Let's talk about Cirrhosis! Learn about the signs and symptoms, the complications, and what you, as the nurse, can do about it.
Over 44,000 people die every year from cirrhosis, so it’s the 9th leading cause of death in the US. Cirrhosis is an incurable form of liver disease that happens slowly due to inflammation and scarring of the liver tissue. When you think of cirrhosis, think of scarring, or “Scarosis”. The main cause is chronic hepatitis C. The other two causes are: drinking too much alcohol, and nonalcoholic fatty liver disease. Nonalcoholic fatty liver disease is when too much fat gets stored in the liver cells, and this can be from obesity or diabetes.
So the liver cells get damaged, they try to fix themselves, but just wind up making scar tissue instead. So instead of having a nice, smooth liver, you’ve got a lumpy mess of a liver with constrictive bands that cut off the flow of blood and bile. Remember bile is made in the liver, and then has to go to the gallbladder to be stored.
So why do we care so much about the liver? What does it do for us?
Our liver detoxifies alcohol and drugs. It breaks down proteins and carbs, and steroid hormones. It makes blood clotting factors, so if your liver isn’t working, you’re gonna have a decrease in every coagulation factor, except factor 8. The liver makes blood proteins, like Albumin, and if you remember, Albumin is the main protein in your blood, and the main thing regulating your oncotic pressure, or the thing that’s keeping your fluids in your blood vessels, and not seeping out into the tissue. So when the liver isn’t making enough Albumin, we’re gonna see edema and ascites. Ascites is when too much fluid builds up in the peritoneal cavity, causing a big swollen belly.
A normal liver will store glucose as glycogen for later use, but with an impaired liver, we could see hypoglycemia or hyperglycemia cause the body’s having a hard time regulating the glucose levels. The liver makes bile, and bile absorbs fat and gets rid of bilirubin. Bilirubin is a yellow pigment that’s a byproduct of your old red blood cells getting broken down. A healthy liver will take that bilirubin and put it in your poop with bile to get rid of it. This is what makes your poop brown. So without that bile, your poop is gonna be pale and clay-colored, because you’re not getting rid of the bilirubin pigment, and that bilirubin is gonna keep building up building up and make your skin and the whites of your eyes yellow.
Let's talk about Cirrhosis! Learn about the signs and symptoms, the complications, and what you, as the nurse, can do about it.
Over 44,000 people die every year from cirrhosis, so it’s the 9th leading cause of death in the US. Cirrhosis is an incurable form of liver disease that happens slowly due to inflammation and scarring of the liver tissue. When you think of cirrhosis, think of scarring, or “Scarosis”. The main cause is chronic hepatitis C. The other two causes are: drinking too much alcohol, and nonalcoholic fatty liver disease. Nonalcoholic fatty liver disease is when too much fat gets stored in the liver cells, and this can be from obesity or diabetes.
So the liver cells get damaged, they try to fix themselves, but just wind up making scar tissue instead. So instead of having a nice, smooth liver, you’ve got a lumpy mess of a liver with constrictive bands that cut off the flow of blood and bile. Remember bile is made in the liver, and then has to go to the gallbladder to be stored.
So why do we care so much about the liver? What does it do for us?
Our liver detoxifies alcohol and drugs. It breaks down proteins and carbs, and steroid hormones. It makes blood clotting factors, so if your liver isn’t working, you’re gonna have a decrease in every coagulation factor, except factor 8. The liver makes blood proteins, like Albumin, and if you remember, Albumin is the main protein in your blood, and the main thing regulating your oncotic pressure, or the thing that’s keeping your fluids in your blood vessels, and not seeping out into the tissue. So when the liver isn’t making enough Albumin, we’re gonna see edema and ascites. Ascites is when too much fluid builds up in the peritoneal cavity, causing a big swollen belly.
A normal liver will store glucose as glycogen for later use, but with an impaired liver, we could see hypoglycemia or hyperglycemia cause the body’s having a hard time regulating the glucose levels. The liver makes bile, and bile absorbs fat and gets rid of bilirubin. Bilirubin is a yellow pigment that’s a byproduct of your old red blood cells getting broken down. A healthy liver will take that bilirubin and put it in your poop with bile to get rid of it. This is what makes your poop brown. So without that bile, your poop is gonna be pale and clay-colored, because you’re not getting rid of the bilirubin pigment, and that bilirubin is gonna keep building up building up and make your skin and the whites of your eyes yellow.
