Objective -To describe the presentation, diagnosis, treatment, and outcome of a case of emphysematous gastritis (EG) in a cat. Case Series Summary -A 15-year-old female neutered domestic short-hair cat presented for a 4-month history of weight loss and intermittent vomiting. Clinicopathologic and imaging findings suggested an underlying primary gastrointestinal (GI) disease, as well as possible hepatobiliary disease. Two days following exploratory laparotomy to obtain GI and liver biopsies, the patient became septic and intracellular bacteria were present on cytology of peritoneal effusion. On radiographs, the stomach was markedly distended with fluid and contained a thin gas opacity surrounding the stomach wall. The patient was taken back to surgery to identify a source of sepsis. At surgery, the patient's stomach was firm and emphysematous on palpation but grossly appeared normal. There were no signs of dehiscence of the previous biopsy sites. Stomach biopsy confirmed the presence of intralesional Gram-positive rods, consistent with microbial EG, and a light growth of a Clostridium sp. was cultured from abdominal fluid, consistent with clostridial peritonitis. During a third surgery for suspected septic peritonitis, a jejunostomy tube was placed for postgastric enteral feeding. The patient ultimately survived to discharge and is clinically stable 10 months later. New/Unique Information Provided -EG is a rare but potentially fatal clinical entity in the human and veterinary literature with only 1 other case reported in cats. Though clostridial organisms have been reported in EG in people, this is the first implication of EG secondary to a Clostridium sp. in the cat. This is also the first report to document the use of a jejunostomy tube for postgastric enteral nutrition to treat EG in the veterinary literature. (J Vet Emerg Crit Care 2018; 28(6): 596-602)

A 10-year-old male neutered mixed breed dog was evaluated for cervical hyperesthesia and tetraparesis. Magnetic resonance imaging of the brain and cervical spinal cord identified an extradural compressive lesion over the body of C2 caused by marked dilation of the vertebral venous sinuses. Following intravenous contrast administration both vertebral sinuses had heterogeneous contrast enhancement consistent with incomplete thrombi formation. An abdominal ultrasound also showed a distal aortic thrombus. A definitive cause for the thrombi formation was not identified, but the patient had several predisposing factors which may have contributed. The patient was treated with a combination of warfarin, clopidogrel, and enoxaparin as well as analgesics. Within 48 h of initiation of warfarin therapy, the tetraparesis and hyperesthesia were markedly improved. Repeat abdominal ultrasound 3 weeks after discharge showed reduction in size of aortic thrombus. Neurologic function remained normal for 6 weeks following initiation of treatment. Seventy-four days following initial diagnosis the patient rapidly declined and passed away at home. Necropsy was declined. This is the first report of vertebral venous sinus enlargement leading to spinal cord compression and tetraparesis in a dog. Additionally, warfarin in combination with clopidogrel and enoxaparin appeared to be a safe and effective treatment for the suspected thrombi reported in this case. Vertebral sinus enlargement secondary to thrombi should be considered as a differential diagnosis in patients presenting with tetraparesis and cervical hyperesthesia.