Bob Childs - ESA/AHA/PHCP Certified Hoof Specialist
News
"The only way to accurately diagnose iron overload is with the correct blood work. Serum iron alone is not accurate. It reflects iron in the diet but not how much is stored. Transferrin is the protein that carries iron in the blood. When transferrin and iron are both measured, the percent transferrin saturation can be calculated by dividing serum iron by transferrin and multiplying by 100. That % is useful in interpreting the third test that is needed, ferritin. Ferritin is a measure of the body’s total iron content. High ferritin can mean iron overload but chronic disease involving inflammation or infection may also elevate ferritin.
With true iron overload, transferrin saturation is high normal or elevated. There is currently only one laboratory in the world that can measure equine ferritin, the comparative hematology laboratory at Kansas State Veterinary Diagnostic Laboratory. "
Read full article here: https://balancedequine.com.au/iron-overload/
How can we protect our horses in the winter months?
Read full article here: https://www.thelaminitissite.org/articles/cold-weather
"Many horses seem to struggle with laminitis during the winter months. Cold weather can cause winter laminitis in horses. Most people associate spring and the flush of grass with the onset of laminitis season however many owners report problems in winter, particularly with horses who have a history of metabolic issues resulting from insulin resistance or Cushing's (PPID)"...
Read full article: https://forageplustalk.co.uk/winter-laminitis
Artikel von Dr. Kellon
Auch Pferde, die sonst überhaupt keine Rehe-Historie mitbringen, können im Winter bei kalten Temperaturen Lahmheiten zeigen, die über das hinausgehen, was Pferde auf buckelig gefrorenem Boden sonst zeigen. Der Grund ist eine Laminitis - aber ohne warme Hufe.
Kälte-induzierte Hufschmerzen treffen Pferde mit Insulinresistenz. IR ist ein bekanntes Risiko für Rehe und auch, wenn das Pferd nicht offensichtlich lahm ist, begünstigt sie Schäden in der Lamina (Lederhaut). Wir haben noch nicht alle Mechanismen erforscht, die sich hinter einem Lederhaut-Schaden aufgrund von hohen Insulinwerten verbergen. Aber ein bekannter Faktor ist ein hoher Wert von Endothelin-1.
Endothelin-1 ist ein Peptid-Hormon, das von den Zellen, die die inneren Blutgefässe umhüllen produziert wird. Es ist der höchst potenteste bekannte gefässverengende Stoff und wird normalerweise durch die Produktion von gefässerweiterndem Stickoxid in Balance gehalten. Eine Verringerung der Blutversorgung durch Kälte während gleichzeitig oder vorangegangen eine hohe Endetholin-1-Aktivität stattfand kann bei IR-Pferden Schmerzen hervorrufen, die gesunde Pferde nicht haben.
Kälte-Stress kann also den Insulinwert steigen lassen. Insulinresistenz ist Teil der metabolischen Anpassung an kaltes Wetter bei verschiedenen Spezies. Forscher haben auch entdeckt, dass Insulinwerte bei Pferden ansteigen bei kälterem Wetter.
Eine Rehe, die durch einen hohen Insulinwert ausgelöst wird ist anders eine Rehe, die andere Gründe hat. Enzymaktivität und entzündliche Prozesse sind hier nicht Teil der Erkrankung. Das erklärt vermutlich warum die üblichen Behandlungsmethoden wie Entzündungshemmer usw. hier nicht oder kaum wirken. Aber es gibt Hilfe.
Das Pferd einzudecken, wenn die Temperaturen unter 7 Grad gehen kann helfen, Kältestress zu vermeiden. Die unteren Beinpartien einzuwickeln und evtl. auch die Hufe mit Schuhen zu schützen kann ebenfalls helfen, die normale Zirkulation aufrecht zu erhalten.
Desweiteren können Kräuter helfen, die einen gesunden Widerstand gegen den Stressor bieten. Jiaogulan (Gynostemma pentaphyllum) ist eine besonders gute Wahl weil dieses Kraut auch bekannt ist für die Unterstützung der Produktion von gefässerweiterndem Stickoxid. Es sollte zweimal täglich, vorzugsweise vor den Mahlzeiten gegeben werden. Die meisten Pferde lieben es und fressen es problemlos als Pulver oder Paste.
