HYPERGLYCEMI

C EMERGENCIES
TAUFAN ARIF, S.KEP., NS., M.KEP
 Hyperglycemic Emergencies
• Diabetes ketoacidosis (DKA) and hyperglycemic hyperosmolar
(HHS) are two extremes in the spectrum of decompensated
diabetes.
• The incidence of DKA is defined as acute hyperglycemia with
acidosis, and HHS is classified as acute hyperglycemia without
acidosis (nonketotic).
• Diabetes is a metabolic disease that results in inadequate uptake
of glucose by cells, resulting in hyperglycemia.
 The Criteria of DKA
1.Blood glucose greater than 250 mg/dL
2.pH less than 7.3
3.Serum bicarbonate less than 18 mEq/L
4.Moderate or severe ketonemia or ketonuria
 The Criteria of HHS
1. Blood glucose greater than 600 mg/dL
2. Arterial pH greater than 7.3
3. Serum bicarbonate greater than 18 mEq/L
4. Serum osmolality greater than 320 mOsm/kg H2O (320 mmol/kg)
5. Absent or mild ketonuria
 Etiology of Diabetic Ketoacidosis
1. Underlying or concomitant infection (40%)
2. Missed insulin treatments (25%),
3. Newly diagnosed, previously unknown diabetes (15%).
4. Other associated causes make up roughly 20% in the various series.
5. Among the other causes are myocardial infarction, stroke, trauma, and
pancreatitis.
Although DKA is primarily a complication of type 1 diabetes, it can
occur (rarely) in some forms of type 2 diabetes under conditions of
extreme stress, including “ketone-prone” type 2 diabetes a disorder found in
African American males (Table 16-5)
 Pathophysiology
Insulin is normally released from the pancreas by beta islet cells (Islets of
Langerhans) in response to an increase in blood glucose. Insulin is necessary
for cellular uptake of glucose by most cells in the body (except brain and
liver cells). Without insulin, the glucose fails to enter cells and
accumulates in the blood, resulting in hyperglycemia and a vascular
inflammatory state. Cells deprived of glucose begin to starve, triggering a
mobilization of stored glucose via the breakdown of protein and fat
(gluconeogesis) and release of stored glucose from the liver
(glycogenolysis).
This triggers a complex series of physiologic processes that account for the
major signs and symptoms associated with DKA and HHS.
 Pathway
increased fatty acid
metabolism & increased liver
insufficient or absent level of increased secretion of
gluconeogenesis (formation of
circulating insulin. counterregulatory hormones
glucose from amino acids and
proteins)

These hormones counteract The pathophysiology of DKA

including glucagon and the
the glucose-lowering effects can be organized into two
stress hormones
of insulin and are released in main components: fluid
(catecholamines, cortisol, and
response to stress and other volume deficit and acidbase
growth hormone).
stimuli. imbalance (Figure 16-2).
 Pathophysiology: Insulin Deficiency

Without insulin, glucose remains in the bloodstream, and cells are deprived
of their energy source. A complex pathophysiologic chain of events follows
(Fig. 33-2).
The release of glucagon from the liver is stimulated when insulin is
ineffective in providing the cells with glucose for energy. Glucagon
increases the amount of glucose in the bloodstream by breaking down stored
glucose (glycogenolysis). Noncarbohydrates (fat and protein) are converted
into glucose (gluconeogenesis).
 Pathophysiology: Hyperglichemia

