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Safad R. Isam
Msn,CollegeOfnursing,universityofBaghdad
Hyperglycemic
Hyperosmolar Syndrome
Main types
Symptoms
Prevention
Organs affected
Treatment
Diabetes Summary
IDDM NIDDM GDM
Polyuria Fatigue weight loss
Polydipsia weakness
Polyphagia
Healthy Physical Weight
Nutrition Exercise Control
Insulin & Medication
Nutritional Therapy
Blood glucose
Monitoring
+ LADA
Complications
Short-term imbalances in blood glucose levels
ACUTE COMPLICATIONS OF DIABETES
Hyperglycemic
Hyperosmolar
Syndrome
(HHS)
Diabetic
Ketoacidosis (DKA)
Hypoglycemia
Hyperglycemic Hyperosmolar Syndrome
HHS is a metabolic disorder of type 2 diabetes resulting from a relative
insulin deficiency initiated by an illness that raises the demand for insulin.
This is a serious condition in which:
hyperosmolarity and hyperglycemia predominate,
with alterations of the sensorium.
Hyperglycemic Hyperosmolar Syndrome
At the same time, ketosis is usually minimal or absent.
The basic biochemical defect is the lack of effective insulin (i.e., insulin
resistance).
Hyperglycemic Hyperosmolar Syndrome
Persistent hyperglycemia causes osmotic diuresis, which results in losses of water
and electrolytes.
To maintain osmotic equilibrium, water shifts from the intracellular fluid space to
the extracellular fluid space.
With glycosuria and dehydration, hypernatremia and increased osmolarity occur.
PATHOPHYSIOLOGY
Causes
HHS often can be traced to
 An infection or a precipitating event such as an acute illness (e.g., stroke)
 Medications that exacerbate hyperglycemia (e.g., thiazides)
 Treatments such as dialysis.
HHS occurs most often in older adults (50 to 70 years of age) who have no known history of
diabetes or who have type 2 diabetes
Occurrence
What distinguishes HHS from DKA?
Ketosis and acidosis generally do not occur in HHS,
partly because of differences in insulin levels.
 In DKA, no insulin is present, and this promotes the breakdown of stored
glucose, protein, and fat, which leads to the production of ketone bodies and
ketoacidosis.
 In HHS, the insulin level is too low to prevent hyperglycemia (and subsequent
osmotic diuresis), but it is high enough to prevent fat breakdown.
What distinguishes HHS from DKA?
Clinical Manifestation
 Hypotension
 Profound dehydration:
- dry mucous membranes,
- poor skin turgor
 Tachycardia
 Variable neurologic signs:
- alteration of consciousness,
- seizures,
- hemiparesis
Assessment and Diagnostic Findings
Diagnostic assessment includes a range of laboratory tests,
including:
 blood glucose
 electrolytes
 BUN
 complete blood count
 serum osmolality
 arterial blood gas analysis
 The blood glucose level is usually 600 to 1200 mg/dL,
 the osmolality exceeds 320 mOsm/kg.
MANAGEMENT
The overall approach to the treatment of HHS is similar
to that of DKA:
 Fluid replacement
 Correction of electrolyte imbalances
 Insulin administration
Management
 Because patients with HHS are typically older, close
monitoring of volume and electrolyte status is important for
prevention of fluid overload, heart failure, and cardiac
dysrhythmias.
 Fluid treatment is started with 0.9% or 0.45% NS, depending
on the patient’s sodium level and the severity of volume
depletion.
Management
 Central venous or hemodynamic pressure monitoring
guides fluid replacement. Potassium is added to IV fluids
when urinary output is adequate and is guided by continuous
ECG monitoring and frequent laboratory determinations
of potassium
Management
 Insulin plays a less important role in the treatment of HHS
because it is not needed for reversal of acidosis, as in DKA.
 Other therapeutic modalities are determined by the underlying illness and the
results of continuing clinical and laboratory evaluation.
 It may take 3 to 5 days for neurologic symptoms to clear, and treatment of
HHS usually continues well after metabolic abnormalities have resolved
Management
After recovery from HHS,
 Many patients can control their diabetes with
Medical Nutrition Therapy (MNT) alone or
with MNT and oral antidiabetic medications.
 Insulin may not be needed once the acute
hyperglycemic complication is resolved.
