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Dogs
Suspected intrapericardial lipoma in a standard schnauzer
  1. Paul Jenkins1,
  2. Soo Kuan1 and
  3. Philip Brain2
  1. 1 Surgery, Small Animal Specialist Hospital, Sydney, New South Wales, Australia
  2. 2 Medicine, Small Animal Specialist Hospital, Sydney, New South Wales, Australia
  1. Correspondence to Dr Paul Jenkins; paul.jenkins{at}sashvets.com

Abstract

A five-year-old, male, neutered standard schnauzer presented for vomiting, diarrhoea and fever. A large intrapericardial fatty mass was identified on advanced imaging. The patient underwent a median sternotomy and exploratory coeliotomy to remove the fatty mass measuring 100 mm x 76 mm x 66 mm, the histopathology of which revealed a large fatty mass with necrosis and inflammation. This is the largest reported intrapericardial fatty mass in the veterinary literature. CT at 28 weeks postoperatively revealed no evidence of recurrence.

  • intrapericardial
  • lipoma
  • schnauzer
  • vomiting
  • effusion

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Background

This is a case report of a pericardial fatty mass with a varied presentation to the four previously described cases within the veterinary literature. One presented for inappetence, two presented for cardiogenic signs and the last was an incidental finding during routine chest radiographs for nocturia.1–4 In the present case report, the patient presented for progressive gastrointestinal signs over a 24-hour period, from inappetence to vomiting. These clinical signs are non-specific, showing that pericardial fatty masses can have a variety of clinical presentation. This report highlights the potential differences in presentation.

In addition, this case describes the largest reported pericardial fatty mass and measures 25 per cent larger than others in the literature. The treatment decision to remove this mass en bloc was the correct decision as the six-month follow-up CT showed no evidence of regrowth.

Case presentation

A five-year-old,male,neutered standard schnauzer initially presented to its regular veterinarian for inappetence, abdominal discomfort and fever (39.4°C). Haematology and biochemistry showed mature neutrophilia (28.28 x 109/l), monocytosis (1.75 x109/l) and decreased urea (2.1 mmol/l). The schnauzer was started on oral metronidazole (13.9mg/kg per os; Metrogyl, Alphapharm) and received an injection of amoxicillin (14.6mg/kg subcutaneously; Betamox LA, Norbrook) and maropitant (1 mg/kg subcutaneously; Cerenia, Pfizer) on the assumption of a bacterial infectious process within the body. It subsequently presented 24 hours later to the emergency service for increased lethargy and vomiting. It had a history of foreign body ingestion with endoscopic removal. On presentation, it had muffled heart sounds and reduced ventral lung sounds. Pulses were of normal quality and synchronous.

Investigations

Limited thoracic ultrasonography was conducted with the use of a methadone (0.2 mg/kg intramuscularly; 10 mg/ml Methadone, Troy Laboratories) sedation, which identified a small amount of pericardial effusion. Pericardiocentesis was carried out and blood cultures were collected, and the fluid was sent to an external laboratory for culture and sensitivity. Inhouse cytology of the pericardial fluid showed degenerate neutrophils with possible intracellular cocci. The patient was treated overnight with intravenous fluid therapy, ampicillin (22 mg/kg intravenously every eight hours; 1 g Ampicyn, Mylan), clindamycin (11 mg/kg intravenously every 12 hours; 150 mg/ml Dalton C Phosphate Clindamycin Injection, Pfizer) and maropitant (1 mg/kg intravenously every 24 hours). The methadone was continued every four hours to provide analgesia for the patient, as the primary clinician had concerns of discomfort. The emergency veterinarian initially opted for a broad spectrum of antibiotic coverage, as initially on inhouse cytology the pericardiocentesis yielded an inflammatory fluid, with suspected bacteria. The initial plan was to use a broad spectrum, awaiting culture and sensitivity results, and then to de-escalate the spectrum based on the results.

The following morning, the patient was internally referred to an internal medicine specialist (PB) for further investigation. A detailed thoracic ultrasound revealed negligible pericardial effusion but identified a mass caudal to the heart, and diagnostic considerations included infection/inflammation (granuloma or abscess), necrosis with an associated neutrophilic pericarditis or neoplasia with effusion. A CT exam revealed a rounded 100 mm x 76 mm x 66 mm space-occupying mass in the caudal pericardium. The majority of the lesion was 15 Hounsfield units with patchy regions of fat attenuation. The mass was surrounded by a 1.5-mm thick capsule (see Fig 1).

FIG 1

CT image reconstructions. Top left: longitudinal view. Bottom left: cyan arrow, capsule around the mass; blue arrow, pericardial effusion; yellow arrow, mass with fat attenuation. Right: frontal view; yellow arrow, mass with fat attenuation. RV, Right Ventricle; LV, Left Ventricle.

Differential diagnosis and treatment

Surgical treatment was elected. The patient was sedated with methadone,1 induced with propofol and maintained on inhalational isoflurane2 in combination with fentanyl3 at continuous rate infusion. A median sternotomy and coeliotomy was performed. The preoperative decision was made to perform a cranial coeliotomy, despite an abdominal CT revealing no penetrating foreign body. The reason for this was the season (summer) which the patient presented; a penetrating grass seed foreign body was part of the differential diagnoses, resulting in a pericardial abscess. The tracts made by a small grass seed may not have been evident on CT. The purpose of the coeliotomy was to examine the concave surface of the diaphragm and the parietal surface of the liver for adhesions. If adhesions were present, then a diagnosis of a penetrating foreign body would be more likely; however, no adhesions were identified. The pericardial effusion was sampled via needle aspiration. The pericardial sac was incised revealing a large soft fatty mass. With blunt dissection and monopolar cautery, the mass and ventral pericardium were removed (see Figs 2 and 3). During the dissection, a small adhesion was identified between the mass and the pericardium. This was suspected to be the region where the pericardiocentesis was obtained from the previous night as there was subtle bruising of the pericardium in the location of the adhesion. The source of the fat was suspected to be from the fat within the myocardial grooves. However, this was not confirmed intraoperatively. Bilateral 20-French thoracic drains (Argyle Trocar Catheter 20 Fr/Ch, Covidien) were placed and sutured with purse string and Chinese fingertrap patterns with size 0 polyamide monofilament non-absorbable suture (Dafilon, B Braun). Two size 1 poly-p-dioxanone monofilament absorbable sutures (MonoPlus, B Braun) in a horizontal mattress pattern were placed around each sternebrae to close the sternotomy. The diaphragm was sutured with size 2–0 glyconate monofilament absorbable suture (Monosyn, B Braun) in a simple continuous suture pattern. The chest was closed and the air was evacuated through the thoracic drains until gentle negative pressure was felt. The muscle layer was closed with 2–0 poly-dioxanone monofilament absorbable sutures in a simple continuous pattern. The subcutaneous tissue was closed with 2–0 poly-dioxanone monofilament absorbable sutures in a simple continuous pattern. The skin was closed with stainless steel staples (Manipler AZ 35 W, B Braun).

FIG 2

Intraoperative photograph. Pericardium has been incised. White arrow, heart; black arrow, mass.

FIG 3

Pericardial mass. Scalpel blade handle: 123 mm.

Outcome and follow-up

Postoperatively, the patient received fentanyl (3 µg/kg/hour), lignocaine (50 µg/kg/hour; 20 mg/ml ilium lignocaine, Troy Laboratories) and ketamine (0.1 mg/kg/hour; 100 mg/ml ketamine injection, Ceva) continuous rate intravenous infusion, and intravenous ampicillin (22 mg/kg intravenously every eight hours). The patient had ongoing nausea for the first three days, which was treated with maropitant (1 mg/kg slow intravenous) and metoclopramide (0.67 mg/kg subcutaneously; 5 mg/ml metoclopramide hydrochloride, Ceva). Three days postoperatively, chest drains were removed due to non-productivity. The patient was discharged eight days postoperatively.

The culture results returned a negative blood culture and a Staphylococcus pseudintermedius positive culture in the pericardial effusion. Histopathology revealed an ‘encapsulated fat necrosis and inflammation’ with no evidence of neoplasia or infection. Thirteen days postoperatively, the patient had a normal sonographic heart. The owner reported a return to previous function and retrospectively noted that there had been an insidious decline in exercise tolerance over a period of 12 months, which had resolved since surgery.

The owner reported continued improvement 28 weeks postoperatively. A repeat thoracic CT scan was performed, which revealed no evidence of recurrence (see Fig 4).

FIG 4

Longitudinal CT reconstruction 28 weeks postsurgery. There is no evidence of recurrence.

Discussion

This case report identifies the largest pericardial fatty mass (100 mm x 76 mm x 66 mm) in the veterinary literature. The described patient presented for vomiting with fever. Fahey and others5 showed a 51 per cent incidence of vomiting in patients with a pericardial effusion.5 They stated that the mechanism of vomiting is poorly understood. However, human literature reports a case of intractable vomiting, refractory to medical therapy associated with an idiopathic pericardial effusion. Theories for the mechanism of vomiting are oesophageal compression and vagus and phrenic nerve involvement.6 The cause of the intractable vomiting may be related to the compression of the vagus nerve associated with the pericardial effusion, resulting in stimulation of the nucleus tractus solitarius within the vomiting centre.6 Despite the patient presenting with acute vomiting, rather than intractable vomiting, the pathogenesis remains poorly understood. The potential for vagus nerve involvement remains uncertain; however, this episode, without appropriate management, may have progressed to intractable vomiting.

Only four cases of pericardial fatty masses have been reported in the veterinary literature. The earliest case report in 1999 described two patients with pericardial fatty masses.4 The first case was a pericardial mass, which was an 80 mm x 70 mm x 30 mm encapsulated adipose tissue mass attached to a pedicle. The second was an 80 mm x 60 mm x 50 mm pericardial hernia post-trauma, which was aetiologically different from neoplasia. The outcome for the first case was excellent at 16-month follow-up.4 The next report, from 2002, described a patient that presented for lethargy, exercise intolerance, inappetence and abdominal distension, and was ultimately euthanased at the owner’s request. Postmortem examination revealed a 60 mm x 35 mm x 35 mm mass attached by a 1-cm stalk and was classified as lipoma on histopathology.2 The third case report identified a 22-mm spheroid intrapericardial mass that was incidentally identified on thoracic radiographs as part of an investigation for nocturia in a geriatric rottweiler.1 The mass was an immobile mass attached to the pericardium.1 The most recent case report was published in 2017; an 18-month-old male German shepherd dog presented with cardiac tamponade resulting from pericardial effusion. There was a 30 mm x 50 mm mass grossly resembling a liver tissue between the parietal and visceral surface of the pericardium.3

The inability to label the source of the mass is a limitation of this case report. Although suspected, it was not possible to definitively diagnose this mass as a ‘lipoma’ because considerable necrosis of adipose tissue affected the ability to determine the original histological aetiology. In addition, morphologically and histologically, it is difficult to differentiate between a lipoma and a normal fat,7 with the histological appearance of lipomas consisting of mature fat cells.8 Based on the histological appearance, it cannot be ruled out that this mass has not started as an encapsulated lipoma that has become strangulated resulting in necrosis and ischaemia.7

Cutaneous and subcutaneous lipomas typically affect middle-aged to older patients9 and are generally non-symptomatic.10 However, when present within a confined space, such as the pericardium, dysfunction can occur secondary to compression or strangulation.10 It is hypothesised the mass in this case was growing insidiously for 12 months, given the reported reduction in exercise tolerance retrospectively identified by the owner. There is a pressure–volume relationship which demonstrates that increased pericardial size and thickening will occur over a more chronic time period from constant pressure. This allows for more pericardial chamber compliance, resulting in tolerance or larger volumes of pericardial fluid compared with acute pericardial effusions.11

The intraoperative pericardial fluid sample yielded a positive culture of S pseudintermedius. Reported bacterial infections of the pericardium included Bacteroides subspecies, Actinomyces subspecies, Streptococcus canis, Pasteurella subspecies and Peptostreptococcus subspecies.12 There was no evidence of infection on histopathology and no bacteria were identified on the Gram stain. It was suspected that this positive culture was a contaminant from the initial pericardiocentesis as the results from the first sample did not display leucocytes, whereas the second did. The inflammatory process on inhouse cytology is assumed to have been caused by the inflammatory nature of the mass.

Pericardial masses diagnosed on ultrasound in conjunction with a pericardial effusion yield a poor prognosis with 5 per cent living a full life.12 The follow-up CT did not reveal any recurrence of disease, suggestive of complete resolution and an excellent clinical outcome. Based on this case and the limited literature on intrapericardial fatty mass, surgical removal is the treatment of choice and offers an excellent outcome.

References

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Footnotes

  • Contributors PJ is the primary author, SK was the primary surgical specialist in the surgery and PB was the internal medine specialist involved in the diagnosis of the lesion.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data statement This is a case report where the data collected from the patient work up has been included in the report. The data is located in a private patient record within a veterinary hostpial server.

  • 1 mg/kg intravenously; 10 mg/ml Methadone, Troy Laboratories.

  • 6 mg/kg intravenously; 10 mg/ml Propofol Sandoz, Sandoz.

  • 7 μg/kg/hour; 50 μg/ml DBL Fentanyl Injection, Hospira.

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