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The Tipping Point: How Venograms Make the Difference Between Success and Failure When Treating Laminitis

R.F. (Ric) Redden, DVM. Venogram technique, indication and interpretation, in Proceedings.
Bain Fallon Memorial Conference October 2006; 28-35.

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


Since 1992 venograms have been used at the International Equine Podiatry Clinic to evaluate horses with lameness problems localized to the foot. This retrograde contrast study can demonstrate structural alterations of the venous as well as arterial supply within the soft tissue and bone early in the course of the disease before the effects of vascular compromise are detected radiographically.1

Venograms have proven to be a valuable tool for making specific diagnosis in horses with foot disease, injuries and diminished horn production. They have been particularly advantageous for treating laminitis as they allow us to identify structural alterations of the solar papillae, lamellar vessels, coronary plexus and terminal arch that can not be seen with other imaging techniques. This has allowed us to follow progressive deterioration of the disease in cases that otherwise might have been considered clinically stable.

Before venogram imaging, radiographs were the only images used routinely to evaluate laminitis and other foot disease syndromes. As a result, veterinarians have been limited to evaluating the significance and severity of the disease during the acute phase, meaning the greatest window of response cannot be effectively utilized. A large majority of cases with significant insult deteriorate, ultimately leaving the horse crippled or resulting in euthanasia. Venograms have added to our knowledge of laminitis and other common foot problems, in large part because for the first time we can see the structural components of the vascular supply to the horse's foot. This procedure is relatively easy, uses basic radiographic equipment and can be performed on the standing horse.

Equipment and Technique

The equipment used at IEPC is a 100/30 MinXray portable unit, asymmetric 6/12 screens, ultra detail film and a 6:1, 106 line/in grid. Several contrast mediums have been used in the past, however we have found that higher concentration produces slightly more information. Reno-60® has been the contrast of choice for the past several years. A variety of catheters have been used. The 21-gauge butterfly is easy to use, easily procured and provides a consistent means of delivering contrast.

Sedation of the horse, local analgesia of the foot and a tourniquet placed over the fetlock is required. The original venogram technique developed at IEPC was a collaboration with Dr. Chris Pollitt using his previous in vitro study model and has since been published with minor modifications.2 The imaging sequence that has been routinely used is soft tissue lateral, lateral with grid, DP with grid, DP with soft tissue detail, followed by a soft tissue lateral. The procedure is technique sensitive in large part because the sequence of film must be taken within a time frame of 45 seconds following contrast injection. Tissue contrast injected retrograde into the palmar vein is quickly absorbed into the interstitial space, significantly reducing the value of the information obtained.

The soft tissue lateral images have proven to be especially valuable because they allow us to see coronary papillae, circumflex vessels, solar papillae and acute and chronic lamellar leakage. The grid used with the higher MAS has proven to be a reliable means of imaging the terminal arch and its tributaries. The soft tissue and hard penetration grid views were implemented to allow us to evaluate normal vascular anatomy and structural alterations within the soft tissues and bone. The soft DP view allows us to evaluate the medial and lateral coronary supply and the medial and lateral circumflex network. The grid view offers further information concerning the terminal arch and tributaries. The soft tissue lateral view taken at the end of the sequence was implemented to allow for adequate filling time required to consistently image lamellar leakage, decreasing the possibility of missing significant structural alterations. More specific beam selection is required to image vascular lesions associated with White Line Disease and Keratomas. Techniques for imaging the equine foot will continue to evolve with increasing experience performing venograms.

Tourniquet failure and perivascular injections are frequent complications encountered in the infancy of procedural skill development. Both complications result in underperfusion and can lead to grossly inaccurate interpretation and misuse of the information. Technique underperfusion should not be confused with stark loss of contrast caused by pathological vascular compromise. The distinction should be well understood before deciding the fate of a laminitic horse based on the information gathered from this valuable tool.


