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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5524_Библиотеки_им_академика_М_И_Перельмана.pdf
318 J. A. Salotto
{ In cases of acute mesenteric ischemia, a CT scan may demonstrate arte-
rial or venous occlusion, thickened bowel loops, or free fluid.
Pneumatosis intestinale, portal venous air, and free air are late findings.
{ A CT scan is highly sensitive for cases of mesenteric ischemia secondary
to embolus, thrombosis of the arterial inflow or thrombosis of the venous
outflow.
{ In most cases, angiography is limited to the minority of cases in which:
findings from less invasive means of imaging are equivocal.
Ö This line of therapy has been selected over operation (e.g., poor
operative risk). Non-occlusive mesenteric ischemia is highly
likely. In this case, a formal angiogram followed by catheter-based
intervention is the most efficient means of diagnosis
and treatment. The hallmark on angiogram of NOMI is diffuse
mesenteric vasospasm with the absence of a complete occlusion.
{ In those patients with crampy abdominal pain, unexplained acidosis, or
bloody stool after an abdominal aortic aneurysm repair, the diagnostic test
of choice is bedside flexible sigmoidoscopy to evaluate the mucosa for
signs of ischemia.
Findings on endoscopy may include: mild colitis with hemorrhagic
mucosa, a moderate colitis with patchy ischemia limited to the
mucosa, or a continuous area of full thickness ischemia.
{ Diagnostic laparoscopy may be considered in the relatively rare instance
in which the diagnosis of AMI is still in question despite imaging with
either CTA or angiography. It is important to remember that the bowel
serosal layer (the only layer of the bowel that is visible via laparoscopy)
is the least susceptible to ischemia. Therefore, normal appearing bowel
serosa does not rule out AMI.
• Treatment
{ Thrombotic vs. embolic
Heparinization.
In the OR: resect dead bowel, restore blood flow to bowel.
Ö bypass for thrombosis.
Ö embolectomy with Fogarty catheters for embolic event.
May anastomose or leave blind ends.
Gastrointestinal Ischemia 319
A second look procedure should generally be performed in 24–48
hours, although the decision is ultimately left to the discretion of the
operating surgeon.
In certain cases where interventional resources and capabilities are
available, therapies including endovascular thrombolysis, mechanical
thrombectomy, angioplasty and stenting may be considered.
{ Mesenteric venous occlusion
Heparinization.
Ö bolus with 5000 U of heparin then begin a continuous infusion
with a goal activated partial-thromboplastin time more than twice
the normal level.
IVF for fluid shifts.
NGT and bowel rest.
Surgical exploration if clinically warranted.
In cases where the clinical picture continues to decline despite full
anticoagulation, there is a role for endovascular clot lysis and mechanical aspiration if interventional radiology is available.
{ Non-occlusive mesenteric ischemia
The treatment mainstay is intra-arterial instillation of papaverine
performed in the interventional radiology suite.
Ö bolus of 60 mg directly into the SMA, then infuse 30–60 mg/hr
until resolution of symptoms.
After vasodilatory therapy, it is necessary to perform a follow-up
angiogram to document resolution.
Adjuncts to intra-arterial therapies include maximizing oxygen delivery
to tissues, improving cardiac output, and minimizing vasoconstrictors.
• Colonic ischemia after repair of an abdominal aortic aneurysm
{ Once this diagnosis of colonic ischemia after an abdominal aneurysm
repair is considered, a bedside flexible sigmoidoscopy is the gold standard
for diagnosis. Findings of mucosal edema, hemorrhage, ulceration, or
necrosis would support the diagnosis.
{ For those patients with mild or moderate findings (hemorrhagic mucosa,
patchy mucosal ischemia), it is appropriate to hydrate and clinically
observe in the absence of sepsis or peritonitis, following up with a repeat
sigmoidoscopy at 12-hour intervals. Caution should be taken with these
320 J. A. Salotto
patients, as delay in resection of a truly ischemic segment may result in
full thickness necrosis and perforation. Any attempt to manage these
patients conservatively should be aborted if the clinical picture worsens.
{ For those patients with severe findings on sigmoidoscopy, the treatment is
returning to the operating room for a colectomy, resecting the necrotic
portions of the bowel and creating a temporary end colostomy.
