Discussion:
To the authors’ knowledge, this report details the successful management
of hypoxemic respiratory failure in a dog with complicated babesiosis.
While definitive evidence of ARDS was not obtained with histopathology,
it remains a likely differential diagnosis. Reports of management of
suspected ARDS are scarce in the veterinary literature, and this report
provides clinical guidance for such patients.
Acute respiratory distress syndrome (ARDS) describes the complex
clinical syndrome of lung injury leading to downstream consequences of
activation of cell-mediated immune pathways, endothelial injury, and
alveolar flooding with protein-rich edema.10,11 This
initial “exudative” phase of lung injury can be initiated secondary to
several pulmonary and extra-pulmonary risk factors, but ultimately leads
to increased vascular permeability, pulmonary edema, atelectasis,
impaired gas exchange/hypoxemia, and respiratory fatigue often requiring
positive pressure ventilation. Consensus definitions of acute lung
injury and ARDS have been proposed previously for small
animals.12 Based on these criteria, the authors
propose that the dog described here fulfilled VetARDS criteria based on
the following: (1) acute onset (<72 hours) tachypnea, (2)
known risk factors (infection/sepsis, multiple transfusions), (3) and
pulmonary capillary leak as evidenced by bilateral lung infiltrates on
thoracic radiographs, proteinaceous fluid within the conducting airways,
and no echocardiographic evidence supporting cardiogenic pulmonary
edema. The fourth criterion, evidence of inefficient gas exchange, was
not directly documented at the time of respiratory decline but arterial
blood gases sampled after 12 hours of MV showed a profound hypoxemia and
coupled with the findings of poor oxygen saturation immediately after
intubation, prior to MV inefficient gas exchange was undoubtedly
present.
The case presented here did have growth of oropharyngeal contaminant
microbes on airway culture, but concurrent aspiration pneumonia cannot
be completely ruled out. Several other factors make bacterial pneumonia
less likely: the radiographic pulmonary changes were not classic for
aspiration pneumonia, the patient presented afebrile, had normal lung
sounds, and the tachypnea at presentation resolved after initial pRBC
transfusion.
Respiratory failure in people with babesiosis that meet ARDS criteria is
unique from other forms of ARDS because of its delayed onset and
relatively rapid resolution when compared to more typical causes. One
patient who survived severe hypoxemic respiratory failure with
initiation of MV was extubated on the 10th day of
treatment and discharged on day 20.4 Another describes
a babesiosis-associated ARDS patient who was extubated on day 4 of
hospitalization.6 The dog described here was on MV for
approximately 2 days, with discharge on day 5 of hospitalization and
developed suspect ARDS several weeks into his disease course.
Respiratory compromise possibly attributable to ARDS has been documented
in 6% of dogs with complicated babesiosis in one study, and only one
dog was reported to recover, representing 3.2% (1/31) of complicated
infections and 1.6% (1/63) of all infections.9 While
the relative severity of respiratory compromise was not specified in the
manuscript, all dogs were treated with oxygen
supplementation.9 In one retrospective canine study of
complicated babesiosis, 38% (32/84) of dogs died, of which 56% (18/32)
had respiratory failure as the listed cause of death.4Another report of respiratory distress and mental obtundation in a dog
with babesiosis had histopathology changes consistent with ARDS on
necropsy.9 Interestingly, previous reports noted thatB. canis vogeli is associated with less severe disease except in
the subpopulation of very young dogs,3 which fits the
scenario presented here.
In people, ARDS historically carried a mortality rate of 40-50%, but
trials in the last 20 years have shown improved outcomes with
“lung-protective” ventilation strategies that include high PEEP and
low tidal volumes to avoid alveolar overdistention and
atelectrauma,13 prone positioning,14neuromuscular blockade,15 and early use of
corticosteroids16 in certain subgroups of patients.
There are no studies specifically evaluating ventilation strategies of
ARDS and their impact on outcome in dogs. The dog in the present report
was managed with ventilation settings adapted from the human ARDSnet
trial.13 In this case, use of PEEP titrated to
FiO2 requirements combined with neuromuscular blockade
resulted in rapidly improved hypoxemia and pulmonary compliance. For the
majority of the patient’s MV, a slightly higher tidal volume (55 mL,
~9.6 mL/kg) was used than the lung-protective tidal
volumes from ARDSnet. It is unknown whether the same tidal volumes used
in people with ARDS should be applied to dogs, as the proportion of
lung:body weight may differ. The tidal volume in this patient was not
reduced further due to hypercapnia.
At the time of initiation of neuromuscular blockade, the dog was
considered heavily sedated. It is standard of care in people to meet
certain criteria of sedation prior to using paralytic agents for MV,
such as the Richmond agitation-sedation score
[RASS].17 Ensuring a RASS of -4 to -5 (deep or
unarousable sedation, respectively) helps avoid inadvertent awake
paralysis in ventilated patients, which may cause ICU delirium and
post-traumatic stress disorder from intensive care.16While human sedation criteria applied to dogs have not been evaluated,
we would have scored the dog a RASS of -5 despite being
tachypneic/dyssynchronous with the ventilator. The amount of sedation
provided was not changed while the dog was paralyzed to avoid awake
paralysis, but an optimal strategy to determine proper sedation prior to
neuromuscular blockade remains unclear for dogs.
The present case report has several important limitations. Confirmation
of ARDS with histopathology and full echocardiography by a cardiologist
were not performed. Given that the dog responded with the therapy
described and tolerated IV fluid administration, the authors feel that
cardiovascular fluid overload is unlikely. Transfusion-related acute
lung injury cannot be ruled out, though a blood type and crossmatch were
performed prior to transfusion. In people this complication is more
commonly associated with products containing soluble antibodies such as
fresh frozen plasma, but activation of primed resident pulmonary
leukocytes by other blood products secondary to severe systemic
inflammation is another proposed mechanism.18 While we
suspect that respiratory failure was already developing prior to blood
transfusion, this cannot be proven. Regardless, receiving multiple
transfusions is listed as a risk factor for ARDS in people as well as
the veterinary consensus definition.12