Hepatic hydatid cyst disease in low- and middle-income countries: Spectrum of imaging findings and complications

Abstract

Hepatic hydatid cyst disease is a significant public health issue in endemic low- and middle-income countries, and imaging plays a pivotal role in diagnosis, classification, management, and follow-up. In resource-limited settings, ultrasound (US) is often the imaging modality of choice, with computed tomography (CT) and magnetic resonance imaging (MRI) usually reserved for complex or atypical cases. This pictorial review illustrates the characteristic and atypical imaging features of hepatic hydatid cysts across US, CT, and MRI, emphasizing practical imaging approaches applicable in low- and middle-income countries. US features include daughter cysts, hydatid sand, and detached membranes, whereas CT provides a more detailed assessment of cyst morphology, calcifications, and complications. MRI offers superior soft-tissue contrast and improved evaluation of biliary involvement and complex disease. Important complications include exophytic growth, rupture, transdiaphragmatic thoracic involvement, perforation into hollow viscera, peritoneal seeding, biliary communication and abdominal wall invasion. The US based World Health Organization-Informal Working Group on Echinococcosis classification is also illustrated, highlighting its role in guiding treatment and follow-up. A structured, image-based approach using available modalities enables accurate diagnosis and effective management, whereas pictorial recognition of key imaging features facilitates early detection and improved outcomes in resource-limited settings.

Key Words: Hydatid cyst; Liver; Imaging; Ultrasound; Computed tomography; Magnetic resonance imaging; Echinococcosis; Complications

Core Tip: Hepatic hydatid disease is highly prevalent in low- and middle-income countries, where imaging is central to diagnosis, staging, and management. This pictorial review demonstrates the spectrum of imaging findings across ultrasound, computed tomography, and magnetic resonance imaging, emphasizing practical, resource-adapted interpretation. Key typical and atypical features, complications, and characteristic radiologic signs are illustrated alongside the World Health Organization-Informal Working Group on Echinococcosis classification to reinforce standardized staging. By focusing on commonly available modalities and real-world diagnostic challenges, this review aims to improve recognition, guide treatment decisions, and enhance diagnostic accuracy, particularly in low- and middle-income countries.

INTRODUCTION

Hydatid disease (HD), or cystic echinococcosis (CE), is a parasitic infection caused by the larval stage of Echinococcus tapeworm. The two primary forms of hepatic HD are CE caused by Echinococcus granulosus, which is characterized by well-defined hepatic cystic lesions (CLs); and the less common but more aggressive alveolar echinococcosis caused by Echinococcus multilocularis which presents as an infiltrative, “tumor-like” mass[1]. HD remains endemic in many low- and middle-income countries (LMICs), particularly in regions where livestock farming and close contact with dogs facilitate transmission, including the Mediterranean Basin, the Middle East, Africa, South America, and parts of Asia[1,2].

Humans are usually infected by ingesting parasite eggs through contaminated food or direct contact with infected dogs. After ingestion, embryos penetrate the intestinal mucosa, enter the portal circulation, and lodge in the liver, where they develop into hydatid cysts. Cysts grow slowly, reaching approximately 1 cm in the first six months and enlarging by approximately 2-3 cm annually; however, in some cases rapid growth rates of up to 4-5 cm per year have been documented[2,3]. The liver is the most frequently involved organ, representing the first filter of the portal circulation but the involvement of other locations in virtually all parts of the body has been described[4-7].

In this pictorial review, we illustrate the spectrum of imaging findings and local complications of hepatic HD based on surgically and laboratory confirmed cases encountered at our institution over the past decade.

IMAGING APPROACH TO HEPATIC HD

Radiologic imaging is the cornerstone for the diagnosis of hepatic CE, whereas serology plays a supportive role. Imaging not only confirms the presence of hydatid cysts but also characterizes morphology, viability, and complications, which directly guide management[8,9].

