Distrubance of Fluid Vol. Regulation

8/9/2019 Distrubance of Fluid Vol. Regulation

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CAPT SAFIA FATIMA

AFIP


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Terminology

Osmolality = No. of solute particles/ KgH2O Temperature independent

Osmolality=2(Na) +urea +glucose

The osmolality of the !" is normally maintainedin the range 2#2$2%& mmol/'g of ater

Osmolarity = No. of solute particles/ H2O

Osmolarity is not commonly used *ecause it istemperature dependent. This is *ecause aterchanges its olume ith temperature


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Osmolal Gap

Osmolal gap = measured plasma osmolality , calc plasmaosmolality

Causes of inc osmolal gap ( > 10 mosm/kg )-

resence of non electrolyte solute other than glucose orurea.

igni0cant discrepancies1 hen the fractional ater contentof

plasma is reduced

Hyperlipdaemia

Hyperproteinaemia


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5


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6


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Water Distribution

Approximately 66% o t!is "ater is in t!e intra#ellular lui$ I F& an$

''% in t!e extra#ellular lui$ ( F&) only *% o bo$y "ater is in t!e


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Distribution O Water

Total *ody ater

natomical !3 4ntracellular

Transcellullar hysiological

lasma 4nterstitial "luid

natomical !3 includes ater e5ternal to the cellmem*ranes through hich all meta*olic e5change occurs

hysiological !3 is the portion of anatomical !3 hose

olume is accessi*le to direct measurement


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Water Inta+e , -oss


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Water .egulation

!" osmolality

6asopressin (7H)

Hypothalamic thirst centre

!" olume


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Water .egulation

4f !" osmolality falls1 there is no sensation ofthirst and asopressin secretion is inhi*ited. dilute urine is produced1 alloing ater lossand restoration of !" osmolality to normal.


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/ormonal .egulation o

0loo$ 1olume


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auses O Water Depletion

An$ lini#al Features


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Water Dei#ien#y

3ater de0ciency may manifest in four forms

ure ater depletion

4sotonic 8uid loss

Hypotonic 8uid loss

Hypertonic 8uid loss

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Water Dei#ien#y

PURE WAER !EP"E#O$%9ody ater loss ithout sodium loss

:ncommon1atient too old or too young or too sic' to drin'

7istur*ance of thirst center Neurogenic1sychogenic

Hypoolemia1!linically 1 may *e euolaemic

High conc. urine (Oliguria) :rinary Na+ decrease

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Water Dei#ien#y

#&OO$#C '"U#! "O&&

Sodium and water loss in the ratio of 140 mmol of Na+ for every

liter of pure water e.g;

lood loss

Serum loss! "urns

#hird spa$e a$$umulation e.g. ileus! pan$reatitis! peritonitis!

$rush in%ury

No $hange in &'( osmolality

No shift of fluid ")w *'( and &'(

e$reased &'( volume

,ypotension

1-


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Water Dei#ien#y

)POO$#C '"U#! "O&&Na+ is lost in e$ess of water

&$essive sweating /omiting! diarrhea! drainage into fistula

ddisons disease

iureti$ therapy

Salt losing nephritis ia"etes insipidus

;ross decrease in !" olume

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O2er!y$ration

4ncrease in total *ody ater ith normal total *odysodium

4t results from e5cessie ater consumption

(polydipsia)3ater into5ication results from imapaired renal free

ater e5cretion as a result of 7H secretion5cess 7H is 'non as 47H(syndrome of

inappropriate 7H secretion)

3ater into5ication *ilutional +yponatremia <hyposmolarity of !3 results in ater moement intothe cells

ymptoms of ater into5ication are related to rate offall in sodium


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auses O Water (x#ess

An$ lini#al Features


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onse3uen#es

Oedema

Hyponatraemia

!ere*ral oedemao conc. of other *lood analytes

o !" osmolality

4ntracellular 8uid shift

4ntracellular oedema

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6asopressin is synthesied *y the supraoptic andparaentricular nuclei of the hypothalamus

