And here I was thinking bicarb was helpful….

For those of you not in conference last Wednesday, there was a brief review of Rhabdo that listed bicarb as a potential treatment.  Feeling like the junior that I was (but of course am no longer), I was hesitant to speak and, instead, waited anxiously for an official senior or an attending to comment.  But no one did…  So I started looking up bicarb and wanted to share some of what I discovered.  It’s kind of long, but hey, so is residency and you all elected to commit yourself to that.

Let’s start with giving bicarb in CPR.  Though we have been giving bicarb since the 1950s, there is scant evidence for it’s effectiveness.  In fact, studies have shown the following:

1. Bicarb actually decreases intracellular pH, while increasing the pH arterially. Theory is that the bicarb is broken down into H+, CO2, and H2O and the H+ goes intracellularly.
2. In animal studies, giving bicarb lowers cardiac perfusion pressure and decreases ROSC after cardiac arrest.
3. In animal studies 12 of 14 studies reviewed concluded that giving bicarb during CPR worsened myocardial performance with the remaining 2 showing no difference.
4. Only 1 RCT for bicarb in CPR in adults was done, which showed no improvement in ROSC or mortality.
5. Out of 19 retrospective reviews, 11 showed no benefit and 8 suggested a worse outcome when Bicarb is given during CPR.

Biochemical explanation (this is the cool part)

Bicarb breaks down into CO2, which can increase the CO2 level in the blood.  If the patient has poor CO2 elimination (aka not breathing), this can lead to increased CO2 levels, especially in cells, leading to worsening intracellular acidosis

Conclusion:  Bicarb during CPR not as helpful as we would think, and may even be harmful!!!!!

This data is so believed, even national guidelines have picked it up.Neonatal resus guidelines (2000) states that “there is insufficient data to recommend routine use of bicarb in the resus of newborns…[it] may be detrimental to myocardial or cerebral function.  The 2005 AHA guidelines no longer recommend bicarb during CPR either.

What about in Hyperkalemia you ask?  Well I’ll tell you.

Traditionally bicarb was one of the mainstays of drugs used to push potassium intracellularly, thus decreasing plasma potassium concentration.  According to a paper from 1977 involving 14 patients, it seems to work.    Since then though, some data has showed less than stellar results.

1. In 12 HD pt’s with hyperkalemia, bicarb therapy + IVF showed no statistically significant change in K until 4 hours (a decrease average of 0.7), and levels returns to baseline by 7 hours (though pH and bicarb levels both increased)
2. Nondiabetic HD patients received a variety of treatments with potassium measured q15 minutes over 1 hour.  Both bicarb and NS failed to show a significant decrease in plasma potassium  Though pt’s receiving bicarb did see an increase in pH and bicarb level

Conclusion:  Though no studies show harm, the administration of bicarb in hyperkalemia does not seem to acutely decrease potassium levels.  In a patient with a  dangerous arrhythmia due to hyperkalemia, calcium starts working in 1-3 minutes to stabilize the myocardium, while the K is pushed into cells by albuterol “immediately”, and  insulin in 10 minutes.  So at the very least, get the calcium, albuterol, and insulin in first.

Next review:  Bicarb in DKA with acidosis

Currently, the ADA says bicarb “may be considered” in patients with pH < 6.9 in DKA.   What about 7.0?  7.1?

            Well, in a retrospective review in Annals of Pharmacotherapy.  Patients with acidosis from DKA who received bicarb (pH<7 with DKA), had no difference in time to pH>7.2, or time to discharge vs standard tx (IVF/Insulin).  Those receiving bicarb did receive more fluid/insulin (significantly significant, but the actual numbers were not different by much).

Another retrospective study of 39 patients with DKA and pH 6.9-7.1 showed no difference in pH, PaCO2, glucose concentration, potassium level, time to normalization of pH, time to clearance of urinary ketone with and without bicarb.

There were no papers that I could find that evaluated patients with pH < 6.9.

Conclusion:  Bicarb unhelpful for pH>6.9 in DKA patients.   Unclear if pH <6.9

Lastly:  Rhabdo

Alkanizing the urine leads to: decreased myoglobin precipitation, less tubule injury from decreased redox cycling of myoglobin and lipid peroxidation, less vasoconstriction due to myoglobin (all in animal studies).

Problematically, bicarb has not shown to be as helpful in actual human studies (though trials are very limited).

