein, hyperammonemia,
and high blood urea nitrogen caused by hepatic
and renal insuffi ciency, cholestasis, and jaun-
dice caused by long-term infusion, accidental
rash-like allergy reactions, and liver function
damage.
The usage and doses are described below.
The infusion volume of 5 % balanced amino
acid injection is 500–2,000 ml/day at a rate of
40–50 drops/min; the infusion volume of 12 %
of balanced amino acid injection is 250–750 ml/
day at a rate of 20–30 drops/min; balanced
amino acid injection should be mixed with fat
emulsion and glucose as an “all-in-one” nutri-
tional fl uid.
(ii) Disease-adaptable amino acid injection
Under normal conditions the ratio of essen-
tial and non-essential amino acids and the
proportion of various amino acids are in bal-
ance. However, in the status of some diseases
amino acid metabolism disorder results in
the defi ciency of or increase in one or several
amino acids and unbalanced proportions. The
improper supply of exogenous amino acids
probably aggravates amino acid metabolism
disorder and the disease worsens. The com-
position of amino acids in disease-adaptable
amino acid injection is determined according to
the metabolism of different disease conditions
and divided into liver disease-adaptable, kidney
disease-adaptable, craniocerebral injury-adapt-
able, and trauma-adaptable types.
A. Trauma-adaptable amino acid injection
(15AA)
Trauma-adaptable amino acid injection,
which contains branched chain amino acids
(BCAAs), is used for patients with amino
acid spectrum disorder and protein metabo-
lism caused by severe trauma and burn. It
supplies the exogenous branched chain
amino acids, which can reduce muscle pro-
tein hydrolysis, promote protein synthesis
in liver, and provide energy in peripheral tis-
sue. The indications include a large area of
burn, trauma, and severe post-surgery infec-
tion. The usage is intravenous (250–750 ml/
day) at a rate of 30–40 drops/min.
Some researchers have studied whether
BCAA- rich injection is benefi cial to the
nitrogen balance of patients with burn or
trauma. In 2004, Gu et al. demonstrated
that BCAAs such as valine, leucine, and
isoleucine were able to be oxidized in skel-
etal muscle to provide energy and regulate
energy substrate, gluconeogenesis substrate,
and muscle protein. The stress reactions of
trauma and burn result in the consumption
of muscle protein and release of alanine,
glutamine, and BCAA. Alanine and gluta-
mine account for two thirds of amino acids
released from muscle, and BCAA is the pre-
cursor of the synthesis of alanine and glu-
tamine. Therefore, the main purpose of the
supplement of BCAA is to reduce muscle
hydrolysis, promote protein synthesis in the
Table 16.67 The dosage forms and characteristics of balanced type amino acid compound injection
Form of medication
Total amino acids
Feature
18AA
5 %
250
500
50
Contains hydrochloride
12 %
250
500
100
18AA-I
7 %
250
500
70
18AA-II
5 %
250
500
50
8.5 %
250
500
85
11.4 %
250
500
114
Osmotic pressure: 1,130, input
from central vein
18AA-III
11.4 %
250
114
Contain 60 mmol/L acetic acid
18AA-IV
3.48 %
250
34.8
Contain 7.5 % glucose, caution
in diabetic patients
18AA-V
3.2 %
250
32
Contain xylitol and hydrochloride
Unit: g/1,000 ml
From the dispensing information of the Clinical Pharmacopoeia [44]
16 Nutrition in Burns

415
liver and other organs, and provide energy
in peripheral tissue when the carbohydrate
cannot be used under the stress status. Thus,
the patients with burn or trauma should use
BCAA-rich injection to recover the nitrogen
balance.
B. Liver disease-adaptable amino acid injection
Patients with severe hepatic insuffi ciency
have amino acids metabolism disorder and
malnourishment presenting as an increase
in plasma aromatic amino acids and sulfur
amino acids and a decrease in BCAAs. The
liver disease-adaptable amino acid injec-
tion contains high amounts of BCAAs,
low amounts of aromatic amino acids and
methionine, which are helpful in the nutri-
tional support of patients with liver diseases.
The clinical applications of liver disease-
adaptable amino acid injection include argi-
nine hydrochloride, and compound amino
acid injection (3AA and 20AA).
C. Kidney
disease-adaptable
amino
acid
injection
Patients with renal diseases need supple-
mentation of essential amino acids, which
can bind with amino acids non-essential
in the blood to reduce urea nitrogen. The
indications include acute and chronic renal
insuffi ciency, and severe renal failure not
caused by renal factors. The contraindica-
tions are amino acid metabolism disorder,
severe liver damage, and contraindications
related to balanced amino acid injection. The
adverse reactions include nausea, vomiting,
palpitations, and chill caused by rapid infu-
sion. The specifi cation is 250 ml (13.98 g).
The usage is intravenous 250–500 ml/day
at a rate of 30–40 drops/min, and the maxi-
mum dose is no more than 1,000 ml/day.
Simultaneously, enough calories should be
supplied to ensure protein synthesis.
3. Technical specifi cations for total nutrient admixture
Glucose, amino acids, and fat emulsion are the main
ingredients of PN solutions. Long-term clinical practice
reveals that single or excessive use of PN solutions may
result in negative effects on patients; they may even hin-
der rather than help. Therefore, reasonable nutritional
preparation should be adopted in clinical nutritional sup-
port to give full play to each type of PN solution and
reduce the incidence of complications. In 1974, Solassol
proposed the concept of “three-in-one” mixed infusion,
which involved a mixture of glucose, amino acids, and fat
emulsion in certain proportions. In 1988, the American
Society for Parenteral and Enteral Nutrition suggested the
total nutrient admixture, which referred to the mixture of
all nutrients for PN, including glucose, amino acids, fat
emulsion, trace elements, and water- and fat-soluble
vitamins.
In recent years, the Nutrition Support Group of the
Chinese Surgical Association and the Chinese Society for
Parenteral and Enteral Nutrition have formulated the
technical requirements for the preparation of total nutri-
ent admixture and have required the units of parenteral
and EN to set up the Pharmacy Intravenous Admixture
Service and provide professional technicians to ensure
medication safety.
(a) Composition of total nutrient admixture
Total nutrient admixture contains the seven main
nutrients that maintain metabolism, including glucose,
amino acids, fat emulsion, trace elements, vitamins,
electrolytes, and water. Glucose and fat emulsion supply
nonprotein calories, and compound amino acid injection
provides a nitrogen source.
(b) Advantages of total nutrient admixture
(i) All nutrients mix in certain proportions to avoid
calorie supply from amino acids and promote
protein synthesis.
(ii) Calories are provided by both glucose and fat
emulsion, which reduce glucose quantity and
avoid the metabolism complications caused by
excessive glucose.
(iii) The adverse reactions caused by a single infu-
sion of certain nutrients are reduced or avoided.
(iv) The low osmotic pressure of total nutrient
admixture diminishes vascular stimulation.
(v) The admixture is sealed after being pre-
pared under the aseptic conditions to avoid
contamination.
(c) Preparation of total nutrient admixture
(i) Ingredients of total nutrient admixture: total
nutrient admixture contains all kinds of nutrients,
provides the actual requirement of nutrients, and
ensures that the nutrients are in the correct
proportions.
(ii) Requirement of calories: as a complement to
EN, the requirement for calories in the total
nutrient admixture is calculated according to the
actual need. When total PN (TPN) is adopted,
the requirement for calories can be calculated
using an indirect calorimeter or by prediction
through formulas. The indirect calorimeter can
measure the correct calories, but because of the
complicated operation, it is often reserved for
severe patients. For common patients prediction
through formulas is also a good alternative.
Although the prediction through formulas can
16.2 Parenteral Nutrition

416
be erroneous compared with actual calories, it is
a simple and easy method and can be calibrated
by the monitoring.
The calorie prediction formula commonly
used for burns patients is the Harris–Benedict
formula listed below:

BEE
W
H
A male
BEE
W
=
+
+
−
(
)
=
+
+
66 47
13 75
5 0033
6 755
655 1
9 563
1 8
.
.
.
.
;
.
.
. 5
4 676
H
A female .
−
(
)
.



calories
BEE
activity coefficient
temperature
coefficient
s
=
×
×
× tress coefficient

Activity coeffi cient: 1.2 for resting; 1.25 for slight
activity; 1.3 for normal activity.
Temperature coeffi cient: 1.1 for 38 °C; 1.2 for
39 °C; 1.3 for 40 °C; 1.4 for 41 °C.
Stress coeffi cient: EE of burn patients can
be calculated according to the formula,
1000 × BSA + 25 × TBSA, proposed by the Third
Military Medical University of China. The daily
EE of adults can also be calculated by weight
as 20–30 kcal/kg. In recent years, the concepts
of “low-energy parenteral nutrition” and “per-
missive under-feeding” have been proposed for
severe burns patients.
(iii) Requirement for nitrogen: the Chinese recom-
mendation is 1.2–1.5 g/(kg·day). The nitrogen
requirement of severe burns patients increases
because of high catabolism and nitrogen loss.
The nitrogen requirement can be calculated by
the nitrogen output in 24-h urine and input in the
previous day, and also by the formula of UUN
(24-h urea nitrogen)+4 (other nitrogen loss) or
estimation of 1–1.5/(kg·day) on the basis of
weight. After the determination of nitrogen
requirement, balanced amino acid injection or
disease-adaptable amino acid injection has been
chosen according to disease status.
(iv) Standards of preparation: the ratio of nitrogen
and nonprotein calories is 1:120–150 kcal,
which means 1 g of nitrogen to 120–150 kcal
of energy. For patients with severe burns the
ratio of nitrogen to nonprotein calories is up to
1:120–150 kcal order to ensure the utilization
of amino acids and avoid the oxidation of
amino acids. Both glucose and fat emulsion are
used for energy supply, and the proportion of
fat in nonprotein calories is 2:1 or 1:1. Patients
on TPN are supplied with the daily require-
ment of vitamins, trace elements, and electro-
lytes. Patients on PN are supplied with the
above nutrients according to the conditions of
the food.
16.2.4
Evaluation of Parenteral Nutritional
Support in Burns Patients [ 42 – 44 ]
16.2.4.1 The Effectiveness of Parenteral
Nutritional Support in Patients
with Severe Burns
We observed 31 patients suffering from severe burns receiv-
ing PN support from 1978 to 1984. We summarized the
respective indications and caution with regard to burn
patients in this section.
All of the 31 cases were adults, 25 had thermal burns, 4
had chemical burns, 1 had an inhalation injury, and 1 had an
electric burn. The TBSA of the patients’ burns ranged from
30 to 95 %. Twenty-fi ve cases were diagnosed with third-
degree burns covering 10–56 % of the TBSA. All 31 patients
were treated with anti-shock, anti-infection, and wound sur-
face cleaning in accordance with the routine method.
Generally, the PN support were applied after shock stage,
same as 3–4 days after burn, in some cases the time were
postponed 1 week after burn. The observation period was
3–7 weeks. Twenty-nine patients survived and 2 died. One
of the patients who was diagnosed with burns covering 90 %
of the TBSA, with third-degree burns covering 56 % of the
TBSA, died of multiple organ dysfunction syndrome
(MODS), and 1 patient who was diagnosed with severe
inhalation injury died of hemoptysis on the 46th day after
the burn.
The objective of PN support is to supply energy for
patients and to recover the albumin reserve of the body of the
patients. Usually, we can evaluate the effectiveness of PN
support by measurement of serum albumin (SAB), prealbu-
min, and the improvement of immune function and the nitro-
gen balance. However, the regular indices of nutrition were
disability for severe burns patients because of high catabo-
lism, water retention in the early burn stage, and the exis-
tence of a wide skin wound. We evaluated the effectiveness
of PN support by observing the nitrogen balance and SAB
level, the speed of wound healing, and complications in the
course of the disease.
1. Observation of the nitrogen balance
Study of the nitrogen balance of severe burns patients
shows that the negative nitrogen balance turns to a posi-
tive nitrogen balance usually following the primary
healing of the burn wound. In this group, the positive
nitrogen balance of 12 cases occurred 15–32 days after
the burn; this was earlier than the primary healing of the
burn wound, which was 7–30 days. The total quantity of
nitrogen of one patient 1 day before reaching a positive
nitrogen balance was 18–32 g, the average was 24.4 g.
The quantity of the total intake of nitrogen of one patient
per day was 15–17 g, the average was 18.8 g, and
40–80 % of the total intake of nitrogen was supplied by
transfusion. It played an important role in changing
16 Nutrition in Burns

417
patients from the negative nitrogen balance status to the
positive nitrogen status in advance. The transfusion fl uid
contained a high proportion of amino acids, which made
up for the insuffi cient nitrogen intake from food
(Table 16.68 ).
2. Changes in serum albumin in burns patients
Many studies show that hypoproteinemia can be cor-
rected by PN support. Many researchers thought that
serum albumin was one index of human nutrition; how-
ever, this should not be regarded as an index of effective-
ness of PN support in patients with a short-term abrosia
after the operation, because the half-life of albumin is
about 20 days. The acute-phase proteins with a shorter
half-life should be used in these patients, such as prealbu-
min (half-life 2 days), fi bronectin (half-life 15 h), and
transferrin (half-life 2 days).
Albumin can be a indication of the nutrition of severe
burned patients, because the term of PN support is very
long in these patients. We observed the serum albumin of
25 cases, and compared the change in serum albumin
before and after the patients received PN support (shown
in Table 16.69 ).
The serum albumin of patients always decreased sig-
nifi cantly in the early stage after the burn, because of the
leak of body fl uid to the wound and tissue space, which
contains plenty of albumin. Hypermetabolism, continued
exudation of the body fl uid, and weakness of the intestine
of burns patients leading to hypoproteinemia, which
weakened the resistance of the body and delayed wound
healing. Thus, the patients with severe burns needed a
high intake of protein, high-calorie food, and PN support.
Table 16.66 shows that all the albumin of the patients
decreased after the burn, and the level of serum albumin
of all the patients increased to some degree regardless of
the level of serum albumin in the early stage after the
burn. The level of serum albumin of patients rises to the
expected level with active PN support, and the percentage
of nitrogen intake of PN of the total intake of nitrogen
was 61.5 % in this case group.
3. The healing time of the burn wound
It is diffi cult to pretest when a burn wound will heal,
because there are many factors that infl uence the process
of wound healing. Second-degree burn wounds heal
according to the normal pathophysiological process and
skin graft survival on third-degree burn wounds can be
regarded as effective treatment. In this group, the average
healed wound comprised 61 % of the total TBSA when
the patients arrived at the point of a positive nitrogen
balance; all the second-degree burn wounds healed, and
the skin grafts survived on the third-degree wounds.
All the facts show that PN support plays an important role
in the process of burn wound healing.
Table 16.69 Changes in serum albumin before and after parenteral nutritional support
Pre-parenteral nutrition (PBD 4–7)
Post-parenteral nutrition (PBD 25–37)
Albumin (g%)
Case no.
Case of albumin
increase
Average value
of increase (g%)
<2
2
2 (100 %)
1.63
2.1–3.0
15
15 (100 %)
1.17
>3.0
8
6 (75 %)
0.68
Table 16.68 Survey of nitrogen balance
Case number
1
2
3
4
5
6
7
8
9
10
11
12
TBSA %
40
58
45
45
70
70
35
95
50
70
90
60
TBSA % of third-degree
36
10
10
38
10
50
40
56
Total dinitrogen (g/day)
Before positive nitrogen balance
20.6
27.7
27.1
18.6
23.7
19.4
19.3
29.2
19.7
31.7
24.7
28.9
After positive nitrogen balance
19.9
23.7
19.9
18.6
18.9
14.9
15.7
14.4
11.2
26.7
29.9
20.5
Total intake of nitrogen (g/day)
Before positive nitrogen balance
18.3
26.8
20.7
16.9
17.8
18.4
15.9
16.7
15.6
14.4
20.8
22.9
After positive nitrogen balance
25.6
27.8
22.9
20.9
22.9
25.7
18.5
19.3
11.4
35.9
32.2
32.1
The proportion of transfusion among the total
nitrogen intake (%)
51
46
54
55
72
76
80
72
44
75
70
44
Time to reached positive nitrogen balance (PBD) 15
22
16
19
20
15
22
32
26
16
16
20
Healed wound area (%) at the time of positive
nitrogen balance
20
55
30
25
40
42
20
59
25
35
27
40
Time of basic wound healing (PBD)
45
40
45
46
31
27
45
56
60
40
Died at
PBD 36
26
Total dinitrogen = nitrogen in urine and feces + nitrogen exuded from the wound (calculation as 25 % of urine and feces nitrogen)
16.2 Parenteral Nutrition

