Diabetic Ketoacidosis/ Hypergylcemic NonKetoacidosis

Deneise Walters
MScN CEN RM RN

The Pancreas

The pancreas
The pancreas is a glandular organ in the upper abdomen,
but really it serves as two glands in one: a digestive
exocrine gland and a hormone-producing endocrine
gland.
Functioning as an exocrine gland, the pancreas excretes
enzymes to break down the proteins, lipids,
carbohydrates, and nucleic acids in food.
Functioning as an endocrine gland, the pancreas secretes
the hormones insulin and glucagon to control blood sugar
levels throughout the day. Both of these diverse functions
are vital to the bodys survival.

Blood Glucose Homeostasis

The endocrine portion of the pancreas controls the

homeostasis of glucose in the bloodstream.
Blood glucose levels must be maintained within certain limits
so that there is a constant supply of glucose to feed the
cells of the body but not so much that glucose can
damage the kidneys and other organs.
The pancreas produces 2 antagonistic hormones to control
blood sugar: glucagon and insulin.

Maintaining homeostatic balance

The alpha cells of the pancreas produce glucagon.
Glucagon raises blood glucose levels by stimulating the liver
to metabolize glycogen into glucose molecules and to
release glucose into the blood. Glucagon also stimulates
adipose tissue to metabolize triglycerides into glucose and
to release glucose into the blood.
Insulin is produced by the beta cells of the pancreas. This
hormone lowers blood glucose levels after a meal by
stimulating the absorption of glucose by liver, muscle, and
adipose tissues. Insulin triggers the formation of glycogen in
the muscles and liver and triglycerides in adipose to store
the absorbed glucose.

Hormones
Maintain homeostatic balance utilizing a feedback mechanism
that involves other hormones, blood or chemicals, and the
nervous system.

Feedback loop mechanism.

Sensors in the endocrine system detect changes in the

hormonal levels.
Hormones are adjusted to maintain normal body levels
.

Regulation of Pancreatic Function

Nerves of the sympathetic division become active during

stressful situations, emergencies, and exercise.
Sympathetic neurons stimulate the alpha cells of the
pancreas to release the hormone glucagon into the
bloodstream.
Glucagon stimulates the liver to begin the breakdown of
the energy storage molecule glycogen into smaller
glucose molecules.

Regulation of Pancreatic Function

Glucose is then released into the bloodstream for the

organs, especially the heart and skeletal muscles, to use
as energy. The sympathetic nerves also inhibit the
function of beta cells and acini to reduce or prevent the
secretion of insulin and pancreatic juice. The inhibition of
these functions provides more energy for other parts of
the body that are active in dealing with the stressful
situation.

Diabetes Mellitus
Type I: autoimmune disease beta cells of the
islets of Langerhans are destroyed by
antibodies
Type II: The cells become insulin-resistant
glucose does not enter the cells as readily

Diabetic Ketoacidosis

Results from lack of insulin

Occurs in people with type 1 diabetes.
Can also occur in type 2 DM in severe stress.
Accounts for approximately 5% mortality
Medical emergency that needs urgent
hospitalization

Role of Insulin
Required for transport of glucose into:
Muscle
Adipose
Liver

Inhibits lipolysis
Absence of insulin

Glucose accumulates in the blood

Liver
Uses amino acids for gluconeogenesis
Converts fatty acids into ketone bodies
Acetone, Acetoacetate, -hydroxybutyrate

COUNTER-REGULATORY HORMONE
EFFECTS

Gluconeogenesis

Breakdown of proteins and conversion of amino

acids into glucose
Glycogenolysis

Breakdown of liver glycogen into glucose

Lipolysis

Breakdown of adipose tissue into fatty acids

What is pathophysiology of
ketoacidosis?
The patient can not utilize glucose from food due to
insufficient insulin.
Energy is provided by fat breakdown (lipolysis)
Some of the free fatty acids released by lipolysis are
converted into ketones by the liver causing a profound
metabolic acidosis.
This patient compensates for this acidosis by
hyperventilation (Kussmaul respiration)

Pathophysiology
Because of acidosis, K ions enter the circulation leading to
hyperkalemia, this is aggravated by dehydration and renal
failure.
So, depending on the duration of DKA, serum K at diagnosis
may be high, normal or low, but the intracellular K stores are
always depleted.
Phosphate depletion will also take place due to metabolic
acidosis.
Na loss occurs secondary to the hyperosmotic state & the
osmotic diuresis.

