• Home
  • Uncategorised

Investigating back pain in horses

  • Super User

Focus - February 2019

Download as PDF

Investigating back pain in horses

Equine orthopaedic expert, Carolin Gerdes, provides a comprehensive overview of investigating back pain in horses, diagnostics and treatment options available

Suspected back pain or dysfunction is a common cause for owners to seek veterinary advice. Cases presenting with perceived back pain are often challenging due to the large number of possible underlying causes (Jeffcott 1980). Back pain may be the primary complaint or could be part of a broader poor performance issue. In order to reach a diagnosis, it is important to have a systematic approach to the diagnostic process, often aiming to systematically rule out common causes of back pain before arriving at the correct diagnosis. Successful treatment requires identifying the underlying problem as well as considering other contributing factors such as lameness, sacroiliac or neck pain, saddle fit and the exercise regime. The main problem encountered when investigating back pain is the lack of a ‘gold standard’ test.

Investigating back pain
Horses exhibiting signs such as rearing, kicking out, bucking or hypersensitivity to grooming or palpation of the back, frequently prompt further investigations into a potential back problem.
The clinical examination is a vital part of investigating horses with suspected back pain. The physical examination should follow a systematic approach and is the same as any other orthopaedic case. It is important to palpate the limbs as well as the head and neck in order to identify possible contributing factors. Horses presenting with back pain sometimes have a strong aversive reaction to back palpation. It is, therefore, advised to leave the thorough palpation of the back until last. Clinical signs of back pain may include reduced mobility, swelling or heat. Pain may be elicited by spinal mobilisation or by pressure applied to the dorsal spinous process and the epaxial musculature. The horse’s back should be approached carefully. Sudden, firm pressure could cause the horse to react with aggression or anxiety, even in absence of back pain, which frequently leads to misinterpretations. Depending on the patient’s temperament, the interpretation of findings during the physical examination can be challenging.
Following the physical examination the horse should be assessed dynamically, ideally both on the lunge and under the saddle. Any asymmetry of the gait should be investigated, as back pain and concurrent lameness is common (Zimmermann et al, 2011). Horses deemed to be unsafe to ride, due to exhibiting dangerous behaviours, can be assessed with tack on the lunge or with a weighted surcingle. The majority of clinical signs associated with back pain have not been measured yet and, therefore, the investigation is primarily subjective.
The ‘gold standard’ for the objective assessment of back movement is 'optical motion capture'. This technique is highly accurate but restricted to the gait laboratory or treadmills and is not applicable for the use in the field. Alternatively, wireless inertial sensors can be used to collect kinematic data. This technique can also be used to assess for gait asymmetries and evaluate interactions between horse and rider (Pfau et al, 2007, 2009). When compared to optical motion capture, inertial sensor data showed a good level of consistency and an acceptable accuracy for back movement (Warner et al. 2010).

Back pain and lameness
Horses compensate hindlimb lameness by adapting spinal movement, which becomes evident as a reduction of range of motion at the lumbosacral junction and extension of the thoracolumbar region (Buchner et al 1996; Alvarez et al 2008). By abolishing the hindlimb lameness with diagnostic local anaesthesia, these asymmetries and reduced range of motion can be reversed (Greve et al 2017).
Saddle slip was observed in a large proportion of horses with hindlimb lameness, probably partly due to asymmetrical epaxial muscling (Greve et al 2013). Furthermore, saddle slip could be corrected by abolishing hindlimb lameness, suggesting that asymmetrical thoracolumbar movement in lame horses is the cause. A study assessing back dimensions of sport horses over time showed that lame horses had a reduced ability to develop normal epaxial musculature (Greve et al 2015).
Due to the close association of lameness, spinal movement and back pain, gait asymmetries should not be overlooked and both should be investigated and treated accordingly.

Diagnostic tests
Diagnostic imaging modalities for the back include radiography, ultrasonography and scintigraphy (bone scan). Standard imaging modalities allow the assessment of the most relevant areas of the back. Gamma scintigraphy might be useful to further assess radiographic and ultrasonographic suspicions or findings. Furthermore, bone scan allows the assessment of bigger breeds, where standard imaging modalities are insufficient due to poor or non-diagnostic image quality. Ultrasonography of the articular process joints of the back is frequently compromised in horses with significant soft tissue coverage. It is important to carefully interpret imaging findings and confirm their clinical significance with diagnostic local anaesthesia or trial medications, where possible.
• Radiography allows the visualisation of the vertebral column, intervertebral articulations (IVAs/’facet joints’) and vertebral bodies to a varying degree, depending on location, equipment and patient size. Latero-lateral views as well as oblique projections can be obtained. Standard radiographs ideally include three to five overlapping latero-lateral radiographs using radiopaque markers, such as coins, for orientation. Collimated views of specific regions of interest can help to increase image quality by reducing scatter. Main limitations of the technique include attenuation and inability to visualise lumbar vertebral bodies. Care should be taken when interpreting or measuring interspinous spaces (ISS). Geometric distortion markedly affects the appearance of the spaces, depending on the shape and the distance of the dorsal spinous processes to the focal spot emitting X-ray beams (Djernæs et al 2017). Furthermore, the head position influences the distance between thoracic dorsal spinous processes and it is therefore advised to acquire back radiographs in a neutral position with the muzzle at shoulder level (Berner et al 2012). To further assess intervertebral articulations, oblique projections are obtained with the beam angled 20˚ from ventral to dorsal and centred 15-20cm ventral to dorsal midline (Butler et al. 2000; Girodroux et al. 2009). The X-ray plate should be aligned perpendicular to the beam and as close as possible to the horse. The highly-curved shape of the ribs is causing superimpositions with to the thoracic IVAs. In the lumbar spine there is superimposition of the transverse processes and abdominal structures.

• Ultrasonography of the back should be combined with the radiographic examination and is particularly useful to examine superficial soft-tissue structures and the intervertebral articulations. To assess all structures of interest, both linear and convex transducers are required. 

For the supra- and interspinous ligaments (SSL and ISL) longitudinal views are most useful. The images are best acquired with a high-frequency linear transducer using a stand-off pad. The head should be kept in a neutral position as high head carriage may cause relaxation of the SSL and therefore a hypoechogenic appearance. Superficial fibres of the SSL have a horizontal orientation whereas deep fibres of the ISL run in caudoventral direction appearing hypoechogenic in comparison. Care should be taken to position the probe exactly midline at the level of the dorsal spinous processes. The aponeuroses of the epaxial musculature can be imaged off-midline with a parallel fibre pattern similar to the SSL.

In the thoracic (saddle) region the SSL is thin and wide, whereas further caudal in the lumbar region the ligament is thick and narrow with a more echogenic, homogenous appearance. The transverse view of the SSL is less useful due to being more prone to artifacts. In order to achieve the best image quality, the transducer should be tilted cranially and caudally. Published scientific data about the ultrasonographic appearance of the SSL in normal horses and horses with back pain offering information about the potential clinical significance is limited (Henson et al 2007). The clinical significance of heterogenous regions in the SSL should therefore be questioned and further tests, such as diagnostic local anaesthesia, should be applied. 

Deep to the ligament the fibrocartilaginous cap, visualised as a hypoechogenic line of approximately 1mm, is visible and runs parallel to the hyperechoic line of the DSP bone surface. The ISS cannot be assessed fully and a statement about potential iminging DSPs should not be made based on ultrasonography alone. The intervertebral articulations can be examined ultrasonographically, both in sagittal and frontal planes, using a convex transducer (Denoix 1999a; Reisinger and Stanek 2005).

The anatomy and ultrasonographic appearance of the joints change slightly from cranial to caudal. The mammillary process is more prominent in the thoracic spine and the joint is positioned further axial and closer to the DSP compared to the lumbar region. Signs of pathology in the intervertebral articulations (see Figure 4) include new bone formation and an enlarged outline of the facet (Denoix and Dyson 2003).
Muscle asymmetries are common in horses with back pain. Measuring the multifidus muscles may add objective information during back investigations and is easily applied. Furthermore, progress made following treatment and training can be measured by re-assessing m. multifidus symmetry (Halsberghe et al 2017).
• Scintigraphy is commonly applied to further image the back in cases where the standard modalities were inconclusive or specific findings require advanced diagnostic imaging. Mild increased radionuclide uptake (IRU) associated with the DSPs is a common finding in horses without clinical signs of back pain (Erichsen et al 2003, 2004). A study of Zimmermann et al (2011) looking primarily at the spinous processes of the thoracolumbar spine showed that the severity of radiographic lesions was associated with scintigraphic abnormalities. DSPs at T14-T17 were most commonly affected. Horses with severe DSP lesions were more likely to have osteoarthritis in the IVAs. But there were also horses with radiographic evidence of ‘kissing spines’ that had no IRU associated with DSPs on bone scan images. Moderate or severe IRU associated with the IVAs was more likely seen in horses with clinical signs of back pain than in normal horses in a study from Gillen et al (2009).
The advantage of applying scintigraphy is the ability to identify dynamic processes of bone modeling and remodeling associated with the entire spine. These processes are either adaptive or pathologic and require careful interpretation, as findings are not necessarily associated with pain. Bone scan is a useful diagnostic tool to help ruling out other regions possibly mimicking back pain, such as the sacroiliac joint region.

Diagnostic local anaesthesia is considered the most important test to confirm that clinical signs of back dysfunction are associated with impingement of DSPs (Walmsley et al 2002). Horses that tolerate injections, are safe to ride and show a consistent, repeatable problem or behaviour are most suitable candidates. The effect of diagnostic local anaesthesia is usually assessed by performing a ridden examination (or other exercise test) before and 10-20 minutes after infiltration of the local anaesthetic solution (Marks 1999; Walmsley et al 2002; Denoix and Dyson 2003). The test is considered positive, if a marked improvement of performance can be recognised by both the rider and the veterinary surgeon. Interpretation difficulties without objective measurements such as interpretation bias should be borne in mind.
In a study of Roethlisberger Holm et al (2006) the back of horses without clinical signs of back pain or lameness was infiltrated with local anaesthetic solution. Kinematics of the back were measured showing an affect on the function of the back. An increased range of motion for dorsoventral flexion-extension resulting in improved flexibility was possibly due to an altered neuromuscular activity by injections made into the multifidus muscle. These findings should be taken into account to avoid false interpretation.

Possible causes of back pain
Underlying causes for back pain can be grouped into three main categories: Pathology-causing primary back pain; pathology causing secondary back pain; and rider/tack-inflicted back pain. Furthermore, problems such as sacroiliac joint region pain, neck pain or rib fractures may result in clinical symptoms similar to the ones of back pain.

Pathology causing primary back pain
• Impinging dorsal spinous processes (‘kissing spines’)
• Arthropathy of the articular process joints in the thoracolumbar spine
• Ventral spondylosis
• Desmopathy of the supra- and intraspinous ligament
• Fractures
• Myopathies

Pathology causing secondary back pain
• Lameness (particularly hindlimb lameness)

Rider or tack-inflicted back pain
• Poor saddle fit
• Unsuitable riding or training techniques (eg. rollkur, overuse of draw reins)
• Poor riding skills (novice, unbalanced riders)
• Lack of fitness/strength of the horse
• Excessive rider weight

An important part of successfully treating back pain is to include physiotherapy in the rehabilitation and to establish a suitable exercise programme depending on the individual case and underlying cause.
There are a number of conservative and surgical treatment options available for primary conditions of back pain. Corticosteroid injections can be employed by infiltrating areas of DSP impingement or by ultrasound-guided periarticular injection of the articular process joints. Other treatment options such as acupuncture, mesotherapy, bisphosphonate medication and extracorporeal shockwave therapy may be considered by some practitioners. Surgical treatment options such as DSP resection or interspinous ligament desmotomy have been described and are available to treat ‘kissing spine’ syndrome.
If lameness has been identified, it is important to diagnose and treat the lameness prior to treating the back in order to achieve successful and long-lasting results.

