European Journal of Radiology 63 (2007) 84–93

Review

Unusual imaging characteristics of complicated hydatid disease

Ahmet Tuncay Turgut a,∗ , Levent Altın b , Salih Topçu c , Bülent Kılıçoğlu d ,
Tamer Altınok e , Erkan Kaptanoğlu f , Alp Karademir b , Uğur Koşar a
a
Department of Radiology, Ankara Training and Research Hospital, Ankara, Turkey
b
Department of Radiology, Numune Training and Research Hospital, Ankara, Turkey
c Department of Thoracic Surgery, Faculty of Medicine, Kocaeli University, İzmit, Turkey
d Department of 4th General Surgery, Ankara Training and Research Hospital, Ankara, Turkey
e Department of Thoracic Surgery, Meram Faculty of Medicine, Selçuk University, Konya, Turkey
f Department of Neurosurgery, Numune Training and Research Hospital, Ankara, Turkey

Received 6 October 2006; received in revised form 31 December 2006; accepted 2 January 2007

Abstract
Hydatid disease, a worldwide zoonosis, is caused by the larval stage of the Echinococcus tapeworm. Although the liver and the lungs are the
most frequently involved organs in the body, hydatid cysts of other organs are unusual. Radiologically, they usually demonstrate typical imaging
findings, but unusual imaging characteristics of complicated cyst of hydatid disease, associated with high morbidity and mortality, are rarely
described in the literature. The purpose of this study is to review the general features of hydatidosis and to discuss atypical imaging characteristics
of the complicated hydatid disease in the human, with an emphasis on structure and rupture of the cystic lesion as well as ultrasonography (USG),
computed tomography (CT), and magnetic resonance imaging (MRI) features of the disease. In our study, the available literature and images of the
cases with complicated hydatidosis involving liver, lung, brain, spine and orbit were reviewed retrospectively. In hydatid disease, there are many
potential local and systemic complications due to secondary involvement in almost any anatomic location in humans. Radiologically, in addition
to the presence of atypical findings such as perifocal edema, non-homogenous contrast enhancement, multiplicity or septations and calcification,
various unusual manifestations due to rupture or infection of the cyst have been observed in our cases with complicated hydatid disease. To prevent
subsequent acute catastrophic results and the development of recurrences in various organs, it should be kept in mind that complicated hydatid
cysts can cause unusual USG, CT, and MRI findings, in addition to typical ones, in endemic areas. Therefore, familiarity with atypical radiological
appearances of complicated hydatid disease may be valuable in making a correct diagnosis and treatment.
© 2007 Elsevier Ireland Ltd. All rights reserved.

Keywords: Brain; Hydatid disease; Liver; Lung; Orbit; Radiology; Spine

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
2. Complicated hydatid cysts of the liver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
2.1. Structure of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
2.2. Rupture of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
2.3. Infection of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
2.4. Imaging of cystic lesion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
2.4.1. USG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
2.4.2. CT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
2.4.3. MRI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
2.4.4. PAIR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87

∗ Corresponding author. Tel.: +90 312 595 36 73; fax: +90 312 434 15 63.
E-mail address: ahmettuncayturgut@yahoo.com (A.T. Turgut).

0720-048X/$ – see front matter © 2007 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ejrad.2007.01.001

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 A.T. Turgut et al. / European Journal of Radiology 63 (2007) 84–93 85

3. Complicated hydatid cysts of the lung . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87

3.1. Structure of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
3.2. Rupture of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
3.3. Infection of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
3.4. Imaging of cystic lesion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
3.4.1. X-ray . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
3.4.2. CT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
4. Complicated hydatid cysts of the brain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
4.1. Structure of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
4.2. Rupture of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
4.3. Infection of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
4.4. Imaging of cystic lesion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
4.4.1. X-ray . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
4.4.2. CT/MRI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
4.4.3. DWI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90
4.4.4. MRS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90
5. Complicated hydatid cysts of the spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
5.1. Structure of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
5.2. Rupture of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
5.3. Infection of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
5.4. Imaging of cystic lesion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
5.4.1. CT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
5.4.2. MRI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
6. Complicated hydatid cysts of the orbit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
6.1. Structure of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
6.2. Rupture of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
6.3. Infection of cystic lesion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
6.4. Imaging of cystic lesion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
6.4.1. USG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
6.4.2. CT/MRI/PAIR . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92
7. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93

