THE EFFECT OF BUFFERED AND NON-BUFFERED ACD BLOOD ON ELECTROLYTE AND ACID-BASE HOMEOSTASIS DURING EXCHANGE TRANSFUSION

(1)

0 These studies ilave been reported in l)art. (Received August .3, 1967; revision accepted for publication January 4, 1968.)

This research was supported in part by a National Institutes of Health Grant

#

HD 00747 and The

Ileniatology Research Fund of the Children’s Orthopedic Hospital and Medical Center.

ADDRESS FOR REPRINTS: (T.K.O., Jr.) Department of Pediatrics, University of \Vashington, Seattle, Washington 98105.

PEDIATRICS, Vol. 41, No. 4. April 1968 802

THE

EFFECT

OF

BUFFERED

AND

NON-BUFFERED

ACD

BLOOD

ON

ELECTROLYTE

AND

ACID-BASE

HOMEOSTASIS

DURING

EXCHANGE

TRANSFUSION

W. E. Pierson, M.D., Cynthia T. Barrett, M.D., and T. K. Oliver, Jr., M.D.

Front the Department of Pediatrics, Unicersity Hospital and Children’s Orthopedic Hospital

and .‘tfedical Center, University of Washington School of Medicine

ABSTRACT. Exchange transfusions have been

per-formed using buffered and non-buffered ACD

1)100(1. In 15 low risk infants receiving unbuffered 1)100(1, severe acidosis occurred ill ne (luring tile transfusion. Other investigators have recently ob-served siniilar findings. In contrast, when blood was buffered prior to exchange transfusion in 26 high risk infants (i.e., with cardiorespiratorv insuf-ficiency

),

acidemia (li(l not occur. Since tile mortal-it of exchange transfusion is increased in infants

with cardiorespiratorv insufficiency, it appears that buffered ACI) blood will lessen the risks.

It is recommended tilat, ACD blood is used for

excilange transfusion in an- infant, the blood

should be buffered immediately prior to transfusion using 10 mM of 1.0-1.2 \I THAM. Pediatrics, 41:802, 1968, ACID-BASE EQUILIBRIUM, HYPEHHILIRU-BIXEMIA, BLOOD TRANSFUSION, ELECTROLYTES,

FETAL ERYTHROBLASTOSIS.

I

r Is . vehl establisileci hut poorly

appre-ciated fact that considerable changes

occur in the electrolyte composition and

acid-base balance of wilole blood when

acid citrate dextrose

(

ACD

)

is used as an

anticoagulant and preservative. Mans’

stud-ies ilave reported metabolic changes in

adults associated witil massive

transfu-SiOfl,1 I)ut relatively few studies have been

performed in neonates vhien large volumes

of blood are given during the course of an

ecilange transfusion. Our interest in thus

sui)ject was first aroused several years ago

\‘ilCll, in the course of studies OIl thermal

regulation, we observed that carbon dioxide

output increased promptly and dramatically

when as little as 20 ml of ACD blood were

infused. \Ve 1)eheved this response to be in

consequence of the acid load of ACD blood

since it did not occur when ileparinized

blood with a more physiologic pH was

given. Because of this observation and the

unquestionable fact tilat tile mortality of

exchlange transfusion is greatly increased in

high risk (usually pre-terni) infants, we

de-cided to study in detail the effects of using

buffered and non-buffered ACD blood

dur-ing exchange transfusion.#{176}

MATERIAL

Non-buffered Blood

Fifteen infants were studied during a

total of 16 transfusions. Two were pre-term

infants weighing 1.7 and 2.2 kg; tile

remain-ing 13 infants were born at term and their

birth weights were above the 25th

percen-tile for gestational All were

coilsid-ered to be healthy except for

hvperbiliru-binemia, which in 13 was associated with

mild to moderate ervthroblastosis fetahis

and in tvo it was idiopathic. The age at the

time of exchange transfusion ranged from 1

to 144 hours, with a median of 36 ilours.

Sam-pies were drawn at the start, mid-way, and

at the end of the exchange transfusion

through a catheter which had been inserted

into the umbilical vein. Capillary samples

were obtained from a warmed heel at 2 and

(2)

ARTICLES

Buffered Blood

A total of 23 infants were given

replace-ment transfusions with ACD blood which

had been buffered with

tris(hydroxy-methyl) aminomethane

(

THAM ). In

ad-dition, tllree infants received blood to

which sodium bicarbonate had been added.

