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LABORATORY TESTS
IN THE
INTENSIVE CARE UNIT
JASSIN M. JOURIA, MD
DR. JASSIN M. JOURIA IS A MEDICAL DOCTOR,
PROFESSOR OF ACADEMIC MEDICINE, AND
MEDICAL AUTHOR. HE GRADUATED FROM ROSS
UNIVERSITY SCHOOL OF MEDICINE AND HAS
COMPLETED HIS CLINICAL CLERKSHIP TRAINING
IN VARIOUS TEACHING HOSPITALS THROUGHOUT
NEW
YORK,
INCLUDING
KING’S
COUNTY
HOSPITAL CENTER AND BROOKDALE MEDICAL
CENTER, AMONG OTHERS. DR. JOURIA HAS
PASSED ALL USMLE MEDICAL BOARD EXAMS, AND
HAS SERVED AS A TEST PREP TUTOR AND
INSTRUCTOR FOR KAPLAN. HE HAS DEVELOPED SEVERAL MEDICAL COURSES AND
CURRICULA FOR A VARIETY OF EDUCATIONAL INSTITUTIONS. DR. JOURIA HAS ALSO SERVED
ON MULTIPLE LEVELS IN THE ACADEMIC FIELD INCLUDING FACULTY MEMBER AND
DEPARTMENT CHAIR. DR. JOURIA CONTINUES TO SERVES AS A SUBJECT MATTER EXPERT
FOR SEVERAL CONTINUING EDUCATION ORGANIZATIONS COVERING MULTIPLE BASIC
MEDICAL SCIENCES. HE HAS ALSO DEVELOPED SEVERAL CONTINUING MEDICAL EDUCATION
COURSES COVERING VARIOUS TOPICS IN CLINICAL MEDICINE. RECENTLY, DR. JOURIA HAS
BEEN CONTRACTED BY THE UNIVERSITY OF MIAMI/JACKSON MEMORIAL HOSPITAL’S
DEPARTMENT OF SURGERY TO DEVELOP AN E-MODULE TRAINING SERIES FOR TRAUMA
PATIENT MANAGEMENT. DR. JOURIA IS CURRENTLY AUTHORING AN ACADEMIC TEXTBOOK
ON HUMAN ANATOMY & PHYSIOLOGY.
Abstract
When patients are brought to the intensive care unit, extensive
laboratory testing is often considered necessary in order to diagnose
and treat critical conditions. However, laboratory tests are not without
risk. Results can be misleading, and the testing itself can be harmful,
such as potentially causing iatrogenic anemia. Medical professionals
need to take a sensible approach to laboratory testing for patients in
the intensive care unit, focusing on the benefits and risks of each test
and being mindful of the probability of disease.
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Policy Statement
This activity has been planned and implemented in accordance with
the policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's
Commission on Accreditation for registered nurses. It is the policy of
NurseCe4Less.com to ensure objectivity, transparency, and best
practice in clinical education for all continuing nursing education (CNE)
activities.
Continuing Education Credit Designation
This educational activity is credited for 2.5 hours. Nurses may only
claim credit commensurate with the credit awarded for completion of
this course activity.
Statement of Learning Need
Clinicians caring for patients in the Intensive Care Unit are required to
interpret laboratory tests and be able to manage safe and appropriate
laboratory testing guidelines. Health professionals working with
critically ill patients need to take an evidenced-based and rational
approach to laboratory testing, including an understanding of the
benefits and risks of each test relative to a disease process.
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Course Purpose
To provide health clinicians with knowledge of different types of
laboratory testing for patients in the ICU as well as the benefits and
risks of varied tests.
Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses
and Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,
Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Please take time to complete a self-assessment of knowledge,
on page 4, sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge
learned will be provided at the end of the course.
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1.
Laboratory test sensitivity refers to the ability of a
a. patient to tolerate a test.
b. test to identify the presence of a disease or condition
correctly.
c. test to identify true negative.
d. test to identify the absence of a disease or condition correctly.
2.
Transfusion of whole blood, packed cells or blood
components has been
a.
b.
c.
d.
3.
shown to offer a survival advantage to patients.
known to reduce production of erythropoietin.
shown to depress new blood cells.
associated with the risk of infection.
True or False: Wellness testing is not an aspect of lab
testing in the ICU setting.
a. True
b. False
4.
Red blood cell transfusion is indicated for a patient
a.
b.
c.
d.
5.
with adequate blood flow (hemodynamic stability).
with acute hemorrhage but only in single units.
with evidence of hemorrhagic shock.
as an absolute method to improve tissue oxygen
consumption.
The Nyquist-Shannon Theorem posits that there is an
appropriate relationship between the number of samplings
and the likelihood that
a.
b.
c.
d.
a test will identify the presence of a disease.
the risk of clinically inappropriate treatments
there will be a medically appropriate solution.
the sample signal will be properly determined.
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Introduction
There are surprisingly relatively few studies that address the question
of what tests are the most effective and offer the most benefit for
patients in the Intensive Care Unit. Evidence and data should drive
medical decisions as much as possible, particularly with critically ill
patients. The Intensive Care Unit is an environment where increased
patient monitoring, data acquisition and frequent testing are very
common. At first glance, one might reasonably believe that the more
data and information one could acquire, the better patient interests
can be served. However, frequent blood draws carry their own perils.
These include anemia, increased need for transfusions of whole blood
or blood components and infection. This course focuses on the
common laboratory tests requested by clinicians caring for critically ill
patients.
Overview Of Laboratory Testing For Critically Ill Patients
Studies focused on laboratory testing in the Intensive Care Unit (ICU)
have revealed that ICU patients had from 40 to 70 mL of blood drawn
daily, amounting to over 1 L of blood during their ICU stay;1 and, also
that conservative blood sampling strategies are not widely used. In a
recent review, the total blood volume removed from ICU patients was
299 ± 355 mL over 48 hours. Utilizing small-volume phlebotomy tube
(SVPT) versus conventional-volume phlebotomy tube (CVPT)
decreased this volume to 174 ± 182 mL.2
Another aspect related to the drawback of frequent blood draws
involved patient discomfort in the ICU setting at a time when they can
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often least endure more discomfort. Frequent blood draws can disrupt
needed sleep and cause additional stress to patients. There is also an
increased risk of false positive or false negative laboratory test results
that can increase the risk of clinically inappropriate treatments.
