What the nurse needs to know about the liver
The liver is a powerhouse of an organ and has many functions which are vital for survival. Today we’re looking at how the liver is structured, what it does, and how we as veterinary nurses can support our hepatic disease patients in practice. Ready to jump in? Let’s go…
Anatomy
The liver is actually the largest gland in the body; it is located in the cranial abdomen and has a unique shape, in order to fit between the stomach and diaphragm. In cats and dogs the liver is made up of six lobes – the left medial, left lateral, right medial, right lateral, quadrate and caudate lobes. These lobes are further divided into lobules; each lobule is wedge-shaped and is made up of hepatocytes, Kupffer cells, sinusoids, a bile channel and a ‘portal triad’ (a bile duct, a branch of the hepatic artery and a branch of the portal vein). The lobules are arranged around a central vein in a hexagonal pattern.
The liver has a unique network of blood vessels called the hepatic portal system; these receive oxygenated and deoxygenated, waste-product containing, blood from the digestive system. Around 80% of the liver’s blood supply comes from the gastrointestinal tract; blood from the GI tract does not directly enter the vena cava to return to the heart and lungs, as it must first be filtered. This filtration occurs in the liver, and so the blood flows from the GI tract to the liver, through the hepatic portal vein. From the hepatic portal vein, the blood flows through the hepatic lobules where it is filtered. The deoxygenated blood from the GI tract is rich in nutrients (from the food which the body has just digested) and provides direct nourishment to the hepatocytes whilst it flows through the liver lobules. Specialised cells within the lobules (known as Kupffer cells) are responsible for the removal of bacteria and other pathogens.
In addition to the filtration of blood through the liver, the hepatocytes also secrete a number of different hormones, as well as bile acids and pigments. These bile components are secreted into channels known as bile canaliculi. These channels merge together to form intrahepatic bile ducts, which in turn merge into the left and right bile duct, and then the common bile duct. The common bile duct connects the liver, gall bladder and small intestine. Bile is stored in the gall bladder and released into the duodenum and plays a vital role in fat breakdown and digestion.
As an animal ages, their liver actually atrophies; the liver of an adult will, therefore, weigh less and be a smaller size than a younger animal.
Functions
The liver is responsible for a lot of vital functions within the body, including:
Filtration of blood from the GI tract
Metabolism/elimination of waste products, medications and toxins from the GI tract
Synthesis of bile
Synthesis of coagulation factors
Processing and removal of expired or damaged blood cells
Storage of glucose (as glycogen)
Synthesis of plasma proteins (albumin)
Breakdown of amino acids to provide energy or create enzymes (deamination)
Conversion of ammonia (a waste product created as a result of protein breakdown) into urea
Metabolism of lipids (synthesis of cholesterol and the production of triglycerides)
Regulation of platelet production
Breakdown of hormones within the body
Diagnostic testing in liver patients
Several diagnostic tests are commonly performed in patients with suspected liver disease. These include:
Biochemistry
Several parameters on our biochemistry panels tell us about the liver. Changes in ALT, ALP, GGT, AST, Total Bilirubin, Cholesterol, Glucose, Albumin, Bile Acids, Ammonia and Urea can all be seen in patients with various liver disorders.
Bile Acid Stimulation Test
The BAST is a dynamic test which involves taking a baseline, fasted serum sample, then feeding the patient and taking a repeat sample 2-hours after eating. Because bile acids are absorbed in the intestine and transported to the liver for processing, measuring bile acid levels is a good indicator of liver and biliary tract function.
Coagulation Times
Because of the liver’s role in synthesising coagulation factors, coagulopathies may be seen in cases of liver disease. Performing coagulation time testing is advisable in hepatic patients, particularly where aspirates or biopsies of liver tissue may be required.
Diagnostic Imaging
Ultrasonography is commonly performed in patients with suspected hepatic disease. This allows evaluation of the hepatic tissue and structure, identification of masses/nodules, and evaluation of the hepatic vasculature. Colour flow Doppler can be used to evaluate blood flow and, in some cases, highlight abnormal vessels such as portosystemic shunts.
Guided aspirates or biopsies can also be taken from the liver using ultrasonography.
Computed tomography or fluoroscopy may also be used to identify abnormal vessels e.g. where a portosystemic shunt is suspected. This can be achieved through the administration of contrast medium, either intravenously or at time of surgery, through catheterisation of a mesenteric vessel (portovenography).
Selected liver diseases
Hepatitis
Hepatitis is inflammatory liver disease; this can be acute or chronic.
Acute hepatitis is often severe and the onset of clinical signs is rapid. It can be caused by viral, bacterial, fungal or protozoal pathogens, or due to immune-mediated disease; infectious causes include leptospirosis and adenovirus.
Clinical signs may include vomiting, diarrhoea, anorexia, lethargy and depression, and jaundice and dehydration may be evident on clinical examination. Abdominal pain is often also present, and in severe cases, signs of coagulopathy (bruising, epistaxis, melena, prolonged haemorrhage from venepuncture sites) or neurological abnormalities (dull mentation, seizures, visual deficits) may be seen.
