A Case Report of Acute Hemolysis after Endovascular Abdominal Aneurysm Repair with Onyx Embolization of Endoleak: A Clinical Conundrum

Abstract

A 75-year-old gentleman with a large degenerative abdominal aortic aneurysm of diameter 7.5 cm underwent standard endovascular aneurysm repair with Endurant (Medtronic) stent graft. He underwent coil embolization of a small penetrating ulcer in the neck of the aneurysm, followed by liquid embolic agent (Onyx 18) injection in the aneurysm sac in view of endoleak. The procedure was uneventful with <100 mL blood loss. However, in the postoperative period, the patient developed a drop in hemoglobin levels with a rising trend of indirect bilirubin and reticulocyte count—suggestive of acute hemolysis. He was managed conservatively with blood transfusion and recovered well. In this case, the one cause of hemolysis could be mechanical damage to the red blood cells by the bare metal part of the stent and the tortuosity of the iliac vessels. No such previous report of acute hemolysis after aortic stent graft deployment has been previously reported.

Keywords

EVAR - abdominal aortic aneurysms - stent graft - hemolysis

Introduction

Endovascular aneurysm repair (EVAR) is the standard of care for treating abdominal aortic aneurysms, especially in elderly patients (above 75 years) and patients with multiple medical comorbidities.[1] The main complications of EVAR, apart from puncture site–related issues, are postprocedural development of endoleak (EL) and re-interventions.[2] Type I EL is usually managed immediately, while type II EL can be followed up with serial imaging, and intervention is needed if there is an increase in the sac size.[3] We present an infrequent complication of EVAR—hemolytic anemia post-stent graft deployment. This complication has not yet been described for EVAR. However, few case reports of hemolytic anemia after stent graft deployment in transjugular intra-hepatic porto-systemic shunt (TIPSS) have been described in the literature.[4]

Case Presentation

A 75-year-old gentleman with a history of comorbidities, including diabetes, hypertension, dyslipidemia, and a background of cigarette smoking, presented with a 7.5 cm fusiform aneurysm of the infra-renal abdominal aorta ([Fig. 1A]). He has a known history of chronic obstructive pulmonary disease and coronary artery disease, for which he underwent coronary bypass surgery 5 years ago. The aneurysm was incidentally discovered during a routine health check-up, and its size necessitated treatment. Notably, the aneurysm sac was located 20 mm from the lowest renal artery (right renal artery). Additionally, there was a small contrast-filled out-pouching suggestive of a penetrating atherosclerotic ulcer (PAU) at the neck of the aneurysm ([Fig. 1B]). After discussion in the aorta multi-disciplinary team, the patient was evaluated and deemed to be at high risk for surgical repair; therefore, standard EVAR with sac and PAU embolization was planned.

Fig. 1 (A) A large fusi-saccular aneurysm of the infra-renal abdominal aorta. Diagnostic angiogram (B) showing the aneurysm with a small penetrating ulcer in the proximal neck of the aneurysm. After deployment of the Endurant IIS stent graft, angiogram (C) showed persistent filling of the ulcer in the neck (type IA endoleak) and persistent filling of the aneurysm sac. Check angiogram (D) shows no residual opacification of the penetrating ulcer and the aneurysm sac after coiling of the PAU and embolization of the sac using liquid embolic agent. CT angiogram (E) done on the following day after Hb drop shows no evidence of any intra- or retro-peritoneal bleed. CT, computed tomography; PAU, penetrating atherosclerotic ulcer.

Bilateral femoral pre-close technique was done, using three suture-based closure devices (Proglide, Abbott) in both common femoral arteries. A 32 × 166 mm Endurant IIS (Medtronic) stent graft with iliac limbs was deployed. Post-deployment angiography revealed ongoing filling of the sac and proximal PAU, likely attributed to inadequate apposition at the proximal landing zone (see [Fig. 1C]). An Echelon 10 (Medtronic) microcatheter was used to selectively cannulate both the PAU and the aneurysm sac via the brachial access. The PAU was successfully embolized with a single detachable long Concerto (Medtronic) coil, while the sac was treated with approximately 3 mL of Onyx 18 (Medtronic) embolizing agent. The final angiogram indicated no further EL (see [Fig. 1D]). The femoral accesses were closed, and hemostasis in the brachial access was achieved via manual compression. Overall, the intra-procedural blood loss was less than 100 mL.

On the morning of postoperative day (POD) 1, the patient exhibited a significant decrease in hemoglobin (Hb) levels, dropping from 11.9 to 9.1 g/dL. The patient remained asymptomatic and hemodynamically stable, maintaining a blood pressure of 100/70 mm Hg. Sonogram of the access site and abdomen revealed no complications related to access or intra-abdominal or retroperitoneal free fluid. However, by the afternoon of POD 1, there was a further decline in hemoglobin levels to 8.5 g/dL. Computed tomography angiogram yielded unremarkable results with no bleeding or EL ([Fig. 1E]). Two units of packed red blood cells (PRBCs) was transfused. Again, a notable drop in hemoglobin was observed on the morning of POD 2, necessitating a repeat transfusion. Hemoglobin levels stabilized on POD 3, and there were no further transfusion requirements from POD 3 onward (refer to [Table 1]).