Cirrhosis
Welcome back to the Nursing School Week by Week podcast. My name is Melanie, and I am so glad you joined me cause today we’re talkin about Cirrhosis. Over 44,000 people die every year from cirrhosis, so it’s the 9th leading cause of death in the US. Cirrhosis is an incurable form of liver disease that happens slowly due to inflammation and scarring of the liver tissue. When you think of cirrhosis, think of scarring, or “Scarosis”. The main cause is chronic hepatitis C. The other two causes are: drinking too much alcohol, and nonalcoholic fatty liver disease. Nonalcoholic fatty liver disease is when too much fat gets stored in the liver cells, and this can be from obesity or diabetes.
So the liver cells get damaged, they try to fix themselves, but just wind up making scar tissue instead. So instead of having a nice, smooth liver, you’ve got a lumpy mess of a liver with constrictive bands that cut off the flow of blood and bile. Remember bile is made in the liver, and then has to go to the gallbladder to be stored.
So why do we care so much about the liver? What does it do for us?
Our liver detoxifies alcohol and drugs. It breaks down proteins and carbs, and steroid hormones. It makes blood clotting factors, so if your liver isn’t working, you’re gonna have a decrease in every coagulation factor, except factor 8. The liver makes blood proteins, like Albumin, and if you remember, Albumin is the main protein in your blood, and the main thing regulating your oncotic pressure, or the thing that’s keeping your fluids in your blood vessels, and not seeping out into the tissue. So when the liver isn’t making enough Albumin, we’re gonna see edema and ascites. Ascites is when too much fluid builds up in the peritoneal cavity, causing a big swollen belly.
A normal liver will store glucose as glycogen for later use, but with an impaired liver, we could see hypoglycemia or hyperglycemia cause the body’s having a hard time regulating the glucose levels. The liver makes bile, and bile absorbs fat and gets rid of bilirubin. Bilirubin is a yellow pigment that’s a byproduct of your old red blood cells getting broken down. A healthy liver will take that bilirubin and put it in your poop with bile to get rid of it. This is what makes your poop brown. So without that bile, your poop is gonna be pale and clay-colored, because you’re not getting rid of the bilirubin pigment, and that bilirubin is gonna keep building up building up and make your skin and the whites of your eyes yellow.
The liver also normally changes ammonia to urea so it can be eliminated through your urine. Ammonia is a byproduct that we get when our body breaks down proteins, but with cirrhosis, the liver can’t metabolize proteins very well, so we’re gonna see an increase in that toxic ammonia. Ammonia is in all kinds of things that you use to clean your house, like toilet bowl cleaners, so no, you don’t want a bunch of this in your body.
So, what makes someone more likely to get cirrhosis? Having a drug habit that involves needles, since hepatitis C is the main cause of cirrhosis, and the main way people get the hepatitis C virus is by sharing needles with someone else who has it.
Also, drinking too much alcohol. For men, “too much” is about 1 ½ ounces of alcohol a day, so that’s about 3 cans of beer, or 3 shots of hard liquor, or 3 glasses of wine a day. For women, it’s less, since women’s livers are easily damaged by alcohol. So “Too much” alcohol for a woman is about half of what a man can drink.
So what are we going to see in a patient with cirrhosis? We could see jaundice, or the yellowing of the skin and eyes. Peripheral edema or even ascites because the liver isn’t making enough albumin, so the fluid is seeping out into the tissue instead of staying in the blood vessels where it belongs. The patient could have an extra large liver and spleen, called “hepatosplenomegaly”. We could see “gynecomastia”, which I call “man-boobs”. This is when a man gets swelling of his breast tissue, and this is because the liver isn’t metabolizing hormones like normal, and there’s an increase in estrogen. In women, we might see them having irregular periods. This buildup of estrogen can also make the palms of their hands turn red, and this is called “palmar erythema”. We may also see something called “spider angiomas” due to the extra estrogen. These are clusters of blood vessels that you’ll see just under the skin on chest, face, neck, and shoulders, and they look like a spider's web with a bright red center.
In the cirrhosis patient, we may also see a severe change in their level of consciousness because of the toxic ammonia building up in their body, and I’ll talk about this more in a minute.
