Transcript Conséquences cardiovasculaires des apnées du sommeil (1)

HPN-LD Complications
• Gallbladder
- Sludge
- Lithiasis - stones
Simplified physiopathology
of sludge & lithiasis during
(H)P N
Cholesterol cristals
GI (upper surgery)
*35% Lithiasis or L/Sludge
Ca-bilirubinate cristals
Octreotide
Messing B et al Gastro 1983; Cano N et al, Lancet 1983 & Gastro 1986
* Roslyn JJ et al , Am J Surg,1984; * Rejasse D et al GCB 1999.
BM0083
Sludge & lithiasis gallblader occurence during and after Exclusive PN,
* indicates lithiasis within the sludge.
Messing et al Gastro 1983
Biliary complications of stones during LT-HPN
- Study
Roslyn 1983/4 Rejasse 1999
- HPN duration
> 3 months
15 (2-204)
- n patients
138
153
- no previous biliary
109
119
- Biliary Lithiasis
38 (35%)
40 (34%)
- Biliary complications
25 (23%)
8 (7%)
Colic/angiocholitis
6
5
Acute cholecystitis
19
1+ 2 pancreatitis
- Causative Factors
Starvation
+
+
Ileopathy
+
borderline
Opiates/anticholinergics
+
absent
- Cholecystectomy
Post-op complications
14 (55%)
1(12%)
Mortality
3 (11%)
0
- Prophylactic Cholecystectomy
yes
yes if...
Roslyn JJ Gastro 1984 & Am L Surg 1984; Rejasse GCB 1999 (A)
Simplified physiopathology
of sludge & lithiasis during
(H)P N
Cholesterol cristals
GI (upper surgery)
Ca-bilirubinate
cristals
Octreotide
Avoiding post op fasting and exclusive HPN may prevent
prophylactic cholecystectomy in - lithiasis negative - HPN patients
HPN-Liver Complications
• liver abnormalities
HPN-Associated-Liver Disease
Elemental liver lesions during HPN
Macrovacuolar steatosis
Portal inflammation
Ductular proliferation
Hepatocyte necrosis
Microvacuolar steatosis
Macrophage proliferation
Extensive fibrosis
25%
Cirrhosis
50%
Glucose based Lipid based
PREVALENCE of CHOLESTASiS in NP
PARENTERAL NUTRITION GLUCIDS & LIPIDS
1
45 – 60 Kcal.Kg.J :
P.A.L.K :
BILIRUBINE :
2
25 à 60%
12 à 30%
30 – 40 Kcal.Kg.J :
P.A.L.K. :
BILIRUBINE :
15 à 25%
5 à 10%.
Allardyce 78, Messing 82, Wagner 83, Bengoa 85
Carpentier 78, Jeejeebhoy 76, Bowyer 85, Beau 88
Natural history of HPNALD
% patients
Cholestasis :
65%
Fct < 50% :
9%
Bili > 60umol/l :
37%
Extensive fibrosis : 26%*
Hypertension portale :16%
Cirrhose :
6%*
Hemorrhage :
2%
Encephalopathy :
5%
occurrence (mo)
6 (2- 155)
10 (2- 117)
19 (3- 100)
26 (2- 148)
35 (7- 95)
37 (26- 77)
42 (24- 65)
104 (16- 155)
* data in 57 patients (calculated for 90) Cavicchi M et al Annal Intern Med 2000
HPN-Associated Liver Disease
 HPNALD in intestinal failure adult patients :
 Increased with HPN duration :
- 26 (17-35)% after 2 years
- 39 (28-50)% after 4 years
- 50 (37-63)% after 6 years
- 53 (39-67)% after 8 years
 Was complicated in 41% of cases
with 2.4(1-6) events per patient
 Was responsible for one among 4 deaths.
