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- Review the anatomy of the gastrointestinal tract
- Describe the characteristics of GI bleeding
- Review causes of upper GI bleeding and lower GI bleeding
- Describe the assessment of a patient with GI bleeding
- Review the prehospital management of the patient with GI bleeding
Squad 15 had just finished cleaning up from their last transport when the alert tones went off for a 42-year-old female with gastrointestinal bleeding. While responding, the two EMTs developed a plan: If the patient was actively bleeding from the rectum, Michael would put absorbent pads on the stretcher while Sarah, his senior partner, obtained vital signs and got a complete history. When the crew walked inside a very clean, modern ranch home, they were directed to a side bedroom where a frail, pale and tired-looking woman was leaning over a garbage can vomiting clots of blood. As her family explained that she had been vomiting blood for two days, Sarah and Michael had to reset in their minds how they would manage this transport. As Michael went outside to get an emesis basin, he turned to Sarah and said, "I thought dispatch said this was for GI bleeding!"
Every year, more than 300,000 patients are hospitalized with gastrointestinal (GI) bleeding1 and countless more are managed in emergency departments. More than 150 out of every 100,000 people experience some sort of GI bleeding annually. Nearly 70% of GI bleeds occur in the upper GI tract and more than 50% of all GI bleeds are caused by peptic ulcer disease. Presently, the mortality from GI bleeding is around 10%, and this rises with age as patients begin to have multiple contributing underlying conditions like hypertension, diabetes and cardiac disease. For individuals younger than age 50, however, the most common cause of GI bleeding is hemorrhoids, which, while uncomfortable, is more of a nuisance than anything else.2
It is essential for EMS providers to understand the different causes of GI bleeding to help perform a thorough patient assessment and provide accurate care. Additionally, understanding how to evaluate GI bleeding helps determine the seriousness, rate and severity of bleeding.
Anatomy of the Gastrointestinal Tract
The gastrointestinal tract, or alimentary canal, is a hollow tube that begins at the mouth and ends at the anus. Materials inside this tract are technically not inside the body, but rather inside the tube. The purpose of the GI system is to break down materials inside this tube so that usable nutrients, minerals and liquids can be removed.
Food and liquids enter the GI tract at the mouth and are passed down through the elastic but muscular esophagus, which squeezes food boluses through with rhythmic muscle contractions. The cardiac sphincter is the valve at the distal end of the esophagus and the beginning of the stomach. One of the most important purposes of the cardiac sphincter is to prevent regurgitation of food and digestive acids from entering the esophagus. Inside the stomach, food is broken down by a variety of acids and muscle contractions. The stomach itself sits just inferior to the diaphragm and is protected by the rib cage; it is also situated just behind liver's left lobe. Once solid materials are broken down in the stomach, they exit through the pyloric sphincter and enter the duodenum, the first of three sections of the small intestine. Food boluses, now called chime, move through the intestinal tract via muscular contractions called peristalsis.
Once inside the 6-7-meter-long small intestine, nutrient and mineral absorption begins and continues as materials are moved continuously through the intestines. In the duodenum, which is the largest in diameter of the small intestine sections, food breakdown is assisted by the introduction of pancreatic enzymes like lipase, amylase and trypsinogen, among others. The pancreas also releases bicarbonate, which buffers the very acidic chime just released from the stomach.
Bile also enters the digestive tract in the duodenum, through the bile duct, and is essential to fat absorption. Most duodenal ulcers occur between the bile duct and the pyloric sphincter.3 Bile is a greenish alkaline fluid produced in the liver and stored in the gall-bladder until needed to aid in fat digestion. The duodenum narrows and connects with the jejunum at the ligament of Treitz, which is considered the transition from the upper to lower GI tract. Absorption of nutrients and minerals continues in the jejunum and the ileum, the final and longest section of the small intestine, making up the final three-fifths of the length.3 The ileum has the thinnest walls of the small intestine and is the most vascular.
For all intents and purposes, nutrient and mineral absorption ends at the ileocecal fold, where the ileum passes all remaining solid materials into the cecum, the first section of the 1.5-meter-long large intestine. Water and salts are absorbed by the large intestine, leaving whatever remains as solid waste. As stated, the cecum is the first section of the large intestine that rests in the lower right abdominal quadrant and receives materials from the ileum. Just inferior, or below the cecum, is the appendix. Materials in the cecum actually move superiorly up the ascending colon, across the transverse colon, down the descending colon along the left abdominal flank, across the sigmoid colon and finally to the rectum and anus.
