RUNNING HEAD: DKA VS.

HHNKS; ARCHIBALD 1

Diabetic Ketoacidosis & Hyperosmolar Hyperglycemia Non-Ketonic Syndrome

Elizabeth Blair Archibald, RN Student

Southwestern Oregon Community College

December 1, 2017
DKA VS. HHNKS; ARCHIBALD 2

Pancreatic Functions: Homeostasis by Negative Feedback

The pancreas is an organ that performs endocrine (hormonal regulation) and exocrine

(digestive regulation) functions. The cells of the pancreas include: alpha cells, beta cells, and delta

cells. All the cells reside in the gland of the pancreas coined the islets of Langerhans. Each cell

secretes a different hormone with a different function. The three hormones are: Glucagon

(secreted by alpha cells), Insulin (secreted by beta cells), and Somatostatin (secreted by delta cells).

Glucagon and insulin affect carbohydrate, protein, and fat metabolism. (Ignatavicius &

Workman, 1260) The function of glucagon is to prevent low blood sugar by causing cells to release

glucose. It has the opposite effect of insulin. The function of insulin is to facilitate the ingestion

of glucose by the cells of the body for energy and nourishment. This is considered a negative

feedback (Ignatavicius & Workman, 1256) mechanism, because insulin negates the effect of

hyperglycemia. Lastly, the function of Somatostatin is to inhibits the release of glucagon and

insulin from the pancreas. (Ignatavicius & Workman, 1260)

Overview of Diabetes

Diabetes can be characterized in many ways. The two most common forms are Type I and

Type II. Both types of diabetes result in poor regulation of serum glucose. Type I Diabetes is an

autoimmune disease where the body attacks the beta cells of the pancreas. This disables the beta

cells, and they are unable to release insulin. As stated previously, insulin is released when blood

sugar levels rise. Without insulin, CBG will continue to rise, and there will be no compensatory

mechanism to balance this metabolic process. The main metabolic effects of insulin are to

stimulate glucose uptake in skeletal muscle and heart muscle and to suppress liver production of

glucose. (Ignatavicius & Workman, 1301)

DKA VS. HHNKS; ARCHIBALD 3

Type II Diabetes can be characterized by two abnormalities: (1) The cells have a decreased

response to insulin, or (2) or the beta cells are not secreting enough insulin. DM II differs from

DM I because not all patients with DM II require insulin. In some cases, patients that have

metabolic syndrome induced DM II can perform lifestyle modifications (diet, exercise,

smoking/ETOH cessation) and control their DM II. In other cases, the patient cannot control the

disease with lifestyle modifications, and require insulin therapy.

No matter the type of diabetes a patient has, glucose regulation is of utmost importance.

Diabetic Ketoacidosis (DKA), and Hyperosmolar Hyperglycemia Non-Ketonic Syndrome

(HHNKS) are both medical emergencies related to lack of glucose regulation that need to be

treated promptly and can lead to death if not corrected.

Pathophysiology of Diabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis (DKA) is severe situation with a sudden onset that occurs when a

person has unrecognized or untreated Type I Diabetes. In breaking down the name DKA, it is first

understood that Type I Diabetes is a disease in which the pancreatic beta cells are destroyed, and

thus they cannot release insulin. Individuals with Type I Diabetes, must inject daily doses of

insulin to ensure normal metabolic processes. Secondly, ketone bodies are defined as a substance

that increase in the blood as a result of faulty carbohydrate metabolism. They increase in persons

with untreated or inadequately controlled DM and are the primary cause of acidosis. (Tabers,

311) Glucose is a carbohydrate. The ketone bodies form because the cells of the body cannot

ingest glucose properly (carbohydrate metabolism) from the lack of insulin. Insulin typically

promotes the formation of fat, and is responsible for inhibiting the breakdown of fat in the body.

Because there is not a sufficient amount of insulin present in the body, fat breakdown is enhanced.

