AETIOLOGY, CLINICAL PRESENTATION
AND OUTCOME OF UPPER
GASTROINTESTINAL BLEEDING –
A STUDY OF 100 CASES
INTRODUCTION
Upper gastro intestinal haemorrhage is a common & serious medical as well as surgical emergency. The most common presenting features of upper gastro intestinal haemorrhage are haematemesis & maelena1.
Haematemesis indicates an upper gastro intestinal source of bleeding (above the ligament of treitz)”. Haematemesis may be red with clots when bleeding is profuse or black (coffee ground) when less severe. Syncope may occur and it is due to hypotension from intravascular volume depletion. Symptoms of anemia suggest chronic bleeding.3
Melaena is the term used to describe the passage of black, foul smelling, tarry, stools containing altered blood.3 Melaena indicates that blood has been present in upper gastro intestinal tract for at least 14 hours2. Melaena develops after as little as 50-100 ml blood loss in the upper gastro intestinal tract. The characteristic appearance is result of action of digestive enzymes and bacteria upon haemoglobin 3.
In USA approximately 115 patients per 100,000 populations are hospitalized each year for the episode of upper gastro intestinal haemorrhage 4. This leads to approximately 250,000 new hospital admissions per year 5. Among them 33-62% are due to peptic ulceration, 4-31% from varices, 3-11% due to gastroduodenal erosion and 1-4% from malignancy2 .
Mortality from bleeding increases with age 6. Mortality of patient admitted to hospital following gastro intestinal haemorrhage is about 10%3. The mortality rate for patients under 60 years of age without any organ failure or malignancy is <1%2. However mortality from a first bleed from varices is around 50%7 and most8 survivors rebleed with an inpatient mortality of about 30%8.
As an immediate management of all cases of recent (within 48 hours) significant gastro intestinal haemorrhage should be admitted into hospital9.
Upper GI endoscopy is the best choice in patient with upper gastro intestinal haemorrhage. Emergency endoscopy enables diagnosis as well as appropriate therapy & provides important prognostic significance.
With the introduction of widespread fibre optic endoscopy service it became clear that many minor mucosal lesions had been missed when diagnosis of the cause of bleeding had relied on clinical and radiological means. From different studies in home and abroad leading causes of upper Gl haemorrhage are-7
1. Duodenal ulcer.
2. Gastric erosion.
3. Gastric ulcer.
4. Ruptured esophageal varices.
5. Gastric cancers.
6. Miscellaneous. . .
It is sometimes very difficult to find out the causes of UGIB from the list of numerous aetiology, which are already mentioned, ranges from curable peptic ulcer disease to killer disease like carcinoma.
Considering the diverse aetiology and its effect which can be minimal to fatal, all cases of recent (within 48 hours) significant gastrointestinal bleeding should be admitted to hospital, the causes of UGIB should be identified as early as possible and treated promptly. In approximately 80% of patients presenting with acute UGIB, bleeding ceases spontaneously and does not recur10. Such cases are often initially treated with intravenous crystalloid or colloid solution & blood is given to restore blood pressure when patients is shocked or when haemoglobin concentration is less then 100g per liter before detecting aetiology3. Knowledge regarding common causes of UGIB in our country is therefore necessary because it is an important problem in our hospital where we deal with these patients frequently.
In Bangladesh endoscope is now available in almost every medical college hospital, in some private clinics and diagnostic centers of the country. For detection of causes of upper GIT bleeding there is no alternative for actual visualization of bleeding points by endoscopy. This will not only solve some of our problems but also provide with an opportunity to make an appraisal of UGIB. However endoscopy is not available in district and upazila hospital where often our junior doctors manage the patients.
Considering all these, the study which has been carried out in 100 patients will help create awareness among all level of medical practitioners and enhance prompt diagnosis or at least early referral. That may reduce sufferings and cost of expensive tests for the poor patient of this country and our doctor can even appropriately manage patients with upper GIT bleeding outside tertiary hospital.
KNOWLEDGE ABOUT UPPER GASTRO-INTESTINAL
HAEMORRHAGE
Most patient with haematemesis and melaena present in the hospital as primary bleeder while some patients (secondary bleeders) who are critically ill develop haematemesis and melaena in the hospital. The mortality is very high in patient with bleeding that develops in the hospital and this is usually a result of systemic diseases. 12
Haematemesis means the vomiting of fresh blood, blood with clots, or blood which has been subjected to digestion by gastric juices. The presence of fresh blood in the vomitus implies recent haemorrhage, often moderately large volume, from the upper alimentary tract, where as the presence of ‘coffee ground’ vomit suggests UGI bleeding, sometimes of smaller volume, over a more prolonged period13.
Melaena is the term used to describe passage of black tarry stool containing altered blood; this is usually due to bleeding from upper GI tract, although haemorrhage from the right side of the colon is occasionally responsible. The characteristic appearance is the result of action of digestive enzymes and bacteria upon haemoglobin. Such stools are tarrying (“sticky”) and have a characteristic odour.14
In case of bleeding from the stomach, the process is initiated by acid pepsin at the initial site. Other factors influencing the production of tarry stool are:
1. Site of bleeding
2. Amount of bleeding
3. Rapidity of bleeding
4. Intestinal transit time
5. Bacterial breakdown of haemoglobin in the intestine.
Haematemesis results from a combination of large amount of blood filling the stomach together with the urge to vomit. So haematemesis generally indicates a more severe bleeding episode than melaena. On the other hand, at least 60ml. blood is required in the upper GIT to produce a single black stool. Melaena usually denotes bleeding from the esophagus, stomach or duodenum but lesion in the jejunum, ileum and even ascending colon may occasionally because melaena provided the gastrointestinal transit time is sufficiently prolonged.
