Inpatient Glycaemic Management

Inpatient glycaemic
management
Straight to the point of care
Last updated: Sep 24, 2021

Table of Contents
Overview 3
Summary 3
Definition 3
Theory 4
Epidemiology 4
Aetiology 4
Pathophysiology 4
Classification 4
Case history 6
Diagnosis 8
Approach 8
History and exam 9
Risk factors 10
Investigations 11
Differentials 13
Management 15
Approach 15
Treatment algorithm overview 21
Treatment algorithm 23
Emerging 34
Patient discussions 34
Follow up 35
Monitoring 35
Complications 35
Prognosis 35
Guidelines 36
Diagnostic guidelines 36
Treatment guidelines 36
Online resources 38
References 39
Disclaimer 46
Inpatient glycaemic management Overview
Summary
Patients with newly discovered hyperglycaemia have significantly higher in-hospital mortality than patients
with a known history of diabetes or normoglycaemic patients.
OVERVIEW
Evidence indicates that the development of hyperglycaemia during acute medical or surgical illness is not a
physiological or benign condition, but is a marker of poor clinical outcome and mortality.
Both hyperglycaemia and hypoglycaemia are associated with higher mortality, independent of known history
of diabetes.
Effective management of hyperglycaemia is associated with a decreased length of ICU and hospital stay.
Tight glycaemic control in the normal range of 4.4 mmol/L to 6.1 mmol/L (80-110 mg/dL) may not be
necessary, however, and may in fact be harmful.
A basal-bolus insulin regimen or a basal insulin regimen may be used in patients admitted to hospital who
are not critically ill. Sliding scale insulin alone should not be used in these patients.
Definition
Inpatient glycaemic management refers to identifying and treating hyperglycaemia in the setting of acute
illness in hospitalised patients with either pre-existing diabetes or new-onset hyperglycaemia. This may occur
in the ICU or in the general ward, and evidence and guidelines differ between these settings. The three
groups of patients to consider are the following:
• Known diabetes mellitus before admission.
• New diagnosis of diabetes mellitus made on admission to hospital: in these cases patients are not
aware they have diabetes but present with hyperglycaemia, and diabetes is diagnosed subsequently.
• Transient hyperglycaemia: this may be related to stress, drug therapy such as corticosteroids, or
parenteral and enteral nutrition, and resolves when the inciting factor is removed.
The prevention and management of hypoglycaemia in the inpatient setting is also addressed. Diabetic
ketoacidosis and non-ketotic hyperosmolar hyperglycaemia are not specifically addressed.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Sep 24, 2021.
BMJ Best Practice topics are regularly updated and the most recent version of the topics
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Inpatient glycaemic management Theory
Epidemiology
Inpatient hyperglycaemia is relatively common. With the increase in obesity and diabetes in the general
population, it is likely that a growing proportion of patients admitted to hospital will have hyperglycaemia.
THEORY
In one study, hyperglycaemia was present in 38% of patients admitted to hospital (26% with a known
history of diabetes; 12% with no history of diabetes before admission).[3] Patients with newly discovered
hyperglycaemia have been shown to have a significantly higher in-hospital mortality (16%) than patients who
have a history of diabetes (3%) or people with normoglycaemia (1.7%).[4]
Aetiology
Increasing evidence indicates that the development of hyperglycaemia during acute medical or surgical
illness is not a physiological or benign condition but is a marker of poor clinical outcome and increased
mortality.[3] [5] [6]
Identification that treating hyperglycaemia may improve clinical outcomes has brought more attention to
this field. The aetiology of inpatient hyperglycaemia is multi-factorial and involves increases in circulating
concentrations of stress hormones, along with possible deleterious effects on vascular, haemodynamic,
and immune systems.[7] In some cases the hyperglycaemia may be due to concomitant therapy, such as
corticosteroids, or to parenteral, and occasionally enteral, nutrition. Hyperglycaemia has been associated
with an increased risk of complications and mortality in patients on parenteral nutrition.[8]
A blood glucose of <3.9 mmol/L (<70 mg/dL) is often used to define hypoglycaemia, <3.0 mmol/dL (<54
mg/dL) as clinically significant hypoglycaemia, and <2.2 mmol/L (<40 mg/dL) for severe hypoglycaemia.
Hypoglycaemia is a known adverse effect of insulin and other antidiabetic medications. In addition, patients
at increased risk of hypoglycaemia include those with reduced nutritional intake, malnutrition, renal or hepatic
impairment, heart failure, malignancy, infection, sepsis, older age, and cognitive impairment.[1] [9] [10]
Pathophysiology
Hyperglycaemia in patients admitted to hospital, with or without a previous history of diabetes, is a complex
condition, usually associated with both insulin resistance and insulin deficiency. Insulin resistance is often
related to inflammation induced by infections or stress hormones and cytokines. Some of these same factors
affect pancreatic beta-cell function and induce insulin deficiency.
Concomitant treatments often exacerbate the problem. Corticosteroid therapy that induces insulin resistance
is a good example. In addition, parenteral nutrition with a high fat load leads to increased free fatty acids,
which in turn affects glucose metabolism.
Hyperglycaemia has multiple consequences, which may affect clinical outcomes. These include altered white
blood cell function, blood flow and reactivity, and oxidative stress. Thus, correction of hyperglycaemia is
theoretically appealing.[11]
Classification
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Sep 24, 2021.
Transient hyperglycaemia
Development of hyperglycaemia is related to the onset of stress (e.g., infection or myocardial infarction),
drugs such as corticosteroids, or enteral and parenteral nutrition, typically with resolution when the inciting
factor is removed.
THEORY
Tests:
• HbA1c is normal if the period of stress or exposure is short (reflecting normal blood glucose before the
illness).
Type 1 diabetes mellitus[1]

May have a genetic predisposition and usually presents at a young age (5-15 years old). May have history of
polyuria, polydipsia, and unintentional weight loss.
Tests:
Two out of the following tests, or the same test performed twice if the patient does not have unequivocal
symptoms of hyperglycaemia:
• Fasting plasma glucose: ≥7 mmol/L (≥126 mg/dL)

• Oral glucose tolerance test: 2-hour plasma glucose ≥11.1 mmol/L (≥200 mg/dL). This test is generally
not necessary
• HbA1c ≥48 mmol/mol (≥6.5%).
In a patient with unequivocal symptoms of hyperglycaemia:
• Random plasma glucose ≥11.1 mmol/L (≥200 mg/dL).

Supporting evidence for type 1 diabetes:
• Plasma and urine ketones: elevated in ketoacidosis

• Fasting C-peptide: usually low but may be in the normal range
• Anti-glutamic acid decarboxylase (GAD) antibodies, islet cell antibodies (ICA), insulinoma-associated
protein-2 (IA-2) antibodies: positive.
Type 2 diabetes mellitus[1] [2]

Usually older age. May have family history. Higher risk in black, Latino, and American Indian people.
May have features of metabolic syndrome (hypertension, obesity, and hyperlipidaemia).
Polyuria, polydipsia, and unintentional weight loss may occur.
May have indication of associated insulin resistance: for example, acanthosis nigricans or polycystic ovary
syndrome (PCOS).
Tests:
Two out of the following tests, or the same test performed twice if the patient does not have unequivocal
symptoms of hyperglycaemia:
5
• Fasting plasma glucose: ≥7 mmol/L (≥126 mg/dL)

• Oral glucose tolerance test: 2-hour plasma glucose ≥11.1 mmol/L (≥200 mg/dL). This test is generally
not necessary
• HbA1c ≥48 mmol/mol (≥6.5%).
THEORY
In a patient with unequivocal symptoms of hyperglycaemia:
• A random plasma glucose ≥11.1 mmol/L (≥200 mg/dL).
Pre-diabetes[1]
Risk factors and history similar to those of type 2 diabetes.
Tests:
• Impaired fasting glucose: fasting plasma glucose 5.55 mmol/L to 6.9 mmol/L (100-125 mg/dL)
• Impaired glucose tolerance: oral glucose tolerance test 2-hour plasma glucose 7.8 mmol/L to 11 mmol/
L (140-199 mg/dL)
• HbA1c: 38 mmol/mol to 47 mmol/mol (5.7-6.4%).
Hypoglycaemia[1]
Blood glucose <3.9 mmol/L (<70 mg/dL). A blood glucose of <3.0 mmol/L (<54 mg/dL) is considered
clinically significant. Multiple studies on inpatient hyperglycaemia use the definition of severe hypoglycaemia
as being a blood glucose <2.2 mmol/L (<40 mg/dL).
Case history
Case history #1
A 56-year-old white man with no prior documented history of diabetes is admitted to hospital for shortness
of breath, fever, and a productive cough. The patient's vital signs are as follows: temperature 38.5°C
(101.4°F); BP 90/60 mmHg; pulse 110 bpm; respiratory rate 22 bpm; and O2 saturation 89% on ambient
air. Chest x-ray (CXR) obtained in the emergency department reveals a right lower lobe consolidation.
Intravenous hydration and appropriate antibiotics for empirical treatment of lobar pneumonia are initiated.
His admission metabolic panel reveals a glucose level of 14.0 mmol/L (252 mg/dL).
Case history #2
A 55-year-old white man presents to the emergency department with a 1-day history of intermittent chest
discomfort. It is characterised as sharp and radiating down his left arm. He is obese but has no notable
abnormalities on examination. An ST-elevation myocardial infarction (MI) is diagnosed, and he is taken
to the catheterisation lab, where he undergoes successful percutaneous coronary intervention. Post-
procedure he is admitted to the cardiac care unit (CCU) for further care. His laboratory results are notable
for a random glucose of 11.2 mmol/L (201 mg/dL) on admission. Two days later, fasting blood glucose is
6.4 mmol/L (115 mg/dL), and HbA1c is 43 mmol/mol (6.2%).
Other presentations
Inpatient hyperglycaemia presents with a wide variety of features and history. Patients may have a
known history of diabetes mellitus preceding admission; a diagnosis of diabetes mellitus established
THEORY
subsequently when a presumed inciting factor is gone and yet the hyperglycaemia persists; or transient
hyperglycaemia, related to, for example, corticosteroids, which usually resolves quickly.
7
Inpatient glycaemic management Diagnosis
Approach
History is extremely important to determine whether a patient has new-onset hyperglycaemia as opposed
to untreated or poorly controlled pre-existing diabetes mellitus. Distinguishing between type 1 diabetes
mellitus and type 2 diabetes mellitus, along with new-onset hyperglycaemia, can help establish a clear plan
for glycaemic control during hospital admission. For example, a higher vigilance for diabetic ketoacidosis is
important in patients with type 1 diabetes.
History
Hyperglycaemia
• Patients known to have diabetes mellitus should have their current medication history reviewed so
that it can be optimised on discharge from hospital.
• In some patients with no prior history of diabetes, medication history may reveal a recent course of
corticosteroid use, which may suggest transient hyperglycaemia.
Hypoglycaemia
• Patients with hypoglycaemia may present with reduced level of consciousness, unusual behaviour,
sweating, tachycardia, seizures, or coma. Recognising these symptoms and signs urgently is
essential to institute immediate management.
• Sedation or beta-blockers may mask symptoms, and counter-regulatory responses may be
impaired.
• Patients at increased risk of hypoglycaemia include older people, malnourished people, those with
cognitive impairment, and those with renal or hepatic failure.[9] [10]
Examination
Patients should undergo a complete physical examination specific to their presenting condition.
Patients with known or suspected diabetes might benefit from the following examinations:
DIAGNOSIS
• Eye examination: a fundus examination with an ophthalmoscope to assess for diabetic retinopathy.
• Vibration sense and microfilament examination: a screening examination, using simple tests
such as pinprick sensation, vibration perception (using a 128-Hz tuning fork), 10-g monofilament
pressure sensation, and assessment of ankle reflexes to assess for signs of diabetic neuropathy.
Tests
• Blood glucose should be checked routinely in all patients admitted to hospital and is the first
indication of hyperglycaemia.
• In patients with pre-existing diabetes or newly discovered hyperglycaemia, capillary blood glucose
(fingerstick) should be checked throughout admission, preferably before meals and at bedtime if
eating, or every 6 hours if taking nothing by mouth. Patients with signs of hypoglycaemia should
have a fingerstick done immediately.
• Hyperglycaemia in hospitalised patients is defined as blood glucose >7.8 mmol/L (>140 mg/
dL).[1] In patients without a prior diagnosis of diabetes, a HbA1c >6.5% suggests that diabetes
was present prior to hospitalisation. A normal HbA1c in the face of new hyperglycaemia suggests
transient hyperglycaemia, whether related to stress, corticosteroids, or parenteral/enteral
nutrition.[10] The oral glucose tolerance test is not usually done during hospitalisation.
• Renal function should be tested to assess for diabetic nephropathy in all patients with
hyperglycaemia and should include serum creatinine, urea, and glomerular filtration rate (GFR)
calculation.
• In patients with type 1 diabetes mellitus and suspected ketoacidosis, serum ketones should be
measured. Of the ketones, beta-hydroxybutyrate is the most sensitive and specific. These tests
may also be useful to monitor progress of recovery from ketoacidosis.
• All patients admitted to hospital with new-onset hyperglycaemia should be assessed after
discharge for the presence of diabetes with a subsequent fasting glucose and/or HbA1c. Abnormal
results need to be confirmed on a separate day. Oral glucose tolerance test may be needed if there
is uncertainty about the diagnosis but is not usually necessary.
History and exam