1. Introduction tion, was described as “complicated” or atypical cyst, if it had

ruptured into the neighbouring cavity spontaneously or iatro-
Hydatid disease or echinococcosis, a systemic zoonosis, is genically [21]. Radiological view of point, the typical findings
caused by the larval stage of the Echinococcus tapeworm. The of hydatid disease are well known, but unusual imaging char-
word ‘hydatid’ which is of Greek origin, literally means a acteristics related with its rare complications are less frequently
‘watery vesicle’ [30]. At present, it remains endemic to many documented in the literature. It is expected that a complicated
parts of the world, most notably the Mediterranean region, hydatid cyst is associated with higher morbidity and mortal-
the Middle East, South America, New Zealand, and Australia ity than uncomplicated counterparts. Therefore, familiarity with
due to the close association between sheep and dogs and atypical radiological features is very important to prevent both
humans [1,2,27,40,41,43]. Humans may become intermediate misdiagnosis and improper diagnostic and therapeutical inter-
hosts through contact with a definitive host, sheep or dog, or ventions in these cases. This paper focuses on the occasional
ingestion of contaminated water or vegetables. In humans, most atypical imaging features related with rare complications of
cases are infected during childhood period, but they do not complicated hydatid disease involving various organs including
present with symptoms until adulthood [45]. Hydatid disease liver, lung, brain, spine, and orbit with an emphasis on struc-
can involve almost every organ of the body; the liver (75%) ture and rupture of the cystic lesion as well as ultrasonography
and lungs (15%) being the predominant locations as well as the (USG), computed tomography (CT), and magnetic resonance
other anatomical regions such as brain (1–2%), spine (1%), and imaging (MRI) characteristics of the disease.
orbit (0.2%) [1,2,40,41,43]. At present, Turkey is one of the
countries where hydatid disease caused by Echinococcus gran- 2. Complicated hydatid cysts of the liver
ulosus or Echinococcus alveolaris and human hydatidosis is still
a major public health problem. E. granulosus is responsible for 2.1. Structure of cystic lesion
unilocular or cystic hydatidosis in man, while E. alveolaris is
the causative organism for multilocular form. The hydatid cyst of the liver has three layers: (1) the outer
Classically, an intact hydatid cyst was classified as simple pericyst is a dense fibrous zone in the liver and other organs;
or typical cyst, but a perforated cyst, with or without infec- (2) the middle laminated membrane is acellular and allows the

