DIABETIC KETOACIDOSIS

Dr. Mohamad dawoud.

 DKA
• Diabetic ketoacidosis(DKA) is an acute, life
threatening complication of DM characterized
by hyperglycemia , ketoacidosis and ketonuria.
• Occurs when absolute or relative insuline
deficiency inhibits the ability of glucose to
enter cells for utilization as metabolic fuel.
• After that the liver rapidly begin the process of
breaking down of fat into ketones to employ as
a fuel source.
• Overproduction of ketones ensues, causing
them to accumulate in the blood and urine
and they turn the blood acidic.
• DKA commonly occurs in patients with type 1
DM.
 etiology
• Lack of or insufficient insulin replacement therapy:
– Undiagnosed, untreated diabetes mellitus
– Treatment failure in known diabetics:  insulin pump failure,
forgotten insulin injection, noncompliance with insulin therapy.
• Increased insulin demand
– Stress: infections, surgery, trauma, myocardial infarction.
– Drugs: glucocorticoid therapy, cocaine use, alcohol abuse.
• In 30% of DKA presented cases are mostly precipitation of
infections ( pneumonia, UTI…) especially in the elderly
populations.
 Pathophysiology of DKA.
• Osmotic diuresis and hypovolemia
• Insulin normally elevates cellular uptake of glucose
from the blood.
• In the insulin-deficient state
of DKA, hyperglycemia occurs.
• Hyperglycemia, in turn, leads to progressive volume
depletion via osmotic diuresis.
• Insulin deficiency
→ hyperglycemia → hyperosmolality → osmotic
diuresis and loss of electrolytes → hypovolemia.
 PATOPHYSIOLOGY OF DKA
• Metabolic acidosis  with increased anion gap.
• Insulin deficiency also increases fat breakdown (lipolysis).
• Metabolic acidosis develops as the free fatty acids generated by lipolysis
become ketones, two of which are acidic (acetoacetic acid and beta-
hydroxybutyric acid). 
• Serum bicarbonate is consumed as a buffer for the
acidic ketones. Metabolic acidosis with an elevated anion gap is therefore
characteristic of DKA.
• Insulin deficiency → ↑ lipolysis → ↑ free fatty
acids → hepatic ketone production (ketogenesis) → ketosis→ bicarbonate
consumption (as a buffer) → anion gap  metabolic acidosis.
• Extracellular potassium shift because of the overall loss of potassium in
urine; A total body potassium deficit occurs but the level of k+ in the blood
is normal even elevated!
 Clinical features
• Polyuria.
• Polydipsia.
• Nausea and vomiting.
• Signs and symptoms of dehydration: dry
mucous membrane, hypotension, decreased
skin turgor.
• Neurological abnormalities:
Altered mental status/lethargy/ coma.
Other specific findings in the DKA:
• Fruity smell from the mouth.
• Rapid onset (<24h).
• Hyperventilation: long, deep breath
(kussmaul’s breathing).
• Abdominal pain.
 diagnostics
• Check serum glucose to confirm hyperglycemia.
• Check BMP for serum bicarbonate, anion gap, electrolytes,
and renal function.
• Check for the presence of ketones.
– Urine ketones: Standard urine dipstick assays detect acetoacetate
and acetone but not beta-hydroxybutyrate.
– Serum beta-hydroxybutyrate.

• Check blood gas analysis for pH. 

• Diagnostic workup to evaluate the underlying
cause: HbA1c, CBC, ECG, infectious workup.
 Electrolytes and renal function in DKA.
• Sodium:
– Hyponatremia is common in both DKA and HHS, due
to hypovolemic hyponatremia
–  and hypertonic hyponatremia
– Always check corrected sodium for hyperglycemia.
• Potassium in DKA: normal or elevated (despite a total body
deficit)
• Magnesium levels are typically low. 
• Phosphorus levels may be falsely elevated despite a total
body deficit.
• BUN and creatinine are often elevated.
 Additional diagnostic workup
• HBA1C
• CBC
• Blood and urine culture.
• Serum lactate.
• Chest x-ray
• Monitor ECG And troponin for cardiac
ischemia.
 management
• IV access with two large-bore peripheral IV lines
• Assess the severity of DKA.
• Fluid resuscitation: initially with isotonic saline (0.9%
NaCl), then 0.45% or 0.9% depending on corrected serum
sodium
• Electrolyte repletion (especially potassium)
• Short-acting insulin(regular insulin) therapy
• IV bicarbonate (only in severe metabolic acidosis)
• Identify and treat the underlying cause.
• Consider admission to the ICU.
• First hour with IV repletion: 0.9% Nacl at 15-
20 ml/kg/h.
• Potassium should be >3.3mEq/l before
insuline initiation.
• Maintain potassium level between 4-5mEq/l.
• Recommended regimen of insulin is:
Regular insulin bolus followed by continuous
regular insulin.
Hyperglycemic hyperosmolar state(HHS).