Chronic hepatitis generally has a subclinical phase of varying duration; often, when the patient presents with clinical signs, the disease is already at an advance stage and generally responds poorly to treatment. The exact cause of chronic hepatitis is unknown, but a genetic component is hypothesised, with several breeds (Dobermans, cocker spaniels and Labrador retrievers) predisposed to the condition.
Clinical signs of chronic hepatitis are variable and generally slow in onset. Lethargy, weight loss, PU/PD, vomiting and anorexia are commonly reported. As the disease progresses, the liver becomes irregularly-shaped and small, and abdominal effusion may be apparent. Jaundice may also be seen, and in severe cases, neurological signs may develop (associated with the build-up of ammonia and other toxins, causing hepatic encephalopathy).
Elevations in ALT is the most common biochemical change seen in patients with acute and chronic hepatitis; elevations in ALP and total bilirubin are also often seen. Additional changes include reductions in urea, glucose, albumin and cholesterol where significant liver dysfunction is present. Elevations in APTT and PT may be present where the production of coagulation factors is impaired, and elevations in ammonia (NH3) level may be seen where neurological signs are present.
A specific type of chronic hepatitis is seen in certain breeds. This is known as copper-associated chronic hepatitis (CACH) and is reported in Bedlington terriers (due to a genetic mutation), West Highland White Terriers, Labrador retrievers and Dalmations. In CACH, copper accumulates within the hepatocytes, causing secondary inflammation and cirrhosis.
Portosystemic shunt
A portosystemic shunt or congenital vascular anomaly is an abnormal vessel which diverts blood from the portal vein to other vessels (such as the caudal vena cava, or azygous vein). This results in venous blood from the GI tract by-passing the liver and returning directly to the systemic circulation. As a result of this, waste products from the GI tract build up in the body, as they are not transported to the liver for removal. The hepatocytes also receive fewer nutrients, as less nutrient-rich blood from the GI tract reaches them.
Congenital PSS’s are reported much more commonly in dogs than cats. They can occur within the liver (intrahepatic) or outside of the liver (extrahepatic). Small breed dogs and cats are more likely to have extrahepatic shunts, whereas larger breeds are more likely to have intrahepatic shunts. Yorkshire terriers are the breed most commonly affected.
Clinical signs are variable and include small body stature/patient size, failure to thrive, poor body condition. Waxing and waning neurological signs are also common, particularly after eating; these include depression, blindness, head-pressing and seizures.
Toxic hepatopathies
Because the liver plays such a vital role in eliminating medications and toxins from the body, it is especially vulnerable to the effects of these toxins. Hepatotoxic medications and substances can cause disease, and most commonly, hepatocellular necrosis is seen. There is an enormous number of substances which are hepatotoxic; the most common medications include anti-seizure medications and non-steroidal anti-inflammatories. Xylitol is perhaps the most common toxicity affecting the liver, though fungi present on corn, maize and wheat also produce toxins which cause liver disease.
Generally, clinical signs are non-specific in the early stages of toxicity and include anorexia, lethargy and vomiting. As toxicity progresses, signs specific for liver disease are seen. These include jaundice, coagulopathy, hypoglycaemia and neurological signs. Xylitol particularly causes rapid and profound hypoglycaemia, leading to seizures and liver failure.
Hepatic lipidosis
Hepatic lipidosis is a well-recognised syndrome in cats, which can occur either due to underlying diseases (e.g. renal disease, pancreatitis, diabetes, IBD and neoplasia) or as a primary/idiopathic problem. Any disease or factors which affects the cat’s voluntary appetite can be associated with the development of hepatic lipidosis.
Hepatic lipidosis is caused by severe calorie or protein restriction, which leads to mobilisation of fatty acids from fat tissue. These fatty acids are converted to ketone bodies and triglycerides by the liver; triglycerides are then converted to lipoproteins, provided sufficient protein is available. Lipoproteins and ketone bodies are used as an alternative energy source during starvation. Where lipoproteins cannot be synthesised, triglycerides build up within the liver. As more and more triglycerides accumulate, they interfere with hepatic function, leading to hepatic failure.
Clinical signs include vomiting, diarrhoea, jaundice and dehydration. Neurological signs may be apparent, and lethargy, weakness and poor coat condition are also commonly seen. The patient’s history usually includes a history of prolonged anorexia or hyporexia or rapid weight loss.
In order to prevent hepatic lipidosis developing, overweight cats should be monitored closely during any weight loss regime, and the rate of weight loss should not exceed 10% of the patient’s body weight per month.
