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CASE REPORT
Year : 2023 | Volume
: 69
| Issue : 4 | Page : 234-236
Celiac artery thrombosis presenting as acute abdomen
M Sharma1, K Natarajan1, A Mahesh Kumar2, P Paramasivan1
Correspondence Address:
Dr. A Mahesh Kumar
Department of Medical Services, Apollo Hospitals, Greams Road, Chennai, Tamil Nadu
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/jpgm.jpgm_331_23
Mesenteric vascular thrombosis, typically of the superior mesenteric artery, is a frequent occurrence in patients with hypercoagulable conditions. Isolated involvement of the celiac artery is rare. Patients with celiac artery thrombosis can present with an acute abdomen or occasionally with acid peptic symptoms. A delay in diagnosis is associated with high rates of morbidity and mortality. We present a rare case of splenic infarction with celiac trunk thrombosis in a 54-year-old patient with underlying antiphospholipid (APLA) syndrome who presented with epigastric pain that was mistaken for symptoms of acid reflux.
Keywords: Celiac artery, gastroesophageal reflux, thrombosis
The celiac artery is a major splanchnic vessel that arises at the level of T12 vertebra from the abdominal aorta.[1] Patients with celiac artery thrombosis present rarely with acute abdomen.[2] Prognosis is dependent on the degree of suspicion, early diagnosis, and prompt treatment to re-establish blood flow.[3] We present the case of celiac trunk thrombosis in a 54-year-old male with underlying antiphospholipid (APLA) syndrome who experienced severe burning pain in his epigastrium along with minor tenderness but no signs of peritonitis.
:: Case PresentationA 54-year-old man with a history of APLA syndrome who was taking acenocoumarin was admitted to the emergency room after missing a dose for two days with complaints of severe burning sensation in the epigastrium. This sensation was of acute onset, had gradually spread over time, was aggravated at time of eating meals, and was relieved on an empty stomach. There was no associated vomiting, abdominal distension, constipation, blood in the stools, or left shoulder pain. Splenic rub or friction fremitus was absent. He denied history of similar episodes in the past. On examination, the patient had a blood pressure of 160/80 mmHg and heart rate of 110 beats/min. The abdomen was soft with mild left upper quadrant tenderness, and normal bowel sounds. Laboratory results indicated elevated arterial lactate at 8 mmol/L (N: 0.5-1.6 mmol/L), C-reactive protein at 26.2 mg/dL (N: 0.8-1 mg/dL), lactate dehydrogenase (375 IU/L), and activated partial thromboplastin time (aPTT) of 85s (N: 30–40s) with normal white blood cells at 8,550/μL (N: 4,500–11,000/μL), packed cell volume at 47% (N: 38.3–48.6%), platelets at 1,35,000/μL (N: 1,50,000–4,00,000/μL). D-dimer levels were within normal limits (0.34 μg/mL; N ≤0.50 μg/mL). The peripheral smear was unremarkable.
Computed tomography (CT) of the abdomen revealed normal stomach, duodenum, and bowel with near total splenic infarct. An abdominal CT angiogram showed partial thrombosis involving the proximal portion of celiac trunk from its origin to a distance of 3.5 cm [Figure 1], as well as in a branch of splenic vein at the level of splenic hilum [Figure 2] and near total infarction of the spleen [Figure 3]. On initial evaluation, no collateral formations were observed. The liver was normal in size, shape, and parenchymal density with no evidence of infarction. The stomach, duodenum, and bowel were normal.
Figure 1: Abdominal CT (sagittal view) showing partial thrombus involving the proximal portion of celiac trunk from its origin to a distance of 3.5 cm (white arrow with label)
Figure 2: Abdominal CT (coronal view) showing partial thrombosis in a branch of splenic vein at the level of splenic hilum (white arrows depicting the portal vein, splenic vein, and thrombus)
Figure 3: Abdominal CT angiogram (axial view) showing total splenic infarction (yellow arrow)The patient was started on unfractionated heparin with activated partial thromboplastin time monitoring (target of 170s; 2 times the baseline aPTT) following a weight-based loading dosage of 8000 units, and eventually switched to oral anticoagulants before being discharged with the advice of the vascular surgeon and hematology team. Patient was initially kept nil by mouth, and once discomfort subsided, liquids were gradually introduced. Patient was discharged on normal diet. On follow-up, 2 weeks later the patient continues to do well on oral anticoagulation.
:: DiscussionThe celiac artery provides oxygenated blood to the structures derived from embryonic foregut, namely the distal esophagus, second part of the duodenum, liver, pancreas, gallbladder, and spleen.[1] Conditions that increase thrombotic tendencies such as atherosclerosis, Behcet's disease, thrombocytosis, protein C, protein S and antithrombin III deficiencies, and malignancies.[4] Other etiologies include APLA syndrome, acute pancreatitis, oral contraceptive drugs, diseases related to hypercoagulability, and surgical trauma.[5]
APLA is a multisystem autoimmune disorder characterized by the presence of APLA antibodies. The pathophysiological hallmark of APLA is thrombosis.[6]
The splenic artery, viz. a branch of the celiac artery, is the primary source of blood supply to the spleen. Hence, celiac artery thrombosis frequently leads to splenic infarction. Abdominal pain associated with splenic infarction has a sudden onset and may subside gradually. Interestingly, in the present patient abdomen on palpation was soft, which is not the usual case with splenic infarction. A similar presentation has been described by Li et al.[7] in 2018 of a patient with infectious mononucleosis having splenic infarction. The present patient presented acutely. Hence, we decided to go ahead with abdominal CT instead of usual abdominal ultrasound and Doppler studies. High levels of lactate could indicate early ischemia even in the absence of true transmural infarct. Several studies have evaluated the possibility of using peripheral blood lactate levels as s surrogate marker for acute mesenteric ischemia. Uncomplicated infarctions respond well to medical management. Surgery is required in situations where the infarct leads to the formation of an abscess or splenic rupture. The opinion of a vascular surgeon was obtained. Since the present patient improved with conservative treatment a close follow-up was advised. On follow-up, 2 weeks later the patient was continuing to do well on oral anticoagulation.
Choi et al.[8] first reported a case of abdominal angina and splenic infarction in a patient with APLA syndrome in 2002. Salaun et al.[9] in 2014 have reported that severe stenosis of visceral and renal arteries led to the diagnosis of primary APLA in a patient. Literature evidence demonstrates reports of mesenteric ischemia associated with APLA.[10] To the best of our knowledge, this is the first report of isolated celiac artery thrombosis and splenic infarction in a patient with APLA syndrome. The patient was treated with intravenous anticoagulation therapy followed by oral anticoagulants prior to discharge. Patient's pro-thrombotic history led to high degree of suspicion initially which resulted in early diagnosis and timely management.
:: ConclusionThis case demonstrates the need for aggressive evaluation of patients with unusual acid peptic symptoms. Early diagnosis and prompt management of celiac artery thrombosis results in favorable prognosis.
Declaration of patient consent
The authors certify that appropriate patient consent was obtained.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
:: References
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