How to Identify and Manage Massive Gastroesophageal Hemorrhage

 

 
 
 

Ryan Gerecht, MD, CMTE | From the August 2014 Issue | Thursday, August 7, 2014


It’s 3 a.m. when you’re dispatched to the home of a 52-year-old male with complaints of abdominal pain and vomiting. He’s well-known to you and your partner for having a long history of alcohol abuse resulting in cirrhosis of the liver. Upon arrival, he states he’s been drinking his normal amount of beer today but has had several episodes of vomiting and diffuse abdominal pain. His initial vitals signs are a blood pressure of 106/52, a heart rate of 128 bpm, a respiratory rate of 20, and an O2 saturation of 94% on room air.

While enroute to the hospital he begins to violently vomit large amounts of bright-red blood, which quickly fills a suction canister and begins to flow onto the stretcher. As you notify the receiving hospital of the sudden decline in your patient’s condition, he quickly becomes unresponsive.

Gastrointestinal Bleeding
Gastrointestinal (GI) bleeding is a relatively common and potentially high-risk presentation for all emergency providers. Bleeding can range from mild to massive, and is typically classified by its source—an upper or a lower GI bleed. Upper GI bleeding involves the esophagus, stomach or the first part of the small intestine called the duodenum. Lower GI bleeding involves the remainder of the intestinal tract. (See Figure 1, p. 58.)

A massive GI bleed results in signs and symptoms consistent with hemorrhagic shock such as hypotension and tachycardia. More than 75% of massive GI bleeding involves an upper GI source. Despite advances in treatment, mortality rates range from 20–39%.1

The most common causes of upper GI bleeding include duodenal ulcers (28%), stomach ulcers (26%) and gastroesophageal varices (10–30%).1–3 Considering all causes of GI bleeding, variceal hemorrhage has the highest mortality rate at 25–50%.4 Up to a third of patients will ultimately die following their first episode of variceal bleeding and prehospital mortality is estimated to be around 3%.3,5,6

Anatomy & Physiology
The systemic venous system carries deoxygenated blood from internal organs directly back to the heart and lungs for reoxygenation and recirculation. However, in the GI tract, an additional venous system called the hepatic portal system directs blood from the majority of the GI tract directly to the liver before allowing this blood to return to the heart. This extra venous system routes blood that’s absorbed man-made or organic chemicals and other potential toxins from the GI tract directly through the liver for detoxification before sending it into the systemic venous system and heart.7

When the pressure in this hepatic portal system becomes elevated, the patient has portal hypertension. It’s caused by any disease state that increases resistance to blood flow through the liver (e.g., blood clots, cancer, certain infections, etc.) but most commonly by cirrhosis—the replacement of normal liver with nonfunctional scar tissue—most commonly caused by alcoholism and hepatitis C.8

Gastroesophageal varices are the direct result of portal hypertension. With increasing resistance to blood flow through the liver, collateral veins develop around the GI tract at sites of communication between the portal and systemic venous systems. (See Figure 2.) This occurs in an attempt to decompress the rising pressure in the portal system.2,5 As these normally small, fragile collateral veins become abnormally enlarged under pressure, they’re called varices. The distal 2–5 cm of
the esophagus extending into the stomach is the most common site for these varices.2 At this location, these vessels lack structural support from surrounding tissue
and, as the pressure and flow increase over time, the varices dilate and eventually may rupture, causing rapidly occurring devastating hemorrhage.2,5

Diagnosis & Treatment
The diagnosis of gastroesophageal varices is made visually through endoscopy, where a tiny camera attached to a long flexible tube is passed through the mouth into the esophagus and stomach. Patients diagnosed with varices will oftentimes be started on daily oral medications such as propranolol, a beta-blocker, to try to decrease the portal pressure and thus reduce the risk of variceal rupture.3,5 If variceal rupture occurs, additional IV medications will be started in the hospital to further decrease portal pressure and blood flow and thus decrease the bleeding.

