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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The abdominal compartment syndrome (ACS) is defined a situation of high degrade abdominal hypertension (IAH) with clinicals signs of multiorganic dysfunction. It's observed like in the intensive care, in particular surgycals and postraumatics, there is ever a bigger frequence of complications presented by criticals patients. The various trials remark a changeable incidence, but the common factor is characterized by a particular severity of scores. All the possibles mechanicals, haemorragicals, infiammatories, and postraumatics causes act, but don't enable the stability among abdominal content, abdominal compliance and parietal tension. The initial triad of effects is constitued by the elevation of diaphragm and the visceral and vascular compression; after this triad provoke a pathophysiologic system that, through various levels, bring to a respiratory, renal and cardiocirculatory dysfunction and to a parietal, hepatic and intestinal ischemia with consequent bacterical translation: sepsis and MOF. The Burch's classification (1996) report four levels of gravity by the slight (< 15 mmHg) to the heavyest (> 35 mmHg): the firsts two levels are of intensivistic competence and for the detention are used conservatives metodics and pharmacological approach; instead in the lasts two levels it's necessary to foresee a surgycal treatment of laparotomy, washing and drainage with following temporary paret's closure. The mortality is now very elevated (29-62%) especially when it's already established a multiorganical dysfunction; therefore it's necessary forward its appearance through the monitorization of abdominal pression (IAP) with the measurement of vescical pression in alls criticals patients at the aim to treat immediately the firsts signs of IAH.
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PMID:[Pathophysiological and clinical trials of the abdominal compartment syndrome]. 1734 91

Three types of historical events are of interest, when dealing with the topic of abdominal compartment syndrome. The first concerns the evolution in the understanding of the pathophysiologic features of a compartment syndrome in general. The symptoms were well described by Richard von Volkmann in the 19th century. The second consists of the experimental studies devoted to measurements of intra-abdominal pressure. Different devices and techniques were used, in particular using detection locations approachable via natural body orifices (bladder/uterus/rectum etc). A third point of interest has come forward after the empirical assessment, in particular by sir Heneage Ogilvie that open laparostomies were beneficial in the healing of great abdominal war wounds, or later, of congenital abdominal wall defects. These three different views on pathology and treatment of life threatening abdominal hypertension have evolved to a concept of abdominal compartment syndrome, that with adequate diagnostic measures and accurate and timely intervention can now be treated with great success.
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PMID:Historical highlights in concept and treatment of abdominal compartment syndrome. 1746 97

Cardiovascular dysfunction and failure are commonly encountered in the patient with intraabdominal hypertension or abdominal compartment syndrome. Accurate assessment and optimization of preload, contractility, and afterload, in conjunction with appropriate goal-directed resuscitation and abdominal decompression when indicated, are essential to restoring end-organ perfusion and maximizing patient survival. The validity of traditional hemodynamic resuscitation endpoints, such as pulmonary artery occlusion pressure and central venous pressure, must be reconsidered in the patient with intra-abdominal hypertension as these pressure-based estimates of intravascular volume have significant limitations in patients with elevated intra-abdominal pressure. If such limitations are not recognized, misinterpretation of the patient's cardiac status is likely, resulting in inappropriate and potentially detrimental therapy. Appropriate fluid administration is mandatory as under-resuscitation leads to organ failure and over-resuscitation the development of secondary abdominal compartment syndrome, both of which are associated with increased morbidity and mortality. Volumetric monitoring techniques have been proven to be superior to traditional intra-cardiac filling pressures in directing the appropriate resuscitation of this patient population. Calculation of the "abdominal perfusion pressure", defined as mean arterial pressure minus intra-abdominal pressure, has been shown to be a beneficial resuscitation endpoint as it assesses not only the severity of the patient's intra-abdominal hypertension, but also the adequacy of abdominal blood flow. Application of a goal-directed resuscitation strategy, including abdominal decompression when indicated, improves cardiac function, reverses end-organ failure, and minimizes intra-abdominal hypertension-related patient morbidity and mortality.
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PMID:Cardiovascular implications of abdominal compartment syndrome. 1746 7

