Transcript Diapositive 1 - UJF) Grenoble

commentaire
 La natrémie PNa reflète l’osmolalité en l’absence
d’osmoles extra et intracellulaires actives ≠ Na et ≠ K
 en pratique, l’osmolalité est partout la même dans
l’organisme
 Na = K en terme d’osmolalité
Commentaire
capital Na
VEC
hydratation extracellulaire
PNa (si = osmolalité)
VIC
hydratation intracellulaire
Vignette
Patient de 87 ans en bonne santé et sans traitement
décès de son épouse,
maison de retraite
anorexie / amaigrissement,
Athymil® 30mg/j
SNG Nutrison énergie® 2000/j
Plasma :
Urée=7 mM, Na=144 mM, K=4,5mM, Glu=6mM, Prot=78g/L,
Créat 55µmol/L, Posm=310 mosm/kg/H2O
mécanisme possible à l’origine du déficit hydrique ?
Vignette
Patient de 87 ans en bonne santé et sans traitement
décès de son épouse,
maison de retraite
anorexie / amaigrissement,
Athymil® 30mg/j
SNG Nutrison énergie® 2000/j
Plasma :
Urée=7 mM, Na=144 mM, K=4,5mM, Glu=6mM, Prot=78g/L,
Créat 55µmol/L, Posm=310 mosm/kg/H2O
Volume urinaire :
Diurèse = 1 L
Ionogramme urinaire :
UNa = 5 mmol/L, UK = 43 mmol/L
Uosmol = 620 mmol/L
Clairance de l’eau libre
Posmol
V = urine volume
Uosmol
osmolurine = Uosmol x V
Cosmol =
Volume of urine
Isotonic to plasma
Cwater =
free solute water
Clairance de l’eau libre
Cosm correspond volume urinaire nécessaire pour
éliminer les osmoles en concentration isotonique au
plasma
Cw = volume d’eau à ajouter ou à retrancher pour obtenir
le volume urinaire réel excrété en sus de Cosm.
Cw = 0 : urines isotoniques au plasma
Cw >0 : excrétion libre d’eau = urines hypotoniques
Cw <0 : réabsorption d’eau = urines hypertoniques
CW = V x (1-Uosm/Posm)
excretion of free water in a polyuric patient without
water intake:  the patient become hypernatremic
failure to ecrete free water in settings of increase
water intake:  the patient become hyponatremic
Quantification of renal water excretion
urea crosses cell membrane readily
urea do not influence PNa and vasopressin (AVP) release
Uurea is a major component of Uosmol
Posmol = 310 mosmolKg, PNa = 144 mmol/L
Uosmol = 620 mosmol, UNa = 5 mmol/L, UK = 43 mmol/L
Diurèse = 1 L
V
=
Cosmol
+
OsmolU
=
Posmol
+
Cwater
Cwater = V x (1-Uosm/Posm) = 1 x (1-620/310) = 1 x (1-2) = -1 litre
L’hypertonie plasmatique n’est pas liée à une diurèse aqueuse ?
Cwater(e)= V x (1-[UNa+UK/PNa])
Cwater(e)= 1 x (1-[5+43/144]) = 1x (1-0.33) = +0.67 litre
L’hypertonie urinaire est liée à une perte rénale d’eau libre (diurèse
osmotique)
renal water excretion quantification and mechanism
CW = V x (1-Uosm / Posm)
CW(e)= V x (1-[UNa+UK] / PNa)
Commentaire
pour interpréter la natrémie
J’analyse la concentration des urines
From fish to philosopher: the story of our environment
Smith H 1953
The early provertebrates resided in a salt water environement whose
composition was similar to that of their own extracellular fluid. Therefore
these animals could ingest salt water freely without altering the
composition of their milieu interieur
As early vertebrates migrated into freshwater streams the
development of a more water impermeable tegument was
necessary to avoid fluid dilution by the hypoosmotic fresh
water environement
the
concentrating
capacity
of
the
mammalian
kidney
contributed to the
evolution of various
biologic
species
including man.
