1. Fluids and Nutrition in the ICU
Dr Paul Healey
John Hunter Hospital, Newcastle
August 2013

2. Bigger than Ben Hur !!

3. Outline Fluids and electrolytes Nutrition The refeeding syndrome
Basic physiology
Assessment of fluid status and fluid responsiveness
Fluids - Crystalloids and Colloids
Fluids - Costs
Evidence to guide fluid delivery
Case studies
Nutrition
Why is nutrition important in ICU patients
Enteral nutrition
Parenteral nutrition
Evidence for nutritional choices
Feed intolerance
Diarrhoea
The refeeding syndrome

4. Why fluid therapy 2nd most common medical therapy
Often prescribed by the most junior member of medical team
There is often confusion as to what end points to aim for with fluid therapy BP HR UO
CVP
Derived numbers such as SVV, VTI, PPV
Fluid prescription is mostly dependent upon your postcode.

5. Historical perspective
1832 – Cholera patient in Scotland who was critically ill and dehydrated given saline based solution instead of blood letting which was standard of care for the time
1876 – Development of Ringer’s solution by Sidney Ringer in London
1876 – Modification of Ringer’s solution to include lactate by Dr Alex Hartmann in the US
1940 – Use of albumin by US army in WWII
1950 – Development of the plastic catheter by Mayo Clinic Anaesthesiology resident Dr David Massa, which allowed widespread use of IV fluid therapy, despite the lack of any evidence of its potential efficacy
Called Ringer’s lactate in US
Called Hartmanns in Commonwealth countries
Ringer – used tap water one day rather than distilled water on experiments in isolated mice cardiac myocytes

6. Some basics
Water
Electrolytes

7. Physiology - Water

8. Physiology - electrolytes

9. Daily fluid and electrolyte requirements - Physiology

10. Physiology - electrolytes

11. Pathophysiology Traditional model – Starling model
Crystalloid – 20 mins intravascular compartment
Colloid – less than expected time in critical illness

12. Pathophysiology Revised model in pathology of critical illness
Importance of the endothelial surface layer (glycocalyx) in transvascular exchange
When ESL in tact and in euvolemia – colloids may sustain plasma expansion better.
However in critical illness with inflammatory degradation of the ESL that causes increased vascular permeablity there is increased trans-capillary escape of albumin and other colloids, which may explain their diminished benefit
In the major trials comparing colloid to crystalloid the ratio of dose was 1: , not 1:3 as was predicted
The increased transcapillary leak will also allow excess crystalloid to accumulate in the interstitial spaces and contribute to reduced organ function

13. Phases of resuscitation
1. Acute resuscitation
Goal is restoration of effective intravascular volume, organ perfusion and tissue oxygenation
Fluid accumulation and a positive fluid balance
2. Maintenance
Goal is maintenance of the intravascular volume
Prevent unnecessary fluid loading and mitigate fluid accumulation
3. Fluid removal
Goal is ‘active de-escalation’ with fluid removal
Secondary organ injury may result from failure to remove unnecessary volume

14. Case 1
75 year old female with septic shock likely secondary to urosepsis, retrieved from Belmont Hospital
Background
OA of knees
Ex-smoker 20 years ago
Management
CTKUB – NAD
3.5 L of Normal saline
IV metaraminol at 20mL/hr
Current observations
HR - 120
BP 65/35
SaO2 96% on 4L via np
ABG – pH 7.15, PaCO2 31mmHg, PaO2 85mmHg, BE -7mmol.L, Lactate 4.5mmol.L
How can I tell if she needs more fluid ??
If she does need more fluid – which one do I give, and how much ??

