|
 
 |
| PRACTICE CHANGING CONTINUING EDUCATION: SURGICAL PRACTICE |
|
| Year : 2014 | Volume
: 1
| Issue : 1 | Page : 28-32 |
|
Abdominal compartment syndrome
Vijayshil Gautam1, Mayur Narayan2
1 All India Institute of Medical Sciences, Patna, Bihar, India
2 R Adams Cowley Shock Trauma Center, Baltimore, Maryland, USA
| Date of Web Publication | 3-May-2014 |
Correspondence Address:
Dr. Vijayshil Gautam
POB 200, Potters Bar, EN6 1XJ, Herts, UK
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2349-0977.131859
Despite being a recognized clinical entity for past more than 100 years, Abdominal Compartment Syndrome (ACS) continues to be an ill understood and under diagnosed condition in surgical practice. It has a high prevalence of upto 50 percent in general surgical or trauma patients receiving intensive care and is associated with twice the death rate. Concurrent medical conditions such as diabetes, ascites, heart failure and a host of others increase the vulnerability both in terms of development of ACS and a poorer outcome. It is also a major cause of death in trauma. Since ACS often clinically mimics the underlying condition, such as abdominal injury or peritonitis/ ascites from any cause, its presentation is confusing. Diagnosis is based on clinical awareness of its potential risk, simple bedside intra-abdominal pressure (IAP) measurement, repeated examination of the abdomen and a 24 × 7 vigil on vital signs. Biochemical markers are non-specific and unreliable. Treatment is very urgent and may involve achieving permissive hypotension, careful management of fluid balance, high quality intensive medical and nursing care, prevention/treatment of sepsis, abdominal drainage and if indicated, decompression surgery by laparotomy, leaving the abdomen open and protected with sterile dressings or a temporary abdominal negative pressure therapy device. Prompt, good and urgent care reduces the risk of adverse outcome. Keywords: Acute abdominal syndrome, ACS, IAH, IAP, APP, critical care, trauma, general surgery, ICU, emergency, post operative complication, intra abdominal hypertension, compartment syndrome, negligence
How to cite this article:
Gautam V, Narayan M. Abdominal compartment syndrome. Astrocyte 2014;1:28-32 |
| Introduction | |  |
Abdominal compartment syndrome (ACS) is met with more commonly in surgical practice than what most clinicians, including surgeons, traumatologists, and intensivists suspect. Unless recognized quickly and treated correctly, it represents a life-threatening complication. A thorough understanding of its etiological factors, pathophysiology, clinical features and principles of management is critical from clinical perspective. The current consensus guidelines [1],[2] and their integration in surgical practice protocols is mandatory for accomplishing improved outcomes in general surgery and trauma patients.
ACS is defined as sustained intra-abdominal hypertension (IAH) ≥20mmHg associated with new-onset organ dysfunction or failure induced by raised intra-abdominal pressure (IAP). Clinically these may be difficult to ascertain, especially in a patient with co-morbidities. Some variations about precise definitions also exist in the literature but persistently high or rising IAP above the patient's baseline, with adverse systemic effects herald impending IAH and ACS. These require urgent and correct treatment.
Sustained, elevated intra-abdominal hypertension (IAH) may develop from many causes including aggressive resuscitation, fluid overload, trauma, and sepsis. These are encountered in the following clinical settings: surgical patients on intensive care units (ICU), postoperative period of abdominal surgery, and on trauma wards. Affected patients may rapidly develop cardiovascular collapse and death from new onset respiratory or renal dysfunction and bowel ischemia.
Early determination of at-risk patients, implementation of damage control principles, and careful use of IV fluids with 4 to 6 hourly monitoring of bladder pressure in the ICU may prevent worsening of IAH into ACS.
