Gastrointestinal Bleeding in the Critically ill Patient

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Chapter 46 Gastrointestinal Bleeding in the Critically ill Patient

George Kasotakis, MD , George C. Velmahos, MD, PhD, MSEd

1 What are the anatomic definitions of upper versus lower gastrointestinal (GI) bleeding?

The GI tract is anatomically divided into upper and lower by the ligament of Treitz. Although this classification has little physiologic significance, it is important to bear in mind that bleeding originating distal to the ligament of Treitz cannot travel backward to the upper GI tract because of the acute angle of the small bowel at this site. Bleeding from the upper GI tract is far more common than in the lower, and this is particularly true in the critically ill.

2 What are hematemesis, coffee-ground emesis, hematochezia, and melena? Are these features helpful in determining the site and rate of bleeding?

image Hematemesis is vomiting of fresh, red blood and indicates bleeding in the upper GI tract. Approximately 50% of patients with upper GI bleeding (UGIB) will present with hematemesis.

image If the blood is older, it can appear like coffee grounds. The return of bright red blood or coffee grounds through a nasogastric tube (NGT) is highly specific for hemorrhage proximal to the ligament of Treitz.

image Hematochezia is used to describe passage of bright red or maroon-colored blood through the rectum and typically indicates a lower tract source. Less commonly (< 15%) it may indicate the rapid transit of torrential hemorrhage from the upper tract.

image Melena is the passage of black, tarry, and usually foul-smelling stool because of degradation of blood components as they traverse the GI tract. It typically signifies upper GI tract bleeding (70%) or, less often, hemorrhage from the proximal lower tract (30%).

3 Do all patients with GI bleeding need to be monitored in the intensive care unit (ICU)?

No, but patients with evidence of active bleeding (ongoing transfusion requirement, hemodynamic instability) or other significant comorbidities should be closely monitored in a high-acuity setting, such as an ICU.

4 What are the most common causes of upper and lower GI bleeding?

See Tables 46-1 and 46-2.

Table 46-1 Causes of Upper Gastrointestinal Bleeding

Cause Prevalence (%)
Peptic ulcer disease 55
Gastritis-duodenitis 20
Esophageal varices 12
Mallory-Weiss tears 8
Neoplasm 3
Angiodysplasia 2

Table 46-2 Causes of Lower Gastrointestinal Bleeding

Cause Prevalence (%)
Diverticular disease 40
Angiodysplasia 20
Colitis 20
Anorectal bleeding (hemorrhoids, anal fissures) 7
Neoplasm 7
Small bowel bleeding 6

5 What risk factors are associated with higher mortality in patients with upper GI tract hemorrhage?

image Shock

image Melena

image Anemia at presentation

image Significant fresh blood in vomit, gastric aspirate, or rectum

image Concurrent sepsis

image Poor general health

image Comorbidities (liver, renal, cardiac disease)

image Large ulcer size

image Persistent bleeding despite endoscopic therapy

image Recurrent bleeding

6 What are the most common causes of GI tract bleeding in critically ill patients?

Although critically ill patients can have any of the usual causes of GI bleeding, they are at particular risk for development of stress-related mucosal disease (SRMD) in the upper GI tract and hypotension-induced colonic ischemia. In addition, the increasing use of rectal tubes for the management of antibiotic- and enteral feeding–associated diarrhea is associated with a rise in incidence of lower GI bleeding (LGIB) due to iatrogenic rectal fissures and ulcers.

7 What are the immediate actions that need to be taken in an acute GI tract hemorrhage in the ICU?

image Ensure patient has at least two large-bore (at least 18 gauge) intravenous catheters.

image Insert Foley and nasogastric catheter (if not already in place), and initiate resuscitation (with crystalloids or blood products) per the local guidelines and policies.

image Consider obtaining a definitive airway in the uncooperative, agitated, or encephalopathic patient at risk for aspiration.

image Aspirate sample from nasogastric tube and perform rectal examination (attempt to localize the source of bleeding).

image If UGIB, initiate medical therapy with intravenous proton pump inhibitors.

image If suspicious of bleeding varices, start an octreotide infusion.

image Consult the endoscopy and/or radiology and surgical services as needed.

image For more details on managing acute GI tract bleeding, see algorithms in Figures 46-1 to 46-3.

image

Figure 46-1 Nonvariceal upper GI tract hemorrhage management algorithm.

image

Figure 46-2 Variceal upper GI tract hemorrhage management algorithm.

image

Figure 46-3 Lower GI tract hemorrhage management algorithm.

8 Does a nonbloody NGT aspirate rule out UGIB?

A bloody nasogastric aspirate indicates an upper source of bleeding. Lavage may also be used to quantify the active bleeding: Bright blood suggests active hemorrhage, whereas darker coffee grounds suggest recent or slower bleeding. However, a negative NGT aspirate is not helpful, as it may miss up to 50% of patients with recent duodenal bleeding. Therefore a nonbloody nasogastric aspirate may indicate bleeding originating in the lower GI tract or one in the upper GI tract that has ceased.