418
16.2.4.2 Evaluation of Parenteral Nutritional
Support in Patients with Severe Burns
1. Clinical data
There were nine burns patients in this group, the aver-
age proportion of the TBSA affected was 42.1 ± 12.6 %,
the average proportion of the TBSA affected by third-
degree burn wounds was 26.71 ± 13.61 % (Table 16.70 ).
All the nine burns patients were cured.
(a) Timing of PN support: from the end of the shock
stage to the inversion point of the nitrogen balance,
the average period was 18 days.
(b) Dosage and compound of the nutrient solution were
shown in Table 16.71 . The nitrogen content was
3.8 g/series. The patients were supplied with two
series of nutrient solutions by injection of the vein at
the beginning of PN support, and then the amount of
solution was increased slowly. The maximum PN
support was a supply of six series per day.
(c) Calories: the calorie demands of the patients were
calculated according to the formula of Curreri and
Wilmore, the proportion of calories supplied by intra-
lipids compared with the nonprotein calories supplied
was 35–45 %.
(d) Other nutrients and nitrogen balance
The electrolyte, vitamin, and trace elements
were supplied regularly. The nitrogen balance was
calculated every day. The amount of urinary nitro-
gen over 24 h × 25 % = amount of nitrogen that
leaked from the burn wound. There were very few
feces throughout TPN; thus, fecal nitrogen was
negligible.
(e) Monitoring items:
(i) Physical signs: the general state of patients and
the condition of the burn wound. Good skin graft
survival could be regard as healing; anything
else should not be regarded as healing.
(ii) Biochemical examination of the blood and urine:
routine blood and urine tests, the electrolyte and
BUN, Cr, CO 2 -cp of blood, serum albumin, trans-
ferrin on a day before the beginning of the TPN and
then on the 1st, 3rd, 5th, 7th, 14th, and 21st days or
until the inversion point of the nitrogen balance.
(iii) Body weight: we measured the weight of
patients on the fi rst day of TPN, and on the 3rd,
7th, and 14th days, or until the day of the inver-
sion point of the nitrogen balance according to
an electronic scale called DT-200.
2. Result:
(a) Seven out of the nine patients who received TPN
achieved inversion of the nitrogen balance at
10–26 days (shown in Table 16.72 ).
(b) An increase in serum albumin of patients occurred in
three cases, it decreased in fi ve cases, and was
unchanged in one case. The transferrin of fi ve out of
nine cases was increasing continuously to some
degree. The examination of liver function, K+, Na+,
Cl−, BUN, and TPN of these patients is normal. The
details are shown in Table 16.73 .
(c) There were complete data for eight out of the group
of nine cases. Six patients’ weight increased, two
patients’ weight decreased, and the maximum
increase in weight was 3.5 kg.
(d) The sero-electrolytes of the nine cases were within
the normal range during the TPN period.
(e) Serum
aminogram
variation:
the
free
sero-
aminograms of six cases were analyzed during the
TPN period. The result showed that free sero-
aminoacid of patients increased signifi cantly after
TPN support. The BCAA, lysine, and methionine of
essential amino acids increased to varying degrees.
The glutamic acid and glycine were signifi cantly
Table 16.70 General information
Case no.
Gender
Age
TBSA (TBSA consisting
of third-degree burn)
Complications
1
Male
38
47 (15)
Null
2
Male
28
10 (8)
Fracture of mandible (oral intake disabled)
3
Male
20
52 (50)
Inhalation injury (tracheotomy)
4
Male
36
40 (35)
Null
5
Male
38
45 (35)
Inhalation injury (tracheotomy)
6
Female
19
35 (20)
Inhalation injury (tracheotomy)
7
Male
40
48 (0)
Null
8
Male
19
47 (0)
Null
9
Female
19
55 (52)
Inhalation injury (tracheotomy)
Table 16.71 Prescription of nutrient solution
Nutrients
Dosage
18FAA (ml)
250
10 % GS (ml)
500
50 % GS (ml)
60
Vitamin C (g)
0.5
10 %KCl (ml)
10
Insulin (U)
10
16 Nutrition in Burns

419
increased too. Therefore, we thought that the nitrogen
source of the nutrient solution based on 18FAA might
prevent the free sero-aminoacid from decreasing in
burns patients to some degree.
3. Conclusion:
(a) One of the characteristics of the metabolism of
patients with severe burns is a severe negative nitro-
gen balance lasting long time, followed by decreased
weight; thus, the patients need a prompt intake of
calories and protein. Although the nutritional support
cannot change the metabolic process, it can shorten
the time of the positive nitrogen balance. The meth-
ods of nutritional support include peroral, enteral ali-
mentation, and PN etc. Some specifi c patients such as
patients with chemical burns to the alimentary canal
can neither take in nutrition via the mouth or intes-
tine, and these patients should receive TPN support.
The data of this series showed that the nutrient solu-
tion whose nitrogen source based on 18FAA with the
proper proportions of nitrogen/calories were supplied
for the patients with severe burns, which could help
the patients to achieve a positive nitrogen balance.
(b) The nitrogen balance of the nutrient solution of this
series based on 18FAA amino acids, which is a type
of balanced nutrition amino acid injection, contains
eight types of essential amino acids and ten types of
non-essential amino acids; the proportion of aromatic
amino acids to the total concentration of amino acids
was 9 %. The nutrient solution of this series was
abundant with nitrogen (15.2 mg/ml), the proper pro-
portions of essential amino acids/non-essential amino
acids (1:0.9), small amounts of electrolytes:
Na + ≤5 mmol/L; Cl - =0, K + =0, CH 3 COO − was about
600 mmol/L. These characteristics ensured that PN
support with this kind of solution could avoid hyper-
chlorine acidosis and could supply a suitable nitrogen
source.
(c) The serial monitoring of serum albumin and transfer-
rin showed that the increase in serum albumin was
not signifi cant and that transferrin increased to some
degree. The metabolic cycle of serum albumin is long
(an average of 21 days), and many factors may infl u-
ence the metabolism of serum albumin; thus, serum
alumin is not a suitable index of evaluation for
TPN. Transferrin is a better index to represent the
protein metabolism of burns patients. In addition, we
should evaluate the patients’ nutritional status using
general information.
(d) Two patients in this series did not achieve a positive
nitrogen balance using TPN support over 28 days.
The TBSA covered by the burn in one of the cases
was 55 %, the proportion of the TBSA covered by
third-degree burn is 52 %, which means that TPN
support cannot supply enough nutrition for patients
with third-degree burns covering more than 50 % of
the TBSA. The proportion of the TBSA of another
patient covered by a burn was 48 %, which was not a
third-degree burn. This means that there are many
Table 16.72 Information on nitrogen balance
Case no.
Nitrogen
intake (g/day)
Elimination
nitrogen (g/day)
Calorie (kcal/day)
Reaching nitrogen
balance (PBD)
Wound healing at
nitrogen balance (%)
Urinary
volume (ml)
1
7.6–22.8
17.4–21.5
1,940–3,020
10
35
1,570–3,250
2
7.6–22.8
15.0–25.7
2,690–3,570
11
7
2,180–3,160
3
7.6–22.8
10.9–25.0
1,740–3,250
26
27
1,900–3,440
4
7.6–22.8
15.4–26.2
1,740–3,250
22
23
2,800–3,010
5
7.6–22.8
9.4–24.4
1,740–3,250
1
30
1,020–3,770
6
7.6–22.8
8.0–20.5
1,420–3,020
13
14
1,260–3,290
7
7.6–22.8
21.4–29.1
1,740–3,020
Negative
/
1,950–4,550
8
7.6–22.8
9.3–21.0
1,420–2,700
17
30
980–3,000
9
7.6–22.8
12.6–26.4
1,190–2,700
Negative
/
2,550–4,600
Table 16.73 Serum protein
before and after total parenteral
nutrition (TPN)
Case no.
Serum albumin (%)
Transferrin (mg%)
Hemoglobin (g/L)
1
2.5–2.5
–
136–123
2
2.7–2.9
115–257
130–106
3
2.5–2.0
206–292
115–104
4
2.6–2.7
115–226
123–98
5
2.9–2.3
196–210
103–98
6
2.9–2.2
–
97–89
7
2.2–3.2
–
106–94
8
3.4–2.8
267–297
133–130
9
2.9–2.5
–
103–82
16.2 Parenteral Nutrition

420
factors that have an impact on the effectiveness of
TPN support besides TBSA and the degree of burn,
such as the prescription of nutritional liquid. We have
revised the prescription to degrade osmotic pressure,
which can reduce the urine of patients, and reduce the
discharge of nitrogen. In addition, we have improved
the technique of transfusion, for example, the appli-
cation of a 3-L bag, which permits the mixing of glu-
cose, amino acids, intralipids, electrolytes, and trace
elements into one or two 3-L bags, and can supply
patients for 24 h. There may be some other factors
that have an impact on the effectiveness of TPN sup-
port and that need investigating in the future.
(e) There are rare burns patients who cannot take in by
mouth at all; thus, we selected this type of patient for
this series to observe the effectiveness of TPN sup-
port. In fact, we can combine the parenteral and
enteral nutrition to support the most severely affected
burns patients.
4. In summary, parenteral nutritional support has been
applied clinically since the 1960s, and has developed con-
stantly with the improving technology. PN support has
created many miracles in the clinic; its effectiveness was
affi rmed and commonly applied in the clinic. However,
some side effects were found by the case group study,
e.g., excessive calorie and nutriment substrate in the nutri-
ent fl uid, and damage to the mucosal barrier caused by
infection and metabolic complications.
Researchers have realized the important contribution of
PN support for patients, and improved the measure-
ment of PN support, such as:
(a) An institute manual for PN, which includes the oper-
ating manual and indication for and monitoring of
nutritional status.
(b) All the nutrient fl uid was prepared as a total nutrient
admixture (TNA), and then the TNA is supplied to
patients via intravenous injection. The prescription of
TNA should, according to the clinical nutriology, be
prepared by trained personnel.
(c) If PN support is for a short period or if the nutrient
fl uid volume is small, the fl uid can be supplied by
infusion with a peripheral vein. For long-term PN
support, had to supply fl uid via the central vein or the
peripherally inserted central catheter (PICC) path.
(d) The calories of nutrient fl uid should be in accordance
with the principle of permissive under-feeding, to
avoid producing complications of metabolism.
(e) The source of calories should include glucose and
lipids. For the patients with severe burns, the propor-
tion of the calories supplied by lipids should be under
30 %.
(f) Supplementation of extrinsic source insulin to con-
trol the level of serum glucose.
(g) The prevailing view applying EN pernasal during the
early stages for patients with a large TBSA. The PN
support should be applied if patients cannot tolerate
pernasal EN.
On the whole, nutritional support for patients with
severe burns cannot depend on only one way; the EN
and PN should be combined together. In the clinic,
the relationship of EN and PN is complementary,
instead of the displacement of each other. We apply
TPN support during the intestinal failure stage, and
we apply EN when the function of the intestines is
partially recovered. In fact, one third burns patients
underwent PN was because of the functional impair-
ment of the intestine or because simple EN was insuf-
fi cient. Thus, the combination of PN and EN can be
used for patients with severe burns, which can
improve the tolerance of the patients, and thus plays
an important role in combined therapy for patients
with severe burns.
16.3
Comparison Between Early Enteral
and Parenteral Nutrition
Shiliang Wang
Advanced “hyperalimentation” has been in use since the end
of 1960s, the complications of catheters, metabolism, and
infection have increased gradually, and attention was paid to
EN again after the 1980s. From the middle of the 1980s, a
series of studies to compare early EN and PN was carried out
at the Burns Institute of the Southwest Hospital (BISH), the
Third Military Medical University (TMMU). More than 700
rats and 200 burns patients were used to comparing EN with
PN. Emphasis was placed on 19 cases of severe burns
(33.05 ± 9.97 years, TBSAB 44.95 ± 9.91 %, deep burn
29.58 ± 1.85 %). Starting nutrition within PBH 2 (in animals)
or PBH 24 (in patients) in the EN or PN group. The supple-
mentation of carbohydrate, lipid, and protein is the same
(animal) or similar (patient) in the EN and PN groups.
As mentioned above in Chap. 15 , there is “enterogenous
hypermetabolism” after a burn injury, i.e., intestinal injury
after a severe burn. Under conventional fl uid resuscitation,
the intestinal blood fl ow may decrease, the vessel permea-
bility increase, and ischemia and reperfusion injury exists.
The energy reservoir of intestinal mucosa cells declines,
proliferation and reparation of intestinal mucosa are sup-
pressed, the intestinal structure and function are injured,
endotoxin translocation induced by intestinal injury is
increased, hormones and infl ammatory mediators are
increased, decomposition of the skeletal muscle is intensi-
fi ed, urinary nitrogen output is increased, and the metabolic
rate is enhanced.
16 Nutrition in Burns

421
The comparison of the effect on an organism between EN
and PN is described in the next section.
16.3.1
Enteral Nutrition Could Reduce
the Decrease in Intestinal
and Viscous Blood Flow, the Increase
in Vessel Permeability and Water
Content, and Ischemia
and Reperfusion Injury [ 1 , 5 , 7 , 8 , 20 ,
45 – 48 ]
1. Enteral nutrition could reduce the blood fl ow decrease in
the intestine, liver, and kidney in rats with third-degree
burns covering 30 % of the TBSA (Tables 16.74 , 16.75 ,
16.76 , 16.77 , 16.78 , 16.79 , 16.80 , 16.81 , 16.82 , 16.83 ,
16.84 , 16.85 , 16.86 , 16.87 , 16.88 , 16.89 , 16.90 , 16.91 ,
16.92 , 16.93 , 16.94 , and 16.95 ).
2. Enteral nutrition could decrease the vessel permeability
of the viscus.
3. Enteral nutrition could decrease the water content of the
viscus (Tables 16.83 , 16.84 , 16.85 , 16.86 , and 16.87 )
4. Enteral nutrition could alleviate ischemia and reperfusion
injury (Tables 16.88 , 16.89 , 16.90 , 16.91 , 16.92 , 16.93 ,
16.94 , and 16.95 )
16.3.2
EN Could Promote Intestinal Mucosa
Proliferation and Reparation,
Maintain Intestinal Structure
and Function, and Reduce Intestinal
Translocation [ 7 , 20 , 27 , 49 – 60 ]
1. Enteral nutrition could promote intestinal mucosa prolif-
eration and reparation (Tables 16.96 , 16.97 , 16.98 , 16.99
and 16.100 ). Enteral nutrition could increase the intesti-
nal mucosa cell PI (S+G 2 +M), expression of thymidine
kinase (TK) activity, and proliferating cell nuclear anti-
gen (PCNA), accelerating the process of intestinal mucosa
cell cycle, promoting the secretion of epidermal growth
factor (EGF), PGE 2 , and intestinal trefoil factor (ITF),
which could proliferate and repair intestinal mucosa epi-
thelium. TEPD could refl ect the integrality of the intesti-
nal mucosa barrier.
Enteral nutrition may accelerate the process of the intes-
tinal mucosa cell cycle compared with PN. Cyclin D and
cyclin E regulate the cell cycle from G 1 (gap1) to S (DNA
synthesis). The expression of cyclin D 1 and cyclin E in the
ileum mucosa cells of burn rats is higher than pre-burn; the
highest is about three times the level pre-burn. The
expression of cyclin D 1 and cyclin E on PDH72 in the PN
group is much lower than in the pre-burn and EN groups.
Table 16.77 Changes in renal blood fl ow in rats with third-degree burns covering 30 % of the TBSA (mv, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
31.2 ± 2.1
13.8 ± 1.7*
11.2 ± 0.8*
21.0 ± 2.5*
24.2 ± 3.5
25.0 ± 2.8*
PN
9.2 ± 0.8
9.0 ± 0.6
13.8 ± 1.7
19.8 ± 2.8
16.2 ± 1.4
vs PN * p < 0.05
Table 16.74 Changes in intestinal mucosa blood fl ow in rats with third-degree burns covering 30 % of the TBSA (mv, x
s
±
, n = 8)
PBD
0
1
2
3
5
7
EN
139.9 ± 8.3
90.4 ± 2.8**
118.0 ± 8.9**
117.3 ± 3.8**
123.9 ± 4.4**
124.9 ± 5.9**
PN
67.8 ± 2.5
92.0 ± 8.5
90.1 ± 6.1
102.3 ± 9.7
91.1 ± 36.2
vs PN ** p < 0.01
Table 16.75 Changes of ileal mucosa blood fl ow in rats with third-degree burns covering 30 % of the TBSA (mv, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
31.3 ± 3.6
19.8 ± 2.0*
20.3 ± 2.4**
20.5 ± 4.4*
27.7 ± 4.0*
21.0 ± 10.0
PN
10.8 ± 2.6
9.8 ± 2.4
13.0 ± 5.1
21.0 ± 4.1
18.8 ± 3.7
vs PN * p < 0.05, ** p < 0.01
Table 16.76 Changes in liver blood fl ow in rats with third-degree burns covering 30 % of the TBSA (mv, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
29.3 ± 1.2
13.0 ± 1.0*
10.5 ± 1.0*
14.5 ± 1.2
17.3 ± 1.4*
25.5 ± 3.0*
PN
10.1 ± 0.7
8.0 ± 0.5
11.7 ± 1.0
13.7 ± 0.8
16.7 ± 2.1
vs PN * p < 0.05
16.3 Comparison Between Early Enteral and Parenteral Nutrition

