Fragmented Coronoid Process or FCP in Dogs
By Cheryl Yuill, DVM, MSc, CVH
The elbow joint is made up of 3 separate bones, the radius, the ulna, and the humerus. Developmental abnormalities may occur in the elbow joint, mostly in medium and large breed dogs. There are three common developmental problems that are often referred to as 'elbow dysplasia', namely a fragmented coronoid process (FCP), and ununited anconeal process (UAP), and osteochondritis dissecans (OCD).
Dogs with elbow dysplasia typically have only one of the three conditions, and it is rare for a single dog to have all three components of elbow dysplasia. This handout will cover the developmental abnormality known as Fragmented Coronoid Process. There are separate handouts in this series of Client Education handouts that cover each of the other conditions.
What is a fragmented coronoid process?
FCP is a developmental defect of one of the coronoid processes, two small bony protrusions on the end of the ulna within the elbow joint. In this condition, one of the coronoid processes develops a fissure or crack and separates from the rest of the bone. It most commonly occurs on the inner, or medial, process. This separation causes pain and joint instability.
Is this condition hereditary?
A genetic component is likely involved, and males appear to be more commonly affected. The problem is usually seen in large breed dogs such as Bernese Mountain Dogs, Golden Retrievers, Labrador Retrievers, Rottweilers, and German shepherds. Some researchers believe that this condition is another manifestation of OCD. FCP has also been associated with excessive calcium levels in the diet and/or with excessively high calorie diets.
What are the symptoms of FCP?
With this condition, lameness usually develops in the foreleg of young dogs that are between 5 and 11 months of age. The dog will have a mild to moderate weight-bearing lameness. Dogs with this disease are lame on the affected leg or legs and they may cry when the elbow is palpated (felt and manipulated). In many cases, the affected joint will be swollen and warm to the touch. The elbow joint will have a decreased range of motion, or decreased mobility, on an orthopedic examination. It is relatively common for the condition to develop in both elbows, although it is usually worse on one side than the other.
How is FCP diagnosed?
Because of the possibility of permanent lameness, your veterinarian will recommend diagnostic testing, in the form of radiographs (x-rays) if any lameness lasts more than 2 weeks in a young, large breed dog. Several radiographs of each affected leg, with the leg in different positions, are necessary in order to get an accurate assessment of various bones and joints. In many cases, this will require a short-acting anesthetic or sedative in order to achieve the optimal positioning for diagnostic purposes. In dogs under 6-7 months of age, x-rays can be challenging to interpret due to the presence of "growth plates." To reach the diagnosis, it may be necessary to have the x-rays examined by a veterinary radiologist.
In some cases, the FCP may not be seen on standard radiographs. Rather, secondary signs associated with degenerative joint disease are seen. With FCP, a diagnosis may be made relatively early in the course of the condition using computerized tomography (a "CT scan").
What is the recommended treatment for FCP?
Surgery is the treatment of choice for this condition, and its aim is to remove any abnormal cartilage or bone and attempt to return the joint to a more normal anatomy and function. The procedure may involve a surgical exploration of the joint or an arthroscopic repair. Arthroscopic repair may be the preferable technique because the smaller incision means that there is less damage done to the supporting structures (the joint capsule and ligaments). Your veterinarian may recommend referral to an orthopedic surgeon for this procedure.
What is the prognosis with and without surgery?
If the joint is not treated surgically, degenerative changes will rapidly develop and the dog will suffer from chronic pain. Surgical treatment of FCP should be performed as soon as possible after diagnosis to minimize the development of degenerative joint disease.
In all cases, some degree of arthritis will develop in the elbow joint, but with surgical treatment, the arthritis will usually be less severe and there will be less pain involved. Medical treatment such as joint protective supplements and/or anti-inflammatory medications will usually be recommended to delay progression of degenerative joint disease.
Will my dog need rehabilitation?
Rehabilitation is an important part of the post-operative care of the dog with FCP and is an important part of the medical management of this condition. In the immediate post-operative period, strict rest is required and anti-inflammatory and pain medication will be prescribed. You will be taught how to perform gentle massage and a type of exercise called "passive range of motion" (PROM) exercise. With this type of exercise, you will move the elbow joint gently through its normal range of motion while your dog is lying on its side, with no weight on the affected joint.
Depending on the specific case, a controlled low-impact exercise program will usually begin about 3 weeks after surgery. Until that time, the dog will require strict exercise restriction, and will only be allowed to go on short leash walks. Your veterinarian will provide you with specific instructions for the optimal rehabilitation program for your dog.
In all cases, it is important to maintain your dog's weight at an ideal level. Since this problem is caused by a developmental defect in the elbow joint, the joint will develop degenerative disease over time. The aim of treatment and rehabilitation is to minimize the degree of arthritis that develops, and to maintain a good quality of life for your dog.
My veterinarian has recommended surgically sterilizing my dog. Why is this?
Since the condition may be hereditary, affected dogs should not be used for breeding. If your dog is a purebred, you should notify your breeder. Many breeders of large breed dogs have their breeding stock cleared for this condition (called elbow certification) prior to using them in a breeding program.
Cruciate Ligament Rupture in Cats
The word cruciate means "to cross over" or "form a cross." The cruciate ligaments are two bands of fibrous tissue located in each knee joint. They connect the femur and tibia (the bones above and below the knee joint). One ligament runs from the inside to the outside the knee joint and the other from the outside to the inside, crossing over each other in the middle.
Hip Dislocation and Post-Op Care in Cats
The hip is a simple "ball and socket" joint that has a wide range of movement in all directions and its efficient function is essential to normal hind limb movement. The joint itself is comprised of the acetabulum which is a cup shaped depression in the pelvis (this forms the "socket") and the femoral head which is part of the femur (thighbone).
Joint Subluxations in Cats
A joint luxation is a dislocation or complete separation between the bone ends that normally articulate to form a joint. Subluxation is the term referring to a partial separation of the joint. The most commonly subluxated joint in cats is the hip, although any joint can be affected.
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QB Brett Hundley - Green Bay Packers
Week 21: bye week
Recent Stats and Projections
Recent Game Summaries
2017 Week 17 vs DET (14 / 24 / 172 / 1 / 2 pass, 3 / 15 / 0 rush)
If there was any lingering doubt about Hundley's general inability to succeed in an NFL offense, this game pretty much put that concern to rest. His continued poor decisions and overall inability to find his receivers put the Packers offense behind the eight-ball too often, and left the defense -- which had its own issues -- in difficult positions. At least the Packers thought they had a competent backup, but Hundley didn't prove he could even do that, much less succeed over an extended absence by the starter.
2017 Week 16 vs MIN (17 / 40 / 130 / 0 / 2 pass, 5 / 48 / 0 rush)
Even though there is a one more game left, this should put a button on Hundley's season and any lingering thoughts Packers fans have as to his fitness as a starting quarterback. Yes, the Vikings defense is fierce, but that aside we saw the same inability to complete passes downfield, the same hesitancy in the pocket and the same poor decisions we've seen all season long.
2017 Week 14 vs CLE (35 / 46 / 265 / 3 / 0 pass, 7 / 31 / 0 rush)
Hundley played two very different games on Sunday, the first half representing the ho-hum, get it done Hundley we tend to see when he's at his most efficient, while the second half made him look really good against an imploding Cleveland Browns defense. Key to Hundley's game was being able to avoid turnovers, as Hundley didn't throw an interception or fumble the ball. His first touchdown, a 30-yard floater to a wide-open Jamaal Williams, came on the Packers first drive. The Browns failed to stay with Williams, who got behind the coverage and was open near the goal line. The Packers didn't find the end zone again until the fourth quarter, and Hundley didn't throw a touchdown again until near the end of that period. That throw--a 1-yard pass to Davante Adams--was a very nice throw, as Hundley saw the coverage was inside, and threw to Hundley's backside shoulder. The touchdown sent the game into overtime, where Hundley again found Adams, this time on what was supposed to be a very conservative screen pass. Randall Cobb and Jordy Nelson did a very nice job blocking, and Adams broke free for a 25-yard touchdown to win the game.
2017 Week 13 vs TB (13 / 22 / 84 / 0 / 1 pass, 7 / 66 / 0 rush)
Hundley came crashing back down to earth after a tremendous Week 12, showing some mobility while gaining yards with his feet, but missing on multiple throws to his receivers throughout the game. Possibly the most egregious came in the first quarter, when he missed a wide open Geronimo Allison on a corner route. While his receiver was absolutely wide open and could have waltzed into the end zone, Hundley airmailed the throw, overshooting Allison by a good bit. So it went on Sunday, and Allison wasn't the only guy Hundley missed on, though it was probably the worst, including the pick he threw early in the second quarter on a pass over the middle to Jordy Nelson. Unlike last week, Hundley seemed much less decisive and some of the yards he gained on the ground, while helpful, also came because he pulled the ball down and took off even though another moment or two might have seen a receiver free. The offense also seemed really conservative compared to last week, even though the defense the Packers faced--in front of a home crowd, no less--was nowhere near as good.
2017 Week 12 vs PIT (17 / 26 / 245 / 3 / 0 pass, 1 / 6 / 0 rush)
Head coach Mike McCarthy finally got an "I told you so" game from Brett Hundley, who was on fire for much of the game against the Pittsburgh Steelers Sunday night. Among the key high notes were his three touchdowns (more than he had for his entire career), a complete lack of turnovers coming off a week where he gave up four, and some excellent throws outside the numbers and downfield. While he was sacked once in the first quarter, fumbling the ball as well, the incident was wiped out by a penalty on Pittsburgh. Aside from that, the offensive line did a good job of keeping him clean and Hundley was adept at getting the ball out when he was pressured. The second half seemed to see him regress a little, as he was sacked four times in the latter two quarters and while some of that was solid defense from the Steelers, some of that was on Hundley as well. While all three of Hundley's touchdown passes were nice, all were helped by either great running after the catch or a defensive breakdown. Randall Cobb's 39-yard score in the first quarter found the receiver wide open as the coverage split off from him and nobody picked Cobb up. Hundley did a nice job recognizing it and not hesitating to hit the wide open receiver for a score. Both the short screen to Jamaal Williams and the deep throw to Davante Adams became touchdowns only because of exceptional efforts by the players and in Williams' case, the blockers ahead of him. Overall Hundley did a solid job, and stepped up when the Steelers were ahead late in the game. Head coach Mike McCarthy was super conservative on the Packers' last drive, though Hundley took a bad sack to start things off, but didn't kill enough of the clock. That, and the defense being out of sorts on the Steelers' final drive, cost the Packers the game and neither of those things were really on Hundley, who might have begun to turn a corner.
2017 Week 11 vs BAL (21 / 36 / 239 / 0 / 3 pass, 3 / 19 / 0 rush)
Hundley had a disastrous opening to the game with interceptions on his first two possessions. He would go on to fumble the ball later and throw another interception. Hundley was a mess, and while some of that was because he was often pressured, plenty of that was Hundley just not being good. He misses receivers, sometimes not even seeing them, makes poor choices and is clearly not ready for prime time even after three years in coach Mike McCarthy's system. While the Packers are sticking with him, and he has played better, it's clear he is not going to get the job done by any means.
2017 Week 10 vs CHI (18 / 25 / 212 / 1 / 0 pass, 2 / 16 / 0 rush)
Hundley's previous three starts were concerning, but this was almost like watching a different quarterback. While far from perfect, Hundley made better reads and decisions, avoided big mistakes and delivered some nice passes, most notably to Davante Adams, both for long gains. While the 42-yard strike was longer, the 19-yard touchdown was a better pass in a more critical moment. The Packers were on the Bears' 19-yard line, on a 2nd and 9, when Hundley rolled out to his right under pressure. He spied Adams at the right-front corner of the end zone and threw a nice pass to Adam's outside shoulder, where only his receiver could get it. While not as sharp a pass as Aaron Rodgers would throw, it was similar in positioning and accuracy and a hopeful step towards seeing more of this in an offense used to it on a regular basis. Hundley did pull a hamstring while running during the game, but played through it and is slated to start against Baltimore next week.
