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The gut-liver axis is now being viewed as a key pathophysiological mechanism leading to complications of cirrhosis. Physicians should be aware of evidence-based medicine regarding how this axis may influence the development of these complications in order to apply this information to practice and improve patient health.

Malnutrition and poor nutritional status in cirrhotic patients is associated with a worse prognosis. Therefore, early intervention to correct nutrient deficiency can prolong life expectancy, improve quality of life, reduce complications, and increase the probability of successful transplantation. Complications of cirrhosis place an enormous toll on both the patient and the health care system. Applying quality measures and addressing specific clinical variables may improve health-related quality of life while reducing the burden of the disease and re-hospitalization rates.

The breakdown of gut-liver axis equilibrium plays a central role in the development of immune disorders involving the small bowel and liver. The gut-liver axis in cirrhosis and portal hypertension is gaining increasing attention as a key pathophysiological mechanism responsible for progression of liver failure and development of complications such as spontaneous infections, HE, and hepatocellular carcinoma. Bacterial overgrowth is common in cirrhosis. Bacterial translocation is thought to cause spontaneous bacterial peritonitis.

Bacterial infection is one of the most frequent complications in cirrhosis and results in high mortality rates. Patients with cirrhosis have altered and impaired immunity, which favors bacterial translocation.

Hepatic encephalopathy | Gastroenterology Report | Oxford Academic

Lipopolysaccharide LPS , a component of the gram negative bacterial cell wall, also translocates into the bloodstream through permeable tight junctions of the gut. This is thought to be one possible trigger of splanchnic vasodilation in the hyperdynamic circulatory state of portal hypertension. The frequency of HE is unrelated to the etiology of cirrhosis. However, increased severity and frequency of encephalopathic episodes are associated with an increased risk of death. Stage 0 applies to those with no detectable abnormalities.

Stage I is classified by anxiety, lack of awareness, decreased attention span, and impaired addition or subtraction. Stage II is characterized by personality changes, inappropriate behavior, loss of time orientation, and lethargy. Stage III patients are confused, with gross disorientation and bizarre behavior, confusion, and somnolence. Patient was the restrained driver with no other passengers in the vehicle.

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He had no loss of consciousness and is GCS 14 on arrival. Patient has no obvious signs of trauma.

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Physical exam reveals a distended abdomen with large veins, gynecomastia, and palmar erythema. There are no focal neurologic deficits, but he is confused. No family is present to provide past medical history. Basic labs are remarkable for hemoglobin CT head is negative. Hepatic encephalopathy HE is a broad spectrum of neuropsychiatric symptoms in a patient with underlying liver disease or porto-systemic shunting 1. Along with exploration of the mechanism of hepatic encephalopathy, this post evaluates commonly missed precipitants of HE in the cirrhotic patient and treatment pearls for the emergency physician.

Increased nitrogen load, decreased toxin clearance, and neurotransmitter alteration are significant contributors to HE. Ultimately, the pathophysiology of hepatic encephalopathy is thought to originate from toxic effects of ammonia, created by bacterial metabolism of protein breakdown in the gut. Ammonia is typically degraded by the liver and excreted by the kidneys. In liver dysfunction, ammonia is allowed to accumulate and readily crosses the blood-brain-barrier, where it is converted to glutamine. This causes astrocyte swelling and cerebral dysfunction 2.

Hepatic encephalopathy is a costly and prevalent disease in the United States and portends a poor prognosis. The Centers for Disease Control estimates 4.

Hepatic Encephalopathy: Information for Patients with Liver Disease

A study extrapolating information from the National Health And Nutrition Examination Survey data conducted between and concluded that over , adults in the United States during that time had cirrhosis 4. With sweeping epidemics of hepatitis C related to IVDU over the last decade, these numbers likely represent an underestimation of data for and beyond. Patients who have grade 3 or 4 HE at the time of their liver transplant have statistically significantly lower 1-year and 5-year survival rates than their counterparts without high grade HE 7.

Correct identification and management of HE can significantly impact the health outcomes of over half a million people. Because HE is frequent, debilitating, recurrent, and associated with poor survival, it is important to highlight clinical pearls and remember that it is often a diagnosis of exclusion.

Maintaining a broad differential is important, and keeping these pearls in the back of your mind may help you correctly identify HE. There are a number of scores used for both HE and cirrhosis.

Hepatic encephalopathy: current challenges and future prospects

The West Haven criteria is the current gold standard for evaluating severity of HE, although there can be some subjectivity when grading 8. There are cognitive and motor testing strategies used by providers, typically not in the ED, that can help assess stages as well. As mentioned previously, detecting HE early can be critically important. Some of the first early clinical signs include mild personality changes like irritability, disinhibition, or apathy. Sleep disturbances can often be detected with excessive daytime sleepiness and yawning.

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  • Minor impairments can lead to falls, impaired driving, and overall decreased quality of life. Motor disturbances typically begin after this in stages Asterixis is common but asterixis of other body parts can be detected as well including of the feet, legs, arms, tongue and eyelids.

