Book: Reptile Medicine and Surgery Second Addition
Hepatic lipidosis is a well-recognized condition that is frequently diagnosed postmortem in numerous of reptiles. Liver disease, and more specifically, hepatic lipidosis, is probably one of the most frequently stated and misunderstood diagnoses made by clinicians and pathologists alike. Metabolic changes that lead to an increase in hepatic fat can lead a pathologist to make a postmortem diagnosis of hepatic lipididosis. Likewise, clinicians may also be forgiven for making a presumptive diagnosis of "fatty liver" when confronted with an obese captive reptile that has been consistently overfed and under exercised. However, the problem is far more complex and extensive than perhaps has been previously appreciated.
THE REPTILE LIVER
The macroscopic appearance of the liver of reptiles is little different from that of other vertebrate animals. The liver comprises 3% to 4% of body weight in most squamate species, generally less in chelonians and crocodilians. However, its size and weight (mass) can fluctuate according to time of year and nutritional or reproductive status. The liver originates (in most species) from the endodermal gut. Usually it consists of two lobes and varies in color from dark brown to black. A gallbladder is usually present. The blood supply to the liver is from the hepatic portal vein and hepatic artery.
The functions ot the reptile liver are similar to those of mammals and birds-essentially fat, protein (including globulin) and glycogen metabolism, and the production of uric acid and dotting factors. However, these functions may vary markedly as the animal progress from egg to juvenile to breeding adult. Mammals and birds tend to store fat in -subcutaneous sites, primarily as a means of thermal in insulation. Such an adaptation is less helpful and, judged from extant species has not evolved within the Reptilia. lnstead, most reptiles store fat in specific fat bodies; these organs are located within the caudoventral coelom. The main role of these fat stores is to provide lipid for vitellogenesis (yolk deposition)and to ad as an energy store during brumation (hibernation) or estivation (dormancy) and fasting (breeding season). Fats are transported from the intestinal tract and the fat bodies to the liver in the form of unesterified fatty acids. All fat transportation away from the liver is in an esterified form, being protein-bound as lipoproteins. These very low-density lipoproteins are recycled as low-density lipoprotein fragments. The formulation of phospholipids and cholesterol is also under hepatic regulation, again from lipid precursors.
DIAGNOSIS OF HEPATIC LIPIDOSIS
One must remember that hepatic lipidosis is a metabolic derangement and not a single clinical disease. A host of factors can predispose to increased hepatic fat. Classically, the high-fat diet (e.g., obese laboratory rats, waxworms) has been implicated in obesity, an increase in the size of coelomic fat bodies, and an increase in hepatic fat. Equally, reduction in activity, which frequently afflicts captive reptiles, must also be considered. Therefore, careful questioning of the keeper or owner with regard to exercise, food items, and feeding frequency is essential. The usual environmental information, particularly with regard thermal provision, is obviously essential. Hepactic disease can be classified as acute or chronic, inflammatory (hepatitis) or degenerative (hepatosis). Hepatic lipidosis is usually chronic, and observant owners and keepers who maintain accurate records may report a gradual reduction in appetite, activity, fecundity and fertility, retarded weight gain or gradual weight loss, brumation (hibernation) problems including post brumation (post hibernation) anorexia, and changes in fecal character and color. However, the underlying liver disease may become clinically apparent only during episodes of increased physiologic demand.
Unfortunately, many caretakers miss these early signs of disease. As a result, veterinary attention is only sought once the animal has deteriorated to a life-threatening condition. When lipidosis is advanced, most affected reptiles are in poor body condition, flaccid, weak, and cachectic. The body weight (mass) is usually below normal, often critically so, although in case of ascites (accumulation of fluid in the abdominal cavity), weight may be artificially maintained or even increased. Reptiles with acute liver disease usually are seen in good body condition but with sudden onset depression and anorexia. As already stated, the early signs of chronic disease may be missed; this; in conjunction with the rapid onset of severe clinical signs, may confuse and convince the clinician that this is an acute hepatitis (an inflammatory change) rather than the end-stage presentation of a chronic hepatosis (degenerative liver disease) figure 56-1.
Although specific therapy for hepatic Lipidosis is usually reserved until the diagnosis has been confirmed histologically and the precise etiology has been identified, much can be done in general to support the reptile with hepatic dysfunction, whether infectious or noninfectious. Medical stabilization with fluid therapy is essential, and the provision of the species specific preferred optimum temperature zone (within which the reptile can select a preferred body temperature) can be instrumental in improvement.
Fluid and nutritional support
The route of therapy is directed by the animal's condition at the time of presentation. Mild to moderate cases of hepatic lipidosis are usually anorectic on presentation but in good condition, and in these cases, oral fluids are adequate. Reptiles with severe disease often need intracoelomic, intravenous, or intraosseous infusion. In cases of severe liver pathology, avoidance of solution that contain lactate may be wise. Other medications may be used at the clinician's discretion, but care should be taken not to invalidate future diagnostic investigations. For example, blood samples should be collected before fluid therapy, and antibiotic medication should be delayed
until after liver biopsy and culture.
In many instances, hepatic lipidosis is a chronic disease that may take months, if not years, to reverse. Therefore, a mean of providing long-term fluid and nutritional support should be explored. Most lizards and snake are easily stomach-tubed; however, most chelonions and some squamates are better served by the placement of an esophagostomy tube with local or light general anesthesia (Figure 56--7). The importance of nutritional support cannot be overemphasized.
CONCLUSIONS AND RECOMMENDATIONS
Hepatic lipidosis of reptiles has traditionally been considered to be associated with overfeeding, obesity, and
under exercised. As in other animals, including humans, excess lipid deposition in the liver can also be from, or following, a number of insults, including toxins, anoxia, and impaired metabolism of carbohydrate and volatile fatty acids.