Test sensitivity is the ability of any test to correctly identify the
presence of a disease or condition (true positives) while specificity is
the ability of any test to correctly identify the absence of a disease or
condition (true negatives). Clinicians should only order those tests that
have a reasonable probability of providing useful information, either
for ruling in or for ruling out a particular diagnosis. Ruling out a
diagnosis with laboratory testing has the highest power for diagnoses
with a low probability.
Wellness Testing
Wellness testing is obviously not an aspect of lab testing in the ICU
setting. Lipid panels or blood glucose screening tests have a definite
place in populations at risk for hyperlipidemia or diabetes. Genetic
screening may make sense for newborns, but it has little application
for patients in the ICU. The general recommendation in the ICU is to
order tests for which, if the results indicate a problem, there is a
medically appropriate solution.
Nyquist-Shannon Theorem
The Nyquist-Shannon Theorem posits that there is an appropriate
relationship between the number of samplings and the likelihood that
the sample values will be properly determined; in other words, there is
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a relationship between how often one should sample a varying
laboratory test.3 For example, blood glucose values will vary based on
meal frequency or if the patient is receiving total parenteral nutrition.
Oversampling (for example) every 30 minutes will not reveal any more
information as compared to sampling 2 hours after a meal. With
oversampling, while sensitivity may be increased, specificity will
necessarily be decreased, which will reduce the accuracy of the test.
Undersampling, on the other hand, can be just as problematic.
Reflexive testing algorithms as well as reflective testing have
significant clinical utility. Using an algorithmic approach, clinicians are
able to order sequential laboratory tests or a laboratory specialist will
get straight to the point of a diagnostic concern through further
testing. There are a number of tools in the laboratory toolbox that can
be effectively utilized in the ICU setting.4 These include the following
strong tools adapted for the ICU setting.
Laboratory Utilization Toolbox
TOOL
TARGET
STRENGTHS
WEAKNESSES
Laboratory Test All tests, but
Formulary
particularly
those with
recognized
(evidencebased) utility
Provides a
uniform policy,
similar to a
pharmacy
formulary.
Exceptions can
be determined as
needed.
Requires a buy-in
from all involved
Combining
Intervention
Combining
interventions
increase the
effectiveness by
allowing one
intervention to
Can be logistically
difficult and
complex,
particularly
because it requires
the involvement
Any test
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complement
another
(buy-in) from all
parties.
Banning
Repetitive
Orders
Daily testing
Powerful way to
reduce automatic
testing. Often
providers are not
aware of
automatic
testing.
Providers are often
concerned about
missing important
data. Indeed,
there is some risk
— i.e., not
ordering
coagulation studies
for patients
Limit Ordering
Privileges to
Specific
Providers
Complex tests,
expensive tests
or those tests
that may provide
questionable
benefits.
Increases cost
effectiveness and
diagnostic yield.
Adds a layer of
bureaucracy and
possibly
competitiveness.
Require Preapproval for
Tests
Complex tests,
expensive tests
or those tests
that may provide
questionable
benefits.
Specialists may
have a better
understanding of
necessary and
effective testing
Time consuming,
adds a layer of
bureaucracy
Change Order
Options
Primarily
computerized
ordering
Difficult to
subvert or “get
around”
Requires
involvement of the
IT department and
universal
cooperation and
use of computer
ordering
Encourage
Reflexive
Testing
Any test where a
less expensive
screening test
can be used
before a more
expensive test
Allows for the
use of ordering
algorithms.
Increases the
efficacy of more
expensive testing
Only useful for
analytes with a
less expensive
screening test
available (eg. TSH
followed, if
necessary with
fT3, fT4, TRH,
etc.)
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These tools are useful to keep in mind when thinking about the specific
tests that may be required for any patient, but particularly to minimize
the testing while maximizing the benefits for ICU patients.
Peripheral Blood Samples
Peripheral blood samples, also called peripheral sticks, may be needed
frequently or intermittently in the ICU, depending on the specific
patient’s condition and needs. Beyond blood tests, the patient will
generally require blood pressure monitoring, temperature
measurements, respiration rates, pulse, fluid intake and output levels
and pulse oximetry.
Frequent blood draws can destroy veins, cause pain and discomfort,
disturb a patient’s rest and, under some circumstances, cause anemia.
Placement of venous, arterial or intraosseous catheters can minimize
the damage and maximize the effectiveness of blood draws. However,
it is also critical to use blood conservation devices and only subject the
patient to blood draws when it is medically necessary.
Anemia is a significant concern in critically ill patients. In critically ill
patients, RBC life span is reduced, there is a decreased production of
erythropoietin and the bone marrow production of new blood cells is
often depressed. Additionally, the inflammatory response increases the
synthesis of hepcidin (a protein that regulates the entry of iron into
the blood circulation), which in turn increases the amount of iron
trapped in macrophages. Transfusion of whole blood, packed cells or
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blood components has not been shown to offer a survival advantage
and has been associated with a number of risks including infection,
febrile, allergic and hemolytic transfusion reactions, transfusionrelated circulatory overload and acute lung injury. In addition, the
significance of RBC storage duration and transfusion-associated endorgan injury and immunomodulatory effects are becoming more
appreciated.
Recent research has shown that institutions involved in blood collection
and transfusion should explore strategies that assure blood
availability, while limiting the use of the oldest RBCs currently
approved by regulation.5 In the last decades, it has become realized
that the use of transfusions does not offer a survival benefit when the
hemoglobin concentration becomes greater than 7 g/dL. The current
recommendations for RBC transfusions in adults are highlighted below.
Indications related to RBC Transfusion in the General Critically
Ill Patient6