• Outcomes
{ Morbidity and mortality of acute mesenteric ischemia remain high despite
advancing surgical and endovascular techniques.
{ After AMI, survival often depends on the age of a patient, comorbidities,
timing of intervention, and the degree and extent of bowel ischemia.
{ Postoperative complications include sepsis, ongoing ischemia requiring
repeat resections, wound infection, and short-gut syndrome in those
requiring extensive small bowel resections.
{ Non-occlusive mesenteric ischemia carries a mortality near 50% due to
underlying cardiac disease.
{ The mortality rate of mesenteric venous thrombosis was quoted by Kumar
et al. to range from 20–50%. Recurrences are most common 30 days after
presentation. These patients require at least six months to a year of
systemic anticoagulation.
{ In a large observational study looking at over 87,000 patients with abdom-
inal aortic aneurysm (AAA) repairs, the mortality of colonic ischemia
post-AAA repair was noted to be around 37%. Those patients undergoing
ruptured, open, or endovascular AAA repair without colonic ischemia
were found to have an overall mortality of 6.7%.
Gastrointestinal Ischemia 321
Practical Algorithm(s) / Diagrams
Diagnostic Algorithm: Suspicion for Acute Mesenteric
Ischemia
History and
Physical: suspect
AMI
IVF, NGT, FC, cultures & antibiotics, labs,
consider heparin
Peritonitis
No
Assess
Risk
Ye s
Operative
Exploration
Consider IR
Factors
Acute
Thrombotic
Event: CAD,
PVD, smoker,
DM,
hypertension,
elderly
Positive for
Embolus, SMA
thrombosis
Acute Embolic Event:
NOMI: cardiogenic
shock,
hypovolemia,
dialysis, digoxin,
cocaine,
vasopressin
MVT: hypercoagulable
states, intraabdominal
inflammatory state,
post splenectomy,
trauma
Afib, Prior Embolus,
recent cath or MI
CT Scan
Angiography
Negative, high clinical
suspicion for AMI
Positive MVT
Heparinization
Fig. 1. Diagnostic algorithm for suspected acute mesenteric ischemia.
322 J. A. Salotto
Treatment Algorithm, Thrombotic and Embolic AMI
Evaluated for AMI: pain out of
proportion to exam, acidosis,
high clinical suspicion given
risk factors
Diagnostic
confirmation
Acute
Thrombotic
Event
IR
capability?
No
Angiography,
angioplasty
and/or
stenting
Clinical Improvement,
Low Suspicion Dead
No
Bowel?
Exploratory
laparotomy
Arterial Bypass
Observe vs. diagnostic
laparoscopy
Resect dead
bowel
Consider Second Look
procedure to re-evaluate bowel
Peritonitis, free air, ongoing sepsis
Diagnostic
confirmation
Acute
Embolic
Event
NoYe s
Catheterdirected
intra-arterial
lysis
No
Ye s
Exploratory
Laparotomy
Exploratory
laparotomy
Embolectomy
Resect dead
bowel
Fig. 2. Treatment algorithm, thrombotic and embolic AMI.
Gastrointestinal Ischemia 323
Treatment Algorithm, Non-Occlusive Mesenteric Ischemia and Superior
Mesenteric Venous Thrombosis
CT-Confirmed MVT Angiography-Confirmed NOMI
Heparinization
Hypercoagulable work-up
No Improvement,
Clinical Deterioration
Consider CatheterDirected
Thrombolysis
No Improvement,
Clinical Deterioration
Papaverine Infusion
Clinical Improvement
Observe clinically
Clinical Improvement
Laparoscopy vs. Laparotomy,
Resect Dead Bowel
IVF Resuscitation
Improve Cardiac Output
Repeat Angiography
No Improvement
Clinical Deterioration
No Improvement,
Clinical Deterioration
Fig. 3. Treatment algorithm, NOMI and SMV thrombosis.
Review of Current Literature with References
• In 2002, a retrospective study out of the Mayo Clinic described their ten-year
experience with the clinical presentation of 58 patients with acute mesenteric
ischemia. 95% presented with abdominal pain, 44% with nausea, 35% with
diarrhea and vomiting, 16% had blood per rectum. The mean white blood cell
count was elevated at 20.3 x 10
Base deficit was elevated in 52% and lactate was elevated in 91%, with a
mean value of 4.7 mmol/L. In this patient population they noted a 32% 30-day
mortality rate (Park WM, Gloviczki P, Cherry Jr KJ et al. Contemporary
management of acute mesenteric ischemia: factors associated with survival.
