Polyuria, polydipsia, weight loss, vomiting, abdominal pain
SGLT2 inhibitors, insulin omission, infection, pregnancy
Steroid use or recent cessation; pituitary disease; pigmentation
Chest pain, fever, diarrhea as precipitants
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← All presentations
DKA, HHS & Adrenal Crisis
Sugar, potassium, volume — and never withhold steroids in the crashing steroid-dependent patient.
Your objective: explain the approach, recognize important warning signs, then test your recall.
Abbreviations explained
- ACS
- Acute coronary syndrome
- OMI
- Occlusion myocardial infarction
- ECG
- Electrocardiogram
- PE
- Pulmonary embolism
- POCUS
- Point-of-care ultrasound
- QTc
- QT interval corrected for heart rate
- LBBB
- Left bundle branch block
- RBBB
- Right bundle branch block
- hs-cTn
- High-sensitivity cardiac troponin
- CTA
- Computed tomography angiography
- ICU
- Intensive care unit
Filter
The jobSugar, potassium, volume — and never withhold steroids in the crashing steroid-dependent patient.
- Bedside glucose, VBG/ketones, and potassium in every sick diabetic or unexplained shock.
- DKA: fluids first, potassium repletion, then insulin. Defer insulin if K⁺ is <3.5 mmol/L.
- HHS: slower osmolar correction, hunt the trigger (infection, MI, stroke), watch sodium and neuro status.
- Steroid-dependent + shock or vomiting: stress-dose hydrocortisone now — do not wait for a cortisol.
Hyperglycemic crises and adrenal crisis are metabolic shock.
DKA requires diabetes/hyperglycemia, ketonemia and metabolic acidosis; blood β-hydroxybutyrate is preferred (glucose may be near-normal on SGLT2 inhibitors). HHS is extreme hyperosmolarity with profound volume loss and a quieter acid-base picture. Adrenal crisis is refractory shock in the steroid-dependent or Waterhouse-Friderichsen patient — give hydrocortisone without waiting for a cortisol. Potassium before insulin if K⁺ is low; fluids are an early treatment in DKA/HHS; individualize volume for heart failure, renal failure and frailty.
Diabetic ketoacidosis Critical
Key: Diabetes history or glucose ≥200 mg/dL, β-hydroxybutyrate ≥3 mmol/L (or urine ketones ≥2+), and pH <7.3 and/or bicarbonate <18 mmol/L. Euglycemic DKA on SGLT2 inhibitors is easy to miss — check ketones when the story fits even if glucose is modest.
Hyperosmolar hyperglycemic state Critical
Key: Glucose ≥600 mg/dL, effective osmolality >300 or total >320 mOsm/kg, β-hydroxybutyrate <3 mmol/L, pH ≥7.3 and bicarbonate ≥15 mmol/L; altered mentation is not required — huge water deficit; correct slowly to avoid cerebral edema.
Adrenal crisis Critical
Key: Shock, hyponatremia, hyperkalemia, or hypoglycemia in a steroid-dependent, pituitary, or meningococcemia patient — hydrocortisone 100 mg IV now.
Precipitant ACS / sepsis / pancreatitis Critical
Key: The crisis is often triggered — ECG, cultures, lipase as indicated. Treat the trigger with the protocol.
Hypokalemia during insulin Critical
Key: Total-body K⁺ is low even when the first value is normal; insulin drives K⁺ in — replace and monitor.
Cerebral edema (especially pediatric DKA) Critical
Key: Headache, bradycardia, or deteriorating GCS during treatment — raise head, mannitol/hypertonic saline, slow the fluids, ICU.
Simple hyperglycemia / missed insulin Common
Key: No acidosis, no ketones, well-appearing — hydration, insulin plan, follow-up. Still hunt infection.
Tick what your patient has — the banner updates as you go.
Volume status
tachycardia, dry mucosa, delayed cap refill
Kussmaul breathing (DKA); focal neuro or coma (HHS)
Abdomen (pancreatitis, surgical mimic); fever; skin (meningococcus, candida)
Medic-alert jewellery; insulin pump in situ
Bedside
- Glucose, VBG, blood β-hydroxybutyrate (urine if unavailable), ECG
- Potassium on the blood gas while the lab is pending
Labs
- Electrolytes with anion gap, osmolality, creatinine, phosphate, CBC, lipase
- Cultures if febrile; troponin if ACS possible; draw cortisol/ACTH before hydrocortisone only if this causes no treatment delay; hydrocortisone confounds subsequent cortisol interpretation
- β-hCG when relevant
Imaging
- CXR; CT only for a suspected surgical or neurologic precipitant
- Do not delay DKA/HHS therapy for imaging
Medication safety reminder
Use this as a first-pass prompt; verify all medications, doses, concentrations, contraindications, weight, pregnancy status, and local protocols before administration.