PATHOPHYSIOLOGY OF DKA

Hyperglycemia
results from:

Blockage of
intracellular glucose
transport
Counter-regulatory
hormone effects

CRH
Excess

Insulin
Deficiency

Hyperglycemia

CLINICAL PRESENTATION
Early Symptoms

Due to hyperglycemia

Polyuria
Polydipsia
Polyphagia
Visual disturbances

Due to muscle breakdown and dehydration

Weight loss
Weakness

CLINICAL PRESENTATION
Later Symptoms
Due to ketonemia
Anorexia
Nausea
Vomiting
Fruity acetone breath
Due to acidosis
Abdominal pain
Kussmaul respirations (deep, regular, sighing)

CLINICAL PRESENTATION
Later Symptoms

Due to hypokalemia

Gastric stasis and ileus

Muscle cramps
Cardiac dysrhythmias

Signs and Symptoms of DKA

Polyuria, polydipsia
Enuresis
Dehydration
Tachycardia
Orthostasis
Abdominal pain
Nausea
Vomiting

Fruity breath
Acetone

Kussmaul breathing
Mental status changes
Combative
Drunk
Coma

DKA - Symptoms
Symptoms develop over several hours

Thirst, Polyuria

Osmotic Diuresis

Fatigue

Dehydration, protein loss

Weight loss

Protein loss, catabolism,

dehydration

Nausea, vomiting

?Ketosis, gastric stasis

Abdominal pain

?ileus, gastric stasis, K deficit

Muscle cramps

?K deficiency

DKA - Signs
Dehydration

Osmotic Diuresis, vomiting

Tachycardia

Dehydration

Hypotension

Dehydration, acidosis

Warm skin

Acidosis (peripheral
vasodilatation)

Hyperventilation

Ketosis, acidosis

Coma, drowsiness Hyperosmolality

Causes of DKA

A. Absolute Insulin Deficiency:

Omission or reduction of insulin
Undiagnosed diabetes

Causes of DKA
B. Relative Insulin Deficiency:
Acute illness:

Infection
Myocardial infarction
Stroke
Trauma
Severe emotional disturbance

Endocrine Disorders

Steroid therapy
Adrenergic agonists
Phaeochromocytoma
Thyroid storm

The Principal Features of DKA

Hyperglycemia
Dehydration
Electrolyte Loss
Ketoacidosis

DKA - Diagnosis
Diagnostic Labs
Determine blood glucose level and test for
ketones
Send blood to laboratory for estimation of
serum electrolytes ,glucose, BUN urea
creatinin, Hb, and WBC,ABG
Send for culture of blood, urine and lung
secretions
ECG

How do I diagnose DKA?

Diagnosis requires all 3 of the following:

High blood sugar (i.e diabetes) Glucose > 11 mmol

*Finger-prick blood glucose can be normal*

Ketones (blood or urine +++)

Acidosis (pH<7.30 or HCO3<15mmol)

Blood Ketone Testing

Indications
Asymptomatic patients with glucose > 16.70 mM
Symptomatic patients with possible DKA
Monitoring in established DKA
To assist in making decision on admission
To assist in making decisions for intensive medical
therapy

Slide
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Principles of DKA management (1)

1.
2.
3.
4.
5.
6.
7.

