Surgical Science, 2013, 4, 354-358
http://dx.doi.org/10.4236/ss.2013.48070 Published Online August 2013 (http://www.scirp.org/journal/ss)
A Prospective Study of Factors Influencing Wound
Dehiscence after Midline Laparotomy
Kusum Meena1, Shadan Ali1, Awneet Singh Chawla2, Lalit Aggarwal1, Suhani Suhani1,
Sanjay Kumar1, Rehan Nabi Khan3
1Department of Surgery, Lady Hardinge Medical College and Smt. Sucheta Kriplani Hospital, New Delhi, India
2Department of Surgery, Safdarjung Hospital, New Delhi, India
3Department of Surgical Disciplines, All India Institute of Medical Sciences, New Delhi, India
Email: shadanali@yahoo.com
Received May 22, 2013; revised June 23, 2013; accepted July 1, 2013
Copyright © 2013 Kusum Meena et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
ABSTRACT
Aim: To evaluate the factors influencing fascial wound dehiscence after midline laparotomy in the patients of perfora-
tion peritonitis with an emphasis on measurement of “intra-abdominal” pressure (IAP) and fascial transforming grow th
factor-beta (TGF-beta). Methods: Hundred eligible adult patients with the diagnosis of perforation peritonitis who u n-
derwent emergency exploratory laparotomy were prospectively recruited. Forty five patients who developed midline
abdominal wound dehiscence were compared with 55 patients without dehiscence. Results: The variables that were
significantly associated with wound dehiscence include anemia, hypo proteinemia, duration of surgery, prolonged
postoperative ileus, wound infection and postoperative pulmonary infection. Age, gender, jaundice, cause of peritonitis,
wound contamination and types of surgery were non significant variables. The mean IAP value in the patients with de-
hiscence was significantly higher than “non-dehiscence” group (p = 0.000). The patients with wound dehiscence
strongly expressed TGF-beta on the day of burst. Conclusion: The patients of peritonitis undergoing prolonged surgery
in the presence of risk factors like anemia, hypo proteinemia, postoperative ileus, wound infection and postoperative
pulmonary infection have high risk of abdominal wound dehiscence.
Keywords: Laparotomy; Perforation Peritonitis; Intra-Abdominal Pressure; Abdominal Wound Dehiscence;
Transforming Growth Fa ctor
1. Introduction
Of all the fall outs of abdominal surgery, dehiscence of
abdominal wound is easily the most notorious [1]. Pro-
foundly distressing both to the patient and the treating
surgeon, it is a common enough complication, with the
morbid consequences and at times, potentially dreadful
outcome [2]. Till recent, however, it has been a subject
little understood with little known about its exact etiopa-
thogenesis, there was little a surgeon could do to take
preventive steps [3].
The present study has endeavored to investigate the
events and contributory factors present in the pre-opera-
tive, per-operative and immediate post-operative period
that facilitate the mechanical forces of disruption and
impede the biological process of healing. While the dis-
ruptive mechanical forces can objectively be measured
by estimating the “intra-abdominal” pressure (IAP), the
impediment to the biological process of healing can be
estimated by the measure of transforming growth factor-
beta (TGF-beta) expression in the healing fascial wound
[4]. The purpose of this study was to evaluate the factors
influencing fascial wound dehiscence after midline lapa-
rotomy in the patients of perforation peritonitis with an
emphasis on measurement of IAP and fascial TGF-beta.
2. Methods
Hundred eligible adult patients with the diagnosis of
perforation peritonitis who underwent emergency ex-
ploratory laparotomy at university college hospital New
Delhi India were prospectively recruited (Table 1). Stan -
dard midline incision and continuous mass closure tech-
nique was used in each case. Based on outcome 45 pa-
tients with midline abdominal wound dehiscence (study
group) were compared with 55 patients without wound
dehiscence (control group). This study protocol was ap-
proved by the Institutional Ethical Committees of the
C
opyright © 2013 SciRes. SS
K. MEENA ET AL. 355
Table 1. Clinical characteristics of dehiscence and “non-
dehiscence ” group.
