STUDY - Technical - New Dacian's Medicine
Gastrointestinal
Bleeding
Translation Draft
From the point of view of direct perception, things are simple, having to do with: 1. hematemesis, which is defined as the bloodshed and 2, melena as the exteriorization of chairs that have become black and pitch-like, by the presence of blood. These clinical manifestations of gastrointestinal haemorrhage (IGI) suggest a proximal source of bleeding. The color of the blood removed depends on the concentration of hydrochloric acid in the stomach and the duration of its contact with the blood.
Thus, if the vomiting occurs shortly after the onset of bleeding, the vomit appears red, and later the appearance will be dark red, brown or black. Precipitated blood clots and acid-degraded blood from the spill will produce a characteristic "coffee grounds" appearance when removed by spillage.
Hematemesis usually indicates proximal bleeding from Treitz's ligament, as blood entering the gastrointestinal tract beyond the duodenum rarely enters the stomach. While bleeding, sufficient to produce hematemesis, usually causes melena, less than half of melena patients have hematemesis.
Melena usually denotes bleeding from the esophagus, stomach or duodenum, but lesions of the jejun, ileum and even the ascending colon can sometimes cause melena provided that the gastrointestinal transit time is sufficiently prolonged. Approximately 60 ml of blood is needed to produce a single black stool, with acute blood loss greater than this amount can cause melena for up to 7 days. Once the color of the stool returns to normal, tests for occult bleeding can remain positive for more than a week.
The black color of the melena comes from the contact of the blood with hydrochloric acid, producing hematin. Such chairs are like fuel oil ("sticky") and have a characteristic smell. This consistency of fuel oil is in contrast to the dark black or grey stools that appear after ingestion of iron, bismuth or licorice extract. HGI, even if it is detected only by positive tests indicating occult bleeding, indicates a potentially serious disease that needs further investigation.
Hematochesia, the passage of red blood through the rectum, generally signifies bleeding from a distal source of Treitz's ligament. However, rapid proximal hemorrhages can cause prolonged rectoragia due to accelerated transit.
Clinical manifestations of gastrointestinal bleeding depend on the size and speed of bleeding and the presence of associated diseases. Blood losses of less than 500 ml are rarely associated with systemic signs (exceptions including bleeding in the elderly and anemic patients, where loss of smaller amounts of blood may cause hemodynamic disorders). Rapid hemorrhage of higher volume causes decreased venous return to the heart, decreased heart rate and increased peripheral resistance due to reflex vasoconstriction.
Orthostatic hypotension greater than a 10 mmHg change usually indicates a 20% or more reduction in blood volume. Associated symptoms may include lipotimia, syncope, nausea, sweating and thirst. When blood loss is 25-40% of blood volume, shock with severe tachycardia and hypotension frequently occurs. Paloare is important and the skin is cold. However, in the presence of beta-adrenergic blockers and calcium channels, these clinical signs can be mitigated.
When assessing rapid bleeding, the initial haematocrit may not accurately reflect the extent of blood loss, as balancing with extravascular fluid and hemodilution often takes more than 8 hours. Common laboratory results include mild leukocytosis and thrombocytosis occurring within 6 hours of the onset of bleeding. Blood urea can be increased disproportionately to creatinine, especially in upper digestive hemorrhages, due to the degradation of blood proteins to urea by intestinal bacteria, as well as a slight reduction in glomerular filtration rate.
Occult haemorrhage, detected by the hemoglobinperoxidase test, is an important way to discover colorectal neoplasia in the early, potentially curable stages. The test should be proposed in patients over 50 years of age as part of the annual check-up. Multiple stools should be examined (usually two samples from three seats), and if any samples are positive further investigations should be carried out.
A positive result may be due to physiological blood loss, peroxidase in the diet, undercooked meat or any cause of upper or lower gastrointestinal bleeding. Ingestion of vitamin C in the amount of more than 500 mg/ day may cause a false negative test. To limit the confusing variables, patients should be tested during a diet with a lot of fiber and a little meat, without ingestion of non-steroidal anti-inflammatory agents (NSAIDs) or vitamin C, although the low daily dose of aspirin (80-325 mg) taken to prevent cardiovascular disease, does not generally lead to false positive results.
