Epipericardial Fat Necrosis: A Case Report

NCBI
04 Dec, 2020 ,

Synnøve Gjelsten Mortensen et.al. report a classic case of epipericardial fat necrosis (EFN) in a 22-year-old male who presented to the ER with left-sided chest pain and shortness of breath. The patient underwent radiologic examinations and findings consistent with EFN with associated thickening of the adjacent pericardium and associated pleural effusion and atelectasis were observed. The patient was started on NSAID therapy which led to the resolution of the symptoms.

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A 22-year-old healthy male was admitted to the ED at Nordland Hospital, Bodø, Norway, with left-sided chest pain intensifying over the last 2 days. At the time of contact with the community emergency primary health system, he felt shortness of breath and was not able to inhale properly due to pain. He had also noticed an increase in resting heart rate. The examining physician found him slightly hypertensive, tachycardic, and tachypnoeic with possibly diminished breath sounds at the affected left side. Point-of-care C-reactive protein (CRP) was 23 mg/L (ref. <5) and an electrocardiogram (ECG) showed sinus rhythm 92 beats per minute, Q-wave in aVF, V3-V6, and peaked T-waves in V2-V6. The patient was referred to a chest X-ray and admitted for further assessment at our ED. The primary suspicion of the referring doctor was pneumothorax.

Upon arrival at the hospital, the pain was described as constant ‘stinging’, 7 to 8 on visual analogue 1 to 10 scale (VAS) and worsened severely when laying down and with inspiration, movements which also made the pain radiate to the left shoulder. Apart from this, he did not feel ill, had no cough, fever, or other symptoms. Clinical assessment was normal, and vital measurements were virtually identical to those reported from the referring doctor. CRP and D-dimer were elevated, and venous blood gas revealed a mild, compensated respiratory acidosis.

Chest X-ray showed no pneumothorax but a small amount of pleural effusion in the left hemithorax and a subtle ill-defined opacity in the left upper lobe anterior to the heart resulting in loss of the left heart contour on the postero-anterior view (so-called silhouette sign).

To rule out pulmonary embolism, a chest CT scan was performed. Pulmonary angiogram showed no evidence of embolism, but a focal inflammatory stranding in a pericardial fat layer lateral to the apex of the left ventricle. The inflammation surrounded an ovoid-shaped structure of fat density with a striking resemblance to the findings in epiploic appendagitis, a subgroup of intraperitoneal focal fat infarctions.

The finding was accompanied by a slight thickening of the adjacent pericardium as well as reactive changes in neighbouring lung parenchyma in terms of subsegmental atelectasis in lingula and basal parts of the left lung and a small amount of pleural effusion.

The radiological findings were consistent with EFN with associated thickening of the adjacent pericardium and associated pleural effusion and atelectasis. Pericarditis was one of the major differentials which should be considered in this situation. The nonspecific X-ray findings did not change the probability regarding pericarditis. However, on the CT exam, one would expect some grade of pericardial effusion and global thickening, or at least more pronounced thickening of pericardium compared to focal changes seen here. EFN was rated as the most probable diagnosis as the CT appearance in total was so typical and almost pathognomonic for this condition.

Transthoracic echocardiography (TTE) showed a hypoechogenic area located in front of the left ventricle and possible highly echogenic adjacent pericardium covering the free wall of the left ventricle. There were no other obvious pathological findings. The patient improved rapidly and was discharged from hospital with ibuprofen as needed.

Heart MRI scan performed 3 weeks later showed a normal heart with neither evidence of oedema in the surrounding fat layers, nor pericardial or pleural effusion, just slightly aggravated small vessels in the epicardial fat at the left pericardio-costal angle as the only remnant of inflammation.