 Frequent SBGM is important in prevention of
recurrence of HHS.
Hyperglycemic hyperosmolar syndrome for nursing

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Hyperglycemic hyperosmolar syndrome for nursing

  • 2. Main types Symptoms Prevention Organs affected Treatment Diabetes Summary IDDM NIDDM GDM Polyuria Fatigue weight loss Polydipsia weakness Polyphagia Healthy Physical Weight Nutrition Exercise Control Insulin & Medication Nutritional Therapy Blood glucose Monitoring + LADA Complications
  • 3. Short-term imbalances in blood glucose levels ACUTE COMPLICATIONS OF DIABETES Hyperglycemic Hyperosmolar Syndrome (HHS) Diabetic Ketoacidosis (DKA) Hypoglycemia
  • 4. Hyperglycemic Hyperosmolar Syndrome HHS is a metabolic disorder of type 2 diabetes resulting from a relative insulin deficiency initiated by an illness that raises the demand for insulin. This is a serious condition in which: hyperosmolarity and hyperglycemia predominate, with alterations of the sensorium.
  • 5. Hyperglycemic Hyperosmolar Syndrome At the same time, ketosis is usually minimal or absent. The basic biochemical defect is the lack of effective insulin (i.e., insulin resistance).
  • 6. Hyperglycemic Hyperosmolar Syndrome Persistent hyperglycemia causes osmotic diuresis, which results in losses of water and electrolytes. To maintain osmotic equilibrium, water shifts from the intracellular fluid space to the extracellular fluid space. With glycosuria and dehydration, hypernatremia and increased osmolarity occur.
  • 8. Causes HHS often can be traced to  An infection or a precipitating event such as an acute illness (e.g., stroke)  Medications that exacerbate hyperglycemia (e.g., thiazides)  Treatments such as dialysis. HHS occurs most often in older adults (50 to 70 years of age) who have no known history of diabetes or who have type 2 diabetes Occurrence
  • 9. What distinguishes HHS from DKA? Ketosis and acidosis generally do not occur in HHS, partly because of differences in insulin levels.  In DKA, no insulin is present, and this promotes the breakdown of stored glucose, protein, and fat, which leads to the production of ketone bodies and ketoacidosis.  In HHS, the insulin level is too low to prevent hyperglycemia (and subsequent osmotic diuresis), but it is high enough to prevent fat breakdown.
  • 11. Clinical Manifestation  Hypotension  Profound dehydration: - dry mucous membranes, - poor skin turgor  Tachycardia  Variable neurologic signs: - alteration of consciousness, - seizures, - hemiparesis
  • 12. Assessment and Diagnostic Findings Diagnostic assessment includes a range of laboratory tests, including:  blood glucose  electrolytes  BUN  complete blood count  serum osmolality  arterial blood gas analysis  The blood glucose level is usually 600 to 1200 mg/dL,  the osmolality exceeds 320 mOsm/kg.
  • 13. MANAGEMENT The overall approach to the treatment of HHS is similar to that of DKA:  Fluid replacement  Correction of electrolyte imbalances  Insulin administration
  • 14. Management  Because patients with HHS are typically older, close monitoring of volume and electrolyte status is important for prevention of fluid overload, heart failure, and cardiac dysrhythmias.  Fluid treatment is started with 0.9% or 0.45% NS, depending on the patient’s sodium level and the severity of volume depletion.
  • 15. Management  Central venous or hemodynamic pressure monitoring guides fluid replacement. Potassium is added to IV fluids when urinary output is adequate and is guided by continuous ECG monitoring and frequent laboratory determinations of potassium
  • 16. Management  Insulin plays a less important role in the treatment of HHS because it is not needed for reversal of acidosis, as in DKA.  Other therapeutic modalities are determined by the underlying illness and the results of continuing clinical and laboratory evaluation.  It may take 3 to 5 days for neurologic symptoms to clear, and treatment of HHS usually continues well after metabolic abnormalities have resolved
  • 17. Management After recovery from HHS,  Many patients can control their diabetes with Medical Nutrition Therapy (MNT) alone or with MNT and oral antidiabetic medications.  Insulin may not be needed once the acute hyperglycemic complication is resolved.  Frequent SBGM is important in prevention of recurrence of HHS.