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Dr Redden's Equine Podiatry Series
In-Depth Laminitis

Venogram Technique, Indication and Interpretation


Written and presented November 2005 by R.F. (Ric) Redden, DVM

(Watch the Digital Venogram video performed by Amy Rucker, DVM.)

Introduction

I developed this clinical protocol out of the need to better understand the degree of vascular damage during different stages of the syndrome. Working with Dr. Chris Pollitt at my clinic, we used his in vitro study to perform the first in-vivo venogram procedure in 1992. It was conducted on a standardbred filly that was owned by the International Equine Podiatry Center. Since that time, I have modified the procedure to meet the requirements of specific breeds, as well as a variety of foot problems that involve the circulatory system.

Basic Steps

  • Sedate the horse.
  • Block the feet just above the fetlock. Use only 4-6cc of blocking agent to prevent transient edema.
  • Place the horse’s feet on approved positioning blocks. This will insure a pure lateral projection.
  • Set the x-ray machine in place, and have all the necessary cassettes and grids within arm’s reach.
  • Take a scout film with soft-tissue detail, using a barium paste marker on the face of the hoof wall.
  • Wrap 4” Elastikon around the fetlock. This will provide an anchor point for the tourniquet and will prevent twisting the skin while applying the tourniquet.
  • Place a tourniquet over the fetlock. Avoid a mid-cannon tourniquet.
  • Catheterize the palmar vein using a 5/8”, 21-gauge butterfly catheter. Be careful not to thread the needle too far into the vein. You risk making a second hole in the vein.
  • Inject 20cc of Reno-60. I recommend using two 12cc syringes instead of one 20cc syringe. A 20cc syringe builds too much back pressure and complicates injection. Injection needs to be completed in less than one minute, as the contrast will leak from the vessels quickly and skew your interpretation.
  • Pull the knee forward slightly while injecting the second syringe. The heel should remain flat on the block. This rocking assures lamellar perfusion and unloads the deep digital flexor tendon (DDF).
  • Clamp a hemostat on the catheter, or apply a stopcock. Quickly tape the hemostat to the leg so it will not be in your way.
  • Take your series of film. This series of film should be completed within 45 seconds.
    • Lateral, soft exposure
    • Lateral, hard exposure with grid
    • DP, hard exposure with grid
    • DP, soft exposure
    • Lateral, soft exposure
  • Soft exposures are needed when there are significantly compromised vessels. Hard exposures offer a diagnostic image of the terminal arch and deeper vessels. The last DP view offers a look at vascular leakage that may not be apparent in the first couple film. Acute and chronic cases will exhibit similar patterns, yet there are distinct differences in the two.
  • Remove the tourniquet and place cotton or gauze over the vessels. Tape in place for 5-10 minutes.
Indications

A venogram is a discovery experience, as it offers a means to track the disease syndrome as it alters the vascular supply. Therefore, it offers unlimited options concerning the medical, surgical and therapeutic regimes necessary to revive the compromised areas. Venograms can be used diagnostically for:

  • Laminitis
  • White Line Disease
  • Keratomas
  • Puncture Wounds

Having performed a few thousand venograms over the years, I have discovered a pattern that appears to be repeatable as laminitis progresses from a mild onset to high-scale cases; whether it is acute or chronic.

Likewise, the venogram offers a reliable means of monitoring the progress of reperfusion in compromised areas. They also help explain why some cases fail to progress in a favorable fashion. Being able to correlate the altered vascular pattern with the clinical picture, growth pattern and tissue response greatly enhances your insight for the planning and treatment stage.

Before this unique discovery experience can be used to reveal how badly areas are compromised, we must first learn the range of norm for specific breeds and age groups. The lateral and DP views are the most valuable views when dealing with laminitis. The 65º, DP reveals another perspective when looking at the circumflex vessel and fimbriae, but this view is not vital for assessing the damage caused by displacement.

