World J Surg (2010) 34:758–764
DOI 10.1007/s00268-010-0393-8
Chronic Corrosive Injuries of the Stomach—A Single Unit
Experience of 109 Patients Over Thirty Years
N. Ananthakrishnan • G. Parthasarathy •
Vikram Kate
Published online: 23 January 2010

Société Internationale de Chirurgie 2010
Abstract
Background Corrosive gastric injuries are not uncommon
in developing countries because acids, which are more
frequently associated with gastric injury, constitute the
major type of offending chemical. The spectrum of gastric
injury may vary from acute to varying types of chronic
gastric involvement.
Methods The 109 consecutive patients with chronic cor-
rosive gastric injuries treated in a single tertiary care su-
perspecialty institute over a period of 30 years were
reviewed with special reference to presentation and prob-
lems in management.
Results Acids contributed to 82.6% of chronic injuries.
Chronic gastric injuries were usually one of five types in
these patients. The majority had prepyloric strictures
(83.5%). The remaining strictures were antral (4.6%), body
(3.7%), pyloroduodenal (2.7%), or diffuse (5.5%).Twenty-
one (22.8%) patients had a delayed gastric outlet obstruc-
tion, and18 patients had a concomitant esophageal stricture
requiring a bypass. Most of the patients with chronic injury
underwent surgical correction with Billroth I gastrectomy
(77.1%), loop gastrojejunostomy (11.0%), and distal gas-
trectomy with Polya reconstruction (3.7%). Other proce-
dures performed were pyloroplasty in 1 patient and colonic
conduit jejunal anastomosis in 6 patients. One patient (1%)
died in the postoperative period.
Conclusions The management of chronic corrosive gas-
tric injury depends on the type of gastric involvement, the
presence of co-existent esophageal stricture, and the gen-
eral condition of the patient. A limited resection of the
N. Ananthakrishnan (&)
G. Parthasarathy
V. Kate
Department of Surgery, Jawaharlal Institute of Postgraduate
Medical Education and Research (JIPMER), Pondicherry, India
e-mail: n.ananthk@gmail.com
123
affected stomach is the ideal procedure for the common
type of gastric injury. In patients whose general condition
prohibits major resection or where the stricture extends to
the antrum the best treatment is a loop gastroenterostomy.
Type III, IV, V strictures require individualized treatment.
Delayed gastric outlet obstruction affects the treatment
plan of combined gastric and esophageal injuries.
Introduction
Corrosive injuries of the stomach are not uncommon in
developing countries, where accidental or suicidal inges-
tion of acids is encountered more often than in developed
countries, where lye or alkaline corrosives are more fre-
quent [1]. The most common occurrences are accidental
ingestion, particularly in children, because of careless
storage of chemicals, and ingestion with suicidal intent,
because of the free availability of caustic agents.
The extent of esophageal and gastric involvement, by
and large, depends on the nature of the corrosive ingested.
Acids affect the stomach more commonly than alkalis do;
they cause mucosal damage by coagulation necrosis, and
they require a longer duration of contact [2, 3]. However,
alkali damage of the stomach has also been reported [4, 5].
Acids are cleared rapidly from the esophagus to the
stomach, where they pool in the prepyloric area in response
to corrosive-induced pylorospasm [6–8]. Prolonged contact
with the prepyloric mucosa results in a prepyloric stricture.
Strictures can also occur in the antrum, the body, or the
pyloroduodenal area. When the volume of the corrosive
ingested is large, the entire stomach becomes scarred,
leading to a diffusely contracted stomach. On the other
hand, alkalis cause liquefaction necrosis, are more viscous,
and tend to adhere to the esophageal mucosa with only a
World J Surg (2010) 34:758–764
relatively small amount reaching the stomach. Thus the
extent of esophageal damage is greater with alkalis than
with acids [3].
Extensive acute injuries are usually fatal. Therefore the
spectrum of acute and chronic gastric injury seen at a ter-
tiary care referral hospital is not reflective of the overall
picture, as patients with the most severe gastric and
esophageal injuries die at peripheral centers.
This article presents a single-center experience of over
30 years in the management of 109 patients with chronic
corrosive gastric injuries, emphasizing the spectrum of
injuries, the extent of involvement, and highlighting the
possible modes of management. We propose a classifica-
tion scheme for chronic corrosive gastric injury to aid in
surgical decision making.
Patients and methods
One hundred nine consecutive patients with chronic injury
to the stomach after ingestion of a corrosive were treated in
our institute from 1977 until 2006. Besides being a post-
graduate teaching and research institute, JIPMER is a
1,000-bed superspecialty tertiary care referral center for
four states. The medical records of the 109 patients were
retrospectively analyzed and the results tabulated. Follow-
up data were based on the follow-up clinical visits and
were retrieved from the medical records. Based on the
nature of the corrosive-induced chronic injury, we pro-
posed a classification system to aid in surgical decision
making.
Chronic corrosive gastric injury was classified into the
following five types:
• type I: short ring stricture of the stomach within one or
two centimeters of the pylorus;
• type II: stricture extending proximally up to the antrum;
• type III: mid gastric stricture involving the body of the
stomach and sparing the proximal and distal parts of the
stomach;
• type IV: diffuse gastric involvement producing a linitis
plastica like appearance; and
• type V: gastric stricture associated with a stricture of
the first part of the duodenum.
Results
The present study was based on 109 patients with chronic
sequelae of corrosive gastric injury, 67% (73 of 109) of
whom had a concomitant esophageal injury. The age of the
patients ranged from 4 to 65 years, with a slight prepon-
derance of males over females (male/female ratio: 60:49).
759
The nature of the offending chemicals is shown in
Table 1. Acids (bathroom cleaning acid, aqua regia, and
sulfuric acid) contributed to over 80% of injuries. In 13
patients the exact nature of the ingested agent could not be
ascertained (Table 1).
Patients with chronic corrosive gastric injury usually
had features of gastric outlet obstruction a few months to a
year after corrosive ingestion. Of the 109 patients, 36 did
not have esophageal involvement. In 38 of those who did
have esophageal involvement, the esophageal injury pre-
ceded the gastric involvement; 14 patients presented
simultaneously with both gastric and esophageal involve-
ment; and the remaining 21 patients had delayed gastric
outlet obstruction that occurred several months after
esophageal obstruction. Of these 21 patients, 17 were
undergoing serial dilatation for esophageal strictures. In
four patients, delayed gastric outlet obstruction occurred
several months after esophageal reconstruction for corro-
sive stricture. These patients presented with progressive
dilatation of the subcutaneous colonic conduit. Cologastric
stenosis was ruled out by endoscopic evaluation. The cause
was probably gastric outlet obstruction resulting in
increased intragastric pressure that created a functional
obstruction at the cologastric anastomosis and consequent
dilatation of the conduit.
The location of the gastric stricture varied and is shown
in Fig. 1. The location of the stricture also influenced
surgical management. The distribution of patients accord-
ing to the various patterns of injury to the stomach was as
follows:
• type I: Of the 109 patients, 91 had a short ring stricture
within 1 or 2 cm of the pylorus (Fig. 2a).
• type II: In 5 patients the stricture extended more
proximally to the antrum (Fig. 2b).
• type III: In 4 patients, there was a midgastric stricture
(Fig. 2c) sparing both the proximal stomach and the
antropyloric segment.
Table 1 Nature of the corrosive ingested
Chronic gastric injury (n = 109)
Acids 90
Aqua regiaa 28
Bathroom acidb 49
Sulfuric acid 13
Alkalis 6
Unknown 13
a
A mixture of hydrochloric and nitric acids used by goldsmiths as a
solvent
b
Concentrated hydrochloric acid
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760 World J Surg (2010) 34:758–764

Fig. 1 Flow chart showing details of management of chronic corrosive gastric injuries

• type IV: In 6 patients there was diffuse gastric enough to undergo both a prolonged esophagocologastric
involvement with an appearance similar to linitis bypass and a gastric resection.
plastica (Fig. 2d). Two patients with type I stricture refused surgery. The
• type V: Although the corrosive damage was usually procedure of choice for a corrosive gastric stricture at our
confined to the stomach, in 3 patients the pyloric institute is a limited gastric resection with a Billroth I
stricture extended into the duodenum or there was a reconstruction in a single layer. This is easily performed
separate stricture of the first part of the duodenum because the strictures are usually short.
