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    Representative lateromedial radiographic image of the right forefoot of a clinically normal horse (part 2; A) and a horse with oligofructose-induced laminitis (part 3; B) and a photograph of the right forefoot of the horse in panel B (C) following placement of a cortical bone screw (diameter, 5.5 mm; length, 38 mm) without (A) or with (group 3; B and C) a washer. For each foot, the screw was aseptically placed through the midline of the dorsal hoof wall into P3 2 cm distal to the coronary band. In part 3 of the study, screw placement (without a washer) for group 2 was the same as that for the horses in part 2. Notice that the screws were inserted through the dorsal cortex of P3 only (ie, unicortically inserted) to prevent inadvertent impingement of the DDFT insertion. R = Right forefoot.

  • 1. Mungall BA, Kyaw-Tanner M, Pollittt CC. In vitro evidence of a bacterial pathogenesis of equine laminitis. Vet Microbiol 2001;79:209223.

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  • 2. Van Eps AW, Pollitt CC. Equine laminitis model: cryotherapy reduces the severity of lesions evaluated seven days after induction with oligofructose. Equine Vet J 2009;41:741746.

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    • Export Citation
  • 3. Lochner FK, Milne DW, Mills EJ, et al. In vivo and in vitro measurement of tendon strain in the horse. Am J Vet Res 1980;41:19291937.

  • 4. Yovich JV, Turner AS, Smith FW. Holding power of orthopedic screws in equine third metacarpal and metatarsal bones: part II. Adult horse bone. Vet Surg 1985;14:230234.

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    • Export Citation
  • 5. van Eps AW, Pollitt CC. Equine laminitis induced with oligofructose. Equine Vet J 2006;38:203208.

  • 6. Pollitt CC. Basement membrane pathology: a feature of acute equine laminitis. Equine Vet J 1996;28:3846.

  • 7. Sherlock C, Parks A. Radiographic and radiological assessment of laminitis. Equine Vet Educ 2013;25:524535.

  • 8. de Laat MA, van Eps AW, McGowan CM, et al. Equine laminitis: comparative histopathology 48 hours after experimental induction with insulin or alimentary oligofructose in Standardbred horses. J Comp Pathol 2011;145:399409.

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    • Export Citation
  • 9. Lopez MJ, Wilson DG, Vanderby R Jr, et al. An in vitro biomechanical comparison of an interlocking nail system and dynamic compression plate fixation of ostectomized equine third metacarpal bones. Vet Surg 1999;28:333340.

    • Search Google Scholar
    • Export Citation
  • 10. Van Epps AW, Pollitt CC. Equine laminitis model: lamellar histopathology seven days after induction with oligofructose. Equine Vet J 2009;41:735740.

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Novel technique for prevention of rotation of the distal phalanx relative to the hoof wall in horses with acute laminitis

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  • 1 1Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada.
  • | 2 2Department of Veterinary Pathology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK S7N 5B4, Canada.

Abstract

OBJECTIVE

To determine the holding capacity of a 5.5-mm-diameter cortical bone screw when placed in the third phalanx (P3) of horses and assess whether screw placement through the dorsal hoof wall into P3 would be tolerated by clinically normal horses and would alleviate signs of pain and prevent P3 rotation in horses with oligofructose-induced laminitis.

ANIMALS

40 limbs from 10 equine cadavers and 19 clinically normal adult horses.

PROCEDURES

In part 1 of a 3-part study, a 5.5-mm-diameter cortical bone screw was inserted by use of a lag-screw technique through the dorsal hoof wall midline into P3 of 40 cadaveric limbs and tested to failure to determine screw pullout force. In part 2, 6 horses had 5.5-mm-diameter cortical bone screws placed in both forefeet as described for part 1. Screws were removed 4 days after placement. Horses were monitored for lameness before and for 2 weeks after screw removal. In part 3, 13 horses were randomly assigned to serve as controls (n = 3) or undergo screw placement without (group 2; 6) or with (group 3; 4) a washer. Following the acquisition of baseline data, horses were sedated and administered oligofructose (10 g/kg) via a stomach tube. Twenty-four hours later, screws were placed as previously described in both forefeet of horses in groups 2 and 3. Horses were assessed every 4 hours, and radiographic images of the feet were obtained at 96 and 120 hours after oligofructose administration. Horses were euthanized, and the feet were harvested for histologic examination.

RESULTS

The mean ± SD screw pullout force was 3,908.7 ± 1,473.4 N, and it was positively affected by the depth of screw insertion into P3. Horses of part 2 tolerated screw placement and removal well and did not become lame. All horses of part 3 developed signs of acute lameness, and the distance between P3 and the dorsal hoof wall increased slightly over time. The change in the ratio of the dorsal hoof wall width at the extensor process of P3 to that at the tip of P3 over time was the only variable significantly associated with treatment.

