Diabetic
Emergencies
Objectives
General Objective:
• Identify the common diabetic complications in an
emergency setting.
Specific Objective:
• Describe diabetic ketoacidosis, hyperosmolar syndrome,
and hypoglycemia.
• Describe their diagnosis, treatment, and prevention.
Introduction
• People with diabetes suffer from diabetic
complications that may arise due to erratic blood sugar
levels, missed meals, accidental overdose of medications,
or too much strenuous exercise. These things could affect
the sensitive body of a person with diabetes and could
lead to serious incidences of hypoglycemia or
hyperglycemia.
Introduction
• Uncontrolled blood sugar often contributes to the
incidence of diabetic emergencies and complications.
Individuals who experience blood sugar levels that are too
high or low for prolonged periods of time may develop
conditions that could lead to a coma.
• Hypoglycemia results from excessively low blood sugar
levels caused by either insufficient food consumption or
the presence of too much insulin.
Introduction
• Diabetic ketoacidosis is a condition that occurs due to an
absence or insufficient supply of insulin, which forces the
body to burn fat and creates ketones that subsequently
accumulate in the body.
• Hyperosmolar syndrome is a diabetic condition that
results from excessively high blood sugar levels, which
cause the blood to adopt a thick consistency.
Hypoglycemia
• Hypoglycemia or low blood glucose is a clinical
state associated with <55mg/dl or low plasma
glucose with typical symptoms.
The Journal of Clinical
Endocrinology & Metabolism
March 1, 2009 vol. 94 no. 3 709-728
Whipples triad
Symptoms consistent with hypoglycemia
Low plasma glucose concentration
Relief of those symptoms after the plasma glucose
level is raised
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Endocrinology & Metabolism
March 1, 2009 vol. 94 no. 3 709-728
Physiological responses
The Journal of Clinical Endocrinology & Metabolism March 1,
Risk factors
insulin doses are excessive, ill-timed, or of the wrong
type
influx of exogenous glucose
insulin-independent glucose utilization
sensitivity to insulin
endogenous glucose production
insulin clearance
The Journal of Clinical
Endocrinology & Metabolism
March 1, 2009 vol. 94 no. 3 709-728
Clinical features
MILD HYPOGLYCEMIA
- mainly adrenergic or cholinergic symptoms
Pallor
Diaphoresis
Tachycardia
Palpitations
Hunger
Paresthesias
The Journal of Clinical
Endocrinology & Metabolism
March 1, 2009 vol. 94 no. 3 709-728
Clinical features
MODERATE HYPOGLYCEMIA (<40 mg/dL)
- mainly neuroglycopenic symptoms
Inability to concentrate Confusion
Slurred speech Irrational behaviour
Slower reaction time Blurred vision
Somnolence Extreme fatigue
The Journal of Clinical
Endocrinology & Metabolism
March 1, 2009 vol. 94 no. 3 709-728
Clinical features
SEVERE HYPOGLYCEMIA (<20 mg/dL )
Associated with severe impairment of neurologic function
Completely disoriented behavior
LOC
Coma
Seizures
The Journal of Clinical
Endocrinology & Metabolism
March 1, 2009 vol. 94 no. 3 709-728
Treatment
MILD HYPOGLYCEMIA
Oral carbohydrates (at least 15gm)
Sources include
• Three glucose tablets (5g each)
• 2 ½ cups of fruit juice
• ½ to ¾ cup regular soda
• 1 cup of milk
If patient is unable to take orally give IV dextrose
The Journal of Clinical
Endocrinology & Metabolism
March 1, 2009 vol. 94 no. 3 709-728
Treatment
MODERATE TO SEVERE HYPOGLYCEMIA
Dextrose - 50mL of 50% dextrose IV bolus after blood
draw followed by 10% dextrose
Glucagon – 1mg IM or SC can be given
Effective in treating hypoglycemia only if sufficient liver
glycogen present
These measures raise blood glucose only transiently
Patient is urged to eat as soon as possible
The Journal of Clinical
Endocrinology & Metabolism
March 1, 2009 vol. 94 no. 3 709-728
Prevention
Patient education
Knowing signs and symptoms of hypoglycemia
Take meals on a regular schedule
Carry a source of carbohydrate
Self monitoring of blood glucose
Take regular insulin at least 30 min before eating
The Journal of Clinical
Endocrinology & Metabolism
March 1, 2009 vol. 94 no. 3 709-728
Diabetic
Ketoacidosis
Acute, major, life-threatening complication of diabetes
Increase in the serum concentration of ketones
Blood glucose level of greater than 250 mg/dL
Blood pH of less than 7.2