Key diagnostic factors
presence of risk factors for hyperglycaemia (common)
• Key risk factors for hyperglycaemia include stress (e.g., severe illness such as myocardial infarction),
infection, corticosteroid use, and poorly controlled diabetes mellitus.
presence of risk factors for hypoglycaemia (common)

• Key risk factors for hypoglycaemia include insulin use, older age, malnourishment, cognitive
impairment, or renal or hepatic failure.[9] [10]
history of diabetes mellitus (common)

• In one study, hyperglycaemia was present in 38% of patients admitted to hospital (26% had a known
history of diabetes and 12% had no history of diabetes before admission).[3]
signs of hypoglycaemia (common)
DIAGNOSIS
• Patients may present with reduced level of consciousness, unusual behaviour, sweating, tachycardia,
seizures, or coma. Recognising these symptoms and signs urgently is essential to institute immediate
management.
Other diagnostic factors

history of recent corticosteroid use (common)
• May suggest transient hyperglycaemia.
signs of diabetic retinopathy (common)

• May suggest longstanding diabetes. Includes intraretinal haemorrhage, cotton wool spots, lipid
exudates, venous beading, and intraretinal microvascular abnormalities.
signs of diabetic neuropathy (common)

• May suggest longstanding diabetes. Includes loss of vibratory sensation; altered proprioception;
impaired pain, light touch, and temperature sensation; gastroparesis, constipation, orthostatic
hypotension, or resting tachycardia.
9
polyuria, polydipsia, or unintentional weight loss (uncommon)
• Hyperglycaemia is usually asymptomatic, but severe or prolonged type 2 diabetes may produce
symptoms.
• May also suggest type 1 diabetes.
Risk factors
Strong
severe illness (hyperglycaemia or hypoglycaemia)
• Particularly severe illness such as myocardial infarction, sepsis, and pneumonia are strong risk factors
for hyperglycaemia.[12] Sepsis can increase serum glucose levels through hormonal changes that
increase hepatic glucose production and reduce peripheral glucose uptake. Patients at increased risk
of hypoglycaemia include those with renal or hepatic impairment, heart failure, malignancy, infection,
or sepsis.[1] [9] [10]
corticosteroid use (hyperglycaemia)

• Corticosteroids oppose insulin action and stimulate hepatic gluconeogenesis. Higher body mass index
(BMI) and increased age increase the risk of corticosteroid-induced hyperglycaemia.[13]
poorly controlled diabetes mellitus (hyperglycaemia)

• Patients with a known history of diabetes mellitus may present with hyperglycaemia.
insulin administration (hypoglycaemia)

• Insulin can induce hypoglycaemia, leading to neuroglycopenia. Hypoglycaemia is associated with
adverse outcomes, especially in ICU patients. Sedation or beta-blockers may mask symptoms of
neuroglycopenia, and counter-regulatory responses may be impaired.
• Compared with sliding scale insulin, basal-bolus insulin use is more frequently associated with
hypoglycaemia.[14]
DIAGNOSIS
changes to corticosteroid or insulin regimen (hypoglycaemia or

hyperglycaemia)
• Iatrogenic factors that may lead to hypoglycaemia include sudden reduction in a corticosteroid dose,
incorrect timing in relation to meals of short- or rapid-acting insulin, and reduction of intravenous
dextrose (glucose) infusion or parenteral nutrition rate.[1]
poor nutritional intake (hypoglycaemia)

• Malnourished people are at risk of hypoglycaemia.[1] [9] [10]
• Changes to nutritional intake may include reduced oral intake, not being able to take food or
medication orally, or unanticipated interruption of nutrition (enteral or parenteral).[1]
older age or cognitive impairment (hypoglycaemia)

• Increased risk of hypoglycaemia.[1] [9] [10] [14]
Investigations
1st test to order
Test Result
random plasma glucose elevated
• Hyperglycaemia in hospitalised patients is defined as blood glucose
>7.8 mmol/L (>140 mg/dL).[1] As a diagnostic screening test, ≥11.1
mmol/L (≥200 mg/dL) accompanied by symptoms of hyperglycaemia
(polyuria, polydipsia, weight loss) is diabetes.
•
• Hypoglycaemia: <3.9 mmol/L (<70 mg/dL); clinically significant
hypoglycaemia: <3.0 mmol/dL (<54 mg/dL); severe hypoglycaemia:
<2.2 mmol/L (<40 mg/dL).
HbA1c ≥48 mmol/mol (≥6.5%)
• The American Diabetes Association has added HbA1c ≥48 mmol/mol suggests chronic
hyperglycaemia; elevated
(≥6.5%) on two separate occasions, or a single HbA1c ≥48 mmol/
HbA1c must be confirmed
mol (≥6.5%) in combination with either a fasting glucose ≥7 mmol/L
(≥126 mg/dL) or a random plasma glucose of ≥11.1 mmol/L (≥200 on a separate occasion
mg/dL), as an additional diagnostic criterion for diabetes. The oral
glucose tolerance test is not usually done during hospitalisation.
HbA1c may be useful in differentiating previously unrecognised
diabetes from transient hyperglycaemia. A normal HbA1c in the face
of new hyperglycaemia suggests transient hyperglycaemia, while an
elevated level suggests longstanding diabetes. HbA1c can also help
assess prior treatment and control of known diabetes.[1]
serum urea nitrogen, creatinine, and glomerular filtration rate may be abnormal in
(GFR) calculation diabetic nephropathy
• Renal insufficiency is a risk factor for hypoglycaemia.
spot urine albumin/creatinine ratio <3.4 mg/mmol (<30
micrograms/mg)
• Microalbuminuria has historically been defined as 3.4-33.8 mg/mmol
creatinine is normal
DIAGNOSIS
(30-299 micrograms/mg) creatinine.
and excludes diabetic
• Macroalbuminuria has historically been defined as ≥33.9 mg/mmol
nephropathy
(≥300 micrograms/mg) creatinine.
serum ketones may be positive
• Need to correlate with clinical picture, because serum ketones may
be elevated in starvation.
• Beta-hydroxybutyrate is elevated when >300 micromol/L (>3 mg/dL).
• Urine ketones are not recommended as they may reflect the patient's
state several hours ago.
11
Other tests to consider
Test Result
post-discharge fasting plasma glucose or HbA1c ≥7 mmol/L (≥126 mg/dL)
or HbA1c ≥48 mmol/mol
• All patients admitted to hospital with new-onset hyperglycaemia
(≥6.5%) is diagnostic of
should be assessed for the presence of diabetes with a post-
diabetes mellitus
discharge fasting glucose or HbA1c.
• Abnormal results need to be confirmed on a separate day.
post-discharge oral glucose tolerance test 2-hour plasma glucose
≥11.1 mmol/L (≥200 mg/dL)
• All patients admitted to hospital with new-onset hyperglycaemia
is diagnostic of diabetes
should be assessed for the presence of diabetes with a follow-up
test. Glucose tolerance test may be needed when diabetes is strongly mellitus
suspected post-discharge, but fasting plasma glucose (<7 mmol/L
[<126 mg/dL]) or HbA1c is not diagnostic.[1]
• Abnormal results need to be confirmed on a separate day.
DIAGNOSIS
Differentials
Condition Differentiating signs / Differentiating tests

symptoms
Transient hyperglycaemia • In corticosteroid-induced • HbA1c normal (reflecting
(e.g., from stress, hyperglycaemia, there is a normal blood glucose before
corticosteroids, clear history of corticosteroid the illness).
parenteral/enteral use (including possible
nutrition) intramuscular injections of
corticosteroids).
Type 1 diabetes mellitus • May have a genetic • HbA1c ≥48 mmol/mol

predisposition and usually (≥6.5%) or
present at young age (5-15 • Fasting plasma glucose: ≥7
years old). May have history mmol/L (≥126 mg/dL) or
of polyuria, polydipsia, and • Oral glucose tolerance test:
unintentional weight loss. 2-hour plasma glucose ≥11.1
mmol/L (≥200 mg/dL).
• Random blood sugar ≥11.1
mmol/L (≥200 mg/dL).
• Plasma and urine ketones:
elevated in ketoacidosis.
• Fasting C-peptide: low or
undetectable, may also be
normal.[1]
Type 2 diabetes mellitus • Usually older age. May • HbA1c ≥48 mmol/mol
have family history of type (≥6.5%) or
2 diabetes. Higher risk in • Fasting plasma glucose: ≥7
black, Latino, and American mmol/L (≥126 mg/dL) or
Indian people. • Oral glucose tolerance test:
• May have features of 2-hour plasma glucose ≥11.1
metabolic syndrome mmol/L (≥200 mg/dL) or
(hypertension, obesity, • Random blood sugar ≥11.1
DIAGNOSIS
hyperlipidaemia). mmol/L (≥200 mg/dL)
• Polyuria, polydipsia, and accompanied by symptoms.
unintentional weight loss • All tests must be repeated in
may occur. the absence of unequivocal
• May have indication of hyperglycaemia.
insulin resistance (e.g., • Fasting C-peptide:
acanthosis nigricans detectable.[1]
or polycystic ovarian
syndrome).
Pre-diabetes • Risk factors and history • Impaired fasting glucose:

similar to those of type 2 fasting plasma glucose
diabetes. 5.55 mmol/L to 7.00 mmol/L
(100-125 mg/dL).
• Impaired glucose tolerance:
oral glucose tolerance test
2-hour plasma glucose 7.8
mmol/L to 11.0 mmol/L
(140-199 mg/dL).
• HbA1c of 38 mmol/mol
to 47 mmol/mol (5.7%
to 6.4%) indicates pre-
13
Condition Differentiating signs / Differentiating tests

symptoms
diabetes or high risk of future
diabetes.[1]
Screening
All patients admitted to hospital with new-onset hyperglycaemia should be assessed for the presence of
diabetes with a subsequent fasting glucose or glucose tolerance test. Measuring HbA1c may also be useful
in differentiating diabetes from stress-induced hyperglycaemia.
DIAGNOSIS
Inpatient glycaemic management Management
Approach
The principles of managing patients with newly diagnosed hyperglycaemia or diabetes remain the same as
those for patients with well-known and established diabetes. However, additional factors must be considered.
Insulin resistance and insulin secretion can be affected by many factors in patients admitted to hospital. In
addition, most inpatients have unreliable oral intake, frequent procedures requiring changes in nutrition,
and new medication schedules. Patients taking oral agents as outpatients may be unable to continue
these medications in hospital due to fluctuating renal function or procedures requiring intravenous contrast
(metformin), heart failure exacerbations (thiazolidinediones), or inability to have oral intake before surgery.
Distinguishing between type 1, type 2 diabetes mellitus, or new-onset hyperglycaemia can help establish a
clear plan for glycaemic control during hospital admission. Patients with newly discovered hyperglycaemia
have been shown to have a significantly higher in-hospital mortality than patients who have a history of
diabetes or people with normoglycaemia.[4] Vigilance is needed for detecting ketoacidosis in patients with
type 1 diabetes. In both the critical and non-critical care venues, glycaemic control should be individualised
to the patient's status and to the resources available to the hospital system.[1] [15] Both hyperglycaemia and
hypoglycaemia are associated with higher mortality, independent of known history of diabetes.[9] [10]
Management strategy and goals remain similar in medical and surgical patients, but hypoglycaemia is
a more frequently encountered problem in medical patients,[14] and outcomes are worse in this group;
therefore, avoidance of hypoglycaemia is essential.
Goals of glycaemic control

Glucose goals and management should be individualised to each patient; hence, management strategies
need to be flexible. Following a study on intensive insulin therapy in the critically ill, published in 2001,
tight glycaemic control became the standard of care for the ICU at that time.[16] Multiple studies have
since investigated the utility of intensive glycaemic control in the ICU setting and have concluded that
intensive insulin therapy may not offer mortality benefits.[17]
Postulated reasons for failure to document reduced mortality in subsequent studies include early study
termination, protocol deviations, and failure to complete enrolment. It is also possible that mortality
secondary to a higher rate of hypoglycaemia in the intensive insulin group offset improvement in mortality
rate.[18] [19] [20]
In another meta-analysis of critically ill patients, intensive glycaemic control was not associated with
significantly reduced hospital mortality but was associated with an increased risk of hypoglycaemia.[21]
In 2008, the American Heart Association recommended a target blood glucose of 5 to 7.8 mmol/L (90-140
mg/dL).[22] However, a large randomised controlled trial subsequently raised concerns about current
intensive blood glucose targets for inpatient glycaemic control and found a higher 90-day mortality for ICU
patients with a blood glucose target of 4.5 to 6 mmol/L (81-108 mg/dL) than for ICU patients with a blood
glucose target of 10 mmol/L (180 mg/dL).[18] This raised concern that there may not be any additional
benefit to lowering blood glucose levels below 7.8 to 10.0 mmol/L (140 to 180 mg/dL) in the ICU setting
and for all hospitalised patients.[23] [24]
MANAGEMENT
A systematic review of 21 trials in ICU, perioperative care, myocardial infarction, and stroke, showed
that intensive insulin therapy did not affect short-term or long-term mortality, infection rate, or length of
stay.[25] [26] Data from several of the trials did, however, document a marked increase in the risk of
15
severe hypoglycaemia, which can also be poorly tolerated, prompting the conclusion that there is no
consistent evidence documenting the improved health outcome of intensive insulin therapy.
The American Diabetes Association and the American Association of Clinical Endocrinologists
recommend the following:[9] [10]
1. A general target blood glucose level of 7.8 to 10.0 mmol/L (140 to 180 mg/dL) for critically ill
patients (preferably by use of an insulin infusion protocol)
2. A target of <7.8 mmol/L (<140 mg/dL) pre-meals for non-critically ill patients, with re-evaluation of
the insulin regimen when the blood glucose level is <5.6 mmol/L (<100 mg/dL), and a change in the
regimen if the blood glucose level is <3.9 mmol/L (<70 mg/dL) unless there is a clear reason, such
as missing a meal
3. A random blood glucose target of 10 mmol/L (<180 mg/dL) for non-critically ill patients.
The Canadian Diabetes Association recommends target glucose levels between 6.0 to 10.0 mmol/L (106
to 180 mg/dL) for most critically ill hospitalised patients.[27]
These are recommended if they can be safely achieved without hypoglycaemia, and with the caveat that
more stringent goals may be appropriate for selected patients.[1]
The American College of Physicians, however, published the following recommendations:[25] [28]
1. Not using intensive insulin therapy to strictly control blood glucose in non-surgical intensive care
unit (SICU)/medical intensive care unit (MICU) patients with or without diabetes mellitus
2. Not using intensive insulin therapy to normalise blood glucose in SICU/MICU patients with or
without diabetes mellitus
3. A target blood glucose level of 7.8 to 11.1 mmol/L (140 to 200 mg/dL) in insulin therapy is used in
SICU/MICU patients.
The authors of this topic feel a target of 11.1 mmol/L (200 mg/dL) may be too lenient and favour
the American Diabetes Association and the American Association of Clinical Endocrinologists'
recommendations. Targets <6.1 mmol/L (<110 mg/dL) for critically ill patients are not recommended.[1]
Greater benefit has been demonstrated for intensive glycaemic control in SICU patients than in MICU
patients.[1] [18] [22] The benefits in patients with myocardial infarction remain controversial, but severe
hyperglycaemia and hypoglycaemia should be avoided.[1] [18] Non-randomised studies suggested that
tight glycaemic control reduced mortality and deep sternal wound infections in patients with diabetes
undergoing cardiac surgery.[1] [29] It has also been suggested by others that elevated A1c in patients
without diabetes who are hospitalised for acute coronary syndrome is associated with increased risk of
mortality, and that perhaps any patient without diabetes with an A1c <6.5% who is admitted to hospital for
acute coronary syndrome should receive an oral glucose tolerance test within 7 to 28 days.[30] [31]
For stroke patients, hyperglycaemia correlates with a poor clinical outcome but the threshold at which
glucose levels predict unfavourable outcomes has not been established, and further controlled studies
are needed to establish optimal glucose levels.[32] In a meta-analysis of critically ill neurological and
neurosurgical patients, tight glucose control (lower ends of target ranges were 4.4 to 5.0 mmol/L [80 to 90
MANAGEMENT
mg/dL], and upper ends of target ranges were 6.1 to 7.8 mmol/L [110 to 140 mg/dL]) was associated with
lower risk of infection and better neurological outcomes (as measured by the Glasgow Outcome Scale,
extended Glasgow Outcome Scale, or modified Rankin Scale), compared with conventional glucose
control (lower end of target ranges was 6.7 mmol/L [120 mg/dL], and upper end of target ranges was
12.0 mmol/L [215 mg/dL]).[33] Target glucoses of <8.6 mmol/L [<155 mg/dL] were also associated with
improved effectiveness of fibrinolysis and reduced haemorrhagic transformation in acute stroke.[34]
Optimum glucose levels have not been established for sepsis and shock.[35]
The benefit of treating corticosteroid-induced hyperglycaemia has not been determined. It is not clear
whether corticosteroid-induced hyperglycaemia (except for transplant patients) is associated with poor
clinical outcome over the short term.
Uncontrolled hyperglycaemia; surgery; or critical illness

In patients with type 1 diabetes, withholding insulin may lead to ketoacidosis. Infusion of glucose for
nutrition, along with insulin administration (e.g., intravenously), is essential.
Insulin is considered the preferred form of treatment for inpatients. Intravenous insulin infusion is the
preferred method of delivering insulin in these situations and is highly recommended in critically ill
patients.[15]
In patients who are not critically ill but have uncontrolled hyperglycaemia, or are to undergo surgery, it
is preferable that insulin be given intravenously. However, this is often not feasible. As such, starting
subcutaneous insulin and stopping oral agents may be an option. Subcutaneous insulin doses can then
be adjusted as needed.
Two randomised trials have shown that a basal-bolus insulin regimen was more effective in controlling
hyperglycaemia than sliding scale insulin alone in non-critically ill patients admitted to hospital.[36] [37]
The American Diabetes Association recommends that either basal insulin or basal plus bolus correctional
insulin may be used in these patients, but that sliding scale insulin alone should not be used.[1] Results of
studies suggest that the following can be used as guides:
• Most patients should discontinue oral anti-diabetic drugs on admission.

• Total daily insulin dose can be initiated at:
• 0.4 unit/kg/day when the admission blood glucose concentration is 7.8 to 11.1 mmol/L
(140-200 mg/dL)
• 0.5 unit/kg/day when the admission blood glucose concentration is between 11.2 and 22.2
mmol/L (201-400 mg/dL)
• 0.3 unit/kg/day in patients >70 years of age or who have serum creatinine >176.8 micromol/L
(>2 mg/dL).
• Half of the calculated dose is to be given as basal insulin, and the other half as mealtime rapid-
acting insulin, with the option to add a rapid-acting correction sliding scale at meals.
Study patients were obese, and doses may need to be lower in insulin-sensitive people such as thin
patients or those with type 1 diabetes.[1]
Other considerations include:
• For patients who were on insulin at home, their home doses can be added up to give their total
MANAGEMENT
daily insulin dose.