CONCLUSIONS AND CLINICAL RELEVANCE

Placement of a 5.5-mm-diameter cortical bone screw through the dorsal hoof wall into P3 had sufficient holding power to counteract the pull of the deep digital flexor tendon in approximately 500-kg horses, and placement of such a screw was well tolerated by clinically normal horses but did not alleviate signs of pain in horses with oligofructose-induced laminitis. Further research is necessary before this technique can be recommended for horses with naturally occurring acute laminitis.

Abstract

OBJECTIVE

To determine the holding capacity of a 5.5-mm-diameter cortical bone screw when placed in the third phalanx (P3) of horses and assess whether screw placement through the dorsal hoof wall into P3 would be tolerated by clinically normal horses and would alleviate signs of pain and prevent P3 rotation in horses with oligofructose-induced laminitis.

ANIMALS

40 limbs from 10 equine cadavers and 19 clinically normal adult horses.

PROCEDURES

In part 1 of a 3-part study, a 5.5-mm-diameter cortical bone screw was inserted by use of a lag-screw technique through the dorsal hoof wall midline into P3 of 40 cadaveric limbs and tested to failure to determine screw pullout force. In part 2, 6 horses had 5.5-mm-diameter cortical bone screws placed in both forefeet as described for part 1. Screws were removed 4 days after placement. Horses were monitored for lameness before and for 2 weeks after screw removal. In part 3, 13 horses were randomly assigned to serve as controls (n = 3) or undergo screw placement without (group 2; 6) or with (group 3; 4) a washer. Following the acquisition of baseline data, horses were sedated and administered oligofructose (10 g/kg) via a stomach tube. Twenty-four hours later, screws were placed as previously described in both forefeet of horses in groups 2 and 3. Horses were assessed every 4 hours, and radiographic images of the feet were obtained at 96 and 120 hours after oligofructose administration. Horses were euthanized, and the feet were harvested for histologic examination.

RESULTS

The mean ± SD screw pullout force was 3,908.7 ± 1,473.4 N, and it was positively affected by the depth of screw insertion into P3. Horses of part 2 tolerated screw placement and removal well and did not become lame. All horses of part 3 developed signs of acute lameness, and the distance between P3 and the dorsal hoof wall increased slightly over time. The change in the ratio of the dorsal hoof wall width at the extensor process of P3 to that at the tip of P3 over time was the only variable significantly associated with treatment.

CONCLUSIONS AND CLINICAL RELEVANCE

Placement of a 5.5-mm-diameter cortical bone screw through the dorsal hoof wall into P3 had sufficient holding power to counteract the pull of the deep digital flexor tendon in approximately 500-kg horses, and placement of such a screw was well tolerated by clinically normal horses but did not alleviate signs of pain in horses with oligofructose-induced laminitis. Further research is necessary before this technique can be recommended for horses with naturally occurring acute laminitis.

In horses, laminitis is a common and often life-threatening condition with multiple possible causes. Regardless of the initiating cause, the end result is mechanical failure of the hoof owing to various degrees of separation of the insensitive part of the hoof wall from the underlying sensitive tissues when mechanical traction is applied across the lamina.1 In both horses with naturally occurring and those with experimentally induced laminitis, it is debatable whether any treatment approach will alter the course of disease once mechanical failure of the hoof has begun. Currently, there is no universally accepted treatment for the prevention of P3 rotation, and most treatments are medical in nature. Research indicates that repair of the laminar tissue occurs quickly in the absence of physical disruption.2 If the anatomic integrity of the hoof could be maintained during the prodromal stages of laminitis, it is possible that complete recovery could occur.

Forces that act on the hoof during weight bearing include a vertical component transmitted down the bony column and rotation of P3 at the distal interphalangeal joint such that the tip of P3 rotates dorsally while being constrained by an opposing tensile force applied through the DDFT. Rotation of the distal tip of P3 occurs when the basement membrane fails and the tension applied by the DDFT is essentially unopposed. In an average-sized (approx 500-kg) horse, the tensile force required to maintain the distal interphalangeal joint in a neutral position during walking is slightly > 400 kg.3 The holding power of 5.5-mm-diameter cortical screws in metaphyseal metacarpal bone is about 800 kg. The forces that act on the distal interphalangeal articulation function much like a pulley system. The roughly 400 kg of tensile force in the DDFT is transmitted around the joint, and that force is opposed by the hoof-P3 complex. From a biomechanical standpoint, if the screw-holding power of P3 is even half that of metaphyseal metacarpal bone, use of one 5.5-mm-diameter screw to anchor the hoof wall to P3 should be strong enough to successfully oppose the pull of the DDFT. In reality, that mechanical advantage should be even more powerful because screws placed in the distal aspect of P3 benefit from simple type 1 lever mechanics. Additionally, the major forces that determine screw-holding power are the size of the screw and thickness of the cortical bone into which it is placed.4 Proportionately, the cortical area of P3 is thicker than that of other bones. Therefore, its holding strength may be sufficient enough that the screw would not have to cross both cortices to maintain adequate holding power, which should translate into less disruption of normal tissues and faster healing.

