Slide 1:INTRA ABDOMINAL HYPERTENSION AND ABDOMINAL COMPARTMENT SYNDROME MURALI


Slide 2:Hammermilk - IAP - 1858 IAP Measurement - rectal bougies - Braune - 1865 pressures - urinary bladder - Odebrecht -1875 Normally intra abdominal pressure - < atmospheric / sub atmospheric


Slide 3:Kron et al - 1984 IAP - Measured 'abdominal compartment syndrome’(ACS)


Slide 5:“progressive, unchecked increase in IAP from a number of disorders leads to multiple organ dysfunction.”


Slide 6:PRIMARY Intraperitoneal: Intraperitoneal haemorrhage, AAA rupture, Acute gastric distension, Bowel obstruction, Paralytic ileus, mesentric vein thrombosis, Pneumoperitoneum, Abscess. Retroperitoneal: Pancreatitis, Retroperitonel haemorrhage, Aortic surgery. Abdominal wall: Burn eschar, Reduction of large hernias, Laparotomy - closure under tension, Abdominal binders .


Slide 7:SECONDARY Due to aggressive fluid resuscitation. Postoperative TERTIARY(chronic) Recurrence of IAP after treating primary & secondary ACS Peritoneal dialysis Morbid obesity Cirrhosis Meigs syndrome


Slide 8:Physiological Sequelae


Slide 9:CARDIAC  cardiac workload  cardiac output Cardiac arrest


Slide 10:CENTRAL NERVOUS SYSTEM  Intracranial pressure  Cerebral perfusion pressure PULMONARY  Intrathoracic pressure  Airway pressures  PaO2  PaCO2


Slide 11:GASTROINTESTINAL  Celiac blood flow  SMA blood flow  Mucosal blood flow RENAL  Urinary output  Renal blood flow  GFR


Slide 12:HEPATIC  Portal blood flow  Mitochondrial function  Lactate clearance ABDOMINAL WALL  Compliance  Rectus sheath blood flow


Slide 13:How to measure IAP ? Ryle’s tube Rectum IVC peritoneal dialysis catheter Urinary bladder


Slide 14:Bladder pressure monitoring through the Foley catheter is: is non-invasive when compared with Intra peritoneal measurements. More reliable & reproducible than clinical judgment . Becoming a standard method for monitoring abdominal pressures . Allows early detection of intra-abdominal hypertension, allowing intervention before ACS develops. IAP Monitoring


Slide 15:The “critical IAP” that causes end-organ dysfunction varies from patient to patient as a result of differences in physiology and preexisting co morbidities. Thus a single threshold value of IAP cannot be globally applied to the decision making of all critically ill patients. “abdominal perfusion pressure” (APP), defined as mean arterial pressure (MAP) minus IAP APP = MAP-IAP


ABDOMINAL COMPARTMENT SYNDROME :ABDOMINAL COMPARTMENT SYNDROME 50 mL of sterile saline is instilled into the bladder via the aspiration port of the Foley catheter with the drainage tube clamped. An 18-gauge needle attached to a pressure transducer is then inserted in the aspiration port, and the pressure is measured. The transducer should be zeroed at the level of the pubic symphysis.


WORLD SOCIETY OF IAH/ACS :WORLD SOCIETY OF IAH/ACS Condition intra abdominal pressure Normal 25mmhg ACS >20mmhg


MANAGEMENT :MANAGEMENT


Slide 19:Management Decompression Laparotomy: early intervention is advantageous Less bowel edema or cell damage, better chance of early closure and early recovery. Can be performed bedside for unstable patients


Management :Management Decompression Laparotomy:


ABDOMINAL COMPARTMENT SYNDROME :ABDOMINAL COMPARTMENT SYNDROME Vacuum-assisted temporary abdominal closure device: thin plastic sheet, a sterile towel, closed suction drains, and a large adherent operative drape. This dressing system permits increases in intra-abdominal volume, without a dramatic elevation in IAP. OPERATIVE DECOMPRESSION


Slide 22:Vacuum pack is removed Dramatic bowel evisceration Replaced with plastic silo dressing


Slide 23:Worsened bowel edema


Slide 24:Management Decompression Laparotomy: Post-operative dressing few days post-op


Slide 25:ABDOMINAL COMPARTMENT SYNDROME SUMMARY The gut is the organ most sensitive to IAH. Measuring IAPs in critically ill patients is important as it can affect management Treatment involves decompression of the abdomen. Since this syndrome affects patients who are already physiologically compromised, a high degree of suspicion and continuous monitoring of bladder pressures are required to prevent the mortality associated with this complex problem.


