05 | Understanding acute and chronic hepatitis in dogs and cats
Today we’re diving into the first conditions in our liver disease series - acute and chronic hepatitis.
These are some of the most common liver diseases that we see, and these patients can present with a wide variety of clinical signs - with some of them requiring very intensive treatment and nursing care.
If you want to know exactly what these conditions are, how they affect our patients, and - most importantly - how to nurse them, this episode is for you.
Acute Hepatitis
Pathophysiology
Acute hepatitis is characterised as acute hepatic necrosis and associated inflammation. There are may causes, including chemical exposure, toxin ingestion, viral and bacterial infections, mycotoxin exposure and immune mediated disease.
The disease varies in severity, from moderately severe signs to fulminant hepatitis, where extensive hepatocellular necrosis occurs - leading to complications like coagulopathies, hepatic encephalopathy, jaundice and hypoglycaemia. The fulminant form of the disease often rapidly progresses and can be fatal.
Unlike other forms of hepatitis (such as chronic, or copper-associated), there are no breed or sex predispositions with acute hepatitis.
Clinical Signs
The signs of acute hepatitis can vary in severity and usually have a very rapid onset, with patients often presenting as an emergency.
Signs include:
Vomiting
Diarrhoea
Anorexia
Lethargy
Dehydration
Abdominal pain
Hepatomegaly
+/- Pyrexia if hepatitis is due to an infectious agent
+/- Jaundice/icterus
+/- Central neurological signs if hepatic encephalopathy is present
+/- Bleeding tendencies and signs of coagulopathy if an acquired coagulopathy is present
Diagnostic Tests
The diagnostic approach to acute hepatitis usually includes bloods for biochemistry and haematology, +/- urine analysis, and abdominal imaging with liver sampling where indicated.
On biochemistry, increases in ALT and AST are the most common laboratory finding, as these enzymes leak from damaged hepatocytes. Increases in ALP and bilirubin are also commonly seen, and as hepatic function declines other biochemical changes may be present, including:
Low glucose
Low BUN
High ammonia
Low cholesterol
Low albumin
Haematological changes are usually non-specific. The patient’s PCV may be normal, increased if haemoconcentration is present, or decreased if haemorrhage secondary to an acquired coagulopathy is present.
WBCs may be increased due to inflammation or decreased in the event of an overwhelming infection causing consumption. We may also see toxic changes to our neutrophils when examining the patient’s blood smear.
Platelets should be assessed prior to any hepatic sampling, may be decreased if consumption is present, or increased in response to haemorrhage
We also need to check the patient’s coagulation status, especially prior to any hepatic sampling (biopsies or surgery). These can be increased if hepatic dysfunction is present - due to a lack of hepatic production of clotting factors.
Once we’ve got our bloods run, imaging is going to be the next step. This is usually achieved with ultrasound, which may reveal diffuse changes in echotexture and changes to the biliary tree and gallbladder if present. Ultrasound also guides FNA and percutaneous needle-core biopsy collection.
Treatment
Management of acute hepatitis varies significantly depending on the underlying cause. It includes the administration of appropriate antibiotics for bacterial infections (such as leptospirosis), or specific antidotes or chelation therapy for toxins where appropriate.
Alongside this, we need to be providing aggressive supportive care, including:
Intravenous fluid therapy
Dextrose supplementation in the event of hypoglycaemia
Lactulose and antibiotics if hepatic encephalopathy is present
Antioxidant therapies
Antiemetics
Analgesics as needed
We also need to be very careful about the dosing we use of many of our medications - since the liver plays such an important role in their metabolism. Always check that dose reductions are not needed in the case of liver dysfunction.
Nursing Considerations
There is a lot to think about when nursing the acute hepatitis patient, including monitoring, fluid balance, nutrition, managing eliminations and managing complications of hepatic dysfunction, alongside general nursing care.
Make sure you’re keeping a close eye on your patient’s routine vitals, neurological status, pain, food and water intake, body weight and comfort levels. Assess their fluid balance regularly, and adjust their fluid therapy plan as needed.
Nutrition is a huge consideration - hyporexia and anorexia are common, so we want to get an appropriate feeding tube in to our patient, and calculate and formulate an appropriate refeeding plan.
In most cases, acute hepatitis recovers spontaneously. However, around 30% of cases can progress to chronic hepatitis - which can begin with a subclinical phase, making the disease harder to spot.
Chronic Hepatitis
Pathophysiology
Chronic hepatitis begins with a subclinical phase of varying length. Clinical signs don’t usually present until the disease is at an advanced stage, making it poorly responsive to treatment.
