AIR MEDICAL ANALYSIS

with DeWayne Miller

Hyperosmolar hyperglycemic state

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS)
are two of the most serious metabolic complications of diabetes
Sep 29, 2011

By DeWayne Miller
You arrive in the emergency department of a small hospital where your patient is waiting. Mr Smith is
a 64 year old of Portuguese descent with type 2 diabetes, chronic hepatitis B, CVA 2 years ago, CAD,
and hypertension. His home medications include metoprolol, aspirin, atorvastatin, lisinopril,
furosemide and metformin. His daughter is at the bedside and reports he had been doing well until
last week when he appeared depressed and had not been taking his medications on time. When she
checked on him today he was dicult to wake and could not sit up in bed. EMS transported to the
hospital.
Now he appears weak, and is very slow to respond. His speech is clear. He is able to move all four
extremities with no unilateral decits. B/P 88/56, pulse is 118, respritory rate 22. Oral temp is 37.4 C.
His lungs are clear, cardiac exam shows S1, S2 without murmur or gallop. His abdomen is soft and
nontender.
Lab results are:
Sodium 138mEq/L
K+ 4.9 mEq/L,
Cl 88 mEq/L,
HCO3 35 mEq/L,
BUN 99 mg/dL
Creatinine 4.3 mg/dL, glucose 1130 mg/dL
Arterial blood gas: pH 7.40
PCO2 35 mmHg
PO2 88 mmHg

WBC 8.4 k
Serum ketones: negative
Urinalysis: 2+ protein, 4+ glucose, no ketones
Is this data complete enough to make a diagnosis? What are the pertinent results to do so?
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two of the most serious
metabolic complications of diabetes. While DKA is more common, HHS has a higher mortality rate. In
adult subjects with DKA overall mortality is <1%, mortality gures for HHS range from 5 to 20%.1,2
Death is usually due in part to a comorbid illness so detection and treatment of the underlying illness
should be included.
HHS is the result of a sustained osmotic diuresis, typically over several days to weeks. It is
characterized by severe hyperglycemia, hyperosmolarity and dehydration without signicant
ketoacidosis. Patients with a lack of mobility are at a higher risk because of their limited access to
water. One of the most common predisposing factors is not recognizing the signs and symptoms of
diabetes and then underestimating the uid requirements of the patient, especially in an assisted
living environment.
HHS has been referred to by several names over the years including hyperosmolar nonketotic state,
hyperosmolar coma, and hyperglycemic hyperosmolar nonketotic coma.
Pathophysiology and Dierential
Biochemical markers comparing HHS to DKA:
HHS

DKA

>7.3

<7.3

Glucose

>600 mg/dl

>250 mg/dl

Ketones

neg to slight

+urine & serum

>15 mEq/L

<15 mEq/L

>320 mOsm/kg

>290 mOsm/kg

pH

Bicarbonate
Serum Osmol

The reason for the absence of ketoacidosis is not completely understood. One theory is that many of
these patients still secrete small amounts of insulin, perhaps just enough to block ketogenesis.
The mean onset age is in the early sixth or seventh decade, but it has presented in all age groups.
Hypokalemia should be anticipated and can pose a life threatening risk if missed. Even if serum
potassium (K+) levels appear normal, total body stores will be low. Once correction of acidosis and

hyperglycemia is started, the serum K+ will drop.

