Diabetes Nursing Guide 2026: DKA, HHS, Insulin, and Blood Glucose Management

Part of the ICU Emergencies Hub — browse every related guide in one place.

This article was created with AI assistance.

Contents: Type 1 vs Type 2 Insulin Types DKA Management HHS Management DKA vs HHS Comparison Oral Antidiabetics Blood Glucose Monitoring Somogyi vs Dawn NCLEX High-Yield

Type 1 vs Type 2 Diabetes

Feature	Type 1	Type 2
Mechanism	Autoimmune destruction of beta cells → absolute insulin deficiency	Insulin resistance + progressive beta cell dysfunction → relative insulin deficiency
Onset	Usually abrupt; often childhood/young adult (but any age)	Gradual; usually adult onset; increasing in youth
Body weight	Usually normal or thin at diagnosis	Usually overweight or obese (80–90%)
DKA risk	HIGH — common; can occur at diagnosis	LOW — rare; usually only under extreme stress (sepsis, surgery)
HHS risk	Very rare	HIGH — the more common crisis in Type 2
Treatment	Insulin required; no oral options that work alone	Lifestyle first; oral agents; GLP-1 agonists; SGLT2 inhibitors; insulin when needed
C-peptide	Very low or absent (no endogenous insulin production)	Normal or high initially (insulin resistance)

Insulin Types: Onset, Peak, Duration

Type	Examples	Onset	Peak	Duration	Use
Rapid-Acting	Lispro (Humalog), Aspart (NovoLog), Glulisine (Apidra)	10–15 min	1–2 hr	3–4 hr	Give 15 min before or with meals; mealtime coverage
Short-Acting (Regular)	Regular (Humulin R, Novolin R)	30–60 min	2–4 hr	6–8 hr	Give 30–60 min before meals; IV for DKA drips; only insulin safe for IV push
Intermediate-Acting	NPH (Humulin N, Novolin N)	1–2 hr	6–12 hr	16–24 hr	Twice daily dosing; cloudy; roll (do not shake)
Long-Acting	Glargine (Lantus, Basaglar), Detemir (Levemir)	1–2 hr	NO peak (flat)	20–24 hr (glargine), 12–20 hr (detemir)	Once daily basal coverage; do NOT mix with other insulins; clear solution
Ultra Long-Acting	Degludec (Tresiba)	1–2 hr	No peak	>42 hr	Flexible dosing; longest duration; once daily

ONLY regular insulin (short-acting) can be given IV. All other insulins are SUBCUTANEOUS ONLY (except in specially designed drips). Giving NPH or long-acting insulin IV causes severe hypoglycemia and potentially death.

Insulin Administration Key Points

Rotate injection sites within the same region each day; document sites to ensure rotation
Absorption fastest in abdomen; slowest in thigh and buttocks
Inject at 90-degree angle for most patients; 45 degrees for thin patients (to avoid IM injection)
NPH is CLOUDY — roll gently to mix (do NOT shake — creates bubbles affecting dose)
Long-acting (glargine/detemir) is CLEAR — do NOT mix with any other insulin in same syringe
If mixing insulins (NPH + regular): draw up CLEAR (regular) first, then CLOUDY (NPH) — "clear before cloudy"
Store unopened insulin in refrigerator; opened vials at room temperature up to 28–30 days

DKA: Diabetic Ketoacidosis

Pathophysiology and Triggers

DKA results from insulin deficiency + counter-regulatory hormone excess (glucagon, cortisol, epinephrine) → uncontrolled lipolysis → free fatty acid ketone production → anion gap metabolic acidosis. Triggers: missed insulin doses (most common), infection/illness, new diagnosis of Type 1, cocaine use, certain medications (steroids, SGLT2 inhibitors).

