Pseudoaortic dissection.

A 72-year-old man was brought to our emergency department (ED) because of upper abdominal pain. Initial vitals at the triage station were significant only for high blood pressure. Computed tomography (CT) of the abdomen with contrast enhancement revealed an intimal flap over his descending aorta, the infrarenal part. The flap was found throughout the descending aorta until its bifurcation. Stanford type B dissection was initially suspected. However, a reconstructed CT discovered an interesting feature of the aorta. A high aortic bifurcation at the level of the second lumbar vertebrae, in conjunction with bilateral common iliac arteries, appeared in pair, masquerading the CT image as infrarenal aortic dissection. Actually, that was a variant in human anatomy. A reconstructed sagittal view of the CT scan is mandatory for a patient with abdomen pain to avoid misinterpretation of the radiographic image.

Bilateral popliteal arterial dissection.

A clinical feature of bilateral popliteal arterial dissection without involving the descending aorta, bilateral iliac, as well as femoral arteries has never been reported in the past literature. We report a 56-year-old man with hypertension and coronary artery disease who presented to our emergency department with complaints of bilateral knee pain after long-distance walking. Physical examination was notable for elevated blood pressure, but there was no palpable pulsation over dorsalis pedis arteries on his feet. Laboratory evaluation revealed a d-dimer level of 35.2 mg/L (FEU) on the day of the test and 1.2 mg/L one and a half months ago (normal level, <0.55). These findings were suggestive of a recent-onset peripheral arterial occlusive disorder. Computed tomography of the aorta showed bilateral popliteal arterial dissection with arterial intimal flap. Abdominal aorta, bilateral iliac, and femoral arteries remained intact with only arteriosclerotic change. Minimally invasive endovascular stent grafting was then performed. The patient had an uneventful recovery.

Recurrent choking as a presenting feature of aortic arch aneurysm.

Aortic arch aneurysm occurs more commonly in the aging population. Rapid expansion and symptomatic patients should undergo aneurysm resection regardless of size. An 87-year-old man was brought to our emergency department because of choking on food during his dinner. The patient did not have hoarseness, dysarthria, dysphagia, as well as other neurologic symptoms. He was finally found to have an aortic arch aneurysm. Swallowing is complex neuromuscular activity consisting essentially of 3 phases: oral, pharyngeal, and esophageal. The pharyngeal phase was mainly mediated by the pharyngeal plexuses of both the glossopharyngeal and vagus nerves. Uncoordinated movement of the pharyngeal muscles because of a stretch of the left vagus nerve or its plexus by an enlarging aneurysm may be the possible mechanism of choking in this patient.

Sonographic diagnosis of spontaneous intramural small bowel hematoma in a case of warfarin overdose.

A 38-year-old man who had been treated with warfarin since mitral valve replacement 10 years earlier presented with acute onset of epigastralgia and melena. Coagulation tests were abnormal with a prolonged prothrombin time of >60 seconds and a prolonged activated partial thromboplastin time of >120 seconds. Abdominal sonographic examination revealed duodenal intramural hematoma that was confirmed on CT. Warfarin therapy was stopped and the patient was treated conservatively with vitamin K and fresh frozen plasma. Recovery was uneventful, and the patient was re-warfarinized 2 weeks later. Duodenal hematoma can be readily diagnosed with bedside sonography.

Neurogenic pulmonary oedema misdiagnosed as acute myocardial infarction in a comatose patient.

INTRODUCTION: We report a case of neurogenic pulmonary oedema (NPO) following massive left cerebral infarct, which was initially misdiagnosed as acute myocardial infarction (AMI). CLINICAL PICTURE: This 52-year-old man presented with acute loss of consciousness with normal brain computed tomography (CT). He was treated as non-ST-elevation AMI complicated with pulmonary oedema based on findings of chest radiograph (bilateral pulmonary oedema), electrocardiogram (marked ST-T changes in leads V3 to V6), and cardiac enzymes [elevated creatinine kinase (CK) and CK-MB]. However, coronary angiogram and serial cardiac enzymes were inconclusive. Anisocoria developed after admission and a repeat brain CT was evident for large left cerebral infarct. TREATMENT: Decompressive craniectomy was carried out. OUTCOME: Mortality. CONCLUSIONS: The diagnosis of NPO can be challenging when it occurs without abnormal findings on preliminary brain CT. It can be mistaken for cardiogenic pulmonary oedema secondary to AMI.