422
Table 16.81 Changes in heart vessel permeability in rats with third-degree burns covering 30 % of the TBSA (μg/100 mg tissue, x
s
±
, n = 6)
PBD
0
6
12
24
48
72
EN
1.5 ± 0.1
1.9 ± 0.1*
3.2 ± 0.2**
4.1 ± 0.2**
3.8 ± 0.3
2.8 ± 0.3
PN
3.2 ± 0.4
4.7 ± 0.2
5.0 ± 0.2
4.3 ± 0.4
3.1 ± 0.3
vs PN * p < 0.05, ** p < 0.01
Table 16.82 Changes in liver vessel permeability in rats with third-degree burns covering 30 % of the TBSA (μg/100 mg tissue, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
2.5 ± 0.2
3.7 ± 0.2
3.2 ± 0.2*
4.2 ± 0.4*
4.1 ± 0.2**
4.0 ± 0.1
PN
4.0 ± 0.2
4.2 ± 0.4
4.8 ± 0.2
4.8 ± 0.2
4.2 ± 0.3
vs PN * p < 0.05, ** p < 0.01
Table 16.78 Changes in ileal vessel permeability in rats with third-degree burns covering 30 % of the TBSA (μg/100 mg tissue, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
1.3 ± 0.5
3.1 ± 0.6
3.7 ± 0.6
2.3 ± 0.8
2.7 ± 0.2
3.0 ± 0.2**
PN
3.8 ± 1.6
3.8 ± 0.5
2.2 ± 2.1
2.1 ± 0.5
5.9 ± 0.6
vs PN ** p < 0.01
Table 16.79 Changes in lung vessel permeability in rats with third-degree burns covering 30 % of the TBSA (μg/100 mg tissue, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
1.0 ± 0.1
1.5 ± 0.1**
4.6 ± 0.2*
4.5 ± 0.2*
4.0 ± 0.1**
3.7 ± 0.2*
PN
2.6 ± 0.2
5.2 ± 0.2
5.1 ± 0.4
4.4 ± 0.1
4.5 ± 0.2
vs PN * p < 0.05, ** p < 0.01
Table 16.80 Changes in renal vessel permeability in rats with third-degree burns covering 30 % of the TBSA (μg/100 mg tissue, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
1.5 ± 0.2
2.4 ± 0.3*
4.9 ± 0.1**
4.6 ± 0.5
4.6 ± 0.3**
4.4 ± 0.2*
PN
3.8 ± 0.5
5.6 ± 0.2
4.9 ± 0.7
6.0 ± 0.1
5.3 ± 0.3
vs PN * p < 0.05, ** p < 0.01
Table 16.84 Changes in lung water content in rats with third-degree burns covering 30 % of the TBSA (%, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
77.1 ± 0.5
78.8 ± 0.5
77.6 ± 0.5*
77.2 ± 0.5*
78.4 ± 0.4
77.9 ± 0.5*
PN
78.8 ± 0.6
79.1 ± 0.5
78.6 ± 0.2
78.9 ± 0.4
79.9 ± 0.8
vs PN * p < 0.05
Table 16.83 Changes in jejunal water content in rats with third-degree burns covering 30 % of the TBSA (%, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
74.1 ± 2.1
77.5 ± 1.9
76.1 ± 1.0
76.0 ± 1.6*
74.1 ± 1.2**
78.6 ± 2.1
PN
75.6 ± 1.9
78.0 ± 0.8
78.8 ± 1.8
78.5 ± 0.6
80.2 ± 2.1
vs PN * p < 0.05, ** p < 0.01
Table 16.85 Changes in renal water content in rats with third-degree burns covering 30 % of the TBSA (%, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
75.5 ± 0.5
76.8 ± 0.6
76.6 ± 0.8
76.2 ± 0.4*
75.5 ± 0.3*
76.8 ± 0.2
PN
76.2 ± 0.8
77.0 ± 0.7
77.8 ± 0.4
76.5 ± 0.4
77.0 ± 0.6
vs PN * p < 0.05
16 Nutrition in Burns

423
Table 16.86 Changes in heart water content in rats with third-degree burns covering 30 % of the TBSA (%, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
75.4 ± 0.5
79.2 ± 0.8
78.6 ± 0.6
77.3 ± 0.4*
78.3 ± 0.5
79.4 ± 0.7
PN
78.8 ± 0.8
79.6 ± 0.5
79.5 ± 0.7
78.4 ± 0.9
79.6 ± 1.0
vs PN * p < 0.05
Table 16.87 Changes in liver water content in rats with third-degree burns covering 30 % of the TBSA (%, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
70.5 ± 0.9
72.6 ± 0.5
71.9 ± 0.5
71.4 ± 0.8*
71.1 ± 0.4
73.0 ± 0.4
PN
72.3 ± 0.5
72.8 ± 0.5
73.9 ± 0.5
71.8 ± 0.4
73.2 ± 0.6
vs PN * p < 0.05
Table 16.89 Changes of lung MDA in rats with third-degree burns covering 30 % of the TBSA (nmol/mg protein, x ± s , n = 6)
PBH
0
6
12
24
48
72
EN
14.9 ± 2.2
24.4 ± 3.4
18.2 ± 2.2*
20.4 ± 3.2
19.9 ± 1.1*
21.0 ± 1.4*
PN
25.1 ± 2.2
26.3 ± 2.2
24.1 ± 1.8
25.1 ± 2.0
26.9 ± 2.2
vs PN * p < 0.05
Table 16.90 Changes in liver MDA in rats with third-degree burns covering 30 % of the TBSA (nmol/mg protein, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
8.9 ± 1.2
16.0 ± 1.4
16.4 ± 3.4
18.2 ± 0.8*
18.2 ± 1.1*
21.7 ± 2.5
PN
17.6 ± 2.8
21.1 ± 4.8
20.8 ± 0.9
23.4 ± 1.2
25.4 ± 3.4
vs PN * p < 0.05
Table 16.91 Changes in renal MDA in rats with third-degree burns covering 30 % of the TBSA (nmol/mg protein, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
6.3 ± 0.5
10.9 ± 1.7
12.9 ± 2.0*
11.3 ± 1.0*
12.7 ± 1.3
13.1 ± 1.2
PN
13.8 ± 1.7
18.8 ± 1.5
15.7 ± 1.7
15.8 ± 1.6
15.5 ± 1.3
vs PN * p < 0.05
Table 16.88 Changes in plasma
MDA in adults with burns
covering 45 % of the TBSA
(μmol/L, x
s
±
)
PBD
1
4
8
14
EN ( n = 10)
6.8 ± 1.5
5.5 ± 0.9**
6.0 ± 0.9**
5.9 ± 1.2
PN ( n = 9)
6.5 ± 1.1
8.4 ± 1.1
7.7 ± 0.7
6.7 ± 1.0
vs PN ** p < 0.01
Table 16.92 Changes in plasma
SOD vitality in adults with burns
covering 45 % of the TBSA
(nU/ml, x
s
±
)
PBD
1
4
8
14
EN ( n = 10)
82.4 ± 18.6
108.9 ± 14.7**
115.4 ± 17.9**
116.1 ± 20.6
PN ( n = 9)
85.9 ± 17.4
66.3 ± 13.7
82.1 ± 21.6
97.4 ± 22.4
vs PN ** p < 0.01
Table 16.93 Changes in liver
SOD vitality in rats with
third-degree burns covering 30 %
of the TBSA (nU/mg protein,
x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
3.5 ± 0.3
2.6 ± 0.2
2.5 ± 0.2*
2.5 ± 0.1*
2.6 ± 0.2*
2.7 ± 0.2*
PN
2.3 ± 0.2
2.0 ± 0.1
2.1 ± 0.1
2.2 ± 0.1
2.1 ± 0.1
vs PN * p < 0.05
Table 16.94 Changes in heart
SOD vitality in rats with
third-degree burns covering 30 %
of the TBSA (nU/mg protein,
x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
4.4 ± 0.6
2.9 ± 0.3*
2.7 ± 0.2*
2.8 ± 0.2
2.9 ± 0.2*
2.7 ± 0.1*
PN
2.2 ± 0.1
2.2 ± 0.1
2.7 ± 0.2
2.2 ± 0.1
2.2 ± 0.1
vs PN * p < 0.05
16.3 Comparison Between Early Enteral and Parenteral Nutrition

424
Cyclin D 1 and cyclin E are measured using Western
blotting, and its relative contents are analyzed using a gel
video scanning system (Tables 16.101 , 16.102 , 16.103 ,
16.104 , and 16.105 ).
Epidermal growth factor could promote the synthesis
of intestinal mucosa DNA, RNA, and protein, accelerate
the process of the intestinal mucosa cell cycle, promote
cell proliferation and differentiation, and speed up the
Table 16.95 Changes in renal SOD vitality in rats with third-degree burns covering 30 % of the TBSA (nU/mg protein, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
3.2 ± 0.3
2.2 ± 0.2
2.2 ± 0.2*
2.0 ± 0.1*
2.3 ± 0.2**
2.1 ± 0.3
PN
2.1 ± 0.3
1.7 ± 0.1
1.7 ± 0.1
1.7 ± 0.1
1.8 ± 0.2
vs PN * p < 0.05, ** p < 0.01
Table 16.96 Changes in intestinal mucosa TEPD in rats with third-degree burns covering 30 % of the TBSA (mv, x
s
±
, n = 8)
PBD
0
1
2
3
5
7
EN
13.5 ± 0.4
6.0 ± 0.2
8.4 ± 0.6
8.7 ± 0.2**
8.7 ± 0.3**
9.0 ± 0.3**
PN
5.3 ± 0.2
8.1 ± 0.3
8.0 ± 0.2
8.0 ± 0.2
8.1 ± 0.3
vs PN ** p < 0.01
Table 16.97 Changes in intestinal mucosa cell PI in rats with third-degree burns covering 30 % of the TBSA (%, x
s
±
, n = 6)
PBD
0
1
2
3
5
7
EN
60.14 ± 6.82
38.38 ± 21.88
29.33 ± 6.83
51.83 ± 4.62*
51.88 ± 4.57*
44.16 ± 11.84
PN
38.60 ± 15.26
35.05 ± 12.56
40.16 ± 13.04
42.28 ± 6.83
45.16 ± 20.68
vs PN * p < 0.05
Table 16.98 Proportional changes of G 0 /G 1 in ileal mucosa cells of rats with third-degree burns covering 30 % of the TBSA (%, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
30.1 ± 7.8
39.7 ± 10.1*
24.3 ± 6.9*
28.3 ± 12.1
21.2 ± 1.6**
43.1 ± 5.5**
PN
21.5 ± 3.8
10.6 ± 1.3
17.1 ± 7.9
74.1 ± 12.7
87.0 ± 8.4
vs PN * p < 0.05, ** p < 0.01
Table 16.99 Proportional changes in S in ileal mucosa cells of rats with third-degree burns covering 30 % of the TBSA (%, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
52.8 ± 6.2
50.0 ± 7.4
59.8 ± 15.0
57.7 ± 11.1
74.3 ± 2.8**
52.3 ± 8.1**
PN
51.1 ± 5.0
69.2 ± 4.4
63.8 ± 12.2
14.5 ± 7.2
9.9 ± 8.3
S period of DNA synthesis in the cell cycle; vs PN ** p < 0.01
Table 16.100 Proliferating cell nuclear antigen (PCNA) immunohistochemistry image pattern analysis in rats with third-degree burns covering
30 % of the TBSA (OD, x
s
±
, n = 6)
PBD
0
1
2
3
5
7
EN
823.5 ± 240.6
717.6 ± 201.4
512.7 ± 109.2
588.4 ± 122.6**
612.7 ± 188.3**
578.4 ± 117.5**
PN
766.5 ± 189.7
466.6 ± 171.3
307.3 ± 154.9
247.4 ± 112.2
311.5 ± 132.4
OD optical density; vs PN ** p < 0.01
Table 16.101 Changes in ileal mucosa cyclin D 1 in rats with third-degree burns covering 30 % of the TBSA ( x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
12,423 ± 5,036
29,539 ± 11,299
16,859 ± 11,927
32,866 ± 11,068
20,530 ± 8,914
35,541 ± 15,634*
PN
19,998 ± 15,097
22,560 ± 11,892
23,787 ± 9,091
28,162 ± 5,809
4,881 ± 3,325
vs PN * p < 0.05
16 Nutrition in Burns

