Computed tomography–derived liver volume is not detectably lower in dogs with histopathologic findings compatible with primary hypoplasia of the portal vein
Abstract
Objective
To compare CT-derived liver volume and noncontrast attenuation variables between dogs with histopathologic findings compatible with primary hypoplasia of the portal vein (PHPV) and dogs without liver disease.
Methods
Medical records were retrospectively reviewed for dogs with abdominal CT and liver histopathology compatible with PHPV. Controls were 121 dogs without liver disease from a published CT reference cohort and were not matched by breed, age, sex, or body weight. Liver volume was evaluated with allometric regression of log-transformed liver volume on log-transformed body weight and group. A body weight–restricted sensitivity analysis was performed.
Results
26 dogs with PHPV-compatible histopathology and 121 controls were analyzed. Affected dogs were substantially lighter than controls (median body weight, 2.13 vs 38.0 kg). In the primary allometric model, the adjusted geometric mean ratio for liver volume in affected dogs versus controls was 0.887 (95% CI, 0.751 to 1.047; P = .156). The body weight–restricted sensitivity analysis was similar (0.923; 95% CI, 0.769 to 1.107; P = .377). Noncontrast hepatic attenuation did not differ significantly between groups, and qualitative CT abnormalities were uncommon.
Conclusions
After allometric adjustment, CT-derived liver volume was not detectably lower in dogs with PHPV-compatible histopathology. This finding should be interpreted cautiously because groups differed substantially in body weight and closely body weight–matched controls were unavailable.
Clinical Relevance
These findings do not support using absence of CT-detectable microhepatia to exclude PHPV. Computed tomography volumetry should be interpreted with body size, vascular imaging, clinical findings, and histopathology, especially when controls are not closely matched by body weight.
Keywords: computed tomography; dog; hepatic attenuation; portal vein hypoplasia; primary hypoplasia of the portal vein
Primary hypoplasia of the portal vein (PHPV) is a congenital microscopic portal vascular disorder characterized histopathologically by small or absent portal venules within portal tracts.1,2 Similar histopathologic changes can occur secondary to reduced portal blood flow caused by macroscopic vascular disorders; therefore, PHPV cannot be diagnosed by histopathology alone without considering imaging and clinical findings.1 Conditions such as congenital portosystemic shunts, arterioportal fistulae, and portal vein thrombosis or obstruction can produce chronic portal hypoperfusion and may mimic PHPV histologically.1,3–9 As a result, diagnosis of PHPV requires an integrated approach that confirms compatible histopathologic findings while excluding macroscopic vascular abnormalities that could account for secondary portal hypoperfusion.1,2,10
Computed tomography is well suited for this diagnostic role because it allows cross-sectional evaluation of the hepatic parenchyma and portal venous system. Computed tomography angiography has been widely used to identify and characterize congenital portosystemic shunts in dogs and can also help detect arterioportal fistulae and portal vein thrombosis.3–9 In dogs suspected of PHPV, CT can therefore provide important information by excluding macroscopic vascular causes of portal hypoperfusion. In addition, CT permits evaluation of liver size, hepatic contour, parenchymal attenuation, contrast enhancement patterns, and secondary findings such as acquired portosystemic shunts, peritoneal effusion, and lymphadenomegaly. Despite this potential clinical value, CT features of dogs with histopathologic findings compatible with PHPV have not been well characterized.
Liver size in dogs with PHPV remains incompletely defined. Previous imaging studies and case reports11–15 have described variable subjective findings, with microhepatia reported in some dogs with PHPV or related portal vascular disorders, whereas other reports did not identify reduced liver size. These discrepancies may reflect differences in imaging modality, patient body size and conformation, observer subjectivity, and disease severity. Radiography and ultrasonography can be useful clinically, but assessment of liver size with these modalities is often subjective and may be limited by superimposition, operator dependence, or lack of standardized quantitative thresholds.
Computed tomography hepatic volumetry provides a more objective method for quantifying liver volume. In veterinary medicine, CT-derived liver volume has been evaluated in dogs without liver disease and in dogs with congenital portosystemic shunts.16–21 Reference data for CT-based liver volume in dogs without hepatic disease have also been reported.16,17,20 These studies support the use of CT volumetry as a reproducible quantitative approach for evaluating canine liver size. However, CT-derived liver volume has not been specifically compared between dogs with histopathologic findings compatible with PHPV and dogs without liver disease.
In addition to liver volume, noncontrast hepatic parenchymal attenuation may provide information about diffuse hepatic composition or parenchymal change. Computed tomography attenuation has been evaluated in dogs with other hepatic or metabolic disorders, including cirrhosis and hepatic steatosis.22,23 However, whether hepatic attenuation differs between dogs with PHPV and dogs without liver disease is unknown. Similarly, the frequency of ancillary CT findings such as hepatic parenchymal heterogeneity, nodules or mass-like lesions, acquired portosystemic shunts, peritoneal effusion, and hepatic lymphadenomegaly has not been established in dogs with PHPV.
