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Pseudothrombophlebitis caused by nontraumatic compartmental syndrome of the calf.

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LETTERS
(4). Studies are currently under way to further investigate
the source of IL-2 inhibitory activity in RA SF.
Paul Emery, MA, MD, MRCP
University of Birmingham
Birmingham, England
Ian R. Mackay, AM, MD, FRCP, FRACP, FRCPA
Royal Melbourne Hospital
Melbourne, Australia
1 . Miossec P, Kashiwado T, Ziff M: inhibitor of interleukin-2 in
rheumatoid synovial fluid. Arthritis Rheum 30: 121-129, 1987
2. Emery P, Gentry KC, Kelso A, Mackay IR: Interleukin-2 inhibitor in synovial fluids. Clin Exp Immunol 72:60, 1988
3. Simmons JA, Wood NC. Nuki G , d’Giovine FS, Duff GW:
Soluble IL-2 receptor in serum and synovial fluid samples from
patients with rheumatic diseases (abstract). Br J Rheumatol 26:
64, 1987
4. Osawa H, Josimovic-Alasevic 0 , Diamantstein T: IL-2 receptors
are released by cells in vitro and in vivo. 1 . Detection of soluble
IL-2 receptors in culture supernatants and serum of mice by an
immunoradiometric assay. Eur J Immunol 16:467469, 1986
Pseudothrombophlebitis caused by nontraumatic
compartmental syndrome of the calf
To the Editor:
Traumatic rhabdomyolysis has long been recognized
as a cause of acute renal failure. Nontraumatic rhabdomyolysis has recently been encountered more frequently and is
probably still underdiagnosed (1,2). Of the many causes of
rhabdomyolysis, nontraumatic compartmental syndrome of
the leg is rarely considered. We recently treated a patient
who experienced an acute episode of myoglobinuria secondary to nontraumatic calf compartmental syndrome, with
resulting deterioration of renal function.
The patient, a 38-year-old black man, was admitted
to our institution because of the gradual onset of painful
swelling of his right calf. Medical history included insulindependent diabetes mellitus, diabetic retinopathy, peripheral
neuropathy, and the nephrotic syndrome. He had no history
of ethanol abuse or of trauma. Radiographs and a bone scan
of the leg showed no abnormalities. Impedance plethysmography of the lower extremities gave a normal result.
Doppler study revealed decreased right popliteal flow. Intravenous heparin treatment was started for possible thrornbophlebitis of the calf.
Renal function was found to be abnormal. The blood
urea nitrogen level was 62 mg/dl, and the creatinine level was
4.0 mg/dl. A renal biopsy was performed and was interpreted
as showing diabetic nephropathy and interstitial nephritis.
Prednisone therapy was started by the attending nephrologist for the latter diagnosis, and the heparin treatment was
discontinued. The patient was discharged and sent for outpatient evaluation of a possible Baker’s cyst.
One month later, the patient was readmitted to our
institution. He then reported worsening of the swelling of his
legs, generalized weakness, and increasing frequency of
urination and nocturia. There was marked pitting edema of
1591
the legs up to the knees. The right calf was slightly larger
than the left, but it was not tender. Examination of the joints
gave normal findings. Neurologic examination showed decreased sensation in both lower extremities, but motor
strength was intact.
Laboratory testing revealed a hemoglobin level of 7.5
gm/dl and a hematocrit value of 24%, with normal indices.
Urine showed traces of occult blood, 2-5 white blood cells
per high power field (HPF), and 0-2 red blood cells per HPF.
Protein excretion was 5 gm in 24 hours. Serum studies
showed the following values: creatine phosphokinase (CPK)
1,314 unitslml, lactate dehydrogenase 574 units/ml, calcium
6.5 mg/dl, phosphorus 5.5 mg/dl, uric acid 8.6 mg/dl, sodium
132 mEq/liter, potassium 5.1 mEq/liter, chloride 102 mEq/
liter, bicarbonate 18 mEqfliter, urea nitrogen 79 mg/dl,
creatinine 7.8 mg/dl, and myoglobin 342 mg/liter.
Impedance plethysmography findings were normal.
Doppler study showed no evidence of deep vein thrombosis
in the thighs, but it did show decreased flow through the right
popliteal vein. Again, treatment with intravenous heparin
was administered. Radiographs of the leg and a bone scan
showed normal results. An electromyogram and nerve conduction studies were performed, and the results confirmed
the presence of peripheral neuropathy of the lower extremities, but no evidence of diffuse myopathy was found. A
biopsy of the right deltoid muscle yielded normal results.
