Successful management of acute intraoperative hyperkalemia during huge liver cancer resection following neoadjuvant chemotherapy: a case report

Introduction

Although intraoperative hyperkalemia caused by necrotic tumor cells as a consequence of neoadjuvant chemotherapy (NAC) for hepatic tumors is relatively rare, it might lead to fatal complications, such as lethal arrhythmias (1). We report here a case of acute intraoperative hyperkalemia in a patient who underwent NAC for a huge hepatocellular carcinoma (HCC), with the development of tumor bleeding prior to surgery. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-213/rc).

Case presentation

A 68-year-old male (170 cm, 62 kg) with a medical history of hepatitis C was admitted for management of HCC. Contrast-enhanced computed tomography revealed a huge HCC measuring 16 cm in diameter located in the right hepatic lobe. Since three courses of NAC with atezolizumab and bevacizumab resulted in partial tumor cell necrosis and intratumoral hemorrhage, we decided to urgently perform right hemi-hepatectomy (laparotomy) (Figure 1). Preoperative laboratory findings included a serum potassium (K⁺) level of 4.8 mmol/L (reference range, 3.6–4.8 mmol/L), blood urea nitrogen of 20.6 mg/dL (reference range, 8–20 mg/dL), creatinine of 0.8 mg/dL (reference range, 0.6–1.1 mg/dL), uric acid of 3.9 mg/dL (reference range, 3.0–7.0 mg/dL), aspartate aminotransferase of 114 U/L (reference range, 13–30 U/L), alanine aminotransferase of 76 U/L (reference range, 10–42 U/L), lactate dehydrogenase of 199 U/L (reference range, 120–245 U/L) and an indocyanine green retention rate at 15 minutes of 16% (reference value, <10%).

Figure 1 Preoperative imaging of the hepatic tumor. (A) Contrast-enhanced CT one month before surgery showed a huge hepatocellular carcinoma measuring 16 cm in diameter in the right hepatic lobe. (B) Non-contrast CT performed immediately before surgery demonstrated the same tumor with intratumoral hemorrhagic components. CT, computed tomography.

Following the establishment of a peripheral venous catheter in the left forearm, an epidural catheter was inserted via the T9/10 inter-vertebral space, and a mixture of 5 mL of 0.2% ropivacaine and 100 µg of fentanyl was administered via the epidural catheter. Subsequently, 60 mg of propofol and remifentanil at a rate of 0.3 µg/kg/min were administered intravenously for anesthesia induction. After confirming loss of consciousness, 50 mg of rocuronium was administered to facilitate tracheal intubation. An arterial blood line was then placed into the left radial artery for continuous blood pressure (BP) monitoring. Intraoperative anesthesia was maintained with 1.5% sevoflurane and remifentanil at a rate of 0.1–0.2 µg/kg/min. Arterial blood gas analysis performed immediately after the start of surgery revealed no evidence of hyperkalemia (Table 1). However, during manipulation of the hepatic tumor and ligation of tumor-feeding vessels, the K⁺ level increased to 6.2 mmol/L, as measured by blood gas analysis. Suspecting spurious results due to potential hemolysis during blood sample collection, a repeat arterial blood gas analysis was carefully conducted, which revealed a further increase in K⁺ level to 6.3 mmol/L (Table 1). Immediate treatment for hyperkalemia was initiated with slow intravenous administration of glucose-insulin (GI) (10 g of glucose and 2 units of insulin), along with calcium supplementation due to the risk of arrhythmia (Figure 2). Considering the potential for ischemia-reperfusion injury and exacerbation of hyperkalemia associated with the Pringle maneuver (PM), which refers to temporary occlusion of both the hepatic artery and portal vein during hepatic resection, the PM was avoided. Bleeding was managed by meticulous surgical and anesthetic techniques, including selective ligation of tumor-feeding vessels, the administration of restricted intravenous fluids to maintain a low central venous pressure, and use of hemostatic agents. Intraoperatively, phenylephrine was infused at 0.5–1 mg/h to maintain mean BP above 60 mmHg. Due to preoperative anemia, 6 units of red blood cells were transfused intraoperatively using a potassium adsorption filter (Kawasumi potassium adsorption filter, Kawasumi Laboratories, Tokyo, Japan). At the end of surgery, his K⁺ level had decreased to 4.6 mmol/L. The total operative time was 436 minutes, and anesthesia time was 506 minutes. Total fluid input was 4,170 mL (including 1,320 mL of transfused blood), estimated intraoperative blood loss was 4,790 mL (including preoperative bleeding and ascites), and urine output was 230 mL. No electrocardiographic changes or alterations in urine color were observed during surgery. Postoperatively, the patient was extubated after confirming the return of spontaneous respiration and transferred to the high-care unit. He was transferred to the general ward on postoperative day (POD) 4. No deterioration in renal function was observed postoperatively. Although the patient developed a stress-related gastric ulcer, which was managed appropriately, he was discharged in an ambulatory condition on POD 33. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Figure 2 Intraoperative clinical course. Trends in serum potassium levels, BP, HR, and interventions such as GI over the course of surgery are shown. ART, arterial blood pressure; BP, blood pressure; GI, glucose-insulin therapy; HR, heart rate; K⁺, serum potassium; SpO₂, peripheral capillary oxygen saturation; SYS-DIA, systolic blood pressure-diastolic blood pressure.