(Fig. 2e). Type II strictures were managed by an antecolic loop
gastrojejunostomy in all patients because the strictures
Of 73 patients with co-existent esophageal injury, the
were long and end-to-end gastroduodenal anastomosis
esophageal strictures required surgery in 18. In patients with
would not have been possible. Four of these patients also
total esophageal obstruction, who were unable to undergo
had an esophageal bypass.
radiological contrast studies, diagnosis of gastric outlet
In four patients with a midgastric stricture (type III),
obstruction was aided by an erect abdominal radiograph
distal gastric resection with a Polya reconstruction was
done after overnight fasting to show a gastric fluid level.
carried out.
Most patients with gastric outlet obstruction were in a
Six patients had diffuse gastric involvement (type IV)
state of malnutrition. Hence it was the policy of the unit to
along with esophageal stricture. In these patients the distal
do a preliminary feeding jejunostomy to build up the
end of the colonic conduit was anastomosed to the proxi-
nutritional status of all patients prior to surgery.
mal jejunum, leaving the stomach in situ as the patients
Details of surgical intervention are shown in Table 2. In
were not fit to undergo total gastric resection.
84/91 patients with type I chronic corrosive gastric injury,
Of three patients with type V stricture involving the
Billroth I gastrectomy was performed. Three of these
duodenum, one had a pyloroplasty and two others were
patients also had a simultaneous esophageal bypass. In 5
treated by a loop gastrojejunostomy.
patients a loop gastrojejunostomy alone was done to bypass
The overall mortality rate for chronic gastric stricture
the strictured region because these patients had concomi-
was 0.9% (1 of 109), with one patient dying after slippage
tant esophageal strictures and underwent an esophagoco-
of the jejunostomy tube and consequent intraperitoneal
logastric bypass. These patients were not considered fit

123
World J Surg (2010) 34:758–764
Fig. 2 a Prepyloric stricture (type I), b stricture extending to the antrum (type II), c midgastric stricture (type III), d diffuse gastric involvement
(type IV), e strictures involving stomach and duodenum (type V)
Table 2 Nature of treatment for chronic corrosive gastric injury
(n = 109)
Management
Loop gastrojejunostomy
Billroth I gastrectomy
Pyloroplasty
Distal gastrectomy (for midgastric stricture)
Colojejunostomy (for diffuse stricture)
Nonoperative
leakage of jejunal contents causing peritonitis. The mor-
bidity rate was also low, with two patients developing
postoperative paralytic ileus. Wound infection was infre-
quent and occurred in 3 patients. One patient developed
carcinoma of the stomach 17 years after acid ingestion
around a gastrojejunostomy stoma.
The long-term outcome of patients depended on the
presence or absence of esophageal involvement. Those
with isolated gastric involvement were relieved of all
symptoms and were nutritionally adequate on follow-up.
For those with concurrent gastric outlet obstruction and
esophageal obstruction, the outcome depended on whether
761
the esophageal obstruction was corrected by dilatation or
bypass.
No.
12
84
Discussion
1
Corrosive injuries of the stomach and esophagus are not
4
infrequent causes of hospitalization in countries like India
6
[1, 2, 9]. In India, hydrochloric acid is readily available
2
over the counter as a cheap toilet cleaner and is the most
common corrosive ingested by lower socioeconomic
groups. The next most frequent corrosive agent implicated
is gold solvent, which is a 3:1 mixture of concentrated
hydrochloric and nitric acid. This preparation is not regu-
lated and is freely available. Alkalis are the cause only in a
minority of people, who have access to caustic soda in an
industrial or laboratory setting, or as a more expensive
toilet cleaner [10]. This is in contrast to the West, where
alkali ingestion is more frequent than acid ingestion [11,
12]. Lack of appropriate regulation in the packaging,
labelling, and child-proofing of these potentially hazardous
substances makes corrosive poisoning a more common
problem encountered in this part of the world.
123
762
Patients with chronic gastric injuries after corrosive
ingestion usually present with features of gastric outlet
obstruction or early satiety. But the overbearing manifes-
tation of a concomitant esophageal stricture may mask an
underlying gastric injury. Physicians must be diligent in
ruling out a concomitant gastric injury in any patient with
corrosive ingestion, as it has a bearing on the management
of the esophageal stricture. This is discussed later. An
upper gastrointestinal endoscopy when possible and a
barium swallow are good means of evaluating the extent
and nature of the gastric injury.
