Endocrinology

Diabetes Overview
• Type 1 Diabetes: autoimmune disease resulting in a failure to secrete sufficient insulin to regulate glucose utilization
• Type 2 Diabetes: most common (80%), characterized by high blood sugar, insulin resistance, and relative lack of insulin
• Gestational Diabetes: diabetes that occurs during pregnancy and resolves after pregnancy, increased risk of T2DM in the future
• Other: due to other endocrine diseases (ie. Cushing’s, acromegaly), medication-associated (ie. steroids), genetic defects and syndromes, diseases
of the exocrine pancrease (CF, pancreatectoy, hemochromatosis), infections (congenital rubella), etc.
Type 1 Diabetes Type 2 Diabetes
Age at onset Younger < 25 yo, beware LADA Typically > 25 yo
May have personal and/or family history of
Family history Often have family history of T2DM
autoimmunity
BMI Often normal Often elevated
Acanthosis nigricans Not present May be present
DKA Can be common Less common
Autoantibodies Present Absent

Risk Factors:
• T1DM:
o Family history of T1DM
o High risk genetic factors
o Other autoimmune diseases → hypothyroidism, adrenal insufficiency (APS II)
o Usually no risk factors or family history in most cases
• T2DM:
o First degree relative with diabetes
o High risk ethnic groups → indigenous canadians, hispanics, asian, south asian, african
o History of impaired glucose tolerance, impaired fasting glucose, or GDM

Diagnostic Criteria – Diagnosis Requires ONE of the Following:

● Fasting plasma glucose (FPG; implies no caloric intake for 8+ hours) > 7.0 mmol/L
● Symptoms of diabetes (BG >14 usually) plus a random plasma glucose value > 11.1 mmol/L
● 2-h 75g OGTT shows a plasma glucose > 11.1 mmol/L
● HbA1c > 6.5%
● If no symptoms of hyperglycaemia need to do a second test → same test on a different day (usually also do HbA1c)
o If the first test is a random PG in an asymptomatic individual need to confirm with an alternate test
● Once results of two different tests are available and both are above the diagnostic thresholds, the diagnosis of diabetes is confirmed

Pre-diabetes – Diagnosis Requires ONE of the Following:

● Fasting plasma glucose (FPG) between 6.1 and 6.9 mmol/L → IFG
Symptoms of Hyperglycaemia
● 2-h OGTT shows a plasma glucose between 7.8 and 11.0 mmol/L → IGT (rarely done, important in CF and
• Polydispia
GDM screening)
• Polyuria
● A1c between 6.0 and 6.4%
• Polyphagia
● Clinical importance → independently predicts future diabetes (need routine screening) and is associated with
• Unexplained weight loss
an increased risk of cardiovascular disease • Visual changes
• Neuropathic symptoms
Physical Exam Findings:
● Central obesity
● Skin tags, acanthosis nigercans
● Poor pedal pulses, peripheral nerves
● Dilated eye exam, cardiac exam

Outpatient Diabetes Management

ABCDES of Diabetes Care:
• Diet (or meal planning)
• Exercise
• Self-monitoring
• Pharmacotherapy after 3 months
• Insulin is signs of metabolic decompensation
● A1c targets < 7.0% (or < 6.5% to decrease risk of CKD and retinopathy)
● BP targets → BP < 130/80 mmHg
● Cholesterol → LDLc < 2.0 mmol/L (or > 50% reduction from baseline)
● Drugs for CV and/or cardiorenal protection → ACEi/ARB, statin, ASA, SGLT2i/GLP1-RA,
● Exercise goals and healthy eating → 150 minutes aerobic activity/week and resistance exercises 2-3 times/week; healthy diet
● Screening for compliations → ECG q3-5y, monofilament, eGFR, ACR and retinopathy yearly
● Smoking cessation
● Self-management, stress, and other barriers → set goals and screen for barriers

A1c Targets:

● Monitoring:
o For an A1c < 7% → meal targets 4-7 mmol/L (typically 5-7), 2 hrs post-meals < 10 mmol/L
o Different targets for frail, elderly, pregnant populations
o Care is interdisciplinary – diabetes educator, dietician, social worker, pharmacist, and other MDs (e.g. family physician, endocrinology,
ophthalmology, nephrology, cardiology, hepatology, vascular surgery)
● ODB Coverage:
o Freestyle libre – insulin
o Dexcom – no
o Test strips – depend on drugs (drugs at risk of hypoglycemia ie. glyburide, gliclazide have more strips)
o Insulin monitoring – ac meals and ohs
o Not insulin monitoring – 3-4x/week
● Continuous glucose monitoring systems:
o Measure glucose in interstitial fluid
o ie. Freestyle libra, Dexcom

Treatments:
● Medications for T1DM:
o Insulin – measured in units (U)
o More concentrated formulations are useful for people on high doses of insulin (less volume for injection)
o Insulin is administered primarily using pens (prefilled) rather than syringes and vials
o Insulin Types:
▪ Insulin comes in two preparations → prandial/bolus (fast onset + short duration) and basal (slow onset + long duration)
▪ Prandial/bolus: rapid-acting: Lispro (Humalog), Aspart (NovoRapid/Fisap), Glulisin (Apidra)
▪ Basal: intermediate-acting: Human NPH; long-acting: Detemir (Levemir), Glargina (Lantus), Degludec (Tresiba)
▪ Premixed: biphasic insulin aspart (NovoMix), insulin lispri/lispro protamine (Humalog Mix25 and Mix50)
o Insulin pumps – Medtronic, Animud, Omnipod
▪ Continuous subcutaneous insulin infusion via a catheter
▪ Delivers basal and bolus insulin:
• Basal rates can be adjusted for time of day
• Boluses given just prior to meals, adjusted according to intake
▪ Advantages → improved diabetic control and more flexible lifestyle
▪ Not completely automatic – administers basal insulin; bolus administered by
patient
▪ Requires carb counting, knowledge of insulin adjustment, and troubleshooting
capacity by the patient
▪ Patient must be alert, competent, and knowledgeable
▪ Offered under Ontario government through ADP for those with DM1 – cost of pump and monthly allowance for supplies
▪ Patients with type 2 diabetes - could also be on pump (self-pay or private drug plan)
● Medications for T2DM:
o Non-Insulin Options:
▪ Metformin (first line therapy) – GI (N/V/D), titration, inexpensive, A1c reduction 1-1.5%
▪ Alpha-glucosidase inhibitor (Acarbose)
▪ DPP IV inhibitor (“-gliptin”) – (e.g. linagliptin, saxagliptin, sitagliptin)
▪ GLP-1 analogues (“-tide”) (e.g. dulateglide, liraglutide, lixisenatide, semaglutide)
▪ Non-sulfonylurea insulin secretagogue (e.g. repaglinide)
 ▪ SGLT2 inhibitor (“-gliflozin”) (e.g. canagliflozin, dapagliflozin, empagliflozin)
▪ Sulfonylurea (e.g. gliclazide, glimepiride, glyburide)
▪ Thiazoledinediones (“glitazone”) (e.g. pioglitazone, rosiglitazone)
o Insulin – injections, pump

● Treatment Algorithm
o If patient is symptomatic → start insulin + metformin
o How far are they from target:
▪ < 1.5% = lifestyle + metformin
▪ > 1.5% = metformin + second agent(SGLT2 (HF)/GLP1 (athesclerosis) ie. Semaglutide = cardiac benefits)

Costs of Diabetes:
● Monitoring costs (test strips, lancets, sensors) → partial reimbursement for test strips/lancets (insulin/DM in pregnancy)
● If on multiple insulin injections need 4 test strips/day, if on medications 1 test is enough
● Medications
● Lifestyle

Hypoglycemia
Diagnosis (Whipple’s Triad)
● Low plasma glucose ** (PG < 4 if on insulin/insulin secretagogues; PG < 3 if non-diabetic)
● Autonomic (tremor, palpitations, sweat, anxiety, hunger, nausea) and/or neuroglycopenic (poor concentration, drawsy, vision changes,
confusion, weak, difficulty speaking, headache, dizzy) symptoms
● Symptoms resolve upon raising the glucose

