Liver lipidosis in cats
Liver lipidosis or fatty hepatosis
Liver lipidosis in cats most often occurs when an animal (especially overweight) remains without food for several days.
With fatty hepatosis, excess lipids begin to accumulate in liver cells, which leads to stagnation of bile, creating prerequisites for the development of liver failure.
The most common causes of liver lipidosis in cats are the following:
a quick transition of an animal to a new food or diet,
an unfamiliar pet in the house,
the appearance of a small child in the family,
stressful situations that force the cat to hide for a long time (for example, the arrival of guests or relatives for a few days, moving to a new place, the postoperative period).
With fatty hepatosis, the animal has a lack of appetite, vomiting, jaundice of the skin and mucous membranes, weight loss, decreased muscle mass, dehydration, lethargy, drowsiness, a desire to hide, increased salivation.
More serious clinical signs include low blood pressure and disorders in blood clotting processes.
The diagnosis is made on the basis of a complete clinical blood test with an assessment of white and red blood cells, a biochemical blood test, a urine test and, if necessary, a blood clotting test.
As additional studies, ultrasound or X-ray examination of the liver, examination of liver aspirates, biopsy can be performed.
Treatment of fatty hepatosis includes intravenous fluids to maintain normal homeostasis (glucose solution, sodium chloride solution, normosol), vitamin K injections to improve blood clotting, taking antibiotics and antiemetic drugs to animals.
In complex cases requiring artificial feeding for several weeks, it is recommended to establish a gastrostomy and blood plasma transfusion in particularly difficult situations.
Treatment of fatty hepatosis is very expensive and, unfortunately, in a large number of cases it cannot save the animal. To reduce the likelihood of a cat's liver lipidosis, the owners should make any changes in the diet or lifestyle of the animal gradually (over several weeks) so that the cat can adapt, closely monitor its appetite, weight and behavior. Early diagnosis of the disease increases the chances of recovery.
Liver lipidosis syndrome in cats manifests itself when more than 50% of hepatocytes accumulate an excessive amount of triglycerides, which leads to severe cholestasis and liver dysfunction.
The cause of the disease is acute or chronic malnutrition (anorexia).
In the absence of treatment - progressive metabolic dysregulation and death.
It can be both a secondary and primary phenomenon.
Most patients have an underlying disease leading to anorexia.
Definition
Synonyms
Fatty liver hepatosis in cats
Fatty liver degeneration in cats
Fatty liver syndrome in cats
Hepatic vacuolization in cats
Vacuole liver degeneration in cats
Genetic aspects
No
Prevalence
The most common hepatopathy in cats, which causes jaundice.
Geographical distribution
Everywhere
Characteristic
Species - cats, rarely dogs (noted in puppies)
Breed predisposition
No
Average age and age range
On average - 8 years
Range - 1-16 years
Mainly among middle-aged cats
Sexual predisposition
In general, it is more common among overweight females
Pathophysiology
Cats have an extraordinary natural tendency to accumulate vacuoles with triglycerides (lipids) in hepatocytes (liver cells).
Protein and energy intake restriction – excessive accumulation of triglycerides in the liver; protein deficiency can play a crucial role, leading to insufficient formation of apoproteins necessary for the mobilization of triglycerides from the liver.
Causal factors - increased peripheral mobilization of fat; increased formation of triglycerides in the liver; damage to B-oxidation of fatty acids; reduction of lipid excretion from liver cells.
Accumulation of triglyceride vacuoles in liver cells – hepatocellular edema, violation of the location of intracellular organelles and structures, violation of their function, further compression.
After, liver failure with severe manifestation.
Affected systems
Hepatobiliary – severe intrahepatic cholestasis, liver dysfunction or insufficiency.
Gastrointestinal – anorexia and vomiting
Musculoskeletal - starvation of peripheral tissues
Nervous - hepatic encephalopathy (Read the article Hepatic encephalopathy in dogs and cats.)
Blood/ lymphatic/ immune - abnormality of erythrocyte forms (poikilocytosis).
Reasons
Idiopathic form of the disease - most often without an underlying cause
Secondary form of the disease
Primary liver disease - portosystemic circulation anomaly; cholangitis/cholangiohepatitis; extrahepatic occlusion of the bile ducts; cholestasis; neoplasia
Diabetes mellitus
Diseases of the small intestine - obstruction, neoplasia, inflammatory bowel disease
Pancreatitis
Urogenital disease - chronic interstitial nephritis, renal failure (acute or chronic); disease of the lower urinary tract of cats
Neurological diseases
Infectious diseases - toxoplasmosis; viral peritonitis of cats; viral leukemia of cats
Hyperthyroidism
Vitamin B12 deficiency
Other systemic pathologies, including toxicosis
Risk factors
Obesity
Anorexia
Negative nitrogen balance – catabolism
Severe rapid weight loss
Signs
Anorexia
Jaundice
Lethargy
Vomiting
Diarrhea or constipation
Weakness
Ptialism (drooling)
Hepatic encephalopathy
Collapse
Anomalies caused by the underlying disease in the absence of treatment
Hepatomegaly
Dehydration
Neck ventroflexia, sedimentation
Blunted thinking
Diagnostics
Differential diagnosis
Primary liver disease - cholangitis / cholangiohepatitis, cholestasis, extrahepatic occlusion of the bile ducts and neoplasia, these are the most important diffdiagnoses; differentiated by abdominal ultrasound, liver aspiration, finally by liver biopsy.
