Page 1490 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 107: Management of the Patient With Cirrhosis 1029

present in the left thorax or bilaterally. Occasionally, fluid accumula- It is defined as a doubling of initial serum creatinine to >2.5 mg/dL or
tion can be massive, leading to severe respiratory compromise, and a 50% reduction of the initial 24-hour creatinine clearance to a level
even cardiac tamponade with systemic hypotension requiring emergent <20 mL/min in less than 2 weeks. Type II hepatorenal syndrome is
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intervention. 21 associated with diuretic resistant ascites and serum creatinine ranging
Diagnosis can be made with thoracentesis to rule out infection or from 1.5 to 2.5 mg/dL. Despite a more protracted course, its prognosis
other etiologies of pleural effusion. The pleural fluid analysis will be is also poor. In both types of hepatorenal syndrome, the diagnosis is
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transudative in nature resembling ascitic fluid. Total protein and albu- clinical and is one of exclusion. Urine electrolytes reveal a urine sodium
min levels may be slightly elevated compared to ascitic fluid, due to the <10 mEq/L and urine sediment is bland without evidence of ATN. 15
greater efficacy of water absorption by the pleura. Spontaneous bacte- Given the high mortality associated with hepatorenal syndrome,
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rial pleuritis should be diagnosed if the pleural fluid absolute polymor- prevention warrants special attention. The administration of albumin,
phonuclear cells (PMN) exceed 250/mm with a positive fluid culture or acting as a volume expander to increase effective circulating volume,
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a PMN count >500/mm with a negative fluid culture in the absence of has been shown to decrease mortality related to renal impairment is
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contiguous foci of infection. This should be treated promptly with IV several studies. Additionally, SBP is a known precipitant of HRS. Based
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antibiotics. Insertion of chest tubes is contraindicated in this setting. 1 on the most recent data, it is recommended that albumin be given to
Medical management of hepatic hydrothorax includes initiation of patients with absolute neutrophil count >250 cells/mm with high
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diuresis with lasix and spironolactone, and therapeutic thoracentesis and clinical suspicion of SBP, who also have a serum creatinine >1 mg/dL,
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paracentesis in symptomatic patients with gas exchange abnormalities. BUN >30 mg/dL, or total bilirubin >4 mg/dL at a dose of 1.5 g/kg
However, caution should be exercised in removing greater than 1.5 L within 6 hours of detection and 1 g/kg on day 3. 26,27 Additionally, it is
of pleural fluid, as it can precipitate reexpansion pulmonary edema. reasonable to administer albumin at a dose of 6 to 8 g/L of fluid removed
Aggressive drainage with insertion of large chest tubes is contrain- if more than 5 L of ascites is removed to maintain circulating volume and
dicated in the management of hepatic hydrothorax due to the risk of renal perfusion. 26
precipitating hypovolemic shock and reexpansion pulmonary edema. Liver transplanation is the only definitive cure for hepatorenal syn-
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In our anecdotal experience, the introduction of smaller bore pleural drome. Initial management of hepatorenal syndrome involves withdrawal
drainage catheters (eg, 10 F biliary drainage catheters) with gravity of diuretics and other nephrotoxic medications. Given that hypovolemia
drainage allows the controlled removal of pleural fluid with stabilization can closely mimic hepatorenal syndrome, administration of a fluid chal-
of gas exchange without hemodynamic derangements. Patients who are lenge and albumin at 1 g/kg body weight up to 100 g/d is recommended.
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refractory to medical management and thoracentesis may require more Other precipitants of hepatorenal syndrome including gastrointestinal
invasive approaches including a TIPS procedure. TIPS has been success- bleed and spontaneous bacterial peritonitis must be promptly diagnosed
ful in treating hepatic hydrothorax when other methods of treatment and treated. Understanding the role of splanchnic arterial vasodilation
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have failed and can be used to bridge patients to liver transplantation. in the pathogenesis of hepatorenal syndrome has led to the use of splanch-
However, it must be recognized that it is a temporizing measure associ- nic vasoconstrictors for treatment of hepatorenal syndrome type I.
