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العنوان
Abdominal Compartment Syndrome
المؤلف
Kamel,Waleed Mohammed Samir
هيئة الاعداد
باحث / Waleed Mohammed Samir Kamel
مشرف / Ahmed Alaa el Din Abdul Majeed
مشرف / Mohamed Ali Nada
الموضوع
Abdominal Compartment Syndrome-
تاريخ النشر
2010
عدد الصفحات
131.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
جراحة
تاريخ الإجازة
1/1/2010
مكان الإجازة
جامعة عين شمس - كلية الطب - General Surgery
الفهرس
Only 14 pages are availabe for public view

from 131

from 131

Abstract

syndrome exists when there increased pressure in a closed anatomic space. The term abdominal compartment syndrome describes the clinical manifestation of pathologic elevation of intra-abdominal pressure ( IAP) which affects a lot of organs. A.C.S. was considered a traumatic surgical disease , but ACS is a problem in many ill patients who have no trauma.In order to understand ACS a clear prospective view of the anatomy of the abdominal wall and cavity should be taken into consideration .
ACS clinical spectrum dramatically impacts patient outcome : the end result of undetected and untreated intra-abdominal hypertension is multisystem organ failure including respiratory , renal , central nervous system manifestations and ends by patient death .
ACS can be divided into the following 3 categories:
• Primary or acute ACS ,
• Secondary ACS
• Chronic ACS .
Normal Intra abdominal pressure (IAP) ranges from subatmospheric to 0 mmhg. The development of ACS requires acute and rapid elevation of IAP. Elevation of intra abdominal pressure causes a ripple effect throughout the body by causing direct pressure effects on intra abdominal and intra-thoracic contents . The cardiovascular , pulmonary , splanchnic , renal and intra cranial systems are most affected . Organ dysfunction severity is proportional to the level of IAP elevation. Cardiovascular dysfunction is a result of elevated IAP that is consistently related with reduction in cardiac output . This can be demonstrated with IAP above 20 mmhg which results in decreased preload through decreased venous return , decreased load through direct pressure effects on the heart from increased intra-thoracic pressure as well as increased after load from increased systemic vascular resistance.Pulmonary dysfunction is a result of increased intrathoracic pressure causing direct pressure effects on the pulmonary parenchyma and it vasculature resulting in decreased compliance and pulmonary hypertension. Renal dysfunction is caused by also direct pressure effects from IAH causin oliguria. GIT dysfunction results from reduction in mesenteric blood flow causing bacterial translocation and intestinal ischemia In addition to reducing arterial blood flow, IAP compresses thin walled mesenteric veins promoting venous hypertension and intestinal edema , decreased intramucosal pH and systemic metabolic acidosis. Hepatic dysfunction is caused by reduced hepatic artery, hepatic vein, and portal vein blood flow due to IAH. Hepatic artery flow is directly affected by decreases in cardiac output as well as along with reduced portal venous flow occurs as a result of both extrinsic compression of the liver as well as anatomic narrowing of the hepatic veins as they pass through the diaphragm. Central nervous system is affected from rapid increased ICP from malignant rapid increase in IAP and ITP(intra-thoracic pressure) resulting in direct compression of paenchymal , vascularcompartments and blocking CSF drainage. Abdominal wall is affected by visceral edema, abdominal packs, and free intraperitoneal fluid which all distend the abdomen and reduce abdominal wall compliance .
Investigations include bedside measurement of IAP as bladder pressure measurements , gastric tonometry & venous pressure measurements . Radiological investigations include
x-ray chest and abdomen , enhanced CT scan abdomen (with or without contrast) , MRI , and sonography.