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SPLENIC HYDATIDOSISA
A Review of Literature

AJAY H BHANDARWAR*, AVINASH N KATARA**, GIRISH D BAKHSHI**,MOTISINGH G

RATHOD***, ABDUL M QURAISHI****
*Associate Professor and Unit Head; **Lecturer; ***Professor and Head, Department of Surgery, Grant
Medical College and JJ Group of Hospitals, Mumbai 400 008. ****Associate Professor, Department of
Surgery, Vasant Rao Naik Medical College and Hospital, Yewatmal, Maharashtra.

Background : Hydatid disease has been recognised since ancient times and has a worldwide
distribution. Echinococcus granulosus is the causative organism in classic hydatid cysts. Splenic
hydatidosis is one of the lesser manifestations of the disease.

Methods : Discussed below is a review of literature, with a focus on the epidemiology, pathology,
clinical presentation, investigations and treatment modalities of splenic hydatidosis.

Results : Our literature review examines different articles published on this topic from 1924 till now,
and summarizes the data obtained.

Conclusion : The incidence of splenic involvement by hydatid cysts in relation to the rest of the
abdominal viscera is very low, constituting 0.5 to 4% of all cases of hydatidosis. Man is an accidental
intermediate host, as entry of the larval forms into humans represents an end stage in its life cycle.
This review discusses in detail the various pathological manifestations, the spectrum of clinical
manifestations and the armamentarium of investigative approaches. Until recently the gold standard
treatment for splenic hydatidosis was splenectomy, as medical therapy seems to be ineffective.
However, the last two decades have shown a tendency towards splenic conservative surgery in
suitable cases, to reduce opportunistic post splenectomy infection.

INTRODUCTION

Hydatid disease has been recognised since ancient times and has a worldwide distribution. Berlot in
1790 is accredited with the first description of a splenic hydatid cyst as an autopsy finding.[1]
Hydatidosis also known as echinococcosis, is a parasitic infection of liver and other organs by flatworm,
echinococcus. Echinococcus granulosus is the causative organism is classic hydatid cysts.

Most hydatid cysts are acquired in childhood but a latent period of five to twenty years occurs before the
diagnosis is made.[2] The growth of hydatid cyst remains indolent yet unremittent by character. As a
very crude estimate hydatid cysts increase their diameter by about two to three centimeters each year.[3]
The rate of growth of hydatids appeared to be dependent not only on immunologic relationship between
the parasites and humans but also on the resistance offered by the enveloping structure.

The incidence of hydatid cysts has decreased in the endemic areas when public health measures and
livestock handling procedures have been enacted. Public education about the disease and its
transmission, including instructions for vigorous hand washing after contact with canine species,
elimination of vegetables grown at ground level from the diet, and discontinuation of the practice of
feeding the entrails of slaughtered animal to dogs, has proven to be of value in decreasing the
occurrence of hydatidosis.[4]

INCIDENCE

Hydatid cysts are endemic in farming regions of Mediterranean, Eastern Europe, Middle East, South
America, Australia and South Africa.[4] In Western Europe and the United States, it is extremely rare.
Hydatid disease of spleen is extremely rare even in endemic areas (0.5-4 percent of all cases of
echinococcosis).[5-7] The incidence of splenic involvement by hydatid cysts in relation to the rest of the
abdominal viscera is very low.[8] The incidence of hydatid cysts of spleen varies widely in sheep raising
countries (Table 1). In India the incidence of splenic hydatid cysts reported by different workers from
different cities is as shown in Table 2.

TABLE 1
Country incidence of splenic hydatid
cysts
Country Incidence (%)
Australia[9] 2.10
Argentina[10] 2.14
Iceland[11] 0.78
Iran[12] 4.00
Uruguay 1.00

TABLE 2
Incidence of splenic hydatid cysts in
Indian Cities
Cities Incidence (%)
Ahmedabad[14] 2.00
Delhi[15] 4.20
Indore[16] 3.30
Nagpur[7] (Central
6.30
India)
Pondicherry[18] 2.70
Srinagar[19] 4.10

A mean incidence of splenic hydatid cyst in India is 4.3% with highest incidence in Central India. The
disease affects all age groups and both sexes with equal frequency.[4]

