Parenteral and enteral nutritionSHANKAR ZANWAR

Parenteral nutrition

History dates back to William Harvey’s(1616) description of circulation to first successful saline infusion(1833) to

Stanley Dudrick 1969 – TPN in puppies – protein hydrolysate and dextrose

EN – formula feeds came in vogue in 1960s and 70s with US manned space program experiments.

Parenteral nutrition Supplying nutrients directly into venous syst. – PN

It delivers – carbohydrates as dextrose, proteins as AA, lipids as intravenous fat emulsions(IVFEs)

Usually delivered over 12-24 hours

Formulations Protein – 4Kcal/g IVFEs – 10Kcal/g (9Kcal fat + 1 Kcal emulsion) Carbohydrates – 3.4Kcal/g Osmolality – 1800-2400mOsmol/L Approx 30-40 gram protein and 1000-1200Kcal

Requirements and administration

Protein – 1-2g/kg/d Restricted in

azotemia needing dialysis Severe HE

Fats -1g/kg/d Restricted if hypertriglyceridemia >400mg/dl But at least 10% of estimated given to supply essen. FA

Remainder of calories by carbohydrates

Fluid req- 20-30ml/kg/d

Started with ½ caloric needs for first 24hr, increased to full over 72 hours – avoids refeeding syndrome.

Prescribing central - PN

Micronutrients Electrolytes, multivitamins

Unmonitored non ICU setting K+ not to exceed >10mEq/hr

Calcium and PO4– sum should be <45 prevent pptn

Withhold Cu and Manganese in cholestasis Selenium in renal compromise

Zinc supplementation in diarrhea, high o/p fistula

Serum glucose level to be maintained in 110-150ml/dl

Peripheral PN Hyperosmolar solution – chemical thrombophlebitis

Osmolality restricted to ≤900mOsmol/L

Thus dextrose conc. should be ≤ 10% and fluid requirement is increased

Infusion rates then become >150ml/hr

Thus limited for pts. with non functioning GI tract good peripheral access Tolerate large amt. of fluids(avoided in renal/CLD) No pressing electrolyte needs Nutritional needs for 5 days to 2 weeks

Monitoring

First few days daily Electrolytes – including Ca, Phosphorus BUN After stabilization weekly and thereafter monthly

CBC monthly

Relevant case Zn, selenium, Cu, chromium, B12,B6

Iron is not a supplement in TPN if IDA features in CBC - iron SOS

Vascular access devices Central catheters

Non-tunneled Tunneled

Peripherally inserted central catheters - PICC

Implantable ports

Non tunneled Short term use Easy to insert More prone to infections

Tunneled When cath. needed for 1-3m Tunneled sub-cutaneously Physical barrier to infection Prevents accidental

dislodgement E.g. – Hickman, Groshog,

Broviac

Implantable ports Placed s.c. in chest wall Require specialized access needle for

infusion Used when therapy needed for long

term

PICC Can be used in IP and home When needed for <6months Less chances of hemothorax

Both have, longer failure free duration, lesser infection rates than CVC

Complications - metabolic

Commonest – hyperglycemia >110-150ml/dl sugars increased morbidity and mortality

Van, Neurology, 2005 sliding scale insulin used, total amount of insulin in next PN =2/3

used in sliding scale Permissive under feeding

Refeeding syndrome Sudden provision of large amount of calories in undernourished ↑insulin↓K, Mag, PO4(intracellular shift) Na retention fluid shifts CHF

and neurological sequelae.

Liver biochemical derangements

↑ AST and ALT – 2X ULN

Steatosis Prominent in periportal areas Mostly asymptomatic Secondary to overfeeding

Cholestasis ↓enteral stimulation ↓cholecystokinin impaired contractility GB stasis sludge and stone

formation calculous and acalculous cholecystitis Catheter sepsis increase risk of cholestasis ↑ALP, GGT & conjugated bilirubin

Patients with short bowel synd. more likely to develop liver disease

Choline deficiency like culprit

Fish oil based TPN with Ω-3 FA containing formulations can reverse PN induced liver disease – studies proven in children

Vanek, Nutr Clin Pract 2012

Catheter related complications Incidence rates 1-20%

Early Hemothorax Pneumothorax Brachial plexus injuries Hematoma Subcutaneous emphysema

Late Sepsis Thrombosis Catheter occlusion Breakage Dislodgement Air emboli

Catheter infection – MC – touch contamination

Catheter tip culture – most sensitive modality

If blood culture +ve for bacteria – treated with cath. in situ

Fungal infection – removal of catheter mandatory

Addition of 1000U/L of heparin in PN prevent thrombus formation ↓ inf risk, but not to be used routinely

Locking antibiotics vs flushing with 100% alcohol both equal

Prophylactic antibiotics for those with recurrent infec.

