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
In which patient might symptoms of hypoglycaemia not be so clear?
- Patients w/ well controlled diabetes have hypoglycaemia more frequently and so might not be symptomatic as soon
- Patients on Beta-blockers. These drugs could mask symptoms (tremor and palpitations)
What investigations should be done in a hypoglycaemic patient?
- GLUCOSE
- U+Es (hypoglycaemia is common in diabetic nephropathy)
- Take C-peptide and serum insulin levels
- Always take blood BEFORE giving insulin
What are some causes of hypoglycaemia?
drugs, organ failure, others
Causes of hypoglycemia
Drugs
-Insulin!!!
-Sulphonylureas common (e.g. Glicazides) (any diabetic drug that’s not metformin
-B blockers (suppress sympathetic NS>less gluconeogenesis)
-Salicyclates
Organ failure
- Hypopituitarism or adrenal failure (normally hypothalamus>pituitary gland (ACTH)> adrenal gland (cortisol)) therefore increase in glucose
- Myxoedema (hypothyroidism)
- Acute liver failure e.g. ALCOHOL
Random causes:
- Sepsis syndrome
- Malaria
- Insulinoma
What must we measure before giving glucose?
Management of hypoglycaemia for CONCIOUS patients?
-Take blood PRIOR to glucose administration (glucose, insulin, C-peptide)
GET THE HYPO BAG!!!!!!
GCS 15 and safe swallow
- 15–20 g oral glucose
-150-200ml fruit juice
-4 or 5 glucose tablets
-2 tubes gel (good for those that cant swallow)
-check 10-15 mins and repeat max 3 times (report if not > 4 mmol)
IF UNRESPONSIVE to previous step
-150ml 10% IV Glucose OR 75ml 20%
or
-IM glucagon (ineffective if depleted glycogen stores)
Then..
- After blood glucose is above 4 mmol/litre, give starchy long acting carb (brown bread)
- ADMIT
- FOLLOW UP (why did this happen)
Management of hypoglycaemia for unconscious patients?
Patients who are unconscious, having seizures, or who are very aggressive:
- ABCDEG assessment
- Stop IV insulin
- initially treat with glucagon (unless contraindicated)
- if glucagon is unsuitable/no response after 10 mins>try IV glucose 150ml 10% or 75ml 20%
Then..
- When they have recovered and blood glucose is above 4 mmol/litre, give starchy long acting carb (brown bread)
- ADMIT
- FOLLOW UP (why did this happen)
What response should you see to treatment of hypoglycaemia?
-Patient should regain consciousness or become coherent within 10mins although complete cognitive recover may take up to 45min
DO NOT GIVE FURTHER BOLUSES WITHOUT REPEATING BLOOD GLUCOSE
What patients would glucagon NOT work for? (a.k.a proffered choice is IV glucose)
Glucagon ineffective in patients with depleted liver glycogen stores:
- prolonged fasting (anorexia)
- adrenal insufficiency
- T1DM
- chronic hypoglycaemia
- alcohol-induced hypoglycaemia
- taking a sulfonylurea;
**cant give repeatedly (use up reserves)
For alcoholics with hypoglycaemia, what should you give in addition to glucose? why?
ALCOHOLICS WITH HYPOGLYCAEMIA
-if alcoholic patient-give IV thiamine with or after IV glucose to prevent Wernikes encephalopathy
How do you diagnose HHS (hyperosmotic hyperglycaemia state)?
Hyperosmotic hyperglycaemia state
1) HYPOVOLEMIA
- cause low Na (water follows glucose and is lost)
2) HYPERGLYCEMIA (blood glucose>30mmol/L)
3) Normal ketones/no academia (ketones <3mmol/L)
With increased osmolality > 320mosmol/kg
-(glucose + urea + 2xNa)