Management
Patients typically present with severe dehydration and some degree of neurological decits ranging
from minimal to frank coma. Assessment should start with the ABCs, along with a thorough history
focused on the precipitating factors. A diagnosis of decompensated diabetes can be made with a
bedside glucose test and clinical presentation. Lab studies should include but not be limited to serum
pH, K+, glucose, and serum and urine ketones.
Fluid Resuscitation
Fluid replacement is the rst priority in managing HHS. An approximate uid decit can be calculated
to guide therapy; the uid decit for an adult is typically 8 to 12 liters.
The initial uid of choice is 0.9% sodium chloride (NS). The initial rate of administration depends on
the clinical state of the patient and any comorbid conditions limiting volume resuscitation. If the
patient is hypotensive and in shock, give 1 to 2 liters of NS until symptoms improve and urine output
is established.
For adults that do not present hypotensive initial rates of 15 to 20 mL/kg/hour for the rst hour can
be used. Then change to 4 to 14 mL/kg/hour and, if the corrected serum sodium is normal to elevated
uid, can be changed to 0.45% sodium chloride. Total uid volumes should not exceed 50 mL/kg in
the rst four hours. Fluids should be calculated to replace the decit over 24 hours for adults or 48
hours for pediatric patients.
Electrolytes:
Potassuim
All patients with HHS have a total body depletion of K+. Serum levels may still be in the normal range
initially. Rehydration and insulin therapy usually results in a rapid decline of serum K+. If initial serum
K+ levels are below 3.3 mEq/L replacement should be started immediately. Rates of administration
should be 20 to 40 mEq per hour until serum levels are above 3.3 mEq/L. Then add 20 mEq/L of
potassium chloride and recheck serum levels every 1 to 2 hours with a goal of 4 to 5 mEq/L. The most
rapid change of serum levels occur in the rst 5 hours of treatment.
Magnesium
Magnesium replacement need only be initiated outside of the ICU setting if the serum level is low. K+
and magnesium regulation is closely related and hypokalemia correction may be dependant on
magnesium.
Insulin
Insulin therapy should be held until serum K+ is > 3.3mEq/L and uid replacement has restored
perfusion. The recommended dose of regular insulin is 0.1 units/kg per hour IV. A bolus of 0.15
units/kg can be given, however studies have failed to show any benet to bolus therapy for adults.
Bolus therapy is not recommended for pediatric patients. Insulin infusions should not be interrupted
once started and serum glucose levels should be checked hourly. Decrease serum glucose levels by

no more than 50 to 75 mg/dL per hour to no less than a serum level of 300 mg/dL. Once that level is
reached D5W should be added to IV uids and the insulin rate can be changed to 0.05 U/kg per hour.
If the glucose level does not improve in the rst hour ensure the adequacy of uid volume
replacement and increase the insulin dose to 0.2 U/kg per hour.
Underlying Pathology
Searching for and treating the underlying illness that precipitated HHS is crucial in the management
of HHS.
Conclusion
It is dicult to predict who is at the greatest risk for complications. Indicators point to overly
aggressive volume replacement during the rst 4 hours. Cerebral edema is uncommon in adults but
is present in >50% of the fatalities in pediatrics with DKA. Little credible data exists on incidence or
predisposing factors of cerebral edema in HHS. It is reasonable to assume gradual correction of
electrolyte abnormalities and water decits would place patients at less risk than rapid changes.
Take home points:
Fluid replacement is the rst priority
Total body K+ stores will be low
Gradually correct hyperglycemia and hyperosmolarity
Frequently reassess LOC, hydration and electrolytes
Find the precipitating illness / cause

References
1. Ennis ED, Stahl EJVB, Kreisberg RA. The hyperosmolar hyperglycemic syndrome. Diabetes Rev
1994;2:115126
2. Lorber D. Nonketotic hypertonicity in di- abetes mellitus. Med Clin North Am 1995;79:39 52
3. American Diabetes Association. Hyperglycemic crises in diabetes. Diabetes Care 2004; 27(Suppl
1):S94102.
4. Marx J.A., Hockberger R.S., Walls R.M., et al; Rosens Emergency Medicine: seventh edition.
Philadelphia, Lippincott Williams & Wilkins, 2010. pp 1644-1646.
5. Nugent. Hyperosmolar hyperglycemic state. Emerg Med Clin North Am (2005) vol. 23 (3) pp. 629-48,
vii

About the author

DeWayne Miller RN, NREMT-P, CFRN has been a ight nurse with West Michigan Air Care for 16 years. He has extensive experience as a
paramedic and as a nurse in the emergency department and ICU. DeWayne teaches critical care transport classes and is an ACLS
instructor at Bronson Methodist hospital. Presently he is collaborating with software developers for the evolution of new computerized
charting techniques and is the orientation training coordinator for Air Care. During his time o he participates in distance running and
endurance sports.

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