the
glomerulus
developed
enabling the fish to filtrate
excess fluid from the blood
the subsequent development of
the tubule in vertebrates was
seminal
for preservation of
sodium
and
excretion
af
excess solute-free water
Réabsorption tubulaire NaCl
apical
basal
apical
basal
112
300
312
312
112
Thin decending limb
permeable for water
375
375
175
(AQP1)
425
425
225
solute impermeable
513
513
313
513
513
313
700
700
500
Thick ascending limb:
diluting segment:
separation of solutes from water
Na+/K+/2ClImpermeable for water:
osmolality decreases along the lenght
The water permeability of the collecting tubules is extremely low
Knoers NEJM 2005
AVP secretion in response to increases in plasma osmolality versus
decreases in blood volume or blood pressure in human subjects
d’après Robertson GL
Relationship between plasma AVP concentrations and plasma osmolality
under conditions of varying blood volume and pressure
d’après Robertson GL
1% de  osmolalité  mécanisme d’adaptation
Knoers NEJM 2005
Thiazide: no impact on
concentrating capacity
Model of urinary concentration
Na+/Cl-
medullar interstitial
tonicity
change in urinary concentration
cotransport
Na+ K+ / Cl-
⇘ Cl-/Na+ reabsorption
Loop diuretics
osmotic diuretics,
interstitial disease
AVP
H2O  AVP release/action:
nephrogenic or central diabetes insipidus
UUrea
Urea réabsorpsion
H2O
⇘ [urea] medullary ⇘ dietary intake of protein
Mechanisms of urine dilution
Na+/Cl-
Glomerular filtration
⇘ age, volume depletion,
CHF, cirrhosis, nephrotic syndrome
H2O
Na+/Cl- delivery of water determined
by glomerular filtration rate,
proximal tubule H2O reabsorption
and Na+/Cl- reabsorption
Thiazide diuretics
⇘ Na+/Cl- reabsorption
alter diluting capacity
not concentrating
capacity
Cl-/Na+
⇘ Cl-/Na+ reabsorption
loop diuretics, osmotic diuretics,
interstitial disease
Collecting duct impermeable to water in
absence of AVPor other antidiuretic
substances
⇗ water permeability by AVP, drugs
Decrease
Suppression
of thirst
Plasmaosmol
280-290 mosmol/KgH2O
Suppression of
vasopressin
Disorder involving
urine dilution with
water intake
Dilute
urine
Hyponatremia
Increase
Stimulation
of thirst
Stimulation of
vasopressin
Disorder involving
urine concentration
without water intake
Concentrated
urine
Hypernatremia
Parikh C
Case description
A 45-year-old male is admitted to ICU for
coma
Medical problems
 active cigarette smoking
chronic psychosis with compulsive behavior
diagnosed 10 yrs ago, (psychogenic polydipsia 10l/d,
medication abuse),
non insulin dependent diabetes
 collagenous colitis
 treatment: neuroleptic, benzodiazepine, sodium
divalproate, diuretic (piretanide), gliclazide
History of case
 24hrs prior to admission: the patient developed a
confusion at home
 admission to the emergency department:
T: 36.6°C, blood pressure : 160/90mmHg,
pulse : 111/min
 coma (Glasgow coma score = 8)
 diuresis: 5l in the first hour
 no other abnormality
Examination upon ICU admission
weight: 85.3kg,
seize:1.6 m,
blood pressure: 160/100 mmHg,
pulse: 110/min,
fever: 38°C
 Glasgow coma score = 8
 no other abnormality
Biology in ICU
PNa
169 mmol/l
pH
7.42
UNa
160 mmol/l
PK
3.1 mmol/l
PaCO2
32 mmHg
UK
31 mmol/l
PCl
132 mmol/l
PaO2
75 mmHg
UCl
202 mmol/l