The enhancement of fat breakdown increases the amount of nonesterified fatty acids in the body
DKA VS. HHNKS; ARCHIBALD 4

that are then sent to the liver. In response to the increase of fatty acids, the liver creates an increased

amount of glycogen (the substance that forms glucose), and more ketone bodies than the body

needs. The result is metabolic acidosis.

DKA, a complication of Diabetes Type I, occurs because there is a lack of sufficient insulin

in the body, and an increased in the hormones that increasing glucose in the blood, such as:

catecholamines, cortisol, glucagon, and growth hormone. (Huether & McCance, 465) The lack

of insulin means that a negative feedback (compensatory mechanism to high levels of glucose) is

not occurring. There is a very specific outline to what defines DKA, and the factors include: A

serum glucose of greater than 250 mg/dl, a serum bicarbonate level of less than 18 mg/dl, a serum

PH of less than 7.30, the presence of an anion gap, and the presence of urine and serum ketones.

(Huether & McCance, 465) DKA can be caused by any situation that imposes stress, such as:

infection, accident, trauma, emotional stress omission of insulin, or medications that antagonize

insulin. (Huether & McCance, 464) Symptoms of DKA, include: lethargy, dry mouth, headache,

increased thirst and urination, gastrointestinal disturbances (weight loss, nausea, vomiting,

abdominal pain, fruity odor to breath), itchy skin, shortness of breath, hyperventilation (bodys

compensatory attempt to eliminate excessive CO2), ketones and glucose in the urine, and dizziness.

Pathophysiology of Hyperosmolar Hyperglycemia Non-Ketonic Syndrome

Hyperosmolar Hyperglycemia Non-Ketonic Syndrome (HHNKS) is severe complication

of Type II Diabetes that has a slow onset, and is caused by lack of insulin and severe fluid depletion.

In breaking down the name HHNKS, it is first understood that Type II Diabetes is a disease that

can be caused by two factors: (1) the tissues (liver, muscle, fat) that are usually responsive to

insulin are not receptive to the insulin, and therefore, the cells do not utilize the available glucose

as readily, called insulin resistance (Huether & McCance, 462); or (2) the beta cells of the
DKA VS. HHNKS; ARCHIBALD 5

pancreas have a decreased formation and a decrease in release of insulin. Secondly, hyperosmolar

is an increase in the concentration of osmotically active particles in a solution (Tabers, 1688)

with the solution being serum. Glucose is considered an osmotically active particle, and therefore,

hyperosmolar and hyperglycemia (elevated serum glucose level) go hand in hand. Lastly, non-

ketonic means that unlike DKA, ketones are not a part of this diabetic complication because in

HHNKS, the pancreas secretes just enough insulin to prevent ketosis, but not enough to prevent

hyperglycemia. (Ignatavicius & Workman, 1336) The people that are at risk for obtaining this

complication are the patients that have Type II Diabetes, and have an active infection, have heart

or kidney disease, have a poor fluid intake, myocardial infarction, sepsis, pancreatitis, stroke, and

some drugs (Ignatavicius & Workman, 1336), or other physiological stressors.

Like DKA, here is a very specific outline to what defines HHNKS, and the factors include:

serum glucose level of greater than 600 mg/dl, a serum PH of greater than 7.30, a serum

bicarbonate level greater than 15 mg/dl, a serum osmolarity greater than 320 mOsm/L, and either

absent of small numbers of ketones in the urine and serum. (Huether & McCance, 465) Glucose

levels are considerably higher and insulin levels are lower in HHNKS than in DKA, and there is

extreme diuresis leading to dehydration, and electrolyte loss. Dehydration and electrolyte loss

contribute to altered CNS functions with neurologic symptoms.

