1. The cause of and nature of the injury.
2. The presence of other injuries and their effects
3. The outcome
4. To review the post mortem or similar fndings
A) To clearly delineate the nature of the intracranial injury.
B) To determine if there were errors in the treatment.
C) To see if there were other ways in which our treatment of head injuries could be improved. During the fifteen month period 371 patients were admitted under our care. There were 269 adult males and 46 females, and 36 boys and 20 girls of 12 years and under. None the less the age distribution (apart from the group 21-30 was remarkably uniform). (Table 1).
Road traffic accidents constitued the major incidence. (Table 2):
Admission policy at the Parireyatwa Hospital decrees that head injuries take priority so that a considerable number of patients with other injuries as well as those of the head are brought into our ward. (Table 3):
|Districution of injuries||Admitted||Died|
|Head Injury Only||213(62%)||27(11%)|
|Head and Upper Limb||29(8%)||4(13%)|
|Head and Lower Limb||24(6%)||3(12%)|
|Head and Thorax||12(3%)||3(24%)|
|Head and Abdomen||3(1%)||2(66%)|
|Head and Multiple Injuries||72(18%)||11(15%)|
These figures are not strictly comparable except to suggest that the chances of dying are slightly greater for those with other injuries that with a head injury only, and for those with a head injury it is just over 10% understandably multiple injuries were commonest in the R.T.A. Group.
The patients were classified according to their Glasgow coma scores which were estimated soon after admission to the ward or Casualty Department and it was frequently impossible to determine exactly how long, post injury this was, patients transferred frrom outside the town had the Coma Score assessed by the referring doctor before their departure. The coma score was measured out of 14 and the patients were divided into three groups on that basis. (Table 4):
|Coma Score||Total Number||Died||Mortality|
|Group I (3-6)||75||35||46.6%|
|Group II (7-10)||79||10||12.6%|
|Group III (11-14)||217||5||2.2%|
As would be expected the mortality was highest in the low coma score and lowest in the high coma score groups. Now 1 hope you will agree that any patient who comes into hospital alive but subsequently demises lias been failed by us as medical science. It is true that at current state of our knowledge we may not have the "know how" to avert death but none the less the patients death represents a failure by us as medical scientists, of equal, if not greater significance, is the question as to whether we are missing any lesions which, in the light of our current knowledge, we could have cured. It is very important therefore that we look closely at the postmortem and other diagnostic findings in an effort to see if we failed and patients in one way or another and to see what other problems there are.
50 patients died overall. 36 of these were the subject of post mortem examination and 5 others had a clear definition of their intracranial status by CT Scanning. Nine patients had neither CT Scan nor autopsy but seven of these had been admitted deeply unconscious and died 48 hours without improvement, so I think we have a fair idea what was going out there.
In group I, where 35 out of 75 patients died, there were three interesting cases:- The patients had normal scans yet they died after four and 21 days, in the third case at autopsy there was only subarachnoid heamorrhage and a very small subdural blood collection and it was difficult to see why these three patients died.
In group II where 10 out of 79 patients died one showed a mild diffuse brain swelling but nothing else, while a second showed small occipital haemorrhage, a small subdural haemorrhage and extensive cerebral oedema. Another patient showed a severe bronchopneumonia with only minor brain change. A fourth patient, a 25 year old male suffered a fractured tibia and fibula as well as a head injury, his conscious level dropped from 14/4 to 9/14 after reduction of the fracture. A Clinical diagnosis of fat embolism was made - post mortem examination confirmed the diagnosis.
Five patients out of 217 died in group III (2.2%) and in some ways these are the most interesting because at admission they all had scores above 11 /14. A young man was admitted following a mine injury in which he temporarily lost consciousness. There was a linear fracture of the frontal region, he died suddenly the following morning and post mortem showed an epidural hematoma. A second case had a pnemothorax, fracture of the long bones and a bilateral subdural effusion all of which were treated. He died suddenly and the pathologist gave the cause of the death as cardiac tamponade. Two patients had diffuse injuries and one died without a post mortem.
Three problems seem to arise from this:
1) Failure to recognise potentially curable lesions.
2) Inadequate care of the patients overall condition.
3) Patients who die intracranial death with little to show for it.
(1) Epidural haematoma, provided it follows the classical pattern is very curable if intervention occurs in time. How can this be facilitated? It is clear that simple clinical observation is inadequate in some cases, where there is easy access to a CT Scanner there should be no problem but where there is not some easier and cheaper method must be employed. Early Angiography is one possibly but it needs a reasonable set up and it is invasive. Basically what is needed is a non invasive, non damaging, easily applied test will show the position of the midline of the brain relative to the centre of the skull - where the midline is centrally placed we can be sure there is no surgical lesion. 1 am suggesting that we try to revamp ultrasound scanning which proved it- self most valuable in the past. There was an instrument called the "Midline" which anyone could use and which could accurately locate the midline structures without difficulty or danger. We used it for many years - unfortunately no one in the northern hemispheres makes it now - though I have tried hard to get one made no one will do so because the first world does not want it. I believe that a cheap reliable model could help us tremendously in the third world. One of these machines in each District Hospital could help the resident doctor to decide whether urgent transfer is necessary.
(2) The second point reveals a different aspect of head injury care - that of care of the airway. When I first came into neurosurgery the importance of airway clearance was not appreciated and I have seen patient literally roaring with laryngeal spasm and tracheal mucous. We eventually got the idea that this had to be removed and started to bronchoscope the patients. We then went over to tracheostomy with very gratifying results and later to endotracheal tubing with what I believe, have been less successful results. In a number of the cases reported here there was evidence of inadequate airway clearance. The patient with cardiac tamponade was a surprise.
(3) In six cases the brain injury appeared minimal and at CT Scanning or autopsy various authors have pointed out how trauma, and particular bruising or the brain with haematoma formation and neuron distracted liberates toxic cytokines as well as electrolytes in the extra cellular fluids with resulting brain swelling and dsyfunction. There were more of these cases than those requiring surgery. This means that while we must tighten up on our diagnosis and observations and on our general and especially airways care, it also means that the main focus of our attention has to be on the development of techniques to mitigate the deleterious effects of these liberated substances that has to be the main thrust of head injury research now.