Compartment Syndrome, Abdominal

Article Last Updated: Jun 28, 2006

AUTHOR AND EDITOR INFORMATION

Section 1 of 10

Authors and Editors Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous References

Author: Richard Paula, MD, Director of Research, Emergency Medicine Residency Program, Tampa General Hospital, University of South Florida at Tampa Richard Paula is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians Editors: James Li, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; 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; 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; Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, YaleNew Haven Hospital Author and Editor Disclosure Synonyms and related keywords: abdominal compartment syndrome, ACS, intraabdominal hypertension, IAH, intra-abdominal pressure, IAP, primary ACS, primary abdominal compartment syndrome, secondary ACS, secondary abdominal compartment syndrome, chronic ACS, chronic abdominal compartment syndrome

INTRODUCTION
Section 2 of 10

Authors and Editors Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous References

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 perfusion, or any organ dysfunction caused by increased abdominal compartment pressure. 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.

As the diagnosis of ACS became easier to establish, it was observed to occur as a consequence of a variety of primary clinical events. 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.

In the emergency department and ICU, ACS 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 ACS.

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. 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.

Frequency
United States According to recent literature, frequency in trauma ICU admissions is anywhere from 515% and is 1% of general trauma admissions.

International 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.

CLINICAL
Section 3 of 10

Authors and Editors Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous References

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.

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 ACS.

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

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)

o o

Penetrating trauma Intraperitoneal hemorrhage

Pancreatitis External compressing forces, such as debris from a motor vehicle collision or after a large structure explosion o Pelvic fracture o Rupture of abdominal aortic aneurysm o Perforated peptic ulcer Secondary: Secondary ACS may occur in patients without an intra-abdominal injury, when fluid accumulates in volumes sufficient to cause IAH.
o o

Large-volume resuscitation: The literature shows a significantly increased risk when more than 3 L are infused. o 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. o Penetrating or blunt trauma without identifiable injury o Postoperative o Packing and primary fascial closure, which increases incidence o Sepsis Chronic
o o o o

Peritoneal dialysis Morbid obesity Cirrhosis Meigs syndrome

DIFFERENTIALS
Section 4 of 10

Authors and Editors Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous References

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 Elder Abuse 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 Pediatrics, Anaphylaxis 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 Urinary Obstruction

WORKUP
Section 5 of 10

Authors and Editors Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous References

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.

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) o Collapse of the vena cava o Bowel wall thickening with enhancement o Bilateral inguinal herniation Abdominal ultrasonography
o o o o

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 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.

Procedures

Percutaneous fluid drainage (paracentesis)

o

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 H2O.
o

TREATMENT
Section 6 of 10

Authors and Editors Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous References

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).

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.

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 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 model.
o o o o

Consultations

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

MEDICATION
Section 7 of 10

Authors and Editors Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous References

The goals of pharmacotherapy are to reduce intra-abdominal pressure. Drug Category: Diuretics Diuretics decrease plasma volume and edema through diuresis. Drug Name 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. 20-80 mg/d PO/IV/IM; titrate to 600 mg/d in severe edema 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 Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

Description

Adult Dose

Pediatric Dose

Contraindications

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 C - Safety for use during pregnancy has not been established. 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. 25-200 mg/d PO in 1-2 divided doses 1.5-3.5 mg/kg/d PO in divided doses q6-24h Documented hypersensitivity; anuria; renal failure; hyperkalemia May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity D - Unsafe in pregnancy 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.

