Nigerian Journal of Paediatrics

2Hypoglycaemia in children Review of the literature

Niger J Paediatr 2016; 43 (2):70 – 77

REVIEW

Elusiyan JBE

Hypoglycaemia in children:

Oyenusi EE

Review of the literature

DOI:http://dx.doi.org/10.4314/njp.v43i2.2

Accepted: 16th March 2016

Abstract : Hypoglycaemia is a

nosed or undertreated hypoglycae-

common metabolic condition in

mia has been found to increase mor-

Elusiyan JBE

(

)

children. It often presents urgent

tality in children when it is present.

Department of Paediatrics and

and therapeutic challenges and it

This review sought to review the

Child Health, Obafemi Awolowo

University, Ile-Ife. Nigeria.

has been documented to affect

subject of hypoglycaemia in chil-

Email: jelusiyan@yahoo.co.uk

many childhood conditions. Its

dren and calls for testing for it in all

clinical presentation is not classi-

sick and admitted children.

Oyenusi EE

cal and requires a high index of

Department of Paediatrics,

suspicion for an early diagnosis

College of Medicine, University of

and prompt management. Undiag-

Lagos/Lagos University Teaching

Hospital, Lagos, Nigeria.

Introduction

whether ‘asymptomatic’ hypoglycaemia causes neuro-

logical dysfunction and damage or not.

The term hypoglycaemia refers to blood glucose level

The plasma glucose concentration is normally main-

below normal. Most of the time low blood glucose con-

tained within a relatively normal range of 3.9 to

centration is not associated with the development of the

8.3mmol/L (70 to 150mgdl), despite wide variations in

classic clinical manifestations of hypoglycaemia. The

glucose influx and efflux such as those that follow meals

and occur during exercise . There is however general

absence of clinical symptoms does not indicate that glu-

cose concentration is normal or has not fallen below

agreement that a value of blood glucose that is less than

optimal level for maintaining brain metabolism. Hypo-

2.2mmol/L (40mgdl) represents hypoglycaemia and

most of the work on hypoglycaemia

3,12-14

glycaemia in the paediatric age group is a common clini-

in the literature

cal finding and is associated with a wide variety of dis-

are based on this cut-off value. Two factors which are

orders . Even in the Tropics, there is a growing aware-

frequently overlooked when interpreting the glucose

ness that hypoglycaemia can complicate many child-

concentrations are the analytic method used and whether

hood illnesses. This has necessitated several recent

whole blood or serum (plasma) was examined. When

work on the problem of Hypoglycaemia among Nigerian

whole blood is used, the value of blood sugar below

children.

4-6

The condition often presents urgent diagnos-

2.2mmol/L represents hypoglycaemia as opposed to

tic and therapeutic challenges.

2.5mmol/L if plasma (or serum) sample is used. This is

because in individuals with a normal haematocrit, fast-

The major long-term sequelae of severe, prolonged hy-

ing whole blood glucose concentration is approximately

poglycaemia are neurologic damage resulting in mental

8 to 15% less than plasma glucose due to the fact that

retardation, transient cognitive impairment, neurological

the water content of plasma (93%) is approximately

12% higher than that of whole blood.

15-17

deficit and recurrent seizure activity. Subtle effects on

In most clini-

personality are also possible but have not been clearly

cal laboratories plasma or serum is used for most glu-

defined.

9,10

Moderate hypoglycaemia has been shown in

cose determination whereas most bedside methods for

neonates to be associated with a considerable increase in

self-monitoring of glucose use whole blood.

adverse neurodevelopmental effects.

Epidemiology

Definition of hypoglycaemia

Hypoglycaemia is said to occur more commonly in pae-

diatric patients than in adults. There are many studies

Although there is a general agreement on the need to

maintain blood glucose concentrations above a ‘critical’

on neonatal hypoglycaemia probably engendered by the

level in young children and neonates, there is no agree-

increased vulnerability of the immature neonatal brain to

damage by hypoglycaemia.

19,20

ment among practising paediatricians and authors as to

the lowest safe concentration of blood glucose.

