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Abdominal Compartment Syndrome-Review
Abstract
Pathophysiological significance of abdominal compartment syndrome (ACS) is hugely unrecognized and is a major cause of ICU mortality especially is left untreated and unrecognized. Abdominal Compartment Syndrome occurs due to increase in abdominal pressure from variety of insults which results in impaired perfusion of abdominal organs leading to Ischemia which inturn causes initiation of acute inflammatory response including cytokine release, free radical formation and decreased production of ATP. Elevated intra abdominal pressure leads to pathophysiological effects on pulmonary, cardiovascular, renal, splanchnic and central nervous system which can mimic or be confused with other conditions such as ARDS or Sepsis. Monitoring of IAP should be done in all patients admitted in ICU who are at risk of developing ACS. Early recognition of ACS and prompt management by non surgical or surgical interventions is of paramount importance in preventing morbidity and mortality.
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The indications for surgical decompression of abdominal compartment syndrome (ACS) are not clearly defined, but undoubtedly some patients benefit from it. In patients without recent abdominal incisions, it can be achieved with full-thickness laparostomy (either midline, or transverse subcostal) or through a subcutaneous linea alba fasciotomy. In spite of the improvement in physiological variables and significant decrease in IAP, however, the effects of surgical decompression on organ function and outcome are less clear. Because of the significant morbidity associated with surgical decompression and the management of the ensuing open abdomen, more research is needed to better define the appropriate indications and techniques for surgical intervention.
Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are increasingly recognised to be a contributing cause of organ dysfunction and mortality in critically ill patients. The number of publications describing and researching this phenomenon is increasing exponentially but there are still very limited data about treatment and outcome.
This review will focus on the available literature from the last years. A Medline and PubMed search was performed using the search terms "abdominal compartment syndrome" and "treatment".
This search yielded 437 references, most of which were not relevant to the subject of this paper. The remaining abstracts were screened and selected on the basis of relevance, methodology and number of cases. Full text articles of the selected abstracts were used to supplement the authors' expert opinion and experience. The abdomino-thoracic transmission of pressure has direct clinical consequences on the cardiovascular, respiratory and central nervous systems in terms of monitoring and management. These interactions are discussed and treatment recommendations are made. IAH-induced renal dysfunction is addressed as a separate issue. Finally, an overview of non-invasive measures to decrease IAP is given.
This paper describes current insights on management of IAP induced organ dysfunction and lists the most widely used and published non-invasive techniques to decrease IAP with their limitations and pitfalls.
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.
Only recently has the important role of abdominal compartment syndrome (ACS) been recognized as a contributing factor to the multiple organ failure commonly seen in severe acute pancreatitis (SAP). Decompressive laparostomy for ACS is a life-saving procedure usually performed through a midline incision followed by a negative pressure wound dressing. High risk of intestinal fistulas and frequent inability to close the fascia with ensuing planned ventral hernia has prompted the search for alternative techniques. Subcutaneous fasciotomy may be effective in early and less severe cases of ACS but it is always accompanied with a ventral hernia.
A patient with SAP developed manifest ACS and was treated with bilateral subcostal laparostomy. Immediately after decompression, the intra-abdominal pressure dropped from 23 mmHg to 10 mmHg, and the respiratory, cardiovascular and renal functions improved markedly leading to full recovery. The abdominal incision including the fascia and the skin was closed gradually over 4 relaparotomies, and during the 6 months' follow up there are no signs of ventral hernia or other wound complications.
Transverse subcostal laparostomy is a promising alternative decompression technique for ACS in SAP. It is feasible, effective and might provide a chance of early fascial closure. Comparative studies are needed to define its role as a decompressive technique for ACS.
Abdominal pressure (80 mm Hg) applied to 12 anesthetized dogs caused an elevation of plasma antidiuretic hormone (ADH) levels to more than twice the basal levels. This elevation of ADH levels was prevented by a prior infusion of dextran which in addition prevented the associated 20% fall in cardiac output. Since other hemodynamic events were unaffected by either the abdominal pressure or the dextran infusion, it is concluded that the effect of abdominal pressure on plasma ADH levels is probably caused by an alteration in cardiac output.
