ABSTRACT
Brazil produced approximately 14.9 million metric tons of chicken meat in 2024, according to data from the Brazilian Animal Protein Association. In this production context, ascites syndrome remains an important cause of carcass condemnation and contributes to morbidity and mortality in broiler flocks. This study aimed to characterize cavitary effusions and investigate associated cardiac, pulmonary, and hepatic histopathological lesions in broiler chickens with ascites syndrome. Forty-five carcasses retained on inspection lines due to free abdominal fluid were evaluated, and liver, heart, and lung samples were collected. Ten clinically healthy birds were included as controls. Effusions were aspirated using sterile syringes and transferred to tubes containing EDTA. Tissue samples were fixed in 10% buffered formalin, paraffin-embedded, sectioned at 5 µm, stained with hematoxylin and eosin, and examined by light microscopy. Effusion analysis revealed predominance of protein-poor transudates with a lymphocyte-predominant cytological profile. Histopathological findings were consistent with pulmonary hypertension and secondary hepatic congestion, while cardiac lesions were observed in a subset of cases. These results reinforce the association between ascites syndrome and chronic hemodynamic disturbances in broilers.
Keywords:
ascites syndrome; broiler chickens; histopathology; portal hypertension; pulmonary hypertension
RESUMO
O Brasil produziu aproximadamente 14,9 milhões de toneladas de carne de frango em 2024, segundo dados da Associação Brasileira de Proteína Animal. Nesse contexto produtivo, a síndrome da ascite permanece uma importante causa de condenação de carcaças e contribui para a morbidade e mortalidade em lotes de frangos de corte. Este estudo teve como objetivo caracterizar os derrames cavitários e investigar as lesões histopatológicas cardíacas, pulmonares e hepáticas associadas em frangos de corte com síndrome da ascite. Quarenta e cinco carcaças retidas nas linhas de inspeção devido à presença de líquido livre na cavidade abdominal foram avaliadas, e amostras de fígado, coração e pulmão foram coletadas. Dez aves clinicamente saudáveis foram incluídas como controle. Os derrames foram aspirados com seringas estéreis e transferidos para tubos contendo EDTA. As amostras de tecido foram fixadas em formalina tamponada a 10%, incluídas em parafina, seccionadas a 5µm, coradas com hematoxilina e eosina e examinadas por microscopia óptica. A análise do líquido efusivo revelou predominância de transudatos pobres em proteínas com perfil citológico predominantemente linfocitário. Os achados histopatológicos foram compatíveis com hipertensão pulmonar e congestão hepática secundária, enquanto lesões cardíacas foram observadas em um subgrupo de casos. Esses resultados reforçam a associação entre a síndrome ascítica e distúrbios hemodinâmicos crônicos em frangos de corte.
Palavras-chave:
síndrome da ascite; frangos de corte; histopatologia; hipertensão portal; hipertensão pulmonar
INTRODUCTION
The poultry industry has become one of the most important segments of global meat production, with world chicken meat output exceeding 139.2 million tons in 2022 (Faostat, 2024) and continuing to expand to meet rising demand. Brazil remains a major contributor to this global output, producing an estimated 15 million tons of chicken meat in 2024, corresponding to more than 11% of total world production. Within this high-output sector, ascites syndrome remains one of the main causes of carcass condemnation, resulting in significant economic losses due to mortality and rejection at slaughter. The condition is particularly prevalent in fast-growing commercial broilers and is commonly associated with pulmonary hypertension and right-sided cardiac overload (Ferreira et al., 2022; Li et al., 2022; Muñoz-Gómez et al., 2025).
Intensive genetic selection for rapid growth and improved feed efficiency has increased metabolic demand without proportional cardiopulmonary adaptation, predisposing modern broilers to hypoxia-related disorders, including ascites syndrome (Vaccaro et al., 2022). The resulting hemodynamic imbalance may lead to fluid accumulation in body cavities, hepatic congestion, and cardiac lesions.
Although ascites syndrome has been widely described, integrated analyses correlating cavitary effusion characteristics with concurrent cardiac, pulmonary, and hepatic histopathological findings in slaughtered broilers remain limited. Such characterization is relevant for improving pathological interpretation and supporting inspection-based diagnosis. Therefore, this study aimed to characterize cavitary effusions in broiler carcasses affected by ascites syndrome and to describe associated histopathological lesions in the heart, liver, and lungs.