The

difficulty with the definition is understandable in view

Hypoglycaemia has also been reported in children be-

yond the neonatal period

3-6,21

of the lack of reliable clinical signs when the blood glu-

. It has been found to also

complicate many emergency paediatric admissions.

3-6,21

cose concentrations fall in newborn infants and young

children and in view of the continuing controversy over

The prevalence of hypoglycaemia in emergencies varies

from one practice to another.

the brain accounts for almost 100% of total basal glu-

In Birmingham , a rate of 6.54/100,000 visits was

cose turnover making most of the endogenous glucose

found among children seeking care at the emergency

production (EGP) in infants and young children ac-

counted for by brain metabolism , unlike in neonates

department while Solomon et al found a rate of 7.1% in

Mozambique. More recent studies done in paediatric

where EGP provides approximately one third of glucose

needs. Thus brief hypoglycaemia may cause profound

emergency admissions of some West African countries

equally documented the occurrence of hypoglycaemia.

22-

brain dysfunction, while prolonged severe hypoglycae-

24.

mia may eventuate in brain death. Therefore, to main-

Prevalence rates of 6.4% in Ile-Ife by Elusiyan et al

and 5.6% in Lagos by Oyenusi et al both in Nigeria and

tain normal blood glucose concentration and prevent

a rate of 13% by Ameyaw et al in Kumasi, Ghana re-

precipitous falls to levels that impair brain function,

spectively were reported. Other studies such as that done

humans have evolved an elaborate gluco-regulatory sys-

by Osier et al

reported a prevalence of 7.3% among

tem.

The prolonged interval between onset of symp-

paediatric admissions in Kenya while a prevalence rate

toms and correct diagnosis reported in most studies indi-

of 18.6% was documented by Wintergerst et al among

cates that the possibility of symptomatic spontaneous

patients admitted to a paediatric intensive care unit of a

hypoglycaemia has not received proper consideration

tertiary hospital in California, United States.

early in the course of many clinical situations. There-

fore, whenever repetitive, episodic, bizarre manifesta-

Some authors reported the prevalence of hypoglycaemia

tions occur at any time, whether after a fast, after an

in studies designed to investigate specific disease enti-

acute illness or shortly after meals, a blood glucose level

ties rather than cohorts ofchildren presenting to the

should be obtained at the time of the symptoms. Only in

emergency room or admitted into the wards with diverse

this way can the diagnosis be established and therapy

problems. For instance, Familusi and Sinnette

docu-

instituted early, thus avoiding the sequelae of prolonged

mented aprevalence rate of 13% in children presenting

hypoglycaemia.

with febrile convulsions at the emergency ward in

Ibadan, Nigeria. Among children with diarrhoea, the

Elucidation of the physiology of glucoregulation in gen-

prevalent rates of hypoglycaemia reported were 4.5%

eral and of glucose counter regulation in particular has

by Bennish et al and Bhattacharya et al 40%, respec-

provided major insights into the pathophysiology of

tively in Asia while in Nigeria, Ntia et al

and Ony-

hypoglycaemia in humans. Nevertheless, there are major

iriuka et al reported prevalence rates of 4% and 4.9%

gaps in our understanding of the causes, mechanisms

and management of many hypoglycaemic states. In the

respectively.

fasted individual, the maintenance of a normal blood

Another clinical condition in which the prevalence of

glucose level is dependent upon (1) adequate supply of

hypoglycaemia has been widely investigated ismalaria.

endogenous gluconeogenic substrates like amino acids,

Comparable prevalence rates of hypoglycaemia between

glycerol, and lactate (2) functionally intact hepatic gly-

16-17% were documented by English et al

in Kenya,

cogenolytic and gluconeogenic enzyme systems, and (3)

Genton et al in New Guinea and Nwosu et al in La-

a normal endocrine system for integrating and modulat-

gos, Nigeria among children with severe malaria. How-

ing these two processes. The adult human being is quite

ever, Onyiriuka et al in Benin, Nigeria and White et al

capable of maintaining a normal blood glucose level

in Gambia

reported higher prevalence rates of 18.3%

even when totally deprived of calories for weeks or, in

and 32% respectively in children with severe malaria.

the case of obese subjects, for months. In contrast, the

normal child exhibits a progressive fall in blood glucose

Pathophysiology

to hypoglycaemic levels when fasted for even short peri-

ods (e.g. 24 to 48 hours).