View References

  • Alvarez CG, Bobbert M, Lamers L, Johnston C, Back W, and Weeren, PV. (2008) The effect of induced hindlimb lameness on thoracolumbar kinematics during treadmill locomotion. Equine Vet. J. 40, 147-152.
  • Berner D, Winter K, Brehm W, Gerlach K. (2012) Influence of head and neck position on radiographic measurement of intervertebral distances between thoracic dorsal spinous processes in clinically sound horses. Equine Vet. J. 44, Suppl. 43, 21-26.
    Buchner H, Savelberg H, Schamhardt H, and Barneveld A. (1996) Head and trunk movement adaptations in horses with experimentally induced fore- or hindlimb lameness. Equine Vet. J. 28, 71-76.
  • Butler J, Colles C, Dyson S, Kold S, Poulus P. (2000) The Spine. In: Clinical Radiology of the Horse. 2nd Edition, Blackwell Science Ltd, pp. 403-454.
  • Coomer, RPC, McKane SA, Smith N, Vanderweerd J-ME. (2012) A Controlled Study Evaluation A Novel Surgical Treatment For Kissing Spines In Standing Sedated Horses. Vet. Surg. 41, 890-897.
    Cousty M, Firidolfi C, Geffroy O, and David F. (2011) Comparison of Medial and Lateral Ultrasound Guided Approaches for Periarticular Injections Of The Thoracolumbar Intervertebral Facet Joints In Horses. Vet. Surg. 40, 494-499.
  • Denoix J-M. (1999a) Lesions of the vertebral column in poor performance horses. In: Proceedings of the World Equine Veterinary Association Symposium. pp 99-107.
  • Denoix J-M. and Dyson SJ. (2003) Thoracolumbar spine. In: Diagnosis and Management of Lameness in the Horse, 1st edn., Eds: MW Ross and SJ Dyson, WB Saunders, St Louis. pp 509-521.
  • Djernæs J, Nielsen J, Berg L. (2017) Effects of X-Ray Beam Angle and Geometric Distortion on Width of Equine Thoracolumbar Interspinous Spaces Using Radiography and Computed Tomography – A Cadaveric Study. Vet Radiol Ultrasound, 58(2),169-175.
  • Erichsen C, Eksell P, Widstro¨m C, Roethlisberger Holm K, Johnston C. Scintigraphic evaluation of the thoracic spine in the asymptomatic riding horse. Vet Radiol Ultrasound 2003;44:330–338.
  • Erichsen C, Eksell P, Roethlisberger Holm K, Lord P, Johnston C. Relationship between scintigraphic and radiographic evaluations of spinous processes in the thoracolumbar spine in riding horses without clinical signs of back problems. Equine Vet J 2004;36:458–465.
  • Gillen A, Dyson S, Murray R. (2009) Nuclear scintigraphic assessment of the thoracolumbar synovial intervertebral articulations. Equine Vet. J. 41 (6) 534-540.
  • Girodroux M, Dyson S, and Murray R. (2009) Osteoarthritis of the Thoracolumbar Synovial Intervertebral Articulations: Clinical and Radiographic Features in 77 Horses with Poor Performance and Back Pain. Equine Vet. J. 41, 130-138.
  • Greve L and Dyson S. (2013) An investigation of the relationship between hindlimb lameness and saddle slip. Equine Vet. J. 45, 570-577.
  • Greve L and Dyson S. (2015) A longitudinal study of back dimension changes over 1 year in sports horses. Vet. J. 203, 65-73.
  • Greve L, Dyson S, and Pfau T. (2017) Alterations in thoracolumbosacral movement when pain causing lameness has been improved by diagnostic analgesia. Vet. J. 224, 55-63.
  • Halsberghe B., Gordon-Ross, P., Peterson, R. (2017) Whole body vibration affects the cross-sectional area and symmetry of the m. multifidus of the thoracolumbar spine in the horse. Equine Vet. Educ. 29 (9) 493-499.
  • Head MJ, ed., (2014) Ultrasnography of the Neck and Back. In: Atlas of Equine Ultrasonography. John Wiley & Sons, Ltd, pp. 199-204
  • Henson F, Lamas L, Knezevic S, Jeffcott L. (2007) Ultrasonographic evaluation of the supraspinous ligament in a series of ridden and unridden horses and horses with unrelated back pathology. BMC Veterinary Research 3(3).
  • Jeffcott L. (1980) Disorders of the thoracolumbar spine of the horse – a survey of 443 cases. Equine Vet. J. 12, 197-210.
  • Marks, D. (1999) Medical management of back pain. Vet. Clin. N. Am.: Equine Pract. 15, 179-194.
    Pfau T, Robilliard J, Weller R, Jespers K, Eliashar E, and Wilson A. (2007) Assessment of mild hindlimb lameness during over ground locomotion using linear discriminant analysis of inertial sensor data. Equine Vet. J. 39, 407-413.
  • Pfau T, Spence A, Starke S, Ferrari M, and Wilson, A. (2009) Modern riding style improves horse racing times. Science 325, 289-289.
  • Quiroz-Rothe,E., Novales, M., Aguilera-Tejero, E. and Rivero,J.L.L. (2002) Polysaccharide Storage Myopathy in the M.Longissimus Lumborum of Showjumpers and Dressage Horses with Back Pain. Equine Vet.J. 34 171-176.
  • Reisinger R and Stanek C. (2005) Sonographische Darstellbarkeit der Intervertebralgelenke an der Brust-und Lendenwirbesäule des Pferdes. Pferdeheilkunde 21, 219-224.
  • Roethlisberger Holm K, Wennerstrand J, Lagerquist U, Eksell P, Johnston C. (2006) Effect of local analgesia on movement of the equine back. Equine Vet. J. 38 (1) 65-69.
  • Walmsley JP, Petterson H, Winberg F, McEvoy F. (2002) Impingement of the Dorsal Spinous Processes in Two Hundred and Fifteen Horses: Case Selection, Surgical Technique and Results. Equine Vet. J. 34, 23-28.
  • Warner S, Koch T, and Pfau T. (2010) Inertial sensors for assessment of back movement in horses during locomotion over ground. Equine Vet. J. 42, 417-424.
  • Zimmermann M, Dyson S, Murray R. (2011) Comparison of Radiographic and Scintigraphic Findings of the Spinous Processes in the Equine Thoracolumbar Region. Vet. Radiolog. & Ultrasound 52, 661-671.
  • Zimmerman M, Dyson S, and Murray R. (2011) Close, impinging and overriding spinous processes in the thoracolumbar spine: the relationship between radiological and scintigraphic findings and clinical signs. Equine Vet. J. 44, 178-184.
Click on images to enlarge
  • Figures 1A & 1B

    A) specimen showing the beam angle lateral 20˚ ventrodorsal (arrow) and the plate position perpendicular to the beam for oblique projections to further evaluate intervertebral articulations of the thoracic spine. B) Lateral oblique projection of the vertebral bodies, intervertebral articulations and dorsal spinous processes in the mid thoracic to cranial lumbar region of a normal horse.

  • Figure 2

    Ultrasound images of the thoracic spine in a normal horse with the high-frequency linear transducer placed in sagittal (1a & 1b) and frontal (2) planes. 1a) the probe is positioned midline showing the SSL and ISL in longitudinal orientation. Note the hyperechogenic lines deep to the ligament of the DSPs indicating the correct position on the midline;1b) the probe is positioned off-midline showing the aponeuroses of the epaxial muscles in longitudinal orientation; 2) the transverse view showing the SSL and DSP centrally and the aponeuroses either side.

  • Figure 3

    Anatomic specimen of lumbar vertebrae superimposed on a correlating ultrasound image. The convex transducer indicates the frontal plane imaging technique for caudal thoracic and lumbar intervertebral articulations. DSP=dorsal spinous process; TP=transverse process; IVA=intervertebral articulation. Note sharp outline of the caudal and cranial articular processes with a clear joint space.

  • Figure 4

    Ultrasound images of a horse with osteoarthritis of the intervertebral articulation at T18/L1. Note the enlargement and rounding of the affected facet joint labeled as T18 visible on both frontal and sagittal plane ultrasound images and the more normally sized joint labeled T17.

Continue reading

The multifaceted role of calcium in milk fever

  • Super User

Large animal - February 2019

Download as PDF

The multifaceted role of calcium in milk fever

John Lawlor, ruminant technical manager, Anchor Life Science Ltd, examines the multifaceted role that calcium plays in milk fever and its associated metabolic issues. A greater understanding of these factors may be one way to capitalise on the post-quota opportunities on Irish dairy farms, he writes

Dairy farming in Ireland has seen many changes over the past 10 years, especially since the dawning of the post-quota era. Milk fever continues to be a major challenge and cost, not only in terms of cow health and lost productivity, but also in terms of scarce labour.
Over the past decade, Irish dairy farmers have embraced new ideas and opportunities to develop their businesses such as: post-quota expansion; more compact calving patterns; and a greater focus on milk from grass. However, a compact calving season when combined with more cows and a lack of skilled labour, means that the calving season is the most stressful time of year on most dairy farms. The calving season also coincides with the period when farms are most exposed to the second most costly disease on the dairy farm, milk fever. It is well established that calcium (Ca) plays a major role when it comes to milk fever and that cows with milk fever are more prone to other costly metabolic issues (Curtis, 1983). Recent research has shown that sub-clinical milk fever has a major unseen cost on farm and is responsible for 80% of the annual cost of milk fever. Reducing the risk of milk fever, clinical and sub-clinical, must be a key priority on Irish dairy farms, due to the large impact it has on herd health, production and profitability.

Milk fever prevalence and economic cost
Over the years, numerous studies have tried to quantify the incidence level and cost of clinical milk fever (blood Ca of <5.5mg/dl). DeGaris and Lean (2009) found that the average incidence level in 10 European studies was 6.2% (range 0-10). Numerous other studies have reported clinical milk fever incidence to be in the order of 5-7% (NAHMS 2002; Goff 2008; Mulligan and Doherty 2008). In 2011, Oetzel estimated the cost of a single case of clinical milk fever at $300. Until relatively recently, our understanding of the incidence level and economic cost of sub-clinical milk fever (blood Ca 5.5-8.0mg/dl) has not been very clear. Work by Reinhardt et al (2011) put the scale of the problem into focus. In this study, Reinhardt found that approximately 50% of second lactation and older cows were in the sub-clinical range and, perhaps surprisingly, that 25% of first lactation heifers were also in the sub-clinical range. A more recent French study (Millemann et al, 2016) found similar results in terms of the level of subclinical milk fever in multiparous cows at 57% and again an incidence level in first lactation heifers of 16%. Oetzel (2011) also found that a case of sub-clinical milk fever costs $125.
Given that many more cows are at risk of sub-clinical milk fever than clinical, these studies demonstrated that 80% of the annual cost of milk fever is coming from the sub-clinical milk fever, not clinical cases.

Calcium in the cow
Ca is the most abundant mineral in the cow, however 99% of it is to be found in bones and, as such, is not readily available to the cow. The cow’s homeostatic mechanism to maintain normal blood calcium operates efficiently most of the time with normal blood Ca levels held within a narrow range (8.5-10mg/dL). The Ca in the cow’s bones is in a state of continuous exchange with the extracellular fluids. There is about 10-11g of Ca available in the extracellular pool, where it plays an important role in muscle contraction and nerve function. A cow can lose 9-13% of her skeletal Ca during the first month postpartum (Ellenberger et al, 1932).
Of the extracellular Ca pool, there is ~2.5-3.5g of Ca which is held within the plasma Ca pool, and which is found as protein-bound Ca, Ca bound in complexes with anions and ionised Ca. Correct muscle and nerve functions rely on the maintenance of an adequate and consistent level of ionised Ca. The plasma pool may need to replenish itself between eight and 10 times per day in early lactation, to support milk production and maintenance of the cow. The remaining calcium pool is the intracellular Ca pool. Intracellular Ca plays a key role in immune function as its signalling is a key early feature in immune cell activation.

Milk fever causes
Milk fever or hypocalcaemia is a common disease of calving or freshly calved cows. The sudden increase in demand for Ca at the onset of lactation, presents a major challenge to a cow’s homeostatic control mechanism. The onset of lactation increases the demand for Ca by several fold. The cow’s normal reserve pool of Ca is about 2.5-3.5g and cows can only afford to lose approximately 50% of this pool before a hypocalcaemia crisis is initiated. With a single litre of colostrum requiring 2.3g of Ca, it is easy to see how a cow can quickly become Ca deficient. It is not so much the sudden demand for Ca that causes milk fever but more so the fact that the cow’s homeostatic system can take 24-48 hours post calving to become fully functional. It is this time-lag that causes the cow to drain Ca from her plasma pool and as this reserve decreases so too does the cow’s blood Ca status, possibly bringing about a case of sub-clinical or clinical milk fever.

Homeostatic mechanism
Ca supply during periods of hypocalcaemia is controlled by two key hormones: parathyroid hormone (PTH) and vitamin D3. PTH is also produced by the thyroid gland and its secretion is stimulated by low blood Ca concentrations. Vitamin D3 itself is quite inactive and must undergo two chemical processes to become active. In the liver it is converted to 25-hydroxy-Vit D3 and undergoes a further chemical conversion in the kidney to 1-25-dihydroxy-Vit D3. The second conversion is reliant on PTH, while the first is reliant on magnesium and may be compromised under conditions of hypomagnesia. As colostrum/milk production increases rapidly, so too does the drain on the cow’s Ca reserve pool, causing the concentration of blood Ca to fall. This then triggers the secretion of PTH by the parathyroid gland and consequently the conversion of 25-hydroxy-Vit D3 to 1-25-dihydroxy-Vit D3.
Bone Ca mobilisation is now stimulated by both PTH and Vit D3 but can take up to 48 hours to respond fully. Absorption of Ca from the intestines is solely under the control of Vit D3 and can take 24 hours of Vit D3 stimulation before calcium absorption increases significantly. It is this 24-48-hour time lag that causes blood Ca levels to drop.

Other important minerals

When it comes to milk fever, the role of magnesium (Mg) cannot be understated. Mg is critical for the release of PTH and in the synthesis of 1-25-dihydroxy-Vit D3. Mg stored in the soft tissues and bone of the cow is unavailable to the cow and so she requires a continuous dietary supply to meet her requirements.
Moderate hypomagnesemia reduces the ability of the cow’s homeostatic control mechanism to function properly and hypocalcaemia occurs. Hypomagnesemia can affect Ca metabolism by:
a) reducing PTH secretion in response to hypocalcaemia; and
b) reducing tissue sensitivity to PTH (Rude, 1978).
Hypomagnesemia can occur in cows either fed an inadequate amount of Mg in the diet or if the diet contains high levels of some other factor that prevents adequate absorption of magnesium, such as potassium.

Potassium (K) binds up Mg in the rumen, which can subsequently inhibit the availability of calcium to the cow. High levels of dietary K are common in Irish grass silages particularly second and third cut silage, which may have received high levels of manure, and which is typically fed to dry cows and youngstock. The recommended dietary K level in the diet of a dry cow is ≤1.8%DM, yet Rogers and Murphy (2000) report that the mean level in Irish grass silages at 2.35% with a range from 0.63%-5.59%. They also report that 11% of Irish grass silages have a K level exceeding >3.1%. Apart from binding Mg, K also has an alkalising effect and can contribute to metabolic alkalosis, a further risk factor for milk fever.

High phosphorous (P) concentrations have been shown to result in increased milk fever risk. Blood P levels, above 2mmol/L, can inhibit the enzyme converting 25-hydroxy-Vit D3 to 1-25-dihydroxy-Vit D3. This can compromise the ability of the cow to produce the hormone necessary for the activation of intestinal Ca transport, which will impair the Ca homeostasis of the cow.

Other risk factors
Metabolic alkalosis
Pre-calving diets supply greater levels of cations (K, Sodium [Na], Ca and Mg) than anions (chlorine [Cl] and sulphate [SO4] and phosphate [PO4]) cause a greater number of positively charged cations than negatively charged anions to enter the blood, which increases blood pH, resulting in a state of metabolic alkalosis. Metabolic alkalosis blunts the response of the cow to PTH (Gaynor 1989; Goff et al, 1991; Phillippo et al, 1994), which increases the risk of milk fever and subclinical hypocalcaemia (Craigie and Stoll, 1947).

Older cows have a decreased capacity to mobilise Ca from their bones (Van Mosel et al, 1993) and possibly a decreased number of 1-25-dihydroxy-Vit D3 receptors in the small intestine (Horst et al, 2003). Lean (2006) found that the risk of milk fever increases by 9% per lactation.

Condition score
Over-conditioned cows (body condition score >3.5 on a 1-5 scale) are at an increased risk of hypocalcaemia (Heuer et al, 1999).
Other common risk factors include: channel island breeds (Harris, 1981); high-yielding cows; lame cows; and cows with a previous history of milk fever (Erb et al, 1985).

Multifaceted role of Ca
Ca plays a critical role to the transitioning cow and its effect is broad based, as Ca plays an important role in a number of key areas for the cow in transition, from muscle and nerve function, to the physical barriers of the innate immune response and also the phagocytic response.

Muscle function
As calcium is required for proper muscle function, cows with low blood calcium levels lose muscle tone and this has a number of negative effects on key muscular functions of the cow.

One of the classic and early indications of milk fever is a cow with an unsteady and staggered walk. Hypocalcaemic cows may be less mobile, leading to lower feed intakes with possible negative effects on energy status. Hypocalcaemic cows can be more prone to slipping, falling and injury leading to higher culling rates.

Impaired rumen activity
Huber et al (1981) found that rumen contractions ceased well before the onset of signs of clinical milk fever in artificially induced hypocalcaemia. Such stasis may be an important factor in the development of hypocalcaemia as even the temporary alimentary stasis can induce acute hypocalcaemia through reduced intestinal absorption of Ca (Moodie and Robertson, 1962). A further study (Jorgensen et al, 1998) showed the negative effects of hypocalcaemia on smooth muscle contractility in cows artificially induced with progressively severe hypocalcaemia. The study demonstrated a significant reduction of contractility even with mild subclinical hypocalcaemia (0.78mmol/L ionised Ca). Reduced feed intakes can lead to an impaired energy status and a higher risk of displaced abomasum.

Innate immunity – physical barriers
Increased mastitis risk
The ability of the teat sphincter muscle to close the teat canal properly post milking is reduced in hypocalcaemic cows which may lead to a higher risk of mastitis. (Kimura et al, 2006). Curtis (1983) reported that cows with hypocalcaemia were eight times more likely to suffer from a case of mastitis.

Tight junction permeability
Ma et al (2000) demonstrated the role extracellular calcium levels play in the permeability of the intestinal tight junction, a key physical barrier to infection. The study was designed to study the role that extracellular Ca++ plays in the modulation of the intestinal epithelial monolayer tight junction barrier. The study demonstrated that extracellular Ca++ is crucial for the maintenance of intestinal epithelial tight junction barrier function.

Innate immunity – phagocytic response
Parturition places a lot of stress on dairy cows and is linked with significant immune suppression and increased susceptibility to infectious disease. The intracellular reserve of Ca is responsible for signalling within the cell and initiation of the immune response to bacterial challenges. Kimura et al, (2006) demonstrated that hypocalcaemia directly reduces immune cell response to an activating stimulus. This study suggested that intracellular Ca stores were being utilised to help sustain extracellular Ca or that when the cow is struggling to maintain Ca homeostasis, the ability to keep endoplasmic reticulum Ca stores fully stocked is compromised. This reduction in intracellular calcium stores in immune cells could blunt intracellular calcium release following an activating stimulus, contributing to the immune suppression seen in hypocalcaemic cows.
A further study by Martinez et al, (2012) demonstrated the link between immune function and calcium status in freshly calved cows. This study found that the neutrophil concentration in blood and the percentage of neutrophils undergoing phagocytosis and oxidative bursts were all reduced in cows with subclinical hypocalcaemia (blood Ca of <8.59mg/dl) compared to normo-calcaemic cows.

The study reported that, not only did the sub-clinical hypocalcaemic group have neutrophils with reduced in-vitro phagocytic and killing activities (graph B) but they also had a smaller leukocyte population in the blood (graph A) because of a sharp decline in neutrophils compared to normocalcaemic cows.

Martinez et al (2012) also found that sub-clinical hypocalcaemic cows had a higher risk of metritis and puerperal metritis compared to normo-calcaemic cows in both study sub populations. Cows were divided at calving based on their calving experience and divided into two groups: low-risk group – cows with a normal calving event; and high-risk group – cows who calved with dystocia, still birth, retained placenta, twins or a combination of issues. The study found that the risk of metritis decreased by 22% for every 1mg/dl increase in blood calcium level recorded over the first three days after calving.

Practical prevention strategies
There are numerous practical proactive preventative strategies available that can help to reduce the risk of milk fever at calving:

  • Low calcium pre-calving diets – restricted dietary Ca will prime the homeostatic response. A target level of less than 30g Ca/day (20g of absorbable Ca) is required but can be difficult to achieve with background levels of Ca in forage; 
  • Anionic salts – addition of anionic salts in the last three weeks pre-calving will prompt a metabolic acidosis in order to counteract cationic elements in the diet and will prime the homeostatic response. This requires two separate dry-cow groups to administer and needs to be adequately mixed into the diet, can be hard to achieve without a diet mixer; 
  • Oral Ca supplementation – Ca boluses given at and 12 hours after calving have become a popular way to support blood Ca levels in the cow, during the period of highest demand. The use of oral Ca supplements allows for a targeted approach of high-risk cow groups within the herd. Liquid, gel and paste oral Ca supplements are also available.

Ca plays a central role in milk fever and having a clear management protocol in place can go a long way to keeping milk fever and its associated metabolic issues at bay. Whilst Ca and its management are key, it is certainly not the only risk factor that needs to be addressed. Energy status, body condition score, and adequate feed barrier space, are just some of the many management areas that require adequate attention and action in order to improve the success of the transition period. Reducing the risk of milk fever, clinical and sub-clinical, must be a key priority on Irish dairy farms, due to the large impact it has on herd health, production and profitability. Optimising Ca status at calving must be a part of any herd management protocol during calving season.

View References

  • DeGaris, P.J., Lean, (2009). Milk fever in dairy cows: A review of pathophysiology and control principles. The Veterinary Journal 176, 58-69.
  • NAHMS (National Animal Health and Monitoring System), (2002). Dairy 2002 Report Part I: Reference of Dairy Health and Management in the United States. Natl. Anim. Health Monit. Syst., US Dept. Agric., Anim. Plant Health Insp. Serv., Vet. Serv., Cent. Epidemiol. Anim. Health, Fort Collins, CO
    Goff, J.P., (2008). The monitoring, prevention, and treatment of milk fever and subclinical hypocalcemia in dairy cows. The Veterinary Journal 176, 50-57.
  • Mulligan FJ and Doherty ML. (2008). Production diseases of the transition cow. The Veterinary Journal, 176, 3-9
    Oetzel, G. R., (2011). An update on hypocalcemia in dairy herds. School of Veterinary Medicine, University of Madison, Wisconsin: 80-85.
  • Reinhardt T A, Lippolis JD, McCluskey BJ, Goff JP & Horst, RL. (2011). Prevalence of subclinical hypocalcaemia in dairy herds. The Veterinary Journal 188, 122-124.
  • Millemann Y, Gillet M, Kirsch P, Besnier P. (2016). Subclinical hypocalcaemia in French dairy cows. Presentation at World Buiatrics Congress, Dublin 2016.
  • Ellenberger HB, Newlander JA, Jones CH. (1932). Calcium and phosphorus requirements of dairy cows. II. Weekly balances through lactation and gestation periods. Vermont Agricultural Experiment Station, Bulletin 342, June 1932.
  • Goff, JP, (2006). Macromineral physiology and application to the feeding of the dairy cow for prevention of milk fever and other periparturient mineral disorders. Animal Feed Science and Technology 126, 237-257.
    Rude, RK, Oldham, SB, Sharp Jr CF, Singer FR. (1978). Parathyroid hormone secretion in magnesium deficiency. J. Clin. Endocrinol. Metab. 47, 800-806.
  • Rogers PAM and Murphy R. (2000). Levels of Dry Matter, Major Elements (calcium, magnesium, nitrogen, phosphorus, potassium, sodium and sulphur) and Trace Elements (cobalt, copper, iodine, manganese, molybdenum, selenium and zinc) in Irish Grass, Silage and Hay. Available at: http://homepage.eircom.net/~progers/0forage.htm
  • Gaynor PJ, Mueller FJ, Miller JK, Ramsey N, Goff JP, Horst RL. (1989). Parturient hypocalcemia in jersey cows fed alfalfa haylage based diets with different cation to anion ratios. Journal of Dairy Science 72, 2525-2531.
    Goff JP, Horst RL, Mueller, FJ, Miller JK, Kiess GA, Dowlen HH. (1991). Addition of chloride to a pre-partal diet high in cations increases 1,25-dihydroxyvitamin D response to hypocalcemia preventing milk fever. Journal of Dairy Science 74, 3863-3871.
  • Phillippo M, Reid GW, Nevison IM. (1994). Parturient hypocalcaemia in dairy cows: effects of dietary acidity on plasma minerals and calciotrophic hormones. Research in Veterinary Science 56, 303-309.
    Craige AH, Stoll IV. (1947). Milk fever (parturient paresis) as a manifestation of alkalosis. American Journal of Veterinary Research 8, 168.
  • van Mosel M, Van’t Klooster AT, van Mosel F, Kuilen JVD. (1993). Effects of reducing dietary [(Na++K+) – (Cl- + SO=4) on the rate of calcium mobilisation by dairy cows at parturition. Research in Veterinary Science 54, 1-9.
    Horst RL, Goff JP, McCluskey BJ. (2003). Prevalence of subclinical hypocalcemia in US dairy operations. Journal of Dairy Science 86 (Suppl. 1), 247.
  • Lean IJ, DeGaris PJ, McNeil DM, Block E. (2006). Hypocalcemia in dairy cows: meta analysis and dietary cation anion difference theory revisited. Journal of Dairy Science 89, 669-684.
    Heuer C, Schukken YH, Dobbelaar P. (1999). Postpartum body condition score and results from the first test day milk as predictors of disease, fertility, yield and culling in commercial dairy herds. Journal of Dairy Science 82, 295-304.
  • Harris DJ. (1981). Factors predisposing to parturient paresis. Australian Veterinary Journal 57, 357-361.
    Erb HN, Smith RD, Oltenacu PA, Guard CL, Hillman RB, Powers PA, Smith MC, White ME. (1985). Path model of reproductive disorders and performance, milk fever, mastitis, milk yield and culling in Holstein cows. Journal of Dairy Science 68, 3337-3349.
  • Huber TL, Wilson RC, Stattleman AJ, Goetsch DD. (1981). Effect of hypocalcaemia on motility of the ruminant stomach. American Journal of Veterinary Research 42, 1488-1490.
    Moodie EW, Robertson A. (1962). Some aspects of calcium metabolism in the dairy cow. Research in Veterinary Science 3, 470-484.
  • Jorgenson RJ, Nyengaard NR, Hara S, Enemark JM and Andersen PH. (1998), Rumen motility during induced hyper- and hypocalcaemia. Acta. Vet. Scand. 39:331-338.
  • Kimura K, Reinhardt TA, Goff, JP, (2006). Parturition and hypocalcemia blunts calcium signals in immune cells of dairy cattle. Journal of Dairy Science 89, 2588-2595.
  • Curtis CR, Erb HN, Sniffen CJ, Smith RD, Powers PA, Smith MC, White ME, Hillman RB and Pearson EJ. (1983). Association of parturient hypocalcemia with eight periparturient disorders in Holstein cows. J. Am. Vet. Med. Assoc. 183, 559-561.
  • Ma TY, Tran D, Hoa N, Nguyen D, Merryfield M and Tarnawski A. (2000). Mechanism of Extracellular Calcium Regulation of Intestinal Epithelial Tight Junction Permeability: Role of Cytoskeletal Involvement. Microscopy Research and Technique 51, 156-168.
  • Martinez N, Risco CA, Lima FS, Bisinotto RS, Greco LF, Ribeiro ES, Maunsell F, Galvão K and Santos JEP. (2012). Evaluation of peripartal calcium status, energetic profile, and neutrophil function in dairy cows at low or high risk of developing uterine disease. J. Dairy Science 95, 7158-7172.
Click on images to enlarge
  • Figure 1

    The removal of Ca++ leads to a rapid drop in epithelial resistance and an increase of intestinal monolayer tight junction permeability (B and C). The increase in tight junction permeability was rapidly reversed by the re-introduction of Ca++ (D).

  • Figure 2

    In-vitro (graph A) phagocytosis (% of neutrophils) and (graph B) oxidative burst (% of neutrophils) in neutrophils of cows considered to have normocalcaemia (Ca >8.59mg/dl) or subclinical hypocalcaemia (Ca ≤8.59mg/dl) in the first three DIM. For panel A, effect of Ca status (P = 0.21), day (P <0.01), and the interaction of Ca status x day (P = 0.03). For panel B, effect of Ca status (P = 0.05), day (P<0.01), and the interaction of Ca status x day (P = 0.12). An asterisk (*) indicates daily means differ (P <0.05).

Continue reading

Assessment of the feline blunt trauma patient

  • Super User

Small animal - February 2019

Download as PDF

Assessment of the feline blunt trauma patient

In this article, Poppy Gant BVSc MRCVS, Queen Mother Hospital for Animals, Royal Veterinary College, reviews the key steps taken in the physical examination of the feline trauma patient, highlighting common injuries and the approach to their emergency management

Cats are commonly involved in road traffic accidents. Of those that survive to presentation, some will require rapid assessment for management of life-threatening injuries. Once considered stable, it is still vital that a thorough physical examination is performed to ensure all injuries are documented.
The initial assessment of a cat involved in a road traffic accident can be separated into primary and secondary surveys. This will ensure that more dramatic injuries, such as major wounds, do not detract from abnormalities of the major body systems that are potentially life threatening. As many blunt trauma cats will have multiple injuries, a secondary survey is required to ensure all injuries are documented. This is essential for owner communications, as certain injuries may necessitate staged diagnostics and interventions, or may have implications for long-term prognosis.

The primary survey should focus on assessment and stabilisation of the cardiovascular and respiratory systems. A full neurological examination should be performed as early as possible, but this may first require basic resuscitation. During this assessment, many patients will likely benefit from active warming and supplemental oxygen therapy.

Blood loss is likely the most common cause of ‘shock’ in blunt-trauma cats. This may be challenging to detect, as cats can present tachycardic or progressively bradycardic and hypothermic. Absence of palpable metatarsal pulses, or even femoral pulses, is a useful indicator of hypotension and should prompt rapid attempts to correct hypovolaemia (Reineke 2016). Serial doppler blood pressure monitoring is useful if available, but resuscitation efforts should not be delayed while obtaining this.
All cats should be assessed for hypovolaemia secondary to haemorrhage, even in the absence of obvious external bleeding. Intracavitary bleeding, which can be assessed using point of care ultrasound, may be seen less frequently in comparison to dogs (Boysen 2004, Lisciandro 2012). A site of, often deceptively, significant haemorrhage is into the inguinal soft tissues following pelvic trauma. The author considers it rare for blunt-trauma cats to require emergency blood transfusion. However, many cats will later become anaemic if significant fluid therapy is required to correct hypovolaemia. Blood transfusions were required in approximately 20% of feline pelvic fracture patients in one referral institute (unpublished data).
If sufficient haemorrhage has occurred to cause hypovolaemia, intravenous crystalloid fluid boluses can be administered while monitoring perfusion parameters, eg. mentation, return or improvement of peripheral pulses and mucous membrane colour. One option is to administer syringes of warm compound sodium lactate (eg. 50ml for a 5kg cat = 10ml/kg) over 10 minutes. Cats are susceptible to volume overload and a full shock ‘dose’ of 40-60ml/kg is unlikely to be required. Failure to at least improve perfusion parameter after two boluses should prompt investigation for ongoing haemorrhage or other causes of shock. Where concurrent hypothermia exists, active warming should be instituted only after starting fluid resuscitation, to avoid vasodilation and worsening of hypotension.

Many causes of dyspnoea are possible, and localisation is key in determining the required intervention. Thoracic trauma is common in these patients, even when there are no other visible injuries. Respiratory rate alone should not be used to exclude significant thoracic trauma and ideally survey radiographs should be performed in all patients (Figures 1 and 2) (Sigrist 2004). Table 1 gives some possible physical examination abnormalities with differentials and suggestions for diagnostics.
feb 2019 table1

Table 1: Potential causes of dyspnoea and recommended follow-up assessment. Differential diagnoses illustrated in italics = more common.

Cats with respiratory injuries can be extremely fragile. Immediate restraint or sedation for radiographs should only be undertaken with great care. Many good resources for the use of thoracic point of care ultrasound are available (Larson 2009, Boysen and Lisciandro 2013) and can offer a much safer option for preliminary diagnostics, although potentially with reduced sensitivity when compared to dogs (Lisciandro 2012). Thoracocentesis can safely be used as both a diagnostic and therapeutic tool, particularly if a pneumothorax is suspected.

An initial assessment of mentation and voluntary motor function (VMF) should, ideally, be performed in all cats prior to analgesia administration. However, the presence of shock may mean basic resuscitation is first required. Table 2 gives seven key areas that should be assessed in the stabilised patient, with potential abnormalities and differentials to consider. 

feb 2019 table2
Table 2: Key abnormalities to consider on neurological exam. SCI = spinal cord injury.

Traumatic brain injury

Reduced mentation, especially in the presence of facial trauma, should prompt concern for raised intracranial pressure (ICP) secondary to brain swelling. Signs of severely raised ICP with impending herniation include bradycardia, hypertension and abnormal respiratory patterns (known as ‘Cushing’s triad’). In the conscious or mildly obtunded patient, bradycardia is more likely secondary to shock. Many resources exist discussing the management of traumatic brain injury (TBI) (DiFazio and Fletcher 2013; Garosi and Adamantos 2011) however the priorities are oxygen therapy, correcting hypotension and elevating the head. Hypertonic saline (3ml/kg) or mannitol (0.25-5g/kg – equivalent to 1.25-2.5ml/kg of a commercial 20% solution) can be considered, especially if initial crystalloid resuscitation fails to improve mentation.

Spinal cord injury
A step-wise assessment for the presence of spinal cord injury (SCI) is given below (Figure 3). If no VMF is witnessed, then significant spinal cord injury cannot be excluded. These patients should be supported on a firm surface (eg. spinal board) and movement minimised until survey radiographs can be performed to assess for unstable vertebral fractures and luxations.

feb 2019 fig3
Figure 3: Step-wise assessment for presence of significant spinal cord injury.

The last step, assessment of ‘deep nociception’, can only be achieved by applying haemostats to the medial and lateral digits of the pelvic limbs. A withdrawal reflex should not be confused with a pain (cortical) response e.g. vocalisation. No data is available in cats but in dogs <5% with displaced vertebral injuries and <25% with non-displaced injuries will have functional recovery (Olby 2003). A full discussion on SCI is provided in several review articles (Eminaga et al. 2011; DiFazio and Fletcher 2013).

Tail pull injury
Luxation/subluxation or fractures of the sacrococcygeal region and stretching of the associated nerve may present as a flaccid tail with or without reduced or absent anal tone (and subsequent faecal incontinence). Absent anal tone increases the likelihood of micturition abnormalities. A lower motor neuron bladder (flaccid detrusor muscle and atonic sphincters) with continuous urinary incontinence may be seen. Alternatively, a paradoxical upper motor neuron bladder (large, difficult to express) is possible when the hypogastric nerve maintains good sphincter tone in the presence of a flaccid detrusor muscle.
Forceps should initially be applied to the distal tail to assess sensation. If no response, then forceps should be applied just caudal to the tail base. Lack of sensation here is associated with a worse prognosis for return of continence but does not preclude it (Tatton 2009). Intact perineal reflex and tail base sensation is a good indicator of early return of bladder function. Prolonged incontinence (>5 days) should prompt discussion of cystotomy tube placement to assist in longer-term bladder management, especially where concurrent pelvic fractures are present. Definitive management of fractures may be required before the outcome of continence is known. If urinary continence does not return within four to six weeks then it is unlikely to do so (Smeak and Olstead 1985). Tail function may take longer to improve and therefore early amputation is not recommended.

If no significant injuries are identified on the primary survey or the patient has been adequately stabilised, a thorough secondary survey should be performed. Common comorbidities in addition to those already discussed include those associated with the head, musculoskeletal system and pelvic injuries.

Head injury
Common injuries include jaw or skull fractures or ocular trauma. Cats with injuries to the jaw may only present with a slightly open mouth or with excess salivation (see Figures 5 and 6). Examination is normally resented and sedation or general anaesthesia may be required. Skull radiographs can be performed to investigate further but owners should be warned that only advanced imaging will allow the full extent of injuries to be determined. Examination of the jaw should include assessment of:
the mandible – both the symphysis and along the ramus;
occlusion and lateral stability of jaw related to the temporomandibular junction;
fractures of maxilla and hard palate; and dentition.
Cats with jaw fractures can be difficult to manage with a prolonged period of recovery. Other than for simple mandibular symphysis fractures, cats are often reluctant to eat and are unlikely to voluntarily meet their caloric requirements. Placement of an oesophagostomy tube should be discussed, especially if performing anaesthesia for other reasons.
Ocular injuries can range from mild globe protrusion to complete proptosis. The prognosis for vision is often not known at presentation but the presence of hyphaema is often associated with a poor prognosis (Figure 4). Globe ruptures tend to occur posteriorly and so may not be evident on physical examination (see Figures 5 and 6).
Cats can frequently present with anisocoria. This may be secondary to:
uveitis (abnormal pupil is miotic due to ciliary body spasm) – topical atropine can be applied to relieve ciliary spasm and pain (Figure 7);
Horner’s syndrome (abnormal pupil is miotic due to loss of sympathetic innervation). This is most likely second order with thoracic or cervical trauma and can often be seen with a brachial plexus avulsion (Figure 8);
optic nerve dysfunction (abnormal pupil is mydriatic due to lack of response to light); and
occulomotor nerve dysfunction (abnormal pupil is mydriatic due to loss of innervation allowing pupil constriction).
Where trauma or opioid medications mean blinking is reduced or not possible, frequent lubrication (eg. Celluvisc TM every two to four hours) should be used prophylactically to reduce the risk of corneal ulceration. Temporary procedures, for example a tarsorhaphy (Figure 6) may be required to protect the corneal surface and provide compression of retrobulbar swelling while pending any resolution of vision. A non-visual, traumatised eye should ideally be enucleated, as there is a link to primary ocular sarcomas in cats with a history of globe trauma (Zeiss et al 2003).

Musculoskeletal system
Pelvic trauma is a common finding in feline blunt-trauma patients and survey radiographs are recommended, even in ambulatory cats (Figure 9). Crepitus on manipulation of the pelvic limbs or palpation of fractures directly via rectal examination can provide an initial indication. Sacroiliac, coxofemoral and distal joint luxations, as well as long bone fractures are also fairly common and may be evident on physical examination or can be assessed on survey radiographs. The abdomen should also be carefully palpated for subtler abdominal wall ruptures (Figure 10).

Urinary system
Urinary tract rupture can also occur with pelvic injury. A palpable bladder and the ability to urinate does not exclude urinary tract trauma (Aumann 1998). Baseline blood work indicating azotaemia and hyperkalaemia and a point-of-care ultrasound indicating abnormal abdominal fluid can help confirm a uroabdomen. Abdominocentesis and fluid analysis can provide further confirmation: in one case series the mean ratio of serum to peritoneal effusion for creatinine and potassium was 2:1 and 1.9:1 respectively (Aumann 1998). The perineal area should also be assessed for subcutaneous leakage from caudal urethral ruptures, but skin necrosis may take 24-48 hours to develop. A contrast study should be performed if there is confirmation of rupture or any uncertainty of patency (Figures 11 and 12). In the author’s institute, an intravenous urethrogram is generally performed prior to a retrograde urethrogram to confirm the ureters are patent.

Wound management
Although definitive wound management may not be possible immediately, all wounds should be covered as soon as possible to minimise the risk of hospital acquired infection. Basic wound management should be performed as soon as possible, and broad-spectrum antibiotics started. It may also be appropriate to take wound culture swabs, especially with open fractures, even if these are not immediately submitted.

Analgesia and sedation/general anaesthesia for further assessment
Depending on the patient, sedation or general anaesthesia may be required to perform parts of the examination or additional diagnostics. When head trauma has occurred, these procedures should be delayed for several days if possible. In the emergency setting, sedatives that can compromise cerebral and renal perfusion, for example, medetomidine and acepromazine, should be avoided. Pure mu opioids often provide sufficient sedation, with the addition of benzodiazepines also being relatively safe. Opioids should not be withheld under any circumstances but may need to be used at lower doses.

Following complete assessment, all injuries and expected prognoses should be communicated to the owner. This initial discussion may be difficult given the potential requirement for multiple staged procedures with unknown prognoses. However, it is vital given the possible time and financial commitments required. Only a thorough physical examination will allow this discussion to take place and ensure owners are fully informed before committing to treatment.

Author contact
Email: pgant@rvc.ac.uk

  • View References

    • Aumann M, Worth L, Drobatz K. Uroperitoneum in cats: 26 cases (1986-1995). Journal of the American Animal Hospital Association.1998; 34(4):315-324.
    • Barnett KC, Crispin SM. Ocular emergencies and trauma. In: Barnett KC, Crispin SM eds. Feline ophthalmology: an atlas and text. London: Saunders, 1998:17-33.
    • Boysen, SR, Rozanski EA, Tidwell AS, Holm JL, Shaw SP, Rush JE. Evaluation of a focused assessment with sonography for trauma protocol to detect free abdominal fluid in dogs involved in motor vehicle accidents. Journal of the American Veterinary Medical Association. 2004; 225(8):1198-204. 
    • DiFazio J, Fletcher DJ. Updates in the Management of the Small Animal Patient with Neurologic Trauma. Veterinary Clinics of North America: Small Animal Practice. 2013 Jul 1;43(4):915-40.
    • Eminaga S, Palus V, Cherubini GB. Acute Spinal Cord Injury in the Cat: Causes, Treatment and Prognosis. Journal of Feline Medicine and Surgery. 2011. 13(11):850-62.
    • Garosi L, Adamantos S. Head Trauma in the Cat: 2. Assessment and Management of Traumatic Brain Injury. Journal of Feline Medicine and Surgery. 2011 Nov;13(11):815-23.
    • Larson MM. Ultrasound of the Thorax (Noncardiac). Veterinary Clinics of North America: Small Animal Practice. 2009;39(4):733-45.
    • Lisciandro GR. Evaluation of initial and serial combination focused assessment with sonography for trauma (CFAST) examination of the thorax (TFAST) and abdomen (AFAST) with the application of an abdominal fluid scoring system in 49 traumatized cats. J Vet Emerg Crit Care 2012;22(2):S11.
    • Olby N, Levine J, Harris T, Munana K, Skeen T, Sharp N. Long-term functional outcome of dogs with severe injuries of the thoracolumbar spinal cord: 87 cases (1996-2001). Journal of the American Veterinary Medical Association 2003; 222: 1502-3.
    • Reineke EL, Rees C, Drobatz KJ. Prediction of systolic blood pressure using peripheral pulse palpation in cats. - PubMed - NCBI. Journal of Veterinary Emergency and Critical Care. 2015 Nov 20;26(1):52-7.
    • Smeak, D.D, Olmstead, M.L. Fracture/Luxations of the Sacrococcygeal Area in the Cat: A Retrospective Study of 51 Cases. Veterinary Surgery. 2nd ed. 1985 Oct;14(4):319-24.
    • Schmiedt C, Tobias KM, Otto CM. Evaluation of Abdominal Fluid: Peripheral Blood Creatinine and Potassium Ratios for Diagnosis of Uroperitoneum in Dogs. Journal of Veterinary Emergency and Critical Care (San Antonio). John Wiley & Sons, Ltd (10.1111); 2001 Dec 1;11(4):275-80.
    • Tatton B, Jeffery N, Holmes M. Predicting recovery of urination control in cats after sacrocaudal injury: a prospective study. - PubMed - NCBI. Journal of Small Animal Practice. 2009 Oct 8;50(11):593–6.
    • Zeiss CJ, Johnson EM, Dubielzig RR. Feline intraocular tumors may arise from transformation of lens epithelium. Veterinary Pathology. 2003; 40(4):355-362.
  • Readers questions and answers

    1. Which of the following would be most likely in a blunt trauma cat with dull ventral lung sounds on auscultation?
    a. Pulmonary contusions
    b. Skull fractures
    c. Diaphragmatic hernia
    d. Pneumothorax

    2. Which of the following treatment protocols would be most beneficial for a patient with suspected head trauma?
    a. Hypotonic saline, oxygen therapy, head elevation, active warming
    b. Hypertonic saline, oxygen therapy, head elevation and active warming
    c. Mannitol infusion, manual ventilation, pelvic elevation and active warming
    d. Normal saline, manual ventilation, pelvic elevation active warming

    3. A blunt-trauma cat presents with a palpable, soft bladder and urine in the carrier. Which of the following differentials is most likely?
    a. Bladder rupture
    b. Urethral rupture
    c. Tail pull injury
    d. May be any of the above

    4. A cat presents with anisocoria with a miotic right pupil and mid-size left pupil. Which of the following is most likely?
    a. Traumatic uveitis of the right eye
    b. Caudal rupture of the right globe
    c. Right sided horner’s syndrome
    d. Periocular trauma around the left eye

    5. Which of the following is most appropriate for sedation of a blunt trauma cat to allow further diagnostics?
    a. Methadone and acepromazine
    b. Methadone and midazolam
    c. Butorphanol and medetomidine
    d. Butorphanol and midazolam

    ANSWERS: C, B, D, A, B.

Click on images to enlarge
  • Figure 1

    Lateral radiograph of a cat with a diaphragmatic hernia.

  • Figure 2

    Lateral radiograph of a cat with large volume pneumothorax.

  • Figure 4

    Cat with mandibular fractures and hyphaema in the right eye. Also note superficial corneal erosion, likely due to opioids suppressing blinking.

  • Figure 5

    Cat with jaw fractures and lagopthalmic eye that was later confirmed to be ruptured.

  • Figure 6

    Same cat with a temporary tarsorhaphy and a mandibular symphysis wire. Unfortunately, extensive maxillary fractures and the requirement for external fixation meant this cat was eventually euthanised.

  • Figure 7

    Cat with traumatic uveitis.

  • Figure 8

    Cat with Horner’s syndrome secondary to a brachial plexus injury.

  • Figure 9

    Survey radiograph of a cat with coxofemoral luxation, sacroiliac luxation, pubic symphysis fracture and ischial fracture. 

  • Figure 10

    Lateral radiograph of a cat with ventral abdominal rupture with gastrointestinal contents. 

  • Figure 11

    Lateral radiograph showing a completed intravenous urethrogram confirming intact ureters and a current retrograde urethrogram confirming a urethral tear.

  • Figure 12

    Fluoroscopic contrast study confirming ureteric rupture.

Continue reading

Celebrating 10 years of IVNA Congress

  • Super User

Nursing - January 2019

Download as PDF

Celebrating 10 years of IVNA Congress

Registration is now open for our very exciting and special 10th IVNA Congress anniversary, which takes place on May 24-26, 2019, at The Grand Hotel, Malahide writes Lorraine McDonnell RVN

This year, the Irish Veterinary Nurses Association (IVNA) celebrates 10 years of Congress with a memorable three-day event in conjunction with our partners Royal Canin, Allianz and Bayer. We have an extensive programme laid out for every nurse to enjoy multiple practical streams in our Friday and Sunday programme, and a full day of lectures on Saturday, followed by our awards, gala dinner and casino night. The 2018 Congress was hugely successful and after analysing all the evaluation forms received and suggestions by our members over the last two years, we set out to deliver one of our most ambitious congress events. For 2019, the exhibition trade show takes place over two days, on Friday and Saturday.Friday is the first practical day, which includes three separate streams. The skin stream starts with Itchy and Scratching – a guide to ectoparasites presented by Doireann Dowling RVN DipVN BA (Hons. Mod.Env.Sci). After lunch, Kerry Lawless from Tick Talk will give an hour-long presentation, followed by Clare Hemmings from Royal Canin on Catering for Nutrition in the Dermatological Patient. After a short break, Doireann Dowling will look through the microscope for the parasitology practical section.Mairead Deacy DipAVN DipHE CVN RVN and Jane Tyrell RVN AdvCert Vphys have teamed up for the Surgical and Physiotherapy stream. Mairead will begin with Surgical Nursing of the Stifle Patient and, following lunch, she will present on the topic of Post-operative Analgesia. Following this, Jane will focus on everyday application of Physiotherapy in Practice.The third Friday stream is hosted by Sinead Sheerin, RVN CertVNECC, focusing on emergency triage, common emergencies presentations, cardio pulmonary and a CPR practical session to close the stream. Following the Friday programme, we will host an opening ceremony in our trade exhibition to celebrate this momentous anniversary with our delegates and sponsors.On Saturday our speakers, Laura Bree MVBDipECVIM-CA and Grainne Lally MVB CertVA, will focus on dealing with the seizing patient from triage, working up the patient and useful diagnostics, anaesthesia and analgesia and long-term management. Our mindfulness lecture, by Dan Tipney, will centre on self-care, stress solutions and mindful practice.After a busy two days, delegates can choose to join a yoga class on Sunday morning, to destress and relax prior to the last day of congress. The Sunday streams will focus on exotics and dentistry. Claire Bloor MA Ed Bsc (Hons) VN RVN PgcE QTLS Cert VN (Dent) and Sara Cowan RVN are teaming up to bring you the dentistry stream. Claire will show us anatomy, physiology and common conditions, moving on to pain management in dental, oral and maxillofacial patients. The practical sessions will deliver probing/charting, scaling and equipment maintenance, and dental radiographing.The exotics stream will be delivered by Garth de Jong. Garth's stream will start with nutrition in the recovering reptile, housing and enrichment for exotic patients, and the practical sessions of the day will be safe handling of exotics. Last year’s winning nominationJennifer Carroll was our winner of Veterinary Nurse of the Year and this was her winning nomination. “I wish to nominate Jennifer Carroll for Veterinary Nurse of the Year. Jennifer is a champion for animals in the Bantry area. She started the Rural Animal Welfare Resources (RAWR) charity, which is an entirely voluntary organisation (with over 20 volunteers) which strives to reduce the number of unwanted domestic animals in Bantry and the surrounding area by performing trap, neuter and return for feral cats while ensuring that they will be fed and sheltered by the farm, etc where they currently live. If this will not be the case, she finds a foster home for all of them. Jennifer personally takes what little spare time that she has, to trap, ensure they are neutered and return the cats. Jennifer never hesitates to help abandoned dogs, cats and other small animals, even fostering them herself if she cannot find a home for them.RAWR has a voucher programme to neuter companion animals at a reduced rate. Jennifer personally contacts vets in other west Cork towns to enlist them to accept RAWR’s vouchers. She has successfully gotten four vets to participate. Last year, 670 cats and dogs were neutered through the programme. Last year, Jennifer initiated a Fix It for a Fiver (FIFF) scheme where, for a two-week period, people can bring in feral cats and have them neutered for €5. She has again recruited other veterinary practices to participate. Through this programme, 203 cats will not be contributing to the feral cat population in west Cork.In addition to her tireless work for abandoned and homeless animals in west Cork, Jennifer is a veterinary nurse par excellence. Jennifer is exceptionally knowledgeable but maybe even more important, she is kind, understanding and sympathetic.My dog, who used to tremble at the vets, now wags her tail upon seeing Jenn. Sometimes she even wants to stop in to say hello on our walks around town. I see other non-human visitors responding positively to her as well.Jennifer’s manner with humans is calming as well, I’ll not forget the support I received when my beloved 18-year-old cat had to be euthanised. She was a truly caring and warm individual.It is clear to me that Jennifer is everything a veterinary nurse should be. She is tireless in her dedication to animals of all types. She loves animals and they love her in return.” Gala dinner and awardsOn Saturday, we will celebrate our awards night with a gala dinner. Three awards will be presented to honour the 2019 Veterinary Nurse of the Year (sponsored by Royal Canin) and the 2019 Student Nurse of the Year (sponsored by Allianz). This year, the third award has been changed to Practice Manager of the Year (sponsored by Bayer). These awards acknowledge outstanding efforts made by veterinary nurses, student veterinary nurses and practice managers, who go above and beyond for their patients, owners, and colleagues alike. These individuals can be nominated by the public or a colleague. The IVNA awards nominations have officially opened. Each winner is selected through the following process: six finalists are selected in each category from all nominations received by March 31, 2019; the winner will be selected by the sponsoring company; no member of the IVNA committee has any input into the overall winners; each winner will receive a holiday gift voucher along with a trophy; the nominator of the winner in each category will also receive a voucher for €50.  If you think someone you know deserves this award for the work they do, please go to our website on www.ivna.ie and fill in the nomination form today.To celebrate the 10th congress anniversary we have special entertainment planned after the gala dinner and awards, with a casino and party night. Join us at the IVNA party let your hair down and hedge your bets in our casino at the blackjack and roulette tables, we have games and more to make this an unforgettable night. It doesn't end there, if you have some energy left after all, that you can dance the rest of the night away with our DJ keeping the party going.As a special thank you for the ongoing support of our members and delegates, we are offering a free ticket to our awards dinner and congress party to those attending the full weekend. Places are limited, so don’t be disappointed and book early to secure a place at what promises to be a memorable and momentous event for Irish veterinary nurses.

Continue reading

Calf health: the good, the bad and the ugly

  • Super User

Focus - January 2019

Download as PDF

Calf health: the good, the bad and the ugly

Hazell Mullins BVM BVS, Abbeyville Veterinary Hospital, Cork, presents three calf health-specific case studies, highlighting the good, the bad and the ugly of all three scenarios, as well as treatment plans and outcomes

Case 1: Scouring CalvesBackgroundCalled out to a 100-cow, spring calving dairy herd in the middle of a busy February. This was a firefighting-type situation as two calves had died overnight and five more were destined for a similar outcome. The good There were raised, individual pens in the centre with small group pens around the outside of house. Sick calves were fed milk plus electrolytes in the middle of the day on two separate occasions. Colostrum management – considered to be good as they were very exact about colostrum administration. Three litres of colostrum were given by bottle as the farmer was nervous of tubing. Calves were fed own mothers’ or frozen, stored colostrum. Cows were vaccinated for Rotavirus/Corona Virus/E. coli and Salmonella. Halofuginone used on every calf as there was a history of cryptosporidium on the farm. The bad Concrete – wet and covered in scour. Poor ventilation – air was ammonia-filled, the building where the calves were housed had very low ceilings leading to poor air speed and lack of fresh air. Housing was slightly over-stocked. No foot dips at the entrance. No measurement IgG to assess the quality of colostrum. The ugly Five moribund calves. Two calves already dead and had not yet been submitted for post mortem. All calves had some form of slight scour. Plan of action Performed a snap test on a scour sample which was positive for Cryptosporidium. Advised farmer to send freshest calf for post-mortem. Dripped all five calves with a bicarbonate spiked drip. Needed to consult with the halofuginone vet adviser regarding its efficacy. Vet Adviser's Plan Take up to five serum tubes from healthy calves ideally between two and five days of age for zinc sulphate turbidity (ZST) testing. The next calf to scour, take a sample to send to regional vet lab, requesting testing for E. coli, Rotavirus, Coronavirus, Cryptosporidium, Salmonella and Campylobacter. Send next deceased calf for post mortem. Results of investigationsNumerous diagnostic tests were performed, starting with a simple farm-side Snap test, which indicated cryptosporidium was the causative agent. On post-mortem and further tests at the regional vet lab, again cryptosporidium was found. To examine failure of passive transfer (FPT) in these calves, the ZST returned results of 80% FPT with readings between 13-19 units, implying that there was certainly room for improvement in colostrum management. ZST is not classed as the most specific test available but does give good indication of IgG levels in calves. Simple serum IgG tests could have been performed, also using a refractometer in practice. I am certainly guilty of not performing these often enough in practice. It involves taking a serum sample, spinning down or letting it rest, and placing a drop on a refractometer. If using a Brix refractometer, a value of over 8% is optimum or on conventional refractometer a reading greater than 5.5g/dL is optimum. In a Moorpark-based study in 2015, Hogan et al wrote that when compared to other tests available for FPT serum total protein was less specific and sensitive than other tests examined but is still very useful for in-house tests. Of course, there is major scope for farmers to use refractometers to measure colostrum before administration and storage with an optimal value of >22% Brix value. The latest data, from a 2018 Irish study by Todd et al, found a worrying figure of 54% of dairy calves having FPT. As vets, we need to encourage the use of these farm-side tests more. But!The elephant in the room in this case was compliance! We should never automatically presume that a product being used on farm is being used correctly. The halofuginone had only been used for four to five days instead of the recommended seven, and had only been started at three to four days ofage instead of after the first feed. Treatment plan- Dose every calf within 24 hours post initial colostrum feed with 7ml halofuginone for seven days.- More vigorous cleaning regimes in place including the use of foot dips, using anti Cryptosporidium disinfectant, and render walls if possible.- Improve drainage in the calf house.- Check colostrum quality using a Brix refractometer on all colostrum prior to feeding.- Ensure strict hygiene with feeding equipment – sterile nipples and buckets after every feed, and change nipples regularly.- Replace or replenish bedding every two days.- Isolate all affected calves to one calf house and keep here until scour is ceased for at least one week. Case 2: Sudden Death in calves BackgroundThis was particularly interesting in terms of unusual disease outbreak that was low down on my differential list due to the farmer’s preventive measures. I was called to a large, 400-cow milking herd towards the end of April. The good Very modern farm facilities. Individual calf pens used for the first week of life. All calves tubed with 3L of stored colostrum mostly within one hour of birth. New calf shed built recently with good ventilation, bright and draught-free, calves moved here at approximately two weeks of age. Automatic calf feeders in place and calves fed on good quality milk replacer (26% whey protein). Vaccination protocols were excellent – Leptospirosis, infectious bovine rhinotracheitis (IBR), bovine viral diarrhoea (BVD), Salmonella and Rotavirus/Corona all administered. The bad High stocking densities, herd expanded in recent years. Poor hygiene in certain areas, especially around feeders. Individual pens used for the first two weeks were very near the sick cow pen. Staff under extreme pressure at the end of spring due to large numbers. Not measuring colostrum quality before storage or administration. The ugly Called to group of four-to-six-week-old calves with sudden onset of inappetence followed by sudden death. Four calves had died overnight. Presented off feed the night before with poor appetite, ears down and lethargic. Injected by farmer with long-acting antibiotic for pneumonia to no avail. Examined four other similar calves in which I found high temperatures, harsh lung sounds on auscultation and a ‘touch’ of scour with no blood present. Treatment plan- Empty calf house and disinfect thoroughly.- Cover ration feeders.- Clean automatic feeder more frequently, including swapping nipples after every feed, and post sterilisation.- Advise/teach farmer to check colostrum quality using a Brix refractometer.- Discussed colostrum storage and thawing methods.- Revised the farmer’s vaccination programme, all eligible in-calf cows given a Salmonella booster, ideally in the window of within three weeks and eight weeks prior to calving.- Calves over three weeks of age were started on a primary course of vaccine using the lower 2ml dose. Plan of action Snap tested the scour, which proved negative to all specified infections. Injected all calves with nonsteroidal anti-inflammatory drugs (NSAIDS) and continued farmers use of antibiotics. Dripped two calves who were unable to stand. Booked the freshest calve into the regional veterinary laboratory for a post mortem. Results of investigationsThe result of the post-mortem confirmed a diagnosis of salmonellosis due to Salmonella Dublin. Signs of pneumonia were found cranioventrally distributed involving abscessation of approximately 30% of the lungs. A large abscess was found in the urachal remnant cranial to the bladder and small white foci were found in the kidney, otherwise referred to as ‘spotted kidney’. S. Dublin was positively cultured from one of the lung abscesses present. On further enquiry from vets at the regional veterinary laboratory in Cork, Salmonella can present with a wide range of pathologies and there is not one finding that is diagnostic, culture is always necessary. Case summaryLessons to be learned from this case are that, despite vaccination, diseases can occur if the infection pressure is high enough. Typically, in Ireland, Salmonella vaccine is primarily used as an anti-abortion vaccine and calves are not generally immune, unless boosters are given closer to calving. The complex presentation of salmonellosis can be confusing to both famers and vets, with very general clinical signs and, unfortunately, not always the textbook blood red scour. After visiting Salmonella-positive farms in Denmark this year, they take their Salmonella prevention very seriously and their biosecurity is second to none. Separate wellingtons for vets/visitors on the farm is commonplace and disinfectant spraying of all personal protective equipment before arrival and departure of the farm is obligatory.Case 3: Bloated CalvesBackgroundThis case was not isolated to one farm outbreak or animal but was a reoccurring issue that I encountered throughout the spring of 2018. It can be frustrating to treat bloat as the etiology is a little complicated and there are no straightforward answers. The main principle of a bloat outbreak involves the excessive fermentation process of high-energy milk or milk replacer in the abomasum resulting in overproduction of gas. The most common bacterial involvement would be Clostridium perfringens A. due to poor storage of colostrum and subsequent bacterial overgrowth. General bloat prevention recommendations: Bloat is worsened by slow abomasal emptying and the osmolality of the milk. Never feed more than 4L in one meal, instead try to aim for smaller, regular meals. Keep osmolality as close as possible to milk’s naturally occurring 12.5% solids, ie. make milk replacer at a rate of no more than 15% (150g mixed in 1L of water). Dehydration, addition of electrolytes or medications to replacers can slow abomasal emptying. Have a strict feeding routine every day. Be careful of iatrogenic vagal nerve damage due to poor tubing technique, this can interfere with abomasal emptying. Try to only tube a calf once, if at all possible. Treatment 5ml penicillin, intramuscular. NSAIDS if in a lot of discomfort. Drench orally with 10ml penicillin, orally. If very distended, get farmer to ‘dog sit’ the calf and extend head to tube but this can be very unreliable. Skip one meal and give non-glucose containing electrolytes if necessary. Feed calves last to ensure correct oesophageal groove open. Recommend to farmers the key feeding points. Curve balls Twists, ie. intestinal intussusceptions/twisted guts/obstructions/foreign bodies. Ruminal bloat – this usually occurs in older calves. Overleaf are pictures of a rumenotomy surgery I performed on a four-month-old bull calf. ConclusionFor younger vets, the ‘text book’ case presentations that we study in vet school do not always translate to real-life situations and this is where help from more experienced vets and vet advisers is vital. Farm animal medicine keeps me on my toes constantly; even when you think you have sussed out a case, a curve ball can be thrown at you at the last minute. In general, calf health is the first building block to a successful farming enterprise and, as vets, we can share our knowledge to help farmers prevent disease and control outbreaks in their calves. As a recent graduate in practice over the past five years, I have realised that every single calf scour, pneumonia outbreak and miscellaneous sick-calf call has contributed to my overall knowledge base. The old saying ‘every day is a school day’ certainly rings true for anyone involved in the exciting world of veterinary medicine. AcknowledgementHazell Mullins BVM BVS, presented at the 2018 CAVI Conference on the topic of calf health, ‘the good, the bad and the ugly’ of some of the real-life cases she has encountered. Hazell would like to thank CAVI organisers for the opportunity to share her professional experiences, enabling her to reach out to younger vets who were in attendance and to help them overcome the pressures of calf health challenges in those first few years in practice.

Click on images to enlarge

Scouring calves.

Sudden death in calves

Bloated calf.

Rumenotomy 1 (top) and Rumenotomy 2 (bottom).

Continue reading

Antimicrobial drug use in calves – implications for antimicrobial resistance

  • Super User

Large animal - January 2019

Download as PDF

Antimicrobial drug use in calves – implications for antimicrobial resistance

Dr Bernadette Earley, Dr Anastasio Arguello, and Dr Mark McGee from Teagasc Grange Animal & Grassland Research and Innovation Centre, Co. Meath, and Aidan Murray, Teagasc, Letterkenny, Co. Donegal explore antimicrobial resistance implications on commercial beef and dairy farms in Ireland

Concern about the use of antimicrobials in food-producing animals is increasing. The following guidelines are recommended to maintain acceptable levels of antimicrobial usage on beef and dairy farms: Develop a herd-health plan in consultation with your veterinarian and Teagasc adviser; Pay attention to colostrum feeding, animal nutrition and animal purchasing policies; Vaccinate animals to reduce the need for antimicrobials and use alternatives to antimicrobials when available; Only give antimicrobials to animals under veterinary supervision; Do not use antimicrobials for growth promotion or to ‘prevent’ diseases in healthy animals; and Improve biosecurity on farms and prevent infections through improved hygiene and animal welfare. What is antimicrobial resistance (AMR)?Antimicrobial, derived from the Greek words anti (against), mikros (little) and bios (life), has a broader definition compared to just the term antibiotic and includes agents (both synthetic or natural), that act against bacteria, viruses, fungi and protozoa. In this paper, antimicrobial is taken to mean antibiotics (and their chemical derivatives) with an antibacterial range of action. Antimicrobial resistance (AMR) is the ability of bacteria (or microbes) to resist the effects of an antibiotic. AMR is one of the leading health concerns in human and veterinary medicine worldwide. AMR occurs when bacteria change in a way that reduces the effectiveness of drugs, chemicals, or other agents designed to cure or prevent infections. AMR can be intrinsic or acquired. Intrinsic or natural resistance is a trait of all bacteria belonging to a specific subspecies, species, genus, family or even higher taxonomic rank. Acquired resistance to antimicrobial drugs can develop in bacteria in two ways: genes can mutate, or genes from other bacteria can be horizontally transferred to them. AMR may cause treatment failure, both in humans and animals. This treatment failure results in a higher morbidity and mortality. Monitoring antimicrobial usageIn Europe, various monitoring programmes have summarised antimicrobial consumption for animals through annual antimicrobial sales data (DANMAP, 2013; ANMV, 2014; MARAN, 2015). These programmes are structured to observe trends at the national level and for comparison of data between years and countries (ECDC/EFSA/EMA, 2015; EMA, 2015). However, a limiting factor of those programmes is that they are unable to provide more precise information, such as usage at farm level, variability between farms, etc.Teagasc study on antimicrobial drug usage in calvesThe main objective of the study described below was to quantify antimicrobial drug usage in calves using health treatment records from Irish suckler beef and dairy farms. In this study, antimicrobial usage refers to the exposure of a given animal or group of animals over a period of time to the active substance in each antimicrobial that was administered. Data sourceData were obtained from a large-scale study on herd-level factors associated with the health and survival of calves on Irish farms (hereafter referred to as the herd-level study). Farmers, enrolled in the herd-level study, recorded birth, disease and health treatment, and death information on their calves using standardised recording sheets. Case definitions were provided to the farmers to assist with the classification of disease. Farmers completed and submitted the project recording sheets on a monthly basis. All health treatment data were reviewed. Long-acting antimicrobials administered more than seven days apart, or other medications administered more than three days apart, were classified as separate disease events. Crude morbidity was defined as calves being treated for at least one disease event, attributed to any cause, excluding injury. Calves treated for illnesses other than diarrhoea, pneumonia, navel infection, or joint infection/lameness were categorised as receiving treatment for ‘other’ disease events. The data collected were the antimicrobial trade name, the pharmaceutical form (oral solution, oral powder, parenteral solutions, tablets, bolus, etc.), the pack size (in L or ml for liquids, in g or kg for solids, in unit number for bolus or tablets, etc.), the total number of packages prescribed and dispensed to the farm, and the prescribed therapy (dose, administration frequency, duration). Antimicrobial usageDefined daily dose for animals (DDDvet) (mg/kg animal/day) and used daily dose (UDDvet) (mg/kg animal) were the technical units used to measure antimicrobial consumption. The DDDvet is defined as the average maintenance dose for the main indication in a specified species and it is provided by the by the European Surveillance of Veterinary Antimicrobial Consumption (ESVAC) project for veterinary antimicrobial usage, whereas the UDDvet is calculated as the amount of an antimicrobial drug administered during a given period (days) divided by the number of calves at risk and their average live weight at the beginning of a treatment. In this way the UDDvet reflects the dose, truly administered by the producer. Treatment incidence (TI) was the indicator used to quantify antimicrobial usage. The TI provides a standardised technical unit of measurement that quantifies how many animals out of a theoretical group of 1,000 animals receive daily an antimicrobial treatment, and the calculations applied were: TIUDD VET = Total active substance administered ×1000UDDvet × standard BW × total calf daysTIDDD VET = Total Active Substance Administered ×1000DDDvet × Standard BW × total calf days The Population Correction Unit (PCU) is a measurement developed by the European Medicines Agency (EMA) and takes into account the animal population as well as the estimated weight of each particular animal at the time of treatment with antimicrobials. The milligrams (mg) of antimicrobial used per PCU was calculated. ResultsThis study provides the first detailed information pertaining to on-farm usage of antimicrobials in suckler beef and artificially-reared dairy calves from birth to six months of age, in Ireland. A total of 123 farms (79 beef and 44 dairy), comprising 3,204 suckler beef calves and 5,358 dairy calves, representing 540,953 and 579,997 calf days at risk, respectively, were included in the study. All calves were raised on farm of origin and most of the studied herds were closed herds. In this study, only animals showing signs of disease were treated with antimicrobials and no mass administration of antibiotics was practiced. On beef farms overall, 12.7%, 5.7%, 2.9% and 20.4% of suckler beef calves were treated with antimicrobials for disease from birth to one month of age, one to three months of age, three to six months of age, and birth to six months of age, respectively. The corresponding values on dairy farms, overall, for calves treated with antimicrobials were 10.2%, 5.3%, 1.9% and 14.8%. The highest risk period for disease in the present study was between birth and one month of age with approximately two-thirds of all disease events occurring during this time period. This is reflected in the proportion of antimicrobials administered to calves at this time (Figure 1).The classes of antimicrobials most frequently prescribed for beef and dairy calves were: tetracyclines, amphenicols, penicillins, 1st and 2nd generation cephalosporins (GC), 3rd and 4th GC, sulfonamides, macrolides, lincosamines, fluoroquinolone, aminoglycosides and spectinomycin (Table 1).A total of 1,770 antimicrobial treatments were prescribed and administered to suckler beef (n=841) and dairy calves (n=929) between birth and six months. From birth to one month, the class of antimicrobial prescribed for most herds irrespective of type of farm, was penicillin (mostly amoxicillin) by the parenteral (non-oral) route (36.7% and 27.3%, beef and dairy, respectively). From one to three months of age, amphenicols (florfenicol) were the most prescribed class of antimicrobial for beef calves (17.7%) and tetracyclines (15.9%), mostly oxytetracycline, for dairy calves. Amphenicols (florfenicol) were prescribed more often in calves in the period from three to six months of age (11.4% and 16.0%, beef and dairy, respectively). The antimicrobials most prescribed for beef calves during the whole period (from birth to six months of age) were penicillins (mostly amoxicillin), tetracyclines (mostly oxytetracycline), amphenicols (florfenicol) and fluoroquinolones (enrofloxacin and marbofloxacin) (41.8%, 30.4%, 29.1% [13.9% and 25.2%] respectively). From birth to six months, penicillins (mostly amoxicillin), amphenicols (florfenicol), tetracyclines (mostly oxytetracycline) and fluoroquinolones (mostly enrofloxacin and marbofloxacin) were more frequently prescribed (34.1%, 29.6%, 22.7% [18.2% and 22.7%), respectively) for dairy calves. Due to their special surveillance in the context of AMR, the third and fourth generation cephalosporins were separated from other beta-lactams, and fluoroquinolones from other quinolones.Fluoroquinolones were the most prescribed antimicrobials with 383 treatments, followed by penicillins (n=374), amphenicols (n=287) and tetracyclines (n=257). The third and fourth generation cephalosporins accounted for a total of seven treatments (Table 1). In the present study the mg/PCU was 8.03, 2.70, 1.43 and 7.25 for suckler beef calves for the treatment periods from zero to one, one to three, three to six, and from birth to six months, respectively. The corresponding values for dairy calves were 9.74, 3.72, 0.95, and 7.11 mg/PCU. The average cost of veterinary services was €41.25 and €43.37 per calf for beef and dairy calves, respectively; corresponding antimicrobial costs were €11.58 and €11.51 per calf.Actions the farmer can take to keep antimicrobials working Only give antimicrobials to animals under veterinary supervision. Always give the right dose, and the number of treatments, as prescribed by your vet. Do not use antimicrobials for growth ‘promotion’ or disease ‘prevention’ in healthy animals. Do not use antimicrobials to treat viral disease. Do not use a ‘stronger’ antimicrobial as first-line treatment. Vaccinate animals to reduce the need for antimicrobials and use alternatives to antimicrobials when available. Improve biosecurity on farms and prevent infections through improved hygiene and animal welfare. In the case of medicines used in food-producing animals, ensure that the Animal Remedies Record is updated on each occasion that a veterinary medicine is administered. Further information is available at www.agriculture.gov.ie/amr/ List of Products containing DAFM Highest Priority Critically Important Antimicrobials (pdf 468Kb) Code of Good Practice Regarding the Responsible Prescribing & Use of ABs in Farm Animals (pdf 1,326Kb) Ireland's National Action Plan on Antimicrobial Resistance 2017-2020 DAFM surveillance on AMR (doc 609Kb) European Commission Guidelines on the prudent use of antimicrobials in veterinary medicines European Commission – 5 year action plan The World Health Organization (WHO) categorises antimicrobials used in human health as ‘critically important’, ‘highly important’ and ‘important’ to human health. The critically important antimicrobials (CIAs) are, therefore, the most important to human health. The CIAs are further categorised into Highest Priority CIAs (HP-CIAs) and High Priority CIAs. Given the importance of HP-CIAs in human health, these antimicrobials should NOT be used prophylactically or as first-line treatment in animals. They should only be used when there are no effective alternative antimicrobials available for the treatment of respective target species and indication. AcknowledgementsFunding from the Department of Agriculture, Food and the Marine (Dr B Earley, project leader) under the Stimulus Fund (11/S/131) is gratefully acknowledged. The authors also wish to acknowledge the participating farmers, their Teagasc advisers, Cynthia Todd and Olivia Butler with data collection, and the administrative staff at Teagasc Grange for their support of this research.

Click on images to enlarge

Antimicrobial drug classes administered to suckler beef (n=654) and artificially reared dairy calves (n=795) from birth to six months of age.

Proportion of antimicrobial treatments (%) for suckler beef and artificially reared dairy calves from birth to six months of age.

Continue reading

The impact of disordered physiology on the provision of veterinary nursing care: chronic renal failure

  • Super User

Nursing - December 2018

Download as PDF

The impact of disordered physiology on the provision of veterinary nursing care: chronic renal failure

Patients are hospitalised for many reasons and it is essential VNs have knowledge and understanding of common disorders and the associated clinical signs in order to justify their chosen nursing interventions, writes Liane Henry RVN

Veterinary nurses are commonly the main care-givers for hospitalised patients. Branscombe (2010) discussed how up-to-date knowledge and skills are relevant to veterinary nurses to provide the highest standards of nursing care to their patients disorders and the associated clinical signs in order to justify their chosen nursing interventions. This article will discuss chronic renal failure (CRF) and how the disruption of normal physiology produces abnormal clinical signs requiring nursing care. Chronic renal failureCRF is a condition that causes pathophysiological and irreversible damage to the parenchyma of the renal anatomy, inhibiting normal function and causing the patient to exhibit abnormal clinical signs. Sparkes (2016) et al stated that renal disease is considered chronic when there is evidence of reduced renal function for a period of three months or more. The International Renal Interest Society published a set of algorithms in 2006 (which have since been modified) to assist the staging of CRF from stages 1-4, in both canines and felines. Patients are classified in the later stages (stages 3-4) of CRF when azotemia is diagnosed, due creatinine levels >140 umol/L in felines and >125 umol/L in canines. Clinical signs and uraemia appear in the later stages of CRF. Hewitson (2009) reported that kidneys react similarly to other body systems when injured. Inflammation occurs in the nephron causing inflammatory cells to populate the area and McLeland et al (2015) reported that these cells are found at all stages of CRF, with incidence increasing with progression of the disease. Cytokines are produced, which activate local mesenchymal cells to proliferate and synthesise extracellular matrix, which contracts and increases in density, causing interstitial fibrosis (Hewitson 2012). Brown et al (2016) reported that these changes are commonly identified in the tubulointerstitial region of the nephron and this continuous accumulation of fibrotic tissue causes reduced function, including tubular degeneration and atrophy. Reduced function in the nephron tubules limits their permeability, resulting in decreased tubular absorption and secretion of materials from the filtrate. Brown et al (2016) stated that pathophysiological changes also occur in the glomerulus of the nephron and McLeland et al (2015) identified global glomerulosclerosis as present when >75% of the capillary tuft was irreversibly damaged, resulting in blood being redirected to remaining viable nephrons causing hypertrophy. Podocytes in the visceral layer of the Bowman’s capsule respond to hypertrophy by adapting in size to cover a larger surface area, which Chakrabarti et al (2012) reported inhibits sufficient filtration through the glomerulus. Affected glomeruli exhibit thickened and wrinkled basement membranes, collapsed capillary tufts and interstitial fibrosis (Brown et al 2016), allowing normally filtered macromolecules to pass through the membrane and enter the Bowman’s capsule, convoluted tubules, loop of Henle and collecting ducts. Hewitson (2012) described how interstitial fibrosis in the nephron affects the vasculature, causing sclerosis in the capillaries, then ischemia and hypoxia. Chakrabarti et al (2012) noted it may be a combination of these factors that contributes to the obsolescence of affected glomeruli. As discussed, this pathogenic process leads to the malfunction of the renal parenchyma causing irreversible nephron loss and clinical signs seen in the affected patient. The kidneys play a vital role in acid-base regulation through the generation of bicarbonate and excretion of acids, such as hydrogen ions, in urine. Damage to the nephron reduces the kidney’s ability to carry out this function, causing a decreased pH in the blood, resulting in acidosis (Welsh and Girling 2010). Korman and White (2013) noted that increased concentrations of gastrin in blood due to poor excretion via the kidneys results in gastric acidity and ulceration. Hypokalaemia is common in cats with CRF due to increased potassium loss and, according to Reynolds and Lefebvre (2013), can induce metabolic acidosis leading to hypergastrinemia, resulting in adverse clinical signs such as ulceration, stomatitis, nausea, inappetence and vomiting. Further clinical signs associated with CRF include hypertension, polyuria, polydipsia, anaemia, and dehydration. An understanding of CRF pathophysiology and clinical signs assists the VN when planning and implementing chosen nursing care and optimises the care plan specific to the patient’s needs. The hypertension linkSystemic hypertension and CRF are strongly linked, with a high incidence of patients presenting with hypertension also showing evidence of CRF. Despite this, there is little evidence to determine whether hypertension causes CRF or vice versa (Jepson 2011). Auto regulation of renal blood pressure may be compromised by systemic blood pressure causing increased glomerular permeability and damage to the convoluted tubules (Jepson 2011). The renin-angiotensin-aldosterone system (RAAS) is noteworthy in CRF. Reynolds and Lefebrve (2013) summarised that activation of the RAAS induces vasoconstriction of the efferent arteriole, contributing to glomerular hypertension, increased cellular matrix, tubular and interstitial inflammation and, ultimately, CRF. Angiotensin II is particularly concerning, as discussed by Rüster and Wolfe (2006), due to its stimulation and proliferation of mesangial, glomerular endothelial and fibroblast cells, causing tubular hypertrophy. The VN should assess hospitalised patients regularly for hypertension using a blood pressure monitoring device. Maltman (2003) advised the readings should be taken in a quiet environment where the patient has acclimatised, with the aim of recording accurate readings unaltered by high stress levels. RehydrationDamage to convoluted tubules and the loop of Henle causes reduced permeability, resulting in several clinical signs for the CRF patient. Polyuria occurs when excess water is excreted in urine due to reduced reabsorption of water from the glomerular filtrate in the convoluted tubules, leading to dehydration then polydipsia in an effort to rehydrate (Korman and White 2013). Breton (2013) discussed diuresis as the gold standard of care for CRF. The VN’s role in the administration and monitoring of intravenous fluid therapy (IVFT) was discussed by Bloor (2015) and care should be taken when calculating fluid requirements to include any fluid losses due to dehydration, vomiting and diarrhoea. In addition, Breton (2013) advised regular reassessment of fluid requirements as the patient becomes rehydrated. Where patients are receiving IVFT for a number of days, Bloor (2015) advised the VN should include daily inspection of the catheter insertion site for signs of infection in the patient care plan. In addition to IVFT, polyuria indicates ample access to litter trays with absorbent litter for cats and numerous toilet walks for dogs. Urine output volumes should be recorded and accounted for in fluid-deficit IVFT requirements and bedding should remain clean and dry to prevent urine scalding (Almond 2017). Proteinuria occurs due to decreased reabsorption in the tubules in combination with systemic hypertension, causing reduced filtration in the glomerulus, leading to proteins being excreted in urine (Beetham and Cattell 1993). Almond (2017) suggested the VN should monitor for proteinuria at regular intervals during hospitalisation and at subsequent visits to the clinic using a urinalysis dipstick, with results recorded. This also provides the opportunity to screen for haematuria or infection, which is a risk for patients with CRF due to dilute urine and some medications (Almond 2017). AnaemiaReduced production of erythropoietin in the peritubular cells results in anaemia for 30-60% of felines with CRF (Reynolds and Lefebvre 2013) and is worsened by shortened red blood cell lifespan and gastrointestinal haemorrhage (Chalhoub et al 2011). Anaemic patients may present with pale mucus membranes and also display clinical signs such as weakness and lethargy (Chalhoub et al 2011). Breton (2013) recommended care when blood sampling these patients including taking the minimum amount of blood required for blood screens or packed cell volume count and suggests applying a pressure bandage to the venipuncture site to prevent haemorrhage. Gastrointestinal signs are major indicators of uraemia and are often the first signs of CFR noted by the owner. Nursing care for the hospitalised CRF patient should include a plan for responding to these clinical signs. Vomiting and nausea can cause inappetence and the attending veterinary surgeon (VS) should be notified where anti-emetics may be required. Clinical signs, such as stomatitis, may be painful and Cherry (2014) suggests the VN pain scores CRF patients regularly. Where the patient is deemed painful, the VS should be notified and analgesics prescribed and administered. Almond (2017) suggested care should be taken when choosing a feed in hospital to reduce the likelihood of diarrhoea and to avoid food aversion due to a quick change in diet. Other clinical signs must also be considered when feeding. Ackerman (2015) noted the effect uraemia has on a patient’s appetite, including reduced sense of smell and taste, and suggested small, warmed, frequent meals may be better accepted. Despite IVFT, fresh water should be available at all times to satisfy polydipsia and a wet-food diet is usually preferable for these patients as it will increase overall water intake (Almond 2017). Newly diagnosed patients should be allowed a slow transition onto a renal diet once discharged from hospital. A study by Plantinga et al (2005) showed renal-specific diets increase longevity in cats with CRF. A thorough clinical history and a holistic approach to nursing these patients will allow the VN to identify the patient’s likes and dislikes to select a diet for use in hospital, as well as recommending an appropriate commercial diet for long-term management. Almond (2017) noted the importance of the VNs continuing role after the patient has been discharged, providing support and advice to owners during the initial weeks following diagnosis, as well as being a familiar face for routine blood and sampling and blood pressure monitoring where a VS consult is not required. Another area for VNs to consider is the patient’s emotional wellbeing during hospitalisation. Cherry (2014) advised the VN should attend to this aspect of patient’s wellbeing to provide holistic nursing care to the patient and suggested low-stress handling, hidey-holes in kennels and the use of pheromones may be beneficial to the feline CRF patient. Cherry (2014) also mentioned the unrivalled benefits of touch and tender-loving-care, for example grooming, which benefits the patient’s mental health and in the case of CRF also provides an appropriate nursing intervention for managing reduced grooming due to stomatitis. CRF is a multifactorial pathophysiological process, causing irreversible loss of nephrons in the kidneys. Chronic and cumulative inflammation, alongside increased production of extracellular matrix production causes tubulointerstitial fibrosis, glomerular sclerosis and vascular sclerosis resulting in abnormal clinical signs, which are thought to further contribute to the disease pathway and to end-stage renal failure. Nursing care for these patients requires a combination of knowledge and understanding of the disease pathway along with a holistic nursing approach, considering all related clinical signs in order to manage the disease, both in hospital and at home.

Continue reading