It is not uncommon to encounter patients with absolute
dysphagia following corrosive injury. In these patients, it
becomes impossible to perform an endoscopy or even a
water-soluble contrast study to assess the extent of gastric
injury. In such cases we have found that a simple plain
abdominal radiograph taken after overnight fasting reveals
a gastric fluid level whenever there is a gastric outlet
obstruction [13]. This is a much cheaper option than a
computed tomography (CT) scan. There are also reports on
the use of a Meckel’s scan to assess the severity of the
gastric injury [14].
The ideal time for surgical intervention for a chronic
corrosive gastric injury is debatable [15]. Hwang et al.
proposed early definitive operation to manage these inju-
ries [16]. Patients with chronic corrosive injuries are gen-
erally poor candidates for prolonged operations because
they suffer severe nutritional deficiency. It is better to
postpone surgery in such patients and resort to jejunostomy
feeds to improve the general fitness status. This may take
up to several months. This period also enables the mucosal
lesions to heal, so that surgical anastomosis can be carried
out with greater safety. Even at the end of this delay, a
subset of the population still will not reach optimal levels
of fitness. Therefore they can endure only less demanding
operations, such as a gastric bypass, as opposed to
resection.
The requirement for gastric resection as prophylaxis
against future malignancy has been overstated in the lit-
erature. There have been reports of malignancy developing
in a scarred esophagus or stomach after corrosive ingestion,
but, in our experience this association has been found to be
tenuous [17–19]. In the over 500 corrosive injuries seen
over a 30-year period, there was only one solitary instance
of cricopharyngeal carcinoma following esophageal burns
from caustic ingestion and one case of perigastroenteros-
tomy carcinoma 18 years after the ingestion of acid. In the
latter case, it is not clear whether the carcinoma was cor-
rosive induced or secondary to chronic bile reflux through
the gastrojejunostomy stoma (stump carcinoma or postga-
stric surgery carcinoma).
The debate over the use of steroids in corrosive burns to
prevent stricture formation has been put to rest with recent
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World J Surg (2010) 34:758–764
meta-analyses [20, 21]. The investigators found no benefit
with the use of systemic corticosteroids in corrosive
ingestion and proscribe their routine use in the prevention
of stricture formation. There is, however, an isolated report
of the use of intralesional steroids in corrosive pyloric
strictures [22].
Once the patient has a stable pyloric or antral stricture,
the preferred operation depends on several factors: (1) the
general condition of the patient, (2) the need for a con-
comitant esophageal reconstruction, and (3) the type of
chronic gastric injury.
In type I gastric injury, a limited resection with a gas-
troduodenal reconstruction is relatively simple to perform.
The strictures are short, and hence the extent of gastric
resection required is minimal. The stomach and the duo-
denum can be brought together in most instances without
tension. Type II or III gastric injury is best treated by a
distal gastrectomy and an antecolic Polya reconstruction. A
type V gastric injury that extends into the duodenum or has
a separate stricture of the duodenum is more difficult to
manage. Resection in such instances involves a major
procedure in a patient with poor general condition. Such
injuries are best managed by an antecolic dependant
gastrojejunostomy.
A loop gastrojejunostomy is used only when absolutely
required for type I, II, or III injuries as it compromises the
possibility of a future gastric pull-up for esophageal
reconstruction. We employ a loop gastrojejunostomy (GJ)
mainly in patients with poor general condition where
resection would be hazardous. When doing a loop gastro-
jejunostomy, the surgeon must be prudent, avoiding a ret-
rocolic or a non-dependant GJ. A retrocolic GJ may
interfere with the middle colic arcade and make mobili-
zation of the colon at a later date for esophageal bypass
more difficult or sometimes impossible. A non-dependant
GJ not only fails to drain the stomach but also produces
recalcitrant bile reflux, compromising the quality of life of
the patient.
It is usually not necessary to combine a vagotomy while
performing a GJ for a corrosive gastric outlet obstruction.
The stomach’s secretory capacity is grossly disrupted after
corrosive ingestion, and the patients undergo what has been
called a ‘‘physiological antrectomy’’ [23]. Type IV gastric
injuries, which involve the entire stomach, create problems
in management. When isolated and in patients whose
general condition permits, they can be managed by a total
gastric resection. However, besides seriously compromis-
ing the general condition of the patient, they are almost
always associated with severe esophageal injuries. We
have treated these patients with colonic bypass for the
esophagus and anastomosing the distal end of the colon
end-to-side to the proximal jejunum, leaving the stomach
in situ. The results have been excellent.
