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Metabolic Alkalosis

Metabolic alkalosis is characterized by a variation  in the pH levels beyond the normal range of 7.35 – 7.45. It is a type of metabolic condition, which practically occurs due to decrease in the concentration of hydrogen ion.


Presentation

Metabolic alkalosis does not present with any specific signs and symptoms. The symptoms which are experienced occur due to hypoventilation and hypokalemia which take place along with it. Due to hypokalemia, individuals often suffer from weakness, arrhythmias, polyuria and myalgia. When there is associated hypoventilation that occurs as compensatory mechanism, individuals suffer from muscle spasm, a short-lived tingling sensation that is short lived and jitteriness. In addition, there may be tremors in hands and light headedness, followed by confusion.

If the patient experiences seizures or has severe problems while breathing accompanied by loss of consciousness, he/she might need an emergency treatment. Such individuals should be immediately taken to emergency room for prompt medical action [6].

Inguinal Hernia
  • Abstract A 2-month-old infant with hereditary hyperekplexia, umbilical and bilateral inguinal hernias and history of poor feeding was noted to have severe normotensive metabolic alkalosis: sodium 132 mmol/L, potassium 3.4 mmol/L, chloride 77 mmol/L, pH[ncbi.nlm.nih.gov]
Hypertrophic Pyloric Stenosis
  • BACKGROUND: This pilot study focuses on regional tissue oxygenation (rSO 2 ) in patients with infantile hypertrophic pyloric stenosis in a perioperative setting.[ncbi.nlm.nih.gov]
  • PURPOSE: Pyloromyotomy has been the treatment of choice for hypertrophic pyloric stenosis (HPS) for the past century.[ncbi.nlm.nih.gov]
  • Does metabolic alkalosis influence cerebral oxygenation in infantile hypertrophic pyloric stenosis?. J Surg Res. 2017 May 15. 212:229-37. [Medline]. Algorithm for metabolic alkalosis.[emedicine.medscape.com]
Food Intolerance
  • Abstract A 7-month-old boy on an oligoantigenic diet because of multiple food intolerances presented with anorexia, failure to gain weight and severe hypochloremic metabolic alkalosis with hyperreninemia.[ncbi.nlm.nih.gov]
Hypotension
  • Abstract We describe a case of medication induced metabolic alkalosis in a maintenance dialysis patient who developed severe hypotension while undergoing a lactate hemofiltration procedure.[ncbi.nlm.nih.gov]
  • On this admission, the patient had recurrent bouts of vomiting induced by psychiatric eating disorder and showed severe volume depletion with hypotension, azotemia and metabolic alkalosis.[ncbi.nlm.nih.gov]
  • […] predisposing factors Fluid and electrolyte imbalances Renal dialysis Respiratory acidosis (primary carbonic acid excess) Respiratory alkalosis (primary carbonic acid deficit) Assessment CIRCULATION May exhibit: Tachycardia, irregularities/dysrhythmias Hypotension[nurseslabs.com]
  • Chloride-resistant alkalosis Causes of chloride-resistant alkalosis can be divided into those associated with hypertension and those associated with hypotension or normotension.[emedicine.medscape.com]
Subcutaneous Nodule
  • A biopsy of the subcutaneous nodule showed a typical appearance of tophus.[ncbi.nlm.nih.gov]
Muscle Twitch
  • People may have irritability, muscle twitching, muscle cramps, or even muscle spasms. Blood is tested to diagnose alkalosis.[merckmanuals.com]
  • Minor muscle twitching is usually the result of less serious, lifestyle-related causes. More severe muscle twitching, however, is often the result of a serious condition.[healthline.com]
  • twitching, weakness Dizziness May exhibit: Hypertonicity of muscles, tetany, tremors, convulsions, loss of reflexes Confusion, irritability, restlessness, belligerence, apathy, coma Picking at bedclothes SAFETY May report: Recent blood transfusions ([nurseslabs.com]
