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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_885_Библиотеки_им_академика_М_И_Перельмана.pdf
308 A. K. Melvin, J. Sandlin and W. L. Biffl
Practical Algorithm(s)/Diagrams
Fig. 1. Tube feed intolerance.
Review of Current Literature with References
• Rohm KD, Boldt J, Piper SN. Motility disorders in the ICU: recent thera-
peutic options and clinical practice. Curr Opin Clin Nutr Metab Care 2009;
12: 161–167.
{ This represents the therapeutic options for motility disorders.
• Nguyen NQ, Chapman MJ, Fraser RJ et al. Erythromycin is more effective
than metoclopramide in the treatment of feed intolerance in critical illness.
Crit Care Med 2007; 35: 483–489.
{ Prospective randomized trial demonstrating an advantage for erythromycin.
Tube Feed Intolerance 309
• Kim H, Stotts N, Froelicher ES et al. Why patients in critical care do not
receive adequate enteral nutrition? A review of the literature. J. Crit Care
2012; 27: 702–713.
{ A pertinent review of existing literature in regards to the nutritional status
of critically ill patients.
• Reignier J, Mercier E, Le Gouge A et al. Effect of not monitoring residual
gastric volume on risk of ventilator-associated pneumonia in adults receiving
mechanical ventilation and early enteral feeding. A randomized controlled
trial. JAMA 2013; 309: 249–256.
{ Evaluation of the utility of measuring gastric residual volumes in patients
on mechanical ventilation and those receiving early enteral feeding.
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Chapter 8-(iii)
Gastrointestinal Ischemia
Jennifer A. Salotto, MD*
* Fellow, Trauma and Acute Care Surgery, Denver Health Medical Center
Take Home Points
• Acute mesenteric ischemia (AMI) is a life-threatening condition which
occurs when perfusion of the viscera fails to meet metabolic demand.
• This disease process exists on a spectrum, ranging from ischemia, necrosis,
and intestinal perforation to sepsis and death.
• Successful outcomes depend on a high index of clinical suspicion, early diag-
nosis and prompt treatment.
• Overall mortality remains high despite broadening options for therapy.
• The four underlying causes of AMI include arterial embolism, arterial
thrombosis, mesenteric venous thrombosis, and non-occlusive mesenteric
ischemia. It is important to distinguish between these causes because the
treatments vary.
• Arterial embolism, specifically to the superior mesenteric artery (SMA), is
the most common cause of AMI and may present with the sudden onset of
Contact information: Denver Health Medical Center, University of Colorado Health
Sciences Center, 777 Bannock Street, MC 0206, Denver, CO 80204; Tel.: 857-928-4766,
email: jennifer.salotto@ucdenver.edu
311
312 J. A. Salotto
abdominal pain or classically, pain out of proportion to exam. Often the
patient can give a history of prior embolic events or arrhythmia. It is treated
with surgical embolectomy.
• SMA thrombosis is seen in patients with risk factors for atherosclerosis.
Treatment is an arterial bypass around the obstruction.
• In those centers with interventional capabilities, endovascular therapy for
AMI is no longer reserved for those at high risk. Patients who do not demonstrate peritonitis or clinical features of bowel ischemia may be candidates for
definitive endovascular therapies including angioplasty, stenting, or thrombolysis. Laparotomy or laparoscopy may be used to assess bowel viability
after an endovascular intervention.
• Non-occlusive mesenteric ischemia is inadequate visceral perfusion in the
absence of an obstructing lesion. It is most commonly seen in ICU
patients with severely depressed cardiac output or those receiving highdose vasoconstrictors such as epinephrine or vasopressin. The mainstay of
therapy is catheter-directed intra-arterial infusion of vasodilators such as
papaverine.
• Mesenteric venous thrombosis (MVT) accounts for a small percentage of all
mesenteric ischemic events and is usually limited to the SMV. MVT is noted
in those with a hypercoagulable state, post-trauma, or post-splenectomy. It
can present in an acute or a chronic form, depending on the etiology.
