Do Creatine Kinase (CK) Levels Influence The Diagnosis Or Outcome In Patients With Compartment Syndrome?

U Ihedioha, S Sinha, A C Campbell 

Department of Orthopaedic Surgery, Monklands Hospital, Airdrie

Correspondence to: Mr S Sinha, Department or orthopaedics, Monklands Hospital, Monkscourt Avenue, Airdrie ML6 0JS  Email: write2satya@hotmail.com

SMJ 2005 50(4): 158-159

 

Abstract

We report a retrospective study in patients with compartment syndrome with the aim to analyse: 1) whether the level of rise in CK levels is a useful marker to the presence of compartment syndrome and; 2) whether an early fasciotomy assists in lowering of the elevated CK levels. The results of our study suggest that although raised CK levels are not diagnostic, they are a useful adjunct in making a diagnosis, and hence CK estimation should be done in all patients with suspected compartment syndrome. Moreover, an early fasciotomy (<12 hours) has a statistically significant influence in lowering elevated CK levels, confirming the view that the earlier the decompression, the lesser the muscle damage. 

Key words: Creatine Kinase, compartment syndrome, fasciotomy

 

Introduction 

Acute compartment syndrome is both a limb- and lifethreatening emergency that requires prompt treatment. Early diagnosis of this condition is of paramount importance, and intra-compartmental pressure (ICP) monitoring is recommended.1,2 However, ICP monitoring requires a clear understanding of the pathophysiology of compartment syndrome for proper clinical correlation. The enzyme creating kinase (CK) is present in striated muscle. When muscle cells disintegrate, CK is released into the bloodstream. Several subtypes of CK exist; some of them are found in striated muscle (CKMM), others in cardiac muscle (CKMB). During rhabdomyolysis, large quantities of CKMM are released and peak concentrations of 100,000 IU/ml or more are not unusual. Because overall degradation and removal are slow, the concentration of CK remains elevated for much longer and in a more consistent manner than that of myoglobin, another key compound released by muscle necrosis. Consequently, CK is more reliable than myoglovin in assessing the presence and degree of damage to muscle.3We report a retrospective study in patients with compartment syndrome with the aim to analyse: 

1. whether the level of rise in CK levels is a useful marker to the presence of compartment syndrome, and 

2. whether an early fasciotomy assists in lowering of the elevated CK levels. 

 

Materials and methods 

We retrospectively reviewed the case notes of patients with compartment syndrome who had undergone: 

i) a fasciotomy, and 

ii) who also had CK levels estimated both on admission and after fasciotomy. 

 

Fifteen patients who fulfilled both these criteria were identified. There were eleven male and four female patients. The mean age in the male patients was 38 (range 24-67) years, while that in the females was 69 (range 43-88) years. The parts involved in decreasing order of frequency were: leg 8, forearm 4, thigh 2, buttock 1.  

 

 The right side was affected in nine cases, the left in four, while in two cases it was bilateral. Compartment syndrome was associated with: 

•fractures in six cases 

•unconsciousness in intravenous drug abusers/ alcoholics in six cases 

•bleeding disorders in two cases 

•seizures in one case. 

 

The mean duration from admission to fasciotomy in these patients was 30 hours (range 6-96 hours). The delay in intervention was mainly because of late orthopaedic referral. The mean hospital stay was 22 days (range 7-90 days). 

 

Results 

The mean CK level on admission was 45,800 IU/ml (range 123-144,310) falling to a post-fasciotomy mean of 14,700 IU/ml (range 70-95,260). But in the eight patients who had their fasciotomy within 12 hours, the mean CK level fell from 65,300IU/ml to 13,300IU/ml, in contrast to patients who had delayed fasciotomy (>12 hours) in whom the CK level fell from a mean of 24,800 IU/ml to 16,400 IU/ml (Fig 1). 

 

The degree of fall in the level of CK in the patients who had early fasciotomy (<12 hours) compared to patients who had delayed fasciotomy (>12 hours) was found to be statistically significant (P<0.05) using the Mann-Whitney test. The seven patients who developed acute renal failure had a much higher mean CK on admission of 78,300 IU/ ml (range 25,130-144,310) than the cohort mean of 45,800 IU/ml. 

 

Discussion 

The symptoms and signs of acute compartment syndrome are pain (usually out of proportion to the apparent injury), tense and swollen compartments, pain on passive stretching of the muscles, and paraesthesia, but none of these are constantly present. Pulselessness is not common, or noted only at a later stage.4 The loss of two-point discrimination is a sensitive sign in differentiating compartment syndrome from raised ICP alone.5 

 

Diagnosis of acute compartment syndrome is based on clinical suspicion and repeated examination. There is a role for ICP measurement, but they are recommended only in doutbful cases, the unconscious or obtunded patient, and in children.6 Plasma creatine kinase levels are elevated in presence of muscle death, but there is no consensus as to what CK level constitutes significant muscle necrosis.7 The primary treatment of acute compartment syndrome is early decompressive fasciotomy.8 

 

Conclusion 

The results of our study suggest that: 

1) Raised CK levels are not diagnostic, but they are a useful adjunct in making a diagnosis of compartment syndrome. 

2) CK estimation should be done in all patients with suspected compartment syndrome. 

3) An early fasciotomy has a statistically significant influence in the lowering of elevated CK levels, confirming the view that the earlier the decompression, the lesser the muscle damage. 

4) Patients with greater increase in their CK levels (>75,000IU/ml) are at a greater risk of developing acute renal failure in compartment syndrome. 

 

REFERENCES 

1 McQueen M. Acute compartment syndrome. Acta Chirurgica Belgica 1998; 98(4): 166-70. 

2 Williams PR, Russell ID, Mintowt-Czyz WJ. Compartmental pressure monitoring - current UK orthopaedic practice. Injury 1998; 29:229-32. 

3 Vanholder R, Sever MS, Erek E, Lameire N. Rhabdomyolysis. J Am Soc Nephrology 2000; 11:1553-61. 

4 Rorabeck CH. The treatment of compartment syndromes of the leg. J Bone Joint Surg. 1984; 66(B):93-97. 

5 Gelberman RH, Garfin SR, Hergenroeder PT, Mubarak SJ, Menon J. Compartment syndromes of the forearm: diagnosis and treatment. Clin Orthop 1981; 161:252-61. 

6 Tiwari A, Haq AI, Myint F, Hamilton G. Acute compartment syndromes. Br J Surg. 2002; 89(4): 397-412. 

7 Slater MS, Mullins RJ. Rhabdomyolysis and myoglobinuric failure in trauma and surgical patients. J Am Coll Surg. 1998; 183(6): 693-716. 

8 Lagerstrom CF, Reed RL, Rowlands BJ, Fischer RP. Early fasciotomy for acute clinically evident post-traumatic compartment syndrome. Am J Surg 1989; 158(1):36-39.

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