Bicarbonate level of 18 mEq/L or less
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Incidence about 1 out of 2000
Usually occurs in younger individuals but can occur in
patients with diabetes at any age
Mortality rates are around 2-5%
No sex predilection
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Mechanism
Absolute or relative insulin deficiency
Increased gluconeogenesis
Elevation of counter regulatory hormones such as
glucagon, cortisol, growth hormone, and catecholamines
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Causes
• Infections
• Inadequate insulin treatment or non-compliance
• New onset diabetes
• Infarction
• Drugs
• Pregnancy
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Classification
Moderate
Mild DKA Severe DKA
DKA
Plasma glucose > 250 mg/dl > 250 mg/dl > 250 mg/dl
Arterial ph 7.25-7.30 7.0-7.24 < 7.0
Serum
15-18 10-<15 < 10
bicarbonate
Urine ketones + + +
Anion gap >10 >12 >12
Alteration in
alert Alert/drowsy stupor/coma
Joint British Diabetes Society guideline for the management
sensorium
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Clinical presentations
• Nausea/vomiting Thirst/polyuria
• Abdominal pain Shortness of breath
• Generalized weakness Malaise/lethargy
• Confusional state
• Fever, dysuria, coughing
• Chest pain
• Palpitations
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Physical findings
Tachycardia
Signs of dehydration - weak and rapid pulse, dry tongue
and skin, hypotension, and increased capillary refill time
Tachypnea/ respiratory distress
Acetone odor in breath
Abdominal tenderness
Lethargy/ obtundation/ cerebral edema/ possibly coma
Fever/ Hypothermia
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Laboratory findings
Hyperglycemia >250mg/dL
Serum ketones +
ABG:
metabolic acidosis
low bicarbonate
low pH (<7.2)
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Serum electrolytes
• Serum potassium may be mildly elevated despite total
body potassium deficit
• The serum sodium level usually is low (1.6meq reduction
in serum sodium for each 5.6mmol/L or 100mg/dL of rise
in serum glucose)
• The serum chloride and phosphorus levels are low
The anion gap is elevated
Plasma osmolarity usually is increased (>290 mOsm/L).
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Others
Leukocytosis (even without infection)
BUN and creatinine are frequently increased
Hypertriglyceridemia/ Hyperlipoproteinemia
Serum assays for β hydroxybutrate more accurately
reflects the true ketone body level
• ECG – for detection of hypokalemia/ hyperkalemia,
myocardial infarction (silent MI in diabetics)
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Differential diagnosis
LACTIC ACIDOSIS
most common cause of metabolic acidosis in hospitalized
patients
presentation is identical to DKA
serum glucose and ketones should be normal
serum lactate concentration should be greater than 5mm
therapy is directed at the underlying cause and optimizing
tissue perfusion
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Differential diagnosis
STARVATION KETOSIS
due to inadequate carbohydrate availability, resulting in
lipolysis and ketone production
blood glucose is usually normal
blood rarely does have large amounts of ketones
arterial pH is normal
anion gap is at most mildly elevated
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Differential diagnosis
ALCOHOLIC KETOACIDOSIS
• anion gap is elevated
• serum and urine ketones are present
• alcoholic ketoacidosis produces an even higher ratio of β-
hydroxybutyrate to acetoacetate than DKA does
• usually, patient is normoglycemic or hypoglycemic
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Differential diagnosis
UREMIC ACIDOSIS
Extremely large elevations in the BUN (>200 mg/dL) and
creatinine (>10 mg/dL) with normoglycemia
pH and anion gap are usually only mildly abnormal
treatment is supportive, with careful attention to fluid and
electrolytes until dialysis can be performed
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Treatment
IV FLUIDS
• 2-3L of 0.9% saline over first 1–3 h (10–15mL/kg per
hour)
• 0.45% saline at 150-300mL/h (if hemodynamically stable
and urine output is adequate )
• change to 5% glucose and 0.45% saline at 100–200 mL/h
when plasma glucose reaches 250mg/dL (14mmol/L).
