Diabetic Ketoacidosis

presented by Ng YH
Definition

• A state of absolute or relative insulin deficiency

• ↑counter regulatory hormone (glucagon, growth hormone, catecholamine-
epinephrine, cortisol)
• ↑gluconeogenesis ↑glycogenolysis, ⌧glucose utilisation by peripheral
tissues→→→Hyperglycemia→→→osmotic diuresis
• ↑lipolysis, ↑unrestrained fatty acid oxidation to ketone bodies→→→metabolic
acidosis

• Ketone bodies: acetone, acetoacetate, B-hydroxybutyrate

Reference
Ooi, S., Manning, P., & National University Hospital. (2004). Guide to the essentials in emergency medicine. Singapore: McGraw-Hill.
Ketone bodies
formation
Diagnostic criteria
• D-capillary Blood glucose ≥ 11mmol or diabetes history( To convert mmol/L to mg/dl, multiply by 18.)
• K-Capillary blood ketones >3mmol/L or urine ketones >2+
• A-pH <7.3 and/ or bicarbonate <15mmol/L / or wide anion gap

• Patients on SGLT-2 inhibitor may develop euglycemic DKA-eg. canagliflozin, dapa and empa
• —>why? (MOA: prevents glucose reabsorption from the proximal renal tubules, resulting in ↑glucosuria and ↓plasma glucose.

• Severity

• Mild ( Venous pH<7.3, HCO3<15mmol/L)

• Moderate ( Venous pH<7.2, HCO3<10mmol/L)
• Severe ( Venous pH<7.1, HCO3<5mmol/L)
Reference
Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic crises in adult patients with diabetes. Diabetes care, 32(7), 1335–1343. doi:10.2337/
Criteria for severe DKA
• HCO3 <5mmol/L
• Blood ketones>6 mmol/L
• Venous pH<7.1
• Hypokalemia on admission ( <3.5mmol/L)
• GCS<12
• Oxygen saturation <92% on air
• SBP<90mmHg
• HR>100 or <60 bpm
• Anion gap >16
**Anion gap= ( Na+K) –( Cl+HCO3)
Precipitating factors

• Type 1 diabetes mellitus, when insulin is interrupted (even for a few hours)

• Type 2 diabetes:
• S - Sepsis
• S - Surgery
• S - Sugar High (Missed insulin)
• S - Substances (Alcohol , Dope-morphine, heroin, marijuana)
• S - Stress
• Others- Pacreatitis/CVA/ACS/endocrinology causes
Symptoms & Signs of DKA
Symptoms Signs
• Polyuria •Dry mucous membranes
• Polydypsia •Cool peripheries
•Delayed peripheral perfusion
• Weight loss (type 1 DM) •Kussmaul breathing(ie, rapid,
• Nausea shallow breathing (sigh
breathing) —> as acidosis grows
• Vomiting more severe, becomes slower,
• Dyspnea deeper, and labored (air hunger)
•Ketotic breath //acetone smell
• Abdominal pain* breath
• Lethargy •Tachypnea
• Confusion •Drowsy
•Coma
• Loss of consciousness
• muscle cramp-?K
• Onset of symptoms can be very
rapid (within a few hours)
 • Many mechanisms have been suggested to underlie the abdominal symptoms
in DKA, namely gastroparesis(esophageal, gastric and gallbladder), rapid
expansion of the hepatic capsule, and mesenteric ischemia precipitated by
volume depletion. Although metabolic stabilization by itself often results in
clinical improvement, in up to 35% of the patients, the precipitant of DKA is
the underlying etiology of the abdominal pain (pancreatitis, hepatitis,
pyelonephritis, pelvic inflamma- tory disease, and gastritis) and surgery is
warranted in 6% of the cases (Fournier's necrotizing fasciitis, acute
cholecystitis, appendicitis and perineal abscess)
• abdominal pain has strong correlation with cause of acidosis and alchohol/
cocaine abuse

Reference
Umpierrez, Guillermo & Freire, Amado. (2002). Abdominal pain in patients with hyperglycemic crises. Journal of critical care. 17. 63-7.
10.1053/jcrc.2002.33030.
Kempegowda P, Chandan JS, Coombs B (2019). Regular performance feedback may be key to maintain good quality DKA management: results from a five-year
Initial treatment: IV fluid

• Most important treatment in diabetic ketoacidosis as mortality

usually results from hypovolemic shock

• Needs around 2-4 liters of resuscitation fluid in the first few hours

• Resuscitation fluid: use normal saline

• Maintenance fluid: use dextrose saline

• May require dextrose 10% to treat acidosis (with higher IV insulin

rate)
Initial treatment: Insulin infusion
• Initial rate at 0.1 units/kg/hour (e.g. 6 units per hour in a 60 kg patient)

• Aim for glucose reduction between 3-5 mmol/L to prevent cerebral oedema
resulting from rapid glucose reduction (especially in children)

• If sugar drops too fast, keep insulin rate but increase glucose rate instead

• If sugar drops too slow or if acidosis is persistent, increase insulin rate

• Continue fixed insulin rate until metabolic acidosis resolves, then can switch to
variable insulin

