DKA Flashcards
DiGNOSIS OF DKA
Blood Glucose >11mmol/L /Diabetic
AND
Blood Ketones>3mmol/L Urine>2+
AND
pH<7.3 / Bicarbonate<15 mmol
Management Plan
Fluids NB. Give 1L as initial first step. Will need ongoing replacement.
- Insulin – fixed rate until BM <14. Don’t hold long acting insulin.
- Consider parameters that would indicate a need for ICU.
- Risk of cerebral oedema and fluid overload.
Monitoring for
response
* Glucose
* Ketones
* PH
* Bicarb
* Potassium
ABC Px of DKA
2 IV
1- fixed rate IV insulin infusion + IV fluids +/- KCL
2- IV Fluids infusion 1L 0.9% soduim chloride over 1h
if on regular Insulin( Tresiba) , prescribe 1-regular basal Insulin, 2-Subcutanous Insulin and 3-Glucose monitoring regularly
If on Mealtime Bolus Insulin( NovaRapid), perscribe 1-Subcutanous insulin and 2-glucose monitoring record
Severe DKA indicators for High dependency Admission
1-Blood-Ketones > 6.0 mmol/L
2-V/A pH < 7.1 / Bicarb < 5 mmol/L
3-Serum K+ < 3.5 mmol/L
4-Systolic BP < 90 mmHg
5- Pulse Rate > 100 / < 60 bpm
6- O2 Sat < 92%
7- GCS < 12 / Abnormal AVPU
Monitoring goals for Admitted DKA
0-Potassium (K+)
1-Bicarbonate: rise of 3mmol/h
2- Glucose fall of 3mmol/h not more than 5mmol/h, if so add 10% dextrose
3- Ketones min fall 0.5mmol/l/h, if less increase insulin infusion
DKA resolution when
Blood ketones < 0.6 mmol/L
Venous pH > 7.3
For At least 6 hours
How to stop the protocol?
When?
* Blood ketones < 0.6 mmol/L + Venous pH >7.3 irrespective of blood glucose for 6 hours.
* How?
Give regular insulin pre-meal, give meal and 1 hour later stop IV insulin (don’t stop
In Primary Adrenocortical insufficiency; high ACTH , Pigmentation, hyperkalemia and hyponatraemia, Managment?
ACTH Stimulation Test ,cause?, Treat Hydrocortisone & Fludrocortisone
In Secondry Adrenocortical insufficiency; deficincy of Glucocorticoids & androgens only (mineralcorticoroids present)
Low ACTH , Pallor, hyponatraemia Only may be Cushingoid
Managment?
ACTH Stim Test
Treat w Hydrocortisone
Presents with :
High ACTH,
pigmentation, Hyperkalaemia and
hyponatraemia
Primary (adrenal
gland affected)
* Autoimmune adrenalitis
* TB, HIV
* Infarction
* Cancer
* Adrenalectomy
* Drugs, eg ketoconazole
* Adrenoleukodystrophy
Presents with:
Low ACTH & Pallor
Hyponatraemia only
Secondary (pituitary)
ACTH deficiency
- Exogenous steroids
withdrawal - Surgery
- Radiation
- Stroke
- Head injury
- Tumor
Addissions disease
ACTH excess, Dark skin, Stress and salt cravings, Na+ low hyponatremia hyperkalemia, orthostatic hypotension, weight loss easily fatigued mc80% Abdo pain, low cortisol
Synacthen Test method
Method
At baseline, time 0 minutes, take cortisol
Give I.M. Synacthen 250mcg (adult dose)
At 30 and 60 minutes take cortisol (serum/gold topped tube).
Interpretation:
Basal Cortisol level should be greater than 180nmol/L
30min or 60min Cortisol should be greater than 420nmol/L (whatever the basal level)
The increment should be at least 170nmol/L, apart from in severely ill patients where adrenal output is already maximal.
If ACTH >200ng/L then diagnosis is primary adrenal failure.
If ACTH <10ng/L then diagnosis is secondary adrenal failure
In patients with both hypothyroidism and adrenal insufficiency an adrenal crisis
can be precipitated if thyroid hormone replacement is initiated before steroid
therapy.
in pnts with adrenal insufficiency free T4 levels = low-normal but TSH levels are high.
This usually normalizes with steroid replacement
Adrenal crisis
Hx: Fatigue, lack of energy, abdominal pain, weight loss, nausea & vomiting, dizziness with postural changes,
collapse, tan, leg spasms
Exam: Hypotension (≥20 mmHg drop in BP from supine to standing position) in severe cases hypovolaemic
shock, abdominal tenderness and guarding, confusion, somnolence, in severe cases delirium or coma
Lab findings:
*Hyponatraemia (in primary and secondary adrenal insufficiency)
*Hyperkalaemia (in primary adrenal insufficiency)
*Pre-renal failure (increased serum creatinine due to hypovolaemia)
*Normochromic anaemia, sometimes also lymphocytosis and eosinophilia
*Hypoglycaemia (primarily in affected children; can cause long-term neurological deficits, if not promptly treated