Risk assessment after acute upper gastrointestinal haemorrhage.

The aim of this study was to establish the relative importance of risk factors for mortality after acute upper gastrointestinal haemorrhage, and to formulate a simple numerical scoring system that categorizes patients by risk. A prospective, unselected, multicentre, population based study was undertaken using standardised questionnaires in two phases one year apart. A total of 4185 cases of acute upper gastrointestinal haemorrhage over the age of 16 identified over a four month period in 1993 and 1625 cases identified subsequently over a three month period in 1994 were included in the study. It was found that age, shock, comorbidity, diagnosis, major stigmata of recent haemorrhage, and rebleeding are all independent predictors of mortality when assessed using multiple logistic regression. A numerical score using these parameters has been developed that closely follows the predictions generated by logistical regression equations. Haemoglobin, sex, presentation (other than shock), and drug therapy (non-steroidal anti-inflammatory drugs and anticoagulants) are not represented in the final model. When tested for general applicability in a second population, the scoring system was found to reproducibly predict mortality in each risk category. In conclusion, a simple numerical score can be used to categorize patients presenting with acute upper gastrointestinal haemorrhage by risk of death. This score can be used to determine case mix when comparing outcomes in audit and research and to calculate risk standardised mortality. In addition, this risk score can identify 15% of all cases with acute upper gastrointestinal haemorrhage at the time of presentation and 26% of cases after endoscopy who are at low risk of rebleeding and negligible risk of death and who might therefore be considered for early discharge or outpatient treatment with consequent resource savings.     

Inhibition of gastric secretion and motility by simulated upper gastrointestinal haemorrhage: a response to facilitate haemostasis?

As gastric acid and pepsin inhibit blood coagulation and platelet aggregation it is surprising that most upper GI haemorrhages stop spontaneously. To investigate this paradox we have studied acid and pepsin secretion, gastric motility and GI hormones after simulated upper GI haemorrhage. In seven healthy volunteers intraduodenal infusion of 160 ml autologous blood decreased pentagastrin stimulated submaximal acid secretion (mmol/h) from 30.0 (3.2) (mean (SE] in the hour preceding infusion to 21.4 (3.7) in the hour following infusion (p less than 0.02), representing a mean reduction in acid output of 30%. Pepsin output (mg/h) was also decreased from 207.5 (67.7) (mean (SE] in the hour preceding blood infusion to 135.7 (54.7) in the hour after infusion (p less than 0.02) representing a mean reduction in pepsin output of 43%. In six volunteers gastric emptying of a liquid meal was delayed after intraduodenal blood infusion compared with intubation alone with the emptying time (min) to half volume (t 1/2) being prolonged at 75.0 (8.2) (mean (SE] after blood infusion compared with 35.5 (6.6) after intubation alone (p less than 0.02). Plasma GIP concentrations (ng/l) increased to peak levels of 127.9 (62.7) (mean (SE] after intraduodenal blood infusion compared with the pre-infusion value of 58.3 (2.3) (p less than 0.02). These changes may represent protective physiological responses to facilitate haemostasis.     

Decreased plasma isoleucine concentrations after upper gastrointestinal haemorrhage in humans.

BACKGROUND: A decrease in arterial isoleucine values after intragastric blood administration in pigs has been observed. This contrasted with increased values of most other amino acids, ammonia, and urea. After an isonitrogenous control meal in these pigs all amino acids including isoleucine increased, and urea increased to a lesser extent, suggesting a relation between the arterial isoleucine decrease and uraemia after gastrointestinal haemorrhage. METHODS: To extend these findings to humans, plasma amino acids were determined after gastrointestinal haemorrhage in patients with peptic ulcers (n = 9) or oesophageal varices induced by liver cirrhosis (n = 4) and compared with preoperative patients (n = 106). RESULTS: After gastrointestinal haemorrhage, isoleucine decreased in all patients by more than 60% and normalised within 48 hours. Most other amino acids increased and also normalised within 48 hours. Uraemia occurred in both groups, hyperammonaemia was seen in patients with liver cirrhosis. CONCLUSIONS: These results confirm previous findings in animals and healthy volunteers that plasma isoleucine decreases after simulated upper gastrointestinal haemorrhage. This supports the hypothesis that the absence of isoleucine in blood protein causes decreased plasma isoleucine values after gastrointestinal haemorrhage, and may be a contributory factor to uraemia and hyperammonaemia in patients with normal and impaired liver function, respectively. Intravenous isoleucine administration after gastrointestinal haemorrhage could be beneficial and will be the subject of further research.     