  • Symptoms of alkalosis can include any of the following: Confusion (can progress to stupor or coma) Hand tremor Lightheadedness Muscle twitching Nausea, vomiting Numbness or tingling in the face, hands, or feet Prolonged muscle spasms (tetany) The health[medlineplus.gov]
Muscle Cramp
  • Symptoms of Diabetic Metabolic Alkalosis Symptoms of diabetic metabolic alkalosis include: light-headedness and dizziness; nausea and vomiting; mental confusion; numbness or tingling in the face and extremities; muscle weakness; myalgia; muscle cramps[battlediabetes.com]
  • People may have irritability, muscle twitching, muscle cramps, or even muscle spasms. Blood is tested to diagnose alkalosis.[merckmanuals.com]
  • See also metabolic acidosis, respiratory acidosis. observations Signs and symptoms of metabolic alkalosis may include apnea, headache, lethargy, muscle cramps, hyperactive reflexes, tetany, shallow and slow respirations, irritability, nausea, vomiting[medical-dictionary.thefreedictionary.com]
  • Finally, symptoms of hypokalemia should be elicited, including muscle cramps, weakness or polyuria. Long-standing hypokalemia may be associated with chronic renal failure. 2.[clinicaladvisor.com]
Carpopedal Spasm
  • […] the cause (too much bicarb, to much loss of acid) use antiemetics, H2 blockers correct electrolyte imbalances give calcium gluconate correct fluid volume depletion give to patient to correct calcium imbalance in patient with carpopedal spasms or tingling[quizlet.com]
  • spasm Type 1 Excludes hysterical tetany ( F44.5 ) neonatal tetany ( P71.3 ) parathyroid tetany ( E20.9 ) post-thyroidectomy tetany ( E89.2 ) alkalosis E87.3 ICD-10-CM Codes Adjacent To E87.3 E85.9 Amyloidosis, unspecified E86 Volume depletion E86.9 Volume[icd10data.com]
Facial Numbness
  • numbness Reduced rate of respiration is one of the initial symptoms of this condition.[hxbenefit.com]
Circumoral Paresthesia
  • paresthesia Muscle twitching, weakness Dizziness May exhibit: Hypertonicity of muscles, tetany, tremors, convulsions, loss of reflexes Confusion, irritability, restlessness, belligerence, apathy, coma Picking at bedclothes SAFETY May report: Recent blood[nurseslabs.com]
Dizziness
  • You are dizzy, confused, or lose consciousness. You have a seizure. Care Agreement You have the right to help plan your care. Learn about your health condition and how it may be treated.[drugs.com]
  • […] vomiting or gastric suction; loss of hydrochloric acid from stomach loss of K excess alkali ingested from antacids(containing HCO3) use of Sodium Bicarbonate during CPR mostly related to movement of Ca (decreased Ca ionization) tingling of fingers and toes dizziness[quizlet.com]
  • […] syndrome Steroid excess Hyperaldosteronism Clinical Shift O2 dissociation curve to left (increased affinity for Hb-O2) Right shift with increase TEMP, 2-3 DPG, H Hypokalaemia, hypocalcaemia, hypochloraemia Symptoms related to HYPOcalcaemia and HYPOkalaemia Dizzy[lifeinthefastlane.com]
  • Symptoms of Diabetic Metabolic Alkalosis Symptoms of diabetic metabolic alkalosis include: light-headedness and dizziness; nausea and vomiting; mental confusion; numbness or tingling in the face and extremities; muscle weakness; myalgia; muscle cramps[battlediabetes.com]
  • […] nausea/prolonged vomiting High salt intake; excessive ingestion of licorice Recurrent indigestion/heartburn with frequent use of antacids/baking soda NEUROSENSORY May report: Tingling of fingers and toes; circumoral paresthesia Muscle twitching, weakness Dizziness[nurseslabs.com]
Insomnia
  • His medications included the anti-hypertensive agents nicardipine hydrochloride, delapril, prazosin; dihydroergotoxin and ticlopidine for cerebral infarction; estazolam for insomnia; azuren-L-glutamine compound and S-M powder.[ncbi.nlm.nih.gov]

