Respiratory Complications Following
Surgical Correction of Brachycephalic
Airway Syndrome
Senior Seminar Paper
Cornell University College of Veterinary Medicine
Blake Hefter
2/12/14
Dr. James Flanders
Dr. Theresa Southard
Keywords: Aspiration Pneumonia, Brachycephalic Airway Syndrome, ALI/ARDS
ABSTRACT
A 10 month old castrated male English bulldog presented to the Cornell University
Hospital for Animals Soft Tissue Surgery Service for surgical correction of a previously
diagnosed urethral prolapse. At that time, the owners were also interested in an
evaluation for Brachycephalic Airway Syndrome. Once anesthetized, the airway of the
patient was evaluated. An elongated soft palate along with everted laryngeal saccules
were visualized. The palate was shortened approximately 1.5 cm and the saccules were
resected. The patient recovered from anesthesia, and was discharged the next day. He
was brought back to the Cornell University Hospital for Animals Emergency Service the
following day for respiratory distress and fever. The owner said he had vomited a few
times since discharge. He went into cardiac arrest while in the emergency room and had
open chest CPR performed. He was successfully resuscitated. He was placed on a
mechanical ventilator in critical care until the owners chose humane euthanasia. We
believe aspiration pneumonia to be the cause of the clinical signs and pathologic changes
observed.
HISTORY
A 10-month-old castrated male English bulldog presented to the Cornell University
Hospital for Animals Soft Tissue Surgery Service on referral for surgical correction of a
urethral prolapse.
According to the owner, for about 1 month prior presentation they noticed what was
described as a purple flower like structure at the tip of the patient’s penis. After
examination by the local veterinarian, it was diagnosed as a urethral prolapse. The local
veterinarian attempted manual reduction, but when it recurred two weeks later, the owner
was referred to the Cornell Universtiy Hospotal for Animals Soft Tissue Surgery Service.
When the client arrived, they wanted the patient to be evaluated for Brachycephalic
Airway Syndrome in addition to the urethral prolapse. The clients owned another bulldog
that had a soft palate resection performed through the Soft Tissue Surgery Service, so
they were aware of the components of Brachycephalic Airway Syndrome.
PHYSICAL EXAM
The physical exam proved there to be a prolapsed urethra. It was manually reduced, but
returned immediately. Additionally, sterterous breathing was noted. The patient was
also noted to be highly overconditioned with a body condition score of 9/9. The
remainder of the exam was unremarkable. Due to the patient’s signalment,
Brachycephalic Airway Syndrome was the top differential for sterterous breathing. If
this were a non-brachycephalic dog, differentials such as foreign body, nasal or laryngeal
mass (abscess, granuloma, neoplasia), laryngeal paralysis, or upper airway infection
would be considered.
TREATMENT
In order to definitely diagnose Brachycephalic Airway Syndrome, evaluation of the
larynx must take place under general anesthesia. The patient was fasted during the
overnight stay in the hospital, and the evaluation took place the following day. While
under anesthesia, the patient was observed to have an elongated soft palate, along with
everted laryngeal saccules. These are two of the six components of Brachycephalic
Airway Syndrome. At the time of evaluation, surgery was performed to correct these
developmental abnormalities. Additionally, the urethral proplapse was corrected. The
patient recovered from anesthesia slightly hypoxic, so he was placed into an oxygen cage.
When his blood oxygen saturation was within the normal reference range, approximately
three hours after surgery, he was taken out of the oxygen cage. At that time, the patient
was bright, alert, and responsive. His vital parameters (temperature, pulse rate,
respiratory rate, mucous membrane color, etc.) were within the normal reference range.
He was fed one can of wet food in small bites. He did well overnight and into the next
morning until 8am when he was observed to vomit and become nauseous. He was given
a dose of metoclopramide, and no further nausea was seen. He was observed to eat more
wet food without difficulty and was discharged to his owner later that morning.
OUTCOME
The owners called the CUHA Emergency Service in the evening on the day of discharge.
They were worried because the patient had vomited twice since being home, was febrile,
and was in respiratory distress. The owners were instructed to bring the patient in for
examination, but since they lived a long distance away they could not come back until the
next morning. The owners dropped the patient off at 6:30 am the next morning to the
care of the Emergency Service. While being stabilized, the dog went into cardiac arrest.
