Hypoglycaemia: Insulin and Conflicts with the Law
Hypoglycaemia: Insulin and Conflicts with the Law
Hypoglycaemia can bring patients into contact with the law in a variety of ways. It can be used as a defence against almost any criminal charge especially those involved with driving or with violence. It has also been used as an offensive weapon. Allegations of murder by insulin are easy to make but difficult to substantiate as methods of analysis that are appropriate for clinical use are not necessarily adequate for forensic purposes.
Hypoglycaemia is not only the most feared complication of diabetes but also the one most liable to bring the patient into contact with the law. It is, however, not confined to diabetic persons on insulin or sulphonylurea therapy but can occur as a sporadic feature of many diseases - or none. Its effect upon brain function takes many forms the most important of which is to produce a change in character such as to convert a normally kind, friendly individual into a thoroughly unpleasant, aggressive - sometime maniacally so - individual capable of committing the most petty or most heinous of crimes. In some it can induce a type of automatism, similar in many respects to sleep walking, in which the sufferer can perform complex actions, including driving a motor vehicle for many miles, without any conscious involvement or memory of it. It is hardly surprising therefore that hypoglycaemia, providing it can be proved to have been present at the time of the offence, is a valid defence acceptable to most jurisdictions in the world.
Hypoglycaemia is always ephemeral - rarely lasting more than a few hours at most and generally much less. Only very rarely is a blood glucose measurement made at the time of the incident, such as an assault or motoring accident, instead the expert called to advise the court in a case in which hypoglycaemia is alleged to have been involved, must rely on clinical acumen aided by past, and occasionally by subsequent, medical records and laboratory data.
Hypoglycaemia can cause death or permanent brain damage. Fortunately this is rare - except with deliberate overdosing or when combined with alcohol - because of the many safeguards built into glucose homeostasis by nature and the long interval between loss of consciousness and irreversible damage occurring. Nevertheless hypoglycaemia is difficult to establish as a cause of death, even when it is suspected, because glucose rapidly disappears from peripheral blood after death. This applies also to the vitreous humour of the eye, mistakenly believed by many forensic pathologists to provide a reliable indicator of ante mortem blood glucose. Death from hypoglycaemia can therefore only be inferred from other circumstances of the case. Consequently it is difficult to estimate how often the ‘dead in bed' syndrome is actually due to hypoglycaemia - or a consequence of adrenaline released in response to it - and how often to other causes of unexpected death in young people.
What evidence there is - and this is mostly derived from the study of patients who have used insulin or sulphonylureas with suicidal intent but also historical records of patients undergoing prolonged insulin coma therapy and experiments on primates - suggests that the adult human being can tolerate profound hypoglycaemic coma for at least three and generally six, rising in some cases to twelve hours before becoming permanently brain damaged or dead.
Abstract and Introduction
Abstract
Hypoglycaemia can bring patients into contact with the law in a variety of ways. It can be used as a defence against almost any criminal charge especially those involved with driving or with violence. It has also been used as an offensive weapon. Allegations of murder by insulin are easy to make but difficult to substantiate as methods of analysis that are appropriate for clinical use are not necessarily adequate for forensic purposes.
Introduction
Hypoglycaemia is not only the most feared complication of diabetes but also the one most liable to bring the patient into contact with the law. It is, however, not confined to diabetic persons on insulin or sulphonylurea therapy but can occur as a sporadic feature of many diseases - or none. Its effect upon brain function takes many forms the most important of which is to produce a change in character such as to convert a normally kind, friendly individual into a thoroughly unpleasant, aggressive - sometime maniacally so - individual capable of committing the most petty or most heinous of crimes. In some it can induce a type of automatism, similar in many respects to sleep walking, in which the sufferer can perform complex actions, including driving a motor vehicle for many miles, without any conscious involvement or memory of it. It is hardly surprising therefore that hypoglycaemia, providing it can be proved to have been present at the time of the offence, is a valid defence acceptable to most jurisdictions in the world.
Hypoglycaemia is always ephemeral - rarely lasting more than a few hours at most and generally much less. Only very rarely is a blood glucose measurement made at the time of the incident, such as an assault or motoring accident, instead the expert called to advise the court in a case in which hypoglycaemia is alleged to have been involved, must rely on clinical acumen aided by past, and occasionally by subsequent, medical records and laboratory data.
Hypoglycaemia can cause death or permanent brain damage. Fortunately this is rare - except with deliberate overdosing or when combined with alcohol - because of the many safeguards built into glucose homeostasis by nature and the long interval between loss of consciousness and irreversible damage occurring. Nevertheless hypoglycaemia is difficult to establish as a cause of death, even when it is suspected, because glucose rapidly disappears from peripheral blood after death. This applies also to the vitreous humour of the eye, mistakenly believed by many forensic pathologists to provide a reliable indicator of ante mortem blood glucose. Death from hypoglycaemia can therefore only be inferred from other circumstances of the case. Consequently it is difficult to estimate how often the ‘dead in bed' syndrome is actually due to hypoglycaemia - or a consequence of adrenaline released in response to it - and how often to other causes of unexpected death in young people.
What evidence there is - and this is mostly derived from the study of patients who have used insulin or sulphonylureas with suicidal intent but also historical records of patients undergoing prolonged insulin coma therapy and experiments on primates - suggests that the adult human being can tolerate profound hypoglycaemic coma for at least three and generally six, rising in some cases to twelve hours before becoming permanently brain damaged or dead.
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