I. Definition.
Acidosis caused by elevated lactic acid in the blood, a metabolite of anaerobic enzymes in the body. Lactic acidosis in diabetic patients due to various causes is called diabetic lactic acidosis. The disease occurs mostly in elderly diabetic patients, with low morbidity and diagnosis rate, and extremely high mortality rate.
II. Morbidity characteristics.
It often occurs in diabetic patients with cardiopulmonary disorders, hypoxia, shock, liver and kidney failure and extreme wasting or malnutrition.
Pathogenesis.
Lactic acid is an intermediate metabolite of glycolysis, and glucose is decomposed into lactic acid under anaerobic conditions. In order to maintain the balance in the body, it can be removed by glycogen isogenesis in the liver and excretion in the kidneys, but when the liver and kidney dysfunction is easy to occur lactic acid accumulation and cause acidosis.
IV. Causes.
(1) Insufficient insulin in diabetic patients can lead to impaired pyruvate oxidation and defective lactate metabolism, so hyperlactatemia exists in general.
(2) The combination of macrovascular and microangiopathy in diabetic patients, resulting in poor perfusion of tissues and organs; the increased level of glycated hemoglobin and decreased oxygen-carrying capacity of hemoglobin can cause local hypoxia and increase lactic acid production.
(3) Liver and kidney dysfunction affects the metabolism, conversion and excretion of lactic acid, which can also lead to lactic acidosis.
(4) Acute complications of diabetes such as infection, ketoacidosis, diabetic non-ketotic hyperosmolar syndrome can cause lactic acid accumulation and lactic acidosis can coexist with ketoacidosis.
(5) Inappropriate use of biguanide hypoglycemic drugs (hypoglycemic, etc.).
V. Clinical manifestations.
History: History of infection, blood loss, shock, hypoxia, alcohol consumption or heavy use of hypoglycemic agents, mostly in people with pre-existing cardiovascular, liver and kidney diseases. The onset of disease is more acute.
Mild cases: may have only weakness, nausea, reduced appetite, dizziness, drowsiness, and slightly deeper and faster breathing.
Moderate to severe cases: there may be nausea, vomiting, headache, dizziness, generalized weakness, lip cyanosis, deep breathing without ketosis, decreased blood pressure, weak pulse, fast heart rate, dehydration, impaired consciousness, weakened limb reflexes, decreased muscle tone, dilated pupils, deep coma or shock.
VI. Ancillary tests.
Blood gas analysis: PH < 7, CO2-CP, [HCO3-] significantly reduced often < 10mmol/L; blood lactate: elevated, often > 5mmol/L, blood pyruvate > 0.2mmol/L, lactate / pyruvate > 3; plasma anion gap [(Na + + K +) -(HCO3- + Cl-)] is enlarged, often > 18mmol/L; blood glucose: normal or elevated blood glucose, but generally ≤ 13.9mmol/L; urinary ketones: negative or weakly positive; plasma osmolality: normal
VII. Diagnostic clues.
Medical history: diabetic patients with an overdose of biguanides (hypoglycemia more than 75mg/d, metformin more than 2000mg/d) after exacerbation; diabetic patients with hepatic and renal insufficiency, hypoxia or surgery and other simultaneous use of biguanides hypoglycemic drugs; diabetic patients with multiple causes of shock and metabolic acidosis should be highly suspected of this disease. There are manifestations of metabolic acidosis such as deep and large breathing and impaired consciousness. Laboratory tests: blood lactate is increased; blood PH is decreased, blood glucose is often increased; blood ketone body is normal; blood osmolality is normal.
VIII. Diagnostic criteria.
1, medical history: most have a history of taking biguanides.
2, clinical symptoms and signs: typical symptoms of metabolic acidosis, including the presence of Kussmaul respiration, varying degrees of impaired consciousness, vomiting, and non-specific abdominal pain.
3. laboratory tests: plasma milk >5 mmol/L, blood AG >18 mmol/L , and significantly lower blood HCO3-, often <10 mmol/L.