For our initial assessment of this patient, we want to look at the color of their skin and eyes, we want to do a full abdominal assessment including looking for ascites and feeling for abdominal pain. We want to do a neurological assessment and get a full set of vitals. Do they have a history of liver disease? Are they heavy drinkers or do they have an injection drug habit?
So what are some complications of cirrhosis? Or, what are some more bad things that can happen because of cirrhosis? Because the liver tries to fix itself and builds up a bunch of scar tissue, it puts pressure on the hepatic veins and blocks them off, so blood can’t flow properly through the liver. This blood starts to back up into the portal vein and causes increased blood pressure in the portal vein. We call this “portal hypertension.” This blood backs up into the GI circulation, in the esophagus, rectum, and abdomen, and these blood vessels aren’t meant to handle high pressures, so they get weak, and can easily break open and bleed out. We call these weak veins that are swollen with blood “esophageal varices” if they’re in the esophagus, and “gastric varices” if they’re in the stomach. If these rupture, it’s a life-threatening emergency. This is really scary, because these patients will literally be spewing blood from their throat, and they can lose liters of blood in a matter of minutes.
So, what would be done for this patient, with esophageal varices? First of all, we want to prevent them from rupturing, so they could have an upper endoscopy done, which is where the doctor puts a tiny camera that’s attached to a long flexible tube down their throat to look for these varices. If varices are seen, they’ll usually put the patient on a beta-blocker, like Nadolol, because remember beta-blockers are gonna decrease blood pressure, and that’s exactly what we want to prevent these varices from rupturing. The doctor may also use endoscopic band ligation or sclerotherapy to reduce the risk of bleeding. Endoscopic band ligation, or just “banding” is when the doc puts an elastic band around the base of the bulging vein, so no more pressure will go into it. Sclerotherapy is something that’s also used to treat varicose veins, but it’s where the doctor injects medicine into the vein, and it makes them shrink.
Another way that we can decrease portal hypertension is by creating another pathway for blood to go past the liver. This is done with a TIPS procedure. TIPS stands for transjugular intrahepatic portosystemic shunt, and this is when a shunt is placed to create a clear pathway for blood to bypass the diseased liver and go straight from the portal vein to the hepatic vein in the liver. This is just a short-term solution to hold a patient over until they can get a liver transplant, since it increases the risk of getting hepatic encephalopathy because the blood is bypassing the liver, so even less of the blood is getting metabolized by the liver, which means even more ammonia is being created.
But what do we do if the esophageal varices actually rupture, and the patient is bleeding from the mouth? First of all, don’t panic. Call for help. If the bleeding is uncontrollable, a balloon tamponade will be placed. You may also hear this called a Sengstaken-Blakemore tube. This is a long tube that’s inserted through the nose or mouth, and has two balloons on it, one that inflates in the stomach, and one that inflates in the esophagus. The balloon that inflates in the esophagus puts mechanical pressure on the veins to stop the bleeding. A balloon tamponade is only a short-term solution since the longer it’s left in, the more the patient is at risk for obstruction of the airway, aspiration, and tissue ischemia. The patient will also be given a blood transfusion to replace the blood that they lost, as well as fresh frozen plasma, since FFP has a ton of clotting factors in it that they’ll definitely need. They may also get octreotide given IV to control the bleeding. Octreotide works by inhibiting the release of glucagon, which is a natural vasodilator.
Another complication often seen with cirrhosis patients is hepatic encephalopathy. I mentioned earlier that because the liver is not metabolizing proteins the way a healthy liver would, there is a buildup of ammonia. This ammonia can actually cross the blood brain barrier and cause severe changes in personality, inappropriate behavior, seizures, coma, and even death if left untreated. This change in mental status is not simply confusion, but worse than that. I heard of one patient who had hepatic encephalopathy for about 5 days, and the whole time she was in the hospital, she thought there was a baby crying in the hospital room with her. She thought the baby needed to be fed or something, but there was nothing she could do to help. Can you imagine? And many of these patients have no recollection of what happened to them while they were in that state. It’s like they just lost days of their lives. Blood tests are often done to show the patient’s ammonia level. One of the first signs of hepatic encephalopathy is if the patient changes their sleep patterns, like they are suddenly sleeping during the day and staying up all night. A more severe symptom of hepatic encephalopathy is called “asterixis” or “liver flap.” You’ll know a patient has asterixis if you tell them to put their hands out in front of them, like they’re stopping a bus, then you push back against their hands briefly. If they have asterixis, they will then start flapping their hands up and down uncontrollably. This is due to the effect that the increased ammonia has on the basal ganglia in the brain, which controls posture and movement.