ated with significant morbidity and mortality. Ultimately, patients with Terlipressin is the most-studied drug. Recent randomized controlled
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refractory hepatic hydrothorax benefit most from liver transplantation. 1 trials have shown improvement in renal function but no survival benefit
with terlipressin and albumin administration. 25,28 Terlipressin, however,
has not yet been approved for clinical use in the United States. There is
HEPATORENAL SYNDROME promising but limited data with the use of other agents targeted at pro-
Patients with decompensated cirrhosis have multiple reasons for renal ducing splanchnic vasoconstriction. A combination of octreotide (inhibi-
dysfunction, occurring at the prerenal, intrarenal, and postrenal level. tor of endogenous vasodilator release) and midodrine (an α-adrenergic
Hepatorenal syndrome, a specific prerenal etiology of renal dysfunction agonist) in the treatment of hepatorenal syndrome has been shown to
in cirrhosis, carries a high mortality, making early diagnosis crucial. improve renal function and hemodynamics. TIPS has alternately been
Hepatorenal syndrome is a diagnosis of exclusion and is characterized studied in management of both hepatorenal syndrome type I and II.
by renal impairment in the setting of advanced liver disease, circulatory There are data suggesting that through portal decompression, it improves
dysfunction, and increased activity of the renin-angiotensin system. renal and circulatory function and may serve as an adjunct to vasocon-
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Other etiologies of renal dysfunction must be ruled out including shock, strictor therapy. Finally, if renal function continues to deteriorate despite
nephrotoxic drugs, prerenal azotemia, and intrinsic renal disease. In medical management, renal replacement therapy can be used as a bridge
1998, the International Ascites Club proposed the major diagnostic cri- to transplantation, which ultimately offers the best option for long-term
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teria for hepatorenal syndrome in the setting of severe liver disease with survival. Typically, patients who require a prolonged course of renal
advanced portal hypertension. This was updated in 2007 and includes replacement therapy extending beyond six weeks are considered for
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the following: (1) cirrhosis with ascites, (2) serum creatinine >1.5 mg/dL, combined kidney/liver transplantation.
(3) no improvement of serum creatinine to <1.5 mg/dL after 2 days of
diuretic withdrawal and volume expansion with albumin, (4) absence ASCITES AND SPONTANEOUS BACTERIAL PERITONITIS
of shock, (5) absence of nephrotoxic drugs, and (6) absence of parenchy-
mal kidney disease indicated by proteinuria >500 mg/dL, microhematu- There are two main factors that lead to ascites in cirrhotic patients:
ria, and normal renal ultrasound. 24 sodium retention and portal hypertension. Systemic vasodilation leads
The pathophysiology of hepatorenal syndrome is thought to derive to decreased renal blood flow and subsequent activation of the renin-
from the dysfunctional circulatory state in cirrhotic patients. Potent angiotensin-aldosterone system. Aldosterone upregulation results in
vasodilators such as nitric oxide cause splanchnic vasodilation. Coupled increased sodium reabsorption in the distal tubule. Additionally,
with a decreased effective circulating blood volume and low systemic vas- decreased renal blood flow leads to decreased glomerular filtration rate,
cular resistance, this causes a reduction in renal perfusion. The kidneys affecting delivery and excretion of sodium. Combined, these mecha-
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perceive a persistent pre-renal state and adapt by activating the sodium nisms involved in sodium balance cause sodium and water retention.
retention mechanisms and the renin-angiotensin system resulting in Portal hypertension contributes to ascites through increased hydrostatic
vasoconstriction. When these adaptive mechanisms are overwhelmed pressure within hepatic sinusoids causing transudation of fluid into the
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glomerular filtration declines and renal failure ensues. 25 peritoneum. 30
Hepatorenal syndrome can be categorized into two types. Type I The mainstay of treatment for ascites includes dietary sodium restric-
hepatorenal syndrome is a rapidly progressive form that occurs in severe tion and diuretic therapy. Daily sodium intake should be restricted to
liver disease and carries a mortality of approximately 80% at 2 weeks. 2 g/d. The most effective diuretic therapy consists of spironolactone
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