2017 Week 9 vs DET (26 / 38 / 245 / 0 / 0 pass, 4 / 22 / 1 rush)
After a bye week, the expectation was that Hundley would look much more confident and competent under center, but that wasn't the case. While he didn't have any massive turnovers, he also didn't find the end zone and he held onto the ball way too long. Worse, he didn't see multiple receivers who were wide open. He's not really seeing the field at all at this point, and that's after a layoff. It took Hundley 38 pass attempts to get 26 completions and total 245 yards - that's an average of 9.4 yards a completion. Mike McCarthy doesn't seem willing to give his quarterback anything challenging, keeping the offense stripped down. And Hundley isn't even doing that well.
2017 Week 7 vs NO (12 / 25 / 87 / 0 / 1 pass, 3 / 44 / 1 rush)
If this is what three years in the Packers' vaunted 'Quarterback School' results in, someone might want to see about cancelling the school's accreditation. Hundley was a mess, with poor timing, no chemistry with his receivers and bad decision-making. And this was with what appeared to be a relatively basic gameplan. Hundley once made a nice play, on his 14-yard touchdown scramble in the middle of the second quarter, which gave the Packers a lead. The thing about that run is, for some reason at least one New Orleans defender seemed uninterested in tackling Hundley at the end of the run. Safety Ken Crawley merely hit Hundley--not even with great force--with his shoulder. Hundley never should have made it into the end zone and one assumes defensive coordinator Dennis Allen will have some words for him in the film room. Maybe Hundley will continue to improve--really he has nowhere to go but up--but if this is just the floor, it's a very, very low floor.
2017 Week 6 vs MIN (18 / 33 / 157 / 1 / 3 pass, 1 / 3 / 0 rush)
Coming in cold off the bench after Aaron Rodgers broke his collarbone in the first quarter, Brett Hundley had some good and some awful moments in his first real action since entering the league as a fifth round pick in 2015. At least one of his three interceptions came off a tipped ball by his receiver, and the last one came in the waning seconds of the game when the Packers were just trying to make something happen. Hundley threw a nice touchdown pass to Davante Adams, who was uncovered. On the play the Minnesota linebackers seemed to get confused on who should be covering Adams, who was tight on the offensive line and ran a slant. The first linebacker released him, but nobody picked him up after that. Hundley stepped up in the pocket to avoid pressure and threw a nice pass to Adams for the score.
2017 Week 4 vs CHI (1 / 1 / 0 / 0 / 0 pass, 0 / 0 / 0 rush)
Hundley came in for the victory lap during the last six minutes of play. He threw one pass and handed the ball off several times before the game ended.
Green Bay Packers Team Links
Footballguys Articles
Austin Lee - October 17
Austin Lee - October 31
Austin Lee - November 7
Austin Lee - November 14
Monday Injury Rounds: Week 11
Jene Bramel - November 13
Injury Expectations | Wednesday Update | Week 11
Ortopedi ( minus muskelskador och senskador. )
ИГРАТЬ
- Passiva stödjevävnader: skelett, brosk, ligament, senor
- Vanligare hos hanhund än tikar
- Stora hundraser (schäfer överrepresenterade)
Patofysiologi: endostal och periostal nybenbildning
Kraftig smärta i de långa rörbenens diafyser vid palpation
Problemen kommer ofta i skov under uppväxten
På RTG ses ökad täthet i delar av diafysens märgkanal (endostet) i de långa rörbenen.
- Störd metafysär blodtillförsel
- Fördröjd benbildning vid tillväxtzoner
- Mikrofrakturer, inflammation, nekros
- Nedsatt AT vanligt förekommade
- Svullnad, värme över tillväxtzoner på långa rörben, ffa distala radius
Röntgen visar nedsatt täthet och intrycket av dubbla tillväxtzoner i metafysen
Smärtlindring är extremt viktigt!
Diagnostiseras med röntgen
Behandling är Ulnaosteotomi, men detta kräver tidig diagnos ( innan radius tillväxtzoner är slutna
-Smärta från höftled, muskelatrofi
2. Biokemiska faktorer - cytokiner
3. Chondrocyter stimuleras frisätta proteaser
4. Dessa bryter bl a ned kollagen
5. Biomekaniska faktorer
6. Uppluckring matrix, broskbitar lossar.
7. Små bitar brosk fagocyteras av synoviocyter
(OA börjar vanligen med skada i ledbroskets yta)
-Otränad för sin uppgift
- Tillfällig, akut överbelastning
- repetetiv låggradig överbelastning
- Nutritionella aspekter (Kosttillskott, Omega-3-fettsyror,Glukosaminoglykaner?)
- Medicinering (NSAID,Pentosan polysulfat (Cartrophen), Opioider, Corticosteroider)
‐ Behandlingsprotokoll varierar med individen/ anpassas individuellt!
- Syftet är att lindra smärta och bromsa utvecklingen av OA ex vid korsbandsskada, OCD, HD, ED, intraarticulaära frakturer, inkongruens ledytor, kollateralligamentsskador.
- Vid grav OA, när konservativ behandling ej har hjälpt: caputresektion, byte av höftled, artrodes (steloperation), amputation
- Kroniska infektioner/reaktiv artrit
- Idiopatisk immunmedierad polyartrit
-FMCP/FPC frakturerad medial coronoideus process/frakturerad processus coronoideus
- Radius och ulna växer i olika hastighet --> ospecifik artrit
- Genetisk predisposition slapphet i ledkapseln
- Dålig kontakt mellan caput och acetabulum - nedsatt kongruens ‐ under skelettets tillväxt
- Onormal belastning - onormal utveckling av
- Instabilitet/subluxation‐ leder till artrosutveckling
Svårt att resa sig, gå uppför trappor, ovilja att
Efter hand sker en fibrotisering av ledkapseln som gör att ledslapphet ej längre kan palperas
- DPO (double pelvic osteotomy)
- TPO (triple pelvic osteotomy)
- Höftledsbyte - hunden ska ha vuxit färdigt
- Resektion av caput femoris - bäst resultat för hundar <20kg
- Motverkar medial rotation av tibia
- motverkar cranial translation av tibia
(säkrast på sövd hund)
caudalt om laterala fabellen
2. Andra handens pekfinger placeras på crista tibia och tummen placeras bakom fibulahuvudet
3. Cranial translation av tibia, prova med olika grader av flexion samt extension av knäleden
Efter kirurgi av korsband så kommer man ändå att ha ett positivt draglåde test. För att testa om operationen gett en stabil led så gör man Tibia compression test
En hund behandlad för korsbandsskada är en hund med OA
-Lateral patellaluxation förekommer, oftast hos
vinklingen av höftleden, som i sin tur påverkar
m quadriceps draglinje
- Kan orsakas av trauma
- I många fall beskrivs hundarna göra "hoppsasteg",
de hoppar över ett eller flera steg med det drabbade
1. Patella kan luxeras manuellt men reluxerar
2. Patella kan luxeras, reluxerar vid tryck med fingrar
eller rörelse av benet (manipulation)
3. Patella ligger luxerad, men kan reluxera vid
4. Patella ligger permanent luxerad, reluxerar ej.
- Grad 1 ofta konservativt
- Grad 2 rekommendera kirurgi om hunden har besvär. Risk för ytterligare deformation av femur och patellarleden.
- Grad 3‐4 kirurgi.
- Ger belastningsfördelning och dämpning av stötvågor mellan kotorna
- Eftersom en disk är deformerbar ger den en viss möjlighet till rörelse mellan kotor.
Boerboel
The greatest WordPress.com site in all the land!
Gesundheit
Der Boerboel wird als eine gesunde Rasse angesehen. Das hat damit zu tun, dass die Rasse Leistungsgezüchtet wurde und immernoch wird (also nicht nach Farbe oder Ausstellungsmeriten selektiert wird). Dadurch konnten nur starke und gesunde Individien ihre Gene weiterführen. Wie jedoch in allen Rassen, so gibt es mehr oder weniger rassetypische Krankheiten, über die man sich bewusst sein sollte. Auch haben nicht alle Züchter den arbeitenden Boerboel bei der Selektion ihrer Zuchttiere vor Augen. Als Welpenkäufer solltest du dich mit nicht weniger als gesunden und untersuchten Elterntieren zufrieden geben, um mit grösster Wahrscheinlichkeit einen gesunden Welpen zu bekommen, der dir lange viel Freude bereitet. Auf dieser Seite haben wir ein paar mehr oder weniger gewöhnliche Krankheiten zusammengestellt, die in dieser Rasse vorkommen.
Hüftdysplasie bedeutet, dass das Hüftgelenk falsch entwickelt ist, also die Gelenkschale zu flach ist. Dies hat Knorpelschäden und Knochenablagerungen (Artrose) zu Folge. Das Gelenk wird unstabiel und das kann zu Lahmheit und Schmerzen führen, oftmals werden die Symptome schlimmer im Alter. In schlimmen Fällen ist das Gelenk vollkommen deformiert und in sehr schlimmen Fällen ist das Einschläfern des Hundes der einzigen Ausweg, egal wie alt der Hund ist. Der Status des Hüftgelenkes wird durch Röntgen beim Tierarzt festgestellt. Die Röntgenbilder werden an den Züchterverein zur Auswertung geschickt.
Hüftdysplasie ist ein Defekt, der sowohl erbliche als auch umweltbedingte Ursachen hat. Das bedeutet, dass sowohl die Zucht aber auch wie der Welpe aufwächst die Entwicklung des Hüftgelenkes beeinflussen. Der Defekt wird polygen vererbt, d.h. dass viele Gene zusammen wirken um eine Eigenschaft in einem hohen oder niedrigen Grad zu vererben. Jedes Gen für sich beeinflusst eine Eigenschaft nur wenig, eine Kombination jedoch kann einen Defekt hervorrufen. Das bedeutet deswegen leider auch, dass es in seltenen Fällen dazu kommen kann, dass ein ganzer Wurf von einem Defekt betroffen ist, obwohl dieser in zurückliegenden Generationen nicht auftritt. Das Risiko für einen defekten Welpen erhöht sich jedoch deutlich, wenn einer oder beide Eltern Dysplasie haben. Es ist sehr wichtig, dass du deinen Hund mit ca 18 Monaten röntgst und deinen Züchter über das Resultat benachichtigst. Hunde, die defekte Welpen hinterlassen sollten aus dem Zuchtprogramm ausgeschlossen werden und ein Züchter muss deswegen den Hüftstatus für den ganzen Wurf wissen, um seine Zucht auswerten zu können. Ausser dem normalen HD-röntgen sollte man ausserdem einen sogenannten PennHip-röntgen machen, der schon gemacht werden kann wenn der Welpe erst 16 Wochen alt ist. Wir empfehlen jedoch den HD-röntgen und den PennHip-röntgen gleichzeitig zu machen. Beim PennHip-röntgen misst man, wie locker das Hüftgelenk ist. Somit kann ermittelt werden, wie hoch das Risiko ist, dass der Hund ist später im Leben Artrose entwickelt. Diese Röntgenbilder werden an ein Institut in den USA zur Auswertung geschickt. Nur vom Institut zertifizierte Tierärzte dürfen diese Röntgenuntersuchung machen. [Hier] findest du Tierärzte in deiner Nähe, die PennHip-röntgen ausführen.