4t is then transported to the posterior pituitary

and stored.6asopressin release from posterior pituitary is

primarily regulated *y changes in plasmaosmolality

The primary site of asopressin action in the'idney is at the collecting duct

6asopressin receptors are classi0ed as 6> and 62

Arginine 1asopressin (A,P-


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Arginine 1asopressin

#t is also kno.n as A!,asopressin

REU"A#O$ O' &ECRE#O$

>.Osmoreceptor mechanism

2.ressure olume mechanism

?.@egulation *y thirst centre

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O&2ORECEPOR 2ECA$#&2

Osmolality of the *lood is the main regulator of6 secretion

s little as a 2A increase in !" osmolalitycauses shrin'age of osmoreceptor cells ith

stimulation of 6 release from the posterior

pituitary lo*e

plasma osmolality a*oe 2#B mOsm/'g is

considered the osmotic threshold for 6 release35


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PRE&&URE ,O"U2E 2ECA$#&2

6 is regulated *y *aroreceptors that respond toalterations in the *lood olume. reduction inplasma olume or arterial pressure1 or *oth1stimulate 6 secretion

Non$osmotic stimuli for 6 release include pain1stress1 sleep1 e5ercise and chemical agents such ascatecholamines1 angiotension 441 opiates1

prostaglandins1 anaesthetics1 nicotine and*ar*iturates

lcohol1 phenytoin1 and glucocorticoids inhi*it 6release 36


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#R& CE$RE

This centre has a higher set$point than theosmoreceptors and respond to osmolalities a*oe2%B mOsm/'g

@esponses inoling 61 thirst1 and the 'idneyare coordinated together to maintain plasmaosmolality ithin a narro range of 2#C to 2%&mOsm/'g

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P)O"O#CA" AC#O$&

!ontrols ater homeostasis hich allos the'idney to rea*sor* ater and concentrate urine

;eneralied asoconstriction that leads to a risein arterial *lood pressure

Daintains *lood pressure during *lood loss

@elease of 6 into pituitary portal systemaugments the action of !@H in stimulating therelease of !TH from the adenohypophysis

5erts contractile in8uence on the uterus

romotes contraction of intestinal musculature 3-


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The vasopressin response to a fall in blood pressure is exponential: it is

relatively small with small decreases in plasma volume, but greater falls

cause a massive increase in vasopressin secretion


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Disor$ers O AD/ A#ti2ity

A!3 !E'#C#E$C)

7e0cient production or action of 6 results inpolyuria caused *y the failure of the renal

tu*ules to rea*sor* solute$free ater 3hen urine output is E2.&/day1 an

inestigation is usually indicated as urine outputmay approach >/hr in complete de0ciency of

6 olyuric states is 'non as dia*etes incipidus.

1


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Deinition7ia*etes insipidus (74) is a disease

characteried *y polyuria and polydipsiadue to decrease secretion or action of

antidiuretic hormone (7H)


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Types O Diabetes Insipi$us

F Neurogenic$ also called central or pituitary1 it iscaused *y a de0ciency of the antidiuretichormone1 asopressin.

F Nephrogenic$ caused *y a defect in thereceptor to the hormone1 asopressin1 locatedin the 'idneys.

F ;estagenic$ caused *y a de0ciency of theantidiuretic hormone1 asopressin1 during

pregnancy.

F 7ipsogenic$ form of primary polydipsia1a*normal thirst and e5cessie inta'e of liGuids.


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/ypot!alami# DiabetesInsipi$us

lso called as neurogenic1 cranial1 or central 74 4t is caused *y failure of pituitary gland to secrete

normal amounts of 6 in response toosmoregulatory factors

Other causes include-Neoplastic diseasesNeurological surgeryHead trauma4schemic or hypo5ic disorders;ranulomatous diseases4nfections

utoimmune diseases 4


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Cont4$

4n the ne*orn1 74 has *een reported inassociation ith asphy5ia1 46H1 intraascularcoagulopathy1 isteria monocytogenes sepsis1

and *acterial meningitis and encephalitis.

ppro5 2BA of cases of 74 are idiopathic


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5ep!rogeni# Diabetes Insipi$us 4t results from the failure of 'idney to respond to normal

or increased concentrations of 6 Primary in+erite* causesThe cause may *e the

incapa*ility of 6 to stimulate cD formation. Dutationin the 6 receptor and mutations in the aGuaporin$2ater channels are thought *e responsi*le

Ac4uire* forms5 of N74 may *e causes *y- Deta*olic disorders (hypo'alemia1 hypercalcaemia1

amyloidosis) 7rugs (lithium1 demeclocycline1 and *ar*iturates) @enal diseases ( polycystic disease and chronic renal

failure) i*iopat+ic.

