Hepatic lipidosis: Winning strategies (Proceedings)
Ginger comes in with her "mom". Complaint: decreased appetite for 1 week, hasn't eaten anything for 2 days now; low energy; retching yesterday and today, only bringing up clear froth, maybe a little yellow at the end; urinating but not defecating for past 4 days; is a strictly indoor cat, "current" on vaccines; very quiet, "not her spunky self!" Ginger is a 4-year-old DSH tabby. She was drinking water on her own. Thinks she has lost weight. Previous exam 9 lbs Today's exam: BW 7 lbs., lethargic, quiet and a little dazed, spiky coat, thin, moderate skin tent with tacky oral mucous membranes, pink, crt 1.5 seconds moderate dental calculus with mild gingivitis, halitosis, yellow hue on soft palate, slightly sunken eyes, mild bilateral crusty ocular discharge, HR=180, RR=48, t=38C (101.5F), BP (Doppler) RH size 3 cuff 148 Thoracic auscultation: no abnormalities; abdominal palpation: doughy abdomen, moderate sized bladder, liver margins easily palpated and rounded, no stool in colon, no evidence of pain; dandruff over tail base.
What is our problem list? Inappetence/ anorexia of 9 days, weight loss (2 lbs, 22%), icterus, dehydration, dental disease, palpable liver margins (hepatomegaly?), depression, vomiting.
What are our differentials? Hepatic Lipidosis-primary vs. secondary to other disorders, cholangiohepatitis, cholangitis, cholecystitis, toxic hepatopathy, extra-hepatic bile duct obstruction, intussusception, gastroenteritis: viral, bacterial, endoparasitic, GI foreign body, pancreatitis, pancreatic cyst or abscess, cholelithiasis, neoplasia (e.g. gastric pushing liver back), hepatic, intestinal lymphoma, adenocarcinoma, pancreatic neoplasia, acute pyelonephritis, diabetic ketoacidosis, or diabetes mellitus FeLV/FIV/FIP. Also, anything that may cause hemolysis including hemobartonella, onions, drug related oxidative injury or IMHA, zinc toxicosis, autoimmune hemolytic anemia.How are we going to help this kitty? What diagnostics and therapeutics do you recommend? Let's collect blood for a CBC, differential, chemistry panel with electrolytes, T4 and lipase, FeLV and FIV, I'd run a PCV/TS, glucose in house, collect urine by agitated cystocentesis for u/a and hook her up to IV fluids at a rate calculated for deficit and maintenance. I'd add 35 mEq KCl to a liter of fluids to start with. We'd start syringe feeding her modestly with a/d to begin with and institute anti-emetic therapy if she appeared nauseous.
The development of lipid vacuoles within hepatocytes does not directly have a noxious effect on the cell. It is believed that the lipid accumulation reflects an underlying metabolic disorder. For example, any systemically ill person is expected to have some fat vacuoles in their hepatocytes. The problem is when the lipidosis is morphologically severe. In a normal feline liver, the fat content is less than 5% of the total hepatic weight. The liver of a cat with lipidosis may double or triple in weight from the accumulated/retained fat.
Fat in the liver is of five types: triglycerides (TG), phospholipids, lipoproteins, cholesterol and cholesterol esters. Lipid vacuolation in lipidosis is predominantly composed of triglycerides. They accumulate in the liver when the rate of hepatic synthesis exceeds their dispersal. Hepatic TGs are produced from fatty acids from systemic circulation (dietary lipids and adipose stores) and from de novo synthesis within the liver. Over nutrition with carbohydrates or protein results in hepatic fat accumulation, as these excess nutrients are stored as triglycerides
Fat metabolism: Regulation of fat metabolism in the adipocyte may be a major factor promoting lipidosis. Many cats developing hepatic lipidosis (HL) are obese. Unrestricted release of fatty acids from excessive adipose fat promotes lipidosis because up to one third of mobilized fat may be residing in the liver at one time. Therefore, in these cats, lipidosis may reflect the liver's inability to match fat dispersal with delivery from systemic sources.
The balance of TG lipolysis and accumulation is modulated by blood glucose concentration as well as hormonal, neural and pharmacological mechanisms. The activity of hormone sensitive lipase and lipoprotein lipase directly regulate adipocyte fat metabolism. Hormone sensitive lipase (HSL) promotes lipolysis. Norepinephrine, epinephrine, growth hormone, glucagons, corticosteroids and thyroxin increase HSL activity. Insulin inhibits HSL. Cats release catecholamines very readily, thus, stress may exacerbate HSL activity and fatty acid metabolism. The absence of insulin would act similarly.