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Champs Elysées

triumphal arch
Fluid and Electrolyte
Management

Department of Gastrointestinal Surgery


Dr. Wang Ailiang
Body water and its distribution



• extracellular( Na+ ) plasma
water
• 25% (5%B.W.)
• Total ( 20% body weight ) (ICF)
• body interstitial fluid
• water 75% (15%B.W.)
• intracellular (K+)
• (40% body weight) (ECF)

Total body water (as percentage of body
weight) in relation to age and sex

Age Male Female


10-18 59 57

18-40 61 51

40-60 55 47

Over 60 52 46
Electrolyte composition of human
body fluids
Positive ion
Negative ion (mmol/L)
(mmol/L)
ECF
Na+ Ca2+<>/sup Cl- HCO3-

(plasma) 140 5 104 24

K+ Mg2+ HPO42- protein


ICF

150 26 100 65
Starling relationshilps

• Plasma proteins (album) account for the


high colloid osmotic pressure of plasma

• It’s an important determinant of


distribution of fluid between vascular
and interstitial compartments
water electrolyte

electrolyte
water
Protein account for the
Capillary wall high colloid osmotic
pressure
Exchange of water and electrolyte
between plasma and interstitial fluid
epicyte
ECF ICF

Ion channel

Enzym (pump)
Mechanism of kidneys to maintain constant
volume and composition of body fluids

• Filtration and reabsorption of sodium:


adjusts urinary sodium excretion to
match changes in dietary intake

• Regulation of water excretion in


response to changes in secretion of
antidiuretic hormone
Blood volume Blood volume

Blood pressure

plasma osmotic thirst plasma osmotic


pressure pressure

Reabsorption Reabsorption
of water ADH↑ ADH↓ of water

urine urine

Regulating and effect of ADH


(antidiuretic hormone)
Osmolality (290mosm/kg H O) 2

• Solutes dissolved in body fluid


contribute to total osmolality in
proportion to their molar concentration

• ECF→ sodium and its salts

• ICF→ salts of potassium


cell cell

Movement of water

electrolyte

ECF ICF

ECF ICF

Balance of osmotic pressure between both sides of epicyte


Control of Osmolality
• Regulation of water intake (thirst) and
excretion (urine volume, insensible loss, and
stool water) ← kidney (regulator)
• water intake↓→ kidney→ urine volume↓ urine
solute concentration↑ (fourfold above plasma
1200-1400mosm/kg H O)2

• water intake↑→ kidney→ urine volume↑ urine


solute concentration↓ (dilute urine 50mosm/kg
H O)
2
Equation
• Osmolality = (Na e++ A-)+(K e++ A- )
TBW
• PNa = (Na e++K e+ )
• TBW
• Na e
+
: exchangeable sodium
• K e : exchangeable potassium
+

• TBW: total body weight


• PNa : plasma sodium concentration
Typical daily solute balances in normal subjects
intake Excretion
concentration Total concentration Total amount
amount
water
Urinary
excretion
ingested 2L water 1.5L

0.4L 400mosm/kgH2O
cell Total solute 600mosm
metabolism
sodium 60meq/L 90meq
Total solute 600mosm
potassium 36meq/L 54meq
sodium 100meq Insensible 10ml/kg/24h
(stools >
Loss (water) 200ml/d)
potassium 60meq ☆

☆ External (insensible )water loss: lungs, skin, stool


Volume disorders
Volume depletion

Volume overload
Recognition and treatment of volume depletion
…… Low BP

Dry mucous membranes Clinical tachycardia


manifestation

Narrow pulse pressure Poor skin turgor


History taking for volume depletion

records Of the history

Analysis
Intake Changes Urine Of
and In Specific The
output Body gravity Chemical
weight Composition
Of
urine
History taking for volume depletion
Intake
and
Changes output
In body
weight

Treatment plan
Urine devised aiming to
Specific Analysis correct volume deficit
gravity Of the chemical and associated
Composition of aberrations in
urine electrolyte
concentrations
Volume depletion

• Simplest form: pure water deficit (water


deficit without accompanying solute
deficit)
• Surgical patients: water and solute
deficit occur together (more often)
Pure water deficit
(unable to regulate intake)

• Debilitated or comatose or increased


water loss from fever
• Tube feedings without adequate water
supplementation
• Diabetes insipidus
• Reflected by hypernatremia
Pure water deficit
(associated findings)

