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M. A. Hardy and C. Yang
Abdominal Emergencies ofParasitic
andUncommon Origin
Abdominal emergencies of parasitic origin
although relatively infrequent do present to the
emergency room at sufcient rate in LMICs not
only to be aware of them but to be able to diagnose and treat them. Although the incidence of
parasitic infections is decreasing in LMICs due
to improved sanitation, access to portable water
and availability of potent antibiotics, peritonitis
secondary to ruptured liver amebic abscess or
typhoid perforation should remain part of the
differential diagnosis of all acute abdomen in
LMICs, while gastrointestinal tuberculosis
(GITB) should be high on the differential list
for abdominal pain or appendicitis. Many of
these parasitic infections may not initially
require surgical intervention. Pre-operative
diagnosis could lead to a non-operative management that may be associated with better
prognosis by being treated with appropriate
antibiotics. The following is a brief summary of
the most common parasitic and less common
diseases that require diagnosis and treatment of
an acute abdomen.
Intestinal Tuberculosis
Epidemiology
Intestinal TB accounts for 11–16% of cases of
extra-pulmonary TB, and accounts for 1–3% of
all TB cases worldwide. It most commonly
affects the ileocecal region, but can involve any
part of the GI tract. There is unclear association
of GI TB with sex predisposition or age of the
patient, but GI TB is commonly seen in populations with lower socio-economic status (SES),
and is associated with illiteracy, malnutrition,
and co-infection with HIV/AIDS. Although the
prevalence rate of GITB is rare in LMICs, it is 20
to 50 times greater than in HICs and should be
looked for. Surgery which should be avoided,
once done, could show the effect on more than
one organ and reveal tuberculous granulomas,
which would prompt a more specic treatment of
these patients.
Diagnosis
Diagnosis of abdominal TB is often delayed
because the clinical presentation is often atypical.
Important part of it includes clinical suspicion on
the basis of relevant history or risk factors for
prior TB.The most common signs and symptoms
are abdominal pain or distention, ascites, and
intestinal obstruction. Other common complaints
include fever, weight loss, melena, abdominal
mass, diarrhea or bowel obstruction, and anorexia
[24]. A family history may not be evident, and
some patients may not manifest any symptoms of
GITB.Symptoms depend on the site of involvement and may include clinical manifestations of
intestinal ulcero-constrictive disease, adjacent
tissue involvement, or chronic inammation.
High-risk populations for tuberculous peritonitis
include Asians, American Indians, alcoholics,
chronic ambulatory peritoneal dialysis patients,
and AIDS patients. Denitive diagnosis can usually be made by laparoscopic guided peritoneal
biopsy.
There is no gold standard for diagnosis of
intestinal TB, which is usually made from a
combination of imaging (CT scans) for extent
and type of GI TB, alongside clinical signs and
laboratory ndings. A high erythrocyte sedimentation rate, anemia, hypoalbuminemia, and leukocytosis raise suspicion for GITB. Puried
protein derivative skin test (PPD) which is readily available in LMICs and interferon-gamma
release assay like T-spot test (not generally available in LMICs) can be positive in 50–80% of
patients, but negative results do not exclude
GITB. Mycobacterium- specic testing modalities for GITB such as quantiferon testing or PCR
assays have high specicity but low sensitivity
and may not be practical in LMIC. Adenosine
deaminase (ADA) levels in ascitic/peritoneal
uid may serve as a good diagnostic marker.
Finally, empirical anti- tuberculosis therapy
(ATT) may be used when clinical suspicion is
high and has been proposed as a diagnostic criterion; there is no recommendation on when to discontinue ATT if used as a diagnostic therapeutic
trial. GITB is often confused with Crohn disease
and has been known to mimic esophageal cancer, esophageal ulcers, gastric ulcers, gastric
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cancer, colorectal cancer, and sarcomas, or other
acute infections such as appendicitis, colitis,
acute cholecystitis, and necrotizing fasciitis.