Elevated intraabdominal pressure (IAP) occurs with intraabdominal bleeding, with tense ascites, or after application of military anti-shock trousers to trauma patients. While changes in renal perfusion with elevated IAP have been documented, there are no data available on blood flow to other viscera. Under pentobarbital anesthesia an inflatable bag was placed intraabdominally to create graded increases in IAP in 9 adult mongrel dogs (20 kg). Hemodynamic parameters and organ blood flow (OBF) using radioactive microspheres were measured at baseline and after increasing the IAP to 20 and 40 mm Hg. The organ blood flow index (OBFI = OBF/cardiac output) was determined for each organ (stomach, duodenum, jejunum, ileum, colon, pancreas, liver, spleen, kidney, and adrenal gland). Elevated IAP caused a decrease in OBF for all organs measured except the adrenal glands where the OBF was increased. The OBFI was decreased significantly for all intraabdominal viscera except the renal cortex and the adrenal gland. These changes in OBF are more marked than can be accounted for by changes in cardiac output alone, suggesting that local control mechanisms may be responsible for changes in OBF. Our data raise the possibility that elevation in IAP may result in visceral ischemia and organ dysfunction.
Intra-abdominal fluid volume and hydrostatic pressure were elevated by positive pressure infusion of Tyrode solution into the peritoneal cavity of anesthetized dogs. The compliance of the peritoneal cavity fell from 10.8 to 0.56 ml X mmHg-1 X kg-1 of body wt as intra-abdominal pressure increased from 0 to 40 mmHg. Intrathoracic pressure also increased as elevated peritoneal pressure caused diaphragmatic bulging. Cardiac output and stroke volume were reduced by 36% after an intra-abdominal pressure rise of 40 mmHg; in contrast, heart rate did not change. Flow in the celiac, superior mesenteric, and renal arteries was reduced by 42, 61, and 70%, respectively. Pressure in the femoral vein increased to 46 mmHg, while flow in the femoral artery decreased by 65%. Whole-body O2 consumption, pH, and arterial PO2 decreased as intra-abdominal pressure rose. The peritoneal cavity, with its high initial compliance, affords the body an ideal location for the temporary accumulation of small to moderate volumes of fluid during episodes of increased vascular pressure or permeability. The marked alterations in the hemodynamic properties of the cardiovascular system are indicative of the physiological changes that occur when intra-abdominal fluid accumulation becomes excessive and peritoneal pressure rises to high levels.
Changes in intra-abdominal pressure (IAP) have significant circulatory effects. However, whether this may influence the gastroesophageal collateral blood flow in patients with cirrhosis has not been studied.
In 14 portal hypertensive cirrhotics, serial hemodynamic measurements were obtained in baseline conditions 30 minutes after the mechanical increase of IAP by 10 mm Hg and 30 minutes after returning IAP to baseline levels.
Increasing IAP caused similar increases in free and wedged hepatic venous pressures (+10.3 mm Hg and +11.0 mm Hg, respectively; P < 0.005), without changing the hepatic venous pressure gradient (HVPG). However, there were significant decreases in cardiac output (-18%; P < 0.005) and hepatic blood flow (-20%; P < 0.05), whereas azygos blood flow, an index of gastroesophageal collateral blood flow, increased markedly (+23%; P < 0.005). The opposite occurred after releasing the high IAP.
In portal hypertensive cirrhotics, acute changes in IAP did not change HVPG but markedly modified splanchnic and systemic hemodynamics. Brief elevations of IAP may have deletereous effects, as shown by the increase in azygos blood flow and the decrease in cardiac output and hepatic blood flow, whereas reduction of a high IAP causes the opposite changes and may be beneficial.
To study the effects of elevated intra-abdominal pressure upon renal function and the renin-angiotensin-aldosterone system.
Two groups of anesthetized, ventilated swine were studied. Intra-abdominal pressure was increased in experimental animals (n = 6) by incrementally instilling an isosmotic ethylene glycol solution into the peritoneal cavity until intra-abdominal pressure was 25 mm Hg above baseline. The intravascular volume was then expanded until cardiac index returned to baseline. Lastly, the solution was drained to decompress the abdomen. Control animals underwent surgical preparation but did not have their intra-abdominal pressure raised. Changes in systemic and pulmonary hemodynamic parameters, renal venous pressure, and urine output were recorded. Venous samples for plasma renin activity, aldosterone, and atrial natriuretic factor were drawn after each change in either intra-abdominal pressure or intravascular volume in experimental animals, and at the same time points in control animals.