Haematochezia is the passage of bright red blood per rectum, generally signifies bleeding from a source distal to the ligament of treitz. However, brisk proximal bleeding can cause haematochezia due to rapid transit.
AETIOLOGY OF UPPER GASTROINTESTINAL BLEEDING
Haematemesis and melaena, the commonest presentation of upper GI haemorrhage results from a variety of causes:
Common Causes:
1. Peptic Ulcer -Duodenal ulcer and Gastric ulcer
2. Erosive gastritis
3. Varices or portal hypertension
4. Reflux oesophagitis
5. Mallory-Weiss tear
6. Vascular malformation
Uncommon causes:
1. Gastric carcinoma, lymphoma, polyp and other gastric tumour.
2. Duodenal and jejunal diverticuli.
3. Aorto-duodenal fistula
4. Primary aortoesophageal fistula
5. Haemobilia following hepatic surgery or trauma
6. Primary blood dyscrasias.
7. Vasculitis.
8. Hereditary hemorrhagic telangiectasia
9. Connective tissue disorder: eg. PAN. 15
10. Uraemia
11. No sources identified
Peptic ulcer is the common cause of upper GI bleeding. In Greece a study conducted in 1534 patients’ shows that peptic ulcer (67%) is the main cause of upper GI bleeding.16
In a study in Thailand on 5000 patients of haematemesis and melaena showed peptic ulcer-51.24%, acute mucosal erosions-31.6 %, cancerous bleeding-1.66%,
gastric polyp-28%, normal study-2.46%, Another study in Jerusalem showed DU-16.9%, esophageal varices-7.5%, erosive gastritis-8,2%, esophagitis-7.5%.17
In one study of American society of gastro endoscopy, shows usually the frequency of haemorrhage is directly related to the duration of disease. However, there is a greater tendency to bleed during the first year 84% as opposed to 5.4%, 5% & 5.9% in subsequent years respectively. In national American Society of Gastroenterology (ASGE) survey on upper GIT involving 2225 patients, six pathological entities were responsible for most bleeding episode. These include in decreasing order of frequency duodenal & gastric ulcer, acute gastritis, oesophageal varices, esophagitis and Mallory-Weiss tear.19 acute gastric erosions & gastritis have become increasingly common and assumed an important position among the causes of upper GI haemorrhage. The study of gastritis has been widened by the use of the fibreoptic endoscope. Massive haematemesis and /or melaena are caused by gastritis in 21.5%, acute haemorrhagic erosive gastritis in 18.5% of the hospitalized patients for upper GI haemorrhage. Massive bleeding in patients with cirrhosis of liver may be due to gastritis and is 22%. Similarly variceal bleeding is much more common, In a survey in England, Scotland & Sweden bleeding from varices was 7.3% but in USA it was 11.2%.20
The proportion of cases of variceal bleeding is greater in countries where alcohol consumption is higher and where hepatitis B virus infection is common.
In recent years UGI bleeding has been associated with the ingestion of NSAIDs taken for arthritis or local motor disorders. Among the patients bleeding from peptic ulceration about 35% had ingested NSAIDs in the week prior to presentation and the majority (84%) over the age 60 year .15 A study of Somerville K 20has shown that 35-55% of elderly patients admitted with upper GI bleeding have taken NSAIDs. Up to 22% of bleeding episode may be due to these drugs with a mortality of 10%.
Vascular anomalies are found throughout the gastrointestinal tract may the source of acute upper GI bleed. The account for about 7% of causes of bleeding vascular ectasias (angiodysplasia) has a bright red stellete appearance. They may be part of systemic condition (hereditary hemorrhagic telangiectasia- CREST syndrome) 21.
In a small but definite proportion of cases no identifiable source of bleeding is found are also have some interest?
Upper gastrointestinal bleeding with no identifiable cause:
1. Lesion missed: Site obscured (blood clots etc)
Gastric fundus not fully examined
2. Inexperienced operator
3. Lesion healed
4. Intermittent bleeding
5. Delay in investigation
6. Site not considered / reached:
Nasopharynx
Second part of duodenum
Biliary tract Pancreas
PATHOPHYSIOLOGY
Ulcer: Ulcers are defined as disruption of mucosa integrity of the stomach or duodenum leading to local defect or excavation due to active inflammation. Ulcer occurs in the stomach or duodenum often chronic in nature. 22
Peptic ulcer: Peptic ulcers are chronic, most often solitary lesions that occur in any portion of the gastrointestinal tract exposed to the aggressive action of acid-pepsin juices.22
Distinctive features of peptic ulcer: 23
1. Usually a single lesion.
2. Tends to be less than 4 cm in diameter.
3. By definition penetrates muscular is mucosa; may perforate gastric wall.
4.Is frequently recurrent, with intermittent healing.
5. Is located in the following sites, with decreasing frequency;
I. Duodenum, first part,
ii. Stomach, usually antrum.
iii. Within barret’s mucosa.
Iv. In the margins of a gastroenterostomy (stomal ulcer)
V. In the duodenum, stomach, or jejunum of patients with
Zollinger-Ellison syndrome.
vi. Within or adjacent to a meckel’s diverticulum that contains ectopic gastric mucosa.
