%0 Journal Article
%T Traumatic Page Kidney Induced Hypertension in Critical Care: Immediately Resolved or Long-Term Resistant Problem
%A E. Brotfain
%A L. Koyfman
%A A. Frenkel
%A A. Smolikov
%A A. Zlotnik
%A M. Klein
%J Case Reports in Critical Care
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/201424
%X Page kidney is a well-known phenomenon causing hypertension, due to compression of renal parenchyma by a subcapsular hematoma, of either traumatic or non-traumatic origin. The main therapeutic approach is based on surgical approach (nephrectomy or hematoma evacuation) and antihypertensive treatment. In this paper we present a post-traumatic case of Page Kidney in a Critical Care unit. We discuss different therapeutical opportunities to extremely elevated systemic blood pressure resistant to traditional drug therapy. 1. Introduction Page kidney is a well-known hypertensive phenomenon caused by compression of renal parenchyma by a subcapsular hematoma [1, 2]. Both traumatic [3¨C5] and spontaneous bleeding etiologies have been reported [1]. The main mechanism responsible for development of resistant hypertension is believed to be renin-mediated [1]. Renal mass lesions and invasive procedures complications may also result with clinical features of Page kidney. The initial management may be divided between antihypertensive treatment only and a combine surgical approach based on drainage of the subcapsular renal hematoma and in extereme cases total nephrectomy [1, 2]. In this paper we describe the case of acute posttraumatic Page Kidney syndrome in a multiple trauma critically ill patient. 2. Case Report An 18-year-old, previously healthy male was admitted to our intensive care department after suffering a motor vehicle accident. His injuries included: skull base fracture; diffuse axonal brain injuries, bilateral lung contusions with left side diaphragmatic rupture and dissection of descending aorta. On admission to ICU he was sedated and mechanically ventilated. His blood pressure was 134/54£¿mmHg and pulse was 69 beats/min. Due to a potentially high risk of rupture and bleeding from the aortic dissection, the patient underwent urgent endovascular stenting. The procedure was completed successfully uneventfully. For the following two weeks the patient was treated for severe traumatic brain injury. Despite adequate sedation and analgesia the patient had become extremely hypertensive (blood pressure 215/100£¿mmHg). CT imaging and ICP monitoring did not reveal any signs of elevated intracranial pressure, or signs of herniation. A detailed clinical workup was performed, and included a repeated abdominal CT, which demonstrated a remarkable subcapsular hematoma of the left kidney (Figure 1), with no active bleeding. There was no biochemical evidence of kidney dysfunction or reduction in GFR. Figure 1: Ct abdomen showed subcapsular renal hematoma around left kidney
%U http://www.hindawi.com/journals/cricc/2013/201424/