The study reported here consisted of 3 parts, the objectives of which were to determine the holding capacity of a 5.5-mm-diameter cortical bone screw when placed through the dorsal hoof wall into P3 of equine cadaveric feet (part 1) and to assess whether placement of a 5.5-mm-diameter cortical bone screw through the dorsal hoof wall into P3 would be tolerated in horses without evidence of P3 pathology (part 2) and would alleviate signs of pain and prevent P3 rotation in horses with experimentally induced acute laminitis from an oligofructose overload (part 3). The hypotheses for the study were that placement of a 5.5-mm-diameter cortical bone screw through the dorsal hoof wall into P3 would provide sufficient strength to prevent mechanical failure (ie, laminar separation) of the hoof under physiologic loading conditions, screw placement would be well tolerated by clinically normal horses, and placement of one 5.5-mm-diameter cortical bone screw (with or without a washer) through the dorsal hoof wall into P3 would result in fewer signs of pain and less P3 rotation than those observed for untreated control horses with oligofructose-induced laminitis.

Materials and Methods

All animal procedures were reviewed and approved by the University of Saskatchewan Animal Research Ethics Board and were performed in accordance with guidelines established by the Canadian Council on Animal Care for humane animal use.

Evaluation of the screw-holding power of P3 (part 1)

From each of 10 horses that were euthanized for reasons other than musculoskeletal disease, the distal portion of all 4 limbs was harvested by disarticulation and removal at the metacarpophalangeal or metatarsophalangeal joint. The limbs were wrapped in towels soaked with saline (0.9% NaCl) solution and stored frozen at −20°C until 24 hours before testing, at which time they were allowed to thaw at room temperature (approx 22°C). Once thawed, each limb was further disarticulated at the distal interphalangeal joint. Lead markers were placed on the dorsal hoof wall at 1-cm intervals, and a lateral radiographic image was obtained. With the lead markers used for reference, a 15-mm-deep hole centered 2 cm proximal to the distal tip of P3 was drilled through the dorsal hoof wall with a 5.5-mm drill bit. For 10 pairs of feet (1 forefoot and 1 hind foot from the same horse), a 4.0-mm drill bit was placed through the previously drilled hole, aligned perpendicular to hoof wall, and used to drill a hole completely through P3. For the remaining 10 pairs of limbs, the same procedure was used to drill a hole into P3 that stopped short of exiting the palmar or plantar cortex of the bone. The depth of each hole was measured and recorded. Each hole was subsequently tapped, and a 5.5-mm-diameter cortical bone screw of appropriate length was inserted.

Each hoof construct was mounted in a steel holding fixture designed specifically for screw pullout studies. The screwhead was inserted into a mounted drill chuck through an articulated fixture designed to ensure that the direction of distraction aligned with the shaft of the screw. Constructs were loaded to failure in distraction at a rate of 1.27 mm/s with a servohydraulic materials testing machine.a Load (N) and stroke displacement (mm) signals were collected from the testing machine at a rate of 10 Hz. Forty pullout trials (20 forefeet and 20 hind feet) were conducted. Data were recorded in a spreadsheet program.b

Assessment of screw placement in P3s of clinically normal horses (part 2)

Six horses (5 mares and 1 gelding) with a mean body weight of 465 kg (range, 368 to 580 kg) and no evidence of preexisting musculoskeletal abnormalities of the forelimbs were purchased. Horses were preconditioned in a paddock and fed free-choice hay for 3 weeks.

Lateral radiographic images of the forefeet were acquired and reviewed to ensure that there was no evidence of preexisting laminitis. On day 0, each horse had the hooves of its forefeet rasped to remove the periople. The forefeet were then placed in foot bags with povidone iodine–soaked cotton overnight (approx 12 hours) to reduce the bacterial burden in the hoof horn. The following morning (day 1), a catheter was aseptically placed in the left jugular vein and the horse was administered phenylbutazonec (4.4 mg/kg, IV) and sodium penicillind (10,000,000 U, IV). Because of behavioral issues, each horse was subsequently sedated with xylazine hydrochloridee (1.1 mg/kg, IV) and then anesthetized for screw placement. Anesthesia was induced with ketamine hydrochloridef (2.2 mg/kg, IV) and maintained with isofluraneg in oxygen delivered via a closed anesthetic system. The horse was positioned in lateral recumbency. An abaxial nerve block was performed biaxially on both forefeet; 3 mL of mepivicaine hydrochlorideh was administered at each site. The hoof wall was aseptically prepared with povidone iodine and alcohol. A 5.5-mm-diameter cortical bone screw was placed by use of the standard lag-screw technique (with the glide hole in the hoof horn) under radiographic guidance in a manner similar to that described for part 1 (Figure 1). The screws were tightened until the horn of the dorsal hoof wall began to visually deform and then untightened by a one-quarter turn of the screwdriver. The foot was then bandaged by the placement of a sterile piece of 4 × 4-cm gauze over the screw, which was held in place with 2-cm-wide adhesive tape.i The procedure was repeated for the contralateral forefoot. All cortical bone screws were placed by the same surgeon (JLC).