Workup

In the preliminary levels, serum electrolytes and arterial blood gas levels will be measured. Following this, a complete medical history should be taken in order to understand the etiology. If no history of medical condition is available, then it must be assumed that metabolic alkalosis is caused either due to diuretics, excessive vomiting, or mineralocorticoid excess [7]. In order to uncover the exact cause, it is necessary to determine the concentration of urinary chloride.

In addition, the serum anion gap should also be calculated in order to distinguish between metabolic compensation and metabolic alkalosis [8]. Along with all the above mentioned laboratory studies, it is necessary to conduct gene analysis to determine underlying conditions such as Bartter syndrome, Liddle's syndrome, Gitelman syndrome and glucocorticoid remediable aldosteronism.

Hypercapnia
  • Low Urine Chloride Gastrointestinal causes Vomiting Nasogastric suction Chloride-wasting Diarrhea Villous adenoma of colon Renal Causes Diuretic use ( Urine Chloride 10 meq/L) Poorly reabsorbable anion Carbenicillin Penicillin Sulfate Phsophate Post-Hypercapnia[fpnotebook.com]
  • Non surgical casuses of chloride sensitive metabolic alkalosis include; diuretics (thiazides, loop, metolazone) and upon the relief of chronic hypercapnia.[surgstudent.org]
  • Posthypercapnia – Hypoventilation (decreased respiratory rate) causes hypercapnia (increased levels of CO2), which results in respiratory acidosis. Renal compensation with excess bicarbonate retention occurs to lessen the effect of the acidosis.[en.wikipedia.org]
  • Posthypercapnia  During respiratory acidosis prolonged co2 retention occurs (chronic hypoventilation and hypercapnia) resulting in increased plasma HCO3 concentration  Due to increased reasbsorption and generation of HCO3  When hypercapnia resolves[slideshare.net]
Bicarbonate Increased
  • RESULTS: Plasma bicarbonate increased from 25.2   2.2 to 29.2   1.9 mmol/L. With increasing inspiratory CO 2 pressure during the HCVR test, RR, V t , Pdi, EAdi and V E increased.[ncbi.nlm.nih.gov]
  • Alkalosis develops when the carbon dioxide content decreases or concentration of bicarbonates increases. In the condition of metabolic acidosis, the kidneys and gastrointestinal tract play a vital role.[symptoma.com]
  • Although acidosis is more common at ICU admission, bicarbonate increases over time (Figure 1 D) [ 3 ]. Alkalosis can be pure or mixed.[ccforum.biomedcentral.com]
  • ABG in Metabolic Alkalosis  Arterial pH increased ( 7.45)  Serum bicarbonate increased ( 26meq/l)  PaCO2 increased  PaCO2 rises 7 mmHg per 10 meq/L bicarbonate rise  PaCO2 0.75 x HCO3 38.  The anion gap is frequently elevated to a modest degree[slideshare.net]
Potassium Decreased
  • Serum potassium: Decreased. Serum calcium : Usually decreased. Prolonged hypercalcemia (nonparathyroid) may be a predisposing factor. Urine pH: Increased, higher than 7.0.[nurseslabs.com]
  • Serum potassium: Decreased. Serum calcium: Usually decreased. Prolonged hypercalcemia (nonparathyroid) may be a predisposing factor. Urine pH: Increased, higher than 7.0.[nurseslabs.com]
Chloride Decreased
  • Serum chloride: Decreased, less than 98 mEq/L, disproportionately to serum sodium decreases (if alkalosis is hypochloremia). Serum potassium: Decreased. Serum calcium : Usually decreased.[nurseslabs.com]
  • Serum chloride: Decreased, less than 98 mEq/L, disproportionately to serum sodium decreases (if alkalosis is hypochloremia). Serum potassium: Decreased. Serum calcium: Usually decreased.[nurseslabs.com]

Treatment

Treatment of metabolic alkalosis depends on the underlying etiology, severity of condition and intravascular volume status of the individual. The aim of treatment is to increase the excretion of bicarbonates and simultaneously decrease its serum concentration.

In case of excessive vomiting, administration of antiemetics is indicated. Constant monitoring of the vital signs is also necessary. If metabolic alkalosis has occurred due to diuretics, the dosage needs to be adjusted accordingly. In such cases, acetazolamide or potassium sparing diuretics may be administered.

If situation demands the constant need for gastric suction, then the gastric secretion can be significantly reduced with the help of H2 blockers or proton – pump inhibitors [9].

It is also necessary to given intravenous administration of hydrochloric acid through the central line. This will correct chloride deficiency and thereby assist normalizing the pH levels. Once the alkalosis is corrected, it will cause improvement in peripheral oxygen unloading [10].

Prognosis

Prognosis of the condition depends on the underlying etiology and the extent of severity. When the condition is not appropriately treated, it can lead to development of arrhythmias and hypokalemia, and the patient can even enter in a comatose phase.

Etiology

Kidney disorders can cause an increase in concentration of bicarbonates. Individuals taking diuretics are also likely to develop metabolic alkalosis. In addition to this, external loss of gastric secretion, such as vomiting, can also lead to development of metabolic acidosis.

Other causative factors include cystic fibrosis, loop diuretics, loss of colonic secretions and posthypercapnia. Short term metabolic acidosis will develop when an excess on an alkali is intravenously administered and the kidneys try to rapidly excrete bicarbonates [2].

Epidemiology

Metabolic alkalosis is a common occurrence amongst hospitalized patients. It has been estimated that 50% of all acid base disorders is constituted by metabolic alkalosis. Mortality occurs in about 45% cases in which the pH measured is 7.55 and in about 80% in which the pH measures is more than 7.65 [3].

