Complications of Critical Illness

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Complications of Critical Illness

• Division of Critical Care Medicine
• University of Alberta

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First, do no harm.
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Outline

• Nutritional support in the ICU
• Abdominal compartment syndrome
• DVT/PE in the ICU
• Ventilator associated pneumonia
• Gastric stress ulceration

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Nutritional Support
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Reasons for Support

• Limit catabolism
• Substrate for healing
• Increase survival

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Calculating Metabolic Needs

• Formula Harris-Benedict Equation
• Nitrogen Balance
• Resting Energy Expenditure

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Harris-Benedict Equation

• Estimates Basal Metabolic Rate (BMR)
• 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
• 25 (mild peritonitis, long bone fracture or
  mild/moderate trauma)
• 50 (severe infection, MSOD, severe trauma)
• 100 (burn of 40 to 100 TBSA)

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Nitrogen Balance

• Measure/estimate all sources of nitrogen output.
• stool, urine, skin, fistulae, wounds, etc.
• Measure all sources of nitrogen input.
• enteral or parenteral nutrition

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Greenfield 1997
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Calculating Nitrogen Balance
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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.

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Metabolic CartIndirect 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.
• Theory - start with a formula, tune it up
  long-term with the metabolic cart!

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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

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Other Clinical Parameters

• Wound healing
• Measured proteins
• Albumin (t½ weeks)
• Prealbumin (t½ days)
• Non-water weight gain

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Enteral vs. Parenteral?

• Use the GI tract whenever possible.
• Contraindications to GI feeds
• large output fistula
• SBO
• severe pancreatitis
• short gut, severe diarrhea, enteritis
• non-functional GI tract

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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!!

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Nutrients

• Fat - essential linolenic, linoleic, arachidonic
  acids
• 9 kcal/gm
• Protein - essential and branched chain AA in TPN
• 4 kcal/gm - not to be included in calorie
  estimates
• no glutamine in TPN due to instability
• Carbohydrates - converted to glucose
• 3.4 kcal/gm (4.0 kcal from endogenous source)
• Trace Minerals
• Chromium, copper, zinc, manganese, selenium, iron
• Vitamins
• Thiamine
• Folate
• Vitamin C

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Rules of Thumb TPN

• Want 25 - 35 solution of dextrose.
• Want 4.25 - 6 AA solution.
• normal 0.8 gm/kg/day up to 2.0 gm/kg/day
• Kcal/nitrogen ratio
• normal 3001
• post-op 1501
• trauma/sepsis 1001
• Lipids 10 - 20 at least twice per week.

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TPN vs. Enteral Advantages?

• Many prospective, randomized studies.
• TPN group had much higher infection rates.
• pneumonia, intraabdominal abscess, line sepsis
• Potential Reasons for TPN Failure
• TPN increases blood glucose if not strictly
  controlled.
• numerous studies now show hyperglycemia increases
  mortality and infectious complications.
• Does not contain glutamine.

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Why Enteral?

• Preservation of villous architecture
• may prevent translocation
• role of translocation unclear in humans
• good study in BMT patients
• Ability to give glutamine
• major fuel of enterocytes
• major nitrogen transfer agent to viscera
• in catabolic stress may be an essential AA

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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.

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Refeeding Syndrome

• In severely malnourished.
• Development of severe electrolyte abnormalities
• phosphorous, potassium, magnesium
• As muscle mass, cell mass, and ATP repleted
• may reach critically low values, cardiac arrest

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Theoretical Advantages of Early 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.

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Energy Requirement in Critical Illness
Different Conditions
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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.

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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.

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Lipid Goals

• High calorie, low volume.
• Suggested max calories - no more than 50 of
  non-protein Kcal, or lt 1 cal/Kg/hr.
• Minimum to prevent essential fatty acid
  deficiency is 2 x 500 cc bottles/week.
• Diprivan (propofol) 1calorie/ml

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Consequences of Overfeeding

• 1. Azotemia - patients gt 65 years and patients
  given gt 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).

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Consequences of Overfeeding

• 6. Hypertonic dehydration - can be caused by
  high-protein 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.

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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. Start feedings conservatively, advance
  gradually, and monitor Mg, Ph, and K closely.

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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.

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Abdominal Compartment Syndrome
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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.

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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.

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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.