Classification
● Severe – sistance needed (includes seizures, coma)
● Mild – autonomic symptoms only
● Moderate – neuroglycopenic symptoms
● Hypo-unaware – no autonomic symptoms at a glucose < 3.5 mM

Treatment
● Mild/Moderate (can self treat) – 15g CHO (glucose preferred) PO, recheck BG in 15 minutes, repeat 15g CHO PO if still < 4 mM
● Severe – 15g CHO PO; retest-retreat per mild/moderate hypoglycemia. If unconscious:
o No IV: 1 mg glucagon SC/IM or 3 mg glucagon intranasally
o IV access: 10-25g (20-50 mL D50W) glucose over 2 minutes
 Hyperglycaemic Emergencies
Hyperglycaemic Emergencies (DKA/HHS):
● DKA (diabetic ketoacidosis)
● HHS (hyperosmolar hyperglycaemic state)
● Common features:
o Insulin deficiency → hyperglycaemia → urinary
loss of water & electrolytes → volume depletion
& electrolyte deficiency & hyperosmolarity
o Insulin deficiency (absolute) & increased
glucagon → ketoacidosis (in DKA)

Diabetic Ketoacidosis:
● pH < 7.3
● Bicarbonate < 15 mmol/L
● Anion gap > 12 mmol/L (Na - [Cl + HCO3])
● Positive serum or urine ketones
● Plasma glucose > 14 mmol/L (may be lower – pregnancy, SGLT2 inhibitor use)
● Precipitating factor

Hyperosmolar Hyperglycemic State: Diabetic Ketoacidosis:

▪ Caused by partial/relative insulin deficiency (may need insulin to tx) ▪ Caused by absolute insulin deficiency = excess counter
▪ More commonly seen in T2DM regulatory hormone/glucagon production (need insulin to tx)
▪ Marked hyperglycaemia, acidosis unusual ▪ More commonly seen in T1DM
▪ Onset is generally gradual ▪ Mild hyperglycaemia
▪ Results in: ▪ Onset is usually sudden
o Blood glucose > 30 mmol/L ▪ Results in:
o Glucosuria, osmotic diuresis, severe dehydration, loss of electrolytes o Blood glucose > 15 mmol/L = polyuria, polydipsia
o Very high serum osmolality (due ↑ BG + severe dehydration) o Lethary
o Beware hypokalemia o Ketonemia, urine ketones, high anion gap acidosis
o Minimal or no ketoacid accumulation (trace urine ketones) o Beware hypokalemia
▪ Significant water deficit (9L), ECVF contraction ▪ 6L water deficit (deplete volume status), ECVF contraction
▪ Often significantly decreased LOC ▪ Consciousness usually intact (depends on level of acidosis)
▪ Can cause neurological complications → seizures and stroke due to ▪ Abdo pain, nausea, vomiting, Kussmaul’s breathing
excessive serum osmolality ▪ Mortality rate < 5%, 5-15% in the community (most common
▪ Mortality rate = 15% (due to neurological complications) cause of death in children with T1DM)

Investigations: #1 test to detect DKA is the anion gap, used to indicate when DKA has resolved and insulin can be started
● Random plasma glucose
● Serum Cr/BUN, Na, Cl, K, HCO3
pH < 7.3, HCO3 < 15, AG > 12
● Serum osmolality, serum ketones (beta-OH butyrate is most prominent ketone)
Positive serum or urine ketones
● Arterial blood gases
PG > 14
● CBC (WBC, Hb)
Precipitating factor
● Urine ketones, urinalysis

Anion Gap Metabolic Acidoses (MUDPILES CAT):

● Methanol
● Uremia
● DKA, alcoholic ketoacidosis, starvation ketoacidosis
● Paracetamol/acetaminophen, paraldyhyde, phenformin
● INH, iron, inborn errors of metabolism
● Lactic acidosis Anion Gap = Na- (Cl + HCO3) – normal ~ 3-13
● Ethylene glycol [(Na + K) - (Cl + HCO3)] – normal ~ 7-15
● Salicylates/ASA Osmolar Gap = 2Na + Flu + BUN ~ 2-6
If high gap consider ethylene glycol or methanol
● CO, cyanide, CHF
● Aminoglycosides
● Toluene

