2016 FALL: Arterial Blood Gas | Is a Partial CCL Tear Surgical? | Deciphering Bronchial Lung Patterns | Ophthalmic Emergencies | Change: Good or Bad? | Continuing Education
Arterial Blood Gas – Why don’t we do them more often?
Myth 1: It’s too hard to obtain the sample.
Arterial blood gases may seem hard to acquire but actually are no harder in medium to large dogs than sampling a vein. Because the artery has a thicker muscular wall, it is can be slightly more difficult to pierce, but by using your finger to anchor the artery, you can make it easier. The most common place to try is the dorsal pedal artery on the medial aspect of the metatarsus. Another common location is the femoral artery or the lingual artery if under anesthesia. The femoral artery must be held off manually for 5 minutes after sampling. When you have a large dog under anesthesia, use this time to practice feeling an artery and even trying to obtain a sample in more controlled circumstances.
Myth 2: It’s too hard to handle the sample.
Arterial samples are handled the same way as venous with a few exceptions. Do not agitate an arterial sample as it can falsely elevate your oxygen content. You do not need to purchase a specific arterial sampling syringe, although those are nice. Aspirate heparin into a tuberculin then evacuate it; this will nicely receive the sample and prevent clot formation. The needle can be pierced into the rubber stopper of a lab tube to prevent further oxygenation. You have about 10 minutes to analyze the sample at room temperature, but if you need longer, the sample can be on ice for 30 minutes without degradation.
Myth 3: I need a special machine to analyze it.
I-STAT cartridges and some other in-house blood analyzers are designed to analyze oxygen and carbon dioxide concentrations. Check with the manufacturer if you are not sure, but any machine that measures pH and bicarbonate is likely to be able to analyze PaO2 and PaCO2.
Why bother if I have a pulse oximeter? Pulse oximeters are wonderful machines but have limitations. Sometimes they have difficulty picking up a signal in animals with pigmented mucosa, icterus or if the patient is not perfusing well. Measuring saturation of oxygen (SaO2) with a pulse oximeter only evaluates oxygenation and not ventilation. This can lead to false assumptions that animals with normal oxygenation do not have lung disease. Many patients can hyperventilate to tolerable SaO2 values but may collapse due to exhaustion if they have to keep hyperventilating.
Myth 4: It’s too hard to interpret arterial blood gases.
With minimal practice, interpreting the basics of oxygenation and ventilation values is not difficult, i.e. determining that the patient is within normal limits or not. The two main values of importance are PaO2 (oxygenation) and PaCO2 (ventilation). The normal value for PaO2 on room air is 80-100 mmHg and for PaCO2, 35-45 mmHg. Most of us will want to perform an arterial blood gas to determine if a patient is hypoxic and needing supplemental oxygen. That would be verified by an arterial blood gas in the following two scenarios:
Scenario 1: The PaO2 is less than 80 mmHg. If you want to verify this finding with a pulse oximeter, you would see a SaO2 of less than 95%.
Scenario 2: The PaO2 is in the 80s but the PaCO2 is less than 30 mmHg. Finding this result indicates that the patient is hyperventilating significantly to normalize their oxygen level.
Both scenarios document a need for oxygen supplementation.
We would like to thank our colleague from BluePearl in Washington, Jennifer Waldrop, DVM, DACVECC, for allowing us to use this article for Companion.
BluePearl criticalists Jordan Scherk, DVM, DACVECC, and Vicki Campbell, DVM, DACVAA, DACVECC, are available 7 days a week from 8 am- 6 pm should you need more information about arterial blood gases or if you would like to consult about a difficult respiratory case.
CCL Partial Tear: Is It a Surgical Case?
Did you know that most dogs have a partially torn cranial cruciate ligament (CCL) before they present with a completely torn CCL? Often, owners will remember a time when their pet cried out or began limping on the affected limb, but the lameness resolved in 12-24 hours. Owners usually forget to include this in the dog’s history because they don’t think the previous lameness is related to the current problem. However, the lameness was probably when their dog’s CCL began to tear.