Once diagnosed, several management techniques are available, including pain control, sedation, positioning, forced diuresis, intra-abdominal percutaneous catheter placement, continuous renal therapy, and decompressive laparotomy.
| Etiology | | |
The underlying etiological principle is the same as compartment syndrome, which is familiar to all clinicians with the knowledge of complications after head injury [3] or circumferential full thickness burn of a limb. The concept of diminishing perfusion pressure applies to the abdomen in the presence of IAH. In critically ill patients it may be easily missed with rapid progression and fatal outcome.
The normal abdominal perfusion pressure (APP) is represented by the formula APP=MAP-IAP, where MAP is mean arterial pressure and IAP is intra abdominal pressure. Patients with morbid obesity, ascites, cirrhosis and many other causes of increased abdominal girth or abdominal wall rigidity, including pregnancy have raised baseline intra-abdominal pressure (IAP), which in healthy individuals is expected to remain below 10 mm of Hg. When the IAP is elevated or rising in an acutely or chronically sustained manner above 20 mm of Hg then the abdominal perfusion pressure may be severely compromised due to the intra-abdominal hypertension (IAH). Abdominal compartment syndrome (ACS) ensues. Additional adverse systemic effects arise. Regression analysis has shown that the correction of APP is a better endpoint for predicting outcome for the patient undergoing resuscitation therapy on the general surgical or trauma wards, than merely the correction of arterial pH, arterial lactate or urinary output.
| Case Report | | |
Mr JSR, a 42-year-old, obese man is brought to the Trauma Centre and Emergency Department of a busy tertiary care hospital with continuous increasing abdominal pain and fluctuating levels of consciousness for the past 3 days. His personal history includes smoking 10 cigarettes a day, and consumption of 15 units of alcohol a week. He is known to have type 2 diabetes and angina, and is noncompliant with medication. His father died of myocardial infarction at the age of 51 years. On arrival, his blood pressure is 90/60 mm of Hg, pulse 120/min, respiratory rate 28/min, and O 2 saturation 89 per cent. He is pale and has poor capillary return. His Glasgow Coma Scale score is fluctuating between 12 and 14. He appears to be restless, uncooperative, and confused. He was reportedly attacked by his neighbour, but no details are available. The patient is unable to provide a detailed history. His abdominal examination is generally unremarkable except for a diffuse nonspecific tenderness and mild distension. Bowel sounds are faint. He has bilateral lower leg oedema, with signs of injury to head and face.
The admitting resident doctor has taken Mr JSR's blood for routine hematology and biochemistry tests. He is posted for a portable X-ray of the abdomen and abdominal ultrasound examination. He is judged too ill to undergo computed tomography (CT) of the abdomen.
He has been started with intravenous infusion of normal saline. No residual urine has been collected via the indwelling urethral catheter applied 30 min ago.
Consider this case history. As a clinician called to see this patient, what diagnostic and therapeutic possibilities would you consider? How would you prognosticate this patient? Would you like to wait for the laboratory test results? Would you consider a 24 × 7 measurement of IAP? What other immediate steps would you like to institute? What would be the roadmap of clinical management?
| Risk Factors | | |
There are several risk factors that predispose a patient to ACS. Broadly, these include diminution of abdominal wall compliance, as in the case of abdominal wall surgery, major trauma or burns, or ventilated patients in the prone position. Factors that increase intraluminal contents in the GI tract, such as gastric distention due to gastro-paresis or ileus, colonic pseudo-obstruction or volvulus also increase the vulnerability. It is important to note that ACS can be the cause as well as the result of intra-abdominal pathology. Increase in the intra-abdominal contents as a result of hepatic dysfunction or cirrhosis with resultant ascites, pancreatitis, or intra-abdominal tumors can contribute to the development of ACS. Another risk factor for ACS is aggressive or large volume fluid resuscitation as part of trauma care or emergency general surgery. Intra venous infusion of 10 L or more resuscitative volume increases the risk for ACS. Other factors such as age, coagulopathy, mechanical ventilation, obesity, peritonitis, and sepsis may all contribute to the development of ACS.
