Abdominal compartment syndrome

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  • 1. Abdominal compartment syndrome Ranjit pandey ranjitpandey17@gmail.com Cist college,Ktm +977-9849464685
  • 2. • Background: Compartment syndrome occurs when a fixed compartment, defined by myofascial elements or bone, becomes subject to increased pressure, leading to ischemia and organ dysfunction. Well recognized to occur in the extremities, it also occurs in the abdomen, and some believe, in the intracranial cavity. The exact clinical conditions that define abdominal compartment syndrome (ACS) are controversial; however, organ dysfunction caused by intra-abdominal hypertension (IAH) is considered to be ACS. The dysfunction may be respiratory insufficiency secondary to compromised tidal volumes, decreased urine output caused by falling renal
  • 3. • ACS was recognized clinically in the 19th century when Marey and Burt observed its association with declines in respiratory function. In the early 20th century, Emerson's animal experiments demonstrated mortality associated with ACS. Initially, cardiorespiratory compromise was thought to be the cause; however, renal failure was hypothesized by Wendt and was later studied by Thorington and Schmidt. More recently, Kron and Iberti developed a simple method of accurately measuring intra-abdominal pressure, leading to a better understanding of the relationship between IAH and ACS.
  • 4. • ACS can be divided into the following 3 categories, which are explained in greater detail in Causes: • Primary or acute ACS: This occurs when intra- abdominal pathology is directly and proximally responsible for the compartment syndrome. • Secondary ACS: This occurs when no visible intra-abdominal injury is present but injuries outside the abdomen cause fluid accumulation. • Chronic ACS: This occurs in the presence of cirrhosis and ascites, often in the later stages of the disease.
  • 5. • The abdominal compartment syndrome represents the pathophysiologic consequence of a raised intra-abdominal pressure. The normal intra-abdominal pressure ranges between 0 and 5 mmHg. When it is mildly increased to between 10 and 15 mmHg, cardiac index is usually maintained or even increased because abdominal viscera are mildly squeezed and venous return increases. Respiratory and renal symptoms are unlikely to occur. Hepatosplanchnic blood flow may decrease [5]. At this point, intravascular volume optimization will probably correct these alterations. When intra-abdominal pressure is moderately increased to between 15 and 25 mmHg the full syndrome may be observed, but usually responds to aggressive fluid resuscitation, and surgical decompression should be considered. At high pressures (< 25 mmHg) surgical decompression associated with fluid resuscitation and transient use of vasoconstrictive agents is mandatory.
  • 6. • Various clinical conditions are associated with this syndrome and include massive intra-abdominal or retroperitoneal hemorrhage, severe gut edema or intestinal obstruction, and ascites under pressure.
  • 7. • Pathophysiology: Organ dysfunction with ACS is a product of the effects of IAH on multiple organ systems. ACS follows a destructive pathway similar to compartment syndrome of the extremity. Problems begin at the organ level with direct compression; hollow systems such as the intestinal tract and portal-caval system collapse under high pressure. Immediate effects such as thrombosis or bowel wall edema are followed by translocation of bacterial products leading to additional fluid accumulation, further increasing intra- abdominal pressure. At the cellular level, oxygen delivery is impaired leading to ischemia and anaerobic metabolism. Vasoactive substances such as histamine and serotonin increase endothelial permeability, further capillary leakage impairs red cell transport, and ischemia worsens.
  • 8. • Although the abdominal cavity (ie, peritoneal and, to a lesser extent, retroperitoneal cavities) are much more distensible than an extremity, they reach an endpoint at which the pressure rises dramatically. This is less apparent in chronic cases because the fascia and skin slowly stretch and thus tolerate greater fluid accumulation. As pressure rises, ACS impairs not only visceral organs, but also the cardiovascular and the pulmonary systems; it may also cause a decrease in cerebral perfusion pressure. Therefore, ACS should be recognized as a possible cause of decompensation in any critically injured patient.