World J Surg (2010) 34:758–764
There have been a few reports on the use of pyloro-
plasty, either a Heineke–Mickulicz type or a Y–V flap
[6, 24].This has not been our practice. Augmentation gas-
troplasty has also been proposed as a means of increasing
the volume of the stomach [25]. Balloon dilatation of the
strictured pylorus has been known to be an insufficient
procedure in managing patients with corrosive burns.
However, Kochhar et al. have reported encouraging results
with the use of endoscopic balloon dilatation for corrosive
pyloric strictures [26].
There needs to be a well laid out policy regarding the
management of combined gastric and esophageal strictures.
When corrosive stricture of the esophagus and stomach
occur simultaneously, treatment can be planned at the same
sitting. If the gastric stricture precedes the esophageal
stricture, it is possible to proceed with a limited gastric
resection with gastroduodenal reconstruction, leaving
esophageal bypass to a later date, should it become nec-
essary. Alternatively, one can leave an indwelling naso-
gastric tube, do a feeding jejunostomy, and take up gastric
or combined gastroesophageal reconstruction on a later
date. However, gastric strictures can present even weeks to
months after esophageal obstruction. In our experience, 21
out of 109 patients (19.3%) developed gastric outlet
obstruction as late as 8 months after the esophageal stric-
ture. The delayed gastric outlet obstruction may result from
mild pyloric stenosis that was overlooked at the time of
esophageal dilatation and that progressed, over months, to
total obstruction. Another possibility is the presence of
subclinical obstruction that is asymptomatic in the presence
of the dysphagia caused by esophageal obstruction; later,
the obstruction becomes functional as the patient starts
eating after successful esophageal replacement. The
delayed occurrence of such strictures has crucial implica-
tions for the management of esophageal stricture when one
contemplates the use of the stomach as a conduit for
esophageal substitution. In patients who have simultaneous
esophageal and gastric presentation, our option has been to
combine esophagocolic replacement with a gastrojejunos-
tomy distal to the cologastric anastomosis.
Delayed gastric outlet obstruction can be a major
problem if an esophageal bypass has been performed. It
usually presents as dilatation of the conduit [27]. The
condition should not be mistaken for cologastric stenosis.
Diagnosis can be confirmed by endoscopy, and the stricture
can be treated by either a distal gastric resection or a
gastrojejunostomy distal to the cologastric anastomosis.
The problem is more complex if delayed gastric outlet
obstruction takes place after a gastric pull-up for esopha-
geal bypass after corrosive injury. In such cases, gastric
resection or gastroenterostomy is seldom feasible, and the
surgeon may have to resort to a jejunal interposition.
Pyloroplasty may be possible in rare instances.
763
The mortality and morbidity from acute corrosive gas-
tric injuries is high and dependent on the severity of initial
damage caused by the corrosive agent, with a significant
proportion of patients succumbing to their injuries either
before reaching tertiary care or soon thereafter. In contrast,
the mortality and morbidity of chronic gastric corrosive
injuries can be significantly reduced by adequate preoper-
ative preparation and a planned protocol of approach
dependent on the type of injury. The risk of malignancy is
low and should not influence the type of surgical inter-
vention. In our center the morbidity was negligible, and the
mortality was under 1% for these patients. The long-term
result, in terms of symptom relief following surgical cor-
rection of a chronic gastric injury, is very good. In fact, the
major determinant of the quality of life and performance
status of a patient with corrosive ingestion is the nature and
extent of the esophageal and pharyngeal injury.
References
1. Ananthakrishnan N, Subba Rao KSVK, Radjendiran P (1993)
Mid-colon esophagocoloplasty for corrosive esophageal stric-
tures. Aust N Z J Surg 63:389–395
2. Subba Rao KSVK, Kakar AK, Chandrasekhar V et al (1988)
Cicatricial gastric stenosis caused by corrosive ingestion. Aust N
Z J Surg 58:143–146
3. Lahoti D, Broor SL (1993) Corrosive injury to the upper gas-
trointestinal tract. Indian J Gastroenterol 12:35–41
4. Bowill EG, Bulawa FA, Olivetti RG (1951) Severe corrosive
gastritis with antral stenosis following ingestion of Saniflusis.