Intestinal sarcoidosis is commonly confused for
GITB, and even on biopsy the two conditions
may be difcult to differentiate. PCR testing for
M. tuberculosis is highly specic for GITB, with
specicity of 95% and can be used for
differentiation.
Management
GITB generally responds to standard anti-TB
drugs, and early initiation of ATT with high
clinical suspicion signicantly reduces morbidity and mortality. The recommendation is the
same as for pulmonary TB, a 6-month therapy
with standard regimen of isoniazid, rifampicin,
pyrazinamide, and ethambutol 3x weekly for
the rst 2months, and isoniazid and rifampin
for an additional 4 months. Full recovery is
sometimes difcult to assess but can be generally seen in 2months. Those with disseminated
disease may require prolonged therapy. Surgery
is only used in patients unresponsive to anti-TB
therapy or for complications such as strictures
or obstruction and for misdiagnosis of appendicitis. In one series of 96 patients with abdominal TB [25], 70 (72.90%) were admitted as
acute intestinal obstruction and 22 (22.9%)
with acute diffuse peritonitis. The emergency
bowel resections in 74 of these patients were
for 34 ileocecal masses, 16 strictures, 10 perforations, and 10 adhesions. Acute intestinal
obstruction was the main acute presentation in
this report from 2006, and although the incidence of GITB in LMICs has decreased since
then, following milk pasteurization in some
areas and improved public health measures,
GITB remains a signicant surgical/medical
problem in LMICs.
Complications
Common complications following treatment are
upper and lower GI bleeding, stula, stricture,
intussusceptions, perforation, anemia, and malnutrition with weight loss or vitamin deciency.
ATT often results in drug-induced liver injury
requiring discontinuation and/or change.
Typhoid
Epidemiology
There are an estimated 11–20 million cases of
typhoid worldwide each year, with approximately 8–15 million cases in LMICs. Typhoid is
most commonly found in developing areas in
Southeast Asia or Africa, primarily in Central
Africa, India, Pakistan, or Bangladesh, and it is
also found less commonly in East Asia, South
America, and in the Caribbean. The risk of
typhoid is high in populations with high poverty,
inadequate sanitation, or lack of access to clean
food and water, as well as in vulnerable groups
such as children.
Diagnosis
The incubation period is 6–30days from exposure, with gradual onset of increasing fatigue
and fever. Other signs and symptoms of
typhoid commonly include prolonged high
fever that peaks in the late afternoon or evening, fatigue, headache, nausea, abdominal
pain, constipation, or diarrhea. Less commonly, patients present with abdominal distention, hepatosplenomegaly, myalgia, dry
cough, sore throat, or a transient, maculopapular rash on the trunk. Signs and symptoms
appear gradually and can be confused with
malaria; typhoid can be clinically suspected
when patients are in areas where typhoid is
endemic when there is a lack of response to
antimalarials. Left untreated or even ineffectively treated, typhoid is often fatal, sometimes with recurrent intestinal perforations
after an original operation and/or with late
symptoms of delirium and “typhoid state”
(lying motionless and exhausted) [26].
Patients with typhoid will have bacteremia,
and the gold standard test for typhoid is positive
multiple blood cultures since a single culture is
positive in only 50% of cases. Multiple cultures
from a large volume of blood and bone marrow
cultures can increase the sensitivity and diagnostic yield and partially neutralizing the antibiotic
effect. Serologic tests and stool and urine cultures have lower diagnostic yield, and are not
substitutes for blood cultures.
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M. A. Hardy and C. Yang
Management
Typhoid responds well to antibiotic therapy, and
uoroquinolones are empirically effective in
adults. Cephalosporins and other newer antibiotics may be preferred now since a resistance of
typhoid to uoroquinolones is emerging in
endemic regions. Azithromycin needs to be
reserved for multidrug-resistant (MDR) typhoid
and should not be used empirically. Treatment
should be initiated as soon as possible, even
before results of blood culture are available
either with oral cexime 400 mg q12hr or IV
ceftriaxone 1gm q12hr or 2gm q24 hr. If there
are any signs of complications or no clinical
improvement after 5days of treatment with PO
cexime and blood culture results and sensitivities are available, it is prudent to give a new antibiotic intravenously. Recommended therapy
depends on the type of typhoid and its sensitivity. For non- resistant typhoid, uoroquinolones
for 14 days are effective and cephalosporins
should be de- escalated to rst-line antibiotics.
