Page 1471 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

1010 PART 9: Gastrointestinal Disorders

expected to have substantial amounts of blood and clots in the stomach. The angiographic diagnosis of acute arterial hemorrhage is based on
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However, prokinetics should not be used routinely, as they were not visualization of extravasated contrast material in the gastrointestinal
shown to affect important outcomes such as units of blood transfused, lumen. Therefore, it only identifies the bleeding site if active bleeding is
length of hospital stay, or the need for surgery. 21 occurring when the study is performed. In addition, the rate of bleed-
In the setting of nonvariceal UGI bleeding, acid suppression with ing must be brisk, in the range of 0.5 to 1 mL/min. In the case of brisk
proton-pump inhibitors is recommended prior to endoscopy, as this may UGI bleeding, angiography may demonstrate a bleeding site in 75% of
downstage the endoscopic lesion and decrease the need for endoscopic patients, with most bleeding episodes originating from a branch of the
intervention. An intravenous bolus followed by continuous-infusion PPI left gastric artery. In the setting of LGI bleeding, the average diagnostic
therapy should be used to decrease rebleeding and mortality in patients yield is decreased to about 60%, with diverticular disease and vascular
with high-risk stigmata who have undergone successful endoscopic ectasia being the most common findings.
therapy. 16,22 In the setting of variceal bleeding, pharmacologic therapy Radionuclide studies occasionally aid in the detection of the bleeding
with a splanchnic vasoconstrictor such as octreotide and empiric antibi- site. The current radionuclide scan of choice is the 99m Tc-pertechnetate-
otic therapy should be initiated. labeled red blood cell scan. The radionuclide scan offers the ability to
detect rates of bleeding of less than 0.5 mL/min, and the 48-hour stability
Hematologic: In order to ensure adequate oxygen-carrying capacity of the tagged red blood cells allows repeated nuclear imaging for 1 to 2 days
in the circulation and to prevent end-organ ischemia, the hematocrit following administration of the radionuclide in the setting of intermittent
should be maintained above 30%. It should be noted that the initial bleeding. However, a positive radionuclide study localizes the bleeding only
hematocrit after an acute GI bleed can be misleading because acute to an area of the abdomen and cannot define the mucosal location of the
hemorrhage produces loss of whole blood, and the hematocrit does not bleeding site precisely. Therefore, a positive result should prompt a repeat
change initially because the initial loss of plasma and erythrocytes is endoscopy or angiography to localize the bleeding site precisely.
equivalent. Within 24 to 72 hours of the initial bleed, plasma is redis-
tributed from the extravascular to the intravascular space, thus resulting ■ REBLEEDING
in a dilution of the red cell mass and a fall in the measured hematocrit. In most instances, the presentation of rebleeding is similar to that of the
Intravenous hydration with crystalloids compounds this dilutional initial episode, and the source is identical to the site of the initial bleed.
anemia so that red cells should be replaced promptly. In most instances, After hemostasis of the initial bleed following spontaneous cessation or
there is sufficient time to allow typing and cross-matching of red cells; therapeutic intervention, the patient should be monitored closely for
however, in the setting of massive exsanguination, the transfusion of rebleeding, especially in the presence of clinical and endoscopic indica-
non–cross-matched type-specific blood may be necessary. In the pres- tors associated with an increased risk of rebleeding (see Table 105-1).
ence of thrombocytopenia, platelets must be transfused to maintain the Most patients who have undergone upper endoscopic hemostasis for
count above 60,000/µL. Any existing coagulopathy should be corrected high-risk stigmata should be hospitalized for at least 72 hours thereafter.
with fresh frozen plasma; however, this should not delay endoscopy Apart from the obvious signs of gastrointestinal blood loss characterized
in most cases. Studies have demonstrated the ability of recombinant by melena, hematemesis, or hematochezia, more subtle signs of rebleed-
activated factor VIIa (rFVIIa) to rapidly correct severe coagulopathy ing may include tachycardia and hypotension owing to a decreasing
in hepatic failure 23,24 ; however, two large studies have not shown a ben- intravascular volume. Therefore, continuous hemodynamic monitoring
efit for factor VIIa for upper gastrointestinal bleeding in patients with should be performed following initial hemostasis, and invasive monitor-
cirrhosis. 25,26 During the process of aggressive intravascular volume ing with a central venous catheter or an arterial line may be considered
resuscitation, fluids and blood products should be warmed to prevent for the patient at high risk for rebleeding. A falling serum hemoglobin
the development of a cold coagulopathy, and the core body temperature concentration on serial measurements may suggest a recurrent bleed.
should be maintained above 35°C.
The management of rebleeding should include immediate repeat endo-
Pulmonary: In the presence of active hematemesis, a nasogastric tube scopic intervention targeted at the initial lesion, followed by radiologic
should be placed to decrease the risk of aspiration. Endotracheal intuba- or surgical intervention, if necessary. Specific pharmacologic and
tion should be performed for airway protection and to decrease the risk endoscopic interventions for long-term secondary prophylaxis against
of aspiration in the following situations: (1) in the presence of active rebleeding will be discussed in the sections that follow.
hematemesis and decreased mental status, (2) prior to an emergent
EGD for active hematemesis, and (3) prior to insertion of an esophageal UPPER GASTROINTESTINAL HEMORRHAGE
tamponade tube. In the setting of shock, intubation and full mechanical
ventilatory support are indicated to decrease the oxygen consumption of With regard to prognosis and treatment, UGI hemorrhage can be
the respiratory apparatus. During the performance of an EGD, signifi- divided into (1) variceal hemorrhage and (2) nonvariceal hemorrhage.
cant hypoxemia may occur, especially in elderly patients and in those
with moderate to severe obstructive pulmonary disease (defined as an VARICEAL HEMORRHAGE
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FEV /FVC ratio of less than 0.6). Probable causes include hypoventila- Variceal hemorrhage presents as a symptom of decompensated cirrhosis
1
tion due to sedative agents, the partial airway obstruction produced by in as many as 50% of patients and accounts for about one-third of all
the endoscope, and aspiration of gastric contents, resulting in broncho- deaths related to cirrhosis. Mortality is related to hepatic disease severity,
spasm and ventilation-perfusion mismatch.
as defined by the Child-Pugh classification (Table 105-3), with an overall
Consultation: Radiology and surgery should be consulted early in the mortality estimated at 50%. There are two distinct phases in the course of
course of management. In the setting of nondiagnostic upper or lower variceal hemorrhage. In the first phase, defined by the initial episode of
endoscopy, radiologic modalities offer diagnostic and therapeutic active hemorrhage, only 50% of patients stop bleeding spontaneously (in
options to achieve hemostasis. Emergent surgical intervention is indi- contrast to nonvariceal hemorrhage, in which 90% cease spontaneously).
cated in the exsanguinating patient who may not be stable enough for The initial bleed is followed by a second phase of an approximately
endoscopic or radiologic evaluation. 6-week duration, defined by a high risk of recurrent hemorrhage, with
the greatest risk of rebleeding being within the first 48 to 72 hours.
When endoscopic evaluation is unable to identify the cause of bleed-
and radionuclide scans. As outlined later, angiography with embo- ■ MANAGEMENT
ing, the two diagnostic radiologic modalities available are angiography
lotherapy or selective infusion of vasoconstrictors offers therapeutic The management of variceal bleeding is outlined in Figure 105-1. In
options as well. addition to multiorgan ischemic injury from hypoperfusion, variceal

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