肝硬化合并非食管胃靜脈曲張破裂出血合并上消化道出血1例

王 芳 賈紅宇

1.浙江省寧波市北侖區(qū)人民醫(yī)院,浙江寧波315800;2.浙江大學(xué)醫(yī)學(xué)院附屬第一醫(yī)院感染科,浙江杭州 310003

肝硬化合并非食管胃靜脈曲張破裂出血合并上消化道出血1例

王 芳1賈紅宇2

1.浙江省寧波市北侖區(qū)人民醫(yī)院,浙江寧波315800;2.浙江大學(xué)醫(yī)學(xué)院附屬第一醫(yī)院感染科,浙江杭州 310003

近年來,隨著飲食結(jié)構(gòu)的改變和人口老齡化的加劇,肝硬化的發(fā)病率有所上升,由于難以治愈,晚期肝硬化甚至比癌癥更可怕.上消化道出血是肝硬化常見并發(fā)癥,其中非食管胃靜脈曲張破裂出血約占30%～40%.若治療不及時(shí),患者有可能因失血性休克而死亡.因此,加強(qiáng)對(duì)患者的關(guān)注和管理,及時(shí)發(fā)現(xiàn)并為出血患者止血,能有效提高患者的生存率.本文對(duì)1例肝硬化合并非食管胃靜脈曲張破裂出血合并上消化道出血患者的臨床表現(xiàn)與診治過程進(jìn)行了分析,現(xiàn)報(bào)道如下.

肝硬化;上消化道出血;非食管胃靜脈曲張破裂出血

Preface

The most common complication in patients with cirrhosis is upper gastrointestinal bleeding. Some of the bleeding patients is caused by esophageal variceal rupture, but another part of bleeding patients are caused by the rupture of non-esophageal variceal bleeding such as the portal hypertension and gastrointestinal ulcer. The clinical manifestations and treatment methods of different causes of bleeding are also different. This study retrospectively analyzed the clinical data of 1 case of hepatic cirrhosis combined with non-esophageal variceal bleeding combined with upper gastrointestinal bleeding in our hospital in September 2016, and to explore the clinical characteristics of the disease.

Case datum

The patient, whose name is Zhang XX, female and 71 years-old, was admitted to our hospital due toquot;fever, cough coupled with weakness for 15 daysquot; on 2016-9-13.

The patient was performed with a cholecystectomy due to quot;gallstonequot; 23 years ago; And she was performed with a splenectomy due to quot; schistosomiasis cirrhosis and hypersplenism quot; 2 years ago (2014).

The patient developed a fever without any distinct inducement 15 days ago with a maximal temperature of 37.6℃,she felt weakness, coughing a little without phlegm, and with a headache occasionally as her body temperature rose, the bilateral frontotemporal parts were the focus of attack, consequently the patient paid a visit to local hospital where she received a cephalosporin anti-infection therapy, but no obvious improvement was achieved, then the patient was transferred to local hospital for hospitalization where the relevant inspections like TB.TSPOT, hepatitis series, HBVDNA, tumor marker were perfected and no anomaly was found. Blood routine findings:WBC 10.5X109/L,HB 99g/L,PLT 102X109/L;Blood Biochemistry findings: Total bilirubin(TB)41.8 μmol/L, Aspartate Transaminase(AST) 56U/L, Albumin(ALB) 19.1g/L, C-reactive protein(CRP):17.60mg/L; Urine routine test findings: occult blood 3+, no anomaly was found in the rest items; Erythrocyte sedimentation rate(ESR):64mm/h; ANA weakly positive; Blood coagulation function: prothrombin time(PT):18.6s,activated partial thromboplastin time(APTT):45.4s;IgG:28.1g/L,IgA:7.12g/L;Chest CT findings: multiple nodules were developed in the inferior lobe of left lung, the lingular segment of left lung was found to have a fiber focus, and enlarged lymph nodes were found inside the mediastinum,hydrothorax at left side, enlarged peritoneal lymph nodes.