Figure 1—
Figure 1—

Representative lateromedial radiographic image of the right forefoot of a clinically normal horse (part 2; A) and a horse with oligofructose-induced laminitis (part 3; B) and a photograph of the right forefoot of the horse in panel B (C) following placement of a cortical bone screw (diameter, 5.5 mm; length, 38 mm) without (A) or with (group 3; B and C) a washer. For each foot, the screw was aseptically placed through the midline of the dorsal hoof wall into P3 2 cm distal to the coronary band. In part 3 of the study, screw placement (without a washer) for group 2 was the same as that for the horses in part 2. Notice that the screws were inserted through the dorsal cortex of P3 only (ie, unicortically inserted) to prevent inadvertent impingement of the DDFT insertion. R = Right forefoot.

Citation: American Journal of Veterinary Research 80, 10; 10.2460/ajvr.80.10.943

Each horse was allowed to recover from anesthesia unassisted and then moved to an indoor stall that was bedded with wood shavings. Each horse received phenylbutazone (2.2 mg/kg, IV) in the evening on days 1 (day of surgery) and 2 and trimethoprim-sulfadiazinej (30 mg/kg, IV, q 12 h for 5 days). On day 4, the screws were removed from both forefeet with the horse unsedated and in a standing position. The screw holes were covered with gauze and tape for 12 hours to allow any bleeding (minimal) to abate and then with a small piece of adhesive tapek that was liberally covered with an acrylic paste.l Each horse was then returned to an outside paddock and monitored by means of physical and lameness examinations once daily for 2 weeks.

Assessment of the efficacy of screws for alleviating signs of pain and preventing P3 rotation in horses with oligofructose-induced acute laminitis (part 3)

Thirteen adult Quarter Horses were purchased and randomly assigned by means of sequentially numbered halter tags to 3 treatment groups. Following induction of acute laminitis by an oligofructose overload, horses assigned to group 1 (control; n = 3) received medical treatment only. Horses assigned to group 2 (n = 6) underwent cortical screw placement (without a washer) through the dorsal hoof wall into P3 as described in parts 1 and 2. Horses assigned to group 3 (n = 4) underwent the same procedure as the horses in group 2, except the screw was placed with a washer (Figure 1). The forefeet of horses in all 3 treatment groups were bandaged in the same manner so that the investigators who monitored the horses remained unaware of (were blinded to) treatment group assignment.

Prior to induction of laminitis (baseline), each horse underwent a physical examination, and lateromedial radiographic images of all 4 feet were obtained. A catheterm was aseptically placed in the left jugular vein, and the horse was sedated with detomidine hydrochloriden (5 mg, IV) and butorphanol tartrateo (5 mg, IV). After the horse became noticeably sedate, it received oligofructose (10 g/kg) through a nasogastric tube as described.5

Twelve hours later, each horse had the hooves of its forefeet rasped to remove the periople, and the forefeet were then placed in foot bags with povidone iodine–soaked cotton for 12 hours to reduce the bacterial burden in the hoof horn. Twenty-four hours after oligofructose treatment, cortical bone screws were placed in both forefeet of each horse in groups 2 and 3, with the horse sedated by use of detomidine (5 mg, IV) and butorphanol (5 mg, IV) and restrained in a standing position. An abaxial nerve block was performed on both forefeet as described in part 2. The hoof wall was treated with povidone iodine and alcohol. In each forefoot, 1 cortical bone screw (diameter, 5.5 mm; length, 38 mm) without (group 2) or with (group 3) a washer was placed through the dorsal hoof wall into P3 2 cm distal to the coronary band on the midline as described in part 2. All screws were inserted through the dorsal cortex of P3 only (ie, were unicortically inserted) to prevent inadvertent impingement of the DDFT insertion. All screws were placed by the same surgeon (JLC).