Ultrasound (US) is generally the first-line modality for screening, staging, and follow-up due to its availability, cost-effectiveness, and suitability for resource-limited settings such as Pakistan. The rise of affordable, portable US devices now allows these examinations to be performed at the point of care, even in isolated rural communities[10]. It enables the identification of characteristic features including daughter cysts, membranes, and calcifications, which form the basis of the World Health Organization-Informal Working Group on Echinococcosis (WHO-IWGE) and Gharbi classification systems that reflect cyst activity and guide treatment[11].

Although US remains the cornerstone of diagnosis and staging in LMICs due to its accessibility and cost-effectiveness, computed tomography (CT) and magnetic resonance imaging (MRI) play complementary roles in evaluating complex disease, complications, extrahepatic extension, and preoperative planning. Accordingly, this review emphasizes US for routine diagnosis while illustrating the additional value of cross-sectional imaging when available. CT is superior for defining anatomy, detecting calcification, and evaluating complications such as rupture, infection, and extrahepatic spread, and is particularly useful for surgical planning[12,13]. However, its performance in precise staging is limited compared with that of US or MRI due to lower soft tissue contrast leading to misclassification. MRI provides excellent soft tissue detail and is especially useful for assessing biliary or neural involvement and differentiating hydatid cysts from simple cysts, although it is less sensitive for detecting calcification[12]. Additionally, diffusion-weighted imaging and fluid attenuation inversion recovery sequences can also reliably differentiate hydatid cysts from simple hepatic cysts[14].

IMAGING FEATURES OF HEPATIC HD

Hepatic hydatid cysts typically appear as well-defined CLs with a fibrous capsule and may contain internal daughter cysts or detached membranes, which are characteristic imaging features[12]. The cyst wall is composed of three layers: The outermost pericyst, which is a product of the host’s inflammatory response and contains inflammatory cells; the exocyst, which is the outer, acellular, protective layer of the parasite itself; and the innermost endocyst, which contains proliferating cells that produce daughter cysts and cyst fluid[15].

On US, hydatid lesions appear as well-defined anechoic avascular cysts, which may be unilocular or multivesicular, with a double-line sign (visualized as two echogenic lines with an intervening hypoechoic layer)[16], internal hydatid sand, daughter cysts, or detached membranes (“water lily sign”), and possible rim calcification[17]. If wall calcifications are present, they can present as hyperechoic rims with posterior acoustic shadowing.

CT reveals well-defined CLs with fluid-to-complex attenuation, internal septations, daughter cysts, membranes, and calcification, and is particularly useful for detecting complications[18,19]. CT further adds value by demonstrating distinct morphological patterns that correlate with pathological stages, including unilocular cystic, multivesicular, collapsed inner wall, partially solidified, solidified, and calcified types, as well as complicated forms[20]. Additionally, hydatid cysts may present atypical patterns, such as exophytic growth; multicystic confluent lesions; or complicated cysts that rupture into the biliary tree, peritoneum, or thoracic cavity[21,22].

MRI usually shows variable T1/T2 signals depending on the cyst content, a hypointense T2 rim representing the pericyst, and characteristic appearances of daughter cysts (attached to the periphery of the endocyst with relative T1 hypointensity to the mother cyst matrix) and low-signal detached membranes (“snake sign”)[18].

The exact morphology varies depending upon the stage of evolution of the cyst. Typically, these cysts start off as simple, fluid-filled unilocular cysts, producing multiple daughter cysts as they mature. Once the parasite dies, the cyst membranes detach and the cyst eventually solidifies or calcifies[23]. This morphological variation is the basis for classifying hydatid cysts into distinct categories, each of which is defined by unique imaging characteristics.

Classification and stage-specific radiologic features of hepatic hydatid cysts

Several imaging-based classification systems have been proposed for hepatic CE. For routine clinical practice, particularly in LMICs, the WHO-IWGE classification is the preferred system because it classifies cysts according to their US morphology, reflects biological activity, and directly guides treatment selection and follow-up[24]. The Gharbi classification, introduced in 1981, was the first widely adopted US-based staging system and remains useful for interpreting older literature[25]. Accordingly, the WHO-IWGE classification forms the basis of current clinical management, while the Gharbi classification is usually used for historical context and comparison.