6


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Clini#al Maniestations

F OI:@41 chronic passage of large olumes of urine

F OI7441 chronic1 e5cessie thirst

F OTH@

feer

irrita*ility

constipation

failure to thrie

lac' of appetiteomiting

high *lood leels of sodium


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Cont4$Neurogenic 74

Hypothalamic tumors- groth

distur*ances1 progressie cache5ia oro*esity1 hyperpyre5ia1 sleepdistur*ance1 se5ual precocity1 oremotional disorders

esions initially causing 74 mayeentually destroy the anterior pituitaryand its associated endocrine a5is


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Patient /istoryHo much 8uid inta'e per day

6oiding patterns

7ietary inta'e7rug history


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-aboratory in2estigations

:rine is usually pale and colorless

:rine analysis and urine electrolytes

:rine speci0c graity aries */ >.BB> and>.B>B

:rine osmolality &B$?BB mosm/'g

erum osmolality may ary idely1depending on hydration status

Other renal function studies usually normal

erum asopressin measurement


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easure

lood glu$ose

'reatinine

otassium

'al$ium

Polyuria diagnosisabnormal

normal

(luid deprivation

test

neurogenic DI

Nephrogenic DI

Primary polydipsia

Non-diagnostic

:rine osmolality (mmol/'g) after-

# h 8uid depriation desmopressin

J ?BB EBB

J?BB J?BB

EBB EBB

?BB$BB JBB


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Diagnosis3ater depriation test4n patients ith seere neurogenic 741

oernight ater depriation results in

eleation of erum and urineosmolality after administration ofasopressin.

4n nephrogenic 74 there is no eLect onserum < urine osmolality afteradministration of desmopressin.


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Diagnosis

dministration of desmopressin4n neurogenic 741 desmopressin ill raise

:rine osmolality< suppress urine out put.

4n nephrogenic 741 desmopressin produces noincrease in :rine osmolality and nosuppression of :rinary out put.

4n normal indiiduals1 desmopressinadministration can cause a asodilatory

response (8ushing1 fall in diastolic 91 rise inH@)1 *elieed to *e mediated *y e5tra renal62 receptors


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Treatmentneurogenic 74dministration of desmopressin1 usually

intranasal.

7esmopressin *inds almost e5clusiely to 62receptors and is more resistant to degradation *y*ody peptidases than endogenous asopressin

Therefore1 the antidiuretic eLects ofdesmopressin last #$>B hr1 compared ith >$? hr

for endogenous asopressin7ose- &$>B mcg intranasal1 gien in single or

diided doses J 2 y/o- B.>&$B.& mcg/'g/2C hr

46/! therapy also aaila*le


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TreatmentNephrogenic 74

nsure a suMcient inta'e of ater toreplace the large urinary ater losses

top causatie medications1 ifapplica*le

o sodium diet

7rugs that reduce polyuria rostaglandin synthesis inhi*itors (indomethacin)

otassium$sparing diuretics (amiloride)


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Management'he$8 serum ele$trolytes fre9uently

fter episodes of dehydration! these patients usually

re9uire repla$ement of large 9uantities of water! "ut not

sodiumNeurogeni$ * prognosis often determined "y the

underlying etiologi$ pro$ess

Nephrogeni$ * good prognosis!#here are isolated

reports of $hroni$ renal failure


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Psy#!ogeni# Or Primary

Poly$ipsia

!hronic1 e5cessie inta'e of ater suppresses6 secretion and produces hypotonic polyuria

sychogenic factors are most commonly

associated ith this disorder1 *ut hypothalamicdisease aLecting the thirst centre may *e acause