Table 1 The temporal course of hemoglobin trend and the blood transfusions

Time	Hb level (gm/dL)
Preprocedural	12.3
Immediate post-procedure	11.8
Postoperative day (POD) 1 morning	9.1
POD 1 afternoon	8.6
2 units of PRBC were transfused
Post-transfusion	10.4
POD 2 morning	8.2
POD 2 afternoon	8.0
Again, 2 units of PRBC were transfused
Post-transfusion	9.6
POD 3 morning	9.7
POD 3 afternoon	10
POD 4	10.2

Abbreviation: PRBC, packed red blood cell.

Laboratory investigations indicated a significant increase in indirect bilirubin, rising from a preprocedural value of 0.5 mg/dL to a post-procedural value of 1.2 mg/dL, accompanied by an isolated elevation of serum glutamic-oxaloacetic transaminase levels ([Table 2]). The post-procedure reticulocyte count was recorded at 2.5% (elevated) and an increased serum lactate level, which collectively suggested acute hemolysis. The patient was observed for an additional 2 days and was ultimately discharged in stable condition on POD 5.

Table 2 Other relevant blood investigations of the patient

Other pertinent laboratory parameters
Iron profile	Normal
Indirect bilirubin	Post-procedural elevation by 1.2 mg/dL
Reticulocyte count	>2.5% (elevated)
LDH	Elevated
Diagnosis: acute hemolysis

Discussion

The most common cause of an acute peri-procedure drop in Hb is usually intra-procedural blood loss.[5] However, blood loss is unlikely here and does not explain hemolysis. Hemolysis post-cardiac valve replacement surgery has been well-documented in the literature. Post-valve surgery, hemolysis can be caused by the shearing force on red blood cells (RBCs), which mechanically breaks them down (schistocytosis), the so-called Waring Blender Effect, and it can also be because of para-valvular leak.[6] [7] In para-valvular leak, a high-velocity regurgitant jet passes through a narrow bottleneck, again causing mechanical injury to the RBCs and subsequent hemolysis.[7]

Similar episodes of hemolysis have also been documented post-TIPSS. Conn introduced the term “naked stent syndrome” for bare metal stents used for TIPSS.[4] Sanyal et al documented an almost 10% prevalence of hemolytic anemia post-TIPSS.[8] They postulated that the fragile RBCs hitting the stent's bare stainless steel metal struts undergo mechanical damage and hemolysis. Sanyal et al also demonstrated how the intra-hepatic part of the TIPSS stent undergoes endothelialization while the intravascular part remains non-endothelialized—so-called naked.[8] Gradually, as covered stents replaced bare metal stents in TIPSS, the prevalence of hemolysis decreased. However, there are still scattered case reports of hemolytic anemia post-TIPSS, even with covered stent grafts.[9] [10]

To our knowledge, hemolysis following aortic stent graft placement has not been previously reported in the literature. This marks our first encounter with hemolysis, after nearly 250 cases of EVAR, encompassing both thoracic and abdominal aneurysms. After excluding blood loss and conducting laboratory investigations that confirmed hemolysis, the most plausible cause in our situation appears to be stent graft-induced. Conceptually, the design of the aortic endograft resembles that of the TIPSS stent graft, where the bare metal component may damage red blood cells, leading to their lysis. Additionally, the graft's bifurcation and the iliac arteries' tortuosity may have further contributed to the mechanical stress. Sanyal et al in their TIPSS study noted that hemolysis is often not significant enough to decrease hemoglobin levels, leading to it frequently going unnoticed.[8] Additionally, genetic heterogeneity in red blood cell membranes of certain individuals makes them inherently fragile and predisposed to a higher risk of breakdown.

An important consideration is whether the intra-aneurysmal injection of the liquid embolic agent may be responsible for hemolysis. Ethylene vinyl alcohol-based liquid embolics have been widely utilized in cerebral circulation, particularly for the embolization of arteriovenous malformations and arteriovenous fistulas. In those cases, the liquid embolic material does not come into direct contact with rapidly flowing blood. However, in our situation, the liquid embolic agent was directly exposed to the high velocity of aortic blood flow. The potential for this to cause hemolysis remains an unresolved question.

Conclusion

To our knowledge, aortic stent graft–induced hemolysis has not been previously described. Management usually involves PRBC transfusion and hemodynamic monitoring till endothelialization happens and there is no further trauma to the blood cells.[9] It is a diagnosis of exclusion, and blood loss–related Hb drop must be ruled out.

Conflict of Interest

None declared.

Author Contributions

A.R.C. drafted the article and prepared images. J.V. edited the draft and images, supervised the work, and finalized the manuscript. A.A. contributed valuable inputs in endovascular management of the patient, edited the draft, and reviewed the manuscript. A.j.A. edited and reviewed the manuscript.

Consent for Publication

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

• References

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Publication History

Article published online:
15 October 2025