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HYDATID DISEASE
DR. SHRIKANT NAGARE
DISEASE
HYDATID
 Hydatid disease describes infection with the larval stage of the
cestode (or tapeworm) Echinococcus spp.
 There are 4 known species of which 3 are of medical importance to
humans:
 Echinococcus granulosus, causing cystic echinococcosis (CE) - most
common of the three
 Echinococcus multilocularis / alveolaris, causing alveolar
echinococcosis (AE) - rare but is the most virulent
 Echinococcus vogeli, causing polycystic echinococcosis- very rare
 Echinococcus oligarthus-very rare
Synonyms
 Hydatid disease. Echinococcosis. Echinococciasis. Tapeworm disease. Hydatidosis.
Sp: Hidatidosis. Equinococia. Fr: L'echinococcose. Maladie hydatique. Ger:
Beckenknochenechinokokkus. Echinokokkose. Blasenwurm-krankheit.
Echinokokken-krankheit.
UNILOCULAR OR CYSTIC HYDATID
DISEASE
 The causative parasite of unilocular cystic hydatid
disease, E. granulosus, is found in sheep-raising
areas.
 To complete its life cycle, E. granulosus requires two
hosts: a canine and a grazing animal.
 In the more common pastoral form, the primary host is
the dog, while herbivores such as sheep, cattle, swine,
or camels serve as intermediate hosts.
 In the less common sylvatic form, the wolf or fox is the
primary host and reindeer or moose are the usual
intermediate hosts.
 Humans are accidental intermediate hosts.
LIFE CYCLE OF E. GRANULOSUS
Eggs in dog’s feces
Swallowed by intermediate host OR MAN
Embryo hatches in duodenum
Burrows in intestinal wall
Enters portal circulation to liver
Trapping and anchoring in liver
Few reaches lungs
Few in systemic circulation & may go
anywhere
 The average rate of growth varies from 1 to 5 cm a
year, being partly determined by the pressure
resistance of its anatomical location. Thus, its rate
of growth is more rapid in the lungs than in the
liver, spleen, or other solid organs, and slowest in
bones.
 If the cyst has room to develop easily, as happens
in the liver, lungs or peritoneum, it almost always
grows as the classic unilocular cyst.
 It can remain latent for a long period, up to 53
years having been reported.
HYDATID CYST STRUCTURE
Three layers:
 The outer pericyst, composed of modified
host cells that form a dense and fibrous
protective zone.
 The middle laminated which is also referred
to as ectocyst allows passage of nutrients.
 The inner germinal layer, where the scolices
(the larval stage of parasite) and the
laminated membrane are produced. This
innermost or germinal layer forms the true
wall of the cyst.
 Daughter vesicles (brood
capsules) are small
spheres that contain the
protoscolices and are
formed from rests of the
germinal layer.
 When vesicles rupture
within the cyst, scolices
pass into the cyst fluid
and may form a white
sediment known as
hydatid sand.
TYPES: I, II, III
 All hydatid lesions start as purely cystic type I
structures, and if they develop daughter cysts or
matrix (or both) they are termed type II cysts.
 When the only remaining hydatid fluid is in
daughter cysts, the lesion can be considered
hypermature as it is probably nearing death by
starvation.
 When formed elements completely replace the
nourishing hydatid fluid, the type II lesion is
starved, dies, and eventually becomes an end-
stage calcified and biologically inert type III
lesion.
Clinical Findings
 Asymptomatic in many cases
 Most symptomatic cysts are 5 cm or more
 Symptoms frequently come from pressure on affected organs
 Jaundice, abdominal pain if in liver
 Cough, dyspnea and chest pain if in lungs
 Other symptoms arise from leakage of cyst contents or
infection of cyst
 Pain, flushing and urticaria
 Anaphylactic reaction
 Fever and sepsis
 Liver is most common organ involved-75% (mostly right lobe)
 The lungs are infected in approximately 15-30% of all patients and are followed
by the kidneys (4%), muscle (4%), spleen (3%), central nervous system (3%),
soft tissues (3%), bone (2%), peritoneum and mesentery (2%), and heart,
mediastinum, pleura, breast, thyroid, salivary glands, omentum, pancreas, orbit
and spinal canal (<1-2%).
HEPATIC HYDATID DISEASE
 Once the parasite passes through the
intestinal wall to reach the portal venous
system or lymphatic system, the liver acts
as a first line defense and is therefore the
most frequently involved organ.
 In humans hydatid disease involves
approximately 75% of cases.
 The right lobe is most frequently involved
portion of the liver.
IMAGING FEATURES
 Depend on the stage of the cyst growth,
i.e. Whether the cyst is unilocular, contains
daughter vesicles; partially calcified or
completely calcified signifying dead
parasite.
PLAIN FILM
 Peripheral crescentic / curvilinear / polycyclic calcifications
(20-30%).
 There may be a fine line of calcification that is well
defined, usually sharp externally, but lacking clarity
internally.
 Only part of the cyst wall may be calcified, giving a
sickle-shaped or crescentic outline.
 Polycyclic calcification can be seen when both mother
and daughter cysts have calcification within their
walls.
 A "crushed eggshell" or "sunburst" type of calcification
may result from prior cyst rupture and collapse.
 Pneumo-hydrocyst ( infection / communication with bronchial
tree).
 Fig. A large calcified unilocular hydatid
cyst in the liver.
 Fig. A solitary calcified liver hydatid causing a localized
bulge in the anteromedial aspect of the right
hemidiaphragm seen on PA (A) and lateral (B) views of
the chest. Calcification in the hydatid wall completely
encircles this smooth, round cyst
 Fig. Heavily calcified endocyst and pericyst
of a biologically inert type III pelvic hydatid.
ULTRASOUND
The ultrasound appearance of hydatid cysts vary
with the stage of evolution and maturity:
1. Well defined anechoic cyst:
 Cyst wall of double echogenic lines separated by
hypoechoic layer.
 Snowstorm sign- multiple internal echogenic foci
settling to most dependant portion of hydatid cyst
due to hydatid sand
2. Multivesicular cyst of racemose /
honeycomb appearance: Multiple septa
between daughter cysts inside mother cyst.
 Wheel spoke pattern: daughter cysts separated by
echogenic material of hydatid matrix composed of
broken daughter vesicles + scolices + hydatid
sand.
 Serpentine linear structures within hydatid matrix.
3. Partial or complete detachment of
endocyst from pericyst : Due to decreasing
intracystic pressure as a sign of degeneration /
trauma / host response / response to therapy.
 Localised split in the wall with floating undulating
membrane.
 Water lily sign: complete detachment of
membrane.
4. Complex heterogeneous mass mimicking
a solid mass.
