The day after admission, blood analysis was requested with significant haemoglobin values of 10.6 and leukocytes of 13,800, chest X-ray without appreciable changes at the bilateral pleural parenchymal level and a normal abdominal ultrasound. The patient's limbs were moving and lab tests, chest X-ray and abdominal ultrasound were pending. In the abdomen, haematoma and excoriation on the right flank wall was observed. Normal breath sounds anteriorly, no crepitations. The patient was complaining, with multiple haematomas in the facial region. The patient was admitted here with a blood pressure of 68/40 mmHg, O 2 saturation of 100% and heart rate of 89 bpm. No free intraperitoneal fluid or presence of ectopic air was observed.Īfter suturing the head and face injuries, the patient was moved to the observation area of the emergency department to receive analgesic treatment and assess progress. Haematoma of anterior abdominal wall in right hemiabdomen was observed. No dilated intestinal loops were observed. Hypodense image seen in the inferior pole in the spleen interpreted as respiratory motion artefact. Liver, pancreas, kidneys and adrenal glands normal. Fracture of costal arches 10 and 11 of the right hemithorax. Heart, pericardium and thoracic aorta without significant changes. Thoracoabdominal CT scan with intravenous contrast medium: lung parenchyma with areas of increased attenuation of predominance in both lung bases with respiratory movement. Nasal bone fracture.Ĭervical CT scan: no vertebral alignment disruption. No focal neurologic deficit.īlood and urine analysis and coagulation study: no significant abnormalities.Ĭranial CT scan with emergency intravenous contrast medium administration: no evidence of foci of intracranial haemorrhage or midline shift. Pain on palpation in right inferior costal cartilage.Ībdominal auscultation: soft abdomen, depressible, erosion in abdominal wall at right flank level with haematoma in said area of approximately 7 × 9 cm in diameter. Lung auscultation: good ventilation in all lung regions. Infranasal and upper lip lacerated contused wounds with loss of teeth in upper jaw. Nasal bone crepitus, periorbital haematoma in right eye and right forehead. The general examination revealed blood pressure of 56/33 mmHg, afebrile, conscious, reactive, agitated, nauseous, O 2 saturation of 94%. Lacerated contused wound in superior maxillary region that communicates with oral cavity with loss of teeth. On arrival at the hospital emergency department, the patient was conscious and presented with a lacerated contused wound to the scalp of approximately 4 cm without skull depression. Clinical, radiological and autopsy data have been analysed and related literature reviewed, with the objective of considering the clinical and medico-legal issues posed by the possible coexistence of these 3 diseases.Īs far as we know, no association between KFS and DS has been described in the literature. In this paper, we present a case of associated vertebral synostosis, DS and traumatic cervical myelopathy (Schneider syndrome). This may present as primary or secondary injury, and is not always identified by routine tests. 4–6 This spinal cord injury may, in the cervical region, constitute Schneider syndrome.ĭown's syndrome (DS) may predispose the development of degenerative cervical myelopathy, 7–9 with the changes increasing with age.īeing 2 conditions that independently tend towards degenerative or traumatic myelopathy, the association between cervical synostosis and DS may involve a high risk of neurologic injury, even in the face of minor trauma. 3 It is known that the existence of vertebral synostosis between 2 or more spinal mobile segments promotes spinal cord injury over the course of a hyperextension, this greater propensity being attributed to adjacent hypermobile block segments. Later on, radiological requirements were added, with the main characteristic being the presence of congenital block vertebrae in the cervical spine. 2 Initially, the diagnostic criteria were clinical (short, stiff neck, and low posterior hairline). Klippel–Feil syndrome (KFS) was described by these two authors in 1912. In the original description, it was attributed to an anterior medullary contusion due to a herniated disc or other causes after a trauma. 1 The typical presentation is that of a greater neurologic deficit in the upper limbs compared to the lower ones. Central post-contusive myelopathy or Schneider syndrome was first described in 1954.
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