Characteristics Dehiscence
group
(n = 45)
“Non–dehiscence”
group (n = 55)
Age (year) mean (range) 33 (17 - 70) 29 (13 - 71)
Sex
Men 36 47
Women 9 8
Primary di ag nos is
Enteric perforation 32 24
Duodenal perforati on 8 14
Blunt abdominal trauma 2 7
Tubercular stricture perforation 1 2
Acute intestinal obstruction
with gangrenous bowel 0
1
Ectopic rupture 0 1
Appendicular perforation 2
6
hospital. All subject signed informed consent.
Main exclusion criteria’s were: age less than 12 years,
patients on steroids/immunosuppressant or anticancer
therapy and patients on anticoagulant therapy
The patient’s nutritiona l status on admission was care-
fully determined. The patient’s were considered mal-
nourished if they had a serum protein level less than 60
g/l. Anemia was defined as hemoglobin level of less than
11 g/l. The presence of peritonitis was confirmed by
presence of clinical symptoms and signs and by the pu-
rulent exudates of abdomen.
The overall hospital stay, the underlying diseases, op-
eration time, the operative procedures performed, the
factors influencing intra abdominal pressure post opera-
tively and post operative mortality were also recorded.
2.1. Measurement of IAP
IAP was measured in all 100 patients from day 0 to day 8.
Readings were taken ever y eight hours.
IAP was first assessed clinically and was graded as
normal, moderate or markedly tense abdomen. Thereafter,
the IAP was measured indirectly by employing the saline
fluid column manometry technique through an indwell-
ing Foley’s catheter. First described by Sedark et al. in
2002, this procedure is easy, quick and inexpensive [5].
Sixty milliliter of saline was instilled into the urinary
bladder via the indwelling catheter. Zero-reference point
was taken at pubic symphysis, keeping Y of Foley’s at
the symphysis. Then Foley’s was connected with gradu-
ated transparent tubing. The distance at which the sterile
saline settles in the tubing was taken to b e the IAP in cm
of H2O.
The following grading was used to categorize the ele-
vated IAP [ 6].
Grade I: 15 - 18 cm H2O
Grade II: 18 - 22 cm H2O
Grade III: 22 - 25 cm H2O
Grade IV: 25 cm H2O or hig her
2.2. Measurement of TGF-Beta
TGF-beta was measured in the fascia from the biopsy
taken at the time of surgery and then on the day burst
abdomen occurred (Bancroft, JD) [7]. Expressed TGF-
beta protein levels were assessed as None (0) when none
of the cells stained, Mild (1+) less than 10% of the cells
stained, Intermediate (2+) 10% to 20% of the cells
stained and Strong (3+) when more than 20% to 25% of
the cells stained following the staining of tissue by im-
munohistochemical staining for TGF β-protein levels by
employing monoclonal antibodies using the Avidin bio-
tin complex technique. TGF-β was localized by means of
immunohistochemical reactions (Figure 1).
2.3. Follow up
All the patients without wound dehiscence were called
one month after discharge for clinical and ultrasono-
graphic scar evaluation.
2.4. Statistical Analysis
The statistical significance of these variables was deter-
mined using unpaired t test, repeated measured ANOVA
test and paired t test. P < 0.05 was considered significant.
3. Results
There were 100 patients in the study, 45 patients with
midline abdominal wound dehiscence and 55 patients
without wound dehiscence. Wound disruption occurred
Figure 1. Photomicrograph showing strong (3+) expression
of TGF-β in biopsy specimen of dehisced fascia.
Copyright © 2013 SciRes. SS
K. MEENA ET AL.
356
on an average of 7 ± 2 days post operatively (range 6 to
9). This necessitated a prolonged hospital stay on part of
patients with wound dehiscence. While the stay in “non-
dehiscence” cases was of five to nine days, it ranged be-
tween 14 to 88 days in patients who had wound dehis-
cence. The mean stay in this group was 22 days. Wound
dehiscence also carried a significantly higher mortality
rate of 15% in comparison to that of 2% in the non de-
hiscence group.