Catheter thrombosis – secondary to vessel wall irritation

Usual component fibrin

Symptoms Neck pain Neck swelling ↓ catheter function Ant chest wall vein distension

Flushing with saline as useful as with heparin in preventionSteiger, JPEN, 2006

Treatment – streptokinase - bolus/ infusion Medication precipitates treated with sodium hydroxide/HCL depending on nature of drug

Enteral nutrition Maintains structural and functional integrity of

GIT

Structural maintenance Villous height Epithelial cell proliferation Brush border enzyme production Secretory IgA production

Functional maintenance Maintaining gap junctions Release of agents like – gastrin, CCK, bile salts,

pancreatic enzymes Mucous secretion and intestinal contractions All these prevent pathogenic bacterial overload

Naso-enteric tube access Indications

Intolerance to gastric feeds d/t gastroparesis Gastric outlet obstruction Esophagectomy/gastrectomy

Risk of aspiration no different from NG feedings Neumann DA, Crit Care Med, 2002

Complications Aspiration pneumonia Nasal mucosal ulceration, bleeds Pharyngitis, otitis, sinusitis Pneumothorax TOF Tube migration and obstruction.

NJ tube placement

Blind techniques Thurlow method

Use of stylet filled NJ tube, cork screw movement in R lat decubitus position, track using stethoscope, success 83%

Use of un-weighted tubes success – 92% vs 56% weighted Magnetic steering technique Self propelled tube – spiral end - 50% success

Endoscopy/ fluoroscopy methods – success 90-100% Over the guidewire technique Through the scope 8-10Fr tubes Hemoclip can be used to keep it in place

Cautions

Prone for clogging

Never check for residual content by aspirating, poor indicator of residual content in jejunum ↑ risk of clogging

Flush NJ tubes after every tube feeding

KCl or theophylline should not be given with feeds may coagulate feeds and obstruct tube

PEG

Endoscopic gastrojejunostomy 2 methods

Jejunal extension through PEG(JET-PEG) Direct – percutaneous jejunostomy (DPEJ)

JET-PEG 9-12 Fr J tube passed through PEG over GW Avg longevity – 120 days Aggressive flushing to avoid clogging Clogging rates 3.5-35% No residual checking >50% Reintervention in 6 mon – MC cause tube

migration Prevention – placing a hemoclip at the distal end

Direct percutaneous jejunostomy Using enteroscope/ pediatric colonoscope

Puncture as in PEG beyond D4

Technical success 68-95%

Best suited when long term access is needed >6 months

Tube left unclamped just after procedure to decompress insufflated air

Enteral feeding should be initiated through pump instead of bolus avoids dumping syndrome

Complications Bleeding Abdo. wall abscess Enteric ulcers Peristomal infection Volvulous and intra peritoneal leakages

Replacement – non balloon, internal bolster type to be used since balloon type may cause obstruction and leakage

Surgical and radiologically placed enteral access Surgical procedure are inferior to endoscopically placed access

Cost savings Less operative time Reduced morbidity

Fluoroscopic access – technically more demanding, Major complication rate higher Though pooled fatality rate compared with endoscopic methods same

Clin Otolarynol, 2009

Enteral feeding Methods

Bolus – 200 – 400ml over short period Intermittent – pump/gravity assisted Continuous –over 12-24hr – using pumps

Monitoring tolerance Pain Distension Nausea Vomiting Stool/flatus Not to check residual volume

Preventing aspiration Head end elevation 30-40⁰ Promotility drugs – metoclopramide/erythromycin When evidenced aspiration on NG change to enteral feeding

Enteral formulations

1. Blenderized formulations Blended table food- high viscosity, osmolality Need functional GI tract Not recommended for small caliber feedings

2. Standard polymeric formulae Lactose free and gluten free Intact macronutrients Contains – 45-60% carbs, 15-20%proteins, 30-40%fat Usually 1kcal/ml – isocaloric 80-85%free water

3. Specialty formulations – for various diseases Diabetic formula Renal or hepatic formula Very little evidence to show survival benefits of these formulae

4. Immune modulating formula – composed of Higher arginine- ↑cell growth, NO substrate Glutamine Ω FA Antioxidants Nucleotides

Should be initiated 5-7d prior to surgery Benefits shown in pts. with burns, on ventilators Benefits include ↓need of antibiotics, MOF rates and LOS

Complications of enteral feeding

GI side effects in 15-30% MC

Nausea and vomiting Abdominal distension Cramping Diarrhea

Except for diarrhea all others can be resolved by slowing the feed rate

Diarrhea – causes

change of medications to liquid form – solvents(sorbitol base) may cause diarrhea

High osmolarity feeds >700mOsmol/Kg Hypoalbuminemia – intestinal wall edema – no data to support IV

albumin helps

Anticholinergics may help ↓ bowel motility

Phenytoin and Ciprofloxacin should be avoided with feeds bind with enteral feed and adheres to tube wall obstruction.

