Page 1491 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

1030 PART 9: Gastrointestinal Disorders

and furosemide in a ratio of 100 mg/40 mg and titrated up to Early broad spectrum antibiotic therapy and discovery of the source
400 mg/160 mg/d. Electrolytes should be monitored with diuretic ther- of infection is crucial, necessitating the evaluation for bacteremia,
apy. Refractory ascites is defined as: (1) ascites not responsive to spontaneous bacterial peritonitis, urinary tract infections, and pneu-
1
sodium restriction and high-dose diuretic therapy in the absence of monia. There are currently no large randomized controlled trials
prostaglandin inhibitors or (2) ascites that recurs rapidly after large regarding the effects of hydrocortisone therapy in cirrhotic patients
volume paracenteses. Tense, refractory ascites can lead to elevated with sepsis. However, studies have shown that cirrhotic patients have a
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abdominal pressures and even abdominal compartment syndrome, high incidence of adrenal insufficiency. A small study conducted by
31
characterized by restrictive chest wall mechanics, hypotension, oliguria, Rodriguez et al in 2006 did show a survival benefit in cirrhotic patients
and mesenteric ischemia. Patients with large, refractory ascites are with sepsis who were administered hydrocortisone. Therefore, treat-
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typically initially managed with repeat large volume paracentesis. While ment with hydrocortisone, should be considered. Similarly, there are
there has been some controversy regarding the benefit of postparacen- also no large randomized controlled trials regarding intensive insulin
tesis volume expanders such as albumin to prevent renal compromise, therapy in this subset of patients, so we recommend that insulin be
it is reasonable to administer albumin at a dose of 6 to 8 g/L of fluid infused to keep blood glucose between 140 and 180 mg/dL in those
removed, if >5 L fluid are removed. In the setting of refractory ascites, with hyperglycemia. Cirrhotic patients with sepsis often present
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patients can be considered for TIPS while awaiting transplantation. with hypoglycemia due to underlying liver dysfunction and therefore
Alternatively, patients with refractory ascites who are not candidates for often do not often need insulin therapy for glycemic control. Further
repeat paracentesis, liver transplantation, or TIPS can be evaluated for randomized controlled trials are needed specifically addressing these
peritoneovenous shunts. 26 issues with respect to critical care management in the cirrhotic patient
All hospitalized patients with chronic liver disease who present with with sepsis.
ascites should undergo a diagnostic paracentesis to assess for spontane-
ous bacterial peritonitis (SBP), which occurs in 15% of hospitalized
cirrhotic patients. An ascitic absolute neutrophil count of >250 cells/mm ACUTE VARICEAL HEMORRHAGE
3
is diagnostic for SBP in the absence of known peritonitis from other Gastroesophageal varices are present in approximately half of patients
etiologies. SBP is a known precipitant of HRS, which is a cause of with cirrhosis. As the development of gastroesophageal varices is a direct
increased mortality in cirrhotic patients; therefore, empiric antibiotic result of portal hypertension, it has been shown that these patients have
treatment is warranted in patients in whom the suspicion for SBP is high a hepatic venous pressure gradient (HVPG) of at least 10 to 12 mm Hg
while awaiting results of the paracentesis. Three of the most common (normal HVPG 3-5 mm Hg) and that the risk for variceal bleeding and
pathogens involved in SBP are Escherichia coli, Klebsiella pneumonia, and rebleeding correlates with severity of disease. Variceal hemorrhage
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pneumococci. Cefotaxime (or similar 3rd generation cephalosporin) is occurs at a yearly rate of 5% to 15% and mortality can be as high as
the treatment of choice, as it provides excellent coverage of these organ- 20% at 6 weeks. Aggressive and early management of cirrhotic patients
35
isms. Coverage can be narrowed once culture data are available. Culture presenting with suspected variceal bleed is critical.
negative neutrocytic ascites should be treated similar to SBP. The The pathophysiology surrounding development of portosystemic
26
administration of albumin has been shown to decrease mortality in sev- collaterals, namely gastroesophageal varices, rests in the underlying
