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  • A 10-year-old male castrated domestic medium hair presented 48 hours prior to ultrasound for an acute onset of hyporexia and vomiting.
  • He was treated for suspected gastroenteritis with outpatient medical management consisting of anti-nausea medication and subcutaneous fluids. He returned 2 days later for diarrhea, persistent anorexia, and progressive, profound lethargy.
  • Initial blood work revealed no abnormalities and an abdominal ultrasound was performed to further evaluate the gastrointestinal signs and the new lethargy.

 

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  • There is a large amount of hyperechoic gas reverberation artifact on initial contact of the transducer with the patient that limits evaluation of intra-abdominal structures (US image 1). This is worse to the left of the midline, but present in all areas of the abdomen.
  • There is no no free fluid within the peritoneal cavity, though the mesentery adjacent to the ileocecocolic junction is mildly hyperechoic and adjacent lymph nodes are slightly hypoechoic (not shown).
  • Diffusely, the small intestinal muscularis layer is minimally thickened with no loss of wall layering or mural nodules/masses (US image 2).
  • The stomach was moderately distended with gas and fluid despite reported prolonged anorexia. No abnormalities of the pylorus are noted (also not shown).
  • Further evaluation with the patient in different recumbency, highlights that the gas is outside of the peritoneal cavity and is superficial to the peritoneal surface. The gas is present within the subcutaneous space (US video).
  • When evaluating the cranial abdomen, there is a small volume of pleural fluid, an irregular pleural margin and decreased aeration of the most caudal lung adjacent to the diaphragm(US image 3).
  • Moderate volume subcutaneous gas is subjectively beyond expected for iatrogenic causes (reported SQ fluid administration), though an origin is not identified sonographically.
  • Small volume pleural effusion and atelectasis or pulmonary infiltrates within the caudal lung lobes. Given subcutaneous gas, the possibility of concurrent pleural/mediastinal/subcutaneous disease should be considered as these structures communicate.
  • Diffuse small intestinal muscularis layer thickening is a change that could represent inflammatory bowel disease or small cell lymphoma. Ileocecocolic inflammation and suspected reactive lymphadenopathy. Consider typhlitis.

On initial examination, the large volume of gas gave the false impression of free peritoneal gas as could occur secondary to gastric perforation and necessitating emergent surgical intervention. However, the lack of peritoneal effusion or diffuse peritonitis was incongruent with a gastrointestinal perforation, prompting more close evaluation of the location of the gas artifact. Given the now suspected SQ gas and the pleural abnormalities, thoracic radiographs were recommended (radiographs 1-2).

 

Lateral thoracic radiograph of this patient, after the abdominal ultrasound exam

Ventrodorsal radiograph of this patient, after the abdominal ultrasound exam

The thoracic radiographs revealed a moderate volume of subcutaneous emphysema, cervical intrafascial gas, pneumomediastinum, pneumoretroperitoneum, and a small volume of pneumothorax. Tracheal laceration secondary to venipuncture or unreported trauma were primary considerations for this large volume of gas, but no underlying cause was determined in this patient. The possibility that the pneumomediastinum was secondary to vomiting was considered, though the clinical signs were not reportedly that severe.

Ultimately, although striking, the changes to the mediastinum, pleural space, etc were considered unrelated to the initial presenting complaining of gastrointestinal signs, though may have contributed to the progressive decline in the patient’s status. Because no prior radiographs were available to review, the possibility of previous pulmonary or mediastinal pathology could not be ruled out.

Over the course of several days, the patient responded well to continued empiric medical management for enteritis/typhlitis and the volume of thoracic gas continued to decline. The patient was discharged and lost to follow-up.

The feline mediastinum divides the thorax into two halves and communicates with both the retroperitoneal space caudally, and the cervical fascia cranially. In veterinary literature, most cases of pneumomediastinum are secondary to an obvious inciting pathologic event. In cats, pneumomediastinum has been described secondary to endotracheal intubation, trauma, neoplasia (pulmonary carcinoma), viral infections (necrotizing bronchopneumopathy), and endoscopy. The authors are unaware of current veterinary literature describing spontaneous pneumomediastinum alone in cats. A human study that was done using cats revealed overdistention and rupture of alveoli could cause subsequent air leaking into the pulmonary interstitium. This led to dissection along the bronchovesicular interface with the mediastinum. This phenomenon is known as the Macklin Effect and has been described as a source of pneumomediastinum. Treatment of pneumomediastinum with or without concurrent pneumothorax may include supplemental oxygen therapy if needed, analgesics and correction of the underlying cause, if determined. Prognosis is excellent depending on the severity/etiology with an 87% survival reported in a retrospective of 45 cases of pneumomediastinum in a cat.

 

References

  • Caceres M, Syed ZA, Braud R, et al. Spontaneous pneumomediastinum: a comparative study and review of the literature. Ann Thorac Surg 2008; 86(3):962–966.
  • Choisunirachon N. What is your diagnosis? Thai J Vet Med. 2015. 45(4): 671-673.
  • Thomas E, Syring R. Pneumomediastinum in cats: 45 cases (2000-2010). J Vet Emerg Crit Care 2013; 23(4): 429–435.