425
migration of crypt cells to the top of villus. PGE 2 could
protect the gastrointestinal tract, promote proliferation
of the intestinal mucosa cell, increase DNA synthesis,
and mitosis of the villus and crypt cell. The ITF could
fi x and support the intestinal mucus, prevent injury, and
accelerate proliferation and migration of mucosa cells.
EN could promote intestinal mucosa secretion of EGF,
PGE 2 , and ITF compared with PN.
2. Enteral nutrition could maintain the intestinal structure
and function (Tables 16.106 , 16.107 , 16.108 , 16.109 ,
16.110 , 16.111 , 16.112 , 16.113 , 16.114 , and 16.115 )
Enteral nutrition is benefi cial to the restoration of the
thickness and its composition of intestinal mucus, and could
maintain intestinal mucosa thickness, villus height, villus
surface area, quantity of intestinal mucosa DNA, protein,
and activity of alkaline phosphatase; it could increase gas-
trin, motilin, and gastrointestinal transit (the intestinal seg-
ment of carbon staining occupied the whole intestine).
The activity of alkaline phosphatase in brush border is
used as marker of differentiated and matured intestinal
epithelial cells, and alkaline phosphatase could partici-
pate in intestinal lipid absorption. Compared with PN, EN
Table 16.102 Changes in ileal mucosa cyclin E in rats with third degree burns covering 30 % of the TBSA ( x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
13,529 ± 4,634
24,404 ± 12,423
23,969 ± 18,006
17,086 ± 5,667
30,414 ± 16,856
30,782 ± 7,708*
PN
27,562 ± 13,988
33,302 ± 14,544
20,473 ± 6,540
29,676 ± 18,483
9,842 ± 3,032
vs PN * p < 0.05
Table 16.103 Changes in ileal mucosa epidermal growth factor (EGF) in rats with third-degree burns covering 30 % of the TBSA (pg/mg protein,
x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
154.9 ± 71.9
172.0 ± 35.0
295.0 ± 110.4
269.3 ± 33.7
421.5 ± 30.8*
292.0 ± 93.4*
PN
354.8 ± 115.1
276.0 ± 96.1
199.1 ± 37.4
276.5 ± 56.2
64.8 ± 44.6
vs PN * p < 0.05
Table 16.104 Changes in intestinal mucosa PGE 2 in rats with third-degree burns covering 30 % of the TBSA (pg/mg tissue, x
s
±
, n = 6)
PBD
0
1
2
3
5
7
EN
8.4 ± 1.3
6.7 ± 0.8
6.4 ± 0.7**
5.0 ± 0.6
4.3 ± 0.5**
3.7 ± 0.6
PN
6.5 ± 2.2
4.7 ± 0.7
4.0 ± 0.6
2.8 ± 0.5
3.0 ± 0.8
vs PN ** p < 0.01
Table 16.105 Changes in intestinal mucosa intestinal trefoil factor (ITF) in rats with third-degree burns covering 30 % of the TBSA (ng/g tissue,
x
s
±
, n = 6)
PBD
0
1
2
3
5
7
EN
369.3 ± 65.6
555.8 ± 209.4
362.2 ± 50.9
258.8 ± 45.7**
258.0 ± 66.1**
129.2 ± 46.2**
PN
588.2 ± 100.3
343.7 ± 51.8
127.7 ± 45.5
98.7 ± 40.3
15.8 ± 4.4
vs PN ** p < 0.01
Table 16.106 Changes in the intestinal mucosa thickness in rats with third-degree burns covering 30 % of the TBSA (mg, x
s
±
, n = 8)
PBD
0
1
2
3
5
7
EN
7.8 ± 0.7
8.4 ± 0.5
6.2 ± 0.4
7.4 ± 0.2
7.5 ± 0.5**
6.7 ± 0.3*
PN
8.6 ± 0.3
7.2 ± 0.4
6.9 ± 0.6
6.3 ± 0.3
5.0 ± 1.3
vs PN * p < 0.05, ** p < 0.01
Table 16.107 Changes in hexose content of intestinal mucosa in rats with third-degree burns covering 30 % of the TBSA (mg/ml, x
s
±
, n = 6)
PBD
0
1
2
3
5
7
EN
2.7 ± 0.6
3.5 ± 0.8
3.1 ± 0.2
2.4 ± 0.4
2.9 ± 0.8**
2.8 ± 0.3**
PN
3.3 ± 0.9
3.0 ± 0.2
1.8 ± 0.4
1.6 ± 0.3
2.0 ± 0.3
vs PN * p < 0.05, ** p < 0.01
16.3 Comparison Between Early Enteral and Parenteral Nutrition

426
Table 16.108 Changes in the intestinal mucosa thickness in rats with third-degree burns covering 30 % of the TBSA (μm, x
s
±
, n = 30)
PBD
0
1
2
3
5
7
EN
466.7 ± 48.0
455.7 ± 25.6
458.0 ± 45.7
423.7 ± 20.6*
404.7 ± 19.8**
396.3 ± 23.9**
PN
451.0 ± 32.0
448.0 ± 35.7
402.0 ± 24.4
374.3 ± 29.6
325.0 ± 27.1
vs PN * p < 0.05, ** p < 0.01
Table 16.109 Changes in the intestinal VH in rats with third-degree burns covering 30 % of the TBSA (μm, x
s
±
, n = 30)
PBD
0
1
2
3
5
7
EN
273.3 ± 24.5
262.0 ± 22.8
263.7 ± 33.1
234.7 ± 20.8*
214.7 ± 14.1*
229.0 ± 16.5**
PN
262.3 ± 23.3
258.7 ± 25.2
221.0 ± 16.5
202.3 ± 18.5
214.7 ± 14.8
vs PN * p < 0.05, ** p < 0.01
Table 16.110 Changes in the intestinal mucosa DNA in rats with third-degree burns covering 30 % of the TBSA (μg/100 mg tissue, x
s
±
, n = 6)
PBD
0
1
2
3
5
7
EN
140.7 ± 23.5
107.7 ± 26.0
63.7 ± 24.5
67.3 ± 19.4*
67.8 ± 14.0*
65.7 ± 12.9
PN
98.4 ± 18.9
94.5 ± 29.3
43.3 ± 12.5
43.0 ± 7.8
49.5 ± 8.9
vs PN * p < 0.05
Table 16.111 Changes in the ileal mucosa protein content in rats with third-degree burns covering 30 % of the TBSA (mg/100 mg tissue, x
s
±
, n = 6)
PBD
0
1
2
3
5
7
EN
14.6 ± 1.3
12.7 ± 2.7
14.3 ± 1.6**
13.2 ± 1.4*
12.2 ± 1.0
12.5 ± 0.6
PN
15.5 ± 1.4
11.6 ± 1.2
11.4 ± 1.7
11.1 ± 0.9
12.8 ± 1.7
vs PN * p < 0.05, ** p < 0.01
Table 16.112 Changes in the activity of ileal mucosa alkaline phosphatase in third-degree burns covering 30 % of the TBSA (U/g tissue, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
4.1 ± 0.4
2.2 ± 0.6
1.8 ± 1.1
2.0 ± 0.4**
2.3 ± 0.5**
3.9 ± 1.2**
PN
2.7 ± 0.5
2.4 ± 0.7
3.2 ± 0.3
1.4 ± 0.3
1.2 ± 0.4
vs PN ** p < 0.01
Table 16.115 Changes in gastrointestinal transit in rats with third-degree burns covering 30 % of the TBSA ( x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
62.0 ± 6.8
21.0 ± 1.9*
25.0 ± 4.3**
30.5 ± 4.3*
43.6 ± 7.2**
28.9 ± 5.7
PN
12.0 ± 3.3
12.5 ± 3.3
22.9 ± 5.9
25.0 ± 7.3
34.1 ± 3.9
vs PN * p < 0.05, ** p < 0.01
PBD
1
4
8
14
EN ( n = 10)
61.9 ± 12.4
82.6 ± 28.6*
72.1 ± 14.6**
75.6 ± 16.8
PN ( n = 9)
63.0 ± 17.9
52.9 ± 16.6
51.3 ± 13.9
62.1 ± 12.5
vs PN * p < 0.05, ** p < 0.01
Table 16.113 Changes in
plasma gastrin in adults with
burns covering 45 %
of the TBSA (ng/L, x
s
±
)
PBD
1
4
8
14
EN ( n = 10)
209.1 ± 46.9
344.0 ± 88.2**
424.6 ± 93.3*
423.2 ± 141.1
PN ( n = 9)
201.2 ± 37.7
210.2 ± 55.1
276.8 ± 71.9
367.9 ± 76.9
vs PN ** p < 0.01
Table 16.114 Changes in
plasma motilin in adults with
burns covering 45 %
of the TBSA (ng/L, x
s
±
)
16 Nutrition in Burns

427
could do much to promote the restoration of intestinal
digesting and absorbing lipid function. The activity of the
ileum mucosa alkaline phosphatase is lower on PBH 24
but higher on PBH 48, 72 in the EN group compared with
the PN group in rats with third-degree burns covering
30 % of the TBSA.
Gastrin could stimulate the secretion of gastric juice,
promote the synthesis of DNA, RNA, and protein of the
gastrointestinal mucosa cell, stimulate cell proliferation;
motilin could promote the motion of the gastrointestinal
tract, refl ecting its motive situation. Filling the stomach
with 10 % activated carbon gel, promptly observing its
moving length in the intestinal tract, so as to compare the
difference in the promotion of intestinal movement
between the EN and PN groups.
3. Enteral nutrition could lessen the intestinal injury post-
burn and reduce the translocation of the intestinal endo-
toxin (Tables 16.116 , 16.117 , 16.118 , 16.119 , and 16.120 )
Enteral nutrition could decrease plasma diamine oxidase
(DAO) and the ratio of urine lactulose to mannitol (L/M),
and lower the plasma content of endotoxin. DAO exists
mainly in the intestinal mucosa cells; the intestinal mucosa is
injured after a burn, the DAO of intestinal mucosa cells is
released into the blood, the injured degree of the intestinal
mucosa could be refl ected by a measured activity change in
plasma DAO. The intestinal mucosa permeability is refl ected
by the urinary ratio of L/M. EN could decrease plasma DAO
and urinary L/M compared with PN.
The normal adult value of plasma DAO activity in various
publications is quite different:
(a) 2.05 ± 1.37 in Journal of Amino-acid and Biologic
Resources , 1996, 18 (6):28–30.
(b) 4.803 ± 1.132 in Practical Medicine Journal , 2005, 21
(9):904.
(c) 0.12 ± 0.06 in Journal of China Emergency Medicine ,
2006, 26 (12):893.
(d) 0.312 ± 0.009 in Journal of North China Coal Medical
College , 2007, 9 (5):292.
The data from Chap. 15 , “enterogenous hypermetabo-
lism” show that the endotoxin level of the portal is obviously
higher than the central vein in burned mini-pigs with third-
degree burns covering 30 % the TBSA, i.e., intestinal
Table 16.116 Changes in plasma diamine oxidase (DAO) activity in rats with third-degree burns covering 30 % of the TBSA (U/ml, x
s
±
, n = 8)
PBD
0
1
2
3
5
7
EN
0.32 ± 0.02
1.14 ± 0.36
1.02 ± 0.27
0.51 ± 0.14**
0.62 ± 0.10
0.61 ± 0.14
PN
1.23 ± 0.53
1.05 ± 0.31
0.88 ± 0.21
0.60 ± 0.14
0.70 ± 0.16
vs PN ** p < 0.01
Table 16.119 Changes in plasma endotoxin in rats with third-degree burns covering 30 % of the TBSA (EU/ml, x
s
±
, n = 8)
PBD
0
1
2
3
5
7
EN
0.17 ± 0.05
0.49 ± 0.06
0.52 ± 0.08
0.64 ± 0.08**
0.73 ± 0.06**
1.02 ± 0.09**
PN
0.45 ± 0.08
0.43 ± 0.04
0.93 ± 0.10
1.05 ± 0.11
1.45 ± 0.11
vs PN ** p < 0.01
Table 16.120 Changes in plasma endotoxin in adults with burns covering 45 % of the TBSA (EU/L, x
s
±
)
PBD
1
4
8
14
EN ( n = 10)
320 ± 76
652 ± 135**
530 ± 205**
438 ± 119
PN ( n = 9)
330 ± 74
853 ± 103
780 ± 145
555 ± 199
vs PN ** p < 0.01
PBD
1
4
8
14
EN ( n = 10)
3.44 ± 0.64
2.58 ± 0.39**
2.20 ± 0.37
2.19 ± 0.52
PN ( n = 9)
3.57 ± 1.21
3.43 ± 0.59
2.57 ± 0.79
2.26 ± 0.90
vs PN ** p < 0.01
Table 16.117 Changes in
plasma DAO activity in adults
with burns covering 45 % of the
TBSA (U/ml, x
s
±
)
PBD
1
4
8
14
EN ( n = 10)
0.195 ± 0.048
0.160 ± 0.045**
0.169 ± 0.028*
0.148 ± 0.034
PN ( n = 9)
0.191 ± 0.040
0.274 ± 0.044
0.213 ± 0.027
0.183 ± 0.048
vs PN * p < 0.05, ** p < 0.01; the normal value of the Department of Surgery, PUMC (Peking Union Medical
College) Hospital is 0.021 ± 0.0016
Table 16.118 Changes in the
ratio of urinary lactulose to
mannitol (L/M) in adults with
burns covering 45 %
of the TBSA x
s
±
(
)
16.3 Comparison Between Early Enteral and Parenteral Nutrition

428
endotoxin translocation should exist after burn injury.
Compared with PN, EN can decrease the endotoxin level
post-burn.
16.3.3
Enteral Nutrition Lowers the Level
of Catabolic Hormone, Decreasing
the Release of Infl ammatory
Mediators [ 7 , 19 , 20 , 50 , 52 , 61 – 63 ]
Enteral nutrition could decrease the level of plasma cortisol,
serum glucagon, plasma TNF, and urine catecholamine, and
increase the level of serum insulin (Tables 16.121 , 16.122 ,
16.123 , 16.124 , 16.125 , 16.126 , 16.127 , and 16.128 ).
Enteral nutrition could raise the level of the anabolic hor-
mone; its serum insulin is higher than in PN.
16.3.4
EN Could Reduce Decomposition
of Skeletal Muscle Protein, Lower
Hypermetabolism [ 7 , 20 , 47 , 50 , 60 , 61 ,
64 – 67 ]
1. Enteral nutrition could reduce decomposition of skeletal
muscle protein. ATP-ubiquitin-dependent 26S protea-
some complex is the main means of protein decomposi-
tion in eukaryotes. The center of the 26S proteasome
complex is the 20S proteasome; both ends consist of a
19S regulator. Two subunits of ATPase (Psmc2 and
Psmc5) and non-ATPase (Psmd1 and Psmd2) exist in the
19S regulator complex. Compared with PN, EN could
markedly reduce the activity and the content of the 26S
proteasome and 19S regulator complex and the subunit
gene expression level of the 19S regulator complex
Table 16.121 Changes in plasma cortisol in rats with third-degree burns covering 30 % of the TBSA (μmol/L, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
31.05 ± 2.57
44.35 ± 3.51*
48.96 ± 3.81**
48.80 ± 3.78*
42.81 ± 4.22*
40.77 ± 2.54*
PN
59.17 ± 5.22
75.02 ± 5.38
68.75 ± 6.62
59.45 ± 6.04
52.27 ± 2.98
vs PN * p < 0.05, ** p < 0.01
Table 16.123 Changes in serum glucagon in rats with third-degree burns covering 30 % of the TBSA (ng/L, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
119.8 ± 6.9
160.9 ± 8.3*
181.0 ± 8.4*
182.2 ± 6.9
162.5 ± 9.5*
172.4 ± 6.6*
PN
195.5 ± 9.8
209.3 ± 8.5
215.3 ± 14.5
192.1 ± 7.1
194.4 ± 6.6
vs PN * p < 0.05
PBD
1
4
8
14
EN ( n = 10)
47.3 ± 11.2
77.9 ± 20.3**
91.6 ± 38.8
86.3 ± 28.6
PN ( n = 9)
49.2 ± 14.7
118.1 ± 22.3
109.7 ± 32.8
108.4 ± 19.9
vs PN ** p < 0.01
Table 16.124 Changes in serum
glucagon in adults with burns
covering 45 % of the TBSA
(ng/L, x
s
±
)
PBD
1
4
8
14
EN ( n = 10)
1.563 ± 0.249
2.331 ± 0.236**
2.252 ± 0.338**
2.237 ± 0.350
PN ( n = 9)
1.678 ± 0.246
3.258 ± 0.463
3.183 ± 0.621
2.957 ± 0.611
vs PN ** p < 0.01
Table 16.125 Changes in
plasma TNF in adults with burns
covering 45 % of the TBSA
(μg/L, x
s
±
)
PBD
1
4
8
14
EN ( n = 10)
1,017.6 ± 332.0
781.8 ± 179.6**
654.6 ± 115.6** 537.7 ± 107.2
PN ( n = 9)
1,114.4 ± 278.4
1,059.0 ± 216.5
830.4 ± 144.9
539.2 ± 111.5
vs PN ** p < 0.01
Table 16.122 Changes in plasma
cortisol in adults with burns covering
45 % of the TBSA (nmol/L, x
s
±
)
PBH
0
24
48
72
EN
3,097.4 ± 213.9
3,719.2 ± 175.4*
5,232.8 ± 346.8*
5,359.5 ± 307.4**
PN
4,910.4 ± 462.7
6,509.8 ± 430.8
6,837.2 ± 336.8
vs PN * p < 0.05, ** p < 0.01
Table 16.126 Changes in urine
catecholamine in rats with
third-degree burns covering 30 %
of the TBSA (nmol/24 h, x
s
±
,
n = 6)
16 Nutrition in Burns

