2016 SPRING: Twinspired 2016 | Local Analgesia | Physical Assessment | Tracheal Collapse | Hyperthyroidism and Kidney Failure | Sudden Paralysis: What a Technician Needs to Know | Pearls from ACVIM Forum 2015 | Feline Anemia Trial
Twinspired 2016 Is Almost Here!
8:00am-12:30pm followed by lunch and live racing
Please save this date and plan on joining us once again for our annual fun-filled daylong CE event at beautiful Churchill Downs!
Enjoy a morning of veterinary CE topics and lectures presented by area specialists from BluePearl Veterinary Partners, Animal Dermatology Clinic, Bluegrass Veterinary Specialists and Metropolitan Veterinary Specialists followed by a fabulous luncheon and live racing in the newly renovated Stakes Room!
Click here to register.
Indications for Local Analgesia
Local analgesia is an underused technique that can greatly enhance the overall analgesia in a patient; lead to use of less systemic drugs; and may be used in situations in which sedation, heavy systemic analgesia or anesthesia is contraindicated. Many animals that present to emergency are in shock, and those that are not in decompensated shock may be in compensated shock. Those in compensated shock are able to compensate because their sympathetic nervous system is maintaining their blood pressure and helping to maintain their oxygen delivery. In the intensive care unit, critically ill animals are dynamic with potentially minute-to-minute changes in cardiac output, blood pressure and oxygen delivery.
Almost all sedatives, analgesics and anesthetics blunt the sympathetic nervous system to some extent. This effect puts animals in the emergency department and critical care unit at risk for decompensation when receiving systemic drugs for analgesia, sedation or anesthesia. Local analgesic techniques may aid in decreasing systemic drug requirements in these patients.
Although shock patients in general are at risk for systemic decompensation with systemic sedatives and anesthetics, there are specific conditions in which these drugs should be particularly avoided or delayed if at all possible. Specific examples include head trauma, pulmonary contusions, pneumothorax, myocardial contusions (and subsequent arrhythmias), diaphragmatic hernia, liver fractures, splenic fractures, urinary tract rupture, severe anemia/hypoproteinemia and neurologic abnormalities. Avoidance of anesthesia and sedation in these cases is beneficial for the reasons indicated:
- Arrythmias: can be worsened or induced
- Head trauma: can alter blood flow to the brain and worsen trauma/neurologic status
- Liver/spleen fractures: Can cause intraoperative hemorrhage and hypotension
- Lungs with pulmonary contusions: more prone to atelectasis and subsequent hypoxemia
- Pneumothorax: can be worsened with positive pressure ventilation
- Urinary tract injuries: can cause severe life-threatening electrolyte disturbances (especially hyperkalemia)
In addition, many anesthetic drugs are protein-bound and become more bioavailable in animals that are acidemic, a common consequence of shock and trauma. Avoidance of anesthesia until full assessment and proper resuscitation is attained is critical. However, sometimes sedation or anesthesia in these cases cannot be avoided. Use of local analgesic techniques in these life-threatening situations frequently decreases the need for systemic drug use and makes for a safer overall procedure.
Because local anesthetics directly block nerve impulses, they decrease pain in an alternative way compared with systemic analgesics. When used preemptively, this decreases the likelihood of wind-up of the pain pathways, ultimately helps prevent hyperalgesia, and aids in the multimodal approach to patient analgesia.