Results from the International Conference of Experts on Intra-Abdominal Hypertension (IAH) and Abdominal Compartment Syndrome (ACS) :Results from the International Conference of Experts on Intra-Abdominal Hypertension (IAH) and Abdominal Compartment Syndrome (ACS) RECOMMENDATIONS Intensive Care Medicine 2007; 33(6): 951-962


Slide 27:Is underdiagnosed in intensive care settings 23% of medical intensivists unaware of bladder pressure measurement procedure by recent survey Decompression laparotomy had never been used by 19.6% or medical intensivists in the same survey Is a common cause of multisystem organ failure Because it occurs in critically ill patients, it is often misdiagnosed as progression of underlying disease Death rates are reported from 40-100% Having an IAP > 12 mmHg at any time during your ICU stay is an independent predictor of poor outcome


Slide 28:Intraabdominal pressure monitoring techniques Despite the impression by some clinicians that they can examine a patient and predict whether they have an elevated abdominal pressure, the fact is clinical judgment for this disorder is no better than the flip of a coin. Several studies have confirmed that even in the hands of a staff level academic surgeon, abdominal exam is completely unreliable at determining the presence or absence of an elevated intra-abdominal pressure.[1, 2] These authors conclude that due to the inaccuracies of physical exam findings, intra-abdominal pressures must be measured by an objective, reliable, reproducible method at an interval that is frequent enough to detect rising pressure and allow interventions to occur prior to the onset of the highly mortal abdominal compartment syndrome. To date, the most reliable method is via pressure transduction through a catheter within the peritoneal cavity. Other less invasive options include pressure transduction through a tube placed in the stomach, bladder, or rectum.[1, 2] Of these options, Obeid et al found bladder pressure to most closely reflect intraperitoneal pressure and to be the most technically reliable.[3] Multiple other authors confirm Obeids‘ findings that bladder pressures most closely tracks peritoneal pressures, whereas stomach pressures are less reliable.[4-7] Bladder pressures taken through a Foley catheter correlate very closely with pressures measured directly in the abdominal cavity and are now considered to be the gold standard method of monitoring intra-abdominal pressure by an international consensus committee ­ the World Society of abdominal compartment syndrome.[8]


Slide 30:Thank you


Slide 31:Primary or acute abdominal compartment syndrome: This occurs when intra-abdominal pathology is directly and proximally responsible for the compartment syndrome. Secondary abdominal compartment syndrome: This occurs when no visible intra-abdominal injury is present but injuries outside the abdomen cause fluid accumulation. Chronic abdominal compartment syndrome: This occurs in the presence of cirrhosis and ascites, often in the later stages of the disease.


Slide 32:Primary (ie, acute) Penetrating trauma Intraperitoneal hemorrhage Pancreatitis External compressing forces, such as debris from a motor vehicle collision or after a large structure explosion Pelvic fracture Rupture of abdominal aortic aneurysm Perforated peptic ulcer Secondary: Secondary ACS may occur in patients without an intra-abdominal injury, when fluid accumulates in volumes sufficient to cause IAH. Large-volume resuscitation: The literature shows significantly increased risk when more than 3 L are infused. Large areas of full-thickness burns: In 2002, Hobson et al demonstrated abdominal compartment syndrome within 24 hours in burn patients who had received an average of 237 mL/kg over a 12-hour period.2 Penetrating or blunt trauma without identifiable injury Postoperative Packing and primary fascial closure, which increases incidence Sepsis Chronic Peritoneal dialysis Morbid obesity Cirrhosis Meigs syndrome


ABDOMINAL COMPARTMENT SYNDROME :ABDOMINAL COMPARTMENT SYNDROME ETIOLOGY Massive volume resuscitation is the leading cause of ACS. Inflammatory states with capillary leak, fluid sequestration, inadequate tissue perfusion, and lactic acidosis can develop ACS. Gastric over distention following endoscopy has resulted in ACS.