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86 A.T. Turgut et al. / European Journal of Radiology 63 (2007) 84–93
passage of nutrients; (3) the inner germinal layer where the sco-
lices, which is the larval stage of the parasite, and the laminated
membrane are produced [30]. Among these layers, the middle
laminated membrane and the germinal layer are known as the
endocyst [21]. The inner-most layer is the germinative or fer-
tile membrane having two major functions: (1) production of
the laminated membrane outward and (2) germination of the
later generation scolices inward [21,30]. Cyst fluid is clear or
pale yellow and antigenic [21]. It has been reported that hepatic
hydatid cysts grow to a mass 1 cm in diameter during the first 6
months and grows 2–3 cm annually thereafter, depending upon
the surrounding tissue resistance [33]. The clinical manifesta-
tions of hepatic hydatid disease depend upon the site, size and
stage of development of the cyst, on the viability of the cyst, and
whether it is secondarily infected or not [30].
2.2. Rupture of cystic lesion
Among the intrahepatic complications of the hydatid dis-
ease, in contrast to contained and communicating types of
ruptures, direct rupture occurs when both the pericyst and endo-
cyst rupture, allowing free spillage of hydatid material into the
surrounding anatomical channels, adjacent organs, or free body
cavities [3]. Hydatid cyst rupture occurs in 50–90% of cases due
to the degeneration of parasitic membranes caused by aging,
chemical reactions, or a host defense mechanism [33]. In the
presence of any rupture or leakage of a hepatic cyst, an allergic
response is evoked due to the spillage of antigenic cyst contents
into the surrounding tissues [30,33]. In hepatic hydatidosis, there
are different types of spontaneous ruptures as following:
1. Rupture into hollow viscera like gastrointestinal tract includ-
ing the stomach, duodenum or small intestine [3].
2. Rupture into the biliary tree causing cholestasis, cholangitis,
biliary colic and jaundice because of the excretion of germi-
native membranes in the stools, in up to 90% of hydatid cysts
[15,30,33].
3. Rupturing into diaphragma or sub-diaphragmatic space, or
thoracic and pericardial cavities resulting in pericardial effu-
sion [3,13,33].
4. Rupturing into pancreatobiliary ducts due to local spread via
the pancreatobiliary ducts and peripancreatic invasion [33].
5. Rupturing into peritoneal cavity, named as “peritoneal seed-
ing”, or retroperitoneal region secondary to spillage of
hepatic hydatid cyst [3,30,33].
6. Rupturing to the skin invasion of the abdominal wall and
development of cutaneous fistula.
7. Rupturing in the bronchia and development of cysto-hepato-
bronchial fistula [30,33].
2.3. Infection of cystic lesion
Bacterial superinfection of hydatid cyst is always secondary
to one of different types ruptures described above in detail and up
to 25% of ruptured cysts may become infected, resulting in liver
abscess [9,35]. Radiological view of point, most of the poorly
defined lesions are accepted as infected [9]. In particular, the
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Table 1
Summary of types of hydatid cysts based on the radiological appearancesa
Type Definition
Type I Simple cysts with no internal architecture
with/without hydatid sand and septa
Type II Cysts with daughter cysts and matrix
Type IIA Round daughter cysts arranged at the periphery
Type IIB Irregularly shaped daughter cysts occupying the
entire mother cyst
Type IIC High-attenuation round or oval masses with
scattered calcifications and occasional daughter
cysts
Type III Calcified cyst
Type IV Complicated cyst with rupture and super-infection
a According to classifications described by Kalovidouris et al. [20] and von
Sinner et al. [45].
presence of gas or air–fluid generally suggests the probability
of infected hydatid cyst [9,35]. Nevertheless, the presence of
air within the cyst establishes the diagnosis of direct or com-
municating rupture does not necessarily imply infection [33]
(Table 1)
2.4. Imaging of cystic lesion
In cases with hepatic hydatid disease, the right lobe of the
liver is most frequently, with characteristic imaging findings
[16,30,45]. As expected, the imaging findings in hepatic hydatid
disease depend on the stage of evolution of the disease. It is
accepted that the presence of calcification having a peripheral
curvilinear or ring-like pattern is suggestive of the death of the
parasite [16,30]. On plain radiographs, calcification occurs in
20–30% of patients [9]. Interestingly, hepatic hydatid cyst may
be asymptomatic and discovered incidentally by radiological
screening [1]. Additionally, it has been reported most of them
are expected to undergo spontaneous abortion and do not need
any active intervention [3].
2.4.1. USG
USG is the primary diagnostic modality for hepatic hydatid
disease and no further imaging modality is required when the
appearance is typical [10,16,19,33,45]. On USG, hepatic hydatid
cysts are seen as well-defined, circumscribed, anechoic lesions
with no infiltration of surrounding liver tissue [3,5,10,16,33].
Gharbi et al. [16] have described various types of hepatic hydatid
cysts according to their evolutionary stages as purely cystic
except for hydatid sand, detached membrane, multiseptated,
peripheral or diffuse distribution of coarse echoes in a complex
heterogenous mass, and calcified wall. On USG, type I hydatid
cysts, an initial stage in the development of the parasite, appear
as a well-defined anechoic mass with or without hydatid sand
and septa, producing small echogenic foci, called the “falling
snowflakes” [35]. In the presence of type II hydatid cysts, a
dividing septa or daughter cysts within a fluid-filled liver mass
is considered as diagnostic for hydatid disease, giving hydatid
cyst a “racemose” or “wheel spoke” appearance [34,45]. The
capsule floats freely in the hepatic hydatid cyst, giving rise to
 A.T. Turgut et al. / European Journal of Radiology 63 (2007) 84–93
Fig. 1. USG of 50-year-old male patient with separation of the cyst wall from the
surrounding liver parenchyma, floating internal membranes, and intraperitoneal
fluid revealing intraperitoneal rupture of a hydatid cyst located in the left liver
lobe.
the “floating membrane” sign, which is equivalent to the radio-
graphical “water lily sign”, when there is a complete detachment
(Fig. 1) [19,34,45]. Type III lesions with dead and calcified cysts
demonstrate strong posterior shadowing at USG study [35]. In
cases with type IV lesions, an undulating membrane manifest-
ing as postural changes is seen due to separation of the endocyst
from the pericyst as a result of contained rupture, called as
“snowstorm” pattern at USG examination [35]. Radiologically,
communicating rupture appears more echogenic than contained
rupture, if there is an intrabiliary rupture, and layering of hydatid
sand can be seen in the biliary channels at USG [35]. It has been
