anesthetic management of diabetic child · anesthetic management of diabetic child essay submitted...

Anesthetic Management of

Diabetic Child

Essay

Submitted for Fulfillment of Master Degree in Anesthesiology

By

Mohammed Gomaa Sobhy M.B.B.CH

Faculty of Medicine, Benha University

Under Supervision Of

Prof.Dr.Hamdy Hassan Eliwa Professor of Anesthesiology and Intensive Care

Faculty of Medicine

Benha University

Dr.Dina Hosny Abd El Hamid Lecturer of Anesthesiology and Intensive Care

Faculty of Medicine

Benha University

Faculty of Medicine

Benha University

6103

I

Abstract

n addition to recognizing the relevant differences among diabetes

treatment regimens, pediatric anesthesiologists must also consider

a child‘s metabolic control, age, size, pubertal development, the

intended surgical procedure, and its length when devising a

perioperative plan.As diabetes treatment options for children

continue to change, such algorithms will need to be updated. Formal

assessment of the impact of such algorithms on clinical outcomes,

satisfaction with care, and cost of care would provide additional

insight into their revision.

Key word

DIABETIC CHILD- GAD65-IDDM- Subcutaneous -MODY

AAcckknnoowwlleeddggmmeenntt

At First, thanks to ALLAH to whom I relate any success in my life.

I wish to express my deepest thanks, gratitude and

appreciation to Prof. Dr. Hamdy Hassan Eliwa,

Professor of Anesthesiology and Intensive Care for his

meticulous supervision, kind guidance, valuable instructions

and generous help.

Special thanks are due to Dr. Dina Hosny,

Lecturer of Anesthesiology and Intensive Care for her help,

encouragement, active participation and support.

MMoohhaammmmeedd GGoommaaaa

List of Contents

Title Page No.

Introduction ................................................................................................ 1

Aim of the Work .......................................................................................... 4

Classification and Diagnosis of Diabetes Mellitus in Children .................. 5

Pathophysiology of Diabetes Mellitus ....................................................... 11

Management of Diabetes Mellitus in Children ......................................... 35

Anesthetic Management ........................................................................... 33

Summary ................................................................................................ 121

References ............................................................................................... 123

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Tabl

es

Table No. Title Page No.

Table (1): Etiologic classification of diabetes mellitus ............................. 6

Table (2): Criteria for the diagnosis of diabetes mellitus ...................... 11

Table (3): Effects of Primary Glucoregulatory Hormones ..................... 23 Table (4): Oral hypoglycemic drugs ………………………………...……. ... 36

Table (5): Guidelines for insulin dose and target blood glucose

ranges ..................................................................................... 39

Table (6): Management of hypoglycemia ............................................... 42

Table (7): Sick day management ............................................................ 43 Table (8): Factors associated with an increased risk of cerebral

oedema .................................................................................... 52

Table (9): Proposed criteria for the diagnosis of cerebral oedema ........ 54

Table (11): Factors affecting insulin absorption. ..................................... 61

Table (11): Insulin Preparations Classified According to Their

Pharmacodynamic Profiles .................................................... 78

Table (12): Broad management goals across the perioperative timeline

…………………………………..……….………………………..…85

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Figur

es

Fig. No. Title Page No.

Fig. (1): Anatomy of the pancreas ....................................................... 19

Fig. (2): Biphasic insulin response to a constant glucose

stimulus 24

Fig. (3): Postprandial glucose flux in nondiabetic controls ................. 26

Fig. (4): Pathogenesis of Type 1 Diabetes ........................................... 31

Fig. (5): Pathogenesis of type 2 Diabetes ............................................ 32

Fig. (6): Algorithm for the management of DKA in children and

adolescents ............................................................................. 46

Fig. (7): A selection of the available insulin injection devices.

