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Complications of parenteral nutrition
Dr Alison CulkinLead Intestinal Failure Dietitian
St Mark’s HospitalPENG PN study day 2018
NCEPOD 2010
http://www.ncepod.org.uk/2010report1/downloads/PN_report.pdf
% of patients
No of patients
Good practice 19.5% 171
Metabolic complications
39.3% 249
Avoidable 49.4% 81
Inappropriately managed
15.5% 30
Session outline
•Catheter related bloodstream infections•Glucose & lipid abnormalities•Parenteral nutrition associated liver disease•Micronutrient deficiencies
Do you have a CVC complications protocol?
YesNo Don’t know
Catheter-related infection (CRI)
O’Grady et al (2011) Guidelines for the prevention of intravascular catheter-Related Infection, Clin Infec Dis, 52:e162
Localised Systemic
Infusate related
Catheter associated
Catheter related
Exit site infection
Tunnel infection
Cuff infection
In tunnelled CVC local infection is rarely associated with systemic infection
Exit site infection
Erythema or induration within 2cm of exit site in absence of bacteraemia
Cuff infection
Isolated infection affecting cuff
Tunnel infection
Erythema or induration > 2cm from exit site
Overgranulation
Granulation tissue at exit site
Treating CRBSI
Removal● Septic shock● Fungal & Staph Aureus infections● Positive blood cultures after 48 hours of treatment● Implanted port
Salvage● Targeted antibiotic therapy via CVC● Seek microbiology guidance● Optimum duration of therapy has not been determined● BIFA statement1
Removal Salvage
1 https://www.bapen.org.uk/pdfs/bifa/recommendations-for-crbsi-diagnosis.pdf
Prevention
Healthcare workers caring for patients with intravenous access devices should be trained and assessed as competent in consistently adhering to practices for the prevention of catheter related bloodstream infections
Loveday et al (2014) epic3 Guidelines, J Hosp Infect, 86 S1, S1
CVC related thrombosis
Affect 35-65% long term devices
● Often asymptomatic
Strategies which may influence incidence
● Avoid dehydration● Use the smallest size CVC possible● Minimise insertion site trauma● Right vs left side placement● Tip position● Tip integrity
Endothelial trauma
StasisPlateletadhesion
Loveday et al (2014) epic3 Guidelines, J Hosp Infect, 86 S1, S1O’Grady et al (2011) Guidelines for the prevention of intravascular catheter-Related Infection, Clin Infec Dis, 52:e162
Virchow’s triad
Reducing thrombosis
Cadman et al (2004) Clin Radiol, 59: 349
48% CVC tips too high on transfer
The risk of thrombosis is significantly increased with proximal SVC tip position
Catheter tip Thrombosis%
Proximal 42
Intermediate 5
Distal 3
Treatment optionsThrombolysis
● Alteplase +/- heparin
Mechanical interventions● Balloon angioplasty
● Venoplasty
● SVC filter
● Recannalisation
Surgical interventions● Thrombectomy
● Venous bypass
Pironi et al (2016) ESPEN Guidelines on chronic IF in adults, Clin Nutr, 35, 247
Session outline
•Catheter related bloodstream infections•Glucose & lipid abnormalities•Parenteral nutrition associated liver disease•Micronutrient deficiencies
HyperglycaemiaBlood glucose monitoring essential• Risk of hyperglycaemia in obese and diabetic patients can be reduced if
initial amounts of glucose in PN are <2g/kg/d until normoglycaemiaachieved1
Workshop case study • 125kg x 2g = 250g = 1000kcal
1. Barazzoni et al (2017) Clin Nutr, 36:355
Glycaemic control in non ICU
Olveira et al (2015) Nutrition, 31:58
N = 605BMI = 25.2±5.5
Kcal/kg = 25.1±5.7Days on PN 13±11
Hyperglycaemia(>10mmol/L)↑ Risk of death Malnourished
Older?Sicker as CRP ↑
& albumin ↓
Hypoglycaemia (<3.9mmol/L)Associated with
↓BMIPN durationHigh blood
glucose variabilityOlveira et al (2013) Diabetes Care, 36:1061
ESPEN: Reduce glucose in PN if blood glucose >10mmol/L (Weiman 2017, Clin Nutr, 36:623)
How often do you measure blood glucose?
Every 4 hours
Every 6 hours
Every 8 hoursOther frequency
Frequency of blood glucose monitoringDoes reducing frequency of blood glucose testing in stable non ICU patients reduce costs without increasing episodes of hyperglycaemia? Pre and post guideline development data collected
n=171 Pre (n=86)
Post (n=85)
P value
Total number of tests 25 23 0.011
Number of tests/patient 3.6 2.9 <0.001
Mean glucose (mg/dL) 126 129 0.005
Conclusion: new guideline reduced number of tests by 20% impacting cost and patient comfort without increasing blood glucose or glycaemic events
Ratliff et al (2018) Nut Clin Pract, in press. https://onlinelibrary.wiley.com/doi/pdf/10.1002/ncp.10020
Rebound hyperglycaemiaRebound hypoglycaemia with cyclical feeding?• Four studies comparing abrupt vs tapered in short term PN and no
difference1
Patients at risk• NBM• On Insulin• Octreotide
1. Stout & Cober (2010) Nutr Clin Pract;25:277
Do you measure blood triglycerides?