5. Egg shell calcification in cyst wall.
 Fig. Transverse ultrasound scan of a liver hydatid
showing pseudotumoral appearance due to the
abundance of echogenic matrix. The fluid-containing
daughter cysts (arrows) indicate the true nature of this
hypermature type II cyst.
 US: Large type I liver hydatid complicated by
detached parasitic membrane, producing the
"snake or serpent sign" (arrows).
CT
1. Well demarcated round low density mass
of fluid attenuation value (3-30 HU).
 Cyst wall of high attenuation on NECT.
 Linear areas of increased attenuation: Detached
laminated membrane.
 Round peripheral fluid collection of lower
attenuation: Daughter cysts.
2. Enhancement of cyst wall + septations.
3. Calcification of cyst wall / internal septa.
 Fig. Transverse CT scan through liver showing Type II
hydatid with matrix (curved arrows) and daughter cysts.
The pericyst is seen where it is calcified (broad arrow).
 Fig. Multiple hydatid cysts are identified on
nonenhanced CT scan in the right and left lobes of the
liver and in the spleen, most of which are Type I except
for a Type II cyst in the anterior right lobe of the liver.
 Fig. CT scan through the kidneys showing exophytic
Type I cyst of the right kidney.
 Fig .Multiple Type I hydatid cysts in the lateral
aspect of the right lobe of the liver and the
peritoneal cavity of the mid-abdomen.
 Fig. CT scan of the liver showing a type II lesion with
predominance of daughter cysts. The "septa" are the
walls of daughter cysts flattened by contact with other
daughters.
 Large hypermature type II hydatid in the right lobe of the
liver causing bulging of the liver capsule. The cyst wall is
faintly calcified and there is abundant matrix and several
daughter cysts (arrows) within the endocyst.
 Thick calcified wall of an old hypermature
liver hydatid with daughter cysts.
 Ruptured type I liver hydatid with detached internal
membranes appearing as a "dancing hand" or a
"serpent" within the cyst fluid
 Type II hydatid cyst in right lobe of liver with multiple
daughter cysts and thick contrast-enhanced cyst wall.
There is one smaller medial cyst caused by outward
proliferation
MRI
 Cyst with hypointense rim (collagenous
pericyst) on T1WI and T2WI.
 Peripheral cysts within cyst hypointense
on T1WI & hyperintense on T2WI.
(Daughter cysts).
 Twisted linear structures within cyst
(collapsed parasitic membrane).
Simple Viable Hydatid Cyst (Type I)
 Fig. MRI of a simple viable type I hydatid cyst of liver. (A) T1-
weighted image. Cyst wall is isointense relative to cyst contents. (B)
T2-weighted image. Cyst wall, consisting of both intact parasitic
membranes and pericyst, is of low signal intensity compared with
high signal of cyst contents.
Hydatid Cyst with Daughter Cysts and/or Matrix
(Type II)
 Fig. MRI of type II hydatid cysts containing daughter
cysts. (A) T1-weighted image shows multiple daughter
cysts containing low-intensity fluid compared with
intermediate signal of hydatid sand of mother cyst. (B)
T2-weighted image. Contents of mother cyst and
daughter cysts have same high signal intensity.
ANGIOGRAPHY
 Avascular area with splaying of arteries.
 Halo of increased density around cyst
(inflammation / compressed liver).
 Fig. Hepatic ARTERIOGRAPHY: noncalcified hydatid cysts
are seen as large avascular filling defects in the inferior
aspect of the right lobe of the liver, with hepatic artery
branches stretched and displaced around them.
CHOLANGIOGRAPHY
 Cysts may communicate with the bile
ducts:
1. Rt Hepatic Duct(55%),
2. Lt Hepatic Duct(29%),
3. CHD (9%),
4. GB(6%),
5. CBD (1%).
Radioisotope Scanning
 Useful in identifying the location, number,
and size of liver hydatids, if ultrasound, CT
or MRI are not available.
 Apart from localizing a "space occupying"
mass, the scans are not specific.
Complications of Cystic
Hydatid Disease
RUPTURE : Trauma, medical treatment, and
degeneration of the endocyst.
Three types of rupture are possible: contained,
communicating and direct.
1. Contained Rupture :
 Rupture of laminated membrane of endocyst, pericyst
remains intact.
 Asymptomatic.
 Contained rupture does not invariably cause
premature death of the cyst and does not predispose
to secondary bacterial infection.
 Fig. Transverse CT scan through the liver showing ruptured Type I hydatid
cysts in child who was treated medically with an oral antihelminthic which
killed the cysts and caused spontaneous rupture.
 Because the cysts did not become smaller and there was no evidence of
biliary obstruction, the rupture was assumed to be contained.
2. Communicating Rupture
 Communicating rupture is possible when biliary
radicals or bronchi perforate the pericyst in the
liver or lung, allowing fluid and formed elements to
escape into the biliary or bronchial tree.
 If air enters the partially evacuated pericyst cavity,
the "floating water lily sign" is seen on upright
chest radiographs.
 Communicating rupture is apparently more
common in lung than liver.
 The distinction between contained and
communicating rupture is not always possible.
 Fig. (A) Longitudinal ultrasound scan of liver showing type I cyst
prior to treatment. (B) Transverse US scan after treatment with an
oral antihelminthic which caused the cyst to rupture.
 The fact that the cyst became smaller and less spherical proves that
this is a communicating rupture even though dilated bile ducts are
not demonstrable.
3. Direct Rupture
 Disastrous consequences.
 Both endocyst and pericyst are torn.
 Lesions near the edge of the liver.
 Fluid and infectious scolices spill into the peritoneal or pleural cavity
causing seeding and often anaphylaxis.
 Direct rupture into many sites has been reported, including the liver,
bile ducts, pleura, lung, gastrointestinal tract, and great vessels.
 Development of small satellite lesions around a cyst.
 Direct rupture usually leads to premature death of the cyst and
theoretically can result in bacterial infection of the pericyst cavity.
 Hydatid cysts in any site which result from rupture are termed
secondary cysts.
 Biliary-bronchial fistulae are a consequence of direct rupture of a
liver cyst through the diaphragm and pleural membranes into the
lung.
 Fig. ERCP showing connection between the biliary
tree and a Type II cyst.
 C collapsed pericyst. Arrow communicating bile duct.
 Fig. Transverse CT scan through false pelvis showing late
sequel of spontaneous direct rupture into the peritoneal
cavity. Secondary Type I and II cysts developed from scolices
that spilled into the peritoneal cavity.
 A ruptured hydatid cyst of the dome of the right lobe of the liver which
presented as a subdiaphragmatic abscess.
 An erect PA chest radiograph shows multiple fluid levels within the ruptured
cyst beneath the right diaphragm, and large daughter cysts floating within
the multiloculated fluid levels. The right hemidiaphragm appears thickened
and moderately elevated and its movement was markedly restricted on
fluoroscopy.