Slide 34:The secondary abdominal compartment syndrome: not just another post-traumatic complication Chad G. Ball,* Andrew W. Kirkpatrick,‡† and Paul McBeth‡From the *Departments of Trauma, Surgery and Critical Care, Grady Memorial Hospital, Emory University, Atlanta, Ga., and the †Department of Critical Care Medicine and the Regional Trauma Program, and the ‡Department of Surgery, Foothills Medical Centre, University of Calgary, Calgary, Alta. The secondary abdominal compartment syndrome (ACS) is defined as the presence of organ dysfunction with concurrent intra-abdominal hypertension (IAH) in a scenario lacking primary intraperitoneal injury or intervention. This state appears to be related to visceral, abdominal wall and retroperitoneal edema and ascites induced by resuscitation. Despite a diverse range of associated causes such as pancreatitis, intra-abdominal sepsis, cardiac arrest, thermal injury and extraperitoneal trauma, this class of ACS is characterized by the presence of shock requiring aggressive fluid resuscitation. Secondary ACS is an extreme condition along a continuum of raised intra-abdominal pressure (IAP) that is pathoneumonic when associated with new overt organ failure. When IAP is above normal but is not associated with organ failure, IAH is diagnosed. Because these conditions are common among critically ill patients, the measurement of IAP is crucial. It is unclear whether preventing IAH reduces progression to ACS or influences outcomes. When overt ACS is confirmed, immediate surgical decompression of the patient's abdomen via a standard laparotomy is usually required. Because many disease processes resulting in critical illness require aggressive fluid resuscitation as a primary therapy, it is likely that secondary ACS is much more common than previously believed. Further study is needed.


RESULTS FROM THE INTERNATIONAL CONFERENCE OF EXPERTS ON INTRA-ABDOMINAL HYPERTENSION (IAH) AND ABDOMINAL COMPARTMENT SYNDROME (ACS) RECOMMENDATIONSINTENSIVE CARE MEDICINE 2007; 33(6): 951-962 :RESULTS FROM THE INTERNATIONAL CONFERENCE OF EXPERTS ON INTRA-ABDOMINAL HYPERTENSION (IAH) AND ABDOMINAL COMPARTMENT SYNDROME (ACS) RECOMMENDATIONSINTENSIVE CARE MEDICINE 2007; 33(6): 951-962


Slide 36:A compartment syndrome is a condition of increased pressure in a confined anatomic space that adversely affects the circulation and threatens the function and viability of the tissues therein. This may arise in any closed compartment within the body. Secondary abdominal compartment syndrome (ACS) is characterized by the presence of shock requiring aggressive fluid resuscitation. Because many disease processes resulting in critical illness require aggressive fluid resuscitation as a primary therapy, it is likely that this condition is much more common than previously believed.


Slide 37:The pathophysiology of secondary ACS affects the entire body and is identical to primary ACS. Cardiac output is reduced owing to decreased preload and right heart volumes. Although increased systemic vascular resistance initially maintains apparent blood pressure, decreases in preload from the pooling of blood in splanchnic and lower extremity vascular beds eventually lead to reduced central venous return.3,35,49–53 Cardiac underfilling also occurs despite apparently increased central hemodynamic measurements (central venous pressure [CVP] and pulmonary artery occlusion pressure). As respiratory compliance decreases, mechanical ventilation with increased ventilatory pressures and decreased volumes becomes difficult.54,55 The partial pressures of oxygen will decrease, and carbon dioxide will increase.56,57 Even modest IAH appears to exacerbate acute lung injury and the acute respiratory distress syndrome (ARDS). When IAP levels greater than 20 mm Hg are applied to critically ill animals, a dramatic exacerbation of ARDS-associated pulmonary edema is evident.58 Furthermore, elevated IAP results in a stiffer chest wall with much lower transpulmonary pressures, and therefore less susceptibility to ventilator-induced lung injury.59,60 Oliguria is a common manifestation of the ACS because renal failure and IAH are dose-dependant.3,19,20 These effects are exaggerated by hypovolemia and positive end-expiratory pressure.56,61 Beyond the heart, lungs and kidneys, almost every other organ system is altered by IAH, even if the effects are not clinically overt. Also, IAH appears to contribute to increased intracerebral pressure (ICP) via transmitted intrathoracic pressure62–65 to the extent that laparotomies have been reported to reduce ICP in patients with secondary ACS.66 Patients in shock are at a particularly high risk for splanchnic malperfusion because even modest elevations in IAP greatly reduce hepatic and splanchnic perfusion.67–70 This effect is exacerbated by prior hemorrhage71 and is observed at much lower IAPs than required to induce other clinical features of ACS. As a result, subtle organ failure, concurrent to multisystem disease compatible with other causes, may be difficult to ascertain.