IAP was assessed in each patient. The sensitivity,
specificity, positive pr edictive value and negativ e predic-
tive value of clinical examination for measurement of
IAP were found to be 86%, 52%, 88% and 47% respec-
tively. When clinical examination was used to assess
three categories of IAP range, viz. IAP between 15-18
cm H2O, 18 - 22 cm H2O and 22 - 25 cm H2O and was
correlated with IAP saline fluid column manometry, the
weighted kappa agreement score was 0.50. These result
showed that clinical method is not an accurate tool for
the assessment of IAP (Table 2).
The mean IAP value in patients with dehiscence on
day 1 was 22.7 cm of H2O, on day 2 was 21.4 cm of H2O,
and on day 3 was 20.3 cm of H2O. The corresponding
readings for “non-dehiscence” group were 19.2, 17.4,
and 15.9 respectively. The difference is statistically sig-
nificant wi t h p v al ue of 0.000 (Table 3).
Table 2. IAP measurements.
Saline fluid column manometry Total number
of patients
Clinical
examination IAP > 18 cm of H2O IAP < 18 cm of H2O
Raised 70 9 79
Normal 11 10 21
Total 81 19 100
Table 3. Values of serial measurement of IAP in the two
group.
IAP Day 1 Number Of
patients Mean
(cm of water) Standard
deviation
Standard
deviation
mean
“Non-dehiscence”
group 55 19.200 2.4601 0.3317
Dehiscence group 45 22.7778 1.4443 0.2153
IAP Day 2
“Non-dehiscence”
group 55 17.4364 2.1323 0.2875
Dehiscence group 45 21.4222 2.4998 0.2236
IAP Day 3
“Non-dehiscence”
group 55 15.9455 2.3603 0.3183
Dehiscence group 45 20.3333 1.6652 0.2482
P = 0.000.
The variables that were significantly associated with
wound dehiscence include anemia (p = 0.001), hypo pro-
teinemia (p = 0.006), duration of surgery (0.003). The
additional postoperative factors that were found to be
significant were prolonged postoperative ileus (p =
0.003), wound infection (p = 0.000) and postoperative
pulmonary infection (p = 0.000). Age (p = 0.096), gender
(p = 0.470), jaundice (p = 0.644), cause of peritonitis (p
= 0.459), wound contamination (0.142) and types of sur-
gery (p = 0.261) were non significant variables (Table
4).
On Day 0, TGF beta was expressed in ten patients in
“non-dehiscence” group and eight patients of dehiscence
group. The p value obtain ed for this was 0.958. This sig-
nified the equivalence of baseline unexpressed TGF-beta
levels in these two groups on Day 0.
Forty one/forty five (91%) patients with wound dehis-
cence strongly expressed TGF-beta on the day of burst as
against mild presence in 8/45 patients on Day 0. The dif-
ference is statistically significant with p value of 0.000
(Table 5).
Wound dehiscence rate was 9% in the patients with
three or less significant risk factors, 46% in the patients
with four to seven risk factors and 100% in the patients
Table 4. Distribution of risk factors in the dehiscence and
“non-dehiscence” group.
Risk Factor Dehiscence
group “Non-dehiscence”
group P Value
Anemia 32 23 0.001
Jaundice 4 1 0.644
Total Protein mean
g/l (SD) 5.141 (0.461) 6.149 (0.393) 0.006
Operating time in
hours (SD) 2.2 (0.351) 1.9 (0.381) 0.003
Wound
contamination 39 18 0.142
Post operative ileus24 0 0.000
Post operative
pulmonary infection12 5 0.000
Table 5. Difference betw een TGF-beta on day 0 and on day
of burst in the wound dehiscenc e group.
