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Compartment syndrome

On the human body, the limbs can be divide into segments, such as the arm and the forearm of the upper limb, and the thigh and the leg of the lower limb. more...

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If these segments are cut transversely, it is apparent that they are divided into multiple sections. These are called fascial compartments, and are formed by tough connective tissue septa.

These compartments usually have a separate nerve and blood supply to their neighbours. The muscles in each compartment will often all be supplied by the same nerve.

Compartment syndrome

Knowledge of these compartments not only simplifies the learning of innervation, it is also important in situations where pressure can build up in one compartment and potentially damage the contents.

This problem is called compartment syndrome and can happen acutely (sometimes caused by a fracture) or gradually, as with an athlete's overuse of a muscle.

Because the connective tissue that defines the compartment does not stretch, a small amount of bleeding into the compartment, or swelling of the muscles within the compartment can cause the pressure to rise greatly. Increased pressure within the compartment compresses the nerves, and also decreases blood perfusion. The pressure in the capillaries is approximately 30mm Hg. If the pressure in the compartment rises above this level the blood supply to the muscles can be completely cut off leading to death of the tissue in the compartment. This is a medical emergency requiring immediate treatment by fasciotomy to allow the pressure to return to normal. Because the pressure in the large blood vessels of the limbs is much greater than the compartment pressure required to cause death of the tissue, a patient whose muscles are dying from compartment syndrome, and who is in danger of losing their limb will usually have intact pulses. Severe pain is the most common symptom of acute compartment syndrome.

When compartment syndrome is caused by from repetitive heavy use of the muscles, as in a runner, it is known as chronic compartment syndrome (CCS). This is usually not an emergency, but the loss of circulation can cause temporary or permanent damage to nearby nerves and muscle.

While CCS was first identified in the 1980s, it has been increasingly recognized as a significant source of chronic leg pain. A common indicator of the condition is muscle fatigue and pain in the calf region after sustained physical exercise (such as running). Once the exercise is stopped, the pain gradually disappears.

CCS can be tested for using by gauging the pressure within the muscle compartments. If the pressure is sufficiently high, a fasciotomy may be required.

Fascial compartments of the body

The thigh is usually divided into three compartments:

  • Anterior - supplied by the femoral nerve, contains the knee extensors and hip flexors.
  • Medial - supplied by the obturator nerve, contains the hip adductors.
  • Posterior - supplied by the sciatic nerve, contains the knee flexors and hip extensors.

The (lower) leg is divided into three compartments also:


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How to recognize and manage ABDOMINAL COMPARTMENT SYNDROME
From Nursing Management, 1/1/04 by Gallagher, John J

Although rare, the expansion of abdominal contents can be fatal. Here's how to recognize warning signs and respond appropriately.

ABDOMINAL COMPARTMENT syndrome is a serious complication that can kill critically ill and injured patients. Like all compartment syndromes, this condition develops when the contents of a relatively confined space-in this case, the abdominal cavity-expand beyond the space's capacity. Increasing pressure reduces blood flow to abdominal organs and impairs pulmonary, cardiovascular, renal, and gastrointestinal (GI) function, causing multiple organ dysfunction syndrome and death.

First described in the 1980s, abdominal compartment syndrome was most often associated with patients sustaining severe abdominal trauma who required extensive resuscitation and surgery. But abdominal compartment syndrome can occur in other patients as well.

Although more awareness has resulted in earlier recognition and treatment, the mortality rate for abdominal compartment syndrome still exceeds 50%. In this article, I'll describe subtle assessment findings that indicate organ system dysfunction caused by abdominal compartment syndrome, and current treatments for abdominal compartment syndrome.

Who's at risk

Patients with severe abdominal trauma account for the largest number of patients who develop abdominal compartment syndrome. Traumatic injury causes bleeding and swelling at the injury site. During resuscitation efforts, restoring perfusion to ischemic organs initiates reperfusion injury, causing more tissue swelling. The large volume of blood products and intravenous (I.V.) fluids used to resuscitate the patient further contributes to tissue edema. Other therapeutic measures, such as the use of pneumatic anti-shock garments, can increase intraabdominal pressure (IAP).

Surgical interventions also can be contributing factors. To assist with hemostasis, surgical packs may be inserted into the abdomen before the abdominal wall is closed. Normal IAP is 0 mm Hg to subatmospheric, but may increase to 15 mm Hg after abdominal surgery. The combination of these factors, along with ongoing bleeding into the abdominal cavity as from coagulopathy (a common complication of traumatic injury), contributes to rising IAP or intraabdominal hypertension and can lead to abdominal compartment syndrome.

