eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Compartment Syndrome, Abdominal

Richard Paula, MD, Director of Research, Assistant Professor of Emergency Medicine, University of South Florida

Updated: Feb 23, 2009

Introduction

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 abdominal compartment syndrome. The dysfunction may be respiratory insufficiency secondary to compromised tidal volumes, decreased urine output caused by falling renal perfusion, or any organ dysfunction caused by increased abdominal compartment pressure.

Abdominal compartment syndrome 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 abdominal compartment syndrome. 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 abdominal compartment syndrome.

As the diagnosis of abdominal compartment syndrome became easier to establish, it was observed to occur as a consequence of a variety of primary clinical events. Abdominal compartment syndrome can be divided into the following 3 categories, which are explained in greater detail in Causes:

• 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.

In the emergency department and ICU, abdominal compartment syndrome is recognized with growing frequency as the cause of morbidity such as metabolic acidosis, decreased urine output, and decreased cardiac output. The cause of these events might easily be mistaken for other pathologic events such as hypovolemia if the clinician is not alerted to the morbidity associated with abdominal compartment syndrome.

Pathophysiology

Organ dysfunction with abdominal compartment syndrome is a product of the effects of IAH on multiple organ systems. Abdominal compartment syndrome 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.

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, abdominal compartment syndrome impairs not only visceral organs but also the cardiovascular and the pulmonary systems; it may also cause a decrease in cerebral perfusion pressure. Therefore, abdominal compartment syndrome should be recognized as a possible cause of decompensation in any critically injured patient.

Frequency

United States

According to recent literature, frequency in trauma ICU admissions is anywhere from 5-15% and is 1% of general trauma admissions.

International

Much of the recent literature on abdominal compartment syndrome has originated from outside the United States, where frequency and morbidity appear to be the same.

Mortality/Morbidity

The morbidity of abdominal compartment syndrome is attributed to its effects on multiple organ systems. Because of this, abdominal compartment syndrome has a high mortality rate even with treatment. Furthermore, abdominal compartment syndrome 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%.
• Malbrain et al recently demonstrated there is also a correlation with merely elevated abdominal pressures and mortality prior to the actual development of abdominal compartment syndrome.¹

Race

Nothing has been published indicating a racial or gender difference in the incidence or mortality of abdominal compartment syndrome.

Age

Abdominal compartment syndrome 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.

Clinical

History

The history varies depending upon the cause of abdominal compartment syndrome (ACS), but abdominal pain is commonly present. Abdominal pain may precede the development of abdominal compartment syndrome 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.

• 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

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 abdominal compartment syndrome.

• Distended abdomen
• Wheezes, rales, increased respiratory rate
• Cyanosis
• Wan appearance

Causes

Abdominal compartment syndrome occurs when the IAP is too high, similar to compartment syndrome in an extremity. The 3 types of abdominal compartment syndrome 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
• 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

Differential Diagnoses

Other Problems to Be Considered

The choice of fluid used to resuscitate patients with serious burns may influence whether the abdominal compartment syndrome develops. At a large Japanese burn center, Oda et al demonstrated hypertonic lactated saline could be used in smaller volumes to maintain adequate urine output and significantly reduce the rate of abdominal compartment syndrome and associated morbidity.³

Workup

Laboratory 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.

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 et al found the following in patients with abdominal compartment syndrome:⁴
  • 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.

Other Tests

• Intraluminal bladder pressure measurement, which is described by Ivatury et al in a 1997 report as follows:⁵

  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.

Procedures

• Percutaneous fluid drainage (paracentesis)
  • Multiple reports document the efficacy of paracentesis in burn patients who develop abdominal compartment syndrome. Although not prospectively validated, it appears to be a superior alternative to decompressive laparotomy in this patient population. It may be performed quickly at bedside and avoids potential complications associated with larger incisions.
  • Paracentesis is also extremely useful in patients with chronic ACS due to large volume ascites.
• Laparoscopic decompression: A group in Taiwan has used this procedure successfully in patients who have experienced blunt abdominal trauma and have an IAP of 25-35 cm H₂ O.⁶

Treatment

Prehospital Care

If abdominal compartment syndrome 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).
• Avoid overly aggressive fluid resuscitation, especially in extremity injuries. The super-resuscitated patient is much more likely to develop abdominal compartment syndrome, and often the prehospital setting is where this begins.⁷

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, abdominal compartment syndrome (ACS) is missed unless it is in the differential diagnosis. Therapy should include fluid resuscitation, transfusion if needed, and appropriate consultation.