IX. Differential diagnosis.
1, diabetic ketoacidosis: mostly seen in acute complications in patients with type 1 diabetes or some type 2 diabetes. Features: deep and rapid breathing, may have ketone odor (rotten apple smell), strong positive urine ketone bodies, significantly elevated blood ketones and blood glucose, pH <7.30.
2, diabetic hyperosmolar coma: mostly seen in elderly diabetic patients without proper control of the disease and massive water loss, also seen in a few type 1 diabetes. Features: blood glucose >33.3mmol/L; plasma osmolality >350mOsm/L, or effective osmolality >320mOsm/L; blood sodium >145mmol/L; normal or high blood ketones, urinary ketones (-) or weakly positive; CO2CP normal or low; blood pH around 7.35 or normal. Signs mostly include neurological signs, especially focal motor nerve disorders, elevated blood pressure, sometimes with stroke and coronary heart, and sometimes coexisting with DKA, which need to be differentiated.
X. Treatment.
1. The higher the blood lactate level, the higher the mortality rate, and the mortality rate of those with blood lactate > 9.0 mmol/L is up to 80%. The patient should be immediately sent to a large hospital for resuscitation.
2.Resuscitation measures.
(1) Remove the cause: drugs (such as biguanide hypoglycemic drugs, etc.) caused by the drug should be immediately discontinued, keep the respiratory tract unobstructed, reduce the stimulation of hypoxia, active control of infection, anti-shock treatment, but prohibit epinephrine and norepinephrine (vasoconstrictor agents can reduce muscle and liver blood flow and lactic acid increased).
(2) Condition monitoring: pay attention to changes in vital signs (blood pressure, respiration, pulse); monitor changes in blood gas, blood lactate, electrolytes, blood glucose, etc.
(3) Infusion therapy: purpose: volume expansion – correction of dehydration, shock, acid drainage, etc.; types: saline, colloid solution, 5% glucose solution, plasma or whole blood if necessary, avoid lactic acid-containing preparations (e.g., sodium lactate, etc.); method: the amount of rehydration depends on the patient’s blood gas analysis, dehydration, and cardiopulmonary function.
(4) Correction of acidosis: PH < 7.0, 5% sodium bicarbonate 400ml-800ml IV, total amount and infusion rate should be determined according to blood PH, CO2-CP, [HCO3-] and cardiac function until blood pH is greater than 7.2, then stop alkaline supplementation. (The alkaline supplementation should not be too much or too fast, otherwise it may aggravate hypoxia and intracranial acidosis).
(5) Insulin therapy: (1) counteract glycogenolysis in the liver and surrounding tissues; (2) reduce anaerobic glycolysis; (3) promote pyruvate dehydrogenase activity, so that pyruvate enters the tricarboxylic acid cycle to increase lactate utilization. Usage: Small dose insulin maintenance intravenous drip method, usage is similar to ketoacidosis, but insulin dosage is small for patients with lactic acidosis!
(6) Dialysis therapy: For elderly patients who cannot tolerate excessive sodium and those with cardiac and renal insufficiency, hemodialysis or peritoneal dialysis can be used to accelerate the excretion of lactic acid and harmful drugs (hypoglycemic).
XI. Prevention.
Once lactic acidosis occurs, the morbidity and mortality rate is extremely high, the response to treatment is poor, and the prognosis is very poor, thus prevention is more important than treatment, specific measures are as follows.
1, in the treatment of diabetes without phenibut. Where diabetic nephropathy, hepatic and renal insufficiency, older people older than 70 years old and those with poor cardiopulmonary function, other biguanides should also be used. Diabetes mellitus
Those with poor control can be treated with insulin.
2, diabetic patients should abstain from alcohol and try not to use drugs that can cause lactic acidosis (lactulose, sorbitol, xylitol, salicylate, isoniazid and other drugs).
3. Actively treat various diseases that can induce lactic acidosis. At the same time, patients with hyperlactatemia (i.e., no acidemia, but lactic acid >2.5 mmol/L) need to be treated promptly for various potential triggers and closely followed up and observed.