429
distinctly decrease the rate of protein degradation in skel-
etal muscle post-burn (Tables 16.129 , 16.130 , 16.131 ,
and 16.132 ).
2. Enteral nutrition could lower hypermetabolism and
reduce urinary nitrogen output (Tables 16.133 , 16.134 ,
and 16.135 ).
Enteral nutrition could clearly reduce REE compared
with PN after PBD 3 (PBH 72). EN REEs are 128.8, 143.6,
and 155.8 % and those for PN are 147.1, 168.4, and 172.7 %
of normal (38.98 ± 2.22 kcal/m 2 ·h, 1,535.19 ± 87.43 kcal/day;
163.09 ± 9.29 kJ/m 2 ·h, 6,423.23 ± 365.81 kJ/day) on PBD 4,
8, and 14 respectively. The average REE value on PBD 4, 8,
and 14 in the EN group is 20 % lower than in the PN group.
Compared with PN, the average value of PBD 1–14 urine
nitrogen in the EN group is lower (4.04 ± 0.65 g/day); the dif-
ferences between EN and PN during PBD 11–14 are clear.
Table 16.127 Changes in serum insulin in rats with third-degree burns covering 30 % (mU/L, x
s
±
, n = 6)
PBH
0
6
12
24
48
72
EN
31.4 ± 2.7
22.2 ± 2.4
22.4 ± 1.5*
18.7 ± 1.6*
24.9 ± 1.7**
20.0 ± 1.0*
PN
22.2 ± 2.8
17.7 ± 1.3
13.8 ± 1.2
16.3 ± 2.1
16.2 ± 1.4
vs PN * p < 0.05, ** p < 0.01
PBD
1
4
8
14
EN ( n = 10)
25.2 ± 10.3
44.1 ± 8.5**
41.5 ± 14.6*
43.5 ± 16.6
PN ( n = 9)
22.7 ± 7.6
25.7 ± 13.1
28.1 ± 11.6
32.5 ± 8.1
vsPN * p < 0.05, ** p < 0.01
Table 16.128 Changes in serum
insulin in adults with burns cov-
ering 45 % of the TBSA (mU/L,
x
s
±
)
PBD
26S activity
26S content
EN
PN
EN
PN
0
240 ± 35.2
240 ± 35.2
30.5 ± 5.3
30.5 ± 5.3
1
250 ± 31.4
261 ± 36.0
32.1 ± 5.1
34.5 ± 4.9
2
1,084 ± 54.6
1,141 ± 60.5
42.6 ± 5.9
51.9 ± 5.8
3
1,405 ± 78.5**
1,613 ± 82.8
48.1 ± 6.2**
59.4 ± 6.3
5
1,087 ± 54.2**
1,230 ± 71.3
40.5 ± 5.7**
52.1 ± 6.8
7
624 ± 40.9**
755 ± 43.5
37.9 ± 4.3
44.4 ± 5.1
vs PN ** p < 0.01
Table 16.129 Changes in the
activity (cpm/100 μg protein·2 h)
and content (arbitrary unit/50 μg
protein·2 h) of 26S proteasome
complex (26S) in the skeletal
muscle of rats with third-degree
burns covering 30 % of the
TBSA ( x
s
±
, n = 8)
PBD
19S activity
19S content
EN
PN
EN
PN
0
176 ± 18.2
176 ± 18.2
19.6 ± 4.2
19.6 ± 4.2
1
203 ± 17.8
212 ± 31.6
25.5 ± 4.2
28.8 ± 4.9
2
711 ± 46.0**
883 ± 47.6
43.2 ± 5.5
45.8 ± 5.9
3
1,080 ± 60.4**
1,294 ± 73.5
47.5 ± 6.1**
57.3 ± 7.2
5
825 ± 54.3**
966 ± 60.3
31.3 ± 4.5**
42.4 ± 5.1
7
634 ± 43.4
670 ± 42.5
22.9 ± 4.9**
35.2 ± 4.8
vs PN ** p < 0.01
Table 16.130 Changes in the
activity (cpm/100 μg protein 2 h)
and content (arbitrary unit/50 μg
protein·2 h) of 19S regulator
complex (19S) in skeletal muscle
of rats with third-degree burns
covering 30 % of the TBSA
( x
s
±
, n = 8)
PBD
Psmc2
Psmd2
EN
PN
EN
PN
0
3,645 ± 589
3,645 ± 589
6,483 ± 410
6,483 ± 410
1
84,734 ± 5,704
89,496 ± 7,689
141,255 ± 21,740
149,521 ± 24,400
2
261,501 ± 14,565
29,305 ± 13,094
349,602 ± 37,599**
370,659 ± 40,534
3
401,459 ± 26,741**
463,170 ± 28,350
551,683 ± 76,584**
606,270 ± 81,943
5
283,974 ± 16,779**
334,577 ± 21,088
393,795 ± 59,221**
412,543 ± 57,580
7
154,625 ± 9,239
162,400 ± 8,679
242,760 ± 32,564**
287,308 ± 30,723
vs PN ** p < 0.01
Table 16.131 Changes in the
gene expression of Psmc2
(ATPase) and Psmd2 (non-
ATPase) (AW108cRNA
molecular no./μg total RNA) in
the skeletal muscle of rats with
third-degree burns covering 30 %
of the TBSA ( x
s
±
, n = 8)
16.3 Comparison Between Early Enteral and Parenteral Nutrition

430
From the serial study mentioned above, it can be con-
cluded that if the intestine can work, EN is better than PN
after burn injury. If the internal environment is basically sta-
ble, and the function of enteral absorption exists, the EN
should be supplied promptly; if the nutritional requirement
cannot be satisfi ed by EN, PN should be given
simultaneously.
16.4
Glutamine and Arginine
Xi Peng
16.4.1
Glutamine
Glutamine (Gln) is a conditionally essential amino acid. In
serious wasting diseases such as trauma, burn or major oper-
ations, the organic demand for Gln outstrips its physiological
production, usually leading to the relative insuffi ciency of
Gln. If exogenous Gln cannot be supplemented in time, the
plasma level of Gln continually decreases, leading to a series
of pathological alternatives such as structural and functional
damage of the intestinal mucosa, immunosuppression, pro-
tein metabolism disorder, etc. [ 68 ]. For patients with wasting
diseases or undergoing severe trauma, pharmaceutics con-
taining Gln are usually used for Gln supplementation.
Currently, oral and intravenous preparations of Gln are
available on the market. Oral preparations include tablets,
powder, capsules and granules, and an intravenous prepara-
tion is Gln dipeptide. For burns patients, high doses of Gln
are required and granule preparation is more convenient.
However, in patients with severe gastrointestinal damage or
intestinal failure, intravenous preparations should be
supplemented.
16.4.1.1 Abnormal Metabolism of Gln in Burns
Patients
Glutamine is the most abundant amino acid in plasma and
cells. The average level of Gln in plasma is 600–900 μmol/L,
which accounts for approximately 60 % of the total body
free amino acids pool. The fl uctuation of the plasma level of
Gln directly affects the total body amino acid level [ 69 ]. The
intracellular concentration of Gln is 30-fold higher than that
in plasma. A large quantity of Gln exists in skeletal muscle
cells; when the plasma level of Gln decreases, it is released
into the blood stream to balance the plasma Gln level.
Therefore, sometimes the plasma level of Gln is normal, and
the Gln level in the skeletal muscle has decreased. However,
a low level of plasma Gln defi nitely suggests a defi ciency
of Gln.
Detection of the plasma Gln level has been considered to
be an important means of investigating the level of Gln in the
body. Before the 1990s, no simple and accurate method had
been developed to detect the plasma Gln level owing to its
instability contributing to the diffi culties in the diagnosis and
treatment of Gln defi ciency. Later, You et al. [ 70 ] fi rst used
reversed-phase high-performance liquid chromatography
(HPLC) in China to measure the level of Gln and its metabo-
lites in plasma and tissues. Nowadays, this method is used in
a variety of Chinese hospitals to determine the plasma Gln
level in burns patients. The results indicate that the plasma
Gln level falls rapidly after burns, and was reduced to
approximately 50 % of the normal plasma level. Moreover,
the decreased level of Gln restored slowly, and the plasma
Gln level was still lower than normal at PBD 14.
The Gln metabolism is complex and specifi c to different
tissues. However, only two enzymes (glutaminase and gluta-
mine synthetase) are directly implicated in the metabolism
of Gln. Gln can be disintegrated into glutamate and NH 3 by
a glutaminase catalyzer, and glutamine synthetase can cata-
lyze the Gln synthesis reaction from glutamate and NH 3 .
These two enzymes have tissue-specifi c distribution,
glutamine synthetase is predominantly distributed in the
Table 16.132 Changes in the rate of protein degradation in skeletal
muscle of rats with third-degree burns covering 30 % of the TBSA
(nmol tyrosine/g wet tissue·2 h) ( x
s
±
, n = 8)
PBD
EN
PN
0
272 ± 23.3
272 ± 23.3
1
275 ± 21.0
279 ± 20.5
2
281 ± 23.7
284 ± 18.9
3
285 ± 22.4
299 ± 25.0
5
293 ± 21.9**
348 ± 24.0
7
319 ± 24.4**
380 ± 26.3
vs PN ** p < 0.01
Table 16.133 Changes in REE in rats with third-degree burns cover-
ing 30 % of the TBSA (kJ/day, x
s
±
, n = 5)
PBH
0
24
48
72
EN
272.7 ± 76.1
412.8 ± 53.9
271.6 ± 73.9
283.5 ± 28.3*
PN
262.5 ± 43.6
262.2 ± 24.0
444.1 ± 56.4
vs PN * p < 0.05
PBD
1
4
8
14
EN ( n = 10)
7,560.2 ± 777.8
8,270.3 ± 753.0*
9,224.5 ± 934.2**
10,012.2 ± 830.6
PN ( n = 9)
(1,806.9 ± 185.9)
(1,976.7 ± 180.0)
(2,204.7 ± 233.3)
(2,393.0 ± 198.5)
7,682.2 ± 781.0
9,447.0 ± 955.8
10,818.0 ± 940.9
11,091.7 ± 1,156.7
(1,836.1 ± 186.7)
(2,257.9 ± 228.4)
(2,585.6 ± 224.9)
(2,650.9 ± 276.5)
vs PN * p < 0.05, ** p < 0.01
Table 16.134 Changes in REE
in adults with burns covering
45 % of the TBSA (kJ[kcal]/day,
x
s
±
)
16 Nutrition in Burns

431
Table 16.135 Changes in urinary nitrogen output in adults with burns covering 45 % of the TBSA (g/day, x
s
±
)
PBD
1
2
3
4
5
6
7
8
9
10
11
12
13
14
EN
( n = 10)
14.0 ± 3.8
15.5 ± 3.8 17.5 ± 6.4
20.4 ± 4.2
19.9 ± 4.5
23.3 ± 5.2
25.7 ± 5.4
25.5 ± 4.5
23.1 ± 5.0 22.2 ± 5.4 21.6* ± 6.0 23.3** ± 7.1 23.7** ± 6.6
21.8** ± 4.9
PN
( n = 9)
13.1 ± 4.6
15.6 ± 3.0 20.5 ± 5.3
22.5 ± 5.2
23.1 ± 7.4
25.6 ± 7.2
28.9 ± 6.6
30.4 ± 7.0
26.1 ± 6.5 26.6 ± 4.7 27.6 ± 4.7
29.4 ± 4.7
31.5 ± 5.1
33.3 ± 9.8
vs PN * p < 0.05, ** p < 0.01
16.4 Glutamine and Arginine

432
skeletal muscle and lung, and glutaminase is primarily
resident in the gastrointestinal tract, kidney, and immune
cells. Therefore, the skeletal muscle is the main tissue of Gln
synthesis, and the gastrointestinal tract, the kidney, and the
immune cells are the consumers of Gln [ 69 ]. Generally, the
balance between the uptake and release of Gln is maintained
and the plasma Gln level is relatively stable. After burns, the
glutaminase and glutamine synthetase are both activated, but
the activity of glutaminase is higher than that of glutamine
synthetase. Although the capacity of Gln synthesis in skele-
tal muscle cells is elevated to a certain extent, and the activity
of glutaminase in the gastrointestinal tract, kidney, and
immune cells has been signifi cantly increased, this leads to
an increase in the requirement for Gln. At this time, Gln in
skeletal muscle is usually released to meet the requirement.
Therefore, delayed supplementation of exogenous Gln will
result in reduction of the lean body mass and a sustained
decrease in Gln in plasma, fi nally leading to the exhaustion
of Gln. This is the theoretical basis for the supplementation
of Gln in burns patients.
16.4.1.2 Clinical Application of Gln in Burns
Patients
Burn is a type of severe trauma and nearly all tissues and
organs show pathophysiological changes after a burn injury.
Not only a large-area skin and subcutaneous tissue are
injured, but extensive hypoxia and ischemia may also lead to
the damage of several organs, immune dysfunction, and
release of numerous infl ammatory mediators, eventually
resulting in persistent hypermetabolism and MODS, or even
death. With increasing study, the critical role of the gastroin-
testinal tract in traumatic stress has been confi rmed, and the
gastrointestinal tract is considered to be “one of the central
organs in traumatic stress” [ 68 ]. The endotoxin translocation
from the gastrointestinal tract plays an important role in the
uncontrollable infl ammatory reaction and refractory hyper-
metabolism after a burn injury. Therefore, how to maintain
gut structure and function, to prevent or reduce endotoxin in
the blood is one of the challenges facing burns treatment.
Recently, for critically ill patients, organ- or tissue- specifi c
nutrients have been used for nutritional support. Gln can pro-
vide carbon and nitrogen for rapid growth and differentiation
cells, such as intestinal mucosal cells and immune cells, thus
contributing to the maintenance of the structure and function
of the gastrointestinal tract and to the improvement of immune
function. Hence, the importance of Gln in clinical practice
has been emphasized. Gln requirement in burns patients is
markedly enhanced and can lead to its relative insuffi ciency.
Timely supplementation of Gln may be benefi cial to the
maintenance of intestinal barrier function, to prevention
against bacteria/endotoxin translocation, and to suppression
of enterogenic infection and enterogenous hypermetabolism
[ 71 ]. Additionally, supplementation of Gln could inhibit
excessive degradation of muscular tissues and promote
protein synthesis, which is critical for the alleviation of hyper-
metabolism after burns. Furthermore, administration of Gln
may be benefi cial to the immune homeostasis in burns
patients. Currently, timely and suffi cient supplementation of
exogenous Gln has been one of the guidelines in the treatment
of burns patients.
Maintenance of Intestinal Mucosa Barrier
The gastrointestinal tract is the main consumer of Gln. After a
burn injury, the alterations of infl ammatory mediators and hor-
mones lead to corresponding alterations of Gln metabolism in
the gastrointestinal tract. Yu et al. [ 72 ] found that nutritional
support with Gln was benefi cial to the improvement of gastro-
intestinal tract injury in mini-pigs with burns. They also
observed a profound improvement in the biochemical and
electrophysiological parameters of the intestinal mucosa, his-
topathological structure, and intestinal immune function,
accompanied by a decreased infection rate. Furthermore,
intra-intestinal administration of Gln could markedly decrease
the damaged permeability and maintain gastrointestinal integ-
rity. The benefi cial effects conferred by Gln are associated
with the nitrogen provided by Gln, which is critical for energy
generation and tissue repair. Additionally, regulation of the
enteric nervous system, protection of the structure and func-
tion of mitochondria, increased secretion of ITF, and mainte-
nance of intestinal barrier function by Gln play important roles
in the protective effects afforded by Gln [ 73 ].
In clinical studies, the intestinal barrier function is mark-
edly improved in patients with severe burns after administra-
tion of Gln, accompanied by an evident decrease in plasma
DAO and endotoxin [ 74 , 75 ]. These fi ndings indicated the
effectiveness of Gln in the maintenance of post-burn intesti-
nal barrier function. Nowadays, consensus has been reached
on the scope, dosage, and time of Gln application. For
patients with massive or small burns, the effectiveness is not
evident. The treatment is favorable in patients with burns
covering 20–70 % of the TBSA. With regard to the dosage of
Gln, 0.5 g/(kg·day) is better for adults. The duration of treat-
ment is also important and treatment lasting at least 7 days is
necessary. Administration of Gln for 2–3 consecutive weeks
in severe burns patient is recommended. A favorable out-
come cannot be achieved with a shorter duration [ 73 ].
Reduction of Hypermetabolism
Hypermetabolism and massive nitrogen loss are the charac-
teristics of severe burns patients in which the nitrogen loss
reaches as high as 30–40 g/day and the metabolic rate is two-
fold higher than the normal level, exceeding the metabolism
level in other diseases [ 73 ]. A rapid fall in Gln in muscles is
observed, which may be closely related to the reduced syn-
thesis of proteins after a burn injury. Nutritional support
without Gln will not reverse Gln exhaustion in muscles.
16 Nutrition in Burns

