Acute GI and Surgical Complications of Ascaris Lumbricoides Infection

Acute GI and Surgical Complications of
Ascaris lumbricoides Infection

Sridhar V. Basavaraju, Peter J. Hotez, MD, PhD
Disclosures
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References
Serious complications related to Ascaris infection have been well documented in the literature. Intestinal obstruction by a bolus
of worms is the most common Ascaris-related emergency. Other acute conditions include hepatobiliary and pancreatic ascariasis
(HPA), acute appendicitis, peritoneal granulomas, small-bowel volvulus, and intussusception ( Table 1 ). Many of these
conditions can often be managed with conservative medical therapy. Occasionally, immediate surgical intervention is required (
Table 2 ).
Global incidence, prevalence, and mortality. A lumbricoides is a staggering worldwide public health problem. In India, the
prevalence of high-intensity Ascaris infection, in which there is a high worm burden, is 768 cases per 100,000 persons; in China,
2179 cases per 100,000 persons; in sub-Saharan Africa, 586 cases per 100,000 persons; and in Latin America, 1802 cases per
100,000 persons.[9] An estimated 8 million persons in Latin America are affected. Globally, there are an estimated 62 million
persons with high-intensity A lumbricoides infection.[9]
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Intestinal obstruction is an especially acute problem in the developing world. The prevalence of Ascaris-related intestinal
obstruction in India is 9.2 cases per 100,000 persons.[9] In 1990, the total number of cases of intestinal obstruction in India was
79,000; the average age of the infected person was 11 years. In China, there were 281,000 reports of Ascaris-related intestinal
obstruction in 1990, and in Latin America and sub-Saharan Africa, there were 95,000 and 38,000 cases, respectively. [9]
There are nearly 730,000 cases of Ascaris-induced bowel obstruction and 11,000 deaths annually worldwide. [9] Ascaris is
especially relevant to clinicians in the United States because of the increased numbers of immigrants from regions where the
parasite is endemic. Since 1990, nearly 3 million persons from Asia and more than 6 million from Latin America have migrated
to the United States.[10]
Causes. While roundworms may be found as high in the intestine as the duodenojejunal flexure, 99% of worms inhabit the
jejunum and ileum.[11] The roundworms do not attach to the intestinal wall. Rather, they maintain their position in the gut lumen
by powerful, continuous muscular movement. [11] In this location, the worms feed on nutrients in the host's intestinal tract. Multiple
worms frequently remain in the intestines for several years without causing disease. There are 4 major factors that result in
Ascaris-related intestinal obstruction[12]:
Multiple worms can form a large bolus, resulting in mechanical obstruction of the bowel lumen. This is the most
frequent cause of Ascaris- related bowel obstruction.
The worm bolus may serve as a lead point in intussusception or a pivot in small-bowel volvulus.
Ascaris worms may inhabit the ileocecal valve, where roundworm secretion of neurotoxins prompts small-bowel
contraction. This action, coupled with high worm burden in the ileocecal valve, can obstruct the intestine.
A host inflammatory reaction to worm-derived hemolysins, endocrinolysins, and anaphylatoxins can be severe enough
to obstruct the gut lumen.
Perforation and peritoneal granulomas. The mechanism of Ascaris-induced small-bowel perforation has been the subject of
considerable debate. Patients in the tropics consistently have histories of diseases associated with ulceration of the intestines.
These include typhoid enteritis, tuberculo-sis, and amebiasis. During extreme conditions, such as inflammation, starvation, or
worm bolus obstruction, some parasites are believed to migrate into the ulcers and to cause perforations. [13]
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Another possible explanation is that the large worm bolus can lead to pressure necrosis and gangrene. [14] The bowel, diseased
in this way, becomes susceptible to rupture by the burrowing action of the worm. [7] When the worm enters the peritoneal cavity,
the host immune response may result in masses of inflamed tissue and granulomas seeded throughout the greater omentum, the
serosal covering of the liver and spleen, and the peritoneum. [15] Granulomas are a host response to dead adult parasites and ova
that are released by the female nematode. [15] Grossly, peritoneal granulomas resemble tubercular lesions, and on radiographic and
other imaging studies, they can mimic lymphoma. [15]
Patient presentation and symptomatology. Surendran and Paulose[14] conducted a 5-year study of intestinal obstruction by A
lumbricoides and categorized small-bowel obstruction resulting from Ascaris as either acute or subacute. Patients with subacute
obstruction in this study experienced diffuse and colicky abdominal pain, fever, vomiting that was more pronounced at the onset
of symptoms, and diarrhea without blood and mucus. Acute obstruction had far more ominous presenting signs and symptoms.
Patients were often ill for several days before presentation. These persons showed signs of severe dehydration and had a toxic
appearance. Vomiting, abdominal pain and distention (Figure 1), fever, leukocytosis, and obstipation were frequently noted.
(Enlarge Image)
. Distended abdomen is characteristic of a child with severe ascariasis. (Reprinted from Despommier D et al. Parasitic Diseases.