Let's move now on to the etiology of upper digestive hemorrhages! A careful history and examination of the oropharyngeal and nasal cavity should help to exclude epistaxis or swallowed blood as a source of hematemesis or melena. The most common causes of upper digestive hemorrhage are: 1. erosive or hemorrhagic gastropathy, 2. duodenal ulcer, 3. gastric ulcer, 4. Mallory-Weiss syndrome, 5. varicose veins or portal hypertensive gastropathy and 6. arteriovenous malformations (MAV).
These entities explain over 90% of all causes of superior HGI in which a specific source can be found. Gastric erosion or hemorrhagic, erosive gastropathy are often associated with aspirin ingestion or other NSAIDs. Peptic ulcers (duodenal or gastric) caused by Helicobacter pilory are the most common causes of upper gastrointestinal bleeding.
Since bleeding may be the initial manifestation of a peptic ulcer, the diagnosis should be taken into account even when a characteristic history of ulcerative disease is not obtained. Concomitant use of NSAID increases the risk of bleeding of peptic ulcer and associated mortality. Bleeding from varicose veins or portal hypertensive gastropathy is characteristically brutal and massive. Bleeding from esophageal or gastric varicose veins is usually the result of portal hypertension, secondary to cirrhosis.
Although alcoholic cirrhosis is one of the most important causes, any condition that causes portal hypertension can cause bleeding from varicose veins. Moreover, while the presence of varicose veins usually means long-established portal hypertension, acute hepatitis or severe fatty infiltration of the liver can sometimes produce varicose veins that disappear once the liver anomaly heals. Although upper digestive hemorrhage in a patient with cirrhosis suggests a varicose source, up to a quarter of those patients will bleed from another lesion, such as erosive gastropathy, peptic ulcer, gastritis or Mallory-Weiss syndrome.
As a result it is essential to promptly determine the cause of bleeding so that appropriate treatment is instituted. Mallory-Weiss fissures (fissures of the esofagogastric mucosa) occur in the region of the esophagogastric junction and are often characterized historically by efforts to vomit or vomit non-hemorrhagic followed by hematemesis. However, a history of snorting may be missing in more than half of patients.
Esophagitis, mainly due to gastroesophageal reflux, can cause bleeding. Esophagitis associated with cancer or given by infections, such as cytomegalovirus, herpes virus or Candida, rarely causes acute bleeding (but, anyway, can cause chronic blood loss). Chronic blood loss can also result from linear cracking of the mucosa in the large hiatal hernia, by sliding, as a result of the cutting effect, caused by differences between intraoracic pressure and intragastritis.
Gastric carcinoma, lymphomas, polyps and other tumors of the stomach and small intestine are unusual causes of HGI. Leiomyoma and leiosarcoma are rare, but they can lead to massive hemorrhage. Bleeding from duodenal and jejunal diverticules is an unusual cause of HGI. The rupture of arterioclotheraortic aortic aneurysms in the small intestine is almost always fatal. The rupture usually occurs after reconstructive arterial surgery with fistula formation between the synthetic graft and the intestinal lumen.
A small or "foreboding" bleed may precede a sudden massive hemorrhage from an aortoenteric fistula. Sudden bleeding may also occur through hemobilia, following surgery or liver trauma. Primary blood discs, vasculitis, hereditary haemorrhagic telangiectasis and connective tissue disorders may cause significant gastrointestinal bleeding. Uremia can cause gastrointestinal blood loss (GI) through telangiectasis along the entire gastrointestinal tract. Pancreatic cancer can sometimes erode in the duodenum and produce upper GI bleeding.
I've reached the etiology of lower digestive hemorrhages. We'll start with the and rectal lesions. Small amounts of bright red blood on the surface of the stool and toilet paper are frequently caused by hemorrhoids or fissures (such bleeding is generally precipitated by the forced passage of a hard chair). Proctitis is another source of rectal bleeding. Another cause is colon damage.
Colon cancer, like colon polyps, usually causes chronic occult blood loss, but occasionally can produce rapid bleeding. Angiodysplasia, a proliferation of the vascular mucosa, is a major source of acute or chronic bleeding in elderly patients. Hemorrhagic diarrhea may be the alarming symptom in patients with ulcerative colitis.
