TUGAS ILMU PENYAKIT DALAM VETERINER SISTEM RESPIRASI

Oleh : Dimas Setiawan 060911158

FAKULTAS KEDOKTERAN HEWAN UNIVERSITAS AIRLANGGA SURABAYA 2012

FELINE BROCHIAL DISEASE Feline Bronchial disease describes a spectrum of inflammatory small airway diseases in the cat characterized by signs that range from chronic or intermittent coughing to lifethreatening respiratory diseases. Siamese cats seem to have an increased incidence of disease and may suffer from a more chronic form of bronchial disease. Any age can be afflicted with bronchial disease. The disease results from inflammation within airways that induces reversible airflow obstruction through smooth muscle constriction and hypertrophy, bronchial wall edema and hyperplasia of submucosal glands. Hyper-responsive airways and reversible airflow obstruction have been documented in some cases. These conditions lead to reduction in airway diameter and increased airway resistance, which cause clinical signs of cough and/or respiratory distress. Affected animals become allergic to allergens present in their immediate environment, including house dust mites and fungal spores and produce IgE antibodies against these molecules. When later exposed to the same allergens, asthmatic cats suffer a form of type I hypersensitivity response localized in the bronchi and bronchioles and resulting in constriction of the airways. Extrinsic and intrinsic forms of the disease exist. The extrinsic form describes the formation of exudate in the airways and thickened airway walls. The intrinsic form describes the increased propensity for the bronchial smooth muscle to contract and lead to airway constriction.

Clinical Signs The most frequent complaints in cats with bronchial disease are coughing and abnormal respirations, such as wheezing, loud breathing or respiratory difficulty. Paroxysmal coughing is commonly reported, and the cough is often described as a dry, retch. Exercise intolerance or episodes of open-mouth breathing after exertion may be noted in some cats. Cats with bronchial disease end toward obesity given an inability to exercise. Bronchitic cats can appear normal at rest and exhibit normal pulmonary auscultation; however, increased tracheasl sensitivity is usually present and post-tussive crackles are typically ausculted. Harsh lung sounds, crackles, or expiration wheezes are evident in some affected cats, and the expiractory phase is prolonged. An abdominal component to respiration may also be notrd. Air trapping may occur distal to obstructed

airways leading to decreased thoracic compressibility and a barrel-shaped appearance to cchest. Auscultation in this area of the lung is quiet with increased resonance on percussion.

Diagnosis The most common clinical signs associated with feline bronchial asthma include dyspnea, tachypnea, orthopnea, paroxysmal coughing, and increased expiratory effort. Furthermore, acute asthmatic patients are frequently severely stressed, may breathe with an opened mouth, and may bilaterally abduct their elbows when in sternal recumbency. Unfortunately, a combination of many of the clinical signs may also be seen with several other potential processes; therefore, clinicians must try to determine whether a patients clinical signs are referable to primary cardiac or primary pulmonary disease. Thoracic radiographs: Findings range from normal to increased bronchial and/or increased bronchial and interstitial patterns with or without alveolar densities. Peribronchial infiltrate is described as 'donuts' on the ventrodorsal view and 'tramlines' on the lateral view. There are often hyperlucent lung areas and flattening and caudal displacement of the diaphragm. There may be air trapping and hyperinflation. Atelectasis of the right middle lung lobe and mediastinal shift to the right have also been noted. Rarely, rib fractures and pneumothorax may be evident. Haematology may reveal increased numbers of circulating eosinophils. Bronchial cytology is variable, with predominant cell types including eosinophils, neutrophils and macrophages. However eosinophils can be found in normal cat airways. Bronchial culture may reveal Mycoplasma species in approximately 25% of cases. If the cat is presented in an acute episode, a rapid response to dexamethasone, bronchodilators and oxygen is highly suggestive of a diagnosis of asthma.

Pathophysiology Although there are many potential causes of asthma, the airways respond to inhaled irritants or immunologic stimuli in a limited number of ways: 1. Airway epithelium may thicken (hypertrophy), evolve to a different structure (metaplastic change), or simply become damaged (erode or ulcerate). 2. The structures responsible for producing mucus (goblet cells and submucosal glands) may enlarge and produce excessive amounts of a particularly thick form of mucus. 3. Bronchial smooth muscle will often spasm and may become hypertrophied.

