DKA Flashcards
Summarise DKA
Diabetic ketoacidosis is characterised by a biochemical triad of hyperglycaemia, ketonaemia, and metabolic acidosis, with rapid symptom onset.
Common symptoms and signs include increased thirst, polyuria, weight loss, excessive tiredness, nausea and vomiting, dehydration, abdominal pain, hyperventilation, and reduced consciousness.
Successful treatment includes correction of volume depletion, ketogenesis, hyperglycaemia, electrolyte imbalances, and comorbid precipitating events, with frequent monitoring.
Complications of treatment include hypoglycaemia, hypokalaemia, pulmonary oedema, and acute respiratory distress syndrome (ARDS).
Cerebral oedema, a rare but potentially rapidly fatal complication, occurs mainly in children. It may be prevented by avoiding overly rapid fluid and electrolyte replacement.
Define DKA
Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment. It is characterised by absolute insulin deficiency and is the most common acute hyperglycaemic complication of type 1 diabetes mellitus.
Describe the epidemiology of DKA
In England, the incidence of hospital admissions for DKA among adults with type 2 diabetes increased 4.24% annually between 1998 and 2013; hospitalisations for DKA in adults with type 1 diabetes increased from 1998 to 2007, and remained static until 2013
Describe the aetiology of DKA
In DKA, there is a reduction in the net effective concentration of circulating insulin along with an elevation of counter-regulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These alterations lead to the extreme manifestations of metabolic derangements that can occur in diabetes. The two most common precipitating events are infection and discontinuation of, or inadequate, insulin therapy. Underlying medical conditions, such as myocardial infarction or pancreatitis, that provoke the release of counter-regulatory hormones are also likely to result in DKA in patients with diabetes.[15] Drugs that affect carbohydrate metabolism, such as corticosteroids, thiazides, sympathomimetic agents (e.g., dobutamine and terbutaline), second-generation antipsychotics, immune checkpoint inhibitors, cocaine, and cannabis may contribute to the development of DKA.[1][16][17] The use of sodium-glucose co-transporter 2 (SGLT2) inhibitors has also been implicated in the development of DKA in patients with both type 1 and type 2 diabetes
Outline the pathophysiology of DKA
Reduced insulin concentration or action, along with increased insulin counter-regulatory hormones, leads to the hyperglycaemia, volume depletion, and electrolyte imbalance that underlie the pathophysiology of DKA. Hormonal alterations lead to increased gluconeogenesis, hepatic and renal glucose production, and impaired glucose utilisation in peripheral tissues, which results in hyperglycaemia and hyperosmolarity. Insulin deficiency leads to release of free fatty acids from adipose tissue (lipolysis), hepatic fatty acid oxidation, and formation of ketone bodies (beta-hydroxybutyrate and acetoacetate), which result in ketonaemia and acidosis. Studies have demonstrated the elevation of pro-inflammatory cytokines and inflammatory biomarkers (e.g., C-reactive protein [CRP]), markers of oxidative stress, lipid peroxidation, and cardiovascular risk factors with hyperglycaemic crises. All of these parameters return to normal following insulin and hydration therapies within 24 hours of hyperglycaemic crises. Elevation of pro-inflammatory cytokines, and markers of lipid peroxidation and oxidative stress, have also been demonstrated in non-diabetic patients with insulin-induced hypoglycaemia.[23] The observed pro-inflammatory and pro-coagulant states in hyperglycaemic crises and hypoglycaemia may be the result of adaptive responses to acute stress, and not hyperglycaemia or hypoglycaemia per se.[1][23][24] It has also been postulated that ketosis-prone diabetes comprises different syndromes based on auto-antibody status, HLA genotype, and beta-cell functional reserve
Describe the classification of severe DKA
The presence of one or more of the following may indicate severe DKA:[2]
Blood ketones >6 mmol/L Bicarbonate <5 mmol/L Venous/arterial pH <7.0 Hypokalaemia on admission (<3.5 mmol/L) Glasgow Coma Scale <12 [ Glasgow Coma Scale ] Oxygen saturation <92% on air (assuming normal baseline respiratory function) Systolic blood pressure (SBP) <90 mmHg Pulse >100 bpm or <60 bpm Anion gap >16 [ Anion Gap ]
Describe a case history for DKA
A 20-year-old man is brought to the accident and emergency department with abdominal pain, nausea, and vomiting with increasing polyuria, polydipsia, and drowsiness since the previous day. He was diagnosed with type 1 diabetes 2 years previously. He mentions that he ran out of insulin 2 days ago. Vital signs at admission are: BP 106/67 mmHg, heart rate 123 beats per minute, respiratory rate 32 breaths per minute, temperature 37.1°C (98.8°F). On mental status examination, he is drowsy. Physical examination reveals Kussmaul’s breathing (deep and rapid respiration due to ketoacidosis) with acetone odour and mild generalised abdominal tenderness without guarding and rebound tenderness. Initial laboratory data are: blood glucose 25.0 mmol/L (450 mg/dL), arterial pH 7.24, PCO2 25 mmHg, bicarbonate 12 mmol/L (12 mEq/L), WBC count 18.5 × 10⁹/L (18,500/microlitre), sodium 128 mmol/L (128 mEq/L), potassium 5.2 mmol/L (5.2 mEq/L), chloride 97 mmol/L (97 mEq/L), serum urea 11.4 mmol/L (32 mg/dL), creatinine 150.3 micromol/L (1.7 mg/dL), serum ketones strongly positive.
