Hypoglycemia, or low blood sugar, is caused by very low levels of blood glucose, below 3.0 mmol/L. It is common in type 1 diabetes and can occur due to overdose of insulin or diabetes medications, excessive alcohol consumption, or certain illnesses. Symptoms range from irregular heartbeat and sweating to confusion and loss of consciousness. Treatment involves giving the person glucose tablets, juice, or an IV glucose solution to quickly raise their blood sugar levels. Preventing hypoglycemia requires education on recognizing symptoms early and always having access to fast-acting carbohydrates.

1. HYPOGLYCEMIA
BY AJUNA NOBLE
BSU STUDENT 2017/2021

2. HYPOGLYCEMIA
• Hypoglycemia is a condition caused by a very low level of blood sugar (glucose),
your body's main energy source.
• Blood glucose less than 3.0mmol/l
• Hypoglycemia, also known as.
• low blood sugar,
• fall in blood sugar to levels below normal.

3. Epidemiology
• Hypoglycemia is common in type 1 diabetes, especially in
• patients receiving intensive therapy, in whom the risk of severe
• Incidence :
• Increased risk among women,
• African Americans,
• those with less than high school education,
• elderly participants .

4. • Hypoglycemia is less frequent in type 2 diabetes than it is in type1.
• Hypoglycemia was reported in 38% of patients withT2DM who added a sulfonylurea or
meglitinide to metformin therapy.

5. Signs and Symptoms
• An irregular heart rhythm
• Fatigue
• Pale skin
• Shakiness
• Anxiety
• Sweating
• Hunger
• Irritability
• Tingling sensation around the mouth
• Crying out during sleep

7. •As hypoglycemia worsens, signs and
symptoms may include:
•Confusion,
•Visual disturbances, such as blurred vision
•Seizures
•Loss of consciousness
•People with severe hypoglycemia may appear as if they're intoxicated.They
may slur their words and move clumsily

8. causes
• Hypoglycemia occurs when your blood sugar (glucose) level falls too low.
• 1) Overdose of insulin or anti-diabatic medicines.
• Possible causes, without diabetes
2.Medications.
• Taking someone else's oral diabetes medication accidentally is a possible cause of
hypoglycemia. Other medications may cause hypoglycemia, especially in children or in
people with kidney failure. One example is quinine which is used to treat malaria.
3.Excessive alcohol consumption.
• Drinking heavily without eating can block your liver from releasing stored glucose into
your bloodstream, causing hypoglycemia.
•

9. 4.Some critical illnesses.
• Severe illnesses of the liver, such as severe hepatitis, can cause hypoglycemia. Disorders
of the kidney, which can keep your body from properly excreting medications, can
affect glucose levels due to a buildup of those medications.
5. Long-term starvation, as may occur in the eating disorder anorexia
nervosa, can result in the depletion of substances your body needs to generate glucose
(gluconeogenesis), causing hypoglycemia.
6.Insulin overproduction. A rare tumor of the pancreas (insulinoma) may cause
overproduction of insulin, resulting in hypoglycemia.

10. 7.Hormone deficiencies.
Certain disorders of the adrenal glands and the pituitary gland can result in a deficiency of key
hormones that regulate glucose production. Children may experience hypoglycemia if they have a
deficiency of growth hormone.
8.Strenous exercises.
9.Prematurity.
10.Sepsis, critical illnesses.

11. Pathophysiology.
• The brain uses glucose as its preferred fuel. When a person's
• plasma glucose level is less than 70 mg/dL (3.9 mmol/L),
• signals are sent from the brain to the pancreas, liver, and
• adrenal glands that collectively raise the plasma glucose level.
• The hormones involved are insulin,glucagon,epinephrine,norepinephrine, Cortisol,
and growth hormone .

13. Patho…conti….
• As plasma glucose levels decline within the physiologic range
• in the fasting state, pancreatic beta-cell insulin secretion
• decreases, thereby increasing hepatic glycogenolysis and
• hepatic (and renal) gluconeogenesis.
• Low insulin levels also reduce glucose utilization in peripheral
• tissues, inducing lipolysis and proteolysis, thereby releasing
• gluconeogenic precursors.
• Thus, a decrease in insulin secretion is the first defense against hypoglycemia.

