The density of beta-intercalated cells and pendrin are both reduced in the case of hypokalemia [ 20 ]. Courtesy of Bruno and Valenti. J Biomed Biotechnol. This is an open-access article distributed under the Creative Commons Attribution License. Two steps are required for metabolic alkalosis to persist. The first step is the generation of metabolic alkalosis and the second step is the maintenance of metabolic alkalosis [ 21 ].
In other words, when faced with metabolic alkalosis, one has to answer two questions. Na citrate is added as an anticoagulant to whole blood or fresh frozen plasma FFP and can be an important source of alkali in patients needing massive amounts of blood products as in those treated with large dose plasma exchange [ 9 ].
Some advocate the use of NaHCO3 to improve athletic performance. Some clinical events activate more than one mechanism for the maintenance of metabolic alkalosis. Metabolic alkalosis is divided into two major categories base on extracellular fluid ECF volume status, metabolic alkalosis with ECF volume contraction, and metabolic alkalosis with ECF volume expansion [ 8 - 9 ].
Urine chloride Ucl - is helpful in differentiating the two categories. Typical causes of metabolic alkalosis associated with ECF volume contraction are vomiting and NG suction.
Diarrhea usually results in non-anion gap metabolic acidosis. Likewise, congenital chloridorrhea also results in metabolic alkalosis. Bartter syndrome is due to a loss of function mutation in the TAL resulting in effects similar to the use of a loop diuretic. Liddle syndrome is a rare genetic cause of severe hypertension due to gain of function mutation of the epithelial sodium channel ENaC resulting in hypokalemia and hyporeninemic hypoaldosteronism [ 8 ].
Excessive perspiration can cause metabolic alkalosis in patients with cystic fibrosis CF [ 31 ]. Unexplained metabolic alkalosis with volume depletion and hyponatremia should raise the possibility of cystic fibrosis; this presentation is more common during a heatwave. Aminoglycoside use in patients with CF can result in metabolic alkalosis due to a Bartter-like syndrome. A typical cause of metabolic alkalosis associated with ECF volume expansion is primary aldosteronism commonly caused by unilateral aldosterone-secreting adenoma or adrenal hyperplasia.
Adrenal carcinoma is rare. Primary aldosteronism manifestations are hypertension, hypokalemia, metabolic alkalosis, and ECF volume expansion [ 9 ]. Metabolic alkalosis is maintained due to autonomous aldosterone secretion. Physical examination helps in evaluating ECF volume status. Most clinicians make the diagnosis of metabolic alkalosis in appropriate clinical settings such as vomiting, NG suction, primary aldosteronism based on history, physical exam, and basic chemistry profile without doing ABGs.
A basic chemistry profile is needed for the diagnosis of metabolic alkalosis. Urea and creatinine help in evaluating renal function. Urine electrolytes are obtained. Obtaining Ucl - concentration from a random urine sample is adequate and hour urine collection is usually not necessary. Patients suspected of having primary aldosteronism require further testing [ 34 ]. Surreptitious diuretic use is an important cause of metabolic alkalosis.
Urine diuretic screening is confirmatory. Bartter and Gitelman syndromes require genetic testing to ascertain the diagnosis. The diagnosis of congenital adrenal hyperplasia due to beta or alpha hydroxylase deficiency requires a specialist consultation [ 35 ].
Pendred syndrome is an autosomal recessive disorder characterized by deafness and thyroid goiter. It is due to mutations in gene SLC26A4. SLC26A4 encodes for pendrin, which is expressed by the thyroid gland, the inner ears, and the apical membrane of beta-intercalated cells in the cortical collecting duct in the kidneys.
Pendred syndrome patients do not have renal abnormalities under basal conditions. They are at risk of developing life-threatening metabolic alkalosis in case of volume depletion or treatment with thiazide diuretics [ 36 ]. If a thiazide diuretic is added to acetazolamide, a profound salt-wasting ensues because acetazolamide downregulates pendrin [ 37 ]. Most patients with mild to moderate metabolic alkalosis are asymptomatic.
The manifestations are usually due to concomitant hypokalemia, hypophosphatemia, hypoventilation, volume depletion, and hypocalcemia. Metabolic alkalosis decreases ionized calcium levels [ 33 ]. Alkalemia also inhibits respiratory drive and shifts the oxygen-hemoglobin dissociation curve to the left.
In patients with metabolic alkalosis associated with volume contraction Cl - -sensitive metabolic alkalosis , it is critical to give isotonic saline 0.
This strategy will lead to NaHCO3 diuresis and the restoration of the acid-base balance. Diuretics should be discontinued if feasible; otherwise, the diuretic doses should be reduced. In some patients, such as those with heart failure or liver cirrhosis, discontinuation of diuretics is not an option. It should only be utilized by experienced clinicians. It can be given orally PO or intravenously IV at a dose of mg, two to three times daily.
