ASSESSMENT OF METABOLIC ACIDOSIS

AFTER FLUID RESUSCITATION

Munar Lubis
Pediatric Emergency Division, Child Health Department
Medical School, Sumatera Utara University/
H. Adam Malik Hospital, Medan
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METABOLIC ACIDOSIS
Frequently observed in pediatric intensive care
Usually associated with primary diseases or occurs as a
result of secondary complications in critically ill patients
Metabolic acidosis in shock;
generally results from anaerobic metabolism due to
impaired tissue perfusion
Serum lactate also be elevated
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Fluid Resuscitation
Vital part of critical care
Almost all of the fluids contain strong ion
(such as sodium and chloride) and,
sometimes, weak acids (such as albumin)

It is easy to imagine that massive

fluid resuscitation can result in metabolic
change that alter a patients acid - base
status

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www2.kumc.edu/ki/physiology/course/figures.htm
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 Acid-base approach

Traditional approaches (Henderson and Hasselbalch,

Siggaard-Andersen);
inadequate for appreciating causative mechanisms
may identify the presence of a metabolic acidosis,
but the categorization ends with a broad differential
based on the presence or absence of an anion gap
expresses the relationship of the bicarbonate/
carbonic acid buffering system to pH
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The Henderson-Hasselbach equation
expresses the relationship of the
bicarbonate/ carbonic acid buffering
system to pH:

pH = pKa + log ([HCO3]/ [H2CO3])

fail to explain certain phenomena, e.g.

hyperchloraemic acidosis

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 Stewart
three independent controlling
variables of H+ concentration:

1. The partial pressure of carbon dioxide (PCO2)

2. The strong ion difference (SID)
3. Concentration of nonvolatile weak acids

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Table 1. Normal acid-base values for pediatric patients

GROUP pH PCO2 TCO2

Preterm 7,35 + 0,04 32 + 3 17,9 + 2,2
infant
Term infant 7,34 + 0,03 37 + 1 20,2 + 0,8
Children 7,41 + 0,04 39 + 3 25,2 + 1,6
Male adult 7,39 + 0,01 41 + 2 25,2 + 1,0

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 Causes of metabolic acidosis
1. Elevated anion gap acidosis
a.Diabetic ketoacidosis
b.Renal failure (acute or chronic)
c.Inborn errors of metabolism
d.Poisons (e.g., hypoxia, sepsis, idiopathic)

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2. Normal anion gap acidosis
a.Infective diarrhea and dehydration
b.Renal tubular acidosis
c.Hyperalimentation
d.Enteric fistules (e.g., pancreatic) or enterostomies
e.Ureterosigmoidostomy
f.Drugs (e.g.,sulfamylon,ammonium chloride,
amphotericin, acetazolamide)
g.Early renal failure (chronic interstitial nephritis)
h.Dilution (rapid volume expansion)
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Assessment of metabolic acidosis
after fluid resuscitation

WHY
??

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 Fluid resuscitation

Aimed at preserving oxygen delivery to the tissues

Superimposed upon a powerful homeostatic response
Intravenous volume expansion fluids must be isotonic with plasma
Until recently, saline and Ringers lactate solution were used
almost interchangebly
Interest in colloids was mainly focus on the colloid component
(gelatin, dextran or starch) rather than the carrier solution

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 The endpoint:
normalization of arterial blood pressure, pulse
pressure, peripheral perfusion, and heart rate
establishment of adequate urine output
a decrease in the metabolic acidosis
If there is no improvement, cardiogenic causes of
circulatory failure must be considered
Arterial blood gases, hematocrit, serum electrolytes,
glucose, and calcium should be reevaluated

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 In the later phases of shock, metabolic acidosis
generally results from anaerobic metabolism due to
impaired tissue perfusion. Serum lactate also be
elevated
Ultimately, improved blood flow will result in a
decrease in acid products of anaerobic metabolism
and only then will pH concentration remain normal

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 Following the initial fluid resuscitation of the critically ill
patient, clinician are often faced with a grumbling,
unexplained base deficit

Skellett et al:
the base deficit was a result of hyperchloremia
alone
This relative hyperchloremia could be accounted for
by the large chloride load secondary to the volume
resuscitation with normal saline
Skellett S et al. Arch Dis Child 2000; 83: 514-6
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 ODell et al:
Hyperchloremic acidosis is common and
substantial after resuscitation for meningococcal
septic shock
ODell et al. Crit Care Med 2007; 35: 2390-4

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How about
colloid

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 The salt content of colloidal solutions also
influences acid base status
Some clinicians are still not aware that almost all
colloids are suspended in saline