stated that an infected hydatid cyst may exhibit poor delimita-
tion, mixed echogenicity, and air–fluid or fluid–fluid levels [35].
In addition, it has been claimed that the presence of the cap-
sule differentiates an infected hepatic hydatid cyst from tumour
[19]. Importantly, it has been reported that hepatic hydatid cysts
appear hyperechogenic on USG examination after successful
medical treatment [10]. Based on these observations, one might
sugesst that USG is not only very helpful for initial diagnosis,
but is also an ideal modality for the follow-up of patients with
hepatic hydatid disease. On USG, increased echogenecity of the
biliary three may indicate the existence of rupture into the biliary
tree [35].
2.4.2. CT
Although USG may be necessary in the diagnosis of visceral
hydatid cysts, it is widely accepted that abdominal CT scan with
a higher rate of accuracy is the diagnostic tool of choice [33]. On
CT scan, hepatic hydatid cyst is seen as a peripherally enhancing
hypodense mass lesion [44]. At CT, a type I hepatic hydatid cyst
is seen as a well-defined hypodense mass with enhancing septa
and cyst wall following contrast material injection [35]. Type II
hydatid cysts can be visualized in three stages depending on the
aging, number, and arrangement of the daughter cysts [20]. Type
IIA lesions contain round daughter cysts arranged at the periph-
ery, while type IIB lesions are irregularly shaped daughter cysts
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87
within the mother cyst, causing a “rosette” appearance [20,35].
On the other hand, type IIC lesions are round or oval masses with
scattered calcifications, representing the degeneration of old cyst
with amorphous content [35]. At CT, however, type III lesions
are seen as round calcified areas [3,35]. Moreover, fluid–fluid
or air–fluid levels can be seen as well in case the cyst ruptures
[45]. In type IV hydatid cysts, contained rupture and undulating
membrane resulting from separation of the endocyst from the
pericyst is easily seen at CT study [35]. Additionally, the pres-
ence of fissures in the cyst wall can also be visualized at CT
scan [35]. Thus, it is clear that CT is very useful especially for
demonstrating calcification, infection and peritoneal seeding.
2.4.3. MRI
In type I hydatid cysts, MRI shows the characteristic low
signal intensity rim of the hepatic hydatid cyst on T2-weighted
images [29]. Typically, cysts are of low intensity on T1-weighted
scans and of high intensity on T2-weighted MRI scans [3]. The
septa and cyst wall enhance after injection of contrast material
and a low signal intensity rim, known as “rim sign” on T2-
weighted MRI, is a characteristic finding of hydatidosis [35].
Therefore, it has been reported that MRI has particular impor-
tance, if the diagnosis of hydatid disease is questionable [3].
At T1- and T2-weighted MRI images, daughter cysts in type II
hydatid cysts manifest hypointense or isointense areas compared
to the maternal matrix [35]. Collapsed parasitic membranes with
low signal intensity with all sequences, secondary to damage or
degeneration of an hydatid cyst, are named as “serpent sign”
or “snake sign” [35]. On T2-weighted MRI, type III lesions
appear as hypointense areas, although the membranes manifest
as hypointense linear regions [35]. Furthermore, it is very sensi-
tive in detecting cyst wall irregularity, which is a sign of reduced
parasite viability [45]. Besides, in cases with biliary communi-
cation due to rupture of the hydatid cyst, the development of
some signal intensity changes have been reported [35].
2.4.4. PAIR
USG- or CT-guided fine-needle aspiration of hydatid cyst
contents followed by infusion of a scolicidal agent, such as
hypertonic (15%) saline injection, and reaspiration, known as
PAIR (puncture, aspiration, injection, reaspiration) therapy, has
been used successfully for hepatic hydatid cysts at some centers
[18]. Today, it is known that PAIR therapy of hepatic hydatid
cysts is the most effective and reliable treatment procedure in
the selected cases in experienced hands [5].
3. Complicated hydatid cysts of the lung
3.1. Structure of cystic lesion
Lung facilitates growth of the cyst due to the negative
pressure and great elasticity and it grows faster than that of liver
by a ratio of 3:1 [1]. In general, lung involvement by hydatidosis
follows hepatic infestation in frequency in adults, whereas it
is the most common site affected in children [14,36]. Hydatid
cyst can develop anywhere in the lung, but it has a predilection
for left side [36]. In pulmonary hydatidosis, the structure of
88 A.T. Turgut et al. / European Journal of Radiology 63 (2007) 84–93
the parasitic element composed of a two-layer wall and liquid
content and endogenous vesiculation is rare in the lung [25,36].
Morphologically, the pericyst is made up of an inner layer
similar to serous membrane, a fibrous middle layer, and an
outer layer with active inflammatory reaction [1,2,14,27,36].
Importantly, the pulmonary tissue around the adventitia in
the simple cyst may be compressed with atelectasis or may
show irreversible inflammatory changes like bronchiectasis and
interstitial sclerosis [21,25,27,36]. In regard to the extent of
the resultant bronchopulmonary lesions, the cyst may be with
a proximal or distal lesion or with a lobar lesion [36].
3.2. Rupture of cystic lesion
Pulmonary hydatid cysts usually remain asymptomatic until
the time of rupture [27]. It has been stated that cyst rup-
ture is mainly due to degeneration of the membranes owing
to age, chemical reaction, or host’s defense mechanisms [34].
All hydatid cysts carry the risk of rupture and perforated pul-
monary hydatid cysts, whether infected or not, are classified
as complicated [27,32]. As expected, the increase in the size
and the number of the pulmonary cysts increases the risk
for rupture [31]. Interestingly, cyst rupture may occur during
anthelmintic therapy or percutaneous aspiration and can lead to
severe complications, such as massive hemoptysis and tension
pneumothorax [27]. According to form of hydatid cyst rupture,
complicated pumonary cysts may be classified as following:
1. Rupturing into bronchus and/or vessels manifests by vig-
orous coughing, hemoptysis and expectoration of a large
amount of salty sputum consisting of mucus, hydatid fluid,
and, occasionally, fragment of the laminated membrane [27].
Expectoration of cystic contents can lead to severe complica-
tions, such as acute respiratory failure, massive hemoptysis,
and anaphylactic shock [36].
2. Rupturing into pleural cavity occurs if a live scolex seeds into
the pleural cavity as a result of an intrapulmonary cyst rupture
[32]. In contrast to perforation into a bronchus, it usually
causes simple or tension pneumothorax, pleural effusion, or
empyema [8,26,27]. It has been proposed that rupture of a
cyst into the pleural cavity or rupture into the bronchial tree