The infants who were given

THA1’sI-buff-ered i)lOOd were divided for purposes of

analysis into three sub-groups, depending

on their clinical status.

RESPIRATORY DIsTiuSS-l1 INFANTS (12

TRANSFUSIONS

)

: All of the infants in this

group ha(l clinical and x-ray evidence of

the idiopathic res)iratOry distress syndrome

(

IRDS

)

of moderate to severe degree

(pCO greater than 50 mm Hg) but did

not receive mechanical respiratory

assis-tance before or during the time of study.

The weights at the time of study ranged

from 730 to 2,540 gm, with a median of

1,290 gn. All of the infants in this group

Ilad idiopathic hyperbilirubinemia and

ranged in age from 2 to 5 days at the time

of exchange transfusion.

ERYTHROBLASTOSIS FETALIS WITHOUT

RE-SPIRATORY DISTRESS-4 INFANTS

(

6 TRANS.

FUSIONS

)

: These infants ranged in weight

from 1,950 to 2,950 gm. Each had

moder-atelv severe disease requiring early

cx-change transfusion. None had evidence of

cardiorespiratory insufficiency.

RESPIRATOR PATIErs-8 iNFANTS (10

TRANSFUSIONS

)

: Each of these infants had

severe respiratorY distress or apneic spells

necessitating continuous mechanical

respi-ratorv assistailce before, during, and after

the exchange transfusion. These infants

ranged in weigilt at the time of exchange

from 1,170 to 1,740 gm

(

median 1,295 gm).

Three had ervthlroi)lastosis fetalis, one had

ABO incompatibility

(

icterus praecox

)

,

and

the renlaiilder had idiopathic

hyperbihiru-i)inenhia.

INFANTS RECEIVING BLOOD BUFFERED WITH

SoDIUM BICARBONATE-3 INFANTS: Two of

the infants in this group ilad idiopathic

liv-perbihirubinemia and one had icterus

prae-cox. None had respiratory insufficiency

clinically or biochemically. The infants

weighed 1,520, 2,740, and 3,280 gm at the

time of transfusion.

Blood samples from the babies who

re-ceived buffered blood were obtained from

catheters which ilad been inserted into an

umbilical artery or vein. Heated capillary

samples were not obtained in infants with

res)iratOry distress because of tile

unrelia-bihitv of this sampling method in that

condition.5

M ETHODS

The exchange transfusion was performed

using conventional techniques. The

vol-umes exchanged in the infants who

re-ceived non-buffered blood ranged between

170 and 200 nIl/kg; tile volumes of buffered

blood used were between 132 and 351 mi/kg

(median 220) . Twenty milliliter increments

were used in occasional infants, although 5

to 10 ml increments were the rule for infants

of low birth weight or those with

respira-tory distress. The duration of tile procedure

ranged between 45 and 105 minutes, most

taking 60 to 90 minutes. The blood was

warmed to just below body temperature

with a warming device. The EGG was

dis-played continuously on an oscilloscope.

Core temperature was monitored using a

thermistor which was placed 4 to 10 cm

be-yond the anus. A radiant heater previously

described maintained these infants in a

neutral thermal environment. Twenty to 100

mg of calcium gluconate were given to

most infants following each 100 ml of blood.

ACD donor blood was used for all

transfu-sions. On two occasions, the blood had

been drawn 2 days before usage. Otherwise,

it was less than 24 hours old. The ACD

solu-tion used was NIH solution A, 72 ml being

added to 480 ml of blood. The final volume

in the bag was 552 ml and in the context of

this report is considered to be a unit of

blood.f

In tile first study, 20 mM of THAM were

added to the bag of donor blood but this

(3)

1l(l(/ Start

J)1I 6.73U±U.U19 7.365±U.UUI

I)(#{176}2III!!) hg > IOU 41.±1.3

ilUO3 II1F(1/i

-

‘23.1 ±U.S

BE. ,nEq/l > -‘2U -U.S ±0.6

Na !IIFA1/1 171 ± I .7 147±1.1

(‘1 mEq/l s(;±’2.U 1U4±1.4

i; IIIE(1/l 5.’2±U.’2 4.’2±0.’2

(‘a iiiEq/l 9.’2 ±U.’2 S.S±U..5

iI(t.’, 4’2.4±I.4 44.4±1.9

Mi(l

7.331 ±0.U’2U

4’2.4 ± I..5

-‘2.5±1.’2

547±1.4

104 ±‘2.(;