Drug selection is an important part of the local anesthetic protocol. Most local anesthetics function by blocking nerve impulses. At a cellular level this occurs by blocking sodium channels in the nerve membrane. When sodium is blocked, the nerve cannot conduct an impulse, and therefore no sensation can be transmitted. Local anesthetics cause analgesia but can also cause complete loss of motor function depending on the properties of the drug, location and myelination of the nerve; or the dose and size of the nerve fibers. Generally, local anesthetics cause nerve blockade in a particular order by first numbing pain, then warmth, touch, deep pressure and finally motor function. However, large peripheral nerves are an exception to this and tend to have motor blockade before sensory blockade, as well as cause proximal extremity analgesia prior to distal extremity blockade. Local anesthetic drugs differ in their side effects, onset of action and duration of action. Consideration of these drug factors should influence drug selection.
|Lidocaine||1-2 mg/kg||Short-acting analgesia for local infiltration, intrapleural and intraperitoneal blocks, and occasionally epidural use|
|Bupivicaine||1-2 mg/kg||Longer-acting analgesia for local infiltration, intrapleural, intraperitoneal and epidural use.|
|Dexmedetomidine||0.001-0.005 mg/kg||Epidural, intraarticular, or perineurally|
|Preservative-free morphine||0.1 mg/kg||Epidural|
If you have any questions about local analgesia, please contact our surgery service in Louisville at 502.244.3036.
We would like to thank our colleague in Utah, Vicki L. Campbell, DVM, DACVECC, DACVAA, for allowing us to use this article for Companion.
Patient monitoring in most practices is the responsibility of the technician. Thanks to technological advances, there is a wide array of equipment available to help technicians monitor parameters such as blood oxygen saturation levels and expiratory carbon dioxide concentrations. It is important to note, however, that these are no substitute for using your five senses when evaluating a patient, and any change in the patient’s physiologic parameters warrants further evaluation. It is also important that you know what to do when an abnormal parameter is identified.
Respiratory rate and pattern
The rate of respiration will increase if the patient’s body perceives an increased need for oxygen or the need to eliminate excess carbon dioxide. An increased respiratory rate can also be seen in patients who are experiencing discomfort, febrile, nervous or excited. A decreased respiratory rate will occur secondary to depression of the respiratory center in the brain due to sedation or disease. In patients with a slowed respiratory rate, it is important to assess the adequacy of their ventilation. In addition to monitoring the rate and pattern, smelling the breath can also indicate oral as well as systemic diseases. Halitosis can be indicative of oral infections. Whereas a “fruity” or acetone smell can be noted in patients with diabetes mellitus.
Other visual clues can help differentiate the cause of an altered respiratory rate such as the activity level of the patient, the posture of the patient, the color of the mucus membranes, and the sounds being made during respiration. Auscultation of the lungs can help assess changes in pulmonary air flow. The presence of an abnormal respiratory rate or abnormal respiratory pattern that can’t be attributed to the patient’s excitement or nervousness warrants further evaluation.
The femoral artery is the best place to determine a dog’s pulse.
The heart rate is the number of cardiac contractions that occurs in one minute. The patient’s heart rate can be determined from auscultating the chest for heart beats and can be affected by the patient’s breed, size and mental status. An increased heart rate suggests anxiety or nervousness or stimulation of the heart secondary to inadequate perfusion or oxygenation of the peripheral tissues. A slowed heart rate is seen in very fit animals, during times of somnolence or sedation, secondary to neurologic inhibition of the heart, and secondary to cardiac conduction abnormalities.
Every heart beat should produce a palpable pulse. Any incongruity between heart rate and pulse rate would suggest a cardiac arrhythmia. A disparity of heart rate from what is expected, given the circumstances under which it is being monitored, warrants further investigation. Similarly, if an arrhythmia is detected the patient should also be evaluated for underlying cardiac disease.
Mucous membrane color
The color of the patient’s mucous membranes can alert you to medical emergencies or help in early detection of a serious illness. The most common location to assess is the oral cavity. Except where pigmented, the mucus membranes in a healthy patient are pink-red in color reflecting the hue of oxygenated red blood cells.
The presence of a bluish color suggests cyanosis, which means the blood is being inadequately oxygenated. Cyanosis can be caused by respiratory or cardiac problems and rarely due to red blood cell dysfunction. The presence of cyanosis should be considered an emergency, and the patient should be evaluated immediately.
