Acute compartment syndrome occurs when the pressure in the closed bone-myofascial muscle compartment rises above a critical level, and venous perfusion through the capillaries is blocked, resulting in microcirculation disorders. Tissue ischemia in the compartment causes irreversible damage to the muscles, nerves, and even bones, and can cause functional disorders, muscle contractures, nerve damage, and nonunion. In addition to trauma, phlebitis after injection, pseudoaneurysm due to blood vessel damage, anticoagulants (e.g., warfarin), and exercise are all known causes of acute compartment syndrome. On the other hand, it commonly occurs after a fracture, leading to serious complications if not treated appropriately. Therefore, when a fracture occurs, care must be taken to determine if acute compartment syndrome has occurred, and capillary circulation must be quickly restored through early diagnosis and decompression.
The transverse sacral fracture is rare; however, if it accompanies neurological injury or instability, difficult surgical treatment may be necessary. We performed surgical decompression and laminoplasty in a patient with neurological deficits and anterior displacement of S2 on S1. The patient showed a successful clinical outcome by neurological improvement.
This study reviews a case of sacral fracture with delayed onset neurological deficit that showed good results after decompressive surgery. The delayed neurological deficit appeared at 4 weeks after injury and it was treated with anterior decompression through transperitoneal approach. A 23-year-old woman was injured in a car accident and had bilateral pubic rami fractures and fractures of the sacral ala on the right side. She was treated with external fixation devices for approximately four weeks, but complained of pain and numbness. The dorsiflexion and plantalflexion of the right ankle was weakened and graded as grade 2. Preoperative pelvic and sacral radiographs, computed tomography, magnetic resonance imaging and electromyelography, and nerve conduction study were performed to identify the region of neurological deficit, and we decided to implement neurological decompression. By transperitoneal approach, we performed bone curratage and decompression around the region of sacral alar slope and S1 foramen. The pain and numbness of the right foot cleared up. Dorsiflexion and plantalflexion of the right ankle improved to grade 5. Anterior decompression by transperitoneal approach proved to bring satisfactory results in a patient, who presented delayed neurological deficit after sacral fracture.
Late-onset progressive myelopathy, years after odontoid fracture, is considered a rarity. Undiagnosed or untreated odontoid fractures may develop into nonunion or malunion, thereby leading to secondary delayed cervical myelopathy. We present a case of a 50-year-old man with malunion of odontoid fracture. We had a good result following one-staged posterior decompression and occipito-cervical fusion.
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Surgical Management of Type II Odontoid Fractures in a Resource-Limited Setting: A Case Series Ntsambi Glennie, Israël A Maoneo, Kisubi Michel, Chérubin Tshiunza, Antoine Beltchika Cureus.2024;[Epub] CrossRef