15. How to assess fluid status and fluid responsiveness
History
Illness history
Comorbidities
Treatment to now – fluid, vasopressors
Examination
Peripheral temperature
Vital signs (HR, BP, RR, capillary refill)
JVP, pulmonary oedema
Signs of end-organ hypoperfusion
Decreased LOC
Myocardial ischaemia
Decreased U/O
Investigations
Pathology (FBC, UEC, LFTs)
ABG – pH, BE, lactate
ScvO2
Other tests
Static variables
CVP
PCWP
Echocardiography – IVC diameter and collapse, LVEDA
Dynamic variables
Passive leg raise
Systolic Pressure Variation/Pulse Pressure Variation – arterial pressure waveform
Stroke volume variation – PiCCO
Echocardiography – cardiac output measures
Clinical studies have suggested that only 50% of haemodynamically unstable critically ill patients are fluid responsive.
SVV and PPV/SPV all require 8-10ml/kg tidal volume for accuracy (12-13% change predicting fluid responsiveness)
The hemodynamic effects of PLR must be
assessed by a direct measure of cardiac output or stroke
volume; assessing the PLR effects solely on the arterial
pulse pressure leads to a significant number of falsenegative
cases [51]. This suggests that in spontaneously
breathing patients, pulse pressure is not of sufficient
sensitivity for detecting changes in stroke volume.

16. Frank-starling principle

18. Goals of resuscitation
HR < 100
Normal RR and gas exchange
MAP >65mmHg (may need to be higher in patients with a history of hypertension)
CVP 8-12 mmHg or mmHg if intubated
Urine output : 0.5ml/kg/hr
Resolution of end-organ hypoperfuion :
Improving LOC
Lactate clearance of 10%
Lactate level < 2.0 mmol/L
ScvO2 >70%
Echocardiography
Filling state – IVC diameter and collapsability
Ventricular filling
Cardiac output

19. Case 1
75 year old female with septic shock likely secondary to urosepsis, retrieved from Belmont Hospital
Background
OA of knees
Ex-smoker 20 years ago
Management
CTKUB – NAD
3.5 L of Normal saline
IV metaraminol at 20mL/hr
Current observations
HR - 120
BP 65/35
SaO2 96% on 4L via np
ABG – pH 7.15, PaCO2 31mmHg, PaO2 85mmHg, BE -7mmol.L, Lactate 4.5mmol.L
How can I tell if she needs more fluid ??
If she does need more fluid – which one do I give, and how much ??

20. What fluid to give ??
The evidence

21. The SAFE-TRIPS study
Cross sectional study of 391 ICUs in 25 countries to describe the types of fluids administered during fluid resuscitation.
Data collected in 2007 and published in 2010.
Findings in a 24 hour period:
37.1% of patients received resuscitation fluid
Main indicators for administering crystalloid or colloid were impaired perfusion (45%) or to correct abnormal vital signs (35%)
Overall
colloid given to more patients than crystalloids (23 vs 15%) and
Colloid given in more episodes than crystalloid (48 vs 33%)
The choice of fluid was most strongly related to location of the prescriber

23. Crystalloids

24. Colloids
Albumin
Semi-synthetic colloids

25. Fluids - costs Normal saline (1 L) Hartman’s (1L) Plasmalyte (1L)
Voluven (500mL)
Albumin 4% (100mL)
Albumin 20% (500mL)
Packed Red Cells (1 U)
$1.15
$1.20
$2.40
$11.60
$65
$345

26. Fluids : The evidence

27. Colloids - Albumin
Albumin is a plasma protein with an average MW of 66kDa. In healthy humans it accounts for 80% of colloid oncotic pressure.
It has been available for human use since the 1940s.
Albumin is prepared by either cold ethanol (Cohn) fractionation or chromatographic purification of pooled donor plasma.
It is heat-treated at 60 C for 10 h and incubated at low pH to inactivate potentially transmissible viruses.
When infused in well hydrated individuals,
4% albumin will expand the plasma volume by an amount equal to the volume infused,
20% albumin will expand the plasma volume by approximately 4-5 times.

28. The SAFE trial (2004) The Saline versus Albumin Fluid Evaluation Study
An international multi-cente RCT of 6997 patients comparing the use of albumin vs NS for fluid resuscitaton in ICU
Conclusions
No difference in 28 day mortality
Possible improved outcome with albumin in severe sepsis : unadjusted RR 0.87 ( ), adjusted RR 0.71 ( )
Possible worse outcomes with albumin in TBI with an increased risk of mortality at 2 years : RR 1.88 ( )
?? ALBIOS trial (20% albumin)
About 1350 patients with severe sepsis or septic shock will be randomized to receive either albumin or crystalloids as fluid therapy. Volume replacement will be performed for both groups according to the early-goal directed therapy. Treated group will receive 60 gr albumin infusion after randomization, and gr albumin daily infusion to maintain serum album level equal or above 30 g/l. Control group will receive crystalloids for the entire study; albumin administration will be allowed only when daily serum albumin level will be lower than 15 g/l. Patients will be treated until the 28th day after randomization or until ICU discharge, whichever comes first.