4.3 ±0.’2 I 4).1± 0.4

41.3±1.3

End

7.315±U.U’25

43 .S ± ‘2.1

‘23 .3 ± I .1

-‘2.7± 1.3

150±1.1

10’2±’2.7

4.7±0.3

9-(1± 0.5

38 .6 ± 1 .4

2 hr Io,ct

7.5U.5±0.018

3’2.1 ±‘2.1

‘26.7±1.8 +3.8±1.’2

148 ± 0.8

105±1.8 4.4±0.’2

9.0±0.3

‘39.4±1.6

44 hr Post

7.4’21 ±U.U14

35 .6 ± I .9

‘23.I ± I .4

+U.5± I .U 146 ±‘2 .4

1(13 ±3.9 4.5±0.’2

8.I ± U .3

40.5±1.7

BUFFERED BLOOD

markedly overcorrected the acidosis

(

pH

7.705). In the next 15 exchanges 15 mM,

were a(ided to each unit, and later, in 8

ex-changes, 9 to 10 mM were added

(

see

Ap-pendix for details

)

. When sodium

bicarbo-nate solution

(

0.9 M

)

was used, 7.5 to 10mM

were added to each unit. No plasma was

re-moved prior to transfusion.

The pH was determined with standard

micro glass electrodes and pCO2 was

ei-titer determined directly with a

Severing-hatis electrode or calculated, as were

bicar-bonate concentration and base excess, from

the nomogram of SiggaardAndersen.b0

\Vllen pCO2 was determined directly,

bi-carbonate concentration and base excess

were calculated from an alignment

nomo-a’ Serum electrolytes and packed cell

volume were performed in (lul)hicate using

micro methods.12

RESULTS

Non-buffered Blood

Tile acid-i)ase and electrolyte values (hiring and following trallsfusion w’itll

Ilon-i)uffered ACD i)lOOd are showli ill Table I.

The 1)ag 1)100(1 was profoundly acidotic

with a iiiean I)hI of 6.750 ± 0.019 due to

tile accumulation of both metabolic acids

III1(i carbon dioxide. The pCO ‘as always

IllOC tilall 100 mii 1-1g. Because the exact

value of pCO VaS iiot known, i)ase excess

(0111(1 not be calculated. However, even if

pCO2 was 200 111111 Hg the base excess

would have been greater than - 20 mEq/l.

The

donor

blood

was also hypernatremie

(171 ± 1.7 mEq/i), hypochloremic (86 ±

2.0 mEq/i), and slightly hvperkalemic (5.

± 0.2 mEq/l) . During the exchange

trans-fusion, there were no significant changes in

the mean acid-base values in the illfants

even though pH and base excess tended to

fall and pCO2 tended to rise. Two hours

after the transfusion, their acid-base values

had changed significantly. The pH and the

base excess had risen to 7.505 ± 0.018 and

3.8 ± 1.2 mEq/l, respectively, and pCO2

had fallen to 32.1 ± 2.1 mm Hg.

Twenty-four hours after the exchange, the blood gas

values were again within normal limits. No

significant changes in electrolyte

concen-trations were observed either during or

fol-lowing the excilange transfusion.

Buffered Blood-Donor Blood

When THAM was added, it neutralized

h)Oth the metabolic and respiratory

compo-nents of the acidotic donor l)lood (Table

II ). The addition of 15mM/unit sornewilat

overcorrected the pH

(

7.497 ± 0.014

)

he-cause of excessive reduction of pCO2

(

28.9

± 2.3 mm Hg). On tile Otiler hand,

IIJ

mM/unit corrected the pCO2 more

appro-priately (42.1 ± 4.3 mm Hg) imt the pH

was undercorrected

(

7.314 ± 0.032

)

be-cause of incomplete buffering of tile

met-al)olic acidosis. In two instances, the

os-‘rABLE I

i’stFAN ( ± S.E. .Iu-n.eF:, FLEcTIIOLYTE AND IIEMATOCIIIT \SLUES IN 1.5 INFANTS WIIO hAD EXCIItNGI

‘l’IIANSIUSIONS \VITII XoNmF1::IwD AC!) BLOOD

I(hilt

(4)

15

1)11

I)(()2 ItlItI lig ilCO3 mhq/1 B.E. mEq/l Na InEq/l (1 niEq/l

K mEq/l

11(1.