Historical US classification: Gharbi system

Before the WHO-IWGE classification, Gharbi et al[25] classified hepatic hydatid cysts according to their US morphology. The system comprises five types: Type I - purely fluid-filled unilocular cysts; type II - cysts with detached membranes (“water-lily sign”); type III - multivesicular cysts containing daughter cysts (“honeycomb” appearance); type IV - heterogeneous pseudo-solid cysts; and type V - cysts with thick calcified walls producing posterior acoustic shadowing. Although largely superseded by the WHO-IWGE classification, the Gharbi system remains valuable for interpreting historical literature and in educational pictorial reviews. The WHO-IWGE stages correlate approximately with the Gharbi types, with CE1 corresponding to Gharbi I, CE2 to Gharbi III, CE3a to Gharbi II, CE4 to Gharbi IV, and CE5 to Gharbi V, while additionally providing information on cyst activity and management, including suitability for interventions such as percutaneous aspiration, injection and reaspiration (PAIR)[3].

WHO-IWGE classification

The WHO-IWGE classification categorizes hepatic hydatid cysts into five stages (CE1-CE5) based primarily on US morphology, reflecting the biological activity and natural evolution of the parasite (Figure 1)[24]. CE1 and CE2 represent active cysts with viable protoscolices, CE3 cysts are transitional, and CE4 and CE5 are considered inactive stages. Owing to its close correlation with cyst viability and treatment strategy, the WHO-IWGE classification is the current standard for staging, therapeutic decision-making, and follow-up.

Figure 1 Ultrasound images showing the World Health Organization–Informal Working Group on Echinococcosis classification of hydatid cysts (cystic echinococcosis 1-3). A: Cystic echinococcosis (CE) 1 hydatid cyst with the presence of echogenic fine “hydatid sand” (arrows); B: CE2 hydatid cysts with the presence of peripheral daughter cysts (arrows); C: Internal detached membranes within a CE3a-type cyst (arrows); D: CE3b hydatid cysts with internal membranes, daughter cysts and a central solid maternal matrix (arrows).

The CL stage represents the earliest, undifferentiated stage in this classification. These are anechoic uniloculated cysts- with no echoes or internal septations- and are difficult to differentiate from simple hepatic cysts by imaging.

CE1 cysts (Gharbi I) represent the early active stage. US typically reveals an anechoic, well-defined cyst containing fine echogenic particles known as “hydatid sand”, which shift with patient position and settle rapidly within the cyst fluid (“falling snowflakes” sign) (Figure 1A). This “sand” basically represents freed scolices and brood capsules of the parasite, which can be confirmed by microscopic evaluation of hydatid fluid aspirate to provide a definitive diagnosis[26]. On CT, these cysts appear as unilocular homogeneous water-attenuating, thick-walled lesions with smooth margins without any internal septations or calcifications. Larger cysts occasionally demonstrate pseudo-wall enhancement due to compression of adjacent hepatic tissue (Figure 2). In contrast, true wall enhancement, typically observed in superinfections, tends to be thicker or more irregular and is often accompanied by surrounding inflammatory changes such as adjacent hepatic edema, fat stranding, or intracystic gas. On MRI, CE1 cysts typically present homogeneous low signals on T1-weighted sequences and high signals on T2-weighted sequences. A defining characteristic is the “rim sign”, which is a thin, peripheral, T1 and T2 hypointense rim that represents the host's fibrotic reaction[27].

Figure 2 Cystic echinococcosis 1 hydatid cyst. A and B: Ultrasound and images showing a lobulated cystic lesion in the right lobe of the liver with a well-defined wall (arrow in A) and an echogenic nodule at its base (arrow in B), most likely corresponding to cystic echinococcosis 1 with hydatid sand; C: Axial computed tomography image depicts a non-specific low-attenuation cyst (arrow) with subtle pseudo-enhancement, highlighting the superior sensitivity of ultrasound for characterization of early-stage disease.