After the hospital,reduced glutathione injection,compound glycyrrhizin injection and ademetionine injection were administered to the patient for liver protection and removing jaundice, and anti-infection therapy through administration of ceftizoxime injection were administered, the patient's condition was not improved, then the therapy was changed to a combined anti-infection therapy by injection ofquot;piperacillin-tazobactam and ciprofloxacinquot; , which failed to improve the patient's symptoms markedly,the patient sensed a pain and discomfort in the left upper abdomen, and had a distinct edema of both lower extremities, as a result she was transferred to our hospital for a further therapy and admitted to our department by the outpatient clinic due to quot; fever of unknown (FOU)quot;.

Various checks were perfected after the patient was admitted on Sep, 13th: Blood coagulation function:international normalized ratio (INR) 1.61, fibrinogen(Fib) 1.93g/L, activated partial thromboplastin time(APTT) 48.0s, prothrombin time (PT) 18.1s, D-dimer 3032ug/L FEU. Blood routine: WBC 11.3X109/L,neutrophile granulocyte percentage 57.1%, lymphocyte percentage 27.1%, monocyte percentage 10.3%, RBC 2.55X1012/L,HB 102g/L, HCT 26.9%, MCV 105.5fL,MCH 40.0pg, PLT 102X109/L. Blood Biochemistry:ALB 20.7g/L, globulin 47.8g/L, Alanine Transaminase(ALT)25U/L, Aspartate Transaminase(AST) 63U/L,cholinesterase 1868U/L, total bile acid 70μmol/L, total bilirubin(TB) 40μmol/L, direct bilirubin 21μmol/L, indirect bilirubin 19μmol/L, adenylic deaminase 22U/L, Gamma-Glutamyl Transferase(GGT) 76U/L, total cholesterol 2.64mmol/L, highdensity lipoprotein-C 0.58mmol/L. CRP 22.5mg/L. Stool routine: occult blood test: negative. Chest CT reexamined on 9-14: a possibility of infectious lesion in left lung, bilateral pleural effusion; left lower pleural thickening. Multiple enlarged lymph nodes in mediastinum; a few aortic and coronary arterial calcifications. Abdominal + lymph nodes color Doppler ultrasound: liver cirrhosis image, postoperative change after cholecystectomy and splenectomy; bilateral cervical lymph nodes can be detected coupled with an unclear border between cortex and medulla. The patient was administered with ademetionine injection and polyene phosphatidylcholine injection for liver protection and removing jaundice after admission, injection of biapenem for anti-infection,supplementation of human albumin and other therapies,the patient's body temperature peak declined, the maximal temperature declined from 39.9℃ to 37.6℃ ,meanwhile, in view of multiple enlarged lymph nodes,a lymph nodes biopsy was appointed for the patient.

But at 17:00, Sep, 18th, the patient excreted about 100g of try stools without any distinct inducement, and vomited 150g of coffee-like liquid,afterwards, about 1200g of black stool were excreted,ECG monitoring and special nursing were administered to the patient, followed by notification of critical illness and fasting, three venous channels were opened,intravenous injections of somatostatin and terlipressin by micropump were administered to reduce the portal vein pressure, followed by injection of omeprazole to suppress acid, and intravenous medication by injection of carbazochrome sodium sulfonate, dicynone,p-aminomethyl benzoic acid and hemocoagulase, and oral medication of thrombin for hemostasis, 1500mL red cells were transfused to the patient, followed by a dilatation and fluid infusion therapy by compound sodium chloride fluid and hydroxyethyl starch fluid and other treatments.

