A case of blunt liver injury with rare hemodynamics: traumatic outflow block

Abstract

Background

Non-operative management (NOM) has become the standard of care for blunt solid organ injury, with angioembolization (AE) playing a key role in achieving hemostasis, particularly in liver trauma. Although the dual blood supply to the liver provides relative protection against ischemia, AE can disrupt this balance and lead to major hepatic necrosis (MHN), a life- threatening complication associated with significant morbidity and mortality. Early identification of patients at risk of developing MHN is critical but remains challenging. While treatment strategies for MHN have been explored, early predictive markers, especially angiographic findings, remain underreported and are not yet established in the literature. We report a rare intrahepatic hemodynamic phenomenon observed on angiography that may serve as an early predictor of MHN.

Case presentation

A 32-year-old man sustained a Grade III liver injury predominantly involving the left hepatic lobe following a motor vehicle collision. Contrast-enhanced CT showed hepatic parenchymal injury with hemoperitoneum. Although no active extravasation was observed, contrast enhancement was noted in the left portal vein branch during the arterial phase. Selective angiography via the left hepatic artery revealed parenchymal enhancement of the left hepatic lobe, followed by retrograde opacification of the left portal vein branch. Notably, contrast did not proceed into the left hepatic vein, suggesting impaired hepatic venous outflow. This hemodynamic pattern, characterized by trans-sinusoidal arterial-to-portal flow without venous drainage, can be termed traumatic outflow block (TOFB), a phenomenon not previously reported in trauma. Despite this atypical flow pattern, AE was performed using gelatin sponge particles. The patient subsequently developed abdominal pain and fever, and CT showed non-perfusion of the lateral liver segment. Emergency surgery confirmed massive hepatic necrosis and lateral segmentectomy was performed. Intraoperatively, there were no observable lacerations or disruptions of the portal vein or hepatic veins. However, the liver parenchyma near the root of the left hepatic vein exhibited substantial contusion and hematoma, suggesting possible venous compression. The patient made an uneventful recovery and was discharged on postoperative day nine.

Conclusions

TOFB is a novel angiographic finding suggestive of hepatic venous congestion and may serve as an early predictor of MHN after embolization. While therapeutic strategies for TOFB remain undefined, early recognition of this hemodynamic pattern could guide selective embolization, prompt monitoring and potentially improve outcomes in patients with severe liver trauma.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12245-025-00979-0.

Background

Over the last 30 years, non-operative management (NOM) has become essential for treating blunt solid organ injuries. Angioembolization (AE) is highly effective in achieving hemostasis for liver trauma, often preventing invasive surgery) [1, 2].

The liver’s dual blood supply from two distinct vascular systems makes it resistant to ischemia [3]. However, severe liver trauma can damage parenchyma, bile ducts, and vessels, limiting peripheral blood flow. In severe liver injury, AE increases the risk of ischemia, and major hepatic necrosis (MHN) is a serious complication. MHN occurs in 16% of embolized liver injuries, requires surgery in 74% of cases, and carries a mortality rate of 11% due to bleeding, infection, or organ failure [4]. It also necessitates interventions like drainage, leading to higher transfusion needs and longer hospital stays [2]. Early identification of MHN is crucial for improving AE outcomes.

While strategies for MHN treatment have been discussed [4, 5], early predictive markers remain underexplored. We experienced a very rare intrahepatic hemodynamic finding on angiography of severe liver injury leading to MHN after embolization. Traumatic outflow block (TOFB) has not been previously reported in liver injury and could be an early predictive finding for MHN.

Case presentation

A 32-year-old man was involved in a frontal motor vehicle collision. He had no history of liver disease and was not taking any oral anticoagulant or antiplatelet medications. Upon arrival at the hospital, his vital signs were stable: respiratory rate 19 breaths/min, heart rate 74 beats/min, blood pressure 114/69 mmHg, and oxygen saturation 100% while receiving 10 L/min of oxygen. In the initial treatment room, the patient’s cardiovascular status was stable, and a traumatic pan CT scan was performed.

