OVERVIEW
Excessive loss of acid or excessive entry of alkali into the body, so that the plasma HCO3- increase, pH value of the acid-base balance disorders mainly manifested as restlessness, perioral and limb numbness, muscle twitching, etc. by the gastrointestinal or urinary H+ excessive loss or a large number of transfers to the intracellular, rehydration of excessive serum HCO3-, etc. caused by the treatment of the primary pathology and the triggering factors are mainly, and at the same time to correct alkalosis
Definition
Metabolic alkalosis is a disorder in which serum bicarbonate concentration and arterial blood pH are elevated.
Mild metabolic alkalosis is usually clinically asymptomatic, or the clinical manifestations are often masked by the primary disease, and there is a lack of characteristic symptoms or signs.
Acute or severe metabolic alkalosis may present with neuromuscular, cardiovascular and metabolic abnormalities.
Classification
Metabolic alkalosis is categorized into chlorine-responsive metabolic alkalosis and chlorine-tolerant metabolic alkalosis, depending on whether or not it can be corrected by supplemental chloride (Cl-).
Chlorine-responsive metabolic alkalosis
Alkalosis can be corrected with Cl- supplementation, and a slight decrease in glomerular filtration rate (GFR) is seen in some patients.
Chlorine-tolerant metabolic alkalosis
Alkalosis is not corrected by sodium chloride (NaCl) or potassium chloride (KCl) supplementation and is often accompanied by hypertension.
Causes
Causes
Excessive acid loss
Loss through the stomach
Excessive loss of hydrogen ions (H+) from the body due to severe vomiting, pyloric obstruction, gastric drainage, etc.
Loss via the kidneys
Heavy use of diuretics: furosemide or thiazide diuretics can lead to increased renal excretion of H+ and Cl-.
Excessive adrenal salicorticotropic hormone: increased secretion of salicorticotropic hormone due to hyperplasia or tumor of the adrenal cortex, and increased secretion of secondary aldosterone due to insufficient extracellular fluid, trauma, etc., can lead to an increase in the renal excretion of H+ and potassium ions (K+), which is usually accompanied by hypertension and hypokalemia.
Excessive entry or decreased excretion of alkaline substances into the body
Massive supplementation of bicarbonate and organic acid fluids, such as excessive intravenous input and rapid correction of NaHCO3 in correction of acidosis; excessive oral or input of lactate and acetate; and massive input of stock blood (anticoagulated by citrate).
Some diseases result in decreased effective blood volume (e.g., heart failure and cirrhosis), chloride depletion, and renal damage, leading to decreased renal excretion of bicarbonate (HCO3-).
In reduced blood volume, the extracellular HCO3- content is relatively constant and is referred to as concentrated alkalosis.
H+向细胞内转移
When the concentration of K+ in the extracellular fluid is too low (hypokalemia), intracellular K+ is transferred to the extracellular, a process that is accompanied by the entry of H+ from the extracellular fluid into the cell. Thus, an imbalance of acid-base balance occurs.
Risk factors
Persons with any of the following risk factors are at high risk for metabolic alkalosis.
Severe vomiting and diarrhea.
Prolonged use of diuretics.
Large amounts of sodium bicarbonate supplementation (e.g., transfusion of large amounts of blood or blood products anticoagulated with citrate).
Severe trauma, burns, after major surgery.
Symptoms
Clinical manifestations directly related to metabolic alkalosis are rare. Patients may be asymptomatic or may present with manifestations of the underlying disease causing metabolic alkalosis or with concomitant electrolyte disturbances.
Major Symptoms
Psychiatric symptoms
Manifestations of agitation, confusion, disorientation, delirium, and confusion.
Coma may occur in severe cases.
Increased neuromuscular excitability
Fatigue, muscle weakness, myalgic spasm.
Muscle twitching of face and limbs, hyperreflexia of tendons.
Cardiac arrhythmias
Various cardiac arrhythmias may occur in metabolic alkalosis, related to the intracellular transfer of K+ and magnesium ions (Mg2+), which may lead to cardiac arrest in severe cases.
Decreased blood pressure may occur.
Thirst and excessive drinking
Thirst, polydipsia, and polyuria occur due to persistent hypokalemia, impaired urinary concentrating function and/or direct stimulation of thirst.
Complications
Hypokalemia
Hypokalemia is both a cause and a possible complication resulting from metabolic alkalosis.
It is mainly characterized by muscle weakness, abdominal distension, cardiac arrhythmia, and some patients may have numbness in the limbs and around the mouth, or even nausea and vomiting, difficulty in swallowing and breathing.
Consultation
Department of Medicine
Emergency Department
The symptoms of agitation, confusion, delirium, and blurred consciousness suggest prompt medical attention.
When sudden convulsions or coma occur, consult a doctor immediately. Or call 120 emergency number.
Endocrinology
When physical examination reveals low blood potassium, or when involuntary twitching of facial and limb muscles occurs, prompt medical attention is recommended.
Gastroenterology
If severe vomiting or diarrhea occurs, it is recommended to consult a doctor promptly.
Nephrology
Long-term use of diuretics, fatigue, irritability, etc., it is recommended to consult the doctor promptly.