Lateral View Points of Interest

The normal foot will have a dense, uniform contrast pattern over the extensor process. I refer to this as the “waterfall.” These vessels continue down the face of PIII in a relatively parallel plane to the bone. Approximately 8-10mm proximal to the apex of PIII, these vessels meet and join the branches of the circumflex network. This network supplies blood to the palmar surface and the rim of the bone. The normal, healthy foot has 10mm of vascular corium ventral to the palmar surface of PIII. The fimbriae are clearly seen penetrating the sole proper. The fimbriae are of great interest, as they are the first vessels to be compressed or crushed as PIII descends, whether it occurs from rotation or sinking.

Sport horses that become foot sore, have thin soles and poor quality horn walls. They often have no more than 6-10mm of soft-tissue space between the palmar rim and the foot side of the shoe. In this case, the fimbriae are not visible on a soft-detail venogram, and the major vessels are compressed tightly between the bone and hoof wall. This may be one explanation why short feet stop growing at a normal rate.

Therefore, I conclude that a healthy sole requires a minimum depth of 15mm; 10mm for the vascular network and a minimum of 5 mm for the non-sensitive, protective sole. This information should be of particular interest to farriers who strive to maintain a healthy, sound foot.

When a foot is trimmed short, small red dots appear along the freshly trimmed sole. These dots are the ends of the individual fimbria. A healthy sole (20mm) will have longer fimbriae than a sole that is only 15mm in depth. This may explain why a long foot will bleed much easier than a short foot that is trimmed to within 15mm of the palmar rim.

The lamellar vessels can be seen superimposed over bone as they coarse downward from the coronary band to the palmar surface.

The hard penetration radiograph clearly reveals the terminal arch as it supplies blood to the bone. If you examine the coffin bone, you will find small nutrient openings along the face of PIII. These openings allow interior vessels to emerge from the bone, linking with the lamellar network. The more upright, sturdy and apparently healthier hoof has fewer and smaller holes than that found in a low-heel, thin-sole horse.

The terminal arch appears to be a major vascular reserve for the bone and laminae, as it can be seen filling even when the dorsal vessels and circumflex network have collapsed. Once the nutrient supply to the bone is gone, the bone no longer has a chance for survival.

DP View Points of Interest

This view helps evaluate the flow pattern over the medial and lateral aspects of the coronary plexis and the circumflex vessels dorsal to the palmar rim. Often the sound, healthy foot that toes outward will have a diminished flow medially over the coronary plexis. Likewise, if the foot toes inward, there will be a diminished flow laterally. This leads me to believe that this is a load-induced deficit.

Many sinkers will list to the medial side, which compresses the coronary supply and the circumflex zone. When they recover from the episode, a very distinctive, deprived growth pattern can be seen along the medial coronary band. In addition, the palmar rim often loses considerable bone due to pressure necrosis. This zone of necrotic bone typically becomes septic and is manifested as a full-blown abscess that migrates to the coronary groove. This focal coronary band separation is often mistaken as sloughing of the hoof.

Overall Points of Interest

Placing the tourniquet over the sesamoid is more dependable than placing it mid-cannon, as it is difficult to shut down the vascular supply that is well protected between the tendons and bone. Performing digital hyperfusion with the tourniquet placed mid-cannon has questionable efficiency simply because it is susceptible to tourniquet failure. It is a misconception that mid-cannon tourniquet placement adequately and consistently prevents blood flow to the digit. Without the advantage of contrast media to reveal what actually happens, we would have no reason to question this thought process.

In my early studies, I found that 50% of my venograms failed to be diagnostic due to mid-cannon tourniquet leak. Trainers also dislike having the tourniquet placed tightly over tendons, and justifiably so. Therefore, the mid-cannon placement has been abandoned.

It is relatively easy to determine when tourniquet leak is present, as the contrast will be visible up to the tourniquet. A properly applied tourniquet will completely preclude the arteries and veins. Radiographs will reveal 2-3cm of non-filled vascular space just below the tourniquet.

Apparently the contrast compresses the blood, pushing it to the limit of the tourniquet. A healthy foot will have the arterial supply filled retrograde. The arteries will appear as a long strand of beads. The contrast apparently affects the perineum of the vessel wall, causing spasms along the entirety of the vessels.