30. Cochrane Review : Albumin

31. The CHEST trial
The Crystlalloid versus Hydroxyethyl Starch Trial (Myburgh et al 2012)
Involved 7000 general ICU patients who were randomized to masked fluid resuscitation with either HES 130/0.4 (Voluven) or normal saline while in the ICU
Conclusions:
Patients in the HES group received slightly less trial fluid (526 +/- 425 vs /- 488 ml per day in the first 4 days), and had higher CVPs
Fewer patients developed new circulatory failure (36.5 vs 39.9% P 0.03)
Ninety-day mortality was not significantly different between the groups, neither in the whole population (18 vs. 17%; P. 0.26) nor in the predefined subgroups.
More patients in the HES group received renal replacement therapy (7.0 vs. 5.8%; P. 0.04)
More patients in HES group had pruritus (4.0 vs. 2.2%; P< 0.001).
Paradoxically, HES preserved urine output better but at the expense of declines in glomerular filtration (increase in creatinine) when compared with isotonic saline

33. The 6S trial Scandinavian Starch for Severe Sepsis/Septic Shock Trial
This trial randomised 804 patients in the ICU with severe sepsis to resuscitation with HES 130/0.42 (Tetraspan) vs. Ringer’s acetate
Conclusions:
Haemodynamic parameters and total doses of trial fluid [median (interquartile range) 44 ml/kg (51) vs. 47 ml/kg (51)] did not differ between the groups.
The patients assigned to HES had higher 90-day mortality (51 vs. 43%; P. 0.03) and
The patients assigned to HES had increased risk of receiving renal replacement therapy (22 vs. 16%; P. 0.04) and red blood cell (RBC) transfusion (58 vs.46%; P< 0.001) compared with those assigned to Ringer’s acetate.
Post-hoc analyses revealed more bleeding events (23 vs. 15%; P ) in patients receiving HES.

36. Cochrane review – Colloids (2013)

37. Case 1
75 year old female with septic shock likely secondary to urosepsis, retrieved from Belmont Hospital
Background
OA of knees
Ex-smoker 20 years ago
Management
CTKUB – NAD
3.5 L of Normal saline
IV metaraminol at 20mL/hr
Current observations
HR - 120
BP 65/35
SaO2 96% on 4L via np
ABG – pH 7.15, PaCO2 31mmHg, PaO2 85mmHg, BE -7mmol.L, Lactate 4.5mmol.L
How can I tell if she needs more fluid ??
If she does need more fluid – which one do I give, and how much ??

38. Other controversies Fluid balance and mortality
Chloride and organ function
Sodium balance
Normal saline vs buffered crystalloid solutions
No fluids

39. Fluid balance
In experimental models of porcine septic shock, more vigorous fluid resuscitation was associated with greater hemodynamic stability, urine output, and preserved RBF; however, despite this apparent physiological benefit, high-volume resuscitation was associated with substantially increased mortality
The majority of human data is post-hoc associative and not causative – however there appears to be a trend (See table)
Increased mortality
Worse respiratory function
Worse renal fuction
Increased LOS

41. Fluids : The Chloride problem
Fluid resuscitation with Normal saline causes hyperchloraemic metabolic acidosis
Shaw et al (2012) Retrospectively reviewed a large clinical database of major abdominal surgical patients treated only with NS vs only Plasmalyte (30,994 in 0.9% saline arm vs 926 in Plasma-Lyte arm). They found after propensity matching, the 0.9% saline group had:
More fluid (1976 ml vs 1658 ml, p <0.001)
More buffer orders (6.3% vs 4.2%, p = 0.02)
Moretransfusions(11.5%vs1.8%,p<0.001)
Increased ventilator days (3.0 days vs 2.5 days, p <0.001)
A 5-fold greater chance of receiving dialysis (1% vs 4.8%, p <0.001)
But the balanced group had longer length of stay in the hospital (6.4 days vs 5.9, p < 0.001)
Yunos et al (2012) conducted a before after trial of 1533 patients in one Australian ICU. This involved comparison of a chloride liberal vs a chloride restrictive approach to IV fluid therapy.
Before – NS, Gelatin, 4% albumin
After – CSL, plasmalyte, chloride poor 20% albumin
Several studies have shown NS, compared to more physiological solutions containing near normal chloride concentrations, is associated with
delayed time to micturition,
decreased urine output
decreased sodium excretion