Treatment and nursing care considerations
Treatment and care considerations for the hepatic disease patient are vast, and include:
Fluid Therapy
Fluid therapy is one of the most important treatments in hepatic patients. This maintains perfusion to the liver and minimises signs such as hypotension, hypovolaemia and renal injury. Where hypoalbuminaemia is present, colloidal oncotic pressure reduces and colloids may be required, to prevent oedema and fluid shifting. Electrolyte supplementation may also be required where anorexia is present, due to the risk of hypokalaemia.
Vitamin K Administration
Vitamin K administration may be required in patients with evidence of coagulopathy, due to the role of vitamin K in the synthesis of coagulation factors. This is generally given as a S/C injection, and stings on administration – so give slowly!
Glucose Administration
Hypoglycaemia may be seen as a result of hepatic failure; where this is present, glucose should be administered. This may be given as a bolus (50% glucose, diluted 50:50 with water for injection) to correct acute hypoglycaemia, and/or as a constant rate infusion where necessary for ongoing support.
Hepatosupportive Agents
A number of hepatopsupportive medications are used to manage chronic liver disorders. These include antioxidant medications and hydrophilic bile acids. These are supportive medications but do not cure severe disease, and so should be used alongside other treatments as necessary.
Antioxidant medications are generally neutraceutical medications and include S-adenosylmethionine, silybin/silymarin, Vitamin E and N-acetylcysteine. These increase the concentrations of glutathione (an antioxidant) within the liver.
Copper Chelating Agents
Medications such as penicillamine may be used in patients with copper-associated chronic hepatitis. This is a copper chelating agent, and gradually removes accumulated copper from the liver. Medications which bind dietary copper may be given to prevent further accumulation; these are not used at the same time as chelating agents and are usually administered after chelator therapy has finished.
Lactulose and Antibiotics
Lactulose and antibiotic agents are commonly administered to hepatic encephalopathy patients, to reduce circulating ammonia levels.
Supportive Treatments
Supportive treatments include appetite stimulants, anti-emetics and analgesia. Their administration is important to promote comfort, maximise patient wellbeing during hospitalisation and encourage voluntary food intake. The veterinary nurse is ideally situated to monitor patients, and discuss with the veterinary surgeon whether these medications can be used, given our pivotal role in inpatient care and monitoring.
Nutrition
Nutritional management is a key part of nursing the liver patient. Anorexia is common, and nutritional support is frequently required. These patients should have their resting energy requirement calculated (for their admitted weight, not ideal weight, to avoid over-feeding) and voluntary food intake measured. Where this falls below 80-85% of RER for 3+ days, a feeding tube should be placed and an appropriate diet administered.
A number of liver disorders have specific dietary requirements. These include:
The administration of a restricted-protein diet in hepatic encephalopathy patients (as ammonia is a by-product of protein breakdown, and contributes to neurological dysfunction)
The administration of a restricted-copper diet in patients with copper-associated chronic hepatitis
The administration of a high-protein diet in patients with hepatic lipidosis. These patients should also be re-fed carefully to prevent re-feeding syndrome.
Monitoring
Patients with hepatic disease require often intensive monitoring and care. Routine assessments and collection of vital parameters should be performed at appropriate intervals, based on the individual patient and their stability.
Neurological monitoring is also vitally important in hepatic disease patients, particularly those with severe liver dysfunction/failure and portosystemic shunt patients. Those at risk of seizures should have a seizure plan written up and attached to the front of their kennel, alongside pre-calculated drug dosages, a needle and syringe and a vial of the drug required.
Accommodation and Recumbency Care
Patients with severe liver dysfunction may be critically unwell and unable to move. These patients should have recumbency care provided at regular intervals, including bladder and bowel management as necessary and turning every 2-4 hours.
Cleanliness and Bathing
Diarrhoea may be seen in the hepatic disease patient, requiring careful management to prevent faecal scalding. In addition, patients with portosystemic shunts require lactulose as part of their management; this may be given orally, or as a retention enema in severe or emergency cases, resulting in diarrhoea.
Managing Bleeding Risk
Coagulopathies may be seen in patients with severe liver dysfunction, due to a reduction in coagulation factor synthesis. These patients should be carefully managed to minimise haemorrhage. Jugular venipuncture should not be performed, pressure bandages should be applied after any peripheral venepuncture, and patients should be kept calm and quiet as much as possible.
Barrier Nursing
As acute hepatitis can be caused by infectious pathogens (such as leptospirosis and distemper), patients with a suspected acute hepatic disease should be barrier nursed, until these have been excluded.
So that is an overview of the structure and function of the liver, as well as some of the common liver diseases we encounter in practice and our role as nurses in their care! What are your experiences with nursing hepatic patients? Be sure to let me know down below!
References
Breton, A. 2019. The Liver. Vetfolio, Available from https://www.vetfolio.com/learn/article/the-liver
Boroffka, S. 2015. The Liver: One Big Brown Organ in Gray Shades. VIN, Available from https://www.vin.com/apputil/content/defaultadv1.aspx?id=7259380&pid=14365&print=1
Merrill, L. 2012. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell
