Understanding the different types of shock helps with providing the right resuscitation for the patient. Is the patient distributive? IV fluids, vasopressors, and antibiotics/source control if you suspect infection. Cardiogenic? Inotropic support and diuresis. The table showing the hemodynamics of the different types of shock is well known and taught to residents and fellows nationwide (Figure 1).
Table 1: Types of Shock and Hemodynamics
Splanchnic steal syndrome/cirrhotic shock
Many of you may not have even heard of this term, but it definitely exists. When I say hepato-renal syndrome, people will spout off type 1 vs type 2 or talk about its poor prognosis. Calling splanchnic steal syndrome hepato-renal is like calling cardiogenic shock cardiorenal syndrome. Cardiogenic shock affects the kidneys, but it does so much more. This is also true for splanchnic steal syndrome, it leads to AKI and renal failure, but there is so much more.
Physiology:
This occurs when there is cirrhosis, especially decompensated cirrhosis which can be multifactorial. In order for this to occur you have to have portal hypertension and an increase in vasodilators.
Portal Hypertension → Increased portosystemic collateral venous flow:
The first part of the problem is portal hypertension. This is due to an increase in resistance of portal blood through the cirrhotic liver caused by collagen deposition in the hepatic acinus and also external compression from nodules and granulomas. The end result is actually an increase in flow through the portal system. This is thought to be due to the dilation of the portosystemic collaterals that occurs with portal hypertension (1).
Increase in vasodilators → Splanchnic artery vasodilation and increased flow:
Cirrhosis leads to an increase in production or a decrease in the breakdown of carbon monoxide (CO), nitric oxide (NO), and prostaglandins (PGs). Other vasodilators include histamine, substance P, estrogen, glucagon, VEGF, and endogenous cannabinoids. In decompensated cirrhosis the is an increase in inducible NO (iNO). NO and iNO are major contributors and preferentially dilate the mesenteric arteries (1).
Blood will go in the path of least resistance and, with dilated splanchnic arteries and veins, blood is shunted to the splanchnic system and back to the heart. The blood is shunted away from the systemic circulation which includes the brain, kidney, adrenals, and extremities. With decreased blood flow to these other organs, the patient develops altered mental status, AKI, and multi-organ dysfunction. Poor organ perfusion leads to shock and lactic acid formation (1).
Other factors to consider:
Ascites/Varices:
One-third of the cardiac output goes to the liver and intestines. This is increased in cirrhotic patients and part of what leads to ascites and gastric/esophageal varices. The varices lead to bleeding and anemia and even hemorrhagic shock and compound the already poor hemodynamics of the patient. The ascites will continue to build and can lead to abdominal hypertension. Abdominal hypertension puts pressure on the intra-peritoneal structures, as well as the retroperitoneal kidneys, and can worsen renal function (1,2).
Figure 1: Normal Hemodynamic Circulation (adapted from McAvoy)
Figure 2: Splanchnic Steal Syndrome/Cirrhotic Shock
Stop calling it hepatorenal:
As far back as 1957, it was described that these patients get renal dysfunction despite having normal renal histology. They also reported recovery of the kidney to normal with the recovery of the hepatic function. This fits a picture similar to cardiogenic shock where there is decreased blood flow to the kidney and increased venous pressure leading to a decreased pressure gradient to create a GFR. The issue is not the kidneys it is the hemodynamics. By calling it hepato-renal we are focusing on one part of a systemic problem. By calling it splanchnic steal syndrome the whole picture can be seen.
Cirrhotic Shock:
I believe that when organ dysfunction due to inadequate oxygen delivery is identified this should be called cirrhotic shock. It should be splanchnic steal syndrome when compensated. This is a hyperdynamic shock with increased cardiac output in some parts of the body, but low blood flow and cardiogenic/hypovolemic-like shock in another, due to the shunt. The mixed venous oxygen saturation is normal or elevated since blood is shunting through the body without delivering oxygen. These patients are also often overall volume overloaded, but due to low oncotic pressure and poor systemic flow can have less intravascular volume. This low intravascular blood does not fully explain the low blood flow to the kidneys and other organs, as overall it is hyperdynamic with normal or elevated cardiac output. In fact, the RV preload and venous volume are usually elevated in these patients.
Breaking down splanchnic steal into its hemodynamic components is difficult using our current definitions. Where does cirrhotic fit into the shock subcategories?
Table 2: Cirrhotic Shock Hemodynamic Profile
As mentioned above, it is hyperdynamic where cardiac output is elevated and systemic vascular resistance (SVR) is low. But, SVR is a calculated number and while it is true the splanchnic circulation has low resistance, the SVR outside of the splanchnic system is most likely elevated. Additionally, CVP is elevated due to the high RV preload, and cirrhotic patients are prone to pulmonary hypertension which does not fit the distributive model. The wedge pressure (PAOP) is variable and can be elevated or normal.