A yellowish discoloration (icterus) of the mucous membranes would be typical of excessive red blood cell destruction (hemolysis) or a hepatic/biliary condition. Pale mucous membranes will occur if perfusion of the peripheral tissues is diminished due to a heart disease or shock or if there are decreased numbers of red blood cells (anemia) circulating in the peripheral blood. Dark red or injected mucous membranes can be seen with toxicities and systemic infection (septicemia).
Capillary Refill Time (CRT)
To determine CRT, first apply pressure to the patient’s gums, then release.
The capillary refill time is the time it takes for blood to refill empty capillaries. It is an indicator of the adequacy of blood delivery to the peripheral tissues. To perform the test, press your finger down on the patient’s gums until they turn white. Release pressure, then note the time it takes for the mucous membrane color to return, i.e. for the compressed capillaries to refill once pressure is released. A normal CRT time is less than 2 seconds. A prolonged CRT would suggest inadequate perfusion of the peripheral tissues typically secondary to heart disease or a shock condition.
Heart and lung sounds
The character of heart and lung sounds on auscultation with a stethoscope can provide significant insight into the status of the patient. The presence of a heart murmur or irregular heart rhythm suggests an underlying heart condition, whereas the presence of crackly or bubbling lung sounds suggests airway disease or pulmonary fluid accumulation. Diminished heart or lung sounds suggest the presence of fluid or air trapped in a compartment between the chest wall and the organ you are trying to auscult.
Pulse strength is the subjective assessment of the ease with which you can identify the patient’s pulse. It reflects the difference between the push of blood against the vessel wall during the ventricular contraction (systole) and that present when the ventricle is relaxed (diastole). A decrease in pulse strength could reflect diminished cardiac contractility or cardiac output secondary to a primary heart condition, a decrease in blood volume (due to dehydration or blood loss), or diminished blood delivery to the palpated site (due to shock or obstruction of the vasculature). An increase in pulse strength typically reflects a decrease in diastolic pressure and can be seen with leaking heart valves. Pulses can be difficult to palpate in overweight pets and in dogs with certain conformations.
Tracheal Collapse: Diagnosis and Treatment
Tracheal collapse is a progressive disease of the cartilaginous rings within the trachea seen often in middle-aged, small-breed dogs. This is most commonly found in Yorkshire terriers, Pomeranians, pugs, Chihuahuas and toy poodles and results in dorsoventral narrowing of the tracheal lumen. The cause is unknown, but a strong genetic predisposition is suspected. Tracheal collapse should be suspected when dogs have a “goose honk” cough, noisy breathing and periodic dyspnea. Coughing episodes are worsened with excitement, anxiety and pressure on the trachea and can result in respiratory distress in severely affected dogs. As the condition progresses, the degree of collapse worsens, causing the cartilaginous rings to become more ovoid. This increases the cough severity and causes exercise intolerance. Severe tracheal collapse can also result in pulmonary hypertension and right-sided heart disease.
Definitive diagnosis and characterization of tracheal collapse is based on a combination of thoracic and cervical radiographs, fluoroscopy and tracheobronchoscopy. Collapse of the cervical trachea is best seen during inspiration, and intrathoracic collapse is seen best during exhalation on radiographs. With tracheobronchoscopy, tracheal collapse severity can be graded from grade I to IV (25-100% collapse). Laryngeal function and main stem bronchial collapse can also be assessed. Samples are often obtained for culture and cytology.
Medical management of tracheal collapse is the most important aspect of treatment, particularly when signs of collapse are first noted. Weight loss, limiting exposure to irritants (dust, cigarette smoke) and utilizing a harness rather than a collar are of paramount importance and can dramatically improve clinical signs. Oral antitussives (butorphanol, hydrocodone, diphenoxylate) are also important medications in helping to limit the clinical signs and progression of the disease. Tapering doses of corticosteroids (prednisone or inhaled fluticasone), bronchodilators (theophylline, terbutaline), and tranquilizers (acepromazine) are also used to treat affected patients. These patients are also predisposed to the development of bacterial tracheitis, necessitating antibiotic treatment if present.
