Should I continue nadolol in my patient with cirrhosis and refractory ascites?

Under certain circumstances, you may need to! Although nonselective beta blockers (NSBBs), such as nadolol and propranolol, have been the cornerstone of medical treatment of portal hypertension in preventing variceal bleeding in patients with cirrhosis for decades, recent reports of their association with worsening survival, increased risk of hepatorenal syndrome and acute kidney injury in patients with refractory ascites or spontaneous bacterial peritonitis [SBP]) 1,2 have added controversy to their routine use in end-stage cirrhosis.

This is because patients with end-stage cirrhosis may be highly dependent on their cardiac output (particularly the heart rate) in maintaining an adequate arterial blood pressure 3-5 and the negative inotropic and chronotropic effects of NSBBs blunt this compensatory mechanism. The result is a drop in the cardiac output that may be particularly significant in the presence of conditions already associated with hypotension, such as sepsis, spontaneous bacterial peritonitis (SBP), or hemorrhage, further increasing the risk of renal hypoperfusion and hepatorenal syndrome.3

Although 2 meta-analysis studies failed to find an association between NSBBs and increased mortality among patients with cirrhosis and ascites, 6,7 serious concerns over the adverse effects of these drugs in at least a subset of patients has not waned.  Some have recommended reducing NSBB dose or discontinuing treatment in patients with refractory ascites or SBP and any of the following parameters: 4

  • Systolic blood pressure <90 mmHg
  • Serum creatinine >1.5 mg/dL
  • Hyponatremia <130 mmol/L

Similar recommendations were made by a 2015 consensus conference on individualizing the care of patients with portal hypertension.

In the absence of randomized-controlled studies, it seems prudent to proceed with more caution when using NSBBs in patients with end-stage cirrhosis and watch closely for any signs of hypotension or renal function deterioration.


  1. Serste T, Njimi H, Degre D, et al. The use of beta-lackers is associated with the occurrence of acute kidney injury in severe hepatitis. Liver In 2015;35:1974-82.
  2. Mandorfer M, Bota S, Schwabl P, et al. Nonselective beta blockers increase risk of hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterol 2014;146:1680-90.
  3. Garcia-Tsao G. The use of nonselective beta blockers for treatment of portal hypertension. Gastroenterol Hepatol 2017;13: 617-19.
  4. Reiberger T, Mandorfer M. Beta adrenergic blockade and decompensated cirrhosis. J Hepatol 2017;66: 849-59.
  5. Giannelli V, Lattanzi, Thalheimer U, et al. Beta-blockers in liver cirrhosis. Ann Gastroenterol 2014;27:20-26.
  6. Facciorusso A, Roy S, Livadas S, et al. Nonselective beta-blockers do not affect survival in cirrhotic patients with ascites. Digest Dis Sci 2018;63:1737-46.
  7. Njei B, McCarty TR, Garcia-Tsao G. Beta-blockers in patients with cirrhosis and ascites: type of betablocker matters. Gut 206;65:1393-4.
  8. De Franchis R. Expanding consensus in portal hypertension. Report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension.  J Hepatol 2015;63:743-52.  

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Should I continue nadolol in my patient with cirrhosis and refractory ascites?

Which non-pharmacological approaches may help symptoms of orthostatic hypotension in my patient with autonomic insufficiency?

A number of simple measures to help reduce the symptoms of neurogenic orthostatic hypotension (nOH) in susceptible patients have been recommended.1

  • Blood volume repletion (a minimum of 64 oz or 2L of water intake daily), depending on cardiac status. In addition, rapid consumption (within 5 min) of 16 oz or 500 ml of water can raise blood pressure by 30 mmHg for about an hour. It’s worth noting that liquids other than water (eg, water plus salt) do not provide the same BP response, likely due to water-induced hypo-osmolar reflex in the portal circulation.2,3
  • Increase salt intake if possible (eg, add 1-2 teaspoons or 2.3-4.6 g of salt per day), as many patients with nOH have an inadequate salt intake.
  • Improve physical conditioning that is not gravitationally challenging (eg, stationary recumbent bicyle, rowing machine).
  • Avoid increased core body temperature (eg hot tubs, prolonged hot showers).
  • Head-up position while sleeping through use of a wedge under the mattress or blocks under the head of the bed so that the head is 6-9 inches (15-23 cm) higher than the feet. This is to minimize nocturnal supine hypertension which can cause pressure diuresis and volume depletion.
  • Compressive garments, preferably either an abdominal binder or thigh high stockings when erect; knee high stocking are not likely to be effective.
  • Smaller, more frequent,  meals not high in carbohydrates in patients with postprandial hypotension.
  • Dietary supplementation with B12 or iron, if deficient.

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  1. Gibbons CH, Schmidt P, Biaggioni I, et al. The recommendations of a consensus panel for the screening, diagnosis, and treatment of neurogenic orthostatic hypotension and associated supine hypertension. J Neurol 2017;264:1567-1582.
  2. Jordan J, Shannon JR, Black BK, et al. The pressor response to water drinking in humans: a sympathetic reflex? Circulation 101:504-9.
  3. Raj SR, Biaggioni I, Black BK, et al. Sodium paradoxically reduces the gastropressor response in patients with orthostatic hypotension. Hypertension 2007;48:329-334.
Which non-pharmacological approaches may help symptoms of orthostatic hypotension in my patient with autonomic insufficiency?