Before After

6.775±0.0’2() 7.497±0.014 >100

->-‘20 -1.0±1.0

178±6.4 140±1.6 76±3.9 77±5.5

5.4±0.3 4.5±0.’2

4’2±1.0 33±0.9

TABLE II

MEAN (±S.E.) ACID-BASE \ALI’ES OF ACI) BLOOD BEFORE AND AFTER BUFFERING

Buffer TIIAM-15 in)! TIJAM -9--JO in)! NaII(’03-7.5--IO n.h

Before After

<6.8 7.314±0.0’3’2 >100 4’2.1±4.3

->-‘20

169±’2.4 145±3.9

7’2±1.9 71±s2.9

6.3±0.5 6.1±0.4

45±.1 39±’2.0*

Before After

<6.8 6.9’26±o.048

>100 >100

>-‘20

174±3.9 ‘20’2±3.1

68±1.4 7’2±3.8

5.3±0.1 4.6±0.6

46±6.7 41±5.3

* Calculated from addition of 1.’2 molar solution (5 exchanges).

molarity of the donor blood was measured

before and after the addition of 10 mM of

isotonic THAM. Osmolarity rose from a

mean of 302 to 359 mOsm/l, the principal

increment being due to an increase in

glu-cose concentration. In contrast to the

ef-fective neutralization of the acidosis in the

donor

blood

by 10 mM THAM, a similar

amount of sodium bicarbonate had but

lit-the effect on the pH. It rose to 6.926 ±

0.048. The explanation lies in the fact that,

although the metabolic component of the

acidosis is improved when sodium

bicar-bonate is added, pCO rises and hence

there is little change in pH.I!

The donor blood used in these studies

was usually type 0 cells re-suspended in

type AB plasma. The initial hematocrit was,

in consequence, somewhat higher than in

usual ACD blood. The dilutional effect of

adding 10 to 15 mM of isotonic

(

0.3 M)

THAM was considerable. For example, the

addition of 15 mM (50 ml) of THAM

re-sulted in a drop of the hematocrit from 42 to

:33.

For this reason, a 1.2 M solution was

used which resulted in a significantly

smaller fall in packed red cell volume.

Thirty-three milliliters of 0.3 M THAM

pro-vides nearly 30 mOsm of glucose per liter.

IIAddition of sodium bicarbonate to an acid

so-lution increases pCO: HA±NaHCO3-* NaAc

+ftCO3.

PATIENTS-Group A: Respiratory Distress

(Table Ill)

In the infants with respiratory distress

and elevated pCO2, there was a progressive

rise in mean pH at tile end of the

transfu-sion and 2 to 15 hours thereafter. This rise

was primarily due to a decrease in pCO.

In three of the nine infants in whom

sequential measurements were performed,

there was no change in pCO2 between the

beginning and end of the transfusion; in

the remaining six, pCO fell significantly.

The pCO1 did not rise in any of the infants

as might have been expected if blood with

a high pCQ has been infused. Following

exchange transfusion, pCO2 either fell

fur-tiler or essentially stabilized, reflecting the

state of the underlying pulmonary disease.

Emergence of a significant metabolic

alka-iosis, a feature in healthy term infants whlo

received unbuffered blood, was not

ob-served in these infants. An example of the

acid-base changes during and following

transfusion is shown in Figure 1.

The hematocrit fell significantly at the

end of tile exchange transfusion, doubtless

a reflection of the low hematocrit in the

donor blood; by several hours

post-ex-change, the hematocrit had risen to

pre-ex-change levels.

Ten of the 11 infants survived. The one

(5)

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Baby G 2 days wt 730gm RDS with apnea

Bilirubin 1.1/19.5

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FIG. 1. Acid-base values from

6.6 6.7 6.8 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9

pH

730 fll infant before Lfl(l after exchange transfusion using ACD blood buffered \Vitil 15 fll\1 TIIA\I.

tile trallsfusiOn, occurred in an infant who

weighed 980 gm and died of severe infection

2 days after the procedure. There was no

evidence of omphalitis at autopsy.