24 mmol/l
Ucreat
2230 µmol/l
Uosmo mes
462 mosm/l
(FiO2 : 45%)
HCO3-
PCa
2.2 mmol/l
Pphosphorus
0.36 mmol/l
PBUN
4 mmol/l
Hb
15.1 g/dl
Pcreat
88 µmol/l
Ht
45%
Pglucose
7.1 mmol/l
WBCs
15 Giga/l
Pprotide
81 g/l
Platelets
285 000 G/l
Palbumin
48 g/l
Prothrombin
ratio
80%
Posmo
335 / 337
calculated
/measured
Evolution during ICU stay
Treatment:
 correction of hydro-electrolytic disorders with 2.5%
glucose over 60 hours
 coma: orotracheal intubation + invasive mechanical
ventilation during 48h
 Recovery of neurologic state
 Day 4 : ICU discharge with PNa : 142 mmol/l
PNa
169 mmol/l
pH
7.42
UNa
160 mmol/l
PK
3.1 mmol/l
PaCO2
32 mmHg
UK
31 mmol/l
PCl
132 mmol/l
PaO2
75 mmHg
UCl
202 mmol/l
24 mmol/l
Ucreat
2230 µmol/l
Uosmo mes
462 mosm/l
(FiO2 : 45%)
PCa
2.2 mmol/l
Pphosphorus 0.36 mmol/l
PBUN
4 mmol/l
Pcreat
88 µmol/l
Pglucose
7.1 mmol/l
Pprotide
81 g/l
Palbumin
48 g/l
HCO3TAP=16
Posmo
calculated
/measured
335 / 337
PNa
169 mmol/l
pH
7.42
UNa
160 mmol/l
PK
3.1 mmol/l
PaCO2
32 mmHg
UK
31 mmol/l
PCl
132 mmol/l
PaO2
75 mmHg
UCl
202 mmol/l
HCO3-
24 mmol/l
Ucreat
2230 µmol/l
Pphosphorus 0.36 mmol/l
TAP=16
TAPc = 14
Uosmo mes
462 mosm/l
PBUN
4 mmol/l
SIDa= 40
SIDe= 39
SIG = 0
Pcreat
88 µmol/l
Pglucose
7.1 mmol/l
Pprotide
81 g/l
Palbumin
48 g/l
Posmo
335 / 337
(FiO2 : 45%)
PCa
2.2 mmol/l
calculated
/measured
PNa
169 mmol/l
pH
7.42
UNa
160 mmol/l
PK
3.1 mmol/l
PaCO2
32 mmHg
UK
31 mmol/l
PCl
132 mmol/l
PaO2
75 mmHg
UCl
202 mmol/l
HCO3-
24 mmol/l
Ucreat
2230 µmol/l
Pphosphorus 0.36 mmol/l
TAP=16
TAPc = 14
Uosmo mes
462 mosm/l
PBUN
4 mmol/l
SIDa= 40
SIDe= 39
SIG = 0
Pcreat
88 µmol/l
PNa-Cl = 37
Nao/Nath=1.21 PNa-Cl = 44 PCl = 125
Pglucose
7.1 mmol/l
PClcorr(H2O)
= 132 x
(140/169)
Pprotide
81 g/l
Palbumin
48 g/l
Posmo
335 / 337
(FiO2 : 45%)
PCa
2.2 mmol/l
calculated
/measured
110
Metabolic diagnosis
Chloride sodium overdose
PO NaCl medication
 after consciousness recovery of the patient, confirmation
of the deliberate dose ingestion
Hypernatremia
Assess volume status
Hypovolemia
⇘ total body Na
⇘ total body water ++
Euvolemia
(no edema)
no change in total body Na
⇘ total body water
Hypervolemia
⇗ total body Na ++
⇗ total body water
UNa analysis
> 20 mmol/L
< 20 mmol/L
variable
> 20 mmol/L
Hypernatremia
Assess volume status
Hypovolemia
⇘ total body water ++
⇘ total body Na
Euvolemia
(no edema)
⇘ total body water
no change in total body Na
Hypervolemia
⇗ total body water
⇗ total body Na ++
UNa analysis
> 20 mmol/L
< 20 mmol/L
variable
> 20 mmol/L
Renal losses
Extra renal losses
Renal losses
Extra renal
losses
Sodium gains
Osmotic or loop
diuretics
Postobstruction
Intrinsic renal disease
Vomiting
Diarrhea
Excess sweating
Fistulae
Diabetes
insipidus
Hypodypsia
Respiratory
dermal
Primary
hyperaldosteronism
Cushing
Hypertonic
dialysis
fluid infusion
Parikh C
hypernatrémie = déficit hydrique / capital
sodé ou osmotique
l’hypernatrémie ne préjuge en aucun cas de ce
capital sodé
sauf urgence vitale, la vitesse de correction
d’une dysnatrémie est parallèle à sa vitesse
d’installation
cas clinique
femme 76 ans errant dans la rue
confusion désorientation temporo-spatiale + soif
TA=100/60mmHg, FC=110/min,
SpO2=98%, T=37.1°C, Poids=62Kg
pli cutané
ordonnance hydrochlorothiazide®: 40mgx2/j.