Nutrition in disease state

1. Intestinal failure - Short bowel syndrome - <200cm remnant Crohn’s disease Post resection

Stages – Stage 1 – fluid shift Stage 2 – adaptive phase enteral nutrition(EN) is imp. Stage 3 – stable

If less than 80cm of SI left with no colon Parenteral nutrition

Citrulline predictor of permanent PN if <20U/L PPV 95% and NPV 86%

Crenn, Gastroenterology, 2000

2. Pancreatitis Multiple trials have proved benefits of EN over PN

Role is limited in situation of severe ileus EN benefits - ↓ mortality, infectious complications, MOF, surgical interventions

Yi F Intern Med. 2012

Early vs late enteral nutrition – controversy Earlier trials and metaanalysis – early feeding was beneficial over late

reducing complications as above Li JY, Timing of nutrition metaanalysis, PLoS One. 2013

RCT by Dutch group(PYTHON trial), no difference in outcomes in very early feeding vs on demand feeds

Prolonged gut rest

Atrophy and ↑gut

mucosa permeability

Overgrowth of pathogenic

bacteria

Increased bacterial

translocation Infected necrosis

NG vs NJ feeding NG at slow rate of infusion is well tolerated as NJ feeding, no difference in

out come measuresKumar A, J Clin Gastroenterol. 2006

Immuno-nutrition Moderate amount of evidence to support immuno-nutrition. 4 RCTs, ↓LOS, ↓ gut permeability, ↓ plasma endotoxin level but no difference in out clinical

comes.Pearce CB, JOP. 2006

Use of probiotics PROPATRIA trial by DPS group – MOF is more common in probiotic group used

in SAP, thus avoided.Besselink MG, et al, Lancet 2008

Liver disease Prevalence in malnutrition in CLD – 50-90%

Raman M, Clini Gastro-hepato 2012

Mortality in CLD in malnourished vs non malnourished – 14.1 vs 7.5%Sam J, Liver Int 2009

Causes of malnutrition and anorexia Stomach compression by ascites ↑TNF α and leptins ↓ Bile salt ↓ fat soluble vitamins Hypoalbuminemia intestinal wall edema Porto-systemic shunting of unmetabolized nutrients ↓glycogen synthesis and insulin resistance ↓ muscle mass

Role of br. chain amino acids(BCAA), metabolism is not in liver, in CLD normal balance b/n BCAA and aromatic AA is disturbed

In CLD, ↑AAA pseudo-neurotransmitters HE

BCAA supplementation ↓ NH3 because BCAA metabolism in muscles supplies C skeleton for formation of glutamine.

RCT with 174 pts. – BCAA ↓ decompensation and death. Marchesini, Gastroenterology 2003

Another RCT – 12 g of BCAA significant ↓ in HE and refractory ascitesMuto, Clin Gastro Hepato 2005

Micronutrients Thiamine – alcoholics and also in Hep C – Korsakoff’s dementia Vitamin A – deficiency considered as risk factor for HCC Vitamin E – steatohepatitis Zinc – prevention of HE Copper and Manganese to be avoided cirrhosis and cholestasis in

PN formula since excreted in bile

EN preferred over PN, ↓ length of stay in ICU and ↓ incidence of sepsis.

Critical illness Goals – avoid catabolic response, prevent oxidative cell injury

and favorable immune response modulation.

Albumin and transferrin are not true indicators of nutrition in critically ill.

Nutrition initiated early EN preferred over PN

EN started within 24 to 48 hours

Can be started even in absence of bowel sounds and failure of passage of stools/ flatus

Rare complication of EN ischemic bowel injury, thus should be avoided in shock/vasopressor use.

Can still be given at slow rate with monitoring of BS, AG and stools/flatus and metab. acidosis

If risk of aspiration high SB feeding may be started.

If EN not feasible PN after 7 days

RCT early(48h) vs late(7 d) PN late – early discharge, less infection, cholestasis, venti/dialysis. (90 day mortality – no diff.)

Casaer, Intensive care med, 2011

Hypocaloric PN to start with – giving 80% of calorie req. prevent hyperglycemia

Long chain Ω-3 FA – immunosuppressive ↓ pneumonia, catheter asso. sepsis, venti need.

PO4 to be supplied adequately component of ATP – diaphragm function venti. needs

Thank you