Diabetes Emergencies and High Glucose States Flashcards
Definition of Diabetic Ketoacidosis (DKA)?
Disordered metabolic state that occurs in the context of an absolute/relative INSULIN DEFICIENCY accompanied by an increase in the counter-regulatory hormones, e.g: glucagon, adrenaline, cortisol and growth hormone
In which types of diabetes can DKA occur?
By definition, can occur in both Type 1 and Type 2 diabetes
Pathophysiology of DKA?
Absolute/relative insulin deficiency causes stress hormone activation:
• Increased lipolysis
This causes increased free fatty acids to the liver and increased KETOGENESIS , leading to acidosis
- Decreased glucose utilisation
- Increased proteolysis
- Increased glycogenolysis
These cause hyperglycaemia, leading to glycosuria (causes electrolyte loss and dehydration)
Main problems in DKA?
There is an acidosis and a degree of hyperosmolarity (this is larger in HHS)
Consequences of DKA in pregnancy?
High risk of fetal loss
Biochemical diagnostic factors in DKA?
Ketonaemia >3 mmol/L or significant ketonuria (>2+ on standard urine stick)
Blood glucose >11.0 mmol/L or known diabetes (the BG is high but not too high in DKA)
Bicarbonate <15 mmol/L or venous pH <7.3
Common precipitants of DKA?
- Infection
- Illicit drugs and alcohol
- Non-adherence with treatment (majority)
- Newly diagnosed diabetes
Types of symptoms and signs of DKA?
Osmotic-related
Ketone-body raised
Assoc. conditions
Osmotic-related symptoms in DKA?
Polyuria and polydipsia
Dehydration
Symptoms of raised ketone bodies in DKA?
- Flushed
- Vomiting
- Abdominal pain and tenderness
- Breathless (Kussmaul’s respiration as they try to correct acidosis)
- Ketone body smell on breath (not everyone can smell these)
Conditions assoc. with DKA?
Underlying sepsis
Gatroenteritis
True coma virtually never occurs
What is euglycaemic DKA?
DKA that occurs at lower than expected or even normal blood glucose levels
Classic glucose levels at DKA presentation?
Median level around 40 mmol/L (normal in a non-diabetic is <6 mmol/L)
This can vary from 10 (e.g: in euglycaemic ketosis) to 100 mmol/L
Classic potassium levels at DKA presentation?
Usually raised to > 5.5 mmol/l; be more wary of the low normal than a high level
Classic creatinine at DKA presentation?
Often raised
Classic sodium levels at DKA presentation?
Often reduced
Classic lactate levels at DKA presentation?
Raised lactate is very common
Classic blood ketones at DKA presentation?
Usually raised to >5:
- Blood measure - β-hydroxybutyrate
- Urine measure (obsolete) - acetoacetate
Other biochemistry at DKA presentation?
Bicarbonate (<10 in the most severe cases)
Amylase is frequently raised but this does not always indicate pancreatitis (can be salivary in origin)
WCC (if it is raised, it does not always indicate infection)
How much fluid loss can occur in DKA?
Variable but can lose up to 12 litres (even higher in HHS)
Risks in DKA to consider?
If the person is semi-conscious, is there an aspiration risk? (consider an NG tube)
Is potassium concerning?
Could the patient be septic?
What is the thromboembolic risk?
Complications of DKA in adults?
Hypokalaemia (can cause cardiac arrest)
Aspiration pneumonia
ARDS (can be a consequence of DKA treatment)
Gastric dilatation
Co-morbidities
Complications of DKA in children?
Cerebral oedema (tends not to occur in adults)
Principles of Mx of DKA?
Replace losses:
- Fluid - initially with 0.9% NaCl; once glucose falls to 15, switch to dextrose
- Insulin
- Potassium
- Phosphate (rarely and bicarbonate (almost never replaced as this would drive more K+ into cells)
Address risks:
- NG tube, if required, to reduce aspiration risk
- Monitor K+
- Prescribe prophylactic LMWH
- If there is sepsis, find the cause (do a CXR, blood culture, etc)
How does insulin deficiency cause DKA?
This switches metabolic balance in a catabolic direction
Liver produces glucose via gluconeogenesis and glycogenolysis; fat in adipose tissue is reduced to triglycerides and fatty acids, by lipolysis, and muscle is degraded to release protein (for gluconeogenesis)
Ketone body levels rise, as does the glucose levels which:
- Increases urine production as it passes the renal threshold (osmotic diuresis)
- Increased losses of electrolytes via urine • Metabolic acidosis
What is Kussmaul respiration?
Involuntary attempt to remove CO2 from the blood that would otherwise form carbonic acid and further worsen ketoacidosis
Methods of monitoring ketones?
