### Nutritional Support in the ICU - Division of Critical Care

```Complications of Critical
Illness
Division of Critical Care Medicine
University of Alberta
First, do no harm.
Outline
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Nutritional support in the ICU
Abdominal compartment syndrome
DVT/PE in the ICU
Ventilator associated pneumonia
Gastric stress ulceration
Nutritional Support
Reasons for Support
Limit catabolism
Substrate for healing
Increase survival
Calculating Metabolic Needs
Formula: Harris-Benedict Equation
Nitrogen Balance
Resting Energy Expenditure
Harris-Benedict Equation
Estimates Basal Metabolic Rate (BMR):
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Male BMR kcal/day = 66.47 + 13.7 (kg) + 5 (cm) - 6.76 (yrs)
Female BMR kcal/day = 66.51 + 9.56 (kg) + 1.85 (cm) - 4.68 (yrs)
Total Caloric Requirements equal the B.E.E. multiplied by
the sum of the stress and activity factors.
Stress plus activity factors range from 1.2 to over 2.
Factors to add to the BMR:
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25% (mild peritonitis, long bone fracture or mild/moderate trauma)
50% (severe infection, MSOD, severe trauma)
100% (burn of 40 to 100% TBSA)
Nitrogen Balance
Measure/estimate all sources of nitrogen output.
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stool, urine, skin, fistulae, wounds, etc.
Measure all sources of nitrogen input.
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enteral or parenteral nutrition
Greenfield 1997
Calculating Nitrogen Balance
Problems with Nutritional
Parameters
UUN will be invalid if creatinine clearance is less than
50.
UUN and prealbumin are not helpful if the patient has
not received goal volumes of feeding consistently for
three to four days prior to the test.
Metabolic Cart
Indirect Calorimetry: Theory
Measures O2 absorbed in lungs
Assumptions of Fick equation, at steady state O2
absorbed equals O2 consumed.
Metabolic rate in cc of O2 per minute.
Conversion 5kcal/liter O2.
24 hour steady state measurement recommended.
the metabolic cart!
Metabolic Cart - Indirect
Calorimetry: Results
RQ or respiratory quotient (CO2 expired/O2
inspired).
0.6 - 0.7 starvation/underfeeding
0.84 - 0.86 desired range/mixed fuel utilization
0.9 - 1.0 carbohydrate metabolism
1.0 + overfeeding/lipogenesis
Other Clinical Parameters
Wound healing
Measured proteins
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Albumin (t½ = weeks)
Prealbumin (t½ = days)
Non-water weight gain
Enteral vs. Parenteral?
Use the GI tract whenever possible.
Contraindications to GI feeds:
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large output fistula
SBO
severe pancreatitis
short gut, severe diarrhea, enteritis
non-functional GI tract
Starting Estimates
Determine number of calories needed.
Determine normal or increased protein needs.
Determine if contraindication to fats.
Determine fluid restrictions.
USE THE GI TRACT IF POSSIBLE!!
Nutrients
Fat - essential linolenic, linoleic, arachidonic acids
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9 kcal/gm
Protein - essential and branched chain AA in TPN
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4 kcal/gm - not to be included in calorie estimates
no glutamine in TPN due to instability
Carbohydrates - converted to glucose
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3.4 kcal/gm (4.0 kcal from endogenous source)
Trace Minerals
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Chromium, copper, zinc, manganese, selenium, iron
Vitamins
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Thiamine
Folate
Vitamin C
Rules of Thumb: TPN
Want 25 - 35% solution of dextrose.
Want 4.25 - 6% AA solution.
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normal 0.8 gm/kg/day up to 2.0 gm/kg/day
Kcal/nitrogen ratio
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normal 300:1
post-op 150:1
trauma/sepsis 100:1
Lipids 10 - 20% at least twice per week.
Many prospective, randomized studies.
TPN group had much higher infection rates.
pneumonia, intraabdominal abscess, line sepsis
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Potential Reasons for TPN Failure:
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TPN increases blood glucose if not strictly
controlled.
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numerous studies now show hyperglycemia increases
mortality and infectious complications.
Does not contain glutamine.
Why Enteral?
Preservation of villous architecture
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may prevent translocation
role of translocation unclear in humans
good study in BMT patients
Ability to give glutamine
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major fuel of enterocytes
major nitrogen transfer agent to viscera
in catabolic stress may be an essential AA
Gastric vs. Post-pyloric Feeds
Route probably not important if patient tolerating feeds.