• Plasma osmolality ↑
• Concentrated urine
• Low urine sodium (severe depletion)
Pure water deficit
(clinical manifestation)

• Depress central nervous system:


lethargy, coma
• Muscle rigidity
• Tremors
• Spasticity
• seizures
Pure water deficit
(Treatment)

• Enough water to restore the plasma sodium


( PNa) concentration to normal
• △Na = ( 140-PNa) ×TBW
• △Na: the total milliequivalents of sodium in
excess of water
• Required water: △Na/140
• Ongoing obligatory water losses must be
satisfied: due to diabetes insipidus, fever etc.
Volume and electrolyte depletion
causes

Gastrointestinal Other:
losses: Excessive diuretic therapy
nasogastric suction Adrenal insufficiency
Enteric fistulas Profuse sweating
Enterostomies Burns
diarrhea Body fluid sequestration
(trauma or surgery)
Volume and electrolyte depletion
(diagnosis)
history

Physical
signs

Records
diagnosis
Of intake
Clinical
And output
findings
Volume and electrolyte depletion
(clinical findings)
• Urine Na+ concentration<10meq/L: aldosterone→
renal tubule→ renal sodium conservation
• Hypertonic urine: >450-500mosm/kg
• Prerenal azotemia: BUN (blood urea nitrogen) ↑ ↑;
serum Cr (creatinine)↑; BUN/ Cr go as high as 20-
25:1; disproportionate rise (normal ratio:10:1)
• Acute tubular necrosis: BUN↑ Cr↑; ratio close to
normal
Combined water-electrolyte deficits
Replacement
therapy

Calculate the Estimate


serum deficit volume deficit
from clinical
signs and
changes in
body weight
Volume overload
ADH [ antidiuretic
Hormone] ← anesthesia
And surgical press

Circulatory
overload
Excessive fluid
Intake [immediate
Postoperative period]
Renal vasoconstriction
And increased
aldosterone
Volume overload
[clinical manifestation]
Gallop rhythm Edema [ sacrum, extremities]
[cardiac failure]

Pulmonary artery clinical Jugular venous distension


And central venous
pressure↑
manifestation

Increased body weight Tachypnea [pulmonary edema]


Volume overload
[management]

mild hyponatremia severe

Sodium restriction Water restriction diuretics


Specific electrolyte disorders

sodium
potassium

phosphorus

calcium
magnesium
Specific electrolyte disorders
(Sodium )
• Hypernatremia: chiefly loss of water
• Hyponatremia: in patients with
hyperlipidemia or hyperproteinemia or
hyperglycemia
• Acute, severe hyponatremia: occasionally
develops in patients undergoing elective
surgery. [excessive intravenous sodium-
free fluid administration]
Specific electrolyte disorders
(Sodium )
• Most cases: treated by administering the
calculated sodium needs in isotonic solutions
• Use hypertonic sodium solutions: Severe
hyponatremia (PNa <120meq/L) produces
mental obtundation and seizures
• Rapid correction→ permanent brain damage
(osmotic demyelination syndrome)
• The increasing speed of serum Na+ not to
exceed 10-12meq/L/h
Specific electrolyte disorders
(potassium )

anabolism
Food K+ Intracellular K+

Small intestine Serum K+


catabolism
Stool, sweat
urine
Normal potassium metabolism
Serum potassium concentration [k+]
[k+]

pH of ECF Size of the


intracellular k+
pool
Function of potassium
body cell plasma body cell plasma

acidosis hyperkalemia hypokalemia alkalosis


Serum and digestive juice
electrolyte ( mmol/L )
Na+ K+ Cl- HCO3-
serum 140 3.5-5.5 104 23-28
saliva 10-40 26 10-30 <10
Gastric
juice
20 10-20 150 0
Pancreatic
juice
140 5 40 110
gall 140 5 100 40
Intestinal
140 5-15 60-110 30-80
juice
Potassium excretion of kidney
Renal artery

Capillary vessel of
glomerulus

Renal corpuscle

proximal convoluted tubule

Renal vein

distal convoluted tubule


Disturbance of potassium metabolism
Disturbance of
potassium metabolism

Hypokalemia:
Hyperkalemia: Diuretics
Renal failure Adrenal steroid excess
Adrenal Renal tubular disorders
insufficiency (potassium wasting)
Deficient dietary potassium
intake
Alcoholic patients
Total parenteral nutrition with
inadequate potassium
replacement
hyperkalemia
• Serum potassium concentration >5.5mol/L
• Treatable problem
• Fatal if undiagnosed
• Blood potassium levels must be closely
monitored in susceptible patients
Hyperkalemia (clinical evidence)
• susceptible patients: severe trauma,
burns, crush injuries, renal insufficiency,
marked catabolism (other causes)
• Nausea and vomiting
• Colicky abdominal pain
• Diarrhea
• ECG changes (electrocardiographic)
ECG changes of Hyperkalemia
(electrocardiographic)
ECG changes

Early changes Further elevation


peaking of T waves QRS like sine wave
Widening of QRS complex (portends imminent
Depression of ST segment cardiac standstill
ECG changes of Hyperkalemia
(electrocardiographic)
ECG changes of Hyperkalemia
(electrocardiographic)
Assessment of hyperkalemia
1 2 3
Assess acidbase Determine the
⑴A true metabolic status rapidity to correct
abnormality?
the elevated
⑵ Elevated by serum potassium
hemolysis, marked
leukocytosis,
thrombocytosis
(platelet >1million/L)
Emergency treatment of hyperkalemia
(five approaches)
1 Infusion: 50% GS +20u insulin (K+ ECF→ICF

2 Intravenous NaHCO3
solution
3 Calcium antagonize the tissue effects of K+

4 Cation exchange resin (orally or enema)

5 Sorbitol to induce
osmotic diarrhea
Hemodialysis for renal failure
Hypokalemia
• Serum potassium concentration <3.5mol/L
• Causes:
renal wasting of potassium,
potassium deficiency,
inadequate dietary intake,
alcoholics,
elderly people with restricted diets
Clinical manifestation
(neuromuscular function related)

• Decreased muscle contractility


• Decreased muscle cell potential
develop
• Paralysis of the muscles of respiration
(can cause death)
Assess of hypokalemia
• Initial goal: identify the cause
• alkalosis→ hypolemia
• Renal losses → hypolemia (no acid-base
imbalance, or persists after alkalosis corrected)
• Renal potassium wasting (urine potassium excretion
>30meq/24h, and serum K+<3.5meq/l ):diuretic
therapy, alkalosis, increased aldosterone activity
• Total body deficit (urine potassium excretion
<30meq/24h)
Treatment of hypokalemia
• Correct the cause
• Given orally (patient can eat), otherwise
Intravenously
• Concentration in solution<40meq/L
• Moderate to severe (K+<3meq/L): administering
rate: 20-30meq/L
• Mild (K+3-3.5meq/L): slowly to avoid hyperkalemia
• Use chloride salt of potassium often
• Refractary to replacement→ coexistent magnesium
deficiency?
calcium
• Mediator of neuromuscular function and
cellular enzyme processes
• Dietary intake (1-3g/d), unabsorbed in feces
• Normal serum concentration: 4.2-5.2meq/L
• Maintained by: humoral factors, mainly
vitamin D, parathyroid hormone, calcitonin
【 acid-base balance 】
bloo d buf fe r s ys tem
bu ffe ri ng ac id bu ffe ri ng ba se
H 2 CO 3 HC O 3 - + H +
H 2 PO 4 - HP O 4 - + H +
HH b H b- + H+
HH bO 2 H bO 2 - + H +
HP r P r- + H+
HCO 3 - H CO 3 - 24 24
20
= = =
=
H 2 CO 3 pH 7O 2 .35-0 .0 3× 40
0. 03 ×PC 1. 2
1 7.45
【 maintaining of acid-base balance 】
pul mon ary e xp ira tio n

pH H 2 CO 3 r esp ir at ory ce nt re ex cit ed


ex agg er ate d and f ast ex pi ra tio n g ive of f CO 2
( pH H 2 CO 3 r ev er se cha ng es )

ren al re gul at io n : th e m os t of all i n aci d-b as e


ba lan ce , ge t r id of f ixe d a ci d and ex ce ss ive
ba se 。 ( se e ne xt pic tu re )
Renal tubule Blood vessel

Bicarbonate radical

exchange reabsorption

glutaminase

ketoglutarate

Acidification of urine Excretion of ammonia

renal regulation for acid-base balance


Acid-base imbalance

met abo lic a ci dos is de cre ase i ncr eas e


me tab oli c

al kal osi s
• ( HC O 3 - )
( H 2 CO 3 )

re sp ir ato ry inc rea se de cr ea se
re spi rat or y
Ac ido si s
al kal osi s
metabolic
path ogen acidosis ( HC O 3
-
)

1 lo ss of a lka li ne ma tte r ↑

2 ac id oid c ome s int o bei ng ↑


3 re na l i ns uff ic ien cy
dy sf un cti on of s ecr eti on o f H + ( ac id os is
of di st al co nvo lu ted t ubu le )
dy sf un cti on of a bso rpt io n of HC O 3 –
( acid os is of pr ox ima l con vo lut ed
tu bul e )
Path ophy siolo gy
① pu lm on ary ex pi ra tio n :
HCO 3 - H 2 CO 3 rel ev ant d efus ed C O 2 、 PCO 2
sti mu late res pi rato ry c en tre 、
ex agg er at ed and f as t expi ra tio n CO 2 PC O 2
HC O 3 - /H 2 CO 3 cl os e to 20/ 1
pH no rm al
co mp ens at ed me tab ol ic ac ido si s
② re nal r egu la tio n :
re na l tub ule g en era te H + an d N H 3 H+
ex cha ng e wit h N a + a nd H + c om bi ned wi th NH 3 t o b e
clinical manifestation
1 ne rve s yst em :
ti red , gid dy , somnolence, h yp oe sth esi a, d ott ine ss
ev en com a, t en don re fl ex wea ke n or dis ap pe ar
2 re spi ra tor y sys te m :
de ep an d f as t b re ath , wi th ke to ne 。
3 ca rdi ov asc ul ar sy ste m :
ru beo si s o f fac e, in cr eas e of he art r ate , low B P
4 ot her :
ac com pa nie d wit h sym pt oms o f s ev ere w ate r
sc arc ity , de cre as e of myo ca rd ial co nt ra cti on
fo rce an d se nsi tiv it y of per ip he ral bl oo d ves sel s
to ca tec ho la min e , ea sy t o h ave a rr yth mia , ac ute
re nal fa il ur e a nd sh oc k. Aci di c uri ne
Dig nosti c pro grame
1 H ist or y + c las si cal c lin ic al
ma ni fes ta tio n
2 B loo d gas a nal ys is
part ly co mp ens at ed : pH , H CO 3 - , PCO 2
de cr eas e ( t o som e ext en t )
unco mp ens at ed : pH H CO 3 - de cre as e
ob vi ous ly , PCO 2 no rm al
• CO 2- CP me asu ra tio n : ob vio us sy mp tom s
<3 0% vol um e ( unc on dit io nal blood gas
analysis )
4 Measuration of bl ood N a + 、 K + 、 Cl - helpful
for diagnosis
trea tmen t
1 mil d : HCO 3 - > 16- 18 mm ol/ L
el imi na te et iol og ic fa cto r, pu lm ona ry
an d r ena l re gul ati on , aci dos is c an be
co rre cte d af ter co rr ec tio n o f
de hyd rat io n wit hou t su ppl eme nt o f b ase 。
2 sev er e : HC O 3 - <1 0m mol /L
HC O 3 - ( mm ol ) = H CO 3 - no rma l( mm ol/ L)-
HC O 3 - mea su red ( mmo l/ L )
×b od y w ei ght ( kg ) ×
* 0. 4
trea tment
* 2- 4h g ive h alf , the n giv e mor e
afte r ca reful ly con side ring the
actu ral situa tion

•To suppl ement pota ssium when


corr ecti ng ac idosis

* ion izat ion o f Ca ++


incr eases in
acid osis , it decr ease s aft er
++
Mela boli c Alk alosis ( HCO 3 - )
pat hogen
1 exc es s los s a ci di ty gas tr ic ju ice :
lo ss of H + 、 Na + Cl - and E CF , HCO 3 -
re abs orp ti on in cre as e ; in re nal t ubu le ,
K+ ex cha ng e wit h N a+ , H+ exc ha ng e w ith
Na + , H+ K+ ex ce ssi ve lo ss , al kal os is an d
hy pok ale mi a.
2 exc es si ve ing es ti on of ba se :
ta ke Na HC O 3 for lo ng ti me to tr ea t
di ges tiv e ul cer
pathogen