Several different factors increase the chance of a CCL tear: age, activity level, anatomy, inflammatory joint disease and trauma. It is important to educate owners of dogs in these risk categories on the signs of a CCL tear, so they can have their dog evaluated by a veterinarian before the CCL is completely torn and the pet suffers from meniscal damage.
Most dogs with a partially torn CCL are lame but functioning very well. Dogs with partially torn CCLs may have either a persistent or intermittent weight-bearing lameness or are worse when they first rise from a recumbent position. Instability between the tibia and the femur is often absent and the dog may or may not have palpable joint effusion. Because the CCL also prevents hyperextension of the stifle joint, the most common clinical sign is discomfort on extension of the stifle joint. This is a major indicator of a partially torn CCL.
If you suspect a partial tear, we recommend taking a radiograph of the affected stifle. Most of these patients have subtle joint effusion and mild osteoarthritic changes on radiographs.
Partially torn CCLs do not go on to heal with exercise restriction and time. Most of these dogs will eventually tear their CCLs completely and possibly tear their medial or lateral meniscus. Dogs that undergo tibial plateau leveling osteotomy (TPLO) surgery when they have a partially torn CCL tend to recover faster and have less osteoarthritis progression after the TPLO than those with a complete tear. There is also evidence that dogs with partially torn CCLs have a lower rate of medial meniscal tears at the time of surgery. With early surgical intervention in this disease process, our patients will have less pain and a faster recovery after their stifle surgery.
Deciphering Bronchial Patterns
Figure 1. Normal canine thorax (a) in which vessel margins and background interstitium are distinctly visible. In the close-up of the hilar region (b), note only the walls of the primary bronchi are visible (white arrows).
Whether you are relatively new to looking at digital radiographs or not, the amount of “background” pattern in the lungs can often be misleading. The interstitium is actually visible on a normal radiograph especially in the caudodorsal lung fields on the lateral projection because of the large size of the lobes and larger amount of superimposed structures. The interstitium appears as the lacy soft tissue opacity between airways and vessels and is more prominent in expiratory images. This opacity, however, should not blur margins of the vessels, and as long as the pulmonary vessels are distinctly visible, you can infer that lung parenchyma is adequately aerated and normal. On top of this background opacity, the walls of the primary bronchi should be visible in a normal patient as opaque double parallel lines leaving the trachea up to the level of the second divisions. Visible bronchial walls should stay thin, linear, and distinct without blurring opacity in the immediate peribronchial parenchyma (Figure 1).
Yes, you WILL see airway walls near the hilus of the lungs in a normal dog, but you should not be able to follow these airways out into the periphery. The hallmark of a bronchial pattern is visualizing airway walls as double parallel lines (side-view, “tram tracks”) or rings (end-on-view, “doughnuts”) in the pulmonary periphery. The best places to look in the pulmonary periphery on the lateral projection are superimposed with and just cranial to the cardiac silhouette, overlying the diaphragm, and just ventral to the vertebral bodies. On the ventrodorsal projection, look lateral to the cardiac silhouette, and overlying the diaphragm caudally. Try to avoid the central hilar portions of the lung fields as these will always look “busy.” The thickening of and excess of visible airway walls in a pathologic state causes the lung fields to overall appear linear and “streaky” (Figure 2). This is a common finding in geriatric patients due to fibrosis from aging or prior disease. Bronchial patterns are typically diffuse in distribution.
Figure 2. Lateral thoracic radiograph of a 1-year-old border collie who presented for coughing, sneezing, oculonasal discharge and fever, diagnosed with infectious tracheobronchitis. Note thickened/fuzzy and prominent airway walls in the pulmonary periphery (white arrows = “tram tracks”, white circles = “doughnuts”).