433
Administration of an appropriate dose of Gln in burns
patients or animals (1.0 g/kg·day for mini-pigs with burns;
0.5 g/kg·day for burns patients) can effectively alleviate
post-burn hypermetabolism. The amount of Gln released
from muscles of mini-pigs will be markedly increased after
burns, which is more than 3.5 times higher than that before
burns. Treatment with exogenous Gln dramatically decreases
the level of Gln released, which is about 1.6-fold higher than
that before burns, accompanied by a decrease in the amount
of stress hormone and urinary nitrogen [ 76 ]. These fi ndings
suggest that administration of Gln might effectively suppress
post-burn hypermetabolism, and inhibit degradation of
proteins and loss of lean body mass, effectively restraining
the post-burn negative nitrogen balance. REE of rats with
burns covering 30 % of the TBSA began to increase on PBD
3 and reached a maximum on PBD 7 followed by a slight
decrease. However, REE was still higher than before burns.
After administration of Gln with 1.0 g/kg·day, the REE was
reduced by approximately 17 % with a maximum of 25 %
[ 77 ]. A multi-center clinical trial indicated that administra-
tion of Gln with 0.5 g/kg·day for 7 consecutive days signifi -
cantly reduced urinary nitrogen and increased the amount of
serum prealbumin and transferrin in patients with burns or
traumas, suggesting that administration of Gln might pro-
mote protein synthesis and inhibit hypercatabolism [ 71 ].
The following three mechanisms may be involved in the
suppression of hypermetabolism by Gln.
1. Glutamine can maintain intestinal barrier function, allevi-
ate the stimulation of the immune system by bacteria/
endotoxin translocation, reduce the release of infl amma-
tory mediators, and inhibit uncontrolled infl ammatory
response.
2. Glutamine promotes anabolism by providing nitrogen for
protein synthesis, and it also accelerates synthesis of
other amino acids that are the precursors of protein
synthesis.
3. Glutamine activates the mTOR signaling pathway, which
leads to phosphorylation of P70 S6k and 4E-BP, resulting
in increased synthesis of proteins. The promotion of the
synthesis of heat shock proteins and metallothioneins
(MT) is critical for the improvement of post-burn cellular
metabolism [ 73 ].
Improvement of Immune Function
Studies indicated that Gln not only enhanced the activity of
immune cells and anti-infection ability, but inhibited exag-
gerated infl ammatory response and cascade effects conferred
by the infl ammatory mediators, exerting immune bidirec-
tional regulation. Immune dysfunction is frequently found in
severe burns patients accompanied by an evident decrease in
the Gln level in the plasma and muscles. The decreased
plasma Gln level causes post-traumatic immunosuppression.
Administration of Gln in burns patients may enhance
cell- mediated immune function and the composition of T
lymphocyte subsets tends to be normal. In addition, Gln is
benefi cial to the regulation of intestinal immune function. Yu
et al. [ 72 ] found that intra-intestinal administration of Gln in
animals with burns could increase the secretion of S-IgA in
the jejunum and ileum and inhibit intestinal bacterial translo-
cation. Gln not only enhances immune function and anti-
infection ability, but suppresses an exaggerated infl ammatory
response and alleviates systemic infl ammatory response syn-
drome (SIRS) caused by immune hyper-function and exag-
gerated infl ammatory responses. Endotoxin has been
considered to be the triggering factor in SIRS and plays an
important role in the occurrence and development of
SIRS. The suppression of an exaggerated infl ammatory
response by Gln arises from its inhibition to endotoxin. The
following mechanisms may be implicated:
1. Glutamine can protect the intestinal barrier function,
inhibit endotoxin translocation, alleviate activity of
immune cells, and suppress infl ammatory response.
2. Glutamine can promote the synthesis of glutathione in the
liver and enhance the ability to clear endotoxin, reducing
the plasma endotoxin level.
3. Glutamine can modulate the sensitivity of immune cells
to endotoxin, especially the macrophages, reduce the
release of infl ammatory mediators, and suppress the
infl ammatory cascade.
4. Glutamine can increase the intracellular glutathione level
and inactivate NF-κB, leading to decreased expression of
NF-κB-dependent cytokines [ 73 ]. Clinical studies indi-
cated that the administration of Gln at 0.5 g/kg·day for
consecutive 7 days in severe burns patients markedly
improved immune function, and the levels of plasma
immunoglobulin and IL-2 were signifi cantly higher than
in the controls. At the same time, the levels of plasma
endotoxin and TNF were markedly decreased [ 78 ]. These
alterations effectively suppressed post-traumatic exagger-
ated infl ammatory responses.
Improvement of Wound Healing
Administration of Gln can increase plasma prealbumin,
transferrin, immunoglobulin and IL-2, improve immune
function and nutritional status, and lead to the promotion of
wound healing in burns patients. The healing time and hospi-
tal stay were shortened by 5 and 9 days respectively [ 75 , 78 ].
Compared with the control group, the healing rate was found
to increase from 81 to 89 % in 30 days by using Gln dipep-
tide, and the healing time of 1 % TBSA was shortened by
0.37 day [ 74 ].
16.4.1.3 Problems in the Clinical Application
of Gln in Burns Patients
Some multi-center clinical trials have confi rmed that criti-
cally ill patients may benefi t from Gln. Administration of the
16.4 Glutamine and Arginine

434
appropriate dose of Gln for adequate duration can
dramatically decrease the infection rate and mortality [ 79 ],
and shorten the hospital stay [ 80 ]. Results in our multi-center
study demonstrated that Gln played an important role in the
maintenance of intestinal barrier function, promotion of pro-
tein metabolism, and improvement of immune function in
burns or trauma patients. The benefi cial effects of Gln in
burns patients have been confi rmed and the focuses of con-
troversy in the application of Gln lie in the indication, dos-
age, and course of the treatment, especially the route of Gln
supplementation. Some specialists speculated that the effi -
cacy of the oral administration of Gln might be lower than
that of intravenous administration, or that it might even be
ineffective [ 81 , 82 ]. This is a major obstacle in the clinical
application of Gln and more studies are needed.
Indications for the Administration of Gln
No evident effectiveness of Gln administration can be
observed in patients suffering from mild or extremely severe
burns. In other words, for patients with mild burns, Gln is not
necessary, and for those with extremely severe burns, favor-
able effectiveness is diffi cult to validate. Generally, adminis-
tration of Gln is recommended in patients with burns
covering 20–70 % of the TBSA, which has been considered
as one of the principles in the application of Gln. Nevertheless,
we should take into account the presence of inhalation injury,
multiple trauma, special burns, and age, in addition to the
patient’s condition on admission. In principle, the use of Gln
is preferable in patients with moderate or severe burns. Liver
and kidney function should be observed when Gln is admin-
istered in patients with severe burns [ 73 ]. These factors
should be taken into account before the application of Gln.
Dosage, Course of Treatment and Management
of Adverse Reactions
Dosage and course of treatment are the key factors implicated
in the effects of Gln on the immune function and nutriture. A
low dose of Gln may lead to ineffectiveness and a high dose
may interfere with the metabolism of other amino acids. We
recommend that Gln administration of 0.5 g/kg·day for at
least 1 week is appropriate for adults with burns. In severe
burns, the treatment may last for 3 weeks [ 73 ].
Glutamine has been confi rmed to be very safe for patients
in clinical practice. To date, no severe adverse reactions have
been observed. A minority of patients may have nausea,
vomiting, and stomach discomfort at the fi rst administration.
These manifestations are transient and they will be resolved
when Gln is used with reduced fi rst dose or several small
doses. A long course of treatment with Gln may cause con-
stipation, which will be resolved after the administration of
water and foods rich in fi ber. The metabolite of Gln (ammo-
nia) may add a burden to the liver and kidney, and liver and
kidney dysfunction may be transiently observed in patients
after a severe burn injury. Administration of Gln cannot
severely affect liver and kidney function. However, in burns
patients with existing liver and kidney dysfunction or failure,
administration of Gln is not recommended.
Routes of Gln Administration
The effectiveness of the oral and intravenous administration
of Gln has been validated. Oral and intravenous administration
of Gln have individual features and should be chosen based
on the purpose of therapy and on the patient’s condition. Gln
has low water solubility and heat instability, leading to its
absence in conventional intravenous formulations. These
defects of Gln are subsequently solved by Gln dipeptide.
With the action of dipeptidase, Gln dipeptide is hydrolyzed
into Gln, contributing to an increase in the plasma Gln level,
followed by improvement in the nitrogen balance, immune
function, and intestinal structure and function, especially in
critically ill patients with intestinal failure. Although the
effectiveness of Gln dipeptide has been validated, it still has
several defects:
1. Long-term administration of exogenous Gln dipeptide
restrains Gln biosynthesis in the liver.
2. Administration of several glucogenic amino acids during
Gln treatment affects the blood glucose level.
3. The Gln dipeptide is relatively expensive, which increases
the medical costs [ 73 ].
Although Gln dipeptide has its own advantages, the ben-
efi cial effects afforded by the intestinal administration of Gln
cannot be neglected. Nowadays, the ineffectiveness of the
oral administration of Gln may be explained as follows:
1. Destruction by gastric acid or degradation by bacteria
leading to a reduced effective dose [ 81 ].
2. Gln is mainly absorbed in the upper gastrointestinal tract
and is ineffective for the diseases of the lower gastrointes-
tinal tract [ 82 ].
The opinions above have not been supported by some
basic and clinical studies in which the effectiveness of the
oral administration of Gln is investigated. Pharmacokinetic
studies indicated that the blood Gln level was signifi cantly
elevated after the oral administration of Gln in healthy vol-
unteers and the blood Gln level was positively correlated
with Gln dosage [ 83 ]. In burns patients, the plasma Gln level
was also increased after supplementation with Gln, which
increased the storage of Gln and prevented depletion [ 84 ].
Oral administration of Gln increases not only plasma Gln
level but also the intracellular Gln concentration in periph-
eral white blood cells [ 85 ]. These fi ndings suggested that
Gln, intra-intestinally administered, can be used by tissue
and cells.
The pH value can affect the stability of Gln, if it is greater
than 3.0. Gln is stable when the pH value ranges from 6.0 to
9.0; more than 90 % of initial Gln volume would be main-
tained after 1 h and about 80 % would remain 4 h later [ 73 ],
16 Nutrition in Burns

435
while the peak time of Gln absorption (Tmax) was at 40 min.
Therefore, the abovementioned pH range does not affect the
absorption of Gln, but Gln is rapidly decomposed when the
pH value is below 3.0; thus, oral administration of Gln should
be avoided under fasting condition (strong acid environ-
ment), and administration of Gln at 30 min after meals (pH
5.0–6.0) is recommended. Additionally, jejunal administra-
tion of Gln through a feeding tube is also feasible.
Degradation of Gln by bacteria deserves no concern. Because
Gln is mainly utilized by eukaryotic cells, and prokaryotes
usually utilize asparagine as a nitrogen source and seldom
make use of Gln. Therefore, oral administration of Gln at the
right time can ensure the effective blood concentration
of Gln.
Although Gln is absorbed in the upper gastrointestinal
tract, it can still exert benefi cial effects on the lower gastro-
intestinal tract. The uptake of Gln in the gastrointestinal tract
can be achieved from either the intestinal wall or blood.
Despite the mucosal cells in the ileum and colon not being
able to take up Gln from the intestine, the increased blood
Gln can meet the requirement of these cells. Therefore, the
effectiveness can be ensured as long as the plasma Gln level
has been elevated. Clinical studies have confi rmed the effec-
tiveness of Gln in the treatment of some digestive diseases
including irritable bowel syndrome and chronic colitis.
In summary, intestinal or intravenous administration of
Gln can meet the requirements of burns patients and exert
benefi cial effects. Intestinal administration and intravenous
administration of Gln have their own advantages and should
be rationally applied at different stages in burns patients.
Studies at our Burn Institute and Peking Union Medical
College Hospital have confi rmed that the advantages of
intestinal administration in the maintenance of intestinal
barrier function are better than those of intravenous adminis-
tration. However, intravenous administration of Gln is supe-
rior to intestinal administration during intestine dysfunction
of the patient especially during the early stages after a burn.
16.4.2
Arginine
Arginine (Arg) is a basic amino acid that is widely involved
in tissue metabolism. It is closely associated with immune
function, protein metabolism, and wound healing. Under
physiological conditions, the synthetic Arg can meet human
needs. After severe trauma, infection or major operations,
the requirement for Arg is dramatically increased, endoge-
nous Arg appears to be insuffi cient, and supplementation of
exogenous Arg is necessary. Therefore, Arg is considered to
be a conditionally essential amino acid. In addition, Arg can
promote blood ammonia into the urea cycle, thus preventing
ammonia poisoning. Polyamine, the intermediate metabolite
of Arg, is an important mucosal protective agent and can
promote gastrointestinal mucosal proliferation. Arg is also
the important substrate in the synthesis of nitric oxide (NO),
which is implicated in the regulation of immune function and
vascular tone.
16.4.2.1 Clinical Application of Arg in Burns
Patients
Improvement of Immune Function
Previous studies found that supplementation of exogenous
Arg to rats could increase thymus size and weight, accompa-
nied by an increase in the number of thymocytes, and that
Arg is benefi cial to weight restoration and wound healing in
rats with burns. Subsequent studies indicated that treatment
with Arg could improve immune function after severe
trauma, infection, and major operations, and can alleviate the
suppression of immune function by stress. Our previous
studies found that rabbits with burns had decreased immune
function,
especially
cell-mediated
immune
function.
Administration of arginine acetate at different dosages
achieved different outcomes. In the group taking 1.2 g/
kg·day and the group taking 2.4 g/kg·day, the immunization
indicators were markedly improved and no evident improve-
ment in immune function was observed in the group taking
0.3 g/kg·day or the group taking 0.6 g/kg·day. The minimum
effective dose of arginine acetate was 1.2 g/kg day (net dos-
age of Arg was 0.9 g/kg·day) The effi cacy of Arg is related
not only to the dosage, but also to the duration of treatment.
Administration of Arg for 3–5 days may achieve unsatisfac-
tory outcomes and a favorable curative effect can be observed
only after 7-day treatment with Arg. Therefore, administra-
tion of Arg for 7–10 days, as a course of treatment, is recom-
mended in clinical practice [ 86 ]. Clinically, the plasma Arg
level in patients with severe burns is positively correlated
with survival rate and negatively correlated with the severity
of infection. Treatment with exogenous Arg (15 g/day) for
14 consecutive days in adults with second-degree burns
could dramatically enhance cell-mediated immune function
and promote anabolism of proteins, which were benefi cial to
patient recovery [ 87 ]. Other studies also showed that the
incidence of infection at the skin graft donor sites was dra-
matically decreased after the administration of Arg [ 88 ].
Improvement of Nutritional Status
Supplementation with Arg accelerates protein synthesis and
down-regulates its degradation, leading to decreased weight
loss or even weight gain. Clinical observations indicate that
supplementation of Arg can reverse the nitrogen balance
from negative to positive post-operatively. Administration of
Arg can effectively increase the storage of nitrogen and alle-
viate post-operative creatinuria and urinary nitrogen loss.
Nowadays, Arg is considered to be the main rate-limiting
amino acid in the restoration of body weight after a burn
injury. Recently, conventional PN and EN have been
16.4 Glutamine and Arginine

