Spontaneous resolution of bilateral congenital patellar luxation in an alpaca cria

Abstract

An 8-day-old alpaca was presented for suspected meconium impaction and abnormal gait and posture. Physical examination revealed bilateral medial patellar luxation. In previous reports, medical treatment of patellar luxation in crias has been associated with a poor to grave prognosis; here we report a case of successful resolution.

The relatively recent introduction of alpaca farming in Canada, starting in the late 1980s, has been mostly for small hobby farm and small-scale fiber production purposes (1). The number of alpacas in Canada is relatively low compared with other livestock species, and clinical research involving alpacas is still in preliminary stages for many aspects of their anatomy and physiology. As such, there is little information relating to orthopedic abnormalities and/or defects in this species such as angular limb deformities, arthrogryposis, hemivertebrae, scoliosis, and luxation of the patella (2,3). Although lateral and medial luxations of the patella have been reported in South American camelids (SACs), the current limited literature reports a higher number of cases of lateral luxation (3,4). In general, untreated unilateral and bilateral patellar luxations are given a poor prognosis for long-term survival (2). However, surgical intervention was reported to be successful in a small number of cases (4–7). Conservative management generally seems to result in an unfavorable outcome (2). The case described herein demonstrates successful resolution of bilateral medial patellar luxation in an alpaca cria over a period of approximately 2 wk, without any noticeable conformational abnormalities observed over an 18-month follow-up period.

Case description

An 8-day-old male alpaca cria (Vicugna pacos) was presented to the Ontario Veterinary College Health Sciences Centre (OVC-HSC) Large Animal Hospital for evaluation of suspected persistent meconium impaction and constantly attempting to defecate. The cria was born at a normal gestational period, the birth had been unassisted and unobserved, and later that day the owner reported seeing the passing of some meconium, but then no feces were seen for 3 d. At that time, it was also noticed that the cria was walking with a hunched back and flexed hind legs; the owner suspected a meconium impaction and administered an enema which did not result in the passage of any feces. Upon examination by the referring veterinarian and digital examination of the rectum some meconium was expelled. Positive contrast radiography using a barium enema was performed to rule out meconium impaction, atresia coli, or a gastrointestinal stricture; no abnormalities were seen and so the cria was referred for further workup.

On presentation, the cria was bright, alert, and responsive, in good body condition, and weighed 12.5 kg. He was vocalizing normally. Vital parameters including heart rate [84 beats/min, reference range (RR): 70 to 100 beats/min] and temperature (38.6°C, RR: 37.8 to 38.9°C) were within normal limits. Moderate tachypnea was present (60 breaths/min, RR: 20 to 30 breaths/min), likely due to the new environment and manipulation during the physical examination (2). Throughout the examination the cria stood with an arched back and raised tail and appeared to be straining frequently to defecate; normal urination was observed. When ambulating, the cria did not fully extend either hind leg and walked with a hopping/bouncing-like movement and continuously arched back (Figure 1). On palpation, the lumbar muscle mass was tense and firm. When walking around the stall both hind limbs remained flexed at the tarsi and stifles. Tail tone and anal tone were within normal limits. Based on the history and clinical findings, the cria was sedated with ketamine (Vetalar; Bioniche, Belleville, Ontario), 1.6 mg/kg body weight (BW), IM, butorphanol (Torbugesic; Wyeth, Guelph, Ontario), 0.1 mg/kg BW, IM, and xylazine (Rompun; Bayer, Toronto, Ontario), 0.3 mg/kg BW, IM, for contrast fluoroscopy of the distal gastrointestinal tract. A barium sulfate (Liquid Polibar Plus; Therapex, Montreal, Quebec) enema was administered for the contrast fluoroscopy, which revealed no abnormalities. Right lateral and ventrodorsal radiographs of the thoracolumbar vertebrae were taken to determine if a congenital or traumatic malformation of the thoracolumbar spine was present but no radiographic abnormalities were identified.

Figure 1.

Typical stance adopted by the cria during hospitalization, showing the “hunched” posture consisting of bilaterally flexed stifle and tarsal joints.

As the spine and distal gastrointestinal tract had been ruled out as the causes for the cria’s abnormal posture and gait, both hind limbs were examined for abnormalities. It was noted that when each stifle was extended, the patellas of both limbs were deviated medially and could not be manipulated into the trochlear groove, and remained medial to the trochlear groove when the limbs were in the flexed position. Using the grading scale developed for patellar luxation in dogs (8), a grade of IV/IV was assigned. The patellas also did not exhibit the normal range of motion when the limbs were flexed and extended and remained proximal and medial to their normal anatomical location. The owner declined to have radiographs of the stifles taken following the barium contrast study and thoracolumbar radiographs. Based on the clinical findings as assessed by the internists and surgery clinician, a diagnosis of bilateral congenital medial luxation of the patellas was made. As per the literature recommendations (2), the owner was given a poor prognosis for normal hind limb function. Further, considering the potential genetic component of the condition, the owner was encouraged not to keep this cria for breeding stock. The owner elected to take the cria home and monitor him, with the option of humane euthanasia should the cria’s quality of life decline.