Upon admission, the owner chose a green code for resuscitation. This means upon arrest
measures up to and including open chest cardiac massage should be attempted. While the
patient was in cardiac arrest and the emergency room doctor was putting on sterile
gloves, closed chest compressions were performed. As soon as the doctors were ready
and the site was prepared, an incision through the chest wall and into the thoracic cavity
was made. The ribs were separated, and cardiac massage was performed. Following
return of spontaneous circulation, the patient was brought into the surgery suite for sterile
lavage and closure of the thoracotomy. At that time, a tracheal tube and arterial catheter
were placed. Postoperative radiographs were performed which revealed diffuse
consolidation in most lung lobes. The patient was attached to the mechanical ventilator
and admitted into the critical care ward.
The patient continued to decline over the next two days, and ultimately the owners chose
humane euthanasia. A full necropsy was performed, which revealed diffuse consolidation
and atelectasis of most lung lobes. Differential diagnoses for these problems are
pneumonia, cardiogenic and non-cardiogenic pulmonary edema, torsion, neoplasia,
airway obstruction, and trauma. Samples of lung were taken for histopathology in an
attempt to determine the underlying cause of the clinical signs. The histopathology
revealed ninety percent of the airspace and interstitum was filled with fibrin, degenerate
neutrophils, and phagocytized bacterial cocci. Fibrinosuppurative pneumonia consistant
with aspiration was the final diagnosis.
DISCUSSION
Aspiration pneumonia is acute or chronic inflammation of the lungs and airways due to
inhalation of irritant material. The most commonly noted irritant materials are food
particles and gastric acid. The pathologic changes seen occur in three stages. The first
stage occurs immediately after aspiration. During this phase, damage to the airways and
pulmonary parenchyma is a result of the aspirate. This direct tissue damage triggers the
activation of cytokines, most notably TNF-a, IL-1, and IL-6, and other inflammatory
mediators. The inflammation then leads to necrosis of type I alveolar cells, pulmonary
hemorrhage, and increased vascular permeability resulting in pulmonary edema.
The second stage begins 4 to 6 hours after aspiration and lasts for 12 to 48 hours. It is
characterized by infiltration of neutrophils into the alveoli and pulmonary interstitium.
The continued leakage of proteins furthers the development of pulmonary edema.
Neutrophil activation, and release of further proinflammatory cytokines add to the
vascular leakage.
The third and final phase involves bacterial colonization of the airways and pulmonary
parenchyma (1)
Clinical signs from aspiration vary widely from patient to patient. Some patients will
have no signs, others can develop a mild pneumonia, and some end in systemic
inflammatory response and ultimately death.
In retrospective study of aspiration pneumonia in 88 dogs, regardless of etiology, 77% of
the cases survived until discharge. The remaining 23% either died in the hospital, or
were euthanized (2)
Depending on what is aspirated, stomach acid, food particles, or both, the pathologic
changes and severity differ. In a study involving intratracheal administration of stomach
acid, food particles, or both, arterial oxygenation was dramatically reduced following
administration of the both acid and food with PaO2/FiO2 ratios meeting the criteria for
clinical Acute Respiratory Distress Syndrome (ARDS) in the 24 hr period following
aspiration. Additionally the inflammatory response following the administration of both
food and acid was more profound than administration of either food or acid.
(3)
Aspiration pneumonia is known to be a causal factor of acute lung injury (ALI) or acute
respiratory distress syndrome. ALI is a syndrome of pulmonary inflammation and edema
resulting in acute respiratory failure. ARDS is the severe manifestation of ALI, with the
major difference between the two being the degree of hypoxemia as defined by the ratio
of arterial oxygen tension (PaO2) to fractional inspired oxygen concentration (FiO2).
ALI and ARDS are similar to aspiration pneumonia since there are many underlying
etiologies, however the pathologic findings in all ALI and ARDS cases are consistent.
Causes of ARDS are aspiration, pneumonia, toxic inhalation, asphyxiation, sepsis, shock,
severe trauma, or drug related toxicity.
The development of ALI/ARDS is secondary to an exaggerated inflammatory response.
The phases of ALI/ARDS are described based on morphologic changes seen in 3 stages,
known as the exudative, proliferative, and fibrotic stage.