The forefeet of all horses in all 3 treatment groups were bandaged as described in part 2. Each horse was returned to a stall. Physical and lameness examinations were performed every 4 hours by an investigator who was blinded to treatment group assignment. After each lameness examination, each horse was assigned a lameness grade as described by Obel.p Briefly, lameness was graded on a scale of 1 to 4, where grade 1 was defined as a horse that shifts weight from one foot to another or incessantly lifts feet and is not evidently lame at a walk but has a visibly shortened stride at a trot, grade 2 was defined as a horse that moves willingly at a walk and trot but has a noticeably shortened and stabbing stride and will allow the foot to be lifted without difficulty, grade 3 was defined a horse that moves reluctantly and resists attempts to lift the affected or contralateral foot, and grade 4 was defined as horse that has marked reluctance or absolutely refuses to move. All horses received trimethoprim-sulfadiazine (30 mg/kg, IV, q 12 h for 5 days) and phenylbutazone (2.2 mg/kg, IV, q 12 h for 5 days). The horses in group 1 received only trimethoprim-sulfadiazine and phenylbutazone in addition to having their forefeet bandaged.

For each horse, lateromedial radiographic images of all 4 feet were acquired at 96 and 120 hours after laminitis induction. Then, each horse was euthanized with an IV overdose of pentobarbital sodium.q Immediately after death was confirmed, all 4 feet were harvested for histologic examination. Histologic sections were prepared by use of a previously described protocol.6 All histologic sections were evaluated by a pathologist (ALA) who was blinded to the treatment group assignment of each horse.

All radiographs were reviewed,r and measurements were obtained by the same investigator (KH). The angle of the dorsal aspect of P3 relative to the dorsal hoof wall (parietal surface angle [P3 angle]) and dorsal hoof width (D) were measured digitally as described7 with some modifications. Briefly, D was measured at the base of the extensor process (D1), midway between the extensor process and tip of P3 (D2), and at the tip of P3 (D3). The change in distance between the first (acquired from baseline images) and subsequent measurements was calculated and recorded. For each image, the ratio of D1 to D3 (D1:D3 ratio) and the change in that ratio from baseline (ΔD1:D3 ratio) were calculated. Data were recorded in a spreadsheet program.b

Statistical analysis

For part 1, multilevel mixed-effects models were used to assess whether the screw pullout force was associated with foot location (forelimb or hind limb), placement of the screw through 1 or both cortices (unicortical or bicortical insertion), and depth of screw insertion into P3. All models included a random effect to control for the analysis of multiple limbs from each horse (ie, repeated measures within horses).

Descriptive data were generated for part 2. For part 3, the data distributions for continuous outcomes (heart rate; P3 angle; changes in D1, D2, and D3; D1:D3 ratio; and ΔD1:D3 ratio) were assessed for normality by means of a Shapiro-Wilk test. Data were normally distributed for all continuous variables except P3 angle. A logarithmic transformation was applied to the P3 angle data to normalize them for regression analysis. Multilevel mixed-effects linear regression models were used to assess the effect of treatment group on each continuous variable. Mixed-effects ordinal logistic regression was used to evaluate the effect of treatment group on the Obel lameness grade. All models included a random effect to account for repeated measures within horses. All analyses were performed with commercially available statistical software,s and values of P ≤ 0.05 were considered significant.

Results

Part 1

The mean ± SD force at failure was 3,908.7 ± 1,473.4 N (range, 1,630 to 6,940 N). The mean ± SD bone thickness engaged by the screw was 15.8 ± 4.4 mm (range, 8 to 27 mm). The mean force at failure did not differ significantly between forefeet and hind feet (P = 0.22) or between feet with unicortical and bicortical screw insertion constructs (P = 0.82). However, the force at failure was significantly (P = 0.006) associated with the depth of screw insertion into P3. The force at failure increased by 187.6 N (95% CI, 54.0 to 321.1 N) for each 1-mm increase in screw insertion depth.

Part 2

All 6 clinically normal horses had an uneventful recovery from anesthesia and were not visibly lame when walking at any time during the observation period, including day 3 when phenylbutazone was not administered. When the horses were walked on a clean dry cement floor without a bandage, close observation revealed that the screwheads moved relative to the dorsal hoof wall as the forefeet were loaded. Screw removal was performed with horses unsedated and in a standing position. No adverse effects were observed. No evidence of lameness was observed at any time during the 2 weeks after screw removal.

Part 3

All 13 horses developed clinical signs consistent with endotoxemia (depression, diarrhea, tachycardia, and a dark-red line at the gingival margins [toxic line]) and acute laminitis (reluctance to move and an increase in digital pulses) following oligofructose administration. All screws were successfully placed without incident and with the horses sedated and restrained in a standing position.