Intra-abdominal pressure (IAP) is the steady-state pressure contained within the abdominal cavity. It is usually in the range of 5-7 mmHg in critically ill adult patients. When trend is for IAP to be elevated above 10-12 mmHg, Grade 1, IAH may be diagnosed [Table 1].
| Measurement | | |
The IAP is best approximated and measured by the bladder pressure noted after instilling the bladder with 25 mL of sterile saline. Measurement should be taken at end-expiration in the supine position. It is important to zero the pressure transducer at the level of the mid-axillary line. Attempts should be made to prevent abdominal muscle contractions that may falsely elevate recordings. The principles and connections for a mechanical system of measurement are similar to those used for monitoring of the central venous pressure. [4],[5],[6] Electronic and intra abdominal devices also exist. The connections are applied to the indwelling Foley's catheter in the bladder and observations are taken every 4 to 6 hours.
| Types | | |
When ACS presents as a result of trauma or disease involving the abdomen-pelvic region, it is known as primary (surgical) ACS. Secondary (medical) ACS does not directly involve the abdomen-pelvic region and occurs, for example, as a result of overaggressive resuscitation especially in patients with co-morbidities. Recurrent ACS is defined as the redevelopment of ACS after initial management, either medical or surgical.
| End Organ and Systemic Effects of Abdominal Compartment Syndrome: Clinical Correlation | | |
Signs and symptoms of ACS can often be subtle and easy to miss. These can be confused both with the causes and effects of ACS. Multiple organ systems may be affected collectively or in isolation, making the diagnosis subtle, yet important.
Increased IAH/ACS can lead to compression of the inferior vena cava, causing decreased venous return and resultant low cardiac output. Pressure transmitted upward can lead to impaired pulmonary function.IAH/ACS can also lead to reduction of renal and mesenteric blood flow causing decreased urine output, acute kidney injury, and intestinal ischemia. The effects of IAH on peritoneal structures have been studied in both human and animal models. For example, in swine, raising IAP to 10 mmHg led to reduced perfusion of the hepatic artery and microvasculature. Increasing IAP to 20 mmHg markedly decreased blood flow through the mesenteric arteries.
The "two-hit" hypothesis of the development of multiple organ dysfunction syndrome and intestinal ischemia has been described. The precipitating trauma or illness (first hit), leads to a mild systemic inflammatory response syndrome and is considered part of the normal physiological reaction to stress. A secondary injury (second hit) tips the body into an exaggerated systemic inflammatory response potentially progressing to multiple organ dysfunction syndrome.
Neurologic Effects
ACS has been implicated in the elevation of intracranial pressure in patients with multiple traumas that includes a brain injury. Increases in intra-thoracic pressure cause obstruction in cerebral venous outflow, leading to vascular congestion. In addition, the ACS-induced decrease in cardiac output may combine with increased intracranial pressure to significantly decrease cerebral perfusion pressure. These events are poorly tolerated in patients who already have impaired cerebral autoregulation. [3]
Cardiovascular Effects
The cardiovascular system is affected as a result of elevated IAP compression of the inferior vena cava, leading to decreased venous return to the heart.IAH can also cause increases in systemic vascular resistance leading to impaired left ventricular function. With decreased cardiac output, the body's attempt to compensate further worsens the cycle and predisposes the patient to ischemia.
Respiratory and Ventilator Effects
Elevated IAP of the abdomen can impede diaphragmatic movement, reduce functional residual capacity, and worsen the increasing oxygen debt. Intubated patients may require increased positive pressure or encounter difficult ventilation as the IAP gets transmitted upward preventing adequate diaphragm excursion. Poor filling pressures can lead to hypoventilation and significant de-recruitment of the lung alveoli, which causes further worsening of the respiratory function. Increases in peak airway pressures during volume ventilation and decreases in tidal volumes in pressure modes on the ventilator settings can be clues to the presence of ACS.