The disease is characterised by fibrosis around the portal triads, infiltration of lymphocytes and plasma cells within the liver, and necrosis/apoptosis of hepatocytes leading to fibrosis and cirrhosis.
The exact cause unknown, but associations with acute hepatitis, and hepatic copper accumulation are reported. There are also several breed associations, including
Dobermans
Cocker spaniels
Labradors
Bedlington terriers
Westies
Dalmations
Welsh Corgis
Keeshonds
Maltese
Clinical Signs
The signs are often vague and non-specific, and are associated with a loss of normal liver function. They include:
PUPD
Weight loss
Vomiting
Anorexia
Lethargy
+/- Jaundice
+/- Ascites (due to portal hypertension)
+/- Neurological signs
+/- Signs of coagulopathy
Diagnostic Tests
Like acute hepatitis, we’ll be diagnosing the condition based on bloodwork, imaging and hepatic sampling.
On biochemistry, increased ALT is most the consistent finding, especially in the subclinical phase of the disease. Elevations in ALP and bilirubin are seen more consistently in the clinical phase of the disease.
On top of this, we can also see changes associated with liver dysfunction (such as increased NH3, low BUN, low glucose, and low albumin).
Haematology may reveal a nonregenerative anaemia of chronic disease, and microcytosis (small red blood cells), but no changes specific to liver disease itself.
Like acute hepatitis, ultrasound is the preferred method of imaging. XRays can show microhepatica but are otherwise non-specific - and if ascites is present a fluid effect will limit the abdominal detail significantly.
On ultrasound, we often see a diffusely abnormal liver with irregular, nodular parenchyma and an irregular surface +/- free abdominal fluid.
A liver biopsy is indicated for definitive diagnosis. As with acute hepatitis, coagulation status should be checked beforehand.
Samples should be submitted for histology, culture and quantitative copper analysis
Treatment
Chronic hepatitis is managed medically with antioxidants, hydrophilic bile acids, copper chelating agents (if required), and corticosteroids alongside supportive therapy.
On top of this, we’ll also need to manage any complications associated with liver dysfunction, such as hepatic encephalopathy, and provide supportive treatment.
Nursing Considerations
Our nursing considerations for the chronic hepatitis patient are similar to patients with acute hepatitis, but usually less severe.
After inpatient treatment, long-term treatment and at-home care will be needed, and the veterinary nurse is ideally placed to support clients with this. This home-care may include dietary adjustments (low copper diets, hydrolysed non-meat protein diets to HE patients), comfort monitoring, monitoring for complications of disease, and medication administration.
So that’s it for this week’s episode on acute and chronic hepatitis! These patients often benefit from many nursing skills, including calculating CRIs, placing feeding tubes and creating nutritional plans, assessing fluid balance and creating fluid therapy plans, sample collection and processing, ultrasonography and radiography, and much more.
Join me next week for part 3 in our liver series - where we’ll be chatting all about copper-associated hepatopathy, and the nursing skills we can use with these patients.
Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it and tag me on instagram (@vetinternalmedicinenursing) so I can give you a shout out, and share it with a colleague who’d find it helpful!
Thanks for learning with me this week, and I’ll see you next time!
References and Resources
Center, S.A. 2023. Hepatotoxins in small animals [Online] MSD Vet Manual. Available from: https://www.msdvetmanual.com/digestive-system/hepatic-diseases-of-small-animals/hepatotoxins-in-small-animals
Center, S.A. 2023. Fulminant hepatic failure in small animals [Online] MSD Vet Manual. Available from: https://www.msdvetmanual.com/digestive-system/hepatic-diseases-of-small-animals/fulminant-hepatic-failure-in-small-animals
Center, S.A. 2023. Canine chronic hepatitis [Online] MSD Vet Manual. Available from: https://www.msdvetmanual.com/digestive-system/hepatic-diseases-of-small-animals/canine-chronic-hepatitis
Gordon, J. 2010. Inflammatory liver diseases in the dog [Online] DVM360. Available from: https://www.dvm360.com/view/inflammatory-liver-diseases-dog-proceedings
Merrill, L. 2012. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell
Rothuizen, J. 2011. Hepatitis in dogs: new concepts in pathogenesis and treatment [Online] VIN. Available from: https://www.vin.com/apputil/project/defaultadv1.aspx?pid=11343&catid=&id=5124413&meta=&authorid=#:~:text=Acute%20hepatitis%20is%20characterized%20by,macrophages%20called%20%22scavenger%20cells%22.
