Complete parenchymal separation of the left hepatic lobe with intact vascular pedicle after blunt trauma: A rare salvageable American Association for the Surgery of Trauma (AAST) Grade V injury

INTRODUCTION

Blunt hepatic injury typically results from two broad mechanical processes. In inertial force-driven trauma, sudden deceleration generates shearing stress at points where the liver is anchored by its ligaments. In contrast, direct compression forces press the parenchyma against the vertebral column and thoracic cage. In deceleration-related trauma, the difference in mobility between the liver tissue and its fixed attachments often leads to lacerations near the ligamentous insertion sites, most notably along the falciform and triangular ligaments.

Studies examining trauma biomechanics have emphasized the role of ligament anatomy in shaping the pattern and trajectory of liver rupture, particularly in injuries involving the falciform and left coronary ligaments.^1,2 While these observations help explain why certain injury patterns occur, their practical value in guiding operative decision-making remains incompletely defined, and such patterns are still underrepresented in clinical literature.

We present an unusual case of complete separation and rotational displacement of the left hepatic lobe caused by inertial forces, in which the displaced segment remained viable and was successfully preserved by orthotopic repositioning. This case underscores the importance of mechanism-based interpretation of blunt liver injuries and illustrates that major hepatic resection is not inevitable in high-grade ligament-associated injuries when vascular integrity is maintained.

CASE REPORT

A 40-year-old male truck driver, restrained, was involved in a high-speed head-on collision with another truck. He presented five days after the injury with abdominal pain and distension. On arrival, his airway and breathing were unremarkable. His heart rate was 100/min, and his blood pressure was 110/60 mm Hg. The Glasgow Coma Scale (GCS) score was 15. He had multiple abrasions on the chest and abdomen. Generalized abdominal tenderness was present on palpation. Contrast-enhanced computed tomography (CECT) of the torso demonstrated a an American Association for the Surgery of Trauma (AAST) Grade V liver laceration with complete separation of segments II and III along the falciform ligament [Figure 1a and b]. The detached lobe rotated inferiorly almost 270 degrees, yet the arterial supply remained intact. The left hepatic vein was not visualized, and gross hemoperitoneum was noted. Laboratory investigations revealed leukocytosis, mild anaemia, and elevated bilirubin. Although the patient was haemodynamically stable, the presence of a Grade V liver injury with complete rotational displacement of segments II–III and gross hemoperitoneum with probable bilious peritonitis associated with a high risk of delayed vascular compromise prompted early laparotomy.

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Figure 1: Contrast-enhanced computed tomography of the abdomen. (a) Coronal reconstruction demonstrating a deep laceration along the falciform ligament with separation of the left hepatic lobe (arrow). (b) Axial section showing inferior displacement and rotational malposition of liver segments II and III (arrow), consistent with an inertial shear injury pattern, with preserved parenchymal enhancement.

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At laparotomy, bilio-hemorrhagic peritoneal fluid was evacuated. A complete parenchymal fracture on the left of the falciform ligament was noted [Figure 2]. The left lobe, involving segments II and III, was separated and rotated inferiorly [Figure 3]. It was contained by surrounding tissue, including bowel and peritoneal adhesions. Despite the marked rotational displacement, the lobe appeared viable, with preserved color and no evidence of venous congestion or ischemia. There was no active bleeding suggestive of left hepatic vein avulsion, and the hilar pedicle appeared intact. Adhesiolysis was performed, the left lobe was de-rotated, and orthotopic repositioning of the lobe was completed [Figure 4a]. No significant bleeding or major bile leak was noted on the surface of the fractured liver. The bilious peritoneal collection was likely due to small intrahepatic biliary channel disruption along the fractured plane. No major bile duct injury was identified intraoperatively. The parenchyma was sutured with catgut to reconstitute liver continuity, and a local hemostatic agent was placed on the surface [Figure 4b]. The patient was kept in the intensive care unit for two days postoperatively and was discharged on postoperative day eight. No bile leak or signs of sepsis were noted, and no reoperation was required. The ultrasound of the abdomen before discharge did not reveal any gross abdominal collection or significant hepatic parenchymal abnormality. A postoperative CECT was not performed due to the patient’s stable clinical course and uneventful recovery. Follow-up was uneventful, and he resumed regular activity for six weeks.

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Figure 2: Intraoperative view following laparotomy demonstrating a deep hepatic parenchymal fracture with exposed raw surface, consistent with high-grade liver injury.

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Figure 3: Intraoperative photograph showing a deep parenchymal fracture along the left side of the falciform ligament with inferior rotation and displacement of the left hepatic lobe (segments II–III)

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Figure 4: (a) Intraoperative photograph demonstrating adhesiolysis and de-rotation of the displaced left hepatic lobe (segments II–III), following separation from surrounding adhesions and restoration toward its anatomical position. (b) Intraoperative photograph following orthotopic repositioning of the left hepatic lobe, demonstrating anatomical parenchymal repair with suturing of the fracture plane and application of a topical hemostatic agent.

