Sektion vedr

Sektion vedr. Heste
Årsmøde 2015 i Middelfart
”Fra føl til den geriatriske hest”
Proceeding
Indhold
Folingen og dens udfordringer v/Hanne Gervi
3
The foal in the first days v/Andy Durham
4
Inflamm-aging og Recurrent Airway Obstruction (RAO) v/Sanni Hansen
7
Therapeutics for respiratory diseases v/Andy Durham
10
General limitations of application and interpretation of Clinical Pathology
v/Andy Durham
14
Metabolic and Endocrine Diseases in the older horse v/Andy Durham
18
En værdig afslutning på livet v/Peter Sandø og Pia Haubro Andersen
23
Fodring igennem livet v/Rasmus Bovbjerg Jensen
25
Når en hest skal obduceres: Hvad gør man…. v/Henrik Elvang Jensen
27
2
Folingen og dens udfordringer
Hanne Gervi Pedersen, Dyrlæge, PhD, Dipl ECAR
Sektion for Veterinær Reproduktion og Obstetrik, Institut for Produktionsdyr og Heste, KU
SUND
E-mail: hgp@sund.ku.dk
Foling hos hoppen er i de fleste tilfælde ikke kompliceret, men i de få tilfælde af dystoki, er
der behov for en hurtig indsats. Dyrlægens vurdering og beslutninger lavet på
folingstidspunktet kan påvirke føllets helbred og overlevelse. Viden om den normale foling og
de problemer der kan opstå i forbindelse hermed er vigtig for at dyrlægen kan give den rette
hjælp i tide. Den gennemsnitlige drægtighedslængde er cirka 340 dage, med en variation på
320–360 dage, hvilket gør det svært at vide hvornår hoppen foler. Uddrivningsfasen foregår
hurtigt hos de fleste hopper og føllet er født indenfor 20–30 minutter efter ruptur af
chorioallantois. Dystoki ses i cirka 4% af folinger hos fuldblod og 10% hos koldblodsracer.
Holdningsfejl hos føllet er den hyppigste årsag til dystoki, hvor specielt hovedet i
sideholdning kan ekstremt svær at korrigere. Tidlig opdagelse af folingskomplikationer og
tidlig og korrekt fødselshjælp er nødvendig for at redde føllets og hoppens liv, og for at
bevare hoppens evne til at blive drægtig på et senere tidspunkt. Undersøgelse af den folende
hoppe kan lettes ved at give epiduralanalgesi og clenbuterol for at afslappe uterus.
Fødselshjælp kan bestå af udretning og fremtrækning, kejsersnit eller føtotomi hvis føllet er
dødt. Komplikationer hos hoppen efter foling inkluderer tilbageholdt efterbyrd, udrivninger
og blødninger i kønsvejen, intussusception af et uterus horn og uterus prolaps.
3
The foal in the first days
ANDY E DURHAM BSc.BVSc.CertEP.DEIM.DipECEIM.MRCVS, RCVS and European
Specialist in Equine Internal Medicine
The Liphook Equine Hospital, Forest Mere, Liphook, Hants GU30 7JG
E-mail: andy.durham@theleh.co.uk
In the first week of life, foals are at increased risk of illness and death. In clinical practice, it is
most helpful to develop a personal protocol of immediate stabilisation therapy, then full
assessment of the foal, and finally more specific therapy depending on the foal’s problem list.
Common neonatal illnesses that lead to illness and collapse in the first week of life comprise:

Septicaemia

Perinatal asphyxia syndrome (PAS)