Morphology:
Ninty eight percent of peptic ulcers are located in the first part of duodenum, or in the stomach in a ratio 4:1, most duodenal ulcer is in the first part of the duodenum within a few cm of pyloric ring. The anterior wall of the duodenum is more often affected than the posterior wall. Gastric ulcers are predominantly located in the lesser curvature in and around the border zone between the corpus and the antral mucosa. Less frequently they may occur on the anterior or posterior wall of the greater curvature of the stomach. In 10 to 20% of patients with gastric ulceration, there may be a coexistent duodenal ulcer. Irrespective of the site, chronic peptic ulcer has a fairly standard gross appearance. Small lesion less than 0.3 cm are more likely to be shallow erosion, those greater than 0.6 cm are likely to be ulcer. Although more than 50% peptic ulcers have a diameter of less than 2 cm, about 10% of benign ulcer greater than 4 cm. Even carcinomatous ulcer is may be less than 4 cm in size. So, size does not differentiate benign from a malignant ulcer.
Histological appearance:
The histological appearance varies from active necrosis to chronic inflammation and scarring to healing. In active ulcers with ongoing necrosis, four zones are demonstrable:
1. The base and margins have a superficial thin layer of necrotic: fibrinoid debris not visible to the naked eye.
2. Beneath this layer is the zone of a nonspecific inflammatory infiltrate with neutrophils predominating.
3. In the deeper layers, especially in the base of the ulcer, there is an active granulation tissue infiltrated with mononuclear leukocytes.
4. The granulation rests on a more solid fibrous or collagenous scar.
GASTRIC PHYSIOLOGY RELATED TO PEPTIC ULCER:
A. Aggressive factors:-
Acid and pepsin:
The gastric mucosa has an extraordinary capacity to secrete acid. The parietal cells scattered along the course of the mucosal glands (oxyntic mucosa) of the body and fundus of the stomach secretes HCL by a process involving oxdative phosphorylation. The estimated concentration of HCL by parietal cells is approximately 160 ml. For each H+ Secreted into lumen, one HCO3– is released into the gastric venous circulation, accounting for alkaline tide, reflection of gastric HCL secretion.
The final step in H+ secretion is accompanied by a proton pump mechanism involving specific hydrogen potassium adenosine triphosphatase (H+K+ ATPase) located in the apical micro villous1 membrane and tubulovesicular apparatus. The major physiological stimulus for gastric acid secretion is ingestion of food. Traditionally regulation of gastric acid secretion has been classified into three phases.
Phases:
Cephalic, gastric and intestinal.
Cephalic phase:
Is initated by the sight of taste, smell, chewing & swallowing of palatable food. This phase is largely mediated by direct vagal stimulation of gastric release.
Gastric Phase:
Induced by food in the stomach.
Intestinal Phase:
Is initiated when food containing digested protein enters the proximal small intestine. The stimulation of acid secretion that occurs at that time is thought to be related to elaboration in the small intestine of a polypeptide quite distinct from gastrin.
The proteolysis effect of pepsin in concert with the corrosive properties of secreted gastric acid contributes to the tissue injury that produce peptic ulcer. Gastric acid catalyzes the cleavage of inactive pepsinogen molecules, converting them to proteolytically active pepsins and also provides the low PH required for pepsin activity.
B. Mucosal Defense:
The mechanism by which the normal stomach & duodenum resists the corrosive effects of acid & pepsin (i.e. the mechanism of mucosal resistance to injury or mucosal defense) have not been defined clearly. However, a variety of factors have been identified that contribute to or compromises mucosal defense.
Factors are-
Gastric Mucus
Bicarbonate (HCO3~)
Prostaglandin
Epithelial barrier
Mucosal blood flow
Neural & muscular component.
Gastric mucus:
Secreted by mucous cells of gastric mucosal epithelium and gastric gland is important in mucosal defense and in preventing peptic ulceration. Mucus secretion is stimulated by mechanical or chemical irritation and by cholinergic stimulation. Gastric mucus is present in two phases: In a stable phase; in gastric juice & as in insoluble mucus gel layer, approximately 0.2 mm thick, which coats the mucosal surface of the stomach. When intact this mucus gel serves as a unstirred water layer that slows ionic diffusion but more impermeable to penetration macromolecule such as pepsins (Mol.wt 34,000). Gel thickness is increased by prostaglandin E & reduced by aspirin & other NSAIDs. Gastric mucus glycoproteins also contain antigenic determinants used to classify ABO blood group substance. Approximately 3/4th of the population secretes gastric juice containing these ABO substances. Such individuals are referred to as secretors.
Bicarbonate (HCO3):
Non parietal gastric epithelial cells secrete HCO3– ions into mucus gel which help create a microenvironment with a substantial H+ ion gradient ranging from PH 1 to 2 in the luminal side of the gel layer toPH 6 to 7 in the zone in contact with gastric mucosal cells. As an unstirred water layer, the mucus gel slows the diffusion of H+ toward the gastric mucosal surface allowing buffering by HCO3– with the gel gastric HCO3– is stimulated by calcium, certain prostaglandin of E&Fseries, cholinergic agents & dibutyryl cyclic guanidine monophosphate. Aspirin & NSAIDs, acetazolamide, adrenergic agents inhibit it.
Epithelial barrier (Tight junction):
Normally the luminal surfaces and intercellular tight millions of the gastric epithelial cells create a gastric mucosal barrier that is almost completely impermeable to diffusion of the H+ from the lumen. There barrier can be interrupted by bile acids, ethanol, & weak organic acids, permitting H+ to diffuse into the gastric tissue. The result may be cell injury and release of histamine from mast cells, further stimulation of acid secretion, and damage to small blood vessels, mucosal haemorrhage, and erosion or ulceration.
