Pregnancy toxemia in a ferret

A pregnant 1.3-kg adult jill of unknown age or stage of gestation was presented with a history of sudden onset of depression, weakness, and anorexia (day 1). The current owners had acquired the jill 1 wk earlier from the local ferret rescue society, with no known medical or reproductive history. Although the owners had been keeping and fostering adult ferrets since the early 1990s, they had had no experience with pregnant jills or new-born kits. Under their care, the jill had been fed the same commercial ferret diet (Premium Ferret Food; Rolf C. Hagen, Montreal, Quebec) as the other ferrets in the home. Despite a few days of stress on arrival in the new environment, the jill had seemed initially to be doing quite well.

At presentation, the ferret was moribund, sternally recumbent, and hypothermic. Rectal temperature was 34.8°C, pulse 140 beats/min, and respirations shallow at a rate of 38 breaths/min. The jill was estimated to be 12% to 15% dehydrated, on the basis of a very prolonged skin tent, sunken dry eyes, and tacky oral mucous membranes. The capillary refill time was prolonged at 3 s, and the rectum contained dark brown feces and mucus. Initial in-clinic diagnostic testing (Glucometer; Roche Diagnostics, Mississauga, Ontario) revealed a blood glucose of 3.3 mmol/L (reference range (1), 6.97 to 10.49 mmol/L) and urine that was positive for ketone bodies on dipstick (Chemstix; Roche Diagnostics). Careful abdominal palpation confirmed that the jill was in late gestation with numerous kits. The list of differential diagnoses included pregnancy toxemia; insulinoma, resulting in hypoglycemic coma; toxicant ingestion; pyometra; trauma; sepsis; and heat prostration. Pregnancy toxemia became the working diagnosis. Supportive care was initiated; contributing factors, such as stress in a new environment, obesity, large litter size, and inadequate late-gestation nutrition, were discussed with the owners. The ferret was immediately administered a balanced electrolyte solution, IV, at a rate of 2 mL/h via a 25-gauge catheter placed in the cephalic vein, with 10 mL of 5% dextrose solution (500 mg of glucose) added to the 1-L bag. Active rewarming was initiated, using hot water bottles and blankets, and 150 mg of glucose in 5% dextrose solution was force-fed by syringe. Within 1 h, minimal improvement was noted, and the owners were informed that an emergency cesarean section under general anesthesia would be required if the jill was to survive (2).

The owners agreed to this plan, despite the risks and the guarded to poor prognosis. By the time surgery commenced 2 h after admission, the jill’s rectal temperature had risen to 35.7°C and hydration status had improved slightly to 10% dehydration. Prior to surgery, she was oxygenated by mask for 5 min (flow rate of 1 L/min), maintained on a heating blanket, and then anesthetized with 1.5% isoflurane at 150 mL/kg bodyweight (BW)/ min by mask. Intravenous administration of electrolyte solution with dextrose was continued at 10 mL/kg BW/h throughout the procedure.

The gravid uterus was carefully exteriorized through a ventral midline incision. A 2-cm incision was made midway along each horn and 6 live kits were milked out of each incision. The 12 kits were dried; warmed, using towels and hot water bottles; and immediately placed in a sealed tank with 100% oxygen supplied via a Bain anesthetic circuit. A routine ovariohysterectomy was then performed. Both the ovarian pedicles and the uterine body were double ligated using 3-0 polydioxanone suture (Ethicon, Norwood, Massachusetts, USA). The linea alba and subcutaneous tissue were closed using 4-0 vicryl (Ethicon) in a simple continuous pattern, and the skin was closed using 4-0 vicryl in a subcuticular pattern. There were no apparent complications. Immediately after surgery, the jill was weighed (BW 0.75 kg), administered butorphanol (Torbugesic; Fort-Dodge Animal Health, Overland Park, Kansas, USA), 0.2 mg/kg BW, IM, once, and the IV flow rate of 10 mL/Kg BW/h was reduced to 2 mL/h. During the recovery period (almost 4 h), the ferret received 100% oxygen by mask and was maintained on hot water bottles. The kits were force-fed, using a syringe and a teat cannula, a mixture of 3 parts milk replacer (KMR milk replacer; PetAg, Hampshire, Illinois, USA) and 1 part whipping cream (40% butterfat). Kits were fed q2h but would not take much. When they returned to pick up the kits, the owners were instructed regarding feeding and caring for the kits at home and warned of the poor prognosis.