Bleeding may also accompany diarrhoea due to infections with Shigella, Salmonella, Campylobacter jejuni, Clostridium difficile, Escherichia coli enterohemorrhagic toxicogenic, amoeba and other parasites. In elderly, diabetic and vascular patients, mesenteric ischemia may be a cause of bloody diarrhoea. Bleeding from colon diverticules is a common cause of lower digestive hemorrhage in patients over 40 years of age.
The usual presence of diverticular hemorrhage is the painless, rapid passage of a brownish colored stool. Meckel's diverticulum, a congenital abnormality, most often distal ileum, is present in about 2% of the population and is an important cause of acute bleeding in young children and adults.
Let me now present some things about the patient's approach "starting" with the one with acute superior HGI. Conduct towards the bleeding patient depends on the location, proportion and rapidity of bleeding. Primary attention to the care of a bleeding patient should be given to maintaining adequate intravascular volume and hemodynamic stability. When first consulted, the patient may be in shock. Before anamnesis and undertake a thorough physical examination, vital signs should be noted, blood group tests and compatibility samples should be performed and a wide venous approach for a saline or erythrocytic infusion established.
A history or symptoms suggestive of ulcerative peptic disease may be a useful clue. Similarly, recent use of NSAID may raise suspicion of erosive gastropathy. If the ingestion of alcohol has been prolonged and there are stigmas of chronic liver disease, esophageal varicose veins can be a source of hemorrhage. A history of gastrointestinal haemorrhage or a family history of intestinal disease or hemorrhagic diathesis may provide diagnostic clues. Recent vomiting contractions, followed by hematemesis, must suggest Mallory-Weiss cracks.
After assessing changes in orthostatism of heart rate and blood pressure, clinical assessment of central venous pressure and the establishment of volemy filling, the patient should be examined for indications of the underlying disease. A source of extraintestinal bleeding should be excluded by careful examination of the oral cavity and nasopharynx. Dermatological examination may reveal characteristic telangiectasis lesions in Osler-Rendu-Weber disease (although they may not be visible if there is severe anaemia). Stigmas of chronic liver disease such as star angiomas, gynecomastia, testicular atrophy, jaundice, ascites and hepatosplenomegalia suggest portal hypertension with bleeding from esophageal or gastric varicose veins as an important potential source.
Initial investigations should include hematocrit, hemoglobin, a careful assessment of the morphological characters of erythrocytes (hypochrome hematitis, microcitation, suggests that blood loss is chronic), leukocyte formula, platelet count. Prothrombin time, partial thromboplastin time are necessary to exclude primary or secondary defects of coagulation. An increase in blood urea and the ratio of blood urea to creatinine may help suggest superior HGI.
X-rays of the abdomen are rarely useful in establishing a diagnosis, except in cases where a visceral perforation or ischemia is suspected or an intestinal occlusion is present. Although initial investigations are valuable and essential, repeated evaluation of laboratory data is important as the clinical course of bleeding is tracked (a diagram of data dynamics is desirable and should include the times when blood products and intravenous fluids have been administered and their sum).
The diagnostic and therapeutic approach of the patient with HGI should be individualized. When there is a history of melena or hematemesis or suspicion of bleeding from the upper GI tract, the patient should be given a nasogastric tube to empty the stomach and determine whether the bleeding is proximal to Treitz's ligament. if the initial nasogastric suction is clear or bilios, a current active bleeding is unlikely and the tube can be removed. If red blood or material is sucked into the "coffee grounds" through the nasogastric tube, the lavage with water or saline solution (at room temperature) should be started.
Stomach irrigation serves two purposes: 1. provide the clinician with an assessment of the speed of bleeding and 2. cleanses the stomach of blood and blood clots before a diagnostic endoscopies that will improve the ability to see all surfaces of the mucosa. The pace of subsequent diagnostic evaluation will depend on the nature of the nasogastric suction, as well as on vital signs, transfusion needs and the number and consistency of the stools. Once the patient is hemodynamically stable, diagnostic endoscopy should be performed to identify the source of bleeding.
Early diagnostic endoscopy may also provide prognostic information on the possibility of the patient re-bleeding and allows endoscopic therapy. When there is evidence of persistent upper GI bleeding, based on continued blood drainage through the nasogastric tube or when hemodynamic stabilisation of the patient fails, the situation should be viewed as an emergency and diagnostic endoscopy should begin as soon as possible. If the source of bleeding is discovered, the endoscope should determine whether endoscope therapy can stop the bleeding.