Nursing Implications

With any type of diabetes, the most important intervention is management of disease by

maintaining a normal blood glucose level, and adequate hydration. The patient should be well

versed in their own understanding about what causes their disease, and how to appropriately

manage the disease to prevent complications, such as: Diabetic Ketoacidosis (DKA) and

Hyperosmolar Hyperglycemia Non-Ketonic Syndrome (HHNKS). The nurse should discuss with
DKA VS. HHNKS; ARCHIBALD 6

all diabetic patients the risks of DKA or HHNKS, and how to prevent these complications. The

patient would need to be aware of the signs and symptoms associated with hyper and hypoglycemia

and DKA or HHNKS. Reviewing proper capillary blood glucose checks, and administration of

insulin is of the upmost importance, as well as having the patient teach back the information to the

nurse to ensure understanding. The patient needs to understand sick day rules and that in the

event of illness they should inform their primary care provider. When sick, CBG needs to be

monitored Q4H, and urine needs to be monitored for ketones when CBG is greater than 240 mg/dL.

When sick, patient should continue to take medications as prescribed (including insulin), maintain

adequate hydration, eat meals at regular times, treat symptoms as directed by PCP, get plenty of

rest, and call the PCP is there is persistent nausea or vomiting, large ketones in the urine, or a fever

that persists for 24 hours. Finally, the nurse needs to discuss diet in detail. A person with diabetes

should not eat many simple carbohydrates because they do not need excess sugar in their diet.

Their diet should include: whole grains, ample protein, lean meats, fruits, vegetable, omega 3 fatty

acids, and nuts. Of course, the diet will not remain perfect, because humans get emotional

satisfaction from eating, but it should be discussed that sweets and junk food should be ingested

in moderation.

Nursing Assessments

As a nurse, it is important to perform a full head to toe exam. Focused assessments would

include: Vitals, auscultation of heart and lungs, a respiratory assessment for adequate airway or

for signs of the body trying to compensate from metabolic acidosis (hyperventilation), and a

cardiovascular assessment for fluid overload or depletion, regular capillary blood glucose check,

central nervous system evaluation (LOC, depression, lethargy, malaise, 12 cranial nerves, reflexes,

peripheral sensations), vision tests, hydration evaluation/fluid status (skin turgor, skin moisture,
DKA VS. HHNKS; ARCHIBALD 7

mucous membrane moisture), pain scale (palliative/provocative factors, quality, radiation/region,

severity, temporal factors), intake and output, thorough gastrointestinal exam (weight loss, nausea,

vomiting, abdominal pain, fruity odor to breath), daily weight check, skin check for pruritus or

breakdown, any sign on infection, signs of hyperkalemia (fatigue, malaise, confusion, muscle

weakness, shallow respirations, abdominal distention/paralytic ileus, hypotension, weak pulse,

abnormal heart sounds), and signs of hypo or hyperglycemia.

Laboratory Values and Diagnostics

It would be important for the nurse to advocate for an HgbA1C (6.5% or less), capillary

blood glucose (70-130 mg/dL pre-meal/peak 180 mg/dL after meal), a urinalysis (negative for

glucose, ketone bodies, or albumin), CMP (BUN 8-21 mg/dL; CREA 0.5-1.2 mg/dL; Lactate 0.5-

1 mmol/L), arterial blood gas (PH 7.35-7.45/PaCO2 35-45 mmHg/PaO2 80-100 mmHg/HCo3 22-

26), electrolytes (NA 135-145 mg/dL, K 3.5-5 mg/dL), serum ketones (negative), serum osmolarity

(275-295 mOsm/kg), urine osmolality (300-900 mOsm/kg of water), urine specific gravity (1.005-

1.030), and anion gap (7-9 mEq/L).

Abnormal laboratory values associated with DKA show: CBG greater than 300 mg/dL,

variable osmolarity, positive 1:2 dilution of serum ketones, serum PH less than 7.35, serum

bicarbonate less than 15 mEq/L, BUN greater than 30 mg/dL, CREA greater than 1.5 mg/dL, and

a positive result for ketones in the urine.

Abnormal laboratory values associated with HHNKS show: CBG greater than 600 mg/dL,

serum osmolarity greater than 320 mOsm/L, negative for serum ketones, serum PH greater than

7.4, serum bicarbonate greater than 20 mEq/L, elevated BUN and CREA, and negative result for

ketones in the urine.

