Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_885_Библиотеки_им_академика_М_И_Перельмана.pdf
328 C. C. Barnett, B. C. Chapman and E. L. Jones
{ Mild pancreatitis (interstitial): Balthazar B (enlargement of pancreas),
Balthazar C (inflammatory changes in pancreas and peripancreatic fat),
without pancreatic or extrapancreatic necrosis.
{ Intermediate (exudative): Balthaazar D (ill defined single fluid collection),
Balthazar E (two or more poorly defined fluid collections), without
pancreatic necrosis; peripancreatic collections are due to extrapancretic
necrosis.
{ Severe (necrotizing): pancreatic necrosis.
Main Body
• Acute Liver Failure
{ An acute injury (<26 weeks) to the liver demonstrated by encephalopathy
and impaired synthetic function (INR >1.49) in a patient without
pre-existing liver disease.
{ Determination of the etiology begins with a careful history, hepatic
function tests (bilirubin, aminotransferases, alkaline phosphatase),
prothrombin time, viral hepatitis serology, autoimmune panel and specific
medication levels as indicated by history.
{ Common patterns of presentation in liver function tests are available in
Table 1.
{ The most common cause is acetaminophen toxicity followed by idio-
syncratic drug reaction and viral hepatitis.
{ Common etiologies can be remembered using the “ABCs” pneumonic:
A — Hepatitis A, Autoimmune, Amanita phalloides (mushroom poisoning).
B — Hepatitis B, Budd-Chiari.
C — Hepatitis C, cytomegalovirus infection.
D — Hepatitis D, Drugs (acetaminophen, isoniazid, halothane, pheny-
toin, labetalol and many others).
E — Epstein-Barr virus.
F — Fatty liver of pregnancy, Reye’s syndrome.
G — Genetic (Wilson’s disease).
H — Hypoperfusion (sepsis), HELLP syndrome, HSV, hepatectomy.
{ The appropriate management is directed towards rectifying the underlying
cause. In addition, aggressive treatment of the common electrolyte
abnormalities (hypokalemia, hyponatremia, hypophosphatemia and hypoglycemia) as well as closely monitoring for cerebral edema (intra-cranial
pressure monitors or transcranial Doppler ultrasound) and treatment when
indicated.
Hepatopancreaticobiliary 329
{ Seizures, acute renal failure and pulmonary infections and edema are
other common complications. Treatment is supportive.
{ Prognosis is most consistently associated with the grade of hepatic
encephalopathy. Spontaneous recovery by gade. Grade I–II (mild to
moderate confusion, minimal asterixis): 70% (mild-moderate confusion, minimal asterixis). Grade III (incoherent, arousable but sleeping):
50% Grade IV (comatose): <20%.
{ Acetaminophen toxicity, hepatitis A, ischemia/shock or pregnancy-related
acute liver failure as well as age 11–39 have higher likelihood of spontaneous recovery in contrast to hepatitis B, autoimmune hepatitis, Wilson
disease, Budd-Chiari or malignancy.
{ Prognostic models include the King’s College Criteria as well as the
MELD but must be used with caution as the sensitivity and specificity
of these models have varied widely in the literature.
{ If consideration is given for liver transplantation, then patients should be
rapidly triaged and transferred to transplant centers.
• Decompensated Cirrhosis
{ Variceal hemorrhage:
Prevention: non-selective beta blocker.
Signs and symptoms: hematemesis and/or melena.
Treatment: Endoscopic variceal band ligation.
{ Ascites
Presentation: circulatory, vascular, functional, and biochemical
abnormalities.
Treatment: diuretics and sodium restriction, therapeutic pericentesis,
and/or TIPS placement.
{ Spontaneous bacterial peritonitis
Prevention: diuretics, aggressive treatment of localized infections,
avoidance of proton pump inhibitors, prophylactic antibiotics.
Presentation: fever, abdominal pain, abdominal tenderness, altered
mental status, positive ascitic fluid bacterial culture and/or an elevated ascitic fluid absolute polynmorphonuclear leukocyte count
3
(≥ 250 cells/mm
).
Treatment: Antibiotics.