To definitively stop variceal hemorrhage, patients undergo endoscopic band ligation, which is placement of a small elastic tourniquet around the varices. An alternative option is endoscopic sclerotherapy, or the injection of an irritating solution in or near the bleeding varices to make them clot.

In 10–20% of cases, hemorrhage is unable to be controlled with endoscopy, and the use of balloon tamponade may be considered as a lifesaving rescue procedure.3,5 This involves placement of a Minnesota or Sengstaken-Blakemore tube—a specialized tube fitted with large balloons that, when inflated, apply direct pressure to bleeding varices in both the stomach and esophagus. (See Figure 3.) In extreme cases, emergency surgery for massively bleeding esophageal varices can be performed.

Prehospital Management
Unlike other sources of massive hemorrhage such as extremity wounds, EMS doesn’t have the tools required to control acute hemorrhage from gastroesophageal varices. Despite these resource limitations, timely and effective EMS triage and treatment can help maximize patient outcomes. The cornerstone of prehospital management for these patients focuses on airway management and volume resuscitation.

Managing the Bloody Airway
There are several critical considerations all providers must address through calculated preparation and execution prior to managing a bloody airway, which can occur from a variety of causes, not just ruptured gastroesophageal varices. Obstacles to intubation include

1. Obscured view of the vocal cords due to uncontrolled hemorrahage into the airway;
2. The increased risk of peri-intubation cardiac arrest when the patient is in hemorrhagic shock;9
3. Pulmonary aspiration and subsequent critical hypoxia caused by blood in the airway; and
4. Increased risk of blood-borne pathogen exposure for the provider.

There are several things providers can do to increase the chances of successfully managing the bloody airway:

Consider alternatives to intubation. The prehospital management of the bloody airway doesn’t necessarily mean intubation. Sometimes less is more. Frequently, the airway can be successfully managed with aggressive continuous suctioning, proper patient positioning, provision of maximal supplemental oxygen, use of nasopharyngeal airways and administration of IV antiemetics such as Zofran (ondansetron).

Have an airway plan and say it out loud. Making and verbalizing an airway plan agreed upon by all providers is critical for any intubation, but particularly important in the bloody airway. This plan should include identifying anticipated anatomic and physiologic difficulties to intubation, a description of the tools that will be utilized for intubation based on these difficulties, the medications to be administered if allowed by protocol and the back-up devices to be deployed if intubation fails.

Choose your medication doses wisely. If forced to perform rapid sequence or medication-facilitated intubation on a patient in hemorrhagic shock, strongly consider using a more hemodynamically stable induction agent such as ketamine or etomidate. Regardless of the medications used, it’s strongly advised to use half of the normal weight-based induction dose to help prevent peri-intubation cardiac arrest.

Maximize preoxygenation, utilize apneic oxygenation and minimize bagging. Preoxygenation is arguably the most important step of any intubation attempt. Your patient won’t die from lack of an endotracheal (ET) tube, but rather from lack of oxygen. You want to do everything possible to prevent having to bag these patients. BVM ventilation frequently forces air into the stomach and increases the risk of aspiration. Utilize a nonrebreather mask and a nasal cannula simultaneously to maximize oxygenation before and during intubation.10 (See “Apneic Oxygenation: How & why to give a non-breathing patient oxygen,” by Joshua Sappenfield, MD, from the JEMS May 2013 issue.) If you must bag in response to critical hypoxia, do so in a disciplined manner—Utilize a counted rate of 10 breaths per minute and only the volume required to achieve chest rise.

Consider oral or nasogastric sump tubes. If allowed by protocol, strongly consider placement of an oral gastric (OG) or nasogastric (NG) tube before intubation. OG or NG tube placement serves to empty the stomach of blood, reducing the risk of aspiration and possibly helping with ventilation post-intubation. The presence of already-bleeding esophageal varices isn’t a contraindication to placement of these devices.11

Suction, suction, suction. Utilize both the onboard and portable suction units simultaneously when resources allow. Additionally, I’ve found the Lipsky Super Suction System beneficial in rapidly removing large volumes of fluid and particulate matter from the oropharynx.