These are the most commonly used injection devices,

although others are also available. Most are available

on prescription. ....................................................................... 58

Fig. (8): Appropriate insulin injection sites. ........................................ 61

Fig. (9): Lipohypertrophy. .................................................................... 61

Fig. (11): Schematic representation of the attempt to mimic

physiologic insulin release following three main meals

using a basal bolus regimen. .................................................. 73

Fig. (11): Diabetes mellitus perioperative management clinical

practice guideline ................................................................... 94

Fig. (12): Preoperative management for split-mixed insulin

regimen ................ 112

Fig. (13): Preoperative management for insulin glargine

(Lantus®) regimen .................. 113

Fig. (14): Insulin pump ........................................................................ 114

Fig. (15): Preoperative management for insulin pump ....................... 115

Fig. (16): Preoperative management for patients on oral drugs

and/or insulin. ...................................................................... 117

Fig. (17): Preoperative management for patients who require

insulin infusion during surgery ........................................... 111

Fig. (18): Intraoperative management ................................................ 115

Fig. (19): Postoperative management. ................................................. 117

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Abbreviat

ions

Abb. Full term

ADA America diabetes association

CGMS Continuous glucose monitoring system

DKA Diabetic ketoacidosis

DM Diabetes mellitus

DPP-4 Dipeptidyl peptidase-4

FPG Fasting plasma glucose

GA General anesthesia

GAD65 Glutamic acid decarboxylase

GIP Glucose-dependent insulin tropic peptide

GLP Glucagon-like peptide

GWB2 Glucowatch biographer

HBGM Home blood glucose monitoring

HgbA1c Glycosylated hemoglobin

HLA Human leucocyte antigen

IAA Insulin autoantibodies

ICA Islet cell autoantibodies

IDDM Insulin-dependent diabetes mellitus

IFG Impaired fasting glycemia

IGT Impaired glucose tolerance

MODY Maturity onset diabetes of youth

NPH Neutral protamine Hagedorn

OGTT Oral glucose tolerance test

SC Subcutaneous

T1DM Type one diabetes mellitus

TDD Total daily dose

Introduction

1

S

INTRODUCTION

urgical operations needing general anesthesia carry a greater

risk to the child with diabetes than to the child without diabetes.

Every such surgical procedure and anesthesia should be taken

seriously and meticulously to prevent preoperative hypoglycemia,

hyperglycemia, or electrolyte disturbance (Rhodes;et al.,6112).

The demographics describing the dramatic increase in the

number of patients with diabetes are well known. Patients with

diabetes require surgical procedures more frequently and have

longer hospital stays than those without the condition . The presence

of diabetes or hyperglycaemia in surgical patients has been shown to

lead to increased morbidity and mortality, with perioperative

mortality rates up to 505 greater than the non-diabetic population

(Dhatariya;et al.,6106).

The reasons for these adverse outcomes are multifactorial, but

include : failure to identify patients with diabetes or hyperglycaemia,

multiple co-morbidities including microvascular and macrovascular

complications, complex polypharmacy and insulin prescribing

errors, increased peri-operative and postoperative infections,

associated hypoglycaemia and hyperglycaemia, a lack of, or

inadequate, institutional guidelines for management of inpatient

diabetes or hyperglycaemia and inadequate knowledge of diabetes

Introduction

2

and hyperglycaemia management amongst staff delivering care

(Rayman G,6102).

Management of glycemic levels in diabetic patients is critical,

as persistent hyperglycemia may lead itself to a number of

complications including cardiovascular disease, nephropathy,

retinopathy, neuropathy, and various foot pathologies (Diabetes

Care,6101).

Diabetes leads to increased morbidity and length of stay of the

surgical patient. The perioperative mortality rate is reported to be up

to 505 higher than that of the population without diabete (Frisch;et

al.,6101).

Surgical procedures may result in a number of metabolic

perturbations that can alter normal glucose homeostasis. The

resulting hyperglycemia due to abnormal glucose balance is a risk

factor for postoperative sepsis, endothelial dysfunction, cerebral

ischemia, and impairedwound healing. In addition, the stress

response may also cause other diabetic pathologies including

diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar

syndrome (HHS) during surgery or postoperatively (Lee;et

al.,6101).