9 What medical therapies are available for the management of GI bleeding?

image Somatostatin analogs: Octreotide is a long-acting somatostatin analog that inhibits glucagon-induced mesenteric vasodilation and has been shown to decrease the risk for persistent bleeding and rebleeding in patients with both variceal and nonvariceal upper tract bleeding. Although somatostatin analogs do not improve mortality rates, they are helpful in reducing bleeding and minimizing transfusion requirements. The recommended dose for octreotide is 250 mcg IV bolus followed by a 250 mcg/hr infusion.

image Proton pump inhibitors (PPI): They have been shown to reduce risk of rebleeding, transfusion requirements, and need for surgical intervention. Their effect on mortality is questionable. They are recommended before endoscopy, as they decrease the likelihood of bleeding or need for intervention during endoscopy. Continuous PPI infusion does not appear to be better than intermittent administration and is less cost-effective. H2-receptor blockers have not proved to be valuable in the management of acute UGIB, as they lack benefit in duodenal ulcers and afford only a weak benefit in bleeding gastric ulcers.

image Vasopressin: This is a potent vasoconstrictor that has been used extensively for UGIB, most commonly for variceal bleeding. However, its unfavorable safety profile has led to its progressively diminishing use. Common adverse events include a significant rebleeding rate when the infusion is stopped and a high rate of complications (myocardial and peripheral tissue ischemia, dysrhythmias, hypertension, and decreased cardiac output).

10 What is the role of endoscopy in the management of UGIB?

Endoscopic assessment constitutes a risk-assessing tool for ongoing or recurrent bleeding by visualizing the offending lesions: Actively bleeding ulcers, nonbleeding visible vessels, and adherent clots require aggressive intervention, as rebleeding is associated with a fivefold to 16-fold increase in mortality. On the contrary, the rebleeding rate of ulcers with a clean base or red or blue spots is low, and endoscopic intervention is not warranted. Newer methods of assessment (combining Doppler evaluation with endoscopy) may provide a more accurate assessment of the bleeding risk.

Endoscopic intervention is beneficial in high-risk patients with UGIB, as it reduces the rate of rebleeding, need for surgical intervention, length of stay, and mortality. Injection of dilute (1:10,000) epinephrine around the bleeding points, laser and argon plasma coagulation, bipolar electrocoagulation and heater probe thermocoagulation, as well as Endoloops and clips, appear to be very effective at achieving hemostasis. Varices may be band ligated or injected with sclerosing agents. Endoscopic suturing and cryotherapy hold promise for even better bleeding control endoscopically.

11 How does ulcer appearance help predict rebleeding or mortality risk?

See Table 46-3.

Table 46-3 Prevalence and Outcomes of Peptic Ulcer Disease Based on Endoscopic Findings

image

12 What is SRMD? Who is at risk?

SRMD represents a continuum of conditions ranging from stress-related injury (superficial mucosal damage) to stress ulcers (focal deep mucosal injuries). Frequently, the terms stress ulcers, stress gastritis, or erosions are used interchangeably. The etiology of SRMD is multifactorial, with a common end pathway being the breakdown of mucosal defenses, typically because of ischemia (decreased prostaglandin and alkaline mucus production). SRMD is typically seen in the acid-producing areas of the stomach (corpus and fundus), unlike peptic ulcer disease (PUD), which is more common in the antrum and duodenal bulb and typically affects the critically ill. Risk factors for SRMD include coagulopathy and respiratory failure requiring mechanical ventilation. Mortality is high, ranging between 20% and 40%.

13 What are the indications for stress ulcer prophylaxis?

image Respiratory failure requiring mechanical ventilation

image Coagulopathy

image Traumatic brain injury

image Burns > 30%

image Patients already taking acid-suppression medications

image Diagnosis of PUD or UGIB in the last 6 weeks

14 What agents are typically used?

PPIs, H2-receptor antagonists, sucralfate (mucosal protective), and misoprostol (a prostaglandin E1 analog) are the agents most frequently used.

15 What are Curling ulcers?

A Curling ulcer is an acute peptic ulcer resulting as a complication from severe burns, when reduced plasma volume leads to sloughing off of the gastric mucosa. They appear to be more prevalent in pediatric patients with burns compared with adults.

16 What are Cushing ulcers?

Cushing ulcers are peptic ulcers (usually in the stomach, or less commonly in the duodenum or distal esophagus) that develop in patients with brain injury. They are thought to arise from gastric acid oversecretion, as a result of intracranial hypertension.

17 What is the role of endoscopy in the management of LGIB?

Urgent colonoscopy for acute LGIB is less established than urgent endoscopy is for acute UGIB. Bowel preparation is generally recommended, as it improves the efficacy of endoscopy to identify the offending lesion and decreases perforation risk. Hemostatic therapy can also be applied endoscopically, by means of epinephrine injection, heater probe and polar electrocoagulation, argon plasma coagulation, hemoclips, and band ligation. Attempts to visualize the entire colon should ideally be made, as more than one source of bleeding may be identified in up to 40% of cases.