Mucosal blood flow:
The gastric mucosa has a rich blood supply consisting of extensively arborising capillaries. A rich blood flow is necessary to provide O2, HCO3–, and nutrients to epithelial cells and to remove back diffused acids. Mucosal blood flow is regulated by local vasoactive mediators, particularly endogenous nitric oxide (generated by endothelial cells), prostaglandins, and neuropeptides, increased blood flow occurs simultaneously with stimulation of acid secretion. Gastric blood flow may be adversely affected by severe medical or surgical stress exogenous agents such as aspirin & alcohol and entry into the lamina propriety of luminal agents such as acid and pepsin.
Prostaglandin:
Prostaglandins are abundant in the gastric mucosa. Administration to animals of various prostaglandins, particularly those of E series has been shown to prevent mucosal injury caused by a wide variety of agents. Endogenous prostaglandins stimulate secretion of gastric mucus, gastric and duodenal HCO3– . They participate in the maintenance of gastric mucosal blood flow and of the integrity of the gastric mucosal barrier and promote epithelial cell renewal in response to mucosal injury.24
Neural and muscular component:
Afferent neurons within the mucosa of the stomach and perhaps the duodenum can trigger a protective reflex vasodilatation when toxins or acid breach the epithelial barrier. In addition muscular is mucosa may serve to limit the injury. Superficial damage limited to the mucosa can heal within hours to days. When damage extends in the sub mucosa, a minimum of several weeks is required for complete healing.
Pathogenesis of peptic ulcer 25:
1. Peptic ulcers are produced by an imbalance between the gastroduodenal defense mechanisms and the damaging forces.
2. Some level of acid pepsin secretion is requisite for the development
of duodenal & gastric ulcreation.
3. For duodenal ulcers, major causal influences appear to be exposure of gastroduodenal mucosa to excessive amounts of acid & pepsin.
4. For Gastric ulcers, the major causal influence appears to be some break down in gastric mucosal defense against acid & pepsin.
Duodenal ulcers:
In general, duodenal ulcer patients have:
1) Increased capacity to secrete acid & pepsin
2) Increased responsiveness to stimuli of acid secretion and
3) In some patients with DU, there is too rapid gastric emptying exposing the duodenal mucosa to an excessive acid load.
Gastric Ulcer:
GU patients as a group have acid secretion rate that is normal or reduced compared with non ulcer subjects, although true achlorhydria almost rever occurs with benign GU. It is suggested from different data that is existence of some primary defect in gastric mucosal resistance like-
o an increased tendency of back diffusion of H+ augmenting some derangement in the gastric mucosal barrier.
o Frequent association of chronic antral gastritis with the ulcer. Gastritis is present in association with ulceration in most cases.
o Gastritis persists even after the ulcer heals, suggesting that gastritis is primary and gastric ulcer secondary.
Helicobacter pylori in gastroduodenal disease:
Helicobacter pylori colonize the gastric mucosa. It is found primarily in the
deeper positions of the mucus gel that coats the gastric mucosa and between the mucus gel layer and apical surfaces of the gastric mucosal epithelial cells. H pylori may adhere to the luminal surfaces of gastric epithelial cells but does not invade the gastric mucosa.
H pylori produce a variety of proteins that appear to mediate or facilitate its damaging effect on the gastric mucosa. Urease produced by H pylori catalyzes the hydrolysis of urea to ammonia and carbon dioxide. Hydroxide ions generated by equilibration of water with ammonia may contribute to gastric mucosal epithelial damage. H.pylori produces surface proteins that are chemotactic for human neutophils and monocytes and secrets platelet activating factors which is also pro inflammatory. H pylori activate monocots which express HLA-DR & IL2 receptors on their cell surfaces and produce superoxides IL1 and TNF. This organism also produces protease and phospholipase, which degrade the glycoprotein lipid complex of the mucus gel layer, this activity reduces the thickness and viscosity of the mucus gel layer overlying the gastric mucosal epithelial cell layer.26‘27
Risk Factors for peptic Ulcer:
Dietary factors:
Dyspepsia may be caused by certain foods, spices beverages. Tovey in 1979, 28 reported that DU is more in rice eating belt in south India compared with wheat eating areas in the north and there is no geographic correlation between habitual consumption of hot spices and the high prevalence of DU in some case.
Alcohol:
Alcohol has not been proved to cause peptic ulceration directly. But according to Hudson30 possibly alcohol ingestion has got some relationship with development of erosive mucosal disease in the stomach leading to bleeding.
Drugs:
Aspirin and other NSAIDs cause acute gastric mucosal damage and precipitate upper GI bleeding.
Cigarette smoking:
Cigarette smoking has been associated with an increased incidence of DU, a
Decreased response to DU therapy and an increased mortality from DU. Cigarette smoking impairs healing and favours recurrence and so is suspected of being ulcerogenic, possibly by suppression of mucosal prostaglandin synthesis29.
Association with blood groups, antigens HLA and secretary status:
Patients with DU have an increased frequency of blood group O and of the non secretary status (absence of secretion of blood group) ABO antigens into the gastric juice), but these association are weak. More over the association with blood group O may relate to preferential binding of group O antigens to H pylori. An increased incidence of HLA-B5 antigen has been reported in white male subjects with DU.
Association of peptic ulcer with some other disease:
1. Gastrinoma and MEN type- 1
2. Chronic obstructive pulmonary disease.
3. crf.