Treatment and Medications

DKA VS. HHNKS; ARCHIBALD 8

Many of the pharmacological interventions are the same for DKA and HHNKS. The main

goals with these two diseases are to correct hypovolemia with fluid therapy, and to correct elevated

blood glucose levels with intravenous insulin. Each facility has its own policy to performing an

insulin drip, but strict monitoring of capillary blood glucose is always imperative to track treatment,

and to prevent hypoglycemia. CBGs are typically performed every hour with an insulin drip.

Once the blood glucose drops to a facility dictated level (usually around 200 mg/dL), 5% Dextrose

will be infused at facility dictated rate concurrently with insulin drip to prevent the patients blood

glucose levels from being depleted to an unsafe level. Electrolyte levels are a concern when a

person has hyperglycemia. When blood glucose levels are high, it is common to also have high

potassium levels. With the correction of CBG to normal levels, it is possible for the potassium

level to drop to an unsafe low level. The nurse needs to be aware of what to assess for with

hypokalemia, including: fatigue, malaise, confusion, muscle weakness, shallow respirations,

abdominal distention, paralytic ileus, hypotension, and weak pulse. The doctor will prescribe a

potassium replacer if needed. Insulin drip is discontinued, and subcutaneous insulin is initiated

when blood glucose levels have normalized.

The only treatment that is specific to DKA is treatment of metabolic acidosis. If acidosis

is extreme in DKA, (PH below 7.0), the patient will be treated with intravenous Sodium

Bicarbonate. Arterial blood gases must be assessed, and once PH is above 7.0, infusion is

discontinued.

Works Cited

Huether, S. E., & McCance, K. L. (2012). Understanding Pathophysiology (5 ed.). (S. Clark,

Ed.) St. Louis, Missouri, United States of America: Elsevier Mosby.

DKA VS. HHNKS; ARCHIBALD 9

Ignatavicius, D. D., & Workman, L. M. (2016). Medical Surgical Nursing (8th Edition ed.). St.

Louis, Missouri, United States of America: Elsevier Mosby.

Taber, C. W. (2013). Taber's Cyclopedia Medical Dictionary (22nd Edition ed.). Philadelphia,

Pennsylvania, United States of America: F.A. Davis.

Patient Information: Diabetic Ketoacidosis

Problem #1 Primary base bicarbonate deficiency related to rapid breathing as evidence by

increased CO2, and decreased PH of arterial blood gas (metabolic acidosis).
Desired Outcome: Patient will display decrease in rate of breathing from tachypnea to

a RR between 12-20 breaths per minute post interventions within the 12-hour shift.

Nursing Interventions Client Response to Intervention

1. Administer 2-5 mEq/kg Bicarbonate 1. Patients bicarbonate level and PH will

intravenously over 5 minutes, once. rise to normal levels. (HCO3= 22-26;

PH=7.35-7.45)

2. Assess respiratory status Q2H: depth, rate, 2. Patients respiratory rate will decrease

effectiveness of breathing, and degree of to 12-20 BPM; slow rate will increase

oxygenation. depth of breathing. SPO2 will remain at

95% saturation or higher.

3. Reevaluate arterial blood gases, electrolytes, 3. ABG PH= 7.35-7.45; PaCo3= 35-45

kidney function, and urinalysis- once per 12-hour mmHg; PaO2 80-100 mmHg; HcO3 22-

shift. 26; Sodium 135 145 mEq/L; Potassium

3.5 5.0 mEq/L; Chloride 97-107

mEq/L; BUN 8-21 mg/dL; Creatinine

DKA VS. HHNKS; ARCHIBALD 10

0.51.2 mg/dL; Urinalysis will be

negative for ketone bodies or glucose.

Evaluation: Patients respiratory rate will decrease to between 12-20 BPM and will effectively

oxygenate the tissues evidence by normal ABG- within the 12-hour shift. Neurologic status

will reflect adequate oxygenation (A/Ox4).