Bleeding from an ulcer can be controlled by injecting a vasoconstrictor, such as epinephrine or a sclerosing agent, or by using electrocautery, most commonly performed with a bipolar or multipolar sample or a heat sample. Such therapy should be tried when there is arterial jet, which is unlikely to spontaneously give way, or when there is a "visible vessel", an arteriole exposed to the base of the ulcer that involves a 50% risk of bleeding. Erosive or hemorrhagic gastropathy (given aspirin or other NSAID) is not usually accessible to endoscopic therapy.
Fortunately, this often improves with the stopping of the aggressor and the administration of H2 receptor antagonists or proton pump inhibitors. Arteriovenous malformations, when they bleed, are frequently treated with bipolar electrocautery, but when detected, they usually do not bleed actively. Mallory-Weiss fissures stop bleeding, usually spontaneously, but may require cauterization or injection therapy if bleeding persists.
Bleeding of esophageal varicose veins usually requires endoscopic intervention. Varicose veins may bleed actively in the jet or very slowly or show signs of recent bleeding through "red tracks" or cherry red spots. So far, the most common approach to stopping bleeding has been sclerotherapy. This involves injecting varicose veins with sclerosing agents such as ethanolamine, sodium tetradecisulphate, sodium moruate and absolute ethanol. The ligation of esophageal varicose veins by banding (similar to rubber band ligation of hemorrhoids) is a technique used in increasing use and is associated with a lower risk of formation of esophageal stricture and systemic toxicity than sclerotherapy.
Systemic infusion of vasopressin together with intravenously administered nitroglycerin decreases portal venous pressure and can be used as adjuvants in the control of varicose vein bleeding. Similarly, systemic somatostatin or its analogues (e.g. octreotide) can decrease portal pressure and help control bleeding from varicose veins without the peripheral vasoconstrictive side effects of vasopressin. If endoscopic or pharmacological measures fail to stop bleeding from varicose veins, Blakemore or Linton tube balloon tamponade can be used to compress varicose veins directly and thus stop bleeding temporarily until definitive therapy can be attempted.
Another approach is the placement of a transjugular intrahepatic portosystemic shunt. This procedure involves placing an expandable metal stent through the liver to connect the porta vein and the hepatic vein. Sometimes upper GI bleeding is too rapid to endoscopically view the source of bleeding (in such cases, angiography, such as selective mesenteric arteriography, may be indicated). Bleeding of this magnitude usually requires surgery, once the source of bleeding is localized, but sometimes intraarterial infusion of vasopressin or angiographic injection of foam-gel or metal claws can stop bleeding.
I will complete this long post by presenting a few things about the patient's approach with acute lower GI bleeding. The most common causes of lower GI hemorrhage vary with age. In all cases, upper GI bleeding should be excluded, if necessary, by nasogastric suction or even diagnosed endoscopy and rectal cough and anoscopy should be carefully performed to exclude anorectal pathology, such as cracks and bleeding from internal hemorrhoids.
A flexible sigmoidoscopy (after a gentle enema with saline solution) should be performed to rule out rectosigmoid disease. In the hemodynamically stable patient, elective colonoscopy should be performed after lavage with an oral solution of polyethylene glycol/ electrolytes or phosphosodium solution. The endoscope therapist can remove polyps, cauterize angiodysplastic lesions and sometimes inject a bleeding diverticulum with epinephrine.
If colonoscopy is negative, but there is recurrent or intermittent lower GI bleeding, a study with marked hematia should be considered. Images can be obtained within 48 hours. If the study shows a suspicious lesion, selective angiography helps locate the bleeding site more accurately. The patient with a lower torrential GI bleeding usually cannot be prepared for colonoscopy, nor can he wait for images with marked hematia (such a patient must undergo a mesenteric angiography, after the nazogastric suction has ruled out rapid upper GI bleeding).
Once the site of bleeding is identified by angiography, surgery is often necessary. Acute upper and lower GI bleeding is a challenge, both diagnostically and therapeutically. It requires an optimal team of emergency and intensive care personnel, internists, gastroenterologists, invasive radiologists and surgeons.
Here I managed to finish this long post! I'll probably work tomorrow on the jaundice presentation (it looks like I'll have some time available, as today). If not, we'll read each other on June 28th...