Yes
No
Once a dayOther frequency
Hypertriglyceridaemia Occurs if metabolic capacity to clear lipid exceeded
1. Llop et al (2003) Clin Nutr, 22:577
n = 260TG <3mmol/L
Days on PN ≥7 daysLipid 0.83±0.37g/kg
TG >3mmol/Ln=68 (26%)
62 (91%) ≥ 1 risk factorAKI
PancreatitisSteroids
Hyperglycaemia
Treatment
• Aim to avoid triglyceride >5mmol/dL, although evidence lacking1
• Take care where blood sampled• May need to discontinue PN for 4 hours• Should resolve on reducing lipid content• Avoid overfeeding from glucose
1. Braga et al (2009) Clin Nutr, 28:378. 2. Llop et al (2003) Clin Nutr, 22:577
Session outline
•Catheter related bloodstream infections•Glucose & lipid abnormalities•Parenteral nutrition associated liver disease•Micronutrient deficiencies
Abnormal LFTs
How common are abnormal LFTs in patients on PN?
Is it the PN?
Abnormal LFTs & short term PN• 58 patients receiving PN • 48 (83%) fistula, obstruction, ileus, failed EN
Baker & Nightingale (2004) Clin Nutr;23:864
• 60% LFTs worsened on PN• 30% LFTs resolved on PN
Abnormal LFTs before PN (34% patients)
• 46% sepsis• 24% underlying liver disease
Abnormal LFTs on PN (9% patients)
What are the causes of abnormal liver function tests?
What can we do to change this?
Causes
LFTsMedications
Sepsis
AKI/CKD
Pre-existing liver disease
Underlying disease
Gallstones
NBM
Gabe & Culkin (2010) Frontline Gastroenterology 1:98
Liver function testsFunction Causes of raised level (liver) Other causes
Bilirubin Breakdown of haem in RBC Cleared by hepatocytes Conjugated and secreted in bile
Hepatic: cirrhosis, viral hepatitis –would be associated with other abnormal LFTs
Prehepatic: ↑ bilirubin production (haemolytic anaemia, internal haemorrhage, Gilberts syndrome)Post hepatic: problem with excretion (obstruction of bile duct eg gallstones)
Alkaline phosphatase (ALP)
Enzyme in the cells lining the biliary ducts of the liver (but also bone & placental tissue)
Marked elevation in cholestasis (often with raised GGT more than ALT/AST), bile duct obstruction or infiltrating disease of the liver
Non liver causes more common if ALP raised in isolation. As ALP also present in bone, levels ↑ when increased bone turnover (adolescence, fracture) Pagets disease (elderly), metastasis and 3rd trimester of pregnancy
Alanine transaminase (ALT)
Aspartate aminotransferase (AST)
Enzymes normally inside hepatocytesALT more specific to the liver
AST also found in cardiac, RBC and skeletal muscle
Usually represent hepatocellular damage (viral hepatitis, paracetamol overdose) where marked ↑ seen
Raised AST may indicate issue with cardiac, RBC and skeletal muscle
Gamma-glutamyltransferase(GGT)
Related to bile ducts. May be ↑ with even minor, sub-clinical levels of liver dysfunction
Most common due to alcohol abuse (isolated ↑ or in combination with AST) Steatosis (fatty liver) or non-alcoholic steatohepatosis (NASH) caused by obesity & hyperlipidaemia
If NASH treat underlying causes such as raised cholesterol and obesity
Newsome et al (2018) Guidelines on the management of abnormal liver blood tests, Gut, 67:6
What can we do?