AETIOLOGY

Echinococcus granulosis is a member of the order Cestoda (flatworm) and family Taenia. The adult form
of echinococcus is a 5 mm long, hermaphrodite which infests the small intestine of carnivorous animals,
typically dogs, foxes and coyotes, the definitive hosts. Eggs are shed in the faeces of these animals and
are incidentally consumed by grazing animals such as cows, sheep, buffalo, zebras, moose, and caribou.
Enzymatic digestion of the shells of these eggs in the duodenum of these intermediate hosts release the
embryonic forms. These migrate through the intestinal wall to enter the portal circulation, from where
they make their way towards the liver or lung. These are filtered here and transformed into the
microscopic larval stage, the protoscolex or scolex. These larval forms are capable of asexual
multiplication within the affected organ. When the host dies or is slaughtered, the ingestion of the
infected organs completes the cycle, and the larval forms mature into adult parasites within the small
intestine of the carnivore.[4]

Man is an accidental intermediate host, as entry of the larval forms into humans represents an end stage
in its life cycle. Consumption of contaminated vegetables or meat, which are not washed or scrubbed
free of eggs, exposes man to the larval forms. An alternate mode of entry is direct contact with dogs,
whose fur has the eggs clinging onto it. Once in the intestine of man, these embryonic forms enter the
portal circulation and can spread to a variety of organs, including liver, lungs, pancreas, spleen, etc.

PATHOLOGY

The spleen undergoes cystic changes less often than any other abdominal viscus. Martin[20] proposed a
simple clinically practical classification of splenic cysts (Table 3).

Hydatid cyst is the only parasitic cyst of the spleen and it is said to be twice as common as the non-
parasitic variety.[13] The frequency of the splenic cysts in hydatid disease varies from one series to
another. In general a mean incidence of 3% is reported.[21,22] In India, a mean incidence of splenic
hydatidosis is 4.3%. The most common sites where hydatid cysts develop are liver (70%), which acts as a
first filter and lungs (15%), which acts as second filter. The other 15% are found in other organs.[23]
Practically no organ is immune to infestation by hydatid disease.[17] The rare sites include thyroid,[24]
omentum[25], pancreas[26], gall bladder[27], central nervous system[28], kidney[29], psoas sheet[30],
retroperitoneal region[31], orbit[32], cervix[32], adductor longus muscle[33], leg[34], heart[35] and
breast[36]. In India the incidence of hydatid cysts at unusual sites is higher as compared with other parts
of the world.[24] Hydatids at these unusual sites present difficulties in clinical diagnosis.

TABLE 3
Martin's Clinical Classification
of Splenic cysts
A. Primary (True) Cysts
a. Parasitic
b. Non-parasitic
Congenital
Neoplastic
B. Secondary (False) Cysts

As quoted by Mills,[37] Dieulafoy (1898) classified hydatid cysts of the spleen into ascending (immobile)
and discending (mobile) types and into cortical, central and juxtasplenic types as per location of the cyst.
Scherb (1904) added the abdominothoracic type. Such splenic echinococcal cyst burrowing into left
pleural space and left hemithorax were reported and detected by ultrasound and MRI, respectively.
[38,39] As per Mills[37], Segond and Potherat divided hydatids into three groups (a) those containing
much fluid but few daughter cysts, (b) those packed with vesicles and (c) suppurating cysts. Torbati[12]
from Iran reported a giant splenic hydatid cyst containing [21] litres of fluid in present series. The largest
cyst ever found was in Australia and it contained 57 litres of fluid.[2]

Anatomical classification of cysts was proposed by Martin (1908) as anterior cyst (gastro-splenic),
posterior cyst (pancreatico-splenic), superior cyst, inferior cyst and parietal cyst. The various
speculations about the possible routes followed by the parasite in order to reach the spleen include
spread through blood stream, lymphatics[40], reflux into spleen from portal vein,[41] from
haemorrhoidal veins after short circuiting the liver and lung filters,[42] through small veins passing
from the splenic flexure of the colon to the lower pole of the spleen,[43] via arterial blood[44], direct
migration from intestine to inferior vena cava through the lower and middle haemorrhoidal veins
without passing through the liver, migration through chyliferous ducts into superior vena cava and
general circulation after penetration of intestinal wall and direct entry into spleen from stomach and
colon across the actual or potential spaces or via lymphatics.[13] Despite these speculations, the most
logic route seems to be escaping of 10-15% of embryos from liver and lung filters into general
circulation, a fraction of which settle down in the spleen. The cyst may lodge in the interior of the spleen
or at its periphery. It may lie beneath the capsule (Fig. 1) or outside it or it may remain attached to the
spleen by a pedicle which may be broad or narrow[38] (Fig. 2).
 Fig.1: A large multilocular cyst with
multiple daughter cysts beneath the
capsule.

