Tag Archives: acid-base

Fluids contribute to acid-base disturbance on ICU

Image from Wikipedia
I enjoyed a paper from Critical Care Medicine this month which relates to a major bugbear of mine: the prescription of 0.9% saline for critically ill patients and the consequent metabolic acidosis this causes. However it did produce some interesting findings that helped me review my own biases here.
In short, an ICU team decided to reduce and where possible eliminate the use of high chloride fluids including 0.9% saline and Gelofusine and replace with lower chloride fluids, mainly Ringer’s Lactate (Hartmann’s solution).
It is known that saline causes a metabolic acidosis by elevating chloride and reducing the strong ion difference. This results in a normal anion gap, hyperchloraemic acidosis. The clinical significance of this is uncertain, but the iatrogenic acidosis is often confused by clinicians as a sign of severe illness, especially those clinicians that don’t look at the chloride or anion gap.
Not surprisingly, changing the fluid policy resulted in less acidosis (and also less hypernatraemia). There was however an increase in severe alkalaemia. The study was not designed to look at patient oriented outcomes.
My observations are:

  • This is an important reminder that saline causes acidosis
  • Because of the possibility of worsening alkalosis, fluid therapy choice should be individualised for an ICU patient based on their known acid-base issues; in some cases, saline may be appropriate.
  • These patients were managed for several days on an ICU. Alkalaemia is common on the ICU for reasons that include hypoalbuminaemia, furosemide use, and iatrogenic hyperventilation. These factors are less relevant in the ED resuscitation population where such a degree of alkalaemia is rarely seen.
  • The authors point out that their results are “consistent with previous acute treatment studies, which were conducted in the perioperative or experimental setting” – isn’t it a shame that ED-based studies are not forthcoming?

The authors point to an additional finding:

Furthermore, our results suggest that routine use of lactate fluids such as Hartmann’s or Ringer’s lactate is associated with a detectable iatrogenic increase in lactate in the first 48 hrs after ICU admission, when, presumably, lactate clearance is less effective.

While this is interesting, the mean [SD] lactate values in the two groups were 1.79 [1.57] and 2.05 [1.61] so while statistically significant I suspect this is clinically irrelevant. And as we know, the cause of a raised lactate is more of a concern than the fact of a raised lactate
A significant benefit of the change in fluid policy was a signficant cost saving, largely due to the omission of Gelofusine.
For me, this study reassures me that my current practice of preferring Ringer’s Lactate to Saline in the resuscitation setting is likely to minimise iatrogenic acidosis without significantly elevating the lactate, in a population rarely afflicted by significant alkalaemia.
The biochemical effects of restricting chloride-rich fluids in intensive care
Crit Care Med. 2011 Nov;39(11):2419-2424
[EXPAND Abstract]

Objective: To determine the biochemical effects of restricting the use of chloride-rich intravenous fluids in critically ill patients.

Design: Prospective, open-label, before-and-after study.

Setting: University-affiliated intensive care unit.

Patients: A cohort of 828 consecutive patients admitted over 6 months from February 2008 and cohort of 816 consecutive patients admitted over 6 months from February 2009.

Interventions: We collected biochemical and fluid use data during standard practice without clinician awareness. After a 6-month period of education and preparation, we restricted the use of chloride-rich fluids (0.9% saline [Baxter, Sydney, Australia], Gelofusine [BBraun, Melsungen, Germany], and Albumex 4 [CSL Bioplasma, Melbourne, Australia]) in the intensive care unit and made them available only on specific intensive care unit specialist prescription.

