The vascular aspects of head injuries / Hugh Cairns.

  • Hugh Cairns
Date:
1942
Catalogue details

Licence: Public Domain Mark

Credit: The vascular aspects of head injuries / Hugh Cairns. Source: Wellcome Collection.

    6/40 page 378
    I — TRAUMATIC OBSTRUCTION OF THE INTERNAL CAROTID ARTERY BY THROMBOSIS OR EMBOLISM PRO¬ DUCING DELAYED HEMIPLEGIA CASE I. L. J. E., a pilot of 23, crash-landed his plane after engine failure on the afternoon of May 16, 1941. He remembers landing and going through a hedge, but was unconscious for probably two or three minutes. The next thing he remembers was being carried away from the burning aircraft and being taken to hospital. On arrival there he recognized the doctor, whom he had known before the accident, and gave a clear account of the accident. Owing to an oedema and lacerations of the neck, his voice was husky, and he had difficulty in swallowing and breathing. He showed the following wounds: (a) Deep laceration 4 cms. long through right eyebrow; bone exposed, (b) Laceration 2 cms, long at the level of the hyoid bone on right side, deep and bleeding freely, (c) Super¬ ficial grazes in the left carotid triangle, (d) Small puncture wound in the left shin. The marked oedema and the inability to swallow were so striking that a tracheotomy set was. prepared (but was not used). The next day, May 17, he had improved, was conversant and coherent, with no abnormal signs in the central nervous system, until suddenly at 10 o’clock that night—about 30 hours after injury — he was heard to ring the bell in the ward and was found in bed, staring before him, with a paralysis of the right side of his face and of his right arm, and he was unable to speak. He could still move his right leg, but it was weak and showed an extensor plantar response. One hour before this he had got out of bed and walked 10 yards to the lavatory. The following morning, May 18, he showed a complete motor and sensory aphasia, wit flaccid paralysis in the right upper limb and a severe weakness of the right lower limb with an extensor plantar reflex. He was alert and was not incontinent, but was still having difficulty in swallowing and could not protrude his tongue. On admission to Hospital on May 19 he was alert and co-operative while being examined, but showed a tendency to relapse into sleep when left alone. The neurological signs were identical with those of the previous day; and in addition there was some impairment of tactile localization on the right side. There was no apraxia. His visual fields appeared full to confrontation. X-ray of the skull was normal. Lumbar puncture showed normal cerebro spinal fluid under normal pressure, with no block on jugular compression. Blood pressure was 120/60 mm. Hg.; pulse rate 72. Op^ratioM.. On May 19, as intracranial haemorrhage was suspected, a burr hole was made over the left temporal region. The subdural space was empty, the brain was soft, of normal colour and under normal tension. Courtsto. His condition remained substantially unchanged apart from the slow march of hypertonus in arm and leg, with no improvement in the aphasia, A week after the accident further tests showed that there
    No text description is available for this image
    No text description is available for this image
    No text description is available for this image