Elevated intra-abdominal pressure significantly (p < 0.05, analysis of variance) increased renal venous pressure, pleural pressure, wedge pressure, and pulmonary artery pressure compared to both baseline and control animals; whereas cardiac index and urine output decreased significantly. Both plasma renin and aldosterone levels increased significantly compared with baseline and controls. Intravascular volume expansion significantly increased urine output and decreased significantly both plasma renin activity and aldosterone levels. Abdominal decompression further significantly decreased both plasma renin activity and aldosterone levels. There were no significant changes in atrial natriuretic factor at any time point.
Elevated intra-abdominal pressure decreases urine output and significantly up-regulates the hormonal output of the renin-angiotensin-aldosterone system. Intravascular volume expansion in combination with abdominal decompression reverses the effects of acutely elevated intra-abdominal pressure upon renal function and the renin-angiotensin-aldosterone system.
To determine whether intra-abdominal pressure (as estimated from urinary bladder pressure) is elevated in patients with central obesity (as measured by sagittal abdominal diameter) and pseudotumor cerebri and whether this increased intra-abdominal pressure is associated with increased pleural pressure and cardiac filling pressure, implying a resistance to venous return from the brain.
Nonrandomized, prospective.
University hospital, operating room.
Intracranial pressure, urinary bladder pressure, sagittal abdominal diameter, transesophageal pleural pressure, central venous pressure, pulmonary artery pressure, and pulmonary artery occlusion pressure.
Six women with pseudotumor cerebri (one with CSF leak, one with lumboperitoneal shunt).
Urinary bladder pressure (22 +/- 3 cm H2O) and sagittal abdominal diameter (29 +/- 3 cm) were significantly elevated in these patients with elevated intracranial pressure (293 +/- 80 mm H2O) compared with a previously reported group of nonobese control patients. The transesophageal pleural pressure (15 +/- 10 mm Hg), central venous pressure (20 +/- 6 mm Hg), mean pulmonary artery pressure (31 +/- 6 mm Hg), and pulmonary artery occlusion pressure (21 +/- 7 mm Hg) were all markedly elevated compared with published normal values and with previous data from obese patients without pseudotumor cerebri.
These data support the hypothesis that central obesity raises intra-abdominal pressure, which increases pleural pressure and cardiac filling pressure, which impede venous return from the brain, leading to increased intracranial venous pressure and increased intracranial pressure associated with pseudotumor cerebri.
To evaluate the performance and verify the safety of the Koala Intrauterine Pressure Catheter (IUPC) in clinical use.
Twenty IUP Koala Catheters were placed in laboring women. IUPC monitoring provided diagnostic information in assessing the pressures generated by the myometrium during the labor and delivery process. Information was recorded pertaining to the catheters' safety, ease of use, accuracy, zeroing, drift and amnioinfusion capability. Comparisons were made to a preexisting IUPC.
The Koala catheter was safe to introduce into the intrauterine cavity. There were no problems with amnioport communications, connectors, placental perforation, unusual patient discomfort or infections with either the Koala or Intran fluid-filled system. The numerical ratings were compared using the Mann-Whitney test and showed no significant difference between the two groups in safety, zeroing and drift. A statistically significant difference at the .01 level for ease of use, accuracy and setup in favor of the Koala was found.
Clinical study of the Koala Intrauterine Pressure Catheter vs. Intran and the other fluid-filled catheters demonstrated the Koala to be as safe and as functionally effective as, or more effective than, standard IUPCs.
IAH causes multiple and profound physiologic abnormalities both within and outside the abdomen. IAP monitoring is easily performed by bladder measurements. Careful monitoring and prompt recognition and treatment of IAP are critical in patients after damage control surgery because IAH is extremely common in these patients. Use of mesh fascial prostheses at the initial celiotomy in high-risk patients may prevent the deleterious effects of IAH. IAH should be considered an earlier manifestation of ACS. Surgical intervention should be indicated by IAH and not delayed until ACS is clinically apparent.
The mechanisms of cellular priming resulting in both adaptive and maladaptive responses to subsequent injury and strategies for manipulating this priming to constructive therapeutic advantage are explored.
A cell is prepared or educated by an initial insult (priming stimulus). Investigations in both laboratory animals and humans indicate that cells, organs, and perhaps even whole patients respond differently to a proximal second insult ("second hit") by virtue of this prior environmental history. The opportunity to achieve the primed state appears to be conserved across almost all cell types. The initial stimulus transmits a message to the cellular machinery that influences the cell's response to a subsequent challenge. This response may result in an exaggerated inflammatory response in the case of the neutrophil (an often maladaptive process) or an improved tolerance to injury by the myocyte (adaptive response). Our global hypothesis is that cellular priming is a conserved, receptor-dependent process that invokes common intracellular targets across multiple cell types. We further postulate that these targets create a language based on the transient phosphorylation and dephosphorylation of intracellular enzymes that is therapeutically accessible.