Cavicchi M et al Annal Intern Med 2000
PROBABILITY OF BEING FREE OF BIOLOGICAL &
HISTOLOGICAL COMPLICATIONS IN HPN-ALD
Cavicchi M et al Annal Intern Med 2000
PROBABILITY OF BEING FREE OF LIVER
COMPLICATIONS ACCORDING TO IV LIDID INTAKE
Cavicchi M et al Annal Intern Med 2000
(Long-term) HPN Associated liver disease:
Main physiopathological components*
Chronic Cholestasis
PN-dependent
LCT (w6) emulsion:
hepatocytes/ macrophages
Patient-dependent
microsteatosis,
phospholipidosis
Macrophages (Kuppffer):
decreased bacterial clearance
Deficit in tauro-Conjugates BS
ductular
lesions
Excluded segment (s),
bacterial translocation
sepsis
Very short bowel/ no ileum
extensive fibrosis, cirrhosis
° BS = Biliary salts
* Hypernutrition per se and through imbalance
between pro & antioxydants promoting peroxidation
of various substrates, notably IV lipids.
BM.HPNALD.ESPEN.
PN « TOXICITY » AND HEPATOPATHY
? EXCESS OF
? DEFICIENCY IN
• Vit. A*
• Selenium
• Cu.
• Vit. E *
• Fe*
• Sulfur AA (glutathion).
• Mn.
• Carnitine
• Choline*
• Alu*
• Phospholipids*
• P.U.F.A (soya)*
• Others micronutrients...
* Strong arguments for implication
• Others
micronutrients...
BM.
(Long-term) HPN Associated liver disease
• Best treatment : prevention through adapted IV
• « no hyperalimentation » with sufficient micronutrients
• if « normonutrition », no more than 33% of energy as lipids
• IV soya lipids : Less than 1g / Kg /d (20 or 30%)
or 100 g / Wk to avoid EFA deficiency
• IV Soya lipids = MCT/LCT. Structured : ?. Olive oil : ≥
• supplement PUFA with -tocopherol (oral + IV)
• Treat « contributive » patient’s covariables
• encourage enteral feeding as much as possible
• avoid or treat sepsis
• treat bacterial overgrowth
• nourish excluded segments especially colon (SCFA)
• decrease or stop some of the trace metals if cholestasis
•Curative : Ursodeoxycholate ;
hope with methyl donors / taurine enriched AA
HPN COMPLICATIONS
3 additional slides
B Messing.
Approved centre for Intestinal failure. Paris
Renal function impairment
Renal focal tubulointerstitial fibrosis with short bowel syndrome: report of a case.
Hebiguchi T et al. Surg Today. 2002;32(7):646-50.
SBS 3yr old. TPN. GH supplementation between 11 and 17yr.
At 20 yr old Hyperuricemia : Renal focal tubulointerstitial fibrosis
morphometric amelioration under Arg supplementation at 23 years of age (2 cycle PN/wk)
Extremely short small bowel induces focal tubulointerstitial fibrosis.
Hebiguchi T et al. J Pediatr Gastroenterol Nutr. 2001;32(5):586-92
Nitric oxide (NO) is synthesized from l-arginine by NO synthase (NOS), and NO is involved in the
regulation of blood flow in the kidney. Arg deficiency in SBS = increased urinary excretion of orotate
Experimental study strongly suggests that arginine deficiency causes focal tubulointerstitial
fibrosis in the kidney after massive SBR in rats
Orotic aciduria and plasma urea cycle-related amino acid alterations in short bowel
syndrome, evoked by an arginine-free diet. Pita AM et al JPEN 2004;28(5):315-23
Four stable SBS (30-100 cm) adult patients : L-amino acid arginine-free diet (egg pattern) for 5 days
(0.9 g protein equivalent/kg/d). Significant decreases in plasma levels of arginine, ornithine, occurred at
day 5, ammonium concentrations remained normal. a peak of orotic aciduria at day 4 (14-fold vs
baseline) and significant decreases in uric acid and urea excretion.
Oral diet provides 5 g of Arg/d is sufficient to prevent Arg deficiency: Pita at al Clin Nutr 2003; 22: 93-8 BM2005
What is your micronutrient-deficiency diagnosis ?
By courtesy of F Marrache and M Lemann MDs, Paris, France
X-ray diffractometry showing Ca-Bilirubinate cristals
BM 0083a