J Vasc Surg 2002; 35: 445–452).
• An observational study by Perry et al. looked at the records of over 89,000
patients undergoing abdominal aortic aneurysm repair from the 2003–2004,
utilizing the Nationwide Inpatient Sample database. They found the overall
incidence of colonic ischemia to be 2.2%. The incidence after ruptured AAA
repair was 8.9%, after open repair incidence was 1.9%, and after endovascular repair incidence was 0.5%. They reported mortality rates increased from
9
/mL and was abnormal in 98% of the patients.
324 J. A. Salotto
two- to four-fold, quoting mortality from colonic ischemia post-AAA around
37% (Perry RJ, Martin MJ, Eckert MJ, Sohn Vr, Steele SR. Colonic ischemia
complicating open versus endovascular abdominal aortic aneurysm repair.
J Vasc Surg 2008; 48: 272–277).
• A systematic review and meta-analysis published in 2010 evaluated the utility
of multi-detector computerized tomography in the evaluation of acute mesenteric ischemia. They included three prospective and three retrospective
studies for a total of 619 cases. They found an overall pooled sensitivity of
93.3% and a pooled specificity of 95.9% and concluded that this modality can
be safely used as a first-line agent in evaluating AMI (Menke J. Diagnostic
accuracy of multidetector CT in acute mesenteric ischemia: systematic
review and meta-analysis. Radiology 2010; 256: 93–101).
• A single-institution retrospective cohort review from the Cleveland Clinic
described 56 of 70 patients with arterial embolic or thrombotic etiologies of
AMI who underwent initial endovascular therapies. Successful endovascular
treatment was achieved in 87%, defined as return of bowel perfusion without
laparotomy, or with laparotomy but without open embolectomy or bypass.
They demonstrated a statistically significant difference between in-hospital
mortality with endovascular treatment (36%) as compared with traditional
open therapy (50%). Factors associated with increased risk of death included
advanced age, history of coronary artery disease, peripheral arterial disease,
and an initial lactate >2.2 mmol/L (Arthurs ZM, Titus J, Bannazadeh M,
Eagleton MJ, Srivastava S, Sarac TP, Clair DG. A comparison of endovascular revascularization with traditional therapy for the treatment of acute
mesenteric ischemia. J Vasc Surg 2011; 53: 698–705).
Chapter 8-(iv)
Hepatopancreaticobiliary
Carlton C. Barnett, MD* Brandon C. Chapman, MD†
and Edward L. Jones, MD
* Professor of Surgery, University of Colorado School of Medicine
†
Surgical Resident, University of Colorado School of Medicine
Take Home Points
• Acute liver failure can be a primary indication for ICU care as well as a
significant co-morbidity and its management is driven by the etiology.
Unfortunately, acute liver failure is resolved in only 40% of cases, leaving a
significant number of patient in need of liver transplantation (Chapter 26).
• Chronic liver failure ( cirrhosis) is a common co-morbidity that complicates
ICU patient care.
• Cirrhosis is divided into two stages: compensated and decompensated. The
median survival of patients with decompensated cirrhosis and a Child-Pugh
score ≥ 12 or a model of end stage liver disease (MELD) score ≥ 21 is ≤ 6
months compared to a median survival of patients with compensated cirrhosis
of >12 years. Decompensated cirrhosis often requires liver transplant for
survival.
†
Contact information: Denver Health Medical Center, University of Colorado Health
Sciences Center, 777 Bannock Street, MC 0206, Denver, CO 80204; Tel.: 303-436-5402,
email: Carlton.barnett@dhha.org; edward.jones@ucdenver.edu; Brandon.Chapman@
ucdenver.edu
325
326 C. C. Barnett, B. C. Chapman and E. L. Jones
• The differential diagnosis of patients with acute jaundice associated with
critical illness can be broadly divided into three groups: extrahepatic bile
duct obstruction, increased bilirubin production (or re-absorption), and
impaired excretion due to hepatocellular dysfunction, hepatitis, or intrahepatic cholestasis.
• Biliary disease can be difficult to diagnose and often takes the form of
acalculous cholecystitis [Chapter 10-(vi)].