1) Sedate the horse.
2) Block the feet just above the fetlock. Use only 4-6cc of blocking agent to prevent transient edema.
3) Place the horse's feet on proper positioning blocks. This will insure a pure lateral projection.
4) Set the x-ray machine in place, and have all the necessary cassettes and grids within arm's reach.
5) Take a scout film with soft-tissue detail, using a barium paste marker on the face of the hoof wall.
6) Wrap 4 inch Elastikon around the fetlock. This will provide an anchor point for the tourniquet and prevent twisting of the skin while applying the tourniquet.
7) Place a tourniquet over the fetlock. Avoid a mid-cannon tourniquet.
8) Catheterize the palmar vein using a 5/8 inch, 21-gauge butterfly catheter. Be careful not to thread the needle to far in to the vein. You risk making a second hole in the vein.
9) 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.
10) Pull the knee forward slightly while injecting the second syringe. The heel should remain flat on the block. This rocking assures lamellar perfusion by unloading the deep digital flexor tendon (DDF)
11) Clamp a hemostat on the catheter. Quickly tape the hemostat to the leg using the loose end of the tape that secures the tourniquet.
12) Take your series of film. All exposures should be taken within 45 seconds. Move quickly.
Radiographic Views
i) Lateral, soft exposure
ii) Lateral, hard exposure with grid
iii) DP, hard exposure with grid
iv) DP, soft exposure
v) 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 films. Acute and chronic cases will exhibit similar patterns, yet there are distinct differences between the two. 13) Remove the tourniquet and place cotton or gauze over the medial and lateral vessels. Tape in place for 5-10 minutes.

A venogram is a discovery experience, offering 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
  • Sore feet with thin soles and poor quality walls

Having performed hundreds of venograms, I have discovered a pattern of a sequence of events that appears to be repeatable in most pathological conditions. Laminitis can progress from mild onset to high-scale case within hours to weeks. Venograms can provide consistent evidence of each stage of the syndrome.

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 65 degree, DP reveals another perspective when looking at the circumflex vessel and papillae, but this view is not vital for assessing the damage caused by displacement.

Interpretation of the Normal Foot

Lateral View
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 papillae are clearly seen penetrating the sole proper. The papillae 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. Conversely, the thin soled horse has a compressed palmar vascular supply, though it appears quite different from compression caused by medial displacement.

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 papillae may not be visible or they are very short relative to their normal length. The major vessels are compressed tightly between the bone and hoof wall. When the papillae are demonstrable they have their normal linear relationship with the solar corium????. This may be one explanation for 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 5mm 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 papillae. A healthy sole (20mm) will have longer papillae than a sole that is only 15mm in depth. This may explain why a long foot will bleed much easier. When trimmed short there is a very thin foot that has half the sole depth it needs.

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 nutrient foramen than that found in a low-heeled, thin-soled 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. The bone no longer has a chance for survival when the terminal arch loses its function.

DP View
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.

Some normal horses have medial listing that apparently compromises the growth centers of the medial horn wall and medial sole, as most will have minimal horn growth in this area. Most sinkers will list to the medial side, which compresses the coronary supply and the circumflex zone. As 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 fetlock 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.

Early studies 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 vascular space void of contrast 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 muscular 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, pulling the catheter
  • Forgetting to rock the leg to allow for total perfusion of the dorsal vessels
  • Removing the catheter prior to taking radiographs
  • Inadequate nerve block

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 papillae 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) = 5 degrees
  • Bone Angle = 50 degrees
  • Coronary Band-Extensor Process (CE) = 8mm
  • Digital Breakover (DB) = 25mm
Adding the bone angle of 50 degrees to the palmar angle of 5 degrees means the hoof angle is 55 degrees.