Gastroenterology 17:436–441
5. Boikan WS, Singer HA (1930) Gastric sequelae of corrosive
poisoning. Arch Intern Med 40:342–357
6. Ciftci AO, Senocak ME, Büyükpamukçu N et al (1999) Gastric
outlet obstruction due to corrosive ingestion: incidence and out-
come. Pediatr Surg Int 15:88–91
7. Lowe JE, Graham DY, Boisaubin EV Jr et al (1979) Corrosive
injury of the stomach: the natural history and role of fibreoptic
endoscopy. Am J Surg 137:803–806
8. Poteshman NL (1967) Corrosive gastritis due to hydrochloric
acid ingestion—report of a case. Am J Roentgenol Rad Ther Nucl
Med 99:182–185
9. Ananthakrishnan N (2008) Corrosive injuries of the esophagus
and stomach. In: Tandon BN (ed) Tropical hepatogastroenterol-
ogy. Elsevier, New Delhi, pp 39–56
10. Zargar SA, Kochhar R, Nagi B et al (1992) Ingestion of strong
corrosive alkalis: spectrum of injury to upper gastrointestinal
tract and natural history. Am J Gastroenterol 87:337–341
11. Ramasamy K, Gumaste VV (2003) Corrosive ingestion in adults.
J Clin Gastroenterol 37:119–124
12. Hugh BT, Kelly DM (1999) Corrosive ingestion and the surgeon.
J Am Coll Surg 189:508–522
13. Ananthakrishnan N, Parthasarathy G, Kate V (2006) Gastric fluid
level after overnight fast: test to diagnose gastric outlet obstruc-
tion in corrosive esophageal stricture. Indian J Gastroenterol
25:269–270
14. Chung DK, Wines MP, Cummins GE et al (2003) Application of
the Meckel’s scan in a case of gastric corrosive injury. Pediatr
Surg Int 19:9–10
123
764
15. Chaudhary A, Puri AS, Dhar P et al (1996) Elective surgery for
corrosive-induced gastric injury. World J Surg 20:703–706
16. Hwang TL, Chen MF (1996) Surgical treatment of gastric outlet
obstruction after corrosive injury—can early definitive operation
be used instead of staged operation? Int Surg 81:119–121
17. Eaton H, Tennekoon GE (1972) Squamous carcinoma of the
stomach following corrosive acid burns. Br J Surg 59:382–387
18. Gonzalez LL, Zinninger MM, Altemeier WA (1962) Cicatricial
gastric stenosis caused by ingestion of a corrosive substance. Am
Surg 156:84
19. Nicosia JF, Thornton JP, Folk FA et al (1974) Surgical man-
agement of corrosive gastric injuries. Ann Surg 180:139–143
20. Pelclova D, Navratil T (2005) Do corticosteroids prevent
esophageal stricture after corrosive ingestion? Toxicol Rev
24:125–129
21. Howell JM, Dalsey WC, Hartsell FW et al (1992) Steroids for the
treatment of corrosive esophageal injury: a statistical analysis of
past studies. Am J Emerg Med 10:421–425
123
World J Surg (2010) 34:758–764
22. Kochhar R, Sriram PV, Ray JD et al (1998) Intralesional steroid
injections for corrosive induced pyloric stenosis. Endoscopy
30:734–736
23. Kaushik R, Singh R, Sharma R et al (2003) Corrosive-induced
gastric outlet obstruction. Yonsei Med J 44:991–994
24. Brown RA, Millar AJ, Numanoglu A (2002) Y–V advancement:
antropyloroplasty for corrosive antral strictures. Pediatr Surg Int
18:252–254
25. Kumar A, Ansari M, Shukla D et al (2006) Augmentation gas-
troplasty using a segment of transverse colon for corrosive gastric
stricture. Int J Colorectal Dis 21:470–472
26. Kochhar R, Sethy PK, Nagi B et al (2004) Endoscopic balloon
dilatation of benign gastric outlet obstruction. J Gastroenterol
Hepatol 19:418–422
27. Ananthakrishnan N, Subba Rao KSVK, Radjendiran P (1991)
Delayed gastric outlet obstruction after esophagocoloplasty—
clinical presentation with massive megacolon. Indian J Thorac
Cardiovasc Surg 7:99