TGF-beta expression Day 0 Day of burst
None (0) 37 3
Mild (1+) 8 1
Intermediate (2+) 0 21
Strong (3+) 0 20
Total 45 45
P = 0.000.
Copyright © 2013 SciRes. SS
K. MEENA ET AL. 357
with eight or more risk factors. The difference is statistic-
cally significant with p value of 0.000.
Patients with seven risk factors had mortality of 25%,
with eight risk factors 40% and with nine or more risk
factors 1 00%.
Follow up
At one month follow up, on clinical and sonographic scar
evaluation none of the patients in the “non-dehiscence”
group developed incisional hernia.
4. Discussion
In the current study, out of 100 patients of generalized
peritonitis, 45 developed wound dehiscence. The vari-
ables that were significantly associated with wound de-
hiscence include anemia, hypo proteinemia and duration
of surgery. The postoperative factors that were found to
be significant were prolonged postoperative ileus, wound
infection and postoperative pulmonary infection. Age,
gender, jaundice, cause of peritonitis, wound contamina-
tion and types of surgery were non significant variables.
The mean IAP value was significantly higher in the de-
hiscence group while strong expression of TGF-beta
level was observed in the healing fascial wound on the
day of burst.
In our study, wound dehiscence rate was 45%. While
some retrospective studies have reported these rates be-
tween 0.2% and 10%, their rates derive from patient
group where few underwent emergency surgery [8,9].
Makela et al. reported an incidence of 10%; their series
include 30% patients operated emergently [10]. Riou et
al. found that 16 (51.6%) of their 31 dehiscence patients
had an emergency surgery [11]. Wound dehiscence is
associated with considerable mortality. While Madson et
al. and Greenberg et al have reported mortality rate in the
range of 10% - 30%, the current study had a mortality of
15% (7/45) in the burst group and 2% (1/55) in the non
burst group [2,3]. Time to dehiscence following surgery
may vary considerably. The reported range is 1 to 28
days with mean of 7 days [2,10,11]. Abdominal wound
dehiscence is associated with a prolonged hospital stay.
Studies report an average stay of 45 days with a range 20
- 90 days in patients managed conservatively [3]. The
mean hospitalization time was only reduced marginally
to 22 ± 10 days and 25 ± 15 days, when wounds were
reclosed following disruption [2,10]. In our study, the
mean period of hospital stay of wound dehiscence pa-
tients was 22 days, with a range between 14 - 88 days.
Currently preferred surgical closure technique is by a
continuous running polypropylene suture using Jenkin’s
technique because of its simplicity, speed, low rate of
wound dehiscence, and its superiority in an infected set-
tings [12,13]. We also follow Jenkin’s technique. In this
series, we did not have a knot slippa ge or suture breakage
in any of our patients. However, cutting through the tis-
sue was a common problem. While a poor application of
technique may be culpable, several studies emphasize the
role of mechanical or biological factors operating at the
wound site in causation of burst [14-16].
Measurement of IAP is critical while studying the ro le
of mechanical factors in wound dehiscence. W e tried two
different approaches: clinical examination and saline
fluid column manometry. The second a more objective
method; allowed us to assess the accuracy of first. Girth
and tenseness of the abdomen, two clinical determinant
of IAP, have however been discounted by several studies
[17,18]. They fared no better in present study. Unlike the
result of Sugrue et al. (weighted kappa agreement 0.70,
we did not observe a significant improvement (weighted
kappa agreement 0.50) despite adding a third category of
IAP in clinical examination [19].
Anemia and hypo proteinemia are known to impair
wound healing [20 ]. Wound infection is a major risk fac-
tor for wound dehiscence [11,12]. Prolonged ileus and
pulmonary infections are known to increase the IAP
[11,21,22]. Both played a significant role in our series.