2,37

The reasons for the differ-

Glucose plays a central role in mammalian fuel econ-

ence are not clear, but it may be that the young individ-

omy and is a source of energy derivable from glycogen,

ual, when fasting, is unable to supply sufficient glucose

fats and protein. Glucose is an immediate source of

to meet the obligatory demands of the body for glucose.

energy providing 38 moles of ATP/mole of glucose oxi-

Although most tissues have the enzyme systems re-

dized. Blood glucose level reflects a dynamic equilib-

quired to synthesize glycogen (glycogen synthase) and

rium between the glucose input from dietary sources

to hydrolyse glycogen (phosphorylase), only the liver

plus that released from the liver and kidney and the glu-

and kidneys contain glucose-6-phosphatase, the enzyme

cose uptake that occurs primarily in the brain, muscle,

necessary for the release of glucose into the circula-

tion . The liver and kidneys also contain the enzymes

adipose tissue and blood elements.

11,34

Hypoglycaemia

thus represents a defect in one or several of the complex

necessary for gluconeogenesis (including the critical

interactions that normally integrate glucose homeostasis

enzymes pyruvate carboxylase, phosphenol pyruvate

carboxykinase, and fructose-1,6- bisphophatase). This

during feeding and fasting.

shows the importance of these organs in glucose ho-

The maintenance of the plasma glucose concentration is

meostasis, particularly with gluconeogenesis. In dis-

critical to survival because plasma glucose is the pre-

eased states affecting these organs, hypoglycaemia will

dominant metabolic fuel utilized by the central nervous

be a major problem unless adequate intake of glucose is

system (CNS) under most conditions. The CNS can

maintained.

neither synthesize glucose nor store more than a few

minutes’ supply of glucose.

Glucose metabolism by

There are multiple potential metabolic fates of glucose

It may be stored as glycogen

(deficient endogenus production), or both.

11,38

transported into cells

There are

majorly. It may undergo glycolysis to pyruvate, which in

conditions in which glucose utilization is increased

turn can be oxidized to carbon-dioxide and water via the

markedly (e.g. exercise, large tumours, infections) and

tricarboxylic acid cycle, converted to fatty acids (and

in which renal losses occur at physiological plasma glu-

cose concentration (i.e. renal glycosuria) . However,

stored as triglycerides), or utilized for ketone bodies

(acetoacetate, B-hydroxylbutyrrate), or cholesterol syn-

because of the normal capacity of the liver to increase

thesis (Fig.1). Finally, glucose may be released into the

glucose production several fold, clinical hypoglycaemia

is rarely the result of excessive glucose efflux alone.

circulation for the immediate metabolic need of the

body. External losses are normally negligible.

Rather, it is commonly the result of hepatic glucose pro-

duction that is either decreased absolutely or inappropri-

Fig 1: Schematic representation of glucose metabolism

ately low relative to the rate of glucose utilization .

Glycogen

In African children with malaria and other infections, an

(2)

(9)

impairment in hepatic gluconeogenesis in the presence

of adequate levels of precursors has been considered the

Glucose-1-p

most likely mechanism

12,14,39

(1)

(8)

Other suggested possible mechanisms of hypoglycaemia

in malaria include accelerated tissue metabolism;

Glucose

Glucose-6-P

Glucose

the

metabolic requirements of the parasites and malabsorp-

tion of glucose probably secondary to changes in

Fructose-6-P

splanchnic blood flow owing to a heavy parasite load in

vessels

41,42

. Sequestration of parasitized red cells in the

(3)

