Hypoglycemia

Dr Seemal Aslam
PGR MW-3
• Glucose a fuel for brain.
• Physiological levels of glucose in fasting state
are 70-110mg/dl
• Glycogenolysis helps brain in fasting state (
~8hr)

• Gluconeogenesis plays its role after

glycogen is depleted.
Counter-regulatory mechanism starts when
glucose level goes just below the physiological
range

1st line defense : decreasing level insulin

2nd line defense : release of glucagon

3rd line defense: release of epinephrine

4th line of defense : release of cortisol and

growth hormone
Symptoms of Hypoglycemia
a) Autonomic symptoms:
• Tremors
• Palpitation
• Anxiety / arousal catecholamine mediated

• Sweating
• Hunger
• Paresthesia Acetylccholine mediated

b) Neuroglycopenic Symptoms :

• Diziness
• Weakness
• Drowsiness
• Confusion
• Altered mental status
Pt tend to forget symptoms due to amnesia during hypoglycemia.
hence history Should always be taken from attendents as well.
Signs of hypoglycemia:
• Diaphoresis
• Pallor
• Increased heart rate
• Raised systolic BP (may or may not be there)
• Ocassinally focal neurological deficit that is transient may be found
CAuSES of HyPoglyCEmiA in ADulTS
Ill or medicated individual
1. Drugs
2. Critical illness
Hepatic, renal or cardiac failure
Sepsis
Inanition
3. Hormone deficiency
Cortisol
Glucagon and epinephrine (in insulin-deficient diabetes)
4. Non–islet cell tumor
Seemingly well individual
5. Endogenous hyperinsulinism
Insulinoma
Functional β-cell disorders (nesidioblastosis)
Noninsulinoma pancreatogenous hypoglycemia
Post–gastric bypass hypoglycemia
Insulin autoimmune hypoglycemia
Antibody to insulin
Antibody to insulin receptor
Insulin secretagogue
Other
6. Accidental, surreptitious, or malicious hypoglycemia
Causes of Hypoglycemia in
1) DRUGs :
insulin
sulphonylurea
Meglitinides
Beta blockers
ACE Inhibitors
Quinolone
Pentamidine

2) Ethanol :
it only inhibits gluconeogenesis but no glycogenolysis hence
hypoglycemia occur after prolonged starvation.
3) Critical illnes:
DM
Sepsis
ESRD
Heart failure
Mechanical ventilation
4) Malnourishment:
absent glycogen and no substrate for gluconeogensis.
5) Cortisol deficiency:
for e.g Addisons Disease
Hypoglycemia in patients with diabetes

Definition:
American Diabetes Association (ADA) Workgroups have
defined hypoglycemia in patients with diabetes as all
episodes of an abnormally low plasma glucose
concentration (with or without symptoms) THAT EXPOSE
THE INDIVIDUAL TO HARM . They did not identify a
specific glucose level that defines hypoglycemia

Alert value: alert value is the value of serum glucose that

should alert the patient for possiblity of developing
clinically significant hypoglycemia and to take possible
prompt actions.( <70mg/dl).
Clinically important biochemical
hypoglycemia:

A glucose level of <54 mg/dL (3 mmol/L) as

sufficiently low to indicate serious, clinically
important biochemical hypoglycemia
 Classification of severity
Severe hypoglycemia – An event requiring the assistance of anothe
person to actively administer carbohydrate, glucagon, or other
resuscitative actions.
●Documented symptomatic hypoglycemia – An event during
which typical symptoms of hypoglycemia are accompanied by a
measured glucose level ≤70 mg/dL (3.9 mmol/L).
●Asymptomatic hypoglycemia – An event not accompanied by
typical symptoms of hypoglycemia but with a measured glucose
level ≤70 mg/dL (3.9 mmol/L).
●Probable symptomatic hypoglycemia – An event during which
typical symptoms of hypoglycemia are not accompanied by
measurement of the glucose level (but that was presumably caused
by hypoglycemia).
●Pseudohypoglycemia – An event during which the person with
diabetes reports typical symptoms of hypoglycemia but has a
measured glucose level >70 mg/dL (3.9 mmol/L).
Risk factors :
Risk factors for hypoglycemia include the following [
●Hypoglycemia-associated autonomic failure (including the
syndromes of impaired awareness of hypoglycemia and of
defective glucose counter-regulation)
●Longer duration of diabetes
●Older age
●Lower levels of glycemia, when achieved with medications
●Erratic timing of meals, including missed meals and low
carbohydrate content of meals
●History of recent severe hypoglycemia
●Exercise
●Alcohol ingestion
●Chronic kidney disease
●Malnutrition with glycogen depletion
STRATEGIES TO MANAGE HYPOGLYCEMIA
• Patient education :
Impementation of flexible insulin therapy.