Meconium impaction

Aspiration pneumonia

Diarrhoea/enterocolitis

Ruptured bladder

Neonatal isoerythrolysis
Once the decision has been made to pursue treatment in a collapsed foal, a cursory
examination is performed as therapy is initiated. The initial examination should includeassessment of demeanour, palpation of extremities, appearance of mucous membranes, and
strength of peripheral pulses. A full clinical examination can then be performed once the foal
has been stabilised/resuscitated.
Fluid therapy
In the first instance, the collapsed neonate will need a rapid infusion of warmed isotonic
fluids to boost circulating volume. Give a 20ml/kg bolus (1 litre for a 50 kg foal) of balanced
isotonic fluids over about 20-30 minutes and re-assess. Most hypovolaemic foals require at
least two 1L boluses and up to 3 or 4 can be given. The benefits of administration of plasma
are enormous whether or not the foal is hypogammaglobulinaemic. One to two litres of
plasma (instead of balanced isotonic fluids) can be given intravenously.
One can tell if enough fluid has been given from clinical signs such as: heart rate returning to
normal limits, urination, an improvement in mentation, warmer legs and ears and stronger
peripheral pulse pressure.
4
Important figures to keep in mind are:
% body weight per day
Volume per 50 kg foal per day
Voluntary milk intake
20-25% bwt /day
10-12 L per day
Maintenance (minimum) fluid
requirements (4-5mls/kg/hr)
10% bwt / day
5 L per day
Feeding tube rate (given hourly)
2-10mls /kg/hr
5 L per day
Mild dehydration deficit
5% bwt deficit
2.5 L per 50 kg foal
Severe dehydration deficit
10% bwt / deficit
5 L per 50kg foal
Nutritional support
Sick foals are prone to hypoglycaemia and glucose or dextrose should be administered to
reach and maintain normoglycaemia if needed. If glucose-saline is not available then this can
be made by adding 25-50 ml of 50% glucose to a 1 litre bag of saline or Hartmann’s
(makes 1.25-2.5% glucose solution).
In mild to moderately sick cases enteral fluids can be supplied entirely as mare's milk (ideal),
milk substitute or oral rehydration mixtures. Oral fluids can be given by stomach tube
which can be sutured in situ if continued use is envisaged. Always tube-feed in sternal
recumbency.
Aim for maintenance requirements (4-5 ml/kg/hr) as milk or milk replacer via the tube in
hourly aliquots (eg. 250 ml/hour for a 50kg foal). However, colic, ileus and bloat are
significant problems. Supply of minimal enteral nutrition is extremely beneficial to enterocyte
function and integrity and even if foals will only tolerate small amounts of milk it is still very
important that it is given. Therefore, begin with as little as 1-2ml/kg hourly (50-100ml/50kg)
and slowly increase if tolerated, whilst supplementing additional fluid requirement
intravenously. Metoclopramide may help prevent GI problems at a dose of 0.25 mg/kg tidqid sc (1 x 10mg ampoule/50 kg).
Anti-inflammatory therapy in foals
The most common reasons for using anti-inflammatories in foals are to control pain, to
reduce cerebral oedema and to control pyrexia.
The main two drawbacks of NSAIDs are gastric glandular mucosal ulceration and the
masking of the pain associated with synovial sepsis. COX2 selective (meloxicam) or specific
(firocoxib) NSAIDs are preferred.
5
Treatment of seizures
Seizures not only cause increased demands for oxygen delivery, glucose utilisation and
perfusion, all of which may be limited in the neonate, but they are also associated with
increased neurological damage. Therefore, it is vital to control ongoing seizures and the firstline of treatment is: 0.11-0.44 mg/kg diazepam or midazolam IV - bolus repeated at 5-20 minute
intervals.
Treatment of meconium impaction
This is a very common cause of colic in foals on day 1 and 2. Pain can often appear severe
but usually responds to mild analgesics. A low volume proprietary enema e.g. ‘Fleet’
phosphate-based enema can be used. In the majority of cases this is all that is required. In
more refractory cases a high volume gravity enema is almost always effective and this could
be supplemented by nasogastric dosing with 60-120ml liquid paraffin. When using a high
volume enema it is vital to bear in mind the weakness and fragility of a foal’s rectum and no
more than gravity pressure should be used to instil the enema. Enema fluid choices include
5% acetyl cysteine or more readily available warm soapy water possibly with a little obstetric
lubricant added works very well. Put 200-400ml of enema solution in a bottle and run it in
to the rectum via a soft rubber flutter valve or Foley catheter following gentle insertion of
the end of the tube a few inches beyond the pelvic brim and hold it there for a few minutes
if possible. A few repeat instillations are often required perhaps every 5 or 10 minutes
before all of the meconium is evacuated. Surgical treatment of these cases is possible but
very rarely required.
Treatment/prevention of gastric ulceration
Sick foals are at a high risk of gastric ulceration. However, the decision to use omeprazole
should be made on an individual case basis that are (i) at an increased risk because they are
receiving NSAIDs and/or (ii) might be showing clinical signs of ulceration (bruxism, dullness)
rather than widespread prophylactic use in all foals.
Ruptured bladder
These cases usually present on the 2nd or 3rd day of life with a depressed foal who is
frequently straining (convex back), with a high respiratory/heart rate and abdominal
distension. Urine may or may not be passed. Ultrasound is very useful for diagnosis and
shows a collapsed bladder and a lot of free abdominal fluid. Serum creatinine will be high but
peritoneal creatinine will be even higher. Low Na+ and Cl- with high K+ are also typical and
must be improved before surgery. Intravenous isotonic fluids should be given alongside
abdominal drainage and surgery can be performed when Na+ is > 120 mmol/L and K+ is <5.5
mmol/L.
6
Inflamm-aging og Recurrent Airway Obstruction (RAO)
Sanni Hansen, DVM, Ph.d.
Faculty of Health and Medical Sciences, Dep. of Large Animal Sciences, Medicine and
Surgery, University of Copenhagen
E-mail: sannih@sund.ku.dk
Recurrent Airway Obstruction
Recurrent Airway Obstruction (RAO) er den hyppigste nedre luftvejslidelse hos heste. I
relation til at sammenligne hestens sundhed er England det land tættest på, der laver
undersøgelser over hestes generelle sundhed (National Equine Health Survey [NEHS]). Den
nyeste rapport fra NEHS placerer RAO som den fjerde hyppigste lidelse med en
sygdomsfrekvens på 6,7 % i år 2015 mod 6,9 % i år 2014, 4,2 % i år 2013 og 3,6 % i år 20102012 (http://www.beva.org.uk/news-and-events/news/view/767).
Lidelsen RAO har i Danmark og resten af verden haft mange forskellige navne både blandt