• For subcutaneous insulin, basal insulin can either be long-acting (glargine, detemir, degludec) or
intermediate-acting (NPH). Use of second-generation basal insulins, such as insulin glargine (300
units/mL) and insulin degludec (100 units/mL and 200 units/mL), have lower peak-to-trough ratios,
17
have longer duration of action than the first-generation basal insulins, and provide less glycaemic
variability. Patients who use these preparations can be continued on these while in hospital.[38]
[39]
• For regimens using long-acting insulin, one half of the total daily dose is given as long-acting insulin
and one half as rapid-acting insulin. Long-acting insulin should be given once- or twice-daily. Rapid-
acting insulin should be given in divided doses before each meal.[36]
• For regimens using intermediate-acting insulin, two-thirds of the total daily dose is given in the
morning (further divided into two-thirds NPH insulin and one third fast-acting insulin), and one third
in the evening (further divided into half fast-acting with the evening meal and half NPH with the
evening meal or preferably at bedtime).
• One study suggests that basal insulin plus sliding scale insulin is an option for patients with type 2
diabetes. In 375 patients with type 2 diabetes randomised to receive basal insulin (glargine) plus
sliding scale insulin (glulisine), basal insulin (glargine) and scheduled mealtime plus correction
sliding scale insulin (glulisine), or sliding scale insulin alone (regular insulin), the two regimens -
basal plus sliding scale, and basal plus scheduled mealtime plus sliding scale - achieved the same
glycaemic control, and performed better than sliding scale alone.[40]
• One randomised controlled trial comparing basal-bolus insulin with or without supplemental short-
acting insulin at bedtime to correct bedtime hyperglycaemia in patients with type 2 diabetes found
no improvement in mean fasting glucoses with the use of the bedtime supplement. Therefore,
correction of bedtime hyperglycaemia with fast-acting insulin is not recommended for inpatients
with type 2 diabetes.[41]
The authors of this topic do not recommend the use of sliding scales alone. However, sliding scales may
be used on occasion for 24 hours to determine the insulin requirements in some patients.
Essentially, the principles of glucose management in patients with newly detected hyperglycaemia remain
the same as those for patients with established diabetes. Avoiding hypoglycaemia and hyperglycaemia is
particularly important, as in some settings this has been associated with worse outcomes.[42]
For patients receiving insulin infusions in the ICU, established computerised protocols that recommend
predetermined changes in infusion rates are increasing in popularity.[1] They facilitate nursing processes,
improve efficiency, and have been shown to reduce glucose variance.[43] Use of the real-time continuous
glucose monitor (CGM) has been shown to lower the incidence of hypoglycaemia but increases nursing
workload.[44] Others have commented on the 'migration' of the outpatient glucose meter to the ICU owing
to its ease of use and speediness. However, results from a central laboratory are obviously more accurate
than those from a handheld device. Perhaps if intensive insulin therapy and tight glycaemic control are
to remain the standard of care, improving the accuracy of the bedside glucose measurement will help to
avoid hypoglycaemia.[45]
The American Association of Clinical Endocrinologists guidelines recommend intravenous insulin for all
critically ill patients with hyperglycaemia above target.[9] [10] A variety of protocols have been published
and, although there are extremely few head-to-head comparisons, the end results are similar in all.[1]
[9] [10] [16] [46] [47] [Yale Insulin Infusion Protocol] (http://care.diabetesjournals.org/content/27/2/461/
F1.large.jpg)
MANAGEMENT
The use of glucagon-like peptide-1 (GLP-1) has been investigated as a potential aid to glycaemic control
in critically ill patients regardless of diabetes status.[48] Compared with insulin or placebo, GLP-1
delivered intravenously effectively lowered glucose concentrations and appears to be associated with
few serious adverse events. Further studies are needed to document its safety and efficacy in critically ill
patients. GLP-1 cannot replace insulin for patients with type 1 diabetes.
Surgery:
• Patients admitted for minor elective surgery who take oral anti-diabetic medication may continue
their oral medication if the procedure is short and the patient is expected to eat later the same day.
• For longer, more complicated procedures, oral medication is usually discontinued in favour of
starting basal-bolus insulin given subcutaneously starting the day of surgery.
• For patients using insulin before hospitalisation, the dose of intermediate-acting insulin is reduced
by 30% to 50% the day of surgery. True basal insulins such as glargine or detemir can usually be
given at or close to their routine dose. Rapid-acting insulins are held while the patient is not eating.
• Long and complicated surgical procedures require intravenous insulin infusion for glucose control
and there are a number of algorithms available. In converting stable post-surgical patients from
intravenous insulin to subcutaneous basal-bolus regimens, the total daily intravenous dose can be
reduced by 20%. Fifty percent of that total is then administered as long-acting insulin once or twice
daily with the other 50% divided into two or three pre-meal injections.
Supportive care:
• Hypoglycaemia must be avoided.[15] In all patients, adequate nutrition and fluid replacement
should be ensured. Total parenteral nutrition may be required in patients who are not eating. In
patients with type 1 diabetes, a glucose-containing intravenous fluid is appropriate, along with
insulin administration.
• Electrolytes should be monitored and corrected as required. Potassium should be added to
intravenous fluids according to local ward protocols to prevent and treat hypokalaemia.
Discharge:
• Measurement of HbA1c is valuable in determining the plan at discharge. A high HbA1c indicates
poor pre-existing control and suggests need for increased or modified antidiabetic therapy (e.g.,
starting insulin or maximising oral agents).[4] [10]
• A wide range of therapy is available for long-term diabetes management. Some patients may need
to continue taking insulin at home until complete recovery allows a transition to other therapies.[15]
• Patients without known diabetes also need follow-up blood sugar levels, possible tests for
diagnosis, and possible continued treatment.
Well-controlled pre-existing diabetes: stable non-critical illness

Insulin is considered the preferred form of treatment for most inpatients. Oral agents may be used
carefully in selected patients whose blood sugars are well-controlled and who are eating normally, if there
are no contraindications and if it can be assured that the patient's feeding status will not be switched to
nil by mouth. Metformin use should be closely monitored given its contraindications (renal impairment,
acute heart failure, contrast studies), and it will probably need to be discontinued. Thiazolidinediones
are not recommended in those patients with fluid retention as part of their presenting condition. Sodium-
MANAGEMENT
glucose co-transporter-2 (SGLT2) inhibitors have been associated with diabetic ketoacidosis, including
euglycaemic diabetic ketoacidosis, and it is recommended to stop them upon admission, and 3 days prior
to scheduled surgery.[49]
19
Medications with hypoglycaemic effects may be difficult to dose appropriately with changes in a patient's
feeding status.
Type 1 diabetes
• Patients admitted to hospital who have well-controlled blood glucose levels can continue taking
their usual insulin regimen if meal consumption remains similar to home intake. A reduction of the
mealtime insulin doses can be made depending on food consumption.
Type 2 diabetes
• There is no strong evidence to suggest whether patients with type 2 diabetes should continue
taking oral anti-diabetic agents if they can as inpatients. Most inpatients would be switched
to basal-bolus insulin regimen. However, physicians could consider allowing well-controlled,
normoglycaemic patients who are eating to continue on their oral anti-diabetic agents if there are no
contraindications and if it can be assured that the patient's feeding status will not be switched to nil
by mouth.
• Several randomised trials show that patients with mild to moderate hyperglycaemia can be
managed with dipeptidyl dipeptidase-4 inhibitors with or without long-acting basal insulin.[50] [51]
[52]
Hypoglycaemia
Patients at risk of hypoglycaemia include older[14] or malnourished patients; and those with cognitive,
renal, or hepatic impairment, heart failure, malignancy, infection, or sepsis.[1] [9] [10] Compared with
sliding scale insulin, basal-bolus insulin is more frequently associated with hypoglycaemia.[14] [15]
Insulin can induce hypoglycaemia leading to neuroglycopenia. Hypoglycaemia is associated with adverse
outcomes, especially in ICU patients. Sedation or beta-blockers may mask symptoms of neuroglycopenia,
and counter-regulatory responses may be impaired. Changes in corticosteroid dosing, reduced glucose or
parenteral nutrition given intravenously, or altered oral nutritional intake may also result in hypoglycaemia.
Oral agents which are insulin secretagogues (sulfonylureas or meglitinides) may also potentially
precipitate hypoglycaemia.
The Endocrine Society, the American Diabetes Association, and the American Association of Clinical
Endocrinologists recommend reassessing the insulin regimen when the patient’s blood glucose is <5.6
mmol/L (<100 mg/dL), and modifying the regimen when the glucose is <3.9 mmol/L (<70 mg/dL).[9] [10]
[53]
Hypoglycaemia should be avoided by regular monitoring of blood glucose and changes in therapy
as needed; for example, reducing an insulin infusion rate promptly. Oral glucose or orange juice may
be given for mild hypoglycaemia in patients taking orally. For severe or refractory hypoglycaemia, or
in patients unable to take orally, 50% glucose should be given intravenously and the blood glucose
monitored closely for the next hour. Some clinicians prefer to use a 10% or 20% glucose solution to
reduce the risk of post-treatment hyperglycaemia or extravasation injury.[54] Alternatively, glucagon can
be given intramuscularly. Newer glucagon formulations are available in some countries; see Emerging
MANAGEMENT
section for more information.
Children
In a randomised trial on paediatric patients undergoing cardiac surgery, tight glycaemic control with
blood glucose targets of 4.4 to 6.1 mmol/L (80 to 110 mg/dL) did not significantly change the infection
rate, mortality, length of stay, or measures of organ failure, compared with standard care.[55] In a trial of
critically ill paediatric patients (cardiac surgery patients excluded) with hyperglycaemia, patients in the
tight glycaemic control group (blood glucose targets of 4.4 to 6.1 mmol/L [80 to 110 mg/dL]) had higher
rates of healthcare-associated infections and significantly higher rates of severe hypoglycaemia compared
with those in the higher blood glucose targets (8.3 to 10 mmol/L [150 to 180 mg/dL]) group. No significant
differences in mortality, measures of organ failure, or the number of ventilator-free days compared with
standard care were observed. The trial was stopped early as critically ill children had no evidence of
benefit from tight glycaemic control, but were at risk of possible harm.[56] Where available, a paediatric
endocrinologist should be consulted when managing hospitalised children with diabetes, particularly if
critically ill.
Treatment algorithm overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
MANAGEMENT
21
Acute ( summary )
critically ill or unplanned surgery or
in ICU: hyperglycaemia
1st insulin + treatment of comorbid illness
plus supportive care
plus follow-up and optimisation of outpatient

anti-diabetic treatment
stable non-critical illness:

uncontrolled hyperglycaemia
1st insulin (subcutaneous or intravenous) +

treatment of comorbid illness

stable non-critical illness: well-

controlled known diabetes
eating normally 1st continuation of usual anti-diabetic

regimen + treatment of comorbid illness
not eating 1st insulin (intravenous) + treatment of

comorbid illness
hypoglycaemia
able to take orally 1st oral carbohydrate + adjustment of diabetic

regimen
2nd glucose or glucagon
unable to take orally 1st glucose or glucagon + adjustment of

diabetic regimen
preoperative: minor elective surgery
1st management of diabetic regimen

MANAGEMENT
Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
MANAGEMENT
23
Acute
critically ill or unplanned surgery or
in ICU: hyperglycaemia
1st insulin + treatment of comorbid illness

Primary options
» insulin neutral: intravenously; consult

institutional protocol
» Effective management of hyperglycaemia

is associated with a decreased length of ICU
and hospital stay.[9] [10] Glucose goals and
management should be individualised to each
patient, therefore, management strategies need
to be flexible.[15]
» Blood glucose targets are 7.8 to 10.0 mmol/L