Approach to Hyperglycaemic Emergencies (DKA): Initial 24 hours:

1. Precipitants • Volume – IV fluids
o Insulin insufficiency (e.g. non-adherence, new onset DM) = #1 cause • Electrolytes – IV potassium
o Infection (e.g. pneumonia, UTI, pancreatitis) • Acidosis – IV iinsulin, when to add glucose to IV,
o Infarction/Ischemia (e.g. MI/CVA = increase in troponin, ECG shows high K) HCO3
• Precipitant – infection, adherene, ischemia, drugs,
o Inflammation (e.g. thyrotoxicosis)
pregnant
o Illegal/Intoxication (e.g. EtOH, cocaine)
• Monitoring
o Iatrogenic (e.g. withholding insulin, high dose steroids, antipsychotics) Next few days:
o Infant (e.g. pregnancy) • Transition to SC insulin and PO diet
• Discharge planning
Investigate and treat underlying
precipitant; don’t assume non-adherence
2. Fluids
o Start an IV (2 18G IVs) and give 0.9NS (NaCl) 1-2 L/hr to correct shock (low bp)
o Reduce IV to500 ml/hr x4 hrs then 250 ml/hr x4 hrs depending on volume status Can have pseudo hyponatremia
in hyperglycaemia
o Once euvolemic determine corrected serum [Na] = Lab[Na] + (0.3 x [glucose - 5])
▪ [Na] > 135 mM give 0.45NS (concerns regarding fluid overload and hyperkalemia)
▪ [Na] < 135 continue 0.9NS
o Add D5W to NaCl when blood glucose < 14 mM which allows you to keep running insulin and maintain BG at 12-14
3. Potassium – generally a low total body K due to polyuria, normal in blood due to lack of insulin
o Add K early as long as renal function appropriate/urine output evident. Insulin shifts K down
o Amount of K in fluids is dependent on initial [K]:
▪ K above 5.0 mmol/L or the patient is anuric (catheterize if not sure, can be euglycemic if pregnant or on an SGLT2 inhibitor) just use
NS and don’t start IV K
▪ K below 3.3, then bolus K before giving insulin (need K > 3.3)
NO insulin bolus in
▪ Between 3.3-5.05, give 20-40 mmol/L KCl IV/hr (based on renal function and level of baseline K)
patients < 20 yo due to the
o Modify K up or down in IVF based on lytes and creatinine done every 4 hours
risk of cerebral edema
4. Acidosis/Osmolarity – insulin (goal is to close the anion gap/stop acidosis)
o Don’t start IV insulin if K < 3.3 mM
o Give regular insulin at 0.1 units/kg by IV bolus then 0.1 units/kg/hr via continuous IV infusion (if pH < 7 need 1 amp/h until pH > 7)
o Start less if you are uncertain of their true body weight (e.g. pregnancy)
o Check poc (fingerstick) glucose q1h and notify MD with the result
o Adjust IV insulin to obtain a BG drop of ~ 3 mM/L and to close the anion gap.
o If less than this, increase insulin by 0.5-1 unit/h; if more than this, drop by 1 u/hour
o Monitor anion gap q4 hours; if blood sugar < 14 and anion gap is not closed, change IVF to D5W/0.45NS (e.g. if on 0.45NS + 20mEq KCl,
then change to D5/0.45NS + 20 mEq KCl)
o Continue insulin infusion and maintain glucose ~ 11 mM on IV insulin and until anion gap is normal and patient can eat
5. Transition to SC Insulin – once the anion gap is closed (BG < 12-14), insulin infusion stable, patient can eat can transition:
o Aim for a meal time, morning is ideal
o Provide SC insulin (short-acting + basal analogue):
Overlap to avoid recurrent DKA
▪ 0.5 to 0.8 units/kg/wt per day by MDI (basal-bolus) insulin
▪ Stop IV insulin infusion 2 hrs after SC insulin started (rapid acting at a meal
o Monitor response and adjust SC insulin doses
6. Monitoring:
o Vitals q1h x4 then re-assess
o Measure ins/outs q1h x 8 hours then re-assess
o Capillary blood (finger stick) glucoses q1h, call results to MD
o Serum lytes, AG, random glucose, BUN, creatinine, + venous blood gases q2h x 4 then re-assess
o Use a flow sheet and try to have one MD follow things for the first 12-18 hours
Effective Serum Osmolality = 2[Na] + [glucose]
o Sips to diabetes diet as tolerated unless a good reason for patient to be NPO ie. Total = 2[Na] + [glucose] + [BUN]
perforated viscous Normally 275-295
Asymptomatic effective < ~ 320
Hyperosmolar Hyperglycaemic State Management:
● Higher mortality → sicker/older patinets, usually significant dangerous precipitant, mortality from precipitant and not HHS = need to
identify ad treat precipitant
● Often established T2DM + older wth CVD (infection, ischemia common causes), can’t correct to quickly to prevent cerebral edema
● Insulin is less important in management, can treat with just volume repletion in some cases
● Once levels normalized can transfer back to anti-hyperglycaemic medication
1. IV fluids
o If in shock start 0.9NS IV 1 L/hr to correct hypotension (ensure no pulmonary edema develops in patients with heart disease/suspected)
o Determine corrected serum [Na]:
▪ [Na] > 135 mM give 0.45NS IV at 250-500 ml/hr
▪ [Na] < 135 continue 0.9NS IV at 250-500 ml/hr
o Monitor volume status closely and adjust IV rate accordingly – pulmonary edema (clinically/O2 sat), BP, PR, neck veins, urine output
 o Add D5W to 0.45NS when blood glucose < 17 mM
2. Potassium
o K < 3.3 start IV K ASAP, don’t start insulin
o K > 5.0 mM and/or patient is anuric (catheterize if not sure), don’t start IV potassium
o If K 3.3-5.0 start KCl 20-40 mmol/L IV per hour
o Follow serum bytes closely
3. Insulin:
o Don’t start IV insulin if K < 3.3 mM
o Give regular insulin 0.1 units/kg/hr via continuous IV infusion (no bolus needed)
o Check poc (fingerstick) glucose q1h and notify MD with the result
o Adjust IV insulin to obtain a BG drop of ~ 3 mM/L
o Change IVF to D5W/0.45NS when blood glucose < 17 mM
o Maintain glucose ~ 15 mM on IV insulin and continue until effective plasma osmolality < 320 mosm/kg and patient is mentally alert (or
back to their baseline mental state)
o Start SC insulin:
▪ 0.5 to 0.8 units/kg/wt per day by MDI (basal-bolus) insulin
▪ Stop IV insulin infusion 2 hrs after SC insulin started
4. Monitoring:
o Vitals + O2 sat q1h x4 then re-assess
o Measure ins/outs q1h x 8 hours then re-assess
o Capillary blood (finger stick) glucoses q1h, call results to MD
o Serum lytes, AG, random glucose, BUN, creatinine, + venous blood gases q2h x 4 then re-assess
o Use a flow sheet and try to have one MD follow things for the first 12-18 hours
o Sips to diabetes diet as tolerated unless a good reason for patient to be NPO
DKA HHS
• Usually T1DM • Usually T2DM
• Symptoms of uncontrolled hyperglycaemia • Symptoms of uncontrolled hyperglycaemia
• Loss of Na, K, and water • Impaired mental acuity (cf. baseline)
• Hypotensive (and acidemic) • Loss of water, Na, K
• Mortality < 5% • Hypotensive (and hyperosmolar)
• Cerebral edema • Mortality ~ 20%
• Labs: • Labs:
o Increased BG level o Really high blood glucose level (> 30 mM)
o Anion gap metabolic acidosis = increased AG, low pH, low serum HCO3 o High effective serum osmolality > ~ 320 mosm/kg
o Ketonemia = beta-OH-butyrate (active ketogenesis), acetoacetate, acetone o AKI = increased serum creatinine
(fruity breath) o Serum Na = variable but usually low
o Ketonuria = urine dipstick misses b-OH-butyrate o HCO3 = variable
o AKI = increased serum creatinine o pH = variable
o Serum Na = variable but usually low • Mechanism:
o Serum osmolality = variable but usually not high o Reduced net effective insulin response → reduced insulin action
o Low total body K o Increased counter-regulatory hormones as per DKA (not as
• Mechanism: much), with increased hepatic glucose production and impaired
o Reduced net effective insulin response → reduced insulin secretion glucose use in periphery
o Increased counter-regulatory hormones (especially glucagon) with o Enough insulin to prevent lipolysis and ketogenesis but still not
increased hepatic glucose production and impaired glucose use in adequate for normal glucose utilization
periphery o Osmotic diuresis → water (dehydration), Na (volume
o Increased lipolysis and muscle breakdown with release of amino acids and contraction), K loss
FFA to liver leading to gluconeogenesis and ketogenesis
o Osmotic diuresis → water (dehydration), Na (volume contraction), K loss