RBC transfusion is indicated for patients with evidence of
hemorrhagic shock.

RBC transfusion may be indicated for patients with evidence
of acute hemorrhage and hemodynamic instability or
inadequate oxygen delivery.

A “restrictive” strategy of RBC transfusion (transfuse when
Hb< 7 g/dL) is as effective as a ‘liberal’ transfusion strategy
(transfusion when Hb < 10 g/dL) in critically ill patients with
hemodynamically stable anemia, except possibly in patients
with acute myocardial ischemia.
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
The use of only Hb level as a trigger for transfusion should be
avoided. Decision for RBC transfusion should be based on an
individual patient’s intravascular volume status, evidence of
shock, duration and extent of anemia, and cardiopulmonary
physiologic parameters.

In the absence of acute hemorrhage RBC, transfusion should
be given as single units.

Consider transfusion if Hb < 7 g/dL in critically ill patients
requiring mechanical ventilation (MV). There is no benefit of a
‘liberal’ transfusion strategy (transfusion when Hb < 10 g/dL)
in critically ill patients requiring MV.

Consider transfusion if Hb < 7 g/dL in resuscitated critically ill
trauma patients. There is no benefit of a ‘liberal’ transfusion
strategy (transfusion when Hb < 10 g/dL) in resuscitated
critically ill trauma patients.

Consider transfusion if Hb < 7 g/dL in critically ill patients
with stable cardiac disease. There is no benefit of a ‘liberal’
transfusion strategy (transfusion when Hb < 10 g/dL) in
critically ill patients with stable cardiac disease.

RBC transfusion should not be considered as an absolute
method to improve tissue oxygen consumption in critically ill
patients.

RBC transfusion may be beneficial in patients with acute
coronary syndromes (ACS) who are anemic (Hb ≤ 8 g/dL) on
hospital admission.
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Fluid And Electrolyte Balance In The ICU
Fluid and electrolyte balance is a critical issue in ICU patients. Often,
fluids can have unwanted effects on multiple organs, particularly in
patients with systemic inflammatory response. Electrolyte imbalances,
especially in patients with kidney dysfunction and impaired excretion
of fluids, are also critically important.
Sodium Overload
One liter of 0.9% saline infusion contains 3.4 g of sodium,
representing about eight 100 g packages of potato chips. Sources of
additional sodium include saline used to dilute medication and to keep
catheters open. This can result in hypernatremia in many patients —
recent studies have indicated that up to 7 % of ICU patients are
hypernatremic on admission. Hypernatremia is associated with disease
severity, kidney injury and dysfunction, mechanical ventilation, ICU
length-of-stay and higher in-hospital mortality. In many ICUs,
hypernatremia is considered a quality-of-care marker.
Chloride
Intravenous infusions such as 0.9% saline, Ringer’s lactate and
Plasmalyte contain 154, 109 and 98 mEq/L of chloride, respectively.
Initial chloride levels in patients are generally lower than initial sodium
concentrations; this can lead to uneven increases is chloride levels as
compared to sodium levels after infusions containing the same
amounts (in mEq/L) of each ion. Extra- to intravascular chloride shifts
can occur due to the combined effects of differences in transmembrane
potentials.
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The renal excretion of both sodium and chloride are often impaired in
many ICU patients, especially those with acute kidney injury (AKI).
This can result in a hyperchloremic metabolic acidosis or strong ion
difference (SID) acidosis, a condition associated with higher mortality,
particularly in septic patients.
Electrolyte overload has renal, hemodynamic, acid-base and
inflammatory consequences. These effects may be direct or indirect.
Fluid overload is also a concern in critically ill ICU patients and can
include renal, pulmonary and other end-organ consequences as well as
acid-base effects. A recent review on electrolyte and fluid imbalances
in critically ill patients recommended a patient-centered approach. This
includes the following approaches.
Fluid Resuscitation
Judicious fluid resuscitation includes timing. There is no evidence that
other than at the onset of injury (i.e., during surgery) or soon after
injury or insult (i.e., during the first hours of septic shock or major
surgery) infusion of supplemental fluids lead to improved results;
rather, the evidence suggests the opposite. Early use of vasopressors
may be beneficial, and repeated or excessive fluids should be avoided.
Acid-Base Monitoring
The acid-base status should be consistently monitored during fluid and
electrolyte resuscitation.
Active De-resuscitation
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Active de-resuscitation can involve the use of diuretics or, if necessary,
hemodialysis to maintain fluid and electrolyte balance.
Potassium
Hypokalemia can be defined as a serum potassium level of < 3.5
mEq/L. Potassium may be given by mouth of by intravenous (IV)
infusion. Potassium is usually replaced intravenously as KCl, which
raises the serum potassium levels quickly. Dosage is usually Oral: 40
meq three times to four times daily; IV: peripheral line 10 meq/hr.
With a central line, the dosage is usually 20 meq/hr. Potassium
bicarbonate/citrate/acetate is less commonly used, but may be used in
patients with metabolic acidosis. In general, every 10 mEq of K+ given
will raise the serum K+ by 0.1 mEq/L. Potassium levels should be
rechecked in 2-4 hours after an infusion. Potassium should be diluted
in saline as it may burn. Dextrose should be avoided as it can increase
potassium excretion. If infusing potassium, a femoral catheter is
recommended as using an internal jugular or subclavian can increase
potassium levels too rapidly.
Hypokalemia is usually secondary to GI losses (i.e., vomiting,
diarrhea) or urinary losses and often co-exists with other electrolyte
abnormalities. Symptoms include muscle weakness, cramps,
rhabdomyolysis, respiratory muscle weakness, anorexia, nausea,
vomiting.
Cardiac arrhythmias (atrial tachycardia, junctional tachycardia, AV
block, ventricular tachycardia or fibrillation) and ECG abnormalities
(PAC, PVC, sinus bradycardia, ST segment depression, decreased
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amplitude of T-wave, increased amplitude of U-wave (mostly in V4V6)) can be evident as well. Signs and symptoms include tetany,
seizures (in children and neonates), electrolyte imbalances
(hypokalemia, hypocalcemia), hypoparathyroidism (hypocalcemia),
vitamin D deficiency, ECG changes (widened QRS, peaked T-waves, PR
interval prolongation), and ventricular arrhythmias including torsades
des pointes.
Magnesium
Hypomagnesemia can be defined
IV MgSO4:
as a serum magnesium level of
1.5-1.9mg/dL: 2g magnesium
sulfate IV
1.2-1.4mg/dL:4g
0.8-1.1mg/dL: 6g
<.8mg/dL: 8g
Torsades des Pointes: 2g IV push
Low K+/Ca2+ with tetany or
arrhythmia
50meq (~6g) of IV Mg2+ given
slowly over 8-24 hrs
< 1.3mEq/L. In general, every 2 g
of MgSO4 will raise the serum Mg2+
by 0.5 mEq/L. Magnesium can be
given by mouth (usually as MgO)
or by IV (as MgSO4). Almost 12%
of hospitalized patients may have hypomagnesemia. It should be
suspected in patients with chronic diarrhea, other electrolyte
imbalances and ventricular arrhythmias.
Phosphorus
Hypophosphatemia can be defined as serum phosphorus of < 2.8
mg/dL. Phosphorus can be given by mouth or by IV.
Hypophosphatemia can occur in alcoholism, refeeding syndrome,
hyperalimentation, “Hungry Bone” syndrome, chronic antacid use,
primary or secondary hyperparathyroidism, Vitamin D deficiency and
Fanconi syndrome. Acute signs and symptoms of hypophosphatemia
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include encephalopathy, respiratory distress, decreased cardiac output,
proximal myopathies, elevated CPK and coagulopathy.
Chronic signs and symptoms of hypophosphatemia include
hypercalciuria and osteomalacia and rickets due to increased bone
resorption. Oral replacement is preferred. The dose should be adjusted
for patients with reduced glomerular filtration rate (GFR) (decreased
dose) and for certain patients with obesity. Phosphate levels should be
rechecked within 12 hours.
Calcium
Hypocalcemia can be defined as a
serum calcium < 8.4 mg/dL or an
ionized calcium < 4.2 mg/dL.
Calcium should only be given IV for
severe or symptomatic
hypocalcemia. Pseudohypcalcemia
should be ruled out by determining
the corrected calcium levels. As a
general rule, every 1 g of calcium
gluconate given will raise the serum
calcium by 0.5 mg/dL. Signs and
symptoms of acute hypocalcemia
Corrected Ca2+ = [(4 – albumin) x
0.8] + measured calcium.
Symptomatic or acute serum Ca2+
<7.5 mg/dL:
- IV Calcium gluconate 1-2 g (amp) over
10-20min.
- Temporary rise for 2-3 hrs, must be
followed by slower infusion
- 50 mL/hr if Ca2+ remains low)
Asymptomatic and serum Ca >7.5
mg/dL or chronic:
Oral therapy: calcium carbonate or citrate
1-2 g/day (500 mg bid-qid)
Consider Vitamin D in following cases:
Hypoparathyroidism: Vitamin D
- Calcitriol: 0.25-0.5 mcg bid
- Vitamin D deficiency: 50,000 IU/week
for 6-8 weeks then 800-1000 IU daily.
include tetany, seizures, bronchospasm, papilledema, and cardiac
symptoms (prolonged QT, hypotension, heart failure, arrhythmia).
There may also be signs of psychiatric manifestations.
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Complete Blood Count
Routine blood tests have not been shown to be of an overall benefit for
many critically ill patients and may actually cause harm. Recently, a
5-step quality improvement project was implemented to eliminate
unnecessary ordering of routine blood tests. The 5-steps used were
identified as:7
1. An educational component regarding the lack of evidence that
routine blood tests were medically justified and that repeated
blood draws could in fact prove deleterious.
2. An added checkbox to the ICU rounds checklist reminding
clinicians of the evidence presented in Step 1.
3. A rubber stamp made for orders and progress notes that read
‘No routine lab work indicated for tomorrow’.
4. Adding a prompt to the electronic ordering system that allowed
for acceptable indications when routine tests such as CBCs,
electrolytes, urea and creatinine were ordered.
5. Re-meeting with the staff reinforcing the first educational
component of the strategy.
It has been shown through studies that there was no increase in timecritical orders, no differences in severity of illness or the duration of
ICU stays. Additionally, studies have shown that fewer blood tests
ordered (over a period of 3 months) are associated with significant
cost savings. The American Board of Internal Medicine and the Critical
Care Societies Collaborative which includes the American Association
of Critical Care Nurses, the American College of Chest Physicians, the
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American Thoracic Society and the Society of Critical Care Medicine
has made the following recommendations:8
 Diagnostic tests — including complete blood counts (CBCs), blood
chemistries, arterial blood gases and ECGs — should only be ordered
as a response to specific clinical questions and not as a matter of
routine.
 A ‘restrictive’ transfusion policy is recommended; hemodynamically
stable patients who are not bleeding and a hemoglobin
concentration of greater than 7 g/dL should not be transfused. An
exception may be patients with acute coronary syndrome. However,
most studies of aggressive transfusions indicate that harm may be
caused in these patients as well.
Critical CBC Values
There are a number of generally accepted critical or ‘alert’ values.
These values may vary slightly in different settings. Individual values
need to be interpreted for each individual patient. The values used at
Massachusetts General Hospital identified as life threatening or that
place the patient at serious risk if left untreated is listed below.9

