Diabetic

Ketoacidosis
Prepared by: Desiree A. Fernandez
 01
Introduction
⋆ Dka is a serious complications of Diabetes Mellitus.
It carries significant risk of death and/or morbidity
especially with delayed treatment.

⋆ With the new advances of therapy. DKA mortality

decreases. Before discovery and use of insulin the
mortality is 100%.

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 02
Epidemiology
⋆ DKA is reported 2-5% of known type 1 diabetic patients in industrialized
countries, while it occurs in 35-40% pf such patients in Africa.

⋆ DKA at the time of first diagnosis of diabetes mellitus is reported in

only 2-3% in western Europe, but is seen in 95% of diabetic childrien
in Sudan. Similar results were reported from other Africa countries.

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 03
Pathophysiology
⋆ Secondary tp insulin deficiency, and the action of
counter-regulatory hormones, blood glucose increases
leading to hyperglycemia and glucosuria.

In the absence of insulin activity the bpdy fails yo utilize

glucose as fuel and uses fats instead. This lead to ketosis
⋆

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⋆ The excess of ketone bodies will cause metabolic acidosis,
the later is also aggravated by Lactic acidosis caused by
dehydration and poor tissue perfusion.

⋆ Vomiting due to an ileus, increased insensible water losses

due to tachypnea will worsen the state of dehydration.

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⋆ The dehydration can lead tp decreased kidney perfusion and acute
renal failure.

⋆ Accumulation of ketoNe bodies contributes to the abdominal pain

and vomiting.

⋆ Thr increasing acodosis leads to acidotic breathing and acetone smell

in th breath and eventually causes impaired consciousness and coma.

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 04
Precipatating Factors
⋆ New onset of type 1 DM: 25%
⋆ Infections 40%
⋆ Drugs
⋆ Omission of Insulin: 20%

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 05
Laboratory Investigations
 ⋆ Venous blood glucose;
⋆ Electrolytes, urea, creatinine, osmolarity and
ketones;
⋆ Urinalysis for ketones;
⋆ Blood tests for infection markers;
⋆ Venous blood gas values.
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 06
Diagnosis
SHOULD SUSPECT DKA IF A DIABETIC PATIENT PRESENTS
WITH:
⋆ Dehydration
⋆ Acidotic (Kussmaul’s) breathing, with a fruity smell (acetone).
⋆ Abdominal pain and distention.
⋆ Vomiting
⋆ An altered mental status ranging from disoriented to coma.

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TO DIAGNOSIS DKA, THE FF. CRITERIA MUST BE FULFILLED:
1. Hyperglycemia: of >300 mg/dl and glucosuria
2. Ketonemia and ketonuria.
3. Metabolic acidosis: pH < 7.25, serum bicarbonate < 15 mmo1/1.
Anion gap > 10.
This usually accompanied with severe dehydration and electrolyte
imbalance.

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 07
Assessment
HISTORY:
⋆ Symptoms of hyperglycemia, precipatating factors, diet and insulin
dose.
EXAMINATION
⋆ Look for signs pf dehydration, acidosis and electrolytes imbalance,
including shock, hypotension, acidotic breathing, CNS status etc.
⋆ Look for the signs of hidden infection (fever strongly suggests
infection) and if possible, obtain accurate weight before starting
treatment.

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 08
Complications
Cerebral Edema
⋆ Intracranial thrombosis or infraction
⋆ Acute tubular necrosis
⋆ Peripheral edema

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 09
Treatment
 ⋆ Careful replacement pf fluid deficits.
⋆ Correction pf acidosis and hyperglycemia via Insulin administration.
⋆ Correction pf electrolyte imbalance.
⋆ Treatment pf underlying cause.
⋆ Monitoring for complications of treatment.
⋆ Manage DKA in the PICU. (Pedia)

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 10
Fluid Replacement
DETERMINE HYDRATION STATUS
A. Hypovolemic shock – administer 0.9% saline, Ringer’s lactate or a
plasma expander as bolus dose of 20-30ml/kg.
B. Dehydration without shock:
1. Administer 0.9% Saline 10ml/kg/hr for an initial hour, to restore
blood volume and renal perfusion.
2. The remaining deficit should be added to ge maintenance and total
being replaced over 36-48hrs. To avoid rapid shift in serum
osmolality 0.9% Saline can be used for the initial 4-6hrs, ff by
0.45% saline
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⋆ When serum glucose reaches 250mg/dl change fluid to 5% dextrose
with 0?45 saline, at a rate that allow complete restoration in 48 hrs
and yo maintain glucose at 150-250mg/dl.