From the point of view of direct perception, things are simple, having to do with: 1. hematemesis, which is defined as the bloodshed and 2, melena as the exteriorization of chairs that have become black and pitch-like, by the presence of blood. These clinical manifestations of gastrointestinal haemorrhage (IGI) suggest a proximal source of bleeding. The color of the blood removed depends on the concentration of hydrochloric acid in the stomach and the duration of its contact with the blood.
Thus, if the vomiting occurs shortly after the onset of bleeding, the vomit appears red, and later the appearance will be dark red, brown or black. Precipitated blood clots and acid-degraded blood from the spill will produce a characteristic "coffee grounds" appearance when removed by spillage.
Hematemesis usually indicates proximal bleeding from Treitz's ligament, as blood entering the gastrointestinal tract beyond the duodenum rarely enters the stomach. While bleeding, sufficient to produce hematemesis, usually causes melena, less than half of melena patients have hematemesis.
Melena usually denotes bleeding from the esophagus, stomach or duodenum, but lesions of the jejun, ileum and even the ascending colon can sometimes cause melena provided that the gastrointestinal transit time is sufficiently prolonged. Approximately 60 ml of blood is needed to produce a single black stool, with acute blood loss greater than this amount can cause melena for up to 7 days. Once the color of the stool returns to normal, tests for occult bleeding can remain positive for more than a week.
The black color of the melena comes from the contact of the blood with hydrochloric acid, producing hematin. Such chairs are like fuel oil ("sticky") and have a characteristic smell. This consistency of fuel oil is in contrast to the dark black or grey stools that appear after ingestion of iron, bismuth or licorice extract. HGI, even if it is detected only by positive tests indicating occult bleeding, indicates a potentially serious disease that needs further investigation.
Hematochesia, the passage of red blood through the rectum, generally signifies bleeding from a distal source of Treitz's ligament. However, rapid proximal hemorrhages can cause prolonged rectoragia due to accelerated transit.
Clinical manifestations of gastrointestinal bleeding depend on the size and speed of bleeding and the presence of associated diseases. Blood losses of less than 500 ml are rarely associated with systemic signs (exceptions including bleeding in the elderly and anemic patients, where loss of smaller amounts of blood may cause hemodynamic disorders). Rapid hemorrhage of higher volume causes decreased venous return to the heart, decreased heart rate and increased peripheral resistance due to reflex vasoconstriction.
Orthostatic hypotension greater than a 10 mmHg change usually indicates a 20% or more reduction in blood volume. Associated symptoms may include lipotimia, syncope, nausea, sweating and thirst. When blood loss is 25-40% of blood volume, shock with severe tachycardia and hypotension frequently occurs. Paloare is important and the skin is cold. However, in the presence of beta-adrenergic blockers and calcium channels, these clinical signs can be mitigated.
When assessing rapid bleeding, the initial haematocrit may not accurately reflect the extent of blood loss, as balancing with extravascular fluid and hemodilution often takes more than 8 hours. Common laboratory results include mild leukocytosis and thrombocytosis occurring within 6 hours of the onset of bleeding. Blood urea can be increased disproportionately to creatinine, especially in upper digestive hemorrhages, due to the degradation of blood proteins to urea by intestinal bacteria, as well as a slight reduction in glomerular filtration rate.
Occult haemorrhage, detected by the hemoglobinperoxidase test, is an important way to discover colorectal neoplasia in the early, potentially curable stages. The test should be proposed in patients over 50 years of age as part of the annual check-up. Multiple stools should be examined (usually two samples from three seats), and if any samples are positive further investigations should be carried out.
A positive result may be due to physiological blood loss, peroxidase in the diet, undercooked meat or any cause of upper or lower gastrointestinal bleeding. Ingestion of vitamin C in the amount of more than 500 mg/ day may cause a false negative test. To limit the confusing variables, patients should be tested during a diet with a lot of fiber and a little meat, without ingestion of non-steroidal anti-inflammatory agents (NSAIDs) or vitamin C, although the low daily dose of aspirin (80-325 mg) taken to prevent cardiovascular disease, does not generally lead to false positive results.