(7)

venules and capillaries of deep tissues may impair local

circulation

43,44

. This may necessitate a transition to an-

Fructose-1,6-P

aerobic glycolysis releasing lactate and increasing glu-

cose consumption . High serum lactate levels in pa-

tients with malaria is thought to indicate lactate produc-

Triose-P

tion by the malaria parasites and anaerobic glycolysis in

TRIGLYCERIDES

tissues where the blood vessels have a heavy parasite

infestation

39,43,46

. Impaired hepatic gluconeogenesis

GLYCEROL

could also lead to high lactate levels from the Cori cy-

cle . Furthermore, the reduced dietary intake and the

FATTY ACIDS

Phosphoenolpyruvate

associated vomiting as well as the increased metabolic

requirement caused by fever in malaria are other sug-

(4)

(6)

gested mechanisms of hypoglycaemia .

Pyruvate

AcetylCoA

Mechanisms of hypoglycaemia in infections

(5)

Oxaloacetate

Citrate

KETONES

Hypoglycaemia in other infective process like pneumo-

nia and septicaemia has been attributed to the increased

LACTATE

TCA cycle

metabolic requirement caused by fever as stated earlier

resulting in increased peripheral glucose utilization.

ALANINE

a-Ketoglutarate

Studies have also shown that increased peripheral utili-

zation of glucose appears to be the primary mechanism

Glutamine

for hypoglycaemia in neonates with bacteraemia

48,49

Inhibition of gluconeogenesis is considered to be pri-

Hexokinase/Glucokinase

marily responsible for the hypoglycaemia in septicaemia

in a report by Filkins and Cornell.

Glycogen synthase

Endotoxins pro-

Phosphofructokinase

duced by organisms in infectious processes have also

Pyruvate kinase

been known to stimulate increased insulin secretion

causing hypoglycaemia

47,50,51

Pyruvate carboxylase

. These toxins can also

Phosphoenol pyruvate carboxylkinase

cause hypoglycaemia by contributing directly to deple-

tion of hepatic glycogen stores . Hypotension and de-

Fructose-1,6-Bisphosphatase

Glucose-6-phosphatase

creased tissue perfusion in septic shock increase periph-

Phosphorylase

eral utilization of glucose because the shift to anaerobic

from aerobic metabolism requires 18 times more glu-

cose to produce the same amount of energy (ATP) .

Mechanisms of hypogyclaemia

Several mechanisms are known to cause hypoglycaemia

Mechanisms of hypoglycaemia in diarrhoeal disease

in children.

Theoretically hypoglycaemia could result

from excessive glucose efflux (excessive glucose utiliza-

Various factors ranging from hyperinsulinaemia,

tion or external losses), deficient glucose influx

hypoxia, fasting, malnutrition, ketosis and impairment

of gluconeogenesis have been suggested as the mecha-

glucose.

nisms of hypoglycaemia in diarrhoeal diseases

13,50,53

Exact cause unknown – Small for gestational age,

Bennish et al noted that plasma levels of counter-

fetal distress, any sick newborn Neonatal sepsis,

regulatory hormones (glucagon, epinephrine and norepi-

Neonatal tetanus etc.

nephrine) were appropriately elevated while gluconeo-

B) Persistent (Neonatal, Infancy and early child hood 0

genic substrates were inappropriately low in the

-2yrs)

children with diarrhoea and hypoglycaemia suggesting

Hyperinsulinism – Islet cell hyperplasia, Nes-

that the hypoglycaemia observed in such patients is of-

sidioblastosis, Islet cell adenoma, leucine sensitiv-

ten due to the failure of gluconeogenesis.

ity, Beckwith – Wieldeman syndrome

Glycogen Storage disease

Mechanisms of hypoglycaemia in malnutrition

Defect in gluconeogenesis

Hormone deficiency – Congenital Adrenal Hyper-

During severe malnutrition, gluconeogenic substrates

plasia, hypothyroidism etc.

such as alanine and lactate are significantly reduced

2,54

Miscellaneous – Galactosaemia, Fructose – intoler-

The capacity to generate glucose by gluconeogenesis is

ance, salycylate intoxication, Reye syndrome, hepa-

markedly diminished and alternate fuels such as ketones

titis

or lactate are also reduced

2,54

. The resultant fatty infiltra-

tion of the liver causes glycogen and gluconeogenic

Older Children 1-18 years: The predominant condi-

substrate depletion. There is also defect in glyco-

tions complicated by hypoglycaemia as seen in the trop-

genolytic pathways and limited lipolysis .

ics include severe malaria, septicaemia, pneumonia and

protein-energy malnutrition.