4. Cirrhosis of liver
5. Alpha 1-antitrypsin deficiency
6. Systemic mastocytosis.
7. Basophilic leukaemia.
Acute erosion and stress ulceration:
Definition: 23
Focal acutely developing gastric mucosal defects may appear following severe stress, whatever its nature-hence the designation stress ulcer. Stress erosions and ulcer are most commonly encountered in patients with shock, extensive burn, sepsis or severe trauma (Curling’s ulcer), in any intracranial conditions that raises intracranial pressure.
Erosion:
Is defined as mere shedding of the superficial epithelium of the stomach and occasionally of the duodenum. When they involve the entire mucosal thickness
they are termed stress ulcer.
Criteria of erosion:
1) Acute gastric ulcer is usually less than 1 cm is diameter, is circular and rarely penetrates beyond the mucosa.
2) The ulcer base is frequently stained a dark brown by the acid digestion of extruded blood.
3) They may occur singly or more often multiply throughout the
stomach and duodenum.
4) Conspicuously absent are scarring or thickening of blood vessels, as seen in chronic peptic ulcer.
5) Healing with complete re-epithelization occurs after the causative factors are removed.
Recurrent ulcer: 21
Recurrent ulcerations occur in approximately 5% of all patients after surgery for peptic ulcer. The risk for recurrence is 3 to 10% after surgery for DU and approximately 2% other GU surgery. Recurrence is more common after vagotomy with enterectomy. When ulcers occur after partial gastric resection, the ulcer is usually located at the anastomosis (stomal or marginal ulcer) or immediately distal in the small intestine.
Aetiology of recurrent ulcer: 30
Inadequate surgical procedures:
Simple gastroenterostomy is the most obvious example of an inadequate surgical procedure in that it fails to reduce vagal stimulation, antral gastritis or parietal cell population. Inadequate vagotomy, inadequate gastric resection, inadequate drainage after gastroenterostomy and pyloroplasty etc. are the common causes of recurrent ulceration.
Unrecognized endocrine factors:
Hypergastrinoma is due to Zollinger-Ellison syndrome and antral
G-cell hyperplasia.
Ulcerogenic agents:
Chronic use of aspirin and other NSAIDS have been associated with recurrent ulcers. In Cirrosis of liver when there is congestive gastropathy intake of NSAIDs 3 1 may lead to develop ulcer31.
Smoking is also associated with recurrent ulcer32.
Tumours of the Stomach:33‘34
| Benign | Malignant |
| 1. Hyperplastic polyp2. Leiomyoma.3. Fibroma.4. Neurofibroma |
5. Heterotypic pancreas.
6. Lipoma.
7. Leiomyoblastoma.
8. Gastric cyst.
9. Vascular tumours.1. Carcinoma of stomach2.Metastatic tumour3. Lymphoma.4. Leiomyosarcoma
5. Sarcoma.
6. Carcinoid
7. Malignant vascular tumor.
8. Haemangiopericytoma.
9. Haemangioendothelioma
10. Kaposis sarcoma.
Clinically recognizable benign gastric lesions probably occur in about 5% of all patients. 50% of the benign tumours discovered incidentally when investigations done for other reasons. Usually these lesions are symptompless. The most common presentations are pain and gastro-intestinal bleeding. The overlying mucosa of the many submucosal tumours tends to ulcerate and massive haemorrhage may result. This most often takes the form of melaena, although haematemesis can also occur. 33
Among the malignant tumours that occur in the stomach, carcinoma is the overwhelmingly, the most important and the most common (90 to 95%). Next in order of frequency lymphoma (4%), characinoid (3%) and malignant spindle cell tumour (2%).
Esophageal varices:
Varies are tortuous dilated veins lying primarily within the submucosa of the distal oesophagus and proximal stomach. Venous channels directly beneath the oesophageal epithelium may also become massively dilated. Oesophageal varices are mainly supplied by the left gastric vein and gastric varices are largely supplied by the short gastric veins and drain into the deep intrinsic veins of the oesophagus.35 Haemorrhage from the oesophageal varices is a major complication of portal hypertension. The bleeding from the varices may occur when the portal pressure exceeds 11 to 12 mm of Hg above the inferior venacaval pressure. However not all patients with pressure above these levels have bleeding varices. The tension on the vessel wall is greater in larger than in small varices for given pressure. Therefore, large varices are more likely to rupture and bleed than are smaller ones36. Oesophageal varices is a common cause of bleeding and carry a mortality rate of 50% and most survivors rebleed an inpatient mortality of 30%36 and most survivors rebleed an inpatient mortality of 30%11, gastric varices develop in the settings of portal hypertension but ten times less than oesophageal varies. Gastric varices lie within 2 to 3 cm of gastroesophageal junction and rarely occur in the absence of esophageal varices.
Oesophagitis:
Injury to the oesophageal mucosa with subsequent inflammation is called oesophagitis. According to aetiology it is of three types:
1. Reflux
5. Infective
3. Others
Reflux oesophagitis:
Consists of esophageal mucosal change caused by reflux of gastric or intestinal contents in the oesophagus. Depending on the causative agents it is referred to as peptic, bile or alkaline oesophagitis.38
The normal anti reflux mechanism consists of the lower oesophageal
sphincter & the anatomic configuration of gastro-oesophageal junction. Reflux occurs only when the gradient of pressure between the lower oesophageal sphincter (LES) and the stomach is lost. It can be caused by increased intra thoracic pressure or by a transient or sustained decrease in LES tone. Decreased tone may be due to:
Primary cause: Due to muscle weakness or to inappropriate sphincter relaxation mediated by inhibitory nerves.
