Disruption of the anterior cruciate ligament characteristically produces marked joint swelling. The ligament is extrasynovial and intracapsular and has a rich blood supply. As the ligament was torn it ruptured into the joint. Blood from the tear irritates the synovial membrane and also enters the joint. These factors produce gradual swelling of the joint over the ensuing hours with significant fluid accumulation in the joint cavity.
The patient had a surgical reconstruction of the anterior cruciate ligament.
It is difficult to find a man-made substance that can act in the same way as the anterior cruciate ligament and demonstrate the same physical properties. Surgeons have devised ingenious ways of reconstructing the anterior cruciate ligament. Two of the commonest methods use the patellar ligament (tendon) and hamstrings to reconstruct the ligament.
The patient had further surgical procedures.
The tibial collateral ligament was explored and resutured. Using arthroscopic techniques, the tear in the medial meniscus was débrided to prevent further complications.
A 45-year-old man with diabetes mellitus visited his nurse because he had an ulcer on his foot that was not healing despite daily dressings.
Diabetes can lead to vascular disease of large and medium arteries, narrowing the lumen and reducing blood supply to the extremities, thereby impairing healing. In addition, diabetes can also affect blood supply to nerves, which leads to peripheral neuropathy. Peripheral neuropathy results in reduced sensation, and therefore minor injuries can often go unnoticed.
This patient has developed an ulcer on his heel, which is a pressure point and likely to be under repeated strain. The nurse examined the ulcer and found that the ulcer was looking infected with pus at the base of the ulcer and asked for a specialist orthopedic opinion, who requested an x-ray and an MRI. The MRI and x-ray both demonstrated infection invading into the calcaneus with destruction of the bone (Fig. 6.141A,B).
The patient required surgical washout with removal of the dead and infected bone (debridement) and was given long-term antibiotic treatment (Fig. 6.141C).
A young woman came to a vascular surgeon with a series of large dilated tortuous veins in her right leg. The rest of her leg was otherwise unremarkable.
A diagnosis of varicose veins was made and the surgeon needed to determine the site of valvular incompetence.
There are typical points where incompetent valves occur between the superficial and the deep veins. In these regions the varicosities tend to become marked. The typical sites are: at the saphena varix—the saphenofemoral junction where the femoral vein is joined by the great saphenous vein; in the midthigh perforating vein between the great saphenous vein and the femoral vein; in the calf the three sites where perforators occur, 5, 10, and 15 cm above the medial malleolus between the great saphenous vein and the deep veins of the calf; and at the junction of the small saphenous vein and the popliteal vein.
The surgeon asked the patient to lie supine on the bed and elevated the leg. A tourniquet was placed around the upper thigh below the saphenofemoral junction and the patient was asked to stand up. No veins were demonstrated filling on the medial aspect of the thigh and lower limb.
The effect of the tourniquet is to compress the great saphenous vein while permitting blood to flow in the deep venous system of the femoral vein and the deep femoral vein.
Because there was no filling of the medial varicose veins below the level of the tourniquet, the surgeon assumed that the valve at the saphenofemoral junction was incompetent and would require surgical treatment.
However, during the tourniquet maneuver the surgeon also noted some veins around the posterior and posterolateral aspect of the calf.