Hematocrit
 >56%
 ≤20%

Platelet counts
 <40,000 (pediatric patients <20,000)
 >999,000

White blood cells
 <1500
 >50,000
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
Hemoglobin
 <6.5 g/dL

INR
 ≥4.0
CBCs after Bleeding Episodes
It is important to remember that many of the variables such as
hemoglobin and the hematocrit can remain unchanged for up to 12
hours. There is no absolute hematocrit or hemoglobin level that
universally should prompt a transfusion, though patients at risk for
myocardial ischemia are generally transfused when Hgb levels fall
below 7 g/dL. As stated above, repeated CBCs should be avoided as
much as possible due to the potential for inducing anemia and have
not been shown to add clinical value. Coagulation studies may also not
be useful because of the time delay in equilibration after hemorrhage
begins.
Coagulation studies may be useful for those patients on warfarin, low
molecular weight heparin, or antiplatelet medications or those patients
with severe preexisting hepatic insufficiency. Total bleeding time may
be useful, but is difficult to perform in a patient with acute
hemorrhage; aPTT and PT tests, if abnormal, require correcting. On
the other hand, arterial blood gas and pH levels can be good indicators
for oxygen imbalance at the tissue level. A pH of less than 7.25
generally requires intervention.
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Blood Chemistries
As with CBCs, blood chemistries should not necessarily be routinely
performed, but only if potentially critical and medically necessary
information can be obtained.