Reasons for Technique Failure
  • Tourniquet leak
  • Perivascular injection
  • Failure to inject the contrast in a timely fashion
  • Failure to take all necessary views in 45 seconds
  • Horse steps off of the blocks
  • Forgetting to rock the leg to allow for total perfusion of the dorsal vessels
  • Removing the catheter prior to taking radiographs
  • Inadequate nerve block
Venogram Interpretation

The range of norm is quite varied, as the vascular network is influenced by load, anatomical variations and pathology. Pathology also has a broad definition as sound horses are often found to have compromised blood flow in areas where other horses have a more prominent, well-filled network. Strong, healthy feet have unique characteristic differences, but all seem to have common anatomical, vascular similarities. Being able to identify a healthy foot requires good experience and an eye for minute details.

Hoof angles are reflections of coffin bone angles, which are influenced by breed as well as congenital and acquired foot problems. Therefore, to speak of our ideal hoof angle we must consider the bone angle, as all healthy feet will have a parallel relationship between the face of the wall and the face of PIII. The efficiency of horn growth centers also influences the mass of the heel.

The digital cushion and sensitive frog rely upon the protection of the horny, heel mass. As a complex unit, all major zones are dependent on the nutrient blood flow. The rate of wear and growth influences, and often alters, the mass of horn protection thereby challenging the integrity of the vascular supply. Trimming and shoeing also greatly influences the perfusion to the digit as the mechanics of the shoes can alter mass-load distribution and nutrient supply to vital growth centers.

Whenever the nutrient supply to the solar plexus is compromised, sole growth is diminished. Once the sole becomes thin, the wall also becomes thinner and more fragile.

Venograms reveal a typical compressed circumflex zone in horses with less than 15mm of sole depth. When the fimbriae are diminished in length or no longer exist along the palmar surface. Pathology exists even though the horse continues to train in a reasonably sound fashion. This is a normal finding for many speed horses, but far from being a healthy venogram.

The scope of this paper is intended to cover the basis for interpreting venograms. A few examples of low to high-scale cases follow.

Consider a healthy, strong foot that would have these soft tissue parameters:

Left Front
  • Horn-Lamellar (H.L.) Zone 15mm/15mm
  • Sole Depth (SD) 20mm
  • Palmar Angle (PA) 5º
  • Bone Angle 50º
  • Coronary Band-Extensor Process (CE) 8mm
  • Digital Breakover (DB) 25mm

Adding the bone angle of 50º to the palmar angle of 5º means the hoof angle is 55º.

The opposite foot is slightly mismatched with the following measurements:

Right Front
  • Horn-Lamellar (HL) Zone 15mm/13mm
  • Sole Depth (SD) 20mm
  • Palmar Angle (PA) 1º
  • Bone Angle (BA) 48º
  • Coronary Band-Extensor Process (CE) 15mm
  • Digital Breakover (DB) 30mm

One would suspect the hoof angle to be 49º, but with the toe backed up hard (note the 15/13 HL measurement), it can actually measure up to 52º. Toe angles only reveal a small part of the big picture. Farriers are often asked to match toes angles on horses with discriminating palmar angles. This often leads to a series of cascading, negative results.

Taking these measurements into consideration with every lateral view on all feet will quickly build a database that helps define the range of norm, and how the foot was last trimmed.

The left foot from above will have uniform, well-defined fimbriae patterns along the palmar surface. The fimbriae will continue along the terminal laminae in the same plane as the face of the bone. When the early stages of laminitis alter PIII placement, the fimbriae will be bent forward due to the download. These early, but subtle, signs of instability can be clearly assessed from a venogram days before significant displacement of PIII can be measured. The return of the fimbriae following adequate mechanical and therapeutic treatment can also be demonstrated within days of a progressive response.

The right foot from above will have a slightly different fimbriae pattern. They will be slightly longer along the toe area and significantly diminished in length from the widest part of the foot to the heel. The growth ring pattern of the hoof wall will confirm that more toe growth has occurred than heel growth. The digital cushion will also be compressed, while the heel tubules will be folded forward with limited structural stability.