2001.[24])
Well-localized masses are occasionally palpated in the abdomen of patients with subacute obstruction and rarely in the distended
bellies of children with acute obstruction. Patients will frequently have a history of worms in fecal matter or vomitus.
Presentation of patients with peritoneal granulomas is similar to that of patients with obstruction.
Diagnosis and treatment. Obtaining plain radiographs of the abdomen should be the first step after obtaining a thorough history
and performing a physical examination. In addition to distended loops of bowel with air-fluid levels, radiographs (in a
longitudinal or transverse cut) will often reveal worms. [12] The mass of worms is described as being in a whirlpool pattern. [12] On a
plain radiograph, perforation may manifest as free air under the diaphragm. Stool studies will often reveal abundant ova and
parasites, along with numerous eosinophils. Blood counts may demonstrate marked leukocytosis, and eosinophilia can approach
25%.[15] Other diagnostic studies, such as radiography following a barium enema, will often show no abnormalities and are thus
not indicated.
Treatment of Ascaris-related bowel obstruction depends on whether the condition is subacute or acute. Tondon and colleagues [16]
examined the use of conservative versus surgical management of GI ascariasis. This retrospective study involved 250 pediatric
patients in central India. All of the patients in the study initially received conservative therapy, which consisted of the
administration of a freshly made hypertonic saline enema. In 239 patients (95.6%), conservative therapy was successful -defined as passage of worms into the colon.[16] Eleven subjects in the study underwent exploratory laparotomy after symptoms did
not abate following conservative management.
Hypertonic enema is effective because the saline concentration serves as an irritant to the worm bolus. The distressed bolus often
breaks apart, and the worms enter the large intestine and rectum. While hypertonic enema is generally regarded as safe, it does
carry the risk of complications, which include perforation of the small or large bowel, massive fluid loss and dehydration, and
subsequent electrolyte abnormalities.
Conventional therapy for subacute obstruction includes administration of intravenous fluids and nasogastric aspiration for 48 to
72 hours.[14] Anthelmintic agents followed by hypertonic enema can then be used to expel the roundworms (Figure 2). [14] There are
a variety of anthelmintic agents that can be administered after intravenous rehydration and nasogastric tube placement.
Previously, piperazine citrate was given in a 75 mg/kg dose. Because of toxicity, this agent has been virtually discontinued in
developed countries.[7]
(Enlarge Image)
. Ascaris (roundworm) collection following anthelmintic therapy in a child. (Reprinted from Despommier D et al. Parasitic
Diseases. 2001.[24])
The anthelmintics of choice are mebendazole and albendazole. These medications are used for intestinal ascariasis as well as
HPA. Mebendazole,100 mg, is given twice daily for 3 days and provides protection against Trichuris trichiura (whipworm) as
well as Ancylostoma duodenale and Necator americanus (hookworm).[7] Alternatively, albendazole may be used; the advantage of
this drug is that it is given in a single 400-mg dose.[7]
These medications are embryotoxic and teratogenic in laboratory animals. For this reason, package inserts for these medications
do not recommend their use in pregnant women and children younger than 2 years. Widespread use in developing countries,
however, suggests that both of these benzimidazole anthelmintics are probably safe for use in young children and in women
during the last 2 trimesters of pregnancy. The World Health Organization endorses the use of albendazole and mebendazole in
those groups.
Surgical management of bowel obstruction is indicated in patients with rectorrhagia or toxicity, in those who are unresponsive to
medical treatment, or when plain abdominal films show several air-fluid levels. [12] Resection with end-to-end anastomosis of the
affected bowel is not necessary unless there is perforation or gangrene. The more common technique for mechanical obstruction
is laparotomy and massaging of the packed worm bolus toward the colon. [12]
When the cause of obstruction is volvulus, management is different. Milking of the bowel in volvulus can damage the small
intestine, so enterotomy is the preferred method of surgical management. [17] Surgical exploration in any patient with Ascarisinduced bowel obstruction can reveal peritoneal granulomas, which can be as large as 20 3 10 cm. [15] Granulomas can be excised
during laparotomy.
While roundworms most commonly reside in the jejunal and ileal lumen, on occasion they may migrate into the duodenum and
ampullary orifice. Ascaris worms can then enter the hepatobiliary tree or the pancreatic ducts, resulting in significant disease of
the liver, gallbladder, and pancreas. While intestinal obstruction is more common in children, adults experience HPA more
frequently.[7] The hepatobiliary duct network in children is smaller and thus more difficult for worm entry. The mean age of
patients who present with HPA is 35 years (range, 4 to 70 years), with a female-to-male ratio of nearly 3:1. [7]
Pregnant women and patients with a history of biliary tree surgery who are infected with Ascaris are at an especially heightened
risk for contracting HPA. Previous surgeries as well as endoscopic sphincterotomy result in widened ampullary diameter; this
facilitates entry for roundworms. [18] HPA has 5 typical presentations, including acute cholecystitis, acute cholangitis, biliary colic,
acute pancreatitis, and hepatic abscess.