3 po ta ssi um de pl eti on :
exc han ge of K + an d N a + ,H + be twe en
in tr ac ell ula r an d e xtr ac el lul ar, intracellular
acidosis, extracellular alkalosis
cel ls of di st al con vo lu ted tu bu le se cre t
ex ce ss ive H+ , HC O3- re ab so rpt ion i nc rea ses ,
ab no rm al aci di ty ur ine ;
4 pe re ira :
fo r exa mp le: n ico ro l ( 速尿 )a nd ur gen t ( 利尿
酸 )e xc re te mor e Cl - tha n Na + i n uri ne , Na + a nd
Pathophysiology
1 pulmonary expiration :
sh al low a nd sl ow br eat h CO 2 expiration
PC O 2 HCO 3 - /H 2 CO 3 close to 20/1 pH normal

2 renal regulation
renal tubule generate H+ and NH3 ; NaHC O 3 reabsorbed
HC O3 - exclude in urine
clinical manifestation
in ge nera l ,n o symp to ms
re sp ir ato ry sy st em : slo w and s hal lo w
br eat h ;
ne rv e sys tem : ph re niti s ( 谵妄 ), in san it y
( 精神错乱 ),h yp erso mi a ( 嗜睡 ) et c.
sp iri tu al ab nor ma l , ev en co ma ;

dia gnosi s b lo od ga s a na lys is ca n mak e


su re di agn os is an d o rd er of se ve rit y
par tl y co mp en sa ted : blo od pH , HCO 3 - ,
PC O 2 ↑
un co mp ens ate d : bl ood pH , H CO3 - in cr ease
treatme nt
1 el imi na te et iol og ic fa cto r :

lo ss of g ast ric j ui ce →iso to nic s alt


so lut io n , co rre ct hy po chl ore mi c
al kal os is , s upp le me nt of K + to co rre ct
hy pok al em ia 。
• Se ver e al kal osi s :
bloo d HCO 3 - 40 -5 0m mol /L, pH >7 .65 ,
Eq ua tio n for s upp le men t of hy dro ch lor ic
ac id:
① su ppl em ent o f h yd roc hl ori c aci d
(m mol )= H CO 3 - mea su red (m mo l/ L)— HC O 3 -
ho pe to r eac h (mm ol /L) ×b od y w ei ght
treatment

② supplement of hydrochloric acid = C l - no rma l


(m mo l/L ) - Cl - me asu re d (mm ol/ L) × vo lu me
of t ota l bod y flu id ( 60% of bo dy
we ig ht ) ×0.2

* Fi rst 2 4h , g ive h al f , not s iut ab le to


be f ast t o c or rec t alk al osi s , if lo ts of
Cl - are me asu re d i n uri ne , i t mea ns
su pp lem en t o f Cl - e no ug h
Respiratory Acidosis
pathogen
vent ilati on of alve olus decrea se,
un abl e to co mpl et ely e xcl ud e C O 2 gen er ated i n
bo dy , bloo d PC O 2 incr ea ses t o c au se hy per ca pni a

① in su ffi ci enc y pul mo nar y vne ti lat io n :


gen er al a ne st he sia is t oo dee p ,e xc ess
nar co tic( 镇静剂 ), ca rd ia c a rre st ,
pn eu mot ho rax , tra ch eos pa sm, m ise mp loy
of l ife -s upp or t m ac hin e etc .
② pu lm ona ry di se ase s , in su ff ici enc y pu lmo nar y
Pathophysiology

1 bl ood e ffe ct ive t o b uf fer :

PCO 2 H 2 CO 3 bl oo d H 2 CO 3 co bi ned w ith


Na 2P O 4 to be N aHP O 3 and Na H2P O 4 , the l att er is
ex cr ete d in ur ine , H 2 CO 3 HC O 3 -

2 re nal r egu la tio n :

Re na l t ub ula r epi th eli al ce ll s g en era te H +


an d NH + 3

H + ,N a + e xch ang e an d H + co mb in ed wit h


NH + 3 to b e NH + 4 H + excreted and Na HC O 3
re ab sor pt ion , HC O 3 - / H 2 CO 3 cl ose t o 2 0/ 1
ag ai n , pH no rma l ra nge 。
clinica l ma nifes tation
dys pn ea, hy po ve ntil at io n, mal ai se ;
ta ch ypn ea ( 气促 ), cy ano si s ( 紫绀 ),
he ad ach e, ch es t d is tre ss ; BP lo w
do wn (s ev ere ), ph re nit is ( 谵妄 ),
co ma ;
diagnos is
his to ry, cl in ic al m an if es tati on ,
bl oo d g as an al ysi s
ac ut e : bloo d pH de cre as e o bv iou sl y,
PC O 2 r ise u p, pl asm a HC O 3 - no rma l
ch ro nic : bl ood p H d ec rea se no t
ob vi ous ly , P CO 2 ri se 、 plas ma HC O 3 -
in cr eas e
treatme nt
radi ca l m et hod : ra pid ly re li eve
ob str uc ti on of re sp ira tor y
tr act , im pro ve p ulm ona ry v ent ila ti on ,
di sch ar ge th e a cc um ula te CO 2 out fr om
bo dy
1 re lie ve ob st ruc ti on of re sp ira to ry
tr act :
for e xam pl e: tr ach ea ca nn ula , lif e-
su ppo rt m ach ine 、 tr ac heo to my an d s o on
2 ate le ct asi s ( 肺不张 ) :
enc ou rag e dee p ins pi rat io n, in fla te
tre atmen t
3 re spi ra tor y dep re ssi on : re sc ue br eat hi ng ( 人
工呼 吸 ), st im ula ns of r esp ir ato ry ce nt re

4 se ver e res pi rat or y a ci dos is : giv e lit tl e


NaHCO3

5 ox yge n sup pl y :

respiratory acidosis , the m ost i mpo rt ant i s t o


im pr ove v ent il ati on , n ot to m ere ly su pp ly
ox yg en of hi gh co nc ent ra tio n, ot he rwi se , i t can
ma ke re fl ex of se ns or of re sp ira to ry ce ntr e to
Resp irat ory a lkalos is

excessive ventilation of alveolus ( 肺泡 ) , CO2


generated in body exsufflate too much , blood
PaCO2 decrease , lead to hypocapnia , blood PH
increase
Clinical manifestation :
tachypnea , giddy ( 眩晕 ) , numb of
hands, feet, and mouth
Respiratory alkalosis

di agn os is :
history + clinical manifestation , blood
gas analysis show: PH↑ , PaCO2 and

HCO3- ↓hypocapnia , blood PH ↑ 。

tr eat me nt :
Use paper bag to cover nose and mouth
If necessary, block autonomous
respiration , life-support machine
control principle of water-electrolyte
metabolism and acid-base disorder
To pr eve nt
2 El eme nta ry d ail y r eq ui rem ent :
wa te r 200 0-2 50 0m l G S10 0- 15 0g NaC l4 -5 g
KC l3- 4g
2 fe ve r : T in cre as e 1 ℃ , lo ss of
hy pot oni c so lut ion t hr oug h s ki n :3-
5m l/k g
sw ea ti ng : mo de ra te swe at in g: los s 50 0-
10 00m l(N aC l3 -4g )
grea t amo un t : l oss 1 000 -1 500 ml
tr ac he oto my : exh ale ev ap or ati ve wa te r
• treatment
• 1 、 estimate the situation of fluid and
electrolyte disorder specifically
• ① is there fluid and electrolyte
disorders ?
• ② is there water deficit ?
• ③ hypertonic dehydration or
hypotonic dehydration ?
• ④ is there acid-base imbalance ?
• ⑤ is there K+ 、 Ca++ deficit ?
• estimate amount and category of
fluid infusion specifically:
• ① supplement of intraday requirement
• ② supplement of extra loss of the other day
• (胃 肠道 等额外 丧失 、内在 性失 液、显 性
出汗 等)
• gastric juice : 2:1 ( 5%GS : 5%GNS )
• intestinal fluid :
7:2:1 ( 5%GNS:5%GS:1.25NaHCO3 )
• with gall and pancreatic fluid : 2:1 (
5%GNS:1.25NaHCO3 )
• pancreatic fluid : 1:1(
5%GNS:1.25NaHCO3 )
• * lose 1000mlgastrointestinal fluid , give KCl
1-2g

③ suppl emen t of t he pa st l oss :
giv e hal f i nt ra day , giv e the ot he r the
se con d, th ir d d ay ca re ful ly co ns ide ri ng he
ac tur al si tu ati on

Nor mal stand ard of flu id an d


elec troly te
uri ne amo un t 40- 50 ml /h
sp ec ifi c gra vi ty 1. 010 -1 .02 0
to ta l c hl ori de >4g /2 4h