PBUN
20 mmol/l
Hb
17.1 g/dl
Pcreat
151 µmol/l
Ht
49%
PNa
123 mmol/l
WBCs
12.5 Giga/l
PK
3.2 mmol/l
Platelets
325 000 G/l
PCl
86 mmol/l
Prothrombin
ratio
80%
CO2T
31 mmol/l
Pphosphorus
1.26 mmol/l
Pglucose
6.1 mmol/l
Pprotide
88 g/l
Pglucose
6.1 mmol/l
Puric aid
620 mmol/l
PBUN
20 mmol/l
Hb
17.1 g/dl
UNa
54 mmol/l
Pcreat
151 µmol/l
Ht
49%
UK
32 mmol/l
PNa
123 mmol/l
WBCs
12.5 Giga/l
UCl
320 mmol/l
PK
3.2 mmol/l
Platelets
325 000 G/l
Ucreat
5600 µmol/l
PCl
86 mmol/l
Prothrombin
ratio
80%
CO2T
31 mmol/l
Pphosphorus
1.26 mmol/l
Pglucose
6.1 mmol/l
Pprotide
88 g/l
Pglucose
6.1 mmol/l
Puric aid
620 mmol/l
cas clinique
diagnostic le plus probable ?
Na+/Cl-
quelques étiologies
Thiazide diuretics
⇘ Na+/Cl- reabsorption
alter diluting capacity
not concentrating
capacity
Commentaire
Pour interpréter la natrémie
J’évalue le capital sodé
J’analyse la concentration des urines
hyponatrémie normovolémique à dilution urinaire optimale
hyponatrémie hypovolémique et déperdition sodée urinaire
hyponatrémie hypovolémique et déperdition extrarénale
hyponatrémie euvolémique par SIADH
hyponatrémie par excès mixte Na + H2O
excès H2O > excès Na
algorithme d’analyse
Hyponatremia
Assess volume status
Hypovolemia
⇘ total body Na
⇘ total body water [< TBNa]
Euvolemia*
(no edema)
no change in total body Na
⇗ total body water
Hypervolemia
⇗ total body Na
⇗ total body water ++
UNa analysis
> 20 mmol/L
< 20 mmol/L
> 20 mmol/L
> 20 mmol/L < 20 mmol/L
*The presence of normal or low BUN or serum uric acid levels are helpful
laboratory correlates of normal ECF volume
Parikh C
algorithme d’analyse
Hyponatremia
Assess volume status
Euvolemia
Hypervolemia
(no edema)
⇗ total body water ++
⇗ total body water
⇗ total body Na
no change in total body Na
Hypovolemia
⇘ total body water
⇘ total body Na
UNa analysis
> 20 mmol/L
< 20 mmol/L
Renal losses
Extra renal losses
Diuretic excess
Mineralocorticoid
deficiency
Salt loss nephropathy
Renal tubular acidosis
Ketonuria
Osmotic diuresis
Cerebral salt wasting
Vomiting
Diarrhea
Third spacing
of fluids
pancreatitis
burns
Malnutrition
> 20 mmol/L
Glucocorticoid
deficiency
Hypothyroidism
Stress
Drugs
SIAD
> 20 mmol/L < 20 mmol/L
Acute or
Nephrotic
Chronique
syndrome
Renal failure Cirrhosis
Cardiac Failure
Parikh C
algorithme d’analyse
Hyponatremia
Assess volume status
Hypovolemia
⇘ total body water
⇘ total body Na
Euvolemia
(no edema)
⇗ total body water
no change in total body Na
Hypervolemia
⇗ total body water ++
⇗ total body Na
UNa analysis
> 20 mmol/L
