A hypercoagulable state has been demonstrated in human falciparum malaria in mild and complicated forms of the disease. Disseminated intravascular coagulation (DIC) was implicated by some authors, but deemed a rare occurrence by others. The possibility of coagulopathy in Babesia canis rossi infections in the canine patient has also been suggested in the literature, but minimal work has been done to evaluate the clinicopathological nature of it in further detail. In the canine babesiosis (CB) pathogenesis thought-process, DIC has been implicated. A DIC-like syndrome, as evidenced by intravascular fibrin deposition and haemorrhage into muscles and tissues was found at post mortem in one study. On the basis of these findings, it was postulated that DIC might be a serious complication of severe Babesia infection in the dog. Clinical DIC (haemorrhagic diathesis) is however seldom seen. It was also hypothesised in the literature that the multiple organ dysfunction syndrome (MODS) demonstrated in the complicated form of Babesia was caused, in addition to tissue damage due to local hypoxia, by microthrombi as a result of a coagulopathy. This needs to be further investigated. Pulmonary thromboembolism (PTE) has not been implicated in CB, however thromboemboli in the lungs were found in dogs with immune-mediated haemolytic anaemia (IMHA) for which a similar mechanism of venous stasis, hypercoagulability and endothelial damage (as found in CB) is proposed. In humans, PTE is believed to be a major underdiagnosed contributor to mortality in 5 to 15% of hospitalised adults. If early diagnosis of PTE can be achieved, the mortality rate can certainly be decreased. A similar situation with resultant serious implications in complicated CB cases may exist. Clinically, PTE is suspected if a patient with a known prothrombotic condition develops sudden dyspnoea and tachypnoea. These clinical symptoms are frequently seen in complicated CB patients and may, in addition to being a compensatory mechanism for the metabolic acidosis and anaemia, be attributed to thrombus-induced mechanical changes in lung function. Pulmonary scintigraphy provides a sensitive means of diagnosing PTE. It was (and some authors still do) believed that a ventilation scintigraphic scan should be done in association with a perfusion scan to increase the specificity and accuracy of diagnoses. However, authors of the recent PISA-PED study in humans proposed that the sensitivity and specificity of a perfusion scan, without a ventilation scan, in patients with suspected PTE was sufficient. The incidence of PTE or the use of pulmonary perfusion scintigraphy in CB dogs has never been studied. The objective of this study was to prospectively evaluate the scintigraphic pulmonary perfusion pattern in hospitalised Babesia dogs in an attempt to ascertain whether a scintigraphic pattern consistent with PTE does indeed occur in these patients. The study consisted of a normal control group of nine mature healthy Beagle dogs aged 36 – 43 months and weighing 9.9 – 15kg and a Babesia group with 14 dogs of a variety of breeds that were naturally infected with Babesia, aged 6 – 103 months and weighing 6.3 – 25.5kg. Pulmonary perfusion scintigraphy was performed after making thoracic radiographs and performing a blood gas analysis in both groups. The scintigraphic images were visually inspected for changes suggestive of PTE. Surprisingly, not a single dog in the Babesia group had segmental or wedge-shaped perfusion defects which would have resulted in a high probability for PTE. The scintigraphic pulmonary perfusion pattern demonstrated was not significantly different between the two groups (p = 1.00). Many dogs in both groups had a mottled appearance on the right and left dorsal oblique images, which was not believed to be consistent with clinically relevant PTE. This study provides baseline data that may be used to further investigate the pulmonary perfusion pattern in Babesia dogs.
Dissertation (MMedVet (Diagnostic Imaging))--University of Pretoria, 2008.