• Hyperglycemia increases the plasma osmolality, and the blood becomes

hyperosmolar.
• Cellular dehydration occurs as the hyperosmolar extracellular fluid
draws the more dilute intracellular and interstitial fluid into the vascular
space in an attempt to return the plasma osmolality to normal.
• Dehydration stimulates catecholamine production in an effort to provide
emergency support. Catecholamine output stimulates further
glycogenolysis, lipolysis, and gluconeogenesis, pouring glucose into
the bloodstream.
 Fluid Volume Deficit With Associated Electrolyte Imbalance
• Polyuria (excessive urination) and glycosuria (sugar in the urine) occur as a result of
the osmotic particle load that occurs with DKA.
• The hyperglycemia causes an osmotic diuresis and hypotonic losses leading to fluid
volume deficits (intracellular and extracellular) and electrolyte losses. This
further increases serum blood glucose, increases urine glucose, and worsens the
osmotic diuresis and ketonemia.
• Urinary losses of water, sodium, magnesium, calcium, and phosphorus cause an
increase in serum osmolality and decreased electrolyte levels.
• Potassium levels may be increased or decreased, depending on the amount of nausea
and vomiting, acid-base balance, and fluid status of the patient.
• This hyperosmolality causes additional fluid shifts from the intracellular to the
extracellular space, increasing dehydration.
 Acid-base Imbalance
Cells without glucose starve and begin to use existing stores of fat and protein to provide
energy for body processes (gluconeogenesis).
Fats are broken down faster than they can be metabolized in the liver, which results in an
accumulation of ketone acids.
These ketone acids are usually cleared in peripheral tissues. If the ketogenic pathway is
overwhelmed ketone acids accumulate in the blood stream where hydrogen ions (H+)
dissociate, causing a profound metabolic acidosis.
Acetone is formed during this process and is responsible for the “fruity breath” found in
these patients.
 Acid-base Imbalance
Metabolic acidosis may be worsened with severe fluid volume deficits because
hypovolemia results in tissue hypoperfusion and production of lactic acids from
anaerobic metabolism.
Excess lactic acid results in what is called increased anion gap (increased body acids).
Sodium, potassium, chloride, and bicarbonate are responsible for maintaining a normal
anion gap in the body which is normally less than 12 to 14 mEq/L (Table 16-6).
The anion gap represents the difference between the cations (Na+, K+) and anions (Cl−,
HCO3−). Ketone accumulation, a by-product of gluconeogenesis, causes an increase in
the anion gap more than 14 mEq/L.
 Acid-base Imbalance
• The normal physiologic response to metabolic acidosis is to produce
bicarbonate to buffer the ketones and H+ ions. The patient with DKA
often has diminished bicarbonate levels because of the osmotic diuresis.
• Breathing becomes deep and rapid to release carbonic acid in the form of
carbon dioxide to restore normal blood pH. This explains the deep rapid
breathing, called “Kussmaul respirations,” often seen in these patients.
• Acetone is exhaled, giving the breath its characteristic fruity odor.
 Gluconeogenesis
• Gluconeogenesis is the process of breaking down fat or protein to make
new glucose.
• Fat is metabolized to ketones. Protein used for gluconeogenesis leaves
no reserve protein available for synthesis and repair of vital body tissues.
• Nitrogen accumulates as protein is metabolized to urea. Urea, added to
the bloodstream, increases the osmotic diuresis and accentuates the
dehydration.
 Hyperosmolar Hyperglychemic States
The pathogenesis of HHS is similar to the pathogenesis of DKA with the following
differences. HHS is classified as hyperglycemia with profound dehydration in the
absence of ketosis. The onset of hyperglycemia in HHS is progressive. Many of these
patients have a history of type 2 DM with some circulating insulin levels.
The extremely severe hyperglycemia in HHS results in profound extracellular fluid
volume contraction, marked intracellular dehydration, and excessive loss of
electrolytes.
Mortality rates are higher with HHS, because of the severe volume loss and because it
occurs more frequently in a chronically ill patients.
Death results from CNS depression of vital body functions (cardiac and respiratory
centers in the brain are depressed), cerebral edema, cardiovascular collapse, renal
shutdown, and vascular embolism.
 Clinical Presentation
DKA HHS
History
Younger with history of type 1 DM or previously Elderly with history of type 2 DM, and preexisting
undiagnosed; pre-existing infection common chronic illness which are associated with decreased renal
glucose excretion, concurrent illness frequently
precipitates viral infections or pneumonia
Signs and Symptoms
Nonspecific: Polyuria, polydipsia, weakness, abdominal Nonspecific: Polyuria, polydipsia, weakness confusion,
cramping, stupor, coma coma
Specific: Nausea, vomiting, anorexia, Kussmaul Specific: : None
respiration, fruity breath
 Clinical Presentation
DKA HHS
Diagnostic Tests
Serum glucose 250 to 800 mg/dL (usually < 500) Serum glucose At least 600 mg/dL oen > 1000 mg/dL
Serum osmolality < 330 mOsm/kg/H2O Serum osmolality > 350 mOsm/ kg/H2O
Ketoacidosis Ketoacidosis
↓ pH Not a feature
Mild: < pH 7.20-7.30 pH > 7.30
Moderate: pH 7.10-7.19 HCO3 > 15 mEq/L
Severe: pH < 7.09 Serum ketones below 2+
HCO3 < 15 mEq/L
Serum ketones > 2+
 Clinical Presentation
DKA HHS
Diagnostic Tests
Serum glucose 250 to 800 mg/dL (usually < 500) Serum glucose At least 600 mg/dL oen > 1000 mg/dL
Serum osmolality < 330 mOsm/kg/H2O Serum osmolality > 350 mOsm/ kg/H2O