A contrast-enhanced CT scan revealed a Grade III [6] liver injury predominantly affecting the left lobe (Fig. 1a, arrow), along with hemoperitoneum. Although no definite extravasation was observed in the arterial phase, contrast enhancement was noted in the left branch of the portal vein (Fig. 1a, arrowhead) in addition to the hepatic artery. No definitive evidence of portal vein injury was observed in the portal phase (Fig. 1b).

Fig. 1.

a Contrast-enhanced CT findings(arterial phase) Liver injury predominantly affects the left lobe (arrow) with hemoperitoneum, consistent with a Grade IIIb injury accompanied by capsular disruption. In the arterial phase, contrast enhancement is observed in the left branch of the portal vein (arrowhead). b Contrast-enhanced CT findings(portal venous phase) Coronal image in the portal venous phase demonstrating no apparent disruption or extravasation of the portal vein. The mid-portion of the splenic vein appears less conspicuous due to contrast timing rather than true vascular disruption. No evidence of splenic veins or pancreatic injury was observed Figure༒;Angiographic findings Retrograde contrast flow from left lateral superior portal vein branch (P2) into left main portal vein branch after staining of liver parenchyma (see Additional file 2)

Emergency transarterial embolization findings

Angiography of the celiac artery and selective angiography of the posterior lateral branch of the left hepatic artery (A2) did not reveal any arterial extravasation. However, after enhancement of the hepatic parenchyma, contrast was observed flowing retrogradely from the left lateral superior portal vein branch (P2) into the left main portal vein branch (Fig. 2, see Additional files 1, 2). Notably, contrast did not opacify the left hepatic vein, suggesting impaired hepatic venous drainage and the presence of trans-sinusoidal arterial-to-portal shunting. Embolization was performed using a microcatheter positioned selectively in the A2 and A3. Uniformly cut gelatin sponge particles (approximately 1 mm in size) were administered until angiographic stasis was observed in both branches, confirming vascular occlusion.

Fig. 2.

Angiographic findings. Retrograde contrast flow from left lateral superior portal vein branch (P2) into left main portal vein branch after staining of liver parenchyma (see Additional file 2)

Postoperative course

CT on postoperative day 1 showed enlargement and non-perfusion in the lateral hepatic segment (Fig. 3). The patient complained of upper abdominal pain accompanied by fever, raising suspicion of major hepatic necrosis (MHN) and biliary peritonitis. Emergency surgery was performed, during which necrosis of the lateral segment of the liver was confirmed (Fig. 4), and a sectionectomy༈S2 + S3༉ was carried out. The patient’s general condition subsequently improved, and he was discharged on postoperative day 9.

Fig. 3.

CT on the day after IVR. Swelling of the lateral area of the liver and poorly contrast-enhanced area were observed, and massive hepatic necrosis was suspected

Fig. 4.

Intraoperative findings. Ischemic findings were observed on the lateral side of S2 and S3 of the liver. A laceration extending to the falciform membrane was also observed

Discussion

In cases of liver trauma involving the vasculatures such as injury to the hepatic artery, portal vein, or hepatic vein, the distribution of contrast medium during imaging can aid in characterizing the lesion as extravasation, contrast blush, or pseudoaneurysm. These findings are indicative of vascular injury and typically necessitate prompt hemostatic intervention. These CT findings are very clearly delineated, and the choice of AE or surgical approach is based on vital signs and coagulation status.

This case report introduces a new hepatic hemodynamic concept: Traumatic Outflow Block (TOFB). TOFB occurs when the hepatic vein is compressed or injured by a hematoma, leading to arterial blood flowing into the portal vein. In this condition, the arterial blood, with no drainage route, eventually flows into the portal vein. While the outflow block phenomenon is recognized in liver transplant complications and Budd-Chiari syndrome [7, 8], it has not been described in trauma. Our case represents TOFB, a unique hemodynamic condition (Fig. 5 Table 1).

