Sepsis is a critical medical condition characterized by life-threatening organ dysfunction resulting from the uncontrolled immune response to infection. It can lead to multiple organ dysfunction syndrome, posing a substantial risk to the lives of critically ill patients [1, 2].
In individuals with sepsis, the combination of inflammatory reactions and oxidative stress often leads to gastrointestinal mucosal ischemia, thereby impacting the functionality of the digestive system. Extensive research has established sepsis as a significant risk factor for gastrointestinal bleeding. Nevertheless, there is a notable scarcity of reports focusing on the alterations in gastric microecology among septic patients who develop gastrointestinal bleeding. This paper present detailed insights into the gastric microecology and the diagnostic and treatment procedures applied to two patients afflicted by sepsis complicated with gastrointestinal bleeding. This contribution aims to enhance our understanding of the underlying causes of gastrointestinal bleeding in such cases and offers valuable guidance for the adjustment of treatment strategies.
Case 1
A 34-year-old female was admitted to the hospital due to a history of "abnormal liver function for over nine years." The elevated liver transaminase levels had been detected more than nine years ago, and a liver biopsy had confirmed the presence of autoimmune cirrhosis. The patient had previously undergone esophageal variceal ligation, splenectomy, and pericardial devascularization.
Upon admission, the patient was conscious, exhibiting moderate jaundice in the skin and sclera, along with slight abdominal distension. No other significant abnormalities were noted during the physical examination. Initial laboratory results showed a hemoglobin level of 91 g/L, a total bilirubin concentration of 263 µmol/L, a prothrombin time of 16.2s, and an activated partial thromboplastin time of 39s. Abdominal contrast-enhanced CT scans revealed the presence of liver cirrhosis, ascites, and signs of portal hypertension with collateral circulation. Furthermore, a liver biopsy confirmed the diagnosis of nodular cirrhosis with intrahepatic cholestasis. Gastroscopy upon admission revealed mild esophageal varices, along with gastric mucosal congestion and edema (Fig. 1A). The primary admission diagnosis: 1. Decompensated stage of liver cirrhosis (Child-Pugh B); 2. Portal hypertension with esophageal varices.
The patient underwent an allogeneic liver transplantation on September 4, 2022, following which she was transferred to the ICU. After surgery, the patient received mycophenolate mofetil and tacrolimus to modulate immune function. Despite these interventions, the bilirubin levels remained elevated after the procedure. Subsequently, percutaneous transhepatic biliary drainage was performed.
Eleven days post-operation, the patient had a high fever (39 ℃) with abdominal distension. Blood cultures identified the presence of Enterococcus faecium and Candida albicans, leading to a diagnosis of sepsis. The anti-infective regimen was promptly adjusted to vancomycin, cefoperazone sodium, and sulbactam sodium. Fifteen days following the transplantation, the patient experienced acute gastrointestinal bleeding, characterized by a profusion of dark stools and decreased blood pressure. Immediate interventions included fluid resuscitation, blood transfusion, and intravenous use of proton pump inhibitors. A subsequent gastroscopy revealed multiple extensive ulcers in the gastric body and pronounced exfoliation-like alterations in the gastric mucosa (Fig. 1B).
Unfortunately, the patient's gastroscopy showed that the lesions of the stomach body were significantly worse than those on admission. Gastric fluid analysis reported a pH level of 6.0. Both next-generation sequencing (NGS) and culture analysis of the gastric fluid disclosed the presence of Klebsiella aerogenes and Pseudomonas aeruginosa, which correlated with the findings from blood cultures. In response to these results, the anti-infection regimen was further adjusted to colistin sulfate, cefoperazone sodium sulbactam sodium, caspofungin, and hemostatic therapy involving the administration of human fibrinogen, human prothrombin complex, fresh frozen plasma, and transfusion of red blood cell suspension. Tragically, two days later, the patient's condition deteriorated drastically, resulting in severe gastrointestinal hemorrhage, hypovolemic shock, disseminated intravascular coagulation (DIC), and ultimately, respiratory and cardiac arrest. Despite extensive rescue efforts, the patient succumbed to her condition.
Case 2
A 29-year-old female patient was admitted to the hospital with a complaint of "abdominal pain persisting for 20 days, dyspnea for one day." The patient had experienced sustained epigastric colic for the preceding 20 days, starting at the 39 + 1 week of her gestation period, which was accompanied by bouts of vomiting. Upon examination, an emergency ultrasound indicated pancreatic enlargement, and laboratory tests revealed a significant elevation in blood amylase and lipase levels. Consequently, a diagnosis of acute severe pancreatitis was established, leading to the performance of an emergency cesarean section. Postoperative blood culture and abdominal drainage identified the presence of carbapenem-resistant Acinetobacter baumannii. Despite initial medical management, the patient's condition worsened, manifesting as aggravated dyspnea. She was subsequently transferred to our hospital following endotracheal intubation. Importantly, the patient had no history of digestive tract disorders.
Upon admission, the patient was in a state of analgesia and sedation. Wet rales could be heard in both lungs. The whole abdomen is distended and tender, and 6 drainage tubes can be seen in the abdomen. Laboratory tests were as follows: hemoglobin 70 g/L, platelet count 18*109/L, prothrombin time 17.7 s, activated partial thrombin time 48.7 s, creatinine 316 µmol/L, lipase 399 IU/L, and pancreatic amylase 92 IU/L. Abdominal enhanced CT: Pancreatic swelling, extensive peripancreatic exudation, peritonitis signs, omentum and mesangial swelling, gastrointestinal wall swelling, stratified enhancement (Fig. 2A). The primary diagnoses upon admission included acute pancreatitis, septic shock, and multiple organ dysfunction syndrome, which encompassed the heart, liver, and coagulation systems.
After admission, the patient was subjected to a regimen that included the administration of tigecycline and colistin sulfate for anti-infective purposes, intravenous noradrenaline to raise blood pressure and other supportive treatments. Over the course of her hospitalization, the patient underwent blood culture and abdominal drainage culture assessments. It was also observed that a small amount of brown drainage fluid could be seen in the gastrointestinal decompression unit. On the third day following her admission, gastroscopy revealed ulcers and numerous dark-brown protuberances in the middle curvature of the gastric body and across the mucosa from the anterior wall to the antrum, indicative of ulcerated gastric mucosa and purulent secretions. This presentation was consistent with suppurative gastritis (Fig. 2B).
Gastric fluid analysis reported a pH level of 6.5. Gastric fluid samples were sent to NGS and culture testing. Subsequent findings indicated the presence of Pseudomonas aeruginosa, Stenotrophomonas maltophilia, Acinetobacter baumannii, Saccharomyces cerevisiae, Aspergillus fumigatus, and Candida albicans. On the sixth day, culture results from the abdominal drainage fluid indicated Candida albicans, while blood cultures identified Pseudomonas aeruginosa. Simultaneously, gastric juice cultures revealed the presence of Stenotrophomonas maltophilia and Candida albicans. In response to these findings, voriconazole antifungal therapy was initiated, accompanied by component blood transfusions. Unfortunately, despite these efforts, there was no significant improvement in the patient's hemodynamic status. Her condition continued to deteriorate, characterized by progressive gastrointestinal bleeding and multiorgan dysfunction. Tragically, the patient's clinical state failed to respond to rescue efforts and was ultimately declared deceased.