Page 129 - Problem-Based Feline Medicine
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8 – THE CYANOTIC CAT  121


           and most cats will be in heart failure, so are poor anes-  If all veins draining an area are obstructed, edema,
           thetic risks.                                  cyanosis and necrosis may occur.
           Thrombolytic therapy using  tissue plasminogen  Cranial vena caval obstruction results in edema of the
           activator reduces time to reperfusion and ambu-  neck, ventral head, cranial thorax and forelimbs.
           lation, however 50% of treated cats died during clin-
           ical trials.                                   Diagnosis

           Pain treatment in the early stages of the disease using  Diagnosis is based on historical and clinical findings.
           oxymorphone (0.05–0.15 mg/kg IM or IV every 6
           hours) and butorphanol (0.02–0.4 mg/kg every 4 hours
                                                          Treatment
           IM or SC) is essential.
                                                          Thrombosis is usually self-limiting once catheters are
           Acetylpromazine (0.05–0.1 mg/kg IV) may be useful
                                                          removed. Broad-spectrum antibiotic cover may be nec-
           as an anxiolytic.
                                                          essary for septic lesions.
           Treatment of the heart failure must also be undertaken.
                                                          Surgical management is by drainage of abscesses and
                                                          hematomas, and debulking of tumors where indicated.
           VENOUS OBSTRUCTION
                                                          Treat the underlying cause of lymphadenopathy using
                                                          antibiotics, chemotherapy or surgical excision where
            Classical signs
                                                          appropriate.
            ● Localized cyanosis and edema referable to
               site of obstruction.                       Prognosis
            ● Edema of neck, ventral head, cranial thorax
               and forelimbs (vena cava obstruction).     Prognosis depends on the primary disease process.


           Pathogenesis
                                                           ABNORMAL HEMOGLOBIN WITH
           Localized peripheral hypoxia resulting from venous  DECREASED OXYGEN-CARRYING
           obstruction is usually the result of thrombosis, phlebitis  CAPACITY
           or venous obstruction from external compression.
            ● Thrombosis is typically caused by blunt trauma
              and perforating injury, such as venepuncture or pro-  ACETAMINOPHEN (USA)/PARACETAMOL
              longed venous catheterization.              (EUROPE, AUSTRALIA) TOXICITY
            ● Phlebitis may result from tissue inflammation
              extending to the veins, or originate from a venous  Classical signs
              intimal lesion.                              ● Salivation, vomiting and depression and
            ● Venous obstruction may be caused by compression  cyanosis.
              by  abscesses, hematomas, tumors or enlarged  ● Subcutaneous edema of face and
              lymph nodes.                                   extremities.
                                                           ● Lacrimation and facial pruritis.
           Clinical signs                                  ● Hematuria and hemolysis.
           Clinical signs depend on the anatomic location and
           the extent of the obstructive process, the collateral ves-
           sel reserve and the capacity of the draining lymphatics.  Pathogenesis

           Large lesions may result in edema and cyanosis in the  Feline hemoglobin is particularly susceptible to oxida-
           area, which is usually short-lived because of large col-  tive damage, and therefore to the formation of methe-
           lateral circulation.                           moglobin and Heinz bodies in erythrocytes.
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