One of the reasons bronchial patterns are often difficult to distinguish is that the abnormal opacity will not be as noticeable adjacent to surrounding interstitium. However, as with many things in radiology lung patterns are not always black and white (pun intended), and mixed patterns such as bronchial and interstitial or intertial and alveolar may exist with certain disease processes. Caution must be taken to ensure an artefactual change is not to blame (i.e. underexposure or an expiratory image causing the appearance of unstructured interstitial opacity).
What does it mean?
Cellular infiltrate from primary airway disease causing wall thickening is often the cause of increased conspicuity and a bronchial pattern on radiographs, but a bronchial pattern may also result from wall mineralization, luminal exudate, thickened bronchial mucosa or peribronchial cuffing (i.e peribronchial interstitial pattern). Depending on the type and stage of the particular disease process, other pulmonary patterns may be concurrently present.
Here is a list of canine/feline differentials to consider – note some of these may be disregarded due to lack of certain endemic infectious diseases here in Utah, but travel history must be considered. Further characterization of airway disease may be obtained with airway sampling (i.e. bronchoalveolar lavage or tracheal wash) with cytology and culture, and in some cases thoracic computed tomography is helpful in better evaluating distribution and severity of disease.
Differentials for a bronchial pattern
- Allergic bronchitis – asthma
- Infectious bronchitis
- Paragonimus kellicoti (lung fluke) – dogs and cats, often with cystic lesions
- Alurostrongylus abstrusus (lungworm) – cats, often with patchy interstitial and alveolar patterns
- Heartworm – often with interstitial pattern, enlarged pulmonary arteries, and right-sided cardiomegaly
- Fungal – Histoplasmosis in cats. Other types often have pulmonary nodules and lymphadenopathy (e.g. caccidiomycosis—this occurs in neighboring states such as Arizona and California)
- Neospora caninum – dogs
- Toxoplasma gondii – cats, often with regions of patchy consolidation
- Other inflammatory bronchitis
- Toxic/inhaled irritant – i.e. smoke inhalation
- Acute lung injury/acute respiratory distress syndrome
- Cushing’s disease, hypercalcemia, hyperparathyroidism – bronchial wall mineralization mimicking a bronchial pattern
- Bronchogenic carcinoma, although often associated with mass lesions
- Pulmonary edema (an interstitial pattern that starts out as peri-bronchial with mild or early disease) – possible manifestation of cats and dogs in congestive heart failure
We would like to thank our colleague from BluePearl in Washington, Ellie Nuth, DVM, DACVR, for allowing us to use this article for Companion.
If you would like to consult with our diagnostic imaging service, our board-certified radiologist, Dainna Stelmach, DVM, DACVR, is available Monday, Wednesday and Friday.
A Sight for Sore Eyes: Ophthalmic Emergencies
Because more than three extraocular muscles are ruptured, compromising the globe arterial irrigation, this eye must be enucleated.
Proptosis, “eye out of the socket,” is the forward displacement of the globe out of the orbit with subsequent entrapment of the eyelids behind the eye. It occurs due to trauma to the head, usually a dog fight. Dogs with wide eyes and shallow orbits are at higher risk. Cats and long-nosed dogs require very severe trauma for the eye to proptose.
Factors to consider before replacing the eye into the orbit:
- Time elapsed since injury
- How many extraocular muscles are ruptured (no more than three)
- Presence of hyphema
- Whether or not the the globe is soft
If the decision is made to replace the globe in the orbit, it should be done immediately. The patient should be stable enough for a short period of general anesthesia. After the area is prepped, infiltrate the lateral canthus with local anesthesia, then perform a lateral canthotomy. This will enlarge the palpebral fissure immediately and allow grasping of the skin on the upper and lower eyelids with Allis forceps; pull gently up and over the globe. Once the eyelids are manipulated over the globe, the eye returns to the orbit. Suture the lateral canthotomy and place a temporary tarsorrhaphy to protect the globe during the first two weeks postsurgery. Topical antibiotic, oral analgesia and anti-inflammatories are in order. Postoperative deviation of the globe occurs due to rupture of extraocular muscles. Strabismus often diminishes over weeks to months.
