HISTORY / CLINICAL SIGNS: ADR X 3 days (progressively worse) according to owners. Inappetant. Stares at water bowl, but will not drink. No known vomiting or diarrhea. Uses litterbox in multi-cat household, so unknown urination habits. Not UTD on vaccines. Not on flea/tick/HW prevention.
PHYSICAL EXAM FINDINGS: BCS 1/9. T 99.2ยฐF (37.3ยฐC). P 140. R 30. mm tacky. CRT 2-3 sec. Delayed skin tent. Moderate dental disease. Flea dirt. Cervical ventroflexion. Generalized muscle cachexia. Intestines distended. Diarrhea w/ hematochezia.
What is on your differential diagnosis list? (What could be causing the cervical ventroflexion?) What diagnostic tests would you order? What empirical treatments, if any, would you start?
.
.
.
(SCROLL DOWN)
.
.
.
DIAGNOSTIC TESTS & RESULTS:
- CBC: PCV 40%. Hypochromic RBC. High WBC (26.9X10^3cells/uL) with mature neutrophilia.
- Chemistry: Low Glu 58mg/dL. High BUN 48mg/dL (. Low Ca 8.1mg/dL. Low Alb 2.7g/dL. High AST 116U/L. High TBil 1.1mg/dL. Low Na 136mEq/L. Low K 2.3mEq/L. Low Cl 113mEq/L. Low CO2 10mEq/L.
- FeLV/FIV: negative
- Urinalysis: Free-catch. Yellow, cloudy. USG 1.019. pH 6.5. Glu 1+. Ketones 4+. Bili 1+. Blood 2+. Protein 3+. SSA/Bumin 2+. Sediment: RBC 0-2/hpf, WBC 1-3/hpf, epithelial cells 8-20/hpf, granular casts 0-1/lpf, moderate bacteria/hpf.
- Abdominal radiographs: Decreased serosal detail. Moderate generalized small bowel distension.
- Abdominal ultrasound: Stomach: gas-distended. SI: mildly fluid/gas-distended, no abnormal wall thickening/layers. Kidney: mineral foci in left renal crest (no pyelectasia).
Based on these findings, what is your diagnosis, recommended treatment, and prognostic outlook?
.
.
.
(SCROLL DOWN)
.
.
.
TREATMENT / PROGNOSIS: While diagnostic test results were pending, this patient was initially stabilized with the following therapies: Dewormer. Flea treatment. IV fluids: LRS + 40mEq/L KCl + 2.5% dextrose. IV ampicillin/sulbactam.
However, this patient did not respond well to therapy over the next 24hr, and based on the poor outlook of the preliminary test results, the owners chose euthanasia.
NECROPSY RESULTS: Kidneys: proximal tubules have incomplete/missing epithelium = mild tubular nephrosis. Parathyroid gland: cells are small w/ scant cytoplasm = atrophy.
DIAGNOSIS: This cat had RENAL TUBULAR DYSFUNCTION, resulting in the epithelial cells and granular casts noted on urinalysis along with the glucosuria (despite hypoglycemia), proteinuria, and ketonuria as well as poor BCS, dehydration, electrolyte derangements, and azotemia noted in this cat. A definitive cause was not confirmed, though renal tubular nephrosis in cats is typically caused by an acquired renal injury followed by Fanconi Syndrome. Though an overall uncommon disorder in cats, Fanconi Syndrome can develop due to primary hypoparathyroidism. Atrophy of this patientโs parathyroid gland was noted on necropsy, so perhaps this cat indeed had Fanconi Syndrome. In dogs, Fanconi Syndrome may also be inherited (as in the Basenji) or caused by renal-toxic drugs. Prognostic outlook is variable due to the severity of subsequent kidney failure.
Any other questions, comments, or suggestions?
BONUS QUESTION: Why do you think this cat had high BUN yet a normal creatinine?
.
.
.
(SCROLL DOWN)
.
.
.
ANSWER TO BONUS QUESTION: A patient with kidney dysfunction is expected to have elevated BUN and creatinine on bloodwork. However, with cachexia and muscle wasting, such a patient may have normal or even decreased serum creatinine. Since creatinine is a waste byproduct of muscle cells, decreased muscle mass means less creatinine is released into the bloodstream.
Unless otherwise stated, these clinical cases are real-life cases that I have managed as a veterinarian in general small animal veterinary practice or else assisted with as a student in vet school. These cases are a great real-world learning tool for vet students and other veterinary professionals. They shall be used for learning purposes and collaboration of knowledge only. These cases are not intended to diagnose or treat any disease by pet owners. – Maranda Elswick, DVM