But the patient still keep bleeding, with hemoglobin declining from the original 101g/L to 39g/L, coagulation function reexamined: INR 3.6, Fib 0.50g/L, APTT 93.6s, PT 39s, D-dimer 4045ug/L FEU.Digestive department doctors, surgeons were invited for a treat together, it was observed by emergency gastroscopy that, there was an active bleeding at the junction of duodenal bulb drop department, which was still not clearly seen after washing, no distinct active bleeding spot was found at the descending part(十二指腸球降部交界處前壁大彎側(cè)活動(dòng)性出血), the bleeding decreased as the active bleeding spot was clipped by two BOSTON titanium clips, three spots around the titanium clips were injected respectively with 3ml of lauromacrogol. No distinct active bleeding was found after washing, a gastric tube was retained before the gastroscopy was withdrawn.

圖1 肝臟CT影像結(jié)果(2016年9月14日)Figure1 Results of liver CT imaging (September 14th, 2016)

圖2 內(nèi)窺鏡檢查結(jié)果(2016年9月19日上午3點(diǎn)50分)Figure 2 Endoscopy results (50 Points at 3a.m. on September 19th, 2016)

The patient persisted excreting black stool and spitting blood repeatedly after the gastroscope therapy, surgeons was invited again and considered a surgery but which was cancelled in view of a high risk, meanwhile the doctor from liver transplantation department was invited for a group consultation and considered the possibility of liver transplantation therapy, which was deterred by its high risk and cost.The patient's relatives were informed of the condition,the program of liver implantation and surgical operation treatment was denied by the relatives after they consulted with each other, then the doctor from Interventional therapy department was invited to consider an interventional therapy, which was not decided until the relatives consulted with each other.

But the patient's oxygen saturation declined to 70% at 13:20, Sep, 19th, coupled with whole body clamminess, active bleeding complicated with shock was considered, the treatment of hemostasis, dilatation and anti-shock was continued, meanwhile supportive therapies like sputum suction, mask oxygeninspiration and so on were administered. The patient's oxygen saturation was progressively lowered at 13:25,coupled with heart rate decreased, cardio-pulmonary resuscitation (CPR), balloon mask oxygen inspiration were administered to the patient, meanwhile, the dosage of hypertensive drugs like dopamine and aramine was adjusted, and the intravenous infusion and dilatation were continued. The patient had no autonomous heart rate at 13:26, the CPR was continued, 1mg of adrenaline and 0.5mg of atropine was intravenously injected, the patient still had no autonomous respiration after being performed with CPR for over 30 minutes, a ventricular escape rhythm was indicated by the heart rate, the relatives gave up endotracheal intubation after consultation and other invasive rescue and ICU, and then the patient was taken home after signing.

Discussion

Liver cirrhosis is a pathologic change shared by various terminal liver diseases, it is usually complicated with portal hypertension, upper gastrointestinal hemorrhage, hypersplenism,hepatorenal syndrome, hepatic encephalopathy and other complications. Upper gastrointestinal hemorrhage is one of the common complications for terminal liver cirrhosis, it has an acute onset and high fatality rate,often leading to hemorrhagic shock or inducing the hepatic encephalopathy, it is the leading cause of death of patients with liver cirrhosis[1-3].The gastrointestinal hemorrhage of patients with liver cirrhosis is mainly caused by esophageal and gastric varices, the nonvarices hemorrhage accounts for a small percentage. It is reported by domestic literatures that, the acute upper gastrointestinal hemorrhage due to esophageal and gastric varices is 43.2%-90% in liver cirrhosis, the portal hypertensive gastropathy is 12.2%-28.9%, the digestive ulcer bleeding is 10.57%-23.8%, all these three were more than 90% of upper gastrointestinal hemorrhage with liver cirrhosis[4]. AA Romcea and other scholars had carried out a retrospective analysis on 1284 patients with liver cirrhosis complicated with upper gastrointestinal hemorrhage, 73% of them were esophageal and gastric varices, while 27% were non-varices hemorrhage[5]. Of the cases with variceal bleeding, 91.7% were from esophageal varices while 18.3% were from gastric varices; The majority of nonvarices hemorrhage in the study was peptic ulcer bleeding, with duodenal ulcer 33.75% and gastric ulcer 21.25%, portal hypertensive gastropathy 17.5%,the rest included acute corrosive gastritis, Mallory-Weiss syndrome, gastric antral vascular ectasia and so on. This result is similar to what the other literatures reported[6-11]. For instance, Pavel Svobodo et al.[12]had studied 137 cases of patients with liver cirrhosis complicated with gastrointestinal hemorrhage,among whom, the varices hemorrhage accounted for 62.8% (esophageal varices 57.7%, gastric varices 5.1%), non-varices hemorrhage accounted for 37.2%(peptic ulcer 18.2%, portal hypertensive gastropathy 9.5%, the others 9.5%). It has been found among all these researches that, most of the liver cirrhosis gastrointestinal hemorrhages are caused by varicosis rupture, non-varices hemorrhage is held about 1/4 to 1/3 of patients, which predominated by peptic ulcer and portal hypertensive gastropathy.