Intubate as a team. With uncontrolled hemorrhage, the intubator can suction the airway and often obtain the necessary view of the vocal cords. To overcome the challenge of placing the ET tube as blood rapidly re-accumulates in the airway, assign a second provider to maintain continuous suction in the oropharynx throughout the intubation attempt. This can be done from both sides of the mouth as resources and equipment allow.12 (See photo on p. 61.)

Build a completely novel suction device. To address rapidly reaccumulating fluids in the airway, Scott D. Weingart, MD, has described a method of transforming the ET tube into a large bore suction catheter. This method involves attaching a neonatal meconium aspirator to the end of the ET tube which allows for continuous removal of blood and secretions throughout the ET tube placement process.13 There are some possible EMS operational limitations to this method, but it does offer the potential to improve airway visualization. (For more details on this device, visit www.emcrit.org/blogpost/ett-as-suction-device.)

Elevate the head of the bed at 30–45 degrees. Gone are the days of always intubating with the patient in the supine position. There’s good evidence that elevating the head of the bed actually improves your view of the vocal cords and prolongs the time until critical apneic desaturation occurs.14,15 It’s also reasonable to assume this semi-upright positioning helps prevent aspiration in patients suffering from a massive upper GI bleed. This technique shouldn’t be utilized for trauma patients requiring spinal precautions.

Ditch the video laryngoscope (for now). EMS use of video laryngoscopes is steadily increasing as multiple studies show improved success with use of these devices compared with direct laryngoscopes in a variety of clinical settings.16 However, excessive blood and secretions in the airway obscure the camera lens at the distal end of the blade. Providers may want to consider direct larygoscopy when faced with a severely bloody airway.17 Future use of video laryngoscopy blades with integrated suction may change this approach.18,19

Protect yourself. The importance of personal protective equipment including eye protection can’t be underestimated.

Recognize when the airway has failed. It takes both courage and confidence to acknowledge unsuccessful attempts at intubation and oxygenation. Providers should rapidly proceed to a backup plan, including cricothyrotomy, as allowed by protocol. Failure to promptly recognize the failed airway can result in devastating consequences.

Volume Resuscitation
The overall resuscitation strategy for the patient with bleeding esophageal varices is similar to that of the critical trauma patient and should include efforts to combat the “lethal triad” of hypothermia, coagulopathy and acidosis.20,21

The initial goal is to restore intravascular volume to maximize organ perfusion and achieve the hemodynamic stability required to proceed with diagnostic and treatment procedures in the hospital. For any patient with acute massive bleeding, it’s preferable to replace hemorrhaged blood with blood product transfusions to both optimize the delivery of oxygen to the tissues as well as replenish clotting factors. However, until these blood products are available, prompt resuscitation with warmed fluids should be initiated in the hemodynamically unstable patient. (See “Stop Fluid Resuscitation? Using blood products for prehospital trauma patients” on pp. 24–25.)

The exact blood pressure target for fluid resuscitating patients is largely unknown and primarily dependent on the patient’s size, age and medical conditions.

It’s particularly important to avoid prolonged hypotension in patients with liver cirrhosis and bleeding esophageal varices, as this can contribute to infection and renal failure. Both are associated with increased risk of rebleeding and death.22 However, we should avoid overly aggressive resuscitation to normalize blood pressure as this may increase liver portal pressures and possibly worsen the uncontrolled esophageal hemorrhage.23

In patients with cirrhosis, excessive crystalloid infusion may be harmful due to their increased risk of fluid shifts out of the vascular system caused by low serum protein levels.20

It’s reasonable to utilize a strategy similar to what’s advocated in the care of a bleeding trauma patient. Permissive hypotension resuscitation calls for incremental fluid boluses to restore or maintain adequate vital organ perfusion. This is typically defined as the presence of a radial pulse or normal mental status, rather than normalization of blood pressure. A systolic blood pressure of approximately 80–90 mmHg is believed to meet this objective in most patients.24

Case Conclusion
Repeat vital signs after hospital notification reveal a blood pressure of 72/40, a heart rate of 132 and an O2 saturation of 90%. You quickly establish a humeral intraosseous (IO) and place bilateral nasal trumpets, a nasal cannula and a non-rebreather mask to maximize oxygenation. Then, with aggressive suctioning, your patient’s O2 saturation improves to 100% indicating you’re successfully managing the airway and can defer intubation until arrival at the ED. You administer 4 mg of Zofran via the IO and initiate a 500 cc fluid bolus.