Intestinal Ischemia
One of the most feared complications of ACS is intestinal ischemia. [7] Increased abdominal pressure leads to compromise of small and large bowel blood supply, with reduction in mesenteric circulation. If not corrected, this can lead to bowel necrosis, lactic acidosis, overwhelming sepsis, and death. Patients may initially present with abdominal distention, pain, and hyperlactemia. Progressing acidosis in the setting of IAH should raise concern about progression to ACS and intestinal ischemia. Urgent decompression of the abdomen should be considered in such cases.
Renal Dysfunction
Elevated IAP can also get transmitted to the renal arteries leading to decreased perfusion of the kidneys. This can lead to decreased urine output or oliguria and onset of acute renal injury even in the setting of a normal blood pressure. Elevation of basic metabolic biochemistry tests such as blood urea nitrogen and creatinine may occur only at a later time causing delay in treatment. The clinician should therefore pay particular attention to the volume of urine produced per hour and initiate therapy as warranted. With rapid deterioration of kidney function, the patient may require temporary continuous veno-venous hemofiltration till ACS is controlled. A low threshold must be applied to starting hemofiltration if indicated.
| Clinical Findings | | |
These have low specificity and sensitivity. [8] It is preferable for the same team of clinicians to frequently examine the patient so any change can be assessed and noted reliably. Signs of ACS on physical examination can range from subtle to glaringly obvious. It is important to know that a thorough, repeated and routine physical examination of the patient can potentially pick up elevated IAH before it develops into ACS and causes organ dysfunction. Gross abdominal distention can occur, with or without the presence of a temporary abdominal closure device. Many of critically ill patients will be intubated in the ITU. The clinical findings may therefore be subtle and confusing, especially during the observation stage of trauma victim and in the early postoperative course after abdominal surgery.
| Differential Diagnosis | | |
Erythema of the distended abdomen in the setting of fever may be an important marker of necrotizing soft tissue infection, which itself is a life threatening condition and should always be considered in the early differential diagnosis. A common mistake in the management of the post-operative patient or open abdomen after stabbing injury is the failure to recognize recurrent ACS. Often, it is difficult to tell the difference between cause and effect-a circular pathophysiology seems to develop between the underlying abdominal condition leading to circulatory and inflammatory response, which makes the situation worse in a vicious spiral. Clinicians should not be misled by the presence of a temporary abdominal closure device (e.g. abdominal negative pressure therapy device -- itself designed and used to lower the intra-abdominal pressure). Elevated IAH/ACS can still occur in this setting. The device may result in elevated IAP leading further to organ dysfunction. Early recognition and rapid adjustment of this device should be performed in sterile condition. Presence of distended abdomen is neither necessary nor diagnostic of ACS.
| Management | | |
Routine bladder pressure measurement (4 to 6 hourly) in abdominal trauma or emergency general surgery patient in the ICU has been suggested. Subsequent measurements can be compared with the baseline measurements in order to recognize developing IAH before the development of ACS. The indirect technique involves applying either a mechanical or electronic pressure measuring manometer or transducer to the indwelling urinary Foley's catheter. [9]
Once IAH or ACS has been identified, the clinical team should consider one or several of the following management options. The first management principle of ACS is to prevent its occurrence. Careful use of fluids, attention to fluid balance and application of the principles of permissive hypotension may aid in the prevention of IAH and ACS. Damage control interventions such as intra-abdominal drainage and surgical techniques such as decompressive laparotomy should be considered by suitably senior and experienced surgeons. Permissive hypotension should be implemented when possible in the trauma or emergency surgery patient. Damage control is a term adopted from the merchant navy that describes the essential steps to get a damaged vessel to shore without having to perform definitive repairs while at sea. All efforts are made to prevent sinking of the ship. Implementation of damage control in trauma or emergency surgery is warranted if the patient appears to be getting worse due to IAH or ACS. Patients, who are in post resuscitation stage of their care, should be considered for early diuresis to help alleviate the problem of overload. In patients who have IAH and with concern for progression to ACS, percutaneous drainage (such as for ascites) may be utilized in order to avoid full surgical decompression. Decompression leaves the patient's abdomen open and carries the potential hazard of complications such as enterocutaneous fistula. The treating clinician must use his clinical judgment in deciding upon the most suited treatment strategy. [10] For patients who have ACS with end-organ dysfunction, surgical decompression by laparotomy and delayed closure remains a difficult but treatment of choice.
| Conclusions | | |
ACS is an important cause of acute general surgical and post-traumatic morbidity and mortality. [11] It is more common than many clinicians expect but relatively easy to diagnose if there is awareness. Early and correct treatment is essential to improve prognosis. ACS is a condition in which the convergent role of surgeons, surgical intensivists, and traumatologists is essential.