Describe some other presentations of DKA
It is now well recognised that new-onset type 2 diabetes can manifest with DKA. These patients are obese and have undiagnosed hyperglycaemia, impaired insulin secretion, and insulin resistance. However, after treatment of the acute hyperglycaemic episode with insulin, beta-cell function and insulin effects improve, so these patients are able to discontinue insulin therapy and may be treated orally or by diet alone, with 40% remaining insulin-independent 10 years after the initial episodes of DKA. These patients do not have the typical autoimmune laboratory findings of type 1 diabetes.[3] This type of diabetes has been labelled as ‘type 1 and 1/2’ or ‘type 1 and a half’ diabetes, ‘Flatbush’ diabetes, or ‘ketosis-prone’ diabetes. Conversely, an extreme hyperosmolar state similar to hyperosmolar hyperglycaemic state (HHS) has been reported in combination with DKA in type 1 diabetes
When should you consider DKA
Consider DKA in:
Patients with known diabetes who are unwell[2][17]
DKA is most common in people with type 1 diabetes but can also present in those with type 2 diabetes.[42][46][47]
Any patient with increased thirst, polyuria, recent unexplained weight loss, or excessive tiredness, AND any of the following:[17][48]
Nausea and vomiting
Abdominal pain[2][49]
Hyperventilation (Kussmaul’s respiration)[50]
Dehydration
Reduced consciousness.
What urgent tests should be done at the bedside
Urgently order a venous blood gas, blood ketones, and capillary blood glucose.[42]
These tests should be done at the bedside.
When should DKA be diagnosed
Diagnose DKA if:[51][17][47][52]
Blood ketones are ≥3.0 mmol/L OR there is ketonuria (more than 2+ on standard urine sticks) AND
Blood glucose is >11.1 mmol/L OR known diabetes
This blood glucose cut-off is recommended in the 2020 Joint British Diabetes Societies (JBDS) guideline “Diabetes at the front door” and supersedes the 11.0 mmol/L cut-off recommended in the 2013 JBDS guideline “The management of diabetic ketoacidosis in adults”.[42][52]
AND
Bicarbonate (HCO3-) is <15.0 mmol/L, AND/OR venous pH is <7.3.
When should you involve senior or critical care support
Ensure continuous cardiac monitoring and involve senior or critical care support if:[42][17]
There is persistent hypotension (systolic blood pressure <90 mmHg) or oliguria (urine output <0.5 ml/kg/hour) despite intravenous fluids
Glasgow Coma Scale <12 [ Glasgow Coma Scale ]
Blood ketones >6 mmol/L
Venous bicarbonate <5 mmol/L
Venous pH <7.0
Potassium <3.5 mmol/L on admission
Oxygen saturations <92% on air
Pulse >100 bpm or <60 bpm
Anion gap >16 [ Anion Gap ]
The patient is pregnant or has heart or kidney failure or other serious comorbidities.
Involve the specialist diabetes team as soon as possible and definitely within 24 hours
Describe some clinical features of DKA
Clinical presentation
Other features of DKA are:
Acetone smell on breath[17]
Smells like pear drops or nail varnish remover
Hypothermia[53]
Suspect sepsis as a precipitant if there is fever as this is not a feature of DKA. Sepsis may also cause hypothermia, however.
What should you ask about in the history of DKA
Ask about causes of DKA. These are:
Infection[17][47]
The most common causes are pneumonia and urinary tract infection.
Suspect sepsis as a cause of DKA if there is fever or hypothermia, hypotension, refractory acidosis, or lactic acidosis.[51]
Discontinuation of insulin (either unintentional or deliberate)[17][47]
Inadequate insulin
Due to:
Malfunctioning insulin pen or pump[54]
Degradation of insulin due to storage at incorrect temperature.[55]
New onset of diabetes[17]
Acute illness
Common causes include myocardial infarction, sepsis, and pancreatitis.[47][15][30]
Physiological stress
This includes:
Pregnancy[17]
Trauma[56]
Surgery
Drugs[17] Corticosteroids[57] Thiazides Sympathomimetics[26] Second-generation antipsychotics[58] Immune checkpoint inhibitors[59] Cocaine, cannabis, and acute intoxication with alcohol[56][60] Sodium-glucose co-transporter 2 (SGLT2) inhibitors.
What should you look for upon examination
Examine the chest:
Look for hyperventilation (Kussmaul’s respiration).[17]
Auscultate for crepitations or reduced air entry.
This may indicate pneumonia as a cause of DKA or pulmonary oedema.
Monitor for pulmonary oedema. This typically occurs several hours after treatment is started and can occur even in patients with normal cardiac function.[42][17]
Assess for signs of dehydration:[17]
Dry mucous membranes Decreased skin turgor or skin wrinkling Slow capillary refill Tachycardia with a weak pulse Hypotension.
Assess conscious level hourly using the Glasgow Coma Scale to monitor for cerebral oedema.[42][ Glasgow Coma Scale ]
Signs include headache, irritability, slowing pulse, rising blood pressure, reducing conscious level. These may occur several hours after starting treatment.[51][61]
Involve immediate critical care input and give mannitol.[62]
Examine the abdomen
Look for an intra-abdominal cause of DKA such as pancreatitis.[47][15][30]
However, DKA commonly causes abdominal pain and may be mistaken for an acute abdomen.[63]
Check the patient’s feet to look for new ulceration or infection.[64]
Check the patient’s skin for rashes, signs of cellulitis, or open wounds that may have precipitated DKA.