ETHICAL ASPECTS
The research was submitted to the Ethics Committee on Animal Use of the Farroupilha Federal Institute, and approved under the number 3452130422
MATERIALS AND METHODS
This observational cross-sectional study was conducted after approval by the Animal Ethics Committee of Instituto Federal Farroupilha (protocol no. 3452130422; approval date: April 13, 2022).
Animals and sampling. The study included 55 commercial broiler chickens (Ross and Cobb strains), weighing between 3 and 5 kg, collected from slaughterhouses operating under the State Inspection Service (SIE) in southern Brazil. Sampling was performed during routine post-mortem inspection. Animals were divided into two groups:
G1 (control group): 10 carcasses without macroscopic evidence of cavitary effusion or other lesions leading to condemnation.
G2 (ascites group): 45 carcasses retained on the inspection line due to the presence of free fluid in the abdominal cavity and/or pericardial sac.
Only birds with evident cavitary effusion at post-mortem examination were included in G2. Carcasses presenting advanced autolysis were excluded.
Sample collection and processing. Cavitary fluids were aspirated using sterile 20mL syringes and transferred to tubes containing ethylenediaminetetraacetic acid (EDTA). Samples were stored at 2-8°C and processed within two hours after collection. Fragments of liver, heart, and lung were collected and fixed in 10% buffered formalin. Tissues were routinely processed, paraffin-embedded, sectioned at 5 µm, and stained with hematoxylin and eosin.
Effusion analysis. Effusions were subjected to physical, biochemical, and cytological evaluation according to established cytological criteria for cavitary effusions (Manaswini, 2023), adapted for avian samples. Classification into protein-poor transudate, protein-rich transudate, aseptic exudate, or septic exudate was based on total protein concentration, total nucleated cell count, and cytological findings. Septic exudates were identified by the presence of structures morphologically compatible with bacteria.
Histopathological evaluation. Examination and documentation were conducted in a light microscope (Novel L3000-T) coupled to a computer (Mosaic V2.2 software) for the identification and description of lesions in cardiac, hepatic, and pulmonary tissues.
Statistical analysis. Data was analyzed using descriptive statistics. Absolute and relative frequencies were calculated for histopathological lesions and effusion classifications.
RESULTS
Among the 45 effusion samples analyzed, protein-poor transudates predominated (68.9%; 31/45), followed by protein-rich transudates (20%; 9/45) and aseptic exudates (11.1%; 5/45). No septic exudates were identified. Cytological evaluation revealed a predominance of lymphocytes in 41 samples, whereas mesothelial cells predominated in three samples and heterophils in one.
In the histological evaluation of the lungs (n = 45), 27 samples exhibited moderate to marked hypertrophy of the parabronchial smooth muscle (Fig. 1). Eleven samples showed mild hypertrophy, and seven showed no evidence of hypertrophy. Marked congestion was observed in 12 samples, moderate congestion in 17, and mild congestion in seven; nine samples showed no evidence of congestion.
Cartilaginous nodules were identified in 13 samples (nine mild and four moderate). Moderate perivascular hemorrhage was observed in two samples, and mild multifocal hemorrhage in one (Fig. 2). Moderate hyperplasia of the parabronchial epithelium was observed in six samples (Fig. 1), and moderate metaplasia in five.
Marked hypertrophy of the parabronchial smooth muscle (asterisk) and epithelial hyperplasia (arrowhead). Objective 20×, Haematoxylin-eosin stain.
Moderate perivascular hemorrhage in lung tissue (arrowhead). Objective 10×, Haematoxylin-eosin stain.
One lung sample showed focal necrosis with negative images suggestive of fungal hyphae, consistent with granulomatous fungal pneumonia. In the control group, five birds presented congestion, four exhibited parabronchial smooth muscle hypertrophy, and one showed connective tissue thickening of the parabronchus. All samples from both groups presented at least one anatomopathological lesion. Pulmonary lesions according to the type of cavitary effusion are presented in Table 1.
In the heart, mild to marked epicardial thickening was observed in 9/45 samples (20%), characterized by fibrin deposition and mixed inflammatory infiltrate composed of lymphocytes, macrophages, and heterophils, consistent with fibrinous pericarditis (Fig. 3). Seven cases were associated with protein-poor transudates and two with aseptic exudates; no cases were associated with protein-rich transudates.