may also lead to secondary larval spread or to allergic and
anaphylactic reaction [27,36].
3. Rupturing into biliary and bronchial trees causes bronchobil-
iary fistula [38]. Although the incidence of hepatic hydatid
cyst has decreased, bronchobiliary fistula still remains a seri-
ous and rare complication with a high morbidity and mortality
[38].
4. Rupturing into vena cava causing recurrent acute pulmonary
embolism, as a rare complication that can be seen when a
cyst directly involves the vena cava [35].
3.3. Infection of cystic lesion
It has been reported that the increase in the size and the num-
ber of the pulmonary cysts increases the risk for infection [31].
Superimposed bacterial infection following cyst rupture results
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in bronchopneumonia characterized by fever and purulent spu-
tum [9]. In general, a complicated cyst ruptured into the bronchus
or pleural cavity is considered to be “infected”, when the patient
exhibited accompanying problems of purulent sputum, leuko-
cytosis, fever, and pericystic pneumonitis. In some cases, lung
abscess and surrounding pneumonia may develop a result of
involvement of the pericyst with infection [9].
3.4. Imaging of cystic lesion
The pulmonary hydatid cysts is diagnosed by various com-
binations of radiological imaging methods including chest
radiography, USG, and CT. Type II daughter cysts are rarely
reported in the pulmonary hydatidosis [9].
3.4.1. X-ray
On chest radiography, uncomplicated cysts are seen as round
opaque lesions, but infection and perforation may change the
radiographic appearance of hydatid cyst, leading a delayed treat-
ment [36]. In these cases, abdominal USG is necessary to assess
for concomitant hepatic or splenic cysts in each case. Radiolog-
ical view of point, it is important to be aware of the fact that
calcification of pulmonary hydatid disease with a frequency of
0.7%, is an extremely rare entity [35,42].
3.4.2. CT
In cases with complicated pulmonary hydatid cyst, CT has
played a major role [6,8,27,32,36]. Kervancıoğlu et al. [21]
reported that CT is extremely useful in establishing the diagnosis
in complicated pulmonary cysts and in making the diffferen-
tial diagnosis from malignant lesions in elderly. For ruptured
pulmonary hydatid cysts complicated with/without infection,
some classical radiographic criteria have been defined as signet
ring sign, water lily sign, crescent or meniscus sign, inverse
crescent sign, serpent sign, air bubble sign, and dry cyst sign
[24,25,32,33]. Among these, “signet ring sign” named due to the
similarity to a shape of ring develops due to a bleb of air dissect-
ing into the wall of cyst [25] (Fig. 2). The appearance of “water
lily sign” consists of the endocyst floating freely within the cyst
fluid secondary to the complete collapse of the aforementioned
membranes [33] (Fig. 3). The presence of air collection between
the laminated membrane and the pericyst owing to the erosions
in the bronchioles included in the pericyst appears a thin and
radioluscent crescent in the upper part of the cyst and has been
named as “crescent or meniscus sign” [33]. The existence of
intracystic small air bubles, especially in the peripheral part of
the cyst which may either be between pericyst and parasitic
membranes or within any part of the cyst, has been described
as “air buble sign” resulting in the shrinkage and rupture of the
cyst and the passage of air into the endocyst [24,33] (Fig. 4).
4. Complicated hydatid cysts of the brain
Although hydatid disease may be located anywhere in the
brain, it is most frequently located in the hemispheres (90–95%
of the cases), particularly in the territory of the middle cere-
bral artery mostly in the postrolandic parts of the hemispheres,
 A.T. Turgut et al. / European Journal of Radiology 63 (2007) 84–93
Fig. 2. CT scan of 22-year-old female patient showing signet ring sign with a
bleb of air dissecting into the wall of cyst (arrow).
pons, ventricular system, aqueduct of Sylvius, the subarachnoid
space of cerebellopontine angle, and intracranial epidural space
[1,2,44].
4.1. Structure of cystic lesion
The wall of cerebral hydatid cyst of the brain is also composed
of pericyst, endocyst, and ectocyst, similar to the hydatid cyst
of the liver [1,40]. Importantly, however, cerebral hydatid cyst
has been shown to grow faster than the liver by a ratio of 3:1,
revealing that brain like the lung tissue facilitates growth of the
cyst as it is a compressible organ [1]. In the brain, it takes 5–16
months for the cyst to grow to a mass, which is 1 cm in diameter
[1]. In a recent study, it has been reported that cerebral hydatid
cyst is seen eight times more often in children than in adults
[42].
Fig. 3. CT scan with water lily sign (arrow) revealing ruptured hydatid cyst
with a peripheral localization of a 14-year-old male patient presenting with the
complaint of expectoration for a duration of 2 days.
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89
Fig. 4. CT scan depicting air bubbles (arrow) within a perforated pulmonary
hydatid cyst of 40-year-old female patient presenting with the complaints of
fever and expectoration and having been treated medicallly with the diagnosis
of pneumonia with a delayed resolution.
4.2. Rupture of cystic lesion
In the vast majority of the cases, cysts are solitary and differ-
ential diagnosis of a cerebral hydatid cyst includes other cystic
lesions such as arachnoid cyst and cystic tumors [1,2,40,44]. In
the brain, multiple cysts can result from spontaneous or iatro-
genic rupture of a viable primary lesion during diagnostic or
surgical procedures (Fig. 5) [1,2,33]. Rupture is an important
complication of hydatid disease of the brain as well and the rate
of intraoperative rupture exceeds about 25% of the cases with
cerebral hydatid cysts [1,2,35,37].
4.3. Infection of cystic lesion
Secondary infection of intracranial hydatid cysts is extremely
rare but an important complication of cerebral hydatidosis [35].
Radiologically, the lesions show enhancement after contrast
material injection when hydatid cysts are infected and differ-
ential diagnosis is difficult in these cases [35].
4.4. Imaging of cystic lesion
4.4.1. X-ray
In cases with cerebral hydatidosis, the plain skull roent-
genograms may demonstrate unilateral enlargement of the vault,
suture separation or erosion of the posterior clinoid process
and calcifications [2,33]. It has been reported that calcification
occurs in less than 1% of cases [35].
4.4.2. CT/MRI
Both CT and MRI demonstrate a well-defined oval or cystic
mass having an attenuation or a signal intensity similar to that
of cerebrospinal fluid [2,27,40,44,45]. Characteristically, the
cystic lesions do not enhance after injection of contrast medium
and there is no associated pericystic edema, although they may
cause extrinsic compression on the ventricular system with
90 A.T. Turgut et al. / European Journal of Radiology 63 (2007) 84–93

