by Kwas Huston, MD
Instructor of Medicine
Johns Hopkins University School of Medicine
Release Date: 2/13/07
Expiration Date: 2/13/09
Dr. Huston has no significant financial interest or relationships to disclose.
The patient is a 50-year-old man who was admitted for a radical retropubic prostatectomy for adenocarcinoma of the prostate. On post-operative day 1, he complained of bilateral lower extremity pain. On examination, he was alert and interactive. His vital signs were stable; he had no fever, no chest pain or dyspnea. Cardiac and pulmonary exams were unremarkable. The new low-midline abdominal incision was unexceptional. Examination of the legs, including neurovascular assessment, also was unremarkable. Shortly after he was examined, the leg pain spontaneously resolved.
On the morning of the second post-operative day, the leg pain recurred and rapidly intensified. His blood pressure remained normal, he had a fever of 38°C, and he was without respiratory compromise. There were associated myalgias. Heart, lung, and abdominal examinations remained unremarkable. There were no palpable cords in the calves and Homans’ sign was negative. He had a new light pink rash over both shins. He had no calf tenderness. The neurovascular assessment was unremarkable. There were no chills, no chest pain, no headache, and no shortness of breath. His symptoms at this point were confined to the lower extremities.
The white blood cell count was normal. Platelets were normal. The hemoglobin level was mildly depressed likely due to surgical blood loss. The basic chemistries were all unremarkable. He had an ultrasound of his lower extremities that showed normal flow and compressibility. Ultrasound showed no evidence of deep vein thrombosis (DVT). Overall, the labs were somewhat reassuring at this point.
Before moving on to the exam findings, we will review the pertinent past medical history. One year before this admission, the patient had a benign prostate biopsy. However, after that biopsy, his PSA started to rise. Therefore, a second biopsy was performed, and it showed an adenocarcinoma of the prostate. In addition, he had had testicular cancer with seminoma 12 years earlier, which had been treated with orchiectomy and radiation therapy. He also has a family history of cancer: His father died of colon cancer; his mother had lung cancer. The patient was not a smoker or a drinker. The extensive past medical history of cancer raised the possibility of current metastasis. However, a preoperative bone and CT scan showed no metastatic extension. The pathology showed a Gleason 3+3 grade 6 adenocarcinoma with negative margins, consistent with moderately differentiated prostate cancer. Nineteen lymph nodes were examined, and all were negative. His tumor, therefore, was confined to the prostate by pathology and imaging studies.
The patient had been in excellent health before the current admission. He lived in Chicago and worked full-time as a lawyer. He exercised regularly by going on regular walks with his wife, four to eight miles at a time. During these walks he had shin splints, but he was able to continue leisure walking despite the discomfort. He had hyperlipidemia, which was managed with simvastatin. He had used atorvastatin in the past, but that had been discontinued because of myalgias. During the surgical procedure, he had venous compression devices placed bilaterally to prevent DVT. This was the routine protocol for prostate surgery at Hopkins. He was placed in a supine position, so he was flat on the operating table. His anesthetic was administered at the L2-L3 level of the spine.
Now, back to post-op day 2. Although the assessment was somewhat reassuring in the morning, his symptoms worsened as the day progressed. By noon, the skin over his shins was pink to light red in color. It was warm to the touch and exquisitely tender. There was diffuse tenderness over the shin, not just the bone. The pink rash went from the proximal third of the tibia distally to the dorsum of the ankles, and it did not have a sharp border. In addition, he said that he had numbness of the first toe bilaterally.
The patient reported that after the morning rounds by the urology team, when he walked from the bed to the chair and to the bathroom, his right foot kept slapping the floor. During the morning hours, the degree of pain over both shins and the dorsum of the right foot was exacerbated. It was particularly severe when he was supine, or when he moved either foot. However, standing up provided some degree of relief.
To add to the exam, he had no evidence of swollen joints in the knees, ankles or toes. At this point, he had new weakness in the right and left foot, he was unable to dorsiflex the right foot or the left great toe. Plantar flexion was normal. He had decreased sensation to light touch on the dorsum of both great toes. He had symmetric posterior tibialis pulses, but a diminished dorsalis pedis pulse on the right and a palpable dorsalis pedis on the left. He had exquisite tenderness to even light palpation of the anterior tibial region, but no calf tenderness. His creatine phosphokinase level was elevated to 7490 UL/L.
Based on the history and physical, we were concerned about progressive neurovascular compromise due to an anterior compartment syndrome. We requested an urgent evaluation by orthopedics, and the patient was taken to the operating room for immediate pressure measurement of his compartments. The right anterior compartment was 70mm Hg; the left was 52mm Hg. Normal is less than 10. Other compartments in the lower leg were normal. He immediately went to the OR for bilateral fasciotomies of the anterior compartments.
