Clinical Significance of Intra-Abdominal Hypertension

Intra-abdominal hypertension (IAH) is defined as steady state pressure in the abdominal cavity. Intra-abdominal pressure (IAP) acts as resistance against blood flow. IAH decreases abdominal perfusion pressure, aggravates hemodynamics and organ dysfunction and raises serious risks of morbidity and mortality. IAP should be a goal of resuscitation, and aggressive treatment should be performed to relieve IAH, including therapeutic open abdomen.

Intra-abdominal hypertension and abdominal compartment syndrome: A review of current concept and trends.

Abdominal compartment syndrome (ACS) and intra-abdominal hypertension (IAH) have been a cause of complications in ICU patients, especially those of trauma and acute abdomen. ACS affects almost every system of the body namely the cardiac, respiratory, renal, CNS and the GIT. It has been under-recognized as it primarily affects patients who are already critically ill and the organ dysfunction may be incorrectly attributed to the primary illness. Since ACS can improve with treatment, it is important that the diagnosis be considered in the appropriate patient. We will review here the definition, classification, incidence, etiology, pathophysiology, clinical presentation, diagnosis and management of intraabdominal hypertension and abdominal compartment syndrome. The method employed for literature search included web search of articles in various international and national bibliographic indices. The websites used for the search include Google, PubMed, NIH.gov, Medscape.com, Science direct and Scopus.

Renal protective effect and its related mechanisms of targeted abdominal perfusion pressure treatment in intra-abdominal hypertension / 国际外科学杂志

Objective To evaluate the renal protective effect of targeted abdominal perfusion pressure (APP) treatment in intra-abdominal hypertension (IAH) and further investigate its related mechanisms.Methods Twelve healthy pigs were randomly divided into experimental group and control group,each group had 6 pigs.All animals were collected urine volume each hour,continuously monitored mean arterial pressure (MAP) and renal cortical blood flow after anesthesia.IAH models were established by intraperitoneally injecting carbon dioxide in all animals,the baseline MAP,intra-abdominal pressure (IAP)and APP were obtained before IAH models established.In both groups,IAP was raised gradually from 0 mm Hg to 10 mm Hg,20 mm Hg and 30 mm Hg.In control group,IAP was maintained at 30 mm Hg for 8 hours with-out any other interventions.In experimental group,the animals were intravenously given with norepinephrine in order to get a target level of APP equal to its baseline values after 15 minutes of the onset of 30 mm Hg IAP.Changes of renal cortical blood flow,serum creatinine,TNF-α,IL-6 and urine IL-18 with the alteration of IAP in both groups were explored.Animals were then sacrificed for renal histopathology after 8 hours of the onset of 30 mm Hg IAP.Results With the increase of IAP,renal cortical blood flow in both groups was significantly decreased (P ＜ 0.01).Compared to its baseline,serum Cr and urinary IL-18 were significantly up-regulated after the maintenance of IAP at 30 mm Hg for 6 hours in both groups (P ＜ 0.05).However,in experimental group,which utilized a strategy of targeted APP,significant improvement of the renal cortical blood flow was observed (P ＜ 0.01),and urinary IL-18 was significantly lower than the control group (P ＜ 0.05).Renal histopathological examination found no obvious abnormalities either in control group or in experimental group.Conclusions The targeted APP treatment may have some renal protective function within the first 8 hours of IAH by improving renal cortical blood flow rather than affecting systemic inflammatory response.

Consecuencias hemodinámicas y respiratorias del síndrome compartimental abdominal en un modelo experimental / Hemodynamic and respiratory alterations in an experimental abdominal compartment syndrome model

Introduction: Abdominal compartment syndrome (ACS) is a severe and under-reported condition among the pediatric population due to inadequate warning and recognition. It can be caused by medical and surgical reasons, resulting in a high mortality rate. objective: To determine the magnitude of the initial hemodynamic and respiratory consequences triggered by the induction of ACS in an experimental model. Methods: The model consisted of twelve anesthetized pigs (4.8 +/- 0.1 kg). The ACS was induced by instillation of colloid solution in the peritoneal cavity to obtain an intra-abdominal pressure (IAP) of 24.9 +/- 0.6 mmHg. In basal conditions and after the ACS induction, a conventional hemodynamic monitoring and transpulmonary thermodilution were performed. At the same time, arterial blood gases and lung mechanics analysis were measured. results: There was a reduction of cardiac output by 16 percent (5.19 +/- 0.33 to 4.34 +/- 0.28 l/min/m², p = 0.01) and abdominal perfusion pressure by 20 percent (72.3 +/- 3.2 to 57.3 +/- 4.0 mmHg, p <0.001) without changes in heart rate, arterial or central venous pressure. In addition there was an approximately 50 percent worsening of respiratory system compliance (1.28 +/- 0.09 to 0.62 +/- 0.04 ml/cmH2O/kg, p = 0.002) associated with a significant increase in intrathoracic pressure and slight decrease in oxygenation. Discussion: In this experimental model, the early development of hemodynamic and pulmonary dysfunction could be observed. A reduction of cardiac output that was not detected by conventional monitoring and a substantial deterioration of lung mechanics, characteristic of restrictive disease, associated with mild alterations in gas exchange were reported. It is essential then to monitor the IAP in patients predisposed to develop ACS, especially in the case of organ dysfunction deterioration, as severe hypotension and hypoxemia are late signs of this complication.

Introducción: El síndrome compartimental abdominal (SCA) es una entidad grave, de escaso reporte en población pediátrica por una inadecuada alerta y reconocimiento. Puede ser originado por causas médicas y quirúrgicas, presentando una elevada mortalidad. objetivo: Determinar la magnitud de las consecuencias hemodinámicas y respiratorias iniciales desencadenadas por la inducción de un SCA en un modelo experimental. Método: Doce cerdos anestesiados (4,8 +/- 0,1 kg). El SCA fue inducido con instilación de solución coloide en cavidad peritoneal para obtener una presión intra-abdominal (PIA) de 25 +/- 5 mmHg. En condiciones basales y posterior a inducción del SCA se realizó monitorización hemodinámica convencional y termodilución transpulmonar. Paralelamente se midió gasometría arterial y análisis de mecánica pulmonar. resultados: Hubo una reducción del gasto cardíaco en 16 por ciento (5,19 +/- 0,33 a 4,34 +/- 0,28 l/min/m², p = 0,01) y de la presión de perfusión abdominal en 20 por ciento (72,3 +/- 3,2 a 57,3 +/- 4,0 mmHg, p < 0,001) sin cambios en frecuencia cardiaca, presión arterial y venosa central. Además ocurrió un deterioro de la compliance del sistema respiratorio cercana al 50 por ciento (1,28 +/- 0,09 a 0,62 +/- 0,04 ml/cmH2O/kg, p = 0,002) asociado a un incremento significativo en las presiones intratorácicas y disminución leve de la oxigenación. Discusión: En este modelo experimental se pudo apreciar el desarrollo temprano de disfunción hemodinámica y pulmonar. Se evidenció una reducción de gasto cardiaco no detectado por la monitorización convencional y un deterioro substancial de la mecánica pulmonar, propia de una enfermedad restrictiva, asociado a alteraciones leves del intercambio gaseoso. Creemos que es fundamental monitorizar la PIA en pacientes predispuestos a desarrollar un SCA, más aún ante empeoramiento de disfunciones orgánicas dado que la hipotensión e hipoxemia grave son signos tardíos de esta complicación.