Correction of shock
Correction of dehydration
Correction of hyperglycaemia
Correction of deficits in electrolytes
Correction of acidosis
Treatment of infection
Treatment of complications

Treatment of Ketoacidosis
Initiation of treatment must be
immediate
Treatment includes

Rehydration
Insulin administration
Electrolyte correction
Stabilization of cardiovascular and
and renal function

DKA MANAGEMENT
Flow Sheet
Hourly Observations
Electrolytes
Glucose
Osmolality
Blood gases
Output
Vital signs
Mental status

What is the nursing management of DKA?

Nursing diagnosis
1-Inadequate airway protection related to decreased level of
consciousness
Intervention:
Maintain patent and protected airway
Mechanical ventilation for deeply comatose
Naso-gastric tube to decrease the risk of aspiration
Respiratory rate and pattern monitoring
Blood gases and oxygen therapy accordingly

What is the nursing diagnosis of DKA? cont

Hypovolemia related to dehydration
Hyperglycemia
Electrolyte depletion related to polyuria
Metabolic acidosis related to ketosis
Potential deep vein thrombosis

DKA MANAGEMENT
INTRAVENOUS FLUID ADMINISTRATION
Normalizes pH
Normal saline, 1 L over 30 min
Then, Normal saline, 1 L over 1-2 h

Treatment of ketoacidosis
Fluids
Most urgent and first line treatment
lowers blood glucose by as much as 18%
Rehydration alone will cause fall in glucose
Increase urine flow
Allow perfusion
Saline given rapidly
1 L in 30min, then hourly for 3 hrs
Then, 0.5 NS @ 300-500 mL/h, guided by urine
output

Treatment of ketoacidosis
Insulin
Aim to switch off gluconeogenesis, lipolysis,
ketogenesis
Insulin regimens
Intravenous infusion
Adults: 6 U/hr
Children 0.1 U/kg/hr

Once glucose fallen to below 15 mmol/L, replace

saline with 10%Dextrose with 20-40 mmol K, reduce
insulin to 3 U/hr

Treatment of ketoacidosis
Potassium
Hypokalemia most common cause of death
Potassium will fall during therapy:
Move into cells resulting from insulin, correction
of acidosis, and restoration of volume
Haemodilution
Urinary loss
Begin with insulin treatment: 20 mmol/h

Treatment of ketoacidosis

Acid-base
Give 100 mmoL with KCl 200 mmol when pH <
7, repeat until pH 7
Symptomatic relief: 50 mmoL with KCl 10 mmol

DKA MANAGEMENT
Electrolytes
Potassium
Level will fall precipitously with treatment
Hold only if peaked T-waves on ECG
20-40 mEq in the first liter of fluid
as chloride
as phosphate
Monitor hourly

DKA: Laboratory Findings

Elevated blood glucose (usually <1,000)
Low bicarbonate level
Anion gap metabolic acidosis
Unmeasured ketoacids
Urine dipsticks - Helpful in determining if there is
ketoacids in urine but not sererity of DKA or response
to treatment

40

DKA: Laboratory Findings

Sodium: low
Osmotic flux of water into extracellular space reduces
serum sodium concentration
Actual sodium: 1.6mEq/L per 100mg/dL rise in glucose over
100
Hypertriglyceridemia low sodium pseudohyponatremia
Phosphate
Depleted in the setting of DKA
Serum level may not accurately represent total body stores
41

DKA: Laboratory Findings

Potassium:
Level varies depending on urinary loss and severity of
acidosis
Potassium moves extracellularly in exchange for
hydrogen ions typical hyperkalemia on presentaion
Total body stores are depleted due to urinary loss

Treatment of ketoacidosis
Clinical measures
Gastric stasis: NG suction in drowsy pts
Infection:
Usual signs lacking
Hyperglycaemia increases risk of sepsis
Use broad spectrum antibiotics after cultures

Risk of thrombosis
Prophylactic SC Heparin 5000 units q6-8hrly in the
unconscious, elderly, hyperosmolar

Hypotension: use plasma expanders

Clinical monitoring

Complications of treatment
ARDS
Sudden dyspnoea, hypoxaemia, diffuse pulmonary
infiltrates
Younger pts, fatal
Mechanisms:
Use of crystalloids
Alveolar defect caused by acidosis and hyperventilation

