|
NEUROMUSCULAR CASE OF THE MONTH - SEPTEMBER 2001
Progressive pelvic limb paresis in a 6 year old FS Rottweiler dog
Contributed by Dr. Michael Podell
The Ohio State University
Columbus, OH 43210-1089
Clinical History
The dog was obtained approximately 1 year ago from a friend. Over the past year, she had been diagnosed with cystic and renal calcium
oxalate calculi (treated with nephrotomy and cystotomy), recurrent lower urinary tract infections (treated with multiple antibiotics and
vulvoplasty), and chronic renal failure. She had recently traveled in the Carolinas. The owner had noticed some exercise intolerance and
dyspnea leading to an inability to rise over the 2 days prior to presentation. Appetite was reduced and the dog was polydipsic. Current
medications included 100 mg nitrofurantoin PO TID for the past 6 weeks and Heartguard Plus monthly year round.
Physical and Neurological Examination
(See video clip) *this is a large file and download time will depend on connection speed*
Weight: 49 kg; T=102.3; HR=160 bpm; RR=panting. The dog was alert and responsive. A grade 3 caudal-ataxia with reluctance to rise was observed, although the dog
was able to walk with support. Evaluation of cranial nerves showed a decreased blink and gag reflexes and laryngeal stridor. Conscious proprioception, hemistanding
and hemihopping, and spinal reflexes were depressed in the pelvic limbs. Nociception was normal. A lower motor neuron disorder affecting L4-S1 and cranial nerves
was suspected.
Diagnostic Testing
No specific abnormalities were observed on CBC. The serum chemistry profile showed an elevation of creatinine (2.1 mg/dl; reference
0.6-1.6) and BUN (31 mg/dl; reference 5-20). Calcium oxalate crystals were reported on urinalysis.
Thoracic radiographs: No visual lesions
Abdominal ultrasound: Hyperechoic calculi in the left and right renal pelvis, left hydroureter, and the urinary bladder was thickened
with mineral densities
Urine culture and sensitivity: Moderate malassezia sp. (confirmed twice)
Thyroid panel: OSU T4=0.74 ug/dl (0.5-2.1 ); TSH = 0.59 ng/ml (0.02-0.25) and MSU Total T4 = 16 (15-50), Total T3= 0.3 (1-2.5), Free
T4 by dialysis=7 (9-40), Free T3=2.8 (2.8-6.5), T4 autoantibody=18 (<20), T3 autoantibody=6 (<10), TSH=29(0-30) and Thyroglobulin
autoantibody=92 (<200).
Nitrofurantoin serum concentration: 0.33 mcg/ml (>1 mcg/ml considered toxic in humans)
EMG: Multifocal spontaneous activity consisting mostly of fibrillation potentials in all distal appendicular muscles and some proximal
appendicular muscles.
MNCV - Conduction block was present within the tibial nerve. MNCV was decreased within the ulnar nerve (44.6 m/sec; reference 51.9
+/- 6.2) as was the distal amplitude (14.9 mV; reference 24.0 +/- 6.48).
|
Muscle and Nerve Biopsies: A fresh frozen biopsy specimen from the cranial tibial muscle showed scattered singular angular atrophied fibers of both fiber
types. Fiber type grouping was not observed. A fascicular biopsy from the peroneal nerve showed edema in the subperineurial area and dissecting between
layers of the perineurium (Fig. 1. Asterisk indicates area of edema, arrow highlights myelin debris) and axonal degeneration (Fig. 2. Right facing arrow
shows nerve fiber undergoing axonal degeneration, left facing arrow shows myelin ovoid). Regenerative changes were not evident. |
Figure 1.
Figure 2.
|
Diagnosis
Peripheral neuropathy possibly associated with nitrofurantoin neurotoxicity or hypothyroidism. Peripheral neuropathy has been reported
in humans following therapy with nitrofurantoin (1-3), most commonly occurring in patients with impaired renal function. Rapid deterioration,
within days, often followed the onset of symptoms. Although the serum concentration of nitrofurantoin was not in the toxic range in
this dog, earlier human studies showed that toxicity is not a dose dependent process. Although highly suggestive of hypothyroidism,
the thyroid panel was not 100% conclusive.
Treatment and Outcome
The dog was treated with Soloxine 1 mg PO BID, Fluconozole 100 mg PO BID, Vitamin E 400 IU daily, Vitamin B-complex (B-100) daily,
and physical therapy. Nitrofurantoin therapy was stopped. There was a gradual improvement in strength and laryngeal function in the
2 months following diagnosis with stable renal function. There has been, however, recurrence of resistant bacterial urinary tract infection.
References
1. Yiannikas C, Pollard JD, McLeod JG. Nitrofurantoin neuropathy. Aust NZ J Med 11:400-405, 1981.
2. Holmberg L, Boman G, Erikson B et al. Adverse reactions to nitrofurantoin (921 reports). Am J Med 69:733-738, 1980.
3. White WT, Harrison L, Dumas J. Nitrofurantoin unmasking peripheral neuropathy in a Type 2 diabetic patient. Arch Intern Med 144:821,
1984.
4. Conklin JD, Wagner DL. Excretion of nitrofurantoin in dog hepatic bile. Br J Pharmac 43:140-150, 1971.
Back to Top
|