Patients with wound dehiscence strongly expressed
TGF-beta on the day of burst as against mild presence on
Day 0. Franz et al. and Mustoe et al. have also shown a
peak of TGF-beta expression on five to seven day at
wound site. Therefore, the wound failure in our patients
is not actually a scar matrix failure [23,24]. We also at-
tempted to correlate the fascial TGF-beta expression with
IAP in dehiscence group. The mean expression of TGF-
beta was found to be 2.53 in dehiscence patients with
IAP < 20 cm of H2O, and 2.48 in dehiscence patients
with IAP > 20 cm of H2O (p value 0.786). Thus, wound
failure occurs in the biochemically active zone adjacent
to the acute wound edge where the sutures are placed. It
this process that is accountable for cutting through of
sutures, and was the factor responsible for wound dehis-
cence in the present series.
Multiple factors contributing to increase in disruptive
mechanical forces were primarily responsible for ab-
dominal wound dehiscence as the biological healing
process of having scar matrix in place was found intact
by revealing the strong expression of TGF-beta in the
specimens of facial biopsies. A preventive attitude to-
wards every risk factor responsible f or wound breakdown
at every stage before, during and after surgery should go
a long way in reducing the incidence of wound dehis-
cence.
Limitations of the present study were small sample
size and single institutional study.
5. Conclusion
The patients of peritonitis undergoing prolonged surgery
Copyright © 2013 SciRes. SS
K. MEENA ET AL.
Copyright © 2013 SciRes. SS
358
in the presence of risk factors like anemia, hypo pro-
teinemia, postoperative ileus, wound infection and post-
operative pulmonary infection have high risk of abdomi-
nal wound dehiscence.
REFERENCES
[1] T. T. Irvin, C. J. Stoddard, et al., “Abdominal Wound
Healing: A Prospective Clinical Study,” British Medical
Journal, Vol. 2, No. 6083, 1977, pp. 351-352.
doi:10.1136/bmj.2.6083.351
[2] G. Madsen, L. Fisher and P. Wara, “Burst Abdomen Clini-
cal Features and Factors Influencing Mortality,” Danish
Medical Bulletin, Vol. 39, No. 2, 1992, pp. 183-185.
[3] A. G. Greenberg and R. P. Saik, “Wound Dehiscence—
Pathophysiology and Prevention,” Archives of Surgery,
Vol. 114, No. 2, 1979, pp. 143-146.
doi:10.1001/archsurg.1979.01370260033004
[4] P. Bradley, M. C. Pickett, P. A. Lawrence, et al., “Tensile
Strength vs Healing Time for Wounds Closed under Ten-
sion,” Archives of Otolaryngology—Head and Neck Sur-
gery, Vol. 122, No. 2, 1996, pp. 565-568.
doi:10.1001/archotol.1996.01890170097017
[5] M. Sedrak and K. Major, “Simple Fluid Column Ma-
nometry to Monitor for the Intra-Abdominal Pressure,”
Contemporary Surgery, Vol. 50, No. 5, 2002, pp. 27-29.
[6] J. M. Bruch, E. E. Moore, F. A. Moore, et al., “The Ab-
dominal Compartment Syndrome,” Surgical Clinics of
North America, Vol. 76, No. 4, 1996, p. 833.
doi:10.1016/S0039-6109(05)70483-7
[7] J. D. Bancroft and M. Gamble, “Theory and Practice of
Histological Techniques,” Churchill Livingstone, London,
2002.
[8] G. V. Poole and N. C. Winston-Salem, “Mechanical Fac-
tors in Abdomina l Wound Closure: The Preventio n of Fas-
cial Dehiscence,” Surgery, Vol. 97, No. 6, 1985, pp. 631-
639.
[9] R. B. Bettman and M. W. Kobak, “Relative Frequency of
Evisceration after Laprotomy in Recent Years,” Journal
of the American Medical Association, Vol. 172, No. 16,
1960, p. 1764. doi:10.1001/jama.1960.63020160001007
[10] J. T. Makela, H. Kiviniemi, T. Juvonen, et al., “Factors
Influencing Wound Dehiscence after Midline Laparo-
tomy,” The American Journal of Surgery, Vol. 170, No. 4,
1995, p. 387. doi:10.1016/S0002-9610(99)80309-2
[11] J. P. Riou, J. R. Cohen and H. Johensen, “Factors Influ-
encing Wound Dehiscence,” The American Journal of
Surgery, Vol. 163, No. 3, 1992, pp. 324-330.
doi:10.1016/0002-9610(92)90014-I
[12] T. E. Bucknall and H. Ellis, “Abdominal Wound Closure-
a Comparison of Monofilamental Nylon and Polyglycolic
Acid,” Surgery, Vol. 89, No. 6, 1981, pp. 672-677.
