Volume 7, Case 7
Kevin H. Higashigawa, Medical Student
Loren G. Yamamoto, MD, MPH
Kapiolani Medical Center For Women And Children
University of Hawaii John A. Burns School of Medicine
A 20 year old male arrives ambulatory to the ED at 12:30 pm accompanied by friends. He is complaining of pain in his left forearm and hand. He states that he became drunk the previous night and fell off a bar stool. He does not remember the event well. He awoke in the morning with pain in his left arm, from the mid-upper arm to his wrist. He complains that he cannot move his elbow, wrist, or fingers. He also complains that he has the sensation of pinpricks in his arm with decreased sensation, and numbness in his left hand.
Consider some of the possible diagnoses:
Exam: VS T 37.3 degrees C, P 96, R 20, BP 158/89. He is generally alert, cooperative and in no acute distress. HEENT unremarkable. Heart regular without murmurs. Lungs clear. Abdomen soft and non-tender. No hepatosplenomegaly. Left upper extremity: AC joint and shoulder non-tender. His ability to move his fingers and wrist is minimal. His radial pulse is good. Capillary refill in the nailbeds is good. Pulse oximetry on all the fingers of his left hand demonstrates a good perfusion pulsation waveform. His forearm appears to be modestly swollen. The skin from his elbow to wrist is tense and warm with slight erythema and superficial peeling. No pallor is noted. Sensation in his wrist and hand is minimal. He also has a large patch of necrotic skin in the shape of a polygon over his left flank.
Radiographs of his left forearm are obtained.
View his forearm radiographs.
(missing image - Forearm radiograph showing normal findings.)
After viewing his radiographs, what work-up would you recommend?
Initially, it was believed that the patient had suffered a fracture of his left forearm (during the fall from the bar stool) complicated by a nerve injury. However, radiographs of his left forearm returned normal. The possibility of cellulitis and sepsis in his forearm was raised. The necrotic lesion on his back suggested disseminated infection, but its polygon shape was inconsistent with sepsis. Upon further questioning, the patient; however, denied any history of fever. The superficial peeling of his forearm resembled a possible chemical or heat burn, but the patient could not remember any such event occurring.
The diagnosis of compartment syndrome (CS) was considered, but no fracture was present and his distal pulses were normal, including pulse oximetry perfusion waveforms in his fingers. Some bloodwork was drawn, including a CBC and blood culture. An IV was started and he was immediately given some antibiotics.
Given that the patient demonstrated good distal pulses and the absence of pallor, is a compartment syndrome possible?
An orthopedic surgeon was consulted. A pressure transducer measured the patient's forearm compartment pressure to be 72 mmHg. This is diagnostic of a compartment syndrome.
Does the presence of normal distal pulses rule out a compartment syndrome? Absolutely NOT!! Avoid this pitfall. A compartment syndrome occurs when venous outflow is impeded, thus arterial pulsation is still present in many compartment syndrome cases.
What compartment pressure is diagnostic of compartment syndrome? What is the definitive treatment for compartment syndrome?
The patient was immediately taken to the operating room for a fasciotomy. Large areas of muscle necrosis were noted. The patient also developed renal insufficiency secondary to severe rhabdomyolysis. After multiple debridement procedures, he was able to regain some forearm, wrist, and hand function, but it was apparent that he suffered permanent neuromuscular deficits.
What are the complications of compartment syndrome? What was the etiology for his compartment syndrome?
Upon questioning one of the patient's friends, it was revealed that the patient had taken 20 or 30 shots of liquor the previous night. After falling off the bar stool, his friends carried him into the back of a pick-up truck where he slept until he awoke the next day. His compartment syndrome was due to him sleeping on his arm in an intoxicated state and compressing it for an extended period of time. Because of his ethanol intoxication, normal body protective reflexes that stimulate the body to move and roll while sleeping were blunted. In retrospect, it was believed that the necrotic lesion on his back was probably due to pressure necrosis resulting from something (in the back of the pick-up truck) pressing upon his flank while he was unconscious.
Discussion
Compartment syndrome is the result of increased pressure within a closed anatomical space. As such, any area of the body which contains a compartment can be affected, namely the hand, forearm, upper arm, entire lower extremity, abdomen, and buttocks. As the intracompartmental pressures increase and exceed the perfusion pressure, tissues become ischemic and may become necrotic without timely intervention. Compartment Syndrome is a thus a limb- (and even life-) threatening condition. Patient prognosis depends upon the timeliness of diagnosis. Therefore, time is critical. It is generally accepted that 6 hours is the upper limit of tissue viability (1).