These changes are associated with cellular infiltration of the bronchial mucosa and submucosa, and this tissue may also become edematous. The resulting clinical signs of cough, wheeze, difficulty breathing and decreased exercise capacity are due to airway narrowing (and airflow reduction) from excessive mucus secretions, airway edema, airway narrowing from cellular infiltrates, and airway smooth muscle constriction. Cough may also result from stimulation of cough-mechanoreceptors located in airway epithelium that is inflamed and contracted. This is an important concept, because the effects of even a small degree of airway narrowing to produce clinical signs can be dramatic. For example, a 50% reduction in the diameter of an airway results in a 16-fold reduction in the amount of air that flows through that airway. It is easy to imagine why any movement that requires an increase in the depth of breathing, such as chasing a mouse, will be tremendously altered if there is a16-fold decrease in the amount of air that comes into the lungs during normal respiration. The important take-home message is that small changes in airway size result in dramatic changes in airflow through that airway. The clinical implications of this finding are twofold. First, relatively small amounts of mucus, bronchoconstriction etc can partially occlude airways and cause a dramatic fall in airflow. On the other hand, therapy that results in relatively small increases in airway size may cause a dramatic improvement in clinical signs.

Treatment Acute Therapy Cat with cyanosis and open mouth breathing, diagnostic tests are kept to minimum initially. Stabilization can be achieved by providing an oxygen and using parenteral administration of the beta-2 agonist terbutaline at 0.01 mg/kg IV,IM or SC. Epinephrine, a sympathomimetics agent, is a potent bronchodilatator but should be used only when cardiac disease has been excluded since alpha and beta-1 adrenergic stimulation can result in adverse side effects of cardiac arrhythmias, vasoconstriction and systemic hypertension. Aminophyllines is a weak bronchodilator and it use in an emergency situation may not be justified since terbutaline is more likely to be effective. Respiratory rate and effort are monitored visually in the first hour of observation to determine therapeutics response. If the cat does not respond to terbutaline initially, use of short-acting corticosteroid often

results in rapid alleviation airway obstruction. Failure to respond terbutaline and corticosteroid indicates that other cause for respiratory distress should be investigated.

Chronic Corticosteroid control airway inflammation by inhibition of phospholipase A, decrease migration of inflammatory cells into the airway, which decrease the concentration of toxic granulation. For example prednisolone is administered at 1 mg/kg PO for 1 2 weeks and the dosage is decresead to 0.5 mg/kg if a good therapeutic response is seen. If the cat remains stable, the disage can be slowly decrease to once daily and then every other day. Cats are relatively resistant to the side effects of corticosteroids, however, an attempt should be made to achieve the lowest dose of the drug that controls signs. Approximately one half of cats require lifelong medication. Cats that cannot be orally medicated can be treated with intramuscular injection of repisitol corticosteroid (methyl prednisolone acetate at 10 20 mg IM every 2 to 8 weeks) or use of inhaled steroids (fluticasone). Alternatively anti-inflammatory drugs might be beneficial in some cats. For example cyproheptadine, a serotonin-receptor blocker, attenuated airway smooth muscle in vitro constriction. In some cases, bronchodilators may allow a reduction of the dose of steroids required to control clinical signs. Terbutaline can be administrated at 0.625 mg PO. Inhaled preparations of beta agonist are also available. Theophylline may provide some relief of signs by prevention of acute attacks of broncho-constriction in predispose cats by suppression of inflammation. Sustained release theophylline can be administered one daily at dosage of 10 mg/kg. Antibiotic should be prescribe based on sensitivity and cytology results if airway infection contributes to bronchial inflammation and hyper-responsiveness.

Prevention Because sympathetic tone is particularly important in achieving bronchodilation in the cat, beta blockers such as propanolol and atenolol should be avoided if bronchial disease is suspected, cigarette smoke, dusty litters, aerosol spray, and exposure to upper respiratory viruses may trigger clinical signs in susceptible cats

Prognosis

Therapy with anti-inflammatories and bronchodilators alleviates acute clinical signs in most cases; however, a significant proportion of cats will suffer a recurrence of signs. Continual medical management should be anticipated for many cats diagnosed with bronchial disease

References Byers, C.G. Feline Bronchial Asthma: Pathophysiology and Diagnosis. Cornell University http://en.wikivet.net Ettinger. Small Animal Internal Medicine.