[13] C. Knight and F. D. Groffen, “Abdominal Wound Clo-
sure with a Continuous Monofilament Polypropylene Su-
ture,” Archives of Surgery, Vol. 118, No. 11, 1923, pp.
1305-1308. doi:10.1001/archsurg.1983.01390110053012
[14] T. P. N. Jenkins, “The Burst Abdominal Wound: A Me-
chanical Approach,” British Journal of Surgery, Vol. 63,
No. 11, 1976, pp. 873-876. doi:10.1002/bjs.1800631110
[15] H. Hogstorm and U. Haglund, “Post-Operative Decrease
in Suture Holding Capacity in Laprotomy Wounds and
Anastomoses,” Acta Chirurgica Scandinavica, Vol. 151,
1985, pp. 533-535.
[16] C. A. Nelson and C. Dennis, “Wound Healing Technical
Factors in the Gain of Strength in Sutured Abdominal
Wounds in Rabbits,” Surgery Gynecology & Obstetrics,
Vol. 93, 1951, pp. 461-467.
[17] M. A. Fusco, S. R. Martin and M. C. Cha ng, “Estimation
of Intra-Abdominal Pressure by Bladder Pressure Meas-
urement: Validity and Methodology,” Journal of Trauma,
Vol. 50, No. 2, 2001, pp. 297-302.
doi:10.1097/00005373-200102000-00016
[18] J. A. Fairclough, J. Mintowt-Czyz, I. Mackie, et al., “Ab-
dominal Girth; An Unreliable Measure of Intra-Abdomi-
nal Bleeding,” Injury, Vol. 6, No. 2, 1984, p. 85.
doi:10.1016/S0020-1383(84)80003-0
[19] M. Sugrue, A. Bauman, F. Jones, et al., “Clinical Exami-
nation is an Inaccurate Predictor of Intra-Abdominal
Pressure,” World Journal of Surgery, Vol. 26, No. 12,
2002, pp. 1428-1431. doi:10.1007/s00268-002-6411-8
[20] D. A. Dubay and M. G. Franz, “Acute Wound Healing:
The Biology of Acute Wound Failure,” Surgical Clinics
of North America, Vol. 83, No. 3, 2003, pp. 463-481.
doi:10.1016/S0039-6109(02)00196-2
[21] C. Webester, L. Neumayer, R. Smout, et al., “Prognostic
Models of Abdominal Wall Dehiscence after Laparo-
tomy,” Journal of Surgical Research, Vol. 109, No. 2,
2003, pp. 130-137. doi:10.1016/S0022-4804(02)00097-5
[22] A. H. P. Niggerbrugge, B. E. Hansen, J. B. Trimbos, et al.,
“Mechanical Factors Influencing the Incidence of Burst
Abdomen,” European Journal of Surgical Oncology, Vol.
161, No. 9, 1995, p. 655.
[23] M. G. Frnz, P. D. Smith, T. L. Wachtel, et al., “Fascial
Incision Heals Faster than Skin: A New Model of Ab-
dominal Wall Repair,” Surgery, Vol. 129, No. 2, 2001, pp.
203-208. doi:10.1067/msy.2001.110220
[24] T. A. Mustoe, G. F. Pierce, A. Thomason, et al., “Accel-
erating Healing of Incisional Wounds in Rats Induced by
TGF β,” Science, Vol. 237, No. 4820, 1987, pp. 1333-
1336. doi:10.1126/science.2442813