Fig. 5.

Hemodynamic patterns in the liver: normal and pathological conditions. Schematic representation of hepatic hemodynamics under different conditions. a Normal liver: portal venous inflow and hepatic venous outflow are well-balanced. b Budd-Chiari syndrome: hepatic venous outflow obstruction (dark blue) causes portal congestion and collateral flow. c Hepatic compartment syndrome (HCS): subcapsular hematoma compresses hepatic parenchyma, leading to reduced portal inflow. d Traumatic outflow block (TOFB): parenchymal compression and venous outflow impairment lead to retrograde portal venous flow after arterial infusion

Table 1.

List of conditions that cause hepatic venous congestion. Comparative features of Budd-Chiari syndrome, hepatic compartment syndrome, and traumatic outflow block (TOFB)

	Budd-Chiari Syndrome	HCS	TOFB
Onset	Chronic or subacute	Subacute or early postoperative phase	Acute (early phase of trauma)
Etiology	Thrombosis of hepatic veins or IVC, often involving central veins	Subcapsular hematoma or postoperative parenchymal swelling	Compression of hepatic veins by laceration or hematoma
Capsular integrity	Intact	Intact	Often disrupted
Imaging modality	Doppler ultrasound, CT, MRI	CT, IVC pressure measurement	Angiography
Treatment	Decompression (e.g., stenting, thrombolysis, surgical shunting)	Decompression (surgical or percutaneous drainage)	Hemostasis (embolization or conservative management)
Clinical implication	Portal hypertension, ascites, hepatic insufficiency	Risk of acute liver failure due to impaired perfusion	Predictor of major hepatic necrosis

A comparison is made between Budd-Chiari syndrome and hepatic compartment syndrome, which are regarded as analogous conditions to traumatic outflow block (TOFB). TOFB manifests during the acute phase of trauma and is caused by venous compression. In contrast, Budd-Chiari syndrome has a chronic course and HCS involves compression of not only the hepatic veins but also the bile ducts. Furthermore, the diagnostic tests and intervention methods required for a definitive diagnosis vary

HCS Hepatic Compartment Syndrome, TOFB Traumatic outflow block

The hemodynamics underlying TOFB is hepatic venous congestion. This phenomenon is hemodynamically similar to the partial hepatic vein occlusion attempted in the treatment of hepatocellular carcinoma. The procedure was to intentionally occlude the hepatic vein in the tumor control area with a balloon, allowing the portal vein to function as a drainage route, and then perform arterial embolization to lose the dual supply [9, 10]. The hemodynamics of TOFB are similar, with arterial embolization being the risk of hepatic infarction. TOFB can occur without hepatic venous injury, often due to compression from a hematoma. As shown in Fig. 6, in this case the injury and hematoma were near the root of the hepatic vein and the venous congestion caused by this injury is thought to have caused the TOFB.

Fig. 6.

Contrast-enhanced CT findings (on arrival). The hematoma and contusion indicated by the red dotted line are compressing the right hepatic vein inflow, as indicated by the blue dashed line

Diagnosis of TOFB based solely on CT imaging in arterial and venous phases is unreliable. Dynamic liver CT with three-phase imaging may help but is impractical in acute trauma. Factors such as shunt flow rate, patient blood pressure during CT, and timing of imaging complicate interpretation, making definitive TOFB diagnosis challenging from static CT images. In contrast, angiography is highly effective for TOFB diagnosis. Characteristic angiographic features include [1] clear opacification of distal hepatic arterial branches during the arterial phase [2], prolonged and diffuse parenchymal staining in the intermediate phase, and [3] retrograde opacification of the portal vein in the venous phase. This dynamic pattern reflects trans-sinusoidal arterial-to-portal shunting caused by hepatic venous outflow obstruction, typically due to perivenous hematoma or congestion. Close observation of contrast flow during hepatic arteriography is therefore essential for recognizing TOFB (Fig. 2 and Additional files 1, 2).

