Metabolic alkalosis resident survival guide

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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 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 increase amount of Bicarbonate(HCO3) in body or decrease amount of carbon dioxide or loss of hydrogen ions it causes alkalosis. Metabolic alkalosis occurs due to trapping of Bicarbonate ions (HCO3) or loss of hydrogen ions in 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 increase 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 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.[1]

Common Causes

Diagnosis

Shown below is an algorithm summarizing the diagnosis and treatment of Metabolic Alkalosis.[1]

 
 
 
 
 
 
 
 
 
 
 
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 TestsABG(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 historyTreatment: 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
 

Do's

  • Maintenance of Airway, breathing, circulation if there is an unstable patient.[10]
  • 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

References

  1. 1.0 1.1 Tripathy S (October 2009). "Extreme metabolic alkalosis in intensive care". Indian J Crit Care Med. 13 (4): 217–20. doi:10.4103/0972-5229.60175. PMC 2856150. PMID 20436691.
  2. Galla JH, Gifford JD, Luke RG, Rome L (October 1991). "Adaptations to chloride-depletion alkalosis". Am J Physiol. 261 (4 Pt 2): R771–81. doi:10.1152/ajpregu.1991.261.4.R771. PMID 1928424.
  3. Babior BM (October 1966). "Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances". Am J Med. 41 (4): 615–21. doi:10.1016/0002-9343(66)90223-3. PMID 5927076.
  4. Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J (November 1996). "Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea". Nat Genet. 14 (3): 316–9. doi:10.1038/ng1196-316. PMID 8896562.
  5. Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG (1995). "Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis". Am J Nephrol. 15 (3): 245–50. doi:10.1159/000168839. PMID 7618650.
  6. Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI (August 1995). "Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty". J Urol. 154 (2 Pt 1): 546–9. doi:10.1097/00005392-199508000-00066. PMID 7609133.
  7. Sabatini S (March 1996). "The cellular basis of metabolic alkalosis". Kidney Int. 49 (3): 906–17. doi:10.1038/ki.1996.125. PMID 8648937.
  8. Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM (January 1992). "A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension". Nature. 355 (6357): 262–5. doi:10.1038/355262a0. PMID 1731223.
  9. Warnock DG (January 1998). "Liddle syndrome: an autosomal dominant form of human hypertension". Kidney Int. 53 (1): 18–24. doi:10.1046/j.1523-1755.1998.00728.x. PMID 9452995.
  10. 10.0 10.1 10.2 Kurtz I (October 1998). "Molecular pathogenesis of Bartter's and Gitelman's syndromes". Kidney Int. 54 (4): 1396–410. doi:10.1046/j.1523-1755.1998.00124.x. PMID 9767561.