Metabolic alkalosis resident survival guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]

Synonyms and keywords: Approach to Metabolic alkalosis, Metabolic alkalosis management, Metabolic alkalosis work-up

Overview

The normal physiological pH of blood is 7.35 to 7.45. An increase above this range is known to be Alkalosis. Metabolic Alkalosis is defined as a disease state where the blood pH is more than 7.45 due to secondary metabolic processes. The primary pH buffers in maintaining chemical equilibrium of physiological Blood pH are alkaline Bicarbonate ions(HCO3) and acidic carbon dioxide(CO2). When there is an increased amount of Bicarbonate(HCO3) in the body or a decreased amount of carbon dioxide or a loss of hydrogen ions, it causes alkalosis. Metabolic alkalosis occurs due to the trapping of Bicarbonate ions (HCO3) or loss of hydrogen ions in the body due to some metabolic causes for example- gastrointestinal loss of hydrogen ions, intracellular shifting of hydrogen ions, renal hydrogen loss, increased bicarbonate ions in extracellular compartment, diuretic induced alkalosis or contraction alkalosis. Patient with normal renal physiology will compensate this increased amount of bicarbonate through excretion. But impaired renal function secondary to chloride depletion, hypokalemia, hyperaldosteronism, reduced glomerular function rate, reduced effective arterial blood volume (EABV)) in heart failure or cirrhosis will lead to metabolic alkalosis. When the physiologic blood pH is above 7.45, it triggers the respiratory center to cause hypoventilation, thus decreased PCO2 leading to compensatory respiratory acidosis. The PCO2elevates from 0.5 to 0.7 mmHg per 1.0 mill mole elevation in plasma bicarbonate concentration. In severe Metabolic alkalosis PCO2 can reach 60 mmHg. The mortality rate with metabolic alkalosis is 45% with arterial blood pH 7.55 to 80% with arterial blood pH of 7.65. Treatment is usually supportive based on cause of the disease.

Causes

Life Threatening Causes

Life-threatening causes of severe metabolic alkalosis (pH 7.55 to 7.65) may result in death (45% to 80%) or permanent disability within 24 hours if left untreated.

• Loss of gastric acid
• Loop or thiazide diuretics

Common Causes

• Chloride depletion or Gastrointestinal loss of hydrogen
  • GI loss: Vomiting (most commonly seen in pyloric stenosis), NG suction , Zollinger-ellison syndrome, Bulimia.
  • Diuretics: Loop and thiazide diuretics.
  • Diarrhea: Villous adenoma, congenital chloride diarrhea
  • Cystic fibrosis.
  • Chloride deficient infant formula.
  • Gastrocystoplasty
  • Post hypercapneic metabolic alkalosis.
• Potassium depletion or Mineralocorticoids excess or Renal loss of hydrogen
  • Dietary potassium depletion.
  • Primary hyperaldosteronism: Conn syndrome or adenoma, hyperplasia, carcinoma, renin or glucocorticoid responsive.
  • Secondary hyperaldosteronism: Reno vascular hypertension, edema (cirrhosis, heart failure, nephrotic syndrome), juxtaglomerular cell(renin producing) tumor, renal cell carcinoma, hemangiopericytoma, nephroblastoma
  • Mineralocorticoid excess due to primary decorticosterone excess (11 beta, 17 alpha hydroxylase deficiency), licorice(glycyrrhetinic acid), liddle syndrome.
  • Bartter and Gitelman syndrome.
  • Laxative
• Reduced Glomerular filtration rate
  • Chronic kidney disease
• ECF volume depletion/ Volume contraction
  • Hypovolemia or massive diuresis with loop diuretics.
• Miscellanous
  • Hypercalcemia due to Milk-alkali syndrome or bone metastasis.
  • Massive blood transfusion.
  • Acetate containing colloid sollution.
  • Exogenous alkali admintration.
  • Combined antacid and cation exchange resin administration.
  • Sodium penicillins.

Diagnosis

Shown below is an algorithm summarizing the diagnosis and treatment of Metabolic Alkalosis.

History: • H/O Cystic fibrosis/Congenital adrenal hyperplasia/CHF/Uncontrolled HTN? • Excess antacid consumption? • Calcium over supplementation? • Beta lactum antibiotic use? • Recent or current diuretic use? • Vomiting or diarrhea? • massive use of licorice? • H/O recent hypercapneic respiratory failure?

Physical Examination: •General appearance: Restlessness/ Irritable/lethargic? • Skin: decreased or normal turgor? • HEENT: Headache/Dizziness? • CVS: Dysrhythmia/Tachycardia? • Respiratory: Hypoxemia, Compensatory hypoventilation, Pulmonary microatelactasis, Increased V/Q mismatch • GI: Nausea/vomiting/diarrhea? • GU: Urine output, frequency? • CNS: Confusion, loss of consciousness/Mental obtundation, Neuromuscular excitability/Muscle cramps, Tremor, tingling and numbness in extremities, Weakness?

Laboratory Tests •ABG(pH >7.45, HCO3 >26 mEq/L, PCO2 compensates for increased HCO3 by decreasing) • Basic metabolic panel • Serum Aldosterone And renin • Urine analysis, Urine pH, Urine Chloride and sodium • Chest X-ray • Abdominal USG/CT to rule out mass

Expanded EABV(No sign of volume depletion or Saline unresponsive) •Treatment: Treat underlying cause.

Contracted EABV(sign of volume depletion or saline responsive) •Treatment: Replace volume with NaCl if depleted, correct electrolyte imbalance, reduction of gastric secretion by H2 blocker or PPI, discontinue diuretics, Acetazolamide, NH4Cl and HCl should be reserved for severe cases.

Rule out by history •Treatment: According to cause with discontinuation of offending agents.

Transient

Renal failure with ingestion

• IV HCO3 • Acute correction of hypercapnea

• Milk-alkali syndrome • HCO3 ingesion

GI loss(low urine Cl)

Renal loss(high urine Cl)

• Gastric: Vomiting, NG suction • Lower bowel: Villous adenoma, chloridorrhea, laxative abuse

• Non-reabsorbed ions: Penicillin • =Impaired tubular transport: Loop and thiazide diuretics, Barrter's and Gitelman's disease, Hypomagnesaemia

High Renin, High aldosterone:• Malignant hypertension • renovascular hypertension • Renin secretin tumor

Low Renin, High aldosterone:• Aldosterone secreting tumor • Adrenal hyperplasia • Glucocorticoid remediable aldosteronism

Low Renin, Low Aldosterone:• Licorice • Liddle's syndrome • Enzyme deficiency

Dos

• Maintenance of airway, breathing, circulation if there is an unstable patient.
• Correction of the underlying cause for HCO3 production.
• Removal of inciting factors that reabsorb HCO3.
• Patient should be monitored carefully with SaO2, vital signs monitor and EKG.
• Consider respiratory support in hypoxemic patient.

Don'ts

• Avoid hyperventilation as it will worsen alkalemia.