The jill was hospitalized overnight for supportive care, pain control, and observation. Cardiac arrhythmia, auscultated postoperatively, was attributed to metabolic imbalances and electrolyte disturbances induced by toxemia and ketoacidosis. By day 2, 17 h postadmission, the jill was 6% to 7% dehydrated and her rectal temperature was 38.5°C; her pulse rate was 230 beats/ min and there was no evidence of arrhythmia; however, she remained very depressed. She was force-fed a small amount of canned kitten food (Science Diet, Hill’s Pet Nutrition, Topeka, Kansas, USA) plus water, 21 h postadmission, and ate reluctantly. Mentation began to improve and she resumed normal bowel movements by 25 h postadmission. Because the surgical incision was clean, the dehydration had been corrected, and there were financial concerns, the ferret was discharged to her owners, approximately 33 h after admission, with instructions on force-feeding food and water, rest, and minimal stress, and information regarding ferret nutrition and the importance of extra fat, protein, and fresh water for late- gestation jills. The owners were advised that the prognosis was still guarded due to potential liver damage.

Despite efforts at proper care and nutrition by the owners, all kits had perished by day 10. However, the dam slowly improved, and 13 d after surgery, she began to eat a normal ferret ration unassisted and became more playful.

Pregnancy toxemia, a disease caused by a negative energy balance in late gestation, is seen commonly in ewes, guinea pigs, and rabbits, and occasionally in cows, ferrets, sows, and many other species (2,3). In the ferret, pregnancy toxemia usually occurs between 32 and 42 d gestation (normal gestation — 41 to 42 d) in primiparous jills carrying > 10 kits (3). Predisposing causes include stress and food deprivation late in pregnancy (3). As in this case, clinical signs include sudden onset of lethargy, hypothermia, dehydration, sternal recumbency with decreased awareness, open glazed eyes, and black tarry stools (3,4). Alopecia is common, and coma and death often ensue (3).

Initial laboratory testing often reveals anemia, azotemia, bilirubinemia, hypoglycemia, hypoproteinemia, high levels of hepatic serum enzymes, and ketonuria (3). Immediate supportive care is required, and early treatment with parenteral fluids containing electrolytes and glucose, with frequent feeding of a high energy, high protein diet may be beneficial. Medical management alone, however, is almost never adequate, and an emergency cesarean section is the treatment of choice (2,3).

Pregnancy toxemia in jills is almost always associated with inadequate nutrition, decreased feed intake, or fasting (2,3). Ferrets require a higher level and quality of protein, more fat, and less fiber than do most other carnivores (5). Rations suitable for pregnant jills must contain > 35% high quality animal-source protein, > 18% fat (including 7% to 15% of linoleic acid), and minimal grain or fiber ingredients (6). Owners should also provide high-calorie nutritional supplements (NutriCal; Evsco Pharmaceuticals, Buena, New Jersey, USA; or Ensure Plus; Abbott Laboratories, Ross Products Division, Columbus, Ohio, USA) to jills that appear to be carrying large litters (2). Without such a high quality ration, the demand for nutrients by the developing kits exceeds the energy resources available to the jill from her diet, and body fat mobilization and hypoglycemia occur (2,3).

Severe hypoglycemia partially accounts for the unresponsive, moribund presentation of many affected jills. In an attempt to increase per gluconeogenesis and offset negative energy balance, the jill mobilizes more triglycerides from fat stores, which are hydrolyzed to release free fatty acids (FFA) (7). Triglycerides are resynthesized from the FFA and, as the ability of the liver to metabolize and export the stored fat is overwhelmed, severe hepatic lipidosis ensues (7). In advanced cases of pregnancy toxemia, the enhanced mobilization of FFAs from triglycerides, combined with a shift in hepatic metabolism from fat synthesis to fat oxidation, causes ketogenesis (7). As ketones begin to accumulate in the extracellular space, they elude complete resorption and spill into the urine, resulting in ketonuria and osmotic diuresis (7). This contributes to the severe dehydration and ketoacidotic state seen in many affected jills.

Prognosis for the toxemic jill depends on the extent of hepatic lipidosis, degree of ketoacidosis, and the quality of postoperative care (3). Body temperature after active rewarming must be closely monitored, as ferrets are very susceptible to heat prostration (2). Although prognosis for such a jill is generally guarded, those that survive the first 24 h postsurgery are likely to recover (2). Prognosis for the kits is extremely poor. If they are born before the 40th d gestation or if there is no foster mother available, they are best euthanized, as the toxemic jill will have no milk (2,3).

Pregnancy toxemia in the ferret is a serious, preventable disease. Many commercial ferret diets are well formulated and adequate to meet the needs of primiparous jills. Ferret owners must be educated on proper nutrition for their pets. Prevention is especially important in a disease where prognosis for both the affected mother and her babies is so poor.