Fig.2: A large hydatid cyst projecting from

the hilum with its long pedicle

A hydatid cyst consists of three layers. The outermost layer is the adventitia (pseudocyst), consisting of
fibrous tissue as a result of the reaction of the liver to the cyst. It is greyish in colour and intimately
blends with the liver, from which it is inseparable. The middle layer is the laminated membrane
(ectocyst), which is formed of the parasite itself. It is whitish and elastic and contains hydatid fluid. This
fluid is crystal clear, with a specific gravity of 1.005 to 1.009. It contains chlorides, sulphates and
phosphates of sodium, sodium and calcium salts of succinic acid, but no albumin. It is slightly alkaline.
When not too old, it also contains hooklets and scolices. The ectocyst grows very slowly and resembles a
child's uncoloured balloon filled with water. It peels very readily from the adventitia unless bacterial
infection has set in. The hydatid fluid is antigenic and highly toxic, and can cause an anaphylactic
reaction in humans, which can be fatal. The innermost layer is the germinal epithelium (endocyst) which
consists of a single layer cells lining the cyst. It is the only living part of the hydatid cyst and secretes the
hydatid fluid internally and the laminated membrane externally. Brood capsules develop from this
germinal epithelium and are attached to its innermost walls by pedicles. The scolices, which are the
heads of the future worms, develop within the brood capsules. Should the laminated membrane become
damaged, it disintegrates, freeing the brood capsules which grow into daughter cysts.

CLINICAL PRESENTATION
The first clinical indication of the presence of hydatid disease of spleen usually is an accidentally
discovered splenomegaly.[45] The symptoms are few, non-specific and comprise mainly a mass in the
abdomen mostly in left hypochondrium and less frequently in the epigastrium, pain which is usually a
dull dragging ache, dyspepsia, constipation due to pressure on colon and dyspnoea due to pushing up
of the left diaphragm. Lumbar backache probably due to scoliosis of lumbar spine and referred pain to
the left shoulder due to a large cyst pushing on the diaphragm are rare presentations.

The symptom complex produced by splenic hydatid cyst are mainly due to mechanical displacement
and pressure effect on the adjacent organs. Approximately 30% of splenic cysts are asymptomatic and
detected incidentally. In addition 40% have no detectable physical signs.[46] We have come across two
patients who developed secondary hypertension probably due to left renal artery compression, as seen
intraoperatively, along with downward displacement of left kidney due to splenic hydatid cysts.
Postoperatively both these patients became normotensive without any antihypertensive treatment.
Rakowski[47] reported a splenic cyst causing hypertension by renal artery compression. Splenic
replacement can occur with very little or practically no splenic tissue left behind. The splenic cyst can
rupture and disseminate all over the peritoneal cavity. Other reported complications of splenic hydatid
cysts in literature are acute abdomen produced by splenic hydatid cysts coexistent with bilateral ovarian
tumour,[48] rupture of longstanding splenic hydatid cyst into bronchial tree,[49] traumatic rupture of
splenic echinococcal cyst with anaphylactic shock.[50] Celdran Uriarte[51] reported a case where splenic
hydatid cyst established fistula to the colon.

INVESTIGATIONS

Laboratory evaluation of patients with hydatid disease often yields non-specific data. Eosinophilia
(above 3%) is not significant in endemic areas.[4] A large battery of serological tests are available but
their importance have been diminished by increased reliance upon modern imaging modalities like
ultrasound (USG), computed tomography (CT) and Magnetic resonance imaging (MRI).

Elevated levels of IgE levels are a non-specific indicator of prior sensitization or active infection with
parasitic organisms, while elevated levels of IgM classes specific to echinococcal organisms may be a
sensitive indicator for recurrent disease.[4] Several serological tests are specific to hydatidosis and are
used to confirm the diagnosis. Serum immunoelectrophoresis is currently the most reliable, with a
sensitivity of approximately 90%.[4] It stays positive for one year after the organism has been eradicated.
Indirect haemagglutinition has a sensitivity of 85%4 but remains positive for several years, decreasing its
usefulness in endemic areas. Complement fixation, enzyme linked immuno-sorbent assay (ELISA) and
western blot analysis have also been used. The Casoni skin test is sensitive but not specific, and also
remains positive for years after eradication of the organism.