4. Infection
 Infection occurs only after communicating or direct
rupture .
 Infection associated with communicating rupture and
biliary obstruction can result in an abscess within the
pericyst cavity or in cholangitis, and probably always kills
the parasite.
 Infection leads to loss of clarity of interior detail of the
cyst, and fluid elements become echogenic by
ultrasound and denser by CT.
 The endocyst is usually seen to have detached from the
pericyst, and occasionally gas is produced in the cyst.
5. Premature death
 This is defined as death of the parasite that is not the
result of starvation of a hypermature Type II lesion; it
may occur after rupture , infection or medical treatment.
 When a Type I lesion dies prematurely after rupture it
may develop directly into a type III lesion.
 The fluid component becomes echogenic on ultrasound
and denser on CT, and there is a loss of clarity of the
internal detail of the lesion.
 The endocyst is usually seen to be detached from the
pericyst.
 Premature death apparently does not produce a
diagnostic change in the MR signal.
 Fig. (A) Hazy or fuzzy contour of an old dead and ruptured
pulmonary hydatid cyst.
 (B) Non-enhanced CT scan reveals sunburst appearance of the
same ruptured and collapsed pulmonary hydatid in the right lower
lobe.
Laboratory Diagnosis
 Indirect fluorescent antibody
 Immunoelectrophoresis,
 Enzyme-linked immunosorbent assay
(ELISA)
 Radioallergosorbent (RAST) test.
 A new dot immunobinding assay (DIA) for
the detection of hydatid antigen-specific
antibodies (HA-DIA) has been described.
Spleen
 Primary or secondary, solitary or multiple.
 Single hydatid cysts may grow to a considerable
size, almost totally replacing the splenic
parenchyma.
 Multiple hydatid cysts of different sizes may also
occur.
 Secondary hydatids of the spleen may result
from extension of a peritoneal hydatid or
metastases from other sites.
 Dense calcification within a large splenic hydatid.
 Multiple type I and II hydatids in both lobes of the liver
and a solitary huge unilocular type I hydatid which has
replaced most of the splenic parenchyma on a
noncontrast CT scan.
 Contrast-enhanced CT scan showing a huge type II
hydatid with numerous daughter cysts, which has
replaced virtually the entire splenic parenchyma.
Pancreas
 Rare- incidence of less than <0.2/100
cases.
 The results of imaging (US, CT and MRI)
are not different from other organs.
Mesentery, Omentum, Peritoneum,
Retroperitoneum and Pelvis
 Primary or secondary hydatids may be found
anywhere along the omentum, mesentery,
peritoneal cavity, retroperitoneum or pelvis in
at least 2% of patients.
 When calcified, they may be detected
radiologically on plain radiographs of the
abdomen and pelvis
 Otherwise, they may be discovered, often as
a chance finding, on ultrasound, CT or MRI
 Calcified mesenteric cysts seen on AP (A) and
lateral (B) views of the abdomen
 A huge, faintly calcified mesenteric hydatid cyst
compressing the greater curvature of the stomach.
 The stomach is displaced to the right and the small
bowel inferiorly by this unusually large hydatid.
 Another huge calcified hydatid cyst overlying the left
upper quadrant and lower hemithorax in a different
patient, causing extrinsic compression on the
esophagogastric junction and fundus of the stomach.
Kidneys and Ureters
 Renal hydatids are almost always primary,
although direct invasion from the liver or
spleen can occur.
 They are usually solitary and occur most
commonly in the upper or lower poles and
only occasionally in the central portion of the
kidney.
 Hydatid cysts of the urinary bladder and
ureters occur rarely and can lead to
obstructive hydronephrosis.
 Calcified Echinococcus cyst of the kidney. An
excretory urogram reveals a calcified mass extending
inferiorly from the lower pole of the left kidney.
 Selective right renal arteriography reveals large
avascular mass in the lower pole. Densities in the
lower part of the lesion represent calcifications.
Lungs
 Intact hydatid cysts of the lungs are
commonly solitary, well-circumscribed,
homogeneous, uncalcified masses.
 They are usually round but may be oval,
elliptical or lobulated .
 They can occur anywhere in the lungs, but
are somewhat more common on the right
side and in the basilar segments of both
lower lobes.
 (A and B) PA and lateral views of the chest showing a
lobulated, elliptical, homogeneous mass in the right upper
lobe. There is umbilication or notching along the medial and
posterior borders of this hydatid (arrows) caused by pressure
on the cyst from adjacent vessels or bronchi.
 The perivesicular air meniscus between the host adventitia and the
parasitic endocyst (the so-called "sign of detachment") (1) is clearly
seen, as is a "cyst within a cyst" or "sign of the double arch" (2).
 The irregular wavy nature of the fluid level produced by the
collapsed hydatid membranes floating on top of the residual hydatid
fluid produces the pathognomonic "floating water lily sign" or "sign of
the Camelot" (3).
 MRI, coronal view, 1 week later of hydatid cyst rupture reveals
globular collapsed parasitic membranes at bottom of the cyst
producing the "sign of the rising sun" (arrows).
 One month later, CT shows an "empty cyst" after complete
evacuation of the parasitic membranes.
 Ruptured pulmonary hydatid cyst
 Chest radiograph 2 weeks later demonstrates the "iceberg sign" indicating
collapsed parasitic membranes which are partially submerged (arrows).
 CT scan one week after shows detached membranes ("whirl sign", black
arrows) with small pleural reaction (white arrows).
 Bronchography : Compression and displacement of the bronchi of
the right lung by the huge pulmonary hydatid. Contrast medium may
enter between the layers of the ruptured hydatid membrane.
Radiographic, CT and MRI signs of
hydatid cysts of the chest.
 "Meniscus sign" (also called "crescent sign" or "sign of
detachment")
 "Water-lily sign" (or "camalote sign")
 "Cyst with fluid level" (or "abscess")
 "Iceberg sign "
 "Double-arch or Cumbo sign"
 "Sign of the rising sun"
 "Serpent sign"
 "Whirl sign"
 "Retained cyst"
 "Empty cyst"
 "Calcification" (heart and mediastinum, rarely)
Complications of thoracic hydatid cysts
1. Rupture and pericystic reaction
2. Infection
a. Air bubbles
b. Abscess
3. Rupture into airways
a. Expectoration of scolices "grape skins" (daughter cysts), salty fluid, hemoptysis
with or without suffocation, allergic reactions or shock
b. Bronchocystic fistula
c. Evidence of biliobronchial fistula
d. Bronchogenic spread
4. Pleural perforation
a. Pleural effusion (may contain "hydatid sand" or "grape skins")
b. Hydropneumothorax, pyopneumothorax, tension pneumothorax
c. "Rounded atelectasis"
5. Vascular spread
6. Overgrowth or spread to mediastinum
Mediastinum
 Rare.
