3. Hypoglycemia
ā¢ Hypoglycemia (abnormally low blood glucose level) occurs when the
blood glucose falls to less than 50 to 60 mg/dL.
ā¢ It can be caused by too much insulin or oral hypoglycemic agents, too
little food.
ā¢ Hypoglycemia may occur at any time of the day or night.
3Prof. Dr. RS Mehta
6. Clinical Manifestations
ā¢ The clinical manifestations of hypoglycemia may be grouped into two
categories: adrenergic symptoms and central nervous system (CNS)
symptoms.
ā¢ In mild hypoglycemia, as the blood glucose level falls, the
sympathetic nervous system is stimulated, resulting in a surge of
epinephrine and norepinephrine.
ā¢ This causes symptoms such as sweating, tremor, tachycardia,
palpitation, nervousness, and hunger.
6Prof. Dr. RS Mehta
7. ā¢ In moderate hypoglycemia, the fall in blood glucose level deprives
the brain cells of needed fuel for functioning.
ā¢ Signs of impaired function of the CNS may include :
ā¢ Inability to concentrate
ā¢ Headache
ā¢ Lightheadedness
ā¢ Confusion
ā¢ Memory lapses
ā¢ Any combination of these symptoms (in addition to adrenergic
symptoms) may occur with moderate hypoglycemia.
7Prof. Dr. RS Mehta
9. Clinical feature
ā¢ Numbness of the lips and tongue
ā¢ Slurred speech
ā¢ Impaired coordination
ā¢ Emotional changes
ā¢ Irrational or combative behavior
ā¢ Double vision
ā¢ Drowsiness.
9Prof. Dr. RS Mehta
10. ā¢ In severe hypoglycemia, CNS function is so impaired that the patient
needs the assistance of another person for treatment of
hypoglycemia.
ā¢ Symptoms may include disoriented behavior, seizures, difficulty
arousing from sleep, or loss of consciousness.
ā¢ Severe hypoglycemia can cause a coma and even death.
10Prof. Dr. RS Mehta
11. Management
ā¢ Immediate treatment must be given when hypoglycemia occurs.
ā¢ The usual recommendation is 15 g of a fast-acting concentrated
source of carbohydrate such as the following, given orally:
ā¢ Three or four commercially prepared glucose tablets
ā¢ 4 to 6 oz of fruit juice
ā¢ 6 to 10 Life Savers or other hard candies
ā¢ 2 to 3 teaspoons of sugar or honey
11Prof. Dr. RS Mehta
12. Management contā¦
ā¢ The blood glucose level should be retested in 15 minutes and
retreated if it is less than 70 to 75 mg/dL (3.8 to 4 mmol/L).
ā¢ If the symptoms persist more than 10 to 15 minutes after initial
treatment, the treatment is repeated even if blood glucose testing is
not possible.
ā¢ Once the symptoms resolve, a snack containing protein and starch
(eg, milk or cheese and crackers) is recommended unless the patient
plans to eat a regular meal or snack within 30 to 60 minutes.
12Prof. Dr. RS Mehta
13. ā¢If the symptoms are more severe, impairing of ability
to take sugar by mouth, patient may need an injection
of glucagon or intravenous glucose.
ā¢Do not give food or drink to someone who is
unconscious, as he or she may aspirate these
substances into the lungs.
ā¢Injection Glucagon 1 mg (subcutaneously or I.M.) is
given if the patient cannot ingest a sugar treatment.
ā¢I.V. bolus of 50 mL of 50% dextrose solution can be
given if the patient fails to respond to glucagon within
15 minutes.
13Prof. Dr. RS Mehta
15. Introduction
ā¢ DKA is caused by an absence or markedly inadequate amount of
insulin. The three main clinical features of DKA are:
ā¢ Hyperglycemia
ā¢ Ketosis
ā¢ Acidosis
15Prof. Dr. RS Mehta
17. ā¢DKA is a major medical emergency and a serious
cause of morbidity in people with Type 1 diabetes.
17Prof. Dr. RS Mehta
18. Epidemiology
ā¢ Diabetic ketoacidosis (DKA) is characteristically associated
with type 1 diabetes.
ā¢ It also occurs in type 2 diabetes under conditions of extreme
stress such as serious infection, trauma, cardiovascular or
other emergencies.
ā¢ DKA is more common in young (<65 years) patients.
18Prof. Dr. RS Mehta
19. Causes
ā¢ Decreased or missed dose of insulin
ā¢ Illness or infection
ā¢ Undiagnosed and untreated diabetes (DKA may be the initial
manifestation of diabetes).
ā¢ An insulin deļ¬cit may result from an insufļ¬cient dosage of insulin
prescribed or from insufļ¬cient insulin being administered by the
patient.
19Prof. Dr. RS Mehta
21. Pathophysiology
ā¢ Without insulin, the amount of glucose entering the cells is reduced
and the liver increases glucose production.
ā¢ Both factors lead to hyperglycemia. In an attempt to rid the body of
the excess glucose, the kidneys excrete the glucose along with water
and electrolytes (eg, sodium and potassium).
ā¢ This osmotic diuresis, which is characterized by excessive urination
(polyuria), leads to dehydration and marked electrolyte loss.
21Prof. Dr. RS Mehta
22. Pathophysiology contā¦
ā¢ The absence of insulin also leads to the release of free fatty
acids from adipose tissue (lipolysis), which are converted in
the liver, into ketone bodies.
ā¢ Ketone bodies are acids; their accumulation in the
circulation leads to metabolic acidosis.
