Endocrine Disorder

1. Hypoglycemia &
Diabetes Ketoacidosis
Prof. Dr. RS Mehta 1

2. 2Prof. Dr. RS Mehta

3. Hypoglycemia
• Hypoglycemia (abnormally low blood glucose level) occurs when the
blood glucose falls to less than 50 to 60 mg/dL.
• It can be caused by too much insulin or oral hypoglycemic agents, too
little food.
• Hypoglycemia may occur at any time of the day or night.
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4. Causes
• Drugs :Insulin,Sulfonylurea,Ethanol
• Critical illness: Hepatic,renal,cardiac failure,starvation
• Endocrine deficiency: Type 1 diabetes
• Non beta cell tumor:
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5. Clinical features
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6. Clinical Manifestations
• The clinical manifestations of hypoglycemia may be grouped into two
categories: adrenergic symptoms and central nervous system (CNS)
symptoms.
• In mild hypoglycemia, as the blood glucose level falls, the
sympathetic nervous system is stimulated, resulting in a surge of
epinephrine and norepinephrine.
• This causes symptoms such as sweating, tremor, tachycardia,
palpitation, nervousness, and hunger.
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7. • In moderate hypoglycemia, the fall in blood glucose level deprives
the brain cells of needed fuel for functioning.
• Signs of impaired function of the CNS may include :
• Inability to concentrate
• Headache
• Lightheadedness
• Confusion
• Memory lapses
• Any combination of these symptoms (in addition to adrenergic
symptoms) may occur with moderate hypoglycemia.
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8. 8Prof. Dr. RS Mehta

9. Clinical feature
• Numbness of the lips and tongue
• Slurred speech
• Impaired coordination
• Emotional changes
• Irrational or combative behavior
• Double vision
• Drowsiness.
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10. • In severe hypoglycemia, CNS function is so impaired that the patient
needs the assistance of another person for treatment of
hypoglycemia.
• Symptoms may include disoriented behavior, seizures, difficulty
arousing from sleep, or loss of consciousness.
• Severe hypoglycemia can cause a coma and even death.
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11. Management
• Immediate treatment must be given when hypoglycemia occurs.
• The usual recommendation is 15 g of a fast-acting concentrated
source of carbohydrate such as the following, given orally:
• Three or four commercially prepared glucose tablets
• 4 to 6 oz of fruit juice
• 6 to 10 Life Savers or other hard candies
• 2 to 3 teaspoons of sugar or honey
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12. Management cont…
• 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).
• 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.
• 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.
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13. •If the symptoms are more severe, impairing of ability
to take sugar by mouth, patient may need an injection
of glucagon or intravenous glucose.
•Do not give food or drink to someone who is
unconscious, as he or she may aspirate these
substances into the lungs.
•Injection Glucagon 1 mg (subcutaneously or I.M.) is
given if the patient cannot ingest a sugar treatment.
•I.V. bolus of 50 mL of 50% dextrose solution can be
given if the patient fails to respond to glucagon within
15 minutes.
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15. Introduction
• DKA is caused by an absence or markedly inadequate amount of
insulin. The three main clinical features of DKA are:
• Hyperglycemia
• Ketosis
• Acidosis
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17. •DKA is a major medical emergency and a serious
cause of morbidity in people with Type 1 diabetes.
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18. Epidemiology
• Diabetic ketoacidosis (DKA) is characteristically associated
with type 1 diabetes.
• It also occurs in type 2 diabetes under conditions of extreme
stress such as serious infection, trauma, cardiovascular or
other emergencies.
• DKA is more common in young (<65 years) patients.
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19. Causes
• Decreased or missed dose of insulin
• Illness or infection
• Undiagnosed and untreated diabetes (DKA may be the initial
manifestation of diabetes).
• An insulin deficit may result from an insufficient dosage of insulin
prescribed or from insufficient insulin being administered by the
patient.
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20. Precipitating events
• Inadequate insulin administration
• Infection(pneumonia,UTI,gastroenteritis)
• Drugs(cocaine)
• Infarction(cerebral,coronary)
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21. Pathophysiology
• Without insulin, the amount of glucose entering the cells is reduced
and the liver increases glucose production.
• 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).
• This osmotic diuresis, which is characterized by excessive urination
(polyuria), leads to dehydration and marked electrolyte loss.
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22. Pathophysiology cont…
• 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.
• Ketone bodies are acids; their accumulation in the
circulation leads to metabolic acidosis.
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23. Clinical feature
Symptom
• Nausea and Vomiting
• Thirst/Polyphagia
• Polyuria
• Abdominal pain
• Altered mental function
• Shortness of breath
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24. Clinical Feature
Signs
• Tachycardia
• Dry mucous membrane
• Hypotension
• Kussmaul respiration
• Abdominal tenderness
• Fever
• Lethargy
• Acetone smell in breath
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25. 25Prof. Dr. RS Mehta