Let's move now on to the etiology of upper digestive hemorrhages! A careful history and examination of the oropharyngeal and nasal cavity should help to exclude epistaxis or swallowed blood as a source of hematemesis or melena. The most common causes of upper digestive hemorrhage are: 1. erosive or hemorrhagic gastropathy, 2. duodenal ulcer, 3. gastric ulcer, 4. Mallory-Weiss syndrome, 5. varicose veins or portal hypertensive gastropathy and 6. arteriovenous malformations (MAV).
These entities explain over 90% of all causes of superior HGI in which a specific source can be found. Gastric erosion or hemorrhagic, erosive gastropathy are often associated with aspirin ingestion or other NSAIDs. Peptic ulcers (duodenal or gastric) caused by Helicobacter pilory are the most common causes of upper gastrointestinal bleeding.
Since bleeding may be the initial manifestation of a peptic ulcer, the diagnosis should be taken into account even when a characteristic history of ulcerative disease is not obtained. Concomitant use of NSAID increases the risk of bleeding of peptic ulcer and associated mortality. Bleeding from varicose veins or portal hypertensive gastropathy is characteristically brutal and massive. Bleeding from esophageal or gastric varicose veins is usually the result of portal hypertension, secondary to cirrhosis.
Although alcoholic cirrhosis is one of the most important causes, any condition that causes portal hypertension can cause bleeding from varicose veins. Moreover, while the presence of varicose veins usually means long-established portal hypertension, acute hepatitis or severe fatty infiltration of the liver can sometimes produce varicose veins that disappear once the liver anomaly heals. Although upper digestive hemorrhage in a patient with cirrhosis suggests a varicose source, up to a quarter of those patients will bleed from another lesion, such as erosive gastropathy, peptic ulcer, gastritis or Mallory-Weiss syndrome.
As a result it is essential to promptly determine the cause of bleeding so that appropriate treatment is instituted. Mallory-Weiss fissures (fissures of the esofagogastric mucosa) occur in the region of the esophagogastric junction and are often characterized historically by efforts to vomit or vomit non-hemorrhagic followed by hematemesis. However, a history of snorting may be missing in more than half of patients.
Esophagitis, mainly due to gastroesophageal reflux, can cause bleeding. Esophagitis associated with cancer or given by infections, such as cytomegalovirus, herpes virus or Candida, rarely causes acute bleeding (but, anyway, can cause chronic blood loss). Chronic blood loss can also result from linear cracking of the mucosa in the large hiatal hernia, by sliding, as a result of the cutting effect, caused by differences between intraoracic pressure and intragastritis.
Gastric carcinoma, lymphomas, polyps and other tumors of the stomach and small intestine are unusual causes of HGI. Leiomyoma and leiosarcoma are rare, but they can lead to massive hemorrhage. Bleeding from duodenal and jejunal diverticules is an unusual cause of HGI. The rupture of arterioclotheraortic aortic aneurysms in the small intestine is almost always fatal. The rupture usually occurs after reconstructive arterial surgery with fistula formation between the synthetic graft and the intestinal lumen.
A small or "foreboding" bleed may precede a sudden massive hemorrhage from an aortoenteric fistula. Sudden bleeding may also occur through hemobilia, following surgery or liver trauma. Primary blood discs, vasculitis, hereditary haemorrhagic telangiectasis and connective tissue disorders may cause significant gastrointestinal bleeding. Uremia can cause gastrointestinal blood loss (GI) through telangiectasis along the entire gastrointestinal tract. Pancreatic cancer can sometimes erode in the duodenum and produce upper GI bleeding.
I've reached the etiology of lower digestive hemorrhages. We'll start with the and rectal lesions. Small amounts of bright red blood on the surface of the stool and toilet paper are frequently caused by hemorrhoids or fissures (such bleeding is generally precipitated by the forced passage of a hard chair). Proctitis is another source of rectal bleeding. Another cause is colon damage.
Colon cancer, like colon polyps, usually causes chronic occult blood loss, but occasionally can produce rapid bleeding. Angiodysplasia, a proliferation of the vascular mucosa, is a major source of acute or chronic bleeding in elderly patients. Hemorrhagic diarrhea may be the alarming symptom in patients with ulcerative colitis.
Bleeding may also accompany diarrhoea due to infections with Shigella, Salmonella, Campylobacter jejuni, Clostridium difficile, Escherichia coli enterohemorrhagic toxicogenic, amoeba and other parasites. In elderly, diabetic and vascular patients, mesenteric ischemia may be a cause of bloody diarrhoea. Bleeding from colon diverticules is a common cause of lower digestive hemorrhage in patients over 40 years of age.
