Diabetes and DKA

 Diabetes Mellitus type 2

that day we discussed with MO and he teach us something new, would like to share it to everyone here who is interested and also a reminder to myself. 

Question : how do we know when to give OHA or insulin in a patient.

Diagnosis criteria

- if symptomatic, one abnormal glucose is diagnostic

- if a asymtomatic, 2 abnormal glucose values required

• symptoms of hyperglycemia
• Fasting blood glucose: >7mmol/L
• Random blood glucose : > 11.1mmol/L (at 2 occasions)
• HbA1c: > 6.4 prediabetic

Targets

• fasting BG: 4.4-6.1
• non fasting 4.4-8
• HbA1c <6.5
• LDL<1.7, HDL<1.1, LDL<1.4(for pt with IHD) <2.6(for normal adult)
• exercise: 150min/wk
• BP: <130/80 (normal renal function), <125/75 (renal impaired)

Types of diabetic medication

New oral hypoglycemic agents (OHA):

- AGIs (acarbose): prevent carbohydrate absorption
- DPP4 inhibitor- sitagliptin: to excrete sugar from urine

reference: https://pubmed.ncbi.nlm.nih.gov/10989161/

What about Diabetes emergency?

DKA: diabetic ketoacidosis

• intro
• pathophysio
• risk factor
• signs and symptoms
• investigations
• management

Introduction:

HHS: insulin deficiency--> no ketoacidosis .

DKA: absolute deficiency of insulin --> serum ketone positives

How ketone is produced?

• glucose, fatty acidglycosis
• insulin will prevent fatty acid to move into the cell for ATP
• no insulin 
• no inhibition of fatty acid transport into kreb
• causes increase promital CoA, unable the kreb cycle to produce ATP 
• lead to increase acetone bodies(ketone body) 
• causes acidosis
• hyperglycemia--> dehydration (osmotic diuresis)--> increase Creatinine (renal failure)
• tips: back to Kreb cycle 😳

pathogenesis of DKA and HHS

differences between DKA and HHS

Risk factor:

1. DMT2- uncontrolled, non compliance to medications, inappropriate adjustment, cessation of insulin, new onset of DM

2. MI

3. infection 

4. trauma

5. congenital factors

Signs and symptoms:

• evolves rapidly (24hours)

• early sign: 
• ketoacidosis sign: 
• nausea, vomiting, abd pain and hyperventilation
• fruity breath
• hyperglycemic signs: polyuria, polydipsia and weight loss

• worsen:
• neurological signs: lethargy, focal deficit, obtundation, seizure, coma

Investigations:

• vital signs:
• cardiorespi status
• mental status
• Physical examination: 
• skin turgor, mucosa, urine output
• VBG (venous blood gas)/ ABG (arterial blood gas): metabolic acidosis
• elevated anion gap and ketonemia
• CBS(capillary blood sugar): >13.9 and <44.4
• serum ketone: >3+
• urine ketone: >2+
• HbA1c: see the baseline
• FBC: to exclude anemia 
• BUN and creatinine: 
• AcuteKidneyInjury(AKI)
• check Na level
• check K level: will raised in the initial stage but as it become severe K often lowered.
• if<3.3 : not for insulin infusion first until it is corrected with KCl 
• ECG
• Blood C+S and urine C+S(culture and sensitivity): rule out the cause of infection
• CXR: to check for any pneumonia/cardio issues

Management:

• stabilise the pt airway, breathing, circulation (ABC)
• insert large IV bore
• cardiac monitoring + pulse oximetry
• fluid resus
• IV NaCL as rapidly possible- especially those with signs of shock (hypovolemic shock: hypotensive, tachycardic)
• typical fluid deficit is 100ml/kg, so an average 60kg man= 6L
• give 1L each hour till 6 hours. reaccess after 12 hours
• (make sure there are no cardiac compromise)

• ivi insulin to reduce cbs
• monitor CBS hourly
• once the CBS <12 , urine ketone<0.3, pH normalised
• start D5(dextrose 5%) infusion to run alongside saline
• DO NOT give insulin if serum potassium is in deficit

• Correct K(potassium) deficit
• if<2.5 fast correct with KCL (2g KCL in 100ml NS over 1hr + 3 T. slow K/hour if tolerated)
• 2.5-3 : 1.5g KCL/pint
• 3-4    : 1g KCL/pint
• 4-5.5 : 0.5g KCL/pint
• > 5.5mmol/L : w/hold potassium replacement
• AIM: potassium 4-5mmol/L

• basic electrolytes and bicarbonate(VBG) till pt stable

• determine the underlying causes and treat
• UTI, pneumonia, MI

• monitor urine output, 
• no urine output, consider catheter bladder drainage (CBD)

• AIM for CBS
• aim for glucose to decrease 2-4 mmol/L/hr, HCO3 increase 3/hr, ketone decrease 0.5/hr
• with IHD: CBS aim 8-10
  normal : CBS aim 4-6 (with concious, acidosis normalised) before changing to s/c insulin
  elderly: CBS 6.5-7 
• once all are normal we can start bridging for insulin to basal bolus insulin
• calculate the total ivi insulin for 24hours and divide by 4
• 1 for basal and another for 3 for short acting insulin
• then proceed with sc(subcutaneous) actrapid and ask pt to eat after the injection. stop ivi insulin 1hour after the bolus insulin injection

LTP: basal bolus insulin recommended

*DKA: diabetic ketoacidosis; BUN: blood urea nitrogen; IV: intravenous; ECF: extracellular fluid; Na: sodium; K: potassium.

overall view of DKA management
reference: uptodate

NOTES:

• Insulin therapy 
• lowers the serum glucose concentration 
• by decreasing hepatic glucose production, the major effect, and 
• enhancing peripheral utilization, a less important effect.
• diminishes ketone production 
• by reducing both lipolysis and glucagon secretion
• may augment ketone utilization. 
• Inhibition of lipolysis 
• reduce the serum glucose concentration. 
• to stop ketone regeneration.

References:

1. Uptodate

2. Sarawak handbook of medical emergencies

3. Oxford clinical medicine