Abstract
Compartment syndrome complicating a ruptured Achilles tendon has previously been reported in a surgically treated patient. However – to our knowledge – this is the first report of compartment syndrome following conservative treatment. A 45-year-old man ruptured his Achilles tendon and elected to have treatment in an equinus cast. Three weeks later, he developed compartment syndrome and despite fasciotomy, required surgical debridement of his anterior compartment. Delay in both diagnosis and subsequent fasciotomy resulted in a poor outcome. Any suspicion of compartment syndrome mandates early compartmental pressure monitoring. The exact aetiology is uncertain but we speculate that the equinus position of his ankle combined with weight-bearing, was a major contributing factor.
Introduction
Compartment syndrome occurs when the compartmental pressure in a fascial compartment exceeds the capillary pressure. This leads to hypoperfusion of intracompartmental tissues and if untreated, causes irreversible damage. There are a number of aetiologies that can be broadly classified as extrinsic (tight bandages and cast, eshar following burns, traction, etc.) and intrinsic (bleeding, swelling, fracture). This case was unusual – to our knowledge, compartment syndrome has not been described in a ruptured Achilles tendon treated in equinus cast.
Case presentation
History, clinical features and investigations
An otherwise healthy 45-year-old Caucasian man of heavy athletic build (120 kg) presented with anterior compartment syndrome, three weeks following non-operative management of his Achilles tendon rupture.
Three weeks previously he had tripped over a tree root while running, heard a ‘tear’ and felt ‘as though he had been kicked in the back of his calf. He could not weight-bear. An ultrasound confirmed the clinical impression of a complete tear of the left Achilles tendon. The patient was counselled as to treatment options and elected to proceed with a non-operative regimen. This entailed a week in a non-weight-bearing equinus cast, followed by six weeks in weight-bearing casts with fortnightly cast changes, the ankle being progressively dorsiflexed from equinus at each application. A further three weeks in a moonboot with heel raises was anticipated. The equinus cast was checked the following day.
Fourteen days after the initial injury (1 week into his weight-bearing cast), the patient presented as the rubber base at the bottom of his cast had worn through exposing the metal beneath. The rubber foot was replaced.
At 18 days, the patient presented with intense pain around the left ankle. His toes were well perfused, the dorsalis pedis pulse was present and capillary refill was less than two seconds. The cast was bivalved. Although there was no calf or shin tenderness, the anterior aspect of the ankle was bruised and tender.
Twenty days after the initial injury, the patient complained of intense and increasing ankle pain, scoring 8/10 on a visual analogue score. He had woken at 02:00 with a severe burning sensation on the dorsum of his foot and the anterior aspect of his lower leg. He reported shooting pains up the lateral side of the knee and that his first webspace had become numb. There was no history of excessive walking or consumption of alcohol during the previous 24 hours. The cast was again bivalved. There was bruising on the anterior aspect of the limb but the limb was not tender.
The patient was sent home with a Plaster of Paris backslab in equinus and instructed to stay non-weight-bearing. However, he returned to hospital on the same day (18 hours post onset of this pain) as the pain was not resolving. The back slab was removed and the leg was elevated. There was increased heat and erythema over the dorsum of his foot and the anterolateral aspect of his lower leg. This area was tender to touch and the distal end of his anterior compartment felt tight. Power (MRC grade) was 1/5 (hallux dorsiflexion), 4/5 (lesser toe dorsiflexion), 5/5 (tibialis anterior) and 5/5 (peroneii). He had comfortable passive range of motion of his toes. Coagulation profile on admission was activated partial thromboplastin time 28 seconds, international normalized ratio 1.1, fibrinogen assay of 4.3 g/L. The admitting doctors considered a diagnosis of compartment syndrome unlikely because of (i) the long time period (3 weeks) from initial injury (tendon rupture) to presentation, (ii) his anterior compartment feeling soft and (iii) the absence of pain on passive stretching of his toes. The patient was admitted for pain management and observation with a working diagnosis of neurapraxia secondary to cast impingement at the fibula neck.
