Page 345 - Clinical Small Animal Internal Medicine
P. 345

313


  VetBooks.ir






               32


               Pulmonary Thromboembolism
               Robert Goggs, BVSc, PhD, DACVECC, DECVECC

               Cornell University College of Veterinary Medicine Companion Animal Hospital, Ithaca, NY, USA


               Pulmonary thromboembolism (PTE) refers to obstruc­  due to interstitial and alveolar edema. The V/Q mis­
               tion of a pulmonary vessel or vessels by a thrombus and   matches occur due to small airway constriction, reduced
               encompasses both  in situ thrombus formation and   surfactant production, and development of pulmonary
               embolization from elsewhere in the vasculature. In small   edema and atelectasis. Small airway constriction occurs
               animals, PTE is the preferred term because these mecha­  in  both  nonperfused  and  nonembolized  areas  of  lung,
               nisms  are  difficult  to  differentiate  clinically  and  both   which may lead to airway closure and alveolar collapse.
               share a common pathophysiology. PTE is associated   Surfactant production is reduced in dogs with experi­
               with numerous diseases and disorders in small animals   mental PTE, leading to fluid transudation into alveoli
               (Table 32.1) and many patients with PTE have more than   (pulmonary edema). Edema may also develop in nonem­
               one predisposing condition. These underlying condi­  bolized regions  due to  increased hydrostatic pressure
               tions can be categorized by how they affect Virchow’s   combined with increased microvascular permeability
               triad, although formation of thrombi  in vivo typically   resulting from neutrophil activation. Rarely, pulmonary
               involves more than one such effect.                infarction and pleural effusion may result from complete
                 The true incidence of PTE in dogs and cats is    occlusion of distal pulmonary vascular branches.
               unknown but it is probably more common than the lit­  The cardiovascular consequences of PTE are depend­
               erature suggests. Difficulties definitively diagnosing   ent upon the extent of vessel occlusion. There is substan­
               PTE antemortem, limited numbers of postmortem      tial reserve capacity in the pulmonary vasculature, which
               examinations being performed, and rapid postmortem   likely accounts for the subclinical nature of many PTE
               fibrinolysis mean  some cases are missed. In a  retro­  events. In healthy dogs, >60% of the pulmonary vascula­
               spective case series of 29 dogs with confirmed PTE,   ture must be occluded before alterations in pulmonary
               there was antemortem suspicion in less than 40% of   vascular resistance (PVR) reduce pulmonary arterial flow.
               dogs in which it was subsequently identified at nec­  Reflex vasoconstriction secondary to alveolar hypoxia,
               ropsy. This study suggested a prevalence of PTE in dogs   humoral factors such as serotonin released from acti­
               of  0.9%  over a  10‐year  period.  In cats, PTE  was  sus­  vated platelets, and neurogenic reflexes may also contrib­
               pected in ~25% cats with respiratory signs and in only   ute. Significant pulmonary vascular occlusion leads to
               14% of  cats in  which it was subsequently  diagnosed   pulmonary hypertension and increased right ventricle
               postmortem. Subsequently, a 24‐year prevalence of   (RV) afterload. Severe, acute changes in RV afterload
               0.06% was reported for PTE in cats.                result in dilation and dysfunction. As the RV dilates, the
                                                                  interventricular septum shifts leftward, impairing filling
                                                                  and reducing diastolic distensibility, a concept known as
                 Pathophysiology                                  ventricular interdependence. Consequent reductions in
                                                                  left ventricular filling decrease cardiac output and may
               Pulmonary thromboembolism frequently results in    lead to signs of forward failure (hypotension, cardiogenic
               hypoxemia, hyperventilation, and dyspnea. Arterial   shock). If the patient survives an acute crisis but has
               hypoxemia in patients with PTE is secondary to abnor­  residual pulmonary hypertension, then clinical signs of
               mal ventilation/perfusion (V/Q) ratios within affected   backward failure (hepatomegaly, ascites, pleural effusion)
               lungs, potentially complicated by diffusion impairment   may develop over the medium to long term.


               Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
               © 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
               Companion website: www.wiley.com/go/bruyette/clinical
   340   341   342   343   344   345   346   347   348   349   350