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DISCUSSION

The pattern of liver parenchymal injury is closely related to the characteristics and direction of the blunt force. Inertial forces applied to a partially fixed organ produce a predictable rupture plane. Jin et al., in an analysis of 53 cases, demonstrated that trauma to the right lobe predominantly results from combined acceleration-deceleration and compression forces. In contrast, left-lobe injuries are more often driven by acceleration and vertical shearing.¹ Liver lacerations are consistently located close to the ligamentous attachment sites, which transmit the majority of shearing force. In our case, with an inertia-driven force, the left lobe moves forward. The falciform ligament fixes the liver to the diaphragm and prevents its movement, which caused the laceration and left lobe to rotate. In such inertial injuries, capsular disruption and ligamentous avulsion at fixation points, including the falciform, coronary, and triangular ligaments, may occur depending on the magnitude and direction of force. In our case, the fracture plane was located along the left side of the falciform ligament, consistent with a ligament-based shear mechanism. However, no gross avulsion of major ligamentous attachments or diaphragmatic detachment was observed intraoperatively, suggesting that the injury propagated along the line of fixation without complete ligamentous disruption. Arkuszewski’s autopsy-based analysis identified three types of liver laceration, all located at or near the ligamentous attachment.² Our patient demonstrated Type A (laceration at the ligamentous attachment alone) and Subtype 2 (laceration parallel to the falciform ligament) rupture, with rotation and separation of segments II-III, preserving viability, which is unique. The delayed presentation resulted in partial containment of the displaced lobe by surrounding adhesions, which may have stabilized the rotational displacement. This contrasts with the case reported by Grošek et al., in which a handlebar injury caused a complex left-lobe laceration with pedicle transection and massive bleeding, ultimately requiring more extensive intervention.³ Differences in the vector direction, area of impact, and energy dissipation determine the injury pattern and vascular consequences, which vary among patients. A thorough understanding of these mechanisms is essential for clinical decision-making. Mechanism-driven classification, such as that proposed by Slotta et al. and Arkuszewski, correlates specific patterns of liver injury with higher rates of operative intervention.^2,4 In hemodynamically stable patients, current guidelines favor nonoperative management (NOM) irrespective of American Association for the Surgery of Trauma (AAST) grade, provided that appropriate monitoring, interventional radiology, and 24 hours of operative intervention facility are available.^5-7 NOM is discontinued when the patient has evidence of ongoing bleeding, haemodynamic instability, or peritonitis. We decided to explore the patient in view of gross anatomical displacement with potential dynamic vascular compromise, even when initial arterial inflow was preserved. Given the rotational displacement, there was a significant risk of progressive venous outflow obstruction, torsion-related ischaemia, and delayed necrosis. Exploration allowed us to assess the viability of the liver lobe directly. Additionally, the patient had generalized abdominal tenderness consistent with peritonitis owing to bilio-haemorrhagic fluid and a possible bile leak.

Rotational displacement of left hepatic lobe segments raises concern for potential avulsion of the left hepatic vein or torsion of the left hilar pedicle. However, these were not observed in our case. Despite rotational displacement, the vascular pedicle remained intact, and perfusion was preserved, indicating that this did not represent true hepatic torsion. Intraoperatively, the fracture plane was noted along the left side of the falciform ligament and appeared anatomically separate from the expected course of the left hepatic vein, which typically lies deeper and posterior within the liver parenchyma. Although the vein was not distinctly visualized as a separate structure due to altered anatomy and surrounding tissue changes, the absence of active venous bleeding and preserved viability of the left hepatic lobe suggested that venous outflow was not compromised. It is likely that rotational movement occurred at the level of the parenchymal fracture rather than the hilar structures, thereby preserving vascular continuity.

Modern management algorithms, including World Society of Emergency Surgery (WSES) and Eastern Association for the Surgery of Trauma (EAST) recommendations, therefore prioritize physiology, ongoing blood loss, associated injuries, and resource availability over CT location alone.^7,8 In our case, localization along the falciform ligament predicted a mechanism of the inertial shear but did not, by itself, operate management or NOM. The final choice of anatomical de-rotation and orthotopic repositioning was made after integrating the mechanism, vascular viability, hemodynamic stability, and the feasibility of safe reconstruction.

CONCLUSION

Patterns of blunt liver trauma should always be interpreted in the context of impact mechanics and ligament anatomy, as this helps anticipate which segments and pedicles may be at risk. A detailed understanding of these mechanisms can convert a seemingly catastrophic injury into a salvageable one by directing attention to preserved inflow and outflow and encouraging liver-preserving strategies when feasible. Localization of liver rupture should never be the sole parameter used to decide whether surgical or conservative management should be used. The decision incorporates haemodynamic status, associated injuries, and time-dependent risks, rather than relying solely on localization.