INTRODUCTION: Omental infarct is a rare cause of acute abdominal pain resulting from vascular compromise of the greater omentum. This condition usually has a nonspecific clinical presentation with right lower quadrant being the most common location and is usually managed conservatively. We present a rare case of idiopathic omental infarct. CASE DESCRIPTION/METHODS: 35-year-old obese caucasian male with past medical history significant for hypertension and GERD presented to the emergency department with chief complaint of right lower quadrant pain which started 3 days ago without any precipitating event. Initial labs were unremarkable with vital signs only significant for elevated blood pressure. CT of the abdomen and pelvis with contrast showed significant inflammation in the right side of the abdomen most likely representing omental infarct. On call general surgeon was consulted who suggested no acute surgical intervention and patient to be managed medically with ciprofloxacin and metronidazole. On call vascular surgeon was consulted; advised there was no immediate need for anticoagulation as there was no evidence of acute vascular issues such as embolization and/or dissection involving the celiac or the superior mesenteric arteries. Following day, the patient improved clinically and was discharged with total of 10 days of antibiotic treatment and to follow-up outpatient with general surgeon. DISCUSSION: Omental infarct is a rare cause of acute abdominal pain. Clinical presentation includes sudden onset of acute abdominal pain located mostly in the right lower quadrant with tenderness and absence of any other GI symptoms. Omental Infarction can be isolated event or in succession to omental torsion. A diagnosis of primary/idiopathic omental infarct is made when no identifiable etiology is determined. Secondary causes of omental infarction include hypercoagulability, vasculitis, abdominal adhesions, cysts, and tumors. Other contributing factors include obesity, local trauma, heavy food intake, coughing, sudden body movements, laxative use, and hyperperistalsis. CT of the abdomen may show focal area of fat stranding, swirling of omental vessels, omental torsion, and/or hyperdense peripheral halo. The disease is often self-limiting and managed conservatively. Complications such as abscess can occur which may require surgical or radiologically-guided drainage.

Upper extremity arterial disease is relatively uncommon compared with lower extremity disease, but presents a unique diagnostic challenge for physicians and technologists. It affects approximately 5–10% of the population. The most common causes of upper extremity arterial disease are atherosclerosis and embolic disease. Some common symptoms of upper arterial disease include dysesthesia, paresthesia, pallor, cold intolerance, ulceration, pain, or weakness in one or both extremities. The vascular system plays a vital role in the delivering of nutrients and clearing metabolic waste products from the peripheral tissues and also helps maintain an individual's systemic core temperature. In a majority of patients, the deep and superficial palmar arches provide the dominant blood supply to the hand. The arches are a continuation of the radial and ulnar arteries. These arches are typically connected in approximately 80% of patients. In order to accurately diagnose upper extremity arterial disease, a noninvasive upper extremity physiologic examination is of importance to determine treatment options for patients. The physiologic examination includes upper extremity segmental pressures known as wrist-brachial index, Doppler waveforms; digital evaluations include photoplethysmography and pressures of the digits known as the digital-brachial index. Physiologic tests are indirect examinations. The upper extremity arterial physiologic examination is always completed bilaterally in order to determine if the disease is present in one or both extremities and also assists in the diagnosis of disease severity. The vascular physiologic examination should focus on the symptoms presented by the patient during the history. However, a complete vascular examination is appropriate given the diffuse nature of the atherosclerotic disease process.

In venous insufficiency states, venous blood escapes from its normal antegrade path of flow and refluxes back down the veins into an already congested leg. Venous insufficiency symptoms are most commonly caused by valvular incompetence in the low-pressure superficial venous system. Patients with venous insufficiency may have signs and symptoms of fatigue, heaviness, aching, cramping, throbbing, itching, lower extremity discoloration, and ulcer. Varicose veins are a sign of underlying venous insufficiency and affect 20–30% of adults. Duplex of the lower extremity venous system to rule out venous insufficiency was performed to determine the prevalence of bilateral great saphenous vein insufficiency in men and women. Great saphenous vein insufficiency is the most common form of venous insufficiency in patients presenting with signs and symptoms.