In 2002, the total child population of the world (1-14

years) was estimated to be 1.1 billion, of whom 0.02% have

diabetes. This means that approximately 4404000 children around

the world have

Introduction

3

diabetes with 204000 new cases diagnosed each year (Diabetes

Atlas,6113).

Recent estimates indicate there were 121 million people in the

world with diabetes in the year 2000 and this is projected to

increase to 366 million by 2030 (Wild;et al.,6111).

The American Diabetes Association (ADA) estimated the

national costs of diabetes in the USA for 2002 to be $US 132

billion, increasing to $US 192 billion in 2020 (Diabetes care,6110).

Goals of anesthetic management of diabetic child are to

minimize physiological stress, to maintain euglycemia, to avoid

ketoacidosis and to minimize the risk of postoperative infection

(Can J Diab,6110).

Anesthesiologist must carefully consider not only the

pathophysiology of the disease, but also each child's specific

diabetes treatment regimen, glycemic control, child metabolic state,

age, pubertal development, intended surgery and its length, and

anticipated postoperative care when devising an appropriate peri-

operative management (Glister and Vigersky,6110).

Optimal management should maintain adequate hydration and

near to normal glycemic control, while minimizing the risk of

hypoglycemia. The stress of surgery may cause acute

hyperglycemia, which increases the risk of postoperative infection

(Van den berghe;et al.,6110).

4

Aim of the Work

T

AIM OF THE WORK

he aim of our study is to discuss the proper anesthetic

management of a diabetic child to maintain euglycemia and

minimize the physiological stress of surgery, thus avoiding the

possible complication in the form of hyperglycemia, hypoglycemia

and ketoacidosis.

5

Chapter (1) Classification and Diagnosis of Diabetes Mellitus in Children

D

CLASSIFICATION AND DIAGNOSIS

OF DIABETES MELLITUS IN CHILDREN

Definition

iabetes is a multisystem disorder caused by a relative or

absolute lack of insulin. The prevalence of diabetes is

approximately 2%. The majority (15%) have type 2 diabetes.

With increasing obesity, reduced exercise and alterations in dietary

habits, the prevalence of diabetes is increasing. For every case of

diagnosed type 2 diabetes, there is another undiagnosed individual

(Sivakumar

and Salim,6102).

Diabetes is diagnosed in the presence of either a blood glucose

concentration of 11.1mmol/L [200 mg/dL] or a fasting glucose

concentration of 2mmol/L [126mg/dL]. The diagnosis of diabetes

when symptoms are present is usually straightforward and a glucose

tolerance test is rarely needed. Glucose tolerance testing may be

indicated following the identification of a borderline blood glucose

concentration (e.g. in the sibling of a child with diabetes, or in children

with disorders such as cystic fibrosis predisposing to diabetes which, in

the early stages, may be asymptomatic) (Lowes and Gregory,6111).

Diabetes is a heterogeneous condition which may be classified

on the basis of pathogenesis. Type 1 diabetes is the most common

form of diabetes in children (Lowes and Gregory,6111).

6


Classification

Recent advances in knowledge of the etiology and pathogenesis

of DM has led to revised classifications. The changes have been made

in an attempt to describe diabetes on the basis of the pathogenic

process that leads to hyperglycemia, as opposed to the criteria such as

age of onset or type of therapy (Powers,6110).

Table 1 presents a recent classification of the pediatric

population (Green,6116).

Table (0): Etiologic classification of diabetes mellitus (Alberti;et

al.,0999).