The Diabolo study was a double-blind, randomized trial conducted in 15 intensive care units ICUs in France [ 39 ]. It involved patients with COPD on mechanical ventilation with pure or mixed metabolic alkalosis. Patients in the active arm were given a large dose of acetazolamide mg twice daily IV. Acetazolamide did not change the primary outcome, which was the reduction in the duration of invasive mechanical ventilation via endotracheal intubation or tracheotomy.
The underlying etiology, such as adrenal adenoma, should be the main focus of treatment. Patients with bilateral adrenal hyperplasia are treated with aldosterone blockers such as spironolactone or eplerenone. Continuous renal replacement therapy CRRT is particularly helpful in the management of severe metabolic alkalosis due to the ability to modify electrolytes in replacement solutions and dialysate [ 3 ].
Infusion of dilute HCl 0. HCl should be placed in a glass container and infused through a central venous catheter; it can cause severe hemolysis and venous thrombosis and should be discontinued once pH is around 7. IV tubing has to be changed every 12 hours. NH4Cl is metabolized into urea and HCl and is associated with central nervous system toxicity and gastrointestinal adverse reactions.
NH4Cl can be also given orally. The etiology of metabolic alkalosis should be addressed. Patients with vomiting should be treated symptomatically and the cause of vomiting should be investigated.
The use of proton pump inhibitors PPIs or H2 blockers may be helpful in patients with ongoing gastric fluid losses [ 43 ]. Exogenous sources of alkali should be identified. Patients should be instructed to avoid licorice or licorice-containing tobacco products. Blanchard et al. Indomethacin was the most efficacious with a 0.
Forty percent of patients receiving indomethacin discontinued treatment due to gastrointestinal adverse reactions. Metabolic alkalosis is the most common acid-base disorder in hospitalized patients, and it is associated with increased mortality.
It is generated by a gain of alkali or loss of acid and is maintained by the failure of the kidneys to excrete excess alkali. Metabolic alkalosis is either associated with volume depletion or volume expansion. Recently, the molecular mechanisms of several genetic disorders associated with metabolic alkalosis have been elucidated such as the Bartter, Gitelman, Liddle, and Pendred syndromes.
Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus. The authors have declared that no competing interests exist.
Videos Figures Images Quizzes Symptoms. Symptoms and Signs. Key Points. Acid-Base Regulation and Disorders. Test your knowledge. Primary aldosteronism is caused by autonomous production of aldosterone by the adrenal cortex due to hyperplasia, adenoma, or carcinoma.
Which of the following is an uncommon symptom of this disorder? More Content. Metabolic Alkalosis By James L. Click here for Patient Education. Acid loss. Diuretic use. Bicarbonate excess. Arterial blood gas ABG and serum electrolyte measurements. Cause treated. Patients with chloride-unresponsive metabolic alkalosis rarely benefit from rehydration alone. Metabolic alkalosis involving loss or excess secretion of Cl is termed chloride-responsive.
Treat the cause and give patients with chloride-responsive metabolic alkalosis 0. Treatment for metabolic alkalosis depends on whether your alkalosis is chloride-responsive or chloride-resistant. It also depends on the underlying cause of the alkalosis. If you have only a mild chloride-responsive alkalosis, you may only need to make an adjustment in your diet, such as increasing your intake of salt sodium chloride.
The chloride ions will make your blood more acidic and reduce the alkalosis. If your doctor determines your alkalosis needs immediate attention, they may give you an IV intravenous drip containing a saline solution sodium chloride. An IV is an almost painless procedure.
It involves inserting a small needle into a vein in your arm. The needle is connected by a tube to a sterile bag containing salt dissolved in water. This is usually done in a hospital setting. If you have chloride-resistant alkalosis, your body may be depleted of potassium. Your doctor will instead look for ways to increase potassium. Metabolic alkalosis may not show any symptoms. People with this type of alkalosis more often complain of the underlying conditions that are causing it.
These can include:. Our body produces carbon dioxide when we convert the food we eat into energy in our cells. The red blood cells in our veins take up the carbon dioxide and carry it to our lungs to be exhaled. When the carbon dioxide gas mixes with the water in the blood, it forms a mild acid, called carbonic acid. The carbonic acid then breaks apart into the bicarbonate ion and hydrogen. Bicarbonate ions are alkaline. By changing the rate of breathing, we can raise or lower the concentration of alkaline bicarbonate ions that are retained in our blood.
The body does this automatically in the process called respiratory compensation. The kidneys can help combat alkalosis by increasing the excretion of bicarbonate ions through the urine. Loss of stomach acids. This is the most common cause of metabolic alkalosis. The gastric juices have a high content of hydrochloric acid, a strong acid.
Its loss causes an increase in the alkalinity of the blood. The vomiting can result from any number of stomach disorders. By figuring out and treating the cause of the vomiting, your doctor will cure the metabolic alkalosis. Excess of antacids. But if you have weak or failing kidneys and use a nonabsorbable antacid, it can bring on alkalosis. Nonabsorbable antacids contain aluminum hydroxide or magnesium hydroxide.
Some diuretics water pills commonly prescribed for high blood pressure can cause increased urinary acid secretion. The increased secretion of acid in the urine can make your blood more alkaline.
0コメント