eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Compartment Syndrome, Abdominal: Treatment & Medication

Author: Richard Paula, MD, Director of Research, Assistant Professor of Emergency Medicine, University of South Florida
Contributor Information and Disclosures

Updated: Feb 23, 2009

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.

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

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

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

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.

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

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

Documented hypersensitivity; anuria; renal failure; hyperkalemia

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.

Adult

5-20 mg/d PO

Pediatric

Not established

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

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

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

More on Compartment Syndrome, Abdominal

Overview: Compartment Syndrome, Abdominal
Differential Diagnoses & Workup: Compartment Syndrome, Abdominal
Treatment & Medication: Compartment Syndrome, Abdominal
Follow-up: Compartment Syndrome, Abdominal
References
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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].

  7. Madigan MC, Kemp CD, Johnson JC, Cotton BA. Secondary abdominal compartment syndrome after severe extremity injury: are early, aggressive fluid resuscitation strategies to blame?. J Trauma. Feb 2008;64(2):280-5. [Medline].

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  9. Simon RJ, Friedlander MH, Ivatury RR, et al. Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction. J Trauma. Mar 1997;42(3):398-403; discussion 404-5. [Medline].

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  27. Pusajo JF, Bumaschny E. Post-operative intra-abdominal pressure Its relation to splanchnic perfusion, sepsis, multiple organ failure and surgical reintervention. Inten Crit Care Dig. 1994;13.

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Further Reading

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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

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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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