If gastric ileus, recent surgery, or need for frequent
procedures where feeds would be stopped if gastric,
post-pyloric may be better.
Refeeding Syndrome
In severely malnourished.
Development of severe electrolyte abnormalities:
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phosphorous, potassium, magnesium
As muscle mass, cell mass, and ATP repleted:
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may reach critically low values, cardiac arrest
Enteral Nutrition
1. Ameliorate the stress response, hypermetabolism,
and hypercatabolism.
2. Provide gut stimulation to prevent atrophy and the
loss of immunologic and barrier functions of the gut.
3. Minimize rapid onset of acute malnutrition.
4. Decrease LOS and complication rates.
Energy Requirement in Critical
Illness: Different Conditions
Total Kcal Goals
25 - 35 kcal/kg is suitable for most hospitalized patients
and is a good rule of thumb.
21 kcal/kg is appropriate for obese patients.
30 - 40 kcal/kg may be necessary for highly stressed
patients.
Total Protein Goals
1.0 g/kg for healthy individuals.
1.2 - 1.5 g/kg for mildly stressed.
1.5 - 2.0 severely stressed/multiple trauma/head
injury/burns.
Lipid Goals
High calorie, low volume.
Suggested max calories - no more than 50% of nonprotein Kcal, or < 1 cal/Kg/hr.
Minimum to prevent essential fatty acid deficiency is 2 x
500 cc bottles/week.
Diprivan (propofol) = 1calorie/ml
Consequences of Overfeeding
1. Azotemia - patients > 65 years and patients given >
2g/kg protein are at risk.
2. Fat-overload syndrome - recommended maximum is
1g lipid/kg/d. Infuse IV lipid slowly over 16 - 24 hours.
3. Hepatic steatosis - patients receiving high
carbohydrate, very low fat TPN are at risk.
4. Hypercapnia - makes weaning difficult.
5. Hyperglycemia - increases risk of infection. Glucose
should not exceed 5 mg/kg/min (4 mg/kg/min for
diabetics).
Consequences of Overfeeding
6. Hypertonic dehydration - can be caused by highprotein formula with inadequate fluid provision.
7. Hypertriglyceridemia - propofol, high TPN lipid loads,
and sepsis increase the risk. If the patient is
hypertriglyceridemic, decrease lipid to an amount to
prevent EFAD (500 cc 10% lipid twice weekly) and
monitor.
Consequences of Overfeeding
8. Metabolic acidosis - patients receiving low ratios of
energy to nitrogen are at risk. Acidosis can cause
muscle catabolism and negative nitrogen balance.
9. Refeeding syndrome - common in malnourished
patients or those held NPO prior to initiation of feeding.
monitor Mg, Ph, and K closely.
Nutritional Goals
Feed as soon as hemodynamically stable, after adequate
resuscitation.
No disease state improves with starvation.
Poor gut perfusion may contraindicate enteral feeds, but
enteral feeds are always preferred when possible.
Abdominal Compartment
Syndrome
Abdominal Compartment
Syndrome
Acute increase in intra-abdominal pressure
Affects renal, pulmonary, and cardiovascular systems
Decreases ventilation, causes hypoxia, decreased blood
flow to lower extremities, and kidney failure.
Abdominal Compartment
Syndrome
Caused by intra-abdominal swelling or hemorrhage.
Increase in volume of retroperitoneum such as with
pancreatitis also seen.
Even reports of retroperitoneal hemorrhage such as with
pelvic fracture or from anticoagulation.
Abdominal Compartment
Syndrome
Early recognition and diagnosis vital to prevent
complications.
Distended, tense abdomen first sign
Bladder pressure confirms elevated pressure and is easy to
perform.
Bladder is direct transmitter of pressure at volumes of less
than 100 cc.
Bladder filled with 50 cc. of sterile saline via foley and
pressure monitor connected to side port with 18 ga.
needle.
Normal pressure up to 10 cm H2O
Abdominal Compartment
Syndrome
Grade I-II can be treated with muscle relaxants as long as
clinical situation improves.
Indication for laparotomy with open abdomen:
Failure of improvement with conservative measures
Venous Thromboembolism in
ICU
Importance of DVT
Prophylaxis
Acute DVT/PE prevention
DVT
Valvular Damage
Recurrence
PE
Post-phlebitic syndrome
Symptomatic proximal DVT can be an extension of
distal DVT that was previously asymptomatic.
Significant number of fatal PE’s NOT preceded by
symptomatic DVT.