26. Management
1.REHYDRATION
In dehydrated patients, rehydration is important for maintaining tissue
perfusion. In addition, fluid replacement enhances the excretion of
excessive glucose by the kidneys.
• Patients may need up to 6 to 10 liters of IV fluid to replace fluid
losses caused by polyuria, hyperventilation, diarrhea, and vomiting.
• 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.
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27. •Moderate to high rates of infusion (200 to 500 mL per
hour) may continue for several more hours.
• When the blood glucose level reaches 250 mg/dL or
less, the IV fluid may be changed to dextrose 5% in
water (D5W) to prevent a precipitous decline in the
blood glucose level.
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28. • Monitoring fluid 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.
• Initial urine output will lag behind IV fluid intake as dehydration is
corrected.
• Monitoring for signs of fluid overload is especially important for older
patients, those with renal impairment, or those at risk for heart
failure.
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29. Management
2.Reversing acidosis
• Ketone bodies (acids) accumulate as a result of fat breakdown.
• The acidosis that occurs in DKA is reversed with insulin, which
inhibits fat breakdown, thereby stopping acid buildup.
• Insulin is given 0.1 U/kg bolus and then continuous 0.1U/Kg/hr.
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30. •Hourly blood glucose values must be measured.
•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.
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31. •Insulin must be infused continuously until
subcutaneous administration of insulin resumes.
•Take insulin or oral anti diabetic agents as usual.
•Test blood glucose and test urine ketones every 3 to 4
hours.
•Report elevated glucose levels (greater than 300 mg)
or urine ketones to the physician.
• Insulin-requiring patients may need supplemental
doses of regular insulin every 3 to 4 hours.
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32. 3.RESTORING ELECTROLYTES
• 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.
• 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.
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33. Some of the factors related to treating DKA that reduce the
serum potassium concentration include:
• Rehydration, which leads to increased plasma volume and
subsequent decreases in the concentration of serum
potassium.
• Rehydration also leads to increased urinary excretion of
potassium.
• Insulin administration, which enhances the movement of
potassium from the extracellular fluid into the cells.
• Cautious but timely potassium replacement is vital to avoid
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34. • IV insulin may be continued for 12 to 24 hours until the
serum bicarbonate level improves.
• 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.
• Continuous insulin infusion is usually sufficient for reversing
DKA.
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35. Complication
1.Cerebral edema
2.ARDS
3.Thromboembolism
4.Disseminated Intravascular Coagulation
5.Acute circulatory failure
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36. Nursing Management
• Nursing care of the patient with DKA focuses on monitoring fluid and
electrolyte status as well as blood glucose levels.
• Administering fluids, insulin, and other medications; and preventing other
complications such as fluid overload.
• Urine output is monitored to ensure adequate renal function before
potassium is administered to prevent hyperkalemia.
• The electrocardiogram is monitored for dysrhythmias indicating abnormal
potassium levels.
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37. •Vital signs, arterial blood gases, and other
clinical findings are recorded on a flow sheet.
•The nurse documents the patient’s laboratory
values and the frequent changes in fluids and
medications that are prescribed and monitors
the patient’s responses.
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38. • As DKA resolves and the potassium replacement rate is
decreased, the nurse makes sure that:
• There are no signs of hyperkalemia on the
electrocardiogram (tall, peaked T waves).
• The laboratory values of potassium are normal or low.
• The patient is urinating (ie, no renal shutdown).
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39. Thank you
Prof. Dr. RS Mehta 39