Case 1

A 10 yr old male castrated mixed-breed dog weighing 31.4 kg was presented to the emergency service for acute onset of nonspecific pain and shivering. A few days prior, the owner noticed his dog licking at his perianal region and signs of discomfort. Aside from this episode, the patient had no relevant previous medical history and was on no medications other than preventives. On presentation, the dog was quiet, alert, and responsive with normal vitals and unremarkable cardiopulmonary auscultation. On physical examination, he was euhydrated and mucous membranes were pink and moist, with a capillary refill time of less than 2 sec. He was noted to have a tense, painful abdomen and a firm right-sided perianal mass measuring ∼4 cm in diameter, displacing the rectum laterally, as well as significant sacral lymphadenopathy. A thoracic and abdominal focused assessment with sonography for trauma (T-FAST and A-FAST) did not reveal presence of free fluid. A venous blood gas did not reveal values out of the normal range, and thoracic radiographs showed no abnormalities. Fine needle aspirates were obtained from the perianal mass, and the patient was hospitalized and treated with methadone 0.2 mg/kg IV q 6 hr and IV fluids (lactated Ringer’s, 2.8 mL/kg/hr). On the following day, the patient was transferred to the oncology service for further evaluation and workup.

On day 2, physical examination was static, with normal vitals and persistent caudal abdominal discomfort and palpable caudal organomegaly. Cytology samples of the perineal mass were reviewed by a clinical pathologist, and the findings were interpreted as carcinoma with mild macrophagic inflammation. Based on the location, these were considered to have originated most likely from an apocrine gland anal sac adenocarcinoma (AGASAC). A complete blood count (CBC), biochemistry panel, and urinalysis were submitted to the laboratory. The CBC results indicated a neutrophilia (9.3k/µL) with left shift (1.3k/µL bands) and monocytosis (0.9 k/µL). The biochemistry panel indicated mild hypoglycemia (75 mg/dL), mildly increased total protein (7.0 g/dL), hyperglobulinemia (3.8 g/dL) with normal albumin levels (3.2 g/dL), and increased alkaline phosphatase (111 U/L). The urinalysis showed no evidence of an active sediment or bacteriuria. Complete laboratory findings are summarized in Table 1. Advanced imaging with a computed tomography scan under general anesthesia was proposed for full staging of a suspect metastatic apocrine gland anal sac adenocarcinoma and for radiation and/or surgical planning purposes.

TABLE 1 Laboratory Diagnostic Findings for Two Cancer-Bearing Patients Diagnosed with Septic Peritonitis

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The computed tomography scan of the thorax and abdomen with contrast confirmed the presence of a right-sided perianal mass partially displacing the rectum, splenic nodules, and multifocal pelvic and intra-abdominal lymphadenomegaly most consistent with metastatic neoplasia. A scant amount of free fluid was noted around a mass that was suspected to be a severely enlarged medial iliac lymph node with abnormal contrast enhancement pattern and cystic appearance. These imaging findings were suspicious for a necrotic and/or abscessed lymph node, with possible content leakage in the peritoneal cavity. There was no evidence of gastrointestinal perforation or presence of gas. After advanced imaging, ultrasound-guided aspirates of the intra-abdominal mass identified as presumptive medial iliac lymph node, splenic lesions, and peritoneal fluid were obtained. Abdominal mass and splenic lesion cytology were supportive of carcinoma, with metastatic AGASAC as a differential. The peritoneal fluid was grossly cloudy and yellow. Nucleated cell count was >298,000/µL, and rare neutrophils contained phagocytized mixed bacteria (small cocci and medium-sized rods). This sample was interpreted as a septic exudate with marked neutrophilic inflammation.

Induction, maintenance, and recovery from general anesthesia occurred without complications. Normal blood pressure measurements were obtained throughout the procedure, and the postrecovery blood glucose^a was 87 mg/dL. Exploratory laparotomy to identify and possibly remove the source of the infection was offered, as was hospitalization for medical management on IV antibiotics, pain medications, and close monitoring. Because of the poor prognosis, humane euthanasia was elected. The patient’s remains were submitted for a teaching necropsy. Gross findings identified a large perianal mass and multiple small nodules in the lungs, liver, spleen, and large sublumbar lymph nodes, which were concerning for a primary perianal neoplasm with widespread metastasis. There was creamy material oozing from one of the sublumbar lymph nodes, which was the most likely cause of the reported septic peritoneal fluid. The microscopic findings confirmed nests of neoplastic cells in the perianal mass, as well as in the sublumbar lymph nodes, spleen, liver, tracheobronchial lymph node, and lungs. Final histopathologic diagnosis was a metastatic AGASAC, with one of the sublumbar lymph nodes leaking necrotic material. E coli was cultured from the material sampled from the sublumbar lymph node. This was the only potential source for the focal secondary septic peritonitis identified.

Case 2

A 9 yr old female spayed American bulldog weighing 37.1 kg was presented to the emergency service for progressive lethargy and multiple daily vomiting episodes of 10 days’ duration. The day after the vomiting started, she was taken to her primary care veterinarian, who performed a CBC, serum chemistry, and urinalysis. At the time, she was started on cephalexin, metoclopramide, and a probiotic. No improvement was seen, and a few days later, she was switched from metoclopramide to maropitant. The owner reported progressive nausea and decreased appetite, as well as worsening lethargy. Bruising was noted in her inguinal area a few days before presentation and attributed to trauma after jumping over a fence. The patient had a history of a left maxillary multilobular osteochondrosarcoma surgically excised 1 yr prior and metastatic pulmonary nodules, as well as a low-grade mast cell tumor (MCT; 0 mitotic figures/high-power field) surgically excised from the lateral thigh of her right pelvic limb 2 mo before presentation. The surgical site of the MCT had healing complications and dehiscence, which had recently resolved. Daily medications included phenylpropanolamine for historical urinary incontinence and piroxicam. Diphenhydramine and famotidine were discontinued ∼2 wk before presentation. The patient had received no prior cytotoxic chemotherapy treatment.

On presentation, the patient was quiet, alert, and responsive, normotensive (135 mm Hg on Doppler measurement), and tachycardic, with estimated dehydration of 5%. Mucous membranes were pink and tacky, with capillary refill time of less than 2 sec. Abdominal palpation was soft and nonpainful. A 1 cm × 4 cm healing wound with healthy granulation tissue was noted on the lateral thigh of the right pelvic limb. Two large and firm masses were palpated on physical examination in the inguinal area and were suspected to represent severe bilateral superficial inguinal lymphadenopathy (the right inguinal lymph node measured 5 cm × 4 cm × 7 cm on necropsy). Diffuse ecchymosis of the skin overlaying the lymph nodes was also noted. On T-FAST and A-FAST, there was a scant amount of peritoneal free fluid that was unable to be sampled. CBC and serum biochemistry were submitted. On CBC, there was a normocytic, hypochromic anemia (hematocrit 36%) and a marked leukocytosis (WBC 84k/µL) characterized by a neutrophilia (32.4k/µL) with left shift (bands 0.8k/µL), eosinophilia (1.7k/µL), basophilia (2.5k/µL), and lymphopenia (0.0k/µL). There were 44.8k/µL nucleated cells consistent with mast cells with moderate anisocytosis and anisokaryosis, indicating mastocytemia. On the biochemistry panel, glucose was normal (120 mg/dL) and there were no other significant abnormalities. Complete laboratory findings are summarized in Table 1. The patient was hospitalized for monitoring and transferred to the oncology service the following day for further evaluation and workup. She was treated overnight with injectable diphenhydramine (2.2 mg/kg intramuscularly q 8 hr), maropitant (1 mg/kg IV q 24 hr), and IV fluids (lactated Ringer’s 2.4 mL/kg/hr).

On day 2, the patient was noted to be dull, reluctant to walk, weak, normothermic, and persistently tachycardic (heart rate: 180–200 bpm). She was noted to have a distended and tense abdomen. Doppler blood pressure measurement was 90 mm Hg. A-FAST indicated a moderate amount of peritoneal free fluid. Abdominocentesis was performed, and a brown cloudy fluid sample was obtained. Peripheral blood glucose was rechecked and within normal limits (107 mg/dL). The fluid analysis was interpreted as neutrophilic and proteinaceous exudate with bacterial sepsis (a single morphologic population of bacterial rods). Low numbers of hypogranulated mast cells were also noted, suggesting the presence of an exfoliating intra-abdominal mast cell neoplasm. Samples were also taken from the inguinal masses/lymph nodes, which were consistent with mast cell neoplasia. Because of the poor prognosis related to both mastocytemia and septic abdomen, humane euthanasia was elected.

Postmortem bone marrow evaluation of the right humerus was performed and, despite having adequate cellularity, indicated no evidence of mast cell infiltration in the bone marrow sample. The patient’s remains were submitted for a teaching necropsy. Gross diagnosis indicated disseminated petechial and paintbrush hemorrhages, septic peritonitis, necrotizing lymphadenitis, and suspect metastases in the inguinal, sublumbar, and medial iliac lymph nodes. Additional findings included a focally extensive caudal pulmonary lobar hemorrhage, multifocal pulmonary nodules, splenomegaly, multifocal hepatic necrosis, and fibrinous capsulitis. The exact cause of the septic peritonitis was not grossly apparent on postmortem examination.

The final diagnosis following microscopic evaluation consisted of systemic mastocytosis, as well as diffuse secondary septic peritonitis and sepsis. The diagnosis of systemic mastocytosis was supported by extensive metastatic disease diagnosed in this case, affecting draining lymph nodes associated with the prior cutaneous MCT including inguinal, medial iliac, and sublumbar lymph nodes, as well as bone marrow, liver, and spleen. Sepsis was supported by disseminated petechial hemorrhages, diffuse peritonitis, pericarditis, necrotizing splenitis with intralesional gram-negative rod bacteria, and numerous E coli bacteria cultured from the peritoneal fluid and liver. Pulmonary findings revealed metastasis of the previously excised multilobular osteochondrosarcoma. Additional investigation with Gram stain and toluidine blue was performed on the splenic samples. Within sections of spleen, there was multifocal to coalescing, flocculent eosinophilic (fibrin) material, often surrounding small amounts of karyorrhectic debris or basophilic stippled material. Interspersed within the fibrinous material were plasma cells and histiocytes, hematopoietic precursors, and, occasionally, small islands of neoplastic mast cells. A few small aggregates of small gram-negative rod bacteria consistent with E coli were present within the described areas of fibrin. The finalized diagnosis was consistent with multifocal to coalescing, severe, subacute fibrinonecrotizing splenitis with intralesional gram-negative rod bacteria and mast cell metastasis.