DIABETIC KETOACIDOSIS

Presented by the students from roll numbers 31 - 40

 Introduction:

 Diabetic ketoacidosis is a medical emergency and potentially life

threatening complication in people with diabetes mellitus

 It happens predominantly in people with type 1 diabetes

mellitus but it can occur in people with type 2 diabetes mellitus
under certain circumstances like inadequate administration of
exogenous insulin or stressful conditions like infections,
infarction, trauma, pregnancy ,drugs like cocaine
The cardinal biochemical features of diabetic
ketoacidosis are:

 Hyperketonaemia (≥ 3.0 mmol/lit) or ketonuria

 Hyperglycemia ( approximately 200mg/dl)
 Metabolic acidosis (venous bicarbonate <15mmol/lit and/or
venous pH <7.3)
Pathophysiology:

 Diabetic ketoacidosis results from relative or absolute insulin

deficiency combined with counter regulatory hormone excess
like glucogan, catecholamines, cortisol and growth hormone
 The decreased ratio of insulin to glucogan promotes
gluconeogenesis, glycogenolysis and ketone body formation in
the liver as well as increase in substrate delivery from fat and
muscle to the liver like free fatty acids and amino acids
 Role of Insulin:

 Insulin deficiency leads to hyperglycemia that causes a profound osmotic

diuresis leading to dehydration and electrolyte loss particularly of sodium
and potassium.
 Potassium loss is exacerbated by secondary hyperaldosteronism as a result
of reduced renal perfusion.
 Activation of glycogenolysis and gluconeogenesis and lipolysis by insulin
lack,all resulting in new glucose production
 There is also decreased peripheral utilisation of glucose secondary to
insulin lack and resistance and there is volume depletion secondary to
osmotic diuresis.
 Ketosis results from marked increase in free fatty acids as a
result of lipolysis and are converted into ketone bodies in the
liver by beta oxidation
 Acidosis occurs as a result of exhaustion of body bases in the
process of buffering ketone bodies which are produced
uncontrollably.
Role of counter regulatory hormones:

 Hypersecretion of epinephrine (EN), glucagon, cortisoland

growth hormone (GH) results in DKA by
a. Inhibiting insulin mediated glucose uptake by muscle-peripheral
utilisation (EN, cortisol, GH)
b. Activating glycogenolysis and gluconeogenesis (EN,glucagon,
cortisol)
c. Activating lipolysis (EN, GH)
d. Inhibiting residual insulin secretion (EN, GH).
Clinical features:
 Symptoms usually develops over 24 hours
 Patients present with polydipsia, polyuria and weakness
 Anorexia, nausea, vomiting and abdominal pain may be there
due to ketonaemia especially in children
 A characteristic type of breathing called kussmaul’s breathing
occurs as a respiratory compensation for metabolic acidosis
 Kussmual’s breathing – Type of hyperventilation characterized
by deep, rapid and labored breathing
 Patients may have altered sensorium some of them may even
comatose.
 Physical findings
 Fruity or musty odour in breath
 Loss of skin turgor, dry tongue, and decreased intra ocular
pressure suggestive of dehydration
 Hypothermia
 Postural Hypotension
 Tachycardia
 Kussmauls breathing
 Abdominal tenderness which resembles acute pancreatitis or
surgical abdomen
 Hyporeflexia because of decreased potassium
 Hypotonia, stupor or coma
 Investigations:
 The following investigations are important but should not delay the
institution of intravenous fluids and insulin replacement
 Venous blood: for urea and electrolytes, glucose, bicarbonate and acid–base
status.
 Urine or blood analysis for ketones
 Electrocardiogram
 Screening for infections: Full blood count, blood and urine culture, C-
reactive protein, chest X-ray.
 Although leucocytosis invariably occurs in Diabetic ketoacidosis, this
represents a stress response and does not necessarily indicate infection.
Indicators of severe diabetic ketoacidosis:

Blood ketones >6 mmol/L

Bicarbonate <5 mmol/L
Venous/arterial pH <7.0 (H+ >100 nmol/L)
Hypokalaemia on admission (<3.5 mmol/L)
 Glasgow Coma Scale score <12
 O2 saturation <92% on air
 Systolic blood pressure <90 mmHg
 Heart rate >100 or <60 beats per minute
 Anion gap >16 mmol/L
The presence of one or more of the features mentioned above are
indicative of severe DKA.
Management
Goals of therapy of diabetic ketoacidosis

 Rehydration
 Reduction of hyperglycemia
 Correction of electrolyte imbalance
 Correction of acid – base imbalance
 Investigation and correction of precipitating factors
 Treatment of complications
Fluid resuscitation
 It is a critical part of treating the patients with DKA as it is a state of
severe dehydration.
1.Intravenous solutions to replace extravascular and intravascular
fluids and electrolyte losses. The usual fluid deficit is minimum 3-5L
and should be replaced intravenously. They dilute levels of both the
glucose and the circulating counter regulatory hormones.

2.Fluids itself leads to correction of acidosis to some extent.

Fluid resuscitation
IV fluids

Determine hydration status

Hypovolemic shock Mild hypotension Cardiogenic shock

Administer 0.9% Nacl Evaluate corrected Hemodynamic monitoring

and /plasma expander serum Na

Serum Na Serum Na normal Serum Na low

0.9% Nacl (4-14mL/kg/hr) depending on

0.45% Nacl (4-14mL/kg/h)
the hydration state
Depending on hydration state
 Insulin recommendations
 Short acting insulin is administered to reverse acidosis and treat hyperglycemia.

When serum glucose reaches 250 mg/dl

Change to 5% dextrose with 0.45 % Nacl at 15-250 mL/hr with adequate insulin (0.05-0.1units /kg/hr IV
infusion)to keep the serum glucose between 150 and 200 mg/dL until metabolic control is achieved .

• Check electrolytes,BUN, creatinine and glucose every 2-4 hrs until stable
• Continue IV insulin until patient is able to eat
• When the patient can eat, initiate a multidose subcutaneous insulin regimen
• Continue IV insulin infusion for 30 to 60 mins after subcutaneous insulin is begun,to ensure
adequate plasma insulin levels
• Continue to look for precipitating causes.
Potassium repletion
Check serum potassium
Serum k+ >5mmol/L Serum k+ 3.3-5 mmol/L
• Give 20-30 mmol of
potassium in very litre of
Don’t give potassium
IV fluid
Monitor every 2 hrs
• Target potassium 4-
5mmol/L
Serum k+ 3.3 mmol/L
• Hold insulin
• Give 40 mmol of
potassium per hr till serum
potassium is >_ 3.3
mmol/L
Correction of acid –base balance
 Its role is controversial and is usually not practiced .

Assess need for bicarbonates

PH ≤ 6.9 PH ≥ 6.9

NaHCO 3 (100 mmol)dilute in 400ml No NaHCO 3

distilled water
Infuse at 200 mL/h with 20 mmol kcl

Repeat HCO 3 administration every 2

hrs till ph >7
Monitor serum potassium
• PHOSPHORUS REPLETION
A sharp drop of serum phosphorus can also occur during insulin treatment
and no treatment is usually necessary.

Complicatons of DKA :- Mortality is <10% .Death

occur due to infection, thrombosis,cerebral edema and
shock