See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/317552397

diabetes ketoacidosis

Presentation · January 2014

CITATIONS READS

0 9,241

1 author:

Abdulmoein Eid Al - Agha

King Abdulaziz University
252 PUBLICATIONS   542 CITATIONS   

SEE PROFILE

Some of the authors of this publication are also working on these related projects:

HYPERTRIGLYCERIDAEMIA-INDUCED ACUTE PANCREATITIS IN AN INFANT: A CASE REPORT View project

metabolic bone diseases in children View project

All content following this page was uploaded by Abdulmoein Eid Al - Agha on 12 June 2017.

The user has requested enhancement of the downloaded file.

 Diabetes Ketoacidosis

Abdulmoein Eid Al-Agha, MBBS, DCH, CABP, FRCPCH

Associate Professor of Pediatric Endocrinology,
King Abdulaziz University Hospital
Website: http://aagha.kau.edu.sa
 Goals & Objectives
• What is DKA?
• Understand the Pathophysiology of DKA
• Criteria of diagnosis
• Clinical and laboratory features
• Discuss the management approach to the
patient with DKA
• Appreciate the complications that occur
during treatment
2
 Diabetic Ketoacidosis (DKA)
• A state of absolute or relative insulin deficiency
aggravated by ensuing hyperglycemia, dehydration,
and acidosis-producing derangements in
intermediary metabolism, including production of
serum acetone.
• Can occur in both Type 1 Diabetes and Type 2
Diabetes
– In type 2 diabetics with insulin deficiency/dependence
• The presenting symptom for ~ 25% of Type 1
Diabetics.
 Diabetes Ketoacidosis
• DKA is the leading cause of morbidity and
mortality in children with diabetes
• Strategies are required to prevent the
development of DKA
• In new-onset diabetes, DKA can be prevented
through earlier recognition and initiation of
insulin therapy
• Caution is necessary in management of
paediatric DKA due to increased risk of cerebral
edema
 Pathophysiology
• Hyperglycemia results from impaired glucose uptake
because of insulin deficiency and excess glucagon with
resultant gluconeogenesis and glycogenolysis.
• Glucagon excess also increases lipolysis with the
formation of ketoacids.
• Ketone bodies provide alternative usable energy sources
in the absence of intracellular glucose.
• The ketoacids (acetoacetate, β-hydroxybutyrate, acetone)
are products of proteolysis and lipolysis
• Hyperglycemia causes an osmotic diuresis that leads to
excessive loss of free water and electrolytes.
• Resultant hypovolemia leads to tissue hypoperfusion and
lactic acidosis
 DKA Criteria of diagnosis
• Hyperglycemia > 250 mg/dl
• Dehydration
• Ketonemia & Ketonuria
• Metabolic Acidosis
– pH < 7.30
– Bicarbonate < 18 mEq/L
 Degree of severity in DKA
Mild DKA Moderate DKA Severe DKA

