OVERVIEW
Hypoglycemia syndrome, also known as late dumping syndrome, is a syndrome caused by low blood glucose levels. Blood glucose concentration is often below 3.36 mmol/l. Severe and prolonged hypoglycemia can lead to extensive neurological damage and complications, so early detection and treatment of this disease is very important. Delayed diagnosis and treatment can lead to irreversible and permanent neuropathy, and in severe cases, death can occur due to cerebral edema.
Causes
Common causes include insulinoma, application of hypoglycemic drugs, extrapancreatic tumors, early diabetes mellitus and gastrointestinal surgery, etc., which make the blood glucose overuse; hormone insufficiency such as cortisol and other enzyme deficiencies such as glycogen deposition; cirrhosis of the liver, hepatocellular carcinoma, severe malnutrition, and late stage of pregnancy, etc., which can lead to malnutrition causing hypoglycemia; and ethanol, propranolol, salicylic acid, etc., which make the insufficient production of blood glucose, which can lead to hypoglycemia as well. In addition, unstable regulation of insulin secretion and/or glucose metabolism by nerves and body fluids, or accelerated gastric emptying due to increased vagal tone can cause functional hypoglycemia.
Symptoms
1. Sympathetic nervous system excitation
After the occurrence of hypoglycemia, it stimulates the increase of adrenaline secretion, and hypoglycemia syndrome may occur, which is manifested as pallor, palpitation, cold limbs, cold sweat, trembling of hands, weakness of legs, weakness of limbs, dizziness, blurred vision, hunger, panic and anxiety, which will be relieved by eating.
2. Disorders of consciousness
Cerebral cortex inhibition, confusion, disorientation, reduced recognition, drowsiness, excessive sweating, tremor, impaired memory, headache, apathy, depression, dream-like state, dementia in severe cases, a few patients may have grotesque behavior.
3. Epileptic symptoms
When hypoglycemia develops to midbrain involvement, muscle tone increases, paroxysmal convulsions, epileptic or epileptiform seizures occur, and most of the seizures are grand mal seizures, or epileptic status quo. When the medulla oblongata is involved, the patient may enter coma, go to the brain rigid state, bradycardia, body temperature does not rise, and various reflexes disappear.
4. Involvement of the pyramidal tract and extrapyramidal system
When the subcortical center is inhibited, there is confusion, restlessness, pain hypersensitivity, clonic choreography, pupil dilation, and even tonic convulsions. Extrapyramidal and pyramidal tract signs are positive, and hemiparesis, hemiplegia, aphasia and monoplegia may be manifested.
5. Cerebellar involvement
Hypoglycemia may damage the cerebellum, which may be characterized by ataxia, motor incoordination, inability to recognize distance, low muscle tone and gait abnormality, etc. Especially in the late stage of hypoglycemia, ataxia and dementia are often seen.
6. Cerebral nerve damage
Hypoglycemia may cause cerebral nerve damage, such as abnormal vision and visual field, diplopia, dizziness, facial nerve palsy, dysphagia and hoarseness.
Examination
1. Fasting blood glucose
Fasting blood glucose should be tested several times, and the blood glucose level is lower than 3.36mmol/l.
2.Glucose tolerance test
Hypoglycemic patients and insulinoma patients tend to have hypoglycemic curve. Occasionally there are normal values and hypoglycemia occurs only during an attack.
3. Measurement of serum insulin and C-peptide
Serum insulin and C-peptide were measured by radioimmunoassay, the normal value was (14±8.7)μU/ml, and C-peptide value was 0.8-4.0mg/ml. insulinoma patients had elevated insulin value, which could be more than 160 μU/ml, and the C-peptide value was also elevated accordingly.
4. Fasting test
Fasting for 24 hours, blood glucose drops and hypoglycemic symptoms appear.
5. Electroencephalography
In the case of prolonged hypoglycemia with cerebral lesions, the electroencephalogram may show slow wave or other abnormal changes.
6. Electromyography
There is denervation of distal muscles with a decrease in the number of motor units. Diffuse denervation fibers, tip and huge motor unit discharges, polyphasic potentials.
Diagnosis
1. Hypoglycemic episodes can be induced by fasting and exertion.
2. Clinical hypoglycemia is rapidly relieved by glucose.
3. Blood glucose levels at the time of the attack are often below 2.24-2.80 mmol/l in adults and children, and below 1.68 mmol/l in newborns.
Treatment
1. Hypoglycemic attack
Intravenous injection of 50% dextrose can quickly relieve hypoglycemic symptoms, and severe glucose should be administered intravenously until the patient can eat. If the symptoms are mild, sweet foods such as sugar water, candies and chocolates can be consumed to relieve the symptoms.
2. Cerebral edema
Patients with prolonged and severe hypoglycemia may have focal cerebral and neurological symptoms such as motor nerve palsy, suggesting that hypoglycemia causes cerebral edema, and need to be actively treated with dehydration. 20% mannitol can be injected intravenously to eliminate cerebral edema.
3. Treatment of etiology
Actively search for the original disease and carry out radical treatment. The key to the treatment of hypoglycemia syndrome lies in the treatment of the primary disease and the elimination of the cause of the disease. If the primary disease and the cause of the disease cannot be completely treated, the symptoms of hypoglycemia will recur.