• Measure IAP if abdominal compartment syndrome is suspected. In an excellent group of articles in 1996, Burch et al developed a grading system.⁸ Patients with higher-grade abdominal compartment syndrome 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 H₂ O
  • Grade II, 15-25 cm H₂ O
  • Grade III, 25-35 cm H₂ O
  • Grade IV, greater than 35 cm H₂ O
• End-organ damage has been observed with IAP as low as 10 cm H₂ O, and multiple studies have found damage at values ranging from 20-40 cm H₂ O. Disparity exists because abdominal compartment syndrome never occurs as an isolated event.
• In 1997, Simon et al demonstrated a significantly lowered threshold for injury from IAH in pigs after hemorrhage and fluid resuscitation.⁹ Oxygen delivery may play an important role.
• In 2000, Cheatham et al found abdominal perfusion pressure (APP) to be a much better predictor of end-organ injury than lactate, pH, urine output, or base deficit.¹⁰ 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 abdominal compartment syndrome.
• Dobutamine was shown to be superior to dopamine in restoring intestinal mucosal perfusion in a porcine model.¹¹

Consultations

• General surgeon
• Orthopedic surgeon
• Obstetrician and gynecologist (OB/GYN)
• Vascular surgeon

Medication

The goals of pharmacotherapy are to reduce intra-abdominal pressure.

Diuretics

Diuretics decrease plasma volume and edema through diuresis.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized to patient. Depending on response, administer at increments of 20-40 mg no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until satisfactory effect achieved.

Dosing

Adult

20-80 mg/d PO/IV/IM; titrate to 600 mg/d in severe edema

Pediatric

1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer >q6h
1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg

Interactions

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently

Contraindications

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

Spironolactone (Aldactone)

For management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.

Dosing

Adult

25-200 mg/d PO in 1-2 divided doses

Pediatric

1.5-3.5 mg/kg/d PO in divided doses q6-24h

Interactions

May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity

Contraindications

Documented hypersensitivity; anuria; renal failure; hyperkalemia

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal and hepatic impairment

Amiloride (Midamor)

Pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. Potassium-conserving (antikaliuretic) drug that, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.

Dosing

Adult

5-20 mg/d PO

Pediatric

Not established

Interactions

Concomitant therapy with potassium supplementation may increase serum potassium levels; if concomitant use of these agents is indicated because of demonstrated hypokalemia, use caution and monitor serum potassium frequently
Lithium generally should not be given with diuretics because may reduce renal clearance and add a high risk of lithium toxicity; concomitant administration of NSAIDs can reduce diuretic, natriuretic, and antihypertensive effects of loop, potassium-sparing, and thiazide diuretics (observe patients closely to determine if desired effect of diuretic obtained); indomethacin and potassium-sparing diuretics, including amiloride, may be associated with increased serum potassium levels; consider potential effects on potassium kinetics and renal function

Contraindications

Documented hypersensitivity; elevated serum potassium levels (>5.5 mEq/L); impaired renal function; acute or chronic renal insufficiency; evidence of diabetic nephropathy

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor electrolytes closely if evidence suggests renal function impairment, BUN >30 mg per 100 mL, or serum creatinine levels >1.5 mg per 100 mL; potassium retention associated with use of an antikaliuretic agent is accentuated in presence of renal impairment and may result in rapid development of hyperkalemia; monitor serum potassium level; mild hyperkalemia usually not associated with abnormal ECG findings

Follow-up

Further Inpatient Care

• Inpatient care in acute abdominal compartment syndrome is directed by critical care physicians and surgeons. It should focus on preventing IAH. If the patient experiences decompensation, abdominal compartment syndrome should be reexamined as a potential cause. IAH may be an ongoing process in any patient with pathology producing intra-abdominal fluid loss.
• Repeat or continuous IAP measurement is indicated.
• Patients with recurrent IAH may require drains to be placed or repeat evacuation.
• The abdomen should be clear of any heavy objects.

Further Outpatient Care

• Outpatient care is directed at the primary etiology of abdominal compartment syndrome. Chronic abdominal compartment syndrome requires lifelong medications and lifestyle changes, which may include the following.
  • Diuretics
  • Fluid restriction
  • Weight loss
  • Avoidance of alcohol

Transfer

• Consider transfer of any patient who requires services not available at the current facility. Patients with abdominal compartment syndrome are frequently admitted to the intensive care unit (ICU). Surgical services of multiple disciplines may be consulted.
• Transfer is indicated for any patient meeting local trauma center guidelines.
• Any patient with documented abdominal compartment syndrome requires an emergent surgical consultation. If a surgeon is not immediately available, the patient must be transferred.