A surgeon can take steps to reduce his patient's risk of abdominal compartment syndrome. For example, he can use staged abdominal repair, delaying full closure of the abdominal wall by inserting a synthetic material to allow for anticipated expansion of the abdominal contents. In this procedure, he performs multiple operative reexplorations for injury repair and irrigation. The final step is closing the abdominal wall.

Besides victims of trauma and surgical patients, others at risk for abdominal compartment syndrome include patients with abdominal aortic aneurysm, bowel obstruction, ascites, and hemorrhagic pancreatitis. Most recently, abdominal compartment syndrome was diagnosed in patients who've undergone massive fluid resuscitation and blood component transfusions, even in the absence of abdominal pathology.

Keeping a watchful eye

As you assess your patient, focus on changes in the GI, renal, pulmonary, and cardiovascular systems, which are most vulnerable to increased IAP. Let's take a closer look.

GI system changes. As you might suspect, the GI system is the first organ system affected by the increase in IAP. Increased pressure on the liver, spleen, and intestines decreases blood flow to these organs, causing tissue hypoxia, acidosis, and cell death. Damage to the intestinal mucosa lets normal bowel bacteria into the bloodstream, placing the patient at risk for sepsis. Similar effects from tissue hypoxia in the liver impair hepatic function.

Physical assessment of the abdomen may not provide much information about the underlying pathology of abdominal compartment syndrome. Diagnostic tools that may be more helpful include arterial blood gas (ABG) analysis, serum lactate, and gastric tonometry.

Arterial blood gas analysis and serum lactate levels can tell you if the patient has cellular acidosis and anaerobic metabolism from inadequate tissue oxygenation. The ABG results quickly reflect changes in acid-base balance. Levels of lactic acid, a by-product of anaerobic metabolism, increase with tissue ischemia, but aren't as sensitive as the ABGs for detecting changes in metabolic acidosis.

Gastric tonometry measures the intramucosal pH of the intestines, providing an indirect measurement of mucosal oxygenation. A device called a gastric tonometer is placed into the patient's stomach, and air is instilled into the balloon at the tip. Carbon dioxide from the gastric mucosa equilibrates through the balloon surface into the air inside the balloon. Every 10 minutes or so, the monitor analyzes the carbon dioxide level in the balloon and calculates the pH of the stomach mucosa.

Renal system changes. Rising IAP increases pressure on the retroperitoneal space, compressing the renal blood vessels and kidneys. When blood flow to and through the kidneys is reduced, so is glomerular filtration rate and urine output. Oliguria occurs when the IAP is 15 to 20 mm Hg; this progresses to anuria when IAP rises to 40 mm Hg. Eventual elevations in blood urea nitrogen and creatinine reflect acute renal failure.

Pulmonary system changes. Pulmonary dysfunction in abdominal compartment syndrome directly results from upward displacement of the diaphragm into the thoracic cavity, which limits normal expansion of the lungs and impairs gas exchange. Watch for less chest expansion, an increasing peak inspiratory pressure in the patient/ventilator system, and elevated arterial PaCO2 (hypercapnia) coupled with decreasing arterial PaO2 and oxygen saturation.

Cardiovascular system changes. Cardiovascular function is impaired in abdominal compartment syndrome for several reasons:

* Increasing IAP compresses the inferior vena cava, decreasing venous return to the heart and lowering preload and cardiac output.

* Increasing TAP also compresses the descending aorta, increasing afterload and further reducing cardiac output.

* Elevation of the diaphragm prevents the heart from contracting effectively, completing the triad of cardiovascular dysfunction.

These alterations are more pronounced in patients who are hypovolemic because vascular volume and venous return are already reduced. Elevated ventilation pressures generated during mechanical ventilation or by the use of positive end-expiratory pressure can have a similar effect.

The patient may have a normal or decreased cardiac output despite a normal blood pressure (BP). Memodynamic parameters such as central venous pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure will be normal or falsely elevated because elevated IAP creates back pressure into the venous system. Also, the patient is at risk for deep vein thrombosis because of reduced venous return from the legs and hypercoagulation related to critical illness.

Neurologic system changes. In a patient with a traumatic head injury and abdominal trauma, rising IAP can spur neurologic changes by impairing venous return to the heart from the superior vena cava and associated veins. Reduced venous return from the brain leads to congestion of the cerebral vessels, raising intracranial pressure (ICP) and reducing cerebral perfusion pressure and brain tissue oxygenation. If you're caring for a head-injured patient who's experiencing refractory elevations in ICP, suspect abdominal compartment syndrome.