Fig. 5. Preoperative axial CT section of 14-year-old female, who had ruptured previously because of the use of cystoperitoneal shunt device with a misdiagnosis of
arachnoid cyst (a) at another center, demonstrating an infected secondary multiple hydatid cysts of the brain (b–d). Note that the resorvoir of the device (arrow) on
the skull and the tip of the ventricular catheter lying in the multiple cystic lesions. (e) Postoperative axial CT section of the complicated hydatid case showing the
healing of the brain after the removal of the ventricular shunt catheter.

subsequent development of hydrocephalus [40,44]. However,
the rim of these cystic lesions may rarely enhance after injection
of contrast medium and may show perifocal edema [2,41].
Radiologically, typical appearance of cerebral hydatid cyst
is a large non-enhancing cyst of CSF density by CT and MRI
by which no pericystic edema and no rim enhancement after
injection of the contrast agent is displayed [2,40]. In particu-
lar, on T2-weighted MRI, the presence of a hypointense rim is
characteristic of cerebral hydatidosis [35]. The cerebral cysts are
usually solitary, though there may be multiple cysts either pri-
marily located within the brain or developing secondarily after
rupture of a primary or mother cyst [40]. In cerebral hydatid
disease, the multiple cysts appear as small and large multiloc-
ular cystic lesions on CT and MRI. From radiological point of
view, the following lesions should be considered in differen-
tial diagnosis: brain abscesses, arachnoid cysts, and cystic brain
tumors. Even today, cerebral cysticercosis and echinococcosis
cause significant diagnostic difficulties, because the definitive
diagnosis of these parasitic diseases is rarely possible in the pre-
operative period in spite of recently developed neuroradiological
techniques [39]. In a correlative MRI and histopathology study,
Chawla et al. [12] found that T2-weighted imaging demonstrated
all the cysts while T1-weighted imaging showed 97% of the cysts
in porcine neurocysticercosis. In the differential diagnosis of
hydatidosis from cerebral cysticercosis, we think that epidemi-
ological information may help to both clinicians and radiologists
in some cases.
In complicated cases, there may be some atypical findings
such as perifocal edema of the surrounding brain or even a fine
enhancement of the surrounding rim after injection of the con-
trast medium, both on CT and MRI [2,40,44]. In these cases,
differential diagnosis is sometimes difficult [35]. It has been
reported that irregularity of the cyst wall contour, isodensity or
heterogeneity of the cyst content, and globular or curvilinear
calcification are among the other atypical appearances of cere-
bral hydatid cyst [44,45]. There is no doubt that awareness of
such unusual findings on CT or MRI can prevent misdiagnosis
and inappropriate premature puncture of the lesion during surgi-
cal intervention. In some cases, the cyst may be hyperdense on
unenhanced CT with a calcified ring surrounding the cyst cavity
or it may be septated [40,44]. Partial or complete calcification
with a frequency of less than 1%, is another rarely described
feature of cerebral hydatid cysts, being anecdotally described in
the literature as CT or MRI findings [7].
4.4.3. DWI
Diffusion-weighted imaging (DWI), a relatively new MRI
technique, is becoming the investigation of choice as it may
improve the differential diagnosis of complicated cerebral
hydatidosis [11,22,23]. It provides information about the molec-
ular translational motion of water, rather than the T1 and T2
effects of tissue [22]. Cerebral hydatid cysts due to E. granulosus
show cerebrospinal fluid-like signal intensity and apparent diffu-
sion coefficient values on DWI, while cerebral lesions due to E.
alveolaris demonstrate contrast enhancement [22]. In particular,
it could be used in the differentiation of a variety of intracra-
nial lesions, including neoplasms, demyelinating disease, and
cerebral cystic lesions including complicated hydatid disease
involving the brain [17,22].
4.4.4. MRS
Recently, magnetic resonance spectroscopy (MRS) has
gained popularity and is becoming the investigation of choice for
cases of cerebral hydatidosis [11,23]. On MRS, the presence of
mildly elevated choline, depressed creatine and N-acetyl aspar-
tate, a large peak of lactate, pyruvate and acetate peaks suggests
the diagnosis of hydatid cyst [11]. Particularly, it is promising in
the differential diagnosis of cystic lesions of the CNS because

