Outcomes, including death, in dogs with pneumothorax following nasogastric feeding tube misplacement in the tracheobronchial tree: 13 cases (2017-2022).

OBJECTIVE: Complications of feeding tube placement are uncommon, but life-threatening pneumothorax has been reported in human and veterinary patients during feeding tube placement. This article describes the development of pneumothorax and the outcome associated with misplacement of nasogastric (NG) tubes in the tracheobronchial tree in 13 dogs. ANIMALS: 13 dogs being treated for various medical conditions that had NG tubes placed in 4 hospitals. PROCEDURES: A review was carried out of the medical records of 13 dogs that developed pneumothorax after misplacement of NG tubes between 2017 and 2022. RESULTS: 14 dogs out of 4,777 (0.3%) developed pneumothorax as an adverse effect of NG tube misplacement in the tracheobronchial tree. One dog was excluded due to incomplete medical records. The feeding tube size ranged from 5F to 10F, and the most common tubes utilized were polyurethane tubes with flushing stylets. Nine out of 13 dogs developed evidence of respiratory compromise after the NG tube was placed. Eleven dogs required thoracocentesis, and 5 dogs had thoracostomy tubes placed. Five dogs suffered cardiopulmonary arrest after developing pneumothorax, with 3 of 5 undergoing cardiopulmonary resuscitation. Two out of 3 dogs that underwent cardiopulmonary resuscitation were discharged from the hospital. Five of 13 dogs were successfully discharged from the hospital, while 5 dogs died or were euthanized because of the pneumothorax. CLINICAL RELEVANCE: Pneumothorax is a rare but potentially life-threatening complication of NG tube placement in dogs and may lead to death if not immediately addressed. Practitioners should be aware of this complication and be ready to perform thoracocentesis quickly if appropriate.

Interleukin-1ß, tumour necrosis factor-α and lipopolysaccharide induce C-type natriuretic peptide from canine aortic endothelial cells.

The N-terminal portion of pro C-type natriuretic peptide (NT-pCNP) has shown promise as a biomarker for sepsis in humans and dogs, however the mechanism of NT-pCNP production in dogs is unknown. Canine aortic endothelial cells were stimulated with lipopolysaccharide, lipoteichoic acid, peptidoglycan, TNF-α, IL-1ß, IL-6, IL-10, IL-21, CXCL-8, IFN-γ, VEGF-A or control (PBS), and NT-pCNP production was measured. Lipopolysaccharide, TNF-α, and IL-1ß significantly stimulated NT-pCNP production in a dose and time dependent manner; IL-1ß resulted in the greatest NT-pCNP concentrations. The other stimulants did not result in significant NT-pCNP production. The addition of serum to the cell culture model did not alter lipopolysaccharide, lipoteichoic acid or peptidoglycan induced NT-pCNP production. These data indicate that lipopolysaccharide, TNF-α and IL-1ß regulate CNP production from canine vascular endothelium and of the stimulants tested, IL-1ß is the predominant inducing factor. These data provide some initial insight into the mechanisms of CNP regulation in dogs.