< 20 mmol/L
Renal losses
Extra renal losses
Diuretic excess
Mineralocorticoid
deficiency
Salt loss nephropathy
Renal tubular acidosis
Ketonuria
Osmotic diuresis
Cerebral salt wasting
Vomiting
Diarrhea
Third spacing
of fluids
pancreatitis
burns
Malnutrition
> 20 mmol/L
> 20 mmol/L < 20 mmol/L
Glucocorticoid
Acute or
Nephrotic
deficiency
Chronique
syndrome
Hypothyroidism Renal failure Cirrhosis
Stress
Cardiac Failure
Drugs
SIADH < 20 mmol/L
Primary polydipsia
Poor dietary intake
Hyponatremia
AVP release due to
«hypovoremia»
AVP release not related to
hypovolemia
Assess volume status
Hypovolemia
⇘ total body Na
⇘ total body water [<TBNa]
Euvolemia
(no edema)
no change in total body Na
⇗ total body water
Hypervolemia
⇗ total body Na
⇗ total body water ++
UNa analysis
> 20 mmol/L
< 20 mmol/L
Renal losses
Extra renal losses
Diuretic excess
Mineralocorticoid
deficiency
Salt loss nephropathy
Renal tubular acidosis
Ketonuria
Osmotic diuresis
Cerebral salt wasting
Vomiting
Diarrhea
Third spacing
of fluids
pancreatitis
burns
> 20 mmol/L
> 20 mmol/L < 20 mmol/L
Glucocorticoid
Acute or
Nephrotic
deficiency
Chronique
syndrome
Hypothyroidism Renal failure
Cirrhosis
Stress
Cardiac Failure
Drugs
< 20 mmol/L
SIAD
 GFR
Primary polydipsia
Poor dietary intake
Absence d’AVP
cas clinique
homme 52 ans, sans antécédent ni traitement
asthénie ++ depuis 2 mois amaigrissement -6kg/3 mois
TA=140/80mmHg, FC=85/min, T=37.2°C
pas de signe clinique de deshydratation
cas clinique
PBUN
4 mmol/l
Hb
13.1 g/dl
Pcreat
111 µmol/l
Ht
39%
PNa
110 mmol/l
WBCs
10.5 Giga/l
PK
2.8 mmol/l
Platelets
285 000 G/l
PCl
79 mmol/l
Prothrombin
ratio
80%
CO2T
24 mmol/l
Pphosphorus
0.86 mmol/l
Pglucose
6.1 mmol/l
Pprotide
62 g/l
Puric aid
320 mmol/l
cas clinique
PBUN
4 mmol/l
Hb
13.1 g/dl
UNa
60 mmol/l
Pcreat
111 µmol/l
Ht
39%
UK
20 mmol/l
PNa
110 mmol/l
WBCs
10.5 Giga/l
UCl
75 mmol/l
PK
2.8 mmol/l
Platelets
285 000 G/l
Uuréet
440 µmol/l
PCl
79 mmol/l
Prothrombin
ratio
80%
CO2T
24 mmol/l
Pphosphorus
0.86 mmol/l
Pglucose
6.1 mmol/l
Pprotide
62 g/l
Puric aid
320 mmol/l
cas clinique
diagnostic le plus probable ?
cas clinique
PBUN
4 mmol/l
Hb
13.1 g/dl
UNa
60 mmol/l
Pcreat
111 µmol/l
Ht
39%
UK
20 mmol/l
PNa
110 mmol/l
WBCs
10.5 Giga/l
UCl
75 mmol/l
PK
2.8 mmol/l
Platelets
285 000 G/l
Uuréet
440 µmol/l
PCl
79 mmol/l
Prothrombin
ratio
80%
CO2T
24 mmol/l
Pphosphorus
0.86 mmol/l
Pglucose
6.1 mmol/l
Pprotide
62 g/l
Puric aid
320 mmol/l
TRT : 2 L NaCl 9% / 12 heures
cas clinique
évolution biologique attendue ?