To help increase the surface area for absorption, the intestines are lined with villi, which are closely packed finger-like structures that protrude toward the center of the intestinal lumen. The number and size of villi decrease in the large intestine until the lining becomes smooth near the rectum.
Irritation or injury at any point along this system can result in GI bleeding into the tract. What that blood looks like and where it exits the tract is determined by where the bleeding actually occurs.
Characteristics of GI Bleeding
Depending on the location and rate of bleeding, identifying gastrointestinal bleeding may be fairly simple, or nearly impossible. Regardless of where bleeding is located, the clinical manifestations are dependent on the rate and volume of blood loss. Patients who have experienced slow or minimal blood loss may only present with abdominal discomfort, and bleeding may not be detected until blood tests show the patient has low hemoglobin.
Moderate to severe blood loss from any source causes hypovolemic shock. The human body responds to hypovolemic shock the same way every time through a series of normal compensatory mechanisms. The release of catecholamines, epinephrine and norepinephrine, increases the heart rate and breathing and triggers peripheral vascular resistance, which is what causes pale, cool and clammy skin. Over time, patients may also present with orthostatic blood pressure changes, which signal a blood loss exceeding 1000 mL.1
Blood exiting the GI tract is the best and most definitive indicator of GI bleeding. It comes in three forms: hematemesis, hematochezia and melena. Hematemesis is bloody vomit, which can come as either frank red blood or "coffee-ground" colored. A patient with hematemesis is bleeding above the ligament of Treitz. Gastric acids rapidly convert hemoglobin to a brown-colored hematin, which is why blood takes on a coffee-ground appearance. When frank blood is vomited, it signals that the blood has had little or no time to mix with gastric acids.1
Bleeding anyplace in the GI tract results in blood from the rectum. Melena, black-colored stool caused by the breakdown of blood, signals the blood had to travel a great distance and time; 90% of the time that signifies an upper GI bleed.1 Hematochezia, maroon-colored, clotted or bright red blood passing from the rectum, suggests a lower GI bleed source.
There are many different causes for GI bleeding. Table I summarizes common causes at various places throughout the GI tract. It is not feasible to try to memorize the pathology of all of these diseases, but it is important to understand the pathology of several of the most common causes.
Upper GI bleeding
PEPTIC ULCER DISEASE
Gastric and duodenal ulcers are both included under peptic ulcer disease (PUD), which is responsible for nearly half of all acute upper GI bleeding1 and affects nearly 4.5 million people annually.4 PUD is closely associated with the bacterium Helicobacter pylori (H. pylori). When H. pylori infects the mucosal lining of the stomach or duodenum, it predisposes the mucosal layer to damage by gastric secretions, alcohol, medications or other bacteria.1 When H. pylori is absent, ingestion of aspirin and nonsteroidal anti-inflammatory drugs, as well as smoking, can cause peptic ulcers to form. Patients who have cirrhosis, chronic obstructive pulmonary disease, renal failure, or who have had an organ transplant have an increased risk for PUD. An ulcer develops as part of the mucosal tissue layer erodes, exposing the underlying tissues, including blood vessels. When the wall of a blood vessel is eroded, bleeding occurs.
Patients with PUD most commonly experience a gnawing or burning epigastric pain 2-3 hours after eating, or it awakens them at night. Nausea is also common, as well as a bloating sensation and abdominal distention. When an ulcer has eroded into a blood vessel and there is bleeding, hematemesis and melena are both common.4
The portal vascular system is the vascular system that drains blood from the gastrointestinal system and delivers it to the liver. Portal hypertension is an increase in blood pressure within this vascular system and is typically caused by liver cirrhosis.