⋆ Pediatric saline 0.18% NA Cl should not ve used even in young

children.

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 11
Insulin Therapy
⋆ Start infusing regular insulin at a rate pf 0.1U/kg/hr using a syringe pump.
Optimally, serum glucose should decrease in a rate no faster than
100mg/dl/hr.
⋆ If serum glucose falls <200 prior to correction of acodosis, change IV fluid
from D5 to D10, but don’t decrease the rate pf insulin infusion.
⋆ The use of initial bolus of insulin (IV/IM) is controversially.
Continue the Insulin infusion until acidosis os cleared:
⋆ pH > 7.3
⋆ Bicarbonate > 15mmol/1
⋆ Normal anion gap 10-12

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 12
Correction of Acidosis
⋆ Insulin therapy stops lipolysis and promotes the metabolism of
ketone bodies.

⋆ Bicarbonate therapy should bot be used unless severe acodosis

(pH<7.0) results in hemodynamic instability. If it must be given, its
must infused slowly over several hours.

⋆ As acidosis is corrected, urine KB appear to rise. Urine KB are not

of prognotic value in DKA.

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 13
Correction of Electrolyte
Imbalance
⋆ Regardless of K concentration at presentation, total bofy K is low. So,
as soon as the urine output is restored, K supplementation must be
added to IV fluid at concentration of 20-40mmol/1, where 50% of it
given as KCI and the rest as K phosphate, avoids excess phosphate
and excess CL.

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 14
Management
⋆ Ongoing clinical assessment of the patient: this involves regular (at least
hourly) monitoring of vital signs and level of consciousness during the acute
phase (JBDS, 2013).The early warning score system should be used as a
guide to determine the patient’s clinical condition and response to treatment,
and escalated to senior or specialist colleagues or medical team as
appropriate;

⋆ Accurate monitoring of fluid balance: this includes accurate intake and output
charts (JBDS, 2013). Prescribed fluids should be administered and patients
monitored for signs of complications related to fluid overload, dehydration
and electrolyte imbalance;

⋆ Insulin therapy: this should be administered as prescribed;

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⋆ Regular monitoring of capillary blood glucose and ketones: this is required
at least hourly (JBDS, 2013) during the acute phase. Nurses should liaise
with the medical team for appropriate adjustment to insulin doses as
required;

⋆ Monitoring of metabolic acidosis and electrolytes: this involves liaising with

the medical team to ensure blood gases and appropriate blood tests are
carried out regularly, results interpreted and action taken, for example
potassium being added to IV infusions if required.

⋆ Support early referral to the diabetes team: this involves liaising with the
medical team to ensure the diabetes team is contacted as soon as possible
after admission. 34
⋆ Provide psychological support for patients: this includes keeping
the patient and relatives fully informed about the patient’s clinical
condition and the care given.

⋆ Diabetes specialist nurse: this nurse has a key role in providing

patient education including sick-day management (see below) and
arranging follow-up support for patients after discharge.

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 15
Patient Education
Patients should be taught This should include specific
how to manage blood information about frequency of
blood glucose monitoring, blood
glucose during periods of
glucose targets, checking for
illness (sick-day
ketones, taking extra quick-acting
management).  insulin, appropriate adjustment of
insulin doses, identifying early
signs and symptoms of DKA and
knowing when to contact the
diabetes specialist team (Kitabchi
et al, 2004)

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 Merry Christmas
and a Happy New Year!
THANK YOU!

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