2016 FALL: Deciphering Bronchial Lung Patterns | Anesthetic Management of Common Complications | Arterial Blood Gas | Hemodialysis and Hemoperfusion | Meet Dr. Elizabeth Goudie-DeAngelis, Anesthesia & Pain Management
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).
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.
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).
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.
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.
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”).
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 New York, 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
Article courtesy of our colleague from BluePearl in Washington, Ellie Nuth, DVM, DACVR.
Anesthetic Management of Commonly Encountered Complications
Elizabeth Goudie-DeAngelis, DVM, MS
The anesthetic plan was carefully formulated specifically for your patient. You took into account underlying pathologies and the procedure you are performing. The induction went well, but now that your patient is under general anesthesia you are encountering complications. Chances are your patient has hypotension, hypothermia, hypoventilation or a combination of the three. The best way to keep your procedures moving forward and your patient stable is to know how to predict, prevent and treat these three common anesthetic complications.
We do not have a way to easily, non-invasively, or accurately measure perfusion (the oxygenation of tissues at the capillary level), so in combination with hemoglobin saturation, we use blood pressure to make an approximation of tissue perfusion. Hypotension is defined as a systolic arterial blood pressure (SAP) under 90 mmHg. Ideally, we attempt to keep this number between 90 – 110 mmHg under general anesthesia because an SAP greater than 90 mmHg correlates to a mean arterial blood pressure (MAP) of 60 mmHg. The MAP is the number we are concerned with. With a MAP in the range of 60-120 mmHg the capillary beds of the kidneys and brain can autoregulate; outside of this range there is concern for inadequate perfusion to these and other important tissues. Hypotension under general anesthesia is caused by some premedications, induction agents (e.g. propofol, alfaxalone) and the inhaled anesthetics.
When faced with low blood pressure, it is easiest to go back to basic physiology to determine what to do next:
Blood pressure= cardiac output * systemic vascular resistance
Cardiac output= heart rate * stroke volume
Stroke volume is determined by preload, afterload and contractility.
If you encounter hypotension, the next step is to determine the cause. If we look at the equation above, a decrease in blood pressure is due to a decrease in output and/or vasodilation. Since inhaled anesthetics cause vasodilation, it is important to minimize their use when hypotension is encountered or expected.
- Minimizing the inhaled anesthetics can be achieved by MAC reducing drugs (e.g. opioids, ketamine, lidocaine) as CRIs or boluses. The use of nerve blocks (e.g. epidurals, dental blocks, ring blocks) can also minimize inhalant requirements.
- A crystalloid fluid bolus of 5 mL/kg for cats and 10 mL/kg for dogs can be used to combat the relative hypovolemia caused by the vasodilation. Fluids support can be administered concurrently with inhalant reduction especially if the patient has indications of hypovolemia (e.g. hemoconcentration).
The heart rate should also be evaluated. While a heart rate of 70 bpm for a dog under general anesthesia is not abnormal, it is always important to also consider what the patient’s resting heart rate was, especially when a low blood pressure is observed. If the heart rate is relatively low for your patient, an anticholinergic can be administered:
- Atropine 0.02-0.04 mg/kg IV
- Glycopyrrolate 0.005 mg/kg -0.015 mg/kg IV
Finally, if minimizing inhalants, addition of fluids, and normalization of the heart rate has not successfully treated the hypotension, the addition of a vasopressor agent can be considered:
- Dopamine: alpha1, beta1, dopaminergic receptors. Increases heart rate and causes vasoconstriction. 5-10 ug/kg/min
- Dobutamine: beta1, beta2 receptors. Increases heart rate and contractility. Causes mild vasodilation. 3-5 ug/kg/min
- Norepinephrine: alpha1, alpha2. Potent vasoconstrictor 0.01 ug/kg/min-0.03 ug/kg/min
- Ephedrine: effects at all adrenergic receptors, possibly greater effects at alpha1. Tachyphylaxis with repeated dosing. 0.01-0.05 mg/kg IV
Hypothermia can cause a number of negative sequelae, especially in the surgical patient. It can occur during general anesthesia because of vasodilation, open abdominal or thoracic cavities, resetting of the thermoregulatory center by general anesthesia, and contact with a cool surface and room. Hypothermia is defined by a rectal temperature less than 99°F in dogs and cats.