In this case, although there was no clear evidence of bleeding in the AE, TAE was performed because CT findings showed a ruptured capsule and intra-abdominal bleeding. The feasibility of embolization needs to be investigated, but the results suggest that TOFB is a predictive finding for MHN. In the cases of TOFB, obstruction occurs in the veins distal to the sinusoids, resulting in blood flow refluxing through the hepatic parenchyma and subsequently entering the portal vein. Within the portal vein, a collision occurs between the hepatopetal portal blood and the hepatofugal arterial blood. In the event of arterial blood being stopped by AE in this situation, it causes ischemia in the occluded hepatic vein unless the portal vein blood flows into the hepatic parenchyma. While hemostasis is the primary goal of AE, the recognition of TOFB—especially when accompanied by retrograde portal vein opacification—may warrant a more conservative and individualized approach. In the absence of active extravasation, deferring embolization should be considered, as the combination of TOFB and portal reflux theoretically increases the risk of major hepatic necrosis. If embolization is deemed necessary, targeting the most distal arterial branches feasible, rather than proximal embolization, may help preserve hepatic viability. TOFB may thus serve as a critical angiographic sign guiding embolization strategy in hepatic trauma.

In the setting of hepatic trauma, another condition very similar to TOFB is hepatic compartment syndrome (HCS). HCS is a rare condition characterized by parenchymal hypertension (> 10–15 mmHg), leading to reduced portal flow and subsequent compression of the hepatic veins [11]. The consequences of HCS are serious, as evidenced by the association of this condition with acute liver failure and hepatic necrosis because of reduced arterial blood flow [12, 13]. It has been documented that HCS can also occur after blunt abdominal trauma and, even though rare, in the early postoperative period after liver transplantation [14]. Typical HCS occurs in cases without hepatic capsular disruption or during the subacute phase when a capsule-like structure, such as a subcapsular hematoma, has formed. The pathophysiology of HCS involves increased intra-parenchymal pressure, which leads not only to compression of hepatic veins but also to reduced portal venous inflow. In contrast, TOFB is observed in the very early phase of hepatic trauma and can also occur in cases with capsular disruption. Thus, TOFB differs from HCS in both the timing of onset and the underlying hemodynamic mechanism. Nonetheless, both conditions share a final common pathway of hepatic ischemia due to impaired outflow and congestion (Fig. 5; Table 1).

Unlike HCS, which represents an emergency state requiring definitive therapeutic intervention due to ongoing hepatic injury, TOFB is considered an angiographic finding that may serve as a predictor of impending hepatic infarction. Although there is currently no established evidence-based intervention strategy for cases in which TOFB is observed, it should at least be recognized as a critical finding indicative of potential progression to MHN.

Recognition of TOFB should not directly prompt surgery but rather guide closer monitoring and earlier imaging, including laboratory tests and ultrasound when appropriate. In our case, surgery was undertaken only after clinical signs of infection and worsening abdominal symptoms, along with imaging evidence of hepatic infarction. Surgical decisions should be based on both TOFB and clinical deterioration, not TOFB alone.

Conclusion

TOFB, caused by venous congestion from hematoma compression or injury, is difficult to diagnose on static imaging but can be identified AE. Its presence may predict MHN following embolization. When TOFB is identified, clinicians should consider deferring embolization if there is no active extravasation. If AE is performed, distal embolization and close follow-up may reduce the risk of MHN. TOFB may serve as a key factor in guiding trauma management.

Abbreviations

NOM

Non-operative management

AE

Angioembolization

MHN

Major hepatic necrosis

TOFB

Traumatic outflow block

HCS

Hepatic compartment syndrome

Authors’ contributions

KS is the lead author, contributing to the study design, data collection, and manuscript writing. JU and NH reviewed the cases and contributed to the execution of the study. All authors were involved in the analysis and interpretation of the data and have read and approved the final manuscript.

Funding

No funding was received for this study.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and accompanying images.

Competing interests

The authors declare no competing interests.