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 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-

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-

Physiological responses

The Journal of Clinical Endocrinology & Metabolism March

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-

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

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-

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-

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 orallyThe Journal of Clinical
give IV dextrose
March 1, 2009 vol. 94 no. 3 709-

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-

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-

 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

 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


Mechanism
 Absolute or relative insulin deficiency
 Increased gluconeogenesis
 Elevation of counter regulatory hormones such as
glucagon, cortisol, growth hormone, and
catecholamines


Causes
• Infections
• Inadequate insulin treatment or non-compliance
• New onset diabetes
• Infarction
• Drugs
• Pregnancy


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

Clinical presentations
• Nausea/vomiting  Thirst/polyuria
• Abdominal pain  Shortness of breath
• Generalized weakness  Malaise/lethargy
• Confusional state
• Fever, dysuria, coughing
• Chest pain
• Palpitations

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 Joint British Diabetes Society guideline for the
 Fever/ Hypothermia 28, Issue 5, pages 508–515, May
Medicine Volume

Laboratory findings
 Hyperglycemia >250mg/dL
 Serum ketones +
 ABG:
 metabolic acidosis
 low bicarbonate
 low pH (<7.2)

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

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)


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 Society guideline for the
Joint British Diabetes

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

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


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


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).

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


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


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.


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
s102

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
10.2337/diacare.27.2007.S94
 Lower levels of counterregulatory hormones and free
fatty acids have been found in HHS than in DKA
s102

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
s102

vs DKA

10.2337/diacare.27.2007.S94
s102

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–
10.2337/diacare.27.2007.S94
10L) should be reversed over the next 1–2 days
(infusion rates of 200–300 mL/h of hypotonic
s102

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
s102

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
s102

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
s102

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
s102

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

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