Cerebral oedema
High mortality
Use of hypotonic replacement fluids

Abdominal pain
Can mimic acute abdomen

DKA DISPOSITION
ICU
Age < 2 years or > 60 years
pH < 7.0
Serious concurrent illness
(Blood sugar > 1000)

Outpatient Management
Alert
No persistent vomiting
Mild acidosis, ketonemia & dehydration

DKA SUMMARY

Laboratory evaluation of the DKA patient is

complex and must be repeated on an
hourly basis until the patient is stable
The most important components of the
management of the DKA patient are fluid
and electrolyte management.
Insulin is an essential but secondary
component of management.
.

Hyperosmolar Non-ketotic
Hyperglycaemia
Accounts for 5-10% of
hyperglycemic comas
Mortality 30-50%, usually
from arterial or venous
thrombosis
Occurs mainly in elderly
persons with type 2 diabetes
When compared with DKA, it
has:
Higher mortality
Higher hyperglycemia

Pathophysiology
Insulin levels are sufficient to suppress
lipolysis and ketogenesis
Insulin levels are inadequate to promote
normal anabolic function & inhibit
gluconeogeneis & glycogenolysis
Cell deprivation triggers counter-regulatory
surge, increasing glucose via enhanced
hepatic glucose generation & insulin
resistance
48

Pathophysiology
Hyperglycemia heightened
inflammatory state exacerbating
glucose dysregulation
Osmotic diuresis dehydration
decreased GFR further glucose
elevation
49

Pathophysiology
Dehydration is a major component
15-20% volume depleted
5-10% in DKA
Greater electrolyte loss due to massive osmotic diuresis

50

Clinical Presentation
Similar to DKA
Polyuria
Polydipsia
Weight loss
Neurologic impairment
Different from DKA
Kussmaul breathing
Acetone breath
Abdominal discomfort, nausea & vomiting are less severe
51

Laboratory Findings
Glucose: >600 mg/dL
HCO3>15
pH>7.3 without evidence of significant ketosis
Level of acidemia is influenced by severity of shock &
starvation
Lab values consistent with acute renal failure,
rhabodmyolysis & pancreatitis

52

Emergency Department Care

Manage the airway as needed, establish
intravenous access, initiate vigorous fluid
resuscitation, and obtain appropriate laboratory and
radiographic studies.
Fluid deficits in hyperosmolar hyperglycemic state
(HHS) are large; the fluid deficit of an adult may be
10 L or more.
Administer 1-2 L of normal saline in the first 2
hours. A higher initial volume may be necessary in
patients with severe volume depletion. Slower
initial rates may be appropriate in patients with
significant cardiac or renal disease.

Emergency management

Caution should be taken to not correct

hypernatremia too quickly, as this could
lead to cerebral edema.
Once serum glucose drops to 15mmol/l,
the patient must receive dextrose in the
intravenous fluid. This may decrease the
risk of developing cerebral edema.

Treatment
Initiate insulin therapy in the ED.
Although many patients with HHS respond to
fluids alone, intravenous insulin in dosages
similar to those used in DKA can facilitate
correction of hyperglycemia.
Insulin used without concomitant vigorous fluid
replacement increases risk of shock.
Replace potassium and magnesium as needed.
Use of insulin may exacerbate hypokalemia.

Treatment
Insulin plays a secondary role
Hyperglycemia can often be corrected via
volume resuscitation
Renal perfusion is improved, GF is
enhanced
Insulin gtt 0.1 U/kg/hr
Patients diagnosed with HHS require
hospitalization, usually to intensive care
unit for close monitoring.
56

Summary Treatment

Rehydration is the most important

treatment
Is performed under close observation of
circulatory status

Insulin concentration is usually low

Blood glucose will drop in parallel with
rehydration
Watch electrolytes

Patients should be monitored closely

Treatment
Treat precipitating event
Identify and treat aggressively
Infections