436
supplemented with Arg, which may intensify the immune
function and increase therapeutic effectiveness. After trauma
or infection, detection of an aminogram indicated that Arg
and BCAA levels were signifi cantly reduced and suggested
that Arg consumption might be increased. Therefore, admin-
istration of exogenous Arg is necessary to meet the require-
ments of wound healing. After administration of Arg (25 g/
day) for 7 days in adults with burns in whom the plasma Arg
level was continuously reduced and slightly higher than that
in controls, it was signifi cantly elevated after Arg treatment
for 14 days [ 89 ]. After severe trauma such as major opera-
tions and burns, the post-traumatic stress may signifi cantly
increase the degradation of proteins. At the same time, the
re-absorption of amino acids, especially Arg and glutamate,
is markedly decreased, which, in combination with increased
degradation of proteins, accordingly leads to a negative
nitrogen balance [ 90 ]. Long-term negative nitrogen balance
may cause damage to immune cells, lead to immune dys-
function, increased incidence of infection, and other compli-
cations. Gastrointestinal nutritional support with Arg
increases the storage of nitrogen, accelerates protein synthe-
sis in muscles, decreases protein degradation, and reverses
the negative nitrogen balance, thus leading to improvement
of immune function. Our previous research had found that
the protein synthesis was dramatically increased in burns or
trauma patients treated with Arg acetate, accompanied by
improvement of immune function [ 91 ].
Improvement of Burn Wound Healing
It has been found that Arg can promote the secretion of growth
hormones, insulin-like growth factor-1 and insulin, etc., ele-
vate protein synthesis, and improve nitrogen balance. In addi-
tion, increased blood fl ow to the wound base and the elevation
of hydroxyproline and collagen synthesis have been observed
after treatment with Arg, which eventually accelerates wound
healing [ 90 ]. After administration of arginine acetate for
14 days in patients with second-degree burns, the incidence of
infection was dramatically decreased, and the levels of type I
and type III collagen and hydroxyproline in the wound were
markedly increased, accompanied by increased synthesis of
DNA in dermal cells [ 87 ]. These effects offered by Arg short-
ened the healing time, improved the survival rate of skin grafts
and decreased the number of operations. However, the inci-
dence of complications and mortality were not profoundly
changed. We consider that administration of Arg in trauma or
burn patients can shorten the healing time and reduce the hos-
pital stay to varying degrees.
16.4.2.2 Dosage, Course of Treatment,
and Management of Adverse
Reactions
The dosage of Arg is a determinant factor in the effi cacy.
Defi ciency of Arg is ineffective and excessive supplementa-
tion is also harmful. Studies indicated that the best effects of
Arg could be achieved with the optimal concentration. The
benefi cial effects may be compromised by a high concentra-
tion of Arg, and mild and transient adverse reactions may be
observed, such as minor gastrointestinal symptoms, hyper-
kalemia, hyperchloremia, hypophosphatemia, and metabolic
acidosis. These symptoms may disappear after withdrawal of
Arg. The doses of Arg varied from disease to disease. Dosage
of 10–15 g/day (0.2–0.3 g/kg·day) is recommended in
patients with trauma or those undergoing surgery, and for
patients with burns, we recommend a dosage of 15–20 g/day
(0.3–0.4 g/kg·day). These regimens have been confi rmed to
be safe for patients. In a multi-center clinical study, arginine
acetate was used at dosage of 0.4 g/kg·day (0.29 g Arg/
kg·day). The total amount of Arg is 17.5 g daily according to
a body weight of 60 kg, which accounts for 2.7 % of total
calories and is within the range of safe dosages of Arg [ 92 ].
Duration of Arg treatment is different in numerous dis-
eases. Evident effectiveness has been observed in surgical
patients treated with Arg for 5–7 days, which is a relatively
short period for burns patients. Severe damage, slow repair,
and a long course of disease are the characteristics of severe
burns. Effectiveness of Arg may be observed in these patients
after long-term treatments. Pharmacokinetic study indicated
that after the consecutive administration of arginine hydro-
chloride (25 g/day), the plasma Arg level on 7th day was
slightly higher than that of the control, and was markedly
increased on the 14th day after commencing treatment with
arginine hydrochloride [ 89 ]. Therefore, treatment with Arg
should be administered for at least 10 days in severe burns
patients. In clinical practice, only minor adverse reactions
have been observed, including nausea, vomiting, and diar-
rhea. These adverse reactions may spontaneously disappear
after withdrawal of Arg. Even though benefi cial effects have
been observed in burns patients treated with Arg, more stud-
ies, especially multi-center, randomized, double-blind clini-
cal trials, are required to confi rm the effectiveness of Arg and
the exact mechanisms involved in treatment with Arg.
16.4.2.3 Application Prospects of Arginine
Acetate in Clinical Practice
Arginine is an inherent material in the body composition
with low toxicity. However, L-arginine and arginine hydro-
chloride, conventionally used in clinical practice, have some
defects. L-arginine is a basic amino acid (pH 10.5–12.0) and
the long-term use of L-arginine at a high dose affects blood
pH. Oral administration of L-arginine produces gastrointes-
tinal irritation. However, arginine hydrochloride is an aci-
doid (pH 4.7–6.2) with a high proportion of chloride
(16.5–17.1 %). Long-term use of arginine hydrochloride
may cause metabolic acidosis and hyperchloremia [ 93 ].
Changing hydrochloride root into acetate may reduce the
incidence of hyperchlorine acidosis. After oral administration
16 Nutrition in Burns

437
of arginine hydrochloride in rabbits with 30 % full- thickness
burns for consecutive 7 days, blood pH, HCO 3 −, and alkaline
reserve were all decreased and the concomitant chloride
level increased, while oral administration of arginine acetate
did not induce evident metabolic acidosis and the chloride
level was lower than that in the arginine hydrochloride group
[ 94 ]. Pharmacological studies indicated that no evident
adverse effects were noted in the nervous system, circulation
system or respiratory system after administration of arginine
acetate. Toxicological studies showed that the median lethal
dose (LD50) of arginine acetate in mice was greater than
12.5 g/kg body weight for intravenous administration and
was greater than 32.0 g/kg body weight for intragastric
administration, which was far higher than the doses used in
clinical practice, suggesting the low toxicity of Arg acetate
[ 95 ]. In a multi-center clinical trial, administration of argi-
nine acetate (0.4 g/kg·day) for 7 consecutive days could sig-
nifi cantly enhance immune function; the CD4/CD8 ratio and
number of NK cells were markedly increased and levels of
plasma IL-2, IL-4, and immunoglobulins were also elevated.
The overall effective rate was 86.36 % in the Arg- treated
group, which was signifi cantly higher than that in the control
group (46.43 %) [ 91 ]. Furthermore, the Arg-treated group
had a low adverse effect rate, and nausea, vomiting, and diar-
rhea were the main manifestations of adverse reactions,
which disappeared after withdrawal of Arg. Liver and kidney
dysfunction are always found in patients with severe trauma
or infection, and the ability to regulate the acid–base balance
and electrolyte metabolism was compromised. For these
patients, treatment with arginine acetate, which has been
confi rmed to be relatively safe, should be selected.
16.5
Glucagon-Like Peptide-2
Fengjun Wang and Yun Zhao
Physiologically, the gut epithelium forms a unique barrier to
protect the host against potentially dangerous luminal con-
tents, including bacteria and toxins. Therefore, over the past
two decades, the gut has been believed to be a central organ
after surgical stress. Failure of intestinal barrier function
often occurs in many clinical conditions, including hemor-
rhagic shock, severe burn injury, and surgically critical ill-
ness, resulting in increased intestinal permeability and
subsequent translocation of bacteria and/or endotoxin from
the gastrointestinal tract. It has been well documented that
increased gut permeability and bacteria and/or endotoxin
translocation play very important roles in the setting of
severe complications such as systemic infl ammatory
response syndrome, sepsis, MODS, and multiple organ
failure (MOF). Therefore, how to accelerate the repair of
damaged intestinal mucosa and maintain the intestinal
barrier function are very important to the comprehensive
treatment of severe burn injury. Although growth factors and
growth hormone have been shown to be effective in promot-
ing the repair of damaged intestinal mucosa, the actions of
both growth factors and growth hormone are universal and
less organ-specifi c. The known target of growth factors and
growth hormone is not only the intestine, but also other
organs. It is inevitable that administration of growth factors
and growth hormone to accelerate the repair of damaged
intestine may have side-effects on other organs. Over the
past decade, glucagon-like peptide-2 (GLP-2) has been
found to be effective and specifi c in promoting the repair of
damaged intestinal mucosa.
16.5.1
The Biosynthesis and Degradation
of GLP-2
GLP-2 belongs to proglucagon-derived peptide (PGDP)
superfamily members encoded by proglucagon (PG) gene. In
mammals, the PG gene is predominantly expressed in pan-
creatic islet A cells, intestinal endocrinal L cells, and within
selected neurons of the brain. However, the expression prod-
ucts of the PG gene in pancreatic A cells and intestinal endo-
crinal L cells are different owing to different tissue-specifi c,
post-translational processing. In pancreatic A cells, the
expression product of the PG gene is mainly glucagon,
whereas in intestinal endocrinal L cells, the expression prod-
ucts of the PG gene are proglucagon-derived peptides,
including glicentin (corresponding to PG 1–69), oxyntomod-
ulin (corresponding to PG 33–69), glicentin-related pancre-
atic peptide (GRPP, corresponding to PG 1–30), glucagon-like
peptide-1 (GLP-1, corresponding to PG 78–107), interven-
ing peptide-2 (IP-2, corresponding to PG 111–122), and
GLP-2 (corresponding to PG 126–158) [ 96 , 97 ]. The differ-
ent expression profi le of PG genes between pancreatic A
cells and intestinal endocrinal L cells is dependent on the
type of prohormone convertases (PCs) involved in the post-
translational processing of the PG gene. The tissue-specifi c
processing of PG is regulated largely by the differential
expression of distinct PCs in pancreatic and intestinal endo-
crine cells. PC2 is expressed in pancreatic A cells, whereas
PC1, also known as PC3, is expressed in intestinal endocri-
nal L cells [ 98 ].
Glucagon-like peptide-2, synthesized and secreted by L
cells in the small and large intestine, is a single-chain poly-
peptide consisting of 33 amino acid residues, ending in an
aspartic acid residue as the C-terminal. The molecular weight
of GLP-2 is approximately 3,900 Da. The amino acid
sequence of GLP-2 is highly conserved across different
mammalian species. The difference between mouse GLP-2
and rat GLP-2 is that the 11th amino acid residue of
N-terminal is different, serine residue in mouse GLP-2 and
16.5 Glucagon-Like Peptide-2

438
aspartic acid residue in rat GLP-2. Similarly, there is only a
single amino acid difference between rat and human GLP-2.
The 19th amino acid residue of N-terminal is threonine in rat
GLP-2, but alanine in human GLP-2 [ 97 ]. The GLP-2-(1- 33),
an intact molecular form of GLP-2, is a major form of intes-
tinal GLP-2 that is released into the circulation. However,
GLP-2-(3-33), a degradation product produced by the actions
of dipeptidyl peptidase IV (DPP-IV), which removes the fi rst
two amino acid residues from GLP-2, is also present in both
the intestine and the circulation. The cleaved GLP-2-(3-33)
is biologically inactive [ 99 ]. DPP-IV is able to remove the
fi rst two amino acids from proteins containing N-terminal
penultimate alanine or proline residues, resulting in
N-terminal cleavage at the position 2 alanine residue of
GLP-2. When the N-terminal position 2 alanine residue is
substituted with glycine to synthesize GLP-2 analog [Gly 2 ]
GLP-2 (1–33), [Gly 2 ]GLP-2 (1–33) is resistant to cleavage
by DPP-IV, with more potent bioactions [ 100 ]. Thus, DPP-IV
is a key enzyme involved in the degradation of the
intestinotropic hormone GLP-2 (1–33) in the circulation
in vivo. The kidney seems to be a very important determinant
of GLP-2 clearance, as levels of immunoreactive GLP-2 are
increased in human patients with renal failure. Similarly,
experimental nephrectomy results in delayed clearance and
increased circulating levels of GLP-2 in rats. Therefore, the
kidney is a major organ for the clearance of both GLP-2 and
[Gly 2 ]GLP-2 from the circulation [ 101 ].
16.5.2
GLP-2 Actions
in the Gastrointestinal Tract
The relationship between GLP-2 and intestinal mucosa
growth can be traced back to the 1970s; however, it has
recently been recognized that GLP-2 can promote the growth
of intestinal mucosa. In the 1970s, hyperplasia of intestinal
mucosa was found in endocrine tumor patients accompanied
by the over-production of proglucagon; however, the dyspla-
sia of intestinal mucosa was gradually restored once the
tumor had been surgically removed. These fi ndings suggest
that the dysplasia of the intestinal mucosa observed in endo-
crine tumor patients might be associated with the over-
production of proglucagon-derived peptides, in which the
type of proglucagon-derived peptides involved was unclear
at that time. In 1996, when Drucker and colleagues reported
that among the proglucagon-derived peptides GLP-2 is able
to promote the proliferation and growth of intestinal mucosa
[ 102 ], the research work on the role of GLP-2 in accelerating
intestinal mucosal growth was started. It was found that the
weight, wall thickness, villous height, and crypt cell prolif-
eration rate of the small intestine were signifi cantly increased
in nude mice subcutaneously implanted with the rodent
proglucagon- producing cell lines InR1-G9, RIN1056A, and
STC-1 for 30 days, whereas the crypt depth and muscle
thickness of the small intestine were not affected, suggesting
that proglucagon-derived peptides might be associated with
the regulation of intestinal mucosa growth. In the next study,
it was also found that among the synthetic proglucagon-
derived peptides, including enteroglucagon, GLP-1, and
GLP-2, only GLP-2 was able to induce similar changes
observed in nude mice bearing the rodent proglucagon-
producing tumors. In contrast, no evidence for cell prolifera-
tion or abnormal histological appearance was observed
following examination of histological sections from the
spleen, kidney, heart, lung, brain, and liver of GLP-2-treated
mice, suggesting that the cell proliferation and histological
structure of the spleen, kidney, heart, lung, brain, and liver
were not affected by GLP-2. These observations that mice
implanted with subcutaneous glucagonoma developed a
small bowel growth led to the identifi cation of GLP-2 as the
proglucagon-derived peptide with intestinotropic activity.
Thus, it is quite clear that among the proglucagon-derived
peptides GLP-2 is the only one to accelerate intestinal
mucosa growth.
Glucagon-like peptide-2 is more effective than other
growth factors in accelerating intestinal mucosa growth.
After discovering the specifi c intestinotrophic activity of
GLP-2, Drucker and colleagues studied the intestinotropic
properties of GLP-2, EGF, insulin-like growth factor I (IGF-
I), IGF-II, and growth hormone (GH), in addition to [Gly 2 ]
GLP-2, a DPP-IV resistant GLP-2 analog, administered by
subcutaneous injection alone or in combination in mice
[ 103 ]. At the doses tested, [Gly 2 ]GLP-2 was the most potent
agent for increasing small and large bowel masses. However,
the actions of GLP-2 on intestinal growth appear to be addi-
tive in the presence of other intestinal growth factors such as
EGF, IGF-I, and IGF-II. Subsequent study demonstrated that
GLP-2 induced increases not only in RNA and protein con-
tent, but also in the activities of intestinal mucosal maltase,
sucrase, lactase, and glutamyl transpeptidase [ 104 ], imply-
ing that GLP-2 not only accelerates the proliferation of intes-
tinal epithelial cells, but also promotes the differentiation of
intestinal epithelial cells. GLP-2 also enhances the small
intestine to absorb glucose by upregulating the transport
activity of sodium-dependent glucose transporter-1 (SGLT-
1) [ 105 ]. Thus, induction of intestinal growth by GLP-2
results in an increased capacity for nutrient digestion and
absorption in vivo. Moreover, the apoptosis of intestinal epi-
thelial cells was also lessened by GLP-2 treatment. GLP-2
increases the growth of the small intestinal villus epithelium
in a gender- and age-independent manner [ 106 ]. The intesti-
nal response to GLP-2, principally mucosal villus hyperpla-
sia, can be seen after administration of GLP-2 via intravenous,
intramuscular, intraperitoneal, or subcutaneous routes [ 107 ].
Glucagon-like peptide-2 not only promotes the growth of
normal intestinal mucosa epithelium, but also accelerates the
16 Nutrition in Burns

