Metabolic alkalosis resident survival guide: Difference between revisions

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{{familytree | | | | | | | | | | | | C01 | | | | | |C01=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}}
{{familytree | | | | | | | | | | | | C01 | | | | | |C01=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}}
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{{familytree | | | | | D01 | | | | | D02 | | | | | D03 |D01=Expanded EABV(No sign of volume depletion or Saline unresponsive) *Treatment:Treat underlying cause.|D02=Contracted EABV(sign of volume depletion or saline responsive) *Treatment:Replace volume with NaCl if depleted, Correct electrolyte imbalance, NH4Cl and HCl should be reserved for severe cases. |D03=Rule out by history}}
{{familytree | | | | | D01 | | | | | D02 | | | | | D03 |D01=Expanded EABV(No sign of volume depletion or Saline unresponsive) *Treatment:Treat underlying cause.|D02=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. |D03=Rule out by history}}
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{{familytree | | | | | |!| | | | | | |!| | E01 | | | | | | | E02 |E01=Transient|E02=Renal failure with ingesion}}
{{familytree | | | | | |!| | | | | | |!| | E01 | | | | | | | E02 |E01=Transient|E02=Renal failure with ingesion}}

Revision as of 07:43, 1 December 2020


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

Synonyms and keywords:

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, hyperaldostrenism, reduced glomerular function rate, reduced effective arterial blood volume in heart failure or cirrhosis will lead to metabolic alkalosis. When the physiologic blood pH is above 7.45, it triggers respiratory centre to cause hypoventilation, thus decreased PCO2 leading to compensatory respiratory acidosis. The PCO2 increases about 0.5 to 0.7 mmHg to every 1.0 mM increase in plasma bicarbonate concerntration. In severe Metabolic alkalosis PCO2 can reach 60 mmHg. The mortality rate with metabolic alkalosis is 45% with areterial 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

  • Chloride depletion or Gastrointestinal loss of hydrogen
    • GI loss: Vomiting (most commonly seen in pyloric stenosis), NG suction , Zollinger-ellison syndrome, Bulimia.[2]
    • Diuretics: Loop and thiazide diuretics.
    • Diarrhoea: Villous adenoma[3], congenital chloride diarrhoea[4]
    • Cystic fibrosis.[5]
    • Chloride deficient infant formula.
    • Gastrocystoplasty [6]
    • Post hypercapneic metabolic alkalosis.
  • Potassium depletion or Minerelocorticoids excess or Renal loss of hydrogen
    • Dietary potassium depletion.[7]
    • Primary hyperaldosteronism: Conn syndrome or adenoma, hyperplasia, carcinoma, renin or glucocorticoid responsive.
    • Secondary hyperaldosteronism: Renovascular hypertension, edema (cirrhosis, heart failure, nephrotic syndrome), juxtraglomerular cell(renin producing) tumor, renal cell carcinoma, hemangiopericytoma, nephroblastoma
    • Minerelocorticoid excess due to primary decorticosterone excess (11 beta, 17 alpha hydroxylase deficiency), licorice(glycyrrhetinic acid), liddle syndrome.[8] [9]
    • Bartter and Gitelman syndrome. [10]
    • 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 adminstration.
    • 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 use? *Recent or current diuretic use? Vomiting or diarrhea? *massive use of licorice? * H/O recent hypercapneic respiratory failure?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Physical Examination: *General appearence: Restlessness/ Irritable/lethargic? *Skin: decreased or normal turgor? *HEENT: Headache/Dizziness? *CVS: DYsarrythmia/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
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Transient
 
 
 
 
 
 
Renal failure with ingesion
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
*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:Penicillins *Impaired tubular transport:Loop and thiazide diuretics, Barrter's and Gitelman's disease, Hypomagnesemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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

  • The content in this section is in bullet points.

Don'ts

  • The content in this section is in bullet points.

References

  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. 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.


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