The evidence base for ACS is well established in the literature starting with the early works of Coombs in 1922. After 80 years, [12] in 2006, [1] a conference of experts provided the foundation for the current thinking about ACS. These were updated in 2013. [2] This topic is considered core competency for several clinical specialties including general surgery, traumatology and intensive care.
In the example of the patient given in the introduction, a high degree of clinical suspicion arising from the poor urinary output and rapid measurement of IAP, using bedside techniques to measure the bladder pressure will confirm the presence of ACS. Clinical examination and imaging including CT and ultra-sound scan [13] is unreliable. Correct and prompt treatment with carefully controlled use of fluid therapy, diuresis, ventilation and application of decompression surgery is the key to patient's survival. Renal function and lactate levels may be abnormal but may be delayed and non-specific. Treatment options have been discussed under management principles above. Patient and relatives must be made aware of poor prognosis and possible complications.
| References | | |
| 1. | Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006;32:1722-32.  |
| 2. | Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML, De Keulenaer B, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: Updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013;39:1190-206. |
| 3. | Bloomfield GL, Dalton JM, Sugerman HJ, Ridings PC, DeMaria EJ, Bullock R. Treatment of increasing intracranial pressure secondary to the acute abdominal compartment syndrome in a patient with combined abdominal and head trauma. J Trauma 1995;39:1168-70. |
| 4. | Lee RK, Critical Care Nurse, 2012;32[1]:19-32, Intra Abdominal Hypertension and Abdominal Compartment Syndrome: A comprehensive overview. |
| 5. | Gestring Mark, Abdominal compartment syndrome, In:UpToDate, Waltham, MA (Accessed March 2014) |
| 6. | Vallee F, Dupas C, Feuvrier V, Mebazaa A, Ferre F, Mari A, Genestal M, Fourcade O, Ann Surg. 2010 Jan;251(1):127-32. doi: 10.1097/SLA.0b013e3181b5919b. Intra-abdominal pressure measurement method via the urinary-tube: bedside validation of a biomechanical model integrating urine column height and bladder urinary volume. |
| 7. | Ivatury RR, Porter JM, Simon RJ, Islam S, John R, Stahl WM. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: Prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J Trauma 1998;44:1016-21. |
| 8. | Sugrue M, Bauman A, Jones F, Bishop G, Flabouris A, Parr M, et al. Clinical examination is an inaccurate predictor of intraabdominal pressure. World J Surg 2002;26:1428-31. |
| 9. | Malbrain ML. Different techniques to measure intra-abdominal pressure (IAP): Time for a critical re-appraisal. Intensive Care Med 2004;30:357-71. [ PUBMED] |
| 10. | Cheatham ML. Nonoperative management of intraabdominal hypertension and abdominal compartment syndrome. World J Surg 2009;33:1116-22. [ PUBMED] |
| 11. | Balogh ZJ, Martin A, van Wessem KP, King KL, Mackay P, Havill K. Mission to eliminate postinjury abdominal compartment syndrome. Arch Surg 2011;146:938-43. |
| 12. | Coombs HC. The mechanism of the regulation of intra-abdominal pressure. Am J Physiol 1922;61:159. |
| 13. | Pickhardt PJ, Shimony JS, Heiken JP, Buchman TG, Fisher AJ. The abdominal compartment syndrome: CT findings. AJR Am J Roentgenol 1999;173:575-9. |
[Table 1]
|
Search Pubmed for