Ketoacidosis Ketoacidosis
↓ pH Not a feature
Mild: < pH 7.20-7.30 pH > 7.30
Moderate: pH 7.10-7.19
Severe: pH < 7.09
HCO3 < 15 mEq/L HCO3 > 15 mEq/L

Serum ketones > 2+ Serum ketones below 2+

Positive urine ketones Minimal urine ketones
Positive anion gap > 12 Variable anion gap
Dehydration Dehydration
 Clinical Presentation
DKA HHS
Diagnostic Tests
Volume depletion (decrease intracellular and extracellular) Severe volume depletion (intracellular and extracellular)
Renal function Renal function
Increased BUN: creatinine ratio Marked increase in BUN: creatinine ratio
Urine ketones +2 ↓ GFR
Electrolyte depletion Electrolyte depletion
Potassium, magnesium, phosphate, calcium Potassium, magnesium, phosphate,
sodium
 Hidration Assessment
1. Hourly intake
2. Blood pressure changes
3. Orthostatic hypotension
4. Pulse pressure
5. Pulse rate, character, rhythm
6. Neck vein filling
7. Skin turgor
8. Skin moisture
9. Body weight
10.Central venous pressure
11.Pulmonary arterial occlusion pressure
12.Hourly output
13.Complaints of thirst
 Nursing Diagnosis
1. Decreased Cardiac Output related to alterations in preload, p. 1128
2. Deficient Fluid Volume related to absolute loss, p. 1132
3. Anxiety related to threat to biologic, psychologic, and social integrity,
4. Disturbed Body Image related to functional dependence on life-sustaining technology,
p. 1136
5. Ineffective Coping related to situational crisis and personal vulnerability,
6. Powerlessness related to lack of control over current situation or disease progression,
p. 1152
7. Deficient Knowledge related to lack of previous exposure to information
8. etc
 Priciples of Management for
Hyperglycemic Emergencies
The management of the patient in acute DKA and HHS revolves around six
primary areas:
1. Fluid replacement
2. Treatment of hyperglycemia
3. Electrolyte replacement
4. Treatment of any underlying disorders
5. Prevention and management of complications
6. Patient/family teaching.
 Fluid Replacement
Treatment of intracellular and extracellular fluid volume deficits is a priority for both DKA and HHS to
restore intravascular volume and prevent cardiovascular collapse.
Initial volume replacement is based on assessment of vascular status.
1. Administer normal saline (0.9%).
The choice of IV fluid depends on the initial blood pressure readings and the serum sodium level.
The presence of hyperglycemia and dehydration masks the true serum sodium level, requiring a correction
of serum sodium levels prior to IV fluid selection.
IV fluids are generally infused at rapid rates (1000 to 2000 mL in the first hour, 1000 mL in the
second hour, and then at 500 mL/h) until fluid volume is restored or initially around 15 to 20
mL/kg/h.  20-40 cc/kgBB/jam (1-2 hours firstly)
2. Titrate the rate of infusion based on urine output, mean arterial blood pressure, and central venous
pressure measurements.
3. Change IV fluid to 5% dextrose with 0.45 NaCl at 150 to 200 mL/h when serum glucose reaches
250 mg/dL. Maintain insulin therapy.
 Treating Hyperglycemic
1. Regular insulin 0.15 U/kg as IV bolus.
2. Initiate low-dose IV insulin at a rate of 0.1 U/kg/h. If serum glucose does not fall by
50 to 70 mg/dL in the first hour, double insulin infusion on an hourly basis until glucose
falls by 50 to 70 mg/dL.
3. Monitor serum glucose levels closely and titrate insulin infusion accordingly. Once
