About This Page
This is a clinician-written, evidence-based guide aligned to the MCC Examination Objectives. It is structured by clinical presentation — the way the MCCQE tests and the way patients actually present. Management reflects current Canadian guidelines (CMA, CFPC, CPS). Always cross-reference with institutional protocols and clinical judgment.
Key points
- First decide whether this is uncomplicated hyperglycemia, DKA, HHS, or another cause of osmotic symptoms such as diabetes insipidus
- DKA is hyperglycemia or known diabetes plus ketonemia and metabolic acidosis; HHS is profound hyperglycemia and hyperosmolality with little or no ketosis
- All acutely unwell hyperglycemic patients need capillary glucose, beta-hydroxybutyrate or ketones, venous blood gas, electrolytes, anion gap, creatinine, osmolality, and trigger search
- DKA and HHS management is fluid first, potassium-aware insulin second, and trigger correction throughout
- New diabetes care includes classification, cardiovascular risk reduction, kidney protection, eye/foot screening, and patient-centred education
Approach to the Presentation
Hyperglycemia may present as incidental glucosuria, polyuria and polydipsia, recurrent infections, blurred vision, weight loss, dehydration, vomiting, abdominal pain, Kussmaul respirations, or altered level of consciousness. The MCCQE1 task is not simply to name diabetes; it is to determine acuity. Start with ABCs, vital signs, mental status, volume status, and bedside glucose. Then look for ketosis, acidosis, hyperosmolality, infection, infarction, pregnancy, steroid exposure, SGLT2 inhibitor use, missed insulin, and social barriers to care. Diabetes Canada guidance anchors acute hyperglycemic emergency management and longitudinal diabetes care in Canada.
Differential Diagnosis
| diagnosis | likelihood | key features | distinguishing test |
|---|---|---|---|
| Diabetic Ketoacidosis | must-not-miss | Nausea, vomiting, abdominal pain, dehydration, Kussmaul respirations, fruity breath, tachycardia, altered mental status; often type 1 diabetes but also type 2 diabetes, pregnancy, infection, MI, missed insulin, or SGLT2 inhibitor use | Venous pH <7.30 or bicarbonate <18 mmol/L with elevated beta-hydroxybutyrate/ketones and anion gap metabolic acidosis |
| Hyperosmolar Hyperglycemic State | must-not-miss | Older patient with type 2 diabetes, profound dehydration, confusion, seizures, focal neurological signs, very high glucose, minimal ketosis | Serum osmolality >320 mOsm/kg, marked hyperglycemia, minimal ketones, pH usually >7.30 |
| Euglycemic DKA | must-not-miss | DKA physiology with only mild-moderate hyperglycemia; associated with SGLT2 inhibitors, pregnancy, fasting, alcohol, or partial insulin treatment | High anion gap metabolic acidosis plus elevated beta-hydroxybutyrate despite glucose often <14 mmol/L |
| New Type 1 Diabetes | must-not-miss | Rapid weight loss, polyuria, polydipsia, fatigue, candidiasis, ketones, lean habitus, personal or family autoimmune disease | Ketones and insulin deficiency; autoantibodies and C-peptide may support classification after stabilisation |
| New Type 2 Diabetes | common | Gradual polyuria, polydipsia, blurred vision, recurrent infections; associated with central adiposity, hypertension, dyslipidemia, gestational diabetes history, or high-risk ancestry | A1c >=6.5%, fasting plasma glucose >=7.0 mmol/L, random glucose >=11.1 mmol/L with symptoms, or 2-hour OGTT >=11.1 mmol/L |
| Steroid- or Medication-induced Hyperglycemia | common | Temporal relationship with glucocorticoids, atypical antipsychotics, tacrolimus/cyclosporine, thiazides, tube feeds, or parenteral nutrition | Medication history plus capillary glucose pattern; A1c helps separate chronic dysglycemia from acute drug effect |
| Stress Hyperglycemia from Acute Illness | common | Hyperglycemia during sepsis, MI, stroke, pancreatitis, trauma, or surgery without known diabetes | A1c and repeat outpatient testing after recovery |
| Gestational Diabetes / Overt Diabetes in Pregnancy | less common | Hyperglycemia detected in pregnancy, especially with obesity, previous gestational diabetes, macrosomia, high-risk ancestry, or PCOS | Pregnancy-specific glucose challenge or OGTT according to local Canadian obstetric pathway |
| Diabetes Insipidus or Primary Polydipsia | less common | Marked polyuria and polydipsia without hyperglycemia; nocturia; hypernatremia in diabetes insipidus | Normal glucose with serum sodium/osmolality and urine osmolality assessment |
| Pancreatic Diabetes | rare | Diabetes after chronic pancreatitis, pancreatic cancer, cystic fibrosis, haemochromatosis, or pancreatic surgery; may have weight loss and steatorrhea | History, pancreatic imaging, exocrine insufficiency markers, and C-peptide if insulin deficiency suspected |
Red Flags & Key History
Symptoms
Vomiting, abdominal pain, Kussmaul breathing, or fruity breath — suggests DKA
Confusion, seizure, focal neurological symptoms, or profound weakness — suggests HHS or severe osmotic/electrolyte disturbance
Pregnancy with hyperglycemia, vomiting, or ketones — lower threshold for DKA and urgent obstetric/endocrine involvement
Chest pain, dyspnea, fever, dysuria, or cough — look for MI, PE, pneumonia, UTI, or sepsis as precipitant
SGLT2 inhibitor use with nausea or malaise — euglycemic DKA can occur without extreme glucose elevation
Polyuria, polydipsia, nocturia, blurred vision, weight change, and recurrent candidiasis — typical symptomatic hyperglycemia