Total bilirubin (neonates and infants)
 For infants between 0 and 3 months: >15 mg/dL
 For infants between 4 and 6 months: >20 mg/dL

Calcium
 <6.5 mg/dL or > 14 mg/dL

Total CO2
 <11 mmol/L or > 40 mmol/L

Glucose
 <40 mg/dL

Magnesium
 <1.2 mg/dL or >5.9 mg/dL

Potassium
 <2.8 mmol/L or >6.0 mmol/L

Sodium
 <120 mmol/L or >160 mmol/L

Serum/Plasma osmolality
 <250 mOsm/kg water or >335 mOsm/kg water

Anion Gap
 The anion gap is used primarily to evaluate metabolic
acidosis, though metabolic acidosis can exist with a normal
anion gap.
 An elevated anion gap suggests the presence of metabolic
acidosis (anion gap >30 mmol/L). The anion gap depends on
both serum phosphate and serum albumin levels; in patients
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with low albumin levels, a falsely normal anion gap may be
present.
 Anion Gap = Na+ – (Cl- + HCO3-)- 12 +/-2
 Every 1g/L decrease in albumin will decrease the
anion gap by ≈0.25 mmol. The corrected anion gap
can be calculated: AG + (0.25 X (40-albuming/L).
 A normal anion gap is ≈12 meq/L.
 Causes of a high anion gap can be caused by ketoacidosis
(diabetic, alcoholic, starvation), uremia (renal failure),
lactic acidosis and toxins (ethylene glycol, methanol,
paraldehyde, salicylates); Mnemonic: KULT. Another
mnemonic is MUDPILES (Methanol, Uremia, DKA,
Paraldehyde, INH, Lactic acidosis, Ethylene glycol,
Salicylate).

Delta values (Delta ratio) or Δ/Δ
 The delta ratio can be used to determine if a mixed acid
base disorder exists.
 If Δ/Δ is < 0.4, suspect hyperchloremic AG acidosis
 If Δ/Δ is <1, suspect High AG and Normal AG acidosis
 If Δ/Δ is 1-2, suspect pure Anion Gap Acidosis, Lactic
acidosis (the average value is 1.6) or DKA. DKA is more
likely to have a ratio closer to 1 because of urinary loss of
ketones.
Arterial Blood Gas
Arterial blood gas samples are often obtained. Levels should be
maintained so that PaO2 is between 60-80mm Hg, representing 92100% saturation. The American Thoracic Society recommends a 6-step
approach to the interpretation of arterial blood gasses.10
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Step 1:
The internal consistence of arterial blood gas (ABG) measurements
should be assessed based on the Henderson-Hasselbach equation.
[H+] = (24 PaCO2)/[HCO3-]. As a rule, the pH is not consistent with the
ABG.
•
If the pH is 7.00, the [H+] = 100 mmol/L
•
If the pH is 7.05, the [H+] = 89 mmol/L
•
If the pH is 7.10, the [H+] = 79 mmol/L
•
If the pH is 7.15, the [H+] = 71mmol/L
•
If the pH is 7.20, the [H+] = 63 mmol/L
•
If the pH is 7.25, the [H+] = 56 mmol/L
•
If the pH is 7.30, the [H+] = 50 mmol/L
•
If the pH is 7.35, the [H+] = 45 mmol/L
•
If the pH is 7.40, the [H+] = 40 mmol/L
•
If the pH is 7.45, the [H+] = 35 mmol/L
•
If the pH is 7.50, the [H+] = 32 mmol/L
•
If the pH is 7.55, the [H+] = 28 mmol/L
•
If the pH is 7.60, the [H+] = 25 mmol/L
•
If the pH is 7.65, the [H+] = 22 mmol/L
•
Determine if there is acidemia or alkalemia present based
Step 2:
on the measured pH levels.
 Acidemia: pH<7.35
 Alkalemia: pH>7.45
•
To determine this, the PaCO2, the HCO3- and the anion gap
need to be determined.
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•
Acidosis or alkalosis may be present with a normal pH
between 7.35 - 7.45.
Step 3:
•
Differentiate between respiratory and metabolic
acidosis/alkalosis. In respiratory-based disorders the pH
and the PaCO2 change in the opposite directions while in
metabolically-based disorders change in the same
direction.
 In respiratory acidosis the pH decreases and the PaCO2
increases.
 In respiratory alkalosis the pH increases and the PaCO2
decreases.
 In metabolic acidosis the pH decreases and the PaCO2
decreases.
 In metabolic alkalosis the pH increases and the PaCO2
increases.
Step 4:
Determine if there is appropriate compensation for the
acidosis and alkalosis. If the observable compensation does
not match the expected compensation, it is likely there may
be more than one acid-base disorder present.
Step 5:
•
If metabolic acidosis exists, calculate the anion gap.
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Step 6:
•
The delta ratio may be used in the assessment of elevated anion
gap metabolic acidosis to determine if a mixed acid base disorder is
present. Albumin levels should be adjusted.
Disorder
Expected Compensation
Correction
Factor
Metabolic acidosis
PaCO2 = (1.5 x [HCO3-]) +8
+/- 2
Acute respiratory
acidosis
Increase in [HCO3-] = ∆ PaCO2/10
+/- 3
Chronic respiratory
acidosis
Increase in [HCO3-] = 3.5(∆
PaCO2/10)
Metabolic alkalosis
Increase in PaCO2 = 40 + 0.6(∆HCO3)
Acute respiratory
alkalosis
Decrease in [HCO3-] = 2(∆ PaCO2/10)
Chronic respiratory
alkalosis
Decrease in [HCO3-] =5(∆ PaCO2/10)
to 7(∆ PaCO2/10)
For mixed and complex acid-base disturbances, the following may be
helpful in determining the underlying causes.

Respiratory acidosis associated with metabolic acidosis may be
characterized by:
 A decrease in pH
 A decrease in HCO3 An increase in PaCO2
 This situation may occur in some cases of cardiac arrest,
intoxications and multi-organ failure
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
Respiratory alkalosis associated with metabolic alkalosis may be
characterized by:
 An increase in pH
 An increase in HCO3 A decrease in PaCO2
 This situation may occur in some cases of cirrhosis (with
diuretics), nausea of pregnancy, chronic obstructive
pulmonary disease (COPD) over-ventilation

Respiratory acidosis associated with metabolic alkalosis may be
characterized by:
 Normal pH
 An increase in PaCO2
 An increase in HCO3 This situation may occur in some cases of COPD (with
diuretics, vomiting, NG suction), severe hypokalemia