Chloramphenicol (50mg/kg in 4 doses), trimethoprim sulfamethoxazole (4–20 mg/kg in 2
doses), or ampicillin/amoxicillin (75–100mg/kg
in 4 doses) are also effective. For multidrugresistant typhoid third-generation cephalosporins for 14 days should be used. For extensive
drug-resistant typhoid (XDR), n a clinically
stable patient azithromycin with 1gm loading
dose, followed by either 500 mg or 1gm PO
q24hr for 7–10 days depending on patient’s
weight (<60kg vs >60kg).
There are also two vaccines available, but they
are generally not available in many endemic
countries and do not have a long-lasting effect.
Ileal perforations occur frequently in children
and young adults where the diagnosis is delayed
because they may be treated for malaria for more
than a week before being diagnosed properly
when they present with peritonitis and with septic
shock. After initial resuscitation with IV uids,
antibiotics, nasogastric decompression, and
blood transfusion if necessary, they are explored
and the area of perforation is usually resected followed by re-anastomoses followed by copious
irrigation of the abdomen with warm saline.
Search for more than one perforation is manda-
tory. Re-exploration may be necessary to look for
a new perforation if patient is not improving in
3–5days. Occasionally a right hemicolectomy is
necessary or a tube ileostomy if the patient cannot tolerate the operation. Patients who present
early have a mortality of about 10% while those
who present late with an abdomen lled with pus
and intestinal content have a mortality of 20–50%
depending on the length of the delay and of postoperative ICU care and sensitivity to the antibiotics. Typhoid remains a dangerous and frequently
fatal disease [27].
Complications
Complications occur in 10–15% of patients, particularly those who have been ill for more than
2weeks. The most common complication is GI
bleeding, usually slight bleeding but can be rapidly fatal depending on location. Intestinal perforation is the most serious complication, requiring
surgery, and occurs in 1–3% of patients, manifesting with worsening abdominal pain, and sign
of septic shock with hypotension and with acute
abdomen. Neuropsychiatric presentations, such
as reduced level of consciousness or encephalopathy, severe agitation, or delirium, are also common in certain countries. Relapse occurs in
5–10% of patients 2–3weeks after resolution of
symptoms, though the relapse is usually less
severe than initial disease. Relapse must be differentiated from reinfection before treatment.
Dysentery
Dysentery can either be bacillary dysentery,
caused by Shigella bacteria, or amoebic dysentery, caused by Entamoeba histolytica.
Amoebic Dysentery (Amoebiasis)
Amoebic dysentery is most common in tropical
areas with poor sanitation, and only 10–20% of
people infected become sick. An estimated 500
million people are infected worldwide, with
between 40,000 and 100,000 deaths. It is
endemic in tropical areas, particularly in developing parts of Central and South America,
Africa, and Asia [28].
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Bacillary Dysentery (Shigellosis)
Bacillary dysentery has approximately 188 million cases annually worldwide and 164,000 associated deaths. Globally, shigella is the second
most common cause of diarrheal deaths.
Prevalence of dysentery is generally highest in
children aged 1–4 years in LMICs, and peaks
between 18 and 23months of age [28]. Since it is
spread by fecal contamination of food and water,
dysentery often appears as an epidemic in impoverished areas with poor sanitation, overcrowding,
or refugee populations. Since 1991, there have
been dysentery epidemics in Angola, Burundi,
Malawi, Mozambique, Rwanda, Tanzania,
Democratic Republic of the Congo, and Zambia.
Diagnosis ofDysentery
The incubation period depends on the pathogen,
generally around 1–4 days, with approximately
50% of detected shigella infections being asymptomatic and up to 90% of E. histolytica infections
being asymptomatic. Early clinical presentation
commonly includes fever, headache, anorexia,
and vomiting, followed by abrupt onset of watery
diarrhea. Often, it resolves within 3–7days and
symptoms are mild in healthy individuals.