Check indication, allergy, route, renal/hepatic risk, interactions, monitoring, and local formulary.
Discharge
- Isolated hyperglycemia without ketosis or HHS features, a clear missed-dose story, reliable insulin access and follow-up.
Admit (ward / HDU)
- Uncomplicated DKA responding on a protocol, new diabetes needing education, HHS with improving osmolality under monitoring.
ICU
- Severe acidosis, shock, HHS with coma, pediatric DKA, adrenal crisis, cerebral edema, or a dangerous precipitant (ACS, sepsis).
Use objective reassessment and the local pathway.
Before the next decision · reassess and hand over
Use these learning prompts with the presentation’s pathway. They are not discharge criteria.
- Reassess: compare symptoms, observations and examination with the initial assessment and response to treatment.
- Warning signs for DKA, HHS & Adrenal Crisis:
- Altered mentation with hyperglycemia or ketones
- K⁺ <3.5 before insulin, or falling K⁺ on treatment
- Steroid-dependent patient with shock or vomiting
- SGLT2 inhibitor + acidosis even with a “normal” glucose
- Headache or falling GCS in a child on a DKA protocol
- Hypotension that does not respond to fluids (think adrenal, sepsis, ACS)
- Reconsider: check unresolved findings and alternative explanations, including the pitfalls below.
- Escalate: communicate deterioration, uncertainty or needs beyond the current setting.
- Plan the transition: identify outstanding results, responsibility for follow-up, patient understanding and specific return advice.
Clinical Pearls
- Fluids, potassium, then insulin. That order prevents the crash.
- SGLT2 + unwell = check ketones even if glucose is not high.
- Hydrocortisone in the crashing steroid-dependent patient is a resuscitation drug, not an endocrine consult.
- Clear ketonemia and acidosis, not just hyperglycemia; saline-related acidosis can keep the anion gap/bicarbonate misleading.
Pitfalls
- Starting insulin before potassium is replaced when K⁺ is already low — ventricular arrhythmia.
- Missing euglycemic DKA because the glucose is 180 mg/dL on an SGLT2 inhibitor.
- Waiting for a random cortisol in adrenal crisis.
- Over-rapid correction of HHS sodium/osmolality.
- Calling DKA abdominal pain “just ketosis” without considering pancreatitis or a surgical abdomen.
- Do not stop insulin just because glucose falls: add dextrose and continue until ketoacidosis resolves. Adult resolution: β-hydroxybutyrate <0.6 mmol/L plus venous pH ≥7.3 or bicarbonate ≥18 mmol/L; ideally glucose <200 mg/dL. The anion gap and urine ketones are not resolution targets.
PRACTICE REFRESHER
Rapid recall
Test your first action and the dangerous diagnoses before revealing the answer.
01 · First move
Before you scroll, what needs to happen first?
Bedside glucose, VBG/ketones, and potassium in every sick diabetic or unexplained shock.
02 · Immediate threats
Name at least two diagnoses that cannot wait.
Diabetic ketoacidosis · Hyperosmolar hyperglycemic state · Adrenal crisis
PRIVATE TO THIS DEVICE
Your learning note
Capture a weak point, a teaching pearl, or a question to take to your next shift.
Review schedule starts when marked reviewed
Selected guidance · source check 2026-09-07. These 2 source links support selected teaching points, not a complete review of this topic. Check population, setting and local protocol before applying a recommendation.
- ADA/EASD and partner societies: adult DKA/HHS consensus (2024)
- Endocrine Society: primary adrenal insufficiency
- Rosen’s Emergency Medicine, 10th ed. (2023) — DKA, HHS, adrenal insufficiency
- ADA/EASD/AACE/JBDS/DTS Hyperglycemic Crises in Adults Consensus Report (2024); ADA Standards of Care 2026
- ISPAD pediatric DKA; Endocrine Society adrenal insufficiency guidance