Discussion:
Since its introduction in 1986, EVL (Endoscopic Variceal Ligation) has
been widely recommended as the first-line treatment for esophageal
varices in liver cirrhosis by clinical guidelines in numerous countries.
When compared to EIS (Endoscopic Injection Sclerotherapy), EVL
demonstrates significant superiority in terms of rebleeding rate,
variceal eradication rate, and complications[1-6].
Consequently, an increasing number of clinicians consider EVL as the
preferred treatment for patients experiencing esophageal variceal
rupture and bleeding. Reported complications of EVL mainly encompass
esophageal stenosis, ulcer bleeding, esophageal perforation, esophageal
hematoma[7-9], pneumonia, and spontaneous
bacterial peritonitis[10-12]. However, there have
been few reports documenting liver function failure following EVL
surgery. Through a comprehensive literature review, we discovered that
only one case of elevated bilirubin levels with subsequent liver
dysfunction after EVL surgery has been documented thus far. This case
involved a 51-year-old female patient with primary biliary cholangitis
(PBC) and esophageal variceal rupture and bleeding, who underwent EVL
treatment. Following the procedure, the patient experienced an increase
in bilirubin levels from 4.0mg/dL to 9.5mg/dL, ultimately necessitating
liver transplantation due to the worsening of liver function
failure[13].
The mechanism behind liver function failure after EVL surgery remains
unclear. In the context of cirrhosis, both hepatic and splanchnic
systemic oxygen uptake (VO2) are reduced[14, 15].
Our hypothesis suggests that the cause of liver failure in patients
after EVL may be attributed to increased portal pressure, decreased
cardiac output, and reduced oxygen delivery following the procedure.
Previous studies have reported that 68% of patients undergoing
endoscopic variceal ligation experience an elevation in portal vein
pressure[16]. It is postulated that the sudden
rise in portal vein pressure could exacerbate liver congestion, impair
oxygen utilization by liver cells, and subsequently lead to liver cell
necrosis. However, a study conducted in 2003 revealed no significant
change in the portal vein pressure gradient before and after EVL surgery
in patients with liver cirrhosis and esophageal variceal rupture and
bleeding[17]. Consequently, further investigation
is required to explore whether an increase in portal vein pressure
occurs after EVL surgery.
As early as 1996, reports emerged highlighting a related phenomenon
wherein EVL surgery may exacerbate liver tissue ischemia and hypoxia.
This study observed a decrease in cardiac output and oxygen delivery
immediately after EVL surgery, although the underlying causes and
implications were not fully understood at the
time[18]. This hypoxic condition is particularly
pronounced in patients with varicose veins and anemia. Research has
shown that patients with liver cirrhosis exhibit a high dynamic
circulation, which enhances oxygen delivery but impairs the uptake and
utilization of oxygen by tissues, resulting in sustained liver cell
hypoxia[19]. Furthermore, all tissues of patients
with liver cirrhosis experience a certain degree of hypoxia due to
arteriovenous shunting[20]. Therefore, a sudden
decrease in cardiac output and oxygen delivery could further intensify
liver cell hypoxia, leading to acute massive necrosis of liver
cells.Overall, the precise mechanisms underlying liver function failure
after EVL surgery necessitate further investigation. The potential
impact of increased portal pressure, reduced cardiac output, oxygen
delivery, and the exacerbation of liver cell hypoxia requires
comprehensive exploration. Future research should focus on elucidating
these mechanisms to enhance our understanding and potentially develop
strategies for mitigating liver function failure following EVL surgery.
Furthermore, there have been reports suggesting the potential
involvement of endogenous nitric oxide in the regulation of systemic
hemodynamics in patients with compensated cirrhosis. Serum nitrate and
nitrite, which are metabolic byproducts of endogenous nitric oxide,
exhibit a sudden decrease in concentration in patients after
EVL[21, 22]. Previous studies have demonstrated
that nitric oxide can alleviate ischemia-reperfusion injury of the liver
and expedite the recovery of liver function[23].
Nitric oxide’s protective effects on liver tissue may play a role in the
context of EVL surgery, although further research is required to
investigate the specific mechanisms and implications of nitric oxide
modulation in this setting.
It has been reported in studies that compared to patients with
Child-Pugh A/B, patients with Child-Pugh C cirrhosis exhibit higher
rates of rebleeding and mortality following
EVL[24]. In the case of our patient, their liver
function reserve was evaluated as Child-Pugh B upon admission. However,
after undergoing emergency EVL, the patient experienced a significant
increase in bilirubin levels and developed coagulation dysfunction. We
speculate that these effects may be attributed to the blockage of
collateral circulation caused by acute bleeding and the impact of EVL
surgery, particularly in the context of poor liver function reserve.
This could exacerbate liver congestion symptoms. Additionally, the
decrease in cardiac output further intensifies the ischemia and hypoxia
experienced by liver cells, ultimately leading to acute necrosis and
liver failure. It is important to note that the occurrence of liver
failure after EVL surgery is relatively rare, and our understanding of
its underlying mechanism is based on plausible pathological and
physiological considerations. Further research is required to delve into
the intricate mechanisms involved and provide conclusive evidence.