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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.
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HHNS is also called.
Hyperosmolar Nonketotic State (HNS)
Hyperosmolar Hyperglycemic Syndrome
Diabetic Hyperosmolar State
Hyperosmolar Hyperglycemic Nonketotic
coma
Hyperosmolar Coma
Nonketotic Hypertonicity.
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How does it occur?
HHNS is most common in adults with type
2 diabetes. Having diabetes means thatthere is too much sugar (glucose) in yourblood. Because type 2 diabetes can be a
silent disease for many years, unless yourblood sugar is checked, HHNS could
happen before you know that you havediabetes.
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HHNS is more common in the Type II NIDDMpatient. This is because the Type II patients
pancreas is able to still produce and secretesome insulin. Therefore, some glucose is stillgetting into the cells.
The glucose entering the cells keeps the amount
of fat being burned for energy to a lesseramount than is seen in DKA. If a significantamount of fat is not being used, then lessketones will be produced as a byproduct of fatbreakdown.
Since a large amount of ketones do not collect andcause acid load in the body, the syndrome is
termed nonketotic.
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CAUSES OF HHNS
Age; HHNS is more common in elderly
individuals with Types 1 and 2 DM
Illnesssuch as infections, MI, GI
bleeds, uremia and arterial thrombosis
Stress
Massive fluid loss from prolonged
osmotic diuresis
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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 andchlorthalidone
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FOUR MAJOR CLINICAL
FEATURES
Severe hyperglycemia
No or slight ketosis
Profound dehydration
Hyperosmolality
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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
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Assessment:
Blood glucose level is from600-1200mg/dl
Postural Hypotension
Profound Dehydration-
(typically 8-12 L) dry mucousmembranes, poor skinturgor)
Tachycardia
Mental status changes
Neurological deficits
Seizures
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Physical findings
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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 shockand coma may occur
Normothermia or hypothermia is common due to
vasodilation
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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 withoutCVA or structural lesion
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HHNS: Physical findings
Degree of lethargy and coma isproportional to the level of osmolality
Those with coma tend to have:
Higher osmolality
Higher hyperglycemia
Greater volume contraction
Not surprising that misdiagnosis of strokeor organic brain disease is common in theelderly
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LABORATORYTESTS
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Essential Laboratory Tests
1. Serum osmolality (concentration ofparticles) 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
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Laboratory Tests
Consider Urinalysis and
culture
Liver and pancreaticenzymes Cardiac enzymes Thyroid function Coagulation profiles
Chest x-ray ECG
Other CT of head LP
Toxicology ABG Of value only if
suspicion ofrespiratorycomponent toacid-base
abnormality Both PCO2and pH
can be predictedfrom bicarbonateconcentrationobtained fromvenous
electrolytes
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The primary goal is REHYDRATION. Thisis to restore circulating plasma volume
and correct electrolyte imbalances. In addition, the precipitating event
should be identified and corrected, andother goals similar to those described for
treatment of DKA should be instituted,includingproviding adequate insulin torestore and maintain normal glucosemetabolism.
Glucose concentration is the majorbiochemical end point because patientswith HHNS do not have ketosis oracidosis.
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Treatment
The first emergency
treatment is
intravenous (IV) fluidsso that your body has
more fluid and your
sodium and potassium
levels can be brought
back to normal.
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Electrolytes
K+
Initial levels may be normal or high in the
presence of acidemia
Levels < 3.3mEq/L represents severe deficitand 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
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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 Rinsulin
Loading dose is optional
Once serum glucose reaches 250-
300mg/dL fluid can be to D5 1/2NS and
insulin can be decreased to 0.05units/kg/h.
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Treatment
Dextrose (50 g) should be givenintravenously 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
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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 notneeded for reversal of acidosis in HHNS.
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Patient Management:
Maintain safety and prevent injury
related to changes in the patients
sensorium secondary to HHNS.
Closely monitor fluid status and urine
output
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Emergency Nursing Care
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Nursing Care
Even though the major complication of
the disease is severe dehydration, HHNS
carries the highest mortality rate of thediabetic emergencies.
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Nursing Care
Establish and maintain a patent airway. manual maneuver
mechanical device including endotracheal intubationmay be necessary
Establish and maintain adequateventilation. provide positive pressure ventilation
Establish and maintain adequateoxygenation Assess the patient for evidence of hypoxia
pulse oximeter
determine the SpO2 reading
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Nursing Care
Provide continuous ECG monitoring cardiac dysrhythmias may occur
patients experiencing HHNS have preexisting cardiovasculardisease making them prone to cardiac dysrhythmias
Initiate an intravenous line of normal saline
Aggressive fluid resuscitation may be necessary insevere cases
Administer a bolus of 500 mL of normal saline inseverely dehydrated patients
Lactated Ringers may also be used
In patients with a history of cardiac disease,congestive heart failure, or renal insufficiency, a250 mL bolus should be used
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Nursing Care
Continuously reassess the patient for aresponse 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.
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How to Prevent HHNS
Ask your provider when you should callabout high blood sugar--for example, ablood sugar higher than 250 milligrams perdeciliter (mg/dL), or 13.9 millimoles per
liter (mmol/L). Report any symptoms of infection, such as
fever, a cough, or cloudy urine right awayto your provider.
Check your blood sugar every 4 hourswhen you are sick. Work with yourhealthcare provider to develop a sick-dayplan.
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