Primary Omental Abscessation or Omental Infarction in Four Dogs
Primary omental abscessation was diagnosed in three dogs after laparotomy. Laparotomy was performed to explore an abdominal mass of unknown origin and chronic fat necrosis diagnosed in one dog as an incidental finding during ovariohysterectomy. Primarily hypoechoic masses not connected to any abdominal structures were visualized with abdominal ultrasound in three dogs. Suppurative inflammation was diagnosed from fine-needle aspirate evaluation in two dogs. Bacteria were cultured from two abscesses despite the absence of organisms on Gram stain, cytology, and histopathology. Foreign material was found in one abscess. All four dogs experienced weight loss and/or an episode of gastrointestinal signs. Primary omental abscessation may be preceded by omental vascular compromise and/or interaction of the omentum with foreign material.
Introduction
Omental abscessation in the absence of recent surgery or intraabdominal infection is uncommon in veterinary and human cases.1 This may be due to the extensive immune system within the omentum itself.2 Indeed, omentalization (i.e., the deliberate placement of the omentum into a desired location by the surgeon) has been used to successfully treat nonresectable abscesses of the canine prostate, uterine stump, and pancreas.3–5 The same properties of the omentum that allow it to effectively wall off areas of infection can also make an omental abscess difficult to detect until it leaks and causes peritonitis, erodes health due to chronic inflammation, and/or creates a space-occupying effect. Suggested etiologies for a primary omental abscess in humans include compromise of omental vasculature by infarction or torsion, foreign body reaction, and hematogenous spread.1 The purpose of this paper is to describe the clinical presentation, diagnostic assessment, and treatment of three dogs with primary omental abscesses and one dog with omental infarction.
Case Reports
Case No. 1
A33-kg, overweight, spayed female golden retriever known to be at least 13 years old was presented after an episode of vomiting. The referring veterinarian identified a large abdominal mass, suspected to be splenic in origin, on abdominal palpation and radiographs. The dog was referred to the Washington State University Veterinary Teaching Hospital the following day.
Case no. 1 had an extensive medical history, with previous diagnoses of cardiomegaly, pulmonary edema, hypertension, arthritis, lumbosacral spondylosis, hypothyroidism, uveitis, glaucoma (with enucleation of the right eye), oral ossifying epulis, and vulvar trichoblastoma. Abdominal ultrasonography was performed as part of the workup for hypertension 16 months earlier, and no significant findings were seen. Fourteen weeks earlier, case no. 1 was presented to the referring veterinarian because of diarrhea, hair loss, difficulty going upstairs, unsteady hindquarters, and a 5-kg weight loss. Current medications were enalapril, furosemide, digoxin, carprofen, levothyroxine sodium, and prednisolone acetate eye drops. Mucous membranes were pale, heart rate was regular with good pulses, lung sounds were clear, and the abdomen was pendulous. A fluid wave and possible intraabdominal mass were palpated. A complete blood count (CBC) was normal. Abnormalities on a serum biochemical panel were elevated blood urea nitrogen (BUN) concentration (34.8 mg/dL, reference range 9 to 27 mg/dL) and amylase activity (1801 U/L, reference range 500 to 1500 U/L). The digoxin dose was reduced and the dog improved.
Upon the dog’s arrival at the Washington State University Veterinary Teaching Hospital, the owner reported the dog had eaten well the night before and was no longer vomiting. Physical examination revealed marked abdominal distension and a nonpainful, approximately 8-cm diameter, round moveable mass in the cranioventral abdomen. Other abnormalities were a grade I/VI systolic heart murmur, mild to moderate dental disease, and ossifying epulis. ACBC revealed a mature neutrophilic leukocytosis (17,600 white blood cells [WBCs]/μL, reference range 5800 to 11,700 WBCs/μL; 15,664 neutrophils/μL, reference range 3000 to 7100 neutrophils/ μL) and mild microcytic, hypochromic anemia (packed cell volume [PCV] 37%, reference range 38% to 59%; mean corpuscular volume [MCV] 52 μ3, reference range 64 to 73 μ3; mean corpuscular hemoglobin 18 picograms, reference range 21 to 26 picograms). Large platelets and a few keratocytes, blister cells, target cells, and schistocytes were seen on a blood smear. Serum biochemical abnormalities were high alkaline phosphatase (ALP) activity (120 U/L, reference range 14 to 72 U/L); high concentrations of BUN (68mg/dL, reference range 9 to 27mg/dL), creatinine (2.6 mg/dL, reference range 0.7 to 1.2 mg/dL), and phosphorus (6.9 mg/dL, reference range 3.3 to 6.0 mg/dL); and low concentrations of albumin (2.4 g/dL, reference range 2.5 to 3.8 g/dL), sodium (149 mEq/L, reference range 163 to 168 mEq/L), and chloride (113 mEq/L, reference range 117 to 120 mEq/L). Activated partial thromboplastin time (aPTT) and partial thrombin time (PTT) were within reference ranges.
Echocardiography revealed moderately increased left ventricular wall thickness with normal systolic function and no obvious cardiac masses. Systolic blood pressure was elevated at 180 mm Hg. Chest radiographs revealed a prominent aortic arch and left ventricular hypertrophy, both consistent with systemic hypertension. An approximately 11-cm diameter spherical mass was seen in the ventral aspect of the cranial third of the abdomen with ultrasound. The mass was composite in nature with hyperechoic swirls of tissue embedded in an essentially hypoechoic tissue matrix. Repeated efforts to show attachment of the mass to the spleen or to the liver were unsuccessful. Aslight amount of free abdominal fluid was present.
Based on the dog’s signalment, red blood cell (RBC) changes, and ultrasound findings, hemangiosarcoma was the primary differential diagnosis for the abdominal mass. Digoxin and furosemide were discontinued because of normal cardiac function and to allow more accurate assessment of renal function. Enalapril was continued for systemic hypertension, but the dose was decreased. Because iatrogenic hyperthyroidism was a potential cause of the hypertension, the thyroxine dose was halved.
Six days later, the dog returned for a scheduled exploratory laparotomy. Packed cell volume was 41%, and total protein was 7.4 g/dL. Serum BUN (31 mg/dL) and creatinine (1.5 mg/dL) concentrations were improved but still elevated. Urine specific gravity was 1.017, confirming renal compromise. Blood pressure was 172 mm Hg systolic, 109 mm Hg diastolic, and 129 mm Hg mean.
A ventral midline abdominal exploratory was performed. A 15-cm diameter mass, estimated to weigh approximately 2 kg, was present in the greater omentum [Figure 1A]. No connections were between the mass and any other organs. Purulent fluid oozed out of the mass during manipulation. A partial omentectomy was performed, and the large vessels were ligated with 2-0 silk suture. A few thin, flexible, linear, blue fragments (approximately 1 × 0.1 cm) of unknown composition were found in association with the mass. A copious amount of purulent material leaked out of the excised mass after it was incised [Figure 1B]. Fluid cytology revealed a pyogranulomatous inflammation with previous hemorrhage and secondary fibroplasia. Rare pieces of extracellular, angular, blue-green material consistent with plant material were also seen.
Cefazolin (22 mg/kg intravenously [IV]) was given at anesthesia induction, every 1.5 hours intraoperatively (two doses), and every 6 hours postoperatively (two doses). Amoxicillin-clavulanic acid (20.5 mg/kg per os [PO] q 12 hours) was then administered for 14 days postoperatively. Postoperative management also included IV fluids and analgesics. Recovery was uneventful with the exception of persistent hypertension.
Histological examination of the omental mass revealed thick bands of connective tissue partially surrounding a central area of inflammation that contained neutrophils, macrophages, and a few eosinophils. Occasional foreign matter consisting of bright pink, thin, angular material was contained in dense granulomas of neutrophils and macrophages. Small numbers of multinucleated giant cells and aggregates of streaming cellular debris were adjacent to some of the foreign material. The occasional honey-combed appearance of the material was suggestive of plant matter. The histological diagnosis was chronic, active, locally extensive omental abscess associated with foreign material. The individual fragments of blue material recovered intraoperatively did not survive the histological preparation process. Other histological findings from biopsies taken intraoperatively included moderate, diffuse, hydropic degeneration with iron granulomas in the liver; moderate, chronic medullary fibrosis in the kidney; and normal pancreas. No organisms were identified on cytology, Gram stain, histological section, aerobic culture, or anaerobic culture of the omental mass or its contents.
Two weeks postoperatively, the dog was doing well. No abnormalities were detected on abdominal palpation. A serum biochemical panel found elevated BUN (45 mg/dL), creatinine (2.6 mg/dL), and potassium (6.0 mEq/L, reference range 4.4 to 5.3 mEq/L) concentrations. Systolic blood pressure ranged from 190 to 220 mm Hg. The dog was started on atenolol for hypertension. Eight days later, the dog became very weak and collapsed. Physical examination by the referring veterinarian revealed a left head tilt, nonpositional nystagmus, disorientation, and severe weakness. The heart rate was 120 beats per minute and steady, pulses were strong, and mucous membranes were pink. After treatment with IV diazepam, intramuscular dexamethasone, and subcutaneous fluids, the dog appeared more comfortable; however, neurological signs and weakness persisted. The dog died later at home. No necropsy was performed.
Case No. 2
A10-year-old, spayed female, miniature schnauzer was presented for assessment of urinary incontinence. Abnormal findings on physical examination were a 15% weight loss compared to the previous year (from 6.7 kg to 5.7 kg); bilateral lenticular sclerosis; a grade 2/6 heart murmur with the point of maximal intensity over the right apex; and a firm, round abdominal mass that did not appear to be associated with any organ. The dog was tense on abdominal palpation but did not appear painful.
A CBC was unremarkable. Alkaline transferase (ALT) activity (142 U/L, reference range 12 to 67 U/L) and glucose (125 mg/dL, reference range 70 to 117 mg/dL) concentrations were elevated. Fecal matter prevented clear visualization of the mass on abdominal radiographs. Results of a fine-needle aspiration (FNA) of the mass, guided by palpation, were consistent with a pyogranulomatous inflammatory response. The owner declined further workup at that time. Diethylstilbestrol was dispensed for presumptive urinary sphincter mechanism incompetence.
Two months later, the dog was presented again for further assessment of the abdominal mass. The dog had been doing well, and urinary incontinence had improved. Body weight had increased to 6.5 kg, and the body condition score was 3 out of 5. Grade 3/5 dental disease was present. On abdominal palpation, the dog tensed such that the mass could not be palpated; but once again, the dog did not seem overtly painful.
A CBC indicated mild hypochromic anemia (PCV 36%; RBCs 5.55 × 106/μL, reference range 5.6 to 8.5 × 106/μL; hemoglobin [Hb] 12.2 g/dL, reference range 13 to 19 g/dL); normal total WBC (10,200 cells/μL) with normal neutrophil (6426 cells/μL) and lymphocyte (2556 cells/μL) concentrations; monocytosis (1020 cells/μL); eosinophilia (204 cells/μL, reference range <100 cells/μL); and thrombocytosis (488,000 platelets/μL, reference range 157,000 to 394,000 platelets/μL). Slight anisocytosis and large platelets were seen on a blood smear. Abnormalities on a serum biochemical panel were elevated ALT (162 U/L) and ALP (165 U/L) activities, increased globulin (4.3 g/dL, reference range 2.7 to 3.8 g/dL) concentration, and decreased BUN (7 mg/dL) and calcium (8.4 mg/dL, reference range 9.1 to 12 mg/dL) concentrations.
Abdominal ultrasound revealed a round mass with a maximum diameter of 2.8 cm cranial to the bladder and in isolation from other abdominal structures. The rim of the mass had alternating hypoechoic and hyperechoic layers suggestive of an intestinal wall, but no intestinal loop could be traced to this structure. The center of the mass was hypoechoic. The spleen contained multiple masses of mixed echogenicity; the largest mass was 2.1 cm in diameter. Enlarged lymph nodes in the mesenteric root retained central hyperechogenicity, suggestive of reactive lymphadenopathy. Ultrasound-guided FNAs were indicative of a suppurative, possibly septic inflammatory response in the mass and mild extramedullary hematopoiesis in the spleen. Chest radiographs were within normal limits.
At surgery, a 5-cm diameter, spherical mass was found in the omentum cranial to the bladder; it was removed via partial omentectomy performed with monopolar electrocautery. A partial splenectomy and liver biopsy were performed. The dog received one dose of cefazolin (22 mg/kg IV) intraoperatively. No additional antibiotics were administered.
Postoperative management included IV fluids and analgesics. One day postoperatively, a CBC and blood smear revealed a neutrophilic leukocytosis (24,500 WBCs/μL; 17,640 neutrophils/μL) with a left shift (3185 band cells/μL, reference range <300 band cells/μL); thrombocytosis (594,000 platelets/μL, reference range 157,000 to 394,000 platelets/μL); hyposegmented polymorphonuclear cells; Dohle bodies; and platelet clumps. The dog was discharged on the second postoperative day, and recovery was uneventful.
The omental mass was filled with a milky, suppurative fluid. Histological diagnosis was a focal, chronic omental abscess. The abscess was cystic with a discrete, dense collagenous wall infiltrated with numerous small blood vessels and aggregates of lymphocytes admixed with large numbers of fibrocytes. The center of the cyst was filled with necrotic tissue and sheets of neutrophils and macrophages with fragments of mineralized necrotic debris. The omentum surrounding the mass had multifocal, extensive areas of necrosis with saponification of adipose tissue and numerous hemosiderophages. Nodular hyperplasia of the spleen, hydropic degeneration of the liver, and mild suppurative hepatitis were also present. No organisms were seen on a Gram stain, cytology, or histopathology from the omental mass, and aerobic cultures were negative. A moderate number of Bacteroides ureolyticus grew on anaerobic culture.
Nine months later, case no. 2 was diagnosed with severe pancreatitis and diabetes mellitus. Abdominal ultrasound showed right lobe pancreatitis with secondary peritonitis and diffuse alterations in hepatic echogenicity. Hepatic FNAs were consistent with mild hepatic vacuolar degeneration, cholestasis, and possible mild hepatic lipidosis. The dog responded to medical treatment for this episode of pancreatitis as well as for another episode experienced 2 months later. One year following the omental abscess, the dog continued under treatment for diabetes mellitus.
Case No. 3
A 1.5-year-old, 37.3-kg, neutered male yellow Labrador retriever was referred to the Washington State University Veterinary Teaching Hospital with a 3-day history of anorexia, depression, fever, and abdominal distention; one episode of diarrhea; and a report of loss of detail on abdominal radiographs. Two months earlier, the referring veterinarian had given the dog dipyrone and sulfadiazine/trimethoprim for diarrhea, which resolved. Weight loss (from 39.5 kg to 36.5 kg over 3 months) was documented at that time. The following month, the veterinarian surgically removed an approximately 1.8-cm diameter mass that had been on the left caudal lumbar area for 2 weeks. The histological diagnosis was focally extensive dermal fibrosis with reactive connective tissue and a necrotic tract.
Upon presentation at the Washington State University Veterinary Teaching Hospital, the dog was depressed, tachycardic, tachypneic, normothermic, and had abdominal distension with a palpable fluid wave. The abdomen was not painful. A CBC revealed a leukocytosis (28,100 WBCs/μL) with neutrophilia (17,141 cells/μL); a left shift (2810 band cells/μL); lymphocytosis (5620 cells/μL, reference range 1100 to 5100 cells/μL); monocytosis (2529 cells/mL); and a mild hypochromic, microcytic anemia (PCV 34%; Hb 12.4 g/dL; MCV 63 μ3; RBC distribution width 17%, reference range 14% to 16%). Anisocytosis was seen on a blood smear. Elevated ALP activity (106 U/L) and decreased albumin (2.2 g/dL), globulin (2.3 g/dL), calcium (7.8 mg/dL), phosphorus (2.9 mg/dL), sodium (117 mEq/L), potassium (4.1 mEq/L), chloride (94 mEq/L), and carbon dioxide (16.2 mmol/L, reference range 18 to 24 mmol/L) concentrations were present on a serum biochemical panel.
Abdominocentesis recovered 2100 mL of a serosanguineous exudate containing >170,000 cells/μL (97% moderately degenerate neutrophils, 3% macrophages) and 3 g/dL protein. On abdominal ultrasound, a 2.5 × 5 × 2.5-cm hypoechoic cluster of tissue was found immediately dorsal and medial to the spleen; it could not be connected to any abdominal structures. An FNA of the mass recovered 84% markedly degenerate neutrophils and 16% macrophages, indicating a suppurative inflammatory response; no organisms were seen. Thoracic radiographs showed a small caudal vena cava indicative of dehydration. Sternal lymphadenopathy, consistent with cranial abdominal disease, was also seen. An approximately 1.5-cm focus of periosteal reaction was present on the ventral third of the left eighth rib.
At surgery, a firm, red, necrotic-appearing, 5-cm diameter mass containing multiple pockets of purulent material was excised from the greater omentum. The abdomen was lavaged, and two Jackson-Pratt drains were placed. An esophagostomy feeding tube was also placed. Postoperative management included IV fluids, hetastarch, analgesics, ranitidine, sucralfate, enrofloxacin (2.4 mg/kg IV q 12 hours), ampicillin (22 mg/kg IV q 8 hours; the first dose was given intraoperatively), and feedings through the esophagostomy tube. Antibiotics were administered for a total of 2 weeks, with a switch to oral medications (enrofloxacin 3.6 mg/kg PO q 12 hours; ampicillin 20 mg/kg PO q 8 hours) 3 days postoperatively.
The morning following surgery, the dog was alert and able to go on a short walk outside. Fifteen minutes later, the dog was recumbent and severely pale and was diagnosed with hemoabdomen. A CBC showed pronounced neutrophilic leukocytosis (51,200 WBCs/μL; 34,816 neutrophils/ μL) with a left shift (10,752 band cells/μL) and monocytosis (2048 cells/μL). Neutrophils had moderate toxic changes and Dohle bodies. Anemia (PCV 15% and 2.4 × 106 RBCs/μL) and hypoproteinemia (1.0 g albumin/dL and 1.7 g globulin/dL) were marked. The PTT was normal, while aPTT was prolonged (18.4 seconds, reference range 8.9 to 12.8 seconds). Treatments included blood transfusions, hetastarch, and lactated Ringer’s solution. The dog was returned to surgery, and bleeding omental vessels were ligated. On the third postoperative day, the dog began to eat voluntarily, and a full recovery eventually occurred.
No organisms were seen on Gram stain of the abdominal fluid sampled during the first surgery. Culture of the abdominal fluid grew many Prevotella species and a few Escherichia coli. Histological examination of the omentum identified severe, chronic, multifocal, pyogranulomatous to abscessing omentitis consistent with a foreign body reaction, although no foreign material was seen. No bacteria or fungal organisms were found with special histological stains.
Four months after surgery for the omental abscess, an approximately 2.5-cm diameter, discoid subcutaneous mass and its accompanying tract (approximately 6.6-cm long) of inflamed tissue was removed from over the left rib cage. A Penrose drain was placed. The quantity and duration (>10 days) of drainage were both greater than expected, and the site took several months to heal. The histological diagnosis was ischemic, fibrotic, moderately inflamed adipose tissue likely secondary to trauma or ischemia. The dog was last seen 3.5 years after the omental abscess and was doing well.
Case No. 4
A 1-year-old, intact female Labrador retriever was seen on emergency for a peracute onset of repetitive, profuse vomiting; abdominal pain; and shock (pale mucous membranes, prolonged capillary refill time, tachycardia, weak pulses, tachypnea, and hypotension). The dog had been fine when placed alone in a fenced-in yard 1 hour earlier. Blood smear and CBC were normal. Serum biochemical abnormalities (after fluid treatment for shock) were elevated ALT (1120 U/L), ALP (81 U/L), and amylase (1415 U/L) activities and decreased concentrations of protein (1.1 g albumin/dL; 2.0 g globulin/dL), calcium (8.6 mg/dL), and potassium (3.6 mEq/L). Canine parvoviral antigen test and fecal smear and flotation were negative. On abdominal radiographs, the stomach was displaced dorsally and to the left, with the long axis nearly perpendicular to the ribs, suggestive of an extraluminal mass or local peritonitis. Treatment included IV isotonic fluids, hetastarch, ranitidine, sucralfate, and ampicillin.
The following day, the dog was markedly improved. A CBC showed leukocytosis (16,000 cells/μL) with neutrophilia (12,800 cells/μL) and eosinophilia (640 cells/μL). A blood smear revealed slight anisocytosis and polychromasia, a few hyposegmented neutrophils, toxic neutrophils, reactive lymphocytes, rare Howell-Jolly bodies, and giant platelets. Elevated ALT (1879 U/L), ALP (131 U/L), and amylase (1415 U/L) activities and hypoproteinemia (3.0 g albumin/dL; 2.1 g globulin/dL) were still present. On a barium contrast study, the stomach was back in its normal position, gastrointestinal transit time was normal, and no evidence of luminal compromise was seen. The dog was discharged on sucralfate and ranitidine. A bland diet was administered, and recovery was complete.
During routine ovariohysterectomy 1 year later, a 1.5 × 2 × 3-cm omental mass was an incidental finding in the superficial leaf of the greater omentum; the mass was excised after surrounding omental vessels were ligated with polydioxanone suture. The histological diagnosis was chronic fat necrosis with focal eosinophilic and granulomatous peritonitis. These changes were consistent with disruption of the vascular supply, and such findings led to a presumptive diagnosis of omental infarction as the cause of the acute abdomen 1 year earlier.
Discussion
Primary omental abscessation and omental infarction are uncommon in dogs. The four dogs of this report were the only cases found during a computerized search of canine and feline medical records from January 1994 to March 2007 at the Washington State University Veterinary Teaching Hospital.
A search of the veterinary literature recovered two other cases of omental abscessation, both in dogs. A 17 × 18-cm, 2.1-kg omental abscess was removed from an 11-year-old, neutered male, German shepherd mixed-breed dog with concurrent discospondylitis.6 Clinical signs included 6 weeks of weight loss and abdominal distension. Cultures from the omental mass, blood, and peritoneal fluid were all positive for Staphylococcus intermedius. Because the original site of infection was not determined in this dog, it is unknown if the infection in the omentum was primary or secondary.
Staphylococcus intermedius was also cultured from a 2.2-kg omental mass removed from a 6-year-old, intact male German shepherd dog with acute ataxia, weight loss, and a palpable abdominal mass. Botryomycosis (i.e., bacterial pseudogranuloma) was the histological diagnosis in this dog.7 Neither of these reports focused on primary omental abscessation in their discussions.
The initiating cause of omental abscessation in case nos. 1, 2, and 3 could not be definitively determined. Rodent models demonstrate that a very large inoculum of bacteria is required to create an intraabdominal abscess in a healthy animal; this dose is such that it can lead to fulminant sepsis and death.8 Based on this observation, together with the rarity of infection in the omentum relative to other sites of the body and the extensive omental antibacterial defense system, the likelihood is strong that omental vascular compromise and/or the presence of foreign material precede most cases of primary omental abscessation.1 During the several months prior to the diagnosis of omental abscess, case no. 1 had a period of weakness, weight loss, and diarrhea; case no. 2 had weight loss; and case no. 3 had an episode of diarrhea and weight loss similar to signs described for one dog in a previous report.7 Though unable to be proven, these episodes possibly represented some initial omental compromise or introduction of foreign material into the abdominal cavity, as discussed below.
Foreign material can reach the omentum via penetration of the peritoneum or luminal organs. No history of pene-trating injury to the abdomen or recent abdominal surgery (case nos. 1 and 2 were spayed >4 years prior to presentation) was reported for any of the dogs. However, a small gastroin-testinal perforation that seals on its own may go unnoticed by the owner or be dismissed as a transient gastrointestinal upset (similar to the gastrointestinal events reported for several of the dogs).9–11 Because marked foreign body reactions can be secondary to miniscule fragments of material, the inability of the surgeon or pathologist to find foreign material does not exclude the possibility that foreign material contributed to abscessation.12
Migrating plant awns, which can penetrate the gastrointestinal tract after ingestion, were suspected in case no. 3 because of subcutaneous masses with associated connective tissue tracts and prolonged drainage after excision.13 One mass was in the lumbar area (a location where inhaled migrating plant awns often lodge), and the other was near a site of costal periosteal proliferation, which can be a sign of foreign body migration.12,14 Ongoing inflammation associated with foreign material would explain why case no. 3 presented with a microcytic, hypochromic anemia despite an apparent acute onset of illness, as well as a historic weight loss.
The presentation and clinical course of illness in case no. 4 resembled that of segmental omental infarction or torsion in humans, who present with an acute abdomen that is often misdiagnosed as appendicitis due to its severity.15 These conditions are usually self-limiting, although they occasionally lead to omental necrosis and abscessation.16 In retrospect, the malposition of the stomach seen on radiographs of this dog was consistent with entrapment and strangulation of the omentum in the epiploic foramen. Resolution of the entrapment would explain the normal stomach position and resolving clinical signs the following day. In a dog operated on for acute abdomen, examination of the omentum for torsion or infarction is advised, especially when no other cause can be found.17
Obesity and cardiovascular disease (both present in case no. 1) are predisposing factors for omental infarction in humans.15 The extensive fat necrosis around the abscess in case no. 2 suggested an earlier bout of pancreatitis may have contributed to omental compromise. This dog later developed diabetes mellitus, which in humans has been associated with impairment of omental vascularization.15
The presentation of dogs with primary omental abscessation varied from acute illness to a persistent abdominal mass with minimal clinical signs. Abdominal distension, but not pain, was reported. When a mass was palpable, no definitive connection with a specific abdominal organ could be made; this suggested an omental origin. The most common abnormalities seen on blood analyses were mild anemia, mild to moderate inflammatory leukogram, and hepatobiliary inflammation, most likely from bacterial or toxic showering from the abscess. Alterations in protein levels were consistent with long-standing inflammation (hypoalbuminemia) or bacterial antigen stimulation (hyperglobulinemia). Postoperative exacerbation of neutrophilia, as identified in case nos. 2 and 3, is explained by granulopoiesis that had been upregulated to compensate for WBC sequestration and consumption in the abscess.18
Radiographic signs associated with an abdominal abscess in veterinary cases may include a soft-tissue mass containing gas or a gas-fluid interface, an air-fluid interface seen with a horizontal beam, and/or loss of serosal detail because of associated effusion.6 A soft-tissue mass was visible on abdominal radiographs in case no. 1, and a loss of detail was noted on radiographs from case no. 3 (similar to previous reports6,7), but the omental origin was not apparent and no gas was observed. Because neoplasia is a potential cause of any abdominal mass, performing chest radiography to look for metastatic disease is appropriate.
Similar to previous reports, abnormal tissue was detected on abdominal ultrasounds of all three dogs with omental masses, although none of the masses could be shown to originate from a specific tissue, including omentum.6,7 In these dogs, the dimensions of the omental masses measured intraoperatively were larger than those measured ultrasonographically. These discrepancies may be because measurements were taken from different reference points, precise margins were difficult to determine, and/or because ultrasound can measure directly through the center of a mass while intraoperative measurement of diameter of an intact mass requires a degree of estimation.
Canine abdominal abscesses generally appear as a hypoechoic mass with an irregular border on ultrasound. Ultrasound penetration of the mass is poor.19 Variations in echogenicity can occur because of differences in fluid viscosity and cellularity, density of granulomatous tissues, gas accumulation, presence of foreign material, and/or calcification.19 This ultrasonic appearance is not unique to abscesses; differential diagnoses include hematoma, primary or metastatic neoplasia with necrosis or hemorrhage, and complex cyst with cellular debris or hemorrhage.19 Magnetic resonance imaging, with its excellent delineation of the omentum and other soft tissues, would likely have been a more effective way to localize the mass to the omentum and assess for local metastases. This definitive procedure would increase the preoperative confidence of the surgeon and pet owner that surgery would successfully eliminate disease.20
Percutaneous FNA of abdominal masses is generally associated with high diagnostic accuracy and minimal complications, especially when under ultrasound guidance.21,22 Fine-needle aspiration was not performed in case no. 1 because of the high suspicion that the mass was a hemangiosarcoma.23 Fine-needle aspirates provided evidence of the suppurative nature of the intraabdominal masses in case nos. 2 and 3. This finding lessened the concern for malignancy but did not rule it out, as areas of necrosis and inflammation can mask underlying neoplasia.24
The presence of an abdominal mass of unknown origin was the main indication for exploratory surgery in all dogs with omental abscesses. Similar to previous reports, the abscess in case no. 1 weighed about 2 kg, demonstrating the remarkable ability of the omentum to wall off an area of inflammation from the rest of the abdominal cavity, even when the source of the inflammation is within the omentum itself.6,7 Partial omentectomy was performed with either electrocautery or sequential suture ligation of omental vessels. A margin of grossly normal omentum should be removed where possible, in case the mass is neoplastic. Perioperative challenges included leakage of purulent material from the mass (which was managed by packing moist laparotomy pads on and around the mass and performing lavage), proximity of the omental mass to the main splenic vessels (which required careful dissection), and postoperative management of abdominal drainage. Care must be taken to ensure that fat in the omentum does not prevent ligatures from completely collapsing encircled vessels. Since some omental tissue remains after removal of the abscess, the potential for future omental disease exists in all cases.
Bacteria cultured from the canine omental abscesses were all normal inhabitants of the oral cavity, intestine, and/or skin. These are all potential entry sites for foreign material, which often carries bacteria indigenous to its point of penetration into deeper tissue.12 Hematogenous spread of bacteria from the oral cavity of a dog with dental disease is also possible.25 Important to note is that positive cultures were obtained in case nos. 2 and 3 even though no microorganisms were identified with Gram stain, cytology, and histopathology. Thus, omental abscesses should be cultured for aerobic and anaerobic bacteria even in the absence of bacterial detection by other means. All dogs received antibiotics, although the duration of administration varied from a single intraoperative dose to 2 weeks. The indication for ongoing antibiotic administration is clear in dogs with purulent material free in the abdominal cavity. When the omental abscess is well-encapsulated, limiting antibiotics to the perioperative period may be sufficient.
Adverse consequences of omentectomy in otherwise healthy patients are not reported. Omentectomy is a recommended part of the treatment of human neoplasms with a high incidence of peritoneal dissemination (e.g., ovarian and advanced colorectal cancers), because the omentum serves as a site of tumor implantation.26 Omentectomy is also performed to prevent blockage of peritoneal catheters in dialysis patients.27 In veterinary medicine, omentectomy has been associated with decreased adhesion formation after abdominal surgery in the horse.28 However, omentectomy may adversely affect intraabdominal bacterial defenses in rats, and it is associated with increased mortality in dogs with experimentally induced drainage of pancreatic juice into the abdomen.29,30
Beneficial properties of the omentum include immune surveillance, sealing of gastrointestinal leaks, promotion of hemostasis, drainage of nonresectable abscesses, and stimulation of wound healing.3,4,31,32 Indiscriminate omentectomy is not recommended, because the omentum, via its inherent activity or through surgical omentalization, can be a key factor in the successful management of potentially life-threatening conditions. Also, the incidence of omental disease is low.
Conclusion
Dogs with primary omental abscessation or omental infarction may be presented with an acute illness or a persistent abdominal mass with few clinical signs, although a history of weight loss and/or gastrointestinal signs may exist. The leukogram may not accurately reflect the actual degree of inflammation or infection, especially in dogs with a chronic abscess. Ultrasound may be more informative than radiographs regarding the nature of the abdominal mass. Fine-needle aspiration is a useful tool to identify suppurative contents of the abscess. Despite absence of bacteria on Gram stain, cytology, and histopathology, aerobic and anaerobic cultures should always be performed. Omental abscesses can be cured with surgical resection and appropriate supportive care. Omental infarction may cause an acute abdomen that responds to medical therapy. The omentum should be examined for sites of infarction or abscessation during exploratory laparotomy for acute abdomen, especially when no other cause can be found.
Citation: Journal of the American Animal Hospital Association 45, 4; 10.5326/0450168
(A) A 15-cm diameter mass was found in the greater omentum of an approximately 13-year-old, spayed female golden retriever (case no. 1). No connections to any other organs were present. (B) After an incision was made into the excised mass with a scalpel blade, the abscess deflated and released a copious amount of purulent material.
