Diabetic

Ketoacidosis (DKA)
 Definition
DKA is caused by
Combination of
absolute or relative insulin deficiency
An increase in counter regulatory hormones Leading to
1) increased gluconeogenesis
2) Accelerated glycogenolysis
3) and Impaired glucose utilization by peripheral tissues, lipolysis
and unrestrained hepatic fatty acid oxidation to ketone bodies
Culminating(reach climax) in hyperglycemia and ketonaemia
Pathophysiology
 Sign and symptoms

significant polyuria, polydipsia, weight loss, dehydration,

weakness and clouding of sensorium(altered sensorium)
GI complaints are common especially in young
Nausea
Vomiting
Diffuse abdominal pain
Hyperventilation with deep rapid breathing and the smell of
acetone on the breath
 Diagnostic criteria

1) Hyperglycemia with blood glucose 11 mmol/l

2) Acidaemia with arterial pH <7.3, bicarbonate <15
mmol/l

3) Ketonaemia >3mmol/l or ketonuria 2+

 Serum amylase level elevated in absence of pancreatitis
Non specific elevation of hepatic transaminases,
creatine kinase, lactate dehydrogenase, and lipase as a
result of hyperglycemic crisis.
Inflammatory marker like CRP - elevated
Leucocytosis up to 15K (not necessary indicate
infection until >25K)
Serum sodium usually low
 Common causes

Insufficient insulin/Non compliance to insulin therapy

Infection: UTI, Respiratory tract infection, skin

infection

Infarction: myocardial, CVA, GIT, peripheral

vasculature
Management
 Investigation
FBC
Urea/electrolytes/creatinine/calcium/magnesium/phosp
hate (to include venous glucose),
Cardiac enzymes,
DIC screen (if septic)
Urinalysis (for ketone bodies and leucocytes)
Serum ketone (beta-hydroxybutyrate)
Serum osmolality
Arterial blood gas
 Futher ivx to look for precipitating
cause
Chest X-ray
Blood cultures and sensitivity
Urine analysis
ECG
ECG Changes on Hyperkalemia
 Management
Supportive measures
Managed in monitored area
Supplemental high-flow oxygen
Monitoring : ECG, Pulse oximetry, Vital signs every 15-30mins, blood
levels of glucose, ketones, potassium, and acid base balance every 1-2
hrs.
Labs ivx : FBC, urea /electrolyte /creatinine /calcium/
magnesium/phosphate (to include venous glucose), cardiac enzyme, DIC
screen(if septic), urinalysis (for ketone and leucocytes), serum ketones
(beta-hydroxybutarate), serum osmolality, and ABG
 Supportive measures(cont)
Consider blood culture
12-lead ECG, CXR, urine dipstick: looking for cause of
DKA
Circulatory support : IV normal saline(basic
resuscitation fluid), switching to 45% NS as perfusion
improves and BP normalizes, then 5% Dextrose in 45%
normal saline as serum glucose level drops. Total fluid
loss in DKA averages 4-6 litres.
Urinary catheter to monitor urine output.
 Specific measures for DKA

Aim: correcting u/l pathophysiologic abnormalities.

Fluid resuscitation
Acid-base and electrolyte correction
Insulin therapy
Identifying a precipitating factors
 Specific measures (cont)

IV volume replacement : correct intra and extravascular volume deficit

and improving renal function. Also lowers blood glucose independently
of insulin therapy
1. If patient in shock :
Septic shock : administer IV Hartmanns solution 20-30ml/kg over 30 mins, start
IV antibiotics and admit to ICU.
Cardiogenic shock : admit to ICU for vasopressors and haemodynamic
monitoring
2. Severe hypovolaemia without shock
Administer 0.9% NaCl 1 L/hr
If BP remain low after 2L of NaCl, consider colloids/Hartmanns solution and
ICU/HDU care.
 Specific measures (cont)

3. Neither hypotensive nor severely dehydrated

Administer 0.9% NaCl 1 L/hr (15-20 ml/kg/h) in first hr
Further fluid therapy - depend on haemodynamic/perfusion status,
sodium level and urinary output
4. Corrected serum sodium is low
Administer 0.9% NaCl 250-500 ml/h depending on hydration status.
If patient is haemodynamically stable and corrected sodium is
normal/elevated, infuse 0.45% NaCl at 4-14 ml/kg/h evenly over 24
hrs with careful monitoring of serum glucose level
Corrected serum sodium =
Measured serum sodium + 0.3 (Venous glucose in mmol/l -5.5)
Switched to 5% dextrose when serum glucose falls below 14 mmol/l
 Specific measures (cont)

Insulin administration
Large doses are not needed (may cause hypoglycemia and hypokalemia in high
doses)
Administer bolus dose of 0.1 units/kg BW of IV SI in adults, followed by a low-
dose continuous infusion of 0.1 units/kg BW/hr in both adults and children or
Give a IV dose of 0.14 units/kg BW insulin if bolus dose is omitted
Adjust infusion rate to obtain a drop of serum glucose level by approx. 3-4
mmol/l per hour.
If not achieved, insulin infusion may be doubled every hour for possible insulin
resistance (occur in sepsis or occult infection)
Blood glucose 14 mmol/l, halve the SI infusion rate to 0.05-0.1 units/kg/h and
start IV D5% - aim for blood glucose level 8-12 mmol/l
Maintain infusion rate until acidosis clear (pH>7.3, HCO3 >15)
 Specific measures (cont)

Restoration of electrolyte balance

Establish that there is urine output of 50 l/hr, then replace as
below:-
Serum K+ <3.3 mmol/l, withhold insulin and give 20-40 mEq
KCL per hour until K> 3.3 mmol/l
Serum K+ 3.3-5.2 mmol/l, give 20-30 mEq K+ in each litre of IV
fluid to keep K+ between 4-5 mmol/l
Can be give as 2/3 KCL and 1/3potassium phosphate
Phosphate replacement is indicated when serum phosphate <0.3 mmol/l
or if patient is anaemic or in cardiorespiratory distress
Serum K+ >5.2 mmol/l, withhold potassium but check serum
potassium every 2 hours
 Specific measures (cont)

Restoration of acid-base balance

Sodium bicarbonate Given only if severe
hyperkalemia with ECG changes or if the arterial pH is
<6.9, since IV volume replacement and later, insulin
will improve the metabolic acidosis.
pH <6.9, give IV 8.4% NaHCO3 100mls with 20 mmol
of KCL over 2 hours.
Monitor ABG and serum K+ every 2 hours.
Repeat IV NaHCO3 and KCL every 2 hours until pH is
7.0
 Possible complication while
managing hyperglycemic crisis
Hypoglycemia
Hypokalemia
Hyperchloraemia
Fluid overload
ARDS
Thromboembolism
Rhabdomyolysis