(140-180 mg/dL) (preferably by use of an insulin
infusion protocol).[9] [10] Targets <6.1 mmol/L
(<110 mg/dL) are not recommended.[1]
» Intravenous insulin is recommended for all

critically ill patients with hyperglycaemia.[15]
Several intravenous insulin infusion protocols
have been devised, the end results are similar in
all studies, and each institution should choose
the one that fits its needs and resources.[1] [16]
[46] [47] [Yale Insulin Infusion Protocol] (http://
care.diabetesjournals.org/content/27/2/461/
F1.large.jpg)
» Hypoglycaemia should be avoided.
» The mortality benefit of intensive glycaemic

control in the ICU is unclear. In critically ill
patients, intensive glycaemic control is not
associated with significantly reduced hospital
mortality but is associated with an increased
risk of hypoglycaemia.[21] Mortality was lower
in ICU patients with a blood glucose target of
≤10.0 mmol/L (≤180 mg/dL) than with 4.5 to
6.0 mmol/L (81-108 mg/dL).[18] There may be
no additional benefit to lowering blood glucose
levels below about 7.8 to 10.0 mmol/L (140-180
mg/dL) in hospital or ICU settings.[23] [24]
» Greater benefit has been demonstrated for

intensive glycaemic control in surgical rather
than medical ICU patients.[1] [18] [22] The
benefits after myocardial infarction remain
controversial.[1] [18] Non-randomised studies
MANAGEMENT
suggested that tight glycaemic control reduced

mortality and deep sternal wound infections
in patients with diabetes undergoing cardiac
surgery.[1]
Acute
» A paediatric endocrinologist should be
consulted for children.
Treatment recommended for ALL patients in
selected patient group
» Supportive care should address electrolyte
imbalances, nutritional needs, and fluid balance.
» Electrolytes should be monitored and corrected

as required. Potassium should be added to
intravenous fluids according to local ward
protocols to prevent and treat hypokalaemia.
» In all patients, adequate nutrition and fluid

replacement should be ensured. Total parenteral
nutrition (TPN) may be required in patients
who are unable to take orally. In these cases
insulin can be added to the TPN or administered
as a separate IV infusion. Patients receiving
continuous enteral support may obtain better
glucose control with a basal insulin plus regular
insulin in place of a short-acting insulin due
to a regular insulin's longer duration of action.
In patients with type 1 diabetes, a glucose-
containing intravenous fluid is appropriate, along
with insulin administration.
» Measurement of HbA1c is valuable in
determining the plan at discharge. A high HbA1c
indicates poor pre-existing control and suggests
need for increased or modified anti-diabetic
therapy (e.g., starting insulin or maximising oral
agents).[4] [10]
» A wide range of therapy is available for long-

term diabetes management. Some patients may
need to continue taking insulin at home until
complete recovery allows a transition to other
therapies.[15]
» Patients without known diabetes also need

follow-up blood sugar levels and possible
continued treatment.
stable non-critical illness:
uncontrolled hyperglycaemia
MANAGEMENT
1st insulin (subcutaneous or intravenous) +

treatment of comorbid illness
Primary options
Eating normally
25
Acute
» insulin aspart: subcutaneously before each
meal
-or-
» insulin glulisine: subcutaneously before
each meal
-or-
» insulin lispro: subcutaneously before each
meal
--AND--
» insulin isophane human (NPH):
subcutaneously twice daily, preferably in the
morning and at bedtime
-or-
» insulin glargine: subcutaneously once daily,
preferably at bedtime
-or-
» insulin detemir: subcutaneously once daily,
preferably at bedtime, or twice daily
-or-
» insulin degludec: subcutaneously once daily
OR
Not eating
» Insulin is recommended for hyperglycaemia in

hospitalised patients.[1] Blood glucose targets
are: <7.8 mmol/L (<140 mg/dL) pre-meals, and
random blood glucose <10.0 mmol/L (<180 mg/
dL).[1] [9] [10] The insulin regimen should be
reassessed when glucose levels are <5.6 mmol/
L (<100 mg/dL), and modified when glucose
levels are <3.9 mmol/L (<70 mg/dL). Use of
insulin on the general ward should be based on
a basal-bolus approach.[1] [36]
» Subcutaneous insulin given before meals is

preferred. Intravenous insulin is appropriate if
the patient is not eating. However, this may be
cumbersome and not feasible in some settings,
and so basal insulin (preferably long-acting
insulins as they are relatively peakless) with or
without correction scale may be used instead.
Use of second-generation basal insulins, such
as insulin glargine (300 units/mL) and insulin
degludec (100 units/mL and 200 units/mL), have
lower peak-to-trough ratios, have longer duration
of action than the first-generation basal insulins,
and provide less glycaemic variability. Patients
MANAGEMENT
who use these preparations can be continued on

these while in hospital.[38] [39]
» General blood glucose targets are 7.8 to 10.0

mmol/L (140-180 mg/dL) for patients using
intravenous insulin.[1]
Acute
» Patients usually discontinue oral anti-diabetic
drugs on admission.
» For patients who were not on insulin at home,

the total daily insulin dose can be initiated at
0.4 unit/kg/day when admission blood glucose
concentration is 7.8 to 11.1 mmol/L (140-200
mg/dL); or 0.5 unit/kg body weight/day when
admission blood glucose concentration is 11.2 to
22.2 mmol/L (201-400 mg/dL). Doses may need
to be lower in insulin-sensitive individuals such
as thin patients or those with type 1 diabetes,
in older people, or those with impaired renal
function.[1] Half of the calculated dose is to be
given as basal insulin, and the other half as
mealtime rapid-acting insulin, with the option
to add a rapid-acting correction sliding scale at
meals.
» For patients who were on insulin at home, their

home doses can be added up to give their total
daily insulin dose.
» Long-acting insulin is given once or twice daily.

Rapid-acting insulin should be given in divided
doses before each meal. Rapid-acting insulin
should not be given if the patient is not able to
eat.[36]
» For regimens using intermediate-acting insulin,

two-thirds of the total daily dose is given in the
morning (further divided into two-thirds NPH
insulin and one third fast-acting insulin), and one
third in the evening (further divided into half fast-
acting with the evening meal and half NPH at
bedtime).[36]
» One study suggests that basal insulin plus

sliding scale is an option for type 2 diabetes. In
375 patients with type 2 diabetes randomised
to receive either basal (glargine) plus sliding
scale insulin (glulisine), basal (glargine) and
scheduled mealtime plus correction sliding scale
(glulisine), or sliding scale insulin alone (regular
insulin), basal plus sliding scale and basal plus
scheduled mealtime plus sliding scale achieved
the same glycaemic control, and performed
better than sliding scale alone.[40]
» The use of sliding scales alone is not

recommended, although they may be used on
occasion for 24 hours to determine the insulin
MANAGEMENT
requirements in some patients.
» Hypoglycaemia should be avoided by regular

monitoring of blood glucose and changes in
therapy as needed (e.g., reducing insulin).
27
Acute
» A paediatric endocrinologist should be
consulted for children.
» In all patients, adequate nutrition and fluid
replacement should be ensured. Total parenteral
nutrition may be required in patients who are
not able to take orally. In patients with type 1
diabetes, a glucose-containing intravenous fluid
is appropriate, along with insulin (intravenous
preferred).
» Potassium should be added to intravenous

fluids according to local ward protocols to
prevent and treat hypokalaemia.

monitoring of blood glucose.
» Measurement of HbA1c is valuable in
determining the plan at discharge. A high HbA1c
indicates poor pre-existing control and suggests
need for increased or modified anti-diabetic
therapy (e.g., starting insulin or maximising oral
agents).[4] [10]
» A wide range of therapy is available for long-

term diabetes management. Some patients may
need to continue taking insulin at home until
complete recovery allows a transition to other
therapies.[15]
» Patients without known diabetes also need

follow-up blood sugar levels and possibly
continued treatment.
stable non-critical illness: well-
controlled known diabetes
eating normally 1st continuation of usual anti-diabetic

regimen + treatment of comorbid illness
Primary options
» insulin aspart: subcutaneously before each

MANAGEMENT
meal
-or-
» insulin glulisine: subcutaneously before
each meal
-or-
Acute
» insulin lispro: subcutaneously before each
meal
--AND--
» insulin isophane human (NPH):
subcutaneously twice daily, preferably in the
morning and at bedtime
-or-
» insulin glargine: subcutaneously once daily,
preferably at bedtime
-or-
» insulin detemir: subcutaneously once daily,
preferably at bedtime, or twice daily
-or-
» insulin degludec: subcutaneously once daily
» Insulin is the preferred form of treatment for

most inpatients. Oral agents may be used in
selected patients.[15]
» Patients on metformin should be closely

monitored given its contraindications (renal
impairment, heart failure, contrast studies) and it
will probably need to be discontinued. Sodium-
glucose co-transporter-2 inhibitors have been
associated with diabetic ketoacidosis, including
euglycaemic diabetic ketoacidosis, and it is
recommended to stop them upon admission,
and 3 days prior to scheduled surgery.[49]
Dipeptidyl dipeptidase-4 inhibitors with or without
long-acting basal insulin may be continued
in non-critically ill hospitalised patients with
mild to moderate hyperglycaemia.[50] [51]
[52] Thiazolidinediones are not recommended
in patients with fluid retention as part of
their presenting condition. Medications with
hypoglycaemic effects may be difficult to dose
appropriately with changes in the patient's
feeding status. General blood glucose targets
are: <7.8 mmol/L (140 mg/dL) pre-meals, and
random blood glucose <10 mmol/L (<180 mg/
dL), if these can be safely achieved without
hypoglycaemia.[1]
» Type 1 diabetes: inpatients who have well-

controlled blood glucose levels can continue
taking their usual insulin regimen.
» Type 2 diabetes: most inpatients are switched

to basal-bolus insulin regimen, but well-
controlled patients who are eating may be
able to continue on oral anti-diabetic agents, if
MANAGEMENT
there are no contraindications and if it can be

assured that the patient's feeding status will
not be switched to nil by mouth. For patients
taking metformin, switching to insulin would be
considered a safer option.
29
Acute
» Patients admitted for elective surgery on
oral anti-diabetic medication usually stop their
oral medications and start on intravenous
insulin intra-operatively or post-operatively, then
transition to subcutaneous basal-bolus insulin
once they start eating.
» Use of insulin on the general ward should be

based on a basal-bolus approach.[1] [36]
» For subcutanous insulin, basal insulin

can either be long-acting (glargine, detemir,
degludec) or intermediate-acting (NPH). Use of
second-generation basal insulins, such as insulin
glargine (300 units/mL) and insulin degludec
(100 units/mL and 200 units/mL), have lower
peak-to-trough ratios, have longer duration of
action than the first-generation basal insulins,
and provide less glycaemic variability. Patients
who use these preparations can be continued on
these while in hospital.[38] [39]
» For regimens using long-acting insulin, one

half of the total daily dose is be given as long-
acting insulin and one half as rapid-acting
insulin. Long-acting insulin should be given once
or twice daily. Rapid-acting insulin should be
given in divided doses before each meal.[36]
» For regimens using intermediate-acting insulin,

two-thirds of the total daily dose is given in the
morning (further divided into two-thirds NPH
insulin and one third fast-acting insulin), and one
third in the evening (further divided into half fast-
acting with the evening meal and half NPH at
bedtime).
» The use of sliding scales alone is not

recommended, although they may be used on
occasion for 24 hours to determine the insulin
requirements in some patients.
not eating 1st insulin (intravenous) + treatment of
comorbid illness
Primary options

» Intravenous insulin is considered appropriate

if the patient is not eating. Targets for patients
using intravenous insulin are 140 to 180 mg/
MANAGEMENT
dL.[1] However, this may be cumbersome and

not feasible in some settings, and so basal
insulin (preferably long-acting insulins as they
are relatively peakless) with or without correction
scale may be used instead.
Acute
» For patients with type 1 diabetes, withholding
insulin may lead to ketoacidosis, and an infusion
of glucose for nutrition, along with insulin
administration (e.g., intravenous) is essential.

therapy as needed (e.g., reducing insulin).
hypoglycaemia
able to take orally 1st oral carbohydrate + adjustment of diabetic

regimen
» Insulin can induce hypoglycaemia leading to

neuroglycopenia.
» Hypoglycaemia is associated with adverse

outcomes, especially in ICU patients. Sedation
or beta-blockers may mask symptoms of
neuroglycopenia, and counter-regulatory
responses may be impaired.
» Orange juice or oral glucose is given, along

with adjustment of regimen (e.g., decrease of
insulin dose).
» For refractory or severe hypoglycaemia,

intravenous glucose or intramuscular glucagon is
needed.
2nd glucose or glucagon
Primary options
» glucose: (50%) 25-50 mL intravenously as

a single dose
OR
» glucagon: 1 mg intramuscularly as a single

dose, may repeat in 20 minutes as needed

neuroglycopenia.