Preparation for medical treatment
Consultation: registration, preparation of documents, common problems
Tips for Consultation: Registration, Preparation of Information, Frequently Asked Questions
Remain in bed or in a comfortable sitting position and remain sedated.
Family members should accompany you to the doctor in case of accidents.
Preparation Checklist
Symptom list
Pay particular attention to the time of onset of symptoms, special manifestations, etc.
Have there been any recent symptoms such as irritability, confusion, etc.?
Is there any weakness in the limbs?
Is there polyuria and thirst?
Is there any cardiac discomfort, such as arrhythmia?
How long have these symptoms been present?
What is the timing and frequency of episodes of these symptoms?
Are there any aggravating or relieving factors for these symptoms?
Medical History Checklist
Have diuretics been used for a long period of time?
Any long-term use of antacids?
Has gastric drainage been performed?
Has low blood potassium been found?
Checklist
Test results in the last six months, which can be brought to the doctor’s office
Laboratory tests: serum electrolytes, arterial blood gases, urine electrolytes, etc.
Imaging tests: abdominal CT, MRI, gastrointestinal imaging, ultrasound
Endoscopy: gastroscopy, colonoscopy
List of medications
Medication used in the last 3 months, if available, bring the box or package to the doctor’s office
Diuretics: hydrochlorothiazide, furosemide, torasemide, bumetanide
Antacids: sodium bicarbonate
Gastrointestinal stimulants: Domperidone
Laxative: magnesium sulfate
Herbs: licorice, rhubarb, senna
Others: carbenicillin sodium salt, Ca2+ supplements, mannitol
Diagnosis
Diagnosis is based on
Medical history
History of prolonged application of diuretics, exogenous antacids.
History of severe vomiting and diarrhea.
History of recent gastric drainage.
Clinical manifestations
Patients with mild metabolic alkalosis may present only with symptoms of the primary disease and lack characteristic signs or symptoms.
Patients with acute or severe metabolic alkalosis may present with the following.
Agitation, confusion, delirium, and confusion, or even coma.
Cardiac arrhythmia.
Facial and limb muscle twitching.
Hyperreflexia of the tendons of the limbs.
Shallow and slow respiration.
Little or no urine.
Laboratory Tests
Serum Electrolytes
Measurement of serum levels of K+, Na+, Cl-, Ca2+, and Mg2+ is helpful in the diagnosis of metabolic alkalosis.
Urine electrolytes
Urine Cl- concentration and pH can be helpful in diagnosing metabolic alkalosis.
HCO3–重吸收试验
Check for normal renal tubular acidification.
HCO3- reabsorption levels decrease less than 25-26 mmol/L in metabolic alkalosis.
Buffer base test
Reflects the body’s total buffering capacity in response to disturbances in acid-base balance and assists in the diagnosis of metabolic alkalosis.
It may be lower than normal in metabolic alkalosis, less than 0.97 to 1.62 mmol/L.
Arterial blood gas analysis
Blood pH and HCO3- levels are measured to determine if there is an acid-base balance imbalance.
In the case of decompensation, blood pH and HCO3- are obviously increased, and PCO2 is normal; in the case of partial compensation, blood pH, HCO3- and PCO2 are increased to some extent.
Liver and kidney function tests
To understand the patient’s liver and kidney function.
Other tests
Depending on the patient’s condition, ECG, ultrasound, X-ray and other tests may be required.
Differential diagnosis
Metabolic alkalosis should be differentiated from metabolic acidosis and respiratory alkalosis.
Metabolic acidosis
Similarities: cardiac arrhythmia, tachycardia, decreased blood pressure, dizziness, drowsiness or coma.
Differences: The blood pH and blood HCO3- of patients with metabolic acidosis are decreased, and the urine can be acidic. Patients with metabolic alkalosis have increased blood pH and blood HCO3-, and urine may be alkaline.
Respiratory alkalosis
Similarities: Increased pH and altered respiratory symptoms.
Differences: Respiratory alkalosis patients’ respiration is from deep and fast to fast and shallow, short, there may be intermittent sigh-like breathing, and there may be sensory abnormalities, such as numbness and pins and needles in the perioral area and the limbs, or even convulsions and spasms. Metabolic alkalosis has shallow and slow respiration, elevated nerve excitability, and hyperreflexia.
Treatment
Aim of treatment: treat the primary disease causing metabolic alkalosis and correct alkalosis.
Treatment principle: according to the patient’s etiology, the severity of the disease and other comprehensive assessment, early diagnosis, early treatment, according to the different etiology of the corresponding comprehensive treatment measures, mild and moderate to treat the primary disease, circulating blood volume is insufficient with saline expansion, restore the ability of the kidneys to excrete the remaining HCO3-, and to correct the initiator of the generation of alkalosis.
General treatment
Rest
Keep the hospital room quiet and tidy, and the patient should rest in bed.
Nutritional supplementation
Recommend a nutritious and easily digestible diet.
If the patient is unable to eat, it can be injected by nasal feeding tube to ensure adequate supply of nutrition.
Disease monitoring
Real-time monitoring of arterial blood gas analysis results and blood and urine electrolyte changes.