22-25

Other cause

include

Mechanisms of drug-induced hypoglycaemia

side effects of drugs or drug overdosages, use of tradi-

tional concoctions as mentioned earlier amongst others.

Hypoglycaemia can also be caused by medications ad-

Hyperinsulinism, secondary to therapy of diabetes or

ministered to patients in the course of an illness. Drug

islet cell adenoma is also an important cause of hypogly-

therapy for malaria particularly quinine, may cause hy-

caemia.

57-59

poglycaemia by stimulating insulin release

. The use

of other cinchona alkaloids like quinidine has also been

Persistent hypoglycaemia

associated with hypoglycaemia . Drug intoxications in

children can also cause hypoglycaemia. Excessive doses

There are few examples of persistent hypoglycaemia in

of salicylates (4 to 6g/day) can distort multiple bio-

children. These include persistent hyperinsulinaemic

chemical reactions to produce metabolic acidosis, hypo-

hypoglycaemia and ketotic hypoglycaemia. It must be

glycaemia or hyperglycaemia

61,62

. Accelerated utiliza-

pointed out that these classes of hypoglycaemia are

tion of glucose due to augmentation of insulin secretion

rarely reported in the tropics probably due to problems

by salicylates and possible interference with gluconeo-

with diagnosis.

genesis may both contribute to hypoglycaemia .

Accidental ingestion of ethanol is a common cause of

Hyperinsulinaemic hypoglycaemia is a heterozygous

poisoning in children in our environment.

In ethanol

condition in which insulin secretion becomes unregu-

intoxication, the liver metabolizes ethanol as a preferred

lated and its production persists despite low blood glu-

cose levels . It is the most common cause of severe and

fuel, and generation of reducing equivalents during the

persistent hypoglycaemia in neonates and children

1,15

oxidation of ethanol alters the NADH/NAD ratio that is

essential for certain gluconeogenic steps . As a result,

This could be monogenic or syndromic.Congenital hy-

gluconeogenesis is impaired and hypoglycaemia may

perinsulinism (HI) has been described under various

ensue if glycogen stores are depleted . Three to five

terms in the past including "idiopathic hypoglycaemia of

percentage of children with alcohol intoxication will

infancy,"

"leucine-sensitive

hypoglycemia,"

"nesidioblastosis."

have hypoglycaemia . Overdosage of other drugs such

It has now become apparentt that

as insulin and oral hypoglycaemic agents can also cause

HI is caused by genetic defects in the pathways that

regulate pancreatic β -cell insulin secretion . Several

hypoglycaemia

65,66

candidate genes mutations have been identified as re-

Cow’s urine concoction (CUC) is a mixture consisting

sponsible for CHI

including ABCC8, KCNJ11,

GLUD1, GCK, HADH1 .

of cow’s urine, tobacco leaves, garlic leaves, basil

In a cohort from Tur-

leaves, lemon juice, rock salt and bulbs of onion . It is

key,mutations in the ABCC8 gene were found to be the

most common cause of CHI . Management of HI is

commonly used in Western Nigeria in the belief that it

controls convulsions or prevents febrile convulsions in

very difficult as current facilities for genetic diagnosis

children but it is known to cause severe hypoglycae-

and appropriate imaging are limited only to very few

mia

27,63,67

. This could be due to the hypoglycaemic activ-

centres in the world and frequently requires difficult

and garlic contained in the mixture.