The leg swelling and increased CPK level in the
absence of a diffuse myopathy led us to consider compartmental syndrome of the right leg as a cause of the rhabdomyolysis. Because of the probability that the exacerbation of
renal dysfunction was caused by myoglobinuria, the renal
biopsy sample taken at the previous admission was reexamined. Microscopic examination of the kidney material
showed the presence of pigmented casts in renal tubules,
which was suggestive of myoglobin. Heparin treatment was
discontinued.
The patient was taken to the operating room, where
compartmental pressures were measured in both calves by
the Wick-catheter technique (3). The left calf showed normal
pressure, at 19.5 cm H,O. The right calf (the affected side)
showed high pressure, at 43 cm H,O.
Fasciotomy and decompression of the calf were
performed. The muscle was gray-pink with yellow streaking,
indicative of areas of muscle necrosis. Microscopic examination of the muscle showed areas of muscle fiber necrosis
among areas of more normal fibers (Figure I).
The patient improved clinically and biochemically.
By the time of hospital discharge, the acute renal failure had
partially resolved, with the creatinine level stabilizing at 4.0
mg/dl. His serum CPK level was also within normal limits.
The etiology of this patient’s rhabdomyolysis was a
compartmental syndrome involving the right calf. In this
condition, increased pressure within a limited anatomic
space causes compromise of circulation, with subsequent
tissue dysfunction. Compartmental syndrome was confirmed
by measuring intramuscular pressures, using the Wickcatheter technique (3). Muscle necrosis was identified in the
biopsy sample of the involved muscle group. After decompressive surgery was done, the patient improved clinically.
Although a ruptured Baker’s cyst was not completely ruled
out by such tests as arthrography, ultrasonography, or
LETTERS
1592
Figure 1. Muscle biopsy of the patient’s right calf, showing necrotic muscle fibers (hematoxylin and eosin stained,
original magnification x 300).
computed tomography, the muscle necrosis and subsequent
clinical improvement suggested that the patient had a pseudothrombophlebitis syndrome resulting from a compartmental syndrome.
Medical causes of compartmental syndrome include
bleeding disorders, post-ischemic swelling, exercise, seizures
and eclampsia, intraarterial administration of drugs, venous
obstruction, muscle hypertrophy, infiltrated infusion, and
the nephrotic syndrome (4). Compartmental syndrome has
been reported as a complication of rhabdomyolysis caused
by alcohol and drug ingestion, among other causes (4). The
possible etiologies of this condition in our patient were the
diabetic peripheral vascular disease, small vein obstruction,
and edema due to the nephrotic syndrome. Our patient may
have been experiencing repeated insults from myoglobinuria
due to compartmental calf syndrome (1,2).
Initially, the patient was thought to have a pseudothrombophlebitis syndrome due to a ruptured or dissecting
Baker’s cyst (3). However, the lack of knee effusion or other
abnormal physical findings associated with the knee, and the
absence of palpable calf masses or tenderness, were evidence against the presence of a Baker’s cyst o r other benign
or malignant tumors that occasionally mimic Baker’s cyst.
Nontraumatic compartmental leg syndrome should
be included in the differential diagnosis of the pseudothrom-
bophlebitis syndrome in which ruptured or dissecting Baker’s cyst, rupture of the plantaris tendon, rupture of the
medial head of the gastrocnemius, or cellulitis is a possible
cause. Furthermore, early diagnosis of compartmental syndrome is important because prompt treatment can preserve
function and viability of the contents within the muscular
compartment and prevent renal damage.
Raymond Wargovich, MD
Antonio J. Reginato, MD
Cooper HospitallUniversity Medical Center
Robert Wood Johnson Medical School
Camden, NJ
I . Grossman RA. Hamilton RW, Morse BM, Penn AS, Goldberg
M: Nontraumatic rhabdomyolysis and acute renal failure. N Engl
J Med 291:807- 81 I , 1974
2. Koffler A, Friedler RM, Massry SG: Acute renal failure due to
nontraumatic rhabdomyolysis. Ann Intern Med 85:23-28, 1976
3. Mubarak SJ, Hargens AR, Owen CA, Garetto LP, Akeson WH:
The Wick-catheter technique for measurement of intramuscular
pressure: a new research and clinical tool. J Bone Joint Surg 58A:
1016-1020, 1976
4. Matsen FA: Compartmental syndromes. Hosp Pract 15:113-117.
1980
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