Gosling P. Emerg Med 2003; 20: 306-15

Stephens R, Mythen M. Trauma 2003; 5: 141-7

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Rehm et al:
Preoperative acute normovolemic hemodilution
with 5% albumin or hydroxyethyl starch solutions
led to metabolic acidosis

Rehm et al. Anesthesiology 2000;93:1174-83

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 Hyperchloremic acidosis
Misnamed as normal saline, saline-based fluids are
nonphysiological in three ways;
the chloride level is higher than of plasma ( 154 mmol/l versus
98-102 mmol/l in plasma )
they lack several substances present in plasma, including
potassium, calcium, glucose and magnesium
they lack the bicarbonate ( or bicarbonate precursor ) buffer
that contributes to the maintenance of normal plasma pH

Each of these may be responsible for disrupting homeostasis,

especially the metabolic acidosis produced by saline infusion
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 Authors have traditionally attributed saline-induced acidosis
to a dilution of bicarbonate by saline, leading to a
reduction in buffering capacity with consequent acid excess

There are several recent studies, however, showing this not

to be the case
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 Physical chemistry explanation:
it is the chloride that causes acidosis

saline is added to blood

increasing the amount of Cl- relative to Na+

To preserve electrical neutrality H2O dissociates,

raising the free H+ concentration and causing a fall in pH
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www.anaesthetist.com/icu/elec/ionz/useful1.htm 23
 Hyperchloremic acidosis

What is its clinical relevance

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 Waters et al sought to determine if the differences that result
from Ringers solution or saline influenced outcome in patients
undergoing aortic reconstructive surgery;

As in other studies, the saline patients developed hyperchloraemic

acidosis and received significantly more blood products
There was no difference, however, in duration of mechanical
ventilation, intensive care unit stay, hospital stay and incidences of
complications between the groups, in particular urea, creatinine and
renal failure

Waters JH et al. Anesth Analg 2001; 93: 817-22

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 The consequences of hyperchloremic metabolic acidosis are
traditionally downplayed and accepted as a necessary evil of
saline resuscitation

Recent studies may change this benign view of iatrogenic

hyperchloremic metabolic acidosis, especially as it pertains to
choice of fluid composition for resuscitation

Study that support the hypothesis that the electrolyte composition

of the solution may play a role in the coagulophaty associated with
starch solutions greater than that of the starch molecule it self has
been reported

Gunnerson KJ. Crit Care. 2005; 9(5): 508516

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 Saline induced acidosis has a side effect profile similar to that
of ammonium chloride abdominal pain, nausea, vomiting,
headache, thirst, hyperventilation, and delayed urination

Aside from avoiding these adverse reactions, the treatment of

metabolic acidosis per se has not yet been shown to improve
clinical outcome and, based on a large retrospective database,
mortality does not appear to be significantly increased

However, there is mounting evidence that iatrogenic metabolic

acidosis may be harmful and should be avoided when possible

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SHOULD METABOLIC
ACIDOSIS
BE TREATED?

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 Despite the known effects of acidemia on the organism in
critical situations, a protective role of acidemia in hypoxic cells
and the risk of alkalemia secondary to drug interventions are
being considered

There is consensus regarding the advantages of alkali and

sodium bicarbonate therapy in cases with normal anion gap

In the presence of high anion gap acidosis, the use of sodium

bicarbonate is not beneficial and has potential adverse effects,
limiting its indication

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 More basic approach:

Treat the underlying cause

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 A number of alternatives exist to reduce the chloride load:
consideration of reduced volume colloid
replacing chloride anions with balanced lactate solutions and suspending
colloids in such solutions other than 0,9% saline

It is likely that balanced lactate solutions help correct a strong ion difference
(SID) and improve acidosis as it is the relative ratios of (strong) ions rather
than their absolute equivalents that determine the overall effects on acid-
base status 31
 If the science and art decision is to administer NaHCO3;

HCO3- deficit (mEq) =

0,3 x BW (Kg) x [HCO3- expected HCO3- observed]

The usual NaHCO3 preparation available worldwide has a

concentration of 0,88 mEq/mL, with pH = 8 and 1461 mOsm/kg
ideally administered through a central venous line or diluted
with distillated water

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 Summary
Metabolic acidosis is usually associated with primary diseases or
occurs as a result of secondary complications in critically ill patients

In the later phases of shock, metabolic acidosis generally results

from anaerobic metabolism due to impaired tissue perfusion
If there is no haemodynamic improvement after fluid resuscitation,
cardiogenic causes of circulatory failure must be considered. Arterial blood
gases is one of assessments that should be reevaluated

All critical care practitioners should recognize fluid resuscitation-

induced hyperchloremic metabolic acidosis
When using a large amount of fluids, careful attention should be paid to this
disorder
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