Forty-eight skeletally mature sheep underwent posterior cruciate ligament reconstruction with free patellar tendon autografts in one knee; the contralateral knee served as a control. Immediate rehabilitation without immobilization followed. Autograft healing was evaluated by histologic, roentgenographic, and biomechanical techniques up to 2 years postoperatively. After implantation, the autograft tissue underwent necrosis and degeneration, followed by a gradual healing process comprising revascularization, cellular migration, and formation of an extracellular matrix. The autograft bone pegs were osseously incorporated by 6 weeks. After an initial loss of strength, the material properties of the operated knee recovered to only about one-third that of the control. Better alignment of the collagen fiber bundles resulted in increased material properties, up to approximately 50% of the control at 52 weeks. After 2 years, the autograft tissue was found to differ structurally and mechanically from a ligament, suggesting that the autograft may never approach normal ligament characteristics. Degenerative alterations, the wide-spread presence of type III collagen, and abnormal accumulations of glycosaminoglycans in the autograft correlated with a maximum stress of 60% and an elastic modulus of 70% of the control. Although ligamentization was not seen, the staging of autograft healing into different phases based on distinct morphologic manifestations (necrosis, revitalization, collagen formation, and remodeling) and correlating with changing mechanical properties may provide a rationale for rehabilitation protocols with a realistic evaluation of the loading capacity of the replacement tissue.

We replaced the posterior cruciate ligament in 30 skeletally mature sheep with a patellar tendon autograft using the central third of the ipsilateral patellar tendon. The healing autograft was compared with the contralateral posterior cruciate ligament and the patellar tendons and posterior cruciate ligaments of nonoperated animals. The collagen fibril diameters were analyzed using transmission electron photomicrographs of fibril cross sections taken at six periods during the 2 years after surgery. The patellar tendon and posterior cruciate ligament were characterized by a broad, nongaussian distribution of collagen fibril diameters. The autografts shifted to a unimodal distribution by an increase of small-diameter collagen fibrils. The frequency of small-diameter fibrils measuring up to 100 nm was 99% after 2 years. At that time, these small-diameter fibrils represented 91.6% of the area covered by collagen fibrils. The mean diameter of the collagen fibrils in the autografts significantly decreased to 45% of the controls at Week 26 and remained at this level until the end of this study. The percentage of area covered by collagen fibrils per 1 micron 2 was 78% of the controls 2 years post-operatively. This study suggests that the patellar tendon autograft could not reproduce the collagen fibril organization of the posterior cruciate ligament. This may be a biologic factor responsible for inconsistent results in posterior cruciate ligament replacement.

A 4-year-old boy broke through the ice of a frozen lake and drowned. The boy was extricated from the icy water by a rescue helicopter that was dispatched shortly after the incident. Although the boy was severely hypothermic, no cardiac response could be induced with field resuscitation measures, including intubation, ventilation, suction, and cardiopulmonary resuscitation.On admission, the primary findings included fixed, nonreacting pupils and asystole. The first core temperature measured was 19.8° C (67.6° F). During active, external warming, the first ventricular beats were observed 20 minutes after admission, and changed 10 minutes later to a sinus rhythm. Continuous monitoring included repeated arterial blood gas and electrolyte tests; prophylaxis for cerebral edema was performed with hyperventilation and administration of sodium Brevimytal and dexamethasone. Seventy minutes after admission, hemodynamics stabilized and the boy was transferred to the pediatric intensive care unit (PICU), where active external warming was continued to raise the core temperature at a rate of 1° C/hour.Adult respiratory distress syndrome developed, and the boy had to be ventilated in the PICU for 10 days. He was discharged home after another two weeks. He recovered fully. The rapid heat loss with the induction of severe hypothermia (<20° C; 68° F) was the main reason for survival in this rare event of a patient with cardiac arrest lasting 88 minutes after accidental hypotherma.

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