H Y P E R O S M O L A R

H Y P E R G L Y C E M I C

N O N K E T O T I C

S Y N D R O M E

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS)

- is a life-threatening emergency. It is caused by very high blood sugar (hyperglycemia). Without prompt treatment HHNS can be fatal.

HHNS is also called.

Hyperosmolar Nonketotic State (HNS) Hyperosmolar Hyperglycemic Syndrome Diabetic Hyperosmolar State Hyperosmolar Hyperglycemic Nonketotic coma Hyperosmolar Coma Nonketotic Hypertonicity.

How does it occur?

HHNS is most common in adults with type 2 diabetes. Having diabetes means that there is too much sugar (glucose) in your blood. Because type 2 diabetes can be a silent disease for many years, unless your blood sugar is checked, HHNS could happen before you know that you have diabetes.

 HHNS is more common in the Type II NIDDM patient. This is because the Type II patients pancreas is able to still produce and secrete some insulin. Therefore, some glucose is still getting into the cells.
The glucose entering the cells keeps the amount of fat being burned for energy to a lesser amount than is seen in DKA. If a significant amount of fat is not being used, then less ketones will be produced as a byproduct of fat breakdown. Since a large amount of ketones do not collect and cause acid load in the body, the syndrome is termed nonketotic.

CAUSES OF HHNS
Age; HHNS is more common in elderly individuals with Types 1 and 2 DM Illness such as infections, MI, GI bleeds, uremia and arterial thrombosis Stress Massive fluid loss from prolonged osmotic diuresis

CAUSES OF HHNS
Hypertonic feedings such as prolonged parenteral nutrition via IV infusion, high-protein or gastric tube feedings Pharmacologic agents such as thiazides, propranolol, phenytoin, steroids, flurosemide and chlorthalidone

FOUR MAJOR CLINICAL FEATURES

Severe hyperglycemia No or slight ketosis Profound dehydration Hyperosmolality

Risk Factors
Older age Poor kidney function Poor management of diabetes-not following the treatment plan as directed Stopping insulin or other medications that lower the glucose levels

Assessment:
Blood glucose level is from 600-1200mg/dl Postural Hypotension
Profound Dehydration(typically 8-12 L) dry mucous membranes, poor skin turgor)

Tachycardia Mental status changes Neurological deficits Seizures

Physical findings

HHNS: Physical findings

Non-specific Clinical signs of volume depletion:
Poor skin turgor Dry mucus membranes Sunken eyeballs Hypotension

Wide range of findings such as changes in vital signs and cognition to clear evidence of profound shock and coma may occur Normothermia or hypothermia is common due to vasodilation

HHNS: Physical findings

Seizures
Up to 15% may present with seizures Typically focal Generalized seizures that are often resistant to anticonvulsants may occur

Other CNS symptoms may include:

Tremor Clonus Hyperreflexia Hyporeflexia Positive plantar response Reversible hemiplegia or hemisensory defects without CVA or structural lesion

HHNS: Physical findings

Degree of lethargy and coma is proportional to the level of osmolality
Those with coma tend to have:
Higher osmolality Higher hyperglycemia Greater volume contraction

Not surprising that misdiagnosis of stroke or organic brain disease is common in the elderly

LABORATORY

TESTS

Essential Laboratory Tests

1. Serum osmolality (concentration of particles) of 320 mOsm/kg 2. Plasma glucose level greater than 33.3 mmol/L (600 mg/dL) 3. Intense dehydration shown by elevated serum sodium levels. 4. No ketoacidosis 5. PH of 7.3 6. HCO3 - greater than 15 mEq/L 7. BUN and creatinine-elevated

Laboratory Tests
Other Consider CT of head Urinalysis and LP culture Toxicology Liver and pancreatic ABG enzymes Of value only if Cardiac enzymes suspicion of Thyroid function respiratory component to Coagulation profiles acid-base Chest x-ray abnormality ECG Both PCO2 and pH
can be predicted from bicarbonate concentration obtained from venous electrolytes

T R E A T M E N T

 The primary goal is REHYDRATION. This is to restore circulating plasma volume and correct electrolyte imbalances. In addition, the precipitating event should be identified and corrected, and other goals similar to those described for treatment of DKA should be instituted, including providing adequate insulin to restore and maintain normal glucose metabolism. Glucose concentration is the major biochemical end point because patients with HHNS do not have ketosis or acidosis.