Group B: Erythroblastosis Fetalis Without

Pulmonary Insufficiency (Table IV)

The characteristic feature in tilese

in-fants with normal ventilation was the

devel-opment of a moderate metabolic aikalosis

following exchange transfusion. Tile mean

values at the end, and 2 to 15 hours

post-transfusion, were 7.439 and 7.454,

respec-tively. The changes were similar to but not

as severe as the post-transfusion alkalosis

seen in term infants receiving unbuffered

i)lOOd. The highest pH was 7.502.

Group C: Respirator Patients (Table V)

As might be expected, there was marked

variation in the acid-base values in the

in-fants who required mechanical ventilatory

assistance. Tile tilree infants with severe

er-ythroblastosis fetalis were markedly

aci-(lotic with

pH

ranging

between <6.8 and

7.260. Each had markedly elevated pCO2.

Acid-base balance tended to improve

foh-lowing excilange transfusion . Nonetheless,

all of these infants died, two of them w’ithin

6 hours following tile prOce(lure.

Those illfallts \Vllo did not ilave

ery-throblastosis fetahis railgedi in age between 3

and 6 days and had received proloilged

chemical as well as ventilator support.

Their pH at the start of transfusion railged

between 7.380 and 7.630, and tile 1)CO2

ranged between 17 and 52 mm Hg.

Acid-base values fluctuated considerably

follow-ing exchange transfusion. The olli\’ feature

common to the group was an increase in

base excess 2 to 15 hours post-exchange.

Only one infant survived; the remaining

deaths occured 2 to 11 days following

ex-change transfusion and appeared to be

un-related to the procedure itself. Of

consider-able interest was the fact that suddell

car-diac arrest occurred on one or more

occa-sions in four infants who were receivmg

ventilatory assistance during the exchange

transfusion. in two infants, blood gases

ob-tained at the time of cardiac arrest showed

no deviation in pH; its genesis remains

(7)

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.4-pH ARTICLES

Group D: Blood Buffered with Sodium

Bicarbonate (Table VI)

Although tile three infants who received

blood to which sodium bicarbonate had

been added had normal or near normal

acid-base values at the start of exchange

transfusion, each developed a metabolic

al-kalosis at the end or by 2 hours following

tile procedure. Moreover, two of the three

infants developed transient hypernatremia

witii serum sodium concentrations of 167

and 171 mEq/l at the end of the transfusion,

presumably in consequence of the sodium

load of the donor blood, which averaged 202

mEq/l. Neither of these infants had clinical

manifestations of hypernatremia and by 10

to 15 hours serum sodium concentration in

each had returned to tile upper limit of

nor-mal.

DISCUSSION

\Vith the exceptioll of a rather sparse

study of acid-base ilomeostasis during

cx-change transfusion published in 1955, tilere

has been remarkably little interest in this

subject ulltil recently.’’ ‘‘ These later

stud-ies deal with the effects of ACD blood

dur-ing and following replacement transfusion

and the data are in general agreement with

those reported here.

Examination of the mean values following

ACD transfusion would suggest that

buffer-ing is not necessary in low risk infants.

How-ever, in one infant, wilo was 10 hlours of age

and vigorous at the start of the exchange

transfusion, a severe metai)Ohic aIld

respira-tory acidosis occurred with a pH of 7.07 at

the end of the procedure

(

Fig. 2) . Although

this infant showed no clinical manifestations

of acidosis an(l had an uneventful recovery,

other illVestigatOrs have observed infants

vith distress associated with pH values

below 7. 10 du ring exchange transfusion .‘‘ 1’

The most devastating report is tilat of

Le-noski and Hodgman, who measured

acid-base balance in 14 apparenti low risk

in-fants and observed cardiac arrest invariai)ly

associated with a pH below 7.07 in four of

these, with death in two. For these reasons,

we believe that, even in low risk infants,

donor blood with a near normal pH should

be used. Although heparinized 1)100(1

pOS-I

FIG. 2. Acid-base values from one infant before, during, and after exchange transfusion using

(9)

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+-ARTICLES

sesses this quality and has a normal

electro-lyte concentration, it has several

disadvan-tages. (1) Protamine sulfate may be

neces-sary post-exchange because of 20

(2 ) Heparin causes the release of free fatty

acids; since these bind with albumin, there

is a theoretical concern that they might

compete with bilirubin for such binding

sites. (3) Heparinized blood is unavailable

in many communities largely because its

storage time is short md it must be drawn

for specific purposes.

The addition of THAM to ACD blood

of-fers no disadvantage apart from reduction

in hematocrit which can be minimized by

adding hypertonic THAM. Although

respi-ratory depression or arrest following large

doses of THAM has been described,2’ there

is no reason to believe that this will occur

when it is added to the donor blood, since

the ventilatory complications of THAM are

believed due to a rapid increase in

cerebro-spinal fluid pH which would not occur

when neutralized blood is given.

Hypo-glycemia, which has been reported following

THAM,22 has not been observed in these

in-fants; (1) because the toxic dose is much

larger, and (

2

) additional glucose is present

both in the THAM solution and the ACD

preservative. Studies have been performed

which indicate that THAM does not

inter-fere with the binding of bilirubin with

albumin.23 Finally, the addition of THAM

to the blood immediately prior to

transfu-sion does not alter the lifespan of the

trans-fused 24

Although

Barrie

has suggested that

so-dium bicarbonate can be added to donor

blood,17

our experience would indicate that

this might be dangerous because of the

re-sultant hypernatremia. The same criticism

can be made of the suggestion of MacRae

and Palavradji,l5 who suggest periodic

infu-sions of sodium bicarbonate during the

ex-change procedure. Furthermore, the

markedly elevated pCO2 of donor blood

buffered with sodium bicarbonate presents

a major threat to the high risk infant with

ventilatory insufficiency because he is

un-able to excrete the added CO2 that is

pro-duced. In this situation, pH will inevitably

fall.f

A metabolic aikalosis was observed

con-sistently 2 hours after the exchange

transfu-sion in the infants who received

non-buff-ered

blood.

This was anticipated and has

been shown to be due to the metabolism of

citrate to 2 Calladine, et al.b6

observed that the alkalosis lasted for

sev-eral days and they believed it to be related

to persistent liypochloremia as well as the

metabolism of citrate. Our studies do not

confirm their observations; hypochioremia

did not occur and the metabolic alkalosis

resolved within 24 hours. Treatment with

ammonium chloride as suggested by

Calla-dine, et al.bn would be unnecessary in our

experience.

In infants who require multiple exchange

transfusions within a short period of time, a

progressive alkalosis may develop. Our data

indicate that the severity of the alkalosis is

no greater when the blood is buffered with

THAM than when it is unbuffered for both

single and multiple exchange transfusions.

Quite unexpected was the

hyperventila-tion 2 hours after the conclusion of the

transfusion with unbuffered ACD blood.

The explanation of this remains obscure; a

delay in buffering of cerebrospinal fluid is

an intriguing possibility. There was no

change in pCO2 in the infants with normal

ventilation (Group B) who received

blood

buffered with THAM.

The overall mortality in the infants who

were transfused with THAM-buffered

blood was high; 8 of 23 (or nearly 35%)

died, although only two infants (9%) died

within 6 hours after the transfusion-the

ar-bitrary period in which death is considered

“due” to the 25 It should be

em-phasized that all but one of the deaths

oc-curred in infants who required ventilatory

assistance. Others have reported a high

If

This hazard is linlited to infants with alveolar

hypoventiiation. A high pCO2 results, m fact, in

rather small amounts of dissolved CO2. For

ex-ample, a pCO2 of 150 mm Hg yields 4.5 ml C02/

(11)

z

F-z

S

z

.5 S

z

C:

z

S

C: S

S

F-S

S

.5

.-S

.-‘--

-L_i_:,1i

z

______

T?

#{149}-C.)

-5 5..

:2:- a’

:‘

JS

mortality in small infants “on respirators.”26

The low mortality in the 11 infants vith

re-spiratory distress not requiring respiratory

aid ( Group A ) is considerably better than

one would expect from the u25 27-29

From the experience reported here,

blood with a near normal pH should be

used in all infants undergoing exchange

transfusion. THAM appears to be superior

_________ to sodium bicarbonate as a buffer of ACD

blood. Other factors which can lead to

seri-ous complications of exchange transfusion

should be controlled. These include

mainte-iiance of a neutral thermal environment

during the procedure as well as the

ex-change of small increments of blood to

mm-_____________ imize the effects on the cardiovascular

sys-tem. ‘#{176}Furthermore, in infants with severe

erythroblastosis fetalis, hypoglycemia prior

__________ to or, more often, following exchange

trans-fusion may occur and must be

appropri-ately treated.31 \Vith precise control of

these variables, we believe that tile

mortal-ity and morbidity of exchange transfusion

can be greatly reduced.