• Is a life threatening condition present

commonly in patients with type 2 DM; it has
a higher mortality rate reaching 5-10%.
• Previously was called hyperosmolar
hyperglycemic coma(HHNC) , terminology
was changed because coma was found in less
than 20%.
 etiology
• Present in patients with type 2 DM who have
concomittant illness that reduce fluid intake .
• Infection is the most common cause.
• Stroke and MI
• Some drugs as glucocorticoids, cocaine, and
alcohol abuse.
• Non compliance with oral hypoglycemics or
insulin therapy.
 pathophysiology
• The pathophysiology of HHS is similar to that
of DKA.
• However, in HHS, there are still small amounts
of insulin being secreted by the pancreas, and this is
sufficient to prevent DKA by
suppressing lipolysis and, in turn, ketogenesis. 
• HHS is characterized by symptoms
of marked dehydration (and loss of electrolytes)
due to the
predominating hyperglycemia and osmotic diuresis
 Clinical features
DKA HHS
DM TYPE 1 TYPE 2
HISTORY OF SEVERE STRESS , + +
ILLNESS, HOSPITALIZATION
POLYURIA , POLYDIPSIA + +

NAUSEA, VOMITING + +/-

DEHYDRATION + SEVERE

ALTERED MENTAL STATUS POSSIBLE POSSIBLE

HYPERVENTILATION + -

FRUITY SMELL + -

ONSET RAPID(<24h) INSIDIOUS(DAYS)

 DIAGNOSTICS
• Plasma glucose level of 600mg/dl or greater.
• Effective serum osmolality of 320mOsm/kg or
greater.
• Profound dehydration up to 9L.
• Bicarbonate concentration greater than
15mEq/L.
• Small ketonuria and low to absent ketonemia.
• Serum PH >7.3
• Some alterations in consciousness.
• Imaging studies include:
• CXR, abdominal x-ray if patient has abdominal pain or
is vomiting.
• CT brain indicated in patients with focal or global
neurologic changes to exclude hemorrhagic strokes,
subdural hematoma, subarachnoid bleeding..
• ECG rule out ischemia and MI.
• CSF cell count, glucose, protein, and culture in patient
with suspected meningitis.
 Difference in lab test between DKA AND HHS
Lab test DKA HHS
GLUCOSE <600mg/dL >600mg/dl

BICARBONATE <18 mEq/l >18mEq/l

ANION GAP Elevated >10 mmol/l Normal <10

URINALYSIS Normal large ketones in Absence of ketones in

urine urine
glucosuria glucosuria
SERUM BETA- elevated normal
HYDROYBUTYRATE
BLOOD GAS PH<7.3 PH>7.3

SERUM OSMOLALITY normal Elevated >320mOsm/kg

 MANAGEMENT
• Fluid resuscitation: First line treatment of
patients with HHS is IV crystalloids with 2 large
bores to rehydrate the patient. Isotonic solution
0,9% is usually used first 1 hour of admission at
15-20 ml/kg/h.
• Check for corrected sodium :
If sodium >135mEq/l then 0.45% Nacl is used.
If sodium <15 mEq/l then 0.9% is used.
• Acute management of airway in altered mental status
patient is essential and a first step to maintain patient life
, patient may be mechanically ventilated to support
respiration and prevent arrest.
• IV rapid insulin infusion is needed to decrease blood
glucose and osmotic pressure, although some patient may
not needed after IV fluid resuscitation.
• Always correction of potassium is of high importance
before insulin administration because of the depletion of
intracellular level of potassium even if the level of
potassium is within normal range.
According to American Diabetes association
recommendations:
• If hypokalemia ( k<3.3 mEq/l) has been excluded,
an IV bolus of regular insulin of 0.1U/kg/h should
be administered.
• Continuous insulin infusion of 0.1U/kg/h.
• Monitor blood glucose every hour.
• Continue IV insulin at a goal glucose level of 250-
300mg/dl.
• Electrolytes replacement and potassium replenish
if k<3.3 at first line before insulin infusion.
• Other electrolytes as Mg , P , and Ca are not routinely
replineshed , only in case of severe decrease could be
added.
• Diagnostics and treatment of the underlying cause
responsible for HHS developpment in the diabetic patient
as pneumonia , UTI and treatment with antibiotics.
• Adjustment of the insuline regimen of the patient if
needed or hypoglycemic drugs with maintaining of
normal diet and physical activity after discharge and
regular follow up.