Congenital anomaly of portosystemic circulation - can rarely be confused; differentiated by ultrasound or colorectal scintigraphy.
Liver toxoplasmosis or viral peritonitis of cats - differentiated by liver biopsy.
Pancreatitis – abdominal ultrasound, serum tests (increased trypsin-like immune active substances, increased amylase, lipase; amylase and lipase are unreliable indicators) and /or direct imaging or biopsy.
Gastrointestinal disease - inflammatory disease (endoscopy and deep biopsy of the intestinal wall), obstruction (radiography, contrast radiography, ultrasound)
Poisoning - suspected according to the survey (administration of oral forms of diazepam or acetominophen (paracetamol)).
Hyperthyroidism - according to the level of serum thyroid hormones.
Hematology / Biochemistry / Urine Analysis
Hematology - poikilocytosis often; mild non-regenerative anemia; hemolytic anemia with severe hypophosphatemia, leukogram reflects the underlying pathology.
Biochemistry – hyperbilirubinemia; increased ALT (ALAT), AST (ASAT), alkaline phosphatase, normal or elevated GGT values; low urea levels; normal creatinine; variable glucose levels (hypoglycemia is rare); variable cholesterol and albumin levels; globulins are usually normal (hyperlobulinemia may occur in the main inflammatory disease); hypokalemia (in severe life-threatening condition); may occur hypophosphatemia (< 2 mg/dl) during the first 72 hours of hospitalization (in the presence of hemolytic anemia).
Urine analysis - lipiduria is common.
Other laboratory tests
Prolonged coagulation time – prothrombin time, partial thromboplastin time and activated clotting time - in 50% of patients.
Fibrinogen is usually normal.
Hyperammonemia - may occur; ammonium urate crystalluria is extremely rare.
Serum bile acids - increase before bilirubin; after the appearance of jaundice, this test is unnecessary.
Visual diagnostic methods
Visual diagnostics
Simple abdominal radiography
Hepatomegaly
There may be other signs that characterize the main problem.
Abdominal ultrasound
Diffuse hyperechogenicity of liver parenchyma is a reflection of abnormal lipid content in hepatocytes; lipid vacuolation of renal tubules complicates the comparison of echogenicity of liver parenchyma with kidney parenchyma; comparison of echogenicity with sickle fat is recommended. It is impossible to distinguish the idiopathic form from the secondary one.
Diagnostic procedures
Fine needle aspiration of hepatic tissue to confirm hepatocellular vacuolization; more than 50% of hepatocytes should contain obvious cytosolic vacuoles.
Aspiration cytology - based on historical and clinical signs, elevated alkaline phosphatase, normal or slightly elevated GGT and diffuse hepatic parenchymal hyperechogenicity; does not exclude underlying liver disease or causal diseases in other organ systems.
Liver biopsy - provides a definitive diagnosis for primary liver disease.
Vitamin K1 (0.5-1% mg / kg / m) should be administered at least 12 hours before the biopsy.
Pathological findings
External - diffuse hepatomegaly with smoothed contours; loose, fatty and yellow-gold liver tissue, may have a mesh appearance; liver biopsy samples float in formalin.
Microscopy – severe diffuse vacuolization of hepatocytes; few large (macrovesicular) or many small (microvesicular) vacuoles; the contents of vacuoles with neutral fats (triglycerides) are confirmed by staining the tissue without filling with paraffin using oil-O-red or Sudan black dyes.
Treatment
Inpatient treatment – supportive therapy for severe illness; discharge home after stabilization and determination of the path of further feeding.
Frequent repeated examinations are mandatory.
Outpatient treatment is indicated only to reduce stress in some cats, which can complicate the course of the disease.
Rehydration - balanced polyionic solutions - at initial management; the use of lactate Ringer with caution (the patient may have impaired lactate metabolism); potassium chloride supplementation is provided according to the accepted rules (See potassium, hypokalemia).
Dextrose supplement is contraindicated while there is no hypoglycemia; it may increase the accumulation of triglycerides in the liver.
Vomiting, nausea and gastroparesis - can be treated with metoclopramide (Cerucal) (0.2-0.5 mg / kg, n / a, every 8 hours, 30 minutes before feeding or as a prolonged intravenous infusion at a rate of 0.01-0.02 mg / kg / hour, or 1-2 mg / kg / day).
Hypophosphatemia
If serum phosphates are < 2.0 mg/dl, correction is started.