7rugs can also aLect thirst centre and may cause

primary polydipsia

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Disor$ers O A1P A#ti2ity

A!4t refers to autonomous1 sustained production of 6in the a*sence of 'non stimuli for its release

4n this syndrome plasma 6 concentrations are

inappropriately increased relatie to a lo plasmaosmolality and to a normal or increased plasmaolume (i.e.1 it occurs under conditions that normallysuppress its secretion)

4-


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auses O SIAD/

U2OUR&

! of *ronchus1 prostate1 pancreas9rain tumours- glioma1 meningioma

6RA#$ PAO"O) Tumours- trauma/!64nfections- a*scess1 meningitis1 encephalitis

PU"2O$AR) PAO"O) Tumours- *ronchial !4nfections- tu*erculosis1 pneumonianeumothora51 hydrothora51 positie pressure entilation

2#&CE""A$EOU&ain (post$op)cute intermittent porphyria;9 yndromeHypothyroidism

7rugs- narcotics1 car*amaepine1 o5ytocin 42


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Pat!op!ysiology O SIAD/

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SIAD/

'EAURE&

The characteristic features are-

Hyposmolar plasma ( J 2B mOsm/'g)

:rine osmolality slightly greater than that of

plasma 4nappropriately eleated urinary sodium

concentration (CB to #B mmol/)

num*er of conditions must *e satis0ed *eforema'ing the diagnosis of 47H. This is todiLerentiate it from other causes of hyponatremiali'e dilutional and depletional hyponatremia

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SIAD/

'EAURE&

4n addition to lo serum sodium and osmolalityalues1 and high urine sodium and osmolalityalues1 the folloing must *e satis0ed-

No eidence of dehydration

No cardiac1 adrenal1 pituitary1 or thyroiddysfunction

No drug or diuretic therapy !linical and *iochemical response to 8uid

restriction

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SIAD/

WAER3"OA!#$ E&

4f the cause for mild hyponatremia remains unclear1 aater$loading test may *e performed. This test ishoeer potentially dangerous in patients ith seerehyponatremia and should not *e performed if serum

sodium concentrations are J >?B mmol/

atients ith 47H hae impaired e5cretion of theater load and fail to dilute their urine

Deasurements of 6 in plasma are usually not neededto ma'e a diagnosis of 47H1 *ut *asal alues ould*e e5pected to *e inappropriately high relatie toplasma osmolality

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/yper2olemi# State5DESCRIPTION:

:yperglycemicstates that pulls

water from $ells

:!luid loss "rome#tracellularspace greaterthan solute loss leading to in$rease

serum osmolality 325.

C$INIC%$PRESENT%TION:

:',(

:'irrhosis

:Nephroti$syndrome

:oop diureti$

:


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(u2olemi# State6

DESCRIPTION:

:Decrease in "luidsin both theintra'ascular andinterstitial space.

:Normal serumosmolality ?375@325A

:Bse of Na+ freesolutions that resultin dilution ofetra$ellular spa$e.

C$INIC%$PRESENT%TION:

:S*,

:,ypothyroidism

:sy$hiatri$disorders

:edi$ations

TRE%T&ENT:

:=ater restri$tion

:*n$rease dietary salt

:#reat S*,:'orre$t underlying $ause


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/ypo2olemi# State5DESCRIPTION:

:Clu$ose in isotoni$solution oidiDed leading

to $ellular swelling.

:$oss o" solute "rome#tracellular spacegreater than e#cess o"(ater resulting in

decrease serum osmolality ?E 375A

C$INIC%$PRESENT%TION

:C* fluid loss

:iureti$s:drenal insuffi$ien$y

:urns

:Sweating

:,ypotoni$

:ehydration

TRE%T&ENT:

:*/ Normal Saline to $orre$tthe etra$ellular fluid defi$it

F*n$rease daily salt inta8eF,ypertoni$ saline solutionto in$rease Na+ levels


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Distrubance of Fluid Vol. Regulation

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