Follow-up conversation (weekly for 6 wk) with the owner revealed that the cria had always nursed very well and maintained a good appetite. The cria continued to show the hopping-like gait for approximately 10 d but during that time the owner noticed that his gait improved gradually and steadily, with a return to a completely normal walking and running stance thereafter. The owner reported that he did not administer any treatments or provide special management conditions. A photograph taken approximately 8 mo following presentation to the hospital showed the cria winning his class at a provincial alpaca show (Figure 2). In the last follow-up 16 mo later, the male alpaca was identified as a high quality fine fleece producer but the owner elected not to use him as reproductive stock.

Figure 2.

Photograph showing the cria winning his class at an alpaca show. Note the normal hind limb anatomy.

Discussion

To the authors’ knowledge, spontaneous resolution of patellar luxation in a cria has not previously been reported. This case suggests that in some instances a favorable prognosis could be given, compared to previous reports (2). However, the underlying etiology, e.g., osseous compared to ligamentous abnormality, should be considered, as the degree of severity of any patellar and femoral groove defect(s) could play a significant role in spontaneous recovery versus surgical intervention.

Patellar luxation can be congenital or acquired, with acquired patellar luxation being almost always traumatic in origin (9). Congenital patellar luxation, in which the patella is located in an abnormal position since the time of birth, can be due to osseous abnormalities of the femoropatellar joint, soft tissue abnormalities of the patellar tendon, collateral patellar ligaments, or quadriceps muscle, or muscular weakness due to prematurity (9). Traumatic events at the time of parturition, including prolonged parturition or malpositioning of the fetus during parturition, could result in rupture of the patellar retinacula, damage to the patellar tendon, or femoral nerve deficit with concurrent quadriceps dysfunction resulting in abnormal patellar location (9). Due to the variety of causes, treatment recommendations and prognosis vary. It is plausible that all of these causes could be present in SACs, although the current literature is quite limited. Anatomy of the stifle joint of SACs more closely resembles that of dogs and sheep than of horses or cattle, consisting of a single compartment with a single patellar ligament attaching the patella to the tibial tuberosity and tibial crest and a larger medial trochlear ridge compared to the lateral. In theory, this should make lateral patellar luxation more common than medial luxation (4,10).

Although most published cases of patellar luxation in SACs are associated with suspected or known trauma to the stifle joint (4,6), cases of congenital luxation with a suspected hereditary component have also been reported (2,5). Patellar luxation has a higher prevalence in certain breeds of dog (11) and is thought to be inherited in the Dutch Kooiker breed (12). In a case series describing diagnosis and surgical repair of patellar luxation in sheep (13), all affected sheep came from 1 herd and were all traced back to a related ram and ewe that were purchased as foundation breeding stock; this is highly suggestive of an inherited component to the disease. In horses, while luxation in adults is generally due to a traumatic incident (14,15), it is thought that there is a congenital hereditary form in miniature horses (16,17) and monogenic autosomal recessive hereditary transmission is suspected in Shetland ponies (18). Based on inferences from other species, it is plausible that patellar luxation has a hereditary component in SACs despite the paucity of current literature.

Patellar luxation and its treatment have been described in beef and dairy calves (19–23), sheep (13), a goat (24), and various horse breeds (14–16,18,25,26). While current recommendations in cattle indicate that surgery is required to correct patellar luxation in cases without femoral nerve injury that are grade III or IV/IV (9), the bilateral patellar dysfunction described in this cria appeared to fully resolve without any surgical intervention (Figure 2).

As the history was highly suggestive of meconium impaction, most of the initial diagnostic workup focussed on ruling out this condition, resulting in most of the client’s budget being spent on diagnostic tests for meconium impaction and radiographs of the lumbosacral vertebrae. This was partly due to the lack of general knowledge of congenital conditions of SACs, and illustrates the importance of performing a complete and thorough physical examination on all neonates regardless of species, including a complete musculoskeletal examination.

Limitations of this case report include the lack of stifle radiographs taken to confirm the bilateral patellar luxation or presence of other osseous abnormalities. Although palpation and observation of the cria’s stance and gait were highly suggestive of medial patellar luxation, radiographs were not performed due to the assumed poor prognosis and reluctance of the owner to financially invest in an animal that potentially would have to be euthanized in the near future. There was limited information available about the periparturient period and so trauma during or shortly after birth could not be ruled out. Also, there was no comprehensive neurological workup and so it was not possible to rule out femoral nerve dysfunction. Another limitation is the lack of regular veterinary rechecks of the cria and radiographic and/or ultrasonographic assessment of the stifle joint during its growing phase.

This is the first reported case of spontaneous resolution of bilateral medial patellar luxation in an alpaca cria. This suggests that some patellar luxations in SACs may be self-correcting, and that surgical correction should not necessarily be undertaken immediately. Although it is difficult to formulate recommendations based on an isolated case, the authors suggest any neonatal SAC exhibiting signs of patellar luxation, in the absence of any other congenital disorders or systemic disease, should be monitored for 3 to 4 wk and surgical correction only performed if there is no improvement during that time. CVJ