The usual presence of diverticular hemorrhage is the painless, rapid passage of a brownish colored stool. Meckel's diverticulum, a congenital abnormality, most often distal ileum, is present in about 2% of the population and is an important cause of acute bleeding in young children and adults.
Let me now present some things about the patient's approach "starting" with the one with acute superior HGI. Conduct towards the bleeding patient depends on the location, proportion and rapidity of bleeding. Primary attention to the care of a bleeding patient should be given to maintaining adequate intravascular volume and hemodynamic stability. When first consulted, the patient may be in shock. Before anamnesis and undertake a thorough physical examination, vital signs should be noted, blood group tests and compatibility samples should be performed and a wide venous approach for a saline or erythrocytic infusion established.
A history or symptoms suggestive of ulcerative peptic disease may be a useful clue. Similarly, recent use of NSAID may raise suspicion of erosive gastropathy. If the ingestion of alcohol has been prolonged and there are stigmas of chronic liver disease, esophageal varicose veins can be a source of hemorrhage. A history of gastrointestinal haemorrhage or a family history of intestinal disease or hemorrhagic diathesis may provide diagnostic clues. Recent vomiting contractions, followed by hematemesis, must suggest Mallory-Weiss cracks.
After assessing changes in orthostatism of heart rate and blood pressure, clinical assessment of central venous pressure and the establishment of volemy filling, the patient should be examined for indications of the underlying disease. A source of extraintestinal bleeding should be excluded by careful examination of the oral cavity and nasopharynx. Dermatological examination may reveal characteristic telangiectasis lesions in Osler-Rendu-Weber disease (although they may not be visible if there is severe anaemia). Stigmas of chronic liver disease such as star angiomas, gynecomastia, testicular atrophy, jaundice, ascites and hepatosplenomegalia suggest portal hypertension with bleeding from esophageal or gastric varicose veins as an important potential source.
Initial investigations should include hematocrit, hemoglobin, a careful assessment of the morphological characters of erythrocytes (hypochrome hematitis, microcitation, suggests that blood loss is chronic), leukocyte formula, platelet count. Prothrombin time, partial thromboplastin time are necessary to exclude primary or secondary defects of coagulation. An increase in blood urea and the ratio of blood urea to creatinine may help suggest superior HGI.
X-rays of the abdomen are rarely useful in establishing a diagnosis, except in cases where a visceral perforation or ischemia is suspected or an intestinal occlusion is present. Although initial investigations are valuable and essential, repeated evaluation of laboratory data is important as the clinical course of bleeding is tracked (a diagram of data dynamics is desirable and should include the times when blood products and intravenous fluids have been administered and their sum).
The diagnostic and therapeutic approach of the patient with HGI should be individualized. When there is a history of melena or hematemesis or suspicion of bleeding from the upper GI tract, the patient should be given a nasogastric tube to empty the stomach and determine whether the bleeding is proximal to Treitz's ligament. if the initial nasogastric suction is clear or bilios, a current active bleeding is unlikely and the tube can be removed. If red blood or material is sucked into the "coffee grounds" through the nasogastric tube, the lavage with water or saline solution (at room temperature) should be started.
Stomach irrigation serves two purposes: 1. provide the clinician with an assessment of the speed of bleeding and 2. cleanses the stomach of blood and blood clots before a diagnostic endoscopies that will improve the ability to see all surfaces of the mucosa. The pace of subsequent diagnostic evaluation will depend on the nature of the nasogastric suction, as well as on vital signs, transfusion needs and the number and consistency of the stools. Once the patient is hemodynamically stable, diagnostic endoscopy should be performed to identify the source of bleeding.
Early diagnostic endoscopy may also provide prognostic information on the possibility of the patient re-bleeding and allows endoscopic therapy. When there is evidence of persistent upper GI bleeding, based on continued blood drainage through the nasogastric tube or when hemodynamic stabilisation of the patient fails, the situation should be viewed as an emergency and diagnostic endoscopy should begin as soon as possible. If the source of bleeding is discovered, the endoscope should determine whether endoscope therapy can stop the bleeding.