 The incidence varies from less than 1% to
about 4%.
 Uncomplicated hydatid cysts of the
mediastinum usually cannot be
differentiated from other cysts (e.g.,
bronchogenic or other duplication cysts or
cystic tumors) on plain film radiography
 septated hydatid cysts (arrows) throughout
the left anterior mediastinum
Heart
 Primary cardiac hydatid disease is
uncommon.
 It occurs in only 0.5 to 2% of all human
cases of echinococcosis
 Primary involvement of the heart usually
occurs via the coronary arteries.
 Large uncomplicated, univesicular Type I
hydatid cyst involving the pericardium and
left ventricular wall
Thoracic Wall
 Uncommon (less than 1%).
 Usually secondary, spreading from cysts
in the lungs or bones of the thoracic cage.
Fig. CT scan showing a
univesicular Type I hydatid
cyst involving the thoracic
wall musculature.
Breast
 Not common.
 Asymptomatic and have no specific local signs.
 The shell-like calcification of a hydatid cyst may
mimic a fibroadenoma in the breast. If there are
daughter cysts, hydatid sand, or collapsed
membranes, the diagnosis can be made by
mammography or ultrasound (and also by CT and
MRI).
 When the cyst is complex or multilocular with
internal sonographic echoes due to debris, it is
difficult to exclude added infection.
Brain
 1 to 4% of all cases of echinococcosis.
 Usually primary, developing from a larva carried to
the brain via the arterial circulation.
 More often supratentorial than infratentorial in
location.
 Most cerebral hydatids are in the white matter,
usually in the parietal lobe .
 Solitary, and grow outward toward the cerebral
cortex or inward toward the ventricles.
 Calcification of the cyst may occasionally be seen
on plain radiographs of the skull.
Fig. 3.118 Hydatid cyst of the brain. Large, calcified hydatid cyst of the left
cerebral hemisphere in a 20-year-old man.
 Fig. Axial MR image of right parietal hydatid
cyst with peripheral rim of low signal intensity.
Skull and Facial Bones
 Cranial hydatids appear to be more
common in the parietal and occipital
regions of the skull.
Fig. Hydatid cyst of the skull.. (A) Grossly expansile blowout lesion of
the cranial vault seen on AP view of the skull. (B) Blowout, expansile,
destructive lesion of the occiput caused by a large hydatid cyst in
another patient.
Fig. Large hydatid cyst involving the right orbit with proptosis of the
eye and compression erosion of adjacent bony structures and right
ethmoid sinus.
Orbital Hydatid Disease
MUSCULOSKELETAL SYSTEM
Bone
Fig. Hydatid disease involving the soft tissues of the thigh .
(A) Multiple large, partially calcified, spherical cysts in the upper thigh of a 20-
year-old man.
(B) A huge noncalcified hydatid in the soft tissues of the midthigh, posterior to
the femur in a young woman. Neither patient had any other demonstrable
hydatid cysts.
Fig. Hydatid disease of the distal femur. AP (A) and lateral (B) views of the
femur show well-defined cystic areas that are circular or oval in the long axis of
the bone. The margins are sharp and there is moderate surrounding sclerosis,
giving a multilocular cystic appearance to the femur. The cortex is slightly
thinned in the diametaphyseal area and there is slight periosteal reaction along
its lateral aspect, suggesting the presence of secondary infection, because
hydatid disease alone does not cause periostitis.
Fig. Hydatid disease of the pelvis presenting as bubbly cystic, expansile lesions with
surrounding reactive sclerosis. (A) A solitary large multilocular cyst in the right iliac bone.
There is expansion of the iliac crest with cortical breakthrough and a thin reactive layer of
bone sclerosis about the lesion. (B) Bubbly cystic, expansile lesion involving the pubis,
ischium, and acetabulum on both sides of the pelvis. Hydatid disease may cross the
pubic symphysis, as in this case, or the sacroiliac or hip joints.
Spine
 Dorsal vertebrae are the most frequently
affected with hydatid disease, especially the
lower six thoracic vertebrae.
 Epidural extension of their disease with resultant
compression of the spinal cord and paraplegia.
Fig. Hydatid disease affecting the body and neural arch of the second lumbar
vertebra and the adjacent disc space. A lateral tomogram clearly shows the well
defined cystic area in the posterior portion of the vertebral body extending into the
pedicle and lamina. There is narrowing of the LI-2 disc space as well.
Ribs and Scapula
 The ribs may become involved via the
bloodstream or by direct extension from a lesion
in the spine or lung.
 In its early stages, a primary rib lesion will
appear as a multilocular cystic area with the
cortex preserved.
 Later, the cortex is expanded and often
perforated, permitting the hydatid tissue to break
out from the bone and form a well-defined soft
tissue mass.
Fig. Hydatid disease involving the lateral
aspect of a rib with associated pleural
extension.
Treatment of Cystic Hydatid
Disease
 The role of surgery in the treatment of
hydatid disease is diminishing, with
increased indications for, and success
with, chemotherapy and with the
introduction of PAIR (Puncture-Aspiration-
Injection-Reaspiration).
ALVEOLAR HYDATID DISEASE
(E. multilocularis)
 Alveolar hydatid disease is an infection caused
by larval stages of the tapeworm, Echinococcus
multilocularis.
 These larvae invade the infected organ, which in
at least 90% of patients is the liver, and cause
great destruction, resembling an infiltrating
malignancy.
Fig. Sonograms of hepatic alveolar echinococcosis-Typical massive necrosis
of the large irregularly marginated lesion with shaggy borders and abnormal
adjacent parenchyma (arrowheads and arrows).
The principal sonographic signs of alveolar hydatid
disease are as follows:
Hepatomegaly
Hyperechoic foci
Calcifications
Cystic, often craggy, necrosis
Dilatation of the biliary tree
Deformity and narrowing of the portal and
hepatic veins
Staging Of Hepatic Alveolar
Echinococcosis
Stage 1. Lesion measuring less than 3 cm
in diameter;
Stage 2. Lesion greater than 3 cm,
confined to less than 3 hepatic segments;
Stage 3a. Lesion with invasion of more
than 3 hepatic segments;
Stage 3b. Invasion of the liver hilum or
suprahepatic vena cava;
Stage 4. Invasion of surrounding organs
and/or distant metastases.
Fig. E. multilocularis involvement of the orbit and brain.
(A) Contrast-enhanced CT reveals a round right palpebral mass (1). (B) A large right
frontal lobe mass is present with posterior displacement of the corpus callosum, posterior
and contralateral displacement of the right frontal horn and contralateral displacement of
the falx cerebri. Nodular and ring-like calcifications are seen within the mass, which
shows partial contrast enhancement and is surrounded by edema (2). Nonenhancing and
noncalcified areas represent alveolar hydatid cysts (3). (C) The inner table of the skull (4)
is irregular anterior to the mass.