Priming is a conserved, receptor-dependent process transduced by means of intracellular targets across multiple cell types. The potential therapeutic strategies outlined involve the receptor-mediated manipulation of cellular events. These events are transmitted through an intracellular language that instructs the cell regarding its behavior in response to subsequent stimulation. Understanding these intracellular events represents a realistic goal of priming and preconditioning biology and will likely lead to clinical control of the primed state.
Major trauma or abdominal injury may lead to the development of increased intra-abdominal pressure (IAP) and the onset of the abdominal compartment syndrome. Although the effect of raised IAP on systemic and splanchnic hemodynamics have been described, the consequences of the resultant gut hypoperfusion in this setting are unknown. Bacterial translocation (BT) occurs after a period of splanchnic ischemia and may contribute to later organ failure. A rodent model was used to examine the effect of raised IAP on ileal mucosal blood flow (MBF) and BT. IAP was increased to 25 mm Hg for 60 minutes and mean arterial blood pressure was maintained with fluid. Animals were killed 24 hours later and examined for BT.
Increased IAP resulted in a decrease of MBF to 63% of baseline despite maintaining normal mean arterial blood pressure. BT occurred principally to the mesenteric lymph nodes after 60 minutes of IAP at 25 mm Hg.
Increased IAP leads to decreased MBF and to BT, which may contribute to later septic complications and organ failure.
To standardise a direct method for measuring intra-abdominal pressure (IAP), to correlate the results with intrarectal pressure, and to compare the results in various conditions.
Prospective open study.
Teaching hospital, Egypt.
34 Subjects in 4 groups: control (n = 11), hernia (n = 8; 6 umbilical and 2 incisional), mass (n = 7; 6 enlarged spleen and 1 carcinoma of sigmoid), and obese (n = 8; a mean of 40% above expected weight).
Measurement of IAP with a Verres needle connected to a pressure transducer with the patient at rest, straining, supine, erect, and before and after anaesthesia. Intrarectal pressure was measured simultaneously.
Reproducibility and correlation between the two measurements.
The hernia group had significantly lower IAP than controls both at rest and on straining (mean (SD) 2.7 (1.5) cm H2O compared with 7.0 (5.09) and 6.1 (2.7) compared with 20.5 (7.9), p < 0.01 in each case). Neither the mass nor the obese group differed from the controls at rest, but the pressure was higher on straining (31.2 (1.4) and 33.5 (2.07) cm H2O, respectively, compared with 21.9 (7.3), p < 0.05 in each case). There was a significant drop in IAP after anaesthesia in all groups, and no significant difference between intrarectal pressure and IAP in any group.
The method of measuring IAP is reproducible. Intrarectal pressure is similar to IAP and can therefore be used instead of it.
The purpose of this study was to determine whether the gut or the liver was the source of tumor necrosis factor (TNF), interleukin-6 (IL-6), and endogenous endotoxin in a porcine model of mesenteric ischemia-reperfusion.
Endotoxin, TNF, and IL-6 levels were measured from the carotid artery (CA), portal vein (PV), and hepatic vein (HV) every 30 minutes for 330 minutes in anesthetized pigs after occlusion of the superior mesenteric artery (SMA; n = 7) and after sham operation (n = 7). In animals subjected to mesenteric ischemia, the SMA clamp was released twice: once at 240 minutes (for 40 seconds) and once at 300 minutes (for the remainder of the experiment).
In control animals, TNF and IL-6 levels remained at baseline at all vascular sites for the duration of the experiment. In the SMA ligation group, TNF levels peaked before release of the SMA clamp. Compared with TNF levels in the CA (27 +/- 3.7 pU/ml, unchanged from baseline), TNF levels were higher in the PV and in the HV (47 +/- 1.7 and 44 +/- 4.0 pU/ml, respectively; p < 0.05). In contrast, IL-6 appeared in the circulation immediately after first release of the SMA clamp. At this instant, compared with levels in the CA (1381 +/- 305 pU/ml), IL-6 levels in the PV and HV were higher (1884 +/- 276 and 1795 +/- 213 pU/ml, respectively; p < 0.05). Endotoxin remained at baseline levels (1.0 +/- 0.3 endotoxin unit/ml) throughout the experiment in both groups of animals, and gut efflux of endotoxin never exceeded gut influx.