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 A.T. Turgut et al. / European Journal of Radiology 63 (2007) 84–93 91

the MRS pattern is different from that seen in other cystic lesions
[23]. Besides lactate, alanine, and acetate, a large resonance of
pyruvate is usually detected in these cases [23]. Kohli et al.
[23] reported that in vivo MRS imaging may be used as an
adjunct to imaging for the diagnosis of cerebral hydatid cysts
and monitoring the response to drug therapy.
5. Complicated hydatid cysts of the spine
5.1. Structure of cystic lesion
Spinal hydatid disease is a significant manifestation of the
disease accounting for more than 50% of cases of the hydatid dis-
ease of the bone, while hydatid disease is located in the osseous
structures in only 1% of all cases [1,2]. It can be located in the
thoracic spine (50%), lumbar spine (20%), sacral spine (20%),
or cervical spine (10%) [2,28,41]. Clinically, unilocular type I
cysts, unilocular type II cysts with daughter vesicles or detached
membranes, and type III calcified cysts are frequently seen in
cases with spinal hydatidosis [35]. Characteristic imaging find-
ings for spinal hydatid disease are: (1) lack of osteoporosis and
sclerosis in the host bone and (2) absence of damage to the disc
space and spread of the disease either via hematogenous route
to the more vascular areas of the vertebra, or via a subperiosteal
and subligamentous path to the paraspinal region that results
in involvement of a contiguous rib and destruction of the adja-
cent costo-chondral junction [28]. Importantly, spinal hydatid
cysts have thinner walls in comparison with the other counter-
parts, owing to the existence of decreased inflammatory response
against them and reduced fibrotic reaction [41].
5.2. Rupture of cystic lesion
In endemic areas, preoperative diagnosis of hydatid disease
is very important, as recurrence due to rupture and dissemina-
tion of the cyst is generally inevitable [2]. In contrast to the
infestation of other tissues in the body, the disease involving
the bones including the vertebral column constitute an appro-
priate microenvironment for the development of viable parasites
[37]. In the bony vertebral hydatidosis, the vesicles resembling a
bunch of grapes at macroscopic examination may grow through
the wall of the mother cyst [37]. Therefore, it is impossible to
remove the extradural lesions involving the spine without caus-
ing rupture of the hydatid cyst in almost 100% of the cases [1,2].
Unfortunately, the recurrence is inevitable in cases of leakage
of the echinococcal crystal clear fluid including the parasites
during the surgical intervention.
5.3. Infection of cystic lesion
It is possible that superimposed pyogenic infections involving
the spine may develop in some cases, especially ones with cyst
rupture. In complicated cases, osseous structures such as verte-
bra constitute a friendly microenvironment for the development
of a chronic infection resistant to treatment.
5.4. Imaging of cystic lesion
5.4.1. CT
The findings of spinal radiography are mostly non-specific,
though they have a characteristic imaging appearance as a single
or multiple, uni- or multilocular, and thin or thick walled struc-
ture containing fluid with similar intensity to that of CSF, with
well-defined borders on CT [2,41]. In contrast to cerebral hydati-
dosis, spinal hydatid cysts show no rim enhancement following
contrast material injection [35]. It has been reported that calci-
fication is rarely seen in spinal hydatidosis [35]. Radiologically,
the typical appearance of spinal hydatid cyst is a large non-
enhancing cyst of CSF density on CT, with no pericystic edema
and no rim enhancement after injection of the contrast medium
[1,2]. Additionally, absence of osteoporosis and sclerosis in the
host bone on CT as well as lack of damage in the next interver-
tebral disc space suggest spinal hydatid disease [2,33,37]. On
CT scan, the existence of calcification in the cyst wall, appear-
ance of microvesicular polycystic vertebra, or the development
of vertebral compression fracture can be observed in the last
stage of involvement of the spine (Fig. 6a and b).
5.4.2. MRI
Nowadays, MRI is the first imaging modality in patients with
myelopathy and/or radiculopathy, with multiple daughter cysts
within a parent cyst, in spinal hydatidosis. On MRI, the involved
bone has a heterogeneous medium to low signal intensity on
T1-weighted images and high signal intensity on T2-weighted

Fig. 6. Axial CT (a) and CT-myelography (b) as well as T1-weighted axial magnetic resonance imaging (c) appearances of the cervical spine of a 37-year-old
paraplegic man who had been operated previously with a diagnosis of spinal hydatid cyst showing spinal cord compression due to a recurrent spinal hydatid cyst
involving paravertebral region as well as prominent destruction of C6 vertebra. Note that there were multiple cystic lesions in the paravertebral area on the left side
due to rupture during previous operation (arrow).