Plasma glucose > 250 > 250 > 250

(mg/dL)
Arterial pH 7.25-7.30 7.00-7.24 < 7.00

Sodium Bicarbonate 15 – 18 10 - <15 < 10

(mEq/L)
Urine Ketones Positive Positive Positive

Serum Ketones Positive Positive Positive

Serum Osmolality Variable Variable Variable

(mOsm/kg)
Anion Gap > 10 > 12 > 12

Mental Status Alert Alert/Drowsy Stupor/Coma

 Clinical Manifestations
• Ketoacidosis is responsible for the initial
presentation in up to 25 – 75 % of children
– Early manifestations: vomiting, polyuria,
dehydration
– More severe: Kussmaul respirations,
acetone odor on the breath
– Abdominal pain or rigidity may be
present & mimic acute abdomen
– Cerebral confusion & coma ultimately
ensue
8
 Symptoms of DKA
• Polyuria
• Polydypsia
• Blurred vision
• Nausea/Vomiting
• Abdominal Pain
• Fatigue
• Confusion
• Coma
 Signs of DKA
• Dehydration
• Tachycardia
• Dry mucous membrane
• Delayed capillary refill
• Poor skin turgor
• Hypotension
• Kussmaul breathing
• Decreased sensorial mental status,
varies from sleepiness, drowsiness,
confusion, semi coma & coma
10
 Laboratory
• Blood glucose
• Urinary/plasma ketones
• Serum electrolytes
• BUN/Cr
• Osmolarity
• CBC, blood culture (if infection is
suspected)
• Venous blood gas
11
 Management
• Correction of the following:
–Dehydration
–Hyperglycemia
–Electrolytes deficits
– Metabolic acidosis
–Underlying precipitating factors
• Infection, omission of insulin,
stress, ….etc
12
 Management
• Fluids
– Avoid impending shock
– Rapid fluid replacement has been associate with
cerebral edema
– Usually necessary to help expand vascular
compartment
• Initially fluid bolus of 10 ml/kg over 30-60 minutes
• Followed by maintainace and deficit replacements
• Fluid deficit should gradually be corrected over 36-
48 hrs
• Start with NS, then to switch to dextrose 5% with
½ NS, when glucose drop to 250 mg/dl
13
 Management
• Insulin should be given through
intravenous route and continued till
acidosis and dehydration resolved
– Insulin drips 0.075- 0.1 U/kg/hr (NO
BOLUS)
– Gradual correction by reducing serum
glucose by 50-100 mg/dl/hr
– Serum glucose often falls after fluid bolus
due to increase in glomerular filtration with
increased renal perfusion
– When acidosis resolved to be shifted to
subcutaneous route
14
 Management
• Dextrose should be added to IVF
when serum glucose < 250 mg/dl
–Blood glucose levels often be
corrected prior to ketoacidosis
–Should not lower insulin infusion
unless, there is rapid correction of
serum glucose or profound
hypoglycemia
– Remember that intravenous insulin &
hydration is the treatment of
metabolic acidosis in DKA patients
15
 Management
Electrolyte replacements
• Potassium:
– Initially, might be false normal or high
values
– Should be added to fluids as soon as
insulin has been started
– Be sure of passing urine, prior of giving
pottasium
– Total body depletion will become more
prominent with correction of acidosis
– Continuous EKG monitoring is standard of care
– Dose of 30-40 mEq/L: in either KCl or KPhos
16
 Management
• Serum sodium and chloride will be corrected gradually
by giving normal saline or 0.45 NS over 48 hours.
• Serum potassium level, is the most important electrolyte
disturbance in patients with diabetic ketoacidosis.
• A patient with a low serum potassium level should be
assumed to have a potentially life-threatening total body
potassium level
• As a result of the potential for hypokalemia-induced
dysrhythmias, not to give insulin until potassium
replenishment is underway
 Management
• Phosphate
– Total body depletion will become more
prominent with correction of acidosis
– Theoretically, has to be corrected but
practically not necessary needed
–Hypophosphatemia may cause
rhabdomyolysis, hemolysis, impaired
oxygen delivery
– Calcium should be monitored during
replacement
18
 Metabolic Acidosis
• Ketosis and lactic acidosis produce a metabolic acidosis;
however, supplemental bicarbonate is not
recommended.
• Acidosis usually resolves with isotonic fluid volume
replenishment and insulin therapy.
• Only indicated in severe metabolic acidosis (pH < 7.0) or
patient is in chock with DKA
• Studies confirmed that bicarbonate therapy may cause
paradoxical intracellular acidosis, worsening tissue
perfusion, hypokalemia, and cerebral edema
 Management
• Bicarbonate is almost never administered
– Bicarb administration leads to increased cerebral
acidosis:
– HCO3- + H+  dissociated to CO2 and H2O
– Bicarbonate passes the BBB slowly
– CO2 diffuses freely  exacerbating cerebral acidosis &
depression
• Indications for bicarbonate use: only in severe acidosis
leading to cardiorespiratory compromise

20
 Management of underlying cause
• In each case, we need to look for precipitating
factors
• Infections especially viral is the most common factor
• Using antibiotics should not be routine in children as
most are viral
• Presence of leukocytosis initially in DKA is due to
dehydration and stress (not usually indicates
infection)
• We need to improve education “sick-day
managements” in order to reduce number of DKA
episodes
 Complication, Cerebral Edema
• Cerebral edema: 0.5-3% of pediatric DKA
– Mortality rate of 20%
– Responsible for 50-60% of diabetes deaths in children
– Permanent neurologic disability rate of 25%
• Typically develops within the first 24 hrs of treatment
• Etiology is still unclear
• Signs & symptoms:
– Headache
– Confusion
– Slurred speech
– Bradycardia
– Hypertension
22
Risk Factors for Developing Cerebral Edema

• Younger age (<5 years)

• New-onset diabetes
• High initial serum urea
• Severe acidosis
• Rapid administration of hypotonic fluids
• IV bolus of insulin
• Early IV insulin infusion (within 1st hour of fluids)
• Rapid drop of glucose
• Usage of bicarbonate
 Cerebral Edema, treatment
• Lower intracranial pressure
– Mannitol or 3% saline
• Imaging to rule out other pathologies
• Hyperventilation & surgical
decompression are less successful at
preventing neurologic morbidity &
mortality

24
 other rare complications
• Thrombosis • Rhabdomyolysis
• Cardiac • Infection
arrhythmias – Aspiration
• Pulmonary pneumonia
edema – Sepsis
• Renal failure

25
 Wishing you
Best Success

View publication stats