**3.3.5 Renal impairments**

*Hepatorenal syndrome* (HRS) is defined as an increase in creatinine to greater than 1.5 g/dL or a decrease in creatinine clearance to below 40 mL/min. HRS is a dreaded complication of cirrhosis, and can develop unexpectedly at any point in the course of illness. Splanchnic vasodilation in the setting of cirrhosis results in reduced effective blood volume and prerenal acute kidney injury. HRS is a diagnosis of exclusion. Two forms exist; type I progresses rapidly, whereas type II progresses over a longer time period; both are fatal without transplant. When diagnosing HRS, other causes of acute kidney injury in cirrhosis must be excluded, including dehydration and over-diuresis, medication effects, and intrinsic renal insults. Diagnostic criteria for HRS include: cirrhosis with ascites, creatinine level of at least 1.5 mg/dL, lack of response to diuretic withdrawal and volume expansion, absence of shock, and absence of nephrotoxic and parenchymal renal etiologies.

A definitive curative treatment for HRS is limited to liver transplantation, but supportive measures aimed at correcting the pathophysiology are in trial. Terlipressin has been studied for HRS in addition to its use in variceal hemorrhage, and has demonstrated the ability to reverse Type 1 HRS. Octreotide and the alpha agonist midodrine can induce splanchnic vasoconstriction, thereby potentially reversing the pathophysiology of HRS. Avoidance of additional renal insults, including diuretics and other nephrotoxic agents, is essential. The TIPS procedure can be used to improve overall circulatory function through portal venous decompression. Finally, renal replacement therapy is often required while patients await transplant.

### **3.3.6 Infectious complications**

Further complications of decompensated cirrhosis include a predisposition to infections, owing to a chronic low-grade inflammatory state produced by excess cytokines and reduced clearance of toxins. Impaired function of macrophages and antigen presenting cells and decreased levels of complement are also implicated. In the setting of septic shock, early goaldirected therapy is warranted, but over-resuscitation of volume can increase portal pressures and lead to exacerbation of portal hypertension. As in acute liver failure, patients with decompensated cirrhosis may benefit from use of glucocorticoids to supplement vasoactive agents (*Fernandez et al., 2006*). Bacterial pathogens are most typical, but fungal infections occur frequently in cirrhosis and should be considered in the differential diagnosis.

#### **3.3.7 Ascites**

*Abdominal ascites* is another notable manifestation of decompensated cirrhosis. Ascites can cause significant morbidity, including abdominal pain and discomfort, dyspnea and orthopnea, hepatic hydrothorax, spontaneous bacterial peritonitis, and abdominal compartment syndrome. Abdominal compartment syndrome is characterized by restrictive lung mechanics, renal and mesenteric vascular compromise, and hypotension due to compression of the inferior vena cava.

Ascites develops in response to renal hypoperfusion, which results in upregulation of the renin-angiotensin-aldosterone system to increase sodium and water retention. Elevated portal pressures produce a capillary hydrostatic pressure gradient, forcing fluid into the abdominal interstitium. Sodium restriction and use of diuretics can be used to manage ascites. Refractory ascites can be managed with serial large-volume paracentesis or placement of a TIPS shunt.