lægfolk og blandt dyrlæger. Astma, bronkitis, engbrystighed og chronic obstruktive
pulmonary disease (COPD) er alle betegnelser, som i flæng er blevet brugt om netop denne
lidelse.
RAO er en lidelse, der rammer de nedre luftveje hos voksne og især ældre heste. Der har
gennem mange år været forsket intensivt på området, men endnu er det ikke lykkedes
forskerne at finde den præcise ætiologi og patogenese for lidelsen. Der er bred enighed om,
at kliniske symptomer fremprovokeres af støv og især svampesporer i muggent hø. Hesten
udviser kronisk hoste, næseflåd, nedsat præstation og besværet vejrtrækning i hvile og under
arbejde. Immunologisk ses et influx af neutrofile granulocytter i bronkier og alveoler,
bronkokonstriktion og en forøget mucus produktion (Robinson, 2001).
Inflamm-aging
Inflamm-aging og immunosenescence er to begreber, der bliver sat mere og mere fokus på
både indenfor human medicin og indenfor hesteforskning. Immunosenescence er defineret
som en dysregulation eller nedsat regulation af immunforsvaret med alderen.
Immunosenescence resulterer i nedsat immunrespons mod infektion og nedsat immunsvar
ved vaccination. Det er primært det adaptive immunsvar, der påvirkes af immunosenescence
(Effros et al., 2003; Horohov et al., 2010).
7
Inflamm-aging er defineret som en forøgelse i kronisk inflammation med stigende alder.
Inflamm-aging påvirker primært det innate (medfødte) immunsvar, hvor makrofagerne
forbliver kronisk aktive og producerer pro-inflammatoriske cytokiner (signalstoffer, IL-1, IL-6
og TNF-alpha), der påvirker kroppen (Adams et al., 2009; Franceschi et al., 2000; Horohov
et al., 2010).
Disse pro-inflammatoriske cytokiner påvirker bl.a. hypothalamus-hypofyse-binyreaksen
(HPA), der som respons forøger produktion af cortisol, et homon med anti-inflamm-aging
virkning. Cortisol dæmper virkningen af de pro-inflammatoriske cytokiner i et forsøg på at
opretholde kroppens balance. En bivirkning, som følge af den stigende cortisol med alderen,
er, at receptorfølsomheden af cortisol falder (Giunta, 2008).
Tilpasningsteori
Lungerne er et helt unikt organ, hvor balancen mellem inflammatorisk respons rettet mod
inhalerede allergener og kroppens behov for udveksling af ilt og kuldioxid skal opretholdes.
Ny human forskning viser, at lungerne har deres egen regulering af især de alveolære
makrofager, der størstedelen af tiden holdes i et hvilende stadie for dermed at undertrykke
inflammationen (Lambrecht, 2006). Dette genfindes hos heste, hvor der ses et fald i proinflammatoriske cytokiner i BAL væsken sammenlignet med cytokiner i blodet (Hansen et al.,
2014; Hansen et al., 2013).
I Danmark og den nordlige del af Europa er heste oftest opstaldet ”traditionelt” i bokse
store dele af året, og de har dagligt få timers adgang til fold. Denne opstaldningsform giver
stor belastning på lungernes immunsvar pga. store mængder af inhalerede allergener.
En teori er, at lungerne adapterer/tilpasser sig opstaldningsmiljøet og de inhalerede
allergener ved at nedregulere udskillelsen af cytokiner i den systemiske cirkulation. Med
alderen nedbrydes/nedreguleres denne adaptation hos udvalgte individer og kan være årsag
til udvikling af RAO. Denne nedregulering svækkes muligvis yderligere med alderen, dels ved
en stigning i cortisol og deraf nedsat følsomhed af receptorerne og dels ukendte arvelige
mekanismer (Ewart and Robinson, 2007).
8
Referencer
Adams, A.A., Katepalli, M.P., Kohler, K., Reedy, S.E., Stilz, J.P., Vick, M.M., Fitzgerald, B.P.,
Lawrence, L.M., Horohov, D.W., 2009. Effect of body condition, body weight and adiposity
on inflammatory cytokine responses in old horses. Veterinary immunology and
immunopathology 127, 286-294.
Effros, R.B., Cai, Z., Linton, P.J., 2003. CD8 T cells and aging. Critical reviews in immunology
23, 45-64.
Ewart, S.L., Robinson, N.E., 2007. Genes and respiratory disease: a first step on a long
journey. Equine veterinary journal 39, 270-274.
Franceschi, C., Bonafe, M., Valensin, S., Olivieri, F., De Luca, M., Ottaviani, E., De Benedictis,
G., 2000. Inflamm-aging. An evolutionary perspective on immunosenescence. Annals of the
New York Academy of Sciences 908, 244-254.
Giunta, S., 2008. Exploring the complex relations between inflammation and aging (inflammaging): anti-inflamm-aging remodelling of inflamm- aging, from robustness to frailty.
Inflammation research : official journal of the European Histamine Research Society ... [et al.]
57, 558-563.
Hansen, S., Baptiste, K.E., Fjeldborg, J., Betancourt, A., Horohov, D.W., 2014. A comparison
of pro-inflammatory cytokine mRNA expression in equine bronchoalveolar lavage (BAL) and
peripheral blood. Veterinary immunology and immunopathology 158, 238-243.
Hansen, S., Sun, L., Baptiste, K.E., Fjeldborg, J., Horohov, D.W., 2013. Age-related changes in
intracellular expression of IFN-gamma and TNF-alpha in equine lymphocytes measured in
bronchoalveolar lavage and peripheral blood. Developmental and comparative immunology
39, 228-233.
Horohov, D.W., Adams, A.A., Chambers, T.M., 2010. Immunosenescence of the equine
immune system. Journal of comparative pathology 142 Suppl 1, S78-84.
Lambrecht, B.N., 2006. Alveolar macrophage in the driver's seat. Immunity 24, 366-368.
Robinson, N.E., 2001. International Workshop on Equine Chronic Airway Disease. Michigan
State University 16-18 June 2000. Equine veterinary journal 33, 5-19.
9
Therapeutics for respiratory diseases
ANDY E DURHAM BSc.BVSc.CertEP.DEIM.DipECEIM.MRCVS, RCVS and European
Specialist in Equine Internal Medicine
The Liphook Equine Hospital, Forest Mere, Liphook, Hants GU30 7JG
E-mail: andy.durham@theleh.co.uk
The most common respiratory diseases affecting the performance horse comprise (in
approximate decreasing order or prevalence) inflammatory airway disease (IAD), infectious
airway disease, recurrent airway obstruction (RAO), exercise induced pulmonary
haemorrhage (EIPH) and pleuropneumonia.
1. Antimicrobial drugs
Airway diseases in young horses might be caused by primary bacterial pathogens such as
alpha or beta haemolytic Streptococci (eg Strep equi zooepidemicus, Strep pneumoniae),
Actinobacillus, Pasteurella or possibly Bordetella. Procaine penicillin (20,000–50,000 IU/kg bid
im) or ceftiofur (1-2 mg/kg bid im) are reasonable choices. Oral sulphonamides (30 mg/kg po
bid) and enrofloxacin (5 mg/kg sid iv or 7.5 mg/kg sid po) may not have an ideal spectrum of
activity for these bacteria. Oral doxycycline (10 mg/kg po bid) is another possible option
although there are questions over its bioavailability in some horses.
In cases of pleuropneumonia the bacterial agents tend to include gram negative, gram
positive, aerobes and anaerobes. Broad spectrum cover is then required such as procaine
penicillin plus gentamicin (6.6 mg/kg sid iv) and metronidazole (15 mg/kg loading dose then
7.5 mg/kg qid po). Enrofloxacin could be used instead of gentamicin but would need to be