A better understanding of intra-abdominal hypertension with relation to the liver is vital to the management of all forms of liver pathophysiology. Supporting good hepatic function within the critically ill patient is important not only in maintaining synthetic function, but also in avoiding the multi-organ complications of liver dysfunction. The resulting reduction in hepato-splanchnic blood flow (HSBF) observed with increasing intra-abdominal pressure has been clearly documented and seen to be exaggerated in animals with established liver disease. Unfortunately the tools required to measure this, remain difficult to apply routinely in the clinical setting and as such goal directed therapy to specifically improve the hepatosplanchnic circulation remains elusive. Given the documented effects of lAP on HSBF and the relatively high incidence of intra-abdominal hypertension and the abdominal compartment syndrome within "liver patients" as a whole, close attention to IAP and timely correction by appropriate medical or surgical means would appear to be essential.
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PMID:Hepatic function and non-invasive hepatosplanchnic monitoring in patients with abdominal hypertension. 1746 8

Significant visceral edema associated with massive fluid resuscitation, paralytic ileus and formation of pancreatic ascites in patients with severe acute pancreatitis (SAP) can lead to abdominal compartment syndrome (ACS) that can contribute to the early development of multiple organ dysfunction syndrome (MODS), especially in the early stages of the disease. The prevalence of intra-abdominal hypertension (IAH) in SAP is about 40% and a manifest ACS occurs in about 10% of the patients warranting close monitoring of intra-abdominal pressure (lAP) in all patients with the severe form of the disease. Although nonsurgical management utilizing percutaneous drainage of ascites or continuous hemodiafiltration may decrease IAP, most patients require decompressive laparostomy and temporary abdominal closure. The primary aim in managing the ensuing open abdomen is delayed fascial closure during initial hospitalization. On many occasions a planned hernia approach, either with early skin grafting over the exposed bowel or managing the ASC primarily with a subcutaneous linea alba fasciotomy, is the only available option. The development of ACS in patients with SAP seems to be associated with increased mortality.
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PMID:Abdominal compartment syndrome and acute pancreatitis. 1746 10

Elevated intra-abdominal pressure (IAP) exerts effects not only on intra-abdominal organs, but also on organs distant to the abdominal compartment. Abdomino-thoracic interaction during intra-abdominal hypertension (IAH) or abdominal compartment syndrome (ACS) interferes with pulmonary, cardiovascular and cerebral function. In accordance with recent guidelines, IAH is defined as IAP above 12 mmHg and ACS as IAP more than 20 mmHg with one or more new organ failures. In this review we will first discuss the effects of elevated IAP on pulmonary dynamics and the relevance for interpreting airway pressures and adjusting ventilator settings. We will then discuss the interaction between abdomino-thoracic pressure transmission and global haemodynamics, the knowledge of which is necessary for correct assessment of cardiac preload and to optimize fluid therapy in the setting of IAH/ACS. A discussion on the relationship between increased IAP, increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP) will follow. Finally, we will review ventilator-induced thoracic pressure swings and their transmission to the abdominal compartment.
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PMID:Abdomino-thoracic transmission during ACS: facts and figures. 1746 20

Non-closure of abdominal fascia and the resultant open abdomen after laparotomy has become a major advance in the management of critically ill or injured patients. The benefits of open abdomen are many and include the prevention of intra-abdominal hypertension and the consequent abdominal compartment syndrome. Appropriately and exquisitely managed, it can provide all the benefits and prevent highly morbid complications of leaving the abdomen open. This review will provide some insights into such management.
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PMID:Management of open abdomen. 1746 21

