Compartment Syndrome is a serious but rarely reported condition in dogs and is typically ascribed to intra-compartmental haemorrhage or neoplasia. This article describes the presentation of a dog with Compartment Syndrome secondary to bacterial cellulitis/fasciitis, a recognised but unusual cause of Compartment Syndrome in humans.
A ‘compartment’ is a section within the body that is surrounded by fascia and contains muscles and nerves. In the case of the limbs there are two segments, each containing an anterior and a posterior compartment (Figure 1). These are formed by tough connective tissue septa and, in most cases, have a distinct nerve and blood vessel supplying the local musculature. Because the fascia layer does not stretch, a small amount of bleeding into the compartment, or swelling of the muscles within the compartment, can cause profound pressure increases leading to ‘Compartment Syndrome’.
Acute Compartment Syndrome
This usually occurs following traumatic injury. Well-recognised causes include limb fractures, crush injury, ischemic reperfusion, haemorrhage, vascular puncture/intravenous drug injection, prolonged limb compression (e.g. casting) and burns. Sepsis, cellulitis, and necrotising fasciitis are rarely described causes of Compartment Syndrome. The inciting insult causes an acute, marked increase in pressure within the compartment resulting in insufficient blood supply to muscles and nerves. Acute Compartment Syndrome is generally classed as a medical emergency that requires surgical correction (fasciotomy).
If untreated, the lack of blood supply often leads to permanent loss of limb function resulting from irreversible muscle and nerve damage. Rhabdomyolysis and subsequent renal failure are also possible complications.
Chronic Compartment Syndrome
This is often an exercise-induced condition. Pressure within the muscles increases to extreme levels during exercise creating a reduction in blood flow. The venules and lymphatic vessels that drain the muscle compartments are subsequently compressed while arterial inflow continues, further compounding the pressure build up. This eventually results in tissue ischaemia and oedema formation.
Chronic Compartment Syndrome is usually not a medical emergency, but the loss of circulation can cause temporary or permanent damage to nearby nerves and muscles.
Diagnosis and Treatment
The first clinical sign is invariably pain, followed later by the development of swelling, bruising, congestion and impaired limb function. Pulse quality is only affected if the relevant artery is contained within the affected compartment. Although direct measurement of compartmental pressure is a relatively straightforward procedure, the diagnosis in humans is most commonly made on clinical grounds (i.e. appropriate history and clinical signs). Surgical fascietomy is the most effective treatment.
Incisions are made in the affected muscle compartments resulting in decompression which relieves pressure on the venules and lymphatic vessels, thus increasing blood flow throughout the muscle. In the case of chronic Compartment Syndrome, conservative management using rest and anti-inflammatories can be considered.
Systemic hypotension and application of external pressure to the affected area (e.g. splints, casts, tight wound dressings) should be avoided as this decreases perfusion pressure to the compartment. Similarly, elevation of the affected limb is contraindicated since this leads to reduced vascular perfusion. Ideally, the affected limb should be positioned at the level of the heart. Supplemental oxygen helps to optimise tissue and neural oxygenation.
History and clinical signs
A seven-year-old, male entire Dogue de Bordeaux was referred to Pride Veterinary Centre for further investigation of acute onset right hind limb swelling. Right hind limb lameness had first been noted four days prior to referral with rapid progression and subsequent development of neurological deficits (knuckling). By the time of referral, the dog had also developed lethargy, anorexia and pyrexia. Staged bilateral tibial plateau leveling osteotomy (TPLO) had been performed eighteen months earlier but there had been no ongoing orthopaedic concerns since that time.
On presentation, the dog was quiet, subdued and in slightly excessive body condition (body weight 67.9kg, body condition score 6/9). Mild tachycardia and tachypnoea were identified and ongoing pyrexia was confirmed (rectal temperature 40o C). Pulse quality was generally good but could not be assessed in the right hind limb due to profound swelling. A very large, ill-defined, firm swelling was present over the right lateral thigh and pelvic area with marked generalised oedema spreading distally and affecting the whole limb. The limb was flaccid and non-weight bearing with absent proprioception and marked reduction in withdrawal strength. Only mild to moderate discomfort was apparent on palpation but this was difficult to interpret in light of the dog’s stoic character.
Haematology revealed moderate mature neutrophilia (24.28x109/l, ref: 2.95-11.64) and lymphopenia (0.27x109/l, ref: 1.05-5.10) consistent with a stress/inflammatory leukogram.
The only serum biochemical abnormalities were creatine kinase and aspartate aminotransferase elevations, the magnitude of which was surprisingly mild given the degree of soft tissue damage.