combined with penicillin/metronidazole. Ceftiofur or cefquinome are also reasonable choices
depending on bacteriology results. If budget is an issue then oxytetracycline (5.0-7.5 mg/kg
bid) may well be effective.
2. Adrenergic agonists
Beta-2 agonists are good bronchodilators and include short-acting agents such as salbutamol,
fenoterol and terbutaline and longer acting agents such as salmeterol and clenbuterol.
Further potential beneficial effects of beta-2 agonists include stimulation of mucociliary
10
clearance, reduction of mucus viscosity, stimulation of surfactant secretion, modulation of
cholinergic transmission and anti-inflammatory properties including inhibition of mast cell
degranulation.
Systemic beta-2-agonists
Clenbuterol is the main drug in its class used in the horse. Long term (> 1 month) use of
beta-2 agonists may result in receptor down-regulation leading to reduced efficacy. Adverse
effects such as tremoring, sweating, nervousness and colic are occasionally seen but generally
pass uneventfully.
The licensed recommended dose of clenbuterol is 0.8 microg/kg q 12h but often a gradual
increase to doses as high as 3.2 microg/kg are helpful.
Inhaled beta-2 agonists
Salbutamol (=albuterol) at 1-2 microg/kg is very short-acting whereas salmeterol 0.2-0.5
microg/kg q 8-12 h has a longer duration of action. The intravenous preparation of
clenbuterol can also be administered by nebulisation at a dose of 0.4 mg/kg bid although this
represents off label use.
3. Glucocorticoids
Glucocorticoids inhibit neutrophil migration into the airways, reduce histamine release from
mast cells, inhibit prostaglandin and leucotriene synthesis (inhibiting bronchoconstriction)
and upregulate and increase the sensitivity of beta-2 adrenoceptors (facilitating
bronchodilation).
Systemic glucocorticoids
Prednisolone and dexamethasone appear equipotent in clinical studies. Administration of
prednisolone at a dose of 1-2 mg/kg prednisolone or 0.05-0.1 mg/kg to control inflamed
airways (IAD/RAO). Interstitial lung disease such as equine multinodular pulmonary fibrosis
may also indicate dexamethasone to initiate therapy glucocorticoids although clinical efficacy
is more variable.
Inhaled glucocorticoids
Several corticosteroids have been administered to horses by inhalation with the intention of
maintaining efficacy whilst reducing the risks of systemic side effects. Beclomethasone
11
dipropionate, is the most widely used. It is has been initially administered at between 5-10
microg/kg bid (representing between 2 and 20 x 250 microg actuations q 12 h for a 500 kg
horse) followed by the minimal effective dose (eg. 2-3 microg/kg sid or 4 to 6 x 250 microg
actuations q 24h per 500 kg). Fluticasone propionate (eg. ‘Flixotide 250 inhaler’) is an
additional more potent inhaled glucocorticoid administered to horses at a dose of 2-4
microg/kg bid (between 4 and 8 x 250 microg actuations q 12h to initiate therapy in a 500 kg
horse). Inhaled fluticasone may result in reduced systemic absorption compared with
beclomethasone.
4. Anticholinergic agents
Parasympathetic hyperactivity is the prime cause of bronchoconstriction in horses. Potent
and rapid bronchodilation can be achieved with antimuscarinic products. Atropine, unlike
other anticholinergic drugs, may also inhibit mucociliary clearance.
Systemic anticholinergics
Atropine is a rapid acting and potent anticholinergic bronchodilator which can be
administered intravenously to horses at 0.01-0.02 mg/kg (5-10 mg per 500kg). Long term
clinical use is to be avoided however due to the risk of colic. An alternative potent acute
bronchodilator is hyoscine or butylscopolamine (“Buscopan”) at a dose of 0.3 mg/kg.
Inhaled anticholinergics
Ipratropium is a highly charged anticholinergic drug which is not absorbed systemically
following inhalation and is therefore not associated with side effects. Ipratropium has been
used at a dose of 0.4-0.8 microg/kg q 6 h by MDI (5-10 x 40 microg actuations of ‘Atrovent
Forte’). The drug has maximal effect by 15 minutes but is fairly short acting and should be
given every 4-6 hours.
5. Other drugs
Frusemide
In addition to potentially beneficial effects in cases of pulmonary oedema and exercise
induced pulmonary haemorrhage, frusemide has been shown to have a significant
bronchodilatory effect in horses with obstructive pulmonary disease. This effect is
prostaglandin mediated and may therefore be abolished if NSAIDs are used concurrently.
12
Frusemide may be administered intravenously, orally or by nebulisation at a dose of 1-2
mg/kg.
Cromoglycate
The main benefit of this drug arises from its effect of inhibition of mast cell degranulation. It
might be of particular usefulness in cases where mast cells are a prominent feature of BAL.
Products still exist carrying licenses for use in humans (Cromogen; Baker Norton, London)
and can be given by nebulisation at a total dose of 0.16 mg/kg sid or by MDI at a starting
dose of 0.04-0.06 mg/kg q 12h (4-6 x 5mg actuations bid per 500kg) and reducing to a
maintenance level. A newer related drug, nedocromil sodium, is also licensed for use in
humans and has been used effectively in horses.
13
General limitations of application and interpretation of Clinical
Pathology
Andy Durham, BSc, BVSc, CertEP, DEIM, Dip.ECEIM, MRCVS, RCVS & European Specialist
in Equine Internal Medicine
The Liphook Equine Hospital, Forest Mere, Liphook, Hants GU30 7JG
E-mail: andy.durham@theleh.co.uk
Reference Intervals
Typically a reference interval is defined by 95% of the normal population, disregarding the
lowest 2.5% and the highest 2.5%. If data is normally distributed, then approximately 95% of
normal individuals will lie within the population mean ± 2 standard deviations and a
reference interval can easily be calculated from that simple formula.
Thus there is a 5% chance that results from a normal individual will lie outside the reference
interval (mean ± 2 SDs) but only a 0.3% chance that a normal individual will lie outside the
mean ± 3 SDs.
The impact of multiple tests should also be considered. If there is a 5% chance that a single
test will be abnormal in a normal individual, then there is a 51% chance that at least one of
14 tests will be abnormal in a normal horse when “panels” are run. However, these normal
individuals that return results outside the reference interval are likely to lie only just outside
the reference interval as the chances of them lying > 3SDs outside the reference interval is
very small indeed (<3 in 1000).
14
The normal population used for calculation of the reference interval must be representative
of the population that are to be tested. Thus if you work with Standardbred Trotters then
reference intervals derived from a retirement home for Icelandic ponies are unhelpful! Some
important differences include:

Hot and warm blooded breeds tend to have higher red cell counts, haemoglobin and
haematocrits than cold blooded breeds.

Geriatric and inactive animals also have lower red cell numbers, haemoglobin and
haematocrits than younger and fitter animals.

Foals and weanlings tend to have higher red cell numbers although cells tend to be
small (low MCV) and so haematocrit and haemoglobin may not be different from
adult horses.

Foals tend to have lower total protein and higher alkaline phosphatase values than
adult horses.
Test accuracy
The accuracy of a test can be described in several ways:

Sensitivity – the probability that a diseased individual will test positive for the disease

Specificity – the probability that a healthy individual will test negative for the disease.

Positive predictive value (PPV) – the probability that a positive test result truly
reflects disease.

Negative predictive value (NPV) – the probability that a negative test result truly
reflects absence of disease.
Sensitivity and specificity are fixed for a particular test. PPV and NPV (the most useful clinical
parameters) are heavily influenced by the likelihood of disease (i.e disease prevalence). A low
probability of disease (eg. random screening) results in a low PPV and high NPV such that
negative test results are generally accurate but positive test results less so. A high probability
of disease (eg. a thorough clinical examination which focuses only on those with a strong
clinical suspicion of disease) results in a high PPV and low NPV such that positive test results
are generally accurate but negative test results less so.
15
Clinical application of bacteriology results
In order to predict the efficacy of antibiotic therapy we need to know the sensitivity of the
pathogen to the intended antibiotic(s) at the concentrations likely to be achieved at the site
of infection. Laboratory testing is important but not without its problems. For example
infections are often mixed and overgrowth of a fastidious organism by a more vigorous coinfector can lead to misleading results. If a submitted swab produces a pure growth of E.coli,
can we be certain that there were no coinfectors? – perhaps a Staphylococcus failed to
survive the culture process or was overgrown?
Even if we did successfully culture the relevant pathogen(s), antibiotic sensitivity testing is
also inevitably a compromise. The usual method for sensitivity testing utilises paper discs
(Kirby-Bauer) impregnated with antibiotics which can be laid onto cultures to look for
inhibition of growth. Ideally, the antimicrobial concentration that diffuses from the disc into
the agar will be closely related to the antimicrobial concentration achieved in vivo at the site
of infection after systemic treatment with that antimicrobial. However, this concept is far
from validated for the vast majority of clinical scenarios and antimicrobial drugs in horses.
Apparent disc sensitivity to an antibiotic may only predict clinical success if at least
equivalent local concentrations are achieved in vivo. Conversely apparent in vitro resistance
may be overcome by achieving higher concentrations in vivo (eg local instillation of
antimicrobial). Where infections are amenable to topical antimicrobial treatment then results
of disc sensitivity testing are almost irrelevant as the local antimicrobial concentrations will
be far higher than the test-discs create locally in the culture medium. Further problems arise
as a result of other differences between the in vitro and in vivo circumstances. For example,
ceftiofur is rapidly metabolised to a metabolite desfuroylceftiofur. While both have
antibacterial efficacy, this may be different for a particular bacterial species. A similar
problem may exist for enrofloxacin and its metabolite ciprofloxacin.
16
Time-dependent artefacts in clinical pathology
Delay between collection of a blood sample and processing can result in ex vivo changes in
biochemical analyte activities and concentrations.
Aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatinine
kinase, total bile acids, ammonia, phosphate and potassium significantly increase
over 24-72hrs post-sampling.
Glucose, lactate, sodium and calcium are reduced in stored whole blood but for
glucose this is minimised by the use of potassium oxalate/sodium fluoride. Serum should be
promptly separated if electrolytes are going to be measured.
17
Metabolic and Endocrine Diseases in the older horse
ANDY E DURHAM BSc.BVSc.CertEP.DEIM.DipECEIM.MRCVS, RCVS and European
Specialist in Equine Internal Medicine
E-mail: andy.durham@theleh.co.uk
What is Pituitary Pars Intermedia Dysfunction?
The dysfunctional pars intermedia secretes excessive peptide products including alpha- and
beta-melanocyte stimulating hormone (
-,
-MSH), corticotropin-like intermediate lobe
peptide (CLIP) and beta-endorphin as well as intermediate peptides such as lipotropins and
adrenocorticotropin (ACTH) (Figure 1). However, despite the fact that ACTH
concentrations tend to be increased in PPID cases, PPID is not synonymous with
hyperadrenocorticism. This paradox is probably explained by the finding that the
immunoreactive measurable ACTH found in PPID cases appears to have impaired bioactivity
compared to that from normal horses.
Figure 1. Simplified cascade of peptide secretion from the pars intermedia
PPID cases are at increased risk of laminitis although the mechanism by which this comes
about is not yet understood. PPID cases tend to be hyperinsulinaemic and insulin resistant
and this is associated with their risk of laminitis. However, the exact origins of IR or
hyperinsulinaemia are not well understood. Few if any of the clinical signs of PPID are well
explained. Aside from laminitis additional clinical signs include excessive hair growth
(hypertrichosis) and/or delayed seasonal shedding, lethargy, mild to moderate muscle
18
wastage, increased sweating, polydipsia and polyuria and increased susceptibility to infections
(including parasites). There is undoubtedly a significant population of subclinical PPID cases,
presumably in the early stages of pathologic development, and also clinically subtle cases
showing, for example, only mild laminitis with no other signs suggestive of PPID.
PPID is clearly an age-related disease with >20% of horses >15 years old affected although it
is clear that younger horses may also be affected with several well described cases between
5 and 10 years of age.
What is Equine metabolic syndrome?
Equine Metabolic Syndrome might be regarded as “a collection of coexisting risk factors,
associated with metabolic and endocrine dysregulation, that signal an increased
susceptibility to laminitis”. Such individuals tend to be from certain breed types, are often
obese, and demonstrate dysregulation of insulin-glucose dynamics (“dysinsulinaemia”) as well
as disordered lipid metabolism.
Both human and equine subjects with metabolic syndrome are generally recognised to fail to
normally regulate the fine and dynamic balance between serum glucose and insulin
concentrations, a status referred to as dysinsulinaemia. Fundamentally this may be an
acquired state associated with obesity and/or may have genetic determinants in certain
breeds.
Pathophysiology of endocrinopathic laminitis
“Dysinsulinaemia” comprises up to 3 related but distinct components: insulin resistance,
hyperinsulinaemia and hyperglycaemia (or glucose intolerance) (figure 2). These are interrelated as described in figure 2 but they are not synonymous and each can exist with or
without the others. Current evidence emphasises the primary pathogenic relevance of
hyperinsulinaemia in laminitis. That is not to say that hyperglycaemia or IR are irrelevant, but
that any effect that they might have is probably by indirectly promoting hyperinsulinaemia.
19
Insulin Resistance
 impaired tissue
glucose uptake
Hyperglycaemia
 receptor
down-regulation
 lipogenesis
 pancreatic insulin
secretion
(glucose intolerance)
 compensatory
pancreatic secretion
 decreased insulin
clearance
Hyperinsulinaemia
Figure 2. Flow diagram illustrating the interrelated components of dysinsulinaemia.
Endocrine testing
PPID and EMS are not mutually exclusive and may coexist. Further supportive clinical signs
may or may not be present – for example obesity in EMS cases and hypertrichosis in PPID
cases. Laboratory tests are usefully considered in 4 categories as below.
1. Tests for hyperinsulinaemia
Sustained hyperinsulinaemia will trigger laminitis. Therefore testing for a predisposition
towards hyperinsulinaemia is logical and features in both EMS and PPID.
a) Fasting hyperinsulinaemia - should be < 20 mU/L in normal horses. Higher results
support EMS and/or PPID although unfortunately most such cases have normal fasting
insulin.
b) Resting hyperinsulinaemia - normal horses with hay rarely > 40 mU/L. However most
laminitis-prone individuals (PPID and/or EMS) return normal results.
c) Oral Sugar testing - the preferred method to test for a predisposition to
hyperinsulinaemia. Returns abnormal results in the majority of laminitis-prone individuals
(EMS and/or PPID). An excessive response means that dietary sugar intake must be
restricted/eliminated. There are 3 main choices:
20
1. Dextrose 1 g/kg BWT