MANAGEMENT

therapy as needed (e.g., reducing an insulin
infusion rate promptly).
» If hypoglycaemia is severe or refractory to oral

treatment, glucose should be given intravenously
31
Acute
and blood glucose monitored closely for the
next hour. Alternatively, glucagon can be given
intramuscularly.
unable to take orally 1st glucose or glucagon + adjustment of
diabetic regimen
Primary options
» glucose: (50%) 25-50 mL intravenously as

a single dose
OR
» glucagon: 1 mg intramuscularly as a single

dose, may repeat in 20 minutes as needed

neuroglycopenia.


therapy as needed (e.g., reducing an insulin
infusion rate promptly).
» Glucose should be given intravenously and

blood glucose monitored closely for the next
hour. Alternatively, glucagon can be given
intramuscularly.
preoperative: minor elective surgery
1st management of diabetic regimen
» Patients admitted for minor elective surgery

who take oral anti-diabetic medication may
continue their oral medication if the procedure is
short and the patient is expected to eat later the
same day.
» For longer, more complicated procedures, oral

medication is usually discontinued in favour of
starting basal-bolus insulin given subcutaneously
starting the day of surgery.
» For patients using insulin before

hospitalisation, the dose of intermediate-acting
insulin is reduced by 30% to 50% the evening
MANAGEMENT
before surgery. True basal insulins such as

glargine, degludec, or detemir can usually be
given at or close to their routine dose. Rapid-
acting insulins are held while the patient is not
eating.
Acute
» Long and complicated surgical procedures
require intravenous insulin infusion for
glucose control and there are a number of
algorithms available. In converting stable post-
surgical patients from intravenous insulin to
subcutaneous basal-bolus regimens, the total
daily intravenous dose can be reduced by 20%.
Fifty percent of that total is then administered
as long-acting insulin once or twice daily with
the other 50% divided into two or three pre-meal
injections.
MANAGEMENT
33
Emerging
Newer glucagon formulations
Newer formulations of glucagon are available in some countries. These formulations are easier to use
in hypoglycaemic emergencies compared with the traditional formulation that requires severe steps for
reconstitution. An intranasal powder inhalation device is approved in the US and Europe for the treatment
of severe hypoglycaemia in adult and paediatric patients aged 4 years and above with diabetes. A pre-filled
subcutaneous autoinjector pen is approved in the US and Europe for the treatment of severe hypoglycaemia
in adult and paediatric patients aged 2 years and above with diabetes. A pre-filled subcutaneous autoinjector
containing the glucagon analogue dasiglucagon is approved in the US for the treatment of severe
hypoglycaemia in adult and paediatric patients aged 6 years and above with diabetes. Dasiglucagon has a
shelf-life of 36 months at refrigerated temperatures, and is stable for up to 12 months at room temperature.
To date, there are no data on the use of these newer formulations in the inpatient setting, and these options
are currently limited to outpatient use. However, the onset of action and efficacy in treating hypoglycaemia is
non-inferior to the more traditional glucagon rescue kit.[57] [58]
Continuous glucose monitoring

Several continuous glucose monitoring (CGM) devices have been approved for hospital use in Europe
(most sample glucose through the intravascular route, and one through the subcutaneous route) and in the
US (intravascular route). However, these are not yet widely available. The more pertinent issue is whether
ambulatory CGMs can be used in the hospital in non-critically ill patients, where fingerstick capillary blood
glucose has been the standard for monitoring. Initial studies on one device suggest that its use can assist in
reducing hyperglycaemia and hypoglycaemia in the non-ICU setting.[59]
Patient discussions
Diabetes education is paramount to the follow-up of a patient with diabetes. Educators can provide
information regarding nutritional goals, dietary modification, and exercise. Educators can re-emphasise
the short- and long-term management of glycaemia. Patients can also be taught about management of
intercurrent illness. [ADA: living with diabetes] (http://www.diabetes.org/living-with-diabetes)
MANAGEMENT
Inpatient glycaemic management Follow up
Monitoring
Monitoring
FOLLOW UP
After discharge, patients should follow up with their primary care providers within 2 to 3 weeks for
assessment of insulin needs and potential use of oral agents. Some patients may not need treatment for
hyperglycaemia after discharge given nutritional and medication adjustments.
Patients with known diabetes should undergo routine follow-up, which should include assessments for
diabetic retinopathy and diabetic neuropathy. Patients without known diabetes need follow-up to assess
their status once the acute illness has resolved: for example, with a fasting blood sugar or glucose
tolerance test.
Complications
Complications Timeframe Likelihood

intravenous fluid overload short term medium
Particularly in those with heart failure or renal impairment.
diabetic ketoacidosis short term medium
Precipitating factors include inadequate insulin therapy and infection. Myocardial infarction or stroke and
certain drugs (corticosteroids, thiazides, sympathomimetic agents, and second-generation antipsychotic
agents) may also provoke diabetic ketoacidosis.
Successful treatment includes correcting volume depletion, hyperglycaemia, electrolyte imbalances, and
comorbid precipitating events, with frequent monitoring.
insulin-induced hypokalaemia short term low
Associated with cardiac arrhythmias. Potassium should be added to intravenous fluids according to local
protocols to prevent and treat hypokalaemia.
Prognosis
Patients with newly discovered hyperglycaemia have been shown to have a significantly higher in-hospital
mortality (16%) than patients who have a history of diabetes (3%) or people with normoglycaemia (1.7%).[4]
Follow-up after discharge from hospital is extremely important in this population, as many of the factors
encountered during the hospital stay may not be evident after hospital discharge. Patients with pre-existing
diabetes mellitus should follow up with their physician for titration of insulin or adjustment/initiation of oral
therapy.
A wide range of therapy is available for long-term diabetes management. Some patients may need to
continue taking insulin at home until complete recovery allows a transition to other therapies.
35
Inpatient glycaemic management Guidelines
Diagnostic guidelines
North America
Standards of medical care in diabetes - 2021 (ht tps://

professional.diabetes.org/content-page/practice-guidelines-resources)
Published by: American Diabetes Association Last published: 2021
Clinical practice guidelines for the prevention and management of diabetes

in Canada (ht tp://guidelines.diabetes.ca/cpg)
Published by: Diabetes Canada Last published: 2018
Treatment guidelines
GUIDELINES
United Kingdom
A good inpatient diabetes service (ht tps://abcd.care/joint-british-diabetes-

societies-jbds-inpatient-care-group)
Published by: Joint British Societies for Inpatient Care Last published: 2020
Inpatient glycaemic management Guidelines
North America
Standards of medical care in diabetes - 2021 (ht tps://

professional.diabetes.org/content-page/practice-guidelines-resources)
Published by: American Diabetes Association Last published: 2021
Preoperative management of endocrine, hormonal, and urologic

medications: Society for Perioperative Assessment and Quality Improvement
(SPAQI) consensus statement (ht tps://www.spaqi.org/web/resources-
position_papers.php)
Published by: Society for Perioperative Assessment and Quality Last published: 2021
Improvement
Clinical practice guidelines for the prevention and management of diabetes

in Canada (ht tp://guidelines.diabetes.ca/cpg)
Published by: Diabetes Canada Last published: 2018
GUIDELINES
Management of hyperglycemia in hospitalized patients in non-critical care
set ting (ht tps://www.endocrine.org/education-and-practice-management/
clinical-practice-guidelines)
Published by: The Endocrine Society Last published: 2012
AACE/ADA consensus statement on inpatient glycemic control (ht tps://

pro.aace.com/disease-state-resources/diabetes/position-and-consensus-
statements/american-association-clinical)
Published by: American Association of Clinical Endocrinologists; Last published: 2009
American Diabetes Association
37
Inpatient glycaemic management Online resources
Online resources
1. Yale Insulin Infusion Protocol (http://care.diabetesjournals.org/content/27/2/461/F1.large.jpg) (external
link)
2. ADA: living with diabetes (http://www.diabetes.org/living-with-diabetes) (external link)

ONLINE RESOURCES
Inpatient glycaemic management References
Key articles
• American Diabetes Association. Standards of medical care in diabetes - 2021. Diabetes Care.
REFERENCES
2021;44(suppl 1):S1-S232. Full text (https://care.diabetesjournals.org/content/44/Supplement_1)
• Moghissi ES, Korytkowski MT, DiNardo M, et al. American Association of Clinical Endocrinologists
and American Diabetes Association consensus statement on inpatient glycemic control. Endocr Pract.
2009 May-Jun;15(4):353-69. Full text (https://journals.aace.com/doi/pdf/10.4158/EP09102.RA)
Abstract (http://www.ncbi.nlm.nih.gov/pubmed/19454396?tool=bestpractice.bmj.com)
• Pasquel FJ, Lansang MC, Dhatariya K, et al. Management of diabetes and hyperglycaemia in the
hospital. Lancet Diabetes Endocrinol. 2021 Mar;9(3):174-188. Full text (https://www.doi.org/10.1016/
S2213-8587(20)30381-8) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/33515493?
tool=bestpractice.bmj.com)
• Finfer S, Chittock DR, Su SY, et al. NICE-SUGAR Study Investigators. Intensive versus conventional
glucose control in critically ill patients. N Engl J Med. 2009 Mar 26;360(13):1283-97. Full text (http://
www.nejm.org/doi/full/10.1056/NEJMoa0810625#t=article) Abstract (http://www.ncbi.nlm.nih.gov/
pubmed/19318384?tool=bestpractice.bmj.com)
• Umpierrez G, Smiley D, Zisman A, et al. Randomized study of basal-bolus insulin therapy in the
inpatient management of patients with type 2 diabetes (RABBIT 2 trial). Diabetes Care. 2007
Sep;30(9):2181-6. Full text (http://care.diabetesjournals.org/content/30/9/2181.long) Abstract (http://
www.ncbi.nlm.nih.gov/pubmed/17513708?tool=bestpractice.bmj.com)
References
1. American Diabetes Association. Standards of medical care in diabetes - 2021. Diabetes Care.
2021;44(suppl 1):S1-S232. Full text (https://care.diabetesjournals.org/content/44/Supplement_1)
2. Diabetes Canada (Canadian Diabetes Association). Clinical practice guidelines for the prevention and
management of diabetes in Canada. 2018 [internet publication]. Full text (http://guidelines.diabetes.ca/
cpg)
3. Umpierrez GE, Isaacs SD, Bazargan N, et al. Hyperglycemia: an independent marker of in-hospital
mortality in patients with undiagnosed diabetes. J Clin Endocrinol Metab. 2002 Mar;87(3):978-82. Full
text (http://jcem.endojournals.org/cgi/content/full/87/3/978) Abstract (http://www.ncbi.nlm.nih.gov/
4. Fonseca V. Newly diagnosed diabetes/hyperglycemia in hospitals: what should we do? Endocr

