Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                

Paper Elektif

Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 10

PAPER

HYPERGLIKEMIA
CHAPTER I

INTRODUCTION

1.1 Background

Non Ketotic Hyperosmolar Hyperglycemia is an acute complication of


diabetes mellitus in which the patient will experience severe dehydration, which
can cause mental confusion, dizziness, seizures and a condition called coma. This
occurs in people with type II diabetes (www.wikipedia.com)

Hyperglycemia, Non Ketogenic Hyperosmolar is a syndrome associated


with relative insulin deficiency, most often occurring in people with NIDDM.
Clinically manifested by severe hyperglycemia resulting in hyperosmolarity and
dehydration, absence of ketosis/present but mild and neurologic disturbances.

1.2 Purpose of Writing

After completing this session, participants are expected to be able to:

- Students can understand Non Ketotic Hyperosmolar Hyperglycemia

- Students can find out the causes of Non Ketotic Hyperosmolar Hyperglycemia

- Students can understand the signs and symptoms of Non Ketotic Hyperosmolar
Hyperglycemia

- Students can understand the management of non-ketotic hyperglycemia


hyperosmolar patients

- Students can understand Non Ketotic Hyperglycemic Hyperglycemic Nursing


Care
1.3 Writing Method

The method used in writing this paper is to seek from various sources and
discuss with groups

1.4 Writing Systematics

The writing of this paper is organized into three chapters with the following
systematics.
CHAPTER II

LITERATURE REVIEW

1.1 UNDERSTANDING

Non Ketotic Hyperosmolar Hyperglycemia is an acute complication of


diabetes mellitus in which the patient will experience severe dehydration, which can
cause mental confusion, dizziness, seizures and a condition called coma. This occurs
in people with type II diabetes

Hyperglycemia, Non Ketogenic Hyperosmolar is a syndrome associated with


relative insulin deficiency, most often occurring in people with NIDDM. Clinically
manifested by severe hyperglycemia resulting in hyperosmolarity and dehydration,
absence of ketosis/present but mild and neurologic disturbances

Hyperglycemic Hyperosmolar Non Ketosis is a coma resulting from


complications of diabetes mellitus in which metabolic disturbances occur which
cause: very high blood sugar levels, increased hypertonic dehydration and without
serum ketosis, common in type II DM.

Nonketotic hyperosmolar hyperglycemic coma is a syndrome characterized by


severe hyperglycemia, hyperosmolar, severe dehydration without ketoacidosis,
accompanied by decreased consciousness (Mansjoer, 2000).

According to Hudak and Gallo (edition VI) hyperosmolar coma is a


complication of diabetes which is characterized by:

1. Hyperosmolarity and severe fluid loss.

2. Mild acidosis.
3. Coma and local seizures often occur.

4. Occurs mainly in the elderly.

5. High mortality rate.

1.2 ETIOLOGY

1. Insulin deficiency

a. DM, pancreatitis, pancreatectomy

b. Pharmacologic agents (phenytoin, thiazides)

2. Increase exogenous glucose

a. Hyperalimentation (tpn)

b. High calorie enteral feeding

3. Increase endogenous glucose

a. Acute stress (ami, infection)

b. Pharmacologic (glucocorticoids, steroids, thyroid)

4. Infection: pneumonia, sepsis, gastroenteritis.

5. Acute illness: gastrointestinal bleeding, pancreatitis and cardiovascular


disorders.

6. Surgery/surgery.

7. Administration of hypertonic fluids.

8. Burns.
Risk Factors:

1. Old adult age group (> 45 years)

2. Obesity (BB(kg)>120% ideal weight, or BMI>27 (kg/m2)

3. High blood pressure (BP> 140/90 mmHg)

4. Family history of DM

5. History of pregnancy with a baby's birth weight > 4000 grams

6. History of DM in pregnancy

7. Dyslipidemia (HDL<35 mg/dl and/or triglycerides>250 mg/dl)

8. Have you ever had TGT (Impaired Glucose Tolerance) or GDPT (Impaired
Fasting Blood Glucose)

Common signs and symptoms in clients with KHNK are thirst, skin feeling
warm and dry, nausea and vomiting, decreased appetite (weight loss), abdominal
pain, dizziness, blurred vision, frequent urination, fatigue, polydipsia, polyuria,
decreased consciousness , (www.tabloid-nakita.com).