Traditionally, the "6 Ps" (pain, paresthesia, paresis, pallor, poikilothermia, and pulselessness) were used to clinically diagnose compartment syndrome. In an effort to generate as many Ps as possible, this series of 6 Ps is really a pitfall because pulselessness and pallor are usually NOT present in a compartment syndrome. Additionally, poikilothermia is not a term which is commonly used. Thus, only 3 Ps remain. Learn the three important Ps of pain, paresthesia and paresis and do not rely on the other three.
Currently, it is generally accepted that pallor and pulselessness are no longer reliable criteria for CS. In the pathophysiology of CS, venous outflow resistance is increased, ultimately leading to a cessation in blood flow. CS is really a venous infarction rather than an arterial infarction. Venous outflow is impeded when the compartment pressure exceeds about 30 mmHg. As the compartment pressure rises, all the veins are compressed and venous outflow is blocked. Since venous outflow is blocked, perfusion of the tissues within the compartment ceases. There may still be arterial pulsation of the larger arteries within the compartment and distal to the compartment because the systolic pressure still exceeds the compartment pressure. In addition, arterial blood may continue to flow through arteriolo-arteriolar shunts (1, 2, 3). Thus, distal pulses may still be present. Pulsation within larger arteries, however, will not result in any capillary circulation, because venous outflow is blocked. Avoid this pitfall. Pulselessness is NOT present in early cases of compartment syndrome. Do not use the presence of pulses to rule out a compartment syndrome, because this will cause the diagnosis to be delayed beyond the point of salvage.
Similarly, pallor may not be evident in a compartment syndrome. The skin outside the compartment may be normally perfused since only intracompartmental perfusion may be affected. Even if the venous outflow of the skin is impeded, the appearance of the skin would be that of venous congestion and NOT pallor.
Pain, however, is a reliable indicator of compartment syndrome. CS should be suspected if the patient complains of severe pain following any injury to an extremity. Often, the pain is more severe than one would expect from the injury. Severe pain after splinting or casting should raise the possibility of compartment syndrome. The pain may occur at rest or with certain movements, such as passive stretching of the muscles or active flexion/extension. The pain can be described as a burning sensation, and it is not usually relieved by pain medication or splinting.
Paresthesia will ultimately develop as nerve conduction slows in hypoxic/ischemic conditions. A later finding in CS, paresis or paralysis may set in as motor neurons start to dysfunction. The extremity may also feel tense or hard (1, 3).
The anterior distal lower extremity is cited as the most common site of compartment syndrome. The reason for this location is probably due to its high frequency of injury. The usual cause of CS is a fracture. However, the incidence of CS following a fracture is actually very small. In the setting of a fracture, compartment syndrome is therefore a diagnosis of low probability but high morbidity. It is also estimated that 30% of limbs will develop CS following vascular injury (1).
According to one study, young men appear to be at higher risk for developing CS. Compared to other patient profiles, young men have relatively larger muscle volume confined to an osseofascial space which ceases to expand after growth is complete. Young men are also more likely to be engaged in activities (for example, sports or fights) which are associated with these injuries (4).
There are two main pathways to increasing intracompartmental pressure: 1) Increasing the fluid content within the compartment, either by hemorrhage or from edema; and 2) Decreasing the compartment size, either by tissue constricture or by external compression (1, 5).
I. Increased fluid content
II. Decreased compartment size
Based on the findings of one orthopedic trauma unit in Edinburgh, Scotland, the following outline reveals the underlying condition and mode and cause of injury of 164 cases of CS between 1988 and 1995, inclusive, with percentage of cases in parentheses (4):
I. Underlying Condition
II. Mode of Injury
III. Cause of Injury
Osseofascial compartments are relatively nondistensible and have a fixed volume. Thus, the introduction of fluid into or external compression of the compartment will undoubtedly raise the intracompartmental pressure. There are several theories which attempt to explain the exact mechanism of the resulting decrease in tissue perfusion. One popular theory states that the increase in intracompartmental pressure leads to a compression of the venous system. As the pressure in the venous system rises, the arteriovenous pressure gradient decreases. Hence, blood has a decreased tendency to flow into the capillaries. The body's compensatory mechanisms to increase perfusion pressure are eventually overwhelmed by increasing intracompartmental pressures. The increased venous outflow resistance ultimately causes a retrograde blood stasis. Blood ceases to perfuse the cells and the tissues become ischemic (2).
A further complication is that hypoxic cells will release vasoactive substances such as histamine and serotonin which serve to increase capillary permeability. As protein leaks into the interstitial space, water is pulled along with it. Thus, the intracompartmental pressures continue to rise. Prolonged ischemia (over 6 hours) will result in rhabdomyolysis and potential loss of limb. Rhabdomyolysis may lead to acute renal failure and eventual death.