the serum glucose reaches 250 mg/dL, the insulin infusion should be decreased to a rate
of 2 to 4 U/h and the IV fluids changed to half normal saline with glucose (D5-1⁄2NS).
This ensures that hypoglycemia does not occur during ongoing treatment of the acute
condition. It is essential that insulin infusion continues in the patient with DKA until the
serum pH is corrected to avoid intracellular hypokalemia. Additional glucose may be
needed to achieve this outcome. Glucose-containing solution should also be started in
the patient with HHS when serum glucose reaches 250 to 300 mg/dL to protect
against cerebral edema.
 Electrolyte Replacement
Electrolyte deficits are usually present in both DKA and HHS due to the osmotic diuresis. Hypokalemia
may be masked by acidosis. Potassium levels rise 0.6 mEq/L for every 0.1 drop in pH.
1. Administer potassium supplements according to serum levels:
 If serum K+ is < 3.3 mEq/L, hold insulin and administer 40 mEq K+/h (2/3 KCl and 1/3 KPO4−)
until K+ is > 3.3 mEq/L.
 If serum K+ is > 5.0, hold K+ and check K+ every 2 hours.
 If serum K+ is > 3.3 mEq/L or < 5.0 mEq/L give 20 to 30 mEq K+ in each liter of volume
replacement.
The rate of potassium chloride infusion should be adjusted according to frequently monitored serum
potassium levels and the urine output.
 Electrolyte Replacement
Monitor magnesium, calcium, and phosphate levels every 2 hours during rehydration.
Total body phosphorous levels are depleted due to osmotic diuresis. This may result in
impaired cardiac and respiratory functions. Phosphate deficiencies are usually corrected
with volume replacement. If needed, the administration of potassium phosphate 20
mEq/L is the best method of phosphate replacement as it replaces both potassium and
phosphate simultaneously. Phosphate replacements should not be administered in patients
with renal failure.
 Electrolyte Replacement
3. Assess need for bicarbonate therapy:
 If pH is < 6.9, dilute NaHCO3 (100 mmol) in 400 mL H2O. Infuse at 200
mL/h.
 If pH is 6.9 to 7.0, dilute NaHCO3 (50 mmol) in 200 mL H2O. Infuse at 200
mL/h.
 If pH is > 7.0, hold NaHCO3
Repeat HCO3 administration every 2 hours until pH is > 7.0. Monitor serum K+ closely.
 Treating Underlying Disorders
1.Investigate precipitating factors utilizing the following tests:
urinalysis, complete blood count, ECG, chest x-ray, and
appropriate cultures.
2.Administer antibiotics as appropriate if infection is suspected.
3.Obtain history from patient and family about the possibility of
missed insulin doses.
 Preventing & Managing Complications
1. Monitor serum glucose, electrolytes (sodium and potassium), and arterial blood gases
every 1 to 2 hours until normal levels are attained.
2. Measure serum phosphate and magnesium initially and repeat as necessary.
3. Monitor temperature, blood pressure, pulse, respiratory rate, pulse oximetry, urinary
output, and central venous pressure at frequent intervals.
4. Evaluate neurologic status at frequent intervals. Institute seizure precautions if
cerebral edema is suspected. Institute measures to avoid aspiration in patients with
altered mental status. Administer dexamethasone and mannitol if appropriate.
5. Titrate fluid replacement carefully to prevent heart failure. Auscultate lung sounds
frequently during fluid replacement.