CE2 cysts (Gharbi III) correspond to the multivesicular active phase. During this stage, the germinal layer actively proliferates to produce daughter cysts that contain viable protoscoleces[28]. US usually reveals a multiloculated CL with internal septa and multiple daughter cysts, producing a “honeycomb” appearance (Figure 1B). On CT, daughter cysts appear embedded within a higher-density maternal matrix. Subtypes include type IIA (peripheral daughter cysts), which have a “spoke wheel appearance”; type IIB (large daughter cysts occupying most of the mother cyst which have a “rosette” appearance); and type IIC (with a relatively high-density maternal matrix). These subtypes reflect the progressive maturity of the cyst[10]. MRI reveals daughter cysts as hypo- or isointense relative to the maternal matrix on T1- and T2-weighted images.

CE3 cysts represent transitional cysts, showing early degeneration. CE3a (Gharbi II) features detached endocyst membranes, producing the classic “water-lily sign” also known as the “camalote sign” on US and CT (Figure 1C and Figure 3)[12]. CE3b is characterized by daughter cysts within a partially solid or collapsed maternal matrix (Figure 1D). The solidified matrix appears echogenic on US and demonstrates increased attenuation on CT. MRI reveals mixed signal intensity depending on the amount of proteinaceous debris and daughter cyst composition. The “snake sign” or “double line sign” has been used to describe detached, floating membranes with low signals on all sequences (Figure 4)[18]. These cysts are at risk for rupture or superinfection and require careful follow-up.

Figure 3 Cystic echinococcosis 3a hydatid cyst. A-C: Ultrasound image, and axial and coronal computed tomography images revealing the characteristic water lily sign indicative of detached membranes of a cystic echinococcosis 3a hydatid cyst (arrows).

Figure 4 Magnetic resonance images of two patients with hepatic hydatid cysts. A and B: Axial T2-weighted (A) and coronal T2-weighted (B) images showing the T2 hypointense endocyst (arrows) giving a “double line” sign; C and D: Axial T2-weighted (C) and coronal T2-weighted image (D) from another patient with a large hydatid cyst in the right lobe of the liver showing the double line sign (arrows) and heterogeneous central T2 signal intensity.

CE4 cysts (Gharbi IV) are degenerative cysts that undergo fibrosis and early calcification[9]. US shows heterogeneous echogenicity without daughter cysts (Figure 5A and B). Calcifications are visualized as hyperechoic foci with posterior acoustic shadowing. CT reveals a heterogeneous, solid lesion with mixed attenuation and no definite cystic areas. The cyst wall is often irregular with the development of calcification (Figure 5C and D). MRI shows variable signal intensity. Subtle calcifications can be identified as drop-out signals on susceptibility-weighted imaging. CE4 cysts are generally inactive and uncommonly develop acute complications. When present, complications are usually related to mass effect or secondary infection rather than intrinsic cyst activity. Rarely, inactive CE4 cysts may demonstrate reactivation, with progression to an active or transitional stage, most commonly resembling CE3b morphology[29].

Figure 5 Cystic echinococcosis 4 hydatid cysts. A and B: Ultrasound images from two different patients showing a cystic echinococcosis 4 degenerative hydatid cyst in the right lobe of the liver (arrows) with a heterogeneous appearance on ultrasound with mixed echoes and no definite daughter vesicles; C and D: Axial (C) and coronal (D) images reveal the characteristic cystic echinococcosis 4 hydatid cyst with crumpled membranes and calcifications (arrows).

CE5 cysts (Gharbi V) are inactive cysts with extensive calcification. US shows calcified, hyperechoic walls with posterior acoustic shadowing. CT usually demonstrates total ring-like wall calcification, matrix calcification, or curvilinear calcifications of internal membranes (Figure 6). On MRI, these heavily calcified cysts demonstrate low signal intensity on all sequences[27]. These cysts are considered dead and rarely require intervention.