For all 13 horses, the heart rate following induction of laminitis was significantly (P < 0.001) increased from that prior to oligofructose administration (baseline) by a mean of 11.2 bpm (95% CI, 6.8 to 15.5 bpm). The mean increase from baseline in heart rate (0.14 bpm; 95% CI, −4.9 to 5.2 bpm) did not differ significantly (P = 0.56) between control (group 1) and treated (groups 2 and 3) horses. All horses became noticeably lame following oligofructose administration, and the maximum Obel lameness grade assigned was 2. Treatment group was not significantly (P = 0.48) associated with lameness grade when time was controlled.

One control horse and 3 treated horses developed signs of severe colic after oligofructose administration. The control horse and 2 of the treated horses failed to respond to rescue therapy (xylazine [200 mg/kg, IV] or detomidine [5 mg, IV] combined with butorphanol [5 mg, IV] and flunixin megluminet [1.1 mg/kg, IV]) after 48, 72, and 96 hours, respectively, and were euthanized for humane reasons with an IV overdose of pentobarbital sodium in accordance with the institutional animal care and use protocol. Radiographic images of all 4 feet were acquired immediately prior to euthanasia, and all 4 feet were harvested for histologic evaluation after euthanasia. The remaining horse with colic responded well to xylazine (200 mg, IV) and flunixin meglumine (1.1 mg/kg, IV) and remained in the study.

Treatment group was not significantly associated with P3 angle when all 4 feet (P = 0.20) or only the forefeet (P = 0.10) of the horses were considered. When the data set was limited to only forefeet, D1 (P = 0.045), D2 (P = 0.03), and D3 (P = 0.08) increased significantly from baseline over time. The calculated variable ΔD1:D3 allowed us to control for individual D1:D3 ratio differences that were present at baseline. Overall, treatment group had a significant effect on ΔD1:D3. There was a significant mean difference in ΔD1:D3 between the control group and groups 2 (−0.06; 95% CI, −0.11 to −0.02; P = 0.001) and 3 (−0.08; 95% CI, −0.13 to −0.03; P = 0.002); however, the mean difference in ΔD1:D3 did not differ significantly (P = 0.38) between groups 2 and 3 (−0.02; 95% CI, −0.06 to 0.02). The interaction between treatment group and time was not significant (P = 0.66).

Histologic examination of at least 10 primary epidermal lamellae from medial, sagittal, and lateral lamellar tissues of each foot revealed similar changes in all horses. Specifically, the secondary epidermal lamellae were longer and narrower, were associated with tapered or pointed rather than rounded tips, and formed more acute angles with the primary epidermal lamellae than expected. Ovoid epidermal cells oriented parallel rather than perpendicular to the basement membrane were inconsistently present, as were epidermal cells that appeared to be more round than oval.8 The magnitude of laminar changes did not differ significantly among the 3 treatment groups.

Discussion

The objective of the first part of the present 3-part study was to determine the force required to pull cortical bone screws (diameter, 5.5 mm) from the P3 of adult horses. Results of a previous study9 indicate that paired (from the same horse) forelimb and hind limb bones of adult horses have similar biomechanical characteristics. The present study did not refute that finding. The pullout force required to remove cortical screws from P3 did not differ significantly between the forefeet and hind feet or between the left and right feet evaluated in part 1. Moreover, the mean pullout force (3,908.7 N) required to remove the screws from the feet of part 1 was sufficient to counteract the forces generated by the DDFT, even in the absence of additional support from laminar tissue. Also, results from part 1 of the present study indicated that screw pullout force was not significantly affected by whether the screw engaged 1 or both cortices. That was an important finding because the DDFT inserts on the palmar or plantar aspect of P3, and inadvertent placement of a screw into that region may result in insertional desmopathy and manifest clinically as lameness and signs of pain. In vivo, screw pullout strength may not equate to DDFT strain owing to the effects of other tissues within the hoof and variations in the ground reaction forces generated by differential loading of the foot during ambulation. Furthermore, a single cycle-to-failure study does not take into account the effect of cyclic strain on the construct over time. Nevertheless, the results from part 1 of the present study indicated that placement of 1 cortical screw through the dorsal hoof wall into P3 was strong enough to allow us to proceed with the subsequent parts of the study.

In part 2 of the present study, we evaluated whether clinically normal horses would tolerate placement of a cortical screw through the dorsal hoof wall into P3. The horses tolerated the procedure extremely well and did not have any evidence of lameness beyond the immediate postoperative period throughout the 2-week observation period. None of the horses developed septic pedal osteitis from the procedure. Furthermore, when the horses were assessed several months after screw removal (data not shown), the acrylic paste had eroded, leaving the holes in the dorsal hoof wall exposed, and the holes had migrated distally with horn growth; no evidence of infection (ie, purulent discharge or lameness) was observed in any of the horses. This was important because an effective, albeit invasive, treatment for acute laminitis should be associated with fewer signs of pain and discomfort than the disease being treated. Moreover, the treatment should not be associated with substantial long-term complications such as P3 sepsis. Results from part 2 of the present study indicated that horses tolerated screw placement well and that short-term screw placement was not associated with any long-term adverse effects, which suggested that the procedure may be beneficial for the treatment of horses with naturally occurring acute laminitis.