Der Umweltfaktor, also der nicht erbliche Faktor der den Defekt verursacht, ist die Art und Weise wie der Welpe die ersten 1,5 Jahre aufwächst. Man muss so einiges beachten, um das Risiko für Hüftdysplasie zu minimieren. Der Welpe sollte ein Futter bekommen, das an Welpen und später an Junghunde angepasst ist. Für Boerboel sollte das Futter ausserdem für grosse Rassen zusammengesetzt sein. Wenn du eigenes Futter machst, solltest du dich genau darüber informieren was ein wachsender Hund an Vitaminen und Mineralien braucht – das unterscheidet sich nämlich vom Bedarf erwachsene Hunde haben. Auch das Eiweiss-Fettverhälltnis im Futter ist wichtig. Wir empfehlen extra Glukosamin und Vitamin C unter das Futter zu mischen. Man sollte jedoch nicht vergessen, dass es zur Zeit keine Forschung gibt, die die positive Beeinflussung dieser Nahrungsergänzungsmittel auf die Entwicklung der Hüftgelenke untersucht. Jedoch wurden positive Erfahrungen von Züchtern und Hundebesitzern berichtet. Während der Welpe aufwächst ist es extra wichtig, dass er schlank bleibt. Schon ein bischen Übergewicht erhöht das Risiko für Dysplasie. Auch die Art und Menge von Bewegung beeinflusst die Entwicklung des Gelenkes. Bis zu einem Alter von frühestens 18 Monaten sollte all Stärke- und Ausdauertraining vermieden werden. Das bedeutet, möchtest du mit deinem Hund Fahrrad fahren, mit ihm Weight Pull trainieren, Taschen tragen lassen, etc so ist es sehr wichtig diese Art von Training nicht zu früh anzufangen. Auch das Spiel mit ruppigen Hunden sowie Bällchen/Stöckchen holen (plötliches und kräftiges Einbremsen) sollten vermieden werden. Das Bedeutet jedoch absolut nicht, dass man den Welpen daran hindern sollte sich natürlich zu bewegen. Alle Alltagssituationen, die der Welpe später meistern soll, sollte er schon als Welpe üben, z.B. (einige) Treppen hoch und runtergehen, an der Leine und ohne Leine gehen, spielen, ins Auto hüpfen und wieder raus, etc. Es ist wichtig dass der Welpe seine Gelenke, Muskeln und Knochen während seiner gesamten Wachstumsphase für normale physische Aktiviteten in seinem eigenen Takt und ohne Zwang benutzen kann. Denk daran, dass der Boerboel eine schwere Rasse ist. Lange oder monotome Belastungen verschleissen Gelenke mehr als bei leichten Rassen. Verschleissschäden oder Dysplasie sind oftmals mit Schmerzen verbunden!
Kaufe nur einen Welpen nach freigeröntgten Eltern. Am Besten ist es wenn sowohl ein HD-röntgen als auch en PennHip-röntgen gemacht wurden. Die Hüftwerte für den PennHip sollten nicht 0,5 übersteigen, der HD-status sollte A oder B alt. 0 oder 1 sein. Verlange, die Untersuchungsresultate zu sehen. Kaufe keine Welpen von Züchtern, die sich weigern die Unterlagen zu zeigen. Sei sehr genau mit der Ernährung und Bewegung des Welpen.
Ellenbogendysplasie bedeutet, dass das Ellenbogengelenk falsch entwickelt ist. Dieser Defekt entwickelt sich immer zur Arthrose. Die Ursachen für diesen Defekt sind entweder Erblich und/oder beruhen auf Umwelteinflüsse, die im Abschnitt “Hüftdysplasie” beschrieben sind. Ellebogendysplasie kan auch von den Krankheiten fragmentierte processus coronoideus (FPC), osteochondrosis dissecans (OD) und/oder ununited processus anconeus (UPC) hervorgerufen werden. Der Status des Ellenbogengelenkes wird durch Röntgen beim Tierarzt festgestellt. Die Röntgenbilder werden an den Züchterverein zur Auswertung geschickt. röntgen gleichzeitig zu machen.
Kaufe nur einen Welpen nach freigeröntgten Eltern. ED-status soll 0 sein. Verlange, die Untersuchungsresultate zu sehen. Kaufe keine Welpen von Züchtern, die sich weigern die Unterlagen zu zeigen. Sei sehr genau mit der Ernährung und Bewegung des Welpen.
Entropion/Ectropion bedeutet, dass das untere Augenlied sich entweder nach innen rollt und am Augapfel schabt oder sich nach aussen rollt und einen höheren Tränenfluss verursacht. Dieser Defekt wird als erblich angesehen und betroffene Individien sollten aus dem Zuchtprogramm ausgeschlossen werden. benachritige deinen Züchter, falls dein Welpe mit Entropion/Ectropion diagnostiziert wurde.
Kaufe nur einen Welpen nach freigetesteten Eltern. Verlange, die Untersuchungsresultate zu sehen. Kaufe keine Welpen von Züchtern, die sich weigern die Unterlagen zu zeigen.
Vaginal Hyperplasi innebär att vävnaden i vaginan reagerar för starkt på östrogenet under tikens löp. Vaginan sväller upp och kan komma fram genom vulvan, vilket ser ut som en tunga. Av den anledningen brukar vaginal hyperplasi även betecknas som slidframfall hos vissa uppfödare. Vaginal hyperplasia anses vara ärftligt och drabbade hundar bör plockas ur avel.
Köp enbart en valp efter en fritestad tik. Kräv att få se veterinärintyg på undersökningen.
Demodex bezeichnet die Haarbalgmilbe, die die Krankheit Demodikose verursacht. Etwas schlampig wird die Krankheit an sich manchmal als Demodex bezeichnet. Die Haarbalgmilbe lebt in den Haarbälgen aller Hunde und werden erst zu einemProblem wenn ein Hund ein geschwächtes Immunsysthem hat und so nicht die Milbe “in Schach halten” kann. In diesen Fällen vermehren sich die Milben ungehindert. Demodikose wird in zwei Formen unterteilt, die lokale Form und die generalisierte Form. Die erste Form kommt meist bei Junghunden vor, die jünger als ein Jahr alt sind und verschwindet normalerweise wieder. Sie macht sich durch kahle Stellen an den Vorderbeinen und dem Gesicht bemerkbar und meistens hat der betroffene Hund keinen Juckreiz. Die andere Form kann sowohl junge als auch ältere Hunde befallen und deckt dann normalerweise den Körper grossflächiger.
Die Sympthome sind wie schon genannt kahle Flecken im Pelz und Juckreiz, manchmal sehr schwerer solcher. Die Krankheit kann so schwer und qualvoll für den Hund werden, dass dieser eingeschläfert werden muss. Das war früher sehr gewöhnlich, heute können ungefähr 90% aler Hunde wieder Symptomfrei werden. Trotzdem ist Demodikose eine der am schwersten zu behandelnden Hautkrankheiten bei Hunden und die Sympthome sind oftmals sehr qualvoll für den betroffenen Hund. Demodikose kann weder Menschen noch gesunde Tiere anstecken. Ein Hund kann für gesund erklärt werden, wenn 2 negative Tests mit einem Intervall von 4 Wochen durchgeführt wurden.
Demodikose wird mittels einer Schabeprobe, die von einem Tierarzt entnommen wird, ermittelt. Die Krankheit ist erblich und wird rezessiv vererbt. Beide Elterntiere müssen also wenigstens Träger der Krankheit sein, damit ein oder mehrere Welpen in einem Wurf an der Krankheit erkranken. Hunde, die an Demodikose erkrankt sind oder kranke Würfe hinterassen haben sollten aus dem Zuchtprogramm ausgeschlossen werden. Dies gilt auch für die Geschister erkrankter Hunde.
Wenn du dir die Elterntiere eines Wurfes anguckst, solltest du eventuelle Sympthome beachten. Kaufe keinen Welpen, wenn du weisst oder vermutest, dass eines oder beide Elterntiere Demodikose haben.
Olika allergier kan förekomma inom rasen, men är dock mer sällsynt. Detta kan vara allt från foderallergier (oftast mot spannmål eller nötkött) till allergier mot olika kvalster eller pollen. Allergier visar sig genom många olika symptom som t ex klåda, kala ställen i pälsen, hudsvamp, magproblem såsom diarré och kräkningar, etc. Symptomen visar sig vanligtvis från ett års ålder, men kan dröja tills dess att hunden har uppnått en högre ålder.
SKK och veterinärer rekommenderar att utesluta individer från avel som själva har allergier, har syskon med allergier eller har lämnat valpar med allergier. Det anses att allergier är ärftliga, men även två friska föräldrar kan lämna allergiska valpar efter sig.
Allergier utreds via blodprov samt hudtester hos veterinären. Det är inte vanligt att man testar Boerboel för allergier inför avel utan tester utförs då misstankar om en allergi uppstått. Det är alltid mycket viktigt att du kontaktar din uppfödare om din valp har en diagnostiserad allergi. En seriös uppfödare tar då föräldrardjuren och eventuella avkommor ur avel samt underrättar de andra valpköparna.
När du tittar på föräldradjuren var uppmärksam på eventuella symptom. Avstå från ett valpköp efter föräldrar där du vet om eller misstänker allergi.
Ibland kan patellan, dvs knäskålen, vara fel utvecklad och den kan då förflyttas antingen inåt eller utåt. Patellan undersöks av veterinär och en sådan undersökning bör göras innan avel. Hundar med fel utvecklad patella bör uteslutas ur avelsprogrammet. Patellaluxation kan ha olika orsaker och ibland kan hunden vara symptomfri. I gravare fall kan hunden börja halta. Hur patellaluxation ärvs ner är inte fastställt än. Patellaluxation förekommer dock oftast bland små raser.
Osteochondros är en ärftlig men icke medfödd tillväxtrubbning som uppstår när valpen växer som fortast, dvs mellan 4 – 6 månaders ålder. Defekten förvärras genom felaktig utfodring eller motion (se även höftledsdysplasi). Underrätta alltid din uppfödare om du misstänker eller har fått diagnosen osteochondros på din valp!
Molossers i allmänhet anses ha lätt för att utveckla hjärtfel. Hjärtfel är sällsynta inom Boerboel, men en seriös uppfödare bör undersöka hjärtstatus på sina avelsdjur innan avel, då hjärtfel anses vara ärftliga. Inom Boerboeln hör förstorad hjärtmuskel till de vanligare hjärtfelen.
Ögonsjukdomar (bortsett från Entropion/Ectropion) förekommer mer sällan inom rasen. Trots det ögonlyser en seriös uppfödare sina avelsdjur enligt gällande rekommendationer, dvs en gång årligen. Mer om olika ögonsjukdomar finns att läsa [här].
Kroksvans kan förekomma, men brukar inte medföra problem för hunden, förutom estetiska. Hundar med kroksvans skall ändå uteslutas ur avelsprogrammet, då kroksvans kan sätta sig i ryggraden hos avkommorna och den drabbade individen måste då avlivas.
Cancer kan förekomma, är dock sällsynt och sjukdomen uppstår i så fall oftast i hög ålder.
Fantasy Football News & Views
Green Bay Packers QB Brett Hundley completed 14-of-24 passes for 172 yards, one touchdown and two interceptions in Week 17 against the Detroit Lions before giving way to QB Joe Callahan, who completed 5-of-7 for 11 yards. RB Jamaal Williams led the charge with 22 rushes for 82 yards, while Hundley chipped with 15 yards. WR Trevor Davis led the team in receiving with 56 yards on three grabs, while WR Randall Cobb had four receptions, 45 yards and a touchdown while also tossing a 10-yard pass to Hundley.
Packers | Brett Hundley to stick as starter Mon Dec 25, 10:40 PM
Green Bay Packers QB Brett Hundley will remain the team's starting quarterback heading into Week 17 against the Detroit Lions. 'I thought he competed at a very high level,' head coach Mike McCarthy said about Hundley's performance in Week 16. He said coaches assigned seven dropped passes after watching film.
Packers | Rough night for Brett Hundley Sun Dec 24, 12:11 AM
Green Bay Packers QB Brett Hundley completed 17 of his 40 pass attempts for 130 yards and two interceptions in a 16-0 loss to the Minnesota Vikings in Week 16. He also ran five times for 48 yards.
Packers | Brett Hundley tosses three TDs in win Sun Dec 10, 07:21 PM
Green Bay Packers QB Brett Hundley completed 35 of his 46 pass attempts for 265 yards, three touchdowns and no interceptions in the Week 14 game against the Cleveland Browns. He also ran 31 yards on seven attempts.