Symptoms include:

1. Somewhat drowsy, frequent incidents of stupor or coma.

2. Polyuria for 1 -3 days before clinical symptoms appear.

3. No hyperventilation and no bad breath.

4. Severely excessive volume depletion (dehydration, hypovolemia).

5. Serum glucose reaches 600 mg/dl to 2400 mg/dl.


6. Sometimes there are gastrointestinal symptoms.

7. Hypernatremia.

8. Failure of the thirst mechanism resulting in inadequate digestion of water.

9. High serum osmolarity with minimal CNS symptoms (disorientation, local


seizures).

10. Damage to kidney function.

11. HCO3 levels less than 10 mEq/L.

12. CO2 levels are normal.

13. The anion gap is less than 7 mEq/L.

14. Serum potassium is usually normal.

15. No ketonemia.

16. Mild acidosis.

1.3 CLINICAL MANIFESTATIONS

Common signs and symptoms in clients with KHNK are thirst, skin feeling
warm and dry, nausea and vomiting, decreased appetite (weight loss), abdominal
pain, dizziness, blurred vision, frequent urination, fatigue, polydipsia, polyuria,
decreased consciousness , (www.tabloid-nakita.com).

Symptoms include:

1. Somewhat drowsy, frequent incidents of stupor or coma.


2. Polyuria for 1 -3 days before clinical symptoms appear.

3. No hyperventilation and no bad breath.

4. Severely excessive volume depletion (dehydration, hypovolemia).

5. Serum glucose reaches 600 mg/dl to 2400 mg/dl.

6. Sometimes there are gastrointestinal symptoms.

7. Hypernatremia.

8. Failure of the thirst mechanism resulting in inadequate digestion of water.

9. High serum osmolarity with minimal CNS symptoms (disorientation, local


seizures).

10. Damage to kidney function.

11. HCO3 levels less than 10 mEq/L.

12. CO2 levels are normal.

13. The anion gap is less than 7 mEq/L.

14. Serum potassium is usually normal.

15. No ketonemia.

16. Mild acidosis.

1.3 CLINICAL MANIFESTATIONS

Typically, these patients are middle-aged or elderly with diabetic type II who
are sometimes undiagnosed. They have a bit of a tantrum, eat little, are observed for
several days to deepen the stupor, and finally bring them to the hospital in a state of
extreme volume depletion. In severe cases, the hyperglycemia that occurs in these
patients may be excessive and by definition exceeds 600 mg/dl. In addition to
extracellular water and sodium losses, there is also an additional free water deficit,
possibly due to failure of the thirst mechanism and resulting from inadequate oral
intake. These patients often have very high sodium and glycose levels, with glucose
levels sometimes exceeding 2000 mg/dl, and very high serum osmolarity.

In our discussion of the mechanism of severe hyperglycemia, one might


surmise that low kidney function must have even more to contribute to the nonketotic
hyperosmolarity hypoglycemic syndrome and indeed, kidney function is generally
worse than before, as in all diabetes-related syndromes. However, it seems logical to
consider the diagnosis to be hyperosmolar only if the anion gap affecting ketoacidosis
is less than 7 mEq/L and to diagnose severe ketoacidosis if the anion gap is greater
than 7 mEq/l.
CHAPTER III

CLOSING

3.1 Conclusion

Not infrequently, patients experience clear hyperglycemia and


hyperosmolarity of diabetic ketoacidosis but without accompanying ketoacidosis.
This is a non-ketotic hyperosmolar hyperglycemic coma syndrome. This syndrome
needs to be known because:

1. Its similarities to and differences from severe diabetic ketoacidosis

2. Is a differential diagnosis

3. Differences in management

3.2 Suggestions

Health is very valuable for the life of living things on earth, so we must
maintain health, prevention is better than cure

You might also like