His symptoms began improving after the fasciotomy. He was in the hospital for a few more days before returning home to Chicago for intensive rehab. By six months after discharge, the sensory and motor function had markedly improved. His foot drop had nearly resolved, although he still had numbness. By one year post-discharge, he was back to his usual activities — and was able to do a 190-mile bike ride. Interestingly, he no longer had the shin splints.
The patient had compartment syndrome. Though initially described in the medical literature in the 1880s, this syndrome has likely been present as long as humans have suffered injuries to their extremities. Compartment syndrome is an increased pressure in a fixed space. A space that is bound by inelastic fascia and bone and has a normal pressure that is less than 10mm Hg; anything over 10 is abnormal. Compartment syndrome is far more common in the lower extremities. It is usually caused by a fracture, sometimes blunt trauma, or even reperfusion after revascularization for an arterial obstruction. There is limited epidemiology. Some papers report the incidence from 1% to 29% after a closed fracture, but it is hard to believe that almost 30% of people have compartment syndromes after fracture. The most frequent cause is a tibial shaft fracture. It also can result from excessive physical training; military recruits, when they are running and marching without rest, can develop compartment syndrome. Removal of an intra-aortic balloon pump can result in compartment syndrome. Other causes, though not common, include snakebites and limb compression. There are reports of compartment syndrome associated with dysfunctional venous compression during surgical procedures as well as surgery in the lithotomy position.
The pathophysiology is ischemia followed by reperfusion, which causes edema. Edema in a fixed space can result in increased pressure elevated above the capillary pressure. Arterial inflow and venous outflow is diminished. This leads to a vicious cycle of ischemia, increased pressure, less outflow, more pressure, and eventually, when the metabolic demands of the tissue are no longer met, necrosis. This process can result in rhabdomyolysis with renal failure, neuropathies, multi-organ failure, and death.
There are four compartments in the lower leg separated by the tibia, fibula and fascia. Any of these can have compartment syndrome; however, the anterior compartment is the most commonly affected. From an anatomical standpoint, that makes sense since this is the tightest compartment. The anterior tibial artery and the deep peroneal nerve reside in the anterior compartment and symptoms correlate with damage to structures in the compartment. Any of the other compartments can have compartment syndrome as well.
Signs and symptoms include:
- Pain. It’s disproportionate, and there’s pain on passive stretching of the involved muscle.
- Swollen and tense compartment.
- Rapid progression of these signs over a short time. This makes sense with the vicious cycle of ischemia and reperfusion.
- Paresthesia. The first thing that goes is two-point discrimination; that is supposed to be an early sign.
- Pulselessness. This is a very late sign. Once you have no pulses, it is bad news.
- Paralysis. This is also a late symptom.
When you think about compartment syndrome, the diagnosis is straightforward. You call someone who knows how to measure compartment pressure. Various devices can be used, but a Stryker needle seems to be most common.
A needle is inserted in the compartment and a small amount of saline is injected, which reveals the pressure required to inject the saline. There is no absolute pressure above which you have to do surgery; however, according to the literature, surgeons seem to agree that if it is over 30, a fasciotomy is needed. If pressure is between 10 and 30, you should think about the clinical symptoms and signs, put that together with the pressure, and make a decision. If someone does not have a pulse, there is nerve involvement, and the pressure is 18, you probably need to do a fasciotomy. There are many small reports on other modalities to make a diagnosis — MRI, near infrared spectroscopy, scintigraphy, laser Doppler flowmetry — but they are investigational only. None of them should be used clinically as they take too long and are not very accurate.
The only real treatment is fasciotomy, usually with delayed closure to close the skin, and then return for skin grafting. With our case, surgeons were able to close the patient in the OR after debridement. They said there was some tension, but they felt that it was not enough to warrant leaving him open. There is not always a good outcome, however. In one study of 36 patients treated with fasciotomy, 45% had good limb functioning, 27% had diminished function, 12% had an amputation, and 15% died. That death rate is comparable to that found by other studies as well. This is a nasty thing that you do not want to miss.
What time is the best time to do a fasciotomy? The earlier the fasciotomy, the better the outcome. If it is more than 12 hours, the damage is considered done.
Our patient did not have a normal compartment syndrome. He had what is called a well leg compartment syndrome. There’s no trauma and the leg looks fine, but you have a compartment syndrome. This occurs in different surgeries: urologic, gynecologic, orthopedic, and general surgery. One estimate of prevalence was 1 in 3500; the literature includes reports of only 16 patients who have had this after urologic surgery. It is most often associated with lithotomy or hemilithotomy position.