When medical management is not successful in controlling clinical signs, more definitive treatment should be considered. Extraluminal placement of prosthetic rings can be performed, although this requires surgery. Recurrent laryngeal nerve damage can be a complication with this approach, and the blood supply to the trachea can be disrupted, causing tracheal necrosis.
Minimally invasive structural support of the trachea is now readily available, reducing risk of complications seen with extraluminal ring placement. Self-expanding nitinol stents can be placed, helping the trachea stay open by relying on the cylindrical shape of the stent. They are particularly advantageous due to the short post-operative recovery, rapid restoration of the airway and minimally invasive nature of placement. Measuring the tracheal diameter and length of stent can be challenging as the stents foreshorten during placement. Final stent width should be 10-20% larger than the maximal diameter of the trachea to prevent stent migration. The stent should be at least 1 cm caudal to the cricoid cartilage and 1 cm cranial to the carina and span the entire length of the collapse. Sizing is performed with the patient under general anesthesia with a measuring catheter in the esophagus, ideally with stent placement immediately following under the same anesthesia.
After stent placement, the patient is recovered and discharged with antitussives, sedatives, a tapering dose of corticosteroids and antibiotics. Aggressive control of the cough should be achieved for at least 4 weeks after stent placement in order to prevent stent fracture or granulation tissue formation. Radiographs are repeated at 1, 3 and 6 months post-placement. It should be noted that cough will persist after placement of the stent due to tracheal irritation, but improvement in quality of life should be noted quickly in appropriately selected patients.
BluePearl is pleased to offer tracheal stenting in our Louisville hospital. For more information, please call and ask to speak with Becca Hodshon, DVM, DACVS-SA at 502.244.3036.
We would like to thank our colleague from BluePearl in Tennessee, Carly Waugh, DVM, DACVIM, for allowing us to use this article in Companion.
Hyperthyroidism and Kidney Failure – a Concern?
Both hyperthyroidism and kidney failure are commonly seen in older cats. Occasionally, they may be present in the same patient. Unfortunately, hyperthyroidism can mask the signs and abnormal laboratory findings in cats with kidney failure making it difficult to confirm the presence of both conditions.
How does hyperthyroidism affect the kidney?
Thyroid hormone appears to enhance the responsiveness of beta-adrenergic receptors in the heart leading to increased heart rate, increased left ventricular contractility, and subsequently increased cardiac output. Thyroid hormone also appears to act on smooth muscle cells within the peripheral arteries causing relaxation and decreased peripheral vascular resistance. The decrease in arterial filling volume induces activation of the renin-angiotensin-aldosterone system, which stimulates increased sodium reabsorption by the kidneys and secondary water retention. The subsequent increase in blood volume increases blood return to the heart (increased preload). The increase in preload in combination with the decreased systemic vascular resistance also increases cardiac output.
An increase in cardiac output increases renal blood flow and, in turn, the glomerular filtration rate (GFR). BUN and creatinine are cleared more effectively from the body. The concurrent presence of kidney failure in cats with concurrent hyperthyroidism as assessed using BUN, creatinine, or even tests on GFR, is masked.
Now if you correct the hyperthyroid state, the patient’s cardiac output, and subsequently the GFR, return to normal. Kidney values once again increase. Azotemia has been reported to occur in 15-49% of hyperthyroid cats after treatment, despite the type of treatment.
Can you predict which cats will develop azotemia post-treatment?
Studies to date have failed to identify a marker that will identify those hyperthyroid cats with concurrent kidney failure. Pretreatment values for BUN, creatinine and even urine SG have failed to be reliable predictors for the development of post-treatment azotemia.
How long after treatment before azotemia would become evident?
Studies have indicated that the GFR will decrease during the first 2-4 weeks after treatment.