In the ED, an NG tube is quickly placed and removes more than 2 liters of blood and stomach contents. After two difficult and prolonged attempts, the patient is successfully intubated via direct laryngoscopy with the head of the bed elevated.

No hypoxia occurrs and no BVM ventilation is required because you maximized the patient’s preoxygenation during transport and apneic oxygenation was used during rapid sequence intubation.

The hospital’s massive blood transfusion protocol is initiated through the IO you placed as the patient continues to be in hemorrhagic shock. The decision is made by the emergency physician to place a Minnesota tube in hopes of temporizing the presumed massive variceal hemorrhage. The patient is then quickly transferred to the ICU for further resuscitation and endoscopy.

Final Thoughts
Massive GI bleeding from any cause, but particularly ruptured esophageal varices, is a deadly and time-sensitive medical emergency. Despite not having the tools to stop the hemorrhage, EMS providers are uniquely positioned to improve patient outcomes through rapid recognition of critical illness, skillful stabilization of the airway and initiation of a calculated resuscitation.

By maintaining a disciplined approach to the bloody airway, EMS providers can successfully manage one of the most difficult situations found in all of medicine. By applying some of the same resuscitation strategies as those utilized in a bleeding trauma patient, EMS providers can begin life-saving management for these critically-ill patients long before they arrive at the hospital.

LEARNING Objectives

  • Understand the anatomy and physiology of bleeding gastroesophageal varices.
  • Learn practical tips and tricks to manage the bloody airway.
  • Recognize a reasonable approach to resuscitating patients with massive gastrointestinal hemorrhage.

KEY Terms
Cirrhosis: The gradual replacement of normal liver tissue with nonfunctional scar tissue, commonly caused by alcohol abuse and hepatitis C.
Gastroesophageal varices: Abnormally enlarged, dilated veins in the distal esophagus and stomach, which result from hepatic portal hypertension often caused by cirrhosis.
Hepatic portal system: System of veins that carry blood from the majority of the GI tract to the liver for “detoxification” before sending it back to the heart for reoxygenation and recirculation.
Massive gastrointestinal (GI) hemorrhage: Bleeding from the GI tract that results in signs and symptoms of hemorrhagic shock.