Measurements and Main Results: Saline prescription decreased from 2411 L in the control group to 52 L in the intervention group (p < .001), Gelofusine from 538 to 0 L (p < .001), and Albumex 4 from 269 to 80 L (p < .001). As expected, Hartmann’s lactated solution prescription increased from 469 to 3205 L (p < .001), Plasma-Lyte from 65 to 160 L (p < .05), and chloride-poor Albumex 20 from 87 to 268 L (p < .001). After intervention, the incidence of severe metabolic acidosis (standard base excess5 mEq/L) and alkalemia (pH >7.5) with an increase from 25.4% to 32.8% and 10.5% to 14.7%, respectively (p < .001). The time-weighted mean chloride level decreased from 104.9 ± 4.9 to 102.5 ± 4.6 mmol/L (p < .001), whereas the time-weighted mean standard base excess increased from 0.5 ± 4.5 to 1.8 ± 4.7 mmol/L (p < .001), mean bicarbonate from 25.3 ± 4.0 to 26.4 ± 4.1 mmol/L (p < .001) and mean pH from 7.40 ± 0.06 to 7.42 ± 0.06 (p < .001). Overall fluid costs decreased from $15,077 (U.S.) to $3,915.

Conclusions: In a tertiary intensive care unit in Australia, restricting the use of chloride-rich fluids significantly affected electrolyte and acid-base status. The choice of fluids significantly modulates acid-base status in critically ill patients.


Salicylate poisoning and pseudohyperchloraemia

Severe salicylate poisoning can cause metabolic acidosis from an accumulation of salicylic acid, lactic acid, and ketone bodies. A high anion gap acidosis is therefore the typical metabolic abnormality seen. A case series illustrates salicylate poisoning presenting with a normal gap (hyperchloraemic) acidosis – one patient had a chloride of 111 mmol/l and the other 123 mmol/l. This can occur when some analysers falsely read an elevated chloride in the presence of high concentrations of salicylate.

Severe salicylate poisoning is classically associated with an anion gap metabolic acidosis. However, high serum salicylate levels can cause false increase of laboratory chloride results on some analyzers. We present 2 cases of life-threatening salicylate poisoning with an apparently normal anion gap caused by an important laboratory interference. These cases highlight that the diagnosis of severe salicylism must be considered in all patients presenting with metabolic acidosis, even in the absence of an increased anion gap.

Falsely Normal Anion Gap in Severe Salicylate Poisoning Caused by Laboratory Interference
Ann Emerg Med. 2011 Sep;58(3):280-1

Complex acid-base problems

Working out the expected compensatory response to an acid base disturbance often reveals a second acid-base problem that was otherwise hidden. I regularly use Winter’s formula when I see a metabolic acidosis, but I have trouble remembering the others, so here they are, from Harwood-Nuss’ Clinical Practice of Emergency Medicine (apologies if you ‘think’ in kilopascals):
Formulas Describing Expected Compensatory Response to Primary Acid–Base Disturbances
Simple Metabolic Acidosis

  • Predicted decreased PCO2 mm Hg = 1.2 × Δ(HCO3-) mEq/L
  • Predicted PCO2 mm Hg = 1.5(HCO3-) mEq/L + 8 ± 2
  • Anticipated PCO2 approximates last two digits of arterial pH

Simple Metabolic Alkalosis

  • Predicated increased Δ PCO2 mm Hg = 0.67 × Δ(HCO3-) mEq/L

Simple Acute Respiratory Acidosis

  • Predicted decreased ΔpH units = 0.8 × Δ PCO2 mm Hg
  • Predicted increased Δ(HCO3-) mEq/L = 0.1 × Δ PCO2 mm Hg

Simple Chronic Respiratory Acidosis

  • Predicted decreased ΔpH units = 0.3 × Δ PCO2 mm Hg
  • Predicted increased Δ(HCO3-) mEq/L = 0.35 × Δ PCO2 mm Hg

Simple Acute Respiratory Alkalosis

  • Predicted increased ΔpH units = 0.8 × Δ PCO2 mm Hg
  • Predicted decreased Δ(HCO3-) mEq/L = 0.2 × Δ PCO2 mm Hg

Simple Chronic Respiratory Alkalosis

  • Predicted increased ΔpH units = 0.17 × Δ PCO2 mm Hg
  • Predicted decreased Δ(HCO3-) mEq/L = 0.5 × Δ PCO2 mm Hg