Progression to dysentery is generally marked by
frequent, small stools with blood or mucus in
nearly half of cases of Shigella diarrhea. At this
point, patients commonly present with fever,
lower abdominal cramps, rectal pain, tenesmus,
bloody stool, and especially dehydration.
Persistent diarrhea associated with malnutrition
is the leading cause of death among children.
Dysentery is often confused with other causes of
diarrhea such as bacterial enteritis and nontyphoidal salmonella, which differ from Shigella
by an abrupt onset, more than four frequently
bloody stools per day, no vomiting at onset, and
fever. The diagnosis can also be conrmed by the
identication of the parasite in fresh stool specimens, ulcer scrapings, and on rectal biopsy.
The current gold standard for diagnosing dysentery is rectal swab and conventional bacterial
culture showing evidence of dysentery-causing
Shigella or amoeba. Bacterial culture provides
information on antibiotic susceptibility to dictate
treatment. Fecal leukocytes can also help differ-
entiate dysentery from other diarrheal diseases,
but are not sufcient replacement for bacterial
culture. In amoebiasis the typical punched-out
ulcer is almost diagnostic on sigmoidoscopy, and
these may be found throughout the colon.
Amoebic dysentery is commonly confused with
other parasites under a microscope, such as nonpathogenic Entamoeba dispar which is 10 times
more common. Unfortunately, most laboratories
are unable to differentiate between E. histolytica
and E. dispar.
Management ofBacterial Dysentery
Current treatment guidelines endorse oral ciprooxacin as rst-line therapy for bacterial dysentery, and parenteral ceftriaxone for severe disease.
In children, oral ciprooxacin 15 mg/kg twice
daily for 3days, or in case of severe disease, parenteral ceftriaxone followed by oral for
10–14days. For adults, rst-line therapy is oral
ciprooxacin 500mg once a day for 3days or for
severe disease, parenteral ceftriaxone for 3days
IV or IM. If there is no improvement after
48 hours of antibiotics, therapy needs to be
adjusted according to susceptibility. Second-line
therapy with β-lactams, cephalosporins, and
azithromycin is appropriate in regions where ciprooxacin resistance is high.
Management ofAmoebic Dysentery
Treatment of amoebiasis in tissue is treated with
nitroimidazoles, such as metronidazole, tinidazole, or nitazoxanide, dehydroemetine, or chloroquine. These should be given 3× a day for
5–10 days. Amoeba infection of the lumen is
treated with diloxanide furoate or iodoquinoline,
though it may require a combination of medications for effective treatment. First-line
recommended therapy is metronidazole (500–
750 mg for 5–10 days for adults, 35–50mg/kg
per day divided into 3 doses for 10days). There
is toxicity associated with nitroimidazoles and
concern for development of resistance [29].
The general surgeon is likely to be faced with
complications arising from amoebiasis wherever
he works in LMICs. Amoebic colonic ulcers heal
with a thin scar but may appear as pseudopolyps
and rarely go on to form an amoebic granuloma
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M. A. Hardy and C. Yang
in the cecum or rectosigmoid and confuse the
surgeon. Amoebic abscess may occur in the lung,
pleura, even in the brain, but it is most common
in the liver which they invade from the colon via
the portal vein and are found most commonly in
alcoholics. When operation is considered in a
patient who has amoebiasis, pre-operative treatment of the disease should be done if at all possible. Colon resection should be avoided because
the bowel is very friable, and diverting ileostomy
may be sufcient for amoebic colitis. Perforation
is rare and the signs of peritonitis may be masked,
and it may be diagnosed primarily by free air on
repeated abdominal lms in a patient who is getting worse on antibiotics. If a bowel resection is
done at any point, a diverting colostomy or ileostomy is almost mandatory because intestine
infested with amoeba does not heal well and
breakdown of the anastomosis is common. The
mortality following colonic resection in fulminant amoebic colitis is high. Occasionally perforation is multiple, especially if antibiotic
treatment has been delayed. Hemorrhage from an
ulcer that invades an artery is very rare, and treatment should consist of blood replacement and
embolization by interventional radiologist, and
avoiding exploration that carries a very high mortality. Amoeba can locate in the appendix and
mimic appendicitis leading to a very difcult
appendectomy with friable bowel which may
require exteriorization of the cecum. Colonic
lesions can occasionally lead to strictures and
rarely stulae. Amebic liver abscess is caused by
extraintestinal spread of Entamoeba histolytica.