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92 A.T. Turgut et al. / European Journal of Radiology 63 (2007) 84–93

images [35]. It has been reported that the daughter cysts are
more hypointense than the parent cyst on T1-weighted images,
while they are of slightly higher signal intensity in comparison
with the parent cyst on T2-weighted images [2,45]. Furthermore,
MRI also demonstrates involvement of the neural structures and
paraspinal muscles by hydatid cysts in such cases (Fig. 6c and
d) [2,28,44]. Anatomically, they can be extradural, subdural,
subarachnoidal or intramedullary [5,28,44]. At present, many
authors suggest that MRI is the diagnostic tool of choice for
depicting such lesions properly [2].
In complicated cases, there may be atypical appearances
such as irregularity of the cyst wall contour, enhancement of
the surrounding rim, isodensity or heterogenity of the cyst
content and surrounding brain edema as well as globular or
curvilinear calcification [1,2]. There is no doubt that aware-
ness of such atypical radiological findings in cases with spinal
hydatidosis can prevent misdiagnosis and complications such
as iatrogenic premature puncture of the lesion during surgery.
As a rule, especially in the areas where the disease is endemic,
the hydatid cyst should be considered in the differential diag-
nosis of a cystic lesion in the spine. In countries like Turkey
where tuberculosis is common, it is important to know that
spinal hydatidosis simulates tuberculosis spondylitis or chronic
osteomyelitis. Radiologically, lack of damage to vertebral bodies
and paraspinal extension are the most common features of spinal
hydatidosis [35].
6. Complicated hydatid cysts of the orbit
6.1. Structure of cystic lesion
6.2. Rupture of cystic lesion
Spontaneous or iatrogenic rupture of the hydatid cysts of the
orbit results secondary implantation cysts due to spillage of the
cyst contents. Even today, surgical intervention is often compli-
cated by the rupture of the cyst in the cases of orbital hydatidosis,
causing severe anaphylactic reaction and secondary hydatidosis
[1,2,37,43]. Especially, puncture of hydatid cyst has some poten-
tial risks of recurrences, due to spillage of scolices [4,43] (Fig. 7).
Recently, it has been suggested that percutaneous treatment of
hydatid cysts, as an alternative to surgery is a safe and effective
treatment method [4].
6.3. Infection of cystic lesion
In the cases with ruptured orbital hydatid cysts, secondary
infection with various infectious pathogens may rarely develop,
resulting in abscess formation [43]. Therefore, the probability
of infected hydatid cyst should be considered in the presence of
a poorly defined lesion in the orbit.
6.4. Imaging of cystic lesion
6.4.1. USG
In a young patient from rural area, presenting with painless
unilateral exophthalmos, orbital USG should be the first diagnos-
tic study within the algorithm [2,4,43]. On USG, hydatid cyst
appears as unilocular and well-circumscribed anechoic lesion
usually located in the supero-lateral and supero-medial angles
of the orbit [43].

As observed in other tissues in the body, the hydatid cyst
of the orbit has (1) the outer pericyst consisting of modified
host cells that form a dense and fibrous protective zone, (2) the
middle endocyst (laminated membrane), which is acellular and
allows the passage of nutrients and (3) the inner ectocyst (lami-
nated membrane) are produced [1,37]. Clinically, patients with
orbital hydatidosis generally present with painless unilateral
exophthalmos.
6.4.2. CT/MRI/PAIR
On CT, it is described as a hypodense, unilocular, well-
defined, thin-walled, homogenous mass encircled with a
hyperdense rim, with densitometric values ranging from +23
to +68 HU [2,4,43]. It has been reported that single or multiple
homogenous retrobulbar massess on CT and/or MRI are typical
findings of orbital hydatidosis [4,43]. In addition, destruction
of the wall of the orbit visible both on plain skull radiography

Fig. 7. Coronal section of orbital CT of a 4-year-old boy showing a giant cystic lesion in a diameter of 30 mm with well-defined borders located at the medial aspect
of the right globe and extraocular muscles. Note that the cystic lesion, with no septation, pushing the globe laterally and the globe had a density of 22.1 HU (a) and
13.8 HU (b), respectively.

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 A.T. Turgut et al. / European Journal of Radiology 63 (2007) 84–93
and CT is another finding compatible with gradual and slow
growth of the orbital lesion [1,2,43]. As mentioned previously,
it has been reported that PAIR therapy is useful alternative to the
surgery for orbital hydatid cysts [4].
7. Conclusions
In conclusion, imaging characteristics and/or serological
findings may provide the correct diagnosis of hydatid disease
at various locations in the human body, but it should be kept in
mind that complicated hydatid cysts can cause unusual USG,
CT and/or MRI findings, in addition to typical ones, especially
in patients living endemic regions, to prevent subsequent acute
catastrophic results and the development of recurrences. In the
differential diagnosis, therefore, familiarity with atypical radio-
logical appearances of complicated hydatid disease in an unusual
location may be valuable in making a correct diagnosis and
treatment.
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