DIABETIC KETOACIDOSIS

1. First Line Management of
Adult Diabetic Ketoacidosis
Patients
OLEH: IKA LUKITA SARI
PEMBIMBING: dr Zakaria Mustari, Sp.PD,
FINASIM

2. Diabetic Ketoacidosis (DKA)
It is a life threatening but reversible complication of
type 1 diabetes due to absolute insulin deficiency. and
the unopposed action of counter-regulatory hormones,
such as glucagon, cortisol, and catecholamines
signed by trias hyperglycemia, acidosis, and ketosis
Ketoacidosis: High anion gap metabolic acidosis due to
excessive blood concentration of ketone bodies
(Ketoanion).

3. Factors that may contribute to
DKA
• Infections, acute medical illnesses involving the
cardiovascular system (myocardial infarction, stroke)
•gastrointestinal tract (bleeding, pancreatitis), diseases
of the endocrine axis (acromegaly,Cushing s‟
syndrome), and stress of recent surgical procedures
can contribute to the development of DKA by causing
dehydration, increase in insulin counter-regulatory
hormones, and worsening of peripheral insulin
resistance.

4. Cont...
• Other factors that may contribute to DKA include
psychological
•problems, eating disorders, insulin pump malfunction,
and illegal substance use.
•It is now recognized that new-onset type 2 diabetes
mellitus can manifest with DKA

5. Material and Method
Literature search
•Data Sources:electronic databases were searched:
MEDLINE (including MEDLINE in-process), CINAHL,
Embaseand the Cochrane Library (from 1980).
Internetsearch engines such as Google Scholar and
EMGoogle, a focused emergency medicine search
engine were also explored.
•Search terms diabetic ketoacidosis (DKA), insulin
therapy, bolus, adult, treatment guideline, and beta-
hydroxybutyrate +/complications

6. Data extraction
Study selection and eligibility criteria
• Full text articles and studies conducted in English
language.
•Abstracts were also be included to assess variety of
treatment guidelines and outcomes.
•Study Type: Meta-analysis, practice guidelines,
systematic review, and randomized control trials in line
with the study end point.
•Population: Adults > 18 years old as this protocol will
primarily be used for adults.

8. Clinical features of DKA
A-Symptoms of DKA:
1-Classic symptoms of hyperglycemia: short period of time:
Polyuria, polydipsia, wt loss and thirst.
2-Other symptoms:
- General weakness, malaise and lethargy.
-Nausea, vomiting and abdominal pain.
-↓ Perspiration.
- Disturbed consciousness and confusion.
3-Symptoms of underlying infections or other conditions;
fever, abdominal pain, dysuria, chest pain…etc.•

9. B- Physical signs of DKA:
a-General signs: Ill appearance and disturbed consciousness.
b-Signs of dehydration:
-Skin: Dry, hot, flushed, and loss of skin turgor.
-Tongue: Dry (sometimes woody tongue).
-Eyes: Sunken eyes and dark circles under the eyes.
c-Vital signs:
-Tachycardia, hypotension and tachypnea.
d-Specific signs:
-Ketotic breath: A strong, fruity breath odour
(similar to nail polish remover or acetone).
-Acidotic breath (Kussmaul's respiration): deep and
rapid.
-Abdominal tenderness.

10. DIAGNOSIS OF DKA

11. Complications of DKA
1-Complications of associated illnesses e.g.
sepsis or MI.
2-Adult respiratory distress syndrome.
3-Thromboembolism (elderly).
4-Complications of treatment:
a-Hypokalemia: Which may lead to:
-Cardiac arrhythmias.
-Cardiac arrest.
-Respiratory muscle weakness.

12. b-Hypoglycemia.
c-Overhydration and acute pulmonary edema:
particularly in:
-Treating children with DKA.
-Adults with compromised renal or cardiac
function.
-Elderly with incipient CHF.

13. d-Neurological complications: Cerebral Edema.
-It occurs only in children with DKA.
-Very dangerous and increases mortality.
-The risk is related to the severity, duration and rapid
correction of DKA.
Mechanism: The brain adapts by producing intracellular osmoles
(idiogenic osmoles) which stabilize the brain cells from
shrinking while the DKA was developing. When the
hyperosmolarity is rapidly corrected, the brain becomes
hypertonic towards the extracellular fluids → water flows
into the cells → cerebral edema

14. Management of DKA
• The main lines of management include:
A-Primary assessment:
-Volume status and degree of dehydration.
-Blood pressure and cardiac condition.
-Degree of consciousness.
-Degree of acidosis.
-Precipitating disease

15. B-Ongoing monitoring:
-Blood glucose (using glucometers) every
hour.
-Electrolytes and pH every 4 hours.
-Urine for glucose and ketones every 4 hours

16. TREATMENT OF DKA
Fluid Resuscitation
•Fluid resuscitation is one of the key elements in
the treatment of DKA as intravascular,
intracellular, and interstitial volumes are all
reduced in hyperglycemic crisis.
•The aim to treatment of DKA is to restore
circulating volume, reduce blood glucose levels,
correct any electrolyte imbalances and to
reduce ketone levels therefore correcting
acidosis.