Packers | Brett Hundley runs for 66 yards Sun Dec 3, 07:09 PM
Green Bay Packers QB Brett Hundley passed for just 84 yards in Week 13 against the Tampa Bay Buccaneers, but he was able to total 66 rushing yards on seven attempts.
Packers | Brett Hundley will be fine Mon Nov 27, 07:19 PM
Green Bay Packers QB Brett Hundley will be fine despite taking a helmet-to-helmet hit during the team's Week 12 game, according to head coach Mike McCarthy.
Packers | Three scores for Brett Hundley Sun Nov 26, 11:55 PM
Green Bay Packers QB Brett Hundley completed 17 of his 26 pass attempts for 245 yards and three touchdowns in a 31-28 loss to the Pittsburgh Steelers in Week 12.
Packers | Brett Hundley remaining starter Mon Nov 20, 10:33 AM
Green Bay Packers QB Brett Hundley will remain the starter after turning it over four times in Week 11, according to head coach Mike McCarthy.
Packers | Brett Hundley struggles Sun Nov 19, 04:44 PM
Green Bay Packers QB Brett Hundley went 21-for-36 for 239 yards and three interceptions against the Baltimore Ravens in Week 11. He also lost a fumble during the game.
Packers | Brett Hundley goes full in practice Fri Nov 17, 04:32 PM
Green Bay Packers QB Brett Hundley (hamstring) practiced in full Friday, Nov. 17, and was removed from the injury report ahead of Week 11 against the Baltimore Ravens.
Packers | Green Bay injury report for Friday Fri Nov 17, 04:30 PM
Green Bay Packers OT Bryan Bulaga (knee), S Morgan Burnett (groin), RB Aaron Jones (knee) and RB Ty Montgomery (ribs) did not practice Friday, Nov. 17, and are out for Week 11 against the Baltimore Ravens. CB Kevin King (shoulder) and OG Lucas Patrick (back) were limited participants and are questionable, while LB Ahmad Brooks (back) and DT Quinton Dial (chest) were full participants and also are listed as questionable. QB Brett Hundley (hamstring) and LB Joe X. Thomas (ankle) practiced in full, and OG Justin McCray (ankle) and LB Nick Perry (foot) were limited. Those four players were removed from the injury report.
Packers | Brett Hundley full go Thu Nov 16, 05:20 PM
Green Bay Packers QB Brett Hundley (hamstring) participated fully in practice Thursday, Nov. 16.
Packers | Brett Hundley full go Wed Nov 15, 04:57 PM
Green Bay Packers QB Brett Hundley (hamstring) was a full participant in practice Wednesday, Nov. 15.
Packers | Hamstring injury for Brett Hundley Sun Nov 12, 08:23 PM
Green Bay Packers QB Brett Hundley (hamstring) suffered a hamstring injury in the Week 10 game against the Chicago Bears.
Packers | Brett Hundley has his best game of '17 Tue Nov 7, 12:29 AM
Green Bay Packers QB Brett Hundley completed 26 of 38 passes for 245 yards in the team's Week 9 loss Monday, Nov. 6, against the Detroit Lions. He also picked up 22 yards on the ground and a touchdown on four rush attempts.
Packers | Brett Hundley struggles in Week 7 Sun Oct 22, 05:58 PM
Green Bay Packers QB Brett Hundley went 12-for-25 for 87 yards and one interception against the New Orleans Saints in Week 7. He also rushed for 44 yards and one touchdown on three carries.
Packers | Brett Hundley tosses three picks Sun Oct 15, 06:53 PM
Green Bay Packers QB Brett Hundley completed 18 of his 33 pass attempts for 157 yards, one touchdown and three interceptions in Week 6 against the Minnesota Vikings.
Packers | Brett Hundley enlightened Tue Jun 27, 08:45 AM
Green Bay Packers QB Brett Hundley said he has a better understanding of the mental aspect of the game. He's expected to play quite a bit during the preseason.
Packers | Brett Hundley was close to being moved Sun Apr 30, 04:49 PM
Green Bay Packers QB Brett Hundley was close to being traded during the second day of the 2017 NFL Draft but likely will be remain with the team for at least one more season.
Packers | Brett Hundley expected to miss next game Sat Aug 20, 11:50 AM
Green Bay Packers QB Brett Hundley (ankle) is not expected to play in the team's third preseason game because of his ankle injury.
Packers | Brett Hundley aggravates ankle injury Thu Aug 18, 09:24 PM
Green Bay Packers QB Brett Hundley (ankle) exited against the Oakland Raiders with an ankle injury Thursday, Aug. 18.
Packers | Brett Hundley expected to play Wed Aug 17, 10:14 PM
Green Bay Packers QB Brett Hundley (ankle) is expected to play in the preseason game Thursday, Aug. 18, against the Oakland Raiders after missing the past two weeks due to an ankle injury. He might start if QB Aaron Rodgers is rested again.
Packers | Brett Hundley taking part in practice Sun Aug 14, 12:56 PM
Green Bay Packers QB Brett Hundley (ankle) is participating in practice Sunday, Aug. 14, for the first time since he suffered an ankle injury Aug. 1.
Packers | Green Bay resting two top QBs Fri Aug 12, 05:20 PM
Green Bay Packers QBs Aaron Rodgers and Brett Hundley will not play in the preseason game against the Cleveland Browns Friday, Aug. 12. QB Joe Callahan will be the starting quarterback for the Packers.
Packers | Joe Callahan to start Sunday Sun Aug 7, 11:21 AM
Green Bay Packers QB Joe Callahan will start the preseason opener against the Indianapolis Colts Sunday, Aug. 7. QBs Aaron Rodgers and Brett Hundley will not play in the game.
Packers | Brett Hundley may miss preseason opener Thu Aug 4, 09:03 PM
Green Bay Packers QB Brett Hundley (ankle) is dealing with an ankle injury that is expected to keep him out of practice Thursday, Aug. 4, and head coach Mike McCarthy said he is ready with an alternative if Hundley can't play in the preseason opener against the Indianapolis Colts Sunday, Aug. 7.
Packers | Brett Hundley may miss practice Wed Aug 3, 06:28 PM
Green Bay Packers QB Brett Hundley (undisclosed) is considered questionable for practice Wednesday, Aug. 3, because of an injury he suffered during practice Monday, Aug. 1.
Packers | Brett Hundley has bright future Tue Jun 21, 01:15 AM
Green Bay Packers QB Brett Hundley has the potential to be a 'solid starter' in the National Football League, according to quarterbacks coach Alex Van Pelt. He has drawn praise within the organization for his competitiveness.
Packers | Aaron Rodgers, others excused Tue Jun 14, 12:23 PM
Green Bay Packers QB Aaron Rodgers and other select veterans have been excused from mandatory minicamp this week by head coach Mike McCarthy. WRs Randall Cobb and Jordy Nelson were also included in that group. 'The approach is different than the past,' McCarthy said. 'So, it's obviously tailored toward the younger players.' QB Brett Hundley will get most of the work with what is left of the No. 1 offense.
Packers | Davante Adams among Packers' inactives Sat Jan 16, 06:54 PM
The Green Bay Packers have declared LB Andy Mulumba, QB Brett Hundley, WR Davante Adams, RB John Crockett, OG Josh Walker, CB Ladarius Gunter, CB Robertson Daniel inactive for Week 19.
Packers | Green Bay wild-card game inactives Sun Jan 10, 03:14 PM
The Green Bay Packers have declared QB Brett Hundley, OT David Bakhtiari, LB Jayrone Elliott, OG Josh Walker, TE Justin Perillo, TE Kennard Backman, CB Sam Shields inactive for Week 18.
Packers | Green Bay Week 17 Inactives Sun Jan 3, 07:10 PM
Green Bay Packers OT David Bakhtiari (ankle), LB Jayrone Elliott (quadriceps), CB LaDarius Gunter, QB Brett Hundley, TE Justin Perillo (hamstring), CB Sam Shields (concussion) and OG Josh Walker are inactive for the Week 17 game against the Minnesota Vikings.
Packers | Week 16 inactives for Green Bay Sun Dec 27, 03:12 PM
The Green Bay Packers have declared LB Andy Mulumba, QB Brett Hundley, OT David Bakhtiari, LB Jayrone Elliott, TE Justin Perillo, TE Kennard Backman, CB Sam Shields inactive for Week 16.
Packers | Week 15 inactives for Packers Sun Dec 20, 02:46 PM
The Green Bay Packers have declared LB Andy Mulumba, QB Brett Hundley, RB John Crockett, OG Josh Walker, TE Kennard Backman, CB Sam Shields, WR Ty Montgomery inactive for Week 15.
Packers | Week 14 Green Bay inactives Sun Dec 13, 03:07 PM
The Green Bay Packers have declared LB Andy Mulumba, QB Brett Hundley, C Corey Linsley, RB John Crockett, CB Ladarius Gunter, LB Nick Perry, WR Ty Montgomery inactive for Week 14.
Packers | Green Bay's Thursday inactives Thu Dec 3, 07:05 PM
The Green Bay Packers have declared FB Aaron Ripkowski, LB Andy Mulumba, QB Brett Hundley, OT Bryan Bulaga, CB Damarious Randall, OT T.J. Lang, WR Ty Montgomery inactive for Week 13.
Packers | Week 12 inactives for Packers Thu Nov 26, 07:26 PM
The Green Bay Packers have declared RB Alonzo Harris, LB Andy Mulumba, QB Brett Hundley, C Corey Linsley, WR Jared Abbrederis, FS Micah Hyde, WR Ty Montgomery inactive for Week 12.
Packers | Week 11 Inactives Sun Nov 22, 03:24 PM
The Green Bay Packers have declared RB Alonzo Harris, LB Andy Mulumba, QB Brett Hundley, WR Jared Abbrederis, CB Ladarius Gunter, OG Lane Taylor, WR Ty Montgomery inactive for Week 11.
Packers | Week 10 Inactives Sun Nov 15, 11:53 AM
The Green Bay Packers have declared LB Andy Mulumba, QB Brett Hundley, RB Eddie Lacy, TE Kennard Backman, CB Ladarius Gunter, OG Lane Taylor, WR Ty Montgomery inactive for Week 10.
Packers | Ty Montgomery leads GB inactives Sun Nov 8, 11:47 AM
The Green Bay Packers have declared LB Andy Mulumba, QB Brett Hundley, TE Kennard Backman, OG Lane Taylor, CB Quinten Rollins, CB Sam Shields, WR Ty Montgomery inactive for Week 9.
Packers | Green Bay inactives for Week 8 Sun Nov 1, 07:29 PM
Green Bay Packers TE Kennard Backman, CB LaDarius Gunter, QB Brett Hundley, WR Ty Montgomery (ankle), LB Andy Mulumba, OG Lane Taylor and OG Josh Walker were inactive in Week 8 against the Denver Broncos.
Packers | Week 6 inactives for Green Bay Sun Oct 18, 03:11 PM
The Green Bay Packers have declared WR Davante Adams, SS Morgan Burnett, RB Alonzo Harris, QB Brett Hundley, LB Nick Perry, NT B.J. Raji, OG Lane Taylor inactive for Week 6.
Packers | Week 5 Inactives Sun Oct 11, 11:39 AM
The Green Bay Packers have declared QB Brett Hundley, WR Davante Adams, LB Jake Ryan, CB Ladarius Gunter, OG Lane Taylor, FS Morgan Burnett, SS Sean Richardson inactive for Week 5.
Packers | Week 4 Inactives for Packers Sun Oct 4, 03:13 PM
The Green Bay Packers have declared QB Brett Hundley, OT Bryan Bulaga, WR Davante Adams, CB Demetri Goodson, LB Jake Ryan, OG Lane Taylor, FS Morgan Burnett inactive for Week 4.
Packers | Week 3 Inactives for Packers Mon Sep 28, 07:07 PM
The Green Bay Packers have declared QB Brett Hundley, OT Bryan Bulaga, CB Demetri Goodson, TE Kennard Backman, OG Lane Taylor, FS Morgan Burnett, SS Sean Richardson inactive for Week 3.
