2016 FALL: Arterial Blood Gas | Deciphering Bronchial Lung Patterns | Ophthalmic Emergencies | Meet Internist Jim Whitehead | 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.
|PaO2 mm Hg||SaO2%|
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.
More information about arterial blood gas interpretation can be found in many books and on VIN. You can also take labs locally and at national conferences to practice sampling and interpretation Any one of our three critical care specialists at BluePearl in Georgia are also available to help in any way. Please let us know if you would like more information or if we can help if you have a difficult respiratory case.
Deciphering Bronchial Patterns
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).
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).
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.
Urgent Care of Ophthalmic Emergencies
Stacy Andrew, DVM, DACVO
Ocular emergencies encompass conditions from fairly benign to vision threatening. To an upset owner, anything can be considered an ocular emergency. We will discuss the most commonly seen emergencies and suggestions on how to handle them.
Corneal wounds are some of the most common emergency presentations regarding the eye. They cause discomfort and can result in blindness if not addressed in a timely fashion. Causes include trauma, dry eye/keratoconjunctivitis sicca (KCS), misplaced eyelashes, chemical exposure and foreign bodies. It is important to perform and/or evaluate the following on ulcer patients:
- Schirmer tear test (to rule out KCS) – before too much manipulation or other testing
- Fluorescein stain – to help determine size and approximate depth (superficial vs. stromal vs. descemetocele)
- Evidence of blood vessel ingrowth
- Evidence of melting or necrosis/liquefaction of the stroma
- Concurrent intraocular changes such as hypopyon, hyphema, flare, miosis
- Sometimes corneal cytology and/or culture and sensitivity
Treatment of the underlying cause is important, especially with KCS, foreign bodies and cilia. Most corneal wounds will heal with medical management including topical antibiotics (for all), serum or other anti-collagenases (if melting), and systemic pain/anti-inflammatory therapy. Atropine is rarely needed and often causes pupil dilation that extends past wound healing – which keeps the pet squinting and the owners calling you! Placement of an Elizabethan collar is usually recommended as well. Non-infected “simple” ulcers should heal in 3-5 days. Superficial chronic corneal epithelial defects (SCCEDs) are unique and usually require debridement and grid keratotomy to heal. Deep stromal ulcers, descemetoceles and lacerations often require surgical therapy or at least intensive medical therapy.
Glaucoma is an increased ocular pressure (IOP) that is incompatible with intraocular health. You cannot diagnose glaucoma without tonometry, but you can have a strong clinical suspicion (based on breed, pupil size), and it’s better to start medications than to withhold them. Dog breeds most often affected with primary or inherited glaucoma include American cocker spaniel, basset hound, Chinese Shar Pei, chow, Norwegian elkhound, and samoyed. Secondary glaucoma can occur with inflammation, lens luxation, neoplasia and trauma. Clinical signs with acute glaucoma are a combination of injected or red eye, dilated pupil, pain and corneal edema.
An accurate diagnosis of glaucoma requires IOP measurement, which can be performed with one of many types of tonometers available. The therapeutic goals are to lower the IOP rapidly in an effort to preserve vision. Medical therapy is often tried first, using medications such as dorzolamide, timolol and possibly latanoprost (not usually used for secondary glaucomas). If the IOP does not improve, surgery may be indicated. Tonometry is also the best way to determine if therapy is working. Unfortunately, glaucoma is rarely cured and many animals lose vision in spite of appropriate therapy. It is important to consider the unaffected eye with primary cases since the second eye often develops glaucoma within 6-24 months after the first eye is diagnosed.
Traumatic proptosis OD in a miniature Australian shepherd. Note the eye is being kept lubricated while awaiting surgery.
Proptosis refers to forward protrusion of the eye in front of or beyond eyelid margins. It usually occurs following trauma such as being hit by a car, bite wounds or overzealous restraint. Proptosis is seen in dogs, cats and horses. Clinical signs include globe protrusion, inability to visualize lid edges, subconjunctival hemorrhage, torn extraocular muscles causing globe deviation, and exposure keratitis/corneal ulceration. Keeping the cornea lubricated until globe replacement can be performed is extremely helpful.