43. Fluids : The Sodium problem
Recommended daily intake = 1 mmol/kg
Point prevalence study across 40 ICUS including 356 patients demonstrated the median total sodium administered was 225 mmol (IQR of mmol) (Bihari et al 2012)
A recent small study of ICU patients (Bihari et al 2013) demonstrated that sodium balance can be independent of fluid balance. After 5 days of mechanical ventilation:
Cummulative fluid balance = -954mL
Estimated cummulative sodium balance = 258 mmol
Serum sodium increased from 140 to 147 mmol/L
Body weight decreased by -2.7 kg (SD 1.4 kg)
TBW decreased by – 3.4 L (SD 1.4 kg)
They postulated that sodium balance may correlate better with increased ECF volume and respiratory dysfunction
Therefore future studies may have to examine sodium balance and morbidity in critical care patients

45. Cochrane Review : Buffered vs non-buffered fluids
14 trials with 706 patients
Included trials of perioperative resuscitation
Excluded trials of colloids, hypertonic fluids and dextrose based fluids
Outcomes
Clinical
Mortality – no statistical difference
Renal function – no statistical difference
Renal replacement therapy – no statistical difference
Post operative nausea and vomitting – no statistical difference
Blood loss – no statistical difference
Red cell and plasma transfusion – no statistical difference
Platelet transfusion – increased in non-buffered fluid group
Metabolic
pH – lower in buffered group by mean of 0.06 ( ). This was not maintained on postoperative day 1
PaCO2 – higher in buffered group post op (1.2mmHg) and day 1 (3.3mmHg)
Base excess – mean difference of 3.5 mmol/L postoperatively and 2.5mmol/l on day 1
Serum sodium – higher post operatively in non-buffered by 2.7 mmol/L, no difference on day 1 post operatively
Serum chloride – higher post operatively in non buffered group 114 vs 107 mmol/l, and on day 1 postoperatively (116 vs 107 mmol/L)

46. No fluid ??
The data and safety monitoring committee recommended halting recruitment after
3141 of the projected 3600 children in stratum A were enrolled. Malaria status (57%
overall) and clinical severity were similar across groups. The 48-hour mortality was
10.6% (111 of 1050 children), 10.5% (110 of 1047 children), and 7.3% (76 of 1044
children) in the albumin-bolus, saline-bolus, and control groups, respectively (relative
risk for saline bolus vs. control, 1.44; 95% confidence interval [CI], 1.09 to 1.90;
P = 0.01; relative risk for albumin bolus vs. saline bolus, 1.01; 95% CI, 0.78 to 1.29;
P = 0.96; and relative risk for any bolus vs. control, 1.45; 95% CI, 1.13 to 1.86; P = 0.003).

49. Case 1
75 year old female with septic shock likely secondary to urosepsis, retrieved from Belmont Hospital
Background
OA of knees
Ex-smoker 20 years ago
Management
CTKUB – NAD
3.5 L of Normal saline
IV metaraminol at 20mL/hr
Current observations
HR - 120
BP 65/35
SaO2 96% on 4L via np
ABG – pH 7.15, PaCO2 31mmHg, PaO2 85mmHg, BE -7mmol.L, Lactate 4.5mmol.L
How can I tell if she needs more fluid ??
If she does need more fluid – which one do I give, and how much ??