What is a methimazole trial?
Because it is the correction of the hyperthyroid state and not the type of treatment that unmasks the azotemia, it is possible to get a preview of the cat’s true kidney function, prior to curing the thyroid condition with radioactive iodine or surgery by performing what has been termed a methimazole trial. To perform a trial, administer methimazole with the goal of dropping thyroid hormone levels into the normal range. Once thyroid levels have normalized, blood tests performed 2-4 weeks later would be expected to demonstrate the BUN and creatinine values that you would see after radioactive iodine therapy or thyroidectomy.
When would a methimazole trial be performed?
We typically recommend the trial be performed in cats 14 years of age or older and in those cats with any suspicion for concurrent kidney disease based on the patient’s history, exam findings and lab test results (significantly elevated BUN value and isosthenuria). Why do we perform the test? It’s all about the owners’ expectations. We feel it is important for owners to be aware that concurrent kidney insufficiency is present prior to encountering the expense of radioactive iodine treatment.
What if kidney failure develops after thyroid treatment?
The good news is that, despite the development of post-treatment azotemia, most cats continue to do fine. In one study, the median survival time in cats treated for hyperthyroidism that developed azotemia post-treatment was similar to treated cats that did not develop azotemia (>500 days). The treatment for kidney failure includes ensuring hydration, feeding an appropriate diet, and addressing the complications of kidney disease such as hypertension.
Is there a preferred treatment for hyperthyroidism?
Radioactive iodine therapy is considered the most consistent and predictable means for curing hyperthyroidism in cats. It is technically simpler than other treatment options and involves only a single injection of the liquid chemical. There is no need to administer tablets or creams for the life of the cat or to feed an exclusive diet. Surgical thyroidectomy carries the risk of damaging the parathyroid glands. Meanwhile, poor client compliance, inadequate dosing, a risk for side effects, and the expense of the medication and recommended thyroid monitoring, associated with the use of methimazole are additional reasons to consider treating hyperthyroid patients with radioactive iodine. In one study, hyperthyroid cats treated with radioactive iodine were shown to live longer than those treated with methimazole despite the radioactive iodine-treated population actually being older in age.
If you have any questions on hyperthyroidism and kidney failure or any thyroid related questions, please contact a member of our internal medicine service at 502.244.3036.
Sudden Paralysis: What Your Technician Needs To Know!
Back or neck pain, a drunken and weak hind limb gait, and sudden hindlimb paralysis are all signs of intervertebral disc disease (IVDD).
IVDD is most commonly seen in short-legged, long-bodied dogs such as dachshunds. Although dachshunds appear to be genetically predisposed to the problem, IVDD can be seen in most medium and small breeds. Degeneration and cracking of the intervertebral disc capsule allows the disc contents to protrude into the spinal cord region. The subsequent pressure causes pain and can damage the spinal cord, causing loss of nerve function to the limbs and body parts caudal to the lesion. IVDD can be acute in onset, wax and wane over time, or prove progressive over hours to days.
With prompt attention and surgery, this patient with rear limb paralysis has a reasonable chance for recovery.
Dye injected into the spinal canal will outline the site where disc disease will occur. The loss of the dye column occurs secondary to swelling of the spinal cord in this region.
The longer the pressure is present on the spinal cord the more serious the damage that can occur. In mild cases, only back pain may be present. The pet may be reluctant to move, arch his or her back, show muscle spasm, or whimper with pain.
As nerve function is lost, the pet will have difficulty walking because the pet will be unable recognize how the paws are being placed on the ground, something called propriceptive deficit. Weakness and loss of voluntary movement of the limbs occurs next, followed finally by a complete loss of any recognition of sensation to the limbs. The more severe the damage is, the less reversible the condition.