Packers | GB inactives for Week 2 Sun Sep 20, 07:39 PM
Green Bay Packers TE Kennard Backman, OT Bryan Bulaga (knee), DL Bruce Gaston, CB Ladarius Gunter, RB Alonzo Harris, QB Brett Hundley and CB Quinten Rollins are inactive for the Week 2 game against the Seattle Seahawks.
Packers | Week 1 Inactives Sun Sep 13, 11:38 AM
The Green Bay Packers have declared RB Alonzo Harris, QB Brett Hundley, TE Kennard Backman, CB Ladarius Gunter, OG Lane Taylor, FS Morgan Burnett inactive for Week 1.
Packers | Brett Hundley impresses Thu Sep 3, 11:36 PM
Green Bay Packers QB Brett Hundley completed 16 of his 23 pass attempts for 236 and four touchdowns in a 38-10 preseason win over the New Orleans Saints Thursday, Sept. 3.
Packers | Matt Blanchard has edge for No.3 QB job Tue Jun 16, 08:35 PM
Green Bay Packers QB Matt Blanchard has looked well ahead of rookie QB Brett Hundley in the competition for the team's No. 3 quarterback job. 'Matt Blanchard had a heck of a day today,' Packers coach Mike McCarthy said Tuesday, June 16. 'I'll just tell you what I told him when I met him in April [at his workout]. I said, 'Why the hell don't you have a job?''
Ortopedi ( minus muskelskador och senskador. )
ИГРАТЬ
- Passiva stödjevävnader: skelett, brosk, ligament, senor
- Vanligare hos hanhund än tikar
- Stora hundraser (schäfer överrepresenterade)
Patofysiologi: endostal och periostal nybenbildning
Kraftig smärta i de långa rörbenens diafyser vid palpation
Problemen kommer ofta i skov under uppväxten
På RTG ses ökad täthet i delar av diafysens märgkanal (endostet) i de långa rörbenen.
- Störd metafysär blodtillförsel
- Fördröjd benbildning vid tillväxtzoner
- Mikrofrakturer, inflammation, nekros
- Nedsatt AT vanligt förekommade
- Svullnad, värme över tillväxtzoner på långa rörben, ffa distala radius
Röntgen visar nedsatt täthet och intrycket av dubbla tillväxtzoner i metafysen
Smärtlindring är extremt viktigt!
Diagnostiseras med röntgen
Behandling är Ulnaosteotomi, men detta kräver tidig diagnos ( innan radius tillväxtzoner är slutna
-Smärta från höftled, muskelatrofi
2. Biokemiska faktorer - cytokiner
3. Chondrocyter stimuleras frisätta proteaser
4. Dessa bryter bl a ned kollagen
5. Biomekaniska faktorer
6. Uppluckring matrix, broskbitar lossar.
7. Små bitar brosk fagocyteras av synoviocyter
(OA börjar vanligen med skada i ledbroskets yta)
-Otränad för sin uppgift
- Tillfällig, akut överbelastning
- repetetiv låggradig överbelastning
- Nutritionella aspekter (Kosttillskott, Omega-3-fettsyror,Glukosaminoglykaner?)
- Medicinering (NSAID,Pentosan polysulfat (Cartrophen), Opioider, Corticosteroider)
‐ Behandlingsprotokoll varierar med individen/ anpassas individuellt!
- Syftet är att lindra smärta och bromsa utvecklingen av OA ex vid korsbandsskada, OCD, HD, ED, intraarticulaära frakturer, inkongruens ledytor, kollateralligamentsskador.
- Vid grav OA, när konservativ behandling ej har hjälpt: caputresektion, byte av höftled, artrodes (steloperation), amputation
- Kroniska infektioner/reaktiv artrit
- Idiopatisk immunmedierad polyartrit
-FMCP/FPC frakturerad medial coronoideus process/frakturerad processus coronoideus
- Radius och ulna växer i olika hastighet --> ospecifik artrit
- Genetisk predisposition slapphet i ledkapseln
- Dålig kontakt mellan caput och acetabulum - nedsatt kongruens ‐ under skelettets tillväxt
- Onormal belastning - onormal utveckling av
- Instabilitet/subluxation‐ leder till artrosutveckling
Svårt att resa sig, gå uppför trappor, ovilja att
Efter hand sker en fibrotisering av ledkapseln som gör att ledslapphet ej längre kan palperas
- DPO (double pelvic osteotomy)
- TPO (triple pelvic osteotomy)
- Höftledsbyte - hunden ska ha vuxit färdigt
- Resektion av caput femoris - bäst resultat för hundar <20kg
- Motverkar medial rotation av tibia
- motverkar cranial translation av tibia
(säkrast på sövd hund)
caudalt om laterala fabellen
2. Andra handens pekfinger placeras på crista tibia och tummen placeras bakom fibulahuvudet
3. Cranial translation av tibia, prova med olika grader av flexion samt extension av knäleden
Efter kirurgi av korsband så kommer man ändå att ha ett positivt draglåde test. För att testa om operationen gett en stabil led så gör man Tibia compression test
En hund behandlad för korsbandsskada är en hund med OA
-Lateral patellaluxation förekommer, oftast hos
vinklingen av höftleden, som i sin tur påverkar
m quadriceps draglinje
- Kan orsakas av trauma
- I många fall beskrivs hundarna göra "hoppsasteg",
de hoppar över ett eller flera steg med det drabbade
1. Patella kan luxeras manuellt men reluxerar
2. Patella kan luxeras, reluxerar vid tryck med fingrar
eller rörelse av benet (manipulation)
3. Patella ligger luxerad, men kan reluxera vid
4. Patella ligger permanent luxerad, reluxerar ej.
- Grad 1 ofta konservativt
- Grad 2 rekommendera kirurgi om hunden har besvär. Risk för ytterligare deformation av femur och patellarleden.
- Grad 3‐4 kirurgi.
- Ger belastningsfördelning och dämpning av stötvågor mellan kotorna
- Eftersom en disk är deformerbar ger den en viss möjlighet till rörelse mellan kotor.
Fpc hund
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Inhaltsverzeichnis Orthopädie
Fragmentierter Processus Coronoideus (FPC)
Sind beide Ellbogengelenke betroffen, beobachtet man ab dem 4. Lebensmonat eine intermittierende, v.a. nach stärkerer Belastung auftretende, manchmal wechselseitige Lahmheit. Typisch ist, dass der mediale Teil des Ellbogengelenkes entlastet und dabei die Pfote leicht nach außen und das Ellbogengelenk körpernah gehalten wird. Bei älteren Patienten sind die Symptome ausgeprägter und oft mit einer Gelenkschwellung auf der medialen, zum Teil auch auf der lateralen Seite vergesellschaftet. Eine besondere Form des FPC kommt bei 5-6 J. alten Hunden, v. a. beim Deutschen Schäferhund und Golden Retriever vor. Die Patienten lahmen akut, reagieren auf Analgetika nicht oder nur kurzfristig. Röntgenologisch wird lediglich eine dezente Sklerosierung kaudal der Inc. trochlearis beobachtet.
Differentialdiagnose
Traumatisch bedingte Frakturen im distalen Gelenkanteil.
Diagnosesicherung
Wegen einer sich rasch entwickelnden sekundären Arthrose ist es notwendig, die Diagnose frühestmöglich durch eine gründliche klinische und röntgenologische Untersuchung zu stellen. Durch eine Computertomographie (CT-Untersuchung) ist die Diagnosestellung heutzutage sehr sicher und schnell möglich. Die Diagnostellung nur anhand von Röntgenbildern ist schwierig, wenn der Proc. coronoideus med. ulnae nicht zu sehen ist und beschränkt sich auf die Interpretation der sekundären Veränderungen wie Sklerose im kaudalen Bereich der Incisura trochlearis in Höhe des Processus coronoideus, sowie einer intraartikulären Stufe infolge des tiefer liegenden Radiuskopfes. In fortgeschrittenem Stadium ist der Proc. coronoideus med. ulnae plump, abgerundet und die proximale Radiusmetaphyse erscheint, zusammen mit dem Radiuskopf, glockenförmig erweitert. Später können Osteophyten am kranialen Rand des Caput radii, am dorsalen Rand des Proc. anconaeus, am medialen Rand des Proc. coronoideus und auch im Bereich des medialen Epicondylus humeri beobachtet werden. Die Röntgenaufnahmen werden im medio-lateralen, im anterio-posterioren Strahlengang und mit gehaltenen Röntgenaufnahmen angefertigt.
Behandlung
Sofortige chirurgische Gelenksrevision oder arthroskopische Entfernung des fragmentierten Proc. coronoideus med. ulnae bevor er weitere arthrotische Veränderungen hervorruft.
Nachbehandlung
Sie ist ein wichtiger Teil des Erfolges. Empfehlenswert ist ein Stützverband über 14 Tg. der alle 2-3 Tg. gewechselt wird. In dieser Zeit ist eine maximale Bewegungseinschränkung obligatorisch. Nach 14 Tg. wird etwas mehr Bewegung erlaubt, aber noch 4 Wo. lang besteht Leinenzwang. Anschließend wird ein langsames Aufbautraining durchgeführt. Stärkere Belastungen sollten erst nach 5-6 Mo. erfolgen.
Abhängig vom Alter des Patienten und von den Gelenkveränderungen zum Zeitpunkt der Operation. Je früher operiert wird, möglichst noch vor der Entwicklung schwerer arthrotischer Veränderungen, desto besser ist das postoperative Ergebnis.
Nur Terminsprechstunde (bitte anrufen)
Vormittags vergeben wir nur in Ausnahmefällen
Behandlungstermine, da wir die Zeit von 8:00
bis 12:00 Uhr für unsere Operationspatienten freihalten.
Cross Reference
Welcome to Eaton's Crouse-Hinds series competitor cross reference
This tool allows you to search for partial or complete catalog numbers with or without dashes. A PDF link attached to each part number will direct you to the complete Crouse-Hinds series catalog page.
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This cross reference is intended to be used as a tool to determine an equivalent Crouse-Hinds series catalog number, based on another manufacturer's catalog number. Catalog numbers of other manufacturers are shown for products that appear to be equivalent in their functional use, though not necessarily interchangeable.
Every effort has been made to ensure the accuracy of this information; however, Eaton will assume no responsibility for errors or omissions which may have occurred.
Information in this cross reference is subject to change.
Use of resting-state functional MRI to study brain development and injury in neonates
Advances in methodology have led to expanded application of resting-state functional MRI (rs-fMRI) to the study of term and prematurely born infants during the first years of life, providing fresh insight into the earliest forms of functional cerebral development. In this review, we detail our evolving understanding of the use of rs-fMRI for studying neonates. We initially focus on the biological processes of cortical development related to resting-state network development. We then review technical issues principally affecting neonatal investigations, including the effects of subject motion during acquisition and image distortions related to magnetic susceptibility effects. We next summarize the literature in which rs-fMRI is used to study normal brain development during the early postnatal period, the effects of prematurity, and the effects of cerebral injury. Finally, we review potential future directions for the field, such as the use of complementary imaging modalities and advanced analysis techniques.
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This work was supported by the National Institutes of Health , USA (Grant nos. K02 NS089852 and UL1 TR000448), Cerebral Palsy International Research Foundation , USA and Dana Foundation , USA.