The diagnosis of splenic hydatidosis is difficult or impossible by conventional radiography alone.[52-54]

If the cyst is calcified hydatidosis may be suggested. Plain radiology of abdomen can reveal a soft tissue
shadow with or without calcification, displacement of left diaphragm upwards, stomach to the right
(Fig. 3) and transverse colon with splenic flexure downwards. Intravenous urography may show
downward displacement of kidney. Displacement of adjacent viscera and organs is also recognised on
ultrasound and computed tomography. Benton55 (1932) thinks that downward displacement of splenic
flexure is almost pathognomonic of splenic enlargement, and Ostro and Makover[56] (1937) have
suggested displacement of neighbouring organs is characteristic of cyst of spleen rather than
splenomegaly from other causes.

Ultrasound and Computed tomography alone or in combination established the definite diagnosis of
splenic hydatid cysts in almost all the cases. These procedures can identify daughter cysts and hydatid
sand, both of which are specific to echinococcal infestation[4] (Fig. 4). Ultrasound is cost effective and
particularly valuable for follow up screening. CT is more accurate than ultrasound in localizing and
delineating extent of the cyst (Fig. 5). Non-calcified benign cysts without daughter cysts cannot be
differentiated per se from other benign cysts on CT and USG.39 Postoperative histopathology will
confirm the parasitic nature of this splenic cyst.
 Fig.3: Plain X-ray of the abdomen showing
displacement of the left dome of
diaphragm upwards, fundic gas shadow to
the right and lateral deviation of the
vertebral column to the right.

Fig.4: Ultrasound of the abdomen showing

Fig. 5: CT scans of the abdomen showing a cross
splenic
section of the large unilocular splenic hydatid cyst.
hydatid cysts with multiple daughter cysts.

TREATMENT

Until recently the gold standard treatment for splenic hydatidosis was splenectomy. Medical treatment
which comprises of Mebendazole (60 mg/kg/day for 6-24 months) or Albendazole (10 mg/kg/day for 6
months) can only complement surgery but cannot replace it. The treatment of hydatid cysts is
principally surgical. However, pre- and post-operative 1-month courses of Albendazole and 2 weeks of
Praziquantel should be considered in order to sterilize the cyst, decrease the chance of anaphylaxis,
decrease the tension in the cyst wall (thus reducing the risk of spillage during surgery) and to reduce the
recurrence rate post-operatively.[4] Intra-operatively, the use of hypertonic saline or 0.5% silver nitrate
solutions before opening the cavities tends to kill the daughter cysts and therefore prevent further
spread or anaphylactic reaction.[4]

Splenectomy is the treatment of choice because there is no effective medical treatment.[4] Since 1980
there has been a trend towards splenic conservation to avoid overwhelming post splenectomy infection
(OPSI). Care should be taken to avoid spilling the contents of the cyst. The lesions can be sterilized by
instillation of 3% sodium chloride solution. If intraperitoneal spillage occurs during the course of
dissection, an anaphylaxis may result, which would require prompt treatment with adrenaline,
antihistaminics and steroids. For conservation of the spleen, enucleation of a unilocular cyst can be done.
Secondary hydatid disease of spleen may be caused by rupture of abdominal cysts (e.g. in the liver) with
dissemination to the spleen.[39] Once ruptured, cysts metastases occurs to the peritoneal surface and
despite its benign, infectious aetiology, hydatid cysts exhibit malignant behaviour and the whole of the
abdomen can get studded with multiple hydatid cysts of different size. Recently Ballaux KE57
performed a hand assisted laparoscopic splenectomy for a large splenic hydatid cyst.

Children are more prone to OPSI. The clinical syndrome of OPSI comprises fulminant bacteraemia,
disseminated intravascular coagulation, multiple organ failure, severe hypoglycaemia and often rapid
death.[58] Its reported incidence after splenectomy varies from 0.9 to 60% with mortality exceeding 50%.
[59] Preservation of spleen should always be tried especially in children[60] to prevent OPSI.

ACKNOWLEDGEMENTS

We would like to thank following persons for their support and guidance Dr. BP Deshraj, Ex-Professor
and Head; Dr. Raj Gajbhiya, Associate Professor, Department of Surgery, Indira Gandhi Medical College,
Nagpur.

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