Keywords
albendazole - ascariasis - intraperitoneal migration - parasitic infection - perforation
peritonitis
Introduction
Ascaris lumbricoides (AL) is the most common parasitic (helminthic) infection affecting humans worldwide
and causing serious medical and social problems, mainly in developing countries, because
here unhygienic disposal of human excreta is common.[1]
[2] Globally, more than 1.4 billion people are infected with AL, out of which an estimated
1.2 to 2 million such cases with 20,000 deaths per year occur in mostly endemic areas.[1]
AL might be a cause of intestinal infection in children with a peak age between 2
and 10 years[3] and cause about 60,000 deaths per year.[4] The mortality rate from intestinal infection caused by AL is 5.7% for those below
the age of 10 years.[5] Most cases of AL are asymptomatic; however, symptoms may appear depending on the
intensity of the infection, the host's nutritional and immunological status, and the
possible complications that may arise.
The main sites of involvement are the lungs during larval migration and the intestine
after the parasite reaches full maturity. Invasion of the biliary ducts and the liver
parenchyma may occur.[6]
[7] The adult worm has also been reported in the pleural cavity, airway, pancreas, peritoneal
cavity, lacrimal duct, middle ear, and femoral artery.[8]
[9]
Intestinal obstruction due to AL is a serious disease with high morbidity and mortality,
especially postoperatively.[10]
[11] Even though a lot of complications were reported from AL infestations worldwide.[12] Hence, reporting such findings with their intervention will help policymakers to
mitigate the challenges in the health care system and also help as a piece of baseline
evidence for future researchers on the issue of interest.
Case Presentation
A 14-year-old boy from a rural locality in North India presented in the emergency
room with a chief complaint of fever for 10 days, followed by abdominal pain associated
with multiple episodes of nonbilious vomiting and abdominal distention. He also had
obstipation for the past 3 days. No history of cough and chest pain. On general examination,
the child appeared ill, was febrile, and had moderate dehydration. On per-abdominal
examination, there was abdominal distention with diffuse tenderness, guarding, and
rigidity. Bowel sounds were absent. Digital rectal examination was unremarkable. The
patient was initially resuscitated in the emergency room, and imaging studies were
performed once the patient was stable. A plain radiograph of the chest and abdomen
was taken in the erect position, which was suggestive of pneumoperitoneum, while the
bilateral lung fields were normal ([Fig. 1]).
Fig. 1 X-ray chest shows gas under the right hemidiaphragm (bowel perforation caused by
Ascaris lumbricoides).
Ultrasonography of the abdomen was suggestive of a collection (approximately 150 mL)
in the right subdiaphragmatic space and right paracolic gutter containing low-level
echoes and air foci. Multiple tubular hyperechoic structures were also noted in the
ileal loops in the periumbilical and left lumbar region, suggestive of intestinal
ascariasis and intestinal perforation ([Fig. 2]). Due to confirmation of diagnosis via clinical signs and symptoms, chest X-ray,
ultrasound of abdomen, and emergency due to peritonitis, no further investigations
like computed tomography abdomen were done.
Fig. 2 Ultrasonography of intestinal Ascaris lumbricoides.
All routine investigation including hemoglobin - 8.6 g/dL, eosinophil count - 550
count/μL, platelets count - normal, leucocyte count - 14000/μL, liver and kidney function
tests, as well as serum electrolytes were within normal range. Widal and malaria parasite
tests were negative.
On performing an exploratory laparotomy, we found Ascaris in the peritoneal cavity
and a perforation of 2*2 cm in the prepyloric region of the stomach. The stomach,
small intestine, and large intestine were loaded with Ascaris ([Fig. 3]).
Fig. 3 Intraoperatively: Ascaris present in the lumen as well as the peritoneal cavity.
Peritoneal lavage was done, and ascarids were removed from the stomach. The whole
small bowel, large bowel, stomach, liver and gallbladder, urinary bladder, spleen,
and other adjacent organs were examined. The entire small bowel was found to be edematous
and inflamed, but there were no signs of impending perforation. The other organs showed
no evidence of worm infection. The perforation was primarily repaired with Graham's
omental patch. Enterotomy was done in the distal ileum, worms were removed from the
small bowel by simply squeezing, and distal loop washes were given to empty the large
intestine ([Fig. 4]).
Fig. 4 Worm retrieved from the lumen and peritoneal cavity.