50. The conclusions
Fluid is a drug, it should be given in appropriate doses, and its use reviewed regularly. In sicker patients its likely that the timing of the dosage is more important
There are 3 phases of resuscitation Resuscitation, Maintenance and Fluid removal – identify where your patient lies and act appropriately
Fluid status and fluid responsiveness is difficult to assess. No one single tool is infallible.
If unsure – fluid bolus 20mL/kg and reassess. But don’t keep giving if no change.
Normal saline is the safe answer
Colloids don’t offer any advantage over crystalloids.
Hopefully more directed research the controversies in the future

51. Nutrition in ICU

52. Why nutrition is important
Critical illness causes an increase in Basal Metabolic Rate by more than 40%
Chronic malnutrition is a common finding in patients admitted to ICU
The predominant pattern of protein catabolism, resulting in skeletal muscle breakdown. This includes such important muscle groups as the diaphragm
The loss of lean body mass (whole body water and protein) ranges from 0.5-1% per day, and is far greater than that from bed rest alone. This can lead to a reduction in muscle fibre cross sectional area of up to 3-4% per day.
In the early phases of critical illness, only skeletal muscle is effected. However if protracted beyond 2 weeks this can effect the cardiac muscle.
Providing adequate nutritional intake in the ICU patient can be a challenge:
Delay in initiation
Difficulty reaching target rates of feeding
Fasting for various procedures
Feed intolerance
Diarrhoea
Hormonal milleau is of catabolic hormones to provide substrates for tissues (glucose, fatty acids, amino acids), with resistance to anabolic hormones (Insulin and IGF 1). This leads to peripheral reduction in substrate availability

53. Some basics

54. Daily requirements Energy 20 – 25 kcal/kg Protein 1-2 g/kg
Carbohydrate
4 g/kg
Fat
1 g/kg
30% non-protein energy calories

56. Case 2
67 year old male admitted to the ICU following a laparotomy for anastamotic leak, 3 days post elective hemicolectomy.
Past History
Bowel Ca on colonoscopy 3 months ago. Normal diet up to operation, no weight loss.
Ex smoker 15 years ago
IHD – AMI 5 years ago
Currently
Intubated and ventilated
Noradrenaline SS at 15 mL per hour
HR 95, BP 100/60, SaO2 98% on FiO2 50%
Has had 3L of Hartmann’s intraoperatively
Last ABG
pH 7.2
PCO2 34mmHg
BE -4.5mmol.L
Lactate 2.1
How are you going to manage his feeding ??

57. Guidelines for nutritional support
ESPEN – European Society for Enteral and Parenteral Nutrition (2006)
Canadian Clinical Practice Guidelines (Updated online regularly – criticalcarenutrition.com)
American Dietetics Association evidenced based guidelines for critical illness (2009)
Society of Critical Care Medicine and American Society of Parenteral and Enteral Nutrition’s joint guideline (2009)

58. Assessment of the patients nutritional status
History
Duration of illness
Likely ongoing hypermetabolic state
Nature of illness
Recent weight loss
Co-morbid disease – Liver, Kidney, GIT, Cancer
Examination
Assessment of metabolic activity (Arousal, vital signs)
Muscle wasting
Signs of micronutrient deficiency (angular stomatitis, glossitis, pale conjunctiva, skin, hair, nails)
Investigation
Pathology
Haemoglobin, Iron stores
Electrolytes
Albumin or Pre-Albumin
Transferrin, Coagulation
Fat soluble vitamin levels
Water soluble vitamin levels
Subjective Global Assessment
Indirect calorimetry
Anthropomorphic measures (mid-arm muscle circumference, skin folds)
Consultation
Dietician
Equations to estimate daily energy requirements (Schofield, Harris-Benedict)

59. Early enteral nutrition
On admission all patients should be assessed for feeding via enteral nutrition.
Exceptions
Tolerating adequate oral diet
<24 hours to oral intake
Palliative care
There are a number of patient groups who are unable to be fed enterally
Bowel obstruction
Ischaemic bowel
Imminent bowel resection
Enteric anastamosis
Enteric fistula
Severe exacerbation of inflammatory bowel disease