References
1. Afessa B. Triage of patients with acute gastrointestinal bleeding for intensive care unit admission based on risk factors for poor outcome. J Clin Gastroenerol. 2000;30(3):281–285.
2. Peura DA, Lanza Fl, Gostout CJ, et al. The American College of Gastroenterology Bleeding Registry: Preliminary findings. Am J Gastroenterol. 1997;92(6):924–928.
3. Sharara AI, Rockey DC. Gastroesophageal variceal hemorrhage. N Engl J Med. 2001;345(9):669–681.
4. Berry PA, Wendon JA. The management of severe alcoholic liver disease and variceal bleeding in the intensive care unit. Curr Opin Crit Care. 2006;12(2):171–177.
5. Garcia-Tsao G, Bosch J. Management of varices and variceal hemorrhage in cirrhosis. N Engl J Med. 2010;362(9):823–832.
6. Nidegger D, Ragot S, Berthelemy P, et al. Cirrhosis and bleeding: The need for very early management. J Hepatol. 2003;39(4):509–514.
7. Rhoades RA, Bell DR: Medical physiology: Principles of clinical medicine. Third edition. Lippincott Williams & Wilkins: Philadelphia, pp. 298–299, 2009.
8. Cirrhosis. (Dec. 3, 2012.) American Liver Foundation. Retrieved April 4, 2014, from www.liverfoundation.org/abouttheliver/info/cirrhosis/.
9. Heffner AC, Swords DS, Neale MN, et al. Incidence and factors associated with cardiac arrest complicating emergency airway management. Resuscitation. 2013;84(11):1500–1504.
10. Weingart S, Levitan R. Preoxygenation and prevention of desaturation during emergency airway management. Ann Emerg Med. 2012;59(3):165–175.
11. Lopez-Torres A, Waye JD. The safety of intubation in patients with esophageal varices. Digestive Diseases. 1973;18(12):1032–1034.
12. Airway control in the massive oral bleed patient. (Aug. 6, 2011.) Emergency Medicine Updates. Retrieved April 2, 2014, from www.emupdates.com.
13. Weingart SD, Bhagwan SB. A novel set-up to allow suctioning during direct endotracheal and fiberoptic intubation. J Clin Anesth. 2011;23(6):518–519.
14. Levitan RM, Mechem CC, Ochroch EA, et al. Head-elevated laryngoscopy position: Improving laryngeal exposure during laryngoscopy by increasing head elevation. Ann Emerg Med. 2003;41(3):322–330.
15. Ramkumar V, Umesh G, Philip FA. Preoxygenation with 20° head-up tilt provides longer duration of non-hypoxic apnea than conventional preoxygenation in non-obese healthy adults. J Anesth. 2011;25(2):189–194.
16. Valenzuela T, Mosier J, Sakles J. Tunnel vision: The role of video laryngoscopy in future advanced airway management. JEMS. 2013;38(1):32–37.
17. Ackermann W, Pott LM, Vaida SJ, et al. The GlideScope video laryngoscope and the Macintosh laryngoscope compared in a simulated difficult airway with immobilization and bleeding—A randomized, prospective, crossover study. Open J of Anesth. 2012;1(2):23–28.
18. Wadman MC, Nicholas TA, Bernhagen MA, et al. Endotracheal intubation with a traditional video laryngoscope blade versus an integrated suction blade in a hemorrhagic airway cadaver model. Stud Health Technol Inform. 2013;184:468–470.
19. Mitterlechner T, Maisch S, Wetsch WA, et al. A suction laryngoscope facilitates intubation for physicians with occasional emergency medical service experience—A manikin study with severe simulated airway hemorrhage. Resuscitation. 2009;80(6):693–695.
20. Mihata RG, Bonk JA, Keville MP. Resuscitation of the patient with massive upper gastrointestinal bleeding. EM Crit Care. 2013:3(2):1–12.
21. Gerecht R. The lethal triad: Hypothermia, acidosis and coagulopathy create a deadly cycle for trauma patients. JEMS. 2014;39(4):56–60.
22. Cardenas A, Gines P, Uriz J, et al. Renal failure after upper gastrointestinal bleeding in cirrhosis: Incidence, clinical course, predictive factors, and short-term prognosis. Hepatology. 2001;34(4):469–475.
23. Bendtsen F, Krag A, Moller S. Treatment of acute variceal bleeding. Dig Liver Dis. 2008;40(5):328–336.
24. Beeson J, Starnes T. Add a little salt: Permissive hypotension in trauma resuscitation. JEMS. 2013;38(4):36–43.

 

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Related Topics: Patient Care, Airway and Respiratory, Massive Gastrointestinal Bleed, Hepatic Portal Venous system, Esophageal varices, Cirrhosis, Jems Features

 

Ryan Gerecht, MD, CMTE

Ryan Gerecht, MD, CMTE, started his career in EMS over 10 years ago as an EMT. Today he’s a flight physician with University of Cincinnati Air Care & Mobile Care and is the assistant medical director for Colerain Township Department of Fire and EMS. He’s the inaugural NAEMSP/Physio-Control EMS medicine medical director fellow, and will begin his EMS fellowship with the University of Cincinnati and Cincinnati Fire Department in July.

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