{ Hepatic encephalopathy
Prevention: avoidance of variceal bleeding, infection, sedatives,
hypokalemia, and hyponatremia.
330 C. C. Barnett, B. C. Chapman and E. L. Jones
Presentation: disturbance in diurnal sleep pattern, asterixis, hyperac-
tive deep tendon reflexes, and transient decerebrate posturing.
Treatment: treatment of predisposing conditions, synthetic disaccha-
rides (lactulose), and non-absorbable antibiotics (rifaximin).
{ Hepatocellular carcinoma
Prevention: surveillance ultrasound every six months.
Presentation: pain, early satiety, obstructive jaundice, a palpable mass,
or marked elevations of serum alpha-fetoprotein (AFP).
Treatment: hepatic resection, radiofrequency ablation, chemoemboli-
zation, or liver transplant determined by the size and number of
lesions as well as patient performance.
{ Hepatorenal syndrome
Prevention: avoid nephrotoxic agents and excessive diuresis.
Presentation: very low rate of sodium excretion, progressive rise in the
plasma creatinine concentration.
Treatment: prognosis is poor without liver transplant.
{ Hepatopulmonary syndrome
Presentation: triad of liver disease, increased alveolar-arterial gradient
while breathing room air, and intrapulmonary vascular dilatations.
Treatment: no effective medical treatments thus requiring liver
transplant.
• Acute Jaundice in the Critically Ill Patient
{ History and physical examination
{ Laboratory evaluation
Normal alkaline phosphatase and aminotransferases — unlikely to be
due to hepatic injury or biliary tract disease. Hemolysis characterized
by an increased reticulocyte count, peripheral blood smear, positive
Coombs test, increased lactate dehydrogenase, and decreased haptoglobin or inherited disorders of bilirubin metabolism should be
considered.
Predominant alkaline phosphatase elevation — suggest biliary
obstruction or intrahepatic cholestasis. Abdominal ultrasound to
evaluate for intra- or extra-hepatic bile duct dilation should be
obtained. Computed tomography or MRI can be used in patients in
whom sonographic findings are equivocal if other intra-abdominal
pathology needs to be excluded, or if ductal dilatation is seen on US
without a clearly defined etiology.
Hepatopancreaticobiliary 331
Predominant aminotransferase elevation — suggests intrinsic hepato-
cellular disease. Serologic testing to evaluate for viral hepatitis,
alcoholic liver disease, and metabolic liver disease should be obtained.
A liver biopsy may also be diagnostic.
{ Differential Diagnosis (See Table 2).
• Acute Pancreatitis (AP)
{ Etiology: Gallstones (45%), alcohol (35%), other rare causes include drug
reactions, pancreatic/ampullary tumors, hypertriglyceridemia, hypercalcemia, hypothermia, congenital abnormalities, trauma, ERCP, and
infectious/parasitic organisms.
{ The diagnosis should be suspected in patients presenting with acute upper
abdominal pain and tenderness, nausea, vomiting, elevated lipase and
amylase.
{ Ultrasound should be considered as initial test in all patients with pan-
creatitis to rule out a biliary etiology.
{ Pancreatic necrosis on contrast-enhanced CT scan is characterized by
focal or diffuse areas of diminished pancreatic parenchymal enhancement
(less than 50 Hounsfield units).
{ Due to the risk of contaminating sterile necrosis, fine needle aspiration
(FNA) should only be performed in patients who show clinical signs of
sepsis, fail to improve on supportive therapy, or regress after an initial
period of improvement.
{ CRP levels greater than 150 have been associated necrosis and an elevated
serum procalcitonin may predict later organ dysfunction.
{ Initial management focuses on aggressive intravascular resuscitation as
sequestration of fluid into extravascular extracellular compartment (thirdspacing) can lead to significant plasma volume.
{ Frequent evaluation of abdominal compartment syndrome should be uti-
lized due to the large amount of fluid required.
{ 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.
{ Patients with mild AP should begin oral supplementation within a few
days of presentation.
{ 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.
332 C. C. Barnett, B. C. Chapman and E. L. Jones
{ Historically, early surgery was thought to improve outcome by removing
necrotic tissue and decrease the stimulus for systemic inflammation; however, this has been disapproved by more recent clinical trials.