• DKA induces a transient heightened insulin resistance, and some patients might
require very high doses of insulin during the initial period
Initial treatment: Potassium
• Patients with diabetes ketoacidosis are universally depleted of
total body potassium (even if blood results shows hyperkalemia)

• Insulin treatment shifts potassium into cells, further worsening

hypokalemia

• Hypokalemia causes constipation, polyuria, paralysis, arrhythmia,

and death

• All patients with diabetes ketoacidosis should receive potassium

replacement as long as they have adequate urine output
Initial treatment: Potassium
• If patient is hyperkalemic, start insulin first then start potassium
replacement once serum potassium is less than 5 mmol/L (normal
3.5-5.3 mmol/L)

• If patient has no urine output, rehydrate the patient with IV fluid

until urine output is adequate, then start potassium replacement

• Patients with chronic renal failure may need more careful potassium
replacement

• If patient is hypokalemic, start potassium replacement at 10 to 20

mmol/hour (0.75 to 1.5g KCL per hour), then start insulin once
potassium > 3.3 mmol/L
Initial treatment: Monitoring
• Admit all patients to either ICU or HDW

• Indications for mechanical ventilation:

✤ Severe metabolic acidosis

✤ Hemodynamics instability

✤ Low GCS

✤ Multiorgan failure

• Monitor:

✤ Hourly: heart rate, blood pressure, capillary blood sugar, urine output

✤ 4-6 hourly: blood gas, potassium, venous blood sugar, ketones (urine or blood)
HDU admission and insertion of central
line in the following circumstances:

• Elderly
• Pregnant ladies
• Heart or kidney failure
• Other serious comorbidities
• Severe DKA
Treatment goals
• Ketonemia reduction > 0.5 mmol/L per hour

• Glucose reduction of about 3 mmol/L per hour

• Bicarbonate improvement by about 3 mmol/L per hour

• Potassium maintained within normal range

• Avoid hypoglycemia

Do not rely on bicarbonate alone to asses the resolution of DKA at this point
due to the possible hyperchloraemia secondary to high volumes of 0.9%
sodium chloride solution. The hyperchloraemic acidosis will lower the
bicarbonate and thus lead to difficulty is assessing whether the ketosis has
resolved. The hyperchloraemic acidosis may cause renal vasoconstriction
and be a cause of oliguria.

Reference
https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-
treatment?search=diabetic%20ketoacidosis&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H14
Initial treatment: Others
• Treat underlying infection/trauma/cardiovascular
event

• DVT prophylaxis with SC heparin or LMWH

• GI bleed prophylaxis with IV ranitidine or proton

pump inhibitors

• Most patients can continue oral feeding if they are

alert, otherwise start NG feeding
Subsequent treatments
• Once ketosis/acidosis resolves:

✤ Switch fixed insulin infusion to variable insulin infusion

✤ Switch dextrose 10% to dextrose saline

✤ No need to monitor ketone/blood gas

• Switching from IV insulin to SC insulin:

✤ Patient is taking orally well or on stable bolus NG feeding

✤ Acidosis resolved (pH > 7.3)

✤ Ketonemia resolved (serum ketone < 0.6 mmol/L)

Discharge plan
• All patients must be seen by diabetes nurse and dietitian

• All patients with type 1 DM must be on basal bolus insulin at discharge

• Most patients with type 2 DM should be on insulin at discharge

• Assess indications for statins, antiplatelets, antihypertensives prior to

discharge
Complications of DKA
• Lactic acidosis

✤ Prolonged dehydration/ shock/ infection/ tissue hypoxia

✤ Should be suspected in pt with refractory metabolic acidosis and a persistent anion gap
despite optimal therapy for DKA

• Arterial thrombosis

✤ Stroke/ MI/ ischaemic limb

• Cerebral edema

✤ More frequent in child>adults

✤ Due to overhydration with free water and excessively rapid correction of hyperglycemia

• Rebound ketoacidosis

✤ Due to premature cessation of IV Insulin / inadequate doses of SC insulin after IVI Insulin
has discontinued.
References

Ooi, S., Manning, P., & National University Hospital. (2004). Guide to the essentials in emergency medicine. Singapore: McGraw-Hill.

Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic crises in adult patients with diabetes. Diabetes care, 32(7), 1335–1343.
doi:10.2337/dc09-9032

Umpierrez, Guillermo & Freire, Amado. (2002). Abdominal pain in patients with hyperglycemic crises. Journal of critical care. 17. 63-7.
10.1053/jcrc.2002.33030.

Kempegowda P, Chandan JS, Coombs B (2019). Regular performance feedback may be key to maintain good quality DKA management: results from a five-
year studyBMJ Open Diabetes Research and Care;7:e000695. doi: 10.1136/bmjdrc-2019-000695

CPG 2015, Management of Type 1 DM in children and adolescents

CPG 2016, Management of Type 2 DM, 5th Ed.

https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-
treatment?search=diabetic%20ketoacidosis&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H14
Scenario
http://jknj.jknj.moh.gov.my/ncd/diabetes/12a-%20Diabetic%20Emergencies-DKA-Case%20Studies.pdf
Thank you