We treat hepatic encephalopathy mainly with lactulose. Lactulose is an osmotic laxative that works by pulling ammonia into the colon, where it’s then put into poop and excreted.
Some diagnostic tests for cirrhosis involve blood work, and this would include a liver function test, or LFT, a complete blood count, or CBC with platelets, so this will look at the white blood cell count, red blood cell count, hemoglobin, hematocrit, and the number of platelets. Remember the liver makes the coagulation factors needed for the clotting cascade, so if the liver isn’t working right, your platelet count will be low, or less than 150,000 per microliter. So a cirrhosis patient is automatically going to be put on bleeding precautions, and along with this, we’ll need to monitor their INR, or International Normalized Ratio to see how quickly their blood is clotting.
The patient’s blood will also be tested for bilirubin, that yellow-pigment that is released when the body destroys old RBCs, and it’ll be tested for the plasma protein, Albumin. They’ll also look at the level of ammonia in the blood, and the serum glucose because they could be hypoglycemic or hyperglycemic, since the liver isn’t storing glycogen properly.
So, real quick, the things that will be higher than normal in the blood are: the LFT, the ammonia, bilirubin, and the INR.
The things that’ll be lower than normal are: The protein albumin, Platelets, WBCs, and RBCs.
In addition to blood tests, the cirrhotic patient will probably have an ultrasound done on their abdomen, and a liver biopsy for a definitive diagnosis, and to test for liver cancer.
So how are we going to treat someone with cirrhosis? Unfortunately, it’s irreversible. Cirrhosis is end-stage liver disease, so there’s no cure, but the goal is just to slow down the formation of scar tissue, and delay further damage to the liver. We’re going to support their nutrition, we want to teach them to eat a high carb diet with low fat, and make sure they’re getting enough calories. These patients can suffer from malnutrition, especially if their cirrhosis was caused by alcoholism, cause they’ve been drinking way more than they’ve been eating. We will remind them that they can’t drink alcohol, obviously, and they also need to make sure they’re not using any drugs that are metabolized by the liver. So they can’t even use acetaminophen or Tylenol, because it’s metabolized by the liver, and would be toxic to their already sick liver.
These patients have edema and possibly ascites in their abdomen because of the low albumin levels, so we’re gonna restrict their sodium intake to less than 2 grams a day, put them on fluid restrictions, and give them diuretics to get rid of some of that extra fluid that they're retaining. If the patient has severe ascites, they may need a paracentesis procedure done. This is when the doctor puts a long needle into their peritoneum to drain out the fluid. And it’s super important that we maintain sterility during this procedure, since this puts patients at a big risk for getting a spontaneous bacterial peritonitis infection, and that would be very bad. I mean, we never want our patients to get an infection, but these patients with cirrhosis are already immunocompromised because they’ve got a low white blood cell count, so we want to maintain that sterile field during a paracentesis.
We are going to be taking daily weights on our cirrhosis patients, and if we suspect ascites, we’ll need to measure their abdominal girth every day to see if it’s getting bigger; this is done by wrapping a tape measure under the patient’s back, and then up over the widest part of their belly. We will document their I’s & O’s, and monitor for any changes in level of consciousness, as that could indicate hepatic encephalopathy. And finally, we’re gonna watch for signs of bleeding, and this can show itself a few different ways. We could see blood in their vomit, and this is called hematemesis (heemuhtehmuhsuhs), or we could see it in their stool, and this is hematochezia (heemuhtuhkeezia), or black tarry stool, which would indicate an upper GI bleed; lightheadedness, or fainting.
If the patient is showing signs of hepatic encephalopathy, they’ll be given lactulose to get rid of some of that ammonia through their feces.
Pop Quiz!
The answer is b, ascitic fluid. This is the fluid that builds up when a person has ascites, which causes abdominal swelling.
The answer is a, lactulose. Lactulose is an osmotic laxative that pulls ammonia into the stool and then gets rid of it. Beta-blockers are used to lower the blood pressure and prevent esophageal varices from rupturing, and the Octreotide is used to control varices that are already bleeding.
The answer is b, coagulation defects, because the liver is not making enough clotting factors, so these patients will be at risk for bleeding.
The answer is c, increased ammonia level, since this is known to cause severe mental changes.
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