The opposite foot is slightly mismatched with the following measurements:

Right Front
  • Horn-Lamellar (HL) Zone = 15mm/13mm
  • Sole Depth (SD) = 16mm
  • Palmar Angle (PA) = 1 degree
  • Bone Angle (BA) = 48 degrees
  • Coronary Band-Extensor Process (CE) = 15mm
  • Digital Breakover (DB) = 30mm

One would suspect the hoof angle to be 49 degrees, but with the toe backed up hard (note the 15/13 HL measurement), it can actually measure up to 52 degrees. 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 papillae patterns along the palmar surface. The papillae 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 papillae will be bent forward due to the download and caudal displacement. 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 papillae 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 papillae 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 due to excessive internal heel loading. 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 should be the primary concern of the vet/farrier team.

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

Interpreting Mid-Scale Damage
The mid-scale case will have an increasing HL zone from the onset. This zone will increase several millimeters before displacement occurs. Closely monitor the HL zone!

The circumflex vessel appears compressed tightly against the palmar surface of PIII. The venograms taken at onset become very valuable as you track the progress or deterioration of the case. They also allow you to evaluate the efficiency of the selected treatment protocol.

Let's look at the racehorse as an example. Many times these athletes have only 6mm of sole depth, a -2 degrees to -3 degrees PA, and very upright pasterns. 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 due to displacement, the horse is normally very lame, as the coffin bone is cutting through the sole corium. The result leaves the circumflex vessel between the wall and the palmar rim. At this stage, the vessels become dysfunctional, and the palmar rim of PIII begins to break down as a result of inadequate nutrient supply.

Some acute cases will have 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 on mid-scale cases.

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. All efforts should be made to mechanically unload the compromised zone. The sooner this is accomplished, the better chance the thin palmar rim will remain viable. A favorable response will have an improved vascular pattern within a few days. If the horse appears clinically stable but the vascular pattern continues to deteriorate, derotation shoeing followed by a DDF tenotomy is a preferred treatment.

Interpreting 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 approximate the distance the CE has increased.

High-scale cases require aggressive therapy, in addition to derotation shoeing and decompression of affected areas. A DDF tenotomy is almost 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 also be absent in this area. Occasionally, there will be a very similar picture along the dorsal vessels. When there is no contrast in these specific zones, I decompress these areas by performing an aggressive wall ablation, pin cast for support and a treatment protocol compatible with new hoof replacement.

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 can 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 have 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 and use the venogram as a valuable prognostic tool.

Successful treatment of laminitis requires following:

    1. Timely, accurate assessment of the damage to the digit. The history, clinical examination, radiographic parameters and venograms are vital discovery exercises.
    2. 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.
    3. Adequate financial commitment, which is also relative to the degree of damage.


    Venograms are a valuable imaging modality for horses with clinical signs of laminitis and other problems localized to the foot. They have allowed us to differentiate pathological vascular lesions from the normal vascular tree and visualize vascular compromise before significant digital displacement can be detected radiographically. When used as a damage indicator, venograms allow us to make more timely decisions concerning treatment. During treatment, venogram imaging can be used to evaluate the correlation between various mechanical treatment protocol concepts and the vascular supply to the vital anatomical areas. They are a valuable prognostic tool that can enhance timely treatment decisions, allude to the duration of long term recovery, and confirm irreversible vascular collapse of the digit.

    Forces that create tensile and sheer strain on the laminae and compressive forces on the sole corium and palmar rim of the coffin bone most probably contribute to the mechanical phase of laminitis that causes a vicious cycle compartmental syndrome. Venogram evidence supports both the concept that DDF forces on the laminae, sole corium and palmar rim contribute to development of the secondary compartmental syndrome and the treatment concept that significantly reducing the tension on the DDF relative to the PA, degree and location of vascular compromise and degree of capsular displacement is an effective treatment in most horses with laminitis. Venograms may confirm cases in the predramal stage of laminitis and distinguish them from cases with similar clinical signs. In the future, accurate assessment of the effects of laminitis, especially in acute cases, before radiographic displacement develops may require venogram imaging.


    1. Redden RF. The use of venograms as a diagnostic tool, in Proceedings. 7th Bluegrass Laminitis Symposium, 1993; 1-6.
    2. Redden RF. A technique for performing digital venography in the standing horse. Equine Vet Educ 2001; 172-178.