DKA Diagnostic Criteria

Blood glucose >250 mg/dL (usually; can be lower in euglycemic DKA from SGLT2i)
Anion gap metabolic acidosis: pH <7.30, bicarbonate <18 mEq/L
Ketones positive in blood (beta-hydroxybutyrate) and/or urine

DKA Management (3 Key Pillars)

Fluids: 0.9% NS 1 L/hr for first 1–2 hours (aggressive rehydration); then 0.45% NS or 0.9% NS 250–500 mL/hr depending on Na; switch to D5-containing fluids when BG reaches 200–250 mg/dL (to allow insulin drip continuation while preventing hypoglycemia)
Insulin: Regular insulin IV drip (0.1 units/kg/hr); start AFTER K+ ≥3.5 (hypokalemia + insulin = fatal hypokalemia); goal: decrease BG by 50–75 mg/dL/hr; transition to SQ insulin with first meal 1–2 hr BEFORE stopping drip (overlap prevents rebound ketosis)
Potassium replacement: K+ drops when insulin given (insulin drives K+ into cells); if K+ <3.5: hold insulin, give K+ first; if K+ 3.5–5.5: add 20–40 mEq K+ to each liter of IV fluid; if K+ >5.5: no K+ replacement, hold until <5.5

Resolution criteria: BG <200 mg/dL AND anion gap closed AND pH >7.30 AND bicarbonate ≥15 mEq/L AND patient can eat. NOT defined by BG alone.

HHS: Hyperosmolar Hyperglycemic State

Pathophysiology and Triggers

HHS = severe hyperglycemia + hyperosmolarity WITHOUT significant ketosis. Residual insulin prevents ketosis but is insufficient to normalize glucose. Profound dehydration from osmotic diuresis. Typical patient: elderly Type 2 diabetic with limited fluid access. Triggers: acute illness (pneumonia, UTI most common), medications (steroids, diuretics), poor fluid intake, undiagnosed diabetes.

HHS Diagnostic Criteria

Blood glucose >600 mg/dL (often 800–1200+)
Effective serum osmolality >320 mOsm/kg
Absent or minimal ketosis
pH >7.30 (no significant acidosis)
Profound dehydration (deficit 8–10 L or more)

HHS Management

Aggressive fluid replacement is the PRIMARY treatment: 0.9% NS 1 L/hr x 2–4 hours, then 0.45% NS
Insulin: Low-dose regular insulin drip (0.1 units/kg/hr after fluid resuscitation begun); BG corrects more from fluids than insulin in HHS
Switch to D5 fluids when BG reaches 300 mg/dL (higher threshold than DKA)
Correct SLOWLY to avoid cerebral edema (more gradual than DKA due to brain adaptation to hyperosmolarity)

DKA vs HHS Comparison

Feature	DKA	HHS
Glucose	>250 mg/dL	>600 mg/dL (often >800–1200)
Ketones	Positive (high)	Absent or minimal
pH	<7.30 (acidosis)	>7.30 (near normal)
Osmolality	Variable (may be normal or elevated)	>320 mOsm/kg (markedly elevated)
Dehydration	Moderate (3–6 L deficit)	PROFOUND (8–10+ L deficit)
Diabetes type	Type 1 (primarily)	Type 2 (primarily), elderly
Onset	Rapid (hours)	Insidious (days to weeks)
Mortality	<1% (in good hospitals)	10–20% (older patients, comorbidities)

Key Oral Antidiabetic Medications

Drug Class	Examples	Mechanism	Key Nursing Points
Biguanides	Metformin (first-line)	Decreases hepatic glucose production; increases insulin sensitivity	Hold 48 hr before/after IV contrast (lactic acidosis risk); hold if SCr elevated (>1.5 male, >1.4 female); GI side effects (give with food); no hypoglycemia alone
Sulfonylureas	Glipizide, glyburide, glimepiride	Stimulates pancreatic insulin release	HYPOGLYCEMIA risk (stimulates insulin regardless of BG); glyburide: highest hypoglycemia risk, avoid in elderly; take with meals
GLP-1 Agonists	Semaglutide (Ozempic/Wegovy), liraglutide (Victoza/Saxenda), dulaglutide (Trulicity)	Incretin mimic: glucose-dependent insulin release, slows gastric emptying, decreases glucagon, appetite suppression	Significant weight loss; nausea common (titrate slowly); do NOT use if pancreatitis history or personal/family hx of MTC thyroid cancer; SQ injection weekly or daily
SGLT2 Inhibitors	Empagliflozin (Jardiance), dapagliflozin (Farxiga), canagliflozin (Invokana)	Blocks renal glucose reabsorption → glucose excreted in urine	Cardiovascular and renal benefits; UTI and genital yeast infection risk; euglycemic DKA possible; hold before surgery and contrast; Fournier's gangrene rare but serious; significant BP and weight reduction
DPP-4 Inhibitors	Sitagliptin (Januvia), saxagliptin, alogliptin	Enhances incretin hormones; glucose-dependent insulin stimulation	Low hypoglycemia risk alone; pancreatitis rare but possible; dose adjust for renal impairment; neutral weight effect