14. • When hypoglycemia is prolonged beyond 4 hours, cortisol and
• growth hormone also support glucose production and limit
• glucose utilization.
• As plasma glucose levels fall to lower levels, symptoms prompt
• the behavioral defense against hypoglycemia, including the
• ingestion of food.

16. Classifications of
Hypoglycemia
• In diabetes mellitus the hypoglycemia is classified as :
• 1) Severe hypoglycemia
• 2) Documented symptomatic hypoglycemia
• 3) Probable symptomatic hypoglycemia
• 4) Asymptomatic hypoglycemia(or hypoglycemic Unawareness)
• 5) Relative hypoglycemia
• • Without diabetes mellitus the hypoglycemia
• 1) reactive(sometimes called "postprandial")
• 2) nonreactive(sometimes called "fasting").

17. •Severe hypoglycemia: which requires the assistance of another
person to administer a carbohydrate (preferably glucose
sublingually or intravenously) or subcutaneous glucagon
•Documented symptomatic hypoglycemia : which occurs when
a patient feels typical hyperadrenergic hypoglycemic
symptoms and verifies the blood glucose level is less than
70mg/dL (3.9 mmol/L) before self treating with 15 grams of a
carbohydrate
•Probable symptomatic hypoglycemia :Typical hypoglycemia
symptoms not accompanied by plasma glucose determination
but likely caused by plasma glucose ≤70 mg/dL (≤3.9 mmol/L)

18. • Asymptomatic hypoglycemia (or hypoglycemic unawareness):
•Here the patient does not develop typical hyperadrenergic symptoms
but has a measured plasma glucose level of lessthan 70 mg/dL
(3.9mmol/L).
• this situation occurs most often in type 1 diabetes in patients
striving for excellent glycemic control (hemoglobin A1c value<7.0%)
who have chronic, frequent episodes of hypoglycemia.

19. •Relative hypoglycemia: in which a patient experiences hyperadrenergic
hypoglycemic symptoms but has a measured plasma glucose level greater than 70 mg/dL (3.9
mmol/L).
• this situation occurs most often in patients who have had months (or
• longer) of hyperglycemia (plasma glucose levels >200 mg/dL[11.1mmol/L] at all times) whose
plasma glucose levels are then lowered by medication or lifestyle changes closer to the
normalrange.
• Hyperadrenergic hypoglycemic symptoms can occur when the
• plasma glucose level in these patients is 120 mg/dL (6.7 mmol/L) or
• even higher.
• If these patients continue to keep their plasma glucose level substantially less than 200 mg/dL
(11.1 mmol/L), the threshold at which they manifest hypoglycemic symptoms will fall to more
typicallevels (<70 mg/dL [3.9mmol/L]).

20. • Reactive hypoglycemia.(postprandial). Refers to low blood sugar that occurs
after a meal. Usually within 4 hours after eating.
• Possible causes, alcohol, gastric bypass surgery, inherited metabolic disorders
tumors of the git.
• Non reactive hypoglycemia. fasting hypoglycemia.

21. Laboratory tests
1. 2) Glucose (RBS)
2. 4) C-peptide
3. 5) Beta-hydroxybutyrate
4. 6) Proinsulin
5. 7) Antibodies for insulin and its receptors
6. 8) Sulfonylurea and meglitinide screen
7. 9) Electrolytes, BUN/Cr, UA
8. 10) liver function tests, cortisol and thyroid levels , growth
9. hormone level

22. Diagnosis.
• History
• Physical exam. Profuse sweating, loss of consciousness, dizziness,
• Investigations.
• Random blood sugar.

23. SIGNS-SYMPTOMS-Physical-Exam
• General : confusion, lethargy
• 2) diplopia
• 3) CVS : tachycardia
• 4) Neurologic: tremulousness, weakness, paresthesias , stupor,
• seizure, or coma
• 5) Mental status: irritability, inability to concentrate, or short-term
• memory loss
• 6) Skin: pale, diaphoresis

24. Management of Hypoglycemia
• The management of hypoglycemia can be divided into three
• phases:
•1. acute intervention to prevent and minimize neurological
•damage .
•2. maintenance therapy to prevent recurrence of hypoglycemia
.
•3. subsequent measures to search for and treat the underlying
cause .