Slide 38:The World Society of the Abdominal Compartment Syndrome (WSACS) defines ACS as a sustained increase in intra-abdominal pressure (IAP) greater than 20 mm Hg concurrent with a new onset of organ dysfunction.1 This state of organ failure frequently affects the cardiovascular, respiratory and renal systems.2–8 The condition is uniformly fatal if left untreated.2–8 It is widely understood that ACS represents the end stage of a pathophysiologic spectrum that begins with normal IAP, proceeds to intra-abdominal hypertension (IAH) and ends with overt ACS. To standardize definitions and facilitate communication and research, the WSACS recently outlined working definitions of the conditions.1,9 They also published evidence-based guidelines for the diagnosis, measurement, management and prevention of IAH and ACS. These documents will be revised regularly and are intended to provide guidance to clinicians. Historically, ACS was often diagnosed when the effects of IAH had become overtly obvious. The signs included severe respiratory distress, elevated peak airway pressures, hypotension, diminished cardiac output and oliguria.2,3,6 Diagnosing IAH and ACS at this point is clearly too late, as evidenced by an increasingly poor prognosis, infectious complications and death.1–16 Because many of the effects of ACS are clinically indistinguishable from those of other common syndromes related to critical illness, it is probable that the influence of abnormal IAP is not infrequently missed in a critically ill patient with multifactorial complications. As a result, clinicians must possess a high index of suspicion and monitor IAP aggressiv


Slide 39:The World Society of the Abdominal Compartment Syndrome (WSACS) defines ACS as a sustained increase in intra-abdominal pressure (IAP) greater than 20 mm Hg concurrent with a new onset of organ dysfunction.1 This state of organ failure frequently affects the cardiovascular, respiratory and renal systems.2–8 The condition is uniformly fatal if left untreated.2–8 It is widely understood that ACS represents the end stage of a pathophysiologic spectrum that begins with normal IAP, proceeds to intra-abdominal hypertension (IAH) and ends with overt ACS. To standardize definitions and facilitate communication and research, the WSACS recently outlined working definitions of the conditions.1,9 They also published evidence-based guidelines for the diagnosis, measurement, management and prevention of IAH and ACS. These documents will be revised regularly and are intended to provide guidance to clinicians. Historically, ACS was often diagnosed when the effects of IAH had become overtly obvious. The signs included severe respiratory distress, elevated peak airway pressures, hypotension, diminished cardiac output and oliguria.2,3,6 Diagnosing IAH and ACS at this point is clearly too late, as evidenced by an increasingly poor prognosis, infectious complications and death.1–16 Because many of the effects of ACS are clinically indistinguishable from those of other common syndromes related to critical illness, it is probable that the influence of abnormal IAP is not infrequently missed in a critically ill patient with multifactorial complications. As a result, clinicians must possess a high index of suspicion and monitor IAP aggressiv


Slide 40:The ACS can also be subcategorized based on its causes. Primary or “surgical” ACS is associated with an injury or disease in the abdomino-pelvic region that requires surgical or angiographic intervention.1 This is also considered to be “classic” ACS. Patients with primary ACS typically have intraperitoneal or retroperitoneal bleeding, solid organ injury, damage control surgery (e.g., packing of liver hemorrhage) or transplantation. Primary ACS also includes bleeding pelvic fractures.1 Secondary or “medical” ACS, the focus of our review, is a fundamentally unique entity because it occurs in patients without a primary intraperitoneal injury or intervention.1 This terminology represents a significant departure from the same descriptors employed in the lexicon of peritonitis.10 Finally, tertiary ACS happens when ACS recurs despite attempts at prophylactic or therapeutic treatment of either primary or secondary IAH or ACS.1,11 Examples may include persistent ACS despite surgical decompression or an entirely new episode of ACS after the fascia has been reapproximated following temporary abdominal closure.


MANAGEMENT :MANAGEMENT


Slide 43:condition


Slide 44:Summary Secondary ACS is defined as the onset of organ failure with concurrent IAH in a patient who has not experienced an injury or intervention. This condition is directly related to visceral, abdominal wall and retroperitoneal edema and ascites induced by resuscitation. As a result, secondary ACS is typically characterized by the presence of shock requiring aggressive fluid resuscitation, and therefore includes patients with almost any form of critical illness. With an incidence approaching 30%, ACS can no longer be ignored. The measurement of IAP must occur more often than it is currently among critically ill patients. Furthermore, when overt ACS is confirmed, patients typically require immediate surgical decompression via a standard laparotomy. In conclusion, IAH and ACS are common; secondary ACS is defined as the onset of organ failure in a patient with IAH > 20 mm Hg; secondary ACS occurs in patients without abdominal trauma or intraperitoneal surgery; shock and aggressive fluid resuscitation are common among patients with secondary ACS; the most common treatment for secondary ACS is an emergent decompressive laparotomy; and monitoring IAP to identify ACS is crucial in all critically ill patients.


