Skip to main content
The Canadian Veterinary Journal logoLink to The Canadian Veterinary Journal
. 2020 Feb;61(2):138–141.

Large-volume pneumoperitoneum and septic peritonitis secondary to splenic abscess rupture in a dog

Jean V Rubanick 1,, Adam H Breiteneicher 1, Kelley Thieman-Mankin 1
PMCID: PMC6973221  PMID: 32020930

Abstract

An 11-year-old spayed female American pit bull terrier mixed breed dog was presented because of hyporexia and abdominal distension. The dog had large-volume free peritoneal gas on imaging and septic neutrophilic exudate on abdominocentesis. Exploratory laparotomy revealed a ruptured splenic mass draining purulent material. A splenectomy was performed and the abdomen was lavaged. Culture samples grew an anaerobic Gram-positive rod. The dog was discharged 4 days after surgery with no residual problems noted 1 week later. To our knowledge, this is the first report of large-volume pneumoperitoneum and septic peritonitis secondary to rupture of a splenic abscess


Splenic abscesses are rare in veterinary patients, with a reported incidence of <1% in 2 reports examining splenic disease (1,2). Including this report, only 4 case reports in the veterinary literature have described splenic abscessation in the dog (35). While splenic abscess rupture with secondary pneumoperitoneum has been reported in the human literature, to the authors’ knowledge, this is the first report in a dog (610).

Case description

An 11-year-old spayed female American pit bull terrier mixed breed dog weighing 23.6 kg was presented to our hospital because of hyporexia, abdominal distension, and marked elevation in alkaline phosphatase (ALP) approximately 10 d before presentation. Fourteen days before presentation, the dog had a laceration on the medial aspect of the left stifle secondary to unknown trauma. The veterinarian repaired the laceration and started the dog on meloxicam, 0.13 mg/kg body weight (BW), PO, q24h, for 5 d and ciprofloxacin, 10.6 mg/kg BW, PO, q24h for 7 d. The dog vomited on the first day of administration of meloxicam and had a decreased appetite thereafter. Six days following repair of the laceration, a complete blood (cell) count (CBC) revealed a stress leukogram and serum biochemistry revealed marked elevation in ALP (>1000 U/L). Mild abdominal distension was also present. The dog was presented to a tertiary facility for diagnostic work-up of the hyporexia and abdominal distension.

On presentation to our hospital, the dog was hyperthermic [rectal temperature 39.8°C; reference range (RR): 37.5°C to 39.2°C]. A grade III/VI left apical systolic heart murmur (previously noted by the veterinarian) and strong, synchronous femoral pulses were present. The dog’s abdomen was tense and slightly distended, but non-painful on palpation.

Abdominal radiographs revealed a large amount of free gas within the peritoneal cavity as well as free fluid and a large gas-filled structure in the mid to left ventral abdomen (Figure 1). Interpretation of thoracic radiographs indicated mild hypovolemia.

Figure 1.

Figure 1

Left lateral (A) and ventrodorsal (B) abdominal radiographs in a dog with splenic abscess rupture and secondary pneumoperitoneum and septic peritonitis. There is a large volume of free peritoneal gas, loss of serosal detail, and a large, gas-filled structure in the left-mid ventral abdomen.

Oscillometric systolic blood pressure was 80 mmHg. Intravenous access was obtained and two 1 L boluses (42.4 mL/kg BW) of a balanced isotonic crystalloid solution (Normosol-R; Hospira, Lake Forest, Illinois, USA) and a 4.2 mL/kg BW bolus of a synthetic colloid (Hespan; B. Braun Medical, Bethlehem, Pennsylvania, USA) were administered to achieve normotension. Venous blood gas and electrolyte analysis showed a metabolic acidosis (BE −8.6) with hyperlactatemia (4.3 mmol/L; RR: < 2.5 mmol/L), anemia (PCV 28%; RR: 30% to 55%), and hypoglycemia (3.8 mmol/L; RR: 4.5 to 6.2 mmol/L). Additional treatments included 50% dextrose (Dextrose; APP Pharmaceuticals, Schaumburg, Illinois, USA), 1 mL/kg BW, to correct hypoglycemia, maropitant (Cerenia; Zoetis Animal Health, Parsippany, New Jersey, USA), 1 mg/kg BW, SQ, for nausea, and ampicillin/sulbactam (Unasyn; West-ward Pharmaceuticals, Eatontown, New Jersey, USA), 50.8 mg/kg BW, IV, and enrofloxacin (Baytril; Bayer, Whippany, New Jersey, USA), 21.4 mg/kg BW, IV, for suspected abdominal sepsis.

Simultaneous with these treatments an abbreviated abdominal ultrasound examination was performed. Large volumes of free peritoneal gas and echogenic swirling peritoneal effusion were present. A focal pocket of fluid and gas was noted to be either within the splenic parenchyma or between the spleen and the body wall (Figure 2). The large volume of free gas was suspected to be due to a gastrointestinal rupture. Abdominocentesis and fluid analysis revealed an exudate with marked septic neutrophilic inflammation. A fluid sample was submitted for bacterial culture and sensitivity.

Figure 2.

Figure 2

An abdominal ultrasound shows focal fluid and gas, likely within the splenic parenchyma.

Complete blood (cell) count showed mild anemia (RBC 4.4 × 106/μL and PCV 30.5%; RR: 5.5 to 8.5 × 106/μL and 31% to 56%, respectively) and a neutrophilia with left shift (neutrophils 12 506/μL and bands 2704/μL; RR: 3000 to 11 500/μL and 0 to 300/μL, respectively). Serum biochemistry revealed mild hypoalbuminemia (24 g/L; RR: 24 to 36 g/L), mild hyperglobulinemia (39 g/L; RR: 17 to 38 g/L), and elevated ALP (675 U/L; RR: 24 to 147 U/L). A coagulation profile showed hyperfibrinogenemia (16.4 μmol/L; RR: 3.4 to 10.7 μmol/L), decreased antithrombin III (102% NHP; reference value > 114%), and elevated D-dimers (1797 ng/mL, RR: 116.2 to 371.5 ng/mL).

In order to address source control, the patient was prepared for an exploratory laparotomy. Pre-medication was performed with fentanyl (Hospira), 4.9 μg/kg BW, IV, and lidocaine (West-ward Pharmaceuticals), 1.9 mg/kg BW, IV. Anesthesia was induced with midazolam (Zoetis Animal Health), 0.2 mg/kg BW, IV, ketamine (Ketaset; Zoetis Animal Health), 2.1 mg/kg BW, IV, and alfaxalone (Alfaxan; Jurox, North Kansas City, Missouri, USA), 0.6 mg/kg BW, IV. The dog was intubated and maintained on sevoflurane (Sevo-Flo; Zoetis Animal Health), 1% to 2%, fentanyl (Hospira), 5 μg/kg BW per hour, lidocaine (West-ward Pharmaceuticals), 2 mg/kg BW per hour, and ketamine 0.6 mg/kg BW per hour. The dog received isotonic crystalloid, 230 mL/h for the first hour of anesthesia and 115 mL/h thereafter, and a synthetic colloid, 115 mL/h.

The exploratory laparotomy revealed what appeared to be a ruptured splenic mass draining purulent material (Figure 3). Suction was used to remove the purulent exudate. No other abnormalities were noted. A splenectomy was performed and the abdomen was lavaged with copious amounts of 0.9% sodium chloride. Samples of the exudate and splenic tissue were immediately submitted for bacterial culture and sensitivity and the spleen was submitted for histopathology. A Jackson-Pratt drain was placed to provide closed active suction and the abdomen was closed routinely. Other than hypotension (mean arterial pressure ranging between 58 and 68 mmHg), no anesthetic complications were encountered. Recovery from anesthesia was uneventful.

Figure 3.

Figure 3

Intraoperative view of what appears to be a ruptured splenic mass draining purulent material.

An anaerobic Gram-positive rod was cultured from samples obtained before and during surgery. The organism failed to grow when subcultured for identification and susceptibility testing. There was no aerobic growth. Histopathology of the splenic “mass” identified severe, locally extensive, chronic necrosuppurative splenitis with intralesional bacteria, consistent with an abscess. There was no evidence of neoplasia in any of the sections examined.

After surgery, the patient was administered fentanyl, 3 μg/kg BW, IV, followed by 3 μg/kg BW per hour for analgesia and administered a bolus of a synthetic colloid, 4.2 mL/kg BW, IV for hypotension, which normalized mean arterial blood pressure. The patient was instrumented with a central venous catheter to optimize fluid therapy and drug administration, an indwelling urinary catheter to monitor urine output, and continuous ECG to monitor for arrhythmias. Isotonic crystalloids and a synthetic colloid were administered throughout the night to optimize intravascular volume and oncotic support, metoclopramide (Hospira), 0.04 mg/kg BW per hour, was administered to promote gastrointestinal motility, pantoprazole (Pfizer, Philadelphia, Pennsylvania, USA), 1.06 mg/kg BW, IV, q24h, was administered to prevent gastrointestinal ulceration, and ampicillin/sulbactam, 50.8 mg/kg BW, IV, q8h and metronidazole (B. Braun Medical), 15.2 mg/kg BW, IV, q12h, were administered for abdominal sepsis. Enrofloxacin (Bayer), 15.2 mg/kg BW, IV, q24h, was continued for abdominal sepsis and maropitant (Zoetis Animal Health), 1 mg/kg BW, IV, q24h, was continued for nausea.

The patient did well overnight. Fluid output matched fluid input and the effusion output from the abdominal drain was within normal parameters. The synthetic colloid was discontinued and all remaining treatments remained the same throughout the day. A coagulation panel, abbreviated chemistry panel, and CBC showed all parameters trending toward normal.

An echocardiogram was performed to investigate the cause of the heart murmur and showed moderate mitral regurgitation (chronic valvular disease, ACVIM stage B2) and mild pulmonary hypertension. A phosphodiesterase inhibitor and an angiotensin-converting enzyme inhibitor were recommended upon recovery.

Urine and effusion output remained within normal parameters and the Jackson-Pratt drain and urinary catheter were removed 2 d after surgery. Fentanyl was discontinued and buprenorphine (Reckitt Benckiser, Hull, England), 0.01 mg/kg BW, IV, q8h, was administered for analgesia. Three days after surgery, all IV medications were discontinued, and the patient was administered oral equivalents. The dog was discharged from the hospital 4 d after surgery. Recheck examination 1 wk later revealed no residual problems.

Discussion

In veterinary patients, free gas within the abdomen is typically gastrointestinal in origin and indicative of septic peritonitis. Splenic abscesses are rare in veterinary patients and, to the authors’ knowledge, this is the first report of splenic abscess rupture with secondary pneumoperitoneum in a dog.

In humans, the reported incidence of splenic abscesses is 0.14% to 0.7% and a review of splenic abscesses over a period of 19 y yielded only 67 cases (11,12). Predisposing factors for development of splenic abscess include immunosuppression, trauma, contiguous infection, hematogenous infection, splenic infarction, and diabetes (1,11,13,14). In veterinary patients, abscesses are generally associated with conditions that compromise vascular supply or drainage and splenic foreign body has been described as a cause of abscessation and secondary septic peritonitis in a cat (15,16). In dogs, leishmaniasis is the only immunosuppressive condition that has been reported as a predisposing factor in a dog with complete splenic abscessation (5). Splenic abscess has been reported to develop weeks after a traumatic event, with subsequent ischemia creating an ideal environment for bacterial growth. While unwitnessed, the dog reported here suffered unknown trauma approximately 2 wk before presentation, as evidenced by a laceration on the stifle, and this could have been the inciting cause of the splenic abscessation.

Based on ultrasound findings, a splenic abscess was considered as a differential diagnosis, but deemed unlikely to be a cause of such a large volume of free peritoneal gas. In the previously reported dog with complete splenic abscessation, ultrasound findings indicated gas bubbles within the splenic abscess itself, but free peritoneal gas was not documented (4). The presentation of pneumoperitoneum secondary to splenic abscess rupture is a unique finding in this case.

Bacterial agents documented in humans with splenic abscess include Staphylococcus aureus, Streptococcus viridans, Klebsiella spp., Escherichia coli, and Salmonella enteritidis (14,17,18). In veterinary patients, Staphylococcus epidermidis, Staphylococcus pseudintermedius, Clostridium spp., and Fusobacterium necrophorum have been documented in splenic abscesses (4,5). Several of these bacteria produce gas and have been associated with emphysematous infections (Klebsiella spp., E. coli, S. enteritidis, Clostridium spp., and F. necrophorum) (1921). In the absence of gastrointestinal rupture and an otherwise negative abdominal exploration, gas originating from bacteria is the most likely explanation of pneumoperitoneum in this dog. Considering that a Gram-positive anaerobic rod was cultured from the fluid samples in this dog and that free air was present, we suspect that the bacteria present were Clostridium spp.

Both fluid samples in this case yielded an anaerobic Gram-positive rod, but subculture did not yield identification. The most common Gram-positive rod bacteria isolated from cats and dogs include Clostridium, Actinomyces, and Eubacterium (19). Anaerobic samples must be handled with extreme care prior to arrival at a laboratory (19). Additionally, cultivation of anaerobic bacteria is laborious and time-consuming and, despite best efforts and practices, may not yield growth or identification (19). More than 70% of cultured anaerobic bacteria are mixed with aerobes and, when involved in an infectious process, there is almost always an average of 2 anaerobic species admixed with aerobes (19). Since anaerobic culture samples are sensitive to handling and they frequently grow with a variety of other bacteria, it is interesting that bacterial culture yielded only an anaerobic Gram-positive rod in this case. This patient had received a course of ciprofloxacin, which ended approximately 1 wk before presentation. Fluoroquinolones have primarily Gram-negative spectrum with some Gram-positive spectrum but are not known for their activity against anaerobes. Although ciprofloxacin therapy was discontinued 1 wk before presentation, it may have interfered with obtaining a positive aerobic culture. Regardless of the etiologic agent in this case, splenectomy and broad-spectrum antibiotics appear to have resulted in definitive resolution.

To the authors’ knowledge, this is the first report of large-volume pneumoperitoneum and septic peritonitis subsequent to splenic abscess rupture in a dog. Splenic abscess is a rare entity and splenic abscess with secondary pneumoperitoneum has been reported in humans. Splenic abscessation should be considered as a differential diagnosis for pneumoperitoneum in dogs.

Footnotes

Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office (hbroughton@cvma-acmv.org) for additional copies or permission to use this material elsewhere.

References

  • 1.Spangler WL, Culbertson MR. Prevalence, type, and importance of splenic diseases in dogs: 1480 cases (1985–1989) J Am Vet Med Assoc. 1992;200:829–834. [PubMed] [Google Scholar]
  • 2.Day MJ. A review of pathological diagnosis made from 87 canine splenic biopsies. J Small Anim Pract. 1995;36:426–433. doi: 10.1111/j.1748-5827.1995.tb02769.x. [DOI] [PubMed] [Google Scholar]
  • 3.Sprada AG, Hartmann HF, Huppes RR, et al. Splenic abscess in a dog. Acta Sci Vet. 2015;43:1–4. [Google Scholar]
  • 4.Abdellatif A, Gunther C, Peppler, Kramer M. A rare case of splenic abscess with septic peritonitis in a German shepherd dog. BMC Vet Res. 2014;10:1–6. doi: 10.1186/s12917-014-0201-z. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Ginel PJ, Lucena R, Arola J, Martin MP, Mozos E. Diffuse splenomegaly caused by splenic abscessation in a dog. Vet Rec. 2001;149:327–329. doi: 10.1136/vr.149.11.327. [DOI] [PubMed] [Google Scholar]
  • 6.Barron-Reyes JE, Chavez-Galvan JC, Martinez-Peralta JA, Lopez-Valdes JC. Rotura esplénica secundaria a absceso, causa poco común de neumoperitoneo. Reporte de un caso. Cir Cir. 2017;85:62–67. doi: 10.1016/j.circir.2016.10.021. [DOI] [PubMed] [Google Scholar]
  • 7.Bauman Z, Lim J. Pneumoperitoneum as a result of a ruptured splenic abscess. J Surg Case Rep. 2013;12:1–3. doi: 10.1093/jscr/rjt111. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.van Nunspeet L, Eddes EH, de Noo ME. Uncommon cause of pneumoperitoneum. World J Gastrointest Surg. 2013;5:329–331. doi: 10.4240/wjgs.v5.i12.329. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Ishigami K, Decker GT, Bolton-Smith JA, Samuel I, Wilson SR, Brown BP. Ruptured splenic abscess: A cause of pneumoperitoneum in a patient with AIDS. Emerg Radiol. 2003;10:163–165. doi: 10.1007/s10140-003-0302-7. [DOI] [PubMed] [Google Scholar]
  • 10.Braat MN, Hueting WE, Hazebroek EJ. Pneumoperitoneum secondary to a ruptured splenic abscess. Intern Emerg Med. 2009;4:349–351. doi: 10.1007/s11739-009-0253-4. [DOI] [PubMed] [Google Scholar]
  • 11.Chun CH, Raff MJ, Contreras L, et al. Splenic abscess. Med. 1980;59:50–65. doi: 10.1097/00005792-198001000-00003. [DOI] [PubMed] [Google Scholar]
  • 12.Chang K, Chua S, Changchien C, et al. Clinical characteristics and prognostic factors of splenic abscess: A review of 67 cases in a single medical center of Taiwan. World J Gastroenterol. 2006;12:460–464. doi: 10.3748/wjg.v12.i3.460. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Tung CC, Chen FC, Lo CJ. Splenic abscess: An easily overlooked disease? Am Surg. 2006;72:322–332. [PubMed] [Google Scholar]
  • 14.Priyadarshini S, Shanmugam D, Palraj KK, Antony T, Thayanidhi P. Salmonella typhi Splenic abscess following blunt abdominal injury: A case report. J Clin Diagn Res. 2016;10:DD01–DD02. doi: 10.7860/JCDR/2016/19789.8156. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Richter MC. Spleen. In: Tobias KM, Johnston SA, editors. Veterinary Surgery Small Animal. St. Louis, Missouri: Elsevier; 2012. pp. 1341–1352. [Google Scholar]
  • 16.Culp WT, Aronson LR. Splenic foreign body in a cat. J Feline Med Surg. 2008;10:380–383. doi: 10.1016/j.jfms.2007.12.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Ooi LL, Leong SS. Splenic abscesses from 1987 to 1995. Am J Surg Pathol. 1997;174:87–93. doi: 10.1016/s0002-9610(97)00030-5. [DOI] [PubMed] [Google Scholar]
  • 18.Martins ACA, Vieira LFDF, Ferraz AAB, dos Santos MA, Jr, Ferraz EM. Abscesso esplênico: Mudança nos fatores de risco e nas opções de tratamento. Rev Col Bras Cir. 2005;32:337–341. [Google Scholar]
  • 19.Greene CE, Jang SS. Anaerobic infections. In: Greene CE, editor. Infectious Diseases of the Dog and Cat. St. Louis, Missouri: Elsevier; 2012. pp. 411–416. [Google Scholar]
  • 20.Tariq T, Farishta M, Rizvi A, Irfan FB. A case of concomitant emphysematous cystitis and Clostridium difficile colitis with pneumoperitoneum. Cureus. 2018;10:1–6. doi: 10.7759/cureus.2897. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Hung PH, Chiu CY, Hsueh PR. Gas-forming splenic abscess due to Salmonella enterica serotype Enteritidis in a chronically hemodialyzed patient. J Microbiol Immunol Infect. 2007;40:276–278. [PubMed] [Google Scholar]

Articles from The Canadian Veterinary Journal are provided here courtesy of Canadian Veterinary Medical Association

RESOURCES