Ununited Anconeal Process, Ununited Medial Coronoid Process, Ununited Medial Epicondyle, Patella Cubiti, and Sesamoidal Fragments of the Elbow
Chapter 85
Timothy M. Lenehan and David C. Van Sickle
Osteoarthritis of the elbow has been recognized by veterinarians for many years to be a developmental disease syndrome in young dogs. It was not until the middle 1950s, however, that progress was made toward defining specific pathologic etiologies, with the elucidation of the problem of "ununited anconeal process." Originally thought to be analogous to patella cubiti in humans,(13) the true nature of these ectopic sesamoid bones was soon realized,(3) thereby categorizing an initial cause of elbow osteoarthrosis. In the early 1960s the term "elbow dysplasia" was offered as an alternative to the term ununited anconeal process, since it was believed by some to better describe the generalized osteoarthritis syndrome that involved the entire elbow joint of animals afflicted with that disease.(2) Thus for several years the term "elbow dysplasia" was used synonymously with ununited anconeal process in the veterinary literature,(6,10,14) in spite of the recognition by multiple authors that secondary degenerative joint disease of the elbow in young dogs did, indeed, occur in joints having intact anconeal processes. In 1966 Ljunggren and co-workers correctly pointed out this misuse of terminology and redefined the syndrome of elbow dysplasia, describing the three causes then known for its development: ununited anconeal process, ununited medial epicondyle, and patella cubiti.(9) Corley further refined terminology by describing elbow dysplasia as "a descriptive term applied to a developmental abnormality of the elbow joint that is manifested as an early osteoarthritis with or without an ununited anconeal process."(4) His definition has been respected by many subsequent authors.(7,8,11) More recently, numerous conditions, both congenital and developmental, have been described that may be incorporated under the heading of elbow dysplasia as defined by Corley. (1,5,12) The frustrations of dealing with the term elbow dysplasia as a definitive diagnosis in a computerized records system and the subsequent inability to decipher epidemiologic features of specific causes of elbow osteoarthrosis have been aptly demonstrated by Hayes and co-workers.(7) While a review of all the causes of elbow dysplasia far exceeds the scope of the immediate discussion, several causes of the syndrome will be reviewed in the following pages. An understanding of this evolution of terminology will hopefully aid the reader who is interested in reviewing the veterinary literature on these topics.
History, Incidence, and Prevalence
The term ununited anconeal process is generally used to describe a failure of the center of ossification of the anconeal process of the ulna to fuse completely with its parent structure. Originally described as an ectopic sesamoid bone in the canine elbow (patella Cubits) in 1956,(34) ununited anconeal. process has at various times been referred to in the veterinary literature as elbow dysplasia, (17) congenital detachment of the processus anconeus,(37) and nonunion of the processus anconeus in the dog. (15) Cawley, in 1959, coined the term ununited anconeal process, which remains in use today.(18) As is common with most disease entities, ununited anconeal process had apparently afflicted dogs for many years prior to its recognition, the condition having been documented retrospectively in the skeleton of a bassett-saluki cross who died in 1936.(23,26) Unfortunately, much of the early veterinary literature and data concerning the disease are to be found under the diagnostic heading of elbow dysplasia, a descriptive term applied to any developmental abnormality of the elbow joint resulting in early secondary degenerative joint disease.(19-22,24,30,31,33,35,36) While various authors recognized the existence of elbow dysplasia both with and without concurrent ununited anconeal process, distinct clinical categorizations were not made early on in the literature. Indeed, often the ultimate cause of the reported elbow dysplasia was an unrecognized osteochondritic lesion or ununited coronoid process. Bearing this in mind, it still seems relatively safe to say that ununited anconeal process is a developmental, noninflammatory joint disease (possibly genetic in nature) characterized by a partial or complete separation of the anconeal process from the proximal end of the ulna. The disease generally presents itself as an intermittent, unilateral, subtle to severe forelimb lameness of gradual onset. When occurring bilaterally (approximately 30% of all cases), (18,32) lameness may shift from one forelimb to the other. While the age of onset of clinical symptomatology will vary (4 months-3 years),(28) the average animal manifests clinical signs early in life. Males are apparently affected more frequently than females, with one report stating a 2:1 ratio.(32) The disease characteristically affects large and giant breeds of dogs and has been reported in the Saint Bernard, Great Dane, Irish wolfhound, Great Pyrenees, Newfoundland, bull mastiff, French bulldog, Labrador, Afghan, pointer, and weimeraner. It has also been reported in two achondroplastic breeds, the bassett hound and dachshund.(26) A disproportionate number of cases have been reported in the German shepherd with several early reports citing its occurrence in closely related animals.(19,21,34) Such incidences in conjunction with one early report postulating a genetic mode of inheritance for elbow dysplasia in the German shepherd have led others to implicate a genetic predisposition for ununited anconeal process in that breed.(20) While it would appear that the German shepherd is at risk for developing elbow dysplasia in general, as is the Saint Bernard and the bassett hound,(24) a genetic predisposition is as yet unproven.
Chronologic Development
The anconeal process is a sharp-edged, slightly hooked piece of bone that forms the proximal end of the trochlea of the ulna. Upon elbow extension beyond 45°, this process fits into the olecranon fossa between the humeral epicondyles and in conjunction with the collateral ligaments and other soft tissue structures confines elbow movements to a sagittal plane. It is a completely intracapsular structure, its only soft tissue attachments (and therefore blood supply) inserting proximocaudally at the point of insertion of the elbow joint capsule in that region. With pathology, the degree of malunion may range from complete separation from its bony attachments to apparent anatomical normalcy (the process in actuality being held in place by a fibrous bridging callus) or any stage in between. While the chronologic development of the anconeal process has not been documented in all dogs, it is believed that in many of the smaller breeds (e.g., beagle) it either develops directly as an extension of the proximal ulna itself or originates from a small, separate center of ossification that rapidly unites with the parent structure.
In direct contrast to this, however, a separate center of ossification has been documented in the German shepherd, Saint Bernard, weimeraner, vizsla, Afghan, English pointer, greyhound, bassett, and dachshund.(35,36) The distinctness of the ossification center and the interval of time before eventual synostosis formation are related to the initial size of the cartilaginous anlage.(26) Using the German shepherd as a model, Van Sickle(35,36) has documented that up to 11 weeks of age the anconeal process is cartilaginous and not visible radiographically. At 12 weeks +/-1 week, a single or multiple density appears in the region of the anconeal process that enlarges or coalesces into a single anconeal ossification center by 12 to 18 weeks. The larger dogs with large anconeal processes require a longer time for osteogenesis. A thin perpendicular dark line between the anconeal ossification center and the diaphysis of the ulna is a physeal plate. By 16 to 24 weeks of age the dark physeal line has been replaced by a dense thin white line indicating unification of the anconeal process with the ulnar diaphysis (Figs. 85-1 and 85-2). Thus, in most breeds, a diagnosis of ununited anconeal process prior to 20 to 24 weeks of age would appear premature (Fig. 85-3).
Presenting Signs
Clinical signs of the disease generally do not appear until 5 to 9 months of age, at which time the animal is usually presented for an intermittent unilateral forelimb lameness of slow onset and progression that is exacerbated by exercise. Affected animals have been reported to manifest a characteristic stance in which their front paws point laterally and their elbows are abducted, with a characteristic abduction or "winging out" of the elbow when gaited.(25) Upon physical examination, some crepitus may be noted while placing the limb through a range Of motion, and the animal may experience mild to moderate discomfort upon hyperflexion and hyperextension. Some of the more chronically affected animals exhibit lateral swelling of the joint capsule in the area of the anconeus muscle, a result of chronic synovitis, osteoarthrosis, and joint capsular thickening. Deep digital palpation of the anconeal process through the anconeus muscle with the elbow in flexion may likewise result in the dog exhibiting pain. A small percentage of animals will remain asymptomatic until 18 to 36 months of age, by which time there is significant evidence of degenerative joint disease and chronic muscle atrophy upon both clinical and roentgenographic examination. With close questioning, one is often able to elicit a history of previous episodes of lameness that resolved spontaneously. The cause for presentation generally relates to a hyperextension injury with fracture of an osteophyte or shearing of a previously nondisplaced process. Several disease entities may occur concurrently with a symptomatic ununited anconeal process, or, alternatively, lameness may be due to panosteitis, osteochondritis, ununited coronoid process, ununited medial epicondyle, or elbow subluxation secondary to physeal disturbances, and the ununited anconeal process may, in fact, be clinically silent. One recent study has strongly suggested that hip dysplasia and ununited anconeal process occur in close association within the same animal,(24) a fact alluded to in the earlier literature.(31) Thus, lameness in these animals may relate to soft tissue trauma due to forelimb sparing of dysplastic hips, or in fact the dysplasia may make these animals more prone to trauma of bony forelimb structures (including the anconeal process). Radiography of the elbow in a flexed position will demonstrate the lesion. (See Figs. 85-4, 85-10, and 85-11)
Several etiologies have been proposed for the development of ununited anconeal process depending on the breed of dog afflicted. There has been a discussion whether or not the condition is inherited or is associated with other developmental diseases such as hip dysplasia or osteochondrosis of the humeral head. While the disease prevalence within certain breeds is high enough to suggest a genetic disease, it is not proven. A logical biomechanical etiology for the physeal fracture is based on force and moment. This theory is supported by the biologic facts that the fracture begins at the ventral portion of the physis adjacent to the articular epiphyseal cartilage of the trochlear notch where tension is the greatest, while compression maintains the integrity of the structure dorsally; and the collagen of the fibroid bone marrow in the ventral portion of the fracture is arranged parallel to the lines of tension.
While ununited anconeal process has been documented to occur with premature closure of the distal ulna in a large breed dog, it is generally believed that shearing forces relating to physeal growth disturbances with secondary elbow subluxation are probably of major significance only in the achondroplastic breeds.
Some authors have implicated fracture of the synchondrosis secondary to a spontaneous avascular necrosis of the anconeal process,(28) while more recently ununited anconeal process has been described as resulting from a basic endochondral ossification defect of the physeal plate, a form of osteochondrosis.(32) Regardless of underlying etiology, the ultimate sequence is fracture of the physis of the developing process, with a failure of synostosis formation and the interposition of a fibrous union. The resultant changes in joint mechanics, in concert with joint exposure to subchondral bone and cartilage fibrillation products due to abnormal wear of the loose or free-floating body, result in the release of chondroitin sulfates, producing a chemical synovitis and resultant secondary osteoarthrosis. Chronic low-grade osteoarthritic pain occurs, with an acute, exquisitely painful episode nonresponsive to medical therapy a logical sequela to a sudden dislodgment of the process.
To understand the gross pathology, it is necessary to know the radiographic progression of the disease. There may be minimal initial displacement of the anconeal process because the fracture separation may extend slowly up through the physis. If the radiograph is taken within 3 weeks of the initial biomechanical insult, there is usually a dark radiolucent area extending 3 mm to 4 mm into the ulnar diaphysis (Fig. 85-4). This area represents osteonecrosis of the trabecular bone due to disruption of the diaphyseal blood vessels. The anconeal process may show little alteration, since its blood supply is separate and comes into the anconeus from the dorsal periosteum (Fig. 85-5). if the trauma is so severe as to result in complete separation of the anconeal epiphysis from the ulnar diaphysis and there is no secondary attachment of the anconeal process to the synovial membrane, the anconeus can undergo complete osteonecrosis.
Grossly, ununited anconeal process is recognized by a disruption of the articular cartilage of the semilunar notch in the area of the physis (Figs. 85-6 through 85-8). There may be some thickening of the joint capsule, and a small degree of marginal cartilaginous osteophytosis may form at the lateral edges of the articular cartilage of the trochlear notch. In chronic cases of ununited anconeal process, the changes of secondary osteoarthrosis are readily apparent. The joint capsule is extremely thick, the articular cartilage of the ulnar trochlear notch and the humeral trochlea is gone and the underlying bone is eburnated, marginal osteophytosis is present, and, if the anconeal process is loose, it will be enlarged and bulbous owing to continual remodeling. In some cases the anconeal process may become ankylosed in the trochlea of the distal humerus.