439
repair of damaged intestinal mucosa. In a rat model of TPN,
co-infusion of GLP-2 with TPN solution normalized the
mass, protein, DNA, villus height, and mucosa thickness in
the small intestine, preventing TPN-induced intestinal hypo-
plasia and maintaining intestinal mucosa integrity in TPN
[ 108 ]. GLP-2 also augments the adaptive response to mas-
sive intestinal resection in the rat [ 109 ]. In a rat model of the
effect of GLP-2 on massive intestinal resection, there was a
signifi cant increase in intestinal diameter, total and mucosal
wet weights, crypt–villus height, sucrase activity, protein
content, and DNA content in the proximal jejunum and distal
ileum in response to resection. There was a signifi cant addi-
tive increment in these parameters in response to ALX-0600,
a potent protease-resistant analog of human GLP-2, in the
proximal jejunum. It has been shown that GLP-2, adminis-
tered in a variety of regimens, reduces mortality and improves
gross and microscopic indices of intestinal injury in experi-
mental enteritis in mice and rats. In experimental enteritis
induced by either dextran sulfate or a nonsteroidal anti-
infl ammatory drug (NSAID) such as indomethacin, GLP-2
treatment signifi cantly improved survival and histological
indexes of disease activity [ 110 ]. These actions of GLP-2 are
mediated by increased epithelial repair and reduced cell
death in the crypt compartment. GLP-2-treated animals also
exhibit decreased MPO activity, cytokine expression, and
bacterial translocation, providing an explanation for the
reduced morbidity and mortality observed in the GLP-2-
treated animals. GLP-2 also enhances mucosal mass follow-
ing ischemia and reperfusion injury to the small intestine.
After ischemia and reperfusion injury to the small intestine,
systemic infusion of GLP-2 for 3 days signifi cantly increased
mucosal DNA content by 41 % and mucosal protein content
by 60 %. In addition, infusion of GLP-2 reduced mortality
by 50 % [ 111 ]. It is suggested that GLP-2 may be benefi cial
to patients with intestinal ischemic syndromes such as necro-
tizing enterocolitis. In enteritis induced by a chemotherapy
drug such as 5-fl uorouracil, GLP-2 treatment also enhances
intestinal recovery [ 112 ], suggesting that GLP-2 administra-
tion might be benefi cial to patients suffering from
chemotherapy- induced enteritis.
16.5.3
GLP-2 and the Repair of Damaged
Intestinal Mucosa in a Burn Injury
To date, there has been very little information available con-
cerning the role of GLP-2 in the repair of intestinal damage
induced by a severe burn injury. Our previous data have
shown that GLP-2 is of benefi t to the repair of intestinal
damage following a severe burn injury. In rats suffering from
full-thickness burn injury covering 30 % of the TBSA,
administration of exogenous synthetic GLP-2 is effective in
attenuating intestinal damage, maintaining the mucosal his-
tological structure and barrier function, and preventing endo-
toxin or bacterial translocation from the gut [ 113 ]. The
mechanism by which GLP-2 accelerates the repair of intesti-
nal damage induced by a severe burn injury has not yet been
elucidated. Our previous studies have demonstrated that
GLP-2 enhances the proliferation of intestinal epithelial cells
by inducing the expression of proliferating cell nuclear anti-
gen and cyclin D in the intestinal mucosa of burned rats
[ 114 ]. In the same model of burned rats, it has also been
shown that GLP-2 inhibits the apoptosis of intestinal epithe-
lial cells following burn injury by downregulating caspase-3
activity and upregulating Bcl-2 gene expression in intestinal
epithelial cells [ 115 ]. Thus, exogenous GLP-2 administra-
tion, by promoting the proliferation and inhibiting the apop-
tosis of intestinal epithelial cells, accelerates the repair of
damaged intestine in severe burn injury. Similar to our stud-
ies, it has also been demonstrated that GLP-2 stimulates gut
mucosal growth and immune response in burned rats. GLP-2
infusion in burned rats prevents the loss of gut protein and
enhances immune function [ 116 ].
16.5.4
The Molecular Mechanisms of GLP-2
Actions
At present, it is certain that GLP-2 is a potent specifi c intes-
tinal growth factor. However, the mechanism underlying the
actions of GLP-2 has remained unclear. In 1999, Munroe and
colleagues [ 117 ], for the fi rst time, reported the cloning and
characterization of cDNAs encoding rat and human GLP-2
receptors (GLP-2R), and found that GLP-2R is a G protein-
coupled receptor superfamily member expressed in the gas-
trointestinal tract. The expression levels of GLP-2R RNA
were highest in the jejunum, followed by the duodenum,
ileum, colon, and stomach, whereas expression was unde-
tectable in other detected tissues including the brain, heart,
kidney, liver, lung, muscle, and spleen. This expression pat-
tern of GLP-2R RNA is clearly concordant with previously
reported functional responses to GLP-2 in the duodenum,
jejunum, ileum, and colon; in contrast, no proliferative or
histological changes were observed in the spleen, kidney,
heart, lung, brain, and liver of GLP-2-treated mice. Thus,
GLP-2R expression is highly restricted to known GLP-2 tar-
get tissues.
The cloned GLP-2R only responds to GLP-2, but not to
GLP-1 or other PGDPs. The GLP-2R response to GLP-2 is
accompanied by the activation of adenylate cyclase, leading
to cAMP accumulation in large amounts. Thus, it is specu-
lated that GLP-2 exerts its gastrointestinal actions through
the specifi c GLP-2R coupling to a cAMP-dependent signal-
ing pathway. When exploring the signaling pathway of
GLP-2R, Yusta and colleagues [ 118 ] found that in baby
hamster kidney cells expressing a transfected rat GLP-2
16.5 Glucagon-Like Peptide-2

440
receptor, GLP-2 increased the levels of cAMP and activated
both cAMP response element- and AP-1-dependent tran-
scriptional activity in a dose-dependent manner. GLP-2 also
stimulated the expression of immediate early genes includ-
ing c - fos , c - jun , junB , and zif268 . The GLP-2R may be cou-
pled to the activation of a mitogenic signaling pathway.
Another in vitro study [ 119 ] demonstrated that GLP-2 sig-
nifi cantly stimulated the proliferation of the human intestinal
epithelial cell line Caco-2, which was accompanied by a sig-
nifi cantly greater abundance of the phosphorylated forms of
both extracellular signal-regulated kinase (ERK)-1 and
ERK-2. The proliferative actions of GLP-2 in the human
intestinal epithelial cell line were inhibited by a global tyro-
sine kinase inhibitor that inhibits both receptor and non-
receptor tyrosine kinases, a phosphatidylinositide 3-kinase
(PI3-K) inhibitor, and a mitogen-activated protein kinase
(MAPK) inhibitor in a dose-dependent fashion. Thus, the
signaling pathways taking part in GLP-2 actions, in which
cAMP-dependent kinase, PI3-K, and MAPK pathways are
all involved, are extremely complex.
Our recent preliminary studies about the mechanisms of
GLP-2 actions in hypoxic intestinal epithelial cells have
demonstrated that the GLP-2-stimulated proliferation of
hypoxic intestinal epithelial cells was accompanied by
increased cAMP content, and that the cAMP upregulation
induced by GLP-2 was mediated by G-protein-coupled
receptor kinase 2 (GRK2). In intestinal epithelial cells
expressing transfected GLP-2R gene, both ERK pathway
and PI3-K pathway were involved in the proliferative actions
of GLP-2, contributing to the increased expression of phos-
phorylated c-Raf, MEK1/2, ERK1/2, p90RSK, and Akt. In
contrast, the p38 MAPK pathway was not involved in the
proliferative actions of GLP-2 in hypoxic intestinal epithelial
cells. However, caveolin-1 was found to be involved in the
signaling pathways mediated by GLP-2R in hypoxic intesti-
nal epithelial cells, leading to increased cell proliferation via
the activated ERK and PI3-K signaling pathways. Yet, there
is still a long way to go to clearly elucidate the molecular
mechanisms of GLP-2 actions in intestinal epithelial cells.
16.6
Eco-immune Nutrition
Chunmao Han
Humanity has always been concerned about health. As early
as 1907, Mentchnikoff (Nobel laureate) at the Pasteur
Institute, was interested in the Bulgarian peasants who drank
fermented milk, confi rming the value of probiotics, which
are benefi cial to humans in following respects:
1. Anti-infection, especially laryngitis, cystitis
2. Prevention from food poisoning, traveling-related diar-
rhea or irritable bowel syndrome
3. Prevention of enteritis problems, Crohn’s disease or
colitis
4. Cancer prevention, especially gastric cancer or colorectal
cancer
5. Prevention of constipation or digestive disorder
problems
6. Helping the patient to recover from disorder after antibi-
otic therapy or surgical operation
7. Relieving stress in life
Only for about 20 years have people placed real emphasis
on probiotics. Nowadays, from the point of view of gut nutri-
tion, probiotics as a nutritional supplement are needed for
both healthy and unhealthy people. Probiotics are at present
widely used as food supplements, and sometimes as a medi-
cine in a clinical scenario. The essence of eco-immune nutri-
tion is to supply probiotics.
16.6.1
The Concept of Eco-immune
Nutrition
In 1996, Swedish scientists, Prof. Stig Bengmark [ 120 ] fi rst
proposed the concept of eco-nutrition immunization, which
means adding elements of a mucosal reconstruction compo-
nent to EN: a new surface-active substance (such as polar
lipids), fi ber, L-arginine, and lactic acid bacteria to mucosal
adhesion (lactic acid bacteria, LAB).
16.6.1.1 Background and Theoretical Basis
The gastrointestinal tract not only has the function of diges-
tion, absorption, and excretion, but is also the largest immune
organ in the body and bacterial bank, which can protect for-
eign antigens and pathogenic micro-organisms as the fi rst
main line of body defense. Once the intestinal barrier func-
tion is damaged, an intestinal fl ora imbalance occurs, leading
to systemic infection, such as bacteremia and endotoxemia,
and even developing into MOF. In recent years, a large num-
ber of experimental and clinical studies found intestinal bac-
teria and endotoxin translocation due to trauma, burns, major
abdominal surgery, acute pancreatitis, and organ transplanta-
tion, which is a very important factor in the development of
MOF. Therefore, a new concept or strategy to prevent and
treat the intestinal barrier dysfunction came into being as
eco-immune nutrition. Studies on the nutritional and meta-
bolic support in critically ill patients found that early EN
support could reduce the hypermetabolism and the incidence
of intestinal infection in surgical or trauma patients. Later
on, it was also proposed that during nutritional support atten-
tion should be focused on the application of other forms,
such as dietary fi ber, glutamine, arginine, linoleic acid, and
short-chain fatty acids, etc., which are known as immune-
enhancing EN [ 121 ]. However, bacterial and endotoxin
translocation occurs mainly in the colon. Since these
16 Nutrition in Burns

441
nutrients mentioned above, except for dietary fi ber, are
absorbed in the small intestine, they cannot be good mucosal
protective agents, especially in the colon. While the dietary
fi ber, although it can reach the colon, cannot function well
owing to a reduction of probiotics in cases of stress. In this
situation, eco-immune nutrition is presented as a new treat-
ment strategy for the rebuilding of the intestinal mucosa
environment in those patients with stress.
16.6.1.2 The Composition of the Eco- immune
Nutritional Agent
Eco-immune nutritional agents are also known as synbiotics,
consisting of probiotics and prebiotics. In 1989, Fuller
defi ned prebiotics (also known as dietary fi ber) as those liv-
ing micro-organisms or substances that can adjust the intes-
tinal fl ora, improve its micro-ecological balance, and thus
benefi t the host. Prebiotics was fi rst proposed by Gibson
referring to those food or agents that stimulate the coloniza-
tion and proliferation and growth of one or several physio-
logical bacteria in the host intestine and thus benefi t the host
without digestion by the gut. The main prebiotics of today
consist of various types of oligosaccharides and fi ber, among
which seven to eight types of prebiotics have been developed
for clinical use. As a probiotic, it should have many charac-
teristics, especially the ability to attach to colon mucosa
cells. Previous studies showed that almost all of the LAB that
were available did not have this ability, and thus did not qual-
ify as a probiotic. In order to colonize in the colon, probiotics
should resist the acidity of the gastric fl uid and insult from
the bile and pancreatic fl uid. Different subtypes of LAB dif-
fer in their ability to resist the digestive fl uid and to attach to
the colon epithelia. Now, those subtypes of Lab that possess
the abovementioned abilities as probiotics are Lactobacillus
acidophilus , Lactobacillus rhamnosus , Lactobacillus reuteri ,
Lactobacillus
plantarum ,
Lactobacillus
bulgaricus ,
Lactobacillus johnsonii , and Lactobacillus delbrueckii , etc.
The experiment of attachment to the human intestinal cell
line Caco-2 and HT-29 in vitro demonstrates that
Lactobacillus rhamnosus GG , Lactobacillus acidophilus
(LA1, NCFB1748, and BG2F04), Lactobacillus plantarum
(299 and 299V), and Lactobacillus reuteri can attach to the
human colon epithelial well. However, there is no evidence
of how well they would do in vivo.
Lactobacillus synbiotics is composed of Lactobacillus
and fi bers. Lactobacillus has been widely used in the food
and beverage processing industry for a long time. In recent
years, studies have found that some Lactobacillus can pro-
mote human and animal health. As an important probiotic, in
addition to the ability to colonize in the colon, the space-
occupying effect of nutrition, anti-infection, immune-
enhancing effects, it may also have the ability of decreasing
serum cholesterol, anti-mutagen activity, improving lactose
metabolism, anti-tumor, and anti-aging and other important
physiological functions. Stig Bengmark made a synbiotics
agent, Cocktail 2000, which mixed several Lactobacillus
probiotics with several key fi bers. Its benefi cial clinical
effects have also been validated recently [ 122 – 125 ].
16.6.1.3 Synbiotics and the Intestinal Mucosal
Barrier
The intestinal mucosal barrier refers primarily to the intesti-
nal mucosal immune barrier, mechanical barriers, and bio-
logical barriers. The intestinal mucosal immune barrier
includes the secretary IgA (SIgA), anti-bacterial adhesion,
and intra-epithelial lymphocyte-mediated immune surveil-
lance. The SIgA can neutralize toxins, viruses, antigens,
with a wide range of protective effects, but its main role is to
prevent the adsorption of bacteria on the surface of intesti-
nal epithelia. The lack of SIgA is related to greater opportu-
nity for bacterial infections after burns and major surgery.
Experimental results show that some Lactobacillus species
have a stronger ability to enhance immunoglobulin pro-
duced in humans and animals. For example, the intake of
Lactobacillus acidophilus can cause the level of SIgA to
increase by four times when the body is stimulated by the
typhus bacilli. Kaila et al. divided 39 patients with acute
rotavirus infection into two groups: Lactobacillus casei GG
treatment group and the placebo group. There was a signifi -
cant increase in IgA secretion in the Lactobacillus casei GG
group; the symptoms were also signifi cantly relieved possi-
bly because of the increasing immune response against rota-
virus, neutralizing toxins. The intestinal mechanical barrier
is primarily composed of intestinal epithelial cells, inter-
celluar junction, and the epithelial cell basement membrane
with a superfi cial bacterial membrane. Lactobacillus bacte-
ria, as important indigenous bacteria, are able to combine
the surface of the intestinal epithelia with specifi c ligands,
with orderly colonization on the surface of the intestinal
epithelia. Lactobacillus bacteria constitute the fi lm, together
with other anaerobic bacteria. On the one hand, they can
protect against intestinal adhesion of other pathogenic bac-
teria. On the other hand, they may inhibit pathogen adhe-
sion, growth, and reproduction by producing organic acids,
hydrogen peroxide, and other substances. Most Lactobacillus
bacteria adhere via the protease-sensitive mechanisms or
lipid teichoic acid, but studies have shown that Lactobacillus
plantarum 299v can adhere to the host intestinal epithelium
via the expression of mannose-specifi c adhesin. In addition,
Lactobacillus can also promote the repair of injured intesti-
nal mucosa and prevent pathogenic bacteria translocation
through the intestinal epithelial cells. Intestinal fl ora and
host form an interdependent, interactive micro-ecological
system that constitutes the biological barrier of the intestinal
mucosa. Experiments in vitro and in vivo showed that
Lactobacillus bacteria can inhibit the pathogenic bacteria or
opportunistic bacteria, maintain the normal intestinal fl ora
16.6 Eco-immune Nutrition