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- Apare la pacienti cu DZ tipII,cu acces limitat
la apa, adesea tarati, cu comorbiditati
multiple
- Hglicemia > 180mg/dl depaseste capacitatea
rinichilor de a reabsorbi glucoza, apare
glicozuria si diureza osmotica
- Daca pacientul nu are acces la apa, depletia
volemica va fi de 8-12 l.
 Clinic: - pacienti varstnici, tarati, cu DZ tipII
- evolutie lenta in zile sau saptamani,
cu stare de slabiciune, oboseala, anorexie,
dureri toracice sau abdominale, tulburari
neurologice, coma
 Factori precipitanti:- HDS, TEP, pancreatita,
ischemie mezenterica, infectii, IMA, arsuri
grave, insuf. renala, rabdomioliza, AVC
- droguri:diuretice, litiu,
betablocante, manitol, cimetidina
glucocorticoizi, neuroleptice, fenitoina, blocantii
canalelor de Ca
- G > 600mg/dl
- Osm >315mOsm/kg
- bicarbonat >15mEq/l
- pH > 7,3
- c.cetonici -/moderat crescuti
-poate exista acidoza metabolica (lactica) datorita
hipoperfuziei; cetoacidoza de inanitie sau din
cauza azotemiei
- Na scazut, dar poate fi normal/crescut, trebuie
corectat in functie de glicemie
Nac=Nam+[16x(G-100)]/100
- Osmolaritate crescuta N:275-295
Osm =[2Na+G]/18
- Uree crescuta
- K, P, Mg scazute
1) Fluide:deficit 8-12 l,rehidratarea singura
poate sa scada G cu 35-70 mg/dl/h
- 0,9%NaCl cu 15-20ml/kg/h prima ora
- 4- 14 ml/kg/h dupa aceea
50% din deficit se corecteaza in primele 12ore
- dupa imbunatatirea TA, diurezei si pulsului
se poate trece la 0,45%NaCl
- La pacientii cu insuficienta cardiaca
repletia volemica este mai lenta
2) Electroliti:
- Potasiu:deficit K 4-6- 10 mEq/kg
!acidoza poate interfera cu determinarea
reala a K!
a) K < 3,3mEq/l: 40mEq/h pana K>3.3mEq/l
b) K 3,5- 5mEq/l:10-20mEq/h (20-30mEq/l)
c) K >5mEq/l nu K, dar control la 2 ore
- Magneziu:corectat in paralel cu K
- Fosfati : daca < 1 mg/dl- 20-30 mEq/l K2PO4
- Bicarbonat: pH < 7
3) Insulina:- dupa repletie volemica(altfel
insulina baga glucoza in celula antrenand si
apa, deci accentueaza depletia volemica
intravasculara ducand la colaps)
± bolus 0,1U/kg urmata de 0,1U/kg/h
-daca glicemia nu scade cu 50 mEq/dl/h in
prima ora, se dubleaza doza la fiecare ora
pana G sscade cu 50-70 mg/dl/h
- G<300mg/dl se adm G5% si se scade insulina
la 0,05U/kg/h,pana
Osm< 315mOsm/l
4) Tratamentul factorilor precipitanti
- Edem cerebral(mai frecvent la copiii cu CAD)
-limitarea repletiei volemice<50ml/kg in
primele 4 ore
-monitorizarea statusului mental
- Hipoglicemie
- Hipokalemie
- Edem pulmonar

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STATUSUL HIPERGLICEMIC HIPEROSMOLAR.pptx

  • 1.
  • 2. - Apare la pacienti cu DZ tipII,cu acces limitat la apa, adesea tarati, cu comorbiditati multiple - Hglicemia > 180mg/dl depaseste capacitatea rinichilor de a reabsorbi glucoza, apare glicozuria si diureza osmotica - Daca pacientul nu are acces la apa, depletia volemica va fi de 8-12 l.
  • 3.  Clinic: - pacienti varstnici, tarati, cu DZ tipII - evolutie lenta in zile sau saptamani, cu stare de slabiciune, oboseala, anorexie, dureri toracice sau abdominale, tulburari neurologice, coma  Factori precipitanti:- HDS, TEP, pancreatita, ischemie mezenterica, infectii, IMA, arsuri grave, insuf. renala, rabdomioliza, AVC - droguri:diuretice, litiu, betablocante, manitol, cimetidina glucocorticoizi, neuroleptice, fenitoina, blocantii canalelor de Ca
  • 4. - G > 600mg/dl - Osm >315mOsm/kg - bicarbonat >15mEq/l - pH > 7,3 - c.cetonici -/moderat crescuti -poate exista acidoza metabolica (lactica) datorita hipoperfuziei; cetoacidoza de inanitie sau din cauza azotemiei - Na scazut, dar poate fi normal/crescut, trebuie corectat in functie de glicemie Nac=Nam+[16x(G-100)]/100 - Osmolaritate crescuta N:275-295 Osm =[2Na+G]/18 - Uree crescuta - K, P, Mg scazute
  • 5.
  • 6. 1) Fluide:deficit 8-12 l,rehidratarea singura poate sa scada G cu 35-70 mg/dl/h - 0,9%NaCl cu 15-20ml/kg/h prima ora - 4- 14 ml/kg/h dupa aceea 50% din deficit se corecteaza in primele 12ore - dupa imbunatatirea TA, diurezei si pulsului se poate trece la 0,45%NaCl - La pacientii cu insuficienta cardiaca repletia volemica este mai lenta
  • 7. 2) Electroliti: - Potasiu:deficit K 4-6- 10 mEq/kg !acidoza poate interfera cu determinarea reala a K! a) K < 3,3mEq/l: 40mEq/h pana K>3.3mEq/l b) K 3,5- 5mEq/l:10-20mEq/h (20-30mEq/l) c) K >5mEq/l nu K, dar control la 2 ore - Magneziu:corectat in paralel cu K - Fosfati : daca < 1 mg/dl- 20-30 mEq/l K2PO4 - Bicarbonat: pH < 7
  • 8. 3) Insulina:- dupa repletie volemica(altfel insulina baga glucoza in celula antrenand si apa, deci accentueaza depletia volemica intravasculara ducand la colaps) ± bolus 0,1U/kg urmata de 0,1U/kg/h -daca glicemia nu scade cu 50 mEq/dl/h in prima ora, se dubleaza doza la fiecare ora pana G sscade cu 50-70 mg/dl/h - G<300mg/dl se adm G5% si se scade insulina la 0,05U/kg/h,pana Osm< 315mOsm/l 4) Tratamentul factorilor precipitanti
  • 9. - Edem cerebral(mai frecvent la copiii cu CAD) -limitarea repletiei volemice<50ml/kg in primele 4 ore -monitorizarea statusului mental - Hipoglicemie - Hipokalemie - Edem pulmonar