Respiratory alkalosis associated with metabolic acidosis may be
characterized by:
 Normal pH
 A decrease in PaCO2
 A decrease in HCO3 This situation may occur in some cases of uremia or
ketoacidosis with vomiting, NG suction, use of diuretics
Patients With Arrythmia And Laboratory Testing
Patients with arrhythmias should have magnesium, phosphate and
calcium levels carefully monitored. Electrolyte abnormalities can cause
or contribute to arrhythmias and cardiac arrest and may hamper
efforts at resuscitation.
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Potassium
The potassium gradient across the myocardial cells can determine the
excitability of the myocardial cell membrane. The potassium gradient
(and the levels of serum potassium) is affected by acid-base balance
— when pH decreases, potassium levels in the serum can increase
because of an intracellular to extracellular shift. This is especially
critical in patients with arrhythmias and comorbidities that can affect
the acid-base balance including, for example, diabetic ketoacidosis.
Hyperkalemia is classified as moderate and severe: moderate (K+ 6-7
mEq/L) and severe (>7 mEq/L) hyperkalemia, which is life threatening
and is seen most commonly in end-stage renal disease. Other causes
include chronic renal failure, metabolic acidosis,
pseudohypoaldosteronism Type II, chemotherapy (with tumor lysis),
rhabdomyolysis, renal tubular acidosis, hemolytic disorders, Addison’s
disease and hyperkalemic periodic paralysis. Signs and symptoms of
hyperkalemia include weakness, generalized fatigue, paresthesias,
ascending paralysis, and respiratory failure. ECG changes include early
findings of peaked T waves (tenting). Later changes include flattened P
waves, prolonged PR interval (first-degree heart block), widened QRS
complex, deepened S waves, and a merging of S and T waves.
Untreated hyperkalemia can result in sine-wave patterns, and
idioventricular rhythms. Asystolic cardiac arrest can rapidly develop.
Diuretics (i.e., furosemide) and resins such as kayexalate may be used
for mild (5-6 mEq/L) hyperkalemia, while moderate hyperkalemia may
be treated with:
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 Calcium gluconate or calcium chloride can be used to reduce the
risk of ventricular fibrillation
 Insulin plus glucose will induce an intracellular shift of potassium
because of the ‘dragging’ effect of glucose
 Alkalizing agents will increase the pH, also inducing an
intracellular shift of potassium
 Diuretics to induce renal excretion of potassium
 Beta-2-adrenergic agonist to promote intracellular uptake
 Binding resins, promoting K-Na exchange in the GI tract
Hypokalemia can be defined as a serum potassium level of <3.5
mEq/L. Common causes include loss from the GI tract, loss from renal
excretion (due to hyperaldosteronism, hyperglycemia (severe),
medications such as K+ depleting diuretics, amphotericin B, etc.),
alkalosis, and malnutrition. Mild hypokalemia can result in weakness,
fatigue, paralysis, respiratory difficulty, constipation, paralytic ileus,
and leg cramps. More severe hypokalemia can result in alterations in
myocardial excitability, changes in ECGs such as the presence of U
waves, T-wave flattening, and arrhythmias including ventricular
arrhythmias. Treatment of hypokalemia is generally by infusion and
minimizing loss.
Sodium
Sodium is the major extracellular ion involved in maintaining serum
osmolality and water/ion shifts between the inter- and extravascular
spaces. Hypernatremia is defined as a serum sodium concentration
greater than 145-150 mEq/L. Hypernatremia can be caused by excess
mineralocorticoid (i.e., hyperaldosteronism), excess glucocorticoid
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(i.e., Cushing’s syndrome), excessive hypertonic saline infusion,
sodium bicarbonate administration and by excess dehydration through
GI or renal losses.
Symptoms of hypernatremia are primarily neurologic in nature and
include altered mental states, weakness, irritability, focal neurologic
deficits, coma and seizures. Treatment reduces the cause(s) of
dehydration and correcting any water deficit with normal saline or 5%
dextrose in half-normal saline. The water deficit is calculated and the
fluid is administered to lower the rate of sodium decrease by 0.5 to 1.0
mEq per hour over the first 24 hours.
Hyponatremia is defined as serum [Na+] levels lower than 130 mEq/L
and is commonly caused by reduced renal excretion of water or
urinary loss of sodium. Reduced renal excretion of water can be
caused by thiazide diuretics, renal failure, depletion of the extracellular
fluid (i.e., by vomiting), Syndrome of Inappropriate Antidiuretic
Hormone (SIADH) secretion, congestive heart failure, cirrhosis (with
ascites), hypothyroidism and adrenal insufficiency. Hypo-osmolar
hyponatremia is the most common, but in uncontrolled diabetes, there
may exist a hyper-osmolar hyponatremia. Hyponatremia is often
asymptomatic, but an acute drop in sodium levels can cause nausea,
vomiting, headache, lethargy, seizures, cerebral edema, coma and
death. Hyponatremia is treated by the administration of sodium and
the volume reduction. For gradual increases in sodium (0.5
mEq/L/hour) unless seizures are present, with seizures of other
neurologic symptoms, the serum level should be corrected more
rapidly, i.e., 2-4 mEq/L/hour.
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Magnesium
Magnesium is one of the most common minerals in the body and is
required for a wide variety and large number of critical reactions. It is
bound to serum albumin and serum levels often do not reflect total
body levels; serum magnesium levels can appear to be normal in the
face of depleted bone stores. In addition, magnesium balance is
closely associated with sodium, calcium and potassium levels.
Hypermagnesemia ([Mg2+] >2.2mEq/L) is most commonly related to
renal failure and is characterized by muscular weakness, paralysis,
ataxia, drowsiness, and confusion. Hypermagnesemia can also produce
vasodilation and severe hypermagnesemia can result in severe
hypotension, bradycardia, cardiac arrhythmias, hypoventilation and
cardiorespiratory arrest. Hypermagnesemia is treated by chelation by
calcium. Severe cases may be treated with dialysis.
Hypomagnesemia ([Mg2+] < 1.3mEq/L) occurs in ~10% of all
hospitalized patients, and commonly results from decreased absorption
or increased loss from the GI and kidneys. The levels of T3/T4 can also
affect magnesium levels. Symptoms of low serum magnesium include
muscular fasciculations or tremors, ocular nystagmus, tetany, altered
mental state and cardiac arrhythmias such as torsades de pointes.
Patients may also have ataxia, vertigo, seizures, and dysphagia.
Severe hypomagnesemia is treated with MgSO4.
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Calcium
Calcium is the most abundant mineral in the body, and, as
magnesium, is involved in a wide number and variety of cellular
reactions and processes. About 50% of all extracellular calcium,
regulated by parathormone and Vitamin D, is bound to albumin while
the other 50 % is in the active, ionized form. The levels of ionized
calcium levels are inversely related to the albumin levels and can
therapeutically act as an ionic antagonist to both magnesium and
potassium.
Hypercalcemia is defined as a serum calcium level of > 10.5 mEq/L or
an ionized calcium level of > 4.8mg/dL. Hypercalcemia is most
commonly due to primary hyperparathyroidism and the presence of a
malignancy. Neurologic symptoms of moderate hypercalcemia include
depression, weakness, fatigue and confusion. More significant
hypercalcemia can be characterized by hallucinations, disorientation,
hypotonicity, seizures, and coma. Further, hypercalcemia can affect
the renal concentration of urine and the resultant diuresis can cause
dehydration.
Serum calcium levels above 15 mg/dL can have cardiac effects
including depressed myocardial contractility, decreased automaticity
and shortened ventricular systole. Hypercalcemia can exacerbate
digitalis toxicity. Hypercalcemic individuals can also become
hypokalemic, contributing to potential arrhythmias. QT interval
shortening is often seen in calcium levels above 13mg/dL along with
prolonged PR and QRS intervals. At serum calcium levels above 15
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mg/dL, atrioventricular blocks can occur, sometimes leading to cardiac
arrest.
Treatment should generally begin if a patient exhibits calcium levels
above 12 mg/dL and is often begun with saline diuresis, with
potassium and magnesium levels constantly monitored. Loop diuretics
may be used along with hydration. In patients with heart failure or
renal insufficiency, hemodialysis may be necessary as may be the use
of chelating agents. Bisphosphonates may be used in some cases,
though these may take up to 72 hours to reach therapeutic efficacy.
Hypocalcemia exists with a serum calcium levels below 8.5 mg/dL or
ionized calcium of less than 4.2 mg/dL. The more common causes of
hypocalcemia are toxic shock syndrome, alterations in magnesium
levels, post-thyroid surgery, tumor lysis syndrome and fluoride
poisoning. Symptoms generally appear with calcium levels below 2.5
mg/dL and include paresthesias of the extremities and face, muscle
cramps, carpopedal spasm, stridor, tetany, and seizures. Signs include
hyperreflexia and positive Chvostek and Trousseau signs. Decreased
myocardial contractility and heart failure can also occur. In addition,
hypocalcemia can exacerbate digitalis toxicity. Treatment is supportive
at first and may be followed with administration of calcium — acutely,
with 10% calcium gluconate or calcium chloride (used cautiously).
Nutrition And Laboratory Blood Values
The American Society for Parenteral and Enteral Nutrition (ASPEN)
along with the Society of Critical Care Medicine (SCCM) has produced a
series of guidelines for nutrition support therapy in critically ill
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patients.11 The following guidelines for adults receiving enteral
nutrition (EN) and parenteral nutrition (PN) are necessary for ICU
clinicians to understand, and are outlined below.
Enteral Nutrition
Traditional nutrition assessment tools (albumin, prealbumin, and
anthropometry) are not validated in critical care. Before initiation of
feedings, assessment should include evaluation of weight loss and
previous nutrient intake prior to admission, level of disease severity,
comorbid conditions, and function of the gastrointestinal (GI) tract.
Nutrition support therapy in the form of enteral nutrition should be
initiated in the critically ill patient who is unable to maintain volitional
intake.
Enteral nutrition is the preferred route of feeding over parenteral
nutrition for the critically ill patient who requires nutrition support
therapy. Enteral feeding should be started early within the first 24-48
hours following admission. The feedings should be advanced toward
goal over the next 48-72 hours.
In the setting of hemodynamic compromise (patients requiring
significant hemodynamic support including high dose catecholamine
agents, alone or in combination with large volume fluid or blood
product resuscitation to maintain cellular perfusion), EN should be
withheld until the patient is fully resuscitated and/or stable.
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In the ICU patient population, neither the presence nor absence of
bowel sounds nor evidence of passage of flatus and stool is required
for the initiation of enteral feeding.
When to Use Parenteral Nutrition
If early EN is not feasible or available the first 7 days following
admission to the ICU, no nutrition support therapy should be provided.
In the patient who was previously healthy prior to critical illness with
no evidence of protein-calorie malnutrition, use of PN should be
reserved and initiated only after the first 7 days of hospitalization
(when EN is not available). If there is evidence of protein-calorie
malnutrition on admission and EN is not feasible, it is appropriate to
initiate PN as soon as possible following admission and adequate
resuscitation.
In a patient expected to undergo major upper GI surgery where EN is
not feasible, PN should be provided under very specific conditions:

If the patient is malnourished, PN should be initiated 5-7 days
preoperatively and continued into the postoperative period.

PN should not be initiated in the immediate postoperative period
but should be delayed for 5-7 days (should EN continue not to be
feasible).

PN therapy provided for a duration of <5-7 days would be
expected to have no outcome effect and may result in increased
risk to the patient. Thus, PN should be initiated only if the
duration of therapy is anticipated to be ≥7 days.
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Dosing of Enteral Feeding
The target goal of EN (defined by energy requirements) should be
determined and clearly identified at the time of initiation of nutrition
support therapy. Energy requirements may be calculated by predictive
equations or measured by indirect calorimetry. Predictive equations
should be used with caution, as they provide a less accurate measure
of energy requirements than indirect calorimetry in the individual
patient. In the obese patient, the predictive equations are even more
problematic without availability of indirect calorimetry.
Efforts to provide >50% - 65% of goal calories should be made in
order to achieve the clinical benefit of EN over the first week of
hospitalization.
If unable to meet energy requirements (100% of target goal calories)
after 7-10 days by the enteral route alone, consideration should be
given to initiating supplemental PN. Initiating supplemental PN prior to
this 7-10 day period in the patient already receiving EN does not
improve outcome and may be detrimental to the patient.
Ongoing assessment of adequacy of protein provision should be
performed. The use of additional modular protein supplements is a
common practice, as standard enteral formulations tend to have a high
non-protein calorie:nitrogen ratio. In patients with body mass index
(BMI) <30, protein requirements should be in the range of 1.2 - 2.0
g/kg actual body weight per day, and may likely be even higher in
burn or multi-trauma patients.
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In the critically ill obese patient, permissive underfeeding or
hypocaloric feeding with EN is recommended. For all levels of obesity
where BMI is >30, the goal of the EN regimen should not exceed 60%
- 70% of target energy requirements or 11 - 14 kcal/kg actual body
weight per day (or 22 - 25 kcal/kg ideal body weight per day). Protein
should be provided in a range ≥2.0 g/kg ideal body weight per day for
patients with BMI 30 - 40, ≥2.5 g/kg ideal body weight per day and for
BMI ≥ 40.
Monitoring Tolerance and Adequacy of Enteral Nutrition
In the ICU setting, evidence of bowel motility (resolution of clinical
ileus) is not required in order to initiate EN in the ICU. Patients should
be monitored for tolerance of EN (determined by patient complaints of
pain and/or distention, physical exam, passage of flatus and stool, and
abdominal radiographs).
Inappropriate cessation of EN should be avoided. Holding EN for
gastric residual volumes <500 mL in the absence of other signs of
intolerance should be avoided. The time period that a patient is made
nil per os (NPO) prior to, during, and immediately following the time of
diagnostic tests or procedures should be minimized to prevent
inadequate delivery of nutrients and prolonged periods of ileus. Ileus
may be propagated by NPO status.
Use of enteral feeding protocols increases the overall percentage of
goal calories provided and should be implemented. Patients placed on
EN should be assessed for risk of aspiration. Steps to reduce risk of
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aspiration should be employed. The following measures have been
shown to reduce risk of aspiration:

In all intubated ICU patients receiving EN, the head of the bed
should be elevated 30° - 45°.

For high-risk patients or those shown to be intolerant to gastric
feeding, delivery of EN should be switched to continuous
infusion.

Agents to promote motility such as prokinetic drugs
(metoclopramide and erythromycin) or narcotic antagonists
(naloxone and alvimopan) should be initiated where clinically
feasible.

Diverting the level of feeding by post-pyloric tube placement
should be considered.

Use of chlorhexidine mouthwash twice a day should be
considered to reduce risk of ventilator-associated pneumonia.
Blue food coloring and glucose oxidase strips, as surrogate markers for
aspiration, should not be used in the critical care setting. Development
of diarrhea associated with enteral tube feedings warrants further
evaluation for etiology.
Selection of Appropriate Enteral Formulation
Immune-modulating enteral formulations (supplemented with agents
such as arginine, glutamine, nucleic acid, ω-3 fatty acids, and
antioxidants) should be used for the appropriate patient population
(major elective surgery, trauma, burns, head and neck cancer, and
critically ill patients on mechanical ventilation), with caution in patients
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with severe sepsis. ICU patients not meeting criteria for immunemodulating formulations should receive standard enteral formulations.
Patients with acute respiratory distress syndrome (ARDS) and severe
acute lung injury (ALI) should be placed on an enteral formulation
characterized by an anti-inflammatory lipid profile (i.e., ω-3 fish oils,
borage oil) and antioxidants. To receive optimal therapeutic benefit
from the immune-modulating formulations, at least 50% - 65% of goal
energy requirements should be delivered.
If there is evidence of diarrhea, soluble fiber-containing or small
peptide formulations may be utilized.
Parenteral Nutrition
If EN is not available or feasible, the need for PN therapy should be
evaluated. If the patient is deemed to be a candidate for PN, steps to
maximize efficacy (regarding dose, content, monitoring, and choice of
supplemental additives) should be used.
In all ICU patients receiving PN, mild permissive underfeeding should
be considered at least initially. Once energy requirements are
determined, 80% of these requirements should serve as the ultimate
goal or dose of parenteral feeding. Eventually, as the patient
stabilizes, PN may be increased to meet energy requirements. For
obese patients (BMI ≥ 30), the dose of PN with regard to protein and
caloric provision should follow the same recommendations given for
EN.
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In the first week of hospitalization in the ICU, when PN is required and
EN is not feasible, patients should be given a parenteral formulation
without soy-based lipids. A protocol should be in place to promote
moderately strict control of serum glucose when providing nutrition
support therapy. A range of 110 - 150 mg/dL may be most
appropriate. Additionally, when PN is used in the critical care setting,
consideration should be given to supplementation with parenteral
glutamine.
In patients stabilized on PN, periodically repeated efforts should be
made to initiate EN. As tolerance improves and the volume of EN
calories delivered increases, the amount of PN calories supplied should
be reduced. PN should not be terminated until ≥60% of target energy
requirements are being delivered by the enteral route.
Adjunctive Therapy
Administration of probiotic agents has been shown to improve outcome
(most consistently by decreasing infection) in specific critically ill
patient populations involving transplantation, major abdominal
surgery, and severe trauma. No recommendation can currently be
made for use of probiotics in the general ICU population due to a lack
of consistent outcome effect. It appears that each species may have
different effects and variable impact on patient outcome, making it
difficult to make broad categorical recommendations. Similarly, no
recommendation can currently be made for use of probiotics in
patients with severe acute necrotizing pancreatitis, based on the
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disparity of evidence in the literature and the heterogeneity of the
bacterial strains utilized.
A combination of antioxidant vitamins and trace minerals (specifically
including selenium) should be provided to all critically ill patients
receiving specialized nutrition therapy.
The addition of enteral glutamine to an EN regimen (not already
containing supplemental glutamine) should be considered in burn,
trauma, and mixed ICU patients.
Soluble fiber may be beneficial for the fully resuscitated,
hemodynamically stable critically ill patient receiving EN who develops
diarrhea. Insoluble fiber should be avoided in all critically ill patients.
Both soluble and insoluble fiber should be avoided in patients at high
risk for bowel ischemia or severe dysmotility.
Pulmonary Failure
Specialty high-lipid low-carbohydrate formulations designed to
manipulate the respiratory quotient and reduce CO2 production are
not recommended for routine use in ICU patients with acute
respiratory failure. Fluid-restricted calorically dense formulations
should be considered for patients with acute respiratory failure. Serum
phosphate levels should be monitored closely and replaced
appropriately when needed.
Renal Failure
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Patients in the ICU with acute renal failure (ARF) or acute kidney
injury (AKI) should be placed on standard enteral formulations, and
standard ICU recommendations for protein and calorie provision
should be followed. If significant electrolyte abnormalities exist or
develop, a specialty formulation designed for renal failure (with
appropriate electrolyte profile) may be considered.
Patients receiving hemodialysis or continuous renal replacement
therapy (CRRT) should receive increased protein, up to a maximum of
2.5 g/kg/d. Protein should not be restricted in patients with renal
insufficiency as a means to avoid or delay initiation of dialysis therapy.
Hepatic Failure
Traditional assessment tools should be used with caution in patients
with cirrhosis and hepatic failure, as these tools are less accurate and
less reliable due to complications of ascites, intravascular volume
depletion