History
A 4-week-old 5.5-kg sexually intact male Nigerian Dwarf goat kid was presented for initial evaluation of vocalization, restlessness, and suspected stranguria. On presentation, the patient’s rectal temperature was at the high end of normal (40.1 °C; reference range, 39 to 40.5 °C), but other findings on physical examination were otherwise unremarkable, and urinary obstruction was excluded after observation of the patient voiding normally. The PCV and plasma total solids concentration were within reference limits. Blood gas analysis revealed mild hyperlactatemia (2.2 mmol/L; reference range, 0.4 to 1.5 mmol/L). The patient was hospitalized overnight for monitoring.
The following day, the patient developed progressive signs of abdominal pain, increased rumination, and frequent regurgitation of small volumes of rumen fluid. Additional physical examination abnormalities included dull mentation, mild tachycardia, and tachypnea with otherwise clinically normal cardiothoracic auscultation. Rumen stratification was palpably clinically normal, and abdominal auscultation revealed 1 rumen contraction/min (reference range, 1 to 2 contractions/min). Results of a CBC were within reference limits. Three-vie w abdominal radiography was performed (Figure 1).
Formulate differential diagnoses, then continue reading.
Diagnostic Imaging Findings and Interpretation
Abdominal radiography revealed the presence of well-defined, curvilinear intramural gas within the wall of the ventral sac and caudoventral blind sac of the rumen and cranial aspect of the reticulum (Figure 2). The rumen was mildly distended with gas and heterogeneous content with minimal granular mineral sediment. There was no evidence of small intestinal dilation. The primary differential diagnosis was ruminal pneumatosis secondary to rumenitis, mucosal ulceration, or traumatic mucosal injury associated with foreign material.
Repeated lateral abdominal radiographic images after lack of clinical improvement with medical management were obtained 72 hours after initial presentation and revealed progressive moderate ruminal fluid distension and persistent ruminal intramural gas (Figure 3). Differential diagnoses at this time included severe progressive ruminal stasis or pyloric outflow obstruction secondary to occult intraluminal foreign body or intussusception. The same differential diagnoses were kept for the ruminal pneumatosis. A single-phase (ie, delayed venous phase), contrast-enhanced abdominal CT examination was performed. Abdominal CT revealed severe thickening of the ventrolateral ruminal wall with intramural gas, irregular mucosal margination, and discontinuous serosal margins surrounded by peritoneal fluid. Additionally, a small amount of peritoneal gas was seen. The small intestine was diffusely moderately fluid distended (Figure 4). The primary considerations for the constellation of findings were ruminal perforation and septic peritonitis, secondary to severe progressive gastrointestinal stasis and emphysematous rumenitis.
Treatment and Outcome
Medical treatment for bloat, ruminitis, abomasitis and peritonitis included IV fluid supplementation (Normosol-R; Hisoura Inc; 50 mL/kg/d with added KCl [20 mEq/L] and 23% calcium gluconate [25 mL/L]), potassium penicillin (22,000 U/kg, IV, q 6 h), ceftiofur (5 mg/kg, IV, q 12 h), pantoprazole (1 mg/kg, IV, q 24 h), sucralfate (10 mg/kg, PO, q 8 h), thiamine (10, mg/kg SC, q 12 h), maropitant (1 mg/kg, IV, q 24 h), and poloxalene (0.5 ounces, PO, once). Despite medical treatment, clinical signs of abdominal pain and rumen dysfunction worsened over the following 4 days. Given the location of the potential ruminal perforation, exploratory celiotomy was performed using a ventral midline approach. At that point, the ventral rumen wall was found to have multiple large necrotic regions. The extent of the lesions precluded surgical resection, and the owners elected euthanasia and necropsy. Gross necropsy identified approximately 6 mL of bright-red, opaque, watery peritoneal fluid. There was a 10 X 6.5-cm irregularly shaped, flat, red focus on the serosa of the ventral rumen, with 2 central 2 to 2.5 X 1.5 to 2-cm gray-green foci. There were multiple 2 to 5 X 1.5 to 4-cm irregularly shaped, discrete, firm, brown plaques on the mucosa of the rumen, predominantly in the ventral sac. Histologically, there was a necrotizing rumenitis, with regions of coagulative necrosis of the rumen, sometimes extending into the submucosa or muscularis and occasionally extending transmurally, with associated inflammation that was predominantly neutrophilic. Variable emphysema was often present in the submucosa and muscularis, most prominently in sections with deeper necrosis. Clusters of bacteria (primarily large, curved, gram-negative bacilli with fewer, smaller, gram-negative bacilli) were present multifocally within the wall, in regions of necrosis with emphysema. There was frequent mineralization at the deep margin of the necrotic tissue, and granulation tissue was often present deep to necrotic regions. In regions with transmural inflammation, necrosis, or both, there was fibrinous serositis.
