J. Forens. Sci. Soc. (1972), 12, 567

Traumatic Subarachnoid Haemorrhage Following Blows to the Neck

A. KEITH MANT Department of Forensic Medicine, Guy's Hospital, London, S.E.I., England

Paper presented at the Sixth International Meeting of Forensic Sciences-Edinburgh, 1972

For many years subarachnoid haemorrhage without severe violence was considered to be OJ' natural origin, even when there was no demonstrable abnormality of the cerebral circulation. During the last decade, however, a more critical examination of cases of apparently unexplained subarachnoid haemorrhage has shown that they may occur after relatively minor trauma to the upper neck, especially i f the recipient of the impact is intoxicated. A series of 8 cases oj'traumatic subarachnoid haemorrhage is described.

Introduction Cases of fatal subarachnoid haemorrhage occurring in the absence of any

demonstrable abnormality of the cerebral circulation have been reported for many years either as single reports or as a series of cases. Where no berry aneurysm was identified it was usually considered that the anomaly of the cerebral circulation had been so small that it escaped detection. The presence of apparently minor trauma in such cases was considered coincidental and it was generally believed that such factors as a rapid rise in blood pressure due to emotional stress prior to the collapse precipitated the massive haemorrhage.

In recent years the relationship of apparently minor trauma to the head and neck has been critically examined and these studies have revealed that trauma rather than being coincidental is the direct cause of the haemorrhage. The conclusion of Ford as late as 1956 that "Evidence of severe trauma to the head and neck is necessary to establish injury as the proximate cause of basal subarach- noid haemorrhage in the absence of skull fractures or cerebral contusions" can no longer be accepted.

In 1967, Simonsen reviewed 75 cases of traumatic subarachnoid haemorrhage, in two-thirds of which no origin of the haemorrhage was demonstrated, a r ~ d he made the important observation that in 72% of the cases the trauma was directed to the region of the base of the skull and that 87% were intoxicated with alcohol and 88% had followed fisticuffs.

I n 1970, Contostavlos presented 3 cases of subarachnoid haemorrhage following trauma to the head and neck in which the haemorrhage had been associated with rupture of the vertebral arteries outside the skull, the blood tracking along the arteries into the subarachnoid space. Contostavlos also found in the Medical Examiner files 6 cases of fatal subarachnoid haemorrhage believed to be due to natural causes in spite of minor trauma, which could have been due to vertebral artery haemorrhage.

In these cases the external injury may appear very superficial and can be masked by the natural skin folds of the neck when a body is in the supine position. Bone injury is usually confined to the transverse process of the first cervical vertebra and this may easily be missed upon routine radiographs of the cervical spine.

Cameron and Mant presented 4 cases in 1970 and these 4 cases are included in the following 8 cases of death from traumatic subarachnoid haemorrhage following apparently minor trauma to the head or neck.

- Case I

During a scuffle between 2 patients in the recreation room of a mental hospital, 1 of the patients was knocked to the floor and kicked on the side of

his neck. He became unconscious almost at once and was dead within a few minutes. The autopsy was carried out within a few hours of the fatality. The external visible injuries upon the deceased appeared to be of a most superficial nature consisting of abrasions on a shoulder, the face and below the right ear (fig. 1). Death was due to a massive subarachnoid haemorrhage. No origin of the haemorrhage was identified when the cerebral vessels were examined. Dissection of the neck revealed bruising beneath the abrasion and haemorrhage related to C. 1 and 2 on the right side. A fracture of the tip of the right transverse process of C. 1 could be palpated. The cervical spine and base of the skull were excised and X-rayed. The radiograph confirmed the fracture (fig. 2) but the full extent of the injury was not apparent until the bone had been defleshed (fig. 3). The blood of the deceased was free of alcohol.

Fig. 1. External visible injuries upon the deceased.

-. . . . . - During a fight the deceased was struck across the back of his neck with a

stick. He collapsed, and died in the ambulance on the way to hospital. There were a number of non-fatal injuries upon the deceased including superficial stabbed wounds. Death was due to a massive subarachnoid haemorrhage. There was deep bruising of the back of the neck and below the occiput with a partial dislocation of the atloido-occipital joint. No fractures were present.