With so many contradictory hemodynamic factors occurring, treating these patients as distributive, cardiogenic, or hypovolemic will lead to worse outcomes. By identifying it as its own profile, we can better individualize these patient's care.
How do you treat this type of shock?
The answer is to approach the patient physiologically. The 3 main focuses are the patient’s volume status, splanchnic vasodilation, and inflammation.
1. Splanchnic vasodilation:
Vasopressors are used to improve vasodilation and can be used in this patient population. The risk of vasopressors is worsening the already decreased flow of the systemic circulation leading to the kidney, brain, adrenals, and extremities. Using medications that can preferentially target the splanchnic circulation is preferred. The 3 medications that are typically used for this are vasopressin, octreotide, and midodrine.
Vasopressin will target the splanchnic vasculature and is why it was used in GI bleeds for so long. Terlipressin is an oral alternative in Europe that has been used with great success but unfortunately is not available in the US. Octreotide can be used as an infusion if variceal bleeding is suspected but subcutaneous or IV push is typically used in this situation. I use 100 micrograms subcutaneously every 8 hours, but 200 micrograms is also an option. And last is midodrine which does not preferentially target the splanchnic system but does help decrease the vasodilation and increased cardiac output (1,2).
2. Volume status:
These patients have the appropriate amount of volume in the body and are even volume overloaded. These patients do have low oncotic pressure and third-spacing. The low albumin due to cirrhosis causes this and the patient will have lower extremity edema, pleural effusions, and ascites. The ascites should be drained if felt to be moderate or large. Draining the ascitic fluid can lead to fluid shifts and hyperoncotic albumin supplementation is needed to prevent this.
Even with the low oncotic pressure and third-spacing these patients usually have increased volume and a dilated IVC with high preload. This hypervolemic state is due to increased circulation, acute kidney injury with decreased removal, and often pulmonary hypertension. The goal is to make the patient euvolemic while also ensuring appropriate blood flow to the rest of the body.
Increasing the oncotic pressure with 25% albumin will help draw in third-spaced flued and improve flood flow to the shunted areas. I will target an albumin >2.5g/dL. Diuretics, typically furosemide/bumetanide are used with a thiazide diuretic or spironolactone to reduce the preload.
Another way to remove fluid is to drain the ascitic fluid or pleural effusions that typically develop in these patients (1,2).
To make things more complicated, these patients are easily prone to hypovolemia with GI bleeding and third-spacing. I recommend ultrasound evaluation of the IVC, venous pulsatility, and the RV/pulmonary artery systolic pressures (3).
3. Inflammation:
In decompensated cirrhosis, there is an increase in inflammatory mediators which leads to vasodilation. Also, there is decreased blood flow to the adrenals and relative adrenal insufficiency is common. Due to this, stress dose steroids are used(1,2).
In the end, the treatment works by improving oncotic pressure, increasing splanchnic vasoconstriction, anti-inflammation, and diuresis/fluid removal.
Other adjunct treatments:
Positioning:
There is some evidence that supine positioning worsens the hyperdynamic profile and having the patient sit up or stand may be beneficial.
NSAIDs:
With COX-1 activation and an increase in prostaglandins leading to vasodilation, indomethacin has been shown to improve the hemodynamic profile. But, the bleeding risk and renal toxicity limit its use.
Figure 3: Treating Cirrhotic Shock
Summary:
It is time to add another shock profile to the list. Cirrhotic shock does not fit the four other previously described types of shock. Trying to fit cirrhotic shock into these categories will lead to worsening systemic ischemia or volume overload. Even when there is a suspected infection as the cause of the shock, helping improve the hemodynamics in these critically ill cirrhotic patients will make a big difference in the outcome. Start thinking about splanchnic steal syndrome and cirrhotic shock in cirrhotic patients in the ICU.
References:
1. Bolognesi M, Di Pascoli M, Verardo A, Gatta A. Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis. World J Gastroenterol. 2014;20(10):2555-2563. doi:10.3748/wjg.v20.i10.2555
2. Fukazawa K, Lee HT. Updates on Hepato-Renal Syndrome. J Anesth Clin Res. 2013;4(9):352. doi:10.4172/2155-6148.1000352
3. McAvoy NC, Semple S, Richards JM, et al. Differential visceral blood flow in the hyperdynamic circulation of patients with liver cirrhosis. Aliment Pharmacol Ther. 2016;43(9):947-954. doi:10.1111/apt.13571
4. Vora RS, Subramanian RM. Hypotension in Cirrhosis. Clin Liver Dis (Hoboken). 2019;13(6):149-153. Published 2019 Jul 2. doi:10.1002/cld.764