AssessMedications
Sepsis & collections
Liver screen
UltrasoundEnergy
requirements
Energy delivered
Lipid delivered
Evolution of lipid emulsionsGeneration Description Lipid types Brands
1st Conventional lipid LCT (soybean oil)LCT (soy/safflower oil) Intralipid
2nd Lipid emulsions with reduced PUFA
MCT/LCTStructured lipids (MCT/LCT)Olive oil
LipofundinStructolipidClinoleic
3rdLipid emulsions with reduced PUFA & specific ω6/ω3 FA ratio
Fish oilSoy/MCT/FOSoy/MCT/olive oil/fish oil
OmegavenLipidemSMOF
ASPEN: Clinical role for alternative intravenous fat emulsions (2012) Nut Clin Pract; 27:150. Raman et al (2017) Nutrients, 9:388
Lipid emulsions
Soya (LCT)High in n-6 → oxidative
stress, immune dysfunction/ inflammation
LCT/MCT Slower release into
bloodstream1
Reported benefitsNitrogen sparing2
Improved liver function3
LCT/Olive oil↓ n-6 ↑ n-9
Vitamin E: antioxidant
Reported benefits4,5
Liver function Oxidative stress
Immune function
Fish Oil↑n-3
Reported benefits immune
function6,7
Reduced length of hospital & ICU
stay8
1. Chambrier et al (2006) Nut Clin Pract, 21:342. 2. Lindgren et al (2001) Clin Nutr, 20:43. 3. Piper et al (2008) Eur J Anaesthesiol, 25:557. 4. Sala-Vila et al (2007) CurrOpin Clin Metab Care 10:165. 5. Wanten (2009) JPEN, 33:450. 6. Wang et al (2009) JPEN, 33:450. 7. Liang et al (2008) World J Gastroenterol, 14:p434. 8. Waitzberg & Torrinhas (2009) Nutr Clin Pract. 24:487
Choice of lipid
Soya (Intralipid)LCT/MCT (Lipofundin)LCT/Olive oil (ClinOleic) LCT/MCT/OO/FO (SMOF)
Lipid emulsions in PN
Which one should we use?Strength of evidence
Critical appraisal
Fish oils: A systematic reviewShort term PN
https://www.ncbi.nlm.nih.gov/pubmed/?term=Abbasoglu+2017+JPEN
Aim: To assess the quality of RCT investigating the use of parenteral fish oil (FO) lipid emulsionsQ: Does administering FO alone or as part of a multi-lipid emulsion improve outcomes
Assessed using Cochrane Collaboration criteria (grades bias as low, high or unknown risk)• Random sequence generation• Allocation blinding• Blinding of participants and personal• Blinding of outcome assessments• Incomplete outcome data• Selective reporting• Other bias
ResultsShort term PN
19 • Inflammatory & immune markers
13 • Infection or sepsis
29 • General clinical outcomes
3 • Clinical outcomes in sepsis
Conclusion: very little high quality evidence that fish oils have a beneficial effect
https://www.ncbi.nlm.nih.gov/pubmed/?term=Abbasoglu+2017+JPEN
Infusion ratesContinuous (over 24 hours)• Enables large volumes to be infused• Associated with continuous insulin secretion & lipogenesis
Cyclic (over 12-16 hours)• Permits mobilisation of free fatty acids from stores during non infusion period• Reduces risk of parenteral nutrition associated liver disease1
• Reduces thrombophlebitis in peripherally-fed patients2
• Enables rehabilitation/physiotherapy • Gradual wean from 24 hours
1. Hwang et al (2000) Hepatogastroenterology, 47:1347. 2. Kerin et al (1991) Clin Nutr, 10:315
Practical management of abnormal LFTsAcute IF (Type 1)• Look for other causes • Do not overfeed• Encourage oral• Daily lipid but what type is best? • Anti-inflammatory & anti-oxidative properties of fish oil is
attractive but limited evidence
Chronic IF (Type 2)• Look for other causes• Do not overfeed• Cyclical feeding• Limit lipid (<1g/kg/day)• Do not increase glucose calories to compensate• Decrease further/stop lipid• Use 2nd or 3rd generation but need more studies
Session outline
•Catheter related bloodstream infections•Glucose & lipid abnormalities•Parenteral nutrition associated liver disease•Micronutrient deficiencies
• Which tests analysed at your Trust?• What has to be sent away?• How long does it take to get results? • How do you interpret the results?
Micronutrients: what should you do?
Checking micronutrients
CRP <30
CRP <20CRP <10CRP <5
Duncan et al (2012) Am J Clin Nutr, 95:64. www.trace-elements.co.uk
A reliable clinical interpretation only if CRP <20 mg/L Zinc <10 mg/L Selenium and vitamins A and D <5 mg/L Vitamins B-6 and C
Vitamin D
• Common deficiency1
• Ergocalciferal 300,000IU IM stat dose• Second dose 3 months later, or by high dose oral therapy • Hospital oral liquid preparation 3,000 units/ml
• 15ml ONCE A WEEK • Does not contain gelatine or peanut oil. Suitable for
vegetarians, vegans, and those with nut allergies. Halal compliant
1. Fan et al (2017) Nutr Clin Pract, 32:258
Selenium Deficiency common1
High risk: CRRT, high U/O, diarrhoea/fistula output, multiple drains, steroids & statins2
Concentrations reduced during APRTreatment • IV 500ug for three days• Dilute 10mL of Selenase® in either 100mL or 250mL of 0.9%
sodium chloride solution or 5% glucose solution and infuse over 30 minutes
• Recheck concentration 4 weeks later• Try oral Selenase® 100-500ug/day• Double dose in PN or change to Nutryelt® or Addaven ®
1. Shenkin A. Selenium in intravenous nutrition. Gastroenterology 2009; 137: S61. 2. Jin et al (2017) Nutrients, 9:440
Zinc • Deficiency common1
• Bound to albumin• Concentrations reduced during APR• Major illness (CRP 100-200mg/L) causes a 40-60% reduction
and by 50% post-operatively2
• High GI losses
Treatment depends on concentration• Oral Solvazinc 45mg 1-3 times per day • Double dose in PN or change to Nutryelt® or Addaven®• Recheck concentration 4 weeks later
1. Jeejeebhoy K. (2009) Gastroenterology, 137: S7. 2. Jin et al (2017) Nutrients, 9:440
Conclusion
Monitoring vital to minimise complications
More robust RCTs required
Look for other causes of abnormal LFTs
MDT approach vital
Perfect area for supplementary prescribing