The salient findings on CT imaging were as follows:
Marked diffuse thickening and increased attenuation of the subcutaneous tissue of the right hind limb extending from the pelvic area to the toes. This was particularly marked around the tarsus and distal tibia and along the lateral and ventral aspects of the thigh (Figure 2a, 2b and 2c).
Large non-enhancing fluid attenuating pockets between the muscles of the right thigh, especially laterally between the biceps femoris and vastus lateralis muscles, and caudally between the semitendinosus/semimembranosus and adductor muscles. A smaller similar fluid pocket was present in between the tibialis cranialis and the long digital extensor muscles along the laterocranial aspect of the right tibia (Figure 2d).
Marked right-sided medial iliac (~ 2.3 x 2.7cm vs R ~ 0.8 x 1.6cm) and popliteal (~2.3 x 1.6cm and 1.5 x 1cm vs. R ~ 1.3 x 0.8cm) and moderate right-sided internal iliac (~0.8 x 1.2cm), external iliac (~1.2 x 1.9cm) and superficial inguinal (~ 1.7 x 1.3cm and 1.1 x 2.7cm) lymph node enlargement (Figure 2e and 2f).
Mild articular/peri-articular soft tissue thickening with mild stifle joint effusion on the left and marked articular/periarticular soft tissue thickening with moderate to marked femoropatellar effusion on the right (Figure 2g).
Additional incidental findings were the presence of metallic surgical implants bilaterally (along the cranial and medial aspects of the tibiae), marked peri-articular new bone formation surrounding the stifles bilaterally (more marked on the right), bilateral coxo-femoral osteoarthritic changes (likely secondary to hip dysplasia), mild right talo-calcaneal osteoarthritic changes and moderate symmetrical and smoothly marginated prostatomegally (consistent with benign hyperplasia).
In conclusion, the imaging findings were consistent with severe right hind limb Compartment Syndrome (involving mainly the thigh and to a lesser extent the craniolateral aspect of the tibia) with severe secondary right hind limb edema (as a result of cellulitis and/or subcutaneous bruising). The right stifle effusion/synovial thickening was potentially consistent with post-operative change, but an infectious process involving the right stifle joint could not be excluded.
Cytology of synovial fluid aspirated from the right stifle joint revealed marked neutrophilic inflammation with degenerative changes. Aspiration of the intramuscular fluid pockets yielded a large volume of serosanguinous fluid, cytology of which also identified marked degenerative neutrophilic inflammation. Cytology of fine needle aspirates taken from the enlarged popliteal lymph node revealed mild lymphoid reactivity and neutrophilic lymphadenitis. No bacteria were identified within the synovial or intramuscular fluids but culture of both these samples yielded a growth of Beta haemolytic Streptococcus group G sensitivity testing of which identified resistance to Marbofloxacin.
Compartment Syndrome secondary to bacterial cellulitis/fasciitis
Given the severity of the CT changes and loss of neuromuscular function, the prognosis for complete recovery was felt to be Compartment Syndrome secondary to bacterial cellulitis/fascitis and, since clinical improvement ensued, this was continued. Prior to receiving the culture results, the dog was treated with broad spectrum intravenous antibiotics, analgesia and anti-inflammatories.
Augmentin and enrofloxacin were chosen in an attempt to provide reasonable gram positive, gram negative and anaerobic bacterial cover along with good tissue penetration. Despite the lack of marked aversion to palpation and manipulation, significant limb pain was highly likely so multiple modal analgesia (methadone and lidocaine) together with non-steroidal anti-inflammatory therapy (meloxicam) was used. Intravenous fluid therapy was continued to maintain adequate hydration and thus optimise tissue perfusion.
Within a couple of days, the dog was much brighter with an improved appetite and normal rectal temperature.
Cautious attempts to weight bear on the right hind limb were being made but marked neurological deficits were ongoing. Medical treatment was continued along with physiotherapy and enrofloxacin was discontinued once the culture results were available. Despite our initial pessimism, the clinical signs continued to improve and the dog was discharged a week later with ongoing oral medications (amoxicillin clavulanate, meloxicam and gabapentin). The swelling and oedema continued to resolve and, over the ensuing weeks, neurological function was eventually restored. The dog went on to make a full recovery and maintains a good quality of life with no long-term complications.
Compartment Syndrome is rarely diagnosed in dogs but should be considered as a potential differential in patients with acute onset limb pain, swelling and oedema. As in humans, surgical intervention is generally required and this is likely to be the case in patients presenting acutely post trauma. On the other hand, the case presented here illustrates the potential for a good outcome following conservative management in selected patients.