Pract. 2006 Jul-Aug;12 Suppl 3:108-11. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/16905526?
39
5. Levetan CS, Magee MF. Hospital management of diabetes. Endocrinol Metab Clin
North Am. 2000;29:745-770. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/11149160?
REFERENCES
6. Finney SJ, Zekveld C, Elia A, et al. Glucose control and mortality in critically ill patients.
JAMA. 2003;290:2041-2047. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/14559958?
7. Inzucchi SE. Clinical practice: management of hyperglycemia in the hospital setting. N Engl
J Med. 2006;355:1903-1911. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/17079764?
8. Pasquel FJ, Smiley D, Spiegelman R, et al. Hyperglycemia is associated with increased hospital
complications and mortality during parenteral nutrition. Hosp Pract (Minneap). 2011;39:81-88. Abstract
(http://www.ncbi.nlm.nih.gov/pubmed/21576900?tool=bestpractice.bmj.com)
9. ACE/ADA Task Force on Inpatient Diabetes. American College of Endocrinology and American
Diabetes Association consensus statement on inpatient diabetes and glycemic control. Endocr Pract.
2006 Jul-Aug;12(4):458-68. Full text (http://care.diabetesjournals.org/content/29/8/1955.full) Abstract
10. Moghissi ES, Korytkowski MT, DiNardo M, et al. American Association of Clinical Endocrinologists
and American Diabetes Association consensus statement on inpatient glycemic control. Endocr Pract.
2009 May-Jun;15(4):353-69. Full text (https://journals.aace.com/doi/pdf/10.4158/EP09102.RA)
11. Fonseca V. Clinical diabetes: translating research into practice. Philadelphia, PA: Elsevier Health
Sciences; 2006.
12. Kornum JB, Thomsen RW, Riis A, et al. Diabetes, glycemic control, and risk of hospitalization with
pneumonia. Diabetes Care. 2008 Aug;31(8):1541-5. Full text (http://care.diabetesjournals.org/
content/31/8/1541.full) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/18487479?
13. Kwon S, Hermayer KL. Glucocorticoid-induced hyperglycemia. Am J Med Sci. 2013 Apr;345(4):274-7.
14. Farrokhi F, Klindukhova O, Chandra P, et al. Risk factors for inpatient hypoglycemia during
subcutaneous insulin therapy in non-critically ill patients with type 2 diabetes. J Diabetes
Sci Technol. 2012 Sep 1;6(5):1022-9. Full text (http://www.ncbi.nlm.nih.gov/pmc/articles/
PMC3570835/pdf/dst-06-1022.pdf) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/23063027?
15. Pasquel FJ, Lansang MC, Dhatariya K, et al. Management of diabetes and hyperglycaemia in the
hospital. Lancet Diabetes Endocrinol. 2021 Mar;9(3):174-188. Full text (https://www.doi.org/10.1016/
S2213-8587(20)30381-8) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/33515493?
16. van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients.
N Engl J Med. 2001 Nov 8;345(19):1359-67. Full text (http://www.nejm.org/doi/full/10.1056/
NEJMoa011300#t=article) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/11794168?
REFERENCES
17. Marik PE, Preiser JC. Toward understanding tight glycemic control in the ICU: a systematic
review and metaanalysis. Chest. 2010 Mar;137(3):544-51. Full text (http://journal.chestnet.org/
article/S0012-3692(10)60130-4/pdf) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/20018803?
18. Finfer S, Chittock DR, Su SY, et al. NICE-SUGAR Study Investigators. Intensive versus conventional
glucose control in critically ill patients. N Engl J Med. 2009 Mar 26;360(13):1283-97. Full text (http://
www.nejm.org/doi/full/10.1056/NEJMoa0810625#t=article) Abstract (http://www.ncbi.nlm.nih.gov/
19. Preiser JC, Devos P, Ruiz-Santana S, et al. A prospective randomised multi-centre controlled trial
on tight glucose control by intensive insulin therapy in adult intensive care units: the Glucontrol
study. Intensive Care Med. 2009 Oct;35(10):1738-48. Abstract (http://www.ncbi.nlm.nih.gov/
20. van Kuijk JP, Schouten O, Flu WJ, et al. Perioperative blood glucose monitoring and control in major
vascular surgery patients. Eur J Vasc Endovasc Surg. 2009 Nov;38(5):627-34. Abstract (http://
21. Wiener RS, Wiener DC, Larson RJ. Benefits and risks of tight glucose control in critically ill adults:
a meta-analysis. JAMA. 2008 Aug 27;300(8):933-44. Abstract (http://www.ncbi.nlm.nih.gov/
22. Deedwania P, Kosiborod M, Barrett E, et al. Hyperglycemia and acute coronary syndrome: a
scientific statement from the American Heart Association Diabetes Committee of the Council on
Nutrition, Physical Activity, and Metabolism. Circulation. 2008 Mar 25;117(12):1610-9. Full text
(http://circ.ahajournals.org/content/117/12/1610.long) Abstract (http://www.ncbi.nlm.nih.gov/
23. Inzucchi SE, Siegel MD. Glucose control in the ICU: how tight is too tight? New Engl J Med.
2009 Mar 26;360(13):1346-9. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/19318385?
24. Moghissi ES. Addressing hyperglycemia from hospital admission to discharge. Curr Med
Res Opin. 2010 Mar;26(3):589-98. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/20078323?
25. Qaseem A, Humphrey LL, Chou R, et al. Use of intensive insulin therapy for the management of
glycemic control in hospitalized patients: a clinical practice guideline from the American College
of Physicians. Ann Intern Med. 2011 Feb 15;154(4):260-7. Abstract (http://www.ncbi.nlm.nih.gov/
41
26. Kansagara D, Fu R, Freeman M, et al. Intensive insulin therapy in hospitalized patients: a systematic
review. Ann Intern Med. 2011 Feb 15;154(4):268-82. Abstract (http://www.ncbi.nlm.nih.gov/
REFERENCES
27. Diabetes Canada (Canadian Diabetes Association). Clinical practice guidelines for the prevention and
management of diabetes in Canada. 2018 [internet publication]. Full text (http://guidelines.diabetes.ca/
cpg)
28. Qaseem A, Chou R, Humphrey LL, et al. Inpatient glycemic control: best practice advice from the
Clinical Guidelines Committee of the American College of Physicians. Am J Med Qual. 2014 Mar-
Apr;29(2):95-8. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/23709472?tool=bestpractice.bmj.com)
29. Kao LS, Meeks D, Moyer VA, et al. Peri-operative glycaemic control regimens for preventing
surgical site infections in adults. Cochrane Database Syst Rev. 2009;(3):CD006806. Full text
(http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD006806.pub2/abstract) Abstract (http://
30. Liu Y, Yang YM, Zhu J, et al. Prognostic significance of hemoglobin A1c level in patients hospitalized
with coronary artery disease. A systematic review and meta-analysis. Cardiovasc Diabetol. 2011
Nov 10;10:98. Full text (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3225330) Abstract (http://
31. Vergès B, Avignon A, Bonnet F, et al; Diabetes and Cardiovascular Disease Study Group of the
Société Francophone du Diabète (SFD), Société Française de Cardiologie (SFC). Consensus
statement on the care of the hyperglycaemic/diabetic patient during and in the immediate follow-
up of acute coronary syndrome. Diabetes Metab. 2012 Apr;38(2):113-27. Abstract (http://
32. Bielen I, Sruk A, Zalac D. Specificity of hyperglycemia treatment in acute stroke patients. Acta
Med Croatica. 2008 Jul;62(3):273-80. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/18843847?
33. Ooi YC, Dagi TF, Maltenfort M, et al. Tight glycemic control reduces infection and improves
neurological outcome in critically ill neurosurgical and neurological patients. Neurosurgery.
2012 Sep;71(3):692-702. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/22688953?
34. Gilo Arrojo F, Herrera Muñoz A, Anciones Rodríguez B. Recommendations for an adequate
glycemic control during hospitalization after a stroke episode [in Spanish]. Avances en
Diabetologia. 2010;26:408-412. Full text (http://www.avancesendiabetologia.org/gestor/upload/
revistaAvances/26-6-5.pdf)
35. Ellger B, Westphal M, Stubbe HD, et al. Glycemic control in sepsis and septic shock: friend or
foe? [in German]. Anaesthesist. 2008 Jan;57(1):43-8. Abstract (http://www.ncbi.nlm.nih.gov/
36. Umpierrez G, Smiley D, Zisman A, et al. Randomized study of basal-bolus insulin therapy in the
inpatient management of patients with type 2 diabetes (RABBIT 2 trial). Diabetes Care. 2007
Sep;30(9):2181-6. Full text (http://care.diabetesjournals.org/content/30/9/2181.long) Abstract (http://
REFERENCES
37. Umpierrez GE, Smiley D, Jacobs S, et al. Randomized study of basal-bolus insulin therapy in
the inpatient management of patients with type 2 diabetes undergoing general surgery (RABBIT
2 surgery). Diabetes Care. 2011 Feb;34(2):256-61. Full text (http://www.ncbi.nlm.nih.gov/pmc/
articles/PMC3024330/pdf/256.pdf) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/21228246?
38. Pasquel FJ, Lansang MC, Khowaja A, et al. A randomized controlled trial comparing Glargine U300
and Glargine U100 for the inpatient management of medicine and surgery patients with type 2
diabetes: Glargine U300 hospital trial. Diabetes Care. 2020 Jun;43(6):1242-1248. Full text (https://
www.doi.org/10.2337/dc19-1940) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/32273271?
39. Suzuki J, Yamakawa T, Oba M, et al. Efficacy and safety of insulin degludec U100 and insulin glargine
U100 in combination with meal-time bolus insulin in hospitalized patients with type 2 diabetes: an
open-label, randomized controlled study. Endocr J. 2019 Nov 28;66(11):971-982. Full text (https://
www.doi.org/10.1507/endocrj.EJ18-0309) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/31270291?
40. Umpierrez GE, Smiley D, Hermayer K, et al. Randomized study comparing a basal-bolus with a
basal plus correction insulin regimen for the hospital management of medical and surgical patients
with type 2 diabetes: basal plus trial. Diabetes Care. 2013 Aug;36(8):2169-74. Abstract (http://
41. Vellanki P, Bean R, Oyedokun FA, et al. Randomized controlled trial of insulin supplementation for
correction of bedtime hyperglycemia in hospitalized patients with type 2 diabetes. Diabetes Care. 2015
Apr;38(4):568-74. Full text (http://care.diabetesjournals.org/content/38/4/568.long) Abstract (http://
42. Svensson AM, McGuire DK, Abrahamsson P, et al. Association between hyper- and hypoglycemia
and 2 year all-cause mortality risk in diabetic patients with acute coronary events. Eur Heart
J. 2005 Jul;26(13):1255-61. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/15821004?
43. Dumont C, Bourguignon C. Effect of a computerized insulin dose calculator on the process of
glycemic control. Am J Crit Care. 2012 Mar;21(2):106-15. Full text (http://ajcc.aacnjournals.org/
content/21/2/106.full.pdf+html) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/22381987?
44. Steil GM, Langer M, Jaeger K, et al. Value of continuous glucose monitoring for minimizing severe
hypoglycemia during tight glycemic control. Pediatr Crit Care Med. 2011 Nov;12(6):643-8. Abstract
45. Klonoff DC. Intensive insulin therapy in critically ill hospitalized patients: making it safe and effective.
J Diabetes Sci Technol. 2011 May 1;5(3):755-67. Full text (http://www.ncbi.nlm.nih.gov/pmc/articles/
PMC3192642) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/21722591?tool=bestpractice.bmj.com)
43
46. Goldberg PA, Siegel MD, Sherwin RS, et al. Implementation of a safe and effective insulin infusion
protocol in a medical intensive care unit. Diabetes Care. 2004 Feb;27(2):461-7. Full text (http://
care.diabetesjournals.org/cgi/content/full/27/2/461) Abstract (http://www.ncbi.nlm.nih.gov/
REFERENCES
47. Adams G, Hunter J, Langley J, et al. Is nurse-managed blood glucose control in critical
care as safe and effective as the traditional sliding scale method? Intensive Crit Care
Nurs. 2009 Dec;25(6):294-305. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/19850481?
48. Pinelli NR, Jones MC, Monday LM, et al. Exogenous glucagon-like peptide-1 for hyperglycemia in
critically ill patients. Ann Pharmacother. 2012 Jan;46(1):124-9. Abstract (http://www.ncbi.nlm.nih.gov/
49. Thiruvenkatarajan V, Meyer EJ, Nanjappa N, et al. Perioperative diabetic ketoacidosis associated with
sodium-glucose co-transporter-2 inhibitors: a systematic review. Br J Anaesth. 2019 Jul;123(1):27-36.
Full text (https://www.doi.org/10.1016/j.bja.2019.03.028) Abstract (http://www.ncbi.nlm.nih.gov/
50. Pasquel FJ, Gianchandani R, Rubin DJ, et al. Efficacy of sitagliptin for the hospital management of
general medicine and surgery patients with type 2 diabetes (Sita-Hospital): a multicentre, prospective,
open-label, non-inferiority randomised trial. Lancet Diabetes Endocrinol. 2017 Feb;5(2):125-133. Full
text (https://www.doi.org/10.1016/S2213-8587(16)30402-8) Abstract (http://www.ncbi.nlm.nih.gov/
51. Garg R, Schuman B, Hurwitz S, et al. Safety and efficacy of saxagliptin for glycemic control in
non-critically ill hospitalized patients. BMJ Open Diabetes Res Care. 2017;5(1):e000394. Full
text (https://www.doi.org/10.1136/bmjdrc-2017-000394) Abstract (http://www.ncbi.nlm.nih.gov/
52. Vellanki P, Rasouli N, Baldwin D, et al. Glycaemic efficacy and safety of linagliptin compared to
a basal-bolus insulin regimen in patients with type 2 diabetes undergoing non-cardiac surgery:
A multicentre randomized clinical trial. Diabetes Obes Metab. 2019 Apr;21(4):837-843. Full text
(https://www.doi.org/10.1111/dom.13587) Abstract (http://www.ncbi.nlm.nih.gov/pubmed/30456796?
53. The Endocrine Society. Management of hyperglycemia in hospitalized patients in non-critical care
setting. 2012 [internet publication]. Full text (https://academic.oup.com/jcem/article/97/1/16/2833111/
Management-of-Hyperglycemia-in-Hospitalized)
54. NHS Diabetes. The hospital management of hypoglycaemia in adults with diabetes mellitus.
September 2013 [internet publication]. Full text (http://www.diabetes.org.uk/Documents/About%20Us/
Our%20views/Care%20recs/JBDS%20hypoglycaemia%20position%20(2013).pdf)
55. Agus MS, Steil GM, Wypij D, et al; SPECS Study Investigators. Tight glycemic control versus
standard care after pediatric cardiac surgery. N Engl J Med. 2012 Sep 27;367(13):1208-19. Full
text (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501680/pdf/nihms415945.pdf) Abstract (http://
56. Agus MS, Wypij D, Hirshberg EL, et al. Tight glycemic control in critically ill children. N Engl J
Med. 2017 Feb 23;376(8):729-41. Abstract (http://www.ncbi.nlm.nih.gov/pubmed/28118549?
REFERENCES
57. Rickels MR, Ruedy KJ, Foster NC, et al. Intranasal glucagon for treatment of insulin-induced
hypoglycemia in adults with type 1 diabetes: A randomized crossover noninferiority study. Diabetes
Care. 2016 Feb;39(2):264-70. Full text (https://www.doi.org/10.2337/dc15-1498) Abstract (http://
58. Christiansen MP, Cummins MJ, Presteelski SJ, et al. A phase 3 comparison of a novel liquid glucagon
autoinjector to glucagon emergency kit for the symptomatic relief of severe hypoglycemia. Diabetes
2018 Jul; 67(Supplement 1). Full text (https://doi.org/10.2337/db18-304-OR)
59. Singh LG, Satyarengga M, Marcano I, et al. Reducing inpatient hypoglycemia in the general wards
using real-time continuous glucose monitoring: The glucose telemetry system, a randomized clinical
trial. Diabetes Care. 2020 Nov;43(11):2736-2743. Full text (https://www.doi.org/10.2337/dc20-0840)
45
Inpatient glycaemic management Disclaimer
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Figure 1 – BMJ Best Practice Numeral Style
Inpatient glycaemic management Disclaimer
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numerals < 1: 0.25
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47
Contributors:
// Authors:
M. Cecilia Lansang, MD, MPH