22Prof. Dr. RS Mehta
23. Clinical feature
Symptom
ā¢ Nausea and Vomiting
ā¢ Thirst/Polyphagia
ā¢ Polyuria
ā¢ Abdominal pain
ā¢ Altered mental function
ā¢ Shortness of breath
23Prof. Dr. RS Mehta
26. Management
1.REHYDRATION
In dehydrated patients, rehydration is important for maintaining tissue
perfusion. In addition, ļ¬uid replacement enhances the excretion of
excessive glucose by the kidneys.
ā¢ Patients may need up to 6 to 10 liters of IV ļ¬uid to replace ļ¬uid
losses caused by polyuria, hyperventilation, diarrhea, and vomiting.
ā¢ Initially, 0.9% sodium chloride (normal saline) solution is administered
at a rapid rate, usually 0.5 to 1 L per hour for 2 to 3 hours.
26Prof. Dr. RS Mehta
27. ā¢Moderate to high rates of infusion (200 to 500 mL per
hour) may continue for several more hours.
ā¢ When the blood glucose level reaches 250 mg/dL or
less, the IV ļ¬uid may be changed to dextrose 5% in
water (D5W) to prevent a precipitous decline in the
blood glucose level.
27Prof. Dr. RS Mehta
28. ā¢ Monitoring ļ¬uid volume status involves frequent measurements of
vital signs (including monitoring for orthostatic changes in blood
pressure and heart rate), lung assessment, and monitoring intake and
output.
ā¢ Initial urine output will lag behind IV ļ¬uid intake as dehydration is
corrected.
ā¢ Monitoring for signs of ļ¬uid overload is especially important for older
patients, those with renal impairment, or those at risk for heart
failure.
28Prof. Dr. RS Mehta
29. Management
2.Reversing acidosis
ā¢ Ketone bodies (acids) accumulate as a result of fat breakdown.
ā¢ The acidosis that occurs in DKA is reversed with insulin, which
inhibits fat breakdown, thereby stopping acid buildup.
ā¢ Insulin is given 0.1 U/kg bolus and then continuous 0.1U/Kg/hr.
29Prof. Dr. RS Mehta
30. ā¢Hourly blood glucose values must be measured.
ā¢IV fluid solutions with higher concentrations of
glucose, such as normal saline (NS) solution (eg, D5NS
or D50.45NS), are administered when blood glucose
levels reach 250 to 300 mg/dL to avoid too rapid a
drop in the blood glucose level.
30Prof. Dr. RS Mehta
31. ā¢Insulin must be infused continuously until
subcutaneous administration of insulin resumes.
ā¢Take insulin or oral anti diabetic agents as usual.
ā¢Test blood glucose and test urine ketones every 3 to 4
hours.
ā¢Report elevated glucose levels (greater than 300 mg)
or urine ketones to the physician.
ā¢ Insulin-requiring patients may need supplemental
doses of regular insulin every 3 to 4 hours.
31Prof. Dr. RS Mehta
32. 3.RESTORING ELECTROLYTES
ā¢ The major electrolyte of concern during treatment of DKA is
potassium. Although the initial plasma concentration of potassium
may be low, normal, or even high, there is a major loss of potassium
from body stores and an intracellular to extracellular shift of
potassium.
ā¢ Further, the serum level of potassium drops during the course of
treatment of DKA as potassium re-enters the cells; therefore, it must
be monitored frequently.
32Prof. Dr. RS Mehta
33. Some of the factors related to treating DKA that reduce the
serum potassium concentration include:
ā¢ Rehydration, which leads to increased plasma volume and
subsequent decreases in the concentration of serum
potassium.
ā¢ Rehydration also leads to increased urinary excretion of
potassium.
ā¢ Insulin administration, which enhances the movement of
potassium from the extracellular ļ¬uid into the cells.
ā¢ Cautious but timely potassium replacement is vital to avoid
33Prof. Dr. RS Mehta
34. ā¢ IV insulin may be continued for 12 to 24 hours until the
serum bicarbonate level improves.
ā¢ In general, bicarbonate infusion to correct severe acidosis is
avoided during treatment of DKA because it precipitates
further, sudden (and potentially fatal) decreases in serum
potassium levels.
ā¢ Continuous insulin infusion is usually sufļ¬cient for reversing
DKA.
34Prof. Dr. RS Mehta
36. Nursing Management
ā¢ Nursing care of the patient with DKA focuses on monitoring ļ¬uid and
electrolyte status as well as blood glucose levels.
ā¢ Administering ļ¬uids, insulin, and other medications; and preventing other
complications such as ļ¬uid overload.
ā¢ Urine output is monitored to ensure adequate renal function before
potassium is administered to prevent hyperkalemia.
ā¢ The electrocardiogram is monitored for dysrhythmias indicating abnormal
potassium levels.
36Prof. Dr. RS Mehta
37. ā¢Vital signs, arterial blood gases, and other
clinical ļ¬ndings are recorded on a ļ¬ow sheet.
ā¢The nurse documents the patientās laboratory
values and the frequent changes in ļ¬uids and
medications that are prescribed and monitors
the patientās responses.
37Prof. Dr. RS Mehta
38. ā¢ As DKA resolves and the potassium replacement rate is
decreased, the nurse makes sure that:
ā¢ There are no signs of hyperkalemia on the
electrocardiogram (tall, peaked T waves).
ā¢ The laboratory values of potassium are normal or low.
ā¢ The patient is urinating (ie, no renal shutdown).
38Prof. Dr. RS Mehta