Type 0 diabetes (β-cell destruction, usually leading to absolute insulin

deficiency) 1. Immune mediated

2. Idiopathic

Type 6 diabetes (may range from predominantly insulin resistance

with relative insulin deficiency to a predominantly secretory defect

with insulin resistance) Other specific types

0. Genetic defects of β-cell function 1. Chromosome 12, HNF-1α (MODY3) 2. Chromosome 2, glucokinase (MODY2)

3. Chromosome 20, HNF-4α (MODY1)

4. Chromosome 13, insulin promoter factor-1 (IPF-1; MODY4)

5. Chromosome 12, HNF-1β (MODY5)

6. Chromosome 2, NeuroD1 (MODY6)

2. Mitochondrial DNA 1. Others

6. Genetic defects in insulin action

1. Type A insulin resistance

2. Leprechaunism

7


3. Rabson-Mendenhall syndrome

4. Lipoatrophic diabetes

5. Others

0. Diseases of the exocrine pancreas

1. Pancreatitis

2. Trauma/pancreatectomy

3. Neoplasia

4. Cystic fibrosis

5. Hemochromatosis

6. Fibrocalculous pancreatopathy 2. Others

1. Endocrinopathies 1. Acromegaly

2. Cushing's syndrome

3. Glucagonoma

4. Pheochromocytoma

5. Hyperthyroidism 6. Somatostatinoma

2. Aldosteronoma

1. Others

2. Drug or chemical induced 1. Vacor

2. Pentamidine

3. Nicotinic acid 4. Glucocorticoids

5. Thyroid hormone

6. Diazoxide

2. β-adrenergic agonists

1. Thiazides

9. Dilantin

10.γ-

Interferon

11.Others

3. Infections

1. Congenital rubella

2. Cytomegalovirus

3. Others

7. Uncommon forms of immune-mediated diabetes 1. ―Stiff-man‖ syndrome

2. Anti-insulin receptor antibodies

3. Others

8


8. Other genetic syndromes sometimes associated with diabetes

1. Down syndrome

2. Klinefelter syndrome

3. Turner syndrome 4. Wolfram syndrome

5. Friedreich ataxia

6. Huntington chorea

2. Laurence-Moon-Biedl syndrome

1. Myotonic dystrophy

9. Porphyria 10. Prader-Willi syndrome

11.Others

9. Gestational diabetes mellitus

Type 1 diabetes (insulin-dependent diabetes mellitus, IDDM)

accounts for 905 of cases in children. It is by far the most common

metabolic abnormality in young people and its onset is usually seen

in late childhood and early adolescence. Patients present with

hyperglycemia, ketoacidosis and are reliant on insulin. Early onset of

type 2 diabetes (noninsulin-dependent diabetes mellitus) is very rare

in childhood and has previously been reported to account for 2–35

of cases (Pinhas-Hamiel;et al.,0993).

However, recent studies have shown the prevalence of this

disorder to be increasing. This may be related to the increasing

prevalence of obesity in children (Glaser,0997).

Down‘s, Turner‘s and Kleinfelter‘s syndromes are associated

with the premature development of diabetes. Diseases affecting the

exocrine pancreas can also eventually result in glucose intolerance.

In children with cystic fibrosis, there is a 2.65 incidence of diabetes

under 11 years of age. Congenital infections such as rubella greatly

9


increase the risk of DM and endocrinopathies. Other causes of

pediatric hyperglycemia include genetic defects in beta cell function

and in insulin action, growth hormone secreting tumors and

Cushing‘s syndrome, all of which are rare but essentially produce a

hyperglycemic picture (Kosch;et al.,6110).

Incidence

The incidence of type 1 diabetes varies within the UK. In

England and Wales, 12 per 100 000 children under 16 years

develop diabetes each year and, in Scotland 25 per 100 000 per

year (Green,6116).

There are approximately 29.1 million people with diabetes in

the United States (roughly 9.35 of the total population). Of these

29.1 million cases, around 225 or 1.1 million cases are

undiagnosed. Furthermore, a study funded by the World Health

Organization (WHO) found that estimated 342 million people

worldwide have diabetes. Between 2010 and 2030, a 695 increase

in the number of adults with diabetes in developing countries and a

205 increase in developed countries are predicted (Danaei;et

al.,6100).

Diagnostic criteria for diabetes in childhood

Diabetes in children usually presents with the characteristic

symptoms of polyuria, polydipsia and weight loss, in association

with glycosuria and ketonuria. In its most severe form ketoacidosis


11

or, rarely, a non-ketotic hyperosmolar state may develop and lead to

stupor, coma and, without treatment, death. The diagnosis is usually

confirmed quickly by measurement of a markedly elevated blood

glucose level. If ketones are also present in blood or urine, treatment

is urgent. Waiting another day to confirm the hyperglycaemia is

dangerous as ketoacidosis can evolve rapidly (Albert;et al.,0999).

