All EMS presentations
Endocrine/MetabolicClinical presentation

Hyperglycemia / possible DKA-HHS

A streamlined, differential-led presentation for rapid clinical review.

Clinical snapshot

Twenty-second review

  • Marked hyperglycemia causes osmotic diuresis and dehydration; DKA adds ketone-driven metabolic acidosis, while HHS produces profound hyperosmolality and neurologic dysfunction.
  • Kussmaul breathing, shock, severe dehydration, vomiting, abdominal pain, altered LOC, or suspected infection raises concern for DKA or HHS.
  • Keep sepsis or medication effect in the differential; overlapping or concurrent illness remains possible.
  • For hyperglycemia / possible dka-hhs, trends and combinations of findings are more informative than one isolated vital sign.
Differentials

Compare the clinical patterns

The repeated material is grouped inside each possibility. Open only the condition you need.

Serious2 conditions
DKATime-sensitive high-risk possibility

HPI

Clarify bgl; ketones if available; diabetes type.

Signs & symptoms

Polyuria, polydipsia, dehydration, tachypnea, vomiting, abdominal pain, or altered mentation.

Focused exam

Assess respiratory pattern, hydration, perfusion, temperature, neurologic status, and medication-delivery devices; Repeat glucose and clinical observations after treatment or during transport.

Brief pathophysiology

DKA may cause hyperglycemia / possible dka-hhs through a time-sensitive process capable of rapid physiological deterioration.

Vital-sign pattern

What the trend may show

Possible pattern

Hyperglycemic emergencies combine elevated glucose with dehydration; DKA often produces compensatory deep, rapid breathing. Normal glucose after treatment does not by itself confirm resolution.

Blood glucose (mmol/L)

Elevated

Marked hyperglycemia supports the syndrome; the absolute value does not distinguish DKA from HHS.

Respiratory rate (breaths/min)

Often rises

Kussmaul respirations are compensation for metabolic acidosis in DKA.

Heart rate (bpm)

Often rises

Tachycardia commonly reflects dehydration and physiologic stress.

Blood pressure (mmHg)

May fall

Dehydration can cause relative or overt hypotension; BP may be preserved early.

Front-load in the triage report

  • DKA: Polyuria, polydipsia, dehydration, tachypnea, vomiting, abdominal pain, or altered mentation.
  • BGL.
  • Ketones if available.
HHSTime-sensitive high-risk possibility

HPI

Clarify ketones if available; diabetes type; insulin adherence.

Signs & symptoms

Polyuria, polydipsia, dehydration, tachypnea, vomiting, abdominal pain, or altered mentation.

Focused exam

Repeat glucose and clinical observations after treatment or during transport; Assess respiratory depth and pattern, hydration, perfusion, mental status, abdomen, infection source, and diabetes medication use.

Brief pathophysiology

HHS may cause hyperglycemia / possible dka-hhs through a time-sensitive process capable of rapid physiological deterioration.

Vital-sign pattern

What the trend may show

Possible pattern

Hyperglycemic emergencies combine elevated glucose with dehydration; DKA often produces compensatory deep, rapid breathing. Normal glucose after treatment does not by itself confirm resolution.

Blood glucose (mmol/L)

Elevated

Marked hyperglycemia supports the syndrome; the absolute value does not distinguish DKA from HHS.

Respiratory rate (breaths/min)

Often rises

Kussmaul respirations are compensation for metabolic acidosis in DKA.

Heart rate (bpm)

Often rises

Tachycardia commonly reflects dehydration and physiologic stress.

Blood pressure (mmHg)

May fall

Dehydration can cause relative or overt hypotension; BP may be preserved early.

Front-load in the triage report

  • HHS: Polyuria, polydipsia, dehydration, tachypnea, vomiting, abdominal pain, or altered mentation.
  • Ketones if available.
  • Diabetes type.
Common1 condition
Uncomplicated hyperglycemiaCommon presentation pattern

HPI

Clarify bgl; ketones if available; diabetes type.

Signs & symptoms

Elevated glucose without major dehydration, acidosis pattern, or neurologic change.

Focused exam

Assess respiratory pattern, hydration, perfusion, temperature, neurologic status, and medication-delivery devices; Repeat glucose and clinical observations after treatment or during transport.

Brief pathophysiology

Uncomplicated hyperglycemia may explain the presenting symptoms through a common clinical mechanism, while serial assessment checks for complications or an alternate cause.

Vital-sign pattern

What the trend may show

Possible pattern

Hyperglycemic emergencies combine elevated glucose with dehydration; DKA often produces compensatory deep, rapid breathing. Normal glucose after treatment does not by itself confirm resolution.

Blood glucose (mmol/L)

Elevated

Marked hyperglycemia supports the syndrome; the absolute value does not distinguish DKA from HHS.

Respiratory rate (breaths/min)

Often rises

Kussmaul respirations are compensation for metabolic acidosis in DKA.