Regular SMBG – before and 2-3 hour after every meal ,

bedtime,midnight and before and after exercise to
document glucose pattern

• Glycemic targets :
Individualized (vary from pateint to patient)

Generally in Type 1 DM HbA1c ≤ 7

Generally in Type 2 DM HBA1C ≤ 7 and <8 in old patients

• Insulin Regimen :

• Type 1 DM ---short acting insulins is better to prevent

nocturnal hypoglycemia than regular insulin
• Type 2 DM --- long acting insulins are better than NPH
• Specific settings
Impaired awareness of hypoglycemia —
If there is a history of impaired
awareness of hypoglycemia, a two- to three-week period of
avoidance of hypoglycemia is advisable since that often restores
awareness

Exercise-induced hypoglycemia —
Exercise-induced hypoglycemia can occur
during, shortly after, or many hours after exercise, and
therefore, patients should remain vigilant for
its occurrence including frequent SMBG or CGM.
Measures to reduce early post-exercise hypoglycemia
include interspersing brief episodes of intense exercise
(which tends to raise plasma glucose concentrations),
adding carbohydrate ingestion (eg, 1 g/kg/h), and
reducing insulin doses
Reversing hypoglycemia
Asymptomatic — For a person with drug-treated diabetes, defensive actions
should be taken when self-monitoring reveals a glucose level ≤70 mg/dL
.Defensive options include repeating the measurement within 15 to 60 minutes
,avoiding critical tasks such as driving, ingesting carbohydrates, and adjusting
the treatment regimen

Symptomatic — Patients with symptomatic hypoglycemia should ingest 15 to

20 grams of fast-acting carbohydrate

3 or 4 glucose tablets
½ cup of juice or regular soda (not sugar-free)
2 tablespoons of raisins
4 or 5 saltine crackers
1 tablespoon of sugar
1 tablespoon of honey or corn syrup
6 to 8 hard candies
Retest blood glucose after 15 minutes if still low then repeat treatment and
take long acting carbohydrate.

Severe — Severe hypoglycemia requires the assistance of another person to

actively administer carbohydrate, glucagon or other resuscitative actions.

With IV access
— Patients already in the hospital can usually be
treated quickly by giving 25 g of 50 percent glucose (dextrose)
intravenously (IV).

Without IV access
Glucagon available -A subcutaneous or intramuscular
injection of 0.5 to 1 mg of glucagon will usually lead to
recovery of consciousness within approximately 15 minute

Glucagon Not available- glucose gel or cake frosting

between teeth and buccal mucosa.or sprinkling of sugar
under tongue.
Hypoglycemia in patients without Diabetes .
• The onset of symptoms of hypoglycemia normally occur at glucose levels
less than 55 mg/dL , although the specific value varies among and within
individuals over time.

• Documenting hypoglycemia in patient without diabetes is not merely low

blood glucose . It is through Whipples Triad
 Diagnostic approach in patiets not having DM but having hypoglycemia

Clinical Evaluation:
• history is taken
• Nature of symptoms
• Timings of symptoms ( fasting or post parandial )
• Underlying illness
• Medication taken by patient or family members
• Social history.

Laboratory Evaluation :
• Glucose level
• Insulin levels
• C-peptide level
• Beta Hydroxybutyrate levels
• Pro-Insulin levels
• Sulfonylurea and meglitinide levels
 if patient is not symptomatic at the time of presentation then
check the timing of sympoms, if symptoms are consistent with
fasting hypo glycemia then go FOR 72 HOUR FASTING
PROVOCATION TEST, and if symptoms are consistent with post
parandial hypoglycemia then its better to go for MIXED MEAL
TEST
Post Parandial hypoglycemia evaluation:
Defined as hypoglycemia within 5 hours after eating meal.
In mixed meal test non liquid meal is taken and pt is
observed for 5 hours. Samples are taken before test and after
every 30 minutes uptill 5 hours.
If severe symptoms occur then before administrating
Carbohydrates blood samples are talken.