It tends to be worse when the ankles are very high (as opposed to low lithotomy, when the ankles are low) because of perfusion pressure. It is not just the absolute pressure in the compartment that needs to be considered, but also the perfusion pressure. If the perfusion pressure and the compartment pressure get too close to one another ischemia can result. It’s estimated that for every centimeter of ankle elevation, there is a 0.78mm Hg decrease in the arteriolar pressure. Our patient, though, was not in lithotomy; he was supine.
Risk factors for well leg compartment syndrome include:
- Lithotomy position
- Procedure duration (longer than 4 hours)
- Trendelenburg position
- Ankle dorsiflexion (increases the pressure in the anterior compartment)
- Being overweight
- Having very muscular lower limbs
- Pneumatic calf compressors (a common perioperative treatment)
- Intraoperative hypotension (It turns out that our patient did have surgery performed with intraoperative hypotension, to reduce bleeding.)
- Vasoconstrictive drugs.
The largest look at well leg compartment syndrome comes from a survey of urologists in the United Kingdom. Of the 260 urologists surveyed, 65 had experience with this entity. Most had seen it just once, though a few had seen it two or three times. Blood loss and hypotension appeared in 10 cases, vascular disease in 5. The outcomes were not very good: 40% had permanent disability, 4 patients died. Legal action was taken in 6 cases. They felt that diagnosis had been delayed in 15 cases; 11 of those 15 had permanent disabilities. Not recognizing this is a big problem. Usually the reason a diagnosis is delayed is because people just don’t know about it; sometimes, though, the symptoms are masked by epidural anesthesia or misdiagnosed as DVT.
There is also an entity called chronic exertional compartment syndrome. It occurs typically in young athletes; the median age is 20 years. Most people are involved in sports — 69% are runners, but skiing, golf, crew, gymnastics, boxing, fencing are also reported. Dancers also can have chronic exertional compartment syndrome. There is a 1:1 male/female ratio. It almost always involves the lower extremities. Basically, it is a compartment syndrome that people get with exercise.
The etiology is thought to be either ischemia or abnormally thick fascia, or a combination of the two. There is evidence for and against those. Basically, there is increased muscle volume and edema with exercise. It is generally bilateral. Exercise gradually brings this on. People complain of tightness, cramping or aching in the anterior compartment with exertion. It is reproduced at a defined degree of exercise. People say: “Every time I hit mile 1.3, it hurts in my shins.” Then it resolves within 15 to 30 minutes of stopping the exercise. So, you can see how this could be easily confused with shin splints. It also can worsen gradually over weeks to months. Occasionally, there will be transient neurologic symptoms, such as paresthesia, numbness or foot drop during the exercise with subsequent improvement at rest. Although physical exam generally is not very helpful, there are reports of detecting muscle herniation in the lateral compartment.
The diagnosis is made by measuring compartment pressures. Pre-exercise pressure is greater than 15, or post-exercise pressure elevation supports the diagnosis. Other modalities really aren’t proven. One study looked at MRIs, saying there is an increased T2 signal in the muscles with exercise, but it had no control group. You have to rule out other overuse syndromes, such as shin splints, tibial stress fracture, muscle strain, popliteal artery entrapment (which is very rare). Although some of these syndromes are more common, you might want to think about the possibility of compartment syndrome when you see a young person with these symptoms. The treatment is fasciotomy. Most patients do very well with fasciotomy. This population tends to be quite athletic, and they usually are able to return to their competitive sport.
Our patient had some risk factors for the well leg compartment syndrome. He had the venous compression devices and hypotensive anesthesia — although, if you look at the record at Hopkins, there are 10,000 patients in the database of radical retropubic prostatectomies, and no patient ever had a similar outcome. They all had venous compression devices. But our patient also had so-called shin splints, which may have been a chronic exertional compartment syndrome. He may have had an anatomically tightened compartment. It is very interesting that the pain from shin splints resolved after fasciotomy, and he no longer has this complaint with exercise. Our hypothesis is that he had a baseline tight compartment with a “second hit” during the surgical procedure, which caused the chronic exertion compartment syndrome to become an acute compartment syndrome.
This case is interesting for a variety of reasons. One is that we were called for a very urgent consult on this patient. As rheumatology consultants, we often exclude rheumatic disease (as in this case) but are still able to provide useful management advice by guiding the evaluation towards a specific non-rheumatic illness. We do not see compartment syndrome commonly, but we need to know how to recognize it and how to treat it — including well leg compartment syndrome and chronic exertional compartment syndrome. This diagnosis must be made immediately to prevent a poor outcome. We are often asked to consult on surgical patients for common ailments such as gout in the post operative period, but other less common diagnostic considerations should be kept in mind, as in this case, where it was essential to recognize and treat acute compartment syndrome on an urgent basis. Fortunately, this resulted in a favorable outcome.