One additional sample showed focal moderate interstitial fibrosis associated with moderate cardiomyocyte atrophy and epicarditis (Fig. 4). No cardiac lesions were identified in the control group.
Moderate epicardial thickening in the organizing phase (arrowhead). Objective 4×, Haematoxylin-eosin stain.
Marked epicarditis with expanded epicardium (arrowhead), fibrin deposition and inflammatory infiltrate (asterisk). Objective 4×, Haematoxylin-eosin stain.
The liver exhibited the greatest diversity of lesions. Of the 45 samples, two showed mild capsular thickening and 14 marked thickening. One sample showed marked inflammatory infiltrate and four moderate infiltrates. Diffuse hepatocellular swelling was observed in four samples, and mild swelling in one (Fig. 5). Three samples presented focal cholangitis, one of which was associated with bile duct necrosis.
Hepatocytes with moderate diffuse cellular swelling. Objective 40×, Haematoxylin-eosin stain.
Focal necrosis with hepatocyte loss and deposition of amorphous proteinaceous material resembling fibrin (arrowhead). Objective 20×, Haematoxylin-eosin stain.
Three samples exhibited focal hepatocellular necrosis with cell loss (Fig. 6). Mild congestion was observed in three samples, moderate congestion in five, and centrilobular congestion in two. In the control group, four liver samples showed no significant lesions, except for one presenting a moderate number of microgranulomas. Hepatic lesions according to the type of cavitary effusion are presented in Table 2. Most birds exhibited more than one histopathological lesion within the same organ.
DISCUSSION
The predominance of protein-poor transudates (68.9%) observed in this study corroborates previous descriptions of ascitic fluid in broilers affected by pulmonary hypertension syndrome, in which increased hydrostatic pressure secondary to right ventricular dysfunction is considered the principal mechanism of fluid accumulation (Wang et al., 2022; Shafi et al., 2025a; Shafi et al, 2025b). The absence of septic exudates further supports the predominantly hemodynamic nature of the effusions identified.
Cytologically, lymphocyte predominance was observed in most samples. Although erythrocytes and mesothelial cells are frequently reported in avian cavitary effusions, lymphocytic predominance has also been described in chronic, non-septic effusions and may reflect prolonged fluid persistence rather than active inflammation (Dzialo et al., 2023). The low frequency of heterophil-predominant samples is consistent with the limited number of exudative processes identified.
Protein-rich transudates (20%) and aseptic exudates (11.1%) were identified in a smaller proportion of birds. These findings suggest that, although hydrostatic imbalance predominated, additional factors such as mild inflammatory stimulation or vascular permeability alterations may have contributed in some cases. However, the absence of microbiological analysis limits definitive interpretation of the exudative component.
Pulmonary histological findings were characterized mainly by parabronchial smooth muscle hypertrophy and congestion. The high frequency of these lesions aligns with established descriptions of pulmonary vascular remodeling in ascitic broilers, in which sustained pulmonary hypertension induces structural adaptation of vascular and parabronchial walls (Guo et al., 2023; Shafi et al., 2025a). The predominance of these lesions in birds presenting protein-poor transudate reinforces the association between pulmonary vascular alterations and hydrostatic effusion formation.
Cartilaginous nodules were detected across different effusion types, suggesting that their occurrence is not exclusively dependent on the nature of the cavitary fluid. Their presence in both transudative and exudative profiles indicates that they may represent chronic structural adaptation rather than acute inflammatory response.
Cardiac lesions were less frequent than pulmonary alterations. Epicardial thickening compatible with fibrinous pericarditis was observed in 20% of cases, predominantly associated with protein-poor transudates. Although right ventricular hypertrophy is classically described in ascites syndrome, only microscopic alterations were evaluated in this study, which may explain the lower frequency of cardiac findings compared to reports emphasizing gross pathology (Julian et al., 1987; Wang et al., 2022).
In the liver, capsular thickening and congestion were the most frequent lesions, supporting the concept of passive venous congestion secondary to right-sided circulatory impairment (Ezzulddin, 2023; Shafi et al., 2025a). The distribution of hepatic lesions among effusion types suggests that vascular compromise plays a central role in hepatic involvement. Hepatocellular necrosis and cellular swelling were observed in a limited number of cases, indicating that parenchymal injury was less prominent than circulatory disturbance.