Blood ketone testing (using optium meter) - measures β-hydroxybutyrate (<0.6 mmol/l is normal)
Urine ketone testing - measures acetoacetate and this indicates levels of ketones 2-4 hours prior
Limitations of urine ketone testing?
Ketonuria persists after clinical improvement, due to mobilisation of ketones from fat tissues
When is hospital admission indicated in T1DM?
- Inability to tolerate oral fluids
- Persistent vomiting
- Persistent hyperglycaemia
- Persistent +ve/increasing levels of ketones
- Abdominal pain/breathlessness
What is Hyperglycaemic Hyperosmolar Syndrome (HHS)?
Hyperglycaemic causes severe dehydration, increases in osmolarity and a high risk of complications, coma and death; diagnosed on features of:
- Hypovolaemia
- Marked hyperglycaemia (without significant ketonaemia or acidosis)
- Osmolarity
It is less common than DKA but the two may present as a mixed picture
Typical features of HHS?
Diabetes can be known but is often not; if it is known, the the treatment is DIET ALONE, i.e: they are not taking drugs for it
Tends to occur in older individuals; for younger patients, it tends to be in non-Caucasian groups
High refined CHO (carbs) intake pre-event
Risk assoc. with HHS?
CV event, e.g: stroke or MI
Sepsis
Drugs like glucocorticoids and thiazide diuretics
Typical biochemistry in HSS?
- Higher glucose than in DKA (~60)
- Significantly elevated osmolarity
- Significant renal impairment
- Na+ may be raised
- Less ketonaemic/acidotic than in DKA
How to calculate osmolarity?
Osmolarity = 2 x (Na + K) + Urea + Glucose
Normal osmolarity?
285 to 295
Compare DKA and HHS?
Differences in treatment of HHS compared to DKA?
- Fluids - used more cautiously as there is a higher risk of fluid overload
- Insulin - used slowly as more sensitive; they may not require any insulin
- Sodium - avoid rapid fluctuations; may consider 0.45% saline (this is halved)
- Co-morbidities more likely - screen for vascular events and sepsis; LMWH is given to all unless contraindicated
Principles of management of HHS?
- Measure/calculate osmolarity frequently
- Assess dehydration severity and use 0.9% saline for fluid replacement WITHOUT insulin (lowers BG to reduce osmolarity)
- Monitory and chart BG, osmolarity and sodium
- Start low dose IV insulin only if significant ketonaemia or ketonuria at presentation OR if BG is falling
- Assess for complications of therapy, e.g: fluid overload, cerebral oedema
- Commence prophylactic anticoagulation
- Identify underlying precipitants, e.g: sepsis, and treat
- Protect heels and check for foot ulcerations daily (CPR for feet)
Production and clearance of lactose?
Originates from rbcs, skeletal muscle, brain and renal medulla; it is the end-product of anaerobic metabolism of glucose
Clearance requires hepatic uptake and aerobic conversion to pyruvate then glucose
Problems with diagnosing lactic acidosis?
Distinguish between hyperlactataemia and lactic acidosis
Normal range of lactate?
0.6-1.2 mmol/L; once >5 mmol/L, lactic acidosis starts to develop
Variability in lactate levels?
Lowest in fasting state In severe exercise, can rise 10 mmol/L
Types of lactic acidosis and causes of each type?
Type A (majority) - assoc. with tissue hypoxaemia:
- Infarcted tissue, e.g: ischaemic bowel
- Cardiogenic shock
- Hypovolaemic shock, e.g: in sepsis (endotoxic shock), haemorrhage
Type B (rare) - may occur in:
- Liver disease
- Leukaemic state
- Assoc. with diabetes, e.g: metformin, severe illness or renal failure
- Rare, inherited metabolic conditions if they are well and non-diabetic
Symptoms and signs of lactic acidosis?
Hyperventilation
Mental confusion
If severe, stupor or coma
Biochemistry findings in lactic acidosis?
Reduced bicarbonate
Raised anion gap
Variable glucose (often raised)
Absence of ketonaemia
Raised phosphate
What is the ion gap?
[Na + K] - [HCO3 + Cl): normal range is 10-18 mmol/L
-vely charged proteins, sulphate, phosphate and some organic acids make up the difference
Uses of the ion gap?
Determining the cause of an acidosis, i.e: conditions with a normal anion gap and those with a high anion gap
Other causes of lactic acidosis?
- DKA
- Starvation
- Uraemia
- Alcohol, ethylene glycol, methol, salicylate (aspirin) or paraldehyde poisoning
Treatment of lactic acidosis?
Treat underlying conditions with fluids and/or antibiotics
Withdraw offending medications
Can also give high-dose vitamins
Summary of the different metabolic emergencies:
- Glucose
- Ketones
- Dehydration
- pH
- SOsm ?