The term abdominal compartment syndrome (ACS) describes the clinical manifestations of the pathologic elevation of the intra-abdominal pressure (IAP). When the IAP exceeds 12 mm Hg it is referred to as intra-abdominal hypertension (IAH) while ACS generally sets in at an IAP in excess of 20 mm Hg. This syndrome is most commonly observed in the setting of severe abdominal trauma and in the aftermath of major abdominal operations. ACS affects mainly the respiratory, cardiovascular, renal, gastrointestinal and the central nervous systems. Fundamental to the development of ACS are the obstruction of venous return to the heart via the inferior vena cava and the splinting of the diaphragm due to elevated IAP. Preventing ACS by the identification of patients at risk and early diagnosis is paramount to its successful management. To this end a high index of suspicion is sine qua non. The management of established ACS requires clinical astuteness and decisiveness with a readily available and generous team support. The purpose of this review is to enhance awareness among clinicians about a subtle condition with a devastating impact on morbidity and mortality if undiagnosed.
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PMID:Abdominal compartment syndrome. 1756 72

The abdominal compartment syndrome (ACS) is a life threatening disorder in critically ill patients caused by rapidly decreasing intra-abdominal pressure (IAP) > 12 mm Hg, which may result in multiple organ dysfunctions with a possibly fatal outcome. Under various causes for the development of an ACS, pelvic trauma, volume resuscitation after severe hemorrhage and reperfusion after aortic aneurysm repair as well as intra-abdominal packing figure at the first place. An increased BMI is a risk factor for patients to suffer from ACS. In addition, excessive volume requirement and significantly increasing airway pressures within the first 24 hrs after admission in the ICU are indicators for an impending ACS. Increased IAP causes venous stasis and arterial malperfusion of all intra- and extra-abdominal organs thus resulting in ischemia, hypoxia and necrosis. In parallel, respiratory, cardiocirculatory, renal, intestinal and cerebral decompensation can be registered. Final multiorgan failure has a mortality around 60-70 %. Timely diagnosis of ACS remains sometimes difficult in spite of clinical indicators such as increased airway pressure, hypoxia, oliguria, shock and acidosis. For the early recognition of intra-abdominal hypertension repetitive measurement of the intra-vesical pressure (> 20 mm Hg) can be helpful. Besides intensive care treatment with artificial ventilation, circulatory support with volume and catecholamines, the decision for a prompt abdominal decompression and open abdominal treatment is life-saving and can preserve further functional damage to vital organ systems.
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PMID:[Abdominal compartment syndrome. A still underestimated problem?]. 1766 Dec 59

Pain is a major clinical manifestation of chronic pancreatitis (CP) and a common indication for surgery in these patients. Pathogenesis of pain in CP is multifactorial and the mechanisms of pain may differ from patient to patient. This can explain why one therapeutic method of treatment of pain does not work in all patients and in different stages of the disease. Two main complimentary pathogenetic theories have been proposed to explain the mechanisms of pain in CP, the neurogenic theory and the theory of increased intraductal/intraparenchymal pressures. According to the neurogenic theory, in CP there are alterations of pancreatic/peripancreatic nerves, exposing them to noxious substances and/or activated immune cells, thereby generating pain ("neuroimmune interaction"). The other theory of intraductal/intraparenchymal hypertension suggests that pain in CP is generated as a result of increased pressures within the pancreatic ductal system and/or pancreatic parenchyma, like the pain in the classic compartment syndrome. The theory of intraductal/intraparenchymal hypertension is strongly supported by the good results of drainage procedures in the surgical management of CP. Pancreatic ischemia, oxygen-free radicals, centrally sensitized pain state, acute exacerbations of CP, development of complications from the pancreas (most commonly, pseudocysts) or adjacent organs (usually, duodenal and/or common bile duct stenosis), etc. are other possible contributing factors. Different patterns of pain have been described in idiopathic (early vs. late onset) and in alcoholic CP. Interestingly, pain is automatically relieved during the natural course of the disease in some patients (the "burn-out" phenomenon), after a relatively long time (from a few years to up to 3 decades). However, this is an unpredictable evolution for the individual patient. Therefore, surgery should be offered when pain is intense and after failure of conservative treatment. Surgical management should be individualized, depending on the particular findings of each patient. The knowledge of the pathophysiologic basis and of natural course of pain in CP is of paramount importance for the surgeon to select appropriate therapy for the individual patient with CP.
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PMID:Mechanisms and natural history of pain in chronic pancreatitis: a surgical perspective. 1766 54


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