Page 229 - Small Animal Internal Medicine, 6th Edition
P. 229

CHAPTER 10   Pulmonary Hypertension and Heartworm Disease   201


            therapy (if there is evidence of cardiovascular shock); and   interstitial pulmonary infiltrates; hilar and mediastinal
            cough suppressants could be useful. Antibiotics are of ques-  lymphadenopathy may also be present. Eosinophilic granu-
  VetBooks.ir  tionable benefit unless there is evidence of concurrent bacte-  lomatosis is treated initially with prednisone (1-2 mg/kg PO
                                                                 q12h);  however,  additional  cytotoxic  therapy (e.g.,  cyclo-
            rial infection. Endothelial changes in survivors regress within
            4 to 6 weeks after an adulticide. Pulmonary hypertension and
                                                                 all dogs respond completely, and relapses are common, espe-
            arterial disease, along with radiographic changes, diminish   phosphamide or azathioprine) may be necessary as well. Not
            over the next several months. Eventually, pulmonary arterial   cially when therapy is reduced or discontinued. The response
            pressure and the contour of the proximal pulmonary arteries   to immunosuppressive drugs after relapse may be poor. Sur-
            normalize, although some fibrosis may remain.        gical removal of a severely affected lung lobe is a strategy
                                                                 sometimes used. Therapy for adult HWs is given when pul-
            Treatment of Dogs With Complicated                   monary disease improves.
            Heartworm Disease                                      Severe pulmonary arterial disease, including PAH and
                                                                 PTE, is more common in dogs with long-standing HW
            PULMONARY COMPLICATIONS                              infection, in those with many adult worms, and in active
            Allergic or eosinophilic pneumonitis develops in a minority   dogs. Severe cough, exercise intolerance, tachypnea or
            of dogs with HWD. It tends to develop early in the disease   dyspnea, episodic weakness, syncope, weight loss, fever, and
            process and is thought to involve an immune-mediated reac-  pallor are common clinical signs; sudden death sometimes
            tion to dying larvae in the pulmonary microvasculature.   occurs. Typical radiographic findings include markedly
            Clinical manifestations of HW pneumonitis include a pro-  enlarged, tortuous, and blunted pulmonary arteries with or
            gressively worsening cough, crackles heard on auscultation,   without pulmonary interstitial and alveolar infiltrates; signs
            tachypnea or dyspnea, and sometimes cyanosis, weight loss,   usually are more severe in the caudal lobes. Marked hypox-
            and anorexia. Eosinophilia, basophilia, and hyperglobulin-  emia occurs in some cases. Thrombocytopenia and some-
            emia are inconsistent findings. HW Ag tests are usually posi-  times hemolysis can occur in dogs with severe pulmonary
            tive,  but  many  cases  do  not  have  circulating  microfilaria.   arterial disease and thromboembolism; DIC develops in
            Diffuse interstitial and alveolar infiltrates, especially in the   some dogs. As for postadulticide PTE, treatment with
            caudal lobes, are common on radiographs; these can be   oxygen, sildenafil, prednisone, strict cage rest, and some-
            similar to those in dogs with pulmonary edema, PTE, blas-  times a bronchodilator (e.g., theophylline) is indicated to
            tomycosis, or metastatic hemangiosarcoma. There is often no   improve oxygenation and reduce pulmonary artery pres-
            clinically relevant cardiomegaly or pulmonary lobar artery   sures. Caution is indicated to avoid systemic hypotension.
            enlargement. Tracheal wash cytology usually reveals a sterile   Antiplatelet therapy (clopidogrel or aspirin) or anticoagulant
            eosinophilic exudate with variable numbers of well-preserved   therapy (unfractionated heparin or low-molecular-weight
            neutrophils and macrophages. Therapy with a glucocorticoid   heparin) could be considered, although benefit of anticoagu-
            (e.g., prednisone, 0.5 mg/kg PO q12h) usually results in   lation must be weighed against risk of bleeding, particularly
            rapid and marked improvement. Prednisone may be contin-  in patients with thrombocytopenia or hemoptysis.
            ued as needed, in gradually tapered doses (to 0.5 mg/kg   After the animal’s condition is stabilized, the typical HW
            every other day) and does not appear to adversely affect the   treatment protocol can commence as recommended by
            adulticide efficacy of melarsomine.                  the American Heartworm Society (macrocyclic lactone
              Pulmonary eosinophilic granulomatosis is an uncommon   and doxycycline; 3-injection melarsomine protocol after 2
            syndrome that has been associated with HWD, although   months).
            some affected dogs have negative HW tests. Its pathogenesis
            is thought to involve a hypersensitivity reaction to HW Ag   RIGHT-SIDED CONGESTIVE
            or immune complexes, or both. Pulmonary granulomas are   HEART FAILURE
            composed of a mixed cell population, with predominantly   Severe pulmonary arterial disease and PAH can cause right-
            eosinophils and macrophages. A proliferation of bronchial   sided CHF. Jugular venous distention or pulsation, ascites,
            smooth muscle within granulomas and an abundance of   syncope, exercise intolerance, and arrhythmias are typical
            alveolar cells in the surrounding area are typical. Lympho-  signs; other physical and auscultatory signs secondary to
            cytic and eosinophilic perivascular infiltrates may also occur.   severe PAH might also occur (see p. 191). Although ascites
            Eosinophilic granulomas involving the lymph nodes, trachea,   is the most common manifestation of right-sided CHF in
            tonsils,  spleen,  gastrointestinal  (GI) tract,  and  the  liver  or   dogs, pleural or pericardial effusion can occur as well. Car-
            kidneys may occur concurrently. The clinical signs of pul-  diogenic pulmonary edema is not expected. Treatment is the
            monary eosinophilic granulomatosis are similar to those of   same as for dogs with severe PAH (sildenafil 1-3 mg/kg PO
            eosinophilic pneumonitis. Clinicopathologic findings vari-  q8-12h), with the addition of abdominocentesis or thoraco-
            ably include leukocytosis, neutrophilia, eosinophilia, baso-  centesis as needed, furosemide (e.g., 1-2 mg/kg PO q12h or
            philia, monocytosis, and hyperglobulinemia. In some cases,   as needed), pimobendan (0.2-0.3 mg/kg PO q12h), an ACEI
            an exudative, primarily eosinophilic pleural effusion devel-  (e.g., enalapril or benazepril 0.5 mg/kg PO q12h), and mod-
            ops. Radiographic findings include multiple pulmonary   erate dietary salt restriction. Clopidogrel or aspirin could be
            nodules of varying size and location with mixed alveolar and   considered, because PTE is one of the major mechanisms of
   224   225   226   227   228   229   230   231   232   233   234