Acute cholecystitis. Calculi in patients with ascariasis are often pigmented with worm fragments, and ova serve as the nidus. [19]
Acute cholecystitis caused by Ascaris infection may also be acalculous. In this scenario, symptoms are from the migration of the
worm into the biliary tree, causing obstruction of bile flow.[19] Patients who have acute cholecystitis often complain of right upper
quadrant pain that is referred across the back, right shoulder, and scapula. [20] Vomiting and low-grade fever (temperature of 37.2C
to 37.8C [99F to 100F]) are frequent presenting symptoms. [20]
Biliary colic. Patients with biliary colic present with symptoms of acute cholecystitis, including right upper quadrant pain,
nausea, and vomiting. Fever and jaundice are absent, however.
Cholangitis. Two types of cholangitis have been described in patients with ascariasis. One type is acute cholangitis, in which
patients typically have high fever (temperature of 38.3C to 40C [101F to 104F]); jaundice; enlarged liver; pronounced
leukocytosis; and elevated levels of liver enzymes, such as alanine aminotransferase (ALT), alkaline phosphatase, and serum
bilirubin.[20] In cases of severe cholangitis, hypotension and metabolic acidosis, as manifestations of endotoxic shock, are possible.
The second type, recurrent pyogenic cholangitis (RPC), is a specific condition characterized by stone formation in the biliary
tree, along with chronic infection. [7] Presentation is similar to that of acute cholangitis. Cholangiograms frequently reveal sludge,
dilation, and strictures in the biliary system. RPC is especially significant in the United States because this disease is prevalent
among immigrants and refugees from Taiwan and southern China. A strong epidemiologic correlation exists between RPC and
recurrent HPA. It is theorized that roundworms, chronically in the bile duct, may impair drainage, resulting in biliary sepsis and
stone formation.[21]
Hepatic abscess. Hepatic abscess formation is a potentially dangerous condition caused by the presence of adult worms or ova in
hepatic tissue. Patients with this condition experience right upper quadrant tenderness, high fever, hepatomegaly, intercostal
tenderness, and edema of the right chest wall. [20] Complications of hepatic abscess include sepsis and rupture into the pleural
cavity.
Acute pancreatitis. The global incidence of acute pancreatitis as a result of Ascaris infection is unknown because many cases go
undiagnosed.[19] The mechanism of acute pancreatitis is similar to that of hepatobiliary disease. Ascension of the parasite into the
pancreatic ducts and calcified worm and ova remains are implicated in pancreatitis. [19] A diagnosis of pancreatic ascariasis is often
made on the basis of a high index of suspicion. Patients present with midepigastric pain that is referred to the back; vomiting of
worms; and elevated levels of pancreatic markers, such as serum amylase and lipase. [22] Furthermore, results of liver function tests
are also abnormally elevated.
Diagnosis and treatment. Following a thorough history and physical examination, blood cell counts, liver function tests
(including measurement of serum aspartate aminotransferase, ALT, alkaline phosphatase, and serum bilirubin), and stool analysis
for ova and parasites should be performed. In all of the hepatobiliary manifestations discussed above, liver enzyme levels are
markedly elevated; patients with hepatic abscess have the greatest increase. [20] Acute pancreatitis will also result in elevated levels
of serum amylase and lipase.
Imaging studies are also indicated. Ultrasonography is a particularly specific and sensitive mode for detecting biliary and
pancreatic ascariasis. Because the technique is not invasive and does not require the use of anesthesia, it is possible to repeat the
test so worm migration may be monitored. In cases of hepatobiliary ascariasis, the longitudinal plane of the ultrasonogram will
reveal a hypoechoic strip containing a central anechoic tube within the common bile duct. [23] The transverse plane may display the
worm inside the tubular duct.[23] In patients with acute pancreatitis, ultrasonography will show an enlarged "echo-poor" pancreas.
[20]
Initial management of biliary colic, cholecystitis, and acute pancreatitis is restriction of oral intake; intravenous fluids;
antibiotics; and analgesics. Anthelmintic therapy (mebendazole, 100 mg orally, twice daily for 3 days) is started once acute
symptoms have remitted.[22] Acute cholangitis is much more severe and requires urgent surgical or endoscopic biliary
decompression and drainage. [20] Hepatic abscess is managed by ultrasound-guided aspiration and removal of pus, along with
antibiotics, analgesics, and anthelmintic agents.
The gold standard of diagnosis and treatment of HPA is endoscopic retrograde cholangiopancreatography (ERCP). This
procedure should be performed if initial conservative management (discussed above) fails to provide relief of symptoms. With
ERCP, worms can be detected virtually everywhere within the duodenum and hepatobiliary and pancreatic trees and can be
extracted using biopsy forceps.[3] Khuroo and associates[20] have suggested that recurrent biliary colic that does not remit with
analgesics is an indicator for emergency ERCP.

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