As a technician, it is important to note the clinical signs in pets presented for back pain or hindlimb difficulties. A loss of voluntary hindlimb movement or any indication that the condition is worsening should be brought to the attention of the veterinarian immediately. Prompt surgical decompression of the pressure caused by the disc material is the best chance these patients have to recover full neurologic function. The longer the damage is present, the poorer the chance for recovery.
The knowledge and experience provided by an alert technician can make all the difference in ensuring the health of pets afflicted with IVDD and the satisfaction of your clients.
Pearls from the ACVIM Forum 2015
Can you trust the urine SG (USG) in dogs with glucosuria?
A recent study evaluated the effect of adding increasing concentrations of glucose to urine samples with varying starting USGs. Predictably they found that the lower the starting nonglucosuric USG, the greater the effect adding glucose had on the subsequent USG. Furthermore, the higher the concentration of glucose added to the urine sample, the greater the change in the subsequent USG. However, the addition of even higher concentrations of glucose to urine samples with low USG failed to cause clinically significant changes in the final USG. Researchers concluded that the presence of glucosuria did not interfere with the assessment of renal concentrating ability. (Behrend et al)
Are all antiemetic medications the same?
Well that depends on your goal. Gastric antral motility (contractions per minute) was measured before, during and hourly after the feeding of a meal in normal dogs given metoclopramide, maropitant, dolasetron or saline 1 hour prior to feeding. Researchers found that all three medications increased gastric motility prior to feeding and then intermittently during hourly measurements performed for 7 hours after feeding. Only metoclopramide increased motility at all time measurements. If the goal is only to inhibit nausea then all three medications can be effective. However, if increasing gastric emptying is also the goal, then metoclopramide may be your drug of choice. (Bogard et al)
So how do the new anti-seizure medications add up?
Phenobarbital still appears to be one of the most effective medications for treating seizures in dogs. Alternative medications continue to be evaluated with the goal of avoiding the short-term side effect of sedation and long-term side effect of potential liver disease. A review of records of dogs receiving zonisamide (40), levetiracetum (16) or phenobarbital (65) as first line therapy for control of seizures found that phenobarbital was more likely to be associated with adverse effects but was also most effective as monotherapy to control seizures. Dogs receiving zonisamide or levetiracetum were ultimately more likely to require additional therapy to reduce seizure frequency. (Waldron et al) In another study evaluating zonisamide alone, approximately 75% of 53 dogs demonstrated a 50% reduction in seizure frequency. (Nomura et al)
Fully-Funded Feline Anemia Trial
BluePearl Veterinary Partners in Louisville is currently recruiting patients for a fully-funded trial to evaluate the safety and efficacy of an oral medication to manage anemia associated with chronic kidney disease in cats. The study consists of two phases: the efficacy phase (28 days) and the maintenance phase (8 weeks).
- Cats, > 1 year old, male or female, > 2.0 kg
- Not pregnant, lactating or intended for breeding
- Diagnosis of chronic kidney disease
- Non-regenerative anemia with PCV < 27% at study days -7 and 0
- Stable concurrent medical conditions
- Cats may be receiving SQ fluids
- Fractious cats
- Positive urine culture on study day -7
- Systolic blood pressure > 165 mmHg on study days -7 or 0
- Previous treatment with erythrocyte stimulating agents (ESA), including erythropoietin (EPO)
- Previous blood transfusion since being diagnosed with CKD
- Severe clinical signs of inflammation not attributed to CKD
- Other significant uncontrolled medical issues
- FeLV+ or FIV+ (if not vaccinated, sponsor will cover the cost to test)
- Obvious signs of GI bleeding
The study medication, diagnostic lab work and examinations will be provided at no cost to owners. Owners will be expected to administer the study medication at home, keep an owner diary and comply with study protocols.
*Note that this study is not funded for diagnostic or treatment costs associated with the underlying renal disease. Those costs must still be assumed by the owner.
For more information, or if you have a patient who may meet the above requirements, please contact Dr. Scott Rizzo, Ali Wight or Sarah Latham at 502.244.3036.