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العنوان
Management of Intra_Abdominal Hypertension & Abdominal Compartmental Syndrome in Intensive Care Unit /
المؤلف
Abdelrahman, Dina Mohamed Fathi.
هيئة الاعداد
باحث / Dina Mohamed Fathi Abdelrahman
مشرف / Sahar Kamal Aboul Ella
مشرف / Mohamed Anwar El Shafei
مشرف / Mohamed Saleh Ahmed
تاريخ النشر
2015.
عدد الصفحات
98 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
العناية المركزة والطب العناية المركزة
تاريخ الإجازة
1/1/2015
مكان الإجازة
جامعة عين شمس - كلية الطب - Anesthesia and Intensive Care
الفهرس
Only 14 pages are availabe for public view

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Abstract

Increased intraabdominal pressure is called intraabdominal hypertension (IAH). Abdominal compartment syndrome (ACS) refers to organ dysfunction caused by intraabdominal hypertension. (See ’Definitions’ above.)
ACS can impair the function of nearly every organ system. Physiologic consequences include impaired cardiac function, decreased venous return, hypoxemia, hypercarbia, renal impairment, diminished gut perfusion, and elevated intracranial pressure. (See ’Physiologic consequences’ above.)
Diagnosis of ACS requires that intraabdominal pressure be measured. Symptoms, physical signs, and imaging findings are insufficient to diagnose ACS. (See ’Diagnostic evaluation’ above.)
Management initially consists of careful observation and supportive care. In some cases abdominal compartment decompression is required. (See ’Ventilatory support’ above and ’Surgical decompression’ above.)
We suggest that surgical decompression is not delayed until the development of ACS (Grade 2C). We evaluate the patient for possible surgical decompression when the intraabdominal pressure is ≥20 mmHg, regardless of whether ACS exists. We make our final decision only after carefully weighing the potential benefits and the perioperative risks related to the individual patient. (See ’Surgical decompression’ above.)
Following surgical decompression, an open abdomen is maintained using a variety of temporary abdominal closure techniques. (See ’Temporary closure techniques’ above.)
Elevated IAP commonly causes marked deficits in both regional and global perfusion that, when unrecognized, result in significant organ failure and patient morbidity and mortality. Significant progress has been made over the past decade with regard to understanding the etiology of IAH and ACS as well as implementing appropriate resuscitative therapy. Routine measurement of IAP in patients at risk is essential to both recognizing the presence of IAH/ACS and guiding effective treatment. Adoption of the proposed consensus definitions and recommendations has been demonstrated to significantly improve patient survival from IAH/ACS and will facilitate future investigation in this area. The ACS is a clinical entity that develops from progressive, acute rises in IAP and impacts multiple organ systems in a graded fashion due to differential susceptibilities. The gut is the most sensitive to IAH and develops evidence of end-organ damage prior to the development of the classic renal, pulmonary, and cardiovascular signs. Intracranial derangements with ACS are now well described. Treatment involves expedient decompression of the abdomen, without which the syndrome of end-organ damage and reduced oxygen delivery may lead to the development of multiple organ failure and, ultimately, death. The scenarios of multiple trauma, massive hemorrhage, and/or protracted operation with massive volume resuscitation are where the ACS is most frequently encountered. However, knowledge of the ACS is also essential for the management of critically ill pediatric patients (especially those with AWD) and in understanding the limitations of laparoscopy. The role of IAH in the etiology of NEC, central obesity comorbidities, and pre-eclampsia/eclampsia remains to be fully studied.