Heart rate (bpm)

Often rises

Tachycardia commonly reflects dehydration and physiologic stress.

Blood pressure (mmHg)

May fall

Dehydration can cause relative or overt hypotension; BP may be preserved early.

Front-load in the triage report

  • Elevated glucose without major dehydration, acidosis pattern, or neurologic change.
  • BGL.
  • Ketones if available.
Mimics2 conditions
SepsisImportant alternative presentation

HPI

Clarify bgl; ketones if available; diabetes type.

Signs & symptoms

Infection and steroids can trigger hyperglycemia and independently cause serious illness.

Focused exam

Assess respiratory pattern, hydration, perfusion, temperature, neurologic status, and medication-delivery devices; Repeat glucose and clinical observations after treatment or during transport.

Brief pathophysiology

Sepsis can resemble hyperglycemia / possible dka-hhs through overlapping symptoms or referred physiology despite a different primary mechanism.

Vital-sign pattern

What the trend may show

Possible pattern

No single vital sign diagnoses sepsis. New tachypnea, abnormal temperature, tachycardia, or falling pressure—especially with altered mentation or poor perfusion—supports organ dysfunction and urgency.

Respiratory rate (breaths/min)

May rise early

Tachypnea is included in NEWS2 and can precede overt hypotension.

Temperature (°C)

High or low

Absence of fever does not exclude sepsis; hypothermia is concerning.

Heart rate (bpm)

Often rises

Tachycardia is common but may be blunted by age or medication.

Blood pressure (mmHg)

May fall

Relative hypotension and trend matter; profound hypotension can be late.

Front-load in the triage report

  • Infection and steroids can trigger hyperglycemia and independently cause serious illness.
  • BGL.
  • Ketones if available.
Medication effectImportant alternative presentation

HPI

Clarify ketones if available; diabetes type; insulin adherence.

Signs & symptoms

Infection and steroids can trigger hyperglycemia and independently cause serious illness.

Focused exam

Repeat glucose and clinical observations after treatment or during transport; Assess respiratory depth and pattern, hydration, perfusion, mental status, abdomen, infection source, and diabetes medication use.

Brief pathophysiology

Medication effect can resemble hyperglycemia / possible dka-hhs through overlapping symptoms or referred physiology despite a different primary mechanism.

Vital-sign pattern

What the trend may show

Possible pattern

Hyperglycemic emergencies combine elevated glucose with dehydration; DKA often produces compensatory deep, rapid breathing. Normal glucose after treatment does not by itself confirm resolution.

Blood glucose (mmol/L)

Elevated

Marked hyperglycemia supports the syndrome; the absolute value does not distinguish DKA from HHS.

Respiratory rate (breaths/min)

Often rises

Kussmaul respirations are compensation for metabolic acidosis in DKA.

Heart rate (bpm)

Often rises

Tachycardia commonly reflects dehydration and physiologic stress.

Blood pressure (mmHg)

May fall

Dehydration can cause relative or overt hypotension; BP may be preserved early.

Front-load in the triage report

  • Infection and steroids can trigger hyperglycemia and independently cause serious illness.
  • Ketones if available.
  • Diabetes type.
Red flags

Findings that should escalate concern

  • Kussmaul breathing, shock, severe dehydration, vomiting, abdominal pain, altered LOC, or suspected infection raises concern for DKA or HHS.
  • DKA or HHS: Polyuria, polydipsia, dehydration, tachypnea, vomiting, abdominal pain, or altered mentation.
Related medications

Medication recognition

MetforminEmpagliflozinInsulin glargineInsulin aspart
Related EMS presentations

Continue the clinical pathway

General MedicalGeneral weakness / malaiseGIAbdominal painNeurologicAltered LOC / confusionGeneral MedicalNausea / vomitingInfectiousFever / suspected infection / sepsisEndocrine/MetabolicHypoglycemia
References

Clinical and academic sources

Curated clinical guidance and peer-reviewed evidence supporting this presentation. Current BCEHS guidance, medical direction, and local policy remain authoritative for practice.

BCEHS Handbook — specific CPGs

  1. E01: Hypoglycemia and HyperglycemiaBC Emergency Health Services Handbook

    Official BCEHS clinical practice guidance for hypoglycemia and hyperglycemia.

Supporting clinical and academic evidence

  1. CEDIS Presenting Complaint List updateCanadian Association of Emergency Physicians

    Presenting-complaint terminology and categorization context. It does not establish a prehospital “top 100” ranking.

  2. Clinical Practice GuidelinesDiabetes Canada

    Canadian evidence-based guidance for diabetes, hypoglycemia, hyperglycemia, and related emergencies.

  3. Management of Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar StateMedical Clinics of North America · 2017

    DKA and HHS physiology, dehydration, electrolyte disturbance, triggers, and emergency priorities.