Slide 45:The following tables summarize the WSACS consensus definitions and recommendations statements as published in Intensive Care Medicine. Further details and the evidence-based medicine support for these guidelines may be found in the published douments. The evidentiary grading utilizes the GRADE system. Details of the GRADE approach can be found at the GRADE Working Group.


Why is it important? :Why is it important? Is underdiagnosed in intensive care settings 23% of medical intensivists unaware of bladder pressure measurement procedure by recent survey Decompression laparotomy had never been used by 19.6% or medical intensivists in the same survey Is a common cause of multisystem organ failure Because it occurs in critically ill patients, it is often misdiagnosed as progression of underlying disease Death rates are reported from 40-100% Having an IAP > 12 mmHg at any time during your ICU stay is an independent predictor of poor outcome


Slide 49:“Open Abdomen” dressing with vacuum style temporary closure


Slide 50:The importance of early, frequent IAP monitoring The evaluation and management of critically ill patients requires assessing multiple pieces of clinical, laboratory and physiologic information. Since intra-abdominal hypertension causes severe physiologic alterations as well as misleading data such as CVP and pulmonary arterial occlusion pressure, it is important for the clinician to know the patients intra-abdominal pressure to be able to assess the entire clinical scenario. In addition, unlike many conditions where supportive care is all that is possible, interventions exist to treat elevated intra-abdominal pressure. For these reasons, all patients at risk of developing IAH should have intra-abdominal pressure measured, trended and recorded. Rising intra-abdominal pressure is a clinically silent process that is not apparent until the disease is well progressed.[1, 2] Detecting intra-abdominal hypertension early requires a high index of suspicion, recognition of early symptoms and a consistently applied method to measure intra-abdominal pressure. Unfortunately, clinical exam is notoriously inaccurate.[1, 2] Kirkpatrick et al conducted a study comparing measured intra-abdominal pressures to physician clinical exam.[1] They found that clinical judgment failed to detect significant intra-abdominal hypertension over 40% of the time. Sugrue, et al found similar results.[2] Both authors conclude that clinical exam is unreliable and recommend routine intra-abdominal pressure monitoring.


Slide 51:Since clinical exam is inaccurate, early detection of increasing intra-abdominal pressure requires a reliable, reproducible method of measuring it. In addition, the method should be simple enough that the nursing staff is willing to take frequent measurements to allow early detection of rising IAP. Since recent literature notes that patients develop ACS in as little as 6 to 8 hours, it is probably reasonable to suggest initial measurements be taken at least every 1 to 2 hours until a clear trend is established (See IAP monitoring algorithm).[3] To date, the most reliable method is via pressure transduction through a catheter within the peritoneal cavity. Other less invasive options include pressure transduction through a tube placed in the stomach, bladder, or rectum.[1, 2] Of these options, Obeid et al found bladder pressure to most closely reflect intraperitoneal pressure and to be the most technically reliable.[4] Other authors confirm Obeid’s findings.[5] Bladder pressures taken through a Foley catheter correlate very closely with pressures measured directly in the abdominal cavity and are becoming the primary method of monitoring intra-abdominal pressure.