Recent steroids, atypical antipsychotics, tube feeds, or parenteral nutrition — medication or iatrogenic hyperglycemia
Signs
Hypotension, tachycardia, poor perfusion, dry mucous membranes, reduced skin turgor
Altered level of consciousness, seizure, or coma
Kussmaul respirations or acetone odour
Fever or focal infection including foot ulcer, cellulitis, pneumonia, or pyelonephritis
Acanthosis nigricans, central adiposity, hypertension, and xanthelasma — insulin resistance phenotype
Lean habitus, vitiligo, thyroid disease, or other autoimmune signs — type 1 diabetes phenotype
Approach to Investigation
First-line
Bedside capillary glucose and ketonesImmediate triage test. Serum or capillary beta-hydroxybutyrate is preferred where available because urine ketones lag behind clinical improvement
Venous blood gasAssess pH and bicarbonate; DKA is usually high anion gap metabolic acidosis and venous pH is adequate for most management
Electrolytes, urea, creatinine, anion gap, and calculated osmolalityCorrect sodium for hyperglycemia; potassium may be normal/high despite total-body depletion
CBC, urinalysis, cultures as indicated, ECG, and chest imaging if symptomaticSearch for infection, MI, stroke, pancreatitis, missed insulin, medication effect, or pregnancy-related trigger
A1cAssesses chronicity and helps distinguish stress hyperglycemia from established diabetes; do not delay emergency care
Second-line
Diabetes classification testsGAD, IA-2, ZnT8 antibodies and fasting or stimulated C-peptide can help classify atypical diabetes after acute stabilisation
Lipase, liver tests, TSH, pregnancy test, toxicology, or cortisol testingUse when clinical picture suggests pancreatitis, thyroid disease, pregnancy, toxin/medication effect, or adrenal crisis
Complication baselineUrine ACR, eGFR, lipid profile, BP, foot examination, retinopathy referral, and cardiovascular risk assessment once stable
Specialist
ICU or high-acuity monitoringSevere DKA, HHS, coma, shock, severe electrolyte disturbance, pregnancy, or major precipitating illness
Endocrinology/diabetes education referralNew type 1 diabetes, recurrent DKA, uncertain classification, technology initiation, or complex insulin regimens
Management Principles
Diabetes Canada Clinical Practice Guidelines: Hyperglycemic Emergencies in Adults1
Immediate stabilisation
- ABCs, cardiac monitoring, frequent neurological checks, two IV lines, strict fluid balance, and trigger identification
- Start isotonic crystalloid promptly unless contraindicated; volume restoration is first-line in DKA and HHS
- Check potassium before insulin; replace potassium first if low
- Do not give bicarbonate routinely; reserve for extreme acidosis with specialist guidance
2
DKA pathway
- IV fluids, potassium replacement according to renal function and potassium, then IV regular insulin infusion
- Add dextrose-containing fluids once glucose falls but ketones/acidosis persist so insulin can continue
- Monitor glucose hourly and electrolytes/anion gap every 2-4 hours until stable
- Transition to subcutaneous insulin only when eating, clinically improved, and acidosis has resolved; overlap IV with basal insulin
3
HHS pathway
- Correct dehydration gradually; fluid deficit is often very large and osmolality should fall safely
- Start insulin after initial fluids and potassium assessment because fluids alone can substantially lower glucose
- Assess for thrombosis, infection, MI, stroke, and renal impairment
4
New diabetes after stabilisation
- Type 1 phenotype or ketosis: initiate basal-bolus insulin, ketone testing, sick-day rules, and urgent follow-up
- Type 2 phenotype: lifestyle and cardiometabolic risk assessment; metformin if appropriate, and consider agents with cardiorenal benefit when indicated
- Address smoking, BP, lipids, kidney protection, immunisations, foot care, eye screening, and medication access
Complications & Pitfalls
- Starting insulin before checking potassium: Insulin shifts potassium intracellularly and can precipitate fatal hypokalemia
- Missing euglycemic DKA: SGLT2 inhibitor users, pregnant patients, and fasting patients may have severe ketosis without very high glucose
- Stopping insulin too early: In DKA, continue insulin until ketosis and anion gap resolve, not merely until glucose normalises
- Over-rapid osmotic correction: Abrupt shifts increase neurological risk, especially in HHS and paediatric DKA
- Failure to find the trigger: Infection, MI, stroke, missed insulin, pancreatitis, steroids, and social barriers commonly precipitate metabolic emergencies
MCCQE1 Exam Tips
- 1If unwell with hyperglycemia, the next best step is bedside glucose, ketones, VBG, electrolytes, and fluids — not outpatient A1c alone
- 2DKA diagnosis depends on ketosis and acidosis; glucose level alone is not enough
- 3Potassium is the safety hinge. Normal potassium in DKA does not mean normal total-body potassium
- 4Add dextrose and continue insulin when glucose corrects before acidosis resolves
- 5HHS is older type 2 diabetes with confusion and profound dehydration; DKA is vomiting, abdominal pain, Kussmaul breathing, and ketones
- 6Include diabetes education, sick-day rules, insulin access, and follow-up for CanMEDS communicator/collaborator stations
- 7Do not classify diabetes purely by age; use phenotype, ketosis, autoimmunity, C-peptide, and clinical course
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