TNF is produced in a partially perfused splanchnic bed during SMA clamping (e.g., pancreas, duodenum, liver, left colon). IL-6 is produced in gut during SMA clamping and is released when the SMA is unclamped. There is no apparent splanchnic release of endotoxin during or after SMA clamping in this model.
Background:
The abdominal compartment syndrome (ACS) is a newly appreciated and potentially fatal consequence of increased intra-abdominal pressure. It can be due to either trauma or surgery, as well as numerous medical conditions. Prolonged, unrelieved elevation of intra-abdominal pressure can produce pulmonary compromise, renal impairment, cardiac failure, shock, and death. A high index of suspicion is imperative. Measurement of the intravesical pressure provides a urometric window for detecting and monitoring this condition.
Conclusions:
Reopening the abdominal incision (decompressive celiotomy) has proven a life-saving intervention. Use of delayed wound closure (staged celiotomy) may prevent development of this condition in high-risk surgical patients. It is urgent that all physicians, and surgeons in particular, be alerted to this potentially lethal complication.
Intraabdominal hypertension and abdominal compartment syndrome are increasingly recognized as potential complications in patients who have significant intraabdominal trauma. Intraabdominal hypertension and abdominal compartment syndrome affect all body systems, most notably the cardiac, respiratory, renal, and neurologic systems. This complication also affects blood flow to various intraabdominal organs and may play a significant role in the sepsis and multiple organ failure syndrome seen in many trauma patients. Nursing knowledge of the risk factors and clinical signs of intraabdominal hypertension and abdominal compartment syndrome can reduce the morbidity and mortality associated with this syndrome.
Sustained intestinal ischemic injury often leads to shock and multiorgan failure, mediated in part by a cytokine cascade. Animal models have also identified a central role of Kupffer cells in amplification of cytokines following intestinal ischemia. To better understand this gut-liver axis, we developed an in vitro model.
Kupffer cells were isolated from rat livers by arabinogalactan gradient ultracentrifugation and adherence purification. Cells were grown in RPMI medium in 5% CO(2). Rat intestinal epithelial cells, IEC-6, were cultured under normoxic or anoxic (90% N(2), 10% CO(2)) conditions for 2, 12, and 24 h. Kupffer cells were then grown in the conditioned medium of the IEC-6 cultures. After 24 h, the medium was replaced with fresh medium. This final Kupffer cell supernatant was tested for tumor necrosis factor alpha and interleukin-6 production by ELISA. Trypan blue exclusion was performed to assess cell viability.
Intestinal and Kupffer cells remained viable during the experimental time. Production of both tumor necrosis factor alpha and interleukin-6 by Kupffer cells increased with increasing ischemia time of the intestinal cells.
Consistent with animal studies of intestinal ischemia, this study found an increase in cytokine production by Kupffer cells following hypoxia of intestinal cells. This in vitro model offers a new tool to study the expression of cytokines, proteins, and messengers involved in the cascade of events that follow intestinal ischemia.
Previous methods described to measure bladder pressure require additional setup, making these techniques complex and time consuming. We describe a simple U-tube technique and investigate its accuracy for measuring intra-abdominal pressure (IAP).
Warm saline was infused into the peritoneum of five pigs to increase IAP. Indirect methods of measuring IAP included bladder, inferior vena cava (IVC), and gastric pressures. Bladder pressure was measured by both the standard and U-tube technique. IVC pressure was measured via a femoral line and gastric pressure was transduced through an orogastric tube. In addition, 30 patients undergoing laparoscopy were prospectively investigated. Insufflated abdominal pressure readings were obtained and compared with bladder pressures measured by the U-tube technique (n = 20) and standard technique (n = 10).
In the animal study, U-tube manometry had the highest degree of correlation (r(2) = 0.98) and the lowest bias (0.51 +/- 1.63 mm Hg). The bladder pressure measured by the U-tube technique was between 0.1 and 0.9 mm Hg less than the directly measured IAP (95% confidence interval). There was a high degree of correlation between IAP and the standard technique for bladder pressure (r(2) = 0.93), IVC pressure (r(2) = 0.93), and gastric pressure (r(2) = 0.90). Strong correlation also existed between the U-tube and standard techniques for measuring bladder pressure (r(2) = 0.96). In humans, a strong correlation between insufflated abdominal pressure and bladder pressure (U-tube technique, r(2) = 0.79; standard technique, r(2) = 0.53) was also encountered.
