Hypoglycemia

Hypoglycemia in non-diabetic subject
Quick Review of hypoglycemia in Diabetic patients

✓ Considered one of the acute complications of DM
✓ More common in type 1 DM due to insulin (Type 1 DM treatment specially basal bolus insulin)
(attack of various degrees occurs at least once a week and life-threatening attack occurs at least once a year)
✓ Causes
• Disharmony between meals or exertion and insulin
• Stress, acute illness, renal impairment (↓↓ insulinase → ↑ insulin action), hypothyroidism
• Drugs → secretagogues (sulfonylurea and meglitinides)

✓ There is No cut off point to define hypoglycemia → ↓↓ blood glucose up to manifestations
based on patient’s threshold/tolerance
✓ Signs and Symptoms
• Neurogenic → fatigue, palpitations, sweating, fine tremors, cold extremities, nervousness, pale
• Neuroglycopenic →agitation, fits, coma, amnesia, permanent brain damage
Hypoglycemia → Defined as plasma glucose low enough for development of symptoms of

hypoglycemia (threshold level is dynamic)
Normal defense against development of hypoglycemia:
1. Suppression of insulin secretion: the first step take place (BG 80-85mg/dl) →allowing for
increase hepatic & renal gluconeogenesis, hepatic glycogenolysis
2. Decrease peripheral utilization.
3. Increase glucagon production: 2nd line defense (when BG 65-70mg/dl) → increase hepatic
gluconeogenesis & glycogenolysis.
4. Catecholamine production → alarming symptoms & signs (Patient with autonomic
neuropathy won’t experience these alarming symptoms) → allowing for increase hepatic
& renal gluconeogenesis, hepatic glycogenolysis, decrease peripheral utilization.
5. In prolonged cases (>4h): GH, cortisol.
Whipple's triad of manifestation with raising BG
• Whipple’s triad Must be documented in non-Diabetic with hypoglycemia
• Either neurogenic or neuroglycopenic
• Triad → Symptoms and/or signs of hypoglycemia + Documented venous sample of
low BG during the attack (patient must be admitted to hospital to capture the event) +
improving of manifestation with raising BG
• Capillary blood glucose (finger-prick) levels are less by 10% than venous/plasma sample
Causes of hypoglycemia in non-diabetics
A) In ill or medicated subject
• Drugs → insulin, insulin secretagogue, alcohol, quinine (anti-malarial), Gatifloxacin
(respiratory quinolones), indomethacin (NSAIDs), pentamidine (anti-parasitic)
• Critical illness → acute liver failure (fulminant hepatitis), renal failure, heart failure, sepsis (septic shock)
• Hormonal deficiency → Glucagon, catecholamines(epi and nore), Cortisol (Addisons disease,
hypopituitarism)
• Tumors other than insulinoma → (Paraneoplastic syndrome → endocrinal and neurological
manifestations) SCC – small cell carcinoma or oat cell carcinoma of the lungs, hepatoma,
sarcomas → tumor cells release substances that act like insulin e.g., Insulin like growth
factor 2
B) In seeming well subject
• Insulinoma (rare) → may be sporadic or part of familial syndromes e.g., MEN-1
• Functional B-cells disorders (very difficult to diagnose) → post gastric bypass (dumping
syndrome), non-insulinoma pancreatogenous hypoglycemia, in children due to genetic
disturbances
• Auto immune hypoglycemia (Hirata Syndrome) → autoantibodies stimulating B-cells to
secrete insulin
• Factitious hypoglycemia (pretending to be ill for the sake of attention → Munchausen
Syndrome) → excluded by sulphonylurea testing in urine if induced by oral hypoglycemic
drug. If induced by insulin, it’s difficult to be detected
Fasting hypoglycemia
The symptoms of fasting hypoglycemia occur several hours after food (e.g., on waking or at
night) or can be precipitated by exercise
Causes:
• Drugs (insulin, sulphonylurea, quinine, salicylates, alcohol)
• Beta cell functional hyperplasia
• Insulinoma. (Incidence 1-2 /million, mostly single, benign, <2cm, may be familial)
• Organ Failure (acute fulminant hepatitis, CRF)
• Hormone deficiency (Addison’s disease, hypopituitarism)
• Non-islet cell tumors (fibrosarcoma, hepatocellular carcinoma, mesothelioma): IGFII
mediated.
• Autoimmune (insulin receptor-stimulating antibodies)
• Infection (septicemia, malaria)
• Inborn errors of metabolism (glycogen storage disease)
Postprandial hypoglycemia: Symptoms usually occur 2–5 hours after food.
• Alcohol
• Overweight & obese with insulin resistance (common) → reactive hypoglycemia due to ↑↑
insulin and ↓↓ glucagon + impaired fasting hyperglycemia → weight loss is the main
treatment to break the vicious cycle
• Late dumping syndrome. (common)
• Inborn errors of metabolism (hereditary fructose intolerance, maple syrup disease)
1.
Approach to a case of hypoglycemia (after sure documentation)
2. Test for circulating oral hypoglycemic agents → to exclude factitious hypoglycemia
3. For patient with fasting hypoglycemia: perform 72h fasting test in hospitalized closely
observed patient
4. For patient with postprandial hypoglycemia: perform mixed meal challenge in
hospitalized closely observed patient
The test end after documentation of hypoglycemia with assessment of insulin, proinsulin, c-peptide
4. Localizing images: Once diagnosis of endogenous hyperinsulinemia as a cause of

hypoglycemia. Dual phases CT, MRI with gadolinium enhancement, US, endoscopic
sonography, somatostatin receptor scintigraphy.
Management:
Immediate (emergency – ABCDE):
• Oral glucose as simple table sugar (the best) or fruit juice. Rule of 15 → give 15g (3
spoons) and measure blood glucose every 15 minutes. If not available give sugary fruit
juices. Chocolates are better avoided due to their contents of fats which impair & delay
intestinal glucose absorption. Glucose gel and tablets (sublingual) may be used (not
available)
• For those with impaired consciousness: IV dextrose 25% 100 ml (25 gm glucose), followed
by glucose infusion 5% or 10 %.
• IM or SC glucagon (1mg) (not available)
• Person with recurrent attacks should have medical ID or wearing bracelets.
Non-pharmacological:
• In fasting cases: frequent day time meals with large amount of uncooked starch at bedtime,
or even overnight glucose infusion.
• In dumping: small frequent meals with avoiding simple sugars.
Cause management:
• Insulinoma
✓ Surgery is the treatment of choice.
✓ Medical: Diazoxide, verapamil, Octreotide (somatostatin receptor analogue)
• Post gastric bypass & Functional islet hyperplasia: frequent feeding, α-glucosidase
inhibitor, diazoxide, or octreotide. (Partial pancreatectomy may be required)
• Replacement of deficient hormones.
• Steroid, immunosuppressive for autoimmune cases.
• Treatment of critical illness.

Hypoglycemia

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Hypoglycemia in non-diabetic subject

Quick Review of hypoglycemia in Diabetic patients

• Drugs → secretagogues (sulfonylurea and meglitinides)

• Neuroglycopenic →agitation, fits, coma, amnesia, permanent brain damage

Hypoglycemia → Defined as plasma glucose low enough for development of symptoms of

4. Localizing images: Once diagnosis of endogenous hyperinsulinemia as a cause of

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