ity of onions

68,69

choices, such as near-total pancreatectomy and/or highly

intensive care with continuous tube feedings

71,73

Some

Common aetiology of hypoglycaemia in Neonates

patients may respond to treatment with diazoxide, a

A) Transient 0-7 days

KATP channel agonist while others may also develop

Hyperinsulinism – Infant of Diabetic mothers,

diabetes in later life following the surgery.

erythroblastosis, discontinuation of intravemous

Ketotic hypoglycaemia is said to be the most common

76,77

form of childhood hypoglycaemia . It is also referred to

diagnosing hypoglycaemia in studies by the authors

as ketotic hypoglycaemia of infancy and classically

A brand of glucometer was found to have a sensitivity of

manifest between the ages of 18 months and 5 years and

96.00% (95% CI =81.81%-99.80%) and a specificity of

may remit spontaneously before the age of 10 years.

96.46% (95% CI=94.17%-98.02%).

The predictive

Typical history is of a child who may miss a meal due to

index of a positive test of 64.9% and the predictive in-

dex for a negative test of a 97.72%. An equally high

an infection usually an upper respiratory tract infection

and then develops hypoglycaemia form of childhood

specificity (99.8%) and moderate sensitivity (75%) of

hypoglycaemia . It is also referred to as ketotic hypo-

another brand of glucometer were observed with high

glycaemia of infancy and classically manifest between

positive predictive and negative predictive values of

94.7% and 98.7% respectively . However it remains

the ages of 18 months and 5 years and may remit spon-

taneously before the age of 10 years. Typical history is

imperative that at least, a sample should be sent to the

of a child who may miss a meal due to Convulsion may

laboratory for confirmation. Furthermore, in newborns,

occur at the time of hypoglycaemia and a presumptive

hypoglycaemia should be tested for in all infant of dia-

diagnosis is made by documenting a low blood sugar in

betic mothers irrespective of weight at birth and gesta-

association with ketonuria, ketonaemia and typical

tional age and in all babies born with a birth weight of

4kg and above . Children on nil per oris too should also

symptoms of hypoglycaemia. Ketotic hypoglycaemia is

prevented by limiting the duration of fasting and main-

have regular blood glucose monitoring. Once hypogly-

taining a high glucose intake during illnesses.

caemia is diagnosed, blood glucose should be deter-

mined frequently 30 minutes after initial correction and

Clinical features of hypoglycaemia

then hourly, 2 hourly and 4 hourly after obtaining two

normal readings form of childhood hypoglycaemia . It

The clinical manifestations of hypoglycaemia are non-

is also referred to as ketotic hypoglycaemia of infancy

specific . In addition, they vary among individuals and

and classically manifest between the ages of 18 months

may vary from time to time in the same individuals

and 5 years and may remit spontaneously before the age

of 10 years . Typical history is of a child who may miss

form of childhood hypoglycaemia . It is also referred to

as ketotic hypoglycaemia of infancy and classically

a meal due to

manifest between the ages of 18 months and 5 years and

Another benefit of bedside determination of blood glu-

may remit spontaneously before the age of 10 years.

cose is to prevent hyperglycaemia which may be caused

Typical history is of a child who may miss a meal due to

by unnecessary glucose administration to children that

Clinical manifestations of hypoglycaemia fall into two

are normoglycaemic or may even be hyperglycae-

mic

24,25,79,80

categories. The first category includes features associ-

ated with the activation of the autonomic system and

epinephrine release usually seen with a rapid decline in

Treatment of hypoglycaemia

blood glucose.

1,15

, These features are sweating, trem-

bling, anxiety, nervousness, weakness, hunger, nausea

The primary objective of treatment is to restore the

blood glucose concentration to the normal range. The

and vomiting.

1,15

The second category includes features

due to decreased cerebral glucose utilization usually

hypoglycaemic child should receive an immediate bolus

associated with slow decline in blood glucose level or

of 0.25g/kg of dextrose as a concentrated solution (10-

prolonged hypoglycaemia.