Secondary causes:
Scleroderma.
Myopathy
Pregnancy
Smoking
Smooth muscle relaxant, (Beta-blocker, aminophyline, nitrates and calcium channel blocker)
Surgical resection
Hiatus hernia.
Infective oesophagitis: 39
Most commonly candidal, rarely viral like CMV, HIV and bacterial.
Candidal oesophagitis
Many Candida species are normal commensal in the throats but become pathogenic and produce oesophagitis in immunodeficiency states. Occasionaly monilial esophagi is occurs in absence of any predisposing
Factor. Patient may be asymptomatic or complain of odynophagia and dysphasia. Rarely candida oesophagitis is complicated by bleeding, perforation & stricture or by systemic invasion.
Mallory-Weiss tear:
This is a longitudinal tear below the gastro-oesophageal junction, which is induced by repetitive and strenuous vomiting. Doubtless, many such lesions may occur and does not cause bleeding. When it is a cause of haematemesis the lesion may often be missed as it can be difficult to see as it is just below the gastro-oesophageal junction, a position that can be difficult for inexperienced endoscopes. Occasionally the lesions continue to bleed and require surgical treatment.
Tambours of the oesophagus: 40
Benign tumour:
1. Leiomyoma.
2. Lipoma.
3. Angioma
4. Inflammatory fibroid polyp.
5. Epithelial papilloma.
Malignant tumour:
1. Carcinoma of oesophagus.
2. Sarcoma: sarcoma of the oesophagus is exceedingly rare, but leiomyosarcoma and rhabdomyosarcoma have been reported.
3. Malignant melanoma.
CLINICAL CORRELATION :
Clinical manifestation depends upon the site, extent and rate of haemorrhage and the presence of coincidental disease.
# Blood loss less than 500 ml is rarely associated with systemic signs exception include bleeding in the elderly or in the anaemic patients in whom smaller amount of blood loss may produce haemodynamic alteration.
# Rapid haemorrhage of greater volume results in decreased venous return to the heart decreased cardiac output and increased peripheral resistance due to reflex vasoconstriction.
# Orthostatic hypotension greater than a change of 10 mm of Hg usually indicates a 20% or a greater reduction in blood volume, concomitant symptoms may include light headedness, syncope, nausea, sweating and thirst.
# when blood loss is 20 to 40% of blood volume shock frequently ensues with
Pronounced tachycardia and hypotension, pallor and cool skin.
# In the settings of rapid haemorrhage, the initial haematocrit may not accurately reflect the magnitude of blood loss, since equilibration with the extra vascular fluid and haemodilution often require over 8 hours. Common laboratory findings include mild leucocytosis and thrombocytosis which develop within 6 hours after the onset of bleeding. BUN may be elevated out of proportion to the creatinine.
Effects of acute haemorrhage:
It depends upon two factors:
1. Amount of blood loss.
2. Speed with which the loss occurs
3. If loss of 500 ml: no sign
4. <20% slight effect.
5. Sudden loss of 35% or more : Death.
But over 50% of blood volume, not necessarily fatal, if greater than 50% , it is always serious.
There is individual variation in the response to blood loss, even though the amount and rate are constant. It is therefore impossible to assess accurately the magnitude of any haemorrhage on purely clinical ground.
Some workers like to use the term-massive, moderate and mild in describing the amount of bleeding in cases of haematemesis and melaena.
Massive haemorrhage has been described as having the following criteria:
1. Active haemorrhage.
2. One or more of the following-
a) Shock
b) Hb below7gm/dl orHct<25.
c) 7 or more units of blood transfusion are required within 24 hours to achieve a stable blood pressure.33
In case of moderate haemorrhage:
Blood loss is roughly assumed to be less than 500 ml. Symptoms and signs like-giddiness, weakness, palpitation, sweating, thirst and postural hypotension etc.
In mild haemorrhage:
GIT haemorrhage not exceeding 500 ml produces very few symptoms and has been described as mild haemorrhage.
Continued or renewed haemorrhage may lead to shock, even though the initial presentation was leveled as mild haemorrhage.
This impending catastrophe is detected by the time tested signs:
1. Increased pulse rate.
2. Decreasing blood pressure.
3. Weakening of peripheral pulse.
4. Increasing pallor, coldness and sweating of skin.
Monitoring of central venous pressure permits the optimal maintenance of blood volume in patients with acute hypovolumia and excellently determines the need for transfusion.
The urine output meassured hourly is also an excellent index of tissue perfusion. A drop in urine output 0.5 ml/kg/hour is a good evidence of moderate to marked hypovolumia, provided there is no existing renal disease. Ordinarily the occurence of anuria during shock is associated with poor prognosis.
Shock:
The major consequences of massive haemorrhage, a state of insufficient microcirculatory flow, under perfusion and cellular hypoxia.
It is clinically characterized by:
Rapid thready pulse.
Hypotension with systolic BP below 100 mm of Hg.
Moist pallor skin.
Collapsed veins.
Rapid shallow breathing.
Anxious, restless, agitated, stupor, coma and death.
Heamatologic and blood volume change:
Haematocrit & Hb% level, these are not reliable indicators of the bleeding; for the Haematocrit to fall, the blood plasma must be equilibrated with extracellular or with adminstered intravascular fluids. It takes few hours (3-4hrs) to changes to occur.
Massive dilution occurs usually after 24 to 72 hrs, average time is 32 hours.