Treatment is systemic anticoagulation.
• Bowel ischemia may occur after an open or endovascular abdominal aortic
aneurysm repair due to disruption of the mesenteric arterial supply or
from dislodgement of thrombus to the mesenteric vessels. Patients will
present with acidosis, abdominal pain and bloody diarrhea in the acute
post-operative period after an abdominal aneurysm repair. Diagnosis is
made with a bedside flexible sigmoidoscopy and the treatment is bowel
resection.
• Methods for assessing intestinal viability include visual inspection of
bowel color and bleeding from divided tissue edges, assessing Doppler
signals within the mesentery, and a fluorescein uptake evaluation. These
tests are not completely reliable: bowel ischemia may progress and the
serosa may appear healthy despite an ischemic mucosa. The decision to
return to the operating room 24–48 hours after first operation for a second
look exploration is left to the discretion of the surgeon. This second look
allows time for demarcation of bowel ischemia and an opportunity to
reassess bowel viability.
Gastrointestinal Ischemia 313
Background
• The arterial and venous anatomy of the GI tract
{ The arterial supply to the gastrointestinal tract stems from the abdominal
aorta’s three major branches, the celiac trunk, the superior mesenteric
artery, and the inferior mesenteric artery.
{ The celiac artery provides blood flow to the foregut, including the stomach
and the duodenum just proximal to the ligament of Treitz.
{ The superior mesenteric artery provides blood flow to the midgut, includ-
ing the jejunum, the ileum, the appendix, the ascending colon, and the
transverse colon. Major named branches include the ileocolic artery, the
appendicular artery, the right colic artery and the middle colic artery.
{ The inferior mesenteric artery supplies blood flow to the hindgut, which
includes the descending colon, the sigmoid colon, and the upper rectum.
Major branches include the left colic artery, the sigmoidal arteries and the
superior rectal artery.
{ The internal iliac artery gives rise to the middle and inferior rectal arteries.
{ There exists a fair amount of redundancy and collatoralization among
the artieral branches of the GI tract. The SMA and the IMA usually
anastomose via the marginal artery of the colon in the area of the
splenic flexure, commonly known as the artery of Drummond. The
marginal artery is absent in approximately 5% of the population. There
are macrovascular collaterals between the left and middle colic artery
within the colonic mesentery and microvascular collaterals within the
bowel wall.
{ The venae rectae form a venous arcade that drains the small bowel and the
proximal colon through the ileocolic, middle colic and the right colic
veins into the superior mesenteric vein. Distally, the left colic, sigmoid,
and rectosigmoid veins drain into the inferior mesenteric vein. The superior
mesenteric vein, inferior mesenteric vein, and splenic vein all converge to
become the portal vein.
• Gastrointestinal physiology
{ The layers of the bowel wall include the serosa, a longitudinal muscle
layer, a circular muscle layer, the submucosa, and the mucosa.
{ The blood vessels of the gastrointestinal system are part of a vascular
system known as the splanchnic circulation, which supplies the gut, the
liver, the pancreas, and the spleen.
314 J. A. Salotto
{ The splanchnic circulation receives approximately 25% of the resting
cardiac output and 35% of the postprandial cardiac output.
{ Normal oxygen supply to the gut can be maintained at only 20% of
maximal blood flow.
{ Decreased oxygen concentration in the gut wall can increase local blood
flow by 50–100%.
{ Mesenteric blood flow is auto-regulated by the autonomic nervous system
as well as by endogenous hormones in the bloodstream such as epinephrine, norepinephrine, vasopressin, and acetylcholine.
{ The mucosa of the intestinal tract itself releases vasodilatory peptide hor-
mones including cholecystokinin, vasoactive intestinal peptide, gastrin,
and secretin. Gastrointestinal glands also release kallidin and bradykinin
which are also powerful vasodilators.