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Bladder Pressure Measurement

• 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
• Grade I 10-15
• Grade II 15-25
• Grade III 25-35
• Grade IV gt35

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Abdominal Compartment Syndrome

• Grade I-II can be treated with muscle relaxants
  as long as clinical situation improves.
• Indication for laparotomy with open abdomen
• Grade III and over
• Failure of improvement with conservative measures

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Venous Thromboembolism in ICU
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Importance of DVT Prophylaxis

• Acute DVT/PE prevention
• Valvular Damage
• Symptomatic proximal DVT can be an extension of
  distal DVT that was previously asymptomatic.
• Significant number of fatal PEs NOT preceded by
  symptomatic DVT.
• Most preventable cause of hospital associated
  death in medical patients?PE.

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Asymptomatic DVT Upon ICU Admission
Patient Population DVT
Surgical ICU 7.5 Harris J Vas Surg 1997 26734-9
Respiratory ICU 10.7 Schonhster Respiration 1998 65173-7
MICU-Resp fail/vent 19 Goldberg Am J Resp CCM 1996 153A94
MICU-Resp fail/vent 6.3 Fraisse Am J Resp CCM 2000 1611109-14
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Natural History of DVT
132 Surgical patients no prophylaxis
70 No DVT (92)
30 DVT (40)
35 Calf with spontaneous lysis (14)
42 Calf only (17)
23 propagation Popliteal/femoral (9)
56 No PE (5)
44 PE (4)
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Incidence of VTEin Major Trauma Without
Prophylaxis

• Lower leg DVT 58, proximal DVT 18
• Vast majority clinically not apparent.

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Autopsy Studies for PE in Critically Ill Patients
PE Autopsy PE Autopsy
Study ICU Setting Present Fatal
Neuhaus 1978 Med/Surg 27 12
Moser 1981 Respiratory 20 0
Pingleton 1981 Medical 23 --
Cullin 1986 Surgical 10 1
Blosser 1998 Medical 7 2
Willemsen 2000 Surgical 8 3
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Thromboembolism Riskin Surgical Patients - No
Prophylaxis
DVT, DVT, PE, PE,
Calf Proximal Clinical Fatal
Low Risk 2 0.4 0.2 lt0.01
Minor Surgery lt 40 no risk factors Minor Surgery lt 40 no risk factors Minor Surgery lt 40 no risk factors Minor Surgery lt 40 no risk factors Minor Surgery lt 40 no risk factors
Moderate Risk 10-20 2-4 1-2 0.1-0.4
Minor surgery risk factors Surgery 40-60 no risk factors Minor surgery risk factors Surgery 40-60 no risk factors Minor surgery risk factors Surgery 40-60 no risk factors Minor surgery risk factors Surgery 40-60 no risk factors Minor surgery risk factors Surgery 40-60 no risk factors
High Risk 20-40 4-8 2-4 0.4-1.0
Surgery gt60, 94 40-60 with additional risk factors (prior VTE, cancer, hypercoagulability) Surgery gt60, 94 40-60 with additional risk factors (prior VTE, cancer, hypercoagulability) Surgery gt60, 94 40-60 with additional risk factors (prior VTE, cancer, hypercoagulability) Surgery gt60, 94 40-60 with additional risk factors (prior VTE, cancer, hypercoagulability) Surgery gt60, 94 40-60 with additional risk factors (prior VTE, cancer, hypercoagulability)
Highest Risk 40-80 10-20 4-10 0.2-5
Surgery with multiple risk factors (age gt 40 yr, cancer, prior VTE) Hip or knee arthroplasty, HFS Major trauma, SCI Surgery with multiple risk factors (age gt 40 yr, cancer, prior VTE) Hip or knee arthroplasty, HFS Major trauma, SCI Surgery with multiple risk factors (age gt 40 yr, cancer, prior VTE) Hip or knee arthroplasty, HFS Major trauma, SCI Surgery with multiple risk factors (age gt 40 yr, cancer, prior VTE) Hip or knee arthroplasty, HFS Major trauma, SCI Surgery with multiple risk factors (age gt 40 yr, cancer, prior VTE) Hip or knee arthroplasty, HFS Major trauma, SCI
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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.

