Neoadjuvant treatment of postoperative gastric cancer combined with portal vein gas

doi:10.21203/rs.3.rs-2615746/v1

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Case Report

Neoadjuvant treatment of postoperative gastric cancer combined with portal vein gas

https://doi.org/10.21203/rs.3.rs-2615746/v1

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Portal vein gas (PVG) is an abnormal accumulation of gas in the portal vein of the liver and is often indicative of a critical condition, with rapid onset, rapid progression and poor prognosis.We report a case of neoadjuvant treatment of postoperative gastric cancer combined with portal vein pneumatosis that improved after conservative treatment.After 4 cycles of SOX chemotherapy, he underwent total gastrectomy + oesophago-jejunal Roux-en-Y anastomosis with postoperative complications of portal vein pneumatization, and was discharged after 14 hours of conservative treatment.Combined with the previous literature reports, the diagnosis and treatment of the disease are analysed and summarised in order to raise vigilance for early diagnosis and treatment, and also to lay the foundation for the diagnosis and treatment of clinically relevant cases.

Portal pneumoperitoneum

neoadjuvant therapy

postoperative gastric cancer

conservative treatment

Male, 67 years old, was first admitted on 17 March 2022 with a diagnosis of gastric cancer (cT4aN2Mx) mainly due to bloody stools for more than 2 months. Considering the patient's advanced stage, the patient was given 4 cycles of SOX (oxaliplatin for injection 150mg dl + tegeo 60mg d1-14) regimen chemotherapy.He had a history of "hypertension" and "cerebral infarction" for 6 years. On 25 July 2022, he underwent a total gastrectomy under general anaesthesia and an oesophago-jejunal Roux-en-Y anastomosis under full robotics.Sudden onset of severe abdominal pain on the 9th postoperative day with full abdominal distension, no rebound pain, muscle tension, negative mobile turbid sounds, drums on percussion, weak bowel sounds, with profuse sweating, poor consciousness and wet and cold extremities.

Test results showed: WBC 12.86 x 109/L, neutrophil count 9.13 x 109/L, glutathione transaminase 23.1 U/L, ghrelin 18.5 U/L, D-dimer 2.739 mg/L, calcitoninogen 0.53 ng/ml, C-reactive protein 13.70 mg/L, lactate 2.22 mmol/L.Routine stool results: 15-20 red blood cells/HPF, 3-5 white blood cells/HPF, 0-1 pus cells/HPF, occult blood (positive), microscopic examination shows fat droplets, amyloid granules, no epithelial cells and muscle fibres. Stool pathology biopsy diagnosis: mucus and degenerated necrotic tissue; stool culture results showed normal total bacterial load, 40% gram-positive streptococci detected, 60% gram-negative bacilli detected, blood culture: negative.Abdominal CT suggested: portal vein, splenic vein, superior mesenteric vein and intrahepatic portal system with pneumatization within the mesenteric vascular travel zone (Figure 1 and Figure 2). Vascular ultrasound findings showed: CDFI: bright, multicoloured portal flow signal, PW: bidirectional, intermittent burr-like changes in the spectrum, and pneumatosis in the portal vein and intrahepatic bile ducts. (Figure 3)

Portal vein, splenic vein, superior mesenteric vein and intrahepatic portal system, pneumatization in the mesenteric vascular zone

CDFI: bright, colourful portal flow signal, PW: bidirectional, intermittent burr-like changes in the spectrum, pneumatization of the portal vein and intrahepatic bile ducts.

Repeat CT: disappearance of pneumoperitoneum in portal vein

After a comprehensive multidisciplinary consultation, no intestinal ischaemia, intestinal necrosis, intestinal and abdominal gas-producing bacterial infections were excluded. Conservative treatment was temporarily given: ①Multi-parameter vital signs monitoring ②Water fasting ③Complete parenteral nutrition ④Anti-infection (meropenem injection 1g IV q/8h, levofloxacin sodium chloride injection 0.5g) ⑤Oral bifidobacterium enteric probiotics ⑥Anticoagulation ⑦Supplementation of human albumin and coagulation factors, etc.Conservative symptomatic treatment was given and vital signs were stable.Approximately 14 hours after the diagnosis of portal pneumoperitoneum, the ultrasound showed no significant abnormalities in intrahepatic blood flow colour, normal internal diameter of the main trunk of the portal vein and slightly thickened walls of the right and left trunks of the portal vein.A repeat CT did not suggest a pneumoperitoneum in the portal vein. (Fig. 4) The bowel function gradually recovered and the transition from complete parenteral nutrition to a fluid diet via the mouth was gradual, and he was successfully discharged on the 20th postoperative day on 15 August 2022.