Neodymium-Yag laser photocoagulation for haemostasis of gastrointestinal non-variceal haemorrhage

Neodymium-Yag laser treatment in 130 patients with upper gastrointestinal bleeding, including spurting arterial bleeding, active oozing or fresh stigmata of bleeding (fresh clot or non-bleeding vessel), permitted overall initial haemostasis in 95% of the patients. Total laser failures (rebleeds) amounted to 22%. Considering only the ulcers with vessels in 36 patients, initial control of haemorrhage was achieved in 83%, but the total failure rate amounted to 50%. A controlled randomized study in 129 patients with oozing bleeding and patients with stigmata of bleeding showed a significant (p less than 0.001) reduction of duration and of the recurrence rate of bleeding and a significant decrease (p less than 0.05) of operative indications. Mortality rates however were not lowered by laser therapy. Complications of lasertherapy did not occur. One hundred thirty-eight gastrointestinal angiomas were treated by Yag laser photocoagulation in 32 patients without complications. Although the results of Yag laser treatment of gastrointestinal bleeding seem promising, endoscopic laser techniques should be improved to optimise the results and to improve the prognosis of life-threatening gastrointestinal bleedings.     

Endoscopic haemostasis of the upper gastrointestinal tract

The realm of endoscopy has gone from that of diagnosis to that of diagnosis and therapy. Therapeutic endoscopy is a rapidly advancing frontier in the field of gastroenterology. Its use in securing haemostasis has recently flourished. Considerable progress has been made. Various experimental techniques have been tried and found lacking, while others, such as laser photocoagulation, electrohydrocoagulation and endoscopic sclerotherapy, are proving to be very useful. The mortality for upper gastrointestinal bleeding has remained high for decades, despite recent advances in medicine. This may be related to the shift in the population toward the older age group. Recent advances in endoscopic haemostasis seem to be showing promise in improving survival rates. This is a result of improved recognition of risk factors, including the stigmata of recent haemorrhage, of early surgical intervention in the elderly, and of the ability to reliably secure haemostasis endoscopically. This chapter gives an account of the various techniques of endoscopic haemostasis and explains the numerous controversies through the discussion of selected experimental and clinical trials.     

Management of upper gastrointestinal haemorrhage

Abstract Endoscopic therapy is the first treatment modality in the management algorithm of upper gastrointestinal haemorrhage. In treating bleeding peptic ulcers, diluted epinephrine is first injected followed by targeted treatment to the vessel. Combination therapy adding thermocoagulation or thrombin/fibrin products has been shown to further improve the rate of haemostasis. There is also some evidence to suggest that adjuvant use of optimal acid suppression using high-dose proton pump inhibitors can reduce recurrent bleeding after initial endoscopic control. In treating acute variceal haemorrhage, early administration of vasoactive agents facilitates endoscopic treatment. These drugs should be continued during and after endoscopic therapy to prevent recurrent in-hospital bleeding. Firm evidence exists to date that band ligation is the endoscopic treatment of choice in the acute control of bleeding varices and their secondary prophylaxis against recurrent bleeding. The role of band ligation as primary prophylaxis for first bleeding remains controversial. Transjugular intrahepatic porto-systemic shunts are used as a rescue procedure when endoscopic treatment fails. In selected patients with recurrent variceal haemorrhage and good hepatic reserves, surgical shunts may be indicated.     

Comparison of emergent endoscopy and upper gastrointestinal series radiography in acute upper gastrointestinal haemorrhage.

A prospective study of early diagnostic procedures in acute upper gastrointestinal haemorrhage was conducted in a series of 76 patients. The diagnostic procedures included upper gastrointestinal series radiography (UGIS) and endoscopy (ENDO). The clinicians' diagnosis and management improved in a statistically significant way as a result of the findings of endoscopy. The findings of UGIS did not significantly improve diagnostic accuracy and resulted in a statistically significant adverse effect on patient management. The results suggest that endoscopy is more effective in promoting early accurate diagnosis and management in patients with acute upper gastrointestinal haemorrhage.     

