Statement regarding the death of Brian Murphy 21st April 2006
On the above date, a consultation regarding the death of Brian Murphy (PM 31/08/2000) took place at the Office of the State Pathologist. During this I was given the following material:
1 Booklet of postmortem photographs
2 Synopsis of the information Professor Harbison was given prior to carrying out the postmortem
3 The result of the toxicology on the deceased
4 The histology result on the lungs
5 That the general evidence was that the deceased was involved in a fracas in which he was kicked and punched
6 The contents of the statements of Dr. Sheridan, Dr. Hussein and Karl Twomey who are witnesses in the case Interpretation of the above
The photographs were of a young man. There were injuries to his face, left knee and back.
There was a laceration (skin split) at the point of his chin and bruising and lacerations of his lips associate with fracture of his upper front teeth. The other injuries were surfaces grazes only. Internal photographs of the head and neck showed bruising around the right eye socket and on the chin. The skull was not fractured and there was no evidence of bleeding into the skull cavity.
In my opinion, these injuries were relatively minor, the most significant were to the chin and mouth and these could have been caused by kicks to the face. These injuries would not normally be expected to cause or even contribute to death.
Death following a head injury most commonly results from severe trauma to the brain or related complications, usually bleeding inside the skull cavity which compresses the brain and its vital centres. There was no evidence from the photographs to suggest that such pathology was responsible for death.
In the absence of the above, the following have to be considered in this particular case:
1 Brain swelling
2 Alcohol-induced apnoea
3 Blood inhalation
4 Underlying natural disease, most likely a cardiac complaint
1 Brain swelling, or cerebral oedema, may complicate even minor head trauma in younger individuals, particularly children and teenagers. Its incidence decreases rapidly thereafter. This is unpredictable and may occur rapidly or, in some instances, may follow a short delay. It can cause a rapid deterioration in conscious level.
2 It is now recognised that alcohol can have a detrimental effect on the outcome following even a relatively minor head injury. Trauma to the brain may cause temporary 'concussion' and a short period, at most a few seconds, of apnoea (stopping of breathing). Alcohol has a depressant effect on the brain and at levels over 100mg in blood has been shown to lengthen the period of apnoea, resulting in cessation of respiration and therefore hypoxic (lack of oxygen) brain damage.
If breathing does not recover, death follows. Even if breathing commences after a delay of a few minutes, the brain may already be irrecoverably damaged.
The information given to me was that he was not breathing when the ambulance men arrived and therefore 'alcohol-induced aponea' is a likely cause for the sudden deterioration in this man's state.
3 Blood inhalation is a recognised complication following head injuries, if the injured party is rendered unconscious and has injuries bleeding into the mouth or back of throat. Blood can obstruct the airways causing hypoxia and death. Histological sections of lung showed some intra-alveolar haemorrhage, but the doctor intubating in Accident and Emergency did not see any airway obstruction. This suggests that any blood inhalation was of a minor degree and was not responsible for his unconscious state or his death.
4 As I did not conduct the postmortem examination on this young man and as I have not been given access to Professor Harbison's report, I can neither confirm or refute the presence of any cardiac disease which could have caused or contributed to this young man's death.
IN SUMMARY: This young man died after an assault. The injuries he received were relatively minor and would not be expected to cause his death. It is most likely that his head injury was complicated by alcohol-induced apnoea and acute brain swelling, resulting in hypoxia/ischaemic brain injury and death.