1.      A retrospective study showed no difference in mortality between saline vs saline- bicarb-mannitol.  CK was lower in the saline group at baseline. And the study didn’t include saline vs saline +bicarb.  And CK levels were low at start.  And no one actually developed ARF

2.      bicarb-mannitol-saline vs saline only showed no difference in outcomes.

3.      Review of 27 articles found no RCT comparing IVF with IVF + bicarb. 8 of the articles found delay to IVF increased risk of ARF.  “No evidence supported a preferred fluid type or that sodium bicarb with or without mannitol was superior to fluid therapy alone”.  Rec: UOP 300ml/hr, bicarb only to correct systemic acidosis, and mannitol only if uop< 300ml/hr despite adequate fluid administration.

4.      Lastly, our excellent EBM on the topic recommends bicarb if Urine pH <6.5 with CK level > 5000 as class III evidence (may be acceptable, possibly useful, considered optional or alternative treatments).  One concern with bicarb is that is that it can lower calcium levels, which may already be low as rhabdo can initially lead to hypocalcemia (BUT DON”T CORRECT IT, as the calcium deposits eventually break down and the pt can develop hypercalcemia).

How does all this effect my clinical practice?

1. I don’t think I’ll be giving bicarb during codes anymore.
2. I’m not convinced that giving bicarb helps in hyperkalemia
3. As long as pH >6.9, no bicarb needed in DKA
4. Bicarb in rhabdo is controversial.  The patient mostly needs fluids, fluids, fluids.

Just so you don’t think bicarb is completely useless, a brief literature search dose reveal that it is still recommended in: TCA overdose, salicylate toxicity, phenobarb, chlorpropamide and chlorophenoxy herbicide poisoning, cocaine overdose, organophosphate poisoning (per Cochrane review 2005, 2 RCT’s, both small.  One no difference, one “slight benefit”.), and lastly, life-threatening acidoses from methanol and ethylene glycol (enhances formate elimination…but it seems like that’s a good time for HD).

What do y’all think?

Resources.

1.     Judy L. Aschner, MD,  Ronald L. Poland, MD  Sodium Bicarbonate: Basically Useless Therapy, Journal of Pediatrics

http://pediatrics.aappublications.org/content/122/4/831.full

2.  Contributors and Reviewers for the Neonatal Resuscitation Guidelines , International Guidelines for Neonatal Resuscitation: An Excerpt From the Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: International Consensus on Science

http://pediatrics.aappublications.org/content/106/3/e29.full

3.  Viallon A, Zeni F, Lafond P, Venet C, Tardy B, Page Y, Bertrand JC.  Does bicarbonate therapy improve the management of severe diabetic ketoacidosis?  Crit Care Med. 1999 Dec; 27 (12: 2690-3)

4.  Duhon B, Attridge RL, Franco-Martinez AC, Maxwell PR, Hughes DW.  Intravenous Sodium Bicarbonate Therapy in Severely Acidotic Diabetic Ketoacidosis (July/August). Annals of Pharmacology. 2013 Jun 4

5.  Scharman EJ, Troutman WG.  Prevention of kidney injury following rhabdomyolysis: a systematic review.  Ann Pharmacology. 2013 Jan;47(1):90-105. doi: 10.1345/aph.1R215. Epub 2013 Jan 16.

6.  Bosch X, Poch E, Grau JM., Rhabdomyolysis and acute kidney injury.  N Engl J Med. 2009 Jul 2;361(1):62-72. doi: 10.1056/NEJMra0801327.

7.  Paul M Wax, GoldFranks Toxicology Emergencies  Antidotes in depth: Sodium Bicarbonate   http://www.accessemergencymedicine.com.newproxy.downstate.edu/content.aspx?aid=6535633

8.  Cooper DJ, Walley KR, Wiggs BR, Russell JA. Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective, controlled clinical study. Ann Intern Med. 1990 Apr 1;112(7):492-8.

9.  Fraley DS, Adler S. Correction of hyperkalemia by bicarbonate despite constant blood pH.   Kidney Int. 1977 Nov;12(5):354-60.

10. Blumberg A, Weidmann P, Ferrari P. Effect of prolonged bicarbonate  administration on plasma potassium in terminal renal failure. Kidney

11.  Allon M, Shanklin N. Effect of bicarbonate administration on plasma potassium in dialysis patients: interactions with insulin and albuterol.  Am J Kidney Dis. 1996 Oct;28(4):508-14.

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