In the presence of mild symptoms, the diagnosis of diabetes

should never be made on the basis of a single abnormal blood

glucose value. Diagnosis may require continued observation with

fasting and/or 2-hour postprandial blood glucose levels and/or an

oral glucose tolerance test (OGTT) (Table 6). In the absence of

symptoms of diabetes, hyperglycaemia detected incidentally or

under conditions of acute infection, trauma, circulation or other

stress may be transitory and should not in itself be regarded as

diagnostic of diabetes (Diabetes Care,6117).

Table (6): Criteria for the diagnosis of diabetes mellitus

(Diabetes Care,6117).

- Symptoms of diabetes plus casual plasma glucose concentration ≥11.1

mmol/L (200 mg/dL) (Casual is defined as any time of day without

regard to time since last meal.)

or

- Fasting plasma glucose ≥2.0 mmol/L (≥126 mg/dL) (Fasting is

defined as no caloric intake for at least 1 h.)

or

- Two-hour post-load glucose ≥11.1 mmol/L (≥200 mg/dL) during an

OGTT


11

The test should be performed as described by WHO [1], using a

glucose load containing the equivalent of 25 g anhydrous glucose

dissolved in water or 1.25 g/kg of body weight to a maximum of 25 g.

An OGTT should not be performed if diabetes can be

diagnosed using fasting and random or postprandial criteria, as

excessive hyperglycaemia can result. It is rarely indicated in making

the diagnosis of type 1 diabetes mellitus in childhood and

adolescence. If doubt remains, periodic retesting should be

undertaken until the diagnosis is established. In the absence of

unequivocal hyperglycaemia with acute metabolic decompensation,

these criteria should be confirmed by repeat testing on a different

day (Alberti;et al.,0999).

Impaired glucose tolerance and impaired fasting glycaemia

Impaired glucose tolerance (IGT) and impaired fasting

glycaemia (IFG) are intermediate stages in the natural history of

disordered carbohydrate metabolism between normal glucose

homeostasis and diabetes. IFG and IGT are not interchangeable and

represent different abnormalities of glucose regulation; IFG is a

measure of disturbed carbohydrate metabolism in the basal state,

whilst the IGT is a dynamic measure of carbohydrate intolerance

after a standardized glucose load (Diabetes Care,6117).

Patients with IFG and/or IGT are now referred to as having

‗pre-diabetes‘, indicating their relatively high risk for development

of diabetes (Hoerger;et al.,6111).


12

Pre-diabetes can be observed as an intermediate stage in any of

the disease processes. IFG and IGT may be associated with the

metabolic syndrome, which includes obesity (especially abdominal

or visceral obesity), dyslipidaemia of the high-triglyceride and/or

low-high-density lipoprotein type and hypertension (Alberti;et

al.,6112).

Individuals who meet criteria for IGT or IFG may be

euglycaemic in their daily lives as shown by normal or near-normal

glycated haemoglobin levels, and those with IGT may manifest

hyperglycaemia only when challenged with an OGTT. Recently, the

European Diabetes Epidemiology Group has recommended revising

the lower cut-off for IFG back to 6.1 mmol/L from the current value

of 5.6 mmol/L due to the two- to fivefold increase in prevalence of

IFG across the world (60)

but the American Diabetes Association

(ADA) continues to recommend 5.6 mmol/L as the cut-off point for

normal FPG (Forouhi;et al.,6113).

Categories of fasting plasma glucose (FPG) are defined as

follows (Diabetes Care,6117):

- FPG <5.6 mmol/L (100 mg/dL) = normal fasting glucose

- FPG 5.6–6.9 mmol/L (100–125 mg/dL) = IFG

- FPG≥2.0 mmol/L (126 mg/dL)=provisional diagnosis of

diabetes.


