Use of cryopoor plasma for albumin replacement and continuous antimicrobial infusion for treatment of septic peritonitis in a dog.

OBJECTIVE: To report the successful management of a dog with septic peritonitis and septic shock secondary to enterectomy dehiscence using novel techniques for identification of intestinal dehiscence and for septic shock treatment. CASE SUMMARY: A 5-year-old castrated male Bernese Mountain Dog presented for lethargy 6 days following enterotomy for foreign body obstruction. Septic peritonitis was identified due to dehiscence of the enterotomy site, and resection and anastomosis were performed using a gastrointestinal anastomosis and thoracoabdominal stapling device. Postoperatively the patient experienced severe hypotension, which responded to norepinephrine constant rate infusion (CRI) after failing to improve with fluid therapy or dopamine CRI. Further treatment included antimicrobial CRI and supportive care including careful fluid therapy. Due to low effective circulating volume paired with intersititial fluid overload and large volume abdominal effusion, fluid therapy consisted of a combination of human serum albumin, canine albumin, synthetic colloids, and isotonic crystalloids. Cryopoor plasma (CPP) was used as a source of canine albumin and intravascular volume. On Day 4, food dye was given through a nasogastric tube due to suspicion of dehiscence of the anastomosis site. Dehiscence was confirmed during abdominal exploratory, and a second resection and anastomosis was performed. Abdominal partial closure with vacuum-assisted closure device was performed. Supportive care was continued with CPP CRI and imipenem CRI. Planned relaparotomy to change the vacuum-assisted closure device was performed 48 hours later, with abdominal closure 96 hours after anastomosis. The patient was discharged on Day 15. Recheck 12 months later was normal. NEW OR UNIQUE INFORMATION PROVIDED: This case includes novel techniques such food dye via nasogastric tube to identify anastomosis dehiscence, use of CPP as a source of canine albumin, and antimicrobial CRI in a dog with septic peritonitis.

Successful treatment of a dog with massive 5-fluorouracil toxicosis.

OBJECTIVE: To describe the clinical presentation and successful treatment of a dog that ingested a lethal dose (approximately 330 mg/kg) of 5-fluorouracil (5-FU). CASE SUMMARY: A 1-year-old male intact German Shepherd dog was presented to the Emergency Service of the Ohio State University Veterinary Medical Center after ingesting 10 g of 5% 5-FU cream. The dog rapidly developed refractory seizures and was managed by inducing heavy sedation with phenobarbital, benzodiazepines, ketamine, and propofol, necessitating 48 hours of mechanical ventilation. Seizure activity continued despite these treatments until IV administration of levetiracetam. The dog was discharged from the hospital 6 days after admission and remains neurologically normal currently, with no further seizure activity after 9 months. NEW INFORMATION PROVIDED: This report documents the first successful treatment of a dog that ingested > 43 mg/kg of 5-FU. In this case, the use of rapid decontamination, heavy sedation with anticonvulsant medications including levetiracetam to control seizures, and mechanical ventilation may have contributed to a positive outcome.

Practical acid-base in veterinary patients.

Acid-base abnormalities are common in critically ill veterinary patients. Rapid recognition of disturbances can be helpful in identifying the underlying cause of the patient's clinical signs, directing diagnostics, and monitoring response to therapy. If acid-base disturbances are left unidentified and untreated, severe physiologic consequences can result, including cardiovascular and neurologic dysfunction, protein and enzyme dysfunction, and electrolyte derangements. Treatment of acid-base disorders is aimed at correcting the underlying disease process.

A review of stress-related mucosal disease.

OBJECTIVE: To review and summarize the human and veterinary literature regarding stress-related mucosal disease (SRMD) pathogenesis, patient risk factors, and therapeutic options for prophylaxis and treatment. ETIOLOGY: SRMD is a common sequela of critical illness in human patients. Development of SRMD results from splanchnic hypoperfusion, reperfusion injury, and exposure of the gastric mucosa to acid, pepsin, and bile acids following breakdown of the gastric mucosal defense system. Human patients with the highest risk of stress ulceration include those with respiratory failure necessitating mechanical ventilation greater than 48 h or coagulopathy. Currently, little is known about the incidence and pathophysiology of SRMD in critically ill veterinary patients. DIAGNOSIS: A presumptive diagnosis can be made in high-risk patient populations following detection of occult or gross blood in nasogastric tube aspirates, hematemesis, or melena. Definitive diagnosis is achieved via esophagogastroduodenoscopy. Lesions are localized to the acid-producing portions of the stomach, the fundus, and body. THERAPY: Therapy is aimed at optimization of tissue perfusion and oxygenation. Pharmacologic interventions are instituted to increase intraluminal pH and augment natural gastric defenses. Histamine(2)-receptor antagonists, proton pump inhibitors, and sucralfate are the mainstays of therapy. In people, clinically significant bleeding may necessitate additional interventions (eg, packed red blood cell transfusions, endoscopic, or surgical hemostasis). PROGNOSIS: Mortality is increased in people with clinically significant bleeding compared to those patients who do not bleed. Institution of prophylaxis is recommended in high-risk patients. However, no consensus exists regarding initiation of prophylaxis, preference of frontline drug class, or indication for discontinuation of therapy. The prognosis of veterinary patients with SRMD remains unknown at this time.