Prevention and treatment of gastrointestinal dysfunction following severe burns: A summary of recent 30-year clinical experience

Table 1 General clinical data of 219 burned patients

	LAB			ELAB
Stage	n	Age (yr)	TBSA (%)	n	Age (yr)	TBSA (%)
1	33	26.5 ± 18.7	65.1 ± 12.4	45	28.5 ± 13.7	91.4 ± 10.2
2	21	27.7 ± 13.8	74.6 ± 10.3	29	26.9 ± 14.6	89.3 ± 8.2
3	35	25.9 ± 16.3	69.5 ± 12.2	56	26.4 ± 13.3	93.1 ± 9.4

TBSA: Total body surface area.

Table 2 GI complications and mortality in LAB patients (%)

Stage	n	AE	SU	SSU	FA	EI	Mortality
1	33	12.1	30.3	3.0	15.1	3.0	12.1
2	21	4.8	19.0	-	4.8	-	4.8
3	35	2.9	8.6a	-	2.9	-	2.9

AE: Abdominal extension; SU: Stress ulcer; SSU: Severe stress ulcer; FA: Flora alteration; EI: Enterogenic infection. Compared with the stage 1,

^aP < 0.05.

Table 3 GI complications and mortality in ELAB patients (%)

Stage	n	AE	SU	SSU	FA	EI	Mortality
1	45	24.4	60.0	11.1	20.0	15.5	55.6
2	29	13.8	48.3	6.9	13.8	10.3	41.3
3	56	7.1a	21.4bc	3.6	8.9	7.1	28.5b

Compared with stage 1,

^aP < 0.05,

^bP < 0.01; compared with stage 2,

^cP < 0.05.

Table 4 Endotoxin, IL-1β, IL-6, IL-8 and TNF-α levels and plasma DAO activity before and after CRRT

	Endotoxin (Eu/mL)	TNF-α(pg/mL)	IL-6 (pg/mL)	IL-8 (pg/mL)	DAO (U/mL)
Before CRRT	0.76 ± 0.13	272 ± 28	518 ± 64	583 ± 51	2.98 ± 0.94
After CRRT	0.045 ± 0.017b	57 ± 15b	98 ± 25b	105 ± 31b	1.27 ± 0.54b

Compared with before CRRT,

^bP < 0.01.