It is usually diagnosed from imaging, and the
gold standard of treatment is metronidazole.
Only about 15% of cases require percutaneous
drainage. The prognosis is good, with almost universal recovery.
Complications
Common complications include dehydration,
liver abscess, post-infectious arthritis (joint pain,
inammation, and stiffness), and hemolytic ureic
syndrome, a rare complication of Shigella.
Bacteremia is a common complication in young
children under the age of 5, as well as leukemia
reaction in children between 2 and 10years old.
The most common neurological symptom is generalized seizures, which leads to increased mortality. Dysentery can result in colon perforation
(primarily in infants or malnourished patients),
intestinal obstruction, toxic mega colon, prostates (in infants and young children), dermatitis,
or even acute myocarditis.
Ascaris
Epidemiology
Worldwide, ascariasis, caused by the parasitic
worm Ascaris lumbricoides, infects approximately 807 million to 1.2 billion people in the
world with more than 60,000 deaths annually and
contributes signicantly to the burden of parasitic
diseases worldwide. Ascaris survives best in
warm, humid areas and is endemic to tropical and
subtropical areas of East Asia, China, subSaharan Africa, and Latin America, particularly
in areas with poor sanitation, or in regions where
human feces is often used as fertilizer.
Diagnosis
People with ascariasis often have no symptoms
other than malnutrition, or mild symptoms such
as abdominal discomfort or pain, nausea, vomiting, bloating, and diarrhea. In children, ascariasis
may present with growth retardation. Severe
infection depends on the passage of larvae; ascaris larvae in the lungs can cause Loefer syndrome (pneumonitis and eosinophilia, with
wheezing, dyspnea, hemoptysis, and fever),
whereas ascariasis migration to the biliary or
pancreatic system can cause cholecystitis, cholangitis, pancreatitis, volvulus, appendicitis, and
intussusceptions. Spontaneous resolution is possible, as the adult parasite lives on average for 1
to 2 years, and cannot multiply in the human
host, after which it dies and is eliminated through
the digestive tract.
The best diagnostic test is a stool exam for
ova, which look like large oval brown trilayered
eggs and parasites. However, eggs will not appear
in stool until a month to 40days after infection,
and if one is infected with a male worm, there
will be no eggs in the stool. Patients may also
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notice a worm in their stool or cough one up and
make their own diagnosis.
Management
Ascaris infection responds well to antihelminthic
therapy, with a single-dose treatment of albendazole of 400mg resulting in over 95% cure rate
and reduction in eggs. Medical therapy should be
repeated after 1–3 months, to target larvae that
have matured to adulthood. Second-line treatment is mebendazole 100mg 2× a day for 3days,
or 500mg as a single dose. For pregnant patients,
pyrantel pamoate 11mg/kg up to 1g is recommended, and second-line therapy is 50 mg/kg/
day piperazine for 5days. Children should also
have vitamin A supplementation. If a patient
presents with active parasite migration through
the lungs, medical therapy is contraindicated due
to increased risk of pneumonitis. It is common
for patients to be reinfected especially with no
change inlocation, hygiene habits, or health education. Since Ascaris can invade various organs,
treatment is directed to those organs, such as
removal for appendicitis or cholecystitis.
Complications
Complications of ascariasis result from parasite
migration, and children are more likely to have
complications than adults. Common complications are rectal bleeding, hepatobiliary disease,
and pancreatic pseudocyst. Depending on worm
burden, heavy ascariasis may cause intestinal
blockage and perforation.
