Pulmonary Thromboembolism

Chapter 27 Pulmonary Thromboembolism



Lynelle R. Johnson, DVM, PhD, DACVIM



KEY POINTS



• Pulmonary thromboembolism (PTE) is a challenge to diagnose antemortem.

• PTE is a complication of diseases associated with hypercoagulability, endothelial damage, and stasis of blood flow.

• Identification of risk factors for PTE and disease associations is important for clinical recognition of this complication.

• Diagnostic results that can be used to support a diagnosis of PTE in a patient include positive D-dimer concentrations, echocardiographic detection of echogenic material in the pulmonary artery or evidence of acute right ventricular overload, and perfusion deficits on nuclear scintigraphy.

• Therapy for PTE includes management of the primary condition, support of oxygenation, and limitation of further growth of the clot with anticoagulants or thrombolytic agents.

• PROPHYLAXIS against thromboembolic complications should be considered in animals hospitalized with serious disease syndromes that have been associated with PTE.


INTRODUCTION


Obstruction of the pulmonary vascular bed can occur through blockage with fat, septic emboli, metastatic neoplasia, parasites (Dirofilaria or Angiostrongylus), or blood clots. It is likely that PTE results most commonly from formation of clot material (in the right side of the heart or at a distant site in the venous system) that breaks free and lodges in the pulmonary vasculature. Thrombosis in situ may also occur in association with pulmonary hypertension, heartworm disease, or other disorders of the pulmonary vasculature. PTE is likely as underdiagnosed in the veterinary population as it is in human medicine. Thrombi undergo 50% reduction in clot volume in the first 3 hours postmortem due to fibrinolytic dissolution; with heparin administration, clot volume is further reduced due to inhibition of further clot formation.1 Thus necropsy confirmation of PTE can be difficult.


Antemortem clinical recognition of PTE is low because clinical signs and physical examination findings mimic those found in a variety of cardiopulmonary conditions. In an early report, PTE was a differential diagnosis for respiratory distress in less than 5% of dogs with PTE confirmed at necropsy.2 In a more recent study,3 PTE was suspected in 65% of dogs that had relevant respiratory signs and a recognized predisposing condition for thromboembolism, suggesting increased awareness of the condition. In dogs, immune-mediated hemolytic anemia, sepsis, neoplasia, amyloidosis, hyperadrenocorticism, and dilated cardiomyopathy are associated with increased risk for PTE, and neoplasia and cardiomyopathy are found most often in cats with PTE.3,5


As has been shown in human and veterinary studies, most veterinary cases have comorbid conditions complicating the primary clinical disease and potentially increasing the risk for thromboembolism. Because PTE is associated with nonspecific clinical symptoms such as tachypnea or difficulty breathing, knowledge of predisposing conditions (Box 27-1) is important for appropriate diagnosis and treatment.



Box 27-1 Disorders Associated With Pulmonary Thromboembolism



• Immune-mediated hemolytic anemia

• Neoplasia

• Sepsis

• Protein-losing nephropathy and enteropathy

• Cardiac disease

• Hyperadrenocorticism

• Central catheter use

• Hemodialysis

• Total parenteral nutrition

• Hip replacement surgery

• Trauma


PATHOPHYSIOLOGY


The key pathophysiologic responses to PTE include alterations in hemodynamics due to increased pulmonary vascular resistance, abnormalities in gas exchange, altered ventilatory control, and derangements in pulmonary mechanics. Rarely, pulmonary infarction contributes to the clinical picture. The pulmonary circulation is normally resistant to changes in blood flow that occur with vascular obstruction because distention of the elastic vasculature allows the pulmonary bed to accept the increase in flow from embolized regions without a change in pressure. However, vascular obstruction from embolization results in both physical obstruction and arterial vasoconstriction due to release of vasoactive mediators. The combination of these events causes a reduction in the cross-sectional area of the pulmonary circulatory bed and increased vascular resistance.


PTE results in hypoxemia primarily from ventilation–perfusion (V/Q) mismatch, although physiologic shunting and reduced diffusion capacity also contribute to reduced arterial oxygen content. Hypoxemia can be present with as little as 13% obstruction of the vascular bed in humans,6 suggesting that even minor embolic disease is physiologically relevant. The severity of hypoxemia will be affected by underlying cardiopulmonary disease, reflex bronchoconstriction, and atelectasis. In the normal lung, most lung units have a V/Q ratio of 1; however, PTE causes a redistribution of blood flow, resulting in a wide spectrum of high, normal, and low V/Q units. Low V/Q units are the most important contributor to hypoxemia. As the degree of vascular obstruction exceeds 50% of the surface area of the circulatory bed, intrapulmonary shunting occurs, leading to venous admixture of blood and decreased oxygen responsiveness.7


Ventilation is controlled by the interaction between the sensors activated by elevated carbon dioxide in the central nervous system (CNS) and decreased partial pressure of arterial oxygen (PaO2) in the periphery with the responders (respiratory muscles). PTE is associated with tachypnea and alveolar hyperventilation, although the mechanisms responsible for hyperventilation remain obscure. Platelet aggregation with release of humoral mediators and cytokines could activate C fibers and irritant receptors to effect breathlessness. Also, embolization of additional organs often occurs,3,8 and obstruction of blood flow in the CNS could affect ventilatory control.


Changes in lung mechanics are likely important contributors to tachypnea, because increased resistance and decreased compliance greatly affect the work of breathing. Experimental studies in dogs have documented increased airway resistance following PTE; 5-hydroxytryptamine likely mediates this bronchoconstriction.9 Lung compliance is reduced in patients with PTE because of pulmonary edema and atelectasis. Pulmonary edema appears to result from increased hydrostatic pressure associated with increased blood flow to nonembolized lung regions and from release of humoral factors that increase microvascular permeability.



HISTORY AND CLINICAL SIGNS


Historical features consistent with PTE included labored breathing, tachypnea, lethargy, and altered neurologic status. Additional clinical signs that may be observed include cough, syncope, and hemoptysis. Altered mental state is reported in 20% of human patients with PTE and may be related to transient hypoxemia or cerebral ischemia. In a report in dogs, abnormal neurologic status was recorded in over one third of affected animals3 and thus may be a common finding with PTE. Importantly, obvious respiratory distress and tachypnea may be absent in some dogs or cats that have pulmonary embolization documented during necropsy.


Information regarding concurrent disease processes is essential to determine the risk of embolization for animals. In dogs with a variety of clinical syndromes leading to PTE, intravenous catheters had been placed in most, exogenous glucocorticoid excess was reported in half, use of cytotoxic agents was found in over one third, 21% had undergone recent surgical procedures, and 10% of dogs had been given blood transfusions.3

Related posts:

  1. Deteriorating Mental Status
  2. Hyperthermia and Fever
  3. Ventilator-Associated Lung Injury
  4. Allergic Airway Disease in Dogs and Cats and Feline Bronchopulmonary Disease

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Pulmonary Thromboembolism

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