Sex distribution
Age distribution

Pathophysiology

Under normal physiological conditions, the lungs along with the kidneys are responsible for the maintenance of the appropriate pH balance. Alkalosis develops when the carbon dioxide content decreases or concentration of bicarbonates increases.

In the condition of metabolic acidosis, the kidneys and gastrointestinal tract play a vital role. In hospitalized patients, sodium bicarbonate has to be given to patients but then it becomes difficult for the kidneys to excrete the excess of bicarbonates, and this leads to development of metabolic acidosis.

Loss of hydrogen ions is yet another phenomenon favoring increase in concentration of bicarbonates. During vomiting or nasogastric suction there is a loss of hydrogen ions, which in turn causes metabolic alkalosis to set in [4].

As a compensatory mechanism, the lungs slow down breathing to retain carbon dioxide and bring the condition back to normality. Such an event causes a decrease in pH levels, because the carbon dioxide is used for formation of intermediate carbonic acid. In addition to respiratory compensation, renal compensation also occurs, though it is less effective [5].

Prevention

Effective management of underlying cause can help prevent onset of metabolic alkalosis. Individuals with healthy lungs and kidneys would generally not experience serious alkalosis. The condition is usually encountered in hospitalized patients. Therefore, carefully correction of the underlying etiology is necessary to prevent the onset of metabolic alkalosis.

Summary

Such a type of phenomenon causes increase in bicarbonate levels. In order to compensate for the increase in bicarbonate ions the arterial carbon dioxide rises due to development of alveolar hypoventilation. Bicarbonate concentration more than 35 mEq/L indicates onset of metabolic acidosis. Treating the underlying etiology can help in an effective management of the condition [1].

Patient Information

Definition: Metabolic alkalosis occurs as a result of increase in bicarbonate concentration that causes the pH level to rise beyond 7.45. Such a kind of event occurs due to loss of hydrogen ions that arises as consequence of  various factors.

Cause: Several factors are known to play a role in causing metabolic alkalosis. It includes kidney diseases that causes improper excretion of excess of bicarbonates, diuretics, severe vomiting which results in loss of hydrogen ions and drugs which contain alkalotic agents. In addition, several disorders such as Liddle's syndrome, Gitelman syndrome, aminoglycoside toxicity and Bartter syndrome also favor the development of metabolic alkalosis.

Symptoms: Symptoms of metabolic alkalosis are associated with the secondary conditions like hypokalemia and hypoventilation. Signs and symptoms include weakness, polyuria, arrhythmias and myalgia. In addition, individuals can also experience tingling sensation, jitteriness and muscle spasms.

Diagnosis: A preliminary physical examination along with gathering of the past medial history is necessary. This is followed by measuring the arterial blood gases and serum electrolytes. Following this the serum anion gap is also calculated. Gene analysis is also indicated in determining several underlying conditions.

Treatment: Treatment is geared towards management of the underlying etiology. In the majority of cases, intravenous administration of hydrochloride is necessary. If medications are the cause, then either alternative drugs are prescribed or their dosage is adjusted.

References

Article

  1. Stewart PA. How to understand acid-base: a quantitative acid-base primer for biology and medicine. [AcidBase.org]. Available at http://www.acidbase.org/index.php?show=sb.
  2. Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol 2006; 19 Suppl 9:S86.
  3. Tentori F, Karaboyas A, Robinson BM, Morgenstern H, Zhang J, Sen A, et al. Association of dialysate bicarbonate concentration with mortality in the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. Oct 2013;62(4):738-46.
  4. Gennari FJ, Weise WJ. Acid-base disturbances in gastrointestinal disease.Clin J Am SocNephrol 2008; 3:1861.
  5. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York 2001. p.559.
  6. Sweetser LJ, Douglas JA, Riha RL, Bell SC. Clinical presentation of metabolic alkalosis in an adult patient with cystic fibrosis.Respirology 2005; 10:254.
  7. Palmer BF, Alpern RJ. Metabolic alkalosis. J Am SocNephrol 1997; 8:1462.
  8. Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am SocNephrol. Jan 2007;2(1):162-74.
  9. Kirsch BM, Sunder-Plassmann G, Schwarz C. Metabolic alkalosis in a hemodialysis patient--successful treatment with a proton pump inhibitor. ClinNephrol 2006; 66:391.
  10. Frick PG, Senning A. The treatment of severe metabolic alkalosis with intravenous N /10 or N /5 hydrochloric acid. Germ Med Monthly 1964; 9:242

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Last updated: 2018-06-22 04:18