13

The corresponding categories for stimulated plasma glucose

when the OGTT is used are as follows:

- 2-hour post-load glucose <2.1 mmol/L (140 mg/dL) =

normal glucose tolerance

- 2-hour post-load glucose 2.1–11.1 mmol/L (140–199 mg/dL)

= IGT

- 2-hour post-load glucose ≥11.1 mmol/L (200 mg/dL)

=provisional diagnosis of diabetes (The diagnosis must be

confirmed, as described above).

Epidemiology of T1DM

Approximately 50–605 of individuals with T1DM are

diagnosed before the age of 15 years. In most Western countries,

T1DM accounts for over 905 of childhood and adolescent diabetes.

However, T2DM is becoming more common and it accounts for a

significant proportion of youth-onset diabetes in certain at-risk

populations (Pinhas-Hamiel and Zeitler,6112).

T1DM incidence varies greatly between different countries,

within countries, and between different ethnic populations.

Epidemiological incidence studies define the ‗onset of T1DM‘ by

the date of the first insulin injection because of the variable time

between the onset of symptoms and diagnosis. Annual incidence

rates for childhood T1DM (0–14 yr age group) comparing different

countries of the world (0.1–43.911004000). Gender differences

in


14

incidence are found in some, but not all, populations (Diabetes

Med,6113).

Incidence rates show a close correlation with the frequency of

human leucocyte antigen (HLA) susceptibility genes in the general

population of white Caucasian ancestry; this locus confers

approximately 505 of the genetic susceptibility to T1DM

(Barker,6113).

In countries where the incidence of T1DM is extremely low,

HLA associations are different from those in white Caucasians. In

addition, a unique, slowly progressive form of T1DM is found in

Japan (Forouhi;et al.,6113).

Migrating populations may exhibit diabetes incidence rates

closer to those of their new country compared with their country of

origin, although this is not universally the case, suggesting that the

interplay between genetics and environmental factors is variable

(Neu;et al.,6110).

From 1995 to 1999, the average annual increase was 3.45. In

Europe the average increase was 3.25 (955 CI 2.2–3.2) from 1919

to 1999, in keeping with the increases reported in other parts of

the world (Diabetes Med,6113).

In some reports there has been a disproportionately greater

increase in those under the age of 5 years. The rising incidence is

unlikely to have a strong genetic basis, as it has occurred over too


15

short a time period. Possible explanations include increased

exposure to infections and wealth-related factors, such as lifestyle

and nutrition (Betts;et al.,6112).

A seasonal variation in the presentation of new cases is well

described, with the peak being in the autumn and winter months.

Seasonality of birth has also been described in some countries,

suggesting a perinatal environmental trigger. Higher incidence rates

have been found in countries with colder climates and in colder areas

of large nations, such as China (Laron;et al.,6112).

Despite familial aggregation, there is no recognisable pattern

of Mendelian inheritance. The risk of diabetes to an identical twin of

a patient with T1DM is about 365 and for a sibling the risk is

approximately 45 by age 20 years and 9.65 by age 60 years,

compared with 0.55 for the general population. The risk is higher in

siblings of probands diagnosed at younger age. T1DM is two to

three times more common in the offspring of diabetic men (3.6–

1.55) compared with diabetic women (1.3–3.65) (Harjustalo;et

al.,6112).

The age of onset of T1DM has decreased in many countries.

This has been accompanied by increased weight and linear growth

prior to the onset of diabetes and the observation that children with

T1DM are heavier and taller than their peers. These epidemiological

findings suggest that insulin resistance is responsible for overloading

the beta cell (the accelerator hypothesis), although this hypothesis


16

remains to be proven and is not universally accepted (Clarke;et

al.,6113).

When the clinical presentation is typical of T1DM (often

associated with diabetic ketoacidosis) but antibodies are absent, then

the diabetes is classified as type 1B (idiopathic). This represents

approximately 55 of T1DM in white populations but is more

common in other parts of the world, such as Japan (Diabetes

Care,6117).

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