This increases the resistance in the portal venous system, which receives blood from the GI tract, including the esophagus and other areas of the body. This pressure build-up forces small veins to become stretched and dilated, causing varicose veins. Nearly all EMS crews have seen varicose veins on a patient's leg. It is the dilated blood vessel that bleeds profusely when nicked and does not stop without pressure being applied. In the intestinal tract, varicose veins can develop anywhere from the anus to the esophagus, although varices in the esophagus are among the most common, accounting for nearly 15% of acute upper GI bleeding.1 Picture a bleeding varicose vein inside the esophagus. Heavy bleeding continues endlessly until well-aimed direct pressure is applied or surgical intervention stops the bleeding. This is why the mortality for esophageal varices is nearly 40%.1
Patients who have become ill and are frequently and forcefully vomiting may develop small longitudinal tears in the proximal stomach near the cardiac sphincter and in the esophagus. Bleeding can occur from these Mallory-Weiss tears that present with bright bloody streaks in the patient's emesis when they vomit again. On occasion, tears can occur prior to the patient first vomiting, and there may be some blood in the patient's initial emesis. This is particularly common when the patient has a preexisting hiatal hernia.5 Mallory-Weiss tears cause roughly 15% of upper GI bleeds, but are typically self limiting.1 Bleeding stops spontaneously for nearly 90% of patients with Mallory-Weiss tears.5
Unfortunately, no specific exam findings can rule in Mallory-Weiss tears. When bleeding is present, focus on looking for clinical signs of shock to determine the severity of bleeding. Obtain a thorough history for clues or recent illnesses with vomiting. In addition to a history of hiatal hernia, excessive alcohol use and use of aspirin are common in these patients.
Another serious consequence of forceful vomiting is Boerhaave's syndrome, which is an esophageal rupture. The rupture occurs because of the rise in intra-esophageal pressure combined with negative intrathoracic pressure associated with vomiting. Shortly after rupture, patients begin to experience severe pain in the chest and neck, which may radiate into the back and abdomen. Often they will continue to vomit with the addition of blood in their emesis. The pain associated with Boerhaave's syndrome is much more severe than with a Mallory-Weiss tear, and is distinguished by the increased pain level. Shortness of breath is also common. Untreated, shock can rapidly develop from either bleeding or infection. When not operated on emergently, there is a 72% mortality rate.6 When the esophagus ruptures, digestive juices can spill into the mediastinum, causing an infection that can rapidly lead to sepsis.
Upon examination, 60% of patients experiencing Boerhaave's syndrome develop subcutaneous emphysema in the neck and chest within the first hour of rupture. Fever can develop later, as can decreased lung sounds on the side of the rupture. Boerhaave's syndrome is distinguished from Mallory-Weiss tears by a chest x-ray and the presence or absence of the clinical signs of shock.
Lower GI Bleeding
Diverticular disease, which includes diverticulosis, is one of the most common GI-related diseases and can affect any part of the intestinal tract; however, the sigmoid colon is involved in nearly 98% of cases.7
Diverticula are small saclike protrusions in the lumen of the intestine that develop from increased intralumen pressure and weakening of the mucosal and submucosal wall layers. These sacs protrude outwards of the lumen, often tunneling along blood vessels that penetrate through the circular muscle fibers around the intestine. These vessels lose protection as they travel along the dome of a diverticulum and are only protected from the lumen contents by a small mucosal layer. Injury to a diverticula can cause heavy bleeding and is responsible for 55% of lower GI bleeds.1 While there can be a significant amount of bleeding, it is often self-limiting and terminates spontaneously.7 Diverticula injury can result from an abscess, nonsteroidal antiinflammatory drug use, seeds, colon motility and even age.
Patients experiencing bleeding from a diverticula often do not experience pain, although they do experience cramping sensations or the urge to defecate, and may pass hematochezia that is either bright red or wine-colored. When the abdomen is examined, tenderness is not typically present with diverticulosis and suggests a different etiology. Firmness may be noted in the left lower quadrant where the sigmoid colon travels toward the rectum.7
Most frequently occurring in the cecum and ascending colon, angiodysplasia is the dilation of a submucosal vein or artery that lacks smooth muscles needed for contraction. The incidence of angiodysplasia increases as people age and vessels become weaker, and it is one of the two leading causes of lower GI bleeding. Because angiodysplasia is a malformation of blood vessels, it can occur anywhere in the intestinal tract and can affect both veins and arteries. Unfortunately, the exact mechanisms by which angiodysplasia develops is unknown.8
Angiodysplasia is often asymptomatic until the patient realizes he is passing blood. It is generally found on routine colonoscopy, but in more than one location. When angiodysplasia does cause bleeding, the rate and amount of bleeding are variable based on which vessel has a lesion. Once a lesion begins to bleed, it chronically bleeds and terminates on its own, leading to intermittent hematochezia and chronic iron deficiency.
Over 10 million people in the U.S. experience hemorrhoid symptoms. It is a common condition where vascular structures in the anus become swollen and inflamed.9 Once irritated, a hemorrhoid becomes prone to painless bleeding during bowel movements. Most often, patients notice red streaks of blood on toilet paper when cleansing themselves, or notice a drop or two of blood in the toilet.