Perioperative side effects of hypothermia include coagulopathies, prolonged anesthetic recovery, increased metabolic oxygen demand, reduced wound healing, increased rate of infection, alterations of protein/enzymatic function, and changes to the metabolism and pharmacokinetics of a variety of drugs. Intraoperatively, patients require less inhaled anesthetics due to changes in solubility of the inhalants. Hypothermia causes profound bradycardia that is often nonresponsive to anticholinergic agents as well as decreased response to alpha1 receptor agonists. Ventilation is impaired by a number of mechanisms, and there is an increased risk of acute lung injury, pneumonia and pulmonary edema.
There are three phases to heat loss due to general anesthesia: 1) An initial and marked drop in core temperature is noted during the first 30 minutes to hour of general anesthesia. 2) The second phase occurs over the next 2-3 hours at a more gradual, linear manner. 3) There is a plateau phase in which there is minimal temperature change. Prevention and early intervention are key to maintaining normothermia throughout an anesthetic episode. Mechanisms to counteract heat loss include warm water blankets on the induction table and surgical table, forced air blankets intraoperatively, and the use of towels and blankets between the patient and metal tables. For patients undergoing celiotomies the use of warmed abdominal lavage can increase the core temperature significantly when the flush is allowed to have contact with the abdomen for 2-6 minutes.
Warming of patients should continue post-operatively, and regular assessment of post-anesthetic patients’ rectal temperatures should be performed particularly if the patient is still sedate, inactive and/or suffered from hypothermia during the anesthetic episode.
Hypoventilation is defined as a partial pressure of carbon dioxide in the arterial system greater than 45 mmHg or an end-tidal carbon dioxide greater than 45 mmHg. Hypoventilation under general anesthesia occurs because of a decrease in tidal volume caused by positioning of patients in dorsal recumbency (particularly over-conditioned patients) and resetting of the medullary respiratory center chemoreceptors by anesthetic drugs. Carbon dioxide levels can be used to evaluate tissue perfusion, gas exchange and cardiac output.
Why are we concerned about hypercapnea under general anesthesia? Aside from the necessity of normal ventilation to ensure appropriate gas exchange including the inhaled anesthetics being used to maintain the patient asleep, we also worry about various pathophysiologic changes. Ventilation gives an indication of tissue perfusion, efficiency of gas exchange and cardiac output. Changes that occur with an increased arterial carbon dioxide level include respiratory acidosis, vasodilation, elevated heart rate and hypnosis with levels greater than 90 mmHg.
Carbon dioxide can be measured using a capnometer or by drawing blood gas samples. A capnometer allows for minute-to-minute measurement of end-tidal carbon dioxide and can be used to easily and rapidly to monitor ventilation. If assisted ventilation via manual IPPV or a mechanical ventilator is being used, evaluation of carbon dioxide levels is paramount to ensure neither hyper or hypoventilation is occurring.
Regardless of the method of ventilation (manual or mechanical) airway pressure should not exceed 20 cmH2O to prevent barotrauma or volutrauma to the patient.
Dr. Goudie-DeAngelis always welcomes anesthesia related questions and would be happy to discuss any of the complications described here. In addition she is available for consults relating to pain management and for anesthesia case management.
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. We at BluePearl 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.
We would like to thank our colleague from BluePearl in Washington, Jennifer Waldrop, DVM, DACVECC, for allowing us to use this article in Companion.
Hemodialysis and Hemoperfusion: Beyond Treatment of Traditional AKI
Christine Iacovetta, BVetMed, DACVECC
Hemodialysis is an extracorporeal therapy used primarily to treat patients with acute renal injury and a select few patients with chronic renal disease. In the face of severe renal dysfunction hemodialysis can be lifesaving; however, there are other indications for hemodialysis that can be equally as lifesaving.
Annie was a 1.5-year-old pit bull mix that thought it would be fun to eat a renal toxic amount of Deramaxx® (33mg/kg) along with some ibuprofen (22 mg/kg). The family presented Annie to her primary vet within 3 hours of ingestion, and she was appropriately decontaminated by induction of emesis and administration of activated charcoal. Intravenous fluid therapy was begun and baseline bloodwork performed. Despite this treatment, over the next 2 days Annie’s creatinine increased from 1.7 mg/dl to 3.5 mg/dl. Using the IRIS Acute Kidney Injury (AKI) grading system, Annie was classified as having Grade III, or moderate to severe injury. At this point Annie was presented to BluePearl in Forest Hills for potential dialysis. Based on her young age, lack of chronic renal disease and known toxin ingestion, Annie was deemed a good candidate for dialysis.