Slide 52:Methods to measure bladder pressure Manometry One of the original methods described to measure bladder pressure via the Foley catheter is the manometry technique.[9-11] The formal method of manometry requires a manometry tube that is placed inline between the Foley and the drain tube. A priming volume of fluid must be infused into the bladder to assure adequate volume to fill the Foley and the manometry tube until equilibrium is reached. It is an absolute requirement to vent this tube to ambient air pressure to avoid inaccuracies that will be introduced by an air-lock or siphon effect that can develop in the distal drain tube.[12] One must also carefully pay attention to where they hold the zero point, the angle of the manometer and avoidance of Foley kinking during the measurement.[12] Once the measurement is completed the tube is removed and the Foley-drain tube system is reconnected. Repeat measurements require breaking the system again and reassembling the vented manometry tube ­ a time consuming proposition. While this technique is accurate, there are significant disadvantages due to the need to recurrently open the system and the time requirements to obtain the pressure (leading to infrequent data acquisition). Another disadvantage is that the information is obtained in centimeters of water and must be converted to mm Hg (divide by 1.36) if one is using any of the current recommendations for intervention. Manometry as is often currently practiced (dumping the urine back into the patient, holding the tube up and observing the height of the fluid column) is fraught with error and should not be used to obtain an intra-abdominal pressure measurement.[11, 12] This method introduces two major items that can lead to error: inadequate volume of infusion to fill the manometry column and siphon effect of the distal drain tube.[12] There must be a volume of infusion not less than 30 or more ml to ensure the manometry tubing can fill up to the level of the true IAP in patients with any significant elevation of pressures ­ failure to have adequate volume may lead to a falsely low measurement of IAP.[12] Unless one pre-fills the system with saline, there may not be an adequate volume of urine in the drain tube to adequately fill the manometer. Another common source of error is the siphon effect. Lifting the drain tube causes urine to run distally as well as proximally back into the bladder. The distal fluid, if caught in a loop of the drain tube, will create a hydrodynamic siphon and “pull” the urine out of the bladder leading to a false elevation in the measured IAP.[12] Since the clinical situation in which these patients are having their IAP measured is always complex, these errors are often overlooked and will lead to misleading data. As with the traditional methods of manometry, additional errors can be introduced unless careful attention is paid to the zero point, the angle of the manometer and avoidance of Foley kinking during the measurement. For these reasons as well as the infectious complications discussed below, simply lifting the urine drain tube and eyeballing the fluid column height should not be relied upon since it may lead to significant inaccuracies. An additional concern with lifting the urinary drain tube and dumping urine back into the patient is that of urinary tract infections. Maki et al demonstrated manipulation of the drainage tube such that it rises above the level of the bladder (and dumps old urine back into the patients bladder) is the single best predictor of catheter associated urinary tract infection caused by handling the catheter (more predictive that violating the sampling port or maintaining a closed system).[13, 14] Data from 40 years ago also notes that systems designed to prevent urine reflux dramatically reduce UTI.[15] Foley catheter and drain tube manufacturers recognize these infection risks and their instructions clearly recommend against lifting the urinary drain tube and causing urine reflux. Since urinary tract infections are a major source of morbidity in the ICU, actions that contribute to an increase in this complication should clearly be avoided, especially when other accurate options for measuring IAP are available (see below). In summary, manometry is fraught with risks of erroneous data acquisition unless a formal vented manometry tube is placed in line and carefully attention to detail occurs. As currently practiced, it also raises significant concerns regarding an increased urinary tract infection rate. Given other accurate and low risk options, this method should likely remain of historical interest but not be routinely applied in a modern ICU


Slide 53:Intra-abdominal pressure monitoring in the operating theatre Intra-abdominal pressure monitoring is commonly done in the operating room during laparoscopic surgery. Typically the patient’s abdomen is inflated with gas to a predetermined pressure and maintained at that pressure during the case. Though well tolerated by most patients, this pressure elevation may cause hemodynamic compromise and tissue hypoxia.[1-4] Given our current understanding of the pathophysiology of abdominal compartment syndrome, there are other indications for intra-abdominal pressure monitoring in the operating theatre. One obvious indication is to obtain baseline IAP data on morbidly obese patients. This provides the clinician insight into the level of IAP that this patient has lived with and adapted to for a prolonged time. If the patient then becomes critically ill during the post-operative period, this baseline pressure will provide insights into when the IAP is becoming elevated.[5, 6] Another use of IAP monitoring in the operating theatre is continuous monitoring of IAP at the time of abdominal wall closure after any major laparotomy or when repairing an infants abdominal wall defect.[4, 7, 8] If the intra-abdominal pressure increases dramatically during abdominal wall closure, the surgeon might consider a staged closure to allow time for any edema to resolve. Finally, surgical procedures done in the prone position can result in elevated IAP that may lead to hemodynamic instability during the case. Intra-abdominal pressure monitoring during this situation will assist the anesthesiologist in shorting through the multiple causes of hemodynamic compromise in such cases.


IAH / ACS MEDICAL MANAGEMENT ALGORITHM :IAH / ACS MEDICAL MANAGEMENT ALGORITHM The choice (and success) of the medical management strategies listed below is strongly related to both the etiology of the patient’s IAH / ACS and the patient’s clinical situation. The appropriateness of each intervention should always be considered prior to implementing these interventions in any individual patient. The interventions should be applied in a stepwise fashion until the patient’s intra-abdominal pressure (IAP) decreases. If there is no response to a particular intervention, therapy should be escalated to the next step in the algorithm