_____

SUMMARY

Exchange transfusions have been

per-formed using buffered and non-buffered

ACD blood. In low risk infants receiving

_________

unbuffered blood, severe acidosis may

occa-sionally occur during the transfusion. In

in-_________

fants with cardiorespiratory insufficiency in

whom the mortality of exchange transfusion

is increased, the use of buffered ACD blood

would appear to lessen the risks. Acidemia

during exchange was not observed in any of

____________ the 26 high risk infants who were exchanged

with buffered blood. We believe that, when

____________ ACD blood is used, 10 mM of 1.0-1.2 M

THAM should be added to each unit prior

_____________ to exchange transfusion in all infants.

REFERENCES

1. Schweizer, 0., and Howland, W. S.: The effect of citrated bank blood on acid-base balance. Surg. Gynec. Obstet., 114:90, 1962. 2. Libvin, M. S., Smith, L. L., and Moore, F. D.:

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3. Unker, S. P., Stetson, J. B., Coe, R. C., Grillo, H. C., and Murphy, A. S.: Citric acid intoxi-cation. J.A.M.A., 157:1361, 1955.

4. Barr, N., Tunnell, R., and Oliver, T. K., Jr.: Unpublished data.

5. Oliver, T. K., Jr. : The use of THAM-buffered ACD blood in high risk infants who require exchange transfusion. J. Pediat., 67:951, 1965.

6. Pierson, \V. E., Oliver, T. K., Jr., Hartmann, J.

R., and Stamm, S. J.: Biochemical changes (luring exchange transfusion of low risk ba-bies. Proceedings of the Thirteenth Annual Meeting, Western Society for Pediatric

Re-search, Portland, Oregon, November 1965.

7. Lubchenco, L. 0., Hansman, C., Dressier, M., and Boyd, E. : Ina-uterine growth as esti-mated from liveborn birthweight data at 24 to 42 weeks of gestation. PEDIATRICS, 32:793, 1963.

8. Candy, C., Grann, L., Cunningham, N., Adam-sons, K., Jr., and James, L. S. : The validity of pH and pCO2 measurements in capillary samples in sick and healthy newborn infants.

PEDIATRICS, 34 :192, 1964.

9. Rodawav, K. A., and Oliver, T. K., Jr. : Incu-bator accessory for exchange transfusion. Lancet, 1:1220, 1965.

10. Siggaard-Andersen, 0. : The pH, log pCO2 blood acid-base nomogram revised. Scand. J.

Clin. Lab. Invest., 14:598, 1962.

1 1. Siggaard-Anderson, 0. : Blood acid-base align-ment nomogram. Scan. J. Clin. Lab. Invest., 15:211, 1963.

12. Meites, S., and Falkner, \V. R. : Manual of

Practical Micro and General Procedures in Clinical Chemistry. Springfield, Illinois: Charles C Thomas, 1962.

13. Graham, B. D., and Heyn, R. M. : Acid-base homeostasis during exchange transfusion of newborn infants with preserved blood.

PEDI-ATRICS, 15:241, 1955.

14. Povey, M. J. C. : pH changes during exchange transfusion. Lancet, 2:339, 1964.

15. Lenoski, E. F., and Hodgman, J. D. : Acid-base homeostasis during exchange transfusion. Proceedings of the Twelfth Annual Meeting, \Vestern Society for Pediatric Research, Salt Lake City, Utah, November 1964.

16. Cailadine, M., Gairdner, D., Naidoo, B. T.,

and Orrell, D. H. : Acid-base changes fol-lowing exchange transfusion with citrated blood. Arch. Dis. Child., 40:626, 1965. 17. Barrie, H. : Acid-base control during exchange

transfusion. Lancet, 2:712, 1965.

18. MacRae, D. J., and Palavradji, D. : Acid-base

balance in exchange transfusion. J. Obstet.