Glaucoma, increased pressure within the eye beyond that compatible with normal ocular function, vision and comfort, is one of the leading causes of blindness in animals and people. It is caused by a disturbance in the flow of fluid within and out of the globe. Once one eye has been affected by primary glaucoma, the second eye will normally be affected within two years. Other causes of glaucoma include inflammation, trauma and intraocular tumors. Glaucoma patients often present with a painful eye and decreased vision. Other presenting complaints include injected conjunctival and episcleral vessels, gray uneven discoloration of the cornea, mid-range mydriatic pupil and elevated intraocular pressure. Glaucoma is one of the ophthalmic conditions with severe visual implications and should be referred to a veterinary ophthalmologist for further management. It is rarely cured, and many animals lose vision despite medical and surgical treatment.
An accurate diagnosis of glaucoma is based on a thorough ocular examination and measurement of the intraocular pressure (IOP) with a tonometer. Normal IOP should be lower than 20-25 mmHg. Acute glaucoma is an ophthalmic emergency and must be treated immediately! If the pressure remains elevated for a few hours, permanent vision loss occurs. The combination of the carbonic anhydraze inhibitor, dorzolamide, and a beta blocker, timolol, works very well together with the prostanoid analogue, latanaprost.
Lens luxation into the anterior chamber may be seen with elevated intraocular pressure or not. It is a true ophthalmic emergency that requires surgery. Prompt surgical removal of the luxated lens is recommended if prognosis for vision is good.
The normal lens position is behind the pupil. When luxation occurs the lens may be displaced completely in front of the pupil (anterior luxation) or behind the pupil to the back of the eye (posterior luxation). The luxation can also be partial (incomplete or subluxation). Lens luxation is observed in young adult dogs usually 4 – 5 years of age. Primary lens luxation is common in terrier breeds such as the wirehaired fox terrier, Jack Russell terrier, Sealyham terrier, Tibetan terrier and terrier crosses. The breeds predisposed to this condition are border collie, Australian blue heeler, German shepherd dog and Shar Pei. Primary lens luxation is bilateral, although the onset of luxation varies between the eyes. Secondary lens luxation and subluxation may occur after the globe has increased in size (buphthalmia) in glaucoma cases or after chronic intraocular inflammation (uveitis, cataracts).
Anterior lens luxation usually manifests with acute tearing (epiphora) and eye pain and redness. Cloudiness of the cornea is present if the intraocular pressure is elevated (glaucoma). If the cornea is clear, the luxated lens can be observed in front of the pupil. The luxated lens can migrate back and forth through the pupil.
Superficial corneal ulcer. Notice the positive fluorescein uptake on the stroma and between the stroma and the epithelium at the ulcer margin.
A deep corneal ulcer, descemetocele, progressed from a superficial ulcer.
Infected anterior stromal corneal ulcer with collagenolysis
Corneal ulcers start as simple superficial ulcers that become deeper. One should be worried if the ulcer is deep (descemetocele) and there is a risk of rupturing. Topical antibiotics and pain management, topical atropine, oral analgesics and anti-inflammatories, are recommended. Use of an E-collar is also recommended. An uncomplicated ulcer should heal within 7 to 10 days. If healing takes longer, the ulcer may be indolent and require debridement and grid keratotomy.
Corneal abscesses occur when a corneal ulcer gets infiltrated by bacteria. The corneal stroma may be greenish yellow and become malacotic or gelatinous. Bacteria such as P. aeruginosa and S. betahemolyticus are involved in progression of the ulcer. Clinical signs of a stromal abscess include increased tearing, severe ocular pain, redness and evidence of a whitish to yellow discoloration of the cornea.
A stromal abscess is an ocular emergency, although it may not require immediate intervention by an ophthalmologist. You can stabilize the eye by establishing strong, frequent (every 2 hours) topical antibiotic therapy (quinolones), anticollagenases (serum, EDTA), systemic antibiotics (Clavamoxâ or Unasynâ) and analgesia. It is often necessary to admit these patients for 24 hours. Surgical repair of the cornea (conjunctival flap) may be necessary if the ulcer progresses to deep layers, and the eye is at risk of perforation or has already perforated.