CPK and serum myoglobin levels may be elevated, indicating rhabdomyolysis. Dipstick urinalysis may be positive for blood, but on microscopic review be negative for RBCs, indicating the presence of myoglobin in the urine (1).
Radiographs of the extremity may show the presence of an underlying fracture, but the absence of a fracture does not rule out a compartment syndrome since there are other etiologies for compartment syndrome. A CT scan may reveal areas of muscle necrosis. A CT scan, however, should not delay the treatment of a compartment syndrome. Once it is suspected, it should be acted upon immediately to maximize the patient's chance of recovery.
A measurement of the compartment pressure should be obtained as soon as a diagnosis of CS is suspected. Commercial pressure measurement devices are available. If none is available, three generic procedures for measuring the intracompartmental pressure are suggested at the end of this case.
The level of intracompartmental pressure which serves as the cutoff point for diagnosing CS is under debate. Some cite 30 mmHg as indicative of CS, whereas others claim that 45 mmHg is an appropriate cut-off (1).
The threshold for developing compartment syndrome is directly affected by the amount of blood flow to that area. As such, hypotensive patients may develop CS at lower intracompartmental pressures. Thus, some advocate the use of perfusion pressure, rather than just intracompartmental pressure, in determining CS. Perfusion pressure = Diastolic BP minus the intracompartmental pressure (7, 8).
McQueen used perfusion pressure measurements of less than 30 mmHg as diagnostic of CS and an indication for fasciotomy (1).
TREATMENT: Since the pathophysiology of CS involves an ischemic event, it may be helpful to give the patient oxygen to increase pO2. The patient should be hydrated intravenously to prevent acute renal failure secondary to rhabdomyolysis (1, 5). The involved extremity should kept at body level so that arterial blood flow is not compromised and venous drainage is unhindered (3).
The definitive therapy for CS is fasciotomy to relieve the intracompartmental pressure. The emergency physician should seek immediate surgical consultation, usually with orthopedics.
COMPLICATIONS: Prognosis ultimately depends upon the speed of diagnosis and treatment. However, even with timely intervention, the patient may still suffer some permanent neuromuscular dysfunction. Volkmann's ischemic contracture is the functionless, claw-hand deformity that results from untreated forearm ischemia. Rhabdomyolysis will occur after approximately 6 hours of warm ischemia and may escalate into a bacterial gangrene infection, loss of limb, and sepsis. Acute renal failure may result from rhabdomyolysis, and if left untreated, will lead to death (6). Following a fasciotomy, there is a risk of infection. The procedure will also leave some cosmetic deformity (1).
CLINICAL PEARLS:
Intracompartmental pressure measurement methods:
The Stryker Stic device is a commercially available product made specifically for measuring intracompartmental pressures. It is fast and accurate, but it is modestly expensive and it is possible that your hospital does not have it.
If you don't have access to a Stryker Stic device, there are three generic alternatives which will probably work with equipment that is available in most hospitals. The three methods described below are:
1. Mercury column manometer method (6,9,10)
The following equipment is needed:
This three-way stopcock is a stopcock that must be able to communicate with three ports simultaneously. Most stopcocks have three ports and only communicate two of these ports at a time (this is confusing because these may also be called 2-way or 4-way stopcocks). However, most such stopcocks can communicate all three ports at a time. If the stopcock is positioned such that the three ports point to 9 o'clock, 12 o'clock and 3 o'clock, the position of the stopcock lever and ports can be described.
View the diagram of the stopcock for clarification.
The stopcocks on the top row have a single lever which always points to the port that is off. The stopcocks on the bottom have a different design with four levers, one of which is labeled "off" and the other three which communicate with each other.
In normal use, the "off" stopcock lever can be placed in any position between 9, 12 and 3 o'clock (the first three positions from left to right on the stopcock diagram). In these positions, the stopcock communicates with two ports at a time, with one port off. However, by forcing the stopcock "off" lever over the hump to the 6 o'clock position, the stopcock will usually communicate all three ports simultaneously (the position on the right of the stopcock diagram).
View a diagram of this mercury manometer method.
Follow this procedure:
2. Electronic transducer method
View a diagram of this electronic transducer manometer method.
Follow this procedure:
3. IV infusion pump method
This method is very simple, but it requires an IV infusion pump with a built in pressure readout. Most modern IV infusion pumps have this feature, which is most commonly used to permit nurses to set limits on IV infusion pressure so that the pump with alarm if a high pressure condition is encountered, usually due to an infiltrated IV or a malpositioned IV catheter. These sophisticated pumps reduce the likelihood of an undetected infiltrated or obstructed IV catheter.
Uppal et al, described the use of the IVAC infusion pump to measure the intracompartmental pressure (11):
References