Most preventable cause of hospital associated death
in medical patientsPE.
Asymptomatic DVT Upon
Patient Population
Surgical ICU
% DVT
7.5%
Harris J Vas Surg 1997; 26:734-9
Respiratory ICU
10.7%
Schonhster Respiration 1998; 65:173-7
MICU-Resp fail/vent
19%
Goldberg Am J Resp CCM 1996; 153:A94
MICU-Resp fail/vent
6.3%
Fraisse Am J Resp CCM 2000; 161:1109-14
Natural History of DVT
132 Surgical patients no prophylaxis
70%
30%
No DVT (92)
DVT (40)
35% Calf with
spontaneous
lysis (14)
42% Calf
only (17)
23% propagation
Popliteal/femoral (9)
56%
44%
No PE (5)
PE (4)
Incidence of VTE
in Major Trauma Without
Prophylaxis
Lower leg DVT 58%, proximal DVT 18%
Vast majority clinically not apparent.
Autopsy Studies for PE in
Critically Ill Patients
PE Autopsy
Present
Fatal
Study
ICU Setting
Neuhaus 1978
Moser 1981
Pingleton 1981
Cullin 1986
Med/Surg
Respiratory
Medical
Surgical
27%
20%
23%
10%
12%
0%
-1%
Blosser 1998
Willemsen 2000
Medical
Surgical
7%
8%
2%
3%
Thromboembolism Risk
in Surgical Patients - No Prophylaxis
DVT, %
Low Risk
PE, %
Calf
Proximal
Clinical
Fatal
2%
0.4%
0.2%
<0.01%
10-20 %
2-4%
1-2%
0.1-0.4%
20-40%
4-8%
2-4%
0.4-1.0%
Minor Surgery < 40 no risk factors
Moderate Risk
Minor surgery risk factors
Surgery 40-60 no risk factors
High Risk
Surgery >60, 94 40-60 with additional risk factors (prior VTE, cancer, hypercoagulability)
Highest Risk
40-80%
10-20%
Surgery with multiple risk factors (age > 40 yr, cancer, prior VTE)
Hip or knee arthroplasty, HFS
Major trauma, SCI
4-10%
0.2-5%
Trauma and Venous
Thromboembolism
Patients recovering from major trauma have
highest risk for developing VTE amongst all
hospitalized patients.
Without prophylaxis, multisystem or major
trauma have a DVT risk exceeding 50%.
PE is the third leading cause of death in
trauma patients that survive beyond the
first day.
Significant Risk Factors and Odds
Ratios for Venous Thromboembolism
Risk Factor (Number at Risk)
Odds Ratio (95%
CI)
*Age  40y (n=178,851)
2.29 (2.07 – 2.55)
Pelvic fracture (n=2707)
2.93 (2.01 – 4.27)
*Lower extremity fracture (n=63,508)
Spinal cord injury with paralysis (n=2852)
*Head injury (AIS score  3) (n=52,197)
*Ventilator days > 3 (n=13,037)
*Venous injury (n=1450)
Shock on admission (BP<90 mm Hg) (n=18,510)
*Major surgical procedure (n=73,974)
3.16 (2.85 – 3.51)
3.39 (2.41 – 4.77)
2.59 (2.31 – 2.90)
10.62 (9.32 – 12.11)
7.93 (5.83 – 10.78)
1.95 (1.62 – 2.34)
4.32 (3.91 – 4.77)
VTE Prophylaxis
Pharmacologic
Unfractionated
heparin
Low molecular
weight heparin
Vit K
Antagonists
Mechanical
Compression
Stockings
Intermittent
Pneumatic
Compression
Devices
IVC filters
INJURED PATIENT
High Risk Factors
(Odds ratio for VTE = 2 – 3)
• Age  40
• Pelvic fx
• Lower extremity fx
• Shock
• Spinal cord injury
• Head Injury (AIS  3)
Does the patient have
contraindication for Heparin?
Yes
Mechanical
Compression
Very High Risk Factors
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(Odds ratio for VTE = 4 - 10)
Major operative procedure
Venous injury
Ventilator days > 3
2 or more high risk factors
Does the patient have
contraindication for Heparin?