Comments
Emphysematous rumenitis was diagnosed in the kid goat of the present report. Young small ruminants in the early rumination stage are susceptible to a variety of disease syndromes affecting the forestomachs and abomasum, which can often lead to signs of severe abdominal pain and tympany.1,2 Reports of associated clinical and postmortem findings of intramural gas predominantly affecting the abomasum and less so the forestomachs have been attributed to various bacterial etiologies, including Clostridium and Sarcina spp, gastric ulceration or perforation, or mucosal damage such as secondary to abrasive feed.1,2 Feeding large amounts of easily fermentable carbohydrates produces a more acidic environment within the ruminant forestomach, which has been demonstrated experimentally to favor bacterial overgrowth of potentially pathogenic bacteria including clostridial species.2
Gastric pneumatosis or emphysema is the general radiologic term for the presence of intramural gastric gas.3 Gastric emphysema is generally considered a benign change associated with a favorable prognosis and is characterized by intramural gas trapping usually consequent to mucosal injury.4 In humans, gastric pneumatosis is encountered infrequently, compared to intestinal pneumatosis, with etiologies including iatrogenic results following feeding tube placement or endoscopy, or sequela of vomiting, gastroenteritis, or ingestion of caustic substances.3 In contrast, emphysematous gastritis refers to intramural gastric gas caused by gas-forming bacteria and is often associated with systemic disease and a guarded prognosis.4 The imaging findings of both gastric emphysema and emphysematous gastritis are similar, with overlapping features. Radiographic and CT findings in emphysematous gastritis include mottled intramural gas and thickened gastric folds, with increased sensitivity for detection of pneumoperitoneum and portal venous gas on CT.5 With gastric emphysema, intramural gas is described as generally curvilinear gas oriented parallel to the mucosa, without associated mural thickening.5
For the goat of the present report, serial radiographic monitoring was useful to detect persistent intramural ruminal gas as well as progressive rumen fluid distension. However, the multichambered ruminant stomach, superimposition of the pyloric outflow tract, and degree of visceral crowding in ruminant species make definitive radiographic evaluation of gastrointestinal tract pathology challenging. CT in this case allowed for better delineation of the gastrointestinal tract margins, excluding differential diagnoses of pyloric outflow obstruction or intussusception. CT was useful for further characterizing the imaging diagnosis, demonstrating a rounded to coalescing intramural gas pattern with regions of rumen thickening, which in concert with the patient’s history of an acute abdomen are consistent with emphysematous rumenitis. The most valuable impact of CT in this case was the demonstration of rumen wall ulceration and pneumoperitoneum, which directed case management in the form of immediate exploratory laparotomy. CT in this case not only facilitated the diagnoses of rumen wall ulceration and septic peritonitis but also allowed for appropriate surgical planning, which is especially important regarding surgical approach in ruminant species given their gastrointestinal tract anatomy.
Intramural gas is more commonly reported to involve the juvenile ruminant abomasum associated with abomasitis and abomasal tympany.1,2 For the case in the present study, the intramural emphysema was predominantly within the rumen near regions of mural necrosis, and pathology of the abomasum was not identified. As the patient was not fully ruminating at 4 weeks of age and ingesta would be presumed to predominantly bypass the rumen via the reticuloruminal fold, the ruminal damage may have been caused by a perforating injury such as from early intake of abrasive ingesta. Alternatively, it is plausible that similar pathogenesis speculated in a previous study2 of abomasitis and abomasal tympany apply, where bacterial overgrowth was triggered by ingestion of highly fermentable carbohydrates with subsequent mucosal damage, mural necrosis, and intramural bacterial invasion with gas production.
Although radiography was important for establishing clinical suspicion for ruminal pathology, CT was essential for determining the diagnosis of pneumoperitoneum and gastric perforation with subsequent septic peritonitis in the current case. This case highlights the challenge and limitations of evaluating the ruminant gastrointestinal tract radiographically, as the pneumoperitoneum and mural defects were not detected on follow-up radiography. However, abdominal radiography still provides valuable information and was integral for the decision to ultimately pursue CT, which prompted immediate surgical intervention in this case. This case emphasizes the utility of multimodality imaging for the evaluation of acute, progressive abdominal signs in small ruminants, as well as the significance of recognizing intramural ruminal gas and differentiating benign ruminal pneumatosis from emphysematous rumenitis using both imaging and clinical features.
Acknowledgments
No external funding was used in the management or report of this case. The authors declare that there were no conflicts of interest.
References
- 1. ↑
DeBey B, Blanchard P, Durfee P. Abomasal bloat associated with Sarcina-like bacteria in goat kids. J Am Vet Med Assoc. 1996;209(8):1468–1469.
- 2. ↑
Panciera RJ, Boileau MJ, Step DL. Tympany, acidosis, and mural emphysema of the stomach in calves: report of cases and experimental induction. J Vet Diagn Invest. 2007;19(4):392–395. doi:10.1177/104063870701900409
- 3. ↑
Spektor M, Chernyak V, McCann TE, Scheinfeld MH. Gastric pneumatosis: laboratory and imaging findings associated with mortality in adults. Clin Radiol. 2014;69(11):e445–e449. doi:10.1016/j.crad.2014.07.007
- 4. ↑
Matsushima K, Won EJ, Tangel MR, Enomoto LM, Avella DM, Soybel DI. Emphysematous gastritis and gastric emphysema: similar radiographic findings, distinct clinical entities. World J Surg. 2015;39(4):1008–1017. doi:10.1007/s00268-014-2882-7
- 5. ↑
Grayson DE, Abbott RM, Levy AD, Sherman PM. Emphysematous infections of the abdomen and pelvis: a pictorial review. RadioGraphics. 2002;22(3):543–561. doi:10.1148/radiographics.22.3.g02ma06543