25. Management.
• If the patient is able to swallow.
• Give oral glucose or sugar 10-20 g in 100-200ml of water every 15 minutes.
• If patient is unconscious
• Give 50% DEXTROSE 20-50 mls iv slowly (3ml/min) or diluted with normal saline
followed by 10% dextrose by drip at 5-10 mg/kg/minute.
• If patient remains unconscious after 30 min consider other other causes of coma.
• Investigate the causes of hypoglycemia.

26. Prevention.
• Educate at risk of hypoglycemia on recognition of early symptoms.
• Advise patients to always have regular meals and always have glucose or sugar
with them for emergency treatment.
• Advise diabatic patients to carry an identification tag.

27. Acute intervention
•it is important if possible to obtain a blood sample for
laboratory glucose measurement before glucose
administration and to save serum for more sophisticated
investigation if the cause of hypoglycemia is not obvious
(i.e. hypoglycemia in a seemingly healthy, nondiabetic
patient).
•If the patient has a history of malnutrition or chronic alcohol
abuse, intravenous (IV) thiamine at a bolus dose of 12 mg/kg
should be given before initiation of glucose treatment, to
avoid precipitatingWernicke’s encephalopathy.

28. Maintenance therapy• The clinical response of hypoglycemia to IV glucose administration
should be rapid.
• Patients with hypoglycemic coma are expected to regain consciousness and become coherent
within 5-10 minutes.
• However, complete cognitive recovery may be delayed for 30-60 minutes after restoration of
norm glycaemia.
• If there is no obvious improvement in symptoms or consciousness within 10-15 minutes, alternative
diagnoses (e.g. stroke or drug overdose) should be reconsidered.

29. •Subsequent Measures
•After initial stabilization, subsequent management should
be directed at searching for the underlying etiology of
hypoglycemia and preventing further attacks .
•Once the underlying cause is established, definitive therapy
should be offered.

30. • Treatment of Non-Diabetes Related
• Hypoglycemia
• Non diabetic hypoglycemia definitive management depends on the underlying etiology.
• Hypoglycemia induced by medications improves promptly once the medication is removed.
• Correction of sepsis and improvement in hepatic and renal function improves hypoglycemia of
the critical illness.
• Deficiencies of counter regulatory hormones can be corrected Switch replacement of relevant
hormone.

31. • Dietary changes are important in the context of hyperinsulinaemic
hypoglycemia, and the frequency and severity of episodes can be
• significantly reduced with frequent smaller volume meals.
• Complex carbohydrates such as bread, rice and pasta should be
• consumed frequently.
• Wherever possible, surgery to remove an insulinoma should be employed, although patient
preference and significant comorbidities may preclude the use of surgery.
• In these cases and in the context of NIPHS (where partial pancreatectomy can also be offered
if diet and/or medical treatment fails, although may be ineffectual if diffuse nesidioblastosis
is present), medical therapies should be used in the knowledge that each has significant
limitations or side effects

32. • Diazoxide is a potassium channel activator, first developed as an
• antihypertensive agent, but now more commonly used in the context of hypoglycaemia
due to inhibition of insulin secretion.
• It is administered at a dose of 5 mg/kg/day (with higher doses in refractory cases up to
15 mg/kg/day) in two or three divided oral doses (e.g. 200-1200 mg/day) .
• somatostatin inhibits insulin production, and analogues can be used in any state of
chronic hyperinsulinaemia.
• Octreotide therapy is effective in reducing hypoglycaemia in over 50% of patients
with an insulinoma and can be administered as a long-acting formulation.
• Octreotide is commenced at a dose of 50 mcg three times daily by SC injection, and can
be titrated to a maximum dose of 500mcg three times daily.