A loop ileostomy was performed in view of an overwhelming worm load. Both proximal
and distal washes were given through the ileostomy and per-rectal washes were also
given. Small bowels were heavily loaded with worms, which were found to be impacted
proximal to the ileocecal junction; thus, an ileostomy was appropriate.
In the initial 3 to 4 days postoperatively, the stoma output was watery, averaging
800 to 1000 mL per day, due to inflammatory fluid. The output also showed the passage
of worms. Gradually, the output became more semisolid. A nasogastric tube that was
placed preoperatively was maintained for 5 days to facilitate healing of the gastric
perforation. Postoperatively, the patient received intravenous pantoprazole twice
daily for acid suppression, along with intravenous albumin, micronutrients, and total
intralipid. Intravenous fluids were administered in higher volumes than usual to compensate
for fluid losses through the stoma. For distal bowel clearance, distal loop stoma
washes were given with normal saline for 3 days.
Postoperatively, the patient was allowed oral intake from the 6th postoperative day.
He was advised to take fluids rich in electrolytes and to follow a high-protein diet.
For acid suppression, tablet pantoprazole 40 mg twice daily was prescribed for 5 days.
Antihelminthic treatment was initiated, which consisted of a single 400 mg dose of
albendazole, 6 mg of ivermectin once daily on an empty stomach, and 50 mg of nitazoxanide
twice daily for 3 days. The patient was successfully discharged on the eighth postoperative
day without any complications.
The patient was advised to follow a high-protein and high-fat semisolid diet to promote
prompt healing and compensate for the losses due to steatorrhea. The patient and caregivers
were counseled and taught about stoma care, using a stoma bag with colostomy paste
and adhesive powder to prevent peristomal skin excoriation.
Upon follow-up after 7 days, the patient reported no complaints regarding bowel habits,
pain, or food tolerance. Mild peristomal excoriation was present on examination, which
was initially managed with zinc oxide-based ointment. Excoriation continued to worsen,
necessitating the application of silver paint. The caretakers were reeducated on the
proper use of the stoma bag with adhesive paste and were advised to continue a semisolid,
high-protein diet and fluids rich in electrolytes. Ultrasonography of the abdomen
and chest was performed to look for any persistent worms in the abdomen as well as
to rule out lung involvement. Patient is now on regular follow-up with a healthy wound
and a healthy functioning stoma.
Discussion
AL is one of the most prevalent soil-transmitted helminths and a neglected tropical
parasite, primarily affecting people in developing countries with tropical climates.
These regions have warm and humid climates, which favor the growth and development
of the parasite. Additionally, poor sanitation, inadequate hygiene practices, and
limited access to medication and health facilities further increase the disease burden.[13]
[14]
[15]
Ascaris enters the human body through the ingestion of embryonated eggs, typically
via contaminated raw vegetables, fruits, and water. The adult worms inhabit the lumen
of the small intestine (jejunum or ileum). Intestinal ascariasis is rarely detected
and is usually an incidental finding.[16] The infections are mostly asymptomatic or may present with mild, nonspecific gastrointestinal
symptoms. However, in heavy worm loads, it can also cause intestinal obstruction,
perforation, and gastrointestinal bleeding.[17]
[18]
Approximately 10 to 14 days after infection, AL larvae may migrate through the lungs,
leading to eosinophilic pneumonia (Löffler's syndrome)—a self-limiting inflammatory
response characterized by pulmonary infiltration and eosinophilia. Adult Ascaris can
cause a variety of gastrointestinal complications, such as small bowel obstruction,
upper gastrointestinal bleeding, intussusception, volvulus, intestinal perforation,
and gastric ascariasis. Extraintestinal involvement can present as acute cholangitis,
hepatic abscess, biliary colic, and acute pancreatitis. Transabdominal ultrasound,
using a high-frequency linear transducer, is a highly sensitive diagnostic modality,
especially when performed by expert hands. Due to the risk of residual worms, which
might lead to a worm bolus and spastic paralysis, anthelmintic therapy should be administered
for 3 to 5 days postoperatively once the bowel movements are established.[19]
[20]
[21]
The bowel has a remarkable capacity for dilatation and can accommodate up to 5,000
worms without producing any symptoms.[22]
[23] However, the most common complication is intestinal obstruction, which may be acute
or subacute, and depends upon the worm load, especially in children. Further gangrene
and perforation may also occur due to pressure necrosis caused by worms.[24] The cause of perforation remains controversial, but in the tropics, patients often
have associated diseases such as typhoid enteritis, tuberculosis, and amebiasis, which
can also cause intestinal ulcerations. The worm may escape into the peritoneal cavity
through perforations at these sites of ulceration.[25] Another possible explanation is that the large worm bolus can lead to pressure necrosis
and gangrene.[7] Intussusceptions due to Ascaris have also been reported.[26]
[27]
[28] Involvement of the appendix can lead to appendicular perforation. A perforation
of Meckel's diverticulum has also been found.