The exudative stage of begins with pulmonary vascular leakage and inflammatory cell
infiltration. The architecture of the lung changes as type I alveolar pneumocytes are
damaged. These pneumocytes are primarily responsible for gas exchange. As they can
no longer perform their function, type II pneumocytes make an attempt to repair the
damaged area in order to allow for gas exchange. Type II pneumocytes primarily
produce surfactant, however during this phase of ARDS they abandon this responsibility.
These changes in pneumocyte function are the cause of hyaline membrane formation
histologically, as well as alveolar collapse. The first phase of ALI/ARDS begins at 24-48
hours post injury, and lasts about 1 week in humans.
Organization of the inflammatory exudate and development of fibrosis characterize the
second phase. Type II pneumocytes continue to increase in numbers in an attempt to
repair the damaged epithelial surfaces. Additionally, fibroblasts proliferate and lead to
narrowing and collapse of the airway. Histologically, changes in the lung becomes more
evident. The pulmonary parenchyma becomes dilated and edematous, the hyaline
membrane formation progresses, and ultimately the airspace fills with fibrin and cellular
debris.
The fibrotic phase is the final stage of ALI/ARDS. This phase involves collagen
deposition in the alveoli, vessels, and interstitium. Little is known about this phase in
veterinary patients due to the current mortality occuring during the first phase of ARDS
being close to 100%.
Additionally, ALI and ARDS are associated with the manifestation of MODS, or multi
organ dysfunction syndrome. No matter the etiology of ALI or ARDS, they are
characterized by a local and exaggerated inflammatory response. These inflammatory
mediators then spill over into the circulation, and if exaggerated enough, SIRS, or
systemic inflammatory response syndrome occurs. The result of this syndrome is the
change in vascular endothelium, blood flow, tissue perfusion, and cellular oxygenation.
Inflammatory mediators such as histamine, interlukens, TNF, and cytokines are not only
the cause of these changes, but also the chemicals that perpetuate the cycle that ultimately
leads to organ dysfunction. (4, 5, 6, 7, 8, 9)
Neither ALI nor ARDS were diagnosed by histopathology in the patient of this report.
Characteristic microscopic changes were not present, however ALI and ARDS cannot be
ruled out. The patient was in distress for only three days before euthanasia was
performed. These microscopic changes may have been starting to occur, but were
arrested when the patient was euthanized. The patient’s clinical signs and diagnostic tests
placed this dog in ARDS. Additionally, there were no histologic signs of MODS,
however the patients bloodwork while in Critical Care suggested multiple organ systems
were also beginning to fail.
Selected References:
1-Marik, P. E. (2001). Aspiration Pneumonitis and Aspiration Pneumonia. The New
England Journal Medicine, (344), 665-671.
2-Kogan, D. A., Johnson, L. R., Jandrey, K. E., & Pollard, R. E. (2008). Clinical,
clinicopathologic, and radiographic findings in dogs with aspiration pneumonia: 88
cases (2004-2006). J Am Vet Med Assoc, 233(11), 1742-7.
3- Raghavendran, K., Nemzek, J., Napolitano, L. M., Knight, P. R. (2011). Aspiration
Induced Lung Injury. Critical Care Medicine, 39(4), 818–826.
4- Declue, A. E., Cohn, L. A. (2007). Acute Respiratory Distress Syndrome in Dogs and
Cats: A Review of Clinical Findings and Pathophysiology. Journal of Veterinary
Emergency and Critical Care, (17.4) 340-47.
5-Tamashefski, J. (1990) Pulmonary Pathology of the Adult Respiratory Distress
Syndrome. Clinics in Chest Medicine, (11), 593–619.
6- Bellingan, G. J. (2002) The Pulmonary Physician in Critical Care * 6: The
Pathogenesis of ALI/ARDS. Thorax, (57.6) 540-46.
7-Anderson, W., Thielen, K. (1992) Correlative Study of Adult Respiratory Distress
Syndrome by Light, Scanning, and Transmission Electron Microscopy. Ultrastruct
Pathology, (16) 615–628.
8-Lopez, A,. Lane, I,. Hanna, P. (1995) Adult Respiratory Distress Syndrome in a Dog
With Necrotizing Pancreatitis. Canadian Veterinary Journal, (36), 240–241.
9-Hunter, T. (2001) Acute Respiratory Distress Syndrome in a 10-year-old Dog.
Canadian Veterinary Journal, (42), 727–729.