Thank you

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Hydatid Radiology

  • 3.  Hydatid disease describes infection with the larval stage of the cestode (or tapeworm) Echinococcus spp.  There are 4 known species of which 3 are of medical importance to humans:  Echinococcus granulosus, causing cystic echinococcosis (CE) - most common of the three  Echinococcus multilocularis / alveolaris, causing alveolar echinococcosis (AE) - rare but is the most virulent  Echinococcus vogeli, causing polycystic echinococcosis- very rare  Echinococcus oligarthus-very rare Synonyms  Hydatid disease. Echinococcosis. Echinococciasis. Tapeworm disease. Hydatidosis. Sp: Hidatidosis. Equinococia. Fr: L'echinococcose. Maladie hydatique. Ger: Beckenknochenechinokokkus. Echinokokkose. Blasenwurm-krankheit. Echinokokken-krankheit.
  • 4. UNILOCULAR OR CYSTIC HYDATID DISEASE  The causative parasite of unilocular cystic hydatid disease, E. granulosus, is found in sheep-raising areas.  To complete its life cycle, E. granulosus requires two hosts: a canine and a grazing animal.  In the more common pastoral form, the primary host is the dog, while herbivores such as sheep, cattle, swine, or camels serve as intermediate hosts.  In the less common sylvatic form, the wolf or fox is the primary host and reindeer or moose are the usual intermediate hosts.  Humans are accidental intermediate hosts.
  • 5. LIFE CYCLE OF E. GRANULOSUS Eggs in dog’s feces Swallowed by intermediate host OR MAN Embryo hatches in duodenum Burrows in intestinal wall Enters portal circulation to liver Trapping and anchoring in liver Few reaches lungs Few in systemic circulation & may go anywhere
  • 6.  The average rate of growth varies from 1 to 5 cm a year, being partly determined by the pressure resistance of its anatomical location. Thus, its rate of growth is more rapid in the lungs than in the liver, spleen, or other solid organs, and slowest in bones.  If the cyst has room to develop easily, as happens in the liver, lungs or peritoneum, it almost always grows as the classic unilocular cyst.  It can remain latent for a long period, up to 53 years having been reported.
  • 7. HYDATID CYST STRUCTURE Three layers:  The outer pericyst, composed of modified host cells that form a dense and fibrous protective zone.  The middle laminated which is also referred to as ectocyst allows passage of nutrients.  The inner germinal layer, where the scolices (the larval stage of parasite) and the laminated membrane are produced. This innermost or germinal layer forms the true wall of the cyst.
  • 8.  Daughter vesicles (brood capsules) are small spheres that contain the protoscolices and are formed from rests of the germinal layer.  When vesicles rupture within the cyst, scolices pass into the cyst fluid and may form a white sediment known as hydatid sand.
  • 9. TYPES: I, II, III  All hydatid lesions start as purely cystic type I structures, and if they develop daughter cysts or matrix (or both) they are termed type II cysts.  When the only remaining hydatid fluid is in daughter cysts, the lesion can be considered hypermature as it is probably nearing death by starvation.  When formed elements completely replace the nourishing hydatid fluid, the type II lesion is starved, dies, and eventually becomes an end- stage calcified and biologically inert type III lesion.
  • 10. Clinical Findings  Asymptomatic in many cases  Most symptomatic cysts are 5 cm or more  Symptoms frequently come from pressure on affected organs  Jaundice, abdominal pain if in liver  Cough, dyspnea and chest pain if in lungs  Other symptoms arise from leakage of cyst contents or infection of cyst  Pain, flushing and urticaria  Anaphylactic reaction  Fever and sepsis  Liver is most common organ involved-75% (mostly right lobe)  The lungs are infected in approximately 15-30% of all patients and are followed by the kidneys (4%), muscle (4%), spleen (3%), central nervous system (3%), soft tissues (3%), bone (2%), peritoneum and mesentery (2%), and heart, mediastinum, pleura, breast, thyroid, salivary glands, omentum, pancreas, orbit and spinal canal (<1-2%).
  • 11. HEPATIC HYDATID DISEASE  Once the parasite passes through the intestinal wall to reach the portal venous system or lymphatic system, the liver acts as a first line defense and is therefore the most frequently involved organ.  In humans hydatid disease involves approximately 75% of cases.  The right lobe is most frequently involved portion of the liver.
  • 12. IMAGING FEATURES  Depend on the stage of the cyst growth, i.e. Whether the cyst is unilocular, contains daughter vesicles; partially calcified or completely calcified signifying dead parasite.
  • 13. PLAIN FILM  Peripheral crescentic / curvilinear / polycyclic calcifications (20-30%).  There may be a fine line of calcification that is well defined, usually sharp externally, but lacking clarity internally.  Only part of the cyst wall may be calcified, giving a sickle-shaped or crescentic outline.  Polycyclic calcification can be seen when both mother and daughter cysts have calcification within their walls.  A "crushed eggshell" or "sunburst" type of calcification may result from prior cyst rupture and collapse.  Pneumo-hydrocyst ( infection / communication with bronchial tree).
  • 14.
  • 15.  Fig. A large calcified unilocular hydatid cyst in the liver.
  • 16.  Fig. A solitary calcified liver hydatid causing a localized bulge in the anteromedial aspect of the right hemidiaphragm seen on PA (A) and lateral (B) views of the chest. Calcification in the hydatid wall completely encircles this smooth, round cyst
  • 17.  Fig. Heavily calcified endocyst and pericyst of a biologically inert type III pelvic hydatid.
  • 18. ULTRASOUND The ultrasound appearance of hydatid cysts vary with the stage of evolution and maturity: 1. Well defined anechoic cyst:  Cyst wall of double echogenic lines separated by hypoechoic layer.  Snowstorm sign- multiple internal echogenic foci settling to most dependant portion of hydatid cyst due to hydatid sand
  • 19. 2. Multivesicular cyst of racemose / honeycomb appearance: Multiple septa between daughter cysts inside mother cyst.  Wheel spoke pattern: daughter cysts separated by echogenic material of hydatid matrix composed of broken daughter vesicles + scolices + hydatid sand.  Serpentine linear structures within hydatid matrix.
  • 20. 3. Partial or complete detachment of endocyst from pericyst : Due to decreasing intracystic pressure as a sign of degeneration / trauma / host response / response to therapy.  Localised split in the wall with floating undulating membrane.  Water lily sign: complete detachment of membrane.
  • 21. 4. Complex heterogeneous mass mimicking a solid mass. 5. Egg shell calcification in cyst wall.
  • 22.  Fig. Transverse ultrasound scan of a liver hydatid showing pseudotumoral appearance due to the abundance of echogenic matrix. The fluid-containing daughter cysts (arrows) indicate the true nature of this hypermature type II cyst.