The pathological and pathophysiologic basis of digestive hemorrhage may be very complicated,including dysfunction of hemostasis, coagulation,fibrinolysis, vascular factor and platelet factor, which remains unclear. Portal hypertension is the necessary condition for peptic ulcer and portal hypertensive gastropathy[8,13], it results the venous return obstruction of multiple organs, the stomach and duodenum are the primary organs involved. When the defense mechanism of mucous membrane is undermined by the increased permeability of gastric mucosa and capillary, and plasma extravasation, the mucous membrane's barrier function is damaged, and the mucous tissue is impaired[14]. Besides, liver cirrhosis leads to a decreased production of blood coagulation factor, thrombocytopenia and coagulation dysfunction,leading to a high incidence of hemorrhage complicated with peptic ulcer and portal hypertensive gastropathy[15]. The incidence of acute upper digestive hemorrhage may be increased by patient's stress situation like infection, oral non-steroidal anti-inflammatory drugs and bad living and dietary habits, such as overeating and overdrinking, alcohol or coarse food.

The patient in this case had schistosomiasis cirrhosis for many years, and received a splenectomy 2 years ago, she had already been in the end stage liver disease. As for this digestive hemorrhage, we first consider the esophageal and gastric varices hemorrhage, but lacked of support from the image evidence, an ulcer bleeding at the junction of duodenal bulb drop department(十二指腸球降部潰瘍出血) was indicated by the emergency gastroscopy after the medical treatment, it was considered that the cause of digestive hemorrhage might be associated with long-term liver cirrhosis, poor liver reserve function,coagulation dysfunction, and thrombocytopenia.

To sum up, the digestive hemorrhage with liver cirrhosis has a relatively high incidence rate, although it is predominated by varices hemorrhage, the incidence rate of non-varices upper digestive hemorrhage is also not low, and the peptic ulcer hemorrhage is also very common. Emergency gastroscopy plays an important role in the identification and diagnosis of upper digestive hemorrhage with liver cirrhosis. We need to broaden the clinical thought in diagnosis and treatment of patients with individualized treatment.

[1] DA Sass, KB Chopra. Portal hypertension and variceal hemorrhage [J].Medical Clinics of North America, 2009, 93(4):837-853.

[2] Gao L, Yang F, Ren C, Han J, et al. Diagnosis of cirrhotic portal hypertension and compensatory circulation using transsplenic portal scintigraphy with(99m) TC-Phytate[J].Journal of Nuclear Medicine: Official Publication, Society of Nuclear Medicine,2010,51(1):52-56.

[3] Shengxing Zhu, Sheng Chang. Clinical application value of preoperative selective partial splenic embolization before splenectomy plus portal-azygous disconnection[J].International Journal of Clinical and Experimental Medicine, 2015, 8(8):9574-9579.

[4] 劉南植 ,尹朝禮.790例門脈高壓食管胃底靜脈曲張內(nèi)鏡檢查分析[J].內(nèi)科急危重癥雜志,2001,7(1):22-23.