Filariasis
Epidemiology
Filariasis is caused by parasitic roundworms
called lariae that dwell in blood and tissue
spread by mosquitoes. Lymphatic lariasis, also
known as elephantiasis, is the most important and
common larial disease, infecting 120 million
people with approximately a billion people at
risk for infection. 70% of cases are found in
India, Nigeria, Bangladesh, and Indonesia,
though the parasite is endemic in around 80 tropical and subtropical countries in Central Africa,
the Middle East, Southeast Asia, and coastal
South America. The main pathogen is Wuchereria
bancrofti, comprising 90% of cases, with the
remaining mostly due to Brugia malayi. In many
countries, men are much more susceptible to lariasis, possibly due to women’s mode of dress
being more covered and protected from infective
mosquito bites.
Diagnosis
From infection by mosquito bite, it may take anywhere from 4weeks to 16months or longer for
clinical manifestation to occur. More than half
the patients with lariasis appear asymptomatic,
despite hidden lymphatic damage, and the duration without symptoms is linked directly to the
patient’s immune competence. Filariasis is characterized by acute, episodic attacks of lymphadenitis and lymphangitis, with fever and malaise,
lasting 3–15 days. There may also be lumps in
subcutaneous tissue, breasts, or testicles. These
acute inammatory episodes, due to the parasite
invading lymph nodes, prevent lymph ow and
result in painful lymphatic trunks with red streaks
in the skin, and swelling for several days, usually
isolated to a single limb.
Filariasis is difcult to diagnose and relies on
history of exposures in an endemic area.
The standard method is identifying microlariae by microscopic exam of a thick blood
smear obtained at night since microlariae
exhibit nocturnal periodicity and are only
detected circulating in the blood at night.
Serologic assays can be used but are frequently
negative because of the timing of the infection.
Recently, ultrasonography has been used to visualize adult worms of W. bancrofti even in asymptomatic males with microlaremia. A highly
sensitive antigen detection assay, the Alere
Filariasis Test Trip is now available and recommended for mapping, monitoring, and transmission assessment of W. bancrofti independent of
periodicity. This is, however, not applicable for
B. lariasis or the other less common pathogens.
Management
The WHO recommends mass drug administration (MDA) of a preventive chemotherapy strat-
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egy, by an annual dose to an entire at-risk
population, to reduce the density of microlariae
in the bloodstream and prevent spread to mosquitoes for long-term eradication of lariasis. A
combination of diethylcarbamazine citrate (DEC)
(6mg/kg), ivermectin (200 mcg/kg) and albendazole (400mg) as a single dose can clear almost
all microlariae in the blood within a few weeks.
17 countries have successfully implemented
MDA and eliminated lariasis as a public health
threat (Cambodia, Egypt, Kiribati, Maldives,
Malawi, Marshall Islands, Palau, Sri Lanka,
Thailand, Togo, Tonga, Vanuatu, Vietnam,
Yemen, Niue, Wallis and Futuna, and the Cook
Islands).
The goals of therapy are to kill the adult
worms and slow the progression of disease, as
well as manage the morbidities and complications. The medical therapy of choice is diethylcarbamazine citrate, which can target both the
adult worm and the microlaria. DEC has a
potent and selective effect on microlaria, allowing them to be phagocytosed by tissue xed
monocytes, starting with a low dose to decrease
risk of adverse effects with a gradual increase in
frequency and dose for 4–21 days [30].
Concurrent corticosteroid treatment should be
considered to minimize allergic reaction to the
disintegration of microlaria. Other medical
therapy includes ivermectin or suramin, which
causes tonic paralysis in nematodes. Mebendazole
or ubendazole also work to kill or immobilize
the parasites, which are then cleared from the gut.
Lymphatic damage is irreversible, so early diagnosis and prevention of progression of disease
are crucial. Exercise and elevating affected limbs
relieve the symptoms. Filariasis-associated adenolymphangitis is treated with repeated courses
of DEC, but the late phase of chronic disease is
not affected by DEC. Surgery is necessary for
hydrocele [31].