15,16

These features are head-

25%) over a minute

1,15,22,23,75,81

. This should be followed

aches, visual disturbances, lethargy, lassitude, restless-

by a continuous dextrose infusion at 8-10mg/kg/min in

ness, irritability, difficulty in thinking, inability to con-

order to avoid rebound hypoglycaemia which may occur

within 30 minutes of the bolus injection

1,15,22,75

centrate and mental confusion. Others include somno-

. Glucose

lence, stupor, prolonged sleep, loss of consciousness,

level should be determined at 15 minutes after the bolus

coma, hypothermia, twitching, convulsion and bizarre

has been given and while the maintenance glucose infu-

neurological signs (motor and sensory), loss of intellec-

sion is running. If hypoglycaemia recurs at this time, a

tual ability, personality changes and outbursts of temper.

bolus of 0.5g/kg of glucose may be given and the

There could also be psychological disintegration with

glucose infusion increased by 25-50% until normogly-

caemia is achieved

15,75

manic behaviour, depression, psychosis, permanent

. High volume rates carry the risk

mental or neurological damage

1,15

of fluid overload manifest in pulmonary oedema and/or

Therefore it is important to consider the possibility of

heart failure. This can be minimized by the use of a cen-

tral venous catheter and concentrated solutions . Enteric

hypoglycaemia in any situation in which the signs or

symptoms are compatible with an inadequate supply of

feeding is encouraged if there are no contraindications.

glucose to the brain .

The glucose infusion and blood glucose determination

are discontinued after two consecutive normal blood

Diagnostic work up

glucose levels measured 30 minutes apart and patient is

eating well

22,23

. Infant of diabetes mothers should be fed

within 30 minutes of birth by the most possible route .

Any child that is sick enough to be admitted to the hos-

pital should be screened for presence of hypoglycaemia.

This is very important because most times, hypoglycae-

Complications of hypoglycaemia

mia is asymptomatic and when symptoms are present,

they are non-specific. Bedside meters have been vali-

A strong association between hypoglycaemia and in-

dated and found to be highly sensitive and specific for

creased mortality and morbidity has been documented

by several authors

3,22-26,82

. Hypoglycaemia appears to be

thors further noted that the hypoglycaemia of hyperin-

a function of the severity of illness in childhood and

sulinism is particularly dangerous because it is associ-

more severely ill children will be more likely to die than

ated with total absence of all brain fuels (low plasma

less severely ill ones.

22,23

Hypoglycaemia is also a major

lactate, ketones and glucose) and thus more easily pre-

disposes the individual to brain damage . The risk of

indicator of a poor prognosis in different disease entities

like cerebral malaria and gastrointestinal infections

13,29-

brain damage from hypoglycaemia is highest when the

33,39,83,84

. Hypoglycaemia has been shown to be inde-

hypoglycaemia is prolonged or recurrent and the effects

have been shown to be more in the younger child .

pendently associated with speech and language impair-

ments and impairment of non-verbal functioning.

Nwosu et al reported that neurological sequelae were

about twice as common in children with cerebral malaria

and concomitant hypoglycaemia. The most frequently

Conclusion

occurring sequelae were cortical blindness, monoparesis,

aphasia, hemiparesis, generalized hypotonia, decerebrate

Hypoglycaemia is a common complication of many

syndrome and cerebellar ataxia

33,39

childhood diseases with varied pathophysiological

In a retrospective multicentre study, Lucas et al found

mechanisms. It is amenable to treatment but can cause

that moderate hypoglycaemia (<2.6mmol/L) may have

permanent neurological sequelae if prolonged or not

serious developmental consequences if present for five

treated promptly. Children who present in emergency

or more days during the first two months of life. This

are at special risk of hypoglycaemia. A high index of

provides compelling evidence that even asymptomatic

suspicion should be maintained when evaluating very

hypoglycaemia could be harmful . Menniet al

re-

sick children for early detection and subsequent prompt

ported that hyperinsulinaemic hypoglycaemia was asso-

and aggressive management.

ciated with psychomotor retardation, learning disability,

seizures and diverse neurological sequelae. The au-

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