DKA and HHS Treatment:

First 24-48 Hours
• IV fluids – IV NS to start
• IV K – don’t start insulin if serum K < 3.3 mM Hyperglycaemic Emergencies Equations:
• IV insulin • Anion Gap = Na - Cl - HCO3 (normally ~ 3-13 mM)
• Precipitant – infection, adherene, ischemia, drugs, pregnant • Effective serum osmolality = 2[Na] + [glucose] (normally < 300)
• Monitoring • Corrected Na = lab[Na] + (0.3 x [glucose - 5])
Next few days
• Transition to SC insulin and PO diet
• Discharge planning

Caution areas:
● Euglycemic DKA – BG may be <14 but evidence of ketoacidosis – Seen in pregnancy, SGLT2 inhibitors
● Calculate metabolic acidoses carefully and make sure to consider/rule out other reasons for anion gap metabolic acidosis
● Check osmolar gap (for ingestions – methanol, ethanol) (2Na + sugar +BUN)
● Check lactate
DKA Diagnostic Difficulties:

Inpatient Diabetes Management

Basic Principles:
● Level of BG control needed
● Monitoring BG and how to write insulin/BG testing orders
● Methods of giving insulin
● What can go wrong with “sliding scale” insulin (often suboptimal management)

Inpatient management:
● Check A1C if not done in past 3 months
Reassess in 24h and revise treatment
● Monitoring:
o ac meals and qhs if eating if glucose not at target. What will
patient go home on?
o Q4-6 hours if on continuous feeds or NPO
o Q1h if on insulin infusion or critically ill
● Set glucose target:
o Tight targets – pregnant? Post-op cardiac surgery? ICU?
o Often cant have tight targets on the wards → 5-10 if no comorbidities making this challenging, 6-15 to avoid
symptomatic hypoglycemia
o Targets individualized: 5-8 mmol/L pre-prandial typically; 5.5-11.1 mmol/L if post-CABG
o Patient comorbidities ie. advanced dementia
● How to reach targets – insulin vs drugs, NPO vs non-NPO (enteral/PN nutrition)
o If in doubt use insulin since no CI, always works at an adequate dose, most flexible in unstable settings
o Oral agents need to ensure no CIs ie. ARF/metformin, HF/glirazones, liver failure/Sus, DPP4s/pancreatitis, SGLT2s/volume/renal etc.
o Oral agents generally need to be help and insulin is the safest option
● Avoid hypoglycaemia
● What to do with insulin:
o Determine other factors ie. will patient be on steroids
o Depends on meals ie. if not eating can hold bolus insulin and only use basal
o Add correction scale to guide how much insulin to give

Basal + Bolus + Correction:

● In hospital may need temporarily holding other antihyperglycemic medications (eg. renal or hepatic impairment)
● Insulin is the treatment of choice
● Basal – covers daily needs of patients regardless of whether they are/aren’t eating
● Bolus – for patients consuming meals
● Correction – help patient get back to normal, never want this without a basal
● Management:
o Starting insulin total daily dose = 0.5 units/Kg body weight (more if obese or insulin resistant)
o Reduce insulin TDD to 0.3 units/Kg in patients > 70 yo, or T1DM, and/or with serum Cr > 2.0 mg/dL
o Give half of daily dose as insulin glargine and half as insulin glulisine
o Give insulin glargine OD, at the same time of the day
o Give insulin glulisine in 3 equally divided doses before each meal (hold if patient NPO)

Basal Plus Correction:

● Start glargine insuli TDD of 0.25 units/Kg
● Reduce insulin TDD to 0.15 units/kg in patients > 70 yo and/or with serum Cr > 2.0
mg/dL (kidney failure so less glucose production increasing the risk for
hypoglycemia)
● Give insulin glargine OD, at the same time of the day
● Supplemental insulin glulisine following the “sliding scale” protocol (IE) for BG >
140 mg/dL

SC Insulin Correction Scale:

● Orders based on if patient has low, medium, or high insulin requirements
● Based on insulin dose can determine if patient is insulin sensitive or insulin resistant
● If not on insulin judgement is based on weight and BMI ie. thin, lean, T1DM = low dose sliding scale; obese + high BMI start at a medium
dose scale then move up to high
● Don’t give insulin until BG is high (8.1 and higher)
● This is reactive and used when the original insulin plan is poor
● If this is needed often need to adjust basal and bolus daily amount

Insulin Adjustment:
● Adjustment depends on how much insulin the patient is on (reflects insulin sensitivity)
● Look at AM and PM sugars to assess basal dose
● General rule of thumb – increase insulin by 10% if mildly high, 20% if high
● Reduce by 20% if low (more aggressive to prevent hypoglycemia)
● If at risk of hypoglycemia need access to a source of glucose at all times

Reassess and Revise:

● Acute start treatment (insulin)
● Reassess in 12-24 hours
● Revise treatment if glucose not at target:
o Not in targets means…
o “Revise” usually means adding in a basal or bolus insulin or increasing doses of the basal and/or correction insulins
o Basal insulins – NPH, long-acting analogs (detemir, glargine)
● What will the patient go home on?

DM1 management in hospital:

● Must have insulin – basal even when NPO; avoid sliding scale alone as the management strategy
● Do not hold their insulin if they are hypoglycemic; treat their hypoglycemia and adjust their insulin dose
● If NPO, ensure they are receiving something with carbohydrates (e.g. tube feeds, dextrose-containing IVF)
● Change default powerchart orders for when MRP is notified: Waiting to be called when BG is over 20 mmol/L x 2 may result in DKA;
modify the orders to be called sooner (BG 14.1 or higher) so that you can avoid DKA
● If patient is on a pump at home, they must be alert, competent, and knowledgeable to resume the
pump (i.e. do not restart in someone with delirium)
● Important to correct hyperglycaemia due to AE:

Insuli on tubę feeds:

● Sliding scale with short acting analogue q6h
● Basal analogue insulin (not Tresiba since half-life is 36h) q12h
● Use the prior 24-48 hrs to determine/adjust long acting dosage
● If ever uncertain a 10% change in insulin is cosidered safe

DKA/HHS Prevention:
● T1DM = education about sick day management, continue insulin when not eating, frequent monitoring when ill
● T2DM = education about sick day management, frequent monitoring when ill

Sick Day Management

● When sick BG levels can fluctuate and be unpredictable
● Should check blood glucose levels more often than usual (for example, every 2 to 4 hours)
● Drink plenty of sugar-free fluids or water
● If type 1 diabetes with blood glucose levels remaining over 14 mmol/L before meals, or if symptoms of DKA check for ketones by
performing a urine ketone test or blood ketone test. Blood ketone testing is preferred over urine testing
● Develop a “Sick Day” plan with your diabetes healthcare team. This should include information on:
o Which diabetes medications you should continue and which ones you should temporarily stop
o Guidelines for insulin adjustment if you are on insulin
o Advice on when to contact your health-care provider or go to the emergency room