Treatment with an initial dose of 0.01-0.03 mmol / kg / hour, intravenous (commercial parenteral phosphate solutions containing phosphate 3 mmol / ml or 93 mg / ml of elemental phosphorus); monitor serum phosphate levels every 3-6 hours, discontinue administration when the level reaches > 2 mg / dl.
With an excess of phosphates – hypocalcemia, mineralization of soft tissues.
Phosphate infusion - lowers the level of ionized calcium if calcium-phosphorus products > 58 mg/dl.
Effect on potassium chloride supplementation - the use of potassium phosphate can lead to iatrogenic hyperkalemia if this source of potassium is not taken into account.
Activity
Most patients reduce their activity on their own.
Mobilization - can improve the mobility of the stomach if gastroparesis is complicated by the installation of a feeding tube.
Diet
Nutritional support is extremely important for recovery!!!!
Feeding tube
Force-feeding is necessary in most cases; simply force-feeding through the mouth, as a rule, leads to aversion from food.
Nasogastric, esophagostomy or gastrostomy intubation is recommended.
Initially, it is necessary to position the nosagastric feeding tube in order to establish the most appropriate path later.
The gastrostomy tube can be installed: blindly, by means of an endoscope or diagnostic laparotomy.
The best way out is without the use of diagnostic laparotomy.
Offer regular food for self-consumption daily.
Food composition
High protein level, high calorie content.
Calories gradually increase within 72 hours, it is necessary to achieve consumption of 60-90 kcal / kg / day.
Supplements are controversial efficacy, but may benefit L-carnitine (250 mg/day), taurine (250-500 mg/day); thiamine (50-100 mg/day) water-soluble vitamins (twice the normal dose); vitamin E (100-400 IU / day); potassium gluconate (with hypokalemia); zinc (7-8 mg/ day); fish oil (2000 mg /day).
When using medical nutrient solutions, it is necessary to add protein and arginine to the composition (without arginine – convulsions and coma).
Vitamin K1 - 0.5-1.5 mg / kg; initially 2-3 doses may be required at intervals of 12 hours; avoid overdose (induction of oxidative damage to red blood cells)
Owner Training
Instructing on the feeding regime using a feeding tube.
Warning owners about the possible need to use a feeding tube for up to 4-6 months without interruptions.
Informing owners that the recurrence of the disease is a rare phenomenon.
Surgical aspects
Diagnostic laparotomy – if necessary, perform a liver biopsy during laparotomy; careful examination during surgery for the presence of the underlying disease. And a biopsy of the pancreas, stomach, intestines, if necessary.
Avoid surgery until the patient is stabilized or clinically improved.
Medicinal preparations
Lactulose (0.5 – 1 ml/ kg orally every 12 hours; it is necessary to adjust the dosage to preserve 2-3 bowel movements during the day with soft faeces); metronidazole (7.5 mg/ kg orally every 8-12 hours); and/or neomycin (22 mg/ kg orally every 12 hours).
Antibiotics – if necessary, control of parallel infections.
Contraindications
Do not use medications that affect hepatic biotransformation or excretion.
Do not use drugs that interact with GABA-benzodiazepine receptors (barbiturates, diazepam).
Stimulating appetite (diazepam, oxazepam and ciproheptadine– - will not provide guaranteed caloric intake, may lead to sedation.
Ursodeoxycholic acid - no indications for use in affected cats.
Patient monitoring
Body weight and hydration status are important indicators when monitoring calorie intake and rehydration.
Serum bilirubin concentrations - improve after 5-7 days of adequate feeding and supplementation.
The activity of liver enzymes - normalization is slow.
Discharge home after vomiting is controlled, gastroparesis resolves, total bilirubin levels decrease, and the feeding system using a feeding tube works stably and without problems.
Removal of the feeding tube is carried out only after the patient shows an active interest in food and is able to eat adequately on his own for at least 1 week.
Extensions
Prevention
Obesity is prevention, the rate of weight loss should not exceed 1.5% per week.
Attentive attitude of obese cat owners to their food consumption during periods of external stress (moving, new animals, new people, home repairs).
Possible complications
Disruption of the feeding tube - obstruction of the gastrostomy tube can be eliminated by papaya juice, soda water or pancreatic enzymes, which can dissolve food accumulations in the tube.
Infection around the insertion site of the tube.
Worsening of hepatic encephalopathy after the inclusion of nutritional support.
DIC syndrome (rare)
Liver failure and death.
Expected course and forecast
The optimal response to auxiliary feeding and the use of supplements is within 1 week.
Full recovery is 14-21 days, sometimes longer.
With the therapy described here, 80% of patients recover.
Secondary disease - recovery depends on the nature and control of the pathological condition that led to anorexia.
Liver lipidosis rarely recurs.
Associated states
Primary liver disease
Pancreatitis
Diabetes mellitus
Neoplasia is systemic or hepatic.
Hepatic encephalopathy in dogs and cats.
Any systemic disease that restricts food intake.
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