Diabetic Ketoacidosis

Introduction

Diabetic Ketoacidosis (DKA) is a life-threatening diabetic emergency that consists of the biochemical triad of;

  1. Hyperglycaemia (BM > 11)

    • Insulin deficiency leads to increased ­glucagon and glycogenolysis which causes hyperglycaemia

  2. Ketonaemia (capillary blood ketones >/= 3)

    • Increased lipolysis leads to increase in fatty acids that are broken down to ketones

  3. Acidaemia (pH < 7.3)

    • Accumulation of ketones cause metabolic acidosis

Hyperglycaemia, vomiting that is often associated with DKA and decreased PO intake can result in severe associated fluid and electrolyte derangement

 

DKA can occur in a known Type 1 Diabetic often secondary to an acute illness/infection or as in this case, it can be the first presentation of the disease.

Clinical Features

 

Symptoms

  • Nausea & Vomiting, Abdominal Cramps

  • Polyuria & Polydipsia

  • Lethargy, Fatigue

  • Symptoms of concurrent illness e.g. gastroenteritis, LRTI

Signs

  • Appearance

    • pale, lethargic, dry, ketotic smell on breath (pear drops)

  • Abnormal Vitals

    • Tachypnoea (Kussmaul’s Breathing)

    • Tachycardia, hypotension (if severe dehydration) altered conscious state, hypoxia = all indicate severe DKA

  • Oliguria/Anuria

  • Signs of concurrent illness e.g. chest sepsis etc

Complications

  • Cerebral oedema

    • esp in paediatrics due to overly quick correction of dehydration and electrolyte abnormalities

  • Severe Acidosis, severe hypokalaemia leading to arrhythmia and death

  • Acute MI or Stroke in older people

 

Differential Diagnosis

 

Other Causes of Metabolic Acidosis

  • Starvation or Alcohol Ketoacidosis

  • Lactic Acidosis

    • organ hypoperfusion or infarction, Liver injury

  • Toxins

    • e.g. methanol, ethylene glycol, iron, aspirin

  • Renal failure causing uraemia

Other Causes of Hyperglycaemia

  • Hyperosmolar Hyperglycaemic state

    • occurs in older pts. Normal pH & ketones

  • Endocrine

    • Steroids. Cushings disease. Glucagonoma,

  • Acute rise in BM due to other critical illness

 

Clinical Investigations

 
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Bedside

  • Capillary BM + Ketones

    • helps make diagnosis and track response to treatment

  • VBG

    • low pH + bicarbonate. Confirms diagnosis. Low PCO2 due to respiratory compensation. High K. Low Na.

    • Patient will need hourly VBGs while being treated for DKA

  • Urine BHCG in all women of child bearing age

  • Urine dipstick

    • ketonuria. May be evidence of concurrent UTI

  • ECG

    • Changes due to High/Low Potassium. Evidence of Myocardial infarction

 
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Laboratory

  • FBC – often a leucocytosis

  • U&E

    • AKI.

    • Potassium usually high initially due to acidosis and lack of insulin driving it into the cells. Drops quickly once treatment is started and patient will need K replacement

  • LFT, CRP & Blood cultures if ? sepsis as underlying source

  • MSU if ? urosepsis

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Radiology

  • CXR if ? Chest sepsis

  • Other imaging as indicated by clinical condition

 

Management & Disposition

Initial Resuscitation

  • DKA patients should be managed in resus with close haemodynamic monitoring

  • Attention to ABC as clinically indicated

Specific Treatment

Following initial resuscitation the treatment priorities are;

  1. Fluid Replacement

  2. Insulin Therapy

  3. Careful monitoring of potassium levels

  4. Seek and treat any underlying illness

 

Every hospital has a DKA protocol. Follow it. Your aim is;

  1. Fall in blood ketones of no more than 0.5 per hour

  2. Maintain serum K within normal range

  3. Avoid Hypoglycaemia

 

Fluid Replacement

  • 1L 0.9% N Saline over 1 hour. Or faster if shocked

  • Will usually need at least another 3 L of N saline (+/- with K replacement) over next 8 hours

Insulin Therapy

  • IV infusion of short acting insulin (actrapid) titrated to blood sugar.

  • When BM is < 14 start concurrent IV Dextrose infusion as insulin infusion needs to continue until pH has normalised and ketones are cleared

Monitor Potassium Levels

  • Once Potassium is < 5mmol/L, 40mmol of KCL should be added to 0.9% N Saline infusion.

    • Max K infusion rate is 20mmol per hour.

Disposition

  • Endocrine Team should be involved early in all patients with DKA and these patients should ideally be admitted under their care

  • Severe DKA should be referred to critical care for admission to HDU until metabolic derangement resolves

References

  1. Brown A, Cameron P. Chapter 11.2 Diabetic Ketoacidosis and Hyperosmoloar Hyperglycaemia State. Textbook of Adult Emergency Medicine. 4th Edition

  2. SJH Prescriber Capsule. Endocrinology. Diabetic Ketoacidosis.

    This blog was written by Dr Deirdre Glynn and was last updated in December 2020

 Before you go have another look at the clinical case and see have your answers to any of the questions changed and if so how?