Positive prognostic indicators for vision and/or recommended replacement:
- < 3 hours since occurrence
- Presence of direct PLR
- Fewer than three extraocular muscles torn (medial rectus most common)
- Absence of hyphema and/or corneal ulceration
- Miotic pupil better than mydriatic pupil
If the pet is stable enough for general anesthesia, the globe should be replaced as soon as possible. Following surgical prep, a lateral canthotomy is performed to allow movement of the upper and lower lids from behind the globe. A temporary tarsorrhaphy is placed, using horizontal mattress sutures and stents, to cover the globe. Remember that the eye may not be completely back in the socket at this time, especially in dogs with very shallow orbits. The goal is to cover the globe and not to force back into normal location. The canthotomy is then closed. Topical antibiotic ointment and systemic anti-inflammatory as well as analgesics are indicated. Sutures are usually left in place for 7-10 days. Following removal of the tarsorrhaphy, lateral deviation of the globe is the most common sequelae.
Anterior Lens Luxation
Anterior lens luxation in a terrier mix dog. Central corneal edema, related to endothelial touch by the lens, is a hallmark of anterior luxation.
Forward movement of the lens into the anterior chamber is an emergency that often requires surgical intervention. Lens luxation is most commonly seen in middle-aged dogs of the terrier breeds including fox terriers, Jack Russell terriers, miniature bull terriers, Sealyham terriers, as well as terrier mixes. It can also be as a primary condition in Australian cattle dogs, border collies, Brittany spaniels, Chinese cresteds, and Shar Peis. In cats, lens luxation is usually secondary to chronic inflammation. Clinical signs with an anterior lens luxation include clouding of the cornea (especially centrally where it touches the endothelium), variable pain, redness and visualization of the lens being out of position. Treatment consists of lowering the pressure within the eye which usually includes surgical removal of the lens via intracapsular lens extraction, and sometimes a sutured-in or sulcus fixation intraocular lens, if there is a reasonable prognosis of vision.
Sudden Vision Loss
Acute blindness due to complete retinal detachment. (Photo courtesy of Dr. Ellen Belknap)
Acute loss of vision can occur with disorders of the eye, brain/nerves or systemic causes and may be sudden or gradual. Vision is usually lost in both eyes concurrently but may be lost in one eye prior to the other. Animals with sudden vision blindness show disorientation, anxiety, behavioral changes, and bump into things in familiar environments. Often (but not always) pupils are dilated. Potential causes include sudden acquired retinal degeneration syndrome (SARDS), immune-mediated retinitis (IMR), retinal detachment, optic neuritis, cortical blindness, toxin ingestion, glaucoma, and metabolic causes (i.e. hypoglycemia, hypoxia, and diabetic cataracts). Diagnostic testing usually includes assessment of menace response and pupillary light responses, maze testing, IOP measurement, systolic blood pressure measurement, CBC/chemisty/UA, and electroretinogram (ERG). Prognosis for return of vision depends on the cause, duration and response to treatment.
FROM THE MEDICAL DIRECTOR
Meet our specialist…
Dr. Jim Whitehead
Dr. Jim Whitehead, Internal Medicine
Jim Whitehead, DVM, DACVIM, joined BluePearl in Gwinnett this past spring from BluePearl in Michigan, where his colleagues and referring veterinarians described him as a “committed, helpful teammate.” Dr. Whitehead received both his undergraduate and veterinary medicine degree from Mississippi State University. He’s excited to be back in the south, close to family and SEC football. Within his field of internal medicine, Dr. Whitehead has special interests in immune-mediated diseases, endocrine diseases and gastrointestinal diseases. In his off time he enjoys golfing and spending time with his family and his rescued pets. He’s also a bit of a foodie who enjoys both cooking and trying out new foods. Get to know Dr. Whitehead…
What’s cutting edge in your specialty that you can offer?