  • 9. • Frequency: • In the US: According to recent literature, frequency in trauma ICU admissions is anywhere from 5-15% and is 1% of general trauma admissions. • Internationally: Much of the recent literature on ACS has originated from outside the United States, where frequency and morbidity appear to be the same. • Mortality/Morbidity: The morbidity of ACS is attributed to its effects on multiple organ systems. Because of this, ACS has a high mortality rate even with treatment. Furthermore, ACS is often a sequela to severe injuries that independently carry high morbidity and mortality rates. • In the early 1990s Eddy and Morris documented an ACS mortality rate of 68%, this has been reflected in the subsequent literature, with similar mortality rates of 25-75%. • Race: Nothing has been published indicating a racial or gender difference in the incidence or mortality of abdominal compartment syndrome. • Age: ACS has been documented in all age groups. The intra-abdominal pressure (IAP) that leads to morbidity (>25 mm Hg) appears to be similar in the pediatric population
  • 10. • First, the increased intra-abdominal pressure is transmitted to the pleural space so that lung compliance decreases. Hypoventilation and alteration of ventilation/perfusion distribution lead to hypoxemia and hypercapnia. When mechanical ventilation is applied, very high inspiratory pressures are often required to deliver tidal volume. Second, the combined increase in abdominal pressure and pleural pressure leads to a decrease in venous return, direct compression of the heart, and increased afterload (especially in the right ventricle). Third, perfusion to the intra-abdominal organs can be critically reduced by the combined effects of the decreased cardiac output, increased interstitial pressure, and increased outflow pressure. This can lead to oliguria and renal failure. Splanchnic ischemia can also occur as reflected by a decreased mucosal pH [1,2], decreased liver metabolism [3], and bacterial translocation [4]. In addition, perfusion of the abdominal wall may be decreased, so that wound healing may be impaired. Finally, intracranial pressure may also be increased due to the decrease in cerebral venous return and
  • 11. • History: The history varies depending upon the cause of ACS, but abdominal pain is commonly present. Abdominal pain may precede the development of ACS and be directly related to a precipitating event, such as blunt abdominal trauma or pancreatitis. • Syncope or weakness may be a sign of hypovolemia. Although abdominal pain and distension are commonly present, patients may not experience abdominal pain; difficulty breathing or decreased urine output may be the first signs of IAH. • Furthermore, patients who develop abdominal compartment syndrome may be unable to communicate because they are often intubated and critically ill.
  • 12. • Increase in abdominal girth • Difficulty breathing • Decreased urine output • Syncope • Melena • Nonsteroidal anti-inflammatory drug (NSAID) use • Alcohol abuse • Nausea and vomiting • History of pancreatitis
  • 13. • Physical: Compartment syndrome in the abdomen is usually suggested by an increased abdominal girth. If this change is acute, the abdomen is tense and tender. Although this may be difficult to recognize in patients with morbid obesity, other patients often have an abdomen clearly out of proportion to their body habitus. This may be easier to visualize with the patient standing or sitting upright. Look for the secondary effects of ACS.