  • 23.  US: Large type I liver hydatid complicated by detached parasitic membrane, producing the "snake or serpent sign" (arrows).
  • 24. CT 1. Well demarcated round low density mass of fluid attenuation value (3-30 HU).  Cyst wall of high attenuation on NECT.  Linear areas of increased attenuation: Detached laminated membrane.  Round peripheral fluid collection of lower attenuation: Daughter cysts. 2. Enhancement of cyst wall + septations. 3. Calcification of cyst wall / internal septa.
  • 25.  Fig. Transverse CT scan through liver showing Type II hydatid with matrix (curved arrows) and daughter cysts. The pericyst is seen where it is calcified (broad arrow).
  • 26.  Fig. Multiple hydatid cysts are identified on nonenhanced CT scan in the right and left lobes of the liver and in the spleen, most of which are Type I except for a Type II cyst in the anterior right lobe of the liver.
  • 27.  Fig. CT scan through the kidneys showing exophytic Type I cyst of the right kidney.
  • 28.  Fig .Multiple Type I hydatid cysts in the lateral aspect of the right lobe of the liver and the peritoneal cavity of the mid-abdomen.
  • 29.  Fig. CT scan of the liver showing a type II lesion with predominance of daughter cysts. The "septa" are the walls of daughter cysts flattened by contact with other daughters.
  • 30.  Large hypermature type II hydatid in the right lobe of the liver causing bulging of the liver capsule. The cyst wall is faintly calcified and there is abundant matrix and several daughter cysts (arrows) within the endocyst.
  • 31.  Thick calcified wall of an old hypermature liver hydatid with daughter cysts.
  • 32.  Ruptured type I liver hydatid with detached internal membranes appearing as a "dancing hand" or a "serpent" within the cyst fluid
  • 33.  Type II hydatid cyst in right lobe of liver with multiple daughter cysts and thick contrast-enhanced cyst wall. There is one smaller medial cyst caused by outward proliferation
  • 34. MRI  Cyst with hypointense rim (collagenous pericyst) on T1WI and T2WI.  Peripheral cysts within cyst hypointense on T1WI & hyperintense on T2WI. (Daughter cysts).  Twisted linear structures within cyst (collapsed parasitic membrane).
  • 35. Simple Viable Hydatid Cyst (Type I)  Fig. MRI of a simple viable type I hydatid cyst of liver. (A) T1- weighted image. Cyst wall is isointense relative to cyst contents. (B) T2-weighted image. Cyst wall, consisting of both intact parasitic membranes and pericyst, is of low signal intensity compared with high signal of cyst contents.
  • 36. Hydatid Cyst with Daughter Cysts and/or Matrix (Type II)  Fig. MRI of type II hydatid cysts containing daughter cysts. (A) T1-weighted image shows multiple daughter cysts containing low-intensity fluid compared with intermediate signal of hydatid sand of mother cyst. (B) T2-weighted image. Contents of mother cyst and daughter cysts have same high signal intensity.
  • 37. ANGIOGRAPHY  Avascular area with splaying of arteries.  Halo of increased density around cyst (inflammation / compressed liver).
  • 38.  Fig. Hepatic ARTERIOGRAPHY: noncalcified hydatid cysts are seen as large avascular filling defects in the inferior aspect of the right lobe of the liver, with hepatic artery branches stretched and displaced around them.
  • 39. CHOLANGIOGRAPHY  Cysts may communicate with the bile ducts: 1. Rt Hepatic Duct(55%), 2. Lt Hepatic Duct(29%), 3. CHD (9%), 4. GB(6%), 5. CBD (1%).
  • 40. Radioisotope Scanning  Useful in identifying the location, number, and size of liver hydatids, if ultrasound, CT or MRI are not available.  Apart from localizing a "space occupying" mass, the scans are not specific.
  • 41. Complications of Cystic Hydatid Disease RUPTURE : Trauma, medical treatment, and degeneration of the endocyst. Three types of rupture are possible: contained, communicating and direct. 1. Contained Rupture :  Rupture of laminated membrane of endocyst, pericyst remains intact.  Asymptomatic.  Contained rupture does not invariably cause premature death of the cyst and does not predispose to secondary bacterial infection.
  • 42.  Fig. Transverse CT scan through the liver showing ruptured Type I hydatid cysts in child who was treated medically with an oral antihelminthic which killed the cysts and caused spontaneous rupture.  Because the cysts did not become smaller and there was no evidence of biliary obstruction, the rupture was assumed to be contained.
  • 43. 2. Communicating Rupture  Communicating rupture is possible when biliary radicals or bronchi perforate the pericyst in the liver or lung, allowing fluid and formed elements to escape into the biliary or bronchial tree.  If air enters the partially evacuated pericyst cavity, the "floating water lily sign" is seen on upright chest radiographs.  Communicating rupture is apparently more common in lung than liver.  The distinction between contained and communicating rupture is not always possible.
  • 44.  Fig. (A) Longitudinal ultrasound scan of liver showing type I cyst prior to treatment. (B) Transverse US scan after treatment with an oral antihelminthic which caused the cyst to rupture.  The fact that the cyst became smaller and less spherical proves that this is a communicating rupture even though dilated bile ducts are not demonstrable.
  • 45. 3. Direct Rupture  Disastrous consequences.  Both endocyst and pericyst are torn.  Lesions near the edge of the liver.  Fluid and infectious scolices spill into the peritoneal or pleural cavity causing seeding and often anaphylaxis.  Direct rupture into many sites has been reported, including the liver, bile ducts, pleura, lung, gastrointestinal tract, and great vessels.  Development of small satellite lesions around a cyst.  Direct rupture usually leads to premature death of the cyst and theoretically can result in bacterial infection of the pericyst cavity.  Hydatid cysts in any site which result from rupture are termed secondary cysts.  Biliary-bronchial fistulae are a consequence of direct rupture of a liver cyst through the diaphragm and pleural membranes into the lung.
  • 46.  Fig. ERCP showing connection between the biliary tree and a Type II cyst.  C collapsed pericyst. Arrow communicating bile duct.
  • 47.  Fig. Transverse CT scan through false pelvis showing late sequel of spontaneous direct rupture into the peritoneal cavity. Secondary Type I and II cysts developed from scolices that spilled into the peritoneal cavity.
  • 48.  A ruptured hydatid cyst of the dome of the right lobe of the liver which presented as a subdiaphragmatic abscess.  An erect PA chest radiograph shows multiple fluid levels within the ruptured cyst beneath the right diaphragm, and large daughter cysts floating within the multiloculated fluid levels. The right hemidiaphragm appears thickened and moderately elevated and its movement was markedly restricted on fluoroscopy.