Histopathologically, the physeal fracture begins with the disruption of the articular cartilage and extends dorsally through the physis, eventually breaking through the dorsal cartilaginous model of the ulna. The rate of the physeal splitting can vary; hence, a ventral endosteal callus of vascular collagenous tissue arranged parallel to the underlying articular cartilage may be present. Since ununited anconeal process is an intra-articular fracture, there is no osteogenic contribution from the articular cartilage, and the healing is largely endosteal (Fig. 85-9). This can result in rapid healing (3 weeks) if the condition is diagnosed early during partial splitting and the limb immobilized. When a complete physeal fracture occurs, the ulnar and anconeal ends of the fracture are constantly moving against each other during locomotion, resulting in a fibro-cartilaginous surface that eventually undergoes endochondral ossification and results in eburnated articular surfaces. The movement between the fracture fragments results in the formation of a bony spur on the dorsal surface of the anconeal process and ulna. With time, another angular spur will form on the cranial edge of the proximal radius. These are the hallmarks of the final stage of ununited anconeal process, namely, secondary osteoarthrosis.
If the detachment is only partial and the animal is young, strict confinement with immobilization has reportedly resulted in fusion in a small number of cases.(25) in the acutely affected young animal with minimal osteoarthritis change, most authorities would agree to elective surgical intervention. A common method of management is removal of the ununited process. While most animals experience a mild residual decrease in range of motion as a result of elbow arthrotomy, it does not significantly affect their ability to function. One report of 16 dogs treated in this manner demonstrated a return to full use of the limb an average of 4 weeks postoperatively, with arthritic changes remaining static and good elbow stability on the average follow-up of 19.5 months.(32) Many surgical techniques employing the lag screw principle (Figs. 85-10 and 85-11) have been described in the literature for replacement of the ununited anconeal process; the average time to union post surgery is 6 to 8 weeks. (16,25,27,29) If the bone stock of the process is initially such that stable fixation is impossible or if nonunion persists for longer than 6 to 8 months post osteosynthesis, the process may be removed. To achieve any reproducible degree of success, however, surgery should be reserved for the young animal with an anatomical anconeal process and minimal osteoarthrosis. In a dog who has a significant pathologic deformity of the process or who manifests obvious signs of osteoarthrosis upon initial presentation, medical therapy is seemingly the rational approach.
Surgical reduction of the process in such cases would seem unwarranted owing to the chronic nature of the disease and the degenerative changes in the process. While removal of the free fragment may relieve symptoms for a while, it is the opinion of many that within 2 to 3 years thereafter the animals once again manifest clinical signs of disease related to the chronic instability produced by progressive weight bearing.* For these animals, salicylates remain the first line of defense, followed by nonsteroidal anti-inflammatory agents. Corticosteroids are the final mode of medical therapy prior to arthrodesis.
* Nunamaker DM, Newton CD: Personal communication, 1983
History, Incidence, and Prevalence
A great majority of the earlier reports discussed above contain references to cases of elbow dysplasia that exhibited either medial-compartment or generalized osteoarthrosis, unexplained by the three working diagnoses at hand, and thus were categorized merely as variants of elbow dysplasia. Singular accounts of these oddities had been the rule until a more thorough understanding of osteochondrosis and particularly its relevance to the medial compartment of the canine elbow joint were brought to light by Olsson and others.(45-48) A more complete categorization of this enigmatic syndrome of elbow dysplasia was then made possible. Whereas for years ununited anconeal process was thought to be the main cause of secondary osteoarthrosis in the elbow joint of young dogs, osteochondrosis of the medial humeral condyle and ununited medial coronoid process are now considered to be the most common causes of canine elbow arthrosis as reported by several authors in various countries.(41,42,47,48,52)
The term ununited medial coronoid process of the ulna was originally used to describe a partial or total failure of the medial coronoid process to unite to its parent structure, thereby resulting in one or multiple bony fragments of various size remaining loosely attached at the medial radio-ulnar articulation within the elbow joint. It is felt by some that the word ununited implies that the process was once united to the ulna by a synchondrosis or separate center (or centers) of ossification and has subsequently become separated in some fashion. This terminology becomes somewhat more compromised in light of reports by several authors who have confirmed (by surgical exploration) the presence of osteoarthrosis in elbows free of any underlying pathology other than obvious erosions and fissures in the cartilage of an otherwise intact medial coronoid process.(42) Furthermore, one report describes a similar yet possibly distinct finding of hypoplasia of the coronoid process in which the entire thickness of the articular cartilage over the coronoid process was necrotic, with no germination cells remaining to reinitiate the growth of the process.(49) In light of the foregoing data, the term fragmented coronoid process has been offered by some as an alternative.(38)
In any event, ununited coronoid process can be considered to be a developmental (and possibly inherited)(41) form of osteoarthrosis in which the basic underlying defect relates to an abnormal medial coronoid process of the ulna. It is a disease of young, rapidly growing large breed dogs as has been described in the rottweiler, Labrador, golden retriever, Newfoundland, German shepherd, Bernese mountain dog, Saint Bernard, Old English sheep dog, flat-coated retriever, chow, and Airedale. It has likewise been described in the bearded collie, sheltie, and one mixed-breed animal. While there seems to be a definite predisposition for males to simultaneously develop osteochondritis dissecans and ununited coronoid process of the elbow joint,(41) a sexual predilection in males for ununited coronoid process alone as yet remains unproven. Onset of lameness in affected animals has occurred as early as 3 months of age(40) and as late as 10 years.(38) Ununited coronoid process has manifested itself as an asymptomatic incidental finding in elbow luxations and fractures as well as in elbow subluxations secondary to physeal arrest of the radius or ulna.(38) In a series of Labrador retrievers exhibiting a combined retinal and skeletal dysplasia, ununited coronoid process has been reported to develop from a separate center of Ossification that has been described as hypoplastic and remaining separated from the ulna by a plate of cystic, necrotic cartilage.(39) It has likewise been reported in dogs with hip dysplasia and osteochondritis dissecans of the shoulder.(38)
While ununited medial coronoid process remains the sole cause of osteoarthrosis in many canine elbows, it nonetheless has been described to occur concurrently with ununited anconeal process, and in one series it has reportedly been accompanied by osteochondrosis of the distal medial humeral condyle in 19 of 19 affected animals.(38) In yet another report of 58 animals with either generalized or medial-compartment osteoarthrosis of the elbow, 40 animals were confirmed at surgery to have ununited coronoid process, while 15 had only osteochondritis dissecans and 3 had both ununited coronoid process and osteochondritis dissecans !(42) Thus it would seem that the separation of the two disease entities either radiographically or upon surgical exploration is by no means an easy task and that the categorization of pure symptomatology for either disease is difficult at best. The frequency of concurrent lesions (particularly that of osteochondritis dissecans) would seemingly lend credence to the theory of a similar underlying etiology, however.(48)
Presenting Signs
Animals generally present at 5 to 6 months of age with an acute or chronic intermittent weight-bearing lameness of one or both forelimbs. These animals have a tendency to stand with the affected forelimb externally rotated (supinated) from the elbow distally.(41) Often a history of osteoarthritis pain can be elicited: the animals seem to be stiff in the affected joints after rest, with lameness exacerbated by prolonged exercise or changes in weather. On physical examination, the dogs generally exhibit pain when the limb is placed through a full range of motion, and there is minimal to moderate joint distension and capsular thickening. Deep palpation in the area of the coronoid process is generally equivocal. Local anesthetics placed intra-articularly have been reported to decrease the amount of lameness only slightly (their efficacy is probably a function of the degree of osteoarthrosis and the number of extra-articular structures involved in the degenerative process).(41)
Radiographic evaluation of affected elbows should include cranial-caudal, lateral (flexed and extended), medial oblique, and lateral oblique projections, which, if negative, should be repeated in 4 to 8 weeks if the dog remains symptomatic.(51,54) Generally, the initial radiographic changes are manifested at 6 to 7 months of age (42,48,51) and consist of medial compartment disease evidenced by erosions and roughened, irregular condylar margins with or without bony spur formation (Fig. 85-12). Occasionally, a free fragment may be seen in the medial joint compartment lying between the radial and ulnar articulations. However, owing to the frequent simultaneous occurrence of ununited coronoid process and osteochondritic lesions, as well as the limited ways in which the medial joint compartment of the elbow can respond to any given insult, radiographic diagnosis of a singular ununited coronoid process or osteochondritis dissecans lesion should be made with some hesitancy. As in other osteoarthritic disease processes, the extent of the radiographic changes often shows no correlation with the age of onset, duration of lameness, or degree of affectation clinically.(42,48,51) However, a generalization has been offered that the degree of osteoarthrosis is greater in the lone ununited coronoid process lesion than in an elbow with a singular focus of osteochondritis dissecans.(42)
Chronologic Development
The elbow joint is a composite joint of complex structure. The humeroradial interface provides the major weight-bearing articulation, with the humeroulnar articulation acting primarily as a stabilizing force by restricting motion to the sagittal plane. The ulnar trochlear notch flares distally into the medial and lateral coronoid processes, both of which are articulating structures that act to increase the joint contact surface area between the antebrachium and the humeral condyles without contributing significantly to weight bearing.(38) Abnormal articulation between the humerus and coronoid process (whether a result of hypoplasia and abnormal wear or partial to complete detachment with fragmentation) will result in cartilage degeneration with its resultant release into the joint of chondroitin sulfates and other breakdown products producing synovitis and effusion. Continued changes in the articular cartilage and eventually in the subchondral bone can lead to a loss of normal articular contour, predisposing the joint to further abnormal movement and perpetuation of the vicious cycle.(46) Thus, the ultimate result is generalized osteoarthritis superimposed on the focal osteoarthritis due to the medial compartment instability and chronic irritation. As in many other forms of osteoarthrosis, the degree of muscle tone apparently plays a role in the progression of the disease process; in one study, it was found that those animals with well-developed musculature (regardless of therapeutic modality) at follow-up seemed to move more easily than their less active and poorly conditioned counterparts.(42)
Numerous surgical approaches have been described for exploration of the medial compartment of the elbow. Transolecranon osteotomy(55) and triceps tenotomy(18) have been advocated, as has osteotomy of the medial epicondyle of the humerus.(43) Olsson originally used a medial approach combined with transection of the pronator teres and flexor carpi radialis in conjunction with desmotomy of the radial collateral ligament, as have others.(44,47,53) Several modifications of this approach have been documented.(40,50) Regardless of approach, thorough inspection of the medial joint compartment is mandatory, since complete retrieval of multiple fragments of the coronoid process is essential (Fig. 85-13); likewise, inadequate exposure would preclude distinction of a coronoid process attached by a fibrous union from one fully attached but exhibiting only degenerative changes in its overlying cartilage. Furthermore, inspection of the medial condyle of the humerus frequently reveals either osteochondritis dissecans or erosion and fibrillation of the opposing cartilage; the size of this "kissing lesion" is proportional to the degree of looseness and size of the free coronoid fragment.(42,47) Curettage of any areas of chondromalacia, eburnation, or osteochondritic lesions should be carried out simultaneously. Synovectomy has been recommended in joints manifesting synovial hyperplasia.(38)
To date, the results of surgical intervention in this disease process have been equivocal. Part of the problem relates to a paucity of reliable follow-up information on animals with singular ununited coronoid process lesions that are treated surgically. Certain trends or correlations may be made. While the time to recovery after surgery averages 3 to 4 months,(38,40-42) one author reports that five of nine animals affected with both osteochondritis and ununited coronoid process and treated only medically were fully recovered within 6 months of initial presentation.(42) It would appear that if any generalizations are to be made, young animals with minimal radiographic changes of osteoarthrosis treated surgically seemingly fare better than older animals or animals in whom a moderate amount of osteoarthrosis is present prior to surgery. One author relates the degree of resolution postoperatively to be determined by the animal's age at presentation, the degree of osteoarthrosis, and the condition of the cartilage at surgery.(38) The possibility of any given surgical approach ultimately resulting of itself in degenerative osteoarthrosis in the elbow has been addressed by only one author, who also presented the only control group of medically treated animals.(42)
There exists in the dog a pathologic entity described as ununited medial epicondyle. The humerus of the dog develops from five principal centers of ossification that ultimately organize to form two major epiphyseal growth plates (physes) located near the proximal and distal humeral epiphysis.(56,58) The majority of longitudinal growth of the humerus is thought to occur at the distal physis, the proximal epiphysis being primarily concerned with the ultimate development of the humeral head and greater and lesser tubercles. The medial epicondylar epiphysis eventually forms the medial epicondyle, a site of origin for many of the carpal and digital flexor muscle groups.(59) Radiographically, the center of ossification of the medial epicondyle appears approximately 4 to 8 weeks after birth (depending on breed) and generally by 6 months of age has fused with the distal humeral epiphysis and metaphysis respectively.(56,58) Thus, early disruption of either the centers of ossification or the epiphyseal plates will result ultimately in a congenital or developmental anomaly.