Subsequently (30 hours after initial pain and 12 hours since admission to hospital), power of lesser toe extension was reduced to 3/5, power of ankle dorsiflexion (tibialis anterior) was reduced to 3/5 with 0/5 for hallux dorsiflexion. He had slight discomfort of passive range of motion of his ankle. The dorsum of the left foot was tender. The anterior compartment felt tense in the mid to lower portion. The anterior compartment pressure measured 110 mmHg with a diastolic blood pressure of 80 mmHg. A diagnosis of compartment syndrome was made.
Operative findings and outcome
The patient underwent four-compartment fasciotomy and application of an external fixator to maintain equinus.
A longitudinal lateral incision halfway between the lateral tibial crest and the fibula revealed tibialis anterior, extensor hallucis longus and extensor digitorum to be grey and dusky around the centre of the muscle bellies extending distally. However, the peronei were healthy, pink and contractile. The muscles of the anterior compartment improved in colour, and regained some sluggish contractility. The skin edges were approximated with a bootstrap suture. An external fixator was applied to anterior tibia and first metatarsal (Figure 1).
Debridement of necrotic anterior compartment with external fixator in place
The day after surgery, the patient reported feeling ‘100% better’ and felt no further pain. However, on further inspection (4 days later) his anterior compartment was largely necrotic and he underwent two debridements with subsequent skin closure. His external fixator was removed at six weeks. His Achilles tendon is intact, but he has a completely deficient anterior compartment. He is currently mobilizing with an ankle foot orthosis.
Discussion
Compartment syndrome develops when intracompartmental pressure within a fascial compartment exceeds the capillary pressure. Perfusion of intracompartmental structures is progressively compromised, eventually leading to necrosis. This pathophysiological process can potentially be resolved in its early phases by the timely incision of surrounding fascia, thereby relieving the compartment pressure and restoring capillary blood flow. 1
The aetiology of compartment syndrome can be broadly classified into extrinsic (tight splints cast, lithotomy position, tight ski boots) and intrinsic (haemorrhage, swelling, fracture.) The mainstay of diagnosis is based around an understanding of the aetiology, pathophysiology and clinical features of pain (out of proportion to clinical scenario; also on passive stretch), paraesthesia, pallor and paralysis. 2
Ulmer 3 examined these features identifying four prospective papers and concluded that they had low sensitivity and positive predicted value but a high specificity and negative predictive value. In our case, the characteristics of pain, paraesthesia and paresis were present. Unfortunately the assessing doctors attributed his symptoms to a proximal peroneal neurapraxia. The absence of pain on passive stretch was held to decrease the possibility of compartment syndrome.
McQueen and Court-Brown 4 monitored 116 consecutive patients with tibial fractures and used a pressure difference of less than 30 mmHg between comp artmental pressure and diastolic blood pressure as an indication for fasciotomy. In that series, one patient underwent a fasciotomy without clinical signs of a compartment syndrome, but operative findings clearly showed the presence of an early compartment syndrome. This indicates that compartment syndrome may occur with a paucity of clinical signs. Compartment monitoring in suspicious scenarios is therefore a potentially limb-saving manoeuvre allowing earlier diagnosis and fasciotomy.
Reed and Hiemstra 5 reported a case of anterior compartment syndrome in a surgically treated Achilles tendon rupture, 57 hours following surgery. In our case the aetiology is uncertain but having excluded bleeding disorders, anticoagulative drugs and bone trauma, we speculate that weight-bearing in a walking cast was responsible. Weiner et al. 6 established the relationship between compartmental pressure and ankle position, and showed a three to sevenfold increase in pressure for both anterior and posterior compartments when plantar flexing the ankle to beyond 37°. Also weight-bearing in an equinus cast could potentially cause the leg to slide down the conical plaster tube.
Conclusion
There are two learning points – firstly, any suspicion (even in the absence of certain objective features) of compartment syndrome mandates prompt further investigation with early intracompartmental pressure monitoring. Secondly, that compartment syndrome can develop in the context of a weight-bearing equinus cast.