L-Arginin ist eine wegbereitende Aminosäure für Stickoxid und kann parallel gegeben werden. L-Citrullin ist eine weitere Aminosäure, die der Körper in L-Arginin umwandelt zur Produktion von Stickoxid. Kältestress ist wird ebenfalls ausgelöst durch oxidativen Stress und Antioxidantien helfen, diese freien Radikalen zu neutralisieren.
Zusätzlich kann Acetyl-L-Carnitin ebenfalls helfen, die Nervenfunktionen und den Glukosestoffwechsel zu unterstützen.
Wenn man versteht, was die Winter-Rehe auslöst, kann man mit simplen Maßnahmen den Kältestress minimieren und den normalen Blutfluss in den Hufen aufrecht erhalten.
Original English text: https://drkhorsesense.wordpress.com/2017/12/17/cold-induced-laminitis
Q: Should I seasonally alter the dose of Prascend in my PPID positive patients?
A: There is clear evidence that pituitary activity increases in the autumn. Some horses test normal throughout the year but positive (for PPID) in the autumn, other horses test routinely positive throughout the year with strong positives in the autumn.
Pergolide decreases pituitary activity, therefore it is logical to consider altering the dose of pergolide during the autumn seasonal rise.
Be aware that if a horse (with PPID) has its ACTH tested in August/September and a loss of endocrine control is identified and the dose of pergolide subsequently increased, by the time ACTH is checked again 30 to 60 days later, the seasonal rise is likely to have peaked and be almost over.
However, if it is established that a horse does lose endocrine control in the autumn, then the dose of pergolide could be increased the following July/August in preparation for the seasonal rise.
It is a logical approach to increase pergolide for the seasonal rise; it needs further research, but many people have adopted this approach already.
Liphook Equine Hospital have produced the graph above based on thousands of ACTH tests to show the seasonal rise and fall of ACTH.
Comments by Gene Ovnicek
"Abscesses that occur at the coronary band and through the sole of the
foot are expected in serious cases and offer the patient a better chance
of recovering to a higher level of soundness with a much greater future
of returning to pre-disease condition. This can only happen when proper
support is given immediately to these patients in the area of the foot
that is naturally redeveloping for that purpose.
I have records of the last 30 cases that have abscessed through the
coronary band and/or through the sole within a short time after the
initial insult of laminitis (1 to 2 months). Our purpose was to record
results of those cases whose abscesses were treated, versus those who
were untreated. Over half of the abscesses were not soaked or encouraged
to dry up. The abscesses at the coronary band were left uncovered. The
sole abscesses were wrapped and protected from dirt and debris only. No
trimming of the sole in the area of the abscess was done to encourage
drainage. The wraps consisted of two layers of prepared Styrofoam blocks
applied with Elasticon tape. The other cases were soaked with Epsom
Salts or Betadine for 2 or 3 days. Some of those cases were cleaned of
debris on the sole where the abscess came through.
There were little to no set backs in healing with those who were untreated. Most cases that were treated by soaking progressed slower and some had reoccurring painful periods. All of the cases that had sole material removed around the abscess site stabilized much later and had even more setbacks. All but 2 cases survived with over 70% returning to their pre-disease purpose. The abscesses associated with laminitis are the 'mechanisms of debridement' and follow a cycle that seems to work well if left to follow its own course of events."
Article by: Nancy S. Loving, DVM March 18 2009, Article # 13802
At the 2008 AAEP Convention, which was held Dec. 6-10 in San Diego,
Calif., Bill Moyer, DVM, professor of sports medicine and head of the
Department of Large Animal Clinical Sciences at the Texas A&M
College of Veterinary Medicine and Biomedical Sciences, presented a
variety of considerations on the state of medical treatment for
laminitis. He stressed that once clinical signs are evident, damage has
already been done: Pain and lameness are preceded by vascular and
structural damage within the hoof laminae (lamellae).
So, he posed the question to the audience, "Is any specific medical
treatment for acute laminitis efficacious in altering the outcome after a
horse has developed clinical signs?"
Is any specific medical treatment for acute laminitis efficacious in
altering the outcome after a horse has developed clinical signs?
The current consensus on effective therapy revolves around addressing
and resolving the initiating cause(s) of laminitis. Other strategies
attempt to alter blood flow in the foot, decrease inflammation, and
avert endotoxemia. Moyer addressed these in his talk.