Originally described by Ljunggren and co-workers in 1966,(57) the term ununited medial epicondyle was offered to describe a form of elbow dysplasia arising from an ununited caudal portion of the medial humeral epicondyle that was seen to occur in an 8-month-old German shepherd. The animal had presented for a progressive right forelimb lameness of 2 months duration. Pain was elicited upon flexion of the elbow joint and with direct digital palpation of the medial epicondyle. While there was noticeable soft tissue swelling in the area of the medial epicondyle, range of motion remained good. Radiographically, both elbow joints manifested 1.5 cm x 0.5 cm islands of bone lying caudal and distal to the medial epicondyles, which were treated by surgical excision of the free fragments and their attendant periosteum in two separate procedures 6 weeks apart. Histologically, both specimens revealed normal cancellous bone that had been united to the epicondyle by a fibrocartilaginous bridge. On 10-month postoperative follow-up the animal manifested intermittent right forelimb lameness (possibly related to incomplete excision of the fragment in the right limb), the left limb remained asymptomatic. No initiating traumatic incident was cited nor underlying etiology offered. Similar to patella Cubits the disease remains enigmatic owing to a paucity of reported cases.
The term patella Cubits was used early on in the medical literature to describe a sesamoid bone or ectopic site of ossification that developed within the triceps tendon.(60) The condition was believed to have evolved either from an early injury to or an inherent developmental defect in the olecranon epiphysis of the ulna. Either process would theoretically lead to a divided epiphysis, part of which separated to form an isolated structure in the triceps tendon reminiscent of a patella.(62,64) The term patella cubiti was first introduced into the veterinary literature by Stiern in 1956.(63) He described an "infrequent condition involving the presence of one or more atypical sesamoid bones incorporated within the elbow joint or the extensor surface of the joint, which at surgery had attachments only to the triceps tendon." In reality, Stiern presented a beautiful description in three German shepherds of what is now considered to be ununited anconeal process. It was not until 1966 that the term patella Cubits was reintroduced by Ljunggren and Co-workers to describe one of the three basic forms of elbow dysplasia in the dog, all believed to be congenital fusion defects affecting the ossification centers of the elbow (i.e., ununited anconeal process, ununited medial epicondyle, and patella Cubits). The authors described a single case of patella Cubits occurring in a 5-week-old Doberman pinscher who had been bilaterally affected since birth. The animal had always been less active than its littermates, had walked at a later age, and had been rated on physical examination to have noticeably diminished olecranon prominences. The animal walked with a stilted gait in its forelimbs, with both elbows held in partial Sexton throughout all phases of the step. Mobile, bony masses were palpable in the triceps tendon proximal to its ulnar attachments. Radiography revealed patella-shaped structures caudal to the humeral condyles that were distinctly separate from the proximal ulna. The animal was followed through 23 weeks of age and the authors concluded that the deformity resulted from a separation of both the unossified proximal ulnar (olecranon) epiphysis and the ossified proximal ulnar metaphysis from the ulnar diaphysis at an early stage in bone development. This separation resulted initially in one and eventually in two separate patella-shaped bones becoming radiographically visible caudal to the humeral Condoles. The condition is seemingly rare, since reports of other cases have not been referenced in the veterinary literature.(65) The underlying etiopathogenesis remains speculative.
Whereas ununited medial epicondyle and patella Cubits have received only cursory review in the veterinary literature (indicative no doubt of their infrequent occurrence), ununited anconeal process and ununited coronoid process have been topics of more detailed discussion in past years. More recently, however, attention has turned toward the categorization of other, less well defined etiologies of elbow dysplasia. Of most significance, perhaps, are those papers concerned with sesamoidal fragments both within and around the elbow joint and their relation to the development of chronic osteoarthrosis.
Numerous authors have mentioned the existence of various sesamoidal fragments lying within those soft tissue structures that are intimately connected with the elbow. In general, most of these fragments have been regarded as incidental findings, with no clinical significance ascribed to them. They often receive notice in the severely osteoarthritic joint, in which one may be hard pressed radiographically to distinguish between sesamoid, osteochondral fragments, and osteophytic avulsion, rendering the categorization of such merely speculative.(74) In the younger animal, free of secondary degenerative joint disease, the task becomes somewhat more clearly definable. In the current literature, four compartments of the elbow have received attention as areas in which sesamoidal fragments are routinely described: the cranial humeroradial articulation, the medial compartment, the lateral compartment, and the trochlear compartment, which houses the anconeal process. Of primary concern in the current discussion are the first three compartments of this composite joint.
Cranial Joint Compartment
Calcified bodies referable to the anterior humeroradial articulation have received little recognition in the veterinary literature. Generally considered benign incidental findings,(72) they have been reported by one author as a cause of lameness in the Afghan hound.(67) The animal manifested lameness of both forelimbs after exercise, with pain on flexion and extension of the elbow joints. No other radiographic abnormalities were noted. The dog was one of a litter of nine animals, three of which exhibited congenital malformation of the elbow joint with multiple proximal radial and ulnar deformities. Three other littermates and both parents were radiographically normal, while the two remaining animals were unavailable for evaluation. The etiology remains unknown.
Lateral Joint Compartment
Similar to calcified bodies in the cranial compartment, sesamoid bones existing in the lateral elbow joint region have generally been regarded as incidental vestigial anomalies of a benign nature, purportedly lying within the annular ligament.(66,76) More recently, however, a series of eight large breed dogs with lameness referable to a sesamoidal fragment attached to the ulnar collateral ligament and lateral Joint capsule has been described. All eight animals were presented at 6 months of age for an intermittent forelimb lameness that progressively deteriorated. Affected animals manifested a tendency to exhibit cubiti varum, and their elbow joints were swollen with pain readily elicitable upon palpation of the lateral (ulnar) collateral ligament in the area of the radial head. Crepitation was not manifested when affected limbs were placed through a range of motion. Anteroposterior and lateral radiographs generally prove unremarkable in this condition, flailing to outline the sesamoid and showing minimal to no changes in the joint consistent with osteoarthrosis. An oblique film with the radius rotated approximately 50° from anteroposterior generally reveals a dense fragment of bone situated on the lateral side of the proximal head of the radius. A standard lateral approach between the tendons of origin of the extensor digitorum communis and lateralis generally reveals the 2 mm x 2 mm to 5 mm x 5 mm smooth, dense sesamoidal fragment, which is firmly adhered to the collateral ligament and joint capsule. Upon removal, the intermittent lameness decreased significantly in one week, with lameness resolving completely in five of eight animals. The authors postulated a mechanical lameness in which the fragment became interposed between humeroradial joint surfaces in the flexion phase of joint movement.(75)
Medial Joint Compartment
While an increased interest in the medial joint compartment of the elbow has arisen in the last several years (referable to the elucidation of osteoarthrosis occurring secondary to ununited coronoid process and humeral condylar osteochondritis dissecans), little has been published concerning the frequency or significance of sesamoid bones occurring within that area. The existence of a calcified body lying just medial to the medial humeral epicondyle at the level of the joint space has been described as a primary cause of lameness in the dog.(68,69,71) To date, the lesion has been found only in the Labrador retriever and English setter, with three of four animals symptomatic between 3 and 11 months of age. One animal exhibited bilateral pathology. All animals were presented for a mild forelimb lameness that deteriorated over time. Physical examination generally revealed minimal to no joint swelling, slight atrophy of shoulder musculature, and pain on passive extension and flexion of the elbow joint. Medial arthrotomy between the origins of the flexor carpi radialis and the flexor digitorum superficialis tendons allowed good exposure for retrieval of the calcified body, which was always intimately connected with the origin of the flexor digitorum profundus and inner connective tissues of the fibrous joint capsule. Upon inspection of the medial joint compartment, secondary changes of osteoarthrosis were minimal to nonexistent in all animals explored, except for an obvious thickening of the involved capsular tissues. Histology revealed a true bony fragment, the site of origin of which was undetermined. Most animals became clinically sound between the 7th and 21st postoperative day, with one dog manifesting slight osteoarthritis changes at 6-month follow-up. Some authors have implied that this is really a flap of cartilage from an osteochondritis dissecans lesion that has subsequently adhered down to the caudomedial joint capsule,(73) but this seems unlikely owing to the osseous nature of the fragment and its often extra-articular situation.(70)
It is apparent from the small number of cases presented and the clinical nature of the material that many questions remain to be answered in the study of sesamoid bones and their functional relation to the elbow joint. Likewise, owing to the very nature of its composite structure and the number of insidious disease processes that have already been described to affect it, as well as the systemic diseases that may simultaneously exist to confuse accurate radiographic or clinical examination, further case studies are desperately needed to solidity the above-mentioned preliminary reports.
HISTORY OF TERMINOLOGY
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UNUNITED ANCONEAL PROCESS
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32. Sinibaldi KR, Arnoczky SP: Surgical removal of the ununited anconeal process in the dog. J Am Anim Hosp Assoc 11: 192, 1975
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34. Stiern RA: Ectopic sesamoid bones at the elbow (patella cubiti) of the dog. J Am Vet Med Assoc 128:498, 1956
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36. Van Sickle DC: "U.A.P." in selected orthopedic problems in the growing dog. Monograph Am Anim Hosp Assoc 12:10, 1975
37. Vaughan LC: Congenital detachment of the processus anconeus in the dog. Vet Rec 74:309, 1962
UNUNITED MEDIAL CORONOID PROCESS
38. Berzon JL, Quick CB: Fragmented coronoid process: Anatomical, clinical and radiographic consideration with case analysis. J Am Anim Hosp Assoc 16:241, 1980
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48. Olsson SE: Osteochondrosis: A growing problem to dog breeders. Gaines Progress 1 - 11, 1976
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53. Wissler J. Sumner-Smith G: Osteochondrosis in the elbow joint in the dog. J Am Anim Hosp Assoc 13:349, 1977
54. Wolfe DA: Surgical connection of osteochondritis dissecans of the medial humeral condyle and ununited coronoid process in a dog. Vet Med Small Anim Clin: 1554, 1976
55. Wood AKW, Bath ML, Mason TA: Osteochondritis dissecans of the distal humerus in a dog. Vet Rec :489, 1975
UNUNITED MEDIAL EPICONDYLE
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68. Grondalen J. Braut J: Lameness in two young dogs caused by a calcified body in the joint capsule of the elbow. J Small Anim Pract 17:681, 1976
69. Long RD, Rogers AJ: Letter to the Editor. J Small Anim Pract 18:157, 1977
70. Olsson SE: Osteochondrosis: A growing problem to dog breeders. Gaines Progress 1-11, 1976
71. Price CJ, King SC: Elbow lameness in a young dog caused by an ossified disc in the joint capsule. Vet Rec 100:566, 1977
72. Prole JH: Letter to the Editor. J Small Anim Pract 14:309, 1973
73. Robbins GM: Some aspects of the radiographical examination of the canine elbow joint. J Small Anim Pract 21:417, 1980
74. Tirgari M: Clinical, radiographical and pathological aspects of arthritis of the elbow joint in dogs. J Small Anim Pract 15:671, 1974
75. Vaananen M, Skutnab K: Elbow lameness in the young dog caused by a sesamoidal fragment. J Small Anim Pract 19:363, 1978
76. Webbon PM, Clayton Jones DG: Radiological refresher: 6. The elbow. J Small Anim Pract 17:395, 1976
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