I am very comfortable and experienced with advanced diagnostics including ultrasound and endoscopic procedures. Endoscopy in particular is my favorite procedure to perform, and I have a lot of experience with foreign body retrieval which I find especially rewarding.
How do you like to work with the primary care veterinarian?
I see myself as a partner in the care of patients and clients, helping primary care veterinarians with challenging cases that need more advanced work-up or treatment. Upon graduating from vet school, I worked in general practice. As a result, I appreciate the experience as well as the challenges I had when referring clients to specialists (including sometimes being nervous talking to a specialist or worrying that I might be wasting their time by referring a patient to them). I can assure you, there is never a case or question that is not important, and I am happy to help out in any way I can.
What was your first job? What did you learn from that job?
As a camp counselor in high school I learned that it really takes a team effort to accomplish great things – whether it’s keeping 100 kids a week entertained and safe, or taking care of the patients in our hospitals.
Was there a teacher or professor that changed your life?
While it was my high school freshman biology teacher, Mrs. Catanzaro, who probably started me down the path to veterinary medicine, I have always tried to embrace the positive attributes of my mentors and colleagues as I have progressed through the years. Specifically, I believe it’s important to never stop learning and never stop trying to get better at what you do. Medicine is a never-ending pursuit of perfection, and it is our responsibility as practitioners to provide the highest level of care to our patients using the best available methods and information we have.
Outside of veterinary medicine, what do you consider yourself to be an expert at?
I hardly consider myself an expert, but I enjoy staying involved with my two boys (7 and 4) and their various activities. I also enjoy working on my old Jeep – sometimes with my boys – and yes, sometimes I get in way over my head, but it’s fun and I enjoy learning as I go with that activity or anything else we are interested in.
What’s the best piece of advice you were ever given, and who gave it to you?
I believe James Herriot said it best when referring to being a veterinarian: “You must attend.” We have a responsibility to our patients to always try our best. Even in the face of overwhelming odds or a poor prognosis, we must still try. We embrace our successes, we mourn our losses, but, no matter what happens at the end of one case, we must be ready for the next one that walks in the door.
What is your favorite part of a typical day?
First thing in the morning – this is the time of day with the greatest potential because we have the whole day in front of us.
Tell us about a case that touched your heart.
Charlie was a 125 lb. bloodhound mix with kidney disease and protein-losing nephropathy. He was the biggest lab (lap?) dog I’ve ever seen, and he was one of the nicest dogs I’ve ever met. Charlie, his owners and I fought his kidney disease for well over a year. To the very end, Charlie was patient, gentle, and kind with us, and I’ll never forget the trust he and his owners had in us.
If you didn’t choose veterinary medicine, what do you think you’d be doing today?
Teaching science somewhere I’m sure. My brother is a teacher; my father is a retired teacher; and my mother is a retired principal and former teacher.
CE Calendar of Events
BluePearl is strongly committed to the veterinary community. One of the ways we demonstrate this commitment is through our continuing education program, which is subsidized in part by our Partners in Education.
All BluePearl CE lectures are free and open to all area veterinary professionals. Registration is required, please. Unless otherwise indicated, programs begin with a light dinner prior to the presentation, which starts at 7:30 pm. To RSVP, please email firstname.lastname@example.org.
For the most current information about BluePearl CE, please check our online events page regularly.
|DATE||TIME||TOPIC & PRESENTER||LOCATION||CE HRS|
|Sept 25||7:15 AM||Best PractiCEs 2016|
Registration closes September 16
To register: http://tinyurl.com/bestpractices2016
|Georgia Tech Global Learning Center||6 hr|
|Oct 18||7:30 PM||DVM CE: Pulmonary Pharmacology|
Tom Walker, DVM, DACVECC
|Sandy Springs||2 hr|
|Nov 15||7:30 PM|
DVM CE: GI Surgeries- common procedures and tips to avoid complications
Cassandra Ruthrauff, DVM, DACVS
|Ippolito’s Suwanee Town Center||2 hr|