61. Early enteral nutrition
Guidelines
Enteral nutrition should be started in the first hours of admission following resuscitation
There is evidence of a possible reduction in treatment time, hospital LOS and infectious complications, compared with delayed EN
Aim to reach 60% of target EN by 5-7 days
ACCEPT trial (Martin et al 2004)
Implementation of a feeding algorithm resulted in increased delivery of nutrition, reduced hospital LOS, and trend to decreased mortality
Clinical outcomes not replicated in later ANZ trial
EDEN trial (Rice et al 2012)
Initial trophic feeds vs full enteral nutrition for the first 6 days in 1000 patients with acute lung injury
No difference in 60 day mortality, ICU LOS, ventilator-free days and infectious complications
The full feeding group had higher use of prokinetic agents, higher rates of feed intolerance, more constipation and more vomitting. They also had higher BSLs and more insulin use.
Study shows that those who receive <33% and those who received more than 66% of calculated requirements had worse outcomes.
Nutrition also provided by catabolism secondary to critical illness
Feeding aims to reduce catabolism, but can not stop it

62. Total Parenteral Nutrition
Involves the provision of complete nutrition via CVC in patients who are unable to tolerate enteral nutrition
Requires the provision of macronutrients, micronutrients and fluid
Indications
General
EN contraindicated
EN fails to meet nutritional requirements
Specific
prolonged bowel obstruction and ileus
short bowel syndrome with severe malabsorption
severe dysmotility
high output intestinal fistulae
anastomotic break down
intolerance to EN
Advantages
Provides nutrition to those patients who are unable to tolerate EN
Disadvantages
Cost
CVC access – requires dedicated lumen
Hyperglycaemia
? Infection
Loss of GIT structure and function
Stress ulceration
GIT barrier fuction
GIT immune function

63. Monitoring
Electrolytes
Renal function/Hepatic function
BSL
Triglycerides at start then weekly (especially in known lipid disorders, pancreatitis, hepatic or renal disease to assess clearance of lipids)
Micronutrient levels - zinc, copper,
selenium, vitamin C, thiamine, vitamin B6 ,
vitamin B12 , and 25-hydroxyvitamin D

65. TPN : Guidelines Guidelines
There is disagreement between guidelines on commencement of PN in critically ill patients
If patients well nourished
European guidelines recommend early (24-48hrs) commencement of PN if patients unlikely to reach EN targets at 3 days
American guidelines recommmend late (7 days) commencement of PN if patient unlikely to reach EN targets, and suggest only use if likely to require for longer than 5-7 days
Canadian guideline recommends against early PN and high dose IV dextrose, and states that timing of PN to be individualised to each patient
If patient malnourished
All guidelines recommend early commencement of PN if patient unlikely to reach EN targets, assessed on a case-by-case basis
All recommend only feeding patients up to the desired intake (20-25 kcal/kg/day)
All recommend regular reassessment of the patients need for PN, and cease when patient is tolerating 60% of desired intake via enteral route

66. TPN : recent trials EPANIC trial (2011)
4640 patients randomised Euro vs North american guidelines
Criticisms
Mortality 11%, a lot of cardiac surgical patients
ICU LOS 3 days
Single centre with old feeding guidelines including large quantities of IV glucose
- Early feeding <48 hrs (not really early)

69. Early PN trial
Early PN trial (2013)

71. Whereas EPaNIC targeted critically
ill patients regardless of adequacy
of planned enteral intake,6 the
Early PN Trial maintained a strict focus
on a narrow subset of patients unlikely
to receive any early enteral nutrition.
Furthermore, it is important to
understand that complete nutrition
therapy did not commence in either
group of the EPaNIC trial until ICU day
3, while the Early PN Trial commenced
early parenteral nutrition on
the first day of ICU care, relative to a
standard care group commencing nutrition
therapy on day 3 or later

73. Nutrition – costs EN - $5 per bag (2 bags per day)
TPN – Approx $250 per bag (1 bag per day)
Feed
Pharmacy compounding
Delivery

74. Case 2
67 year old male admitted to the ICU following a laparotomy for anastamotic leak, 3 days post elective hemicolectomy.
Past History
Bowel Ca on colonoscopy 3 months ago. Normal diet up to operation, no weight loss.
Ex smoker 15 years ago
IHD – AMI 5 years ago
Currently
Intubated and ventilated
Noradrenaline SS at 15 mL per hour
HR 95, BP 100/60, SaO2 98% on FiO2 50%
Has had 3L of Hartmann’s intraoperatively
Last ABG
pH 7.2
PCO2 34mmHg
BE -4.5mmol.L
Lactate 2.1
How are you going to manage his feeding ??
Does this patient need TPN ??