It depends upon:
1. State of body hydration
2. Preexisting anemia.
3. Recurrent or continued bleeding.
Therefore, extent of blood loss cannot be ascertained by haemoglobin percentage, haematocrit or erythrocyte count. Even after cessation of bleeding, the Hb%, Hct or erythrocyte count continue to fall till a steady state is attained.
White cells:
Polymorphonuclear leucocytosis (10,000 to 20,000 / mm3) occurs in 2 to 5 hours following GI bleeding white cell count becomes normal in 3 to 4 days. There is shift to left in myeloid series.
Platelet:
Count rises within an hour after a brisk haemorrhage.
Reticulocyte count:
Reticulocytosis begins after 24 hrs, and attains peak value (5-15% or more) 4 to 7 days after GI bleeding. Persistence of reticulocytosis after 10-14 days suggests continued bleeding. Change in Hct parallels the changes in haemoglobin.
Cardiac changes:
MI especially in those with coronary artery disease & elderly, arrhythmia and CCF.
Renal and adrenal complication:
1. Acute tubular necrosis.
2. Adrenal haemorrhage and insufficiency in case of prolonged shock.
Cerebral effects:
1. Cerebral hypoxia leading to restlessness, anxiety, apathy, sleepiness, confusion, disorientation, delirium and coma.
2. Cerebral vascular thrombosis especially in elderly and atherosclerotic.
Hence prompt correction of shock and early ambulation after bleeding is desirable in elderly people.
Hepatic effect:
1. Hepatic coma may be precipitated in patient with cirrhosis of liver perhaps due to the effect of shock on liver and absorption of nitrogenous products from gut.
2. Centrilobular hepatic necrosis.
3. Change in liver function test.
Effect of recumbence:
Hypostatic pneumonia may occur especially in patients with chronic chest disease and also in elderly patients following prolonged recumbency.
DIAGNOSTIC APPROACH
Upper GI hemorrhage is a medical as well as surgical emergency which needs immediate resuscitation of the patient, early detection of the cause of bleeding and appropriate treatment. Accurate diagnosis is a prerequisite for improvement in patient care and management. The first priority of any case of upper GI haemorrhage is resuscitation. The second priority is the history, physical examination and investigation.
History:
It is not always possible to diagnose with certainty the causes of dyspepsia merely from history and examination, either in the routine setting or in the bleeding patient41
However, history from the patient, attendance & family doctor may give some clues to the diagnosis.
1. History of antecedent epigastria pain or discomfort and antacid consumption suggests peptic ulcer disease.
2. Aspirin and other NSAIDs consumption suggest erosive gastritis or
gastric erosion.
3. Symptoms and signs of aneamia indicate chronic blood loss, where as
anorexia, weight loss and epigastric discomfort and asthenia suggests Carcinoma stomach.
4. Past history of jaundice or ascites suggests variceal bleeding.
5. Dysphagia and discomfort during swallowing suggests benign or malignant oesophageal tumours or oesophagitis,
6. Prolonged forceful retching or vomiting of non bloody materials followed by blood vomiting suggests Mallory-Weiss tear.
7. Presence of bleeding disorder, anticoagulant therapy or hereditary telangiactasia suggests the possible cause of bleeding.
8. Presence of fresh clotted blood into the stool for 24 hours after the onset of bleeding suggests either persistent bleeding or bleeding near to the colon not from upper GIT.
9. Clots in stool indicate massive haemorrhage.
If the patient had a haematemesis or fresh melaena in the previous 24 hours, this two is significantly correlated with the mortality which fits with previous studies showing that a major haemorrhage with postural drop in BP, shock or fresh melaena with or without a haemetemesis will be associated with an increase in mortality.42
Physical Examination:
1. Examination should evaluate the patients general condition and assess the signs of shock and hypovolumia (as for example; pulse. BP respiratory rate, temperature, skin condition and level of consciousness),
2. Signs of chronic liver disease if present are of crucial importance since patient bleeding from portal hypertension have a high mortality (upto 50%). In the presence of liver failure or ascites, variceal bleeding carries an even higher mortality.
3. Epigastric tenderness suggests peptic ulceration, oesophagitis, and hiatus hernia.
4. A palpable epigastria mass with Virchow’s node suggests gastric cancer.
5. Petechiae or ecchymosis suggests a haemorrhagic disorder.
6. Melanin spots, telangiectasia, neurofibromatosis and other mucocutaneous lesions give clues to the causes of bleeding.
7. Purpura together with splenomegaly or enlarged lymph nodes suggests blood dyscrasias.45
8. The presence of aortic valvular disease may be associated with mucosal vascular abnormalities of the intestinal tract.
Investigation:
1. Blood for:
I. Grouping and cross matching for patient management.
II. Hb%
III. ESR – Increased in aplastic anaemia and malignancy.
IV. Total count of WBC-Increased after haemorrhage or leucopenia in case of aplastic anaemia
V. DC-Neutrophilia after haemorrhage
VI. Platelet count- Increased after haemorrhage.
VII. BT, CT, VonWF & APTT: When haematological causes are suspected for upper gastrointestinal haemorrhage.
2. Liver function tests?
When liver disease is suspected to be the cause of upper gastrointestinal haemorrhage, the following tests should be done.
I. Serum total protein with albumin and globulin ration. In liver disease serum total protein is reduced with alteration of albumin and globulin ratio.