Figure 6 Cystic echinococcosis 5 hydatid cyst disease. A: Ultrasound image showing a cystic echinococcosis 5 hydatid cyst with dense peripheral calcification revealing posterior acoustic shadowing (arrow); B: Computed tomography axial image showing a densely peripherally calcified cyst in the liver (arrow); C: Ultrasound image of another patient with a type V hydatid cyst in the right lobe of liver showing marked posterior acoustic shadowing (arrow); D: Computed tomography axial image shows a densely calcified lesion in the right lobe of the liver (arrow) corresponding to a calcified inactive hydatid cyst.

LOCAL COMPLICATIONS OF HEPATIC HYDATID CYSTS

Mass effect

Hepatic hydatid cysts can lead to a range of local complications, which are particularly important in active type I and II cysts because of their growth potential. Mass effect is a common consequence of large cysts compressing adjacent structures and has been reported to be the most common radiological complication in up to 38% of cases[19]. Compression of vascular structures, particularly the portal vein (Figure 7), may result in atrophy of the affected lobe and compensatory hypertrophy of the uninvolved liver. Similarly, large cysts can cause biliary duct dilatation either by extrinsic compression or by perforation into the ducts[21].

Figure 7 Magnetic resonance images showing mass effect of a hydatid cyst on the portal vein. A and B: Axial T2-weighted images showing a cystic lesion in the liver compressing the bifurcation of the intrahepatic portal vein (arrow in A). The cyst has a T2 hypointense rim (arrow in B); C and D: Axial T1 pre-contrast (C) and axial T1 post-contrast (D) images show some T1 hyperintensity within the cyst (arrow in C) with mild pericystic enhancement (arrow in D).

Biliary complications

Biliary involvement is one of the most common and important complications of hepatic hydatid cysts. Large cysts can compress nearby bile ducts, causing obstruction, dilatation, or cholestasis, whereas cyst rupture into the biliary system can lead to direct communication (Figure 8). The rupture risk increases with size, and 80% of cysts more than 7.5 cm in size rupture into the bile ducts[30]. Microerosion from pressure may lead to the formation of small fistulas, whereas wide perforations allow the contents of the cyst - including hydatid sand, daughter cysts, or germinal membranes - to enter the biliary tree, causing obstruction and jaundice. Small biliary communications may be difficult to detect on imaging (Figure 9), but MR cholangiography can demonstrate ducts entering the cyst, and US or CT may reveal dilated ducts with echogenic or high-density intraluminal material[22,31,32].

Figure 8 Computed tomography images of a patient with biliary hydatid disease. A: Axial computed tomography (CT) image showing moderate intrahepatic biliary dilatation (arrow); B: Axial CT image shows at least three well-defined cystic lesions present in the liver and porta hepatis (arrow), consistent with hydatid cysts; C: Coronal CT image shows extension of hydatid disease into the common bile duct, likely due to biliary rupture with extrahepatic biliary dilatation (arrow).

Figure 9 Biliary complications of hydatid cyst. A: Ultrasound images show a large characteristic case of cystic echinococcosis 3a hydatid cyst disease with internal floating membranes (arrows); B: A fluoroscopic exam performed after catheter placement and the percutaneous aspiration injection and reaspiration procedure shows opacification of the biliary tree, suggesting a fistula with biliary communication (arrow); C: Axial computed tomography image shows a large cyst in the right lobe of the liver (arrow); D: Coronal computed tomography image showing floating internal membranes within the cyst (arrow).

Rupture and peritoneal seeding

Rupture of hydatid cysts can be internal (contained), communicating, or direct. Internal rupture occurs when the endocyst detaches from the pericyst but the outer wall remains intact; this rupture is often observed in degenerating or treated cysts- and signals parasite death. Communicating rupture involves the passage of cyst contents into the biliary tract and is observed in type I, II, and IV cysts. Direct rupture, where both the endocyst and pericyst breach, can cause peritoneal dissemination, anaphylaxis, or secondary disease[21,22]. Rupture is more likely in subcapsular cysts due to the minimal surrounding tissue (Figure 10).