Discussion

Reportedly, tumor lysis syndrome (TLS) might occur in hepatic tumors due to necrosis of hepatocytes following procedures such as radiofrequency ablation or transarterial chemoembolization (2). However, the occurrence of hyperkalemia during open surgery that is attributed to TLS following chemotherapy remains relatively uncommon. In the present case, intraoperative hyperkalemia was considered to be a consequence of partial tumor cell necrosis, likely triggered by two factors: the presence of intratumoral hemorrhage following NAC, and the massive size of the tumor (16 cm in diameter) (Figure 1). Furthermore, during hepatic surgery, various surgical maneuvers might reduce hepatic blood flow, causing ischemic necrosis of hepatocytes (3). In addition, surgical manipulation, such as ligation of feeding vessels and compression of the liver, might have promoted the release of K⁺ from necrotic tumor tissue in this case. Subsequently, the released K⁺ might have entered the systemic circulation via surrounding venous structures, contributing to the rapid increase in serum K⁺ by 1.3 mmol/L within approximately two hours from the start of surgery. Since exclusion of TLS was a consideration in evaluating the cause of hyperkalemia in this case, we ideally should have measured intraoperative phosphorus and uric acid levels to more definitively rule out the diagnosis of TLS. However, the rapid clinical course and focus on immediate stabilization limited our ability to obtain a full panel of biochemical markers intraoperatively.

In standard hepatic resections, temporary occlusion of the hepatic artery and portal vein, i.e., the PM, is commonly employed to reduce intraoperative bleeding (4). However, this technique might induce ischemia-reperfusion injury in hepatocytes, potentially exacerbating hyperkalemia through additional K⁺ release from ischemic liver tissue (5,6). Previous animal studies demonstrated that hepatic blood flow occlusion induces hyperkalemia due to K⁺ release secondary to ischemia (7). Given the risk of fatal cardiac arrest due to worsening hyperkalemia, we intentionally avoided use of the PM following the detection of hyperkalemia in this case, based on a combined decision by the surgical and anesthesia teams. Additionally, transfusion of packed red blood cells might also contribute to hyperkalemia due to hemolysis (8). This could also contribute to hyperkalemia, particularly when large volumes of stored blood are rapidly transfused. In the present case, a potassium adsorption filter was utilized during transfusion, which likely prevented further exacerbation of hyperkalemia (9). Although aggressive fluid therapy is often employed to enhance renal perfusion in cases of hyperkalemia, fluid administration was intentionally restricted during the surgery in this case to avoid elevation of hepatic venous pressure and minimize bleeding during liver resection. The reduced urine output observed intraoperatively might have been a contributory factor to the hyperkalemia; however, the patient did not develop acute kidney injury, and no subsequent deterioration in renal function was observed during his postoperative course.

In recent years, systemic drug (chemo) therapies for advanced HCC have expanded, and the number of cases undergoing NAC with the aim of tumor shrinkage or downstaging has been increasing (10). While TLS is a known complication of chemotherapy, particularly in hematologic malignancies such as Burkitt lymphoma, it is relatively rare in the treatment of solid organ tumors (11). Moreover, the occurrence of hyperkalemia during hepatic resection following NAC for HCC is extremely rare. As the use of systemic drug therapies continues to increase, the number of patients undergoing NAC is expected to increase. In such cases, particularly when signs of necrosis of hepatocytes, such as hemorrhage, are present, meticulous perioperative management becomes essential.

