Chart — Endocrine
Diabetes Assessment Findings Chart
Key assessment findings in diabetes nursing — hyperglycemia, hypoglycemia, DKA, HHS, and chronic complications — with likely cause, clinical significance, and nursing action for each finding.
Source: ADA Standards of Medical Care; Endocrine Society Guidelines; AACE Consensus Statements; clinical nursing practice standards.
Educational use only. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Hyperglycemia
| Finding | Likely Cause | Clinical Significance | Nursing Action |
|---|---|---|---|
| Polyuria (excessive urination) | Osmotic diuresis — high glucose draws water into urine | Volume depletion; dehydration; electrolyte loss | Measure I&O; assess for dehydration; notify provider if glucose >250 mg/dL; assess for DKA/HHS |
| Polydipsia (excessive thirst) | Cellular dehydration from hyperosmolar state | Compensatory response to osmotic diuresis and dehydration | Encourage fluid intake if patient can drink; monitor glucose trend; assess fluid status |
| Polyphagia (excessive hunger) with weight loss | Cells starved of glucose despite hyperglycemia (insulin deficiency — Type 1) | Classic Type 1 DM symptom; starvation at cellular level | Assess glucose; insulin administration per protocol; nutrition consult if significant weight loss |
| Blurred vision | Osmotic lens swelling from hyperglycemia | Usually resolves with glucose control; distinguish from retinopathy | Assess glucose; document and report if new or worsening; ophthalmology referral for known DM |
| Slow wound healing / skin infections | Impaired leukocyte function, reduced perfusion, neuropathy | Infection risk; DFU (diabetic foot ulcer) risk; sepsis risk | Skin and foot assessment with each visit; glucose control; wound care protocol; culture if infected |
Hypoglycemia
| Finding | Likely Cause | Clinical Significance | Nursing Action |
|---|---|---|---|
| Diaphoresis (sweating), shakiness, tachycardia | Sympathetic nervous system activation in response to low glucose | Adrenergic (early) hypoglycemia signs — glucose typically <70 mg/dL | Check glucose IMMEDIATELY; Rule of 15 (15g carbs → recheck in 15 min); if unable to swallow: IV D50W or glucagon |
| Confusion, slurred speech, irritability | Neuroglycopenia — brain glucose deprivation | Moderate hypoglycemia; glucose typically <54 mg/dL; escalation risk | Check glucose; do NOT give oral carbs if confused (aspiration risk); IV D50W; notify provider; continuous monitoring |
| Seizure or loss of consciousness | Severe neuroglycopenia — critical brain glucose deprivation | Severe hypoglycemia — medical emergency | IV D50W 25–50 mL STAT; if no IV access: glucagon IM/SQ; notify provider immediately; monitor neuro status; prevent aspiration |
| Nocturnal hypoglycemia (night sweats, nightmares) | Insulin peak during sleep; prolonged fasting; delayed meal | Overnight hypoglycemia may be missed; can lead to hypoglycemia unawareness | Bedtime glucose check protocol; adjust insulin timing per provider; consider 3 AM check; educate patient/family |
DKA Signs
| Finding | Likely Cause | Clinical Significance | Nursing Action |
|---|---|---|---|
| Kussmaul respirations (deep, rapid, labored breathing) | Respiratory compensation for metabolic acidosis — body blowing off CO₂ | Classic DKA sign; pH typically <7.3; metabolic acidosis confirmed | Assess respiratory rate and depth; check ABG/BMP; notify provider; prepare for IV insulin and fluid protocols |
| Fruity or acetone breath | Exhaled acetone (ketone byproduct) | Ketoacidosis present — Type 1 DM most common; also Type 2 under severe stress | Check blood/urine ketones; glucose; BMP; notify provider if DKA suspected |
| Nausea, vomiting, abdominal pain | Ketone effect on GI tract; gastroparesis; DKA systemic effects | Worsens dehydration; common DKA presentation; may mimic surgical abdomen | IV access; NPO; antiemetics per order; BMP; notify provider; prepare DKA protocol |
| Altered mental status in DKA | Acidosis, dehydration, hyperosmolarity contributing to CNS depression | May indicate severe DKA or cerebral edema (rare, seen in pediatric DKA) | Neuro assessment; notify provider immediately; rehydrate cautiously; avoid rapid glucose normalization |
HHS Signs
| Finding | Likely Cause | Clinical Significance | Nursing Action |
|---|---|---|---|
| Profound dehydration (skin tenting, dry mucous membranes, hypotension) | Massive osmotic diuresis from extreme hyperglycemia (>600 mg/dL) | Fluid deficit 8–10 liters typical; electrolyte losses massive | IV fluid resuscitation (NS or 0.45% NaCl per protocol); strict I&O; monitor electrolytes; urine output ≥0.5 mL/kg/hr goal |
| Neurological changes (confusion, focal deficits, seizures) | Hyperosmolarity-induced CNS dysfunction; cerebral dehydration | Hallmark of HHS vs DKA; neurological symptoms correlate with osmolality elevation | Neuro assessment q1–2h; notify provider; rehydrate gradually; osmolality monitoring; ICU-level care |
| Absent or minimal ketones (no fruity breath, no Kussmaul respirations) | Residual insulin sufficient to suppress lipolysis and ketogenesis (unlike DKA) | Key differentiator from DKA — HHS is hyperosmolar without significant acidosis | Confirm with labs (pH >7.3, bicarbonate >15, minimal ketones); treat as HHS protocol — slower rehydration |
Chronic Complications
| Finding | Likely Cause | Clinical Significance | Nursing Action |
|---|---|---|---|
| Peripheral neuropathy (numbness, burning, tingling feet) | Chronic hyperglycemia damages peripheral nerves (polyol pathway, oxidative stress) | Loss of protective sensation → unnoticed foot injuries → DFU → amputation | Foot assessment each visit; patient education (no bare feet); podiatry referral; glucose control; pain management |
| Diminished or absent pedal pulses; claudication | Peripheral arterial disease (PAD) from atherosclerosis accelerated by DM | Critical limb ischemia risk; amputation risk; wound healing impaired | Vascular assessment; ABI (ankle-brachial index); vascular surgery referral; antiplatelet therapy per order; no compression without ABI |
| Foamy urine, proteinuria, elevated creatinine | Diabetic nephropathy — glomerular damage from chronic hyperglycemia | CKD progression; end-stage renal disease (ESRD) risk; metformin hold if eGFR <30 | Monitor BMP/eGFR; urine albumin-to-creatinine ratio; BP control; ACE inhibitor/ARB per order; nephrology referral |
| Visual changes, floaters, vision loss | Diabetic retinopathy — proliferative neovascularization from VEGF release | Leading cause of blindness in working-age adults; irreversible if advanced | Annual dilated eye exam; refer to ophthalmology; aggressive glucose and BP control; educate patient on symptoms |
Related Resources
Diabetes Mellitus FundamentalsType 1 vs Type 2, diagnostic criteria, and nursing overview
Open →Diabetic Ketoacidosis (DKA)DKA pathophysiology, labs, and treatment
Open →Hyperosmolar Hyperglycemic State (HHS)HHS vs DKA and emergency management
Open →Glycemic Targets ReferenceGlucose goals, hypoglycemia thresholds, and critical values
Open →Standards & sources
Fact-checked Jun 20, 2026This page is written to align with ADA Standards of Medical Care; Endocrine Society Guidelines; AACE Consensus Statements. It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →