ABSTRACT
Neurogenic pulmonary edema (NPE) is a potential complication of a central nervous system (CNS) insult such as intracranial hemorrhage, uncontrolled generalized seizures, head trauma, tumors, and neurosurgical procedures. The proposed etiology is massive sympathetic discharge following a CNS event. The pathogenesis is not completely understood. However, there are two theories on how NPE occurs: the blast theory and the permeability defect theory. There is evidence for both theories, and NPE is probably the result of a combination of the two. The treatment is mainly supportive with the use of mechanical ventilation and alpha-adrenergic blocking agents while managing increased intracranial pressure. A thorough understanding of the pathophysiological mechanisms behind the development of NPE aids in the management of these patients to prevent further complications.
Subject(s)
Central Nervous System Diseases/complications , Cerebral Hemorrhage/complications , Pulmonary Edema/etiology , Respiratory Insufficiency/etiology , Adrenergic alpha-Antagonists/therapeutic use , Central Nervous System Diseases/physiopathology , Central Nervous System Diseases/therapy , Cerebral Hemorrhage/physiopathology , Cerebral Hemorrhage/therapy , Combined Modality Therapy , Female , Humans , Middle Aged , Nursing Assessment , Patient Care Planning , Postoperative Care , Pulmonary Edema/diagnosis , Pulmonary Edema/physiopathology , Pulmonary Edema/therapy , Respiration, Artificial , Respiratory Insufficiency/diagnosis , Respiratory Insufficiency/physiopathology , Respiratory Insufficiency/therapyABSTRACT
PURPOSE: To review the incidence and repair of inferior mesenteric arterial (IMA) type II endoleaks after endovascular repair of abdominal aortic aneurysms. MATERIALS AND METHODS: Fifty patients who underwent endovascular repair of abdominal aortic aneurysms were examined. If an endoleak was identified at 30-day postoperative computed tomography, conventional arteriography was performed to identify and eliminate its source. After the exclusion of attachment site leaks, a catheter was placed selectively in the superior mesenteric artery (SMA). If retrograde filling of the IMA and aneurysm was identified, coil embolization was attempted through the SMA and middle colic artery. Intrasac pressures were measured at embolization. RESULTS: Eight of 50 patients (16%) had type II endoleaks that were attributed to retrograde flow in the IMA. Intrasac measurements demonstrated systemic pressure in six patients and one-half systemic pressure in two patients. The IMA was embolized through the SMA and left colic artery in seven patients and through the translumbar aorta in one patient. CONCLUSION: Retrograde flow in the IMA is responsible for many type II endoleaks. Systemic pressures are transmitted into the aneurysm sac from the IMA. The IMA can be embolized successfully with an SMA approach in most patients.