The purpose of this study was to compare CT-derived liver volume, with explicit consideration of body weight, and noncontrast hepatic attenuation variables between dogs with histopathologic findings compatible with PHPV and dogs without liver disease. Secondary objectives were to describe qualitative CT findings in dogs with PHPV-compatible histopathology and to evaluate the influence of body size on CT-derived liver volume by use of allometric regression.
We hypothesized that CT-derived liver volume would be lower in dogs with PHPV-compatible histopathology after body weight adjustment and that noncontrast hepatic attenuation variables would differ between groups.
Methods
Study design
This retrospective comparative cross-sectional study was designed to compare CT-derived liver volume and noncontrast attenuation variables between dogs with histopathologic findings compatible with PHPV and dogs without liver disease. The primary outcome was body weight–adjusted CT-derived liver volume from the allometric regression model. Secondary quantitative outcomes were liver volume-to-body weight ratio, noncontrast hepatic parenchymal attenuation, splenic parenchymal attenuation, and hepatic-to-splenic attenuation ratio. The hepatic-to-splenic attenuation ratio was considered exploratory because splenic attenuation could be influenced by pre- and perianesthetic drugs. Qualitative CT findings in dogs with PHPV-compatible histopathology were recorded descriptively as secondary observations.
Because the control group was derived from a previously published CT reference cohort and was not matched to the PHPV group by breed, age, sex, or body weight, exploratory allometric analyses were planned to evaluate the influence of body weight on CT-derived liver volume. No a priori sample size calculation was performed because this study used all eligible dogs that met the final case definition during the study period.
Ethics statement
This retrospective study used deidentified clinical imaging and medical record data generated during routine patient care, and no animals underwent additional procedures for research purposes. Therefore, IACUC approval was not required.
PHPV case selection
Medical records from a referral veterinary hospital were retrospectively reviewed to identify dogs with available abdominal CT examinations and liver histopathology reports describing PHPV or PHPV-like hepatic vascular abnormalities between February 12, 2019, and November 4, 2024. Dogs were eligible for inclusion in the PHPV group when the original diagnostic histopathology report included an explicit diagnosis of PHPV or a diagnostic interpretation that the microscopic findings were suspicious for or compatible with PHPV, consistent with published descriptions of PHPV and PHPV-like microscopic portal vascular abnormalities.1,2
Liver tissue was obtained by laparoscopic liver biopsy. At least 2 biopsy specimens were collected from separate liver lobes in each dog and submitted for diagnostic histopathologic examination. Histopathologic classification was based on the original diagnostic reports rather than centralized blinded rereview by a single study pathologist. Histopathologic features abstracted from the original diagnostic reports included hypoplasia or narrowing of portal or interlobular veins, hypoplasia or narrowing of central veins, hepatic lobular or hepatocellular atrophy, arteriolar proliferation, venous arterialization, copper staining results when available, and concurrent hepatic lesions. Arteriolar proliferation was recorded but was not required as an isolated inclusion criterion because the case definition was based on the reporting pathologist’s integrated diagnostic interpretation, in conjunction with published descriptions of PHPV, rather than on any single microscopic feature.1,2
Dogs were excluded when CT image quality or patient size precluded reliable hepatic volumetry. Dogs were also excluded when the histopathology report did not meet the prespecified PHPV case definition, including reports with only equivocal, minimal, or nonspecific vascular changes or an alternative primary diagnosis. To reduce the risk of including dogs with secondary portal hypoperfusion caused by macroscopic or clinically relevant vascular disorders, multiphasic CT studies were reviewed for congenital portosystemic shunts, portal vein thrombosis, portal venous obstruction, and macroscopic arterioportal or arteriovenous fistulae. Dogs were excluded when any of these abnormalities were identified. Dogs were also excluded when the histopathology report described venous arterialization or raised concern for arteriovenous shunting.
Control group
The comparison group consisted of 121 dogs without liver disease from a previously published CT reference cohort.20 That cohort was originally assembled to define reference data for CT-derived liver volume in dogs without hepatic disease and included dogs with no clinical history, clinical signs, clinicopathologic abnormalities, or CT findings suggestive of hepatobiliary disease. The control cohort was reused in the present study as a previously assembled reference population rather than as a contemporaneously enrolled, breed-, sex-, age-, or body weight–matched control group. Control data used in the present analysis included body weight, CT-derived liver volume, noncontrast hepatic attenuation measurements, and splenic attenuation measurements when available.
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