fast overnight

mix dextrose in chopped hay

measure glucose and insulin 2 hours after eating the test-feed

glucose > 7 mmol/L (and preferably >8 mmol/L) indicates a valid test

insulin > 85 mU/L at 2 hours indicates an excessive insulin response
2. Dextrose 0.5 g/kg BWT

test as above using lower dose

insulin > 60 mU/L at 2 hours indicates an excessive insulin response
3. Karo Light Corn Syrup 0.15 mL/kg BWT

administer by dosing syringe

measure insulin 60-90 minutes after dosing

insulin > 60 mU/L indicates an excessive insulin response

insulin > 45 mU/L is suspicious
2. Tests for insulin resistance
Insulin resistance can be a caused by obesity (EMS), lack of fitness (EMS) and/or PPID and
promotes hyperinsulinaemia (figure 2). Response to exogenous insulin must be measured
and the simplest way to achieve this is to measure glucose before and after an insulin bolus.

measure baseline glucose

inject 0.1 U/kg soluble (neutral) insulin iv

measure glucose at 30 minutes after the insulin

monitor for hypoglycaemia (eg. muscle tremors, sweating) for a further 30
minutes (and treat with iv dextrose as required), or give a preventative iv
bolus of 30mL 50% dextrose per 100 kg BWT after the 30 minute sample

normal horses have a ≥50% decrease in plasma glucose in response to this
test so smaller decreases are indicative of insulin resistance
21
3. Further, more specific tests for PPID
Although horses with PPID are likely to return abnormal results to the tests above, this is
also the case for EMS cases and therefore further testing is needed to establish whether or
not PPID is present (remember horses may be suffering from EMS and/or PPID!).
a. Basal plasma ACTH - highly specific for PPID (i.e. normal horses rarely test positive)
although some PPID cases may test negative. Cut-offs must be adjusted for higher values in
the late summer/autumn. Sensitivity of basal ACTH for detecting PPID appears to be at its
maximum during this seasonal increase. The sample should be chilled as soon as possible
after collection and definitely by 3 hours. Ideally the plasma is separated by centrifugation
although whole blood or gravity-separated plasma is acceptable as long as the samples
remain chilled (and do not freeze).
b. TRH stimulation test – highly sensitivity test for PPID but cannot be interpreted during
the seasonal increase period (July to November). TRH injection often provokes mild reactions
in the horse including a cough, yawn, flehmen or mild tremors but nothing serious has been
reported.