Gvnaec. Brit. Comm., 72:384, 1965. 19. Boda, D., Toth, C., Muranve, L., and Eck. E.:

Acid-base and electrolyte changes during cx-change transfusion. Act:i Paediat., 56:217, 1966.

20. Bentley, T. H. P., Jr., Ziegler, N. R., and Krivit, W. : The use of heparinized blood for exchange transfusion in infants. J. Dis.

Child., 99:24, 1960.

21. Nahas, G. (;., Fink, B. R., Ploski, W. S., and Tencick, R. E. : The depressant effects of Tris( hydroxymethyl)aminomethane and of mannitol on respiration. Ann. N. Y. Acad. Sci., 109:783, 1963.

22. Bennett, T., and Tarail, R. : The hypoglycemic

activity of 2-amino-2-hydroxymethyl-1,

3-propanediol. Ann. N.Y. Acad. Sci., 92:651, 1961.

23. Goldberg, A. R., Schwartz, I., and Verosky, M.: Equilibrium dialysis of

Tris(hy-droxymethyl)aminomethane (THAM

)

in

serum and albumin. Fed. Proc., 21 : 173, 1962.

24. Nahas, C. (;., Manger, W. M., Mittelman, A.,

and Ultmann, J. E. : The use of 2-amino-2hydroxymethyi-1, 3-propanediol in the correction of addition acidosis and its ef-feet on sympathoadrenal activity. Ann. N. Y. Acad. Sci., 92:596, 1961.

25. Boggs, E. 11., Jr., and Westphal, M. C., Jr.: Mortality of exchange transfusion. PEDIAT-RIC5, 26:745, 1960.

26. Thomas, D. V., Fletcher, C., Sunshine, P.,

Schafer, 1. A., and Klaus, M. A.: Prolonged

respirator use in pulmonary insufficiency of

newborns, J.A.M.A., 193:183, 1965.

27. Jablonski, WI. J.: Risks associated with

cx-change transfusion. New Eng. J. Med.,

266:155, 1962.

28. Dique, J. C. A., Stable, W. C., and Wrench,

D. L. : Exchange transfusion in very small infants. Med. J. Aust., 2:344, 1962.

29. Taylor, W. C. : Mortality and morbidity of cx-change transfusion. Canad. Med. Ass., J.,

87:1267, 1962.

30. Phibbs, R. H., Johnson, P., and Tooley, W. H.: Circulatory changes in newborns with cry-throblastosis fetalis with and without hy-drops. Pediat. Res., 1:321, 1967.

31. Barrett, C. T., and Oliver, T. K., Jr.: Hvpo-glycemic and hyperinsulinism in infants with erythroblastosis fetalis. New Eng. J. Med., ill press.

Acknowledgment

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APPENDIX

THAM is prepared in the following manner

for use in buffering ACD blood. There is no

pediatric preparation available commercially;

therefore, it is necessary to add 250 ml 10%

dextrose in water solution to a bottle

contain-ing 36 gm of THAM powder. The resulting

so-lution is 1.2 Molar. Eight milliliters of the

THAM solution (equalling 9.6 mM) are added

to each unit of blood. Sterile techniques should

be used. A freshly made solution of THAM

should be used on each occasion.

AN EIGHTEENTH CENTURY FATHER ASKS HIS SON TO GET HIS HAIR CUT

The current antipathy of many boys toward

barbers is a common cause of friction between

fathers and sons. It may comfort today’s

fa-filers to learn that other fathers in other times

veie similarly bothered, as is evident in the

let-ter below written almost 200 years ago by

Flenry Fox to his son at Eton.

One thing you know I much wanted to see your

hair cut to a reasonable and gentlemanlike short-ness. You an(1 5OfllC Eton boys wear it as no other

people in the world do. It is effeminate, it is ugly

and it must be inconvenient. You gave me hopes

that if I desired it, you would cut it. I will, dear Ste

(

Steven

),

be much obliged if you will.’

Once again, plus #{231}achange, plus c’est Ia

m#{234}mechose!

NOTED BY T.E.C., JR., M.D.

REFERENCE

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1968;41;802

Pediatrics

W. E. Pierson, Cynthia T. Barrett and T. K. Oliver, Jr.

TRANSFUSION

ELECTROLYTE AND ACID-BASE HOMEOSTASIS DURING EXCHANGE

THE EFFECT OF BUFFERED AND NON-BUFFERED ACD BLOOD ON

Services

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