Na/H2O for Residents

From UBC Wiki

Sodium & Water Assessment & Therapeutics for Pharmacy Practice Residents

Updated August 2015

Instructor

Peter Loewen, B.Sc.(Pharm), ACPR, Pharm.D., FCSHP | Peter.Loewen@ubc.ca phone 604-827-1814

Pre-Session Objectives

PRIOR TO arriving at the session, participants should be able to describe

  1. The distribution of total body water (TBW)
  2. The influence of changes in TBW on serum Na concentration
  3. The pathophysiology and clinical presentation of diabetes insipidus and SIADH
  4. The clinical parameters for assessing Extracellular Fluid (ECF, “volume”) Status and Intracellular Fluid (ICF) status.

Preparation for the session

  1. Loewen’s Sodium & Water Assessment & Therapeutics 1-pager
  2. McGee S, Abernethy WB, Simel DL. Is this patient hypovolemic? JAMA 1999;281:1022-9. –the classic article on this subject.
  3. Try the self-assessment questions below
  4. Read the cases
  5. Install “MedCalc”, "MedMath", “Mediquations”, or equivalent on your phone and find the fluid&lytes tools in there.

Pre-session self-assessment

  • Take a crack at trying to apply the 1-pager approach to one or two of the cases. This is will start to develop your APPROACH, even if you aren’t able to fully diagnose and solve the problems identified pre-session. We probably won’t get through all of them in the class time available but you’re equipped with plenty of practice situations to deal with.

Pre-Session Self-Assessment Questions

1. The proportion of Total Body Water (TBW) that is intracellular is approximately

(a) 1/3
(b) 2/3
(c) 1/8
(d) 20%

2. Loss of extracellular fluid (e.g. blood) typically causes which of the following effects ACUTELY (ie, within the first 1-2 hours):

(a) a rise in serum sodium concentration
(b) a drop in serum sodium concentration
(c) excretion of very dilute urine
(d) no effect on serum sodium concentration

3. Which of the following drugs may cause diabetes insipidus (circle as many as apply)

(a) demeclocycline
(b) carbamazepine
(c) sertraline
(d) lithium
(e) enalapril

4. SIADH may be defined as

(a) euvolemic hyponatremia with excretion of concentrated urine
(b) hypervolemic hyponatremia with oliguria
(c) euvolemic hyponatremia with excretion of dilute urine
(d) euvolemic hypernatremia with excretion of dilute urine

5. Which of the following is not a direct measure of a patient’s volume status

(a) symptoms of severe postural dizziness
(b) postural change in HR
(c) serum creatinine/BUN ratio
(d) serum sodium concentration
(e) postural change in SBP
(f) JVP

By the end of the session, and upon further learning and reflection residents should be able to

  1. Describe the difference between water and volume, dehydration, and volume depletion
  2. Using physical assessment and laboratory parameters, diagnose the type of water-related defect a patient exhibits (e.g. hypovolemia, hyponatremia, hypernatremia, SIADH)
  3. Demonstrate an APPROACH to evaluating water-related problems in a patient and their potential causes
  4. Design a detailed therapeutic plan for treating the water-related disorder, including:
  • Selecting and writing orders for an appropriate crystalloid solution (if required) or other drug therapy.
  • Quantitative determination of quantities of crystalloid required and infusion rates
  • Writing orders for (or conducting themselves) an appropriate monitoring plan.

Required Skills

  1. assess your patient for postural BP and HR changes
  2. assess your patient's jugular venous pressure | JVP