Extracorporeal therapy would benefit Annie in two ways. First hemodialysis would reduce the level of creatinine and urea in her bloodstream along with other metabolites that build up when renal function is declined. Although her renal values were not as high as is typical when hemodialysis is instituted they had continued to increase, and early therapy can improve outcome. Second, and more importantly hemoperfusion was recommended with the goal to remove any circulating toxin that was still present in Annie’s bloodstream. Hemoperfusion is a blood purification method that includes a charcoal filter. Large, protein-bound molecules like nonsteroidal anti-inflammatory drugs (NSAID) are not easily removed during standard hemodialysis. The addition of a charcoal filter allows binding and removal of these molecules from the bloodstream while the blood is returned to the patient.
Hemoperfusion can be lifesaving when used to remove toxic substances from the circulation. Beyond NSAIDs, other toxins such as barbiturates, amanita ingestion, and vincristine can be treated with hemoperfusion. Smaller molecules like ethylene glycol, other chemotherapeutics, aminoglycosides and certain cardiac drugs can be removed with traditional hemodialysis.
Annie was treated with one session of hemodialysis with hemoperfusion. Although hemoperfusion is normally only performed once, it was unknown if Annie’s renal values would continue to increase which could require further hemodialysis sessions. Luckily Annie’s renal values were maintained, and she continued to feel well. She did not require further extracorporeal therapy and could be managed with intravenous fluids until she was transitioned home. Annie is currently doing well at home with normal renal values.
FROM THE MEDICAL DIRECTORS
We hope you had a relaxing summer and are ready for the change in seasons.
We are anticipating some exciting changes around here that will allow us to better serve you, your clients and patients. Renovations to our downtown hospital will begin soon as well as the build-out of our new Brooklyn hospital. Several new clinicians have joined our team, along with a new anesthesiology service. Learn more about anesthesiology in this edition of Companion.
We would also like to take this time to let you know about, and welcome, our most recent BluePearl hospital, located in Paramus! We wish our New Jersey colleagues all the best and look forward to working together to serve the primary care veterinary community.
As always, thank you for your support and we hope to see you soon.
Marc Greenberg, DVM, MS, DACVS-SA
Timothy Rocha, DVM, DACVIM-Oncology
Meet Elizabeth Goudie-DeAngelis, DVM, MS
Anesthesiology and Pain Management
Elizabeth Goudie-DeAngelis, DVM, MS
Dr. Elizabeth Goudie-DeAngelis attended Ross University and completed her clinical year at the University of Missouri. She worked in emergency medicine briefly before starting an internship at BluePearl Veterinary Partners in New York. Dr. Goudie is thrilled to be able to return to BluePearl after completing her 3-year comparative anesthesia residency and master’s degree at the University of Minnesota. “My interest in pharmacology and physiology as well as deep concern for pain management in our veterinary patients made anesthesia a perfect fit. I am passionate about my specialty and love to share my anesthesia knowledge with colleagues and technicians alike.”
What keeps you interested in cases day-after-day?
Anesthesia is like flying; the more prepared you are for take-off and landing, the smoother the flight in between. There is such a variety in patients’ underlying pathologies and co-morbidities that it’s hard to get bored. It is like a puzzle to keep the patient as close to normal homeostasis as possible during the anesthetic episode. By using a multimodal approach to analgesia and anesthesia as well as advanced monitoring modalities, we always aim to have the patients in a more stable place postop than when they came to us.
How do you go about helping ease the concerns of a client?
Owner communication is not something most people associate with anesthesiologists. That being said, I really enjoy speaking with owners prior to an anesthetic episode especially when the owner has serious concerns for the welfare of their pet. Often, these owners avoid a procedure because of concerns about anesthesia; they may have had a previous pet that was lost during an anesthetic episode, or they themselves may have had a complicated anesthesia. I find that most of these owners just want a knowledgeable source to listen to their concerns and give them a calm and confident description of the anesthetic plan. That is the role I hope to fill for these owners.
How do you like to work with the primary care veterinarian?
I am here to offer support. I hope to form a strong relationship with the primary care community offering lectures, round-table discussions of case management, and anesthetic setup guidance. Without the primary care community we would not be able to keep so many patients healthy day to day or see the cases that do need more advanced care. I am here for complicated cases that require more advanced anesthetic care, for owners that want specialty anesthetic management or may need more support during an anesthetic episode, and even to discuss anesthetic management of a future anesthetic case.