Patient Information: Early Onset Diabetic Ketoacidosis

Problem #2 Imbalanced Nutrition: Less than body requirements r/t cells inability to
utilize insulin to obtain glucose as evidence by polyuria, polydipsia, polyphagia, and
hyperglycemia.
Desired Outcome: Patient will state that they have a decrease in thirst, a decrease in urine

output, and a decrease in hunger within 12 hours of treatment initiation. This will be achieved

by lower blood glucose levels from 350 mg/dL to 200 mg/dL.

Nursing Interventions Client Response to Intervention

1. Check CBG 4 times per 12-hour shift (before 1. CBG will be 200 mg/dL or below. It

each meal and at HS). will not fall below 100 mg/dL.

2. Initiate continuous infusion of insulin per 2. CBG will be 200 mg/dL or below. It

doctor order and facility policy. Discontinue all will not fall below 100 mg/dL. These

previous orders for insulin and hyperglycemia levels will be confirmed every hour while

agents. patient is on an insulin drip.

Start infusion rate: Use HUMULIN R at

concentration of one (1) unit per 1 ml (100 units /

DKA VS. HHNKS; ARCHIBALD 11

100 ml NS)

Greater than 110 but less than 140 = 0.5 units/hour

Greater than 141 but equal or less than 200 = 1

units/hour

Greater than 201 but equal or less than 300 =2

units/hour

Greater than 301 but equal or less than 400 = 3

units/hour

Greater than 401 but equal or less than 500 = 4

units/hour

Greater than 500 = 5 units per hour + 10 units

Humulin R bolus

3. Administer a diet that is low in simple 3. Patient will avoid simple

carbohydrate, and high in fiber, protein, lean carbohydrates, to stabilize CBG with

meats, whole grains, and fresh vegetables three proper diet.

times per 12-hour shift.

Evaluation: Patients CBG will remain below 200 mg/dL and above 100 mg/dL for entirety of

12-hour shift. These levels will be confirmed every hour while patient is on an insulin drip.

Patient Information: Early Onset Diabetic Ketoacidosis

Problem #3 Acute Pain related to metabolic decompensation as evidence by

abdominal pain, nausea, and vomiting rated at 8/10 pain.
DKA VS. HHNKS; ARCHIBALD 12

Desired Outcome: Patient will display a decrease in gastrointestinal upset from 8/10 to 6/10

within 2-hours of initiated interventions.

Nursing Interventions Client Response to Intervention

1. Administer pain medications as ordered by 1. Patient will state a decrease in pain

doctor. Example: 2.5 mg Morphine IV over two from 8/10 to 7/10. Pain will not resolve

minutes. until metabolic acidosis is corrected, but

Morphine will assist until that occurs.

2. Administer anti-nausea medications as ordered 2. Patient will state a decrease in nausea,

by doctor. Example: 0.15 mg/kg Ondansetron IV and will discontinue vomiting. GI

over 2 minutes. disturbances will not resolve until

metabolic acidosis is corrected, but

Ondansetron will assist until that occurs.

3. Provide a warm blanket and soft music to 3. Patient will relax enough to get some

comfort and distract patient. sleep.

Evaluation: Patient will have a decrease in pain with Morphine from 8-10 to 7-10. With anti-

nauseas and distraction methods (blanket/music), pain level will decrease from 7/10-6/10.

Patient Information: Hyperglycemic Hyperosmolar Non-ketonic Syndrome

Problem #1 Fluid volume deficit related to osmotic diuresis as evidence by polyuria,

polydipsia, flushed/dry skin, sunken eyes, and prolonged skin turgor.

DKA VS. HHNKS; ARCHIBALD 13

Desired Outcome: Patient will display signs of improved hydration within 12 hours of

treatment. This will be evident with decrease in PU/PD, the improvement of skin hydration,

and change in eye presentation (not sunken in).

Nursing Interventions Client Response to Intervention

1. Administer a continuous infusion intravenous 1. Fluid therapy will decrease serum

0.9% NS @ 200 ML/HR for 12 hours. osmolarity by 20 mOsm/kg.