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Significant Risk Factors and Odds Ratios for
Venous Thromboembolism
Risk Factor (Number at Risk) Odds Ratio (95 CI)
Age ? 40y (n178,851) 2.29 (2.07 2.55)
Pelvic fracture (n2707) 2.93 (2.01 4.27)
Lower extremity fracture (n63,508) 3.16 (2.85 3.51)
Spinal cord injury with paralysis (n2852) 3.39 (2.41 4.77)
Head injury (AIS score ? 3) (n52,197) 2.59 (2.31 2.90)
Ventilator days gt 3 (n13,037) 10.62 (9.32 12.11)
Venous injury (n1450) 7.93 (5.83 10.78)
Shock on admission (BPlt90 mm Hg) (n18,510) 1.95 (1.62 2.34)
Major surgical procedure (n73,974) 4.32 (3.91 4.77)
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VTE Prophylaxis
Pharmacologic
Unfractionated heparin
Low molecular weight heparin
Vit K Antagonists
Mechanical
Graduated Compression Stockings
Intermittent Pneumatic Compression Devices
IVC filters
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INJURED PATIENT

• High Risk Factors
• (Odds ratio for VTE 2 3)
• Age ³ 40
• Pelvic fx
• Lower extremity fx
• Shock
• Spinal cord injury
• Head Injury (AIS ³ 3)

• Very High Risk Factors
• (Odds ratio for VTE 4 - 10)
• Major operative procedure
• Venous injury
• Ventilator days gt 3
• 2 or more high risk factors

Does the patient have contraindication for
Heparin?
Does the patient have contraindication for
Heparin?
Yes
No
Yes
No
LMWH and Mechanical Compression
Mechanical Compression and serial CFDI OR
Temporary IVC filter
Mechanical Compression
LMWH
Prophylactic dose
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Patient Assessment
Assess Bleeding Risk
High
Low

• Mechanical Prophylaxis
• Graduated compression 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 dose unfractionated heparin (LDUH)
• Low molecular weight heparin (LMWH)
• Combination of LMWH and mechanical prophylaxis
  for high risk patients

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Patient Assessment
Bleeding Risk Thrombosis Risk Prophylaxis Recommendation
Low Moderate LDH 5000 units SC bid
Low High LMWH Dalteparin Enoxaparin
High Moderate GCS or IPC ? LDUH when bleeding risk subsides
High High GCS or IPC ? LMWH when bleeding risk subsides
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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

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Ventilator Associated Pneumonia (VAP)
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VAP Definition

• Infection of the lung that occurs 48 hours or
  more after intubation.
• Categorized into two groups
• Early onset occurring 48-72 hours after
  intubation.
• Late onset occurring more than 72 hours after
  intubation.
• Accounts for 47 of all ICU infections.

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VAP Risk Factors

• Age gt60
• Male
• Traumatic injuries
• Chronic lung disease
• ARDS
• Micro aspiration of oropharyngeal contents
• Continuous sedation

• Paralytics
• Nasogastric tube
• Low endotracheal cuff pressure
• Supine head position
• H2 blockers
• Sinusitis
• Severity of illness
• Duration of ventilation

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VAP Prevention

• Infection control
• 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 prevent spread of VAP.
• Noninvasive ventilation
• Allows selected patients to preserve normal
  mucociliary defenses.

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VAP Prevention

• Patient positioning
• Lateral rotation of patients while in bed reduces
  the risk of aspiration.
• Keeping the head of the bed gt30 degrees also
  reduces the risk of aspiration.
• Endotracheal cuff pressure and suctioning
• A persistent endotracheal intracuff pressure of
  lt20 cm H2O allows more micro aspiration.
• Continuous subglottic suctioning is used to
  remove the pool of secretions that develops
  around the endotracheal cuff.

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VAP Prevention

• Healthcare provider education
• 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.

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Gastric Stress Ulcers
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Stress Ulcerations - Definition

• 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.

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Stress Ulcerations Risk Factors

• 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.

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Stress Ulceration - Prevention

• H2 blockers
• 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.

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Stress Ulceration Prevention

• Proton pump inhibitors
• Mechanism of action is by inactivation of the
  H-K-ATPase pump.
• At least equally effective as H2 blockers.
• Nutrition
• 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.

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Stress Ulceration Risk of VAP

• 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.

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Summary

• First, do no harm
• Nutritional support in the ICU
• Abdominal compartment syndrome
• DVT/PE in the ICU
• Ventilator associated pneumonia
• Gastric stress ulceration