Portal venous gas (PVG), also known as pneumoperitoneum, is an unspecified radiological sign that manifests as an abnormal accumulation of gas in the portal vein of the liver. PVG often occurs in patients with intestinal ischemia or necrosis and is characterized by rapid onset, rapid progression, poor prognosis and high mortality ^[1][11], often suggesting exacerbation of the disease and ischemic necrosis of the intra-abdominal organs, and is an indication for emergency surgical exploration ^[2].Considered a life-threatening sign in the past, it has been called the "god of death" and was first described by Wolfe and Evens in 1955 in necrotizing small bowel colitis in infants^[3], while HPVG in adults was first described by Susman et al. in 1960 ^[4].The mortality rate of HPVG is high, with a Japanese study showing intestinal ischaemia in 53% of 1590 patients with HPVG and an overall hospital mortality rate of 27.3% ^[5].With advances in medical technology, imaging as well as laboratory tests have improved to help diagnose and monitor changes in the disease in a more timely manner. Generally HPVG does not appear independently of the disease progression and active management of the cause of the disease can result in a lower mortality rate from HPVG.

The clinical presentation of HPVG is not specific and the main symptoms are abdominal pain, bloating, nausea and vomiting, making it more difficult to differentiate from other diseases.The pathogenesis of HPVG is still unclear, but there are two possible mechanisms ^[6]: (1) increased pressure in the intestinal lumen and damage to the intestinal mucosal barrier, allowing gas from the intestinal lumen to enter the portal vein; (2) abnormal proliferation of gas-producing bacteria in the intestinal lumen and abdominal cavity, resulting in the production of large amounts of gas into the portal system.In addition, medical manipulation can also lead to HPVG. Endoscopy and treatment, haemodialysis and chemotherapy have also been reported to cause HPVG, and an unexplained HPVG in a post-operative patient has also been reported ^[7].In the past, the main reliance was on plain radiographs, which have low resolution and detection rates. CT is now considered to be a more objective and reliable imaging tool for this disease, mainly showing a blighted hypodense shadow along the portal vein, and may be preferred, as well as for objective dynamic monitoring of HPVG treatment efficacy ^[8].CT imaging of HPVG should not directly determine clinical or surgical treatment, but rather the severity of the disease and can be used to find the cause and differential diagnosis.Ultrasound is highly sensitive and effective for the detection of HPVG and can be used for early diagnosis, with the main manifestations including hyperechoic granules flowing within the hepatic portal vein and hyperechoic plaques in the liver parenchyma.Colour Doppler ultrasound of the portal system is cheaper than CT and is not radiologically harmful. Pan et al^[9] concluded that the sensitivity of ultrasound for HPVG detection is higher than that of CT, mainly because ultrasound allows dynamic observation of the lesion in real time, has a higher sensitivity to gases and secondly there is a partial volume effect of bubbles on CT images.However, ultrasonography often relies on the examiner's personal experience and is less stable, while the presence of significant abdominal signs in the patient significantly interferes with the examiner's manoeuvre. Therefore, some studies have concluded that colour Doppler ultrasonography and abdominal CT are currently considered to be the most sensitive diagnostic imaging tools for this disease ^{[8] [10]}.

A review of the published literature found intestinal ischaemia and necrosis to be one of the most common causes.Hussain et al ^[11]reported 275 cases of PVG, the proportion of various causes being intestinal ischaemia and mesenteric vasculopathy (61.44%), gastrointestinal inflammation (16.26%), obstruction and dilatation (9.03%), sepsis (6.6%), medical origin injury and trauma (3.01%) and cancer (1.8%) and primary HPVG (1.8% ).This patient was treated conservatively with significant relief of symptoms and signs after 14 hours, and imaging suggested disappearance of HPVG, thus ruling out intestinal ischaemic disease causing pneumatosis in the portal vein and thus avoiding surgery.

