Cirrhosis: Clinical sciences

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Introduction0:00–1:14

Cirrhosis refers to chronic progressive fibrotic changes of the liver parenchyma that occur in response to chronic injury and inflammation.
A variety of conditions can cause this injury, including viral hepatitis, chronic alcohol use, autoimmune disease, and hereditary conditions like hemochromatosis or alpha-1 antitrypsin deficiency, and the ensuing fibrotic changes eventually impair liver function.
Early in the disease process, cirrhotic patients remain relatively asymptomatic and are considered to have compensated cirrhosis, while those who present with symptoms are considered to have decompensated cirrhosis.
Complications due to cirrhosis include spontaneous bacterial peritonitis, ascites, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome, which can be life-threatening, therefore it’s important to quickly identify these patients who may suddenly decompensate.Now, if you suspect cirrhosis, first perform an ABCDE assessment to determine if your patient is unstable.

Unstable patient1:14–5:08

Keep in mind that cirrhosis is never unstable unless it's decompensated and the patient develops complications. If this is the case, you may need to secure the airway, breathing, and circulation, which might require intubating the patient, and starting mechanical ventilation.
Next, obtain IV access and, if your patient is hypotensive, start IV fluids for volume resuscitation. If there are signs of blood loss, they might even need a transfusion of blood products, such as packed red blood cells, platelets, and even fresh frozen plasma.
You should also continuously monitor vital signs. Additionally, if you suspect decompensated cirrhosis complications, it’s important to identify the underlying cause and complication.
To do so, start by performing a focused history and physical examination, and depending on the suspected complication, you may want to order labs or ultrasound.Alright, if your patient presents with abdominal distension and a palpable fluid wave, and ultrasound reveals free fluid in the peritoneal cavity, that’s ascites.
On the other hand, if your patient has fever and abdominal pain, and labs reveal a positive ascitic fluid culture with PMN predominance, your patient has spontaneous bacterial peritonitis.
If you notice signs of blood loss, such as melena, hematochezia, and hematemesis, with anemia on labs, think of variceal bleeding.
If instead your patient presents with neurologic signs, such as altered mental status and flapping tremor, also known as asterixis, that’s hepatic encephalopathy.
Lastly, if your patient has dark urine and oliguria, and their labs show elevated creatinine, but there’s no evidence of an intrinsic kidney disease, you should think of hepatorenal syndrome, keeping in mind that it’s a diagnosis of exclusion.
Once you’ve identified your patient’s specific complication, the management includes treatment of the underlying cause and complication, including consulting the appropriate specialists and the surgical team.
For definitive treatment, consider liver transplantation.Now, here’s a clinical pearl to keep in mind! Active variceal bleeding in a cirrhotic patient carries a high mortality rate and can be challenging to manage.
Not only is the presence of variceal bleeding associated with advanced disease in the first place, but variceal bleeding, by its very nature, is under increased pressure from portal hypertension.
Further, cirrhotic patients typically have coagulopathy and thrombocytopenia, so their ability to clot is impaired, and gaining control of the bleeding is not easy.
Hypotension and hemorrhagic shock may ensue, and volume resuscitation is challenging since albumin is already low. So, you should use colloids, albumin, and blood products to achieve hemodynamic stability.
Finally, immediately call the endoscopy team to stop the bleeding.Ok so let’s go back to the ABCDE assessment where your patient is instead stable and cover compensated cirrhosis.

