Forensic Aspects of Hypoglycaemia

First Edition

Vincent Marks

• Editore: CRC Press
• Anno: 2019
• ISBN:
  9781351678087
• Edizione: 1
• Argomento: Derecho
• Categoria: Ciencias forenses

The Forensic Aspects of Hypoglycaemia succinctly covers the medicolegal considerations of hypoglycaemia in a variety of scenarios including driving fatalities, petty crime, homicide and suicide. Covering the definitions and diagnosis of hypoglycaemia to its bearing on criminal behavior, this book draws on the author's extensive experience and contains a wealth of information for physicians and lawyers, including cases from the author's past and notable cases in the public domain.

1

The Control of Blood Glucose in Health and Disease: Hypoglycaemia

Introduction

No one definition of hypoglycaemia satisfies all situations; context is important. Literally, hypoglycaemia means ‘abnormally low blood glucose concentration’; in other words, it is a numerical value below an arbitrarily defined ‘normal’ or reference value. It may be completely asymptomatic.

Medically, hypoglycaemia is a physical sign (consequence) of disease and is, itself, able to cause characteristic signs and symptoms. These are described as a hypoglycaemic attack and by patients on antidiabetic therapy as a ‘hypo’. In them, a ‘hypo’ is a characteristic set of symptoms regardless of whether their blood glucose concentration is demonstrably low or not.

To the clinical scientist, hypoglycaemia is the blood glucose concentration below which certain well-defined physiological reactions occur which may, or may not, be accompanied by subjective symptoms.

To the clinical biochemist, hypoglycaemia is the level of blood glucose below the 95% confidence limits for the normal, healthy population: with an intermediate zone of uncertainty.

Most clinicians distinguish between hypoglycaemia arising in diabetic people due to treatment (iatrogenic) and those who are not diabetic (spontaneous). For most clinical purposes, a blood glucose concentration below 2.5 mmol/L in people under the age of 60, and below 3.0 mmol/L in older people, must be treated as hypoglycaemia worthy of investigation.

Hypoglycaemia is important in a forensic context because it can produce profound but ephemeral effects upon brain function that can cause the sufferer to behave in a bizarre and totally uncharacteristic way that brings them into conflict with the law. It can also lead to permanent brain damage or death.

The typical signs and symptoms of hypoglycaemia are shown in Table 1.1. Patients on antidiabetic therapy are advised about the signs and symptoms of hypoglycaemia and warned that unless they abort the progression of symptoms by taking something sugary by mouth, they will probably experience more serious symptoms and possibly become unconscious.

Table 1.1Most Common SIGNS and Symptoms of Acute and Subacute Neuroglycopenia

SIGNS and symptoms	Approximate frequency (%)	Comment
SWEATING	80	Often profuse
Inner trembling	65	Occasionally associated with objective tremor
Blurred and/or double vision	50
RAPID HEART BEAT and/or pounding heart	50
Anxiety	50
Hunger	50
Feeling unwell with or without headache	40
UNSTEADINESS	40	May be mistaken for drunkenness
Difficulty concentrating	70
SLURRED and/or DIFFICULT SPEECH	30	May be mistaken for drunkenness
Drowsiness	30
Confusion	30
Note: The most common SIGNS (shown in capitals) and symptoms (subjective) of acute neuroglycopenia observed at onset of hypoglycaemia in patients and volunteers made hypoglycaemic with insulin. In patients with sub-acute neuroglycopenia (unawareness of hypoglycaemia), only those shown in bold occur.

For some patients in whom hypoglycaemia develops spontaneously, e.g. those with insulin secreting tumours of the pancreas, the symptoms to which it gives rise are often the reason for the patient seeking medical advice; in others, it is an incidental finding. In those for whom it is the cause of seeking help, it is possible to distinguish four distinct syndromes: two of which (acute neuroglycopenia and subacute neuroglycopenia) have many features in common and two (chronic neuroglycopenia and hyperinsulin neuronopathy) which are quite distinct.

The symptomatology of acute neuroglycopenia is identical to that produced by hypoglycaemia resulting from an insulin injection given to either a healthy or diabetic person. The symptomatology of subacute neuroglycopenia resembles that of the unawareness of hypoglycaemia that often develops after prolonged use of insulin* therapy by diabetic patients.

Normal Glucose Homeostasis

The concentration of glucose, unlike most substances that are routinely measured in the blood, fluctuates throughout the day depending on whether the patient is fasting or has recently eaten. In healthy people, the changes are relatively small despite large fluctuations in supply and demand. This is largely due to an elaborate system of control collectively described as glucose homeostasis.1

The adult body seldom contains less than 8 g, or more than 28 g, of glucose at any one time, despite enormous fluctuations in supply, such as immediately following a carbohydrate-containing meal, or in demand, such as during rigorous exercise. This quantity of glucose can be looked upon as constituting a hypothetical glucose pool confined within a hypothetical glucose space.2 This is equal in volume to all of the water contained in the blood and interstitial fluid but excludes the much larger volume of water contained within the cells.

In the recently fed person, glucose enters the glucose pool from food by the enzymatic breakdown in the intestines of more complex dietary carbohydrates such as starches. In doing so, it stimulates the release of endogenous insulin into the circulation. In the fasting subject, the only source of blood glucose is preformed glycogen in the liver and newly synthesized glucose from the liver and, to a lesser extent, the kidneys.

Glucose enters the cells by a process known as facilitated transport that uses, depending on the tissue involved, one or more of the seven or eight genetically determined glucose transporter proteins. The blood-brain barrier, for example,3 uses mainly GLUT1 to transport glucose from the blood into the interstitial fluid of the brain and GLUT3 to transfer glucose from the exterior to the interior of the neurons. Most tissues, such as muscle and adipose tissue, use the insulin-sensitive protein, GLUT4, to transport glucose from interstitial fluid into the cells. This means that without insulin, glucose is excluded from access to the enzymes that convert it into energy, fatty acids and glycogen in most tissues apart from the brain and the red cells of the blood.

Within the physiological range, the more insulin there is in the blood the faster glucose is transported from it into the cells where it is destroyed. Under experimental conditions, there is a maximum concentration of insulin above which no further increase in blood glucose uptake occurs.

Glucose Space

The glucose space is a constant in any individual person, and consequently the amount of glucose in the pool is directly proportional to its concentration in the blood (see the next section, Blood Glucose). The concentration is homeostatically controlled through a series of rather-com...