Measuring IAP

Intra-abdominal pressure can be measured directly or indirectly. It's measured directly via a catheter similar to that used for peritoneal dialysis. Inserted into the peritoneal space, the catheter is attached to a water manometer or pressure transducer. Though accurate, this method isn't often used because it's invasive and not always available.

Indirect methods such as bladder pressure measurement are more common. Bladder pressure measurement is easy to perform, repeatable, and the most widely accepted method to measure IAP.

Bladder (intravesical) pressure measurement has several limitations. Preexisting contracted or neurogenic bladder can cause erroneous readings. Elevating the head of the bed, abdominal packing, adhesions, or pregnancy all can falsely elevate bladder pressure measurements.

Because clinical examination is notoriously unreliable in detecting increases in IAP until significant organ dysfunction exists, measure bladder pressure in any patient at risk for abdominal compartment syndrome, especially unconscious patients. Take measurements every 2 to 4 hours and report elevations of 10 mm Hg or greater, and any clinical findings reflective of organ system dysfunction, to the physician.

Treating the syndrome

Surgical decompression of the abdomen, the treatment of choice for abdominal compartment syndrome, is usually performed in patients with an IAP greater than 25 mm Hg and evidence of related organ system compromise. However, the decision may be made to operate based on elevated IAP alone because of the potential for organ system failure.

Abdominal decompression consists of opening (or reopening) the abdominal wall and fascia to reduce pressure. Once the abdomen is open, the surgeon sews a temporary closure in place to give abdominal contents room to expand. The materials used include soft pliable plastic sheeting, large sterilized I.V. bags, occlusive vacuum dressings, and mesh or tissue spacers designed for this purpose. This surgical procedure may be performed in the operating room, but may also be performed easily in the intensive care unit at the bedside (with adequate procedural sedation and analgesia) when necessary.

To prepare the patient for abdominal decompression, optimize oxygenation and ventilation. Mechanical ventilator modes may be changed and settings adjusted to counter the detrimental effects of increasing IAP on the pulmonary system. In an effort to limit or counteract cardiovascular effects of increased IAP, the surgeon may order fluid resuscitation with isotonic fluids to increase preload. Maintaining mild hypervolemia helps maintain or improve cardiac output and BP. A large-bore central vascular catheter may be inserted to infuse large volumes of fluid.

Monitor the patient for reperfusion asystole, a possible complication of abdominal decompression that occurs when by-products of anaerobic metabolism (lactic acid) that have accumulated in poorly perfused areas are rapidly transported back to the central circulation and the myocardium. As a preventive measure before and during surgery, administer an I.V. infusion of 2 liters of 0.45% sodium chloride solution containing sodium bicarbonate and mannitol to counter acidemia. Even with this measure, however, the patient still is at risk for hemodynamic instability and possible cardiac arrest, so keep a crash cart nearby.

Rapid restoration of venous return from the legs can cause a pulmonary embolus (PE) originating from thrombus formation in the legs. If Doppler ultrasound of the legs reveals a thrombosis, the surgeon may place an inferior vena cava filter to prevent PE during surgery.

After abdominal decompression surgery, continue to measure the patient's IAP and assess organ system function for improvement. Monitor the surgical site for infection and perform wound care as ordered. As tissue edema resolves, the patient will be scheduled for surgical closure of the abdomen. If this can't be accomplished within a week, the surgeon may use mesh to close the abdomen and perform skin grafting.

Meeting the challenge

Caring for the patient at risk for abdominal compartment syndrome is a challenge. By understanding which patients are most likely to develop the syndrome and vigilantly watching for organ system changes that indicate rising IAP, you can steer your patient clear of more serious complications.


Cheatham, M.: "Intraabdominal Hypertension," New Horizons. 7(1): 96-115, Spring 1999.

Fritsch, D., and Steinmann, R.: "Managing Trauma Patients with Abdominal Compartment Syndrome," Critical Care Nurse. 20(6):48-58, December 2000.

Maxwell, R., et al.: "Secondary Abdominal Compartment Syndrome: An Underappreciated Manifestation of Severe Hemorrhagic Shock," Journal of Trauma. 47(6):995-999, December 1999.

McNelis, J., et al.: "Predictive Factors Associated with Development of Abdominal Compartment Syndrome in the Surgical Intensive Care Unit," Archives of Surgery. 137(2):133-136, February 2002.

By John J. Gallagher, RN, CCNS, CCRN, MSN

John J. Gallagher is a clinical nurse specialist in emergency and critical care at Croze r-Chester Medical Center in Upland, Pa.

Copyright Springhouse Corporation 2004
Provided by ProQuest Information and Learning Company. All rights Reserved

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