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Treatment
INSULIN
• if serum K+ is <3.3mmol/L, do not administer insulin until
it is corrected to >3.3mmol/L
• bolus of IV (0.1 units/kg) or IM (0.3 units/kg) short-acting
insulin followed by 0.1 units/kg/hr by continuous IV
infusion
• Increase 2- to 3-fold if no response by 2–4h
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Treatment
INSULIN
• IV regular insulin should be given until the acidosis
resolves and the patient is metabolically stable
• Intermediate or long-acting insulin, in combination with
SC short-acting insulin, should be administered as soon as
the patient resumes eating
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Treatment
MONITOR
Blood glucose every 1–2 h;
Serum electrolytes and anion gap every 4 h for first 24 h.
Blood pressure, pulse, respirations, mental status, fluid
intake and output every 1–4 h.
Joint British Diabetes Society guideline for the management
of diabetic ketoacidosis Diabetic Medicine Volume 28, Issue
5, pages 508–515, May 2011
Hyperosmolar
Hyperglycemic
State
The condition is characterized by
• Hyperglycemia
• Hyperosmolarity
• Dehydration without significant ketoacidosis
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Incidence is 1.7 case per 10000
Mortality rate is high (10-20%) and usually due to a co-
morbid illness
(HHS) has a mean age of onset early in the seventh
decade
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Pathophysiology
Relative insulin deficiency and inadequate fluid intake
Insulin deficiency increases hepatic glucose production
(through glycogenolysis and gluconeogenesis) and
impairs glucose utilization in skeletal muscle
Hyperglycemia induces an osmotic diuresis that leads to
intravascular volume depletion, which is exacerbated by
inadequate fluid replacement
Lower levels of counterregulatory hormones and free
fatty acids have been found in HHS than in DKA
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Clinical features
HISTORY
Usually elderly individual, type 2 DM
Mental confusion, lethargy, and coma
Absence of nausea, vomiting, abdominal pain
Frequent precipitants – pneumonia, sepsis, stroke MI,
etc.,
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vs DKA
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Treatment
IV FLUIDS
1–3L of 0.9% normal saline over the first 2–3 h. If the
serum sodium >150 meq/L, 0.45% saline should be used.
After hemodynamic stability is achieved, the IV fluid
administration is directed at reversing the free water
deficit using hypotonic fluids (0.45% saline initially then
D5W).
The calculated free water deficit (which averages 9–10L)
should be reversed over the next 1–2 days (infusion rates
of 200–300 mL/h of hypotonic10.2337/diacare.27.2007.S94
solution).
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Treatment
INSULIN
• IV insulin bolus of 0.1units/kg followed by IV insulin at a
constant infusion rate of 0.1units/kg per hour.
• If the serum glucose does not fall, increase the insulin
infusion rate by twofold
• Glucose should be added to IV fluid when the plasma
glucose falls to 250 mg/dL, and the insulin infusion rate
should be decreased to 0.05–0.1units/kg per hour.
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Treatment
INSULIN
The insulin infusion should be continued until the patient
has resumed eating and can be transferred to a SC insulin
regimen
To avoid cerebral edema the blood glucose level should
be maintained between 250-300mg/dl until
hyperosmolarity and mental status improve and the patient
becomes clinically stable
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Treatment
POTASSIUM REPLETION
ECG monitoring for hyperkalemia or hypokalemia
If K+ < 5.5 give 10-20mEq/hr
If K+ < 3.5 give 40-80mEq/hr
Administer half as chloride and half as phosphate salts
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Monitoring
EKG
Vital signs
1-2 hourly glucose
Serum electrolytes: 2-6 hourly
BUN and creatinine: 6-24 hourly
Ketones: 6-24 hourly
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Pathogenesis of DKA and HHS:
stress, infection, or insufficient insulin. FFA, free fatty acid
Conclusion
• Diabetic emergencies are common in patients with
diabetes, and the effects can be devastating.
However, with continued emphasis on the timely and
appropriate identification and management of diabetic
emergencies, hopefully this may change.
• It is therefore important for those with diabetes to keep
their sugar levels normal to prevent complications and to
be able to live normal, healthy lives.