eral studies. Based on the most recent data, it is recommended that albu- physiology of portal hypertension. Splanchnic vasodilation that results
min be given in patients with absolute neutrophil count >250 cells/mm in increased portal inflow, coupled with intrahepatic resistance to flow,
3
with high clinical suspicion of SBP, who also have a serum creatinine leads to formation of portosystemic variceal collaterals. Variceal wall
>1 mg/dL, BUN >30 mg/dL, or total bilirubin >4 mg/dL at a dose of tension is the primary factor determining risk of variceal hemorrhage.
1.5 g/kg within 6 hours of detection and 1 g/kg on day 3. 26,27 This, in turn, is determined by vessel diameter and pressure within the
vessel. Variceal hemorrhage is directly proportional to HVPG and typi-
SEPSIS cally occurs when the HVPG >12 mm Hg. 35,36
The treatment of acute variceal hemorrhage requires emergent criti-
Patients with cirrhosis have a low-level inflammatory state compared cal care management and aggressive resuscitation. Early airway protec-
with the noncirrhotic population. Additionally, in the setting of sepsis tion with elective intubation prevents pulmonary complications from
and an exaggerated proinflammatory state, compromise of the liver’s aspiration pneumonia secondary to massive hematemesis and inability
ability to clear endotoxins and cytokines results in worsened systemic to protect the airway, as these patients often have concomitant encepha-
function. Infections are more common in cirrhotic patients possibly lopathy. Obtaining intravenous access is important given the cumula-
10
due to decreased complement levels, impaired antigen presenting ability, tive effect of the cirrhotic hemodynamics with low systemic vascular
and impaired macrophage clearance of antibody-coated bacteria. The resistance often combined with massive blood loss. At least two large
most common infections occurring in cirrhotic patients are spontane- bore IVs should be placed or central access should be obtained. Blood
ous bacterial peritonitis, urinary tract infections, pneumonia, cellulitis, transfusions should be initiated when the Hgb concentration falls below
and bacteremia. These bacterial infections precipitate an abnormally 7 g/dL. Overaggressive volume resuscitation has been associated with
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enhanced inflammatory state with high levels of IL-6 and TNF-α. increased portal pressure, rebleeding, and high mortality. Additionally,
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Given the high mortality rate in patients with cirrhosis and sepsis, early cirrhotic patients often have hematologic derangements including defi-
diagnosis and treatment is imperative. cient factor levels and thrombocytopenia, further predisposing them
Early goal-directed therapy may play a role in the sepsis of cirrhosis, to bleeding. Fresh frozen plasma and platelets can be administered as
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but the components of resuscitation remain controversial. Volume infu- clinical evaluation and hematologic parameters necessitate the use of
sion should be guided by objective measures of response, such as rising these products.
blood pressure, central venous oxyhemoglobin saturation values, stroke The use of prophylactic antibiotics has been shown to decrease the
volume, or falling lactic acid levels. Since excessive intravascular volume rate of bacterial infections, including SBP, and also to improve survival.
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risks worsened portal hypertension, advancing ascites, and variceal Either a PO quinolone or IV ceftriaxone should be initiated and contin-
distention, dynamic fluid-responsiveness predictors may be helpful in ued for 7 days. Immediate pharmacologic strategies to decrease portal
limiting fluid therapy to settings where benefit is likely (see Chap. 34). pressures and induce splanchnic vasoconstriction include initiation of the
Judging the endpoints of resuscitation can be challenging since cirrhotics somatostatin analogue, octreotide. Octreotide may be used as a drip with
may have values for cardiac output, stroke volume, and central venous initial 50 µg bolus followed by 50 µg/h continuous infusion. Terlipressin,
saturation that are higher than those in healthy individuals, while mean a synthetic analogue of vasopressin, is effective in controlling variceal
systemic blood pressure tends to be lower. bleeds with a documented mortality benefit, but is not yet available in the

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