The blood alcohol was 250mg/100ml. When the brain was examined after fixation the cerebral vessels presented no abnormality and no bleeding point was disclosed.

Case 3 The deceased in this case was a 17 year-old youth who was the front seat

passenger in a motor car which was involved in a collision. He was conveyed at once to hospital but died on admission. The external injuries were of a superficial nature, abrasions of the knees and superficial glass lacerations of the face. The outer side of the left shoulder was contused. Death was due to a

Fig. 2. X-radiograph of the cervical spine and base of skull.

Fig. 3. The first cervical vertebra, after defleshing, showing full extent of injury,

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massive basal subarachnoid haemorrhage. There were no visible injuries to the side of the neck but dissection revealed deep bruising over the left transverse processes of C. 1 and 2 and a slight subluxation of the atloido-occipital joint. The base of the skull and the cervical spine were removed. Injection of the left vertebral artery disclosed a rupture at C. 1 level. There were no fractures. Traces of alcohol only were present in the blood and urine.

Case 4 The deceased was a woman of 68 years, suffering from osteoarthritis and a

moderate degree of kyphosis. She fell over, striking her forehead, and died shortly afterwards. Autopsy revealed very early bruising of the left forehead. There was a massive subarachnoid haemorrhage with a subluxation of the atloido-occipital joint on the left side. No alcohol was present.

Case .5 The deceased was a woman of 36 years. She had been out drinking with her

boy friend and got intoxicated. When they returned home they had a quarrel and he hit her on the angle of the jaw. He said that her head rolled after he had struck her. She rapidly lost consciousness and died. Autopsy disclosed bruising of the left ear and upper neck, and bruising of the upper neck on the right side. There was a massive subarachnoid haemorrhage. No rupture or anomaly of the cerebral vessels was disclosed by examination of the brain after fixation. Blood alcohol was 138mg/ 100ml and urine alcohol level 188mg/100ml.

Case 6 The deceased, a man of 55 years, was a heavy drinker who became aggressive

when he had been drinking. On the night of his death he returned home after a drinking bout and as a result of his behaviour his wife telephoned her son for assistance. When the son arrived his father became aggressive towards him.

His son struck him on both sides of the neck with the flat or side of the hand and he collapsed and died within a few minutes.

At autopsy both ears were found to be bruised and the bruising extended downwards on both sides on to the neck. On the left side the bruising extended through all the soft tissues to the base of the skull and there was a large haema- toma related to the transverse processes of C. 1 and C. 2 and a subluxation of the atloido-occipital joint on the left side. Death was due to a massive basal subarachnoid haemorrhage.

The cervical spine and base of the skull were removed together with the adjacent soft tissues. The vertebral arteries were injected with radiopaque media and subsequent radiography revealed a filling defect on the left side between C. 1 and C. 2 due to a haematoma and a rupture of the vertebral artery at the foramen magnum. The artery was then injected with a dyed gelatine solution and after fixation dissection confirmed the absence of bone injury and revealed a rupture of the vertebral artery as it entered the foramen magnum. The urine alcohol level was 249mg/100ml giving a calculated blood alcohol level of 186mg/lOOml.

Case 7 The deceased was a man of 19 years. During a dispute on the football field

he was struck on the side of the neck by the fist of an opposing player. He collapsed at once and died some minutes later.

At autopsy there was bruising over the right angle of the jaw which extended downwards into the neck and through the soft tissues to the cervical spine. There was a partial dislocation of C. 1 and C. 2 and a fracture of the right transverse process of C. 1 which was not apparent on radiography. Death was due to a massive basal subarachnoid haemorrhage. Blood alcohol was negative.

The deceased was a heavy drinker of 41 years. He returned to his lodgings one evening intoxicated and made advances to his landlord's pregnant wife. His landlord struck him several times with his fist. He colla~sed and was then made comfortable upon the settee in the room in which th'e fracas had taken place, and was found dead in the same position the next morning.