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    • Extrapyramidal symptoms and Parkinsonian-like features may also occur. Although rare, focal neurologic deficits, most commonly hemiplegia, can occur with normal imaging 8. Ammonia can be obtained but should be interpreted in the broader clinical context. Liver patients frequently exhibit coagulopathy and thrombocytopenia, so a low threshold to order CT head even in the absence of significant trauma is reasonable 5 , 8 , 9.

      Though the pathophysiology of HE is thought to center heavily on accumulation of ammonia within the CNS, it is a common misconception that an elevated ammonia level can be used solely to diagnose HE. Rather, HE is a diagnosis of exclusion that should be made clinically after alternative explanations for altered mental status AMS are ruled out.

      The relation of ammonia elevation to degree to cerebral dysfunction has proven weak at best. Ammonia can lead to both false positive and false negative results. One study by Gundling and colleagues of 59 patients found results of ammonia testing were inaccurate in The same study found that a significant number of patients with grades 3 and 4 HE had normal or only mildly elevated ammonia levels The authors concluded that a single ammonia level had little utility in diagnosing HE.

      Yet another study found that of patients with clinical HE only The method of collecting a blood sample for ammonia can also variably affect the sample Ammonia may be falsely elevated in the case of difficult venipuncture, not placing the sample immediately on ice, or delayed time to analysis due to spontaneous release of ammonia by red blood cells in standing samples 14 , Some liver experts even suggest that ammonia does not add any diagnostic or prognostic value to patients with HE, and therefore does not need to be routinely checked 8.

      Rather than rely on ammonia level, we suggest thorough history and physical examination in conjunction with search for inciting factors for HE and alternative explanations for AMS. It is important to identify common precipitants and understand their pathogenesis in order to correctly identify, diagnose, and address the underlying precipitant. The most common precipitants of HE previously reported are GI bleed and infection 18 , A recent study by Pantham and colleagues sought to examine the frequency of most common precipitating factors resulting inhospitalizations.

      The most common causes of mortality in this group of patients was infection, GI bleed, and multi-organ dysfunction. Patients with underlying chronic liver disease, particularly advanced liver disease, have a dysfunction of host defense mechanisms including immunological deficits in factors produced by the liver specific complement factors and immunoglobulins It has been reported that neutrophil dysfunction and macrophage dysfunction occur in liver disease, contributing to a reduction in bacterial clearance by the liver A dysregulation of inflammatory cytokines has also been shown to exist in underlying liver disease, and are exacerbated by underlying infection 9.

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      In this setting, proinflammatory cytokines likely enhance ammonia production, contributing to the development of HE 9. Patients with underlying liver disease are more susceptible to developing an infection, with a decreased ability to fight infection, and infections aggravate liver damage in an already damaged liver. Although outside the scope of an ED provider to understand the pathogenesis of infection in HE in detail, it is important to appreciate the complexity and thus value in early diagnosis and treatment considering the high risk of mortality due to infection in cirrhotic patients.

      Additionally, length of stay in patients with HE triggered by infection is longer, highlighting the impact on morbidity as well as mortality Finally, a few studies have examined the most common infections identified in HE, and some debate exists. For the purpose of ED diagnosis, it is important to recognize the most commonly reported including respiratory tract infection Pneumococci, Pseudomonas , urinary tract infection E. The hydration status of patients with liver disease is challenging to balance but vital to maintain.

      Triggers of dehydration include aggressive diuresis, lactulose related diarrhea, large volume paracentesis, poor PO intake, and overdiuresis post transjugular intrahepatic portosystemic shunt TIPS procedure 20 , 21 , Additionally, many patients with liver disease have diabetes as a comorbidity, placing them at greater risk of dehydration Dehydration can lead to acute kidney injury, which is critical in patients with liver disease who are at risk of developing hepatorenal syndrome.

      Further, even in mild cases of HE, fluid intake declines and maintaining appropriate oral intake can be challenging, contributing to dehydration. In patients with liver disease who experience dehydration, there is typically a reduction in renal perfusion and glomerular filtration rate, which lead to a decrease in excretion of ammonia and urea and thus increased circulating levels of ammonia The kidneys can be overlooked in ammonia hemostasis but are an important contributor as they maintain acid-base hemostasis.

      For example, they play an important role in the pathogenesis of HE in the setting of hypokalemia. Decreasing levels of potassium cause an increase in the release of hydrogen ions, thus indirectly generating ammonia. Hypokalemia can be traced back to excessive stooling from lactulose in patients with liver disease and subsequent dehydration A study by Bajaj and colleagues demonstrated that lactulose induced diarrhea was associated with recurrent HE and was associated with prerenal azotemia and dehydration The exact mechanisms are still under review 25 , Dehydration, also common in HE and liver disease, can also exacerbate constipation.

      Can My Patient Drive?