DKA - QStation

• Jonathan Phillips - August 3, 2005
• Introduction
– The diagnosis of uncontrolled diabetes mellitus
is usually suspected from the clinical history.
Hyperglycemia and in DKA a high anion gap
metabolic acidosis with ketonuria and
ketonemia. DKA is primarily seen in DM-1 but
can be seen in DM-II, usually in africanamerican.
– DKA and Nonketotic hyperglycemia (NKA) are
related disorders that differ clinically according
to the presence of ketoacidosis and the degree
of hyperglycemia.
– In NKA there is little or no ketoacid
accumulation, the plasma osmolality may reach
380 and neurologic abnormalities are frequently
present, include coma in 25 to 50%.
– In DKA, metabolic acidosis is often the major
finding while the plasma glucose is below 800.
• Precipitating Factors
– DKA and NKA typically occur after a
precipitating event like infection, volume
depletion, trauma, increased levels of
catecholamines, cortsol, and glucagon. These
hormones promote both glucose and ketoacid
• Clinical Presentation
– The signs and symptoms of DKA and NKH are
related to the degree of hyperosmolality,
volume depletion, and in DKA, metabolic
– The earliest symptoms of marked
hyperglycemia are polyuria, polydipsia and
weight loss, nausea, vomiting and abdominal
pain which is limited to DKA.
– The presence of pain is associated with the
severity of the metabolic acidosis, but not the
severity of hyperglycemia or dehydration.
Patients with ketoacidosis may have a fruit odor
due to exhaled acetone and deep respirations
called Kussmaul respirations.
– Neurologic deterioration primarily occurs in
patients with osmolality above 320 to 330,
which develops in NKA.
• Posm=2xNa+(Glu/18)
• Laboratory Findings
– Hyperglycemia- may exceed 1000 in NKH and
generally below 800 in DKA.
– Plasma sodium may vary
– Plasma potassium- patients deficit averages
3 to 5 mg/kg. However, initially serum levels
may be normal to high due to hyperosmolality
and insulin deficiency which promote water out
of the cell and potassium with it.
– For every 1 meq/L of K for every 100 mg/dl of
– Plasma Bicarb and anion gap generally severe
in DKA and generally normal in NKH. Both
insulin and glucogon excess contribute to the
development of ketoacidosis.
– Amylase and lipase are often elevated in DKA
for reasons unknown. Even greater than 3 fold
does not make the diagnosis of acute
pancreatitis with a normal CT.
• Treatment
– Therapy in DKA and NKH is similar.
Monitoring initial labs should include CMP,
CBC, ABG, UA, and blood cultures if findings
suggest fever or localizing symptoms. Glucose
should initially be measured every one to two
hours. BMP and ABG every 2-6 hours.
– Normalization of the anion gap reflects
disappearance of ketoacid anion in the plasma
and correction of the ketoacidosis. Ketonemia
and ketouria may persist for more than 36 hours
due to slower removal of acetone.
– Insulin lowers the plasma glucose concentration
by decreasing hepatic glucose production rather
than enhancing peripheral utilization and
diminishes ketone production by reducing both
lipolysis and glucogon secretion.
– Appropriate insulin therapy lowers plasma
glucose by approx. 65 to 125 mg/dl an hour.
Fluid repletion lowers the glucose by 35 to
70 mg/dl. The combined effect results in a fall
between 100-200mg/dl an hour in DKA but be
more pronounced in patients with NKH who
are much more volume depleted.
– Patients are treated with regular insulin IV, a
loading dose or 15 to 20 units followed by
continuous infusion of 7 units an hour. Some
patients are relatively resistant to lower level
doses of insulin and hourly dose should be
increased if glucose reduction is not seen.
– Insulin infusion is generally discontinued and
standard insulin therapy begun when two goals
are reached.
• The glucose falls below 250 mg/dl to decrease the
risk of cerebral edema
• Ketoacidosis has resolved, evidenced by
normalization of the anion gap, which most often
occurs within the first 5-10 hours of therapy
– Fluid replacement
• The average loss is 3-6 liters in DKA and up to 8-10
in NKH, due to glucose osmotic diuresis. The aim of
therapy is to replete the extracelluar fluid volume
without inducing cerebral edema due to rapid
reduction in the plasma osmolality. Fluid is begun
with isotonic saline. If patient is in shock, fluids
should be wide open. Usually 500 ml for 4 hours
then 250 ml for 4 hours. When glucose goes
between 250-300, patients should be switched to 1/2
NS to replace free water deficit.
• Potassium is added to fluid when levels fall below
4.5 meq/l. Potassium repletion is even more urgent
in those patients with massive deficits who are
hypokalemic prior to therapy, 40 KCL in 1/2 NS
should be added.
• Sodium- when reversing the hyperglycemia with
insulin, this will lower plasma OSM causing water
to move from extracellular fluid into cells and raise
sodium concentration. Thus a patient with a normal
sodium will probably become hypernatremeic
during therapy with insulin and isotonic saline.
• Metabolic acidosis- insulin promotes the
metabolism of ketoacid anions resulting in the
regeneration of bicarbonate which decreases the
anion gap.
• Metabolic acidosis- insulin promotes the
metabolism of ketoacid anions resulting in the
regeneration of bicarbonate which decreases the
anion gap.
• Concerns
– Cerebral edema is a complication of therapy in
uncontrolled DM (DKA) that occurs within 24
hours after treatment has been initiated.
Headache is the earliest sign, but marked
neurologic dysfunction can occur. More than
1/2 of these patients will either die or have
permanent neurologic damage. Almost all
patients are below 20 years of age.
• Questions
– 1) What is the major finding in diabetic
A. Respiratory alkalosis
B. Respiratory acidosis
C. Metabolic acidosis
D. Metabolic alkalosis
– 2) When should potassium be added to fluid?
A. 3.5
B. 4.0
C. 4.5
D. 5.0
– 3) What is the standard infusion rate of insulin
per hour?
A. 5 units
B. 7 units
C. 9 units
D. 12 units
– 4) What physical finding is exclusive to DKA
and not seen in NKH?
A. nausea
B. vomiting
C. abdominal pain
D. weight loss

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