Why Na and H2O Matter in Pharmacotherapy Practice

  • Your patient is on multiple antihypertensives and today complains of dizziness on rising. BP reasonably well controlled. Should you decrease the dose of an antihypertensive?
  • Your patient with parkinson's disease seems to be developing postural hypotension. Does he need midodrine?
  • You're consulted about a patient with severe hyponatremia and recent SSRI initiation. Is the hyponatremia drug-induced?
  • Your CHF patient needs to be started on ACE-I. Her SCr is 155. How worried about a rise in SCr upon starting ACE-I are you?
  • Your CHF patient is stable on ramipril 10mg, B-blocker, and furosemide 40mg. Lately his SCr has been creeping up. Physicians intends to decrease the ramipril dose because everybody knows ACE-I can cause renal failure. Is this a good idea?
  • Your patient with HTN is admitted to hospital with CAP and has a serum Na of 129. Admitting physicians documents that the patient's HCTZ is being held due to "HCTZ-induced hyponatremia" and that it should not be restarted. Is this sensible?
  • Your patient has recurrent angina despite amlodipine+NTG patch. You believe metoprolol will be indicated, but are worried about his standing BP of 110/70 and postural drop. Can his anti-ischemic therapy be augmented?
  • Ever been asked to "please procure some demeclocycline"? Know what conivaptan is?
  • Your vancomycin-treated patient is starting to show signs of GFR decline. Is it due to vancomycin?

Common Misconceptions and Sticking Points

  1. Explain why serum sodium is a reflection of your patient's ICF.
  2. Explain how giving your patient too much free water causes their serum sodium to go down. EXPLANATION | EXPLANATION (HD)
  3. Explain how causing your patient to lose free water (eg, by administering a loop diuretic) causes their serum sodium to go up. EXPLANATION | EXPLANATION(HD)
  4. Explain why giving your hypovolemic hyponatremic patient normal saline causes their serum sodium to go up.
  5. Explain why it is a mistake to believe that hypernatremia causes ICF contraction, or hyponatremia causes ICF expansion.

Further reading on Na/H2O management

  1. The mysterious origins of the “8 glasses of water a day” rule
  2. What would happen to you if you drank seawater?
  3. Freda BJ, Davidson MB, Hall PM. Evaluation of hyponatremia: A little physiology goes a long way. Cleveland Clin J Med 2004;71:639-50.
  4. Zarychanski R, et al. Association of Hydroxyethyl Starch Administration With Mortality and Acute Kidney Injury in Critically Ill Patients Requiring Volume Resuscitation: A Systematic Review and Meta-analysis. JAMA 2013;309:678–88.
  5. Sushrut et al. Mortality after Hospitalization with Mild, Moderate, and Severe Hyponatremia. Am J Med (2009) 122, 857-865.
  6. Chawla A, et al. Mortality and Serum Sodium: Do Patients Die from or with Hyponatremia? Clin J Am Soc Nephrol 6: 960–965, 2011.
  7. Nemerovski C, Hutchinson, DJ. Treatment of hypervolemic or euvolemic hyponatremia associated with heart failure, cirrhosis, or the syndrome of inappropriate antidiuretic hormone with tolvaptan: a clinical review. Clinical therapeutics. 2010;32(6):1015-32.
  8. Hilton AK, Pellegrino VA, Scheinkestel. Avoiding common problems associated with intravenous fluid therapy. MJA 2008;189:509-513.
  9. Bagshaw SM, Townsend DR, McDermid RC. Disorders of sodium and water balance in hospitalized patients. Can J Anesth 2009;56:151–167.
  10. Reynolds RM, Padfield PL, Seckl J. Disorders of sodium balance. BMJ 2006;332:702-5.
  11. Yeates KE, Singer M, Morton AR. Salt and water: a simple approach to hyponatremia. CMAJ 2004; 170:365-9.
  12. Oster JR, Singer I. Hyponatremia, hypoosmolality, and hypotonicity: tables and fables. Arch Intern Med 1999;159:333-6.
  13. Milionis HJ, Liamis GL, Elisaf MS. The hyponatremic patient: a systematic approach to laboratory diagnosis. CMAJ 2002;166:1056-62.
  14. Adrogue HJ, Madias NE. Hyponatremia. New Engl J Med 2000;342:1581-9.
  15. Halperin ML, Goldstein MB. Fluid, Electrolyte, and Acid-Base Physiology: A problem-based approach. W.B. Saunders Co, Philadelphia. 1999.
Retrieved from "https://wiki.ubc.ca/index.php?title=Na/H2O_for_Residents&oldid=375024"