• The management of biliary obstruction can be treated via endoscopic or
percutaneous approaches and surgery is rarely indicated except in cases of
life-threatening hemorrhage from biliary-arterial fistula.
• Acute pancreatitis is an inflammatory condition of the pancreas that ranges
from mild edema to life-threatening necrosis. The mortality rate for severe
acute pancreatitis has been reported as high as 15–30%. Early aggressive
resuscitation is required to minimize morbidity and mortality.
• Contrast enhanced computed tomography (CT) should not be routinely
performed in patients with acute pancreatitis and is indicated only in patients
who show clinical signs of sepsis, fail to improve on supportive therapy, or
regress after an initial period of improvement.
• Antibiotic prophylaxis has not been shown to reduce mortality, protect against
infected necrosis, or reduce the need for surgical intervention and is not
routinely indicated in patients with severe acute pancreatitis, including those
with sterile pancreatic necrosis.
• Enteral nutrition has been shown to lower the incidence of infections,
reduced surgical interventions to control pancreatitis, and a reduced length
of hospital stay. It is the preferred route of nutritional support in patients with
severe acute pancreatitis and can be given via nasogastric or nasojejunal
routes.
• Early surgical debridement of necrotic pancreatic tissue is only indicated for
FNA-proven infected necrosis or patients with surgical complications such as
massive bleeding or bowel perforation.
• Measurements of intra-abdominal pressure should be done liberally as
abdominal compartment syndrome (ACS) has been reported in up to 55% of
patients with severe pancreatitis [Chapter 8-(vi)].
Background
• Acute liver failure is defined as either encephalopathy or hepatic synthetic
dysfunction (INR > 1.49) in a patient without a history of pre-existing liver
disease and lasting < 26 weeks in duration.
Hepatopancreaticobiliary 327
• The most common cause of acute liver failure is acetaminophen overdose
followed by idiosyncratic drug reaction.
• Cirrhosis develops as a result of progressive hepatic fibrosis that is character-
ized by distortion of the hepatic architecture and formation of regenerative
nodules. Although early treatment of the cause of liver disease may improve
or reverse cirrhosis, advanced cirrhosis is irreversible.
• Patients with cirrhosis who have not developed major complications are
classified as compensated cirrhosis
• Decompensated cirrhosis is a life-threatening condition that is characterized
by one of the following complications: variceal hemorrhage, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatocellular carcinoma,
hepatorenal and hepatopulmonary syndrome.
• Patients with bleeding, infection, alcohol intake, medications, dehydration,
and constipation are at increased risk of developing decompensated cirrhosis.
• The MELD score is based on three biochemical variables: serum bilirubin,
serum creatinine, and either international normalized ratio (INR) or prothrombin time. It has been shown to accurately predict 3-month mortality
from liver disease and should be used for allocation of liver donors.
• Eighty percent of daily bilirubin production is derived from hemoglobin. Heme
from senescent red blood cells is converted to bilverdin via the rate limiting
enzyme heme oxygenase. Bilverdin is subsequently converted to unconjugated
bilirubin via bilverdin reductase and is carried to the liver via binding to
albumin. Unconjugated bilirubin is taken up in the hepatocytes via facilitated
diffusion and is conjugated by uridine diphosphoglucuronosyltransferase
(UGT), which is secreted across the canalicular membrane of the hepatocyte
via canalicular multi-drug resistant protein 2 (MRP2). Bacterial enzymes in
the intestine reduce bilirubin into urobilinogen and stercobilinogen.
• Although not routinely indicated, contrast enhanced CT of the abdomen is the
gold standard for diagnosing acute pancreatitis and its associated complications. Necrosis is characterized by focal or diffuse areas of diminished
pancreatic parenchymal enhancement (<50 Hounsfield Units).
• Pancreatic necrosis is associated with pancreatic infection in up to 30–70% of
cases, which is the most important risk factor for death.
• Several prognostic scoring systems including Ranson’s Criteria, Glascow
(Imrie) score, and APACHE II have been developed to predict clinical
outcomes of acute pancreatitis, but frequent clinical assessment is mandatory.
• The Balthazar score is used in CT severity index (CTSI) for grading of acute
pancreatitis and includes grading of pancreatitis (A-E) and the extent of
pancreatic necrosis.