Homme 70 kg, PNa = 110 mmol/L
Uurée= 440 mmol/L, UNa = 60 mmol/L, UK = 20 mmol/L
Uosmol  [440 + 2x(60+20)] = 600 mmol/L
TRT : 2 L NaCl 9% / 12 heures = 600 mmol NaCl
SIADH en euvolémie  élimination des 600 mmol
[Uosmol=600 mmol/L]  600 mmol = 1 litre de diurèse
Apports = 2 L  gain net H2O = (2L - 1L) = 1L
T0,
H2O = 0,6 x P  42L et PNa = 110 mmol/L
TotNa = H2O x PNa = 4400 mmol
H12, [H20 = 42L + DH2O (1L)] = 43L
Natot = 4400 (euvolémie)
PNa= 4400/43 = 102 mmol/L
En cas d’hyponatrémie avec dilution urinaire
inadéquate, si l’hypersécrétion d’AVP n’est pas
volodépendant, des apports isotoniques au
plasma mais hypotoniques aux urines aggravent
l’hyponatrémie
Hoorn Nephrol Dial Transplant 2006
cas clinique
Enfant 15 ans, Poids 40 kg / 1m70
PNa = 105 mmol/L,  Posmol = 220 milliosmol/KgH2O
Uurée= 15 mmol/L, UNa = 10 mmol/L, UK = 10 mmol/L
diurèse 1200 mL dès H1
cas clinique
diagnostic le plus probable ?
Enfant 15 ans, Poids 40 kg / 1m70
PNa = 105 mmol/L,  Posmol = 220 milliosmol/KgH2O
Uurée= 15 mmol/L, UNa = 10 mmol/L, UK = 10 mmol/L
diurèse 1200 mL dès H1
 Uosmol = [15 + 2x(10+10)] = 55 mmol/L
H2O = 0,6.P.[(140/PNa) – 1] = 11 L
CH2O = 1 - 55/220 = +740 mL/L
Si TRT : alimenter Uosmol,(600 mmol)
2 L NaCL 9% : en 12 heures + KCl
Furosémide 20 mg  Uosmol = Posmol
Inhibition de CH2O positive
TRT : « let it be » mais attention à K+
Élimination de la charge hydrique en 9 h
en cas d’hyponatrémie, si la dilution urinaire est
adéquate le furosémide inhibe le pouvoir de
dilution des urines et s’oppose à l’excrétion
d’eau libre
Commentaire
 intrication des désordres hydro-électrolytiques et
acidobasiques +++
 Evaluation des compartiments hydriques et de la
volémie +++ (impact diagnostique et pronostique) +++
 Cl- anion noble (UCl et PCl)
Commentaire
Pour interpréter la natrémie
J’évalue le capital sodé
J’analyse la concentration des urines
hyponatrémie = excès d’eau / capital sodé ou
osmotique
hypernatrémie = déficit hydrique / capital
sodé ou osmotique
la natrémie ne préjuge en aucun cas de ce
capital sodé
examen clinique = estimation du capital sodé
uricémie ou évolution de la FeNa sous perfusion
de sérum salé peuvent faciliter cette estimation.
traitement de l’hyponatrémie volodépendante =
correction du déficit sodé
sauf urgence vitale, vitesse de correction d’une
dysnatrémie parallèle à vitesse d’installation
hypoxie, hypokaliémie : déterminants majeurs
des complications neurocérébrales associées aux
dysnatrémies et à leur correction