{ Open necrosectomy has been associated with a high morbidity (34–95%)
and mortality (11–39%); thus, 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.
{ A recent randomized control trial comparing a “step-up approach,”
characterized by initial percutaneous drainage followed by minimally
invasive retroperitoneal necrosectomy if needed, to open necrosectomy
demonstrated a lower complication rate, less organ failure, lower rates
of incisional hernias, lower incidence of diabetes mellitus, and 35% of
patients were successfully treated with percutaneous drainage alone.
{ Complications of acute pancreatitis include abdominal compartment
syndrome, acute respiratory distress syndrome (ARDS), pancreatic and
peri-pancreatic fluid collections, pancreatic necrosis, pancreatic pseudocyst, and pancreatic abscess.
Practical Algorithm(s) / Diagrams
Table 1. Common laboratory derangements in liver failure.
Chronic
Toxic or
Test
Aminotransferases (IU/L) 1000–10,000 100–1000 50–150 35–150 35–1000 35–100
Alkaline phosphatase
(IU/L)
Total Bilirubin (mg/dL) 2–10 2–60 2–60 2–60 0.5–2.5 0.5–10
PT Prolonged Prolonged Prolonged May be Pro longed Normal Normal
Responsive to Vit K No No No Yes Yes Yes
Examples:
ischemic Viral Alcohol
150–450 150–450 150–1000 300–3000 50–150 150–3000
Acetaminophen
overdose,
Shock or
Sepsis
Hepatitis
A, B
or D
Alcohol
biliary obstruc-
tion
Pancreatic or
Ampullary
Carcinoma
Acute biliary
obstruction Infiltrating cancer
Cholangiocarcinoma,
Choledocholithiasis,
Hepaticolithiasis
Mycobacterium
avium-
intracellulare
infection
Hepatopancreaticobiliary 333
334 C. C. Barnett, B. C. Chapman and E. L. Jones
Table 2. Differential diagnosis and management of acute jaundice.
Classification for acute jaundice associated with critical illness
Primary etiology Examples Treatment
Extrahepatic bile
duct obstruction
Choledocholithiasis Decompression,
Common Bile Duct Stricture
Traumatic or iatrogenic
common bile duct injury
Acute pancreatitis
Malignancy (ampullary
stone retrieval,
stricture dilation,
stent placement
via ERCP or
PTC
carcinoma)
Increased bilirubin
production
Massive transfusion Treat underlying
Resorption of blood collections
condition
(hematomas,
hemoperitoneum)
Acute hemolysis (DIC, Immune
mediated)
Impaired excretion
due to
hepatocellular
dysfunction,
hepatitis, or
intrahepatic
cholestasis
Drug or alcohol-induced
hepatitis
Drug-induced intrahepatic
cholestasis
Drug-induced hepatocellular
necrosis
Discontinue
offending agent
Gilbert’s syndrome No intervention
needed
Sepsis and other causes of
inflammation
Treat underlying
cause
Viral hepatitis
Total parenteral nutrition Consider Enteral
nutrition
Ischemic Hepatitis Treat underlying
cause and
maximize
cardiac output to
improve tissue
oxygenation
Adapted from Vincent, Jean-Louis; Abraham, Edward; Kochanek, Patrick; Moore, Frederick A.; Fink,
Mitchell P. (2011-05-12). Textbook of Critical Care: Expert Consult Premium (Kindle Locations
8657–8658). Elsevier Health Sciences. Kindle Edition.
Hepatopancreaticobiliary 335
Review of Current Literature with References
• Ostapowicz et al. published a prospective cohort study in 17 tertiary care
centers as part of the U.S. Acute Liver Failure Study Group. Over a 41-month
period, they analyzed 308 consecutive patients and reported that acetaminophen overdose was the most common cause of acute liver failure (39%)
followed by idiosyncratic drug reactions (13%) and hepatitis A/B (12%).
Survival at three weeks was just 67% and 29% underwent transplantation.
Transplant-free survival ranged from 68% in acetaminophen toxicity to 25%
for drug reactions and 17% of indeterminate cause. Ann Intern Med. 2002;
137(12): 947.