[5] AA Romcea, M Tanu, A Seicean, et al. The etiology of upper gastrointestinal bleeding in cirrhotic patients [J].Clujul Medical, 2013, 86(1):21-23.

[6] Svoboda P, Ehrmann J, Klvana P, et al. A different view of acute upper gastrointestinal bleeding in liver cirrhosis patients [J].Vnitr Lek, 2010, 56(11):1116-1121.

[7] Kim YD, Cheon GJ, Kim MY, et al. Changes in the Clinical Outcomes of Variceal Bleeding in Cirrhotic Patients: A 10-Year Experience in Gangwon Province, South Korea[J].Gut and Liver,2012,6(4):476-481.

[8] Woo Jin Chung. Management of portal hypertensive gastropathy and other bleeding [J].Clinical and Molecular Hepatology, 2014, 20(1):1-5.

[9] 吳開春.亞太地區(qū)非靜脈曲張性上消化道出血專家共識(shí)意見解讀(三):內(nèi)鏡止血的補(bǔ)救措施[J].中華消化雜志,2012,32(2):82-83.

[10] Sung JJ, Chan FK, Chen M, et al. Asia-Pacific Working Group consensus on non-variceal upper gastrointestinal bleeding [J].Gut, 2011, 60(9):1170-1177.

[11] R Marmo, MD Piano, L Cipolletta, et al. 1039 Mortality From Non Variceal Upper Gastrointestinal Bleeding in Patients With Liver Cirrhosis: an Individual Patient Data Meta-Analysis[J].Gastrointestinal Endoscopy,2013,77(5):AB180-AB180.

[12] Pavel Svobodaa, Michal Konecnyb, Arnost Martineka, et al. Acute upper gastrointestinal bleeding in liver cirrhosis patients[J].Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub,2012,156(3):266-270.

[13] Hwang JH, Fisher DA, Ben-Menachem T, et al.The role of endoscopy in the management of acute nonvariceal upper GI bleeding [J]. Gastrointest Endosc, 2012,75(6):1132-1138.

[14] 張東偉,許樹長(zhǎng),王志榮,等.內(nèi)鏡下金屬鈦夾與注射止血治療急性非靜脈曲張性上消化道出血療效觀察[J].中華實(shí)用診斷與治療雜志,2013,27(9):931-932.

[15] 劉文平,黃彩云.國產(chǎn)奧美拉唑治療急性非靜脈曲張性上消化道出血的Meta分析[J].中國循證醫(yī)學(xué)雜志,2013,13(6):723-727.

A case of upper digestive bleeding by liver cirrhosis complicated with non-esophageal and gastric varices rupture hemorrhage

WANG Fang1JIA Hongyu2
1.Ningbo Beilun People's Hospital, Ningbo 315800, China; 2. The First Affiliated Hospital of Zhejiang University Medical College, Hangzhou 310003, China

In recent years, with the change in diet structure and the intensification of population aging, the incidence of liver cirrhosis has increased. Due to cirrhosis of the liver can't be cured, so the risk of advanced cirrhosis is more terrible than cancer. Upper gastrointestinal bleeding is a common complication of cirrhosis, of which nonesophageal variceal bleeding (NEVB) accounts for about 30%-40%.If the treatment is not timely, NEVB patients may die from hemorrhagic shock. Therefore, to strengthen the NEVB patient's attention and management, and timely detection of bleeding patients and hemostasis, can effectively improve the survival rate of patients. In this paper, the clinical manifestation and diagnosis of a case of hepatic cirrhosis combined with non-esophageal variceal bleeding combined with upper gastrointestinal bleeding were analyzed, and reported as follows.

Liver cirrhosis; Upper gastrointestinal bleeding; Non esophageal gastric varices bleeding

R575.2 [文獻(xiàn)標(biāo)識(shí)碼] A [文章編號(hào)] 2095-0616(2017)22-253-05

2017-09-07)