There are both internal and external hemorrhoids. Internal hemorrhoids occur in the rectum around the perianal arteries, which are in a denervated, or nerveless, section of tissue. Because it is denervated, there is no pain associated with the inflammation or bleeding.9 On occasion, an internal hemorrhoid can become large enough to pass through the anus and become strangulated, which will cause pain and discomfort. External hemorrhoids occur outside of the anus and can become painful, as the area does contain nerves. A thrombosis can develop beneath the hemorrhoid, which is a common cause of discomfort. Straining during defecation can cause tears in internal or external hemorrhoids. The associated bleeding is generally very limited and in a small quantity; however, the first time someone sees blood in the toilet or on the toilet paper, they may become worried and contact 9-1-1. Often, if they cleanse themselves a second time, there will be no blood.
Completing an accurate and thorough assessment is extremely important when managing patients with GI bleeding. Like any assessment, there are two components: a thorough history and an accurate physical exam. Using these together, determine the patient's hemodynamic stability and then determine a treatment plan.
When speaking with patients, work with them to determine not only the onset of bleeding, but the onset of any abdominal discomfort as well. Follow the OPQRST mnemonic (Figure 1) to learn as much as possible about any discomfort the patient may have. A good history will help correlate what the patient says to what condition they may be experiencing.
Also pay particular attention to any prior history of GI bleeding; 60% of patients who have repetitive GI bleeding continue to bleed from the same site.1 Determine if the patient has had digestive tract or abdominal surgery; ask when and for what reason. Seek out conditions in a patient's medical history that can contribute to GI bleeding, such as liver cirrhosis, hypertension, alcohol abuse and the use of aspirin or nonsteroidal antiinflammatory drugs. Try to determine if there have been recent changes in the patient's bowel habits, as change may indicate a time line for when intestinal dysfunction began.
Pay particular attention when taking a SAMPLE history, as subtle clues may help identify what is causing the bleeding. For example, patients with peptic ulcer disease often feel discomfort several hours after eating, and excessive alcohol intake can exacerbate many causes of GI bleeding. Patients with complaints of recent severe vomiting who are not vomiting blood may be experiencing Mallory-Weiss tears. The presence or absence of pain can help rule in or out different conditions: Mallory-Weiss tears do not often present with pain, while Boerhaave's syndrome is associated with severe pain.
A complete physical exam is appropriate for all prehospital patients. Unfortunately, the detailed physical exam does not always reveal a great deal of information when evaluating GI bleeding. A detailed physical exam allows you to look for evidence of hypovolemic shock, and repeat assessments enable monitoring over time.
When evaluating the abdomen, begin by determining the presence of pain. Pain is discomfort that the patient feels constantly or comes and goes spontaneously without stimulation.
The simplest way to identify symptoms of hypovolemic shock is to look at the patient's skin and monitor his or her vital signs. Before vital signs begin to exceed normal limits, patients who are bleeding experience peripheral vasoconstriction and present with pale, cool, clammy skin. Even slightly pale skin may suggest some degree of vasoconstriction. Profound vasoconstriction may nearly eliminate blood flow to the distal extremities, at which point cyanosis of the fingers and toes may develop.
Carefully monitor vital signs. As patients progress through hypovolemic shock, their heart rate and respiratory rate steadily increase. As long as a patient is compensating, his blood pressure and mental status remain relatively unchanged. Decompensated shock is identified when the blood pressure and mental status decline. Typically, a 40% blood loss is required for blood pressure to decline.
While the resting blood pressure changes late in hypovolemic shock, an early sign that a patient has serious GI (or any internal) bleeding is a change in orthostatic blood pressure. Positive orthostatic blood pressure changes exist when the patient's blood pressure decreases by at least 10 mmHg and the heart rate increases by 20 beats per minute after it is measured with the patient supine and then one minute after moving the patient to a seated or standing position. Orthostatic changes are associated with a 15% blood loss.
Capable providers should also obtain a baseline 12-lead EKG. Even though the patient may not be experiencing cardiac symptoms, the loss of blood can strain the heart. When a patient has a preexisting cardiac condition, blood loss can trigger an ischemic myocardial event such as angina or MI.