The objective of part 3 of the present study was to determine whether placement of a cortical screw (diameter, 5.5 mm) through the dorsal hoof wall into the P3 of horses with experimentally induced acute laminitis would help alleviate signs of pain and prevent P3 rotation. Results indicated that placement of cortical screws into the P3 of forefeet of horses restrained in a standing position was feasible, even in horses that were in the prodromal phase of acute laminitis. It is likely that many horses with acute laminitis develop lamellar inflammation before veterinary intervention; therefore, the timing of cortical screw placement relative to laminitis induction (24 hours) for part 3 was purposely selected to approximate typical clinical situations.

During part 3 of the present study, heart rate and the Obel lameness grade were used as surrogate measures for pain. All horses became tachycardic following oligofructose administration to induce laminitis, and cardiovascular compromise may have contributed to the tachycardia. Treatment group had no significant effect on either heart rate or Obel lameness grade, perhaps because all horses developed laminar inflammation and signs of systemic compromise regardless of the assigned treatment. Those results also suggested that placement of cortical screws through inflamed lamellae had no negative effects in acutely laminitic horses, which provided further evidence that the procedure might be clinically applicable.

Previous research indicates that repair of equine laminar tissue occurs quickly in the absence of physical disruption.10 Thus, during development of the cortical screw placement protocol described in the present study, we envisioned that the screws would remain in situ only during the acute phase of laminitis. The lack of substantial P3 rotation (as measured by the angle of the dorsal aspect of P3 relative to the dorsal hoof wall [P3 angle]) for the horses of part 3 of the present study might have been a function of the brevity of the trial, and more rotation may have occurred had the horses been observed for a longer duration. Owing to the lag-screw hole in the dorsal hoof wall and the shape of the screwhead, some rotation of P3 was possible before the screwhead fully engaged the hoof horn. It was theorized that placement of a washer under the screwhead would prevent that rotation. Despite the lack of substantial P3 rotation in the horses with induced laminitis, increases in D1, D2, and D3 measurements and the ΔD1:D3 ratio over time were indicative of laminar inflammation, which was subsequently confirmed by histologic examination. However, the mean ΔD1:D3 ratios for the horses that underwent screw placement (groups 2 and 3) were significantly lower than that for the control horses.

It is important to note that, in the present study, fully threaded screws were placed by use of the lag-screw technique, tightened until dorsal horn compression was visibly evident, and then backed out by a one-quarter turn of the screwdriver. This method was devised to prevent dorsal laminae compression because, in a pilot study, horses developed signs of substantial postoperative pain when the cortical screws were fully tightened (data not shown). Furthermore, placement of fully threaded screws without use of the lag-screw technique might result in implant breakage because the pivot point is the lamellar junction. The observation that the screwheads moved when the forefeet of the horses of part 2 were weight bearing attested to the effectiveness of the lag-screw technique.

Nevertheless, even with use of the lag-screw technique and not fully tightening the screws during placement, should horses develop substantial lamellar edema or P3 rotation, it is possible that the pressure exerted on the dorsal hoof wall by the screw-head as it acts to counter the pull of the DDFT and limit the potential space between the hoof horn and dorsal surface of P3 could create excessive pressure on those structures and be manifested as signs of pain. Additionally, 1 screw was placed in each forefoot of the horses of the present study, and although that screw appeared to be adequate for prevention of P3 rotation, it might not be sufficient to counter the yaw and roll of P3 within the hoof capsule. Control of those forces might be better achieved by placement of a screw with a washer on both sides of midline (ie, 2 screws/foot).

A major limitation of the present study was the low number of horses evaluated. Ethically, it was difficult to justify the use of > 3 control horses because of the extreme systemic effects induced by oligofructose administration; indeed, 1 control horse and 2 treated horses had to be euthanized because of severe systemic disease and endotoxemia. It is possible that our findings were the result of selection bias.

Results of the present 3-part study suggested that a cortical bone screw (diameter, 5.5 mm) placed by use of the lag-screw technique through the dorsal hoof wall into P3 had sufficient holding power to prevent P3 rotation in the absence of dorsal lamellae integrity. The procedure was well tolerated by clinically normal horses, and screw placement in horses during the prodromal phase of laminitis did not appear to be detrimental. None of the horses, including the control horses that did not undergo screw placement, had measurable rotation of P3 relative to the dorsal hoof wall, which might have been a reflection of the short observation period (5 days) or inadvertent selection bias. However, screw placement did significantly decrease the magnitude of the ΔD1:D3 ratio, which suggested that it had a stabilizing effect on P3. Nevertheless, studies with longer observation periods than that of the present study and studies involving horses with naturally occurring laminitis are necessary before the screw placement procedure described in this study can be recommended as a treatment option for horses with acute laminitis in clinical practice.