17. Type of fluid
The ADA recommends emergency guidelines will recommend
initial fluid resuscitation of 1.5 liters 0.9% normal saline bolus
within the first hour followed by 0.45% NaCl at 250-500
mL/hr, with 0.9% NaCl used in cases with hyponatremia
• Advantages:
-Available all the time.
-Rapid expansion of extracellular compartment.
-Slow decline of extracellular osmolarity.
-Slow rate of cerebral edema evolution.
• Disadvantages: May accentuate hypernatrimia if present.
• Indications:
-All cases of DKA.

18. Maintenance Fluid
• Recommendations on fluid maintenance varied among authors. Chaithongdi et al.
has recommended that the fluid replacement goal should be met within 12-24
hours, while Kitabchi et al.2 similarly recommends goals for fluid replacement
should correct estimated deficits within the first 24 hours. Kitabchi recommends
that 0.45% normal saline infused at 250-500 ml/hr is appropriate if corrected
serum
• sodium is normal or elevated; 0.9% normal saline at a similar rate if corrected
serum sodium is low (2009). Similarly, once glucose has fallen below
hyperglycemic levels, intravenous infusion is switched to a solution containing
glucose to facilitate the closure of the anion gap, such as D5W to avoid
hypoglycemia.

20. INSULIN THERAPY
• Treatment of hyperglycemia in DKA through an insulin drip is
a well-established treatment practice. In a Cochrane review,
Fisher, Shahshahani, &Kitabchi established that insulin falls
fastest in the first two hours in DKA with insulin given
intravenously, and that this is the preferred route.
• The data also confirmed the efficacy of low-dose insulin
therapy for DKA. Wagner et al. 27 established the use of very
low dose insulin treatment for DKA. The results of their study
indicated that very low dose insulin was useful to prevent the
rapid fall in blood glucose or rapid electrolyte displacement.

21. • Type of insulin : Regular : Rapid or short acting
insulin U-40 & U-100.
• Regimen:
Initial bolus: 0.1 U/kg body wt given IV.
Maintenance: 0.1 U/kg/body wt /hour:
a- IV Infusion set: Add 100 units of regular insulin
+500 ml saline i.e. every 5 cc fluid contains 1 unit
of insulin
b-IV infusion set is not available: IM route.

22. Sodium Bicarbonate
Due to the extreme acidosis that can result in metabolic pathways in DKA,
sodium bicarbonate has been considered in treatment to correct this pH
abnormality.
• Jearreat reported that sodium bicarbonate in DKA is controversial, and not
usually used. In a study done comparing sodium bicarbonate for metabolic
acidosis in DKA, the authors showed that the patients who received sodium
bicarbonate did not have improved glycemic control or clinical efficacy. There
was also evidence that the bicarbonate administration prolonged
hospitalization, as well as increased the risk for cerebral edema.
•In a review done by Kitabchiet al., it was reported that multiple studies done
have not shown any beneficial effects of using sodium bicarbonate, and they
do not recommend it in pH >6.9. However, in extreme acidosis with pH
values.

23. Potassium Therapy
• Initially: Mild to moderate hyperkalemia occur in
patients with DKA.
• Later on: After initiation of:
Insulin therapy
Correction of acidosis lead to hypokalemia.
Volume expansion & hydration

24. Rational of potassium therapy
• In the 1st
2 liters of fluid → add no potassium.
• If urine output confirmed → add KCl from 3rd
liter on.
If serum potassium:
< 3 mEq/L → add 20 – 40 mEq KCl/liter to IV saline.
3-5 mEq/L → add 10 – 20 mEq KCl/liter to IV saline.
> 5 mEq/L → add no potassium.
• Patient with oliguria or renal insufficiency: K levels must be
frequently monitored with continuous ECG evaluation.
• The infusion continues until the patient can tolerate oral
potassium supplement (15 CC potassium syrup/ 8 hours).

25. A Guide Protocol

26. 6-Order the rehydration program as follow (normal
saline):
– First 4 hours : 50% of the calculated total fluid deficit.
– Next time for up to 24h: 50% of the calculated total
fluid deficit.

27. CONCLUSION
• Timely first line management of DKA is very critical to save patients lives. It s crucial to‟ ‟
follow the correct guidelines in the emergency department is to expedite diagnosis, guide
treatment with evidence-based rationale, and improve continuity of care between the
emergency department and the ICU. Also, a treatment guideline will help to address gaps in
practice and provide a continuum of treatment between the emergency department and the
intensive care unit.
• Furthermore, a combination of communication techniques should be used and factors such
as socioeconomic status and level of heath literacy should be taken into account to ensure
the best outcome for the patient, and to prevent future readmissions with DKA. The
healthcare professional should ensure that they have the ability to provide support and
education to people at risk of developing DKA and those that have had an episode of DKA; it
is important to re-enforce the ongoing education to help reduce both the initial occurrence
and recurrence of this often preventable life-threatening condition.

28. Thank you