• Wiesner et al. prospectively applied the MELD score to estimate the 3-month
mortality to 3,437 adult liver transplant candidates with chronic liver disease
who were added to the OPTN waiting list at 2A or 2B status between
November 1999 and December 2001. Twelve percent of the patients died
during the 3-month follow-up period and the waiting list mortality increased
directly in proportion to the listing MELD score. Patients with a MELD score
< 9 had a mortality of 1.9% versus patients with a score ≥ 40 having a mortality
of 71.3%. Thus, the MELD score can accurately predict 3-month mortality
and should be used for allocation of donor livers. Gastroenterology. 2003;
124: 91–96.
• A meta-analysis of 263 patients from six randomized controlled comparing
enteral nutrition with parenteral nutrition in patients with acute pancreatitis
demonstrated the enteral nutrition was associated with a significantly lower
incidence of infections (RR 0.45; 95% CI 0.26–0.78, p = 0.004), reduced
surgical interventions to control pancreatitis (0.48, 0.22–1.0, p = 0.05), and a
reduced length of hospital stay (mean reduction of 2.9 days, 1.6 to 4.3 days,
p < 0.001). There were no significant differences in mortality (RR 0.66,
0.32–1.37, p = 0.03) or non-infectious complications (0.61, 0.31–1.22,
p = 0.16) between the two groups. Based on these findings, enteral nutrition is
the preferred route of nutritional support. BMJ, doi:10.1136 / bmj.
38118.593900.55 (published 2 June 2004)
• A meta-analysis of 502 patients from eight studies comparing the clinical
outcomes of patients with severe acute pancreatitis treated with prophylactic
antibiotics compared with that of patients not treated with antibiotics demonstrated no protective effect of antibiotic treatment on mortality (RR 0.76;
95% CI 0.49–1.16), protection against infected necrosis (0.79: 0.56–1.11), or
surgical intervention (0.88; 0.65–1.20). However, there was a benefit to nonpancreatic infections (0.60; 0.44–0.82). Based on these findings, antibiotic
336 C. C. Barnett, B. C. Chapman and E. L. Jones
prophylaxis is not routinely indicated in patients with severe acute pancreatitis. Am J Surg. 2009; 197: 806–813.
• In a multicenter study, 88 patients with necrotizing pancreatitis and suspected
or confirmed necrotic tissue were randomly assigned to undergo primary
open necrosectomy or a step-up approach consisting of percutaneous drainage followed, if necessary, by minimally invasive retroperitoneal necrosectomy.
The primary end-point was a composite of major complications (new onset
multiple organ failure or multiple systemic complications, perforation of a
visceral organ or enterocutaneous fistula, or bleeding) or death and occurred
in 31 of 45 patients (69%) assigned to open necrosectomy and in 17 of 43
patients (43%) assigned to the step-up approach. However, the rate of death
did not differ significantly between the groups. The step-up approach should
be considered in patients with infected necrotic tissue. N Engl J Med. 2010;
362(16): 1491–1502.
Chapter 8-(v)
Colorectal
Robert T. Stovall, MD*
* Assistant Professor of Surgery, University of Colorado School of Medicine
Take Home Points
• Acute colonic pseudo obstruction (ACPO) is a result of an ongoing process.
This process should be identified and corrected.
• To diagnose acute colonic pseudo obstruction, mechanical obstruction and
toxic mega-colon must be excluded as the cause.
• Toxic mega colon (TMC) is a potentially lethal final common pathway of
severe colon inflammation that can be caused by a variety of initial processes.
• The diagnosis of TMC is clinical — a dilated, non-obstructed colon in the
setting of and causing severe systemic toxicity.
Background
• Acute colonic psuedo obstruction (ACPO) ( Ogilvie’s syndrome) can compli-
cate the course of many medical and surgical patients, but the exact incidence
is unknown.
• It is believed to be more likely in elderly patients.
Contact information: Denver Health Medical Center, 777 Bannock Street, MC 0206,
Denver, CO 80204. Tel.: 303-436-4029, email: robert.stovall@dhha.org
337