The risk factors for TLS include tumor type and characteristics, host-related factors, preexisting renal insufficiency, dehydration, and metabolic abnormalities (12). TLS is diagnosed based on the Cairo-Bishop criteria, which emphasize a combination of laboratory findings—such as marked elevations in uric acid, potassium, and phosphate levels—and clinical features, including acute renal failure. In cases with tumor lysis tendencies induced by NAC and when the tumor size is huge, as in the present case, patients are considered to be at high clinical risk for TLS (13). However, TLS typically develops within 12 to 72 hours after initiation of treatment. Therefore, while the mechanism of hyperkalemia is similar to TLS (tumor cell lysis and release of intracellular potassium), the biochemical profile and clinical context in this patient do not meet the full diagnostic criteria for TLS. Treatment of TLS requires intravenous hydration, correction of metabolic abnormalities, management of renal impairment, administration of uric acid-lowering agents, continuous electrocardiographic monitoring, and blood tests every 6 to 8 hours. During surgery, monitoring of electrocardiographic changes, urine output, color, and blood gas analysis provides useful information. In this case, continuous electrocardiographic monitoring was performed throughout the surgery. Particular attention was paid to detecting electrocardiographic changes suggestive of hyperkalemia, such as peaked T waves, QRS widening, or arrhythmias. Fortunately, no such abnormalities were observed during the period of elevated K⁺ levels. Several studies show that the risk of arrhythmias rises when K⁺ exceeds 6.0 mmol/L, with life-threatening events more likely above 7.0 mmol/L (14,15). Management of hyperkalemia involves prompt intervention to prevent complications: GI, calcium supplementation, and renal replacement therapy, such as hemodialysis or hemofiltration, when renal function deteriorates and to identify its cause (Table 2).

Conclusions

In conclusion, we encountered a case of rapidly developing hyperkalemia during surgery for a huge HCC exhibiting tumor necrosis following NAC. Cases of considerable tumor size and preoperative administration of chemotherapy carry a potential risk of acute electrolyte disturbances, such as hyperkalemia. Therefore, vigilant intraoperative monitoring of electrolytes, electrocardiography, and the appropriate selection of surgical techniques are essential for early detection and timely therapeutic intervention.

Acknowledgments

The authors appreciate and thank the patient and the Keijinkai Hospital operating room staff.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-213/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-213/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-213/coif). I.K. serves as an unpaid editorial board member of AME Case Reports from May 2025 to December 2027. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Mirrakhimov AE, Ali AM, Khan M, et al. Tumor Lysis Syndrome in Solid Tumors: An up to Date Review of the Literature. Rare Tumors 2014;6:5389. [Crossref] [PubMed]
2. Lehner SG, Gould JE, Saad WE, et al. Tumor lysis syndrome after radiofrequency ablation of hepatocellular carcinoma. AJR Am J Roentgenol 2005;185:1307-9. [Crossref] [PubMed]
3. Siu J, McCall J, Connor S. Systematic review of pathophysiological changes following hepatic resection. HPB (Oxford) 2014;16:407-21. [Crossref] [PubMed]
4. Romano F, Garancini M, Uggeri F, et al. Bleeding in Hepatic Surgery: Sorting through Methods to Prevent It. HPB Surg 2012;2012:169351. [Crossref] [PubMed]
5. Kato M, Sawada T, Kita J, et al. Erythropoietin ameliorates early ischemia-reperfusion injury following the Pringle maneuver. World J Gastroenterol 2010;16:4838-45. [Crossref] [PubMed]
6. Pietsch UC, Herrmann ML, Uhlmann D, et al. Blood lactate and pyruvate levels in the perioperative period of liver resection with Pringle maneuver. Clin Hemorheol Microcirc 2010;44:269-81. [Crossref] [PubMed]
7. Kolovrat M, Gojkovic S, Krezic I, et al. Pentadecapeptide BPC 157 resolves Pringle maneuver in rats, both ischemia and reperfusion. World J Hepatol 2020;12:184-206. [Crossref] [PubMed]
8. Rapido F, Brittenham GM, Bandyopadhyay S, et al. Prolonged red cell storage before transfusion increases extravascular hemolysis. J Clin Invest 2017;127:375-82. [Crossref] [PubMed]
9. Cid J, Ramiro L, Bertran S, et al. Efficacy in reducing potassium load in irradiated red cell bags with a potassium adsorption filter. Transfusion 2008;48:1966-70. [Crossref] [PubMed]
10. Wang Z, Zhang G, Wu J, et al. Adjuvant therapy for hepatocellular carcinoma: current situation and prospect. Drug Discov Ther 2013;7:137-43.
11. Abu-Alfa AK, Younes A. Tumor lysis syndrome and acute kidney injury: evaluation, prevention, and management. Am J Kidney Dis 2010;55:S1-13; quiz S14-9. [Crossref] [PubMed]
12. Wilson FP, Berns JS. Tumor lysis syndrome: new challenges and recent advances. Adv Chronic Kidney Dis 2014;21:18-26. [Crossref] [PubMed]
13. Howard SC, Jones DP, Pui CH. The tumor lysis syndrome. N Engl J Med 2011;364:1844-54. [Crossref] [PubMed]
14. Fonseca C, Garagarza C, Silva G, et al. Hyperkalemia management: a multidisciplinary expert panel's perspective on the role of new potassium binders. Heart Fail Rev 2025;30:271-86. [Crossref] [PubMed]
15. Halperin ML, Kamel KS. Potassium. Lancet 1998;352:135-40. [Crossref] [PubMed]