Pregnancy

Precautions

Drug Name

Description

Adult Dose Pediatric Dose Contraindications Interactions Pregnancy Precautions Drug Name

Description

Adult Dose Pediatric Dose

5-20 mg/d PO Not established

Documented hypersensitivity; elevated serum potassium levels (>5.5 mEq/L); impaired Contraindications renal function; acute or chronic renal insufficiency; evidence of diabetic nephropathy 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, potassiumsparing, 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 B - Usually safe but benefits must outweigh the risks. 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

Interactions

Pregnancy

Precautions

FOLLOW-UP

Section 8 of 10

Authors and Editors Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous References

Further Inpatient Care

Inpatient care in acute ACS is directed by critical care physicians and surgeons. It should focus on preventing IAH. If the patient experiences decompensation, ACS 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 ACS. Chronic ACS requires lifelong medications and lifestyle changes, which may include the following.
o o o o

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 ACS 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 ACS 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 ACS. Primary fascial closure has been prospectively demonstrated to significantly increase the incidence of ACS in postlaparotomy patients, specifically those who undergo damage-control surgery. Various types of surgical mesh are helpful to decrease the incidence of ACS. In a recent series, 100% of patients who developed ACS had primary fascial closure. Prevention is also focused on earlier treatment of IAH. Many authors now recommend managing IAH before full ACS develops. This can only be accomplished by proactive IAP measurement and monitoring. Recent controlled, randomized studies have highlighted the possibility of preventing ACS 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.

Complications

The complications are 2 fold. First are the complications from ACS 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. o Respiratory distress and failure: Initial signs of ACS include elevated peak airway pressures in intubated patients with decreased tidal volumes. o Bowel ischemia o Increased intracranial pressure: Decompressive laparotomy has been shown to reduce intractable elevated ICP in patient with IAH. o Failing cardiac output and refractory shock: ACS factitiously elevates central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) in patients who are hypovolemic or euvolemic. Secondary effects of ACS 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 ACS is much more effective than treating it.
o

Prognosis

When untreated, ACS is almost uniformly fatal. At Vanderbilt from 1984-1996, the mortality rate for patients with documented ACS 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
Section 9 of 10

Authors and Editors Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous References

Medical/Legal Pitfalls

ACS may be hidden in patients with critical injuries. Failure to consider ACS prevents diagnosis and treatment. Many disease processes can contribute to ACS. Consider IAH and document intra-abdominal pressures in any of the following patients:
o o o o

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
o

o o

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.

http://www.emedicine.com/emerg/topic935.htm http://ajcc.aacnjournals.org/cgi/reprint/12/4/367 ==> patfis ACS

Clinics
Print ISSN 1807-5932

Clinics vol.62 no.6 So Paulo 2007

doi: 10.1590/S1807-59322007000600019

LETTER TO THE EDITOR

Abdominal compartment syndrome due to warfarin-related retroperitoneal hematoma

Mnica Mourth de Alvim Andrade; Marcelo Batista Pimenta; Bruno de Freitas Belezia; Rafael Lodi Xavier; Augusto Motta Neiva Hospital Municipal Odilon Behrens - Belo Horizonte, MG/ Brazil Email: monicamourtheaa@yahoo.com.br

INTRODUCTION
Retroperitoneal bleeding is a rare complication of anticoagulant therapy. The clinical consequences depend on the rate of blood loss and on the total amount of blood that is lost into the retroperitoneum.1 Once diagnosed, this condition requires immediate suspension of the anticoagulant, correction of the coagulation disorders and fluid restoration.1,2