Figure 10  Hydatid cyst disease with rupture and transdiaphragmatic spread. A and B: Axial computed tomography (A) and coronal computed tomography (B) images showing subcapsular rupture of hydatid disease in the right lobe of the liver involving segment VII (arrow in A) with transdiaphragmatic extension into the ipsilateral right thoracic cavity (arrow in B).

Imaging may reveal floating membranes (water-lily sign) on US or CT, and serpentine or tubular structures in the biliary tree on US or MR. Finally, peritoneal seeding (Figure 11) is usually secondary to hepatic cyst rupture, surgery, or trauma. Peritoneal HD is often multiple and asymptomatic until large, with an overall incidence of approximately 13% in patients with abdominal HD. CT and MRI are valuable for assessing the entire peritoneal cavity and identifying cysts of varying stages[33,34].

Figure 11  Hydatid cyst disease with intraperitoneal dissemination. A-C: Axial, coronal and sagittal computed tomography images showing at least two hydatid cysts with daughter cysts with a typical rosette appearance in the left and right lobes of the liver (arrows in A). Coronal and sagittal sections show diffuse dissemination of hydatid disease into the peritoneum (B and C).

Presence of fat and gas

Although uncommon, some hepatic hydatid cysts may contain macroscopic fat or fat-fluid levels. Two main mechanisms have been suggested: Degeneration of hydatid membranes as part of the natural aging process - or as an indirect sign of cyst - biliary communication. On CT, fat within the cyst may appear as low-attenuation globules or as a fat-fluid level[21,35].

Secondary (superinfection) infection of hydatid cysts is often secondary to rupture. Infected cysts display thickened, enhancing walls on CT and MRI, with patchy enhancement of adjacent hepatic parenchyma. Gas or air–fluid levels within the cavity are best detected via CT (Figure 12). Importantly, intracystic gas is not specific for infection and may also be seen following prior interventions such as surgery, PAIR, or aspiration procedures[36,37]. On MRI, the presence of diffusion restriction within the cyst contents may suggest superimposed purulent infection; however, diffusion-weighted imaging findings in infected hydatid cysts have not been systematically validated, and restricted diffusion may also be encountered in degenerative (CE4) hydatid cysts[38].

Figure 12  Fat and gas within hydatid cyst disease. A and B: Computed tomography (CT) axial and coronal CT images showing a focal fat density lobule within the hydatid cyst in the right lobe of the liver (arrows); C and D: Axial CT sections from two different patients showing air specks and air-fluid levels within the hydatid cyst (arrows). This was iatrogenic due to surgical deroofing of the cyst in C and due to superinfection of the cyst in D.

Exophytic growth

Exophytic growth occurs via the bare area of the liver or gastrohepatic ligament, allowing the extension of the cyst into the thoracic or peritoneal cavities. Transdiaphragmatic spread into the lung, mediastinum, or even heart occurs in 0.6%-16% of cases, most commonly from cysts in the posterior right lobe[39]. Imaging may reveal diaphragmatic elevation, pleural effusion, atelectasis, or consolidation. Direct migration produces an hourglass-shaped cyst crossing the diaphragm, best appreciated on coronal or sagittal MRI. Cyst perforation into the lung can cause parenchymal consolidation, bronchial fistula, or expectoration of cyst membranes, whereas pleural involvement can lead to empyema or multiple pleural cysts[36]. Additionally, there may be exophytic extension and involvement of the abdominal wall (Figure 13)[40].

Figure 13  Hepatic hydatid disease with exophytic involvement of the abdominal wall. A: Computed tomography axial image showing a multicystic hydatid cyst in the right lobe of the liver involving segments IV and V (arrow); B and C: Axial and sagittal computed tomography images showing extension of the lesion from the subcapsular location of the liver and into the anterior abdominal wall (arrows).