No
Yes
No
LMWH*
* Prophylactic dose
LMWH* and
Mechanical
Compression
Mechanical
Compression and
serial CFDI
OR
Temporary IVC filter
Patient Assessment
Assess Bleeding Risk
High
Mechanical Prophylaxis
stockings (GCS)
 Intermittent pneumatic
compression devices (IPC)
Delayed prophylaxis until high risk
bleeding abates
Screen for proximal DVT with
Doppler US in high risk patients
Low
Low dose unfractionated
heparin (LDUH)
Low molecular weight
heparin (LMWH)
Combination of LMWH and
mechanical prophylaxis for
high risk patients
Patient Assessment
Bleeding
Risk
Thrombosis
Risk
Low
Low
Moderate
High
High
Moderate
High
High
Prophylaxis
Recommendation
LDH 5000 units SC bid
LMWH
 Dalteparin
 Enoxaparin
GCS or IPC  LDUH when
bleeding risk subsides
GCS or IPC  LMWH when
bleeding risk subsides
Vena Caval Filters
5 filter types-all equal efficacy
Pulmonary embolism 2.6%-3.8%
Deep Venous Thrombosis 6%-32%
Insertion site thrombosis 23%-36%
Inferior caval thrombosis 3.6%11.2%
Postphlebitic syndrome 14%-41%
Ventilator Associated
Pneumonia (VAP)
VAP Definition
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Infection of the lung that occurs 48 hours
or more after intubation.
Categorized into two groups:
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Early onset – occurring 48-72 hours after
intubation.
Late onset – occurring more than 72 hours
after intubation.
Accounts for 47% of all ICU infections.
VAP Risk Factors
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Age >60
Male
Traumatic injuries
Chronic lung disease
ARDS
Micro aspiration of
oropharyngeal
contents
Continuous sedation
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Paralytics
Nasogastric tube
Low endotracheal cuff
pressure
H2 blockers
Sinusitis
Severity of illness
Duration of ventilation
VAP Prevention
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Infection control
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Monitoring pneumonia rates and organism
surveillance lower the overall rate.
Strict adherence to hand washing, universal
precautions and barrier precautions for patients
infected or colonized with multidrug-resistant bacteria
Noninvasive ventilation
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Allows selected patients to preserve normal
mucociliary defenses.
VAP Prevention
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Patient positioning
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Lateral rotation of patients while in bed reduces the
risk of aspiration.
Keeping the head of the bed >30 degrees also
reduces the risk of aspiration.
Endotracheal cuff pressure and suctioning
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A persistent endotracheal intracuff pressure of <20
cm H2O allows more micro aspiration.
Continuous subglottic suctioning is used to remove
the pool of secretions that develops around the
endotracheal cuff.
VAP Prevention
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Healthcare provider education
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Ongoing education of hospital staff that
focuses on semi recumbent positioning,
avoidance of gastric over distention,
appropriate use of sedation, routine oral
hygiene, and proper endotracheal tube and
ventilator circuit management results in a
striking decrease in the incidence of VAP.
Gastric Stress Ulcers
Stress Ulcerations - Definition
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Stress ulcerations are mucosal erosions
that are usually shallow and cause oozing
from superficial capillary beds.
Deeper lesions can occur and erode into
the submucosa causing massive
hemorrhage or perforation.
Most common cause of GI bleeding in ICU
patients.
Stress Ulcerations – Risk Factors
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There are two major risk factors for clinically
significant bleeding due to stress ulcers:
mechanical ventilation more than 48 hours and
coagulopathy.
The risk of clinically important bleeding in
patients without either of these risk factors was
only 0.1%.
Burns, renal failure, and head injury are also
minor contributors to the risk of bleeding.
Stress Ulceration - Prevention
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H2 blockers
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Block the stimulatory effects of histamine on
parietal cells.
Continuous infusion provides better control of
gastric pH over bolus infusion but is not more
protective.
Also effective if given orally or NG.
Stress Ulceration – Prevention
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Proton pump inhibitors
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Mechanism of action is by inactivation of the H-KATPase pump.
At least equally effective as H2 blockers.
Nutrition
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Several studies have reported that enteral nutrition
reduces the risk of bleeding.
This effect is not seen with TPN.
If patient is tolerating enteral feeding, then additional
stress ulceration prophylaxis is unlikely to be needed.
Stress Ulceration – Risk of VAP
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Agents that raise the gastric pH may
promote the growth of bacteria in the
stomach.
These organisms then can reflux back up
into the trachea and cause VAP.
The jury is still out on the association
between acid suppression and VAP but
caution is warranted.
Summary
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First, do no harm
Nutritional support in the ICU
Abdominal compartment syndrome
DVT/PE in the ICU
Ventilator associated pneumonia
Gastric stress ulceration
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