75. Feed intolerance

76. Possible causes of feed intolerance
-> NG not in correct position
-> intra-abdominal pathology
-> opioids
-> interruptions of feed for procedures/OT
-> gastric paresis
-> ileus
-> sepsis
-> electrolyte abnormalities

77. Feed intolerance : treatments
Gastric residual volumes (GRVs)
Guidelines
Optional monitoring of GRVs
Suggest mL as the limit for possible feed intolerance
GRV monitoring trial : Reignier et al 2013
Open label RCT of 452 patients in 9 French ICUs comparing no GRV monitoring to 6 hourly monitoring with a 250mL limit
No difference in VAP, acquired infections, duration of MV, ICU LOS or mortality rates
Proportion of patients receiving their full calorie goal was higher in no monitoring group, and rates of vomitting higher
Prokinetic agents
Should not be used routinely
Evidence suggests that when used in a feeding algorithm for feed intolerance, it may improve clinical outcomes, and does improve feed tolerance, gastric emptying and EN delivery
Metoclopramide should be the first choice. Small number of trials that show less feed intolerance with dual therapy

78. Feed intolerance : treatments
Post pyloric feeding
Guidelines
Should be considered if easy access to bedside insertion
Consider in patients on heavy sedation, nursed supine or evidence of feed intolerance with high gastric aspirates.
Meta-analysis : Zhang et al (2013)
No benefit in terms of mortality, new-onset pneumonia or aspiration
PPF delivers higher proportions of estimated energy : WMD 12% (5-18%), and reduce GRV : WMD -170mL (-290 to -46mL)
ENTERIC trial : Davies et al (2012)
Compared early PPF with gastric feeding in 181 ICU patients
Demonstrated no difference in caloric intake, mortality, VAP, vomitting or diarrhoea.

79. Diarrhoea management Diarrhoea is common in ICU
Prevalence is approximately 40-70% depending on definition
It results in
patient discomfort,
Reduced nutrition
electrolyte and fluid disturbances,
increased nursing work,
wound contamination
skin excoriation
The causal factor may be obvious
Infectious diarrhoea – eg Rotovirus, salmonella, campylobacter
Clostridium difficile
GIT disease and surgery
Faecal impaction
Most often the cause is multifactorial
Enteral feeds
Laxatives
Medications
Electrolytes

82. Refeeding syndrome
Defined as the potentially fatal shifts in fluids and electrolytes that may occur in malnourished patients receiving artificial refeeding, whether enterally or parenterally
The hallmark biochemical feature of refeeding syndrome is hypophosphataemia.
However, the syndrome is complex and may also feature
abnormal sodium and fluid balance;
changes in glucose, protein, and fat metabolism;
thiamine deficiency;
hypokalaemia;
hypomagnesaemia
With the restoration of glucose as a substrate, insulin levels rise and cause cellular uptake of ions.
Depletion of intracellular ATP and 2,3 DPG results in tissue hypoxia and failure of cellular energy metabolism
Manifestatiosn include
Cardiac and respiratory failure
Seizures and paraesthesias
Insulin has an anti-natriuretic effect – coupled with increased Na and fluid can lead to overload in refeeding syndrome

83. Refeeding syndrome - risk
Patients who begin feeding with disturbances of K, Mg PO4 and Ca

84. Refeeding syndrome - management

85. Conclusions Start feeding early in appropriate patients
Assess risk of refeeding syndrome, check daily and increase feeds slowly. Supplement with thiamine and multi-vitamin
Refer to dieticians – and read their input
Parenteral nutrition
Liase with treating team, intensivist, dietician and pharmacist
Consider if patient cannot use enteral route, is severely malnourished or not tolerating enteral feeds after 5-7 days
DON’T stop feeds for intolerance, assess patients, use prokinetics and continue feeds
Diarrhoea is common. Exclude the common causes, remove potential contributors and treat consequences

86. References
Many days and nights of fun in the ICU