The management of patients with upper gastrointestinal bleeds (UGIB) presenting in extremis is enough to make any physician have melena. In an effort to preserve your own clothes, make your life easier by classifying the condition in terms of variceal versus nonvariceal.
edited by Amal Mattu, MD
The management of patients with upper gastrointestinal bleeds (UGIB) presenting in extremis is enough to make any physician have melena. In an effort to preserve your own clothes, make your life easier by classifying the condition in terms of variceal versus nonvariceal. Varices are present 85% of the time in patients with Child-Pugh Class C (severe) cirrhosis, but do not be fooled by the lack of cirrhosis. Primary biliary cirrhosis patients develop varices long before the establishment of cirrhosis. It is simple plumbing; varices develop and subsequently bleed as a result of increased portal pressure due to increased resistance to flow from the fibrous reorganization of the liver’s architecture. Variceal hemorrhage is directly proportional to the hepatic venous pressure gradient (HVPG). The control of bleeding varices is therefore aimed at decreasing the HVPG. Inevitably, variceal bleeders require endoscopic banding.
Variceal bleeding frequently is intermittent and resolves spontaneously in 40% to 50% of patients. Rebleeding will occur (in 30% to 40%) in the first 6 weeks, with peak incidence in the first 5 days. Consider the patient who is currently not bleeding as a disaster waiting to happen. Be aggressive!
There are objective criteria that can assist you in risk stratifying your patients. Adverse outcomes have been associated with five initial findings: hematocrit <30%, systolic blood pressure <100 mm Hg, bloody nasogastric lavage, history of cirrhosis or ascites on exam, and history of vomiting red blood. Many of these are intuitive; if your patient is hypotensive with bright red blood in the nasogastric (NG) tube and a hematocrit of 20%, then there is an ominous outcome looming. However, do not overlook the subjective report of hematemesis. Trust your patients! Do not rely on a negative nasogastric lavage or the absence of melena. Hematemesis, whether subjective or objective, has a relative risk of 2.4 and needs to be taken seriously. Furthermore, look for ascites, as patients with a history of cirrhosis or ascites have poor prognosis with a 36% complication rate.
Now that you know that your patient has the potential for a less than optimal outcome, take action to improve his or her chances. You only have to worry about five things: airway protection, volume resuscitation, bleeding tamponade, prevention of organ dysfunction, and minimization of infection. Naturally, you are a master of the As and Bs, but let us focus on the nuances of this patient’s circulation.
Volume resuscitation requires prompt but cautious intervention. Overly aggressive saline resuscitation can lead to increased ascites that will further increase the HVPG, further exacerbating bleeding. Do not be shy about plasma expanders; the average patient requires 4 units of packed red blood cells (PRBCs), 3 units of fresh frozen plasma (FFP), and 11/2 units of platelets. Aim for a hemoglobin of 8 g/dL and systolic blood pressure to 100 mm Hg, but not higher, as higher HVPGs cause more rebleeding and increased mortality. Obviously, the patient with rapid ongoing bleeding or ischemic heart disease requires a higher hemoglobin level. Control bleeding first with FFP and platelets, but do not waste your patient’s money on recombinant factor VIIa, because there is no benefit.
Now is a great time to break out that new handheld computer and your newest drug reference guide! Vasopressin is a potent splanchnic vasoconstrictor that reduces blood flow and decreases the HVPG; however, it has side effects. Give nitrates to decrease some of these untoward effects if the blood pressure can tolerate it. Octreotide also causes splanchnic vasoconstriction, but watch out for tachyphylaxis. Forget about b-blockers; they are only useful to prevent the occurrence of bleeds in outpatients and will complicate your management by blunting the compensatory increase in heart rate.
Interestingly, while vasoconstrictors make intuitive sense, antibiotics also play an important role in patients with variceal bleeds. Cirrhotic patients with UGIB are at increased risk of severe bacterial infections, which lead to early recurrence of hemorrhage and greater mortality. Fifty percent develop spontaneous bacterial peritonitis, 25% urinary tract infections, and 25% pneumonias. Give short-term prophylactic antibiotic therapy whether or not ascites are present. Norfloxacin or ciprofloxacin is the preferred oral medication, but ceftriaxone is the preferred intravenous medication in the severely cirrhotic patient. Forget about lactulose or lactitol; it has no benefit and only angers the nurses.
Unfortunately, despite your efforts, 10% to 20% of patients cannot have their bleeding controlled despite endoscopic or pharmacologic intervention and may need emergent shunt therapy. If your on-call gastroenterologist is on the golf course with nine holes to go, have your interventionalist’s and surgeon’s numbers readily available. Balloon tamponade is an effective device to control excessive bleeding temporarily; however, it has potentially lethal complications including aspiration, migration, necrosis, and perforation with a mortality rate of 20%. Only use it if your patient will be definitively getting TIPS (Transjugular Intrahepatic Portosystemic Shunt) therapy within 24 h of placement.
With these tips in mind, you should be able to satisfactorily sign this patient out to your colleague, and thanks to the ever-increasing practice of emergency department boarding, receive this patient again during next day morning’s sign out.
Suggested Readings –
- Abraldes J, Bosch J. The treatment of acute variceal bleeding. J Clin Gastroenterol. 2007;41(S3):S312–S327.
- Corley D, Stefan A, Wolf M, et al. Early indicators of prognosis in upper gastrointestinal hemorrhage. Am J Gastroenterol. 1998;93(3):336–340.
- Garcia-Tsao G, Sanyal A, Grace N, et al. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46(3):922–938.
- Sorbi D, Gostout C, Peura D, et al. An assessment of the management of acute bleeding varices: A multicenter prospective member-based study. Am J Gastroenterol. 2003;98(11): 2424–2434.9
This article is an excerpt from the book “Avoiding Common Errors in the Emergency Department” (Lippincott Williams & Wilkins, 2010)