• Pathophysiology of acute mesenteric ischemia
{ The musocal and submucosal layers are most vulnerable to ischemia.
Mucosal edema and hemorrhage may progress to sloughing and ulceration of the mucosa.
{ As ischemia progresses, these ulcers go on to full thickness necrosis and
eventually to perforation.
Main Body
• Etiology and presentation of acute mesenteric ischemia
{ Mesenteric ischemia occurs when perfusion of the gastrointestinal tract
fails to meet metabolic needs.
{ Mesenteric arteries are subject to atherosclerosis in the same manner as
both systemic and coronarey arteries. The same risk factors apply and
should be solicited in the evaluation of the patient with suspected AMI.
{ There are four etiologies for acute mesenteric ischemia: embolus, arterial
thrombosis, non-occlusive ischemia, and venous thrombosis. An additional specific etiology of AMI occurs in patients who have had an
abdominal aortic aneurysm repair in which the inferior mesenteric artery
has been sacrificed, resulting in ischemic colitis. It is important to distinguish between each of these entities as the treatments vary.
{ In an acute embolic occlusion, the SMA is the most common destination
for mesenteric emboli due to the acute angle from which it comes off the
aorta. These emboli tend to lodge a few centimeters distal to the origin
of the SMA, usually after the takeoff of both the first jejunal branches
Gastrointestinal Ischemia 315
and the middle colic artery. Consequently, with an embolic event, both
the proximal jejunum and transverse colon are spared. This is in contradistinction to the pattern of injury observed in the case of an acute
thrombosis (discussed below).
{ Superior mesenteric artery thrombosis occurs in the most proximal
SMA, (usually within 2.5 centimeters of the ostia of the SMA off of
the aorta) due to turbulent flow at the bifurcation (as seen in both
carotid and femoral arterial disease). Given the more proximal nature
of these occlusions, larger lengths of bowel are generally affected,
including the proximal jejunum and transverse colon. For this reason,
thrombotic occlusions, as compared to emboli, are associated with a
higher mortality.
{ Mesenteric venous thrombosis is generally limited to the superior mesen-
teric vein, and can be classified as either primary or secondary. Primary
MVT is idiopathic, while secondary can be attributed to a prothrombotic
state, an intra-abdominal inflammatory state such as pancreatitis, postoperative states (especially post-splenectomy), and in conditions of venous
stasis including cirrhosis and portal hypertension. Oral contraceptives are
also responsible for episodes of MVT in younger women.
{ Clinical manifestations of MVT will depend on the size and location of
the thrombus and the extent of the bowel involved. Acute venous thrombosis carries a risk of bowel necrosis, whereas chronic thrombosis allows
time for collaterals to develop and therefore has a more subtle onset and
a benign course.
{ Non-occlusive mesenteric ischemia is malperfusion of the gastrointestinal
tract in the absence of an obstruction. This form of AMI is most often
noted in elderly patients with cardiogenic shock requiring agents such as
vasopressin which constrict splanchnic blood flow.
{ Both open and endovascular repair of abdominal aortic aneurysm can be
complicated by AMI. During an aortic abdominal aneurysm repair, the
inferior mesenteric artery (IMA) may be sacrificed. If little or no collateralization to the colon exists preoperatively, the loss of the IMA blood
supply may result in colonic infarction. GI ischemia may also result from
disruption and embolization of thrombus within the aneurysm. Finally,
low-flow states associated with aortic clamping and/or hypotension
secondary to aortic rupture may predispose the colon to ischemia. Patients
who have undergone emergent repair of a ruptured AAA have a much
greater likelihood of developing colonic ischemia when compared with
those undergoing elective repair.
316 J. A. Salotto
• History and physical exam
{ Signs and symptoms of AMI exist on a spectrum dependent upon the
severity of the ischemia: signs and symptoms of early ischemia are
usually relatively non-specific, whereas the presentation of a patient with
bowel necrosis and perforation is rarely subtle, including tachycardia,
hypotension, peritonitis, leukocytosis, and the accumulation of the
byproducts of anaerobic metabolism.