Autopsy revealed a linear bruise below the left ear and deep bruising of the soft tissues extending to the cervical spine with a haematoma related to C. 1 and C. 2. There was a partial subluxation of C. 1 and C. 2. Radiograph revealed no fractures but confirmed the subluxation. No fractures were found on sub- sequent dissection. Death was due to a massive basal subarachnoid haemorrhage. Injection of the left vertebral artery revealed a rupture between C. 1 and C. 2. The blood alcohol was 305mg/100ml and the urine alcohol 390mg/100ml.

Discussion The relationship between apparently minor impacts to the side of the upper

neck and jaw and traumatic subarachnoid haemorrhage would appear to have been established conclusively (Contostavlos, 197 1 ; Cameron and Mant, 1972). The reasons why this relationship was not recognized for so long would appear due to a variety of factors which can be briefly summarized : (1) I t is accepted that natural fatal subarachnoid haemorrhage may occur spontaneously in the absence of any demonstrable congenital or acquired defect of the cerebral circulation. (2) Subarachnoid haemorrhage arising from developmental aneurysms of the cerebral circulation may be precipitated by emotional stress causing a rise in blood pressure. (3) There may be no visible external injury or, if one is present, it may be so superficial as to escape notice or it may be masked by the hypostasis. (4) The haemorrhage is due to a ruptured vessel outside the skull and the site of the injury is outside those areas normally dissected during a routine post- mortem examination. Partial subluxation of'the atloido-occipital joint or upper cervical spine may be easily missed unless specifically looked for.

Rupture of the vertebral artery appears to be due to its sudden stretching associated with a partial dislocation of the upper cervical spine or atloido- occipital joint and may be also associated with a fracture of the tip of the transverse process of the atlas.

A subluxation and subseauent vertebral arterv iniurv would amear more i J , L L

likely to occur when the normal neuromuscular control of the neck muscles is lowered, leading to a slow and inadequate response to the blow. Amongst the factors likely to influence this response are surprise, disease, old age, arthritis and soporific or hypnotic drugs. The relationship of traumatic subarachnoid haemorrhage to alcohol has been well established for many years as the result of both animal experiments (Thomas 1937) and the data obtained from fatal cases, (Simonsen, 1967; Contostavlos, 1971 ; Cameron and Mant, 1972). In this short series alcohol levels were significantly high in 4 of the 8 cases. Of the other cases, 1 was an elderly arthritic lady, 1 was a road traffic accident, another the result of a kick and the fourth occurred on a football field.

The best technique for demonstrating the source of bleeding in both trau- matic and other subarachnoid haemorrhage is by post-mortem arteriography before removal of the brain. This technique has been used by Contostavlos but is rarely possible in this country due to lack of facilities in autopsy theatres. Once the subarachnoid haemorrhage has been recognized after removal of the calvarium the vertebral arteries should be injected with radiopaque media. The vertebral arteries may be approached either at C. 6 or at their origins from the subclavian artery. Radiographs may reveal fractures of the transverse process of the atlas but often this fracture is only apparent after dissection.

An alternative method is to remove the cervical spine and part of the base of the skull with the attached muscles and to inject the arteries in the laboratory.

Two further steps may then be undertaken. The vessels may be filled with dye- in a gelatine base and then the whole specimen is fixed in formalin and dissected or the specimen may be defleshed. There are many methods available for defleshing bones of which we have found the quickest, simplest and least destructive to be the use of household meat tenderizer, which contains papain and trypsin. Papain by itself was not efficient. The specimen is sprinkled with tenderizer and then sealed in a plastic bag and placed in an oven at 50°C until the bones start to separate after about 5 days. The bulk of the soft tissues is then removed with forceps and the specimen placed in hydrogen peroxide solution. After 5-7 days the remaining soft tissues can be easily detached and the bones examined in detail.

I wish to thank Dr. J. hl. Cameron for permission to include 3 of his cases. (nos. 2 ,5 and 7) in this paper.

References CAMERON, J. M., and MANT, A. K., 1972, Med. Sci. €9 Law, 12, 66. CONTOSTAVLOS, D. L., 1971, J. Forens. Sci., 16,40. FORD, R., 1956, J. Forens. Sci., 1, 1 17. SIMONSEN, J., 1967, J. Forens. Med., 14, 146. THOMAS, C. B., 1937, Arch. Ne~rol Psychiat., 38, 321.