Endoscopy of the esophagus, stomach, and duodenum or endoscopy of the large bowel are generally recommended within 24 hours and may allow treatment as well as diagnosis.An upper GI bleed is more common than lower GI bleed. An upper GI bleed occurs in 50 to 150 per 100,000 adults per year. A lower GI bleed is estimated to occur in 20 to 30 per 100,000 per year. It results in about 300,000 hospital admissions a year in the United States. Risk of death from a GI bleed is between 5% and 30%. Risk of bleeding is more common in males and increases with age. Classification
Gastrointestinal bleeding can be roughly divided into two clinical syndromes: upper gastrointestinal bleeding and lower gastrointestinal bleeding. About 2/3 of all GI bleeds are from upper sources and 1/3 from lower sources. Common causes of gastrointestinal bleeding include infections, cancers, vascular disorders, adverse effects of medications, and blood clotting disorders. Obscure gastrointestinal bleeding (OGIB) is when a source is unclear following investigation. Upper gastrointestinal
Upper gastrointestinal bleeding is from a source between the pharynx and the ligament of Treitz. An upper source is characterised by hematemesis (vomiting up blood) and melena (tarry stool containing altered blood). About half of cases are due to peptic ulcer disease (gastric or duodenal ulcers). Esophageal inflammation and erosive disease are the next most common causes. In those with liver cirrhosis, 50–60% of bleeding is due to esophageal varices. Approximately half of those with peptic ulcers have an H. pylori infection.
Etiology
Microbiology
Of the microflora characterised in aggressive periodontitis, approximately 65-75% of bacteria are Gram-negative bacilli, with few spirochaetes or motile rods present. Aggressive periodontitis is often characterised by a rapid loss of periodontal attachment associated with highly pathogenic bacteria and an impaired immune response. Various studies have associated Aggregatibacter actinomycetemcomitans, formerly known as Actinobacillus actinomycetemcomitans, with aggressive periodontitis. An early study dating back to 1983 explains its prevalence and documents its role in localised aggressive periodontitis.Virulence factors are the attributes of microorganisms that enable it to colonise a particular niche in its host, overcome the host defences and initiate a disease process. Fives Taylor et al. (2000) have categorised the virulence factors of Aggregatibacter actinomycetemcomitans as follows. Samaranayake notes the evidence for the specific involvement of Aggregatibacter actinomycetemcomitans includes: an increased incidence of it found in subgingival plaque obtained from lesional sites, high level of its antibody which tends to fall following successful treatment, its possession of a wide range of potentially pathogenic products and its elimination with concordant disease regression, following treatment with successful periodontal therapy and adjunctive tetracycline.Porphyromonas gingivalis is a Gram-negative anaerobe associated with the pathogenicity of periodontal disease, and aggressive periodontitis is no exception. Greater numbers of both Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans were found in active, destructive periodontal lesions in comparison to non-active sites.Capnocytophaga spp are implicated as prime periodontal pathogens, especially in localised aggressive periodontitis.