33. • Summary Of Management
• Obtain blood glucose concentration as soon as possible (usually with a meter and strips,
if available):
• For symptomatic patient known to have diabetes and with a low glucose value, <70
mg/dL, administer treatment. If a glucose test cannot be performed, do not delay.Treat
as if hypoglycemia has been confirmed.
• If the glucose is low (<55 mg/dL) and the patient is a not a diabetic, draw blood for
glucose, insulin, C-peptide, and an oral hypoglycemic agent screen and then treat
• Do not delay treatment if symptomatic hypoglycemia is suspected but rapid blood
glucose measurement is not available or blood for diagnostic studies cannot be
collected

34. • If conscious and able to drink and swallow safely (ie, administer a rapidly absorbed carbohydrate
(eg, 3 to 4 glucose tablets or a tube of gel with 15 grams, 4 to 6 oz. fruit juice or non-diet soda, or a
teaspoon of honey or table sugar).
• for altered mental status, is unable to swallow, or does not respond to oral glucose administration
within 15 minutes, give an IV bolus of 12.5 to 25 g of glucose (25 to 50 mL of 50 percent dextrose).
• Measure a blood glucose 10 to 15 minutes after the IV bolus.
• Re-administer 12.5 to 25 grams of glucose as needed to maintain the blood glucose above 80
mg/dL.
• If glucose cannot be given by parenteral or oral routes, give glucagon 1 mg IM or SQ. Response
may be transient and should be followed by careful glucose monitoring and oral or intravenous
glucose administration

35. • Give additional maintenance glucose by mouth or IV. IV
• dextrose infusion should ensure delivery of 6 to 9 mg/kg per
• minute of glucose.
• • Amounts needed vary depending upon the cause and severity
• of the symptomatic hypoglycemia. Once the patient is able to
• ingest carbohydrate safely, providing a mixed meal (including
• carbohydrates, such as a sandwich) is the preferred means of
• maintaining glucose levels.
• • Measure a blood glucose 10 to 15 minutes after the initial IV
• bolus and monitor every 30 to 60 minutes thereafter until stable
• (minimum of 4 hours).

36. •Differential Diagnosis
• seizure disorder
•Drug/alcohol intoxication
•Psychosis, depression
•Stroke
•Poisoning.

37. • Complications
•recurrent/persistent psychosocial morbidity(Emotional
liability ,
•irritability, depression.
•Fear of hypoglycemia-barrier for diabetic control.
•Seizure
•permanent neurologic deficit (including cognitive
impairment)
•Coma
•Death

38. Nursing concerns.
•Low blood sugar.
•coma
•seizure
•Confusion
•General body weakness
•.dizziness.

39. Nursing care plan.
NURSING
DIAGNOSIS
GOAL INTERVENTION
.
RATIONAL.
unstable blood sugar
related to low plasma
glucose conc evidenced by
blood sugar less than
3.0mmol./l
Restore the normal
glucose levels from
3.0mmol/l to at least
6.0mmol./l in the next
30 minutes
Monitor blood sugar.
Educate patient on the
early symptoms of
hypoglycemia.
Administer dextrose 10%
5-10 mg/kg/minute
Dextrose 10% replaces
the low sugar.
Acute Confusion related
low glucose levels in the
brain evidenced
Fluctuation in level of
consciousness
Patient regains
normal reality
orientation and
level of
consciousness in
the next 10
minutes.
Administer 10% dextrose
solution by drip at 5-
10mg/kg/minute until the
patient regains
consciousness.
Monitor the blood
glucose over hours.
dextrose 10% restores
blood glucose level
,which later restores
consciousness.

40. NURSING DIAGNOSIS GOAL INTERVENTION
Activity intolerance related to low
blood sugar evidenced by
shortness of breathe, dizziness,
rapid pulse.
Treat the underlying cause with in
the next 30 min.
• .Administer iv glucose 10%.
• Advise the patient to have small
frequent meals.
Imbalanced nutrition less than
body requirements related to
insufficient levels of glucose
evidenced by weight loss.
Treat the underlying cause within
the next 30 minutes.
• Administer dextrose 10% iv
slowly.
• give small frequent meals .
• Find out the cause of
hypoglycemia.
• Treat the cause of hypoglycemia.