6. Administer anticoagulants as ordered. Hyperosmolar patients are at great risk for
developing thrombosis.
 Surveillance for Complications
The patient in DKA can experience a variety of complications, including fluid
volume overload, hypoglycemia, hypokalemia or hyperkalemia, hyponatremia,
cerebral edema, and infection.
1. Fluid Volume Overload. Neck vein engorgement, dyspnea without exertion,
and pulmonary crackles on auscultation signal circulatory overload. Reduction
in the rate and volume of infusion, elevation of the head of the bed, and
provision of oxygen may be required to manage the increased intravascular
volume. Hourly urine measurement is mandatory to assess kidney function
and adequacy of fluid replacement.
2. Hypoglycemia. Hypoglycemia is defined as a serum glucose level lower than
70 mg/dL.24 Most acute care hospitals have specific procedures for
management of the hypoglycemic patient (Box 33-7). the frequency of glucose
testing has lengthened to 2- to 4-hour intervals. A comparison between the
physical symptoms expected with hypoglycemia and those of hyperglycemia is
provided in Box 33-8.
 Surveillance for Complications
3. Hypokalemia and Hyperkalemia. Hypokalemia can occur within the first hours of rehydration and
insulin treatment. Continuous cardiac monitoring is required, because low serum potassium
(hypokalemia) can cause ventricular dysrhythmias. Hyperkalemia occurs with acidosis or with
overaggressive administration of potassium replacement in patients with renal insufficiency. Severe
hyperkalemia is demonstrated on the cardiac monitor by a large, peaked T wave; flattened P wave;
Ventricular fibrillation can follow.
4. Hyponatremia. Sodium elimination from the body results from the osmotic diuresis and is compounded
by the vomiting and diarrhea that can occur during DKA. Clinical manifestations of hyponatremia
include abdominal cramping, postural hypotension, and unexpected behavioral changes. Sodium
chloride is infused as the initial IV solution. Maintenance of the saline infusion depends on clinical
manifestations of sodium imbalance and serum laboratory values.
5. Risk for Cerebral Edema. Alterations in level of consciousness, pupil reaction, and motor function may
be the result of fluctuating glucose levels and cerebral fluid shifts. Confusion and headache are signs
that may signal cerebral edema.
6. Risk for Infection. Dehydration, hypovolemia, and hypophosphatemia interfere with oxygen delivery at
the cell site and contribute to inadequate perfusion and tissue breakdown. Repositioned every 1 to 2
hours. Oral Care may be needed
 Patient & family Education
SKILLS FOR DIABETIC MANAGEMENT
1. Blood glucose monitoring
2. Insulin administration
3. Diet therapy
4. Meal planning
5. Exercise therapy
6. Urine ketone testing
7. Sick day management
8. Recognition of signs and symptoms of hypoglycemia and hyperglycemia
9. Proper treatments for hypoglycemia and hyperglycemia

Expected Outcomes
10. The patient or caregiver will be able to verbalize essential aspects of diet therapy, meal planning, exercise therapy,
sick day management, signs and symptoms of hypoglycemia and hyperglycemia, and proper treatments for
hypoglycemia and hyperglycemia.
11. The patient or caregiver will be able to demonstrate blood glucose monitoring, insulin administration, and urine
ketone testing.
MATUR SUWUN