Deterrence/Prevention

• The literature is replete with recommendations directed primarily at postsurgical care regarding prevention of abdominal compartment syndrome.
• Primary fascial closure has been prospectively demonstrated to significantly increase the incidence of abdominal compartment syndrome in postlaparotomy patients, specifically those who undergo damage-control surgery. Various types of surgical mesh are helpful to decrease the incidence of abdominal compartment syndrome.
• In a recent series, 100% of patients who developed abdominal compartment syndrome had primary fascial closure.
• Prevention is also focused on earlier treatment of IAH. Many authors now recommend managing IAH before full abdominal compartment syndrome develops. This can only be accomplished by proactive IAP measurement and monitoring.
• Recent controlled, randomized studies have highlighted the possibility of preventing abdominal compartment syndrome by avoiding pure crystalloid resuscitation in trauma and burn patients. O'Mara et al demonstrated a significant decrease in IAP in burn patients; they compared lactated Ringer infusion using the Parkland formula to a colloid combination of FFP and lactated Ringer.¹²

Complications

• The complications are 2 fold. First are the complications from abdominal compartment syndrome itself, and almost any organ system may be involved.
  • Renal failure: This is not prevented by intraureteral stents, which suggests direct compression of renal parenchyma and decreased renal perfusion as causes.
  • Respiratory distress and failure: Initial signs of abdominal compartment syndrome include elevated peak airway pressures in intubated patients with decreased tidal volumes.
  • Bowel ischemia
  • Increased intracranial pressure: Decompressive laparotomy has been shown to reduce intractable elevated ICP in patient with IAH.
  • Failing cardiac output and refractory shock: Abdominal compartment syndrome factitiously elevates central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) in patients who are hypovolemic or euvolemic.
• Secondary effects of abdominal compartment syndrome occur immediately after evacuation. Many cases of hypotension and even asystole have been observed. Theories to explain these effects include reperfusion syndrome and suddenly decreased systemic vascular resistance (SVR). Volume resuscitation immediately before decompression has been shown to significantly decrease these events.
• Preventing abdominal compartment syndrome is much more effective than treating it.

Prognosis

• When untreated, abdominal compartment syndrome is almost uniformly fatal.
• At Vanderbilt from 1984-1996, the mortality rate for patients with documented abdominal compartment syndrome was 68%. Most of the population was male (70%), and most had experienced blunt trauma (80%).

Patient Education

• For excellent patient education resources, visit eMedicine's Circulatory Problems Center; Esophagus, Stomach, and Intestine Center; and Liver, Gallbladder, and Pancreas Center. Also, see eMedicine's patient education articles Aortic Aneurysm, Abdominal Pain in Adults, Pancreatitis, Chronic Kidney Disease, Sepsis (Blood Infection), and Cirrhosis.

Miscellaneous

Medicolegal Pitfalls

• Abdominal compartment syndrome may be hidden in patients with critical injuries. Failure to consider abdominal compartment syndrome prevents diagnosis and treatment. Many disease processes can contribute to abdominal compartment syndrome. Consider IAH and document intra-abdominal pressures in any of the following patients:
  • Intubated patients who have high peak and plateau pressures and are difficult to ventilate
  • Patients who have GI bleeding of pancreatitis and are not responding to intravenous fluids (IVF), blood products, and pressors
  • Patients who have severe burns or sepsis with decreasing urine output and are not responding to IVF and pressors
  • Any patient with contradictory Swann-Ganz readings

Special Concerns

• Reperfusion syndrome
  • Sudden loss of blood pressure after abdominal decompression: No clear etiology exists; however, it may be due to a combination of factors, including the following:
    • Washout of products of anaerobic metabolism (eg, lactic acid), which may be directly tissue toxic
    • Sudden loss of SVR, similar to what occurs when military antishock trousers (MAST) are removed too quickly
  • Evidence indicates preloading patients with volume immediately before decompression, which has been shown to ameliorate the syndrome.
  • At Vanderbilt, the teams have decreased the toxicity of reperfusion syndromes by adding mannitol and sodium carbonate (NaCO₃) to the IVF bolus.

References

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2. Hobson KG, Young KM, Ciraulo A. Release of abdominal compartment syndrome improves survival in patients with burn injury. J Trauma. Dec 2002;53(6):1129-33; discussion 1133-4. [Medline].

3. Oda J, Ueyama M, Yamashita K, Inoue T, Noborio M, Ode Y. Hypertonic lactated saline resuscitation reduces the risk of abdominal compartment syndrome in severely burned patients. J Trauma. Jan 2006;60(1):64-71. [Medline].

4. Pickhardt PJ, Shimony JS, Heiken JP, et al. The abdominal compartment syndrome: CT findings. AJR Am J Roentgenol. Sep 1999;173(3):575-9. [Medline].

5. Ivatury RR, Diebel L, Porter JM, Simon RJ. Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am. Aug 1997;77(4):783-800. [Medline].

6. Chen RJ, Fang JF, Lin BC, Kao JL. Laparoscopic decompression of abdominal compartment syndrome after blunt hepatic trauma. Surg Endosc. Oct 2000;14(10):966. [Medline].

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Keywords

abdominal compartment syndrome, ACS, intra-abdominal hypertension, IAH, intra-abdominal pressure, IAP, primary ACS, primary abdominal compartment syndrome, secondary ACS, secondary abdominal compartment syndrome, chronic ACS, chronic abdominal compartment syndrome

Contributor Information and Disclosures

Author

Richard Paula, MD, Director of Research, Assistant Professor of Emergency Medicine, University of South Florida
Richard Paula, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

James Li, MD, Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Eddy Lang, MDCM, CCFP (EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

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