Pt w/ Glucose disturbance Flashcards
In which group of patients does DKA occur?
T1DM
Pathophysiology of DKA?
What are the clinical features of DKA?
Pathophysiology of DKA
-too much glucose>body uses up all insulin>intracellular lack of glucose>break down fatty acids>ketones>acidemia>vomiting (to try and lose H+)>dehydration> electrolyte inbalance
VARIABLE
- Polyuria and Polydipsia are important hx factors (has lead to dehydration over past few days)
- Signs of dehydration
- Sweet smelling breath
- Weight loss and weakness
- Hyperventilation - respiratory compensation for the metabolic acidosis - Kussmaul’s respiration (deep and sighing)
- Abdominal pain (DKA can be an acute abdomen)
- Vomiting (this makes dehydration worse)
- Confusion and coma
- Low BP (due to acidosis and dehydration)
What investigations should you do if you’re considering DKA?
Bedside tests
- Urine (ketones strongly positive. Note may be raised in starvation)
- Septic screen (urine and blood cultures)
Bloods BLOOD GLUCOSE (usually high but might be low in severe academia) ABG - assess degree of metabolic acidosis (↓pH, ↓HCO3-, often ↓CO2 due to compensation
Plasma ketones
FBC - WCC might be up in infection
U+E (look for AKI)
Imaging
-CXR (to check for cause
Special tests
-Determine cause
What is required for diagnosis of DKA?
D -Diagnosis of diabetes or BG >11mmol/L
K -Ketones (blood finger prick ketone >3mmol/L or urine ++)
A -Acidosis on ABG (<7.3 or bicarb <15)
note: patients on SGLT2 inhibition’s (flozin) may be euglycemic
What are some common precipitants of DKA?
Infection, non-compliance with treatment, Newly diagnosed diabetes, stress
What are the two main principles of DKA management?
REHYDRATION AND INSULIN THERAPY
Describe DKA management (5 steps)
DKA MANAGMENT
Place 2 wide bore cannulas and start fluid replacement through one (0.9% NaCl)
-NG tube (to prevent aspiration-big cause of death)
1) FLUIDS 0.9% NaCl (1,2,2,4)
-Consider initial bolus 500ml if hypotensive BP <90
-When BP over 90 start 1224 Regime:
1L over 1hr → 1L over 2hr → 1L over 2hr → 1L over 4hr
2) INSULIN THERAPY
- IV infusion of insulin ACTRAPID
- soluble insulin mixed with NaCl (e.g. 50U in 50ml)
- concentration of 1 unit/mL
- at fixed rate of 0.1units/kg/hr
3) POTASSIUM
-Add 40mmol KCL AFTER first bag if potassium <5.5mmol/L ‘pre empt’
(NB: must never give >20mmol K+ over 1 hr, thats why you give in 2nd bag-slower 2 hourly rate)
4) GLUCOSE
- once the blood glucose level falls to 14mmol/l, give 10% dextrose (rate of 1L 8 hourly)
- give alongside fluids and insulin (do not stop insulin)
5) TREAT CAUSE
- due to stress (infection/PE/poor compliance/wrong dose insulin)
Why do we need to replace potassium in DKA management?
When do we replace potassium?
- Insulin will cause potassium to shift into intracellular compartment
- do not give potassium replacement in first litre or if serum potassium is >5.5mmol/L but consider giving after
*can also cause hypomagnesium
What are the targets for the insulin therapy?
How often should you check these targets?
TRAGETS DKA
- Blood ketones should drop by 0.5 mmol/litre/hour -Blood-glucose concentration should fall by at least 3 mmol/litre/hour (Give 10% dextrose when BG<14mmol/L
- Monitor blood-ketone and blood-glucose concentrations HOURLY and adjust the insulin infusion rate accordingly.
What should you monitor throughout DKA management?
Cap glucose, ketones and urine output, serial VBGs
Consider arterial line for regular ABGs
How long do we give IV insulin therapy for in DKA?
What do we do when it is done?
STOPPING DKA THERAPY CRITERIA: (different to start)
- capillary blood ketones <0.6mmol/L
- Venous pH >7.3
- AND nd the patient is able to eat and drink
*ideally give SC fast-acting insulin and a meal, and stop the insulin infusion 1 hour later.
What complications are associated with DKA treatment?
- Hypoglycaemia from over-treatment with insulin
- Cerebral oedema - occurs mainly in children
- Serum phosphate can fall (moves IC with K+)
- Serum Mg can fall
- Hyperchloraemic acidosis can occur
- Thromboembolism (give prophylaxis)
Who should be assessed for hypoglycaemia?
ALL PATIENTS SHOULD HAVE BLOOD GLUCOSE CHECKED especially…
- those with collapse or reduced consciousness
- those with infection
ALL UNCONSCIOUS PATIENTS SHOULD BE ASSUMED TO BE HYPOGLYCAEMIC UNLESS PROVEN OTHERWISE
What glucose levels would suggest hypoglycaemia
What level is classed as SEVERE?
Glucose <4mmol/L
ALWAYS TAKE A CAPILLARY SAMPLE and then confirm with the LAB
Lab sample:
<2.2mmol/L is defined as SEVERE ATTACK
< 1.5 = coma
How does hypoglycaemia present?
The SYMPATHETIC system becomes overactive leading to:
- Tachycardia
- Hypertension
- Shaking
- Sweating
- Pallor
- Palpitations and anxiety
When it becomes severe (plc <2.6mmol/L) neuro sx: (slurred, blurred, confused)
- Confusion
- Slurred speech/blurred vision
- Drowsiness
- Odd behaviour
- Focal neurological deficit
- Coma/siezures
Others
-Nausea and vomiting