Treatment
The first emergency treatment is intravenous (IV) fluids so that your body has more fluid and your sodium and potassium levels can be brought back to normal.

Treatment
Electrolytes
K+

Initial levels may be normal or high in the presence of acidemia Levels < 3.3mEq/L represents severe deficit and are at risk for dysrhythmias. Replacement can begin once urinary output is assured.
Replace at a rate of 10-20mEq/h.

Na+ Replaced rapidly w/ the amount of NS required for fluid resuscitation.

Treatment
Insulin
As in DKA IV administration preferred over IM or SubQ due to poor adsorption. IV infusion at rate of 0.1 units/kg/h R insulin Loading dose is optional Once serum glucose reaches 250300mg/dL fluid can be to D5 1/2NS and insulin can be decreased to 0.05units/kg/h.

Treatment
Dextrose (50 g) should be given intravenously every 8 hours and insulin dose adjusted accordingly (decreased 1 to 3 U/h) based on plasma glucose measurements every 4 hours. Bicarbonate therapy is contraindicated in absence of acidosis

Patient Management:
Similar to treatment for DKA Includes fluid replacement, correction of electrolyte imbalances, and insulin administration Insulin plays a less critical role in the treatment of HHNS than it does for the treatment of DKA because insulin is not needed for reversal of acidosis in HHNS.

Patient Management:

Maintain safety and prevent injury related to changes in the patients sensorium secondary to HHNS.
Closely monitor fluid status and urine output

Emergency Nursing Care

Nursing Care

Even though the major complication of the disease is severe dehydration, HHNS carries the highest mortality rate of the diabetic emergencies.

Nursing Care
Establish and maintain a patent airway.
manual maneuver mechanical device including endotracheal intubation may be necessary

Establish and maintain adequate ventilation.

provide positive pressure ventilation

Establish and maintain adequate oxygenation

Assess the patient for evidence of hypoxia pulse oximeter determine the SpO2 reading

Nursing Care
Provide continuous ECG monitoring
cardiac dysrhythmias may occur patients experiencing HHNS have preexisting cardiovascular disease making them prone to cardiac dysrhythmias

Initiate an intravenous line of normal saline

Aggressive fluid resuscitation may be necessary in severe cases Administer a bolus of 500 mL of normal saline in severely dehydrated patients Lactated Ringers may also be used In patients with a history of cardiac disease, congestive heart failure, or renal insufficiency, a 250 mL bolus should be used

Nursing Care
Continuously reassess the patient for a response to the fluid administration and for evidence of over-hydration Assess the blood glucose level of any patient with preexisting disease who presents with signs and symptoms of dehydration or an altered mental status, especially the elderly, regardless of a positive history of diabetes mellitus.

How to Prevent HHNS

The best way to prevent HHNS is to: Take your diabetes medicines exactly as prescribed. Talk with your healthcare provider if you have questions about your care. Use your home glucose monitor to check your blood sugar as often as your provider recommends. Keep your regular appointments with your provider (usually every 3 months).

How to Prevent HHNS

Ask your provider when you should call about high blood sugar--for example, a blood sugar higher than 250 milligrams per deciliter (mg/dL), or 13.9 millimoles per liter (mmol/L). Report any symptoms of infection, such as fever, a cough, or cloudy urine right away to your provider. Check your blood sugar every 4 hours when you are sick. Work with your healthcare provider to develop a sick-day plan.