II. Prothrombin time -It is increased in chronic liver disease & in patients on oral anticogulant.
III. Serum bilirubin, SGPT is mildly increased in cirrhosis of liver.
IV. Viral markers- HBsAg, Anti-HCV, HBeAg.
3. USG of hepatobiliary system in CLD to see hepatic echotexture, splenic size and portal vein diameter.
4. BUN is helpful indicating previously unrecognize chronic renal failure.
5. Nasogastric aspiration:
Is done:
I. To determine the site of bleeding.
II. To determine whether there is any active bleeding or not.
If there is no aspirate through nasogastric tube, it means there is no active bleeding. If the patient shows the features of active bleeding despite negative aspiration indicates that the bleeding is from below the ligament of treitz46.
If red blood or coffee ground materials is aspirated from the nasogastric suction, saline aspiration should be instituted.
Irrigation serves two puroses:
-Assessment of rapidity of bleeding.
-Clear the stomach of old clot prior to possible endoscopy.
6. Upper GI endoscopy:
Endoscopes have revolutionized the examination of the gastrointestial tract. Because of the flexibility of the instrument & controllability of the instrument tip, the operator can steer the endoscope around multiple bends under visual control. A channel permits the passage of a variety of endoscopic tools, such as biopsy forceps, cytology brushes, wash tube, injecting devices and electro cautery probes and snares. The video endoscope is a modification of the original fibre endoscope in which a charge coupled device on the tip of the instrument transmits the image to a TV screen. This system is being used increasingly because it permits storage, analysis and transmission of the endoscopic images.
Upper Gl bleeding and oesophagogastroduodenoscopy: 47, 48
Endoscopy within first 12 to 24 hours of an upper gastrointestinal haemorrhage is useful in planning rational therapy by visualizing the bleeding source.
In formations obtained include-
1. Location of the bleeding source.
2. Whether bleeding is continuing.
3. Whether bleeding is arterial.
4. Which of the multiple lesions a bleeding and
5. Whether a visible vessel is present in an ulcer base.
Recognition of bleeding type:
1. Visible active bleeding.
2. Stigmata of recent haemorrhage:
a) Presence of adherent clots, which can not be washed off with a
powerful jet of water.
b) Presence of a visible vessel or an ulcer whose base is hemorrhagic,
Contraindication of upper GIT Endoscopy:
Virtually there is no contraindication but relative contraindication are:
1. Profund shock
2. Severely compromised cardiopulmonary state
3. Large zenker diverticula of the pharynx.
4. Anterior osteophytic proliferation of the cervical spine
5. Coma
6. Non cooperative patient
Complications:
1. Perforation
2. Bleeding
3. Transient suppression of respiration due to medication
4. Cardiovascular complication
5. Infection
6. Aspiration.
Indication for endoscopy in case haematemesis and melaena:
1. As a first procedure and it is the general recommendation to scope all patients within 24-48 hours of admission following acute episode of bleeding.
2. To locate the exact site of bleeding.
3. When surgery is contemplated.
4. When rebleeding occurs often acute self limited blood loss.
5. When portal hypertension or aortoenteric fistula is suspected.
6. For therapeutic purpose of haematemesis & melaena.
a) In varices-both therapeutic and prophylactic sclerotherapy and banding.
b) In Focal -non variceal bleeding.
Electro coagulation
Thermal heat probe technique
LASER photo coagulation.
7. When radiology fails to detect any lesion.
8. To confirm radiological finding.
9. When biopsy is indicated.
Endoscopy versus X-Ray:
Upper gastro-intestinal radiology using conventional single contrast barium meal is impressingly disappointing as compared with endoscopy in patients with haematemesis and melaena. It is the double contrast barium meal, which is not yet well practiced in Bangladesh, has got superiority regarding accuracy of radiological findings of the GI tract. Endoscopy diagnose over 90% of cases, whereas double contrast radiology diagnose over 80 %49. Moreover a good x-ray machine with television monitoring is much more expensive than an endoscopy. Besides a medical doctor can be trained with a fairly short times for endoscopy 50.
MANAGEMENT
Acute upper gastrointestinal bleeding is a medical as well as surgical emergency. The patient should be hospitalized immediately.
Steps of management:
1. Intravenous access: The first step of management is to gain intravenous access using at least one large bore canulla.
2. Initial clinical assessment of the patient:
i. Assessment of the cardiorespiratory status: Severe bleeding causes tachycardia with hypotension and oliguria. The patient is cold, is sweating and may be agitated.
ii. To seek evidence of liver disease: Jaundice, cutaneous stigmata, hepatosplenomegaly and ascites may be present in decompensated cirrhosis.
iii. Co morbidity: The presence of cardiorespiratory, cerebrovascular or renal disease is important, because these may be worsened by acute bleeding and because these disease increase the hazards of endoscopy and surgical operation.
3. Blood tests: These include:
A full blood count. Chronic or subsequent bleeding leads anaemia but the haemoglobin concentration may be normal after sudden major bleeding until haemodilution occurs.
1. Urea and electrolytes. This may show evidence of renal failure. The urea rises as the absorbed products of luminal blood are metabolized by the liver.
2. Liver function tests.
3. Prothrombin time, if there is clinical suggestion of liver disease or in patients.
4. Cross matching of at least 2 units of blood.
4. Resuscitation:
I). Intravenous crystalloid fluid or colloid are given to restore the blood pressure but normal saline should be avoided in patients with liver disease because it can cause ascites.
II). Blood transfusion.
Indication of blood transfusion is:
1. When the patient is in shock- signs of hemorrhagic shock indicate the urgent need to reestablish an adequate circulation to vital organs.
2. Continuing bleeding, as eviden