As our research into neoadjuvant treatment of gastrointestinal tumours continues, the potential for medically induced bowel injury due tIt is now believed that there is a wide variation in the treatment of HPVG with different etiologies, and that there are usually two types of treatment, surgical and conservative, based mainly on the patient's etiology and condition [13].se of hepatic portal vein gas in a right hemi-colon cancer with liver metastases after two cycles of oxaliplatin combined with cetuximab treatment.However, the incidence of HPVG may also be increased by surgical stress, postoperative bowel dysfunction and low immunity in this neoadjuvant patient treated preoperatively with a 4-cycle SOX regimen, and it is not clear that chemotherapeutic factors caused HPVG.

It is now believed that there is a wide variation in the treatment of HPVG with different etiologies, and that there are usually two types of treatment, surgical and conservative, based mainly on the patient's etiology and condition^[13].If the patient's vital signs are stable and there are no signs of peritonitis, the patient should first be actively treated for the primary disease, and while conservative treatment is carried out, the abdominal signs, CT and laboratory tests should be monitored dynamically to help predict the prognosis and evaluate whether there is intestinal ischaemic necrosis, and if there is no improvement or intestinal necrosis, surgical treatment should be actively carried out to reduce mortality.In this case, the patient had sudden onset of severe postoperative abdominal pain as the first symptom, and the presence of HPVG was first detected on imaging. The main consideration was that the intestinal spasm caused dilatation of the lumen, increased pressure in the intestinal lumen, and edema or ischemic necrosis in part of the intestinal canal, allowing intraluminal gas to enter the portal system, leading to the development of HPVG.After 14 hours of conservative treatment with ① multiparametric vital signs monitoring ② water fasting ③ complete parenteral nutrition ④ anti-infection ⑤ oral bifidobacterium entericum probiotics ⑥ anticoagulation ⑦ supplementation of human albumin and coagulation factors, the imaging examination suggested the disappearance of HPVG. After early aggressive and effective treatment, the pain was reduced and surgery was eventually avoided.

Although an increasing number of cases are reported to have improved with conservative treatment of HPVG, the possibility of intestinal necrosis cannot be ignored.The need for conservative treatment or urgent open surgery for HPVG depends on the circumstances, such as the clear presence of manifestations of peritoneal irritation, ascites or shock, in order to ensure life safety and to improve the prognosis by surgical intervention as soon as possible.Neoadjuvant therapy is also a non-negligible factor, and preoperatively we should adequately assess the gastrointestinal toxic reactions caused by the drugs in order to reduce the aggravation of postoperative complications.More research is needed in the future to investigate the pathogenesis of HPVG and its relationship with drugs.HPVG progresses rapidly. In this case, HPVG was probably caused by increased pressure in the intestinal lumen due to intestinal spasm and gas entering the hepatic portal vein. 14 hours after conservative treatment, ultrasound and CT findings did not suggest HPVG.Clinicians should therefore be more aware of the disease and must be on high alert to monitor changes, diagnose and treat early, reduce unnecessary interventions and adopt individualised treatment plans to reduce patient mortality.

Acknowledgements:

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Ethical Approval：

Ethics approval and consent to participate The work has been approved by the Ethics committee of the Hebei Medical University.

Competing interests：

Each co-author certifies that he has no commercial association that may constitute conflict of interest in connection with the submitted article. The authors declare that they have no competing interests.

Authors' contributions:

XueFeng Zhao responsible for the ideas and materials of the article.

HaoRan Fu responsible for writing and revising articles.

All persons gave their informed consent prior to their inclusion in the study.

All authors reviewed the manuscript.

All persons gave their informed consent prior to their inclusion in the study.

Funding:

There was no funding source for this work. This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Availability of data and materials:

The corresponding author had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

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No competing interests reported.

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Neoadjuvant treatment of postoperative gastric cancer combined with portal vein gas

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