Granulomatous peritonitis in ascariasis is reported to be due to the presence of dead
adult worms in the peritoneal cavity or by an inflammatory reaction to the eggs in
the peritoneum.[17] There are only two reports in the literature on duodenal perforation possibly caused
by ascariasis presenting as an acute abdomen.[17]
[18] In a report by Louw,[23] a bleeding duodenal ulcer with ascariasis adherent to the ulcer site was found on
endoscopy. A gastric outlet obstruction due to an Ascaris worm bolus has also been
reported.[24] An extensive literature search revealed only one report[23] from Nigeria on the possible occurrence of gastric perforation caused by Ascaris.
Very few case reports have been published previously, especially in pediatric patients
([Table 1]).
Table 1
Review cases
|
Study
|
Year
|
Age/sex
|
Symptoms
|
Durations
|
Intraoperative findings
|
Management
|
Outcomes
|
Complications
|
|
Gupta et al[1]
|
2012
|
48 y/m
|
Abdominal pain and vomiting
|
2 d
|
Gastric perforation
|
Graham's omental patch repair
|
Discharged
|
Discharge on anthelminthics
|
|
Refeidi[17]
|
2007
|
35 y/m
|
Epigastric pain with nausea, anorexia, constipation, and vomiting
|
6 d
|
Giant duodenal perforation with worm at peritoneal cavity
|
Graham's omental patch repair
|
Discharged
|
Ventilatory support, metabolic acidosis, wound infection
|
|
Anand et al[2]
|
2014
|
27 y/f
|
Pain in abdomen, vomiting
|
3 d
|
Ileal perforation
|
Primary repair
|
Discharged
|
Discharge on anthelminthics
|
|
Darlington and Anitha[16]
|
2018
|
4 y/m
|
Peritonitis features
|
4 d
|
Ileal perforation with volvulus
|
Ileostomy
|
Discharged
|
Discharge on anthelminthics
|
|
Molla et al[29]
|
2023
|
2 y/f
|
Vomiting, abdominal distension, and loss of appetite
|
6 d
|
Ileal perforation
|
Primary repair
|
Discharged
|
Discharge on anthelminthics
|
|
Sarmast et al[18]
|
2011
|
35 y/f
|
Epigastric pain with nausea
|
3 d
|
Peptic perforation
|
Graham's omental patch repair
|
Discharged
|
Discharge on anthelminthics
|
|
Xie et al[30]
|
2025
|
61 y/m
|
Epigastric pain, nausea, and vomiting
|
1 mo
|
Gastric perforation
|
Graham's omental patch repair
|
Discharged
|
Discharge on anthelminthics
|
|
Agrawal et al[31]
|
2017
|
5 y/f
|
Abdominal pain and vomiting of worms
|
4 d
|
Gangrenous small bowel with intraperitoneal worms, duodenal perforation
|
Graham's omental patch repair with resection and anastomosis
|
Discharged
|
Discharge on anthelminthics
|
|
Tejareddy et al[32]
|
2017
|
20 y/m
|
Abdominal pain and vomiting, blood in stool
|
7 d
|
Jejunal perforation
|
Primary repair
|
Discharged
|
Discharge on anthelminthics
|
Abbreviations: f, female; m, male.
In our case, we found that the stomach was distended, and small and large bowels were
highly loaded with Ascaris, which caused obstruction at the distal ileum, which was
decompressed surgically by enterotomy. More often, recurrent infestations lead to
malnutrition and growth retardation in children in endemic areas. Surgical complications
due to ascariasis are rare in adults.[23] Improvements in sanitation, hygiene, and health education, along with adequate therapy,
are used to control and reduce the intensity of infection.
Infestation with roundworms is widespread in developing countries, and although the
majority of intestinal obstructions can be treated conservatively, in some cases,
surgery may be required. Patients with complete obstruction and bowel perforation
are candidates for explorative laparotomy after initial resuscitation. Postoperative
follow-up and further plans for deworming are recommended to ensure patient safety.