  • 49. 4. Infection  Infection occurs only after communicating or direct rupture .  Infection associated with communicating rupture and biliary obstruction can result in an abscess within the pericyst cavity or in cholangitis, and probably always kills the parasite.  Infection leads to loss of clarity of interior detail of the cyst, and fluid elements become echogenic by ultrasound and denser by CT.  The endocyst is usually seen to have detached from the pericyst, and occasionally gas is produced in the cyst.
  • 50. 5. Premature death  This is defined as death of the parasite that is not the result of starvation of a hypermature Type II lesion; it may occur after rupture , infection or medical treatment.  When a Type I lesion dies prematurely after rupture it may develop directly into a type III lesion.  The fluid component becomes echogenic on ultrasound and denser on CT, and there is a loss of clarity of the internal detail of the lesion.  The endocyst is usually seen to be detached from the pericyst.  Premature death apparently does not produce a diagnostic change in the MR signal.
  • 51.  Fig. (A) Hazy or fuzzy contour of an old dead and ruptured pulmonary hydatid cyst.  (B) Non-enhanced CT scan reveals sunburst appearance of the same ruptured and collapsed pulmonary hydatid in the right lower lobe.
  • 52.
  • 53. Laboratory Diagnosis  Indirect fluorescent antibody  Immunoelectrophoresis,  Enzyme-linked immunosorbent assay (ELISA)  Radioallergosorbent (RAST) test.  A new dot immunobinding assay (DIA) for the detection of hydatid antigen-specific antibodies (HA-DIA) has been described.
  • 54. Spleen  Primary or secondary, solitary or multiple.  Single hydatid cysts may grow to a considerable size, almost totally replacing the splenic parenchyma.  Multiple hydatid cysts of different sizes may also occur.  Secondary hydatids of the spleen may result from extension of a peritoneal hydatid or metastases from other sites.
  • 55.  Dense calcification within a large splenic hydatid.
  • 56.  Multiple type I and II hydatids in both lobes of the liver and a solitary huge unilocular type I hydatid which has replaced most of the splenic parenchyma on a noncontrast CT scan.
  • 57.  Contrast-enhanced CT scan showing a huge type II hydatid with numerous daughter cysts, which has replaced virtually the entire splenic parenchyma.
  • 58. Pancreas  Rare- incidence of less than <0.2/100 cases.  The results of imaging (US, CT and MRI) are not different from other organs.
  • 59. Mesentery, Omentum, Peritoneum, Retroperitoneum and Pelvis  Primary or secondary hydatids may be found anywhere along the omentum, mesentery, peritoneal cavity, retroperitoneum or pelvis in at least 2% of patients.  When calcified, they may be detected radiologically on plain radiographs of the abdomen and pelvis  Otherwise, they may be discovered, often as a chance finding, on ultrasound, CT or MRI
  • 60.  Calcified mesenteric cysts seen on AP (A) and lateral (B) views of the abdomen
  • 61.  A huge, faintly calcified mesenteric hydatid cyst compressing the greater curvature of the stomach.  The stomach is displaced to the right and the small bowel inferiorly by this unusually large hydatid.
  • 62.  Another huge calcified hydatid cyst overlying the left upper quadrant and lower hemithorax in a different patient, causing extrinsic compression on the esophagogastric junction and fundus of the stomach.
  • 63. Kidneys and Ureters  Renal hydatids are almost always primary, although direct invasion from the liver or spleen can occur.  They are usually solitary and occur most commonly in the upper or lower poles and only occasionally in the central portion of the kidney.  Hydatid cysts of the urinary bladder and ureters occur rarely and can lead to obstructive hydronephrosis.
  • 64.  Calcified Echinococcus cyst of the kidney. An excretory urogram reveals a calcified mass extending inferiorly from the lower pole of the left kidney.
  • 65.  Selective right renal arteriography reveals large avascular mass in the lower pole. Densities in the lower part of the lesion represent calcifications.
  • 66. Lungs  Intact hydatid cysts of the lungs are commonly solitary, well-circumscribed, homogeneous, uncalcified masses.  They are usually round but may be oval, elliptical or lobulated .  They can occur anywhere in the lungs, but are somewhat more common on the right side and in the basilar segments of both lower lobes.
  • 67.  (A and B) PA and lateral views of the chest showing a lobulated, elliptical, homogeneous mass in the right upper lobe. There is umbilication or notching along the medial and posterior borders of this hydatid (arrows) caused by pressure on the cyst from adjacent vessels or bronchi.
  • 68.  The perivesicular air meniscus between the host adventitia and the parasitic endocyst (the so-called "sign of detachment") (1) is clearly seen, as is a "cyst within a cyst" or "sign of the double arch" (2).  The irregular wavy nature of the fluid level produced by the collapsed hydatid membranes floating on top of the residual hydatid fluid produces the pathognomonic "floating water lily sign" or "sign of the Camelot" (3).
  • 69.  MRI, coronal view, 1 week later of hydatid cyst rupture reveals globular collapsed parasitic membranes at bottom of the cyst producing the "sign of the rising sun" (arrows).  One month later, CT shows an "empty cyst" after complete evacuation of the parasitic membranes.
  • 70.  Ruptured pulmonary hydatid cyst  Chest radiograph 2 weeks later demonstrates the "iceberg sign" indicating collapsed parasitic membranes which are partially submerged (arrows).  CT scan one week after shows detached membranes ("whirl sign", black arrows) with small pleural reaction (white arrows).
  • 71.  Bronchography : Compression and displacement of the bronchi of the right lung by the huge pulmonary hydatid. Contrast medium may enter between the layers of the ruptured hydatid membrane.
  • 72. Radiographic, CT and MRI signs of hydatid cysts of the chest.  "Meniscus sign" (also called "crescent sign" or "sign of detachment")  "Water-lily sign" (or "camalote sign")  "Cyst with fluid level" (or "abscess")  "Iceberg sign "  "Double-arch or Cumbo sign"  "Sign of the rising sun"  "Serpent sign"  "Whirl sign"  "Retained cyst"  "Empty cyst"  "Calcification" (heart and mediastinum, rarely)
  • 73. Complications of thoracic hydatid cysts 1. Rupture and pericystic reaction 2. Infection a. Air bubbles b. Abscess 3. Rupture into airways a. Expectoration of scolices "grape skins" (daughter cysts), salty fluid, hemoptysis with or without suffocation, allergic reactions or shock b. Bronchocystic fistula c. Evidence of biliobronchial fistula d. Bronchogenic spread 4. Pleural perforation a. Pleural effusion (may contain "hydatid sand" or "grape skins") b. Hydropneumothorax, pyopneumothorax, tension pneumothorax c. "Rounded atelectasis" 5. Vascular spread 6. Overgrowth or spread to mediastinum
  • 74. Mediastinum  Rare.  The incidence varies from less than 1% to about 4%.  Uncomplicated hydatid cysts of the mediastinum usually cannot be differentiated from other cysts (e.g., bronchogenic or other duplication cysts or cystic tumors) on plain film radiography
  • 75.  septated hydatid cysts (arrows) throughout the left anterior mediastinum
  • 76. Heart  Primary cardiac hydatid disease is uncommon.  It occurs in only 0.5 to 2% of all human cases of echinococcosis  Primary involvement of the heart usually occurs via the coronary arteries.