Stable patient5:08–14:36

First, obtain a focused history and physical examination, as well as labs, including CBC, CMP, PT, PTT, and possibly ammonia level.
In compensated cirrhosis, the remaining healthy liver parenchyma is still able to compensate for systemic demands of liver function.
As a result, these patients are usually asymptomatic, and they haven’t developed overt complications from cirrhosis; some may present with varices, but they haven’t had any episodes of variceal bleeding.
Now, since these patients are asymptomatic, they may come to clinical attention on routine lab evaluation. Lab findings might include elevated hepatic transaminases AST and ALT, alkaline phosphatase or ALP, bilirubin, clotting studies like PT and PTT, and ammonia levels; as well as decreased albumin and thrombocytopenia.
The combination of these signs, symptoms, and lab findings should lead you to suspect compensated cirrhosis. To confirm the diagnosis, obtain an abdominal ultrasound, as well as ultrasound with elastography.
Additionally, you can obtain a liver biopsy, which is the gold standard for diagnosis. Abdominal ultrasound will reveal a small nodular liver, as well as the absence of ascites, while ultrasound with elastography may show increased liver stiffness.
Lastly, liver biopsy is not always done, but it may help confirm the diagnosis by showing regenerative nodules and fibrotic tissue.
Okay, now that you’ve confirmed the diagnosis of compensated cirrhosis, let's turn our attention to management. First, you’ll want to treat the underlying cause of cirrhosis.
For example, if your patient has viral hepatitis, start them on antiviral medications; or if they use alcohol, encourage abstinence and get them specialty treatment for alcohol use disorder.
Also be sure to encourage additional lifestyle modifications, like weight loss for those with steatohepatitis, as well as avoiding heavily processed foods, and limiting hepatotoxic and nephrotoxic medications, like NSAIDs.
Offer vaccination for Hepatitis A and B, and screen for hepatocellular carcinoma every 6 months by obtaining an ultrasound with or without measuring blood concentrations of alpha-fetoprotein.
You should also screen for esophageal varices at the time of diagnosis and every 2 to 3 years thereafter. In addition, calculate your patient’s MELD-Na score and Child-Pugh scores.
Lastly consult the surgical team for transfer to a transplant center as your patient could be a candidate for liver transplant.
Transplant is the only definitive treatment for cirrhosis. On the other hand, let’s take a look at decompensated cirrhosis.
Here, a patient with previously compensated cirrhosis develops an acute deterioration in liver function and progresses to decompensated cirrhosis.
As a result, their focused history and physical examination may reveal symptoms like progressive abdominal fullness, anorexia, and weight loss, as well as weakness, fatigue, confusion, and even prior episodes of overt complications like variceal bleeding.
Additionally, physical findings might include jaundice, palmar erythema, spider angiomata, and a distended abdomen with a palpable fluid wave suggestive of ascites.
Lab findings might include elevated hepatic transaminases, AST and ALT, alkaline phosphatase or ALP, bilirubin, clotting studies like PT and PTT, and ammonia levels; as well as decreased albumin and thrombocytopenia.
Now, here’s a high-yield fact to keep in mind! The hepatic transaminases are elevated in a variety of liver disorders, besides cirrhosis, and indicate the presence of hepatocellular injury.
However, they are a poor indicator of the degree of liver fibrosis and do not correlate with the severity of clinical manifestations.
In fact, in advanced cirrhosis, most of the viable hepatocytes have been replaced by fibrotic tissue, meaning that the liver releases less AST and ALT.
Therefore, while we should check these values when performing a workup for cirrhosis, we should not use them for diagnosis or prognosis of cirrhosis.
Now, the presence of this spectrum of signs, symptoms, and lab findings should lead you to suspect decompensated cirrhosis.
To confirm this diagnosis, obtain an abdominal ultrasound, as well as ultrasound with elastography, and perform a diagnostic paracentesis followed by laboratory analysis of the ascitic fluid, including albumin and total protein levels.
Finally, you can obtain a liver biopsy, which represents the gold standard for diagnosis. Abdominal ultrasound will reveal a small nodular liver, and in some patients could reveal ascites, while ultrasound with elastography may show increased liver stiffness.
Next, use the ascitic fluid results to calculate the Serum Ascites Albumin Gradient, or SAAG, and check total ascitic protein levels.
SAAG equal to or greater than 1.1, along with a total ascitic protein of less than 2.5 g/dL, are suggestive of ascites due to portal hypertension from cirrhosis.
While not necessary in all cases, liver biopsy can confirm the diagnosis by showing fibrotic tissue and regenerative nodules.
Okay, now that you’ve confirmed the diagnosis of decompensated cirrhosis, let's turn our attention to management. First, be sure to give appropriate management of their specific complications.
For instance, manage ascites with diuretics and therapeutic paracentesis, which is used to remove fluid from the peritoneal cavity.
Also, encourage lifestyle modifications, such as salt restriction to help prevent further fluid accumulation, and consider starting the patient on albumin replacement.
Once you’ve addressed the patient’s complications, you’ll want to treat the underlying cause of cirrhosis. For example, if your patient has viral hepatitis, start them on antiviral medications; or if they use alcohol, encourage abstinence and get them specialty treatment for alcohol use disorder.
Also be sure to encourage additional lifestyle modifications, like weight loss for patients with steatohepatitis, as well as avoiding heavily processed foods, and limiting hepatotoxic and nephrotoxic medications, like NSAIDs.
Offer vaccination for Hepatitis A and B, and screen for hepatocellular carcinoma every 6 months by obtaining an ultrasound with or without measuring blood concentrations of alpha-fetoprotein.
You should also screen for esophageal varices at the time of diagnosis and every 2 to 3 years thereafter, as cirrhosis with associated portal hypertension increases the risk of variceal bleeding.
Lastly, calculate your patient’s MELD-Na and Child-Pugh scores, and consult the surgical team for potential liver transplant.Alright, as a quick recap… Cirrhosis is chronic liver damage from a hepatocellular injury that results in scarring, fibrosis, and compromised liver function.

Review14:36–16:39

Early in the disease process, cirrhotic patients remain asymptomatic and are considered to have compensated cirrhosis, while patients who develop decompensated cirrhosis present with symptoms and complications, such as ascites, spontaneous bacterial peritonitis, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome.
If suspecting cirrhosis, first do an ABCDE assessment to determine whether the patient is unstable or stable. If unstable, it’s decompensated cirrhosis, so first stabilize the airway, obtain IV access, and start fluid resuscitation.
Next, perform history and physical, and order labs and ultrasound to identify complications. Once identified, treat the complications and consult surgery for a possible liver transplant.
On the other hand, stable patients can have compensated or decompensated cirrhosis. To differentiate them, assess for the presence of symptoms and complications, and confirm the diagnosis by obtaining abdominal ultrasound, ultrasound with elastography and liver biopsy, as well as diagnostic paracentesis if decompensated.
Cirrhosis management includes treating the underlying cause, as well as educating patients on lifestyle modifications, vaccinating against hepatitis A and B viruses, and screening for complications.
In addition, consult for liver transplant. Finally, patients with decompensated cirrhosis require
Cirrhosis: Clinical Sciences: Video and Causes | Osmosis