2. Measure intake and output by recording 2. Output will not drop below 30

milliliters of all fluids administered IV and orally, ML/HR. Urine will be a light-yellow

and milliliters of all voided urine in each 12-hour color. Patient will consume of their

shift. body weight in ounces of water per day.

(Example: 100 # = 50 ounces of water).

3. Offer sugar free jello and ice chips every hour. 3. Patient will take hydration tactics well,

and display compliance with

interventions.

Evaluation: Patients hydration status will improve with the listed interventions, and be evident

by decreased thirst, moist skin, and bright alert eyes.

Patient Information: Hyperglycemic Hyperosmolar Non-ketonic Syndrome

Problem #2 Unstable blood glucose level related to cells inability to absorb glucose as
evidence by CBG reading of over 600 mg/dL.

Desired Outcome: Patients blood glucose will decrease over 12-hour shift from 600

mg/dL to between 100-200 mg/dL.

DKA VS. HHNKS; ARCHIBALD 14

Nursing Interventions Client Response to Intervention

1. Check CBG every hour. 1. CBG will be 200 mg/dL or below. It

will not fall below 100 mg/dL.

2. Initiate continuous infusion of insulin per doctor 2. CBG will be 200 mg/dL or below. It

order and facility policy. Discontinue all previous will not fall below 100 mg/dL. These

orders for insulin and hyperglycemia agents. levels will be confirmed every hour when

insulin drip is utilized.

Start infusion rate: Use HUMULIN R at

concentration of one (1) unit per 1 ml (100 units /

100 ml NS)

Greater than 110 but less than 140 = 0.5 units/hour

Greater than 141 but equal or less than 200 = 1

units/hour

Greater than 201 but equal or less than 300 =2

units/hour

Greater than 301 but equal or less than 400 = 3

units/hour

Greater than 401 but equal or less than 500 = 4

units/hour

Greater than 500 = 5 units per hour + 10 units

Humulin R bolus

3. Assess for signs of hypoglycemia: anxiety, 3. Patient will be relaxed, be free of

tremors, and slurring of speech every hour. tremors, and speak without slurring.
DKA VS. HHNKS; ARCHIBALD 15

Evaluation: CBG levels will normalize, and remain between 100-200 mg/dL within the 12-

hour shift.

Patient Information: Hyperglycemic Hyperosmolar Non-ketonic Syndrome

Problem #3 Ineffective health management (learning need) related to patient not

understanding type 2 diabetes, as evidence by patients lack of managing disease adequately,
stating confusion, and early signs of HHNKS.

Desired Outcome: Patients will understand type 2 diabetes and understand how to

manage the disease by the end of the 12-hour shift. He will state

Nursing Interventions Client Response to Intervention

1. Teach patient in his/her own language 1. Patient will state that Type 2 Diabetes is a

about Type 2 Diabetes and HHNKS once disease that results in the body not having

upon admission, and then as needed for enough insulin, or not being able to utilize

complete understanding. insulin, and that therefore, the patient must

administer synthetic insulin every day and

monitor CBG levels daily. Patient states

understanding that HHNKS is a complication of

mismanaged DM2.

2. Ensure that patient knows how to 2. Patient will accurately demonstrate how to

measure CBG and that levels will be obtain a CBG at the right time each day. The

between 100-200 mg/DL, one time, upon patient will state why obtaining a regular CBG is

admission, and then as needed for accurate mandatory for this disease, and at what levels the

disease management. CBG should remain.

DKA VS. HHNKS; ARCHIBALD 16

3. Ensure that the patient can properly 3. Patient will accurately demonstrate how to

administer insulin, once, upon admission, administer SQ insulin into abdominal fat.

then as needed for accurate disease Patient will demonstrate that he/she can do this

management. at the right time and in the right amount each

day.

Evaluation: Patient education will be successful, because patient will effectively teach back

what Type 2 Diabetes is, and how to manage it through frequent CBG checks, and insulin

administration.