Diabetic Emergencies: DKA, HS, Hypoglycemia

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

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 

March 1, 2009 vol. 94 no. 3 709-728
Clinical features
MILD HYPOGLYCEMIA
- mainly adrenergic or cholinergic symptoms
Pallor
Diaphoresis
Tachycardia
Palpitations
Hunger
Paresthesias
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

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

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
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
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

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

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

5, pages 508–515, May 2011
Causes
• Infections
• Inadequate insulin treatment or non-compliance
• New onset diabetes
• Infarction
• Drugs
• Pregnancy

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
sensorium
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

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
5, pages 508–515, May 2011
Laboratory findings
Hyperglycemia >250mg/dL
Serum ketones +
ABG:
metabolic acidosis
low bicarbonate
low pH (<7.2)

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).
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)

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
5, pages 508–515, May 2011
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

5, pages 508–515, May 2011
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

5, pages 508–515, May 2011
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

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).

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

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

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.

5, pages 508–515, May 2011
Hyperosmolar
Hyperglycemic
State
The condition is characterized by
• Hyperglycemia
• Hyperosmolarity
• Dehydration without significant ketoacidosis
10.2337/diacare.27.2007.S94
Diabetes Care January 2004vol. 27 no. suppl 1 s94-s102
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
10.2337/diacare.27.2007.S94
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
10.2337/diacare.27.2007.S94
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.,
10.2337/diacare.27.2007.S94
vs DKA
10.2337/diacare.27.2007.S94
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).
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.
10.2337/diacare.27.2007.S94
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
10.2337/diacare.27.2007.S94
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
10.2337/diacare.27.2007.S94
Monitoring
EKG
Vital signs
1-2 hourly glucose
Serum electrolytes: 2-6 hourly
BUN and creatinine: 6-24 hourly
Ketones: 6-24 hourly
10.2337/diacare.27.2007.S94
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.

Diabetic Emergencies: DKA, HS, Hypoglycemia

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Diabetic

The Journal of Clinical

The Journal of Clinical

The Journal of Clinical Endocrinology & Metabolism March 1,

The Journal of Clinical

The Journal of Clinical

The Journal of Clinical

The Journal of Clinical

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Arterial ph 7.25-7.30 7.0-7.24 < 7.0

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

Joint British Diabetes Society guideline for the management

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