CASE DESCRIPTION
A 49-year-old female patient was admitted to hospital complaining of progressive and severe abdominal pain for the past 3 days. She had been taking warfarin due to a prior diagnosis of deep venous trombosis of the lower extremities. Upon admission her abdomen was mildly distended, her intravesical pressure (IVP) was 45 cm H2O and her blood pressure (initially 70/40 mmHg) rose to 110/80 mmHg after rapid administration of 1000ml of saline solution. The blood count ordered upon her arrival showed a hemoglobin level of 4.1g/d, and an international normalized ratio (INR) of 4.4. CT of the abdomen and pelvis showed a large retroperitoneal and pelvic hematoma [figure 1]. Initially, a conservative approach was adopted: the patient received 1200ml of packed red cells (PRC), 1000ml of fresh frozen plasma and 3500ml of crystaloid solution. However, after the first 12 hours of observation she developed oliguria, seizures, shock and respiratory failure. Serial physical examinations revealed marked abdominal distension and IVP rose to 60cm H2O. The clinical picture resembled abdominal compartment syndrome (ACS) and a decision for decompressive laparotomy was made. As soon as the abdominal cavity was opened the ventilatory and hemodynamic parameters improved significantly, which confirmed ACS. A large retroperitoneal hematoma was seen but not explored, since the purpose of the procedure was only for decompression. A laparostomy with a Bogot bag was performed [figure 2] and the patient was sent to the intensive care unit where she stayed for 12 days, with progressive improvement in hemodynamic and ventilatory parameters. During this period she received another 600ml of PRC and by the 10th day all coagulation parameters were in the normal range. She then underwent serial closure of the laparostomy according to our service protocol and by the end of 29 days the abdomen was totally closed. A duplex scan confirming deep venous thrombosis of the left lower extremity was ordered after internal medicine and vascular surgery consultations. Because the patient had not had an episode of pulmonary embolism and because inadequate control of anticoagulation was considered to be the probable cause of the retroperitoneal hematoma, systemic anticoagulation with heparin was reintroduced. As

an outpatient she was kept on warfarin for another 6 months without any further bleeding complications.

DISCUSSION
Oral anticoagulants have had an expanding role in cardiovascular and thrombotic disorders. Major indications for warfarin use are nonvalvular atrial fibrillation, venous thrombosis, rheumatic heart disease, mechanical heart valve prosthesis, and pulmonary, cerebral or systemic embolism.3-5 Warfarin therapy is associated with a variety of hemorrhagic complications that are usually associated with inadequate control of anticoagulation.2 This is probably what happened to the patient reported above, since her INR was 4.4. Spontaneous retroperitoneal hematomas are rare; Brathwaite CE et al. described only one case of a retroperitoneal hematoma out of 13 patients that required termination of anticoagulation due to hemorrhagic complications6. Stephan D and colleagues evaluated 928 patients that were on chronic anticoagulation with warfarin in a retrospective cohort study. They found an incidence of first bleeding episodes of 17.3 events/100 patient-years for minor bleeding, 7.5 events/100 patient-years for serious bleeding, 1.1 events/100 patient-years for life-threatening bleeding and 0.2 events/100 patient-years for fatal bleeding5. Four variables demonstrated an independent relation to the risk of a first episode of bleeding according to this study: mean prothrombin time ratio (PTR) of 2.0 or greater, short duration anticoagulation (during the first three months of anticoagulation therapy, the risk of bleeding is higher than

after the forth month), high PTR variability and the presence of three or more comorbid conditions.5 Another study showed an incidence of major bleeding in patients treated with coumarin derivatives of 1.4 per 100 patient-years.7 Abnormal and sudden increase in the volume of any component of the intra-peritoneal or extra-peritoneal spaces can cause intraperitoneal hypertension.8 When associated with organ dysfunction (elevated airway pressure, cardiac output reduction, and oliguria) it meets the criteria for ACS.9,10 This usually occurs when the intra-abdominal pressure, measured by IVP, is above 20-25 cm H2O.9,11 The volume increase is mainly due to abdominal trauma, but may also be caused by significant intra-abdominal bleeding or collections, retroperitoneal hematomas, difuse peritonitis, peritoneal edema due to vigorous volemic ressucitation, packing of the abdominal cavity (damage control), pancreatitis, pneumoperitoneum and neoplasms.11-13 Treatment consists of prompt surgical decompression and volemic resuscitation.8,10-14 The mortality rate varies from 29 to 62% and is usually due to multiple organ failure and sepsis.10,14,15 In regard to the case presented above, a nonoperative approach to a retroperitoneal hematoma was attempted first. However, after fluid and blood replacement, the patient presented with a full-blown clinical picture of ACS, which led to a straightforward decision for a laparostomy. A review of the literature reveals little data regarding the duration of withholding warfarin, subsequent thromboembolic complications, and the risk of rebleeding on resumption of warfarin treatment in these patients. Ananthasubramaniam K et al. studied these considerations in patients with prosthetic heart valves hospitalized with a major bleeding event. The mean duration of warfarin withholding during hospitalization in their study was 15 4 days and none of their patients received other antithrombotic therapies during hospitalization. All of their patients resumed warfarin therapy when they were deemed stable by their primary physicians and did not have any thromboembolic events or significant rebleeding episodes.16 Little data exist about recurrent bleeding after resumption of warfarin therapy, but it appears to be common within 5 months of the resumption of anticoagulation. Those whose first bleeding was from a gastrointestinal source are particularly at risk for a second event.5,16 Aggressive treatment of the bleeding source and the risk-benefit ratio of continued anticoagulation need to be considered. An alternative for these high risk rebleeding patients is early caval filter placement.6 In conclusion, a large retroperitoneal hematoma is a severe and potentially fatal complication of anticoagulant therapy. Patients with this sort of complication require constant monitoring of hemodynamic and ventilatory parameters, diuresis and intravesical pressure, since they are at risk for developing ACS.