72 hour fasting test:

This test can be initiated at home
Date the onset of test
Discontinue unnecassory mediction
Allow calorie free and caeffine free beverages
Collect samples for blood glucose , C-peptide levels,insulin,
BHOB, pro insuline every 6 hour and if glucose goes
<60mg/dl take samples every 1-2 hour.

Test is ended when blood glucose levels fall to ≤ 45mg/dl

Interpretation of test

• Insulin level : insulin level of 3 mU/ml when serum glucose

<55mg/dl indicates hyperinsulinemia

• C-peptide level: normal individuals have 0.2 nmol/L at 45mg/dl

,insulinoma pts have higher values than 0.2

• Plasma –BHOB: as insulin is antiketogenic hence its level is ≤ 2.7

mmol/L

• Glycemic response to Glucagon: insulin tends to store glycogen in

liver eve during starvation.hence in pts of insulinoma there is
25mg/dl or more rise is glucose levels when glucagon is given.
• Overall if patient has low BHOB and positive response
to glucagon they have insulin or insulin like factors.

• Plasma insulin values are high in patients with

exogenous insulin administration, whereas plasma C-
peptide and proinsulin values are low
FACTITIOUS HYPOGLYCEMIA.
Factitious (or factitial) hypoglycemia occurs secondary to the surreptitious use
of insulin or insulin secretagogues (sulfonylureas, meglitinides)

Nondiabetic — Nondiabetic subjects with factitious hypoglycemia can present

with a clinical syndrome that appears similar to insulinoma

Diabetic — Factitious hypoglycemia among patients with diabetes is probably

more common than the incidence

Patients with diabetes and factitious hypoglycemia usually appear to have

brittle diabetes . They typically have repeated episodes of hypoglycemia
despite a reduction in dose or even cessation of insulin therapy.

Laboratory tests — In persons for whom insulin or an oral insulin

secretagogue has not been prescribed, the diagnosis of factitious hypoglycemia
can usually be established by documenting the presence of hypoglycemia and
by simultaneously measuring plasma insulin, C-peptide, proinsulin, and
insulin secretagogues

Interpretation of tests — The interpretation of the test results is the same as

when the tests are done during a spontaneous episode of hypoglycemia or
during a 72-hour fast
Insulin secretagogues — Factitious hypoglycemia caused by sulfonylureas or
meglitinides biochemically MIMICS THE INSULINOMA response since these
drugs stimulate insulin secretion. Patients with insulinoma and insulin
secretagogue-induced hypoglycemia can have plasma insulin, C-peptide, and
proinsulin values above or within the normal overnight fasting range

Exogenous insulin — In individuals with factitious hypoglycemia caused by

exogenous administration of insulin, plasma insulin values are high (often above
100 microU/mL), whereas plasma C-peptide and proinsulin values are low

TREATMENT
Long term — The long-term treatment of factitious hypoglycemia involves
changing abnormal behavioral patterns.

Acute — The acute management of factitious hypoglycemia is similar to the

management of hypoglycemia during the treatment of diabetes:
●Patients with symptomatic hypoglycemia should ingest carbohydrates. Fifteen
to 20 grams of oral glucose is typically sufficient. Glucose may be ingested in the
form of tablets, juice, milk, other snacks, or a meal.
●Treatment of severe hypoglycemia, when the patient is unconscious or unable
to ingest carbohydrate, requires a subcutaneous or intramuscular injection of
glucagon (0.5 to 1 mg).
●Patients brought to the hospital can be treated more quickly by giving 25 g of
50 percent glucose (dextrose) intravenously (IV).
 Artifactual hypoglycemiA

Glucose in serum is low but patient does not have hypoglycemic

symtpoms.
cause is usually wrong sampling of blood or few disorders of blood.
proper collection of sampling is using collecting tube having sodium
flouride in blood ,put on ice , and centrifuges immedietly to separate
RBCs from serum.