As a rule, laminitis appears to have a more detrimental effect on the steeper of the two feet, and it should be the primary concern of the vet/farrier team.

A mild onset may simply alter the direction of the fimbriae, but this is very significant. It demands immediate mechanical therapy to reverse the forces at play.

Mid-Scale Damage
The mid-scale case will have an increasing HL zone from the onset. This is your first clue that this case is going to be tough. Closely monitor the HL zone!

The circumflex vessel will be compressed tightly against the palmar surface of PIII. The first lateral film taken at onset becomes very valuable as you track the progress or deterioration of the case.

What if a speed horse that won his last race had 6mm of sole depth, a 2º to 3º PA, and a very upright pastern, then became lame? The compressed circumflex on a super thin-footed horse will appear somewhat different than a compressed circumflex vessel caused by displacement. The sole proper is much thinner and the shortest of feet will not displace the vessels proximal to the palmar rim. Performing many venograms on thin-footed horses will help you distinguish “no foot compression” from “displacement compression.”

When the vessels are acutely compressed 8-10mm, the horse is normally very lame, as the coffin bone is cutting through the sole corium. Basically, this is trapping the circumflex vessel between the wall and the palmar rim. At this stage, the vessels become dysfunctional.

There may be a slight forward projection of the circumflex, which defines the folding nature of the network as PIII pushes distally. The coronary vessels may show reduced flow over the extensor process and the medial coronary plexus may have a stark loss of contrast. The terminal arch will appear quite normal.

This degree of damage may occur within hours of the syndrome, or it may take several days of slow displacement. Either way, it should be considered an emergency and demand great respect from the vet/farrier team. The new goal is to unload the compressed zone mechanically. The sooner this is accomplished, the better chance the thin palmar rim will remain viable.

High-Scale Damage
Once the circumflex vessels are displaced several millimeters and prolapsed over the apex, very serious compromise exists. Considering most healthy feet have 20mm of sole with 10mm of vascular space beneath PIII, when the vessels are 5mm proximal of the apex, 15-20 mm of displacement has occurred. The CE will reveal an increase of 15mm, the sole depth will decrease by 15mm, and the HL zone will be increased by 10-15mm. All high-scale cases will experience a rapid increase in the HL zone. Very serious cases that swell 10-15mm within 24 hours will have stark loss of contrast down the face of PIII along the palmar surface, and significantly diminished supply in the terminal arch. The coronary plexus will be broken. The proximal coronary plexus zone will remain intact, followed by a separation over the extensor process. This zone will match the distance the CE has increased.

High-scale cases require aggressive therapy, in addition to derotation shoeing and decompression of effected areas. A DDF tenotomy is most always indicated. A partial or full wall ablation and pin cast may also be viable options.

Venograms will often reveal stark loss of contrast along the medial quarter. The circumflex vessel will be absent in this area. Occasionally, there will be a very similar picture along the dorsal vessels. When there is no contrast in specific zones, I decompress these areas by performing an aggressive wall ablation.

Often high-scale cases reveal stark loss of contrast throughout the hoof area, it appears like a tourniquet has been placed around the coronary band. There will be a small area of the heel bulb that will perfuse, even when the foot is sloughing. The terminal arch will be absent as well. Once the nutritional supply to the bone no longer exists the prognosis is very grave. Amputation of the digit is the only other option for cases that has total vascular shutdown to the soft-tissue and bone.

Using the very basic parameters to help you plan your treatment options can greatly enhance your ability to treat this disease, as well as become a valuable prognostic tool.

Successful treatment of laminitis requires:

  • Timely, accurate assessment of the damage to the digit. The history, clinical examination, radiographic parameters and venograms are vital discovery exercises.
  • Timely, effective reversal therapy. The mechanical, therapeutic and surgical protocols are based on the evidence provided by the discovery exercises. This evidence varies greatly based on the degree of damage.
  • Adequate financial commitment, which is also relative to the degree of damage.