He explained that evidence is lacking about blood flow-altering agents
having any effect on increasing laminar circulation. While use of
digital nerve blocks might improve blood flow by inhibiting constriction
of blood vessels, numbing the pain stops the horse from protecting his
feet. Increased weight bearing exacerbates laminitis.
Acepromazine increases digital blood flow by direct action on vascular
smooth muscle, but studies have not shown improvement in lamellar blood
flow.
Isoxsuprene has vasodilating properties, while pentoxyfylline requires
weeks of administration to decrease blood viscosity. It does this by
acting on platelets to increase red blood cell flexibility. Both these
medications are absorbed poorly when administered orally.
Nitroglycerin placed over digital blood vessels might increase blood
flow, but it has not been shown to increase lamellar blood flow after
the onset of clinical signs. Coupling this ineffectiveness with
potential risks to the person handling the drug makes nitroglycerin a
poor therapeutic choice.
Heparin removes red blood cells from the system to decrease blood
viscosity and thereby improve blood flow, but researchers have not
examined its use in acute cases.
Inflammation is not always a component of laminitis, but when it is,
non-steroidal anti-inflammatory drugs (NSAIDs) have been used. Moyer
said there is humane justification for judicious use of NSAIDs, but one
should be aware of downsides. Pain relief might increase mobility that
exacerbates tearing of the lamellae.
Phenylbutazone (Bute) might reduce inflammation and pain, and it is
affordable, but it does not prevent laminitis if given during the
developmental stage and has not been shown to alter the course of acute
cases.
Flunixin meglumine (Banamine) provides both anti-inflammatory and
anti-endotoxin effects. However, if flunixin and phenylbutazone are
given together, there is an increased risk of loss of serum protein,
gastric ulcer disease, and/or colitis.
There is anecdotal support for use of dimethyl sulfoxide (DMSO) for its
anti-inflammatory properties and ability to scavenge oxygen-derived free
radicals, which form during hypoxia (deprivation of an adequate supply
of oxygen) and reperfusion (restoration of blood flow to tissues
following an incident or hypoxia). Damage can occur when blood flow is
restored to tissues following an incident of reduced blood and oxygen
supply. However, Moyer noted there is no evidence of hypoxia or
reperfusion in this disease.
Anti-endotoxin drugs (flunixin meglumine, ketoprofen, and polymyxin B)
might be warranted as there is an association between endotoxemia and
the development of laminitis. Endotoxin causes insulin resistance with
decreased use of glucose by the lamellar tissue. While they might not
necessarily be effective in treatment of laminitis, anti-endotoxic drugs
might be life-saving.
Moyer said caretakers and veterinarians should address environment and
ground surface, housing, causes of obesity, and management of the foot
itself. He recommends explaining to clients that the pathogenic
mechanisms of laminitis are not well-understood and that a horse's
clinical appearance might correlate with the outcome, but it is not
always an accurate predictor due to potential for complications.
In general, controlled studies do not exist regarding the efficacy of various treatments for laminitis, and some therapies have additional risks beyond their failure to improve the situation.
Endotoxemia and the roll of ET-1 in acute Laminitis
"Although administration of a low-dose of endotoxin to horses causes a
significant decrease in laminar perfusion and digital blood flow, there
have been no repeatable models of endotoxemia that consistently induces
acute laminitis. However, diseases that are often complicated by
laminitis are accompanied by endotoxemia (intestinal strangulating
obstruction, anterior enteritis, enterocolitis, pleuropneumonia, and
metritis). In a study in our laboratory, we demonstrated a significant
decrease in digital arterial blood flow from 30 min to 2 h after
administration of a low dose (35 ng/kg over 30 min) of endotoxin to
conscious horses. There was a concomitant decrease in digital arterial
blood pressure from 30 min to 1.5 h after endotoxin infusion. These
digital hemodynamic effects were accompanied by a significant increase
in cephalic venous plasma ET-1 concentrations. These findings suggest
that perhaps endotoxin does play a role in initiation of the early
hemodynamic alterations in laminitis, and that this may be at least
partly mediated through increased synthesis and release of ET-1."
Authors: Susan C. Eades, DVM, PhD; Ashley M. S. Holm, DVM; and Rustin M. Moore, DVM, PhD
Kathryn Watts
says: "As with humans, diet and exercise are the only way that insulin
resistance, which causes high levels of circulating insulin, can be
managed."
Read the article: Laminitis: New Study on Sugar and Starch as a Cause