Fluid And Electrolyte Management Surgery

Champs Elysées

triumphal arch

Fluid and Electrolyte Management

Department of Gastrointestinal Surgery Dr. Wang Ailiang

Body water and its distribution • • •

water

extracellular( Na+ ）

plasma

• 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 10-18

Male 59

Female 57

18-40

61

51

40-60

55

47

Over 60

52

46

Electrolyte composition of human body fluids Positive ion (mmol/L) ECF (plasma)

ICF

Negative ion (mmol/L)

Na+

Ca2+<>/sup

Cl-

HCO3-

140

5

104

24

K+

Mg2+

HPO42-

protein

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 pressure Reabsorption of water

urine

thirst

ADH↑

plasma osmotic pressure

ADH↓

Reabsorption of water

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) • water intake↑→ kidney→ urine volume↑ urine solute concentration↓ (dilute urine 50mosm/kg H O) 2

2

Equation • Osmolality ＝ (Na e++ A-)+(K e++ A- ) TBW • PNa

＝ (Na e++K e+ )

•

TBW

• Na • K

e

e +

+

: exchangeable sodium

: exchangeable potassium

• TBW: total body weight • PNa : plasma sodium concentration

Typical daily solute balances in normal subjects Excretion

intake concentration

Total amount

water

concentration

Total amount

Urinary excretion

ingested cell metabolism

2L 0.4L

Total solute

600mosm

sodium

100meq

potassium

60meq

water

1.5L

Total solute

400mosm/kgH2O

600mosm

sodium

60meq/L

90meq

potassium

36meq/L

54meq

Insensible Loss (water) ☆

10ml/kg/24h (stools ＞ 200ml/d)

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

Volume disorders Volume depletion

Volume overload

Recognition and treatment of volume depletion ……

Dry mucous membranes

Narrow pulse pressure

Low BP

Clinical manifestation

tachycardia

Poor skin turgor

History taking for volume depletion records

Intake and output

Of

Changes In Body weight

the

Urine Specific gravity

history

Analysis Of The Chemical Composition Of urine

History taking for volume depletion Intake and Changes In body weight

output

Treatment plan Urine Specific gravity

Analysis Of the chemical Composition of urine

devised aiming to correct volume deficit and associated aberrations in 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 losses: nasogastric suction Enteric fistulas Enterostomies diarrhea

Other: Excessive diuretic therapy Adrenal insufficiency Profuse sweating Burns Body fluid sequestration (trauma or surgery)

Volume and electrolyte depletion (diagnosis) history

Physical signs

Records Of intake And output

diagnosis Clinical 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 2025:1; disproportionate rise (normal ratio:10:1) • Acute tubular necrosis: BUN↑ Cr↑; ratio close to normal

Combined water-electrolyte deficits Replacement therapy

Calculate the serum deficit

Estimate volume deficit from clinical signs and changes in body weight

Volume overload

Excessive fluid Intake [immediate Postoperative period]

ADH [ antidiuretic Hormone] ← anesthesia And surgical press

Circulatory overload

Renal vasoconstriction And increased aldosterone

Volume overload [clinical manifestation] Gallop rhythm [cardiac failure]

Pulmonary artery And central venous pressure↑

Increased body weight

Edema [ sacrum, extremities]

clinical manifestation

Jugular venous distension

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 sodiumfree 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

urine

Stool, sweat Normal potassium metabolism

Serum potassium concentration [k+] [k+]

pH of ECF

Size of the intracellular k+

pool

Function of potassium body cell

acidosis

plasma

hyperkalemia

body cell

hypokalemia

plasma

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 Pancreatic juice

20

10-20

150

0

140

5

40

110

gall

140

5

100

40

Intestinal juice

140

5-15

60-110

30-80

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: Renal failure Adrenal insufficiency

Diuretics Adrenal steroid excess Renal tubular disorders (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 Widening of QRS complex Depression of ST segment

QRS like sine wave (portends imminent cardiac standstill

ECG changes of Hyperkalemia (electrocardiographic)

ECG changes of Hyperkalemia (electrocardiographic)

Assessment of hyperkalemia 1 ⑴A true metabolic abnormality?

⑵ Elevated by hemolysis, marked leukocytosis, thrombocytosis (platelet >1million/L)

2 Assess acidbase status

3 Determine the rapidity to correct the elevated serum potassium

Emergency treatment of hyperkalemia (five approaches) 1 2

Infusion: 50% GS +20u insulin (K+ ECF→ICF 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 H 2 CO 3 H 2 PO 4 -

HP O 4 - + H +

HH b HH bO 2

H b+ H+ H bO 2 - + H +

HP r H CO 3 -

HCO 3 20 = = H 2 CO 3 1

bu ffe ri ng ba se HC O 3 - + H +

P r24 =

pH 7O 2 .35-0 .0 3× 40 0. 03 ×PC 7.45

+ H+ 24

= 1. 2

【

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 （ pH

H 2 CO 3

g ive of f CO 2

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 me tab oli c

de cre ase

i ncr eas e

al kal osi s （ HC O 3 - )

• （ H 2 CO 3 ) • re sp ir ato ry re spi rat or y Ac ido si s al kal osi s

inc rea se

de cr ea se

metabolic acidosis （ HC O ) path ogen 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 esu 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 :35m l/k g sw ea ti ng ： mo de ra te swe at in g: los s 50 010 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

•