Complications
Severe disease manifests with painful and visible
disgurement including acute dermatolymphangioadenitis (ADLA) and elephantiasis, referring
to gross enlargement of the body, particularly the
limbs. Male urogenital disease such as hydrocele
and lymph scrotum have been reported, concurrent with other symptoms due to larial abscesses
in the genital area, which swell until rupturing.
Tropical pulmonary eosinophilia rarely occurs as
an extreme immune response, characterized by
high eosinophil count, asthma-like attacks, splenomegaly, and restrictive lung disease.
Schistosomiasis
Epidemiology
Schistosomiasis is a parasitic disease caused by
trematode worms, commonly Schistosoma man-
soni, S. haematobium, or S. japonicum, that
infects approximately 250 million people worldwide causing around 25,000 to 200,000 deaths
globally per year. Freshwater snails release the
larvae, and people become infected on skin contact with infected usually still water, with adult
worms living in the blood vessel releasing eggs.
It is endemic to tropical and subtropical regions,
particularly agricultural or shing populations or
areas without adequate sanitation or access to
clean water, with more than 200 million cases in
Africa, particularly sub-Saharan Africa. There is
also considerable morbidity in the Middle East,
South America, and Southeast Asia. Adolescents
have the highest intensity of infection by wading
and swimming in still waters and are targets for
screening and mass drug administration
campaigns.
Diagnosis
About 60% of infected patients are symptomatic,
but only 10% result in serious disease requiring
treatment. Adult worms in the blood vessels are
relatively harmless– the only clinical manifestations are terminal dysuria, hematuria, and rarely
dysentery. The symptoms can be divided into
three phases: acute disease, subacute disease, and
chronic disease. In acute disease, clinical manifestation is a sudden presentation with a swimmer’s itch or cercarial dermatitis (a local
inammatory, itchy, maculopapular skin eruption
is evident at the site of cercarial penetration),
bronchopneumonia, myalgia, and Katayama syndrome (a delayed hypersensitivity reaction that
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coincides with worm maturity, characterized by
fever, arthralgia, and vasculitic skin eruption).
Acute symptoms usually resolve spontaneously
after 2–10weeks, but can progress to weight loss,
dyspnea, diarrhea, toxemia, hepatosplenomegaly,
and widespread rash. In the subacute phase, species- and organ-specic lesions form in certain
organs depending on egg location, leading to
granulomatous, cell-mediated inammation in
affected organs. In chronic disease, brosis
replaced granulomas, leading to reduction of
symptom severity, though urinary, hepatointestinal, cardio-pulmonary, or ectopic clinical
manifestations may persist. Morbidity is generally more aggressive in the chronic phase after
healing, and the most serious manifestations,
namely, brotic lesions, glomerulonephritis,
amyloidosis, and bladder or rectal malignancy,
usually occur many years after initial infection
and treatment.
Symptoms depend on inammation secondary to schistosomiasis in either intestinal, hepatosplenic, or urogenital locations. Intestinal
schistosomiasis manifests as abdominal pain,
diarrhea, blood in stool, and hepatomegaly,
associated with uid accumulation in the peritoneal cavity. Hepato-splenic schistosomiasis
manifests as hepatic brosis and portal hypertension, which occasionally lead to the development of esophageal varices, ascites, delayed
growth, and severe anemia. Urogenital schistosomiasis is characterized by hematuria,
increased frequency of micturition, and dysuria.
Untreated urogenital schistosomiasis leads to
brosis of the bladder and ureter, and possibly
the kidney in advanced cases. Women, particularly in communities where women do household chores in unclean bodies of water, may
develop urogenital schistosomiasis with genital
lesions, vaginal bleeding, pain during intercourse, and vulvar nodules. In men, urogenital
schistosomiasis causes pathological degradation
of urogenital structures leading to infertility and
other long-term consequences [32].
Schistosomiasis is diagnosed by stool or urine
sample and identication of parasite eggs during
active or late chronic infection, though during
acute infection the low worm burden makes these
methods relatively ineffective. Acute infection
with its mild symptoms is often confused for
malaria, salmonellosis, or acute hepatitis.