  • 77.  Large uncomplicated, univesicular Type I hydatid cyst involving the pericardium and left ventricular wall
  • 78. Thoracic Wall  Uncommon (less than 1%).  Usually secondary, spreading from cysts in the lungs or bones of the thoracic cage. Fig. CT scan showing a univesicular Type I hydatid cyst involving the thoracic wall musculature.
  • 79. Breast  Not common.  Asymptomatic and have no specific local signs.  The shell-like calcification of a hydatid cyst may mimic a fibroadenoma in the breast. If there are daughter cysts, hydatid sand, or collapsed membranes, the diagnosis can be made by mammography or ultrasound (and also by CT and MRI).  When the cyst is complex or multilocular with internal sonographic echoes due to debris, it is difficult to exclude added infection.
  • 80. Brain  1 to 4% of all cases of echinococcosis.  Usually primary, developing from a larva carried to the brain via the arterial circulation.  More often supratentorial than infratentorial in location.  Most cerebral hydatids are in the white matter, usually in the parietal lobe .  Solitary, and grow outward toward the cerebral cortex or inward toward the ventricles.  Calcification of the cyst may occasionally be seen on plain radiographs of the skull.
  • 81. Fig. 3.118 Hydatid cyst of the brain. Large, calcified hydatid cyst of the left cerebral hemisphere in a 20-year-old man.
  • 82.  Fig. Axial MR image of right parietal hydatid cyst with peripheral rim of low signal intensity.
  • 83. Skull and Facial Bones  Cranial hydatids appear to be more common in the parietal and occipital regions of the skull.
  • 84. Fig. Hydatid cyst of the skull.. (A) Grossly expansile blowout lesion of the cranial vault seen on AP view of the skull. (B) Blowout, expansile, destructive lesion of the occiput caused by a large hydatid cyst in another patient.
  • 85. Fig. Large hydatid cyst involving the right orbit with proptosis of the eye and compression erosion of adjacent bony structures and right ethmoid sinus. Orbital Hydatid Disease
  • 87. Fig. Hydatid disease involving the soft tissues of the thigh . (A) Multiple large, partially calcified, spherical cysts in the upper thigh of a 20- year-old man. (B) A huge noncalcified hydatid in the soft tissues of the midthigh, posterior to the femur in a young woman. Neither patient had any other demonstrable hydatid cysts.
  • 88. Fig. Hydatid disease of the distal femur. AP (A) and lateral (B) views of the femur show well-defined cystic areas that are circular or oval in the long axis of the bone. The margins are sharp and there is moderate surrounding sclerosis, giving a multilocular cystic appearance to the femur. The cortex is slightly thinned in the diametaphyseal area and there is slight periosteal reaction along its lateral aspect, suggesting the presence of secondary infection, because hydatid disease alone does not cause periostitis.
  • 89. Fig. Hydatid disease of the pelvis presenting as bubbly cystic, expansile lesions with surrounding reactive sclerosis. (A) A solitary large multilocular cyst in the right iliac bone. There is expansion of the iliac crest with cortical breakthrough and a thin reactive layer of bone sclerosis about the lesion. (B) Bubbly cystic, expansile lesion involving the pubis, ischium, and acetabulum on both sides of the pelvis. Hydatid disease may cross the pubic symphysis, as in this case, or the sacroiliac or hip joints.
  • 90. Spine  Dorsal vertebrae are the most frequently affected with hydatid disease, especially the lower six thoracic vertebrae.  Epidural extension of their disease with resultant compression of the spinal cord and paraplegia.
  • 91. Fig. Hydatid disease affecting the body and neural arch of the second lumbar vertebra and the adjacent disc space. A lateral tomogram clearly shows the well defined cystic area in the posterior portion of the vertebral body extending into the pedicle and lamina. There is narrowing of the LI-2 disc space as well.
  • 92. Ribs and Scapula  The ribs may become involved via the bloodstream or by direct extension from a lesion in the spine or lung.  In its early stages, a primary rib lesion will appear as a multilocular cystic area with the cortex preserved.  Later, the cortex is expanded and often perforated, permitting the hydatid tissue to break out from the bone and form a well-defined soft tissue mass.
  • 93. Fig. Hydatid disease involving the lateral aspect of a rib with associated pleural extension.
  • 94. Treatment of Cystic Hydatid Disease  The role of surgery in the treatment of hydatid disease is diminishing, with increased indications for, and success with, chemotherapy and with the introduction of PAIR (Puncture-Aspiration- Injection-Reaspiration).
  • 95. ALVEOLAR HYDATID DISEASE (E. multilocularis)  Alveolar hydatid disease is an infection caused by larval stages of the tapeworm, Echinococcus multilocularis.  These larvae invade the infected organ, which in at least 90% of patients is the liver, and cause great destruction, resembling an infiltrating malignancy.
  • 96. Fig. Sonograms of hepatic alveolar echinococcosis-Typical massive necrosis of the large irregularly marginated lesion with shaggy borders and abnormal adjacent parenchyma (arrowheads and arrows).
  • 97. The principal sonographic signs of alveolar hydatid disease are as follows: Hepatomegaly Hyperechoic foci Calcifications Cystic, often craggy, necrosis Dilatation of the biliary tree Deformity and narrowing of the portal and hepatic veins
  • 98. Staging Of Hepatic Alveolar Echinococcosis Stage 1. Lesion measuring less than 3 cm in diameter; Stage 2. Lesion greater than 3 cm, confined to less than 3 hepatic segments; Stage 3a. Lesion with invasion of more than 3 hepatic segments; Stage 3b. Invasion of the liver hilum or suprahepatic vena cava; Stage 4. Invasion of surrounding organs and/or distant metastases.
  • 99. Fig. E. multilocularis involvement of the orbit and brain. (A) Contrast-enhanced CT reveals a round right palpebral mass (1). (B) A large right frontal lobe mass is present with posterior displacement of the corpus callosum, posterior and contralateral displacement of the right frontal horn and contralateral displacement of the falx cerebri. Nodular and ring-like calcifications are seen within the mass, which shows partial contrast enhancement and is surrounded by edema (2). Nonenhancing and noncalcified areas represent alveolar hydatid cysts (3). (C) The inner table of the skull (4) is irregular anterior to the mass.