Scribd
Upload
38 views26 pages

Diebetic Ketoacidosis DKA Amanuel

Uploaded by

sanbetoamalo89
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
38 views26 pages

Diebetic Ketoacidosis DKA Amanuel

Uploaded by

sanbetoamalo89
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 26

Presenter: Amanuel (R1)

Moderator: Ahmed (MD, Endocrinologist)

Yekatit 12 Hospital Medical College


Department of Internal Medicine
May 2021 1
Outline of presentation
 Introduction

 Epidemiology

 Pathogenesis

 Clinical manifestations

 Diagnosis

 Management

2
Introduction
 Acute metabolic complication of decompensated diabetes.
 A medical or diabetic emergency

 Triad of uncontrolled hyperglycemia, metabolic acidosis &


increased total body ketones characterizes DKA.

 It results from the combination of absolute or relative


insulin deficiency and an increase in counter regulatory
hormones.

 Most patients with DKA have autoimmune type 1 diabetes

 However, patients with type 2 diabetes are also at risk


during the catabolic stress of acute illness such as
trauma, surgery or infections.
3
Introduction

4
Epidemiology
 Recent epidemiological studies indicate that
hospitalizations for DKA in the U.S. are increasing.

 Responsible for more than 150,000 admissions per


year at an estimated annual direct medical expense
and indirect cost of 2.4 billion USD (CDC).

 Most patients with DKA were between the ages of 18


and 44 years (56%).

 45 & 65 years (24%), with only 18% of patients 20


years of age.

 Two-thirds of DKA patients were considered to have


type 1 diabetes & 34% to have type 2 diabetes.
5
Epidemiology
 50% were female, and 45% were nonwhite.

 Common cause of death in children and adolescents


with type 1 diabetes.

 Accounts for half of all deaths in diabetic patients


younger than 24 years of age.

 In adult subjects with DKA, the overall mortality is


1% (much lower than HHS).

 However, a mortality rate 5% has been reported in


the elderly and in patients with concomitant life-
threatening illnesses. 6
Pathogenesis

7
8
9
Clinical manifestations

10
Pathogenesis
Diagnostic criteria Mild Moderate Severe

Plasma glucose >250 >250 >250

Serum osmolality Variable Variable Variable

Urine or serum Positive Positive Positive


ketones

Arterial pH 7.25–7.30 7.00–7.24 <7.00

Serum bicarbonate 15-18 10-15 <10

Anion gap >10 >12 >12

Mental status Alert Alert/drowsy Stupor/coma


12
Diagnostic Studies in DKA
 CBC  Chemistry
 Leukocytosis   Glucose, A1C
 (infection vs
cortisolemia)   Bicarbonate
  Anion gap (HAGMA)
 Amylase/Lipase   Creatinine (dehydration~ATN)
 To evaluate for   K+ (early) ~  K+ (late)
pancreatitis   Na+ (pseudo-hyponatremia)
 DKA by itself
can also  Serum ketones (sens. & spec.)
increase them  Positive
(glycerol)  Urinalysis ~ Nitroprusside assay
• Ketones (for DKA); Leukocyte
 EKG and Troponin esterase, WBC (for UTI)
 Evaluate for
possible MI, K+  CxR (PA), cultures if indicated13
14
Steps in managing DKA
 Airway

 Breathing

 Circulation

 Disability

 Exposure

 Definitive management of DKA

 Discharge and follow-up 15


Definitive management of DKA
 Baseline Ix

 Volume

 Insulin

 Potassium

 Identify and treat precipitating cause (the 7 I’s)

 Treat complications if any

 Monitoring
16
Goals: DKA management
 Treatment goals:
 BG: 150-200 mg/dL
 Serum bicarbonate ≥15 mEq/L
 Venous pH > 7.3
 Calculated AG ≤ 12 mEq/L
 K+ level = 4-5 mEq/L

 Resolved DKA: when BG< 200 mg/dL and 2 of the above


criteria have occurred.

 Euglycemic DKA: occurs when the patient presents with


acidosis and ketosis but has a glucose ≤200 mg/dL, has
become an emerging concern. 17
18
19
Pitfalls in DKA management
1. Inconsistencies in the maintenance (IV fluid and IV
insulin) and transition phases of DKA management.

2. Untimely discontinuation of IV insulin prior to AG


normalization

3. Insufficient dosing of SC insulin


 Risk for recurrent hyperglycemia and rebound DKA
 Administering SC basal insulin early in the course of DKA
management has been investigated as a feasible and effective
method for preventing rebound hyperglycemia.

4. False negative and false positive urinary ketones


 The preferred laboratory value to examine for DKA is serum
beta-hydroxybutyrate.
 In DKA, the ratio of the hydroxybutyrate to acetoacetate or
acetone changes in response to the increased ketones.
20
Possible Complications of DKA
 The majority of the complications are DKA treatment-related.

 Electrolyte disturbances (mainly due to urinary loss)


• Low serum levels (Na+, K+, Mg2+ and phosphate)

 Cerebral edema Vs hypoglycemia


 Rare, but life threatening unless treated
 Usually in children & adolescent patients
 Symptoms: Headache, altered mental status
 Treat with mannitol, hyperventilation (MV)

 Shock, myocardial infarction, VTE, cardiac arrhythmias,


pulmonary edema/ARDS, hemolysis and myoglobinuria 21
22
References

23
Newer Concepts about DKA
• Focus on ketones & acidosis
• Bedside monitoring of blood ketones 3-BHBA
• Use venous pH rather than arterial
• Cautious fluid replacement in children and young adults, CHF, CRF, Elderly,
Pregnant
• S/C long acting insulin should be continued
• Metabolic treatment targets
- Decreased blood ketone by 0.5 mmol/hr
- Decrement of RBS by 50-75 mg/dL/hr
- Increased HCO3 by 3 mmol/hr
- K+ between 4.0 & 5.0 mmol/L
Points to remember
• Leukocytosis (up to 12,000/mm3) may be present without infection
• Leukocytosis > 12,000/mm3 is indicative of infection
• Fever may be absent in the presence of infection
• Generalized abdominal pain with severe acidosis – not necessarily
indicative of abdominal process
• Focal abdominal pain with less severe acidosis is indicative of abdominal
process
• A high amylase level – unreliable indicator of acute pancreatitis
• High serum glucose levels may lead to dilutional hyponatremia
Points to remember (Cont’d)
• High triglyceride levels may lead to factitious low glucose levels
• High levels of ketone bodies may lead to factitious elevation of creatinine
levels
• No direct correlation exists between the degree of acidosis,
hyperglycaemia, and the disturbances in the level of consciousness
• Avoid hypoglycaemia during the course of DKA management – rebound
ketosis
• Avoid precipitous fall of BS in the first few hours – cerebral oedema

You might also like