Intestinal schistosomiasis can be detected in stool
samples using the Kato-Katz technique to identify eggs. For urogenital schistosomiasis, the gold
standard is a ltration technique using nylon,
paper, or polycarbonate bers. In regions where
S. mansoni is endemic, the circulating cathodic
antigen (CCA) test is an appropriate alternative.
PCR-based detection of parasite DNA in stool
and urine and ultrasonography for pathological
changes are also used in high-resource areas for
higher sensitivity but are frequently not available
in LMICs.
Management
The gold standard and mainstay of medical treatment is oral praziquantel 20mg/kg PO TID for
1day (at intervals of 4–6hours), which is effective against all 6 types of Schistosoma adult
worms, and safe in children over the age of 4 and
pregnant women after the rst trimester. Adverse
effects are minimal, nausea, itch and rash, and
likely due to immune response to dying and dead
worms. If there is a co-infection of schistosomiasis with T. solium (pork tapeworm), praziquantel
can induce seizures, cerebral infarction, or permanent eye lesions. The limitations of praziquantel are that reinfection is common, and drug
tolerance is of increasing concern. There is also a
MAD campaign to eradicate schistosomiasis,
with an annual single dose of praziquantel in
endemic populations targeting adolescents that
has been effective in China and Egypt. However,
limitations of praziquantel and concerns of relying on a single drug impede scalability and efcacy of this campaign. In spite of a decrease in
prevalence of hepato-splenic schistosomiasis
thanks to mass-treatment with praziquantel,
severe cases of portal hypertension are not exceptional due to esophageal varices. Operative interventions may be indicated for portal hypertension
with a spleno-renal shunt or splenectomy. In
Brazil hepatosplenic schistosomiasis is a serious
clinical presentation of this disease, associated
with splenomegaly, liver brosis, and portal
hypertension, and is responsible for approxi-
336
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M. A. Hardy and C. Yang
mately 7% of schistosomotic patients. The surgical treatment of portal hypertension in
schistosomotic deals with preserved hepatic
function as compared to cirrhosis, and therefore
decompression of portal vein might interfere
with hepatic function. Recent focus therefore has
been on splenectomy, division of the left gastric
vein, devascularization of great gastric curvature,
and postoperative endoscopic variceal sclerosis,
as a surgical option to esophageal varices in hepatosplenic schistosomiasis [33]. In urogenital
involvement cystoscopy may be indicated with
irrigation and fulguration as necessary and stenting of the ureter in rare cases.
Complications
Complications include infertility, spontaneous
abortion, and urinary tract obstruction leading to
ESRD and bladder cancer, commonly squamous
cell carcinoma. Chronic inammation results in
complications such as anemia of chronic disease,
malnutrition, and growth retardation or failure to
thrive. Patients with schistosomiasis are also susceptible to co-infection with other parasitic, bacterial, or viral infections endemic in the area,
particularly HPV, Hepatitis B and C, and HIV.
Conclusion
In this chapter we have briey summarized the
difcult problem of diagnosing and managing
patients with acute abdomen and IAI in LMICs
primarily because of frequently decient infrastructure. This includes shortage of trained staff
inlocal and sometime in regional hospitals, difculties and delays in transferring patients to
regional or tertiary health facilities when
needed, and lack of appropriate equipment,
instruments, supplies, and medications at the
local hospitals and even at regional hospitals.
This chapter initially proposes in general terms
the best ways to address these problems before
proceeding to describe briey the epidemiology,
diagnosis, and management of very common
general surgical conditions with which every
general surgeon in LMICs or in HICs must
become well acquainted. The chapter then
describes in greater detail the most common
parasitic, protozoan, and bacterial causes of
acute abdomen and IAI in LMICs with which
local general surgeons are much more familiar
than the visiting surgeons or residents from
HICs. The chapter also emphasizes the collaboration between local and visiting surgeons at the
level of surgical and medical health care delivery while maintaining the teaching and learning
communication that care of patients with IAIs
and acute abdomens engenders.
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