Blood Glucose Monitoring Targets

Setting	Target BG
Non-critically ill hospitalized (ADA 2024)	140–180 mg/dL for most patients; 100–140 mg/dL for select patients (cardiac surgery, CABG)
ICU/Critically ill	140–180 mg/dL; hypoglycemia (<70) is associated with higher mortality than mild hyperglycemia
Outpatient Type 1/2 (fasting/preprandial)	80–130 mg/dL (ADA); A1C <7% for most
Postprandial (1–2 hr after meals)	<180 mg/dL
Hypoglycemia threshold	<70 mg/dL = hypoglycemia requiring action

Somogyi Effect vs Dawn Phenomenon

Feature	Somogyi Effect	Dawn Phenomenon
What is it?	Rebound hyperglycemia after nocturnal hypoglycemia; hypoglycemia triggers counter-regulatory hormones → AM hyperglycemia	Natural early AM rise in BG from nocturnal growth hormone and cortisol secretion (liver releases glucose); no prior hypoglycemia
Pattern	BG LOW at 2–3 AM then HIGH in morning	BG normal or slightly low at 2–3 AM then RISES before wake time
Treatment	REDUCE evening insulin dose (too much was causing nocturnal hypo)	INCREASE insulin dose or shift timing; bedtime snack may help
How to diagnose	Check BG at 3 AM — if low, then AM high = Somogyi	Check BG at 3 AM — if normal/high, then higher AM = Dawn phenomenon

NCLEX High-Yield Points

ONLY regular insulin can be given IV; all others are subcutaneous only
When mixing insulins: clear first (regular), then cloudy (NPH)
DKA = glucose >250 + ketones + acidosis; HHS = glucose >600 + no significant ketones + profound dehydration
DKA potassium: check K+ BEFORE starting insulin — if K+ <3.5, hold insulin and replace K+ first
Hold metformin 48 hr before/after IV contrast and if SCr elevated (lactic acidosis risk)
Sulfonylureas (glyburide, glipizide) cause hypoglycemia; avoid glyburide in elderly
Somogyi: too much PM insulin → nighttime hypoglycemia → rebound AM hyperglycemia; fix = reduce PM insulin
Dawn phenomenon: natural cortisol/GH rise causes AM hyperglycemia without nighttime hypo; fix = increase insulin
BG target in hospitalized patients: 140–180 mg/dL (tight control <110 increases hypoglycemia mortality)

Get The ICU Notebook Newsletter

Clinical tools and career insights for ICU nurses. One email per week, no fluff.

Yes, send it free

No spam. Unsubscribe any time.

Diabetes Nursing Guide 2026: DKA, HHS, Insulin, and Blood Glucose Management

Type 1 vs Type 2 Diabetes

Insulin Types: Onset, Peak, Duration

Insulin Administration Key Points

DKA: Diabetic Ketoacidosis

Pathophysiology and Triggers

DKA Diagnostic Criteria

DKA Management (3 Key Pillars)

HHS: Hyperosmolar Hyperglycemic State

Pathophysiology and Triggers

HHS Diagnostic Criteria

HHS Management

DKA vs HHS Comparison

Key Oral Antidiabetic Medications

Blood Glucose Monitoring Targets

Somogyi Effect vs Dawn Phenomenon

NCLEX High-Yield Points

Related Articles