Controlled trial of cimetidine in upper gastrointestinal haemorrhage.

One hundred and one patients were studied in a double-blind controlled trial to assess the role of oral cimetidine in preventing the continuation or recurrence of acute upper gastrointestinal haemorrhage from various sources, chiefly peptic ulcer. The dose of cimetidine was 800 mg on entering the study followed by 400 mg six hourly. The source of bleeding was identified endoscopically in 96% of patients, peptic ulcer comprising 70%. Bleeding continued or recurred in 11 of 51 (21.5%) of patients on cimetidine and in 12 of 50 (24%) of patients on placebo. Analysis of the effect of cimetidine according to age or severity of bleeding showed no significant advantage for the drug.     

Determination of fibrin-fibrinogen degradation products in gastric aspirate from patients with upper gastrointestinal haemorrhage

During a 3-year period, 157 patients with upper gastrointestinal haemorrhage were admitted. In 54 of them gastric blood was made available for study of the level of fibrin-fibrinogen degradation products (FDP) to reveal the prevalence of increased local fibrinolytic activity. In all patients except three, FDP in systemic and gastric blood was identical, at less than or equal to 40 micrograms/ml. Two patients with erosive gastroduodenitis and one with a gastric ulcer had high levels of FDP in blood aspirated from the stomach. The present results would suggest that increased local fibrinolytic activity is very seldom involved in the induction and/or maintenance of upper gastrointestinal haemorrhage.     

Comparison of inpatient and outpatient upper gastrointestinal haemorrhage

Background and aims Inpatients developing upper gastrointestinal (GI) haemorrhage are at increased risk of death. This study was performed to elucidate differences in inpatients and outpatients.Patients/methods Three hundred and sixty-two patients who needed esophagogastroduodenoscopy for upper GI bleeding were identified from endoscopy charts. Patients characteristics, bleeding parameters, clinical presentation, pre-existing medication, and laboratory data were compared between patients who were admitted because of upper GI bleeding and patients who developed bleeding while in hospital for other reasons.Results/findings Hospital mortality was 39.0% in inpatients vs. 11.1% in outpatients (p<0.01). Death due to bleeding was observed in 9.5% of inpatients vs. 2.5% of outpatients (p<0.01). Whereas peptic ulcer was the most common source of bleeding in both, variceal bleeding was the most common cause of death because of haemorrhage in both. Recurrent bleeding was associated with mortality in outpatients (p<0.001), but not in inpatients (p=0.11). Rates of bleeding recurrence and need for surgery was similar in both groups. Inpatients suffered more often from renal disease, pulmonary disease, diabetes mellitus, coagulopathy, or immunosuppression, and were treated more frequently with acetylsalicylic acid, glucocorticoids and heparin. The frequency of pre-existing disease was higher in inpatients.Interpretation/conclusion Higher mortality after GI bleeding in inpatients than in outpatients is due to a generally higher prevalence of co-morbidity rather than a single or a few risk factors.     

Bacteremia after upper gastrointestinal endoscopy.

During 24 months, 200 upper gastrointestinal endoscopies were performed on 193 patients. Blood cultures were obtained before and five and 30 minutes after the procedure using thiol (50 ml) and trypticase soy broth (100 ml) media. The mean endoscopic time was 34 minutes. Sixteen patients developed bacteremia (8%). Twelve groups of microorganisms were detected in positive blood cultures: Streptococcus (5 species), Lactobacillus sp, Veillonella alcalescens, Staphylococcus aureus, Staph epidermidis, Propioni-bacterium acnes, Corynebacterium acnes, and Bacillus subtilis. Seven patients had positive blood cultures at five and 30 minutes, eight at five minutes, and one at 30 minutes only. There was no clear correlation of bacteremia with the age or previous history of the patient, biopsy, active bleeding, endoscopic time, or findings. A follow-up study of all patients for six months to two years indicated no complications related to endoscopy and/or bacteremia.