{ It is necessary to have a high clinical suspicion for AMI when evaluating
an ICU patient with abdominal pain. The history, physical, and labs may
be non-specific. Exam may be confounded by sedation, paralytics, or
delirium.
{ The hallmark of AMI is pain out of proportion to physical exam.
{ Both weight loss and food fear suggest chronic stenosis of mesenteric
vessels due to atherosclerosis.
{ Additional clinical findings include diffuse abdominal pain, nausea, vom-
iting, anorexia, diarrhea, melena or hematochezia.
{ Pain may become localized and patient may develop tenderness, rebound
and guarding with bowel ischemia or perforation.
{ Onset of abdominal pain may be sudden in onset (embolic/thrombotic) or
insidious (SMV thrombosis).
{ Certain aspects of the history may aid in differentiation between the
different types of AMI.
Embolic: atrial fibrillation, prior embolic events, recent peripheral or
coronary catheterization, valvular heart disease, myocardial ischemia
or infarction.
Thrombotic: older age, hypertension, smoking, diabetes, CAD/PVD,
food fear, weight loss.
SMV Thrombosis: trauma, hypercoagulable state, post-splenectomy,
pancreatitis, family history of deep vein thrombosis or pulmonary
embolus.
NOMI: cardiogenic shock, hypovolemia, heart failure, vasocon-
strictors, cocaine, digoxin, dialysis.
• Early interventions
{ Initiate intravenous fluid resuscitation with close attention to endpoints of
resuscitation [see Chapter 5-(iv)]. Maintain NPO status.
{ Labs should include a complete blood count, basic metabolic panel,
amylase and lipase, lactate and an arterial blood gas. Labs may indicate
Gastrointestinal Ischemia 317
an anion-gap metabolic acidosis. Correct electrolyte abnormalities and
acid-base abnormalities.
Laboratory derrangements occur relatively late in the course of
ischemia.
Do not wait for lab abnormalities before pursuing further diagnostic
or interventional modalities.
{ Obtain an EKG to evaluate cardiac rhythm.
{ Obtain blood cultures and initiate broad-spectrum antibiotics with
coverage against intestinal pathogens (typically gram negative rods and
anaerobs).
{ If suspicion is high and bleeding risk is low, initiate systemic anticoagula-
tion empirically.
{ Obtain an upright CXR to assess for intra-peritoneal air (suggesting
intestinal perforation).
{ Abdominal films may show semi-opaque indentations of the bowel lumen
(“thumb-printing”) which is indicative of mucosal edema.
{ For patients requiring vasopressors in the face of suspected mesenteric
ischemia, use dopamine or epinephrine.
• Diagnosis
{ Patients with shock and/or diffuse peritonitis (i.e. “acute abdomen”) do
not require any additional diagnostic maneurvers and should undergo
exploratory laparotomy promptly.
{ In the remainder of cases, diagnositic imaging studies include CTA,
angio graphy, duplex ultrasonography, endoscopy, and laparoscopy.
{ A mesenteric duplex is rarely helpful in the evaluation of acute mesenteric
ischemia due to the presence of bowel gas.
{ Although contrast angiography has traditionally been considered the gold
standard for diagnosis of mesenteric ischemia, it is costly, invasive, potentially nephrotoxic, and may not be readily available. In the absence of a
hybrid operating room, it may also delay operative intervention.
{ Thin-slice computed tomography angiography (CT-A) has replaced tra-
ditional angiography as a fast and highly sensitive means of diagnosing
arterial and venous occlusions of the mesenteric vasculature. It easily
rules out other sources of abdominal pain.
{ CT-A may be considered in cases where the patient is hemodynamically
stable and does not show any evidence of peritonitis, warranting a prompt
surgical intervention.