Acknowledgments

Supported by the Townsend Equine Health Research Fund at the Western College of Veterinary Medicine.

The authors declare that there were no conflicts of interest.

The authors thank Dr. Keri Thomas for assistance with lameness assessment in the horses of parts 2 and 3 of the study.

ABBREVIATIONS

bpm

Beats per minute

CI

Confidence interval

DDFT

Deep digital flexor tendon

P3

Third phalanx

Footnotes

a.

Universal Materials Testing Machine 1137-5500 Retrofit, Instron, Canton, Mass.

b.

Excel, Microsoft Canada Inc, Mississauga, ON, Canada.

c.

Butequine, Bioniche Animal Health Canada Inc, Belleville, ON, Canada.

d.

Penicillin G, Fresenius Kabi Canada, Toronto, ON, Canada.

e.

Rompun, Bayer Healthcare, Mississauga, ON, Canada.

f.

Vetalar, Bioniche Animal Health, Belleville, ON, Canada.

g.

Isoflo, Abbott Laboratories, Montreal, QC, Canada.

h.

Carbocaine, Pfizer Animal Health, Pfizer Canada Inc, Kirkland, QC, Canada.

i.

Tensoplast, BSN Medical GmbH, Hamburg, Germany.

j.

Tribrissen 48%, Intervet Canada Corp, Kirkland, QC, Canada.

k.

Micropore, 3M Canada, London, ON, Canada.

l.

Equilox I Gold 14 oz, Side-by-Side Cartridge, Equilox International Inc, Island, Minn.

m.

Becton Dickinson Angiocath, Infusion Therapy Systems Inc, Sandy, Utah.

m.

Dormosedan, Pfizer Animal Health, Pfizer Canada Inc, Kirkland, QC, Canada.

o.

Torbugesic, Ayerst Laboratories, Pierrefonds, QC, Canada.

p.

Obel N. Studies on the histopathology of acute laminitis. PhD thesis. Almqvist & Wiksells, Uppsala, Sweden, 1948.

q.

Euthanyl Forte, Bimeda-MTC Animal H Inc, Lavaltrie, QC, Canada.

r.

RadiANT DICOM viewer, Medixant, Poznan, Poland.

s.

STATA SE, version 14, Stata Corp LP, College Station, Tex.

t.

Banamine, Intervet Canada Corp, Kirkland, QC, Canada.

References

  • 1. Mungall BA, Kyaw-Tanner M, Pollittt CC. In vitro evidence of a bacterial pathogenesis of equine laminitis. Vet Microbiol 2001;79:209223.

    • Search Google Scholar
    • Export Citation
  • 2. Van Eps AW, Pollitt CC. Equine laminitis model: cryotherapy reduces the severity of lesions evaluated seven days after induction with oligofructose. Equine Vet J 2009;41:741746.

    • Search Google Scholar
    • Export Citation
  • 3. Lochner FK, Milne DW, Mills EJ, et al. In vivo and in vitro measurement of tendon strain in the horse. Am J Vet Res 1980;41:19291937.

  • 4. Yovich JV, Turner AS, Smith FW. Holding power of orthopedic screws in equine third metacarpal and metatarsal bones: part II. Adult horse bone. Vet Surg 1985;14:230234.

    • Search Google Scholar
    • Export Citation
  • 5. van Eps AW, Pollitt CC. Equine laminitis induced with oligofructose. Equine Vet J 2006;38:203208.

  • 6. Pollitt CC. Basement membrane pathology: a feature of acute equine laminitis. Equine Vet J 1996;28:3846.

  • 7. Sherlock C, Parks A. Radiographic and radiological assessment of laminitis. Equine Vet Educ 2013;25:524535.

  • 8. de Laat MA, van Eps AW, McGowan CM, et al. Equine laminitis: comparative histopathology 48 hours after experimental induction with insulin or alimentary oligofructose in Standardbred horses. J Comp Pathol 2011;145:399409.

    • Search Google Scholar
    • Export Citation
  • 9. Lopez MJ, Wilson DG, Vanderby R Jr, et al. An in vitro biomechanical comparison of an interlocking nail system and dynamic compression plate fixation of ostectomized equine third metacarpal bones. Vet Surg 1999;28:333340.

    • Search Google Scholar
    • Export Citation
  • 10. Van Epps AW, Pollitt CC. Equine laminitis model: lamellar histopathology seven days after induction with oligofructose. Equine Vet J 2009;41:735740.

    • Search Google Scholar
    • Export Citation

Contributor Notes

Address correspondence to Dr. James L. Carmalt (james.carmalt@usask.ca).