18 What is the role of angiography in the management of GI tract bleeding?

Angiography can identify and localize bleeding accurately, but this requires a bleeding rate of at least 0.5 to 1 mL/min to be positive. This can be problematic because of the intermittent nature of bleeding. However, it has the advantage of not requiring bowel preparation. When the bleeding site is identified, it may be treated with intraarterial infusion of vasopressin or super-selective embolization.

19 What is the role of a tagged red blood cell scan in the workup of LGIB?

If bleeding is clinically significant, yet too slow or intermittent to be picked up by colonoscopy, a tagged red blood count scan can be performed. Typically, 20 mL of the patient’s own red blood cells are tagged with technetium and subsequently reinjected into the patient. Then scintigraphy identifies the bleeding in 15% to 70% of cases, as an area of increased uptake. This study is more sensitive than angiography in detecting bleeding, as it requires a rate of only 0.1 mL/min of bleeding. However, it cannot localize the precise area of hemorrhage and has no therapeutic role.

20 What is the role of surgery in the management of LGIB?

Surgery is typically employed for hemorrhage in the setting of massive or recurrent bleeding not amenable to endoscopic intervention. It is required in 20% of patients with diverticular bleeding and usually reserved for patients with high transfusion requirements. Efforts should be made to accurately identify and mark the bleeding site before surgery, so that selective, rather than subtotal, colectomy can be performed.

21 What is ischemic colitis (IC)? What are the risk factors?

IC constitutes a wide spectrum of clinical diseases of the large bowel, ranging from superficial mucosal ischemia to bowel gangrene and perforation, and the more severe forms carry a high mortality. Nonocclusive IC usually results from low cardiac output, whereas occlusive disease can be due to arterial embolism or thrombosis, or venous thrombosis. Risk factors for development of IC include cardiovascular surgery or disease, cardiac arrhythmias, hypovolemia, and medications with vasoconstrictive properties.

22 How does IC manifest, and how is the diagnosis made?

The clinical features of IC are protean and nonspecific: Diffuse or localized crampy abdominal pain and passage of bright red or maroon blood per rectum are very common. As superficial ischemic changes progress to transmural ischemia, bowel gangrene, and perforation, patients may present with peritonitis. Plain abdominal radiographs may demonstrate thumbprinting, indicating submucosal edema. Computed tomography may reveal thickened colonic wall or pneumatosis (air in the wall of the colon). No laboratory tests exist to aid in early diagnosis of IC, but in advanced disease lactic acidosis and elevated lactate dehydrogenase, creatine phosphokinase, and amylase levels may be present. Definitive diagnosis is made by colonoscopy, which can also provide information about the degree and extent of involvement, but it is contraindicated in the presence of peritoneal signs.

23 What is the treatment of IC?

For the least severe forms of IC, treatment is largely supportive and revolves around resuscitation, cardiac function optimization, and prophylactic broad-spectrum antibiotics. In patients with IC of thrombotic etiology, systemic anticoagulation or catheter-directed thrombolysis may be considered. In patients with severe physiologic derangements and viable bowel, surgical revascularization may be attempted. If bowel necrosis or perforation has occurred, surgical intervention is warranted for resection of the affected part of the colon.

Key Points Gi Bleedingimage

1. Always insert a nasogastric tube to rule out UGIB, even in cases that present with copious fresh blood from the rectum.

2. Early endoscopy is key in both upper and lower GI tract bleeding for diagnosing, risk-stratifying, localizing, and treating bleeding.

3. Do not forget about stress ulcer prophylaxis in critically ill patients with the appropriate indications. Remember to discontinue it when the indications cease to exist.

4. A systematic approach is key in managing all patients with GI bleeding.

Bibliography

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2 Cappell M., Friedel D. Initial management of acute upper gastrointestinal bleeding: from initial evaluation up to gastrointestinal endoscopy. Med Clin North Am. 2008;92:491–509.

3 Ferguson C.B., Mitchell R.M. Nonvariceal upper gastrointestinal bleeding: standard and new treatment. Gastroenterol Clin North Am. 2005;34:607–621.

4 Green B.T., Rockey D.C. Lower gastrointestinal bleeding-management. Gastroenterol Clin North Am. 2005;34:665–678.

5 Laine L., Peterson W.L. Bleeding peptic ulcer. N Engl J Med. 1994;331:717–727.

6 Reissfelder C., Sweiti H., Antolovic D., et al. Ischemic colitis: Who will survive? Surgery. 2011;149:585–592.

7 Rockey D.C. Gastrointestinal bleeding. Gastroenterol Clin North Am. 2005;34:581–588.

8 Spirt M.J. Stress-related mucosal disease: risk factors and prophylactic therapy. Clin Ther. 2004;26:197–213.

9 Yüksel I., Ataseven H., Köklü S., et al. Intermittent versus continuous pantoprazole infusion in peptic ulcer bleeding: a prospective randomized study. Digestion. 2008;78:39–43.

10 Zaman A., Chalasani N. Bleeding caused by portal hypertension. Gastroenterol Clin North Am. 2005;34:623–642.

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