POSITRON EMISSION TOMOGRAPHY/CT IN HEPATIC HD

Positron emission tomography/CT is not routinely used for the diagnosis of hepatic HD but may be useful in selected cases with suspected superinfection, atypical imaging features, or equivocal disease activity. Active or infected cysts may demonstrate mild-to-moderate fluorodeoxyglucose uptake, whereas inactive or calcified cysts typically show no significant uptake (Figure 14); a characteristic “doughnut sign” has also been described in the literature[41]. Positron emission tomography/CT may additionally aid in detecting extrahepatic disease. However, its role in LMICs is limited by cost and availability, and US, CT, and MRI remain the primary imaging modalities.

Figure 14  Positron emission tomography/computed tomography images of hydatid cysts in two patients. A: Plain computed tomography (CT) axial image showing a cystic lesion with wall calcification (arrow); B: Fused positron emission tomography/CT axial image shows no evidence of fluorodeoxyglucose activity within the lesion (arrow); C: Plain CT axial image shows another hydatid cyst in segment VI of the liver with peripheral calcification (arrow); D: Fused positron emission tomography/CT axial image shows no corresponding fluorodeoxyglucose activity (arrow).

RADIOLOGICAL MANAGEMENT OF HEPATIC HYDATID CYSTS

Radiological intervention plays a key role in the management of hepatic hydatid cysts, particularly in patients who are poor surgical candidates or in resource-limited settings. Generally, cysts less than 5 cm in size are considered for medical management with albendazole, whereas larger cysts are often considered for intervention[42,43]. Percutaneous drainage under US or CT guidance allows controlled evacuation of the contents of the cyst, minimizing the risk of rupture and anaphylaxis[44]. The PAIR technique - puncture, aspiration, injection, and re-aspiration - involves cyst puncture, aspiration of fluid, instillation of a scolicidal agent (most commonly 95% ethanol or 20% hypertonic saline), and removal of residual contents (Figure 15)[45]. PAIR is most effective in treating CE1 and selected CE2 cysts, whereas calcified or completely inactive cysts (CE4-CE5) are generally not suitable. Scolicidal agents should be used with caution, and cystobiliary communication should be excluded (e.g., by aspiration of bile or contrast injection) before instillation to avoid severe biliary complications such as chemical or sclerosing cholangitis[45-47].

Figure 15  Percutaneous aspiration injection and reaspiration procedure fluoroscopic images. A 15-year-old girl presented with cystic echinococcosis 2 hydatid cysts in the right lobe of the liver and was diagnosed via ultrasound. Fluoroscopic images from percutaneous puncture, aspiration, injection and reaspiration performed for the management of hydatid cysts with post-procedure film. The cavity was rinsed with 100 mL of 20% hypertonic saline multiple times, and 20 mL of absolute alcohol was also injected into the cyst after aspiration. A: Aspiration; B: Injection; C: Reaspiration; D: Post-procedure film.

Imaging guidance is crucial for accurate needle placement, avoiding vascular or biliary structures, and for monitoring complications such as infection, bleeding, or biliary communication. Follow-up imaging with US or CT is used to assess cyst resolution, recurrence, or residual daughter cysts. In select cases, radiological interventions may serve as adjuncts to surgery, reduce cyst size preoperatively, or provide definitive therapy in high-risk patients, emphasizing the critical role of imaging in both diagnosis and minimally invasive management[48].

IMAGING DIFFERENTIALS OF HEPATIC HYDATID CYSTS

The imaging appearance of hepatic HD may overlap with several cystic hepatic lesions, particularly in early or complicated stages (Table 1). CE1 cysts may closely mimic simple hepatic cysts on CT because of similar fluid attenuation; however, simple cysts lack any internal architectural evolution or complexity and show no associated stage-related changes at follow-up, whereas hydatid cysts may demonstrate progressive structural changes over time. US may be particularly valuable in differentiating the two[49].

Table 1 Imaging differentials of hepatic hydatid disease with key distinguishing imaging features.