Keep the airway open, let the patient’s head tilted to one side to facilitate the discharge of respiratory secretions and prevent asphyxia.
Pay close attention to 24-hour urine output.
Observe the patient’s respiration, heart rate, muscle tone, and neuropsychiatric status.
Correct electrolyte disorders
For chlorine-sensitive alkalosis, electrolyte disorders should be actively corrected, and Na+, K+ and Cl- should be supplemented.
For those with predominantly hypokalemia or coexisting hypokalemia and hypochloremia, KCl supplementation is the mainstay.
If hypokalemia is predominant, supplementation of NaCl is the mainstay, with appropriate supplementation of KCl.
Treatment of underlying etiology
The underlying etiology of alkalosis should be addressed, including treatment of the condition causing the vomiting, cessation or reduction of gastric fluid loss, reduction of the acid content of gastrointestinal secretions, and discontinuation of labeled diuretics or thiazide diuretics if possible.
Discontinue all exogenous bases if possible, including organic anionic sodium or potassium salts that are metabolized to bicarbonate (e.g., citrate or lactate).
If effective blood volume is insufficient, blood volume needs to be replenished as soon as possible.
对于真性动脉血容量不足但不伴心力衰竭和肝硬化的患者，应通过补充液体来纠正。通常给予等渗盐水补充细胞外液及血管内容量。
对于心力衰竭、肝硬化、肾病综合征和肺源性心脏病等患者，禁用等渗盐水治疗，应给予氯化钾或添加保钾利尿药进行治疗。
Medication
Acid medications
In patients with severe alkalosis, alkalosis can be ameliorated.
Commonly used drugs are ammonium chloride, dilute hydrochloric acid, arginine hydrochloride.
Real-time monitoring of the patient’s electrolyte status is required. Ammonium chloride is contraindicated in patients with hepatic and renal failure.
H2受体阻断药
For patients with prolonged vomiting or prolonged nasogastric tube suction, H2 receptor blocking drugs can help inhibit gastric acid secretion and reduce hydrochloric acid loss.
Commonly used drugs are cimetidine and ranitidine.
Carbonic anhydrase inhibitors
For patients with chlorine-tolerant alkalosis, they can inhibit carbonic anhydrase activity in renal tubular epithelial cells and excrete large amounts of alkaline urine.
Commonly used drugs such as acetazolamide.
Saline or glucose
For patients with metabolic alkalosis with insufficient circulating blood volume, to supplement the effective circulating blood volume and correct alkalosis.
Calcium gluconate
In patients with tetany, 10% calcium gluconate can be injected intravenously.
Other treatments
Hemodialysis
Hemodialysis may be considered in patients with severe metabolic alkalosis that is difficult to correct, or in patients with renal failure.
Prognosis
Cure
The prognosis of metabolic alkalosis is related to the severity of the primary disease, the functional status of the kidneys and the degree of alkalosis.
Mild cases can be cured with active and effective treatment. Severe cases and those with serious primary diseases and poor renal function have a poorer prognosis if not treated in time, and severe cases can lead to death.
Harmfulness
Metabolic alkalosis can lead to abnormal function of multiple organs, damage the nervous system, etc., and may lead to a variety of complications.
Hypokalemia.
Cardiac arrhythmias with risk of cardiac arrest.
Neurological damage, patients experience agitation, confusion, blurred consciousness, etc., and even coma.
Daily
Daily Management
Dietary management
Light diet.
Avoid spicy and stimulating food.
Eat small and frequent meals and adjust the recipes reasonably.
It is advisable to consume potassium-containing foods, such as bananas, soy milk and spinach.
Reduce the intake of alkaline substances.
Regular life
After the disease is stabilized, you can exercise appropriately under the guidance of physician.
Avoid exertion and take rest.
Quit smoking and drinking.
Maintain mental health
Understand the relevant knowledge of the disease, eliminate fear, and maintain a good physical and mental state.
Family members should guide and comfort the patient.
Disease monitoring
Observe changes in the patient’s condition and pay attention to his/her mental state, including drowsiness, delirium, coma, or even mental confusion.
Observe the depth and frequency of respiration, and observe the knee tendon reflexes and the presence of hand and foot twitching.
The patient’s arterial blood gas analysis, serum electrolytes, urine electrolytes and other indicators should be strictly controlled to achieve the ideal range.
If necessary, follow the doctor’s instructions for regular review in the hospital for blood gas analysis and blood and urine electrolytes.
Prevention
Regular screening of high-risk groups and establishment of good living habits are important measures to prevent metabolic alkalosis.
Regular physical examination and screening for high-risk groups
People with digestive system diseases such as severe nausea and vomiting.
Those who apply diuretics for a long time.
People with excessive intake of alkaline substances, including those who have been taking medication such as sodium bicarbonate for a long time.
People with metabolic disorders.
Preventive Measures
Balanced diet, rational diet planning, avoid overeating.
Exercise appropriately, aiming at 30 minutes or more of moderate exercise at least 5 days a week.
Timely replenishment of micronutrients after exercise.
Timely treatment of primary diseases, such as kidney diseases and metabolic disorders.