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Accelerated Hypertension After Resuscitation of Hypovolemic Shock From Retroperitoneal Hemorrhage: Do We Think of “Page Kidney”? FREE TO VIEW

Abhisekh Sinha Ray, MD; Meenakshi Ghosh, MD; Sreeparna Ghosh, MBBS; Pinelopi Kapitsinou, MD
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Southern Illinois University School of Medicine, Springfield, IL

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A141. doi:10.1016/j.chest.2016.02.147
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SESSION TITLE: Critical Care

SESSION TYPE: Case Report Poster

PRESENTED ON: Sunday, April 17, 2016 at 11:45 AM - 12:45 PM

INTRODUCTION: Hypertensive urgency in anuric patients is frequently driven by either volume overload or activation of the renin-angiotensin-aldosterone system (RAAS). We report a case of RAAS mediated accelerated hypertension in a patient, who was resuscitated from hypovolemic shock from severe retroperitoneal bleed.

CASE PRESENTATION: 76 year old male with recurrent nephrolithiasis, chronic kidney disease (CKD), prior left nephrectomy in setting of abdominal aortic aneurysm rupture was admitted to a community hospital for ureteral obstruction. Following an unsuccessful attempt of retrograde ureteral stenting, he underwent percutaneous nephrostomy which was complicated by retroperitoneal hemorrhage and hypovolemic shock. He was aggressively resuscitated with crystalloids, 6units PRBC and later started on vasopressor. Upon transfer to ICU of a tertiary center, he remained hypotensive (BP 96/52) and anuric. Labs showed acute kidney injury on CKD (Creatinine 6.27mg/dl), metabolic acidosis (bicarbonate 19mmol/L) for which continuous renal replacement therapy (CRRT) was initiated. Over next 12hrs, he developed accelerated hypertension, with SBP in 220-240 range, not responding to ultrafiltration by CRRT. CT scan revealed right renal subcapsular hematoma (9x6 cm) causing mass effect on renal parenchyma with extension into retroperitoneal pelvic space. Due to high risk of rebleeding, percutaneous drainage was not done; an angiotensin receptor blocker was started to inhibit RAAS. This allowed normalization of BP, but there was no significant recovery in renal function requiring long term dialysis.

DISCUSSION: The ‘Page Kidney’, a rare pathophysiologic condition of accelerated hypertension evoked by RAAS activation, was first described by Dr. Irvin H Page in 1939 who reproduced this by compressing canine kidneys in cellophane. Later, it was described in young football-player having hypertensive crisis after developing subcapsular hematoma. Rather than true compression of major renal vessel, this renovascular hypertensive response is mediated by microvascular ischemia from parenchymal compression causing alterations in small-vessel hemodynamics. CT scan, MRA, US-doppler are key diagnostic tools.

CONCLUSIONS: Although trauma was the primary etiology of ‘Page Kidney’; procedural complications including hematoma, urinoma, lymphocele became more common causes at present. Nephrectomy had been traditionally considered treatment of choice. Currently kidney preserving approaches including radiology guided percutaneous drainage with or without angiographic embolization and laparoscopic decortication represent first line options. RAAS blockade is an effective approach to control BP in ‘Page Kidney’ either as initial therapy or when procedural contraindication exists.

Reference #1: Page IH. The production of persistent arterial hypertension by cellophane perinephritis. JAMA. 1939;113(23):2046-2048

Reference #2: Bakri RS et al. Three ‘Pages’ in a chapter of accidents. Nephrol Dial Transplant. 2003;18(9):1917

DISCLOSURE: The following authors have nothing to disclose: Abhisekh Sinha Ray, Meenakshi Ghosh, Sreeparna Ghosh, Pinelopi Kapitsinou

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