Differential diagnosis	Key differentiating imaging features
Simple hepatic cyst	Homogeneous water attenuation, thin smooth wall, no enhancement, no calcification, no septations or evolution on follow-up
Pyogenic liver abscess	Thick irregular rim enhancement, diffusion restriction, perilesional inflammatory edema, possible intralesional gas, clinical fever/right upper quadrant pain
Amoebic liver abscess	Solitary lesion with shaggy/ill-defined wall, peripheral enhancement, surrounding inflammatory changes, clinical fever/right upper quadrant pain
Cystic metastases	Irregular wall thickening with enhancing solid components, heterogeneous internal architecture, often known primary malignancy
Biliary cystic neoplasm	Multiloculated cystic lesion with enhancing septations and mural nodules or papillary projections
Hydatid disease	Cystic lesion with variable internal architecture depending on stage, typically without dominant solid enhancing components or aggressive inflammatory features

Hepatic abscesses typically show thick, irregular rim enhancement with diffusion restriction, perilesional inflammatory edema, and possible intralesional gas, reflecting active infection, features not observed in uncomplicated HD. Unlike hydatid cysts, they lack internal daughter cysts and membranes and typically have ill-defined, shaggy, irregular walls. Abscesses also show surrounding parenchymal inflammatory changes, such as a hypoechoic halo on US or low-attenuation edema on CT[50,51].

Cystic or necrotic hepatic neoplasms such as metastases and biliary cystadenoma/cystadenocarcinoma are suggested by the presence of enhancing solid components, mural nodules, multiloculations and internal septations, which are uncommon in HD and favor a neoplastic etiology[52,53].

Alveolar echinococcosis (AE), caused by Echinococcus multilocularis, is an important, although less common, differential diagnosis. Unlike CE, AE typically presents as an ill-defined, infiltrative hepatic mass with numerous small cystic spaces within a heterogeneous solid matrix, often mimicking a slow-growing malignancy. Distinguishing features include the absence of a well-defined capsule, irregular central necrosis, coarse or punctate calcifications, biliary or vascular invasion, and adjacent organ extension. On CT and MRI, AE usually demonstrates minimal or peripheral enhancement, with a low-signal-intensity peripheral fibrotic rim on T2-weighted MRI and, in some cases, delayed peripheral fibroinflammatory enhancement[54,55].

CHALLENGES IN LMICs

LMICs face a unique set of challenges that significantly influence the imaging-based diagnosis and characterization of hepatic HD. These regions often have a relatively higher disease burden due to increased exposure to livestock and close contact with dogs, which serve as definitive hosts in the life cycle of Echinococcus granulosus[56,57]. Limited access to advanced imaging modalities, such as CT and MRI, results in a heavy reliance on US, which, although cost-effective and widely available, is inherently operator-dependent and subject to variability in interpretation[19,58]. This is further compounded by the absence of standardized imaging protocols, including inconsistent application of classification systems such as those proposed by the World Health Organization[59].

Additionally, the lack of structured screening programs and poor healthcare accessibility, particularly in remote areas, contribute to delayed clinical presentation, with patients often presenting at advanced stages characterized by large, complex, or complicated cysts. Financial constraints also limit access to follow-up imaging, hindering adequate monitoring of disease progression and treatment response[57,59]. Collectively, these factors not only complicate accurate diagnosis but also shape the spectrum of imaging findings observed in LMICs and endemic regions, with a higher prevalence of advanced and atypical presentations than in high-income settings.

CONCLUSION

Hepatic hydatid cysts exhibit a wide spectrum of imaging appearances, reflecting their stage, activity, and potential complications. A combined understanding of WHO-IWGE and Gharbi classification, along with descriptive CT/MRI morphology enables accurate diagnosis, staging, and management. US remains the primary modality for detection and follow-up, particularly in LMICs, while CT and MRI provide complementary information on cyst morphology, calcification, daughter cysts, biliary involvement, and local or distant complications. Recognition of mass effect, biliary communication, rupture, infection, exophytic growth, transdiaphragmatic spread, and peritoneal seeding is essential for guiding treatment and preventing morbidity. Familiarity with these imaging patterns allows radiologists to provide comprehensive assessment, optimize patient management, and improve outcomes in endemic regions.