Hypoglycemia

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• In animals which have chronic low [plasma glucose], blood glucose may have to drop very low before clinical signs are exhibited.
• Cause: various eg pancreatic tumors, drugs, severe infection, endocrine and gastrointestinal disease.
• Signs: ataxia, weakness, disorientation, seizures.
• Diagnosis: biochemistry.
• Treatment: glucose (oral or intravenous), and correct underlying cause.

• Weakness/collapse.
• Neurological signs.
• Seizures.

• Trembling clonic convulsions collapse + loss of consciousness coma death.

• Neonate.
• Senior.

• Dependent upon costs of treatment of primary disease.

• General anesthesia/surgical procedures - hypoglycemia must be controlled pre-operatively, eg continuous glucose infusions.

• Neonatal hypoglycemia - dystocia, hypothermia, hypoxia, failure to feed/maternal rejection/maternal agalactia, dehydration, diarrhea may be causes.
• Starvation - more common in neonate/juvenile.

Primary disease

• Liver disease, particularly large hepatomas .
• Renal failure .
• Sepsis - 'bacterial shock' .
• Cardiac disease .
• Adrenocortical insufficiency .
• Glycogen storage diseases .
• Functional islet cell tumor (insulinoma ).
• Extrapancreatic neoplasia (most common - hepatic tumors).
• Severe polycythemia.

Exogenous agents

• Excessive insulin dosage - 'Insulin Shock' during treatment for Diabetes mellitus .
• Oral hypoglycemics.
• Drug ingestion, eg ethanol , propranolol , salicylates .

• Neonatal/juvenile animals have immature mechanisms for regulating blood glucose.

• Overactivity, cold, other stresses.
• Hard work - appears as functional disorder.

• A biochemical abnormality rather than a disease resulting in decreased extracellular glucose concentrations CNS signs.

• Normal glucose levels are dependent upon:
  • Hormones:
    • Normal/reduced levels circulating insulin.
    • Normal/raised levels circulating glucagon, growth hormone, epinephrine, cortisol.
  • Functional liver synthesizing glycogen and regulating gluconeogenesis/glycogenolysis.
  • Supply of precursors for hepatic gluconeogenesis.
• The brain = most obligate user of glucose. Hypoglycemia reduced glucose availability to central and peripheral nervous system seizures, lethargy, weakness, ataxia, disorientation.
• Prolonged, severe hypoglycemia irreversible brain damage rarely death (since diabetogenic hormones, eg glucagon and adrenaline antagonize insulin effects and increase [blood glucose]).

Specifics

• Neonatal hypoglycemia - gluconeogenesis limited in neonate and limited glycogen stores rapidly deplete - relies upon regular feeding - may develop hypoglycemia after only 12 hour fast.
• Starvation - severe malnutrition decreased hepatic glycogen, decreased fat stores decreased gluconeogenesis hypoglycemia.
• Glycogen storage diseases - genetic abnormality deficiency in enzymes/defective enzymes involved in glycogen degradation hypoglycemia.
• Exogenous agents: direct drug action hypoglycemia.
• Bacterial shock depletion of glycogen stores, increased peripheral use of glucose, decreased gluconeogenesis + ?circulatory factors hypoglycemia.
• Extrapancreatic tumors:
  • Secretion of Insulin/insulin-like/insulin precursor.
  • Accelerated glucose utilization.
  • Inhibited glucose release from liver. hypoglycemia.
• Functional islet cell tumor insulin secretion hypoglycemia.
• 'Insulin shock': overdose, inappetance/starvation or sudden increase in exercise/stress levels during treatment with insulin may hypoglycemia.

• Episodic weakness and collapse.
• Seizures/neurological signs.

• Episodic weakness or collapse (often only a few seconds).
• Increasing signs with syncope over days or weeks.
• Episodes are often associated with:
  • Exercise, or
  • Feeding:
    • Within 2-6 hours of eating (peak insulin release).
    • A long time after last meal (glycogen reserves exhausted).

• Signs occur when plasma [glucose] <2 mmol/l: severity relative to rate of fall of blood [glucose], not absolute blood [glucose].
• Confusion, apparent blindness.
• Muscle tremors, weakness, incoordination, ataxia.

• Seizures.

• Persistently decreased fasting blood [glucose]: <3 mmol/l .
• Insulinoma:
  • Intravenous glucose tolerance test: glucose half-life of < 20 minutes  (rarely used).
  • Increased plasma [insulin] >20 mIU/l .
  • Insulin:glucose ratio > 4.2mIU/mol .
  • Decreased [fructosamine]: <250-350 mmol/l .
  • Decreased glucose with normal or elevated insulin concentration.

Radiography/ultrasonography

• Chest and abdomen:
  • Look for large intra-abdominal tumor, eg hepatoma .
  • Exclude lung metastasis .
  
   Insulinomas are usually small and not detected with radiography or ultrasound.

• History and clinical signs.

• Biochemistry - measurement of low [blood glucose].

• Trauma.
• Brain neoplasia .
• Lead poisoning .
• Idiopathic epilepsy .

Infections

• Cryptococcosis , Toxoplasmosis .

Congenital

• Hydrocephalus.

Acquired

• Myasthenia gravis .
• Tetanus .
• Discospondylitis .
• Polymyositis.
• Polyarthritis.

Cardiovascular disorders

• Arrhythmias .
• Congenital defects .
• Heartworm.
• Hemangiosarcoma .
• Warfarin-induced coagulopathy .
• Bacterial endocarditis.

Metabolic disorders

• Hepatic encephalopathy .
• Hypocalcemia .
• Anemia .
• Hypoadrenocorticism .
• Hypokalemia .
• Uremia, eg renal failure .
• Pheochromocytoma .

• Control seizures if necessary .

• Glucose administration:
  Either Inject 1ml/kg of 40-50% glucose solution by slow iv injection (care since may stimulate massive insulin release).
  Or If animal conscious, give meal containing glucose.
• Cannot be used for long-term control.

• Treatment of primary disease.

• Surgical excision of tumor and any metastatic disease (if possible) .
• 60% in right duodenal lobe; 40% in left pancreatic lobe.
• Rarely encapsulated, invasive.
• Mostly malignant; may metastasize to regional/local lymph nodes and/or liver.
• Surgery often gives remission for 12-24 months.
• Post-operative complications - pancreatitis, temporary or permanent diabetes.

Diet

• Give small meals high in protein and low in simple sugars 5-6 times daily .

Exercise

• Restrict.

Diabetogenic drugs

• Prednisolone (0.5-1 mg/kg daily in divided doses).
• Diazoxide :
  • Non-diuretic benzothiadiazine antihypertensive drug which suppresses insulin secretion.
  • 10 mg/kg PO daily in divided doses, increasing up to 40 mg/kg daily if necessary.
• Octreotide :
  • Long-acting somatostatin analogue which inhibits insulin synthesis and secretion.
  • 10-20 ug SC q8-12h.
  • Only effective in some cases.
  • Close monitoring required.

• Biochemistry for glucose (and others according to primary disease) to assess response to treatment.

• Dependent upon treatment for primary disease.

• Dependent upon primary disease.
• Insulinoma - surgery often gives remission for 12-24 months.

• Dr David Bruyette DVM DipACVIM

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