The accuracy of the U-tube manometry technique for measuring intra-abdominal pressure is comparable to previously described techniques. The U-tube technique is simple, does not require additional equipment, and can be performed by any member of the medical team.
Authors inform about the group of 8 patients with abdominal compartment syndrome (ACS) occurred as a complication in large blunt injury of abdominal cavity. To the ACS diagnose, the measurement of intracystic pressure is used routinely, whose values correlate fully with values of intraabdominal pressure (IAP). In case of increasing values of IAP over 25 mm Hg with positive clinical signs of ACS, authors indicate decompression laparotomy with temporary closing of abdominal cavity by sterile plastic foil or Ethizip. This preventive temporary laparostomy is recommended also in serious injuries of abdominal cavity in patients with fatal haemorrhage, treated by the method of staged laparotomy with tamponade of abdominal cavity and with massive blood and volume resuscitation.
This review will set forth the new consensus definitions for intra-abdominal pressure, intra-abdominal hypertension, and the abdominal compartment syndrome from the World Congress on the Abdominal Compartment Syndrome in December 2004. The review will explore the challenges in diagnosis, pathophysiology, and recent concepts in the treatment of abdominal compartment syndrome.
Intra-abdominal pressure greater than 12 mm Hg may exert adverse physiologic sequelae, progressing to intra-abdominal hypertension and full-blown abdominal compartment syndrome as intra-abdominal pressure increases. The first challenge is to recognize that abdominal compartment syndrome may be a potential problem in critically ill patients. Intra-abdominal pressure monitoring is essential for this. Continuous monitoring of intra-abdominal pressure and abdominal perfusion pressure adds real-time measurements and can be performed by way of the stomach or bladder. Intra-abdominal hypertension occurs in approximately 35% of patients in the intensive care unit, and abdominal compartment syndrome in approximately 5%.
Massive resuscitation is increasingly recognized as a major contributor to abdominal compartment syndrome. Prophylactic decompression and temporary abdominal closure have important roles in preventing tertiary or recurrent abdominal compartment syndrome. Failure to recognize and treat intra-abdominal hypertension will result in increased risk of renal impairment, visceral and intestinal ischemia, respiratory failure and death.
Managing the abdominal compartment syndrome associated with severe acute pancreatitis by the open abdomen method is associated with considerable morbidity and resource utilization.
A technique of subcutaneous anterior abdominal fasciotomy is described for the first time in two patients with severe acute pancreatitis.
Following the procedure, the intra-abdominal pressure decreased from 30 mmHg immediately to 23 mmHg and to a sustained level of 12-14 mmHg in the first patient, and from 35 mmHg immediately to 23 mmHg and to a sustained level of 14-19 mmHg in the second patient.
The subcutaneous anterior abdominal fasciotomy is a promising method for safe and effective abdominal decompression with sustained effect and avoiding the morbidity associated with the alternative open abdomen techniques.
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.
To investigate the differences in incidence, time course and outcome of primary versus secondary intra-abdominal hypertension (IAH), and to evaluate IAH as an independent risk factor of mortality in a presumable risk population of critically ill patients.
Prospective observational study.
General intensive care unit of a university hospital.
A total of 257 mechanically ventilated patients at presumable risk for the development of IAH were studied during their ICU stay and followed up for 90-day survival.
Repeated measurements of intra-abdominal pressure (IAP).
IAP was measured intermittently, via bladder. IAH (sustained or repeated IAP > or = 12 mmHg) developed in 95 patients (37.0%). Primary IAH was observed in 60 and secondary IAH in 35 patients. Patients with secondary IAH demonstrated a significant increase of mean IAP during the first three days (mean DeltaIAP was 2.2 +/- 4.7 mmHg), whilst IAP decreased (mean DeltaIAP -1.1 +/- 3.7 mmHg) in the patients with primary IAH. The patients with IAH had a significantly higher ICU- (37.9 vs. 19.1%; P = 0.001), 28-day (48.4 vs. 27.8%, P = 0.001), and 90-day mortality (53.7 vs. 35.8%, P = 0.004) compared to the patients without the syndrome. Patients with secondary IAH had a significantly higher ICU mortality than patients with primary IAH (P = 0.032). Development of IAH was identified as an independent risk factor for death (OR 2.52; 95% CI 1.23-5.14).
Secondary IAH is less frequent, has a different time course and worse outcome than primary IAH. Development of IAH during ICU period is an independent risk factor for death.