REFERENCES
1. Surez G, Valera Z, Gmez MA, Docobo F, Alamo JM. Etiology and diagnosis of severe retroperitoneal hematoma: threrapeutic options and surgical indication. Cir Esp. 2005;78:328-330. [ Links ] 2. Andrews FJ. Retroperitoneal haematoma after paracetamol increased anticoagulation. Emerg Med J. 2002;19:84-85. [ Links ] 3. Chan TY, Miu KY. Hemorrhagic complications of anticoagulant therapy in Chinese patients. J Chin Med Assoc. 2004;67:55-62. [ Links ] 4. Fanikos J, Grasso-Correnti N, Shah R, Kucher N, Goldhaber SZ. Major Bleeding complications in a specialized anticoagulation service. Am J Cardiol. 2005;96:595-598. [ Links ] 5. Fihn SD, McDonell M, Martin D, Henikoff J, Vermes D, Kent D et al. Risk Factors for complications of chronic anticoagulation: a multicenter study. Ann Intern Med. 1993;118:511-520. [ Links ] 6. Brathwait CE, Mure AJ, O'Malley KF, Spence RK, Ross, SE. Complications of anticoagulation for pulmonary embolism in low risk trauma patients. Chest. 1993;104:718-20. [ Links ] 7. Cannegleter SC, Rosendaal FR, Briet E. Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses. Circulation. 1994;89:635-641. [ Links ] 8. Decker G. Abdominal compartment syndrome. J Chir. 2001;138:270276. [ Links ] 9. Sieh KM, Chu KM, Wong J. Intra-abdominal hypertension and abdominal compartment syndrome. Langenbecks Arch Surg. 2001;386:53-61. [ Links ] 10. Hunter JD, Damani Z. Intra-abdominal hypertension and the abdominal compartment syndrome. Anaesthesia. 2004;59:899907. [ Links ] 11. Wysocki A. Abdominal compartment syndrome: current view. Przegl Lek. 2001;58:463-465. [ Links ] 12. Majchrzak C. Abdominal compartment syndrome: a case review. Perianesth Nurs. 2002;17:413-417. [ Links ] 13. Walker J, Criddle LM. Pathophysiology and management of abdominal compartment syndrome. Am J Crit Care. 2003;12:367710. [ Links ]

14. Moore AF, Hargest R, Martin M, Delicata RJ. Intra-abdominal hypertension and the abdominal compartment syndrome. Br J Surg. 2004;91:1102-1110. [ Links ] 15. Stagnitti F, Calderale SM, Priore F, Ribaldi S, Tiberi R, De Pascalis M et al. Abdominal compartment syndrome: patophysiologic and clinic remarks. G Chir. 2004;25:335-342. [ Links ] 16. Ananthasubramaniam K, Beattle JN, Rosman HS, Jayam V, Borzak S. How Safety and for How Long Can Warfarin Therapy Be Withheld in Prosthetic Heart Valve Patients Hospitalized with a Major Hemorrhage? Chest. 2001;119:478-484. [ Links ]

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