DKA and HONK Flashcards
What is DKA?
Who gets it and why?
Diabetic ketoacidosis
Patients with undiagnosed T1DM
Patients with T1DM who miss insulin doses or are unwell with D+V, infection, trauma
Describe pathophysiology of DKA
No insulin produced
So no glucose can get into cells, it’s all in the blood
So you get hyperglycaemia
But the cells aren’t getting any glucose, so are telling the body they need energy
They body responds by producing energy via gluconeogenesis using fat
Fat –> glyerol + fatty acids
The fatty acids are used by the cells for energy, the byproduct is ketones
Ketones result in acidaemia resulting in metabolic acidosis
What’s the triad of DKA?
Hyperglycaemia
Ketonaemia
Metabolic adiosis
Presentation of DKA?
Nausea, vomiting Abdo pain Reduced consciousness Seizures Shock: tachyC, P, hypotension Polyuria Dehydration: dry mucous membranes, slow CRT
Investigations of DKA?
BMs
Bloods: hyperglycaemia, hyperkalaemia or hypo, ketones
ABG: metabolic acidosis, pH below 7.3
What would indicate a case of DKA is very serious?
Blood ketones over 6 mmol/L
Bicarbonate level below 5 mmol/L
Venous/arterial pH below 7.0.
Hypokalaemia on admission (under 3.5 mmol/L)
Glasgow coma scale (GCS) less than 12.
Oxygen saturation below 92% on air
Systolic BP below 90 mm Hg.
Pulse rate over 100 or below 60.
Management of DKA?
IV NaCl 0.9% bolus (x2) 100ml/kg
Add K+ to this when urine output increases
Insulin actrapid 0.1um/kg/hr
Dextrose 5% when glucose falls
Complications of DKA?
Acidosis + dehydration = shock = circulatory collapse = death
Hypo or hyperkalaemia = cardiac arrhythmias
Cerebral oedema
Pulmonary oedema
VTE
What is a complication that type 2 diabetics get?
HHS
Hyperosmolar hyperglycaemic state
Describe the pathophysiology of HHS?
Precipitated by illness (infection, dehydration) or not taking meds in a type 2 diabetic
Severe hyperglycaemia - glucose is osmotically active so water follows it
This increases osmolarity in blood, water leaves the cells to be with the glucose in the bloodstream
The kidneys are unable to reabsorb all the excess glucose in the blood, so lots of glucose is excreted. Lots of water follows this glucose to be excreted (polyuria) This is called osmotic diuresis
This leaves the person dehydrated, with high conc of glucose and other ions in the blood. This draws much of remaining water in cells out, leaving them dehydrated
When this happens in brain can be really bad
Presentation of HHS?
Over a few days Often precipitated by illness Fatigue Weight loss Polyuria and polydypsia Dehydration Reduced consciousness, confusion Focal neurological deficit Seizures Coma
Investigations of HHS?
Urinalysis ++ glucose
Severe hyperglycaemia (30+)
High serum osmolality
Bloods: renal function and electrolytes
No ketones, no acidosis on ABG
Why is there no ketoacidosis in HHS?
In type 2 diabetes there is still insulin produced, which prevents the body turning to gluconeogenesis using fat (which is what produces the ketones)
Management of HHS?
ABCDE
IV 0.9% NaCl
Aim for fall in blood glucose by 5mmol/L/hour
Replace lost electrolytes
If fluid no longer lowering glucose, use insulin
Encourage drinking as soon as able
Treat underlying cause
Complications of HONK?
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