Fibrin deposition and inflammatory infiltrates were occasionally identified in hepatic tissue. However, without microbiological or molecular investigation, it is not possible to determine whether these findings reflect secondary infectious processes or non-specific inflammatory reactions.
Cholangitis and granulomatous lesions were observed in isolated cases. Given the absence of microbiological or etiological investigation, these findings cannot be directly attributed to ascites syndrome and may instead reflect unrelated inflammatory or infectious processes, including possible ascending biliary infection or chronic focal inflammatory responses occurring independently of the primary cardiopulmonary alterations.
Overall, the findings of this study indicate that cavitary effusions in broilers were predominantly hydrostatic in origin and closely associated with pulmonary vascular alterations and secondary hepatic congestion. Inflammatory lesions were present but not predominant, reinforcing the central role of cardiopulmonary dysfunction in the pathogenesis of fluid accumulation in this cohort.
CONCLUSION
Cavitary effusions in broiler chickens were predominantly characterized as protein-poor transudates, with a lower frequency of protein-rich transudates and aseptic exudates. Pulmonary lesions were mainly represented by parabronchial smooth muscle hypertrophy and congestion, while hepatic alterations were characterized predominantly by capsular thickening and vascular congestion. Cardiac lesions were less frequent and consisted primarily of epicardial thickening compatible with fibrin deposition. Inflammatory alterations were identified in a limited number of cases. The distribution of histopathological findings indicates that cavitary effusions in the evaluated birds were primarily associated with pulmonary and hepatic circulatory disturbances.
REFERENCE
- DZIALO, M.; BRYLA, A.; DEMORANVILLE, K.J. et al Concerted phenotypic flexibility of avian erythrocyte size and number in response to dietary anthocyanin supplementation. Front. Zool., v.20, n.9, 2023.
- EZZULDDIN, T.A. Ascites in broiler: updates. J. Appl. Vet. Sci., v.8, p.23-29, 2023.
- FERREIRA, H.M.; VIEIRA, F.T.; GOMIDE, A.T.M. et al Condenação de carcaças de frangos de corte por síndrome ascítica em um abatedouro-frigorífico no Estado do Espírito Santo, Brasil. Ars Vet., v.38, p.91-93, 2022.
- FAOSTAT: crops and livestock products - poultry meat production. Rome: FAO, 2024.
- GUO, D.; ZHANG, J.; YUFENG, H. et al Transcriptomic study on the lungs of broilers with ascites syndrome. Animals, v.13, p.175, 2023.
- JULIAN, R.J.; FRIARS, G.; FRENCH, H. et al The relationship of right ventricular hypertrophy, right ventricular failure, and ascites to weight gain in broiler and roaster chickens. Avian Dis., v.31, p.346-354, 1987.
- LI, L.; QIUFENG, J.; LINGLI, C. et al Changes in the expression of macrophage migration inhibitory factor (MIF) and key enzymes of energy metabolism in the myocardium of broiler chickens with ascites syndrome. Animals, v.12, p.2488, 2022.
- MANASWINI, R. Ascitic fluid cytology - rewarding tool in the discovery of unknown. Ann. Clin. Cytol. Pathol., v.11, p.45-52, 2023.
- MUÑOZ-GÓMEZ, V.; SHAW, A.; ABDYKERIMOV, K. et al Economic impact of chicken diseases and other causes of morbidity or mortality in backyard farms in low- and middle-income countries: a systematic review and meta-analysis. BMC Vet. Res., v.21, n.151, 2025.
- SHAFI, M.; BABA, O.K.; MIR, S.M. et al Exploring pathology of ascites in broiler chickens reared in cold climatic conditions of central Kashmir. Int. J. Adv. Biochem. Res., v.9, p.200-207, 2025a.
- SHAFI, M.; KHAN, S.S.; MIR, S.M. et al Pathological evaluation of naturally occurring ascites syndrome in broilers: a case series from Kashmir Valley. Int. J. Biol. Sci., v.7, p.25-33, 2025b.
- VACCARO, L.A.; PORTER, T.E.; ELLESTAD, L.E. The effect of commercial genetic selection on somatotropic gene expression in broilers. Front. Physiol., v.13, p.935311, 2022.
- WANG, E.; LI, Q.; SONG, W. et al Pathogenesis and prevention of ascites syndrome in broilers. Animal Health Perspectives, v.2, p.273-279, 2022. (Cap.35).