Professor of Medicine
Director of Endocrinology, Main Campus, Department of Endocrinology, Diabetes and Metabolism,
Cleveland Clinic, Cleveland, OH
DISCLOSURES: MCL is a consultant for the Sanofi group of companies.
Keren Zhou, MD
Clinical Assistant Professor of Medicine
Research Director, Endocrinology and Metabolism Institute, Department of Endocrinology, Diabetes and
Metabolism, Cleveland Clinic, Cleveland, OH
DISCLOSURES: KZ declares that she has no competing interests.
// Acknowledgements:
Dr M. Cecilia Lansang and Dr Keren Zhou would like to gratefully acknowledge Dr Suzanne Quinn, Dr Ajay
Rao and Dr Vivian Fonseca, previous contributors to this monograph.
DISCLOSURES: SQ, AR and VF declare that they have no competing interests.
// Peer Reviewers:
Guillermo E. Umpierrez, MD
Professor of Medicine
Division of Endocrinology, Metabolism and Lipids, Emory University School of Medicine, Atlanta, GA
DISCLOSURES: GEU is an author of a number of references cited in this monograph.
Daniel Morganstein, MBBS, MA (Cantab), MRCP, PhD

Consultant Diabetologist
Beta Cell Unit, Chelsea and Westminster NHS Trust, London, UK
DISCLOSURES: DM declares that he has no competing interests.
Sean Dinneen, MBBCh, FRCPI, FACP

Senior Lecturer in Medicine
National University of Ireland, Consultant in Diabetes and Endocrinology, Galway University Hospitals,
Galway, Ireland
DISCLOSURES: SD declares that he has no competing interests.

Inpatient Glycaemic Management

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Inpatient Glycaemic Management

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Inpatient glycaemic

Straight to the point of care

Last updated: Sep 24, 2021

• Known diabetes mellitus before admission.

Type 1 diabetes mellitus[1]

• Fasting plasma glucose: ≥7 mmol/L (≥126 mg/dL)

• Random plasma glucose ≥11.1 mmol/L (≥200 mg/dL).

• Plasma and urine ketones: elevated in ketoacidosis

Type 2 diabetes mellitus[1] [2]

May have features of metabolic syndrome (hypertension, obesity, and hyperlipidaemia).

Polyuria, polydipsia, and unintentional weight loss may occur.

• Fasting plasma glucose: ≥7 mmol/L (≥126 mg/dL)

In a patient with unequivocal symptoms of hyperglycaemia:

• A random plasma glucose ≥11.1 mmol/L (≥200 mg/dL).

History and exam

presence of risk factors for hypoglycaemia (common)

history of diabetes mellitus (common)

signs of hypoglycaemia (common)

Other diagnostic factors

signs of diabetic retinopathy (common)

signs of diabetic neuropathy (common)

corticosteroid use (hyperglycaemia)

poorly controlled diabetes mellitus (hyperglycaemia)

insulin administration (hypoglycaemia)

changes to corticosteroid or insulin regimen (hypoglycaemia or

poor nutritional intake (hypoglycaemia)

older age or cognitive impairment (hypoglycaemia)

Other tests to consider

Condition Differentiating signs / Differentiating tests

Type 1 diabetes mellitus • May have a genetic • HbA1c ≥48 mmol/mol

Pre-diabetes • Risk factors and history • Impaired fasting glucose:

Condition Differentiating signs / Differentiating tests

Goals of glycaemic control

Uncontrolled hyperglycaemia; surgery; or critical illness

• Most patients should discontinue oral anti-diabetic drugs on admission.

Other considerations include:

daily insulin dose.

Well-controlled pre-existing diabetes: stable non-critical illness

section for more information.

Treatment algorithm overview

1st insulin + treatment of comorbid illness

plus supportive care

plus follow-up and optimisation of outpatient

stable non-critical illness:

1st insulin (subcutaneous or intravenous) +

plus supportive care

plus follow-up and optimisation of outpatient

stable non-critical illness: well-

eating normally 1st continuation of usual anti-diabetic

not eating 1st insulin (intravenous) + treatment of

able to take orally 1st oral carbohydrate + adjustment of diabetic

2nd glucose or glucagon

unable to take orally 1st glucose or glucagon + adjustment of

preoperative: minor elective surgery

1st management of diabetic regimen

1st insulin + treatment of comorbid illness

» insulin neutral: intravenously; consult

» Effective management of hyperglycaemia

» Blood glucose targets are 7.8 to 10.0 mmol/L

» Intravenous insulin is recommended for all

» Hypoglycaemia should be avoided.

» The mortality benefit of intensive glycaemic

» Greater benefit has been demonstrated for