Manage airway and breathing as with any other patient. Supplemental oxygen is appropriate; however, for the majority of patients a nasal cannula may be used. Titrate oxygen levels to maintain a pulse oximetry over 94%. Recent research has demonstrated that unnecessary high-flow oxygen can oversaturate the blood with oxygen and actually impair oxygen and carbon dioxide exchange at the cellular level.10
Volume resuscitation with intravenous fluids is appropriate when patients display clinical signs of hypovolemia, including tachycardia and hypotension. Advanced providers should establish IV access and administer fluid boluses as permitted by local protocols to maintain a systolic blood pressure of at least 90 mmHg systolic.
When permitted, inserting a nasogastric (NG) tube is very beneficial. There is no evidence that inserting an NG tube can worsen GI bleeding, including with esophageal varices, and it can actually help support the diagnosis.
After inserting a NG tube, aspirate the stomach contents. If there is coffee-ground to black coloration, there is support for an upper GI bleed and mortality is just under 10%. However, if there is bright red blood in the NG aspirate and bloody stool, mortality rises to just over 30%. From a patient management perspective, placing the NG tube can relieve nausea and vomiting by removing the stomach-irritating blood.
While not often used in prehospital care, the medications IV octreotide and IV vasopressin given as continuous infusions can help control GI bleeding and prevent recurrence. Prehospital providers who provide interfacility transport may see these medications being infused. Octreotide is administered 25-50 g/hr for at least 24 hours and is particularly beneficial in managing angiodysplasia.11 Twenty units of vasopressin administered over 20 minutes is beneficial in controlling acute upper GI bleeds, particularly with severe esophageal varices when surgery is delayed. It is important to note that, while vasopressin is beneficial in extreme circumstances, it does not decrease mortality.11
Sarah and Michael were able to obtain their patient's blood pressure and heart rate while she was lying in bed as her blood pressure changed from 110/84 to 92/60 and her heart rate increased from 94 to 112 beats per minute. In speaking with her, they learned she was trying to break herself of long-standing alcoholism and had not had a drink in over a week. She had been taking aspirin for her "pains all over." They secured her to their cot in a position of comfort and Sarah established an IV, initiated a fluid bolus of normal saline and administered Zofran to control the patient's nausea and vomiting. In the emergency department, the patient was diagnosed with esophageal varices and was taken to the operating room for repair.
Table I: Causes of GI Bleeding
UPPER GI BLEEDING
LOWER GI BLEEDING
Small and large intestine
Figure 1: OPQRST
1. Morton PG, et al. Critical Care Nursing, A Holistic Approach, 8th edition. Philadelphia, PA: Lippincott, Williams & Wilkins, 2005.
2. Chico MD, Gavin F. Lower gastrointestinal bleeding, http://emedicine.medscape.com/article/188478-overview.
3. Drake R, Vogl W, Mitchell A. Gray's Anatomy for Students, St. Louis, MO: Elsevier, 2005.
4. Lee TH. Peptic Ulcer Disease, http://emedicine.medscape.com/article/181753-overview.
5. Wong KS, Louis M. Mallory-Weiss Tear, http://emedicine.medscape.com/article/187134-overview
6. Long C, Ezenkwele UA. Esophageal Perforation, Rupture, and Tears, http://emedicine.medscape.com/article/775165-overview.
7. Goss B, Farina G. Diverticular Disease. http://emedicine.medscape.com/article/774922-overview.
8. Thomson A. Angiodysplasia of the colon, http://emedicine.medscape.com/article/170719-overview.
9. Thornton SC. Hemorrhoids, http://emedicine.medscape.com/article/195401-overview.
10. American Heart Association, Post-Cardiac Arrest Care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Peberdy MA, Callaway CW, Neumar RW, et al. Circulation 122:S768-S786, 2010.
11. Marx JA. Rosen's Emergency Medicine, 7th Edition, Chapter 22. Gastrointestinal Bleeding, Philadelphia, PA: Mosby, 2010.
Kevin T. Collopy, BA, CCEMT-P, NREMT-P, WEMT, is an educator, e-learning content developer and author of numerous articles and textbook chapters. He is also a flight paramedic for Spirit Ministry Medical Transportation in central Wisconsin and a lead instructor for Wilderness Medical Associates. Contact him at email@example.com.
Michael Curtis, MD, is an emergency department physician and EMS medical director with Ministry Health Care in Wisconsin.
Scott R. Snyder, BS, NREMT-P, is the EMS education manager for the San Francisco Paramedic Association in San Francisco, CA, where he is responsible for the original and continuing education of EMTs and paramedics. Scott has worked on numerous publications as an editor, contributing author and author, and enjoys presenting on both clinical and EMS educator topics. Contact him at firstname.lastname@example.org.