Uveitis occurs when the uveal tract, rich in vascularization, gets inflamed. Protein, red and white cells leak to the usually transparent intraaocular fluid, making it turbid. The condition may be present in one or both eyes. Bilateral involvement is seen more frequently in patients with infectious, parasitic, neoplastic or autoimmune diseases.
There are many causes of uveitis; it is frequently considered an ocular manifestation of a systemic disease. Among the causes are trauma, cataract formation, infections and tumors. Some of the infections in dogs include Rocky Mountain spotted fever, Lyme disease, ehrlichiosis, anaplasmosis, infected uterus, viral hepatitis and systemic fungal infections. In cats the causes include feline leukemia virus (FeLV), feline immune deficiency virus (FIV), feline infectious peritonitis (FIP), toxoplasmosis and bartonellosis.
Symptoms of uveitis include eye pain, squinting, redness, tearing, elevation of the third eyelid, cloudiness of the cornea and a small pupil. On occasions there is pus or blood inside the eye.
Diagnosis of uveitis requires a complete systemic workup to include blood and urine testing and thorax and abdomen imaging; however, approximately 60% of the cases are a diagnosis of exclusion. Possible sequela include attachment of the pupillary opening to the lens capsule, secondary glaucoma (high intraocular pressure), secondary cataract formation and retinal detachment. The eye may become blind and painful in which case surgical removal (enucleation) will be recommended. Emergency treatment should include topical eye medication to control intraocular inflammation, analgesia, systemic anti-inflammatories and antibiotics, and possibly medications to prevent glaucoma. If there are no corneal ulcers prednisone acetate and atropine are recommended.
We would like to thank our colleague from BluePearl in Massachusetts, Clara Williams, DVM, DACVO, for allowing us to use this article for Companion.
If you would like to consult with our ophthalmologist about a case, Deborah Rowley, DVM, MS, DACVO, is available Wednesday, Thursday and Friday.
FROM THE MEDICAL DIRECTOR
Why is change often associated with a negative connotation?
Change, along with death and taxes seem to be the only inevitable parts of life sometimes. How is it that we can embrace change with optimism rather than cynicism?
Whether experiencing changes in practice ownership, doctors, or staff, it is important to recognize some of these transitions as improvements rather than changes for the worse. It is natural to shy away from certain modifications because for many consistency equals comfort. As leaders of our field, it is valuable to embody the positive aspects of change and learn to apply them in a way that will allow everyone to promote a healthy and productive working environment.
Approach future developments with optimism and open-mindedness rather than resistance. Change is inevitable, and the right attitude can make all the difference.
Jordan Scherk, DVM, DACVECC
Diagnosis and Treatment of Respiratory Distress
1 hour of CE credit
Topic: Diagnosing and Treating Respiratory Distress in the Dog and Cat
Through various case studies in this one hour lecture, Dr. Scherk, DVM, DACVECC will speak about initial assessment, prompt stabilization, and treatment of respiratory distress in the dog and cat. In addition, Dr. Stelmach, DVM, MS, DACVR will review thoracic imaging techniques and offer suggestions for visually evaluating the functioning capability of the lungs and heart.
|Speakers:||Dr. Jordan Scherk, DVM, DACVECC
Dr. Dainna Stelmach, DVM, MS, DACVR
|Date:||Wednesday, October 26, 2016|
|Time:||6:30PM Complimentary dinner
|Venue:||BluePearl Veterinary Hospital in Midvale
308 W 7200 S
Midvale UT 84047
|RSVP:||Allie Carnett at 801.871.0600 or
|Brought to you by our Partners in Education:
Antech Diagnostics, Hill’s Pet Nutrition, Elanco, Stokes Pharmacy, Trupanion, Zoetis