The proximal humerus is the third most common site for primary sarcoma of bone. Since the 1970’s the treatment of primary bone sarcoma has changed from amputation to limb salvage. This has been due to advances in chemotherapy, imaging and surgical techniques. The literature has shown that the survival after limb salvage is similar to that of amputation. The optimum method of reconstruction of the shoulder remains controversial. The aim of our study was to review the cases of primary bone sarcoma of the proximal humerus treated at Middlemore Hospital.

The New Zealand Bone Tumour Registry was searched for all lesions of the proximal humerus, with the diagnosis of chondrosarcoma, Ewing’s sarcoma or osteosarcoma. These records were reviewed for presentation status, biopsy, and type of reconstruct ion, chemotherapy, complications and recurrence. Outcomes measured in months of disease free survival and overall survival.

The Bone Tumour Registry identified 29 patients who were treated at Middlemore Hospital with the primary diagnosis of Ewing’s sarcoma, chondrosarcoma or osteosarcoma of the proximal humerus. Results were available for 26 of the 29 patients (90% follow-up). Of these 29 patients six had chondrosarcoma, four Ewing’s sarcoma and 19 osteosarcoma. The patients with chondrosarcoma had an average age of 50 years. three patients were treated with endoprosthesis (mean survival 48 months) and one with vascularised fibula reconstruction (status 27 months ANED). Of the four patients with Ewing’s sarcoma, two had surgical reconstruction, one with intercalary allograft reconstruction (status 96 months ANED) and one with endoprosthesis (status 84 months ANED). The 19 patients with osteosarcoma had an average age 27 years, 15 patients were treated surgically. Three had endoprosthetic reconstruction (mean survival 29 months), two allograft prosthetic composite reconstruction (mean survival 23 months), three vascularised fibula reconstruction (mean survival 217 months), one total shoulder replacement and proximal humeral autograft (status 68 months ANED), one hemiarthroplasty (status 21 months DOD) and one proximal humeral allograft (status 31 months ANED). 4 patients were treated with primary amputation (mean survival 55.25 months).

The mean overall survival for limb salvage surgery in our institution is 74 months compared to 55.25 months for amputation; this is consistent with the published literature. Function of a salvaged upper limb is superior to amputation. A salvaged limb is socially and emotionally more acceptable for patients than amputation. Limb salvage remains the priority in the treatment of primary bone tumours of the proximal humerus.

Elevated intracompartmental pressure (ICP) results in tissue damage due to impaired microcirculatory function. The nature of microcirculatory impairment in elevated ICP is not well understood. This study was designed to measure the effects of increased ICP on skeletal muscle microcirculation, inflammation and cell viability using intravital videomicroscopy.

Twenty adult male Wistar rats were randomised to four groups: the control group (control) had no intervention; while three experimental groups had elevated ICP maintained for fifteen (15m), 45 (45m), or ninety (90m) minutes. Compartment pressure was continuously monitored and controlled between 30¡V40mmHg in the posterior hindlimb using saline infusion into the anterior hindlimb. Mean arterial pressure was maintained between 80 and 120mmHg. Fasciotomy was then performed and the Extensor Digitorum Longus muscle studied using intravital videomicroscopy. Perfusion was measured by comparing the numbers of continuous, intermittent, and nonperfused capillaries. Inflammation was measured by counting the number of activated (rolling and adherent) leukocytes in post-capillary venules. Muscle cellular Injury was measured using fluorescent vital staining of injured cell nuclei.

Perfusion: The number of continuously perfused capillaries decreased from 77 ± 3/mm (control) to 46 ± 10/mm (15m),40±10/mm(45m)and27±8/mm(90m)(p< 0.05). Non-perfused capillaries increased from 13 ± 1 (control) to 16 ± 4 (15m), 30 ± 7 (45m), and 39 ± 5 (90m) (p< 0.05). Inflammation: Activated leukocytes increased from 3.6 ± 0.7/(100ƒÝ)2 (control) to 5.9 ± 1.3 (15m), 8.6 ± 1.8 (45m), and 10.9 ± 3.0/(100ƒÝ)2 (90m) (p< 0.01). Injury: The proportion of injured cells increased from 5 ± 2 % in the control group to 12 ± 3 (15m), 16 ± 7 (45m) and 20 ± 3 % (90m) (p< 0.05).

As little as fifteen minutes of 30mmHg ICP caused irreversible muscle damage and microvascular dysfunction. With increased duration, further decreases in capillary perfusion and increases in injury are noted. A severe inflammatory response accompanies elevated ICP. The role of inflammation in compartment syndrome is unknown, but may contribute to cell injury and reduced capillary perfusion.