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Hypoglycemia hub

Workflow for acute hypoglycemic crisis in dogs and cats. Covers dextrose bolus, CRI preparation, and glucagon CRI for refractory insulinoma cases.

  • Insulinoma caution, avoid large dextrose boluses. In suspected insulinoma, a bolus of IV dextrose can stimulate further insulin release from the tumor, triggering a cycle of dextrose → hyperinsulinism → rebound hypoglycemia. Give the minimum bolus needed to resolve clinical signs, then maintain with a CRI. Consider glucagon CRI instead.
  • Goal is resolution of clinical signs, not normalisation of glucose. Target low-normal euglycemia (not high normal). Hyperglycemia in an insulinoma patient stimulates more insulin.
  • Do not use 5% dextrose in water as the sole fluid. It can cause severe, potentially fatal hyponatremia. Add 50% dextrose to a balanced isotonic crystalloid (LRS or 0.9% NaCl) instead.

Common causes at a glance

Most common. GP practice
  • Exogenous insulin overdose, diabetic patient, anorexia, vomiting after insulin
  • Insulinoma, middle-aged to older dog, episodic collapse, BG < 60 mg/dL
  • Neonatal / toy breed, inadequate substrate, cold, missed meals
  • Sepsis, non-insulin-mediated excess glucose utilisation
  • Hypoadrenocorticism, loss of cortisol counterregulatory mechanisms
  • Xylitol toxicity, stimulates insulin release; also causes hepatic necrosis
Clinical signs

Neuroglycopenic: altered mentation, dullness, weakness, ataxia, blindness, seizures, recumbency. Prolonged neuroglycopenia → permanent neuronal damage, especially irreversible blindness.

Adrenergic (counter-regulatory): pacing, vocalising, restlessness, trembling, vomiting, panting, tachypnea, diarrhea.

Diagnosis: BG ≤ 60 mg/dL. Clinical signs often don't appear until < 50 mg/dL. Whipple's triad: low BG + compatible signs + resolution with treatment.

Treatment checklist

  1. 1

    Confirm hypoglycemia

    Point-of-care glucometer. Note: glucometers may under- or overestimate BG, especially at abnormal haematocrits. If haematocrit is out of range or result is unexpected, confirm with laboratory. Blood from medial aspect of ear is more accurate than paw pad or mucous membrane. Separate serum within 30 min or use a sodium fluoride tube to arrest ongoing glycolysis in the sample.

  2. 2

    Dextrose bolus. IV (preferred)

    Dilute 50% dextrose at least 1:2 with sterile water or saline before administering, undiluted 50% dextrose is hyperosmolar and causes severe phlebitis. Give over 5 minutes. Improvement in neuroglycopenic signs expected within 1–2 minutes of IV supplementation.

    Parameter Value
    Dose (g/kg): 0.25–0.5 g/kg
    As 50% dextrose (mL/kg): 0.5–1 mL/kg of 50% dextrose
    Dilution: Minimum 1:2 (1 mL dextrose 50% : 2 mL saline/water)
    Rate: Give over 5 minutes IV

    No IV access? Karo syrup, pancake syrup, or honey applied to oral mucous membranes as a temporary bridge only, absorption is slow and unreliable. Obtain IV access immediately. Risk of aspiration in obtunded patients.

  3. 3

    Dextrose CRI, maintenance

    Once signs resolve, transition to a dextrose CRI to maintain low-normal euglycemia. Add 50% dextrose to an isotonic crystalloid (LRS or 0.9% NaCl). Never use D5W as the sole fluid, hyponatremia risk. Continue until underlying cause is identified and resolved (hours to days depending on aetiology).

    Target concentration Recipe (per 1 L crystalloid)
    2.5% dextrose Add 50 mL of 50% dextrose to 950 mL crystalloid
    5% dextrose Add 100 mL of 50% dextrose to 900 mL crystalloid

    Start at 2.5–5% and adjust based on serial BG. If >10% dextrose is needed to maintain euglycemia, use a central line to prevent peripheral phlebitis. Monitor BG every 1–2 hr while adjusting rate.

  4. 4

    Feed the patient, as soon as alert enough

    Small, frequent meals low in simple sugars (higher in complex carbohydrates and protein). Institute as soon as the patient can eat and swallow safely. Oral feeding is the most physiologic method of glucose maintenance and should replace the CRI once tolerated.

  5. 5

    Glucagon CRI, for insulinoma or refractory hypoglycemia

    Preferred over large dextrose boluses in patients with confirmed or suspected insulinoma, bypasses the dextrose → insulin release cycle. Stimulates hepatic glycogenolysis and gluconeogenesis directly. Titrate to the lowest rate that resolves clinical signs and maintains low-normal euglycemia. Note: dose is in nanograms, not micrograms or mg.

    Reconstitute: Per manufacturer instructions → 1000 ng/mL solution in 0.9% NaCl
    Bolus: 50 ng/kg IV
    CRI: 5–40 ng/kg/min, start low, titrate to effect

    Median glucagon CRI doses are higher in non-survivors, use the lowest effective rate. Units are nanograms (ng), do not confuse with micrograms (µg) or milligrams (mg).

  6. 6

    Glucocorticoids, cause-specific only

    Antagonise insulin effects and stimulate gluconeogenesis. Appropriate for paraneoplastic or endocrine-induced hypoglycemia. Contraindicated if infection is the cause (sepsis-induced hypoglycemia).

    Hypoadrenocorticism: Dexamethasone 0.1–0.2 mg/kg IV (does not interfere with cortisol assay)
    Insulinoma (chronic): Prednisone 0.25–0.5 mg/kg PO q12h (cats: prednisolone preferred)

    Dexamethasone is the preferred initial glucocorticoid for suspected hypoadrenocorticism, use before ACTH stimulation test because it will not be measured by the cortisol assay. Do not give prednisone or prednisolone before ACTH stim.

  7. 7

    Treat the underlying cause

    • Insulin overdose: discontinue insulin, feed as soon as able, monitor BG q1–2h; restart insulin at 25–50% reduced dose when eating and BG stable
    • Insulinoma: surgical excision ± prednisone, diazoxide, or toceranib for medical management; dietary management (small frequent low-GI meals)
    • Hypoadrenocorticism: aggressive 0.9% NaCl resuscitation, dexamethasone, ACTH stim test, then long-term mineralocorticoid (DOCP or fludrocortisone)
    • Sepsis: source control, broad-spectrum antimicrobials, supportive care, do NOT give glucocorticoids
    • Neonatal / toy breed: feed frequently, keep warm; recheck BG and repeat supplementation as needed
    • Xylitol toxicity: dextrose supplementation + liver protective support; monitor liver values 24–72h post-ingestion for delayed hepatotoxicity
  8. 8

    Monitoring

    • BG every 1–2 hr while on IV dextrose, more frequently during bolus phase
    • Mentation, neurologic status, watch for signs of persistent neuroglycopenia
    • Electrolytes, hypokalemia common with insulin-mediated cases
    • Liver values if xylitol toxicity, paraneoplastic, or prolonged hypoglycemia
    • Once stable: insulin level drawn during a hypoglycemic episode if insulinoma suspected (high or normal insulin with low BG is diagnostic)
    • Thoracic radiographs for metastatic disease if insulinoma confirmed

Sources

  • Koenig A. Hypoglycemia. In: Silverstein DC, Hopper K, eds. Small Animal Critical Care Medicine. 3rd ed. St. Louis, MO: Elsevier; 2023. Chapter 75. Primary source for all doses, dextrose preparation tables, glucagon CRI protocol, and cause-specific management.