  • 14. • Distended abdomen • Wheezes, rales, increased respiratory rate • Cyanosis • Wan appearance
  • 15. • Causes: ACS occurs when the IAP is too high, similar to compartment syndrome in an extremity. The 3 types of ACS have different and sometimes overlapping causes. • 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
  • 16. • 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 a significantly increased risk when more than 3 L are infused. – Large areas of full-thickness burns: In 2002, Hobson demonstrated ACS within 24 hours in burn patients who had received an average of 237 mL/kg over a 12-hour period. – Penetrating or blunt trauma without identifiable injury – Postoperative – Packing and primary fascial closure, which increases incidence – Sepsis
  • 17. • Chronic – Peritoneal dialysis – Morbid obesity – Cirrhosis – Meigs syndrome
  • 18. • DIFFERENTIALS Section 4 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography • Abdominal Pain in Elderly Persons Abdominal Trauma, Blunt Abdominal Trauma, Penetrating Abortion, Complications Acute Coronary Syndrome Acute Respiratory Distress Syndrome Adrenal Insufficiency and Adrenal Crisis Alcohol and Substance Abuse Evaluation Alcoholic Ketoacidosis Anaphylaxis Anemia, Acute Angioedema Appendicitis, Acute Bulimia Cholangitis Cholelithiasis Congestive Heart Failure and Pulmonary Edema Constipation Cushing Syndrome Delirium Tremens Diabetic Ketoacidosis Diaphragmatic Injuries Dissection, Aortic Diverticular Disease
  • 19. • Pediatrics, Appendicitis Pediatrics, Bacteremia and Sepsis Pediatrics, Child Sexual Abuse Pediatrics, Foreign Body Ingestion Pediatrics, Gastrointestinal Bleeding Pelvic Inflammatory Disease Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum Pneumothorax, Tension and Traumatic Pregnancy, Delivery Pulmonary Embolism Respiratory Distress Syndrome, Adult Sexual Assault Shock, Cardiogenic Shock, Hemorrhagic Shock, Hypovolemic Shock, Septic Spinal Cord Injuries Spontaneous Bacterial Peritonitis Superior Vena Cava Syndrome Thrombocytopenic Purpura Trauma, Lower Genitourinary Trauma, Upper Genitourinary
  • 20. • Electrical Injuries Esophageal Perforation, Rupture and Tears Foreign Bodies, Gastrointestinal Foreign Bodies, Rectum Gas Gangrene Gastroenteritis Hantavirus Cardiopulmonary Syndrome Hernias Hyperosmolar Hyperglycemic Nonketotic Coma Hypothyroidism and Myxedema Coma Inflammatory Bowel Disease Leishmaniasis Malaria Mesenteric Ischemia Mononucleosis Myocardial Infarction Necrotizing Fasciitis Pancreatitis
  • 21. • Lab Studies: • Comprehensive metabolic panel (CMP) • Complete blood cell count (CBC) • Amylase and lipase assessment • Prothrombin time (PT), activated partial thromboplastin time (aPTT) if the patient is heparinized • Test for cardiac markers • Urinalysis and urine drug screen • Measurement of serum lactate levels: At many institutions, the sample must be kept on ice. • Arterial blood gas (ABG): This is a quick way to measure the pH, lactate, and base deficit.
  • 22. • Imaging Studies: • Examine the abdominal series for evidence of free air or bowel obstruction. – Realize plain abdominal radiographic studies are often useless in identifying abdominal compartment syndrome. • Abdominal CT scanning can reveal many subtle findings. In 1999, Pickhardt found the following in patients with ACS: – Round-belly sign - Abdominal distention with an increased ratio of anteroposterior-to-transverse abdominal diameter (ratio >0.80; P <0.001) – Collapse of the vena cava – Bowel wall thickening with enhancement – Bilateral inguinal herniation • Abdominal ultrasonography – An aortic aneurysm, particularly when large, may be detected. – Bowel gas or obesity makes performing the study difficult.
  • 23. • Other Tests: • Intraluminal bladder pressure measurement, which is described by Ivatury in a 1997 report as follows: • Measurement of intraluminal bladder pressure consists of instilling about 50 mL of saline into the urinary bladder through the Foley catheter. The tubing of the collecting bag is clamped, and a needle is inserted into the specimen-collecting port of the tubing proximal to the clamp and is attached to a manometer. Bladder pressure measured in mm Hg is the height at which the level of the saline column stabilizes with the symphysis pubis as the zero point.
  • 24. • The diagnosis of this syndrome is difficult because it usually occurs in critically ill patients with other causes of circulatory or respiratory failure. One should always consider the abdominal compartment syndrome when confronted with acute circulatory failure with wide systolic-diastolic pressure variation and elevated filling pressures. After exclusion of cardiac tamponade and increased pleural pressure (tension pneumothorax, status asthmaticus, etc), the intra-abdominal pressure should be measured.
  • 25. • Current methodology for intra-abdominal pressure assessment relies on the measurement of bladder pressure. Alternative methods include indirect estimations of inferior vena cava pressure, rectal and gastric pressure measurements, and direct measurement of the intra-abdominal pressure by direct puncture. In experimental conditions, bladder pressure is closely related to abdominal pressure [8]. Indeed, Yol et al [9] found good agreement between bladder pressure and intra-abdominal pressure.
  • 26. • In this issue, Johna et al [10] challenged the value of bladder pressure measurements. During laparoscopic cholecystectomy, the authors simultaneously measured intra-abdominal pressure by direct puncture and bladder pressure. The two pressures were clearly not identical, because bladder pressure systematically overestimated the true abdominal pressure; this could lead to an over-diagnosis of intra-abdominal compartment syndrome. Although these data were obtained using a rigorous methodology (and the authors rightly point out that the amount of fluid used to prime the Foley catheter should be limited to 50 ml in order to avoid bladder distension), one should be aware of some limitations. First, although ethical considerations precluded the application of intra-abdominal pressures higher than 15 mmHg, it is, however, dangerous to extrapolate these results to higher pressure levels, at which clinical manifestations of the intra- abdominal compartment syndrome are much more serious. Second, bladder pressure may be higher than the abdominal pressure in some conditions.
  • 27. • When patients are lying in a flat position, the bladder pressure will represent the sum of the exogenously applied pressure (gas pressure) and the pressure exerted by the viscera (which can be roughly estimated as the height of these viscera), whereas the directly measured intra-abdominal pressure only takes into account the pressure of the insufflated gas. Third, bladder pressure increments reflected increments in intra-abdominal pressure on an individual basis, which could advocate the use of very early bladder pressure monitoring in patients at risk of developing an intra- abdominal compartment syndrome. Finally, most clinical studies have used bladder pressure measurements [2,11], so that clinical manifestations have been classified according to bladder pressure levels rather than to directly measured intra-abdominal pressure levels. The study by Johna et al [10] highlights that bladder pressure measurements require cautious interpretation, but we still think that they remain an easy, safe, and valuable tool for diagnosing the abdominal compartment syndrome in critically ill patients.
  • 28. • Prehospital Care: If ACS is suspected, the focus of prehospital care is to immediately transport the patient to the emergency department. • Remove any constricting garments. • Do not place anything on the patient's abdomen (eg, life packs, bundles of blankets, oxygen tanks).
  • 29. • Emergency Department Care: The first priority of the emergency medicine physician is to determine the diagnosis. In any patient with the aforementioned mechanisms of injury or pathology, ACS is missed unless it is in the differential diagnosis. Therapy should include fluid resuscitation, transfusion if needed, and appropriate consultation.
  • 30. • Measure IAP if ACS is suspected. In an excellent group of articles in 1996, Burch et al developed a grading system. Patients with higher-grade ACS are shown to have end-organ damage, which is evidenced by splenic hypercarbia and elevated lactate levels, even if they appear clinically stable. The following grading system has become accepted if IAH is present: – Grade I, 10-15 cm H2O – Grade II, 15-25 cm H2O – Grade III, 25-35 cm H2O – Grade IV, greater than 35 cm H2O
  • 31. • End-organ damage has been observed with IAP as low as 10 cm H2O, and multiple studies have found damage at values ranging from 20-40 cm H2O. Disparity exists because ACS never occurs as an isolated event. • In 1997, Simon demonstrated a significantly lowered threshold for injury from IAH in pigs after hemorrhage and fluid resuscitation. Oxygen delivery may play an important role. • In 2000, Cheatham found abdominal perfusion pressure (APP) to be a much better predictor of end-organ injury than lactate, pH, urine output, or base deficit. The APP is equal to the mean arterial pressure minus the IAP. • Pharmacologic therapy is less effective than mechanical drainage. Pressors have a role but may not be equally effective in treating ACS. • Dobutamine was shown to be superior to dopamine in restoring intestinal mucosal perfusion in a porcine mo
  • 32. • Consultations: • General surgeon • Orthopedic surgeon • Obstetrician and gynecologist (OB/GYN) • Vascular surgeon