History
A5-year-old female alpaca was evaluated for uterine prolapse and inability to rise. The owners reported that the alpaca had given birth unattended 2 days prior, had been recumbent and unable to rise since giving birth, and had begun prolapsing its uterus earlier the day of presentation.
On presentation to the hospital, the alpaca was nonambulatory. Its pelvic limbs were abducted, with stifle joints outward and plantar surfaces of the feet contacting the ground on either side of its body (ie, frog legged). The alpaca was not able to maintain adduction of its pelvic limbs while recumbent and was not able to support weight on its pelvic limbs. The alpaca’s uterus was prolapsed, edematous, and erythematous. The remaining findings on physical examination were unremarkable. Neurologic examination revealed signs of deep pain perception in all 4 limbs. The alpaca was able to stand on its front limbs and place them appropriately while its pelvic region was supported. Conscious proprioception was absent in the pelvic limbs. The patient had decreased extensor tone of both pelvic limbs. Motor function was present in all 4 limbs. Panniculus response was appropriate, and no reaction was elicited upon palpation of the vertebral column or limbs. No muscle atrophy or abnormal swellings were noted.
Assessment
Anatomic diagnosis
In this alpaca, pelvic limb paresis with clinically normal spinal reflexes was consistent with peripheral neuropathy.
Likely location of the lesion
The lesion was most likely a lower motor neuron lesion affecting the pelvic limbs, consistent with nerve root dysfunction between L4 and S3. Caudal spinal cord lesion could not be ruled out based on clinical findings.
Etiologic diagnosis
Differential diagnoses included peripheral neuropathy due to pelvic compression from parturition (eg, obturator nerve or sciatic trauma), neoplasia resulting in compression of the spinal cord, systemic illness leading to septic shock and generalized weakness, inflammation of the spinal cord secondary to aberrant parelaphostrongylus tenius migration, bacterial meningitis, spinal cord trauma, and metabolic derangements secondary to end-stage pregnancy, parturition, and milk production such as hypocalcemia, hypokalemia, ketosis, hypertriglyceridemia, hyperglycemia or hypophosphatemia. The diagnostic plan included electrolyte and blood gas panels and biochemical analyses to evaluate general health and potential metabolic causes of muscle weakness. A lumbosacral CSF sample was obtained to investigate an inflammatory or infectious cause. Additional imaging such as CT was declined by owners.
Diagnostic Test Findings
Biochemical analyses revealed mildly low serum concentrations of sodium (137.4 mEq/L; reference range, 142 to 156 mEq/L), bicarbonate (10.4 mmol/L; reference range, 19 to 29 mmol/L), sorbitol dehydrogenase (SDH; 2 U/L; reference range, 3 to 10 U/L), and cholesterol (8 mg/dL; reference range, 12 to 58 mg/dL) and high concentrations of glucose (290 mg/dL; reference range, 100 to 132 mg/dL) and cortisol (1.59 µg/dL; reference range, 0.7 to 1.3 µg/dL), consistent values observed secondary to a stress response within our hospital population. Results for CSF analysis were unremarkable. After 1 week the patient had shown minimal response to physical therapy involving hobbles and a sling 3 times daily for 5 to 10 minutes and treatment with dexamethasone (13.6 mg, IV, q 24 h) and fenbendazole (50 mg/kg, PO, q 24 h for 4 days).
The owners elected euthanasia for the alpaca after 7 days of treatment. Euthanasia was performed via intravenous administration of 20 mL of pentobarbital-phenytoin solution for large animals.
Postmortem examination revealed gross hemorrhage and edema enveloping the obturator nerve, heterogenous discoloration of the endometrium with suppurative material located in the left uterine horn as well as pale tan lesions in the cortex of both kidneys. Histopathology of the obturator nerve revealed Renaut body mucoid tissue, which is consistent with damage due to external compression of the nerve. Both obturator nerves showed axonal degeneration. The final diagnosis was bilateral obturator nerve paralysis and endometritis with ascending infection to the kidneys resulting in pyelonephritis. Other differential diagnoses for pyelonephritis would include hematogenous spread or cystitis. However, signs of neither sepsis with septic emboli nor cystitis were identified during the postmortem examination, thus making them less likely differential diagnoses.
Comments
Although obturator nerve paralysis is a common postpartum complication in cattle, it is not well described in camelids. Though “calving paralysis” in cattle is sometimes referred to as obturator nerve paralysis, 1 study1 indicated that more nerves are generally involved, as cattle that have only damage to the obturator nerve are still able to rise. This is explained by the innervation of the adductor muscles of the rear legs; Though the obturator nerve innervates many of the adductors, the semimembranosus and semitendinosus, are innervated by branches of the sciatic nerve and also adduct the rear legs.1 This alpaca’s inability to rise is suggestive of damage to more than just the obturator nerve. In 1 study,1 when the nerve root of L6 was sectioned surgically it resulted in the recumbency that is usually associated with calving paralysis. The L6 nerve root supplies the sciatic nerve, which could have been consistent with the presentation of the alpaca of the present report, because this neural tissue was included in the area of the spinal cord to which the lesion was localized. Treatment for calving paralysis involves ensuring proper footing, hobbling the pelvic limbs to prevent excessive pelvic limb abduction, and anti-inflammatory drugs, such as steroids or NSAIDs. These management strategies can be adapted to camelids as the suspected pathogenesis is the same. Response to treatment depends on complete versus partial damage to the nerve. To the authors knowledge there is no published data documenting this disease process or treatments in species other than cattle.
Acknowledgments
The authors declare that there were no conflicts of interest. No third-party funding or support was received in connection with this case or the writing or publication of the manuscript.
References
Cox VS, Breazile J. Experimental bovine obturator paralysis. Vet Rec. 1973;93(4):109–110. doi:10.1136/vr.93.4.109