Bleeding from an ulcer can be controlled by injecting a vasoconstrictor, such as epinephrine or a sclerosing agent, or by using electrocautery, most commonly performed with a bipolar or multipolar sample or a heat sample. Such therapy should be tried when there is arterial jet, which is unlikely to spontaneously give way, or when there is a "visible vessel", an arteriole exposed to the base of the ulcer that involves a 50% risk of bleeding. Erosive or hemorrhagic gastropathy (given aspirin or other NSAID) is not usually accessible to endoscopic therapy.
Fortunately, this often improves with the stopping of the aggressor and the administration of H2 receptor antagonists or proton pump inhibitors. Arteriovenous malformations, when they bleed, are frequently treated with bipolar electrocautery, but when detected, they usually do not bleed actively. Mallory-Weiss fissures stop bleeding, usually spontaneously, but may require cauterization or injection therapy if bleeding persists.
Bleeding of esophageal varicose veins usually requires endoscopic intervention. Varicose veins may bleed actively in the jet or very slowly or show signs of recent bleeding through "red tracks" or cherry red spots. So far, the most common approach to stopping bleeding has been sclerotherapy. This involves injecting varicose veins with sclerosing agents such as ethanolamine, sodium tetradecisulphate, sodium moruate and absolute ethanol. The ligation of esophageal varicose veins by banding (similar to rubber band ligation of hemorrhoids) is a technique used in increasing use and is associated with a lower risk of formation of esophageal stricture and systemic toxicity than sclerotherapy.
Systemic infusion of vasopressin together with intravenously administered nitroglycerin decreases portal venous pressure and can be used as adjuvants in the control of varicose vein bleeding. Similarly, systemic somatostatin or its analogues (e.g. octreotide) can decrease portal pressure and help control bleeding from varicose veins without the peripheral vasoconstrictive side effects of vasopressin. If endoscopic or pharmacological measures fail to stop bleeding from varicose veins, Blakemore or Linton tube balloon tamponade can be used to compress varicose veins directly and thus stop bleeding temporarily until definitive therapy can be attempted.
Another approach is the placement of a transjugular intrahepatic portosystemic shunt. This procedure involves placing an expandable metal stent through the liver to connect the porta vein and the hepatic vein. Sometimes upper GI bleeding is too rapid to endoscopically view the source of bleeding (in such cases, angiography, such as selective mesenteric arteriography, may be indicated). Bleeding of this magnitude usually requires surgery, once the source of bleeding is localized, but sometimes intraarterial infusion of vasopressin or angiographic injection of foam-gel or metal claws can stop bleeding.
I will complete this long post by presenting a few things about the patient's approach with acute lower GI bleeding. The most common causes of lower GI hemorrhage vary with age. In all cases, upper GI bleeding should be excluded, if necessary, by nasogastric suction or even diagnosed endoscopy and rectal cough and anoscopy should be carefully performed to exclude anorectal pathology, such as cracks and bleeding from internal hemorrhoids.
A flexible sigmoidoscopy (after a gentle enema with saline solution) should be performed to rule out rectosigmoid disease. In the hemodynamically stable patient, elective colonoscopy should be performed after lavage with an oral solution of polyethylene glycol/ electrolytes or phosphosodium solution. The endoscope therapist can remove polyps, cauterize angiodysplastic lesions and sometimes inject a bleeding diverticulum with epinephrine.
If colonoscopy is negative, but there is recurrent or intermittent lower GI bleeding, a study with marked hematia should be considered. Images can be obtained within 48 hours. If the study shows a suspicious lesion, selective angiography helps locate the bleeding site more accurately. The patient with a lower torrential GI bleeding usually cannot be prepared for colonoscopy, nor can he wait for images with marked hematia (such a patient must undergo a mesenteric angiography, after the nazogastric suction has ruled out rapid upper GI bleeding).
Once the site of bleeding is identified by angiography, surgery is often necessary. Acute upper and lower GI bleeding is a challenge, both diagnostically and therapeutically. It requires an optimal team of emergency and intensive care personnel, internists, gastroenterologists, invasive radiologists and surgeons.
Here I managed to finish this long post! I'll probably work tomorrow on the jaundice presentation (it looks like I'll have some time available, as today). If not, we'll read each other on June 28th...
Let's hear it for good!
Dorin, Merticaru