Collect baseline ACTH

Inject 1 mg TRH iv

Collect further ACTH sample at exactly 10 minutes
4. Further, more specific tests for EMS
Currently there are no commercially available tests for EMS other than those for
dysinsulinaemia (1.) or insulin resistance (2.) above. Work is ongoing into use of various
“adipokines” which are adipose-derived endocrine factors that can interfere with insulin
sensitivity, and adiponectin seems the most promising. Typical EMS cases may show low
serum adiponectin concentrations.
22
En værdig afslutning på livet?
Peter Sandøe og Pia Haubro Andersen
Professorer ved henholdsvis Københavns Universitet og Sveriges Lantbruksuniversitet
E-mail: pes@sund.ku.dk og pia.haubro.andersen@slu.se
Alle heste skal dø på et tidspunkt; og i vores del af verden vil dette tidspunkt næsten altid
blive afgjort af hestens ejer og oftest i dialog med en dyrlæge. Nogle gange er det i princippet
ikke til diskussion, at hesten skal herfra. Det gælder hvis hesten akut er ramt af en
lidelsesvoldende sygdom og skade, som ud fra en fra en veterinærfaglig vurdering ikke kan
behandles på en måde, så den bliver kureret eller i det mindste kan leve videre med en
tilfredsstillende livskvalitet. Her forlanger den danske dyreværnslov, at dyret skal aflives.
Dog er der plads til fortolkninger, og disse fortolkninger er i vidt omfang lagt i hænderne på
dyrlægen. Nogle gange vil dyrlægen blive udsat for pres for at handle i strid med sin bedste
faglige vurdering. I den en ene ende af spektret kan dyrlægen blive mødt af krav fra ejer om
at få en hest aflivet af dyreværnsmæssige grunde, selv om hesten godt kan leve videre med en
tålelig livskvalitet, men hvor ejer ønsker aflivning af hensyn til at kunne få udbetalt en
forsikringspræmie. I den anden ende af spektret bliver dyrlæger mødt med et krav om
behandling til en hest, som ud fra et kvalificeret fagligt skøn burde aflives af
dyreværnsmæssige grunde; men hvor ejer ikke kan give slip.
Andre gange er situationen mere kompliceret. Her har ejeren et valg, med hensyn til om
hesten skal aflives (eller slagtes) eller leve videre. Ofte vil dyrlægen fungere som rådgiver for
ejeren, der som grundlag for sin beslutning kan have brug for at få svar på en lang række
spørgsmål, herunder: Hvis hesten er syg, hvad er så behandlingsmulighederne? Hvor gode
chancer er der for, at hesten kommer sig? Hvordan har hesten det, og hvad er dens
muligheder for at opnå en god livskvalitet? Hvad kommer det til at koste? Hvad betyder det
for fremtidig brug af hesten? Hvilke muligheder er der i forhold til forsikringen?
Der vil også være situationer, hvor hesten ikke er syg, men hvor ejer ikke længere magter at
passe hesten. Her vil nogle ejere vælge at få hesten aflivet frem for at forsøge at sælge den.
Dette hænger sammen med, at ejeren ønsker at tage ansvar for dyret lige til det sidste – på
23
tilsvarende måde som ejere af hunde og katte ofte vælger at få deres dyr aflivet frem for at
forsøge at finde et nyt hjem til dem, når de ikke længere er i stand til at passe dem.
Der vil være stor forskel mellem, hvordan ejere ser på muligheden for aflivning (eller
slagtning) af deres hest. Dette hænger bl.a. sammen med hestens dobbelte status som brugsog familiedyr. For nogle ejere er hesten primært en brugsgenstand, mens den for andre
primært er et elsket familiemedlem. Situationen bliver ikke mindre kompliceret af, at
dobbeltheden ofte slår ud som ambivalens: Den samme ejer, der opfatter hesten som et
elsket familiemedlem, vil typisk også gøre sig økonomiske og praktiske overvejelser.
At fungere som rådgiver i forbindelse med afslutningen på hestens liv er således ikke altid
nogen nem rolle for dyrlægen. Dels vil dyrlægen skulle forholde sig til ejere med meget
forskellige og ofte ambivalente ønsker og holdninger. Dels har dyrlægen via sin profession og
i kraft af lovgivningen en rolle at spille i forhold til at sikre hestens velfærd.
Set fra hestens synsvinkel må det afgørende være, at den ikke skal lide unødigt, inden den
bliver aflivet, og at selve aflivningen foregår på en god og rolig måde. Desuden kan man også
argumentere for, at det set fra hestens synsvinkel kan være en skam at komme herfra, hvis
alternativet er, at den ellers kunne have fortsat med at leve et godt liv. Heste gør sig
formodentlig ikke tanker om fremtiden, men derfor kan de stadig have en mulig fremtid, som
man ved aflivning eller slagtning kan tage fra dem.
Om hestens afslutning på livet kan kaldes værdig afhænger af kvaliteten af processen set med
de berørte menneskers øjne. Om hesten ender med at få en værdig afslutning på livet vil
derfor i høj grad afhænge af samspil og kommunikation mellem ejer og dyrlæge. En værdig
afslutning på hestens liv er en, hvor dyrlæge og ejer har et godt samarbejde, hvor
kommunikationen lykkes, og hvor både ejer og dyrlæge efterfølgende har det godt med
beslutningen og måden, den blev truffet på. Desværre kan det ske, at både samarbejde og
kommunikation mislykkes til skade for ejer, hest og dyrlæge.
I præsentationen vil vi diskutere, hvad der kendetegner en god afslutning på livet set fra
hestens synsvinkel og dyrlægens rolle i den forbindelse. Endvidere vil vi diskutere, hvad
dyrlæger kan gøre for at sikre et vellykket samarbejde med og kommunikation til hestens
ejer op til en beslutning om, hvor vidt en hest skal aflives. I forhold til det sidste vil vi
fokusere på forskellige metoder og tilgange, som dyrlæger kan lære at gøre brug af.
24
Fodring igennem livet
Rasmus Bovbjerg Jensen, Cand.agro, PhD
Institut for Klinisk Veterinær og Husdyrvidenskab, Det Sundhedsvidenskabelige Fakultet
Københavns Universitet
E-mail: ralle@sund.ku.dk
Hestens fordøjelsessystem er fra naturens side designet til at udnytte fibre, og det er
velkendt at grovfoder bør udgøre den væsentligste del af hestens foderration. Der findes en
lang række af kraftfoder- og tilskudsprodukter på det danske marked. Disse produkter kan
anvendes som supplement til grovfoderet for at opnå en balanceret ration, således at
behovet for eksempel energi, protein, vitaminer og mineraler dækkes. Fodring gennem livet
er et meget bredt emne, og behov og normer for forskellige næringsstoffer kan findes i
forskellige bøger (for eksempel Geor et al 2013). Dette indlæg vil i stedet for belyse noget af
den nyeste forskning inden for ernæring af heste i relation til fodringsmanagement under
danske forhold.
Fodring igennem livet strækker sig fra før hesten er født, hvor fostret er påvirket af
metabolisk-programmering til den gamle hests ændrede behov, som blandt andet er et
resultat af den fodring, den har været udsat for gennem årene. Kulhydrater udgør langt
største delen af foderrationen for alle heste, ung som gammel. Der er dog stor forskel på
hvilken type af kulhydrater forskellige heste fodres med, og kulhydraterne kan groft inddeles
i stivelse+sukker samt fibre. Stivelse er dog ikke bare stivelse, og fibre er ikke bare fibre,
hvilket ofte bliver glemt i forbindelse med sammensætningen af foderrationen. Balancen
mellem fibre og stivelse er blandt andet vigtig i relation til tarmsundhed og præstation
(glykogen), og det er et hyppigt diskussionsemne blandt forskere.
En balanceret foderration sikrer optimal præstation ved at mindske risikoen for sygdomme
og holde hesten rask, samt gøre den i stand til at opnå sit fulde potential (for eksempel
laktation, vækst eller konkurrence). Helt grundlæggende er det nødvendigt at vide, hvad man
fodre med, for at kunne fodre optimalt. Kraftfoderproducenterne oplyser energi og
næringsstofindhold på sækken, mens det for grovfoderets vedkommende er nødvendigt med
25
en grovfoderanalyse (laboratorier er angivet nedenfor). Optimal fodring igennem livet er
med til at sikre sunde og raske heste.
Anbefalede litteratur:
Geor RJ, PA Harris and M Coenen (2013): Equine Applied and Clinical Nutrition - Health,
Welfare and Performance. Saunders Elsvier, Edinburgh, UK.
Grovfoderanalyser:
Eurofins Steins Laboratorium A/S: www.eurofins.dk
BLGG AgroXpertus: www.blgg.agroxpertus.dk
26
Når en hest skal obduceres: Hvad gør man? Hvad kan
man selv? Hvad kan patologer?
Henrik Elvang Jensen, Professor, dr.med.vet., Det Sundhedsvidenskabelige Fakultet,
Københavns Universitet
E-mail: elvang@sund.ku.dk
Præsentation ved SvHs Årsmøde 2015.
27
12-10-2015
Når en hest skal obduceres:
-hvad gør man?
-hvad kan man selv?
-hvad kan patologer?
Henrik Elvang Jensen
Professor, dr.med.vet.
Det Sundhedsvidenskabelige Fakultet
Københavns Universitet
Sektionsteknik
• Sektionsværktøj
• Eksvisceration
• Præparation af de enkelte organer og væv
• Eksempler på læsioner
1
12-10-2015
2
12-10-2015
3
12-10-2015
4
12-10-2015
5
12-10-2015
6
12-10-2015
Knogler og led
Neoplasmer
Respirationsvejene
GI-kanalen
7
12-10-2015
8
12-10-2015
Hest: kronis, erosiv artrose i haseled
Klassiske artroser hos hest
Hest:
Ringfod (kron- +/- kodeled)
Intraartikulær
Periartikulær
Spat (flade glideled i haseled)
Osteoartrosis chronica erosiva
sicca ankylopoetica tarsi
9
12-10-2015
10
12-10-2015
Granulosacelletumor
Knogler og led
Neoplasmer
Respirationsvejene
GI-kanalen
• Hyppigste ovarieneoplasme hos hest
• Unilaterale, glat overflade, runde, > 20-30 cm
• Massive, cystiske eller polycystiske (rød-brunt
indhold)
• Består af granulosa og thecaceller (ofte med
hormonproduktion)
• Meget sjældent maligne
• Differentialdiagnoser: andre primære
ovarieneoplasmer (sjældne)
11
12-10-2015
12
12-10-2015
13
12-10-2015
Maligne melanomer hos hvide, grå og
skimlede heste
Huden i reg. perinei og under halen
Lnn. reg. axillaris
Musakulaturen under skulderbladsbrusken
Reg. parotidea
Alle andre organer
Hos alle dyrearter => knudeformede nydannelser
14
12-10-2015
15
12-10-2015
Halicephalobus gingivalis
Knogler og led
Neoplasmer
Respirationsvejene
GI-kanalen
16
12-10-2015
Hest, 20 år, akut purulent sinusitis (og
rhinitis)
LUFTVEJE, generelt,
betændelses typer
97
Hest, ethmoidalt hæmatom
LUFTVEJE, næsehule og sinus
99
Hest, pony (shetland), 6 år, kronisk
purulent sinusitis og empyem
LUFTVEJE, generelt,
betændelses typer
98
Hest, 20 år,næse-polyp med nekrose
ved apex
LUFTVEJE, næsehule og sinus
100
17
12-10-2015
Hest, emfysem
LUFTVEJE, lunger, emfysem
Hest, alveolært emfysem
LUFTVEJE, lunger, emfysem
105
Lunger (pneumoni hos hest )
• Føl og unge heste
– Fokal pneumoni
104
Hest, alveolært emfysem
bronchiolitis, COPD
LUFTVEJE, lunger, emfysem
106
Føl, kronisk lobulær (og multifokal)
pyogranulomatøs bronchopneumoni, R. equi
• Akut følsyge
– Broncho- eller bronchointerstitiel pneumoni
• Equin influenza
• Equin herpesvirus infektion
– EHV-4 (rhinopneumoni)
– EHV-1 (abort, føtale infektioner, encephalomyelitis (”herpeslammelse”),
(rhinopneumoni))
• Adenovirus og andre virus
• Rhodococcus equi (multifokal eller kranioventral)
– Interstitiel pneumoni
• Pneumocystis carinii
• Voksne heste
– Interstitiel pneumoni
• Pneumonia lardea
LUFTVEJE, lunger, pneumoni,
hest
107
LUFTVEJE, lunger, pneumoni,
hest
108
18
12-10-2015
Føl, 3 uger, kronisk pyogranulomatøs
bronchopneumoni, R. equi
LUFTVEJE, lunger, pneumoni,
hest
109
Hest, pneumonia lardea
LUFTVEJE, lunger, pneumoni,
hest
111
Føl, kronisk, bronchopn. og lymphadenitis,
R. equi
LUFTVEJE, lunger, pneumoni,
hest
110
Hest, samme som foregående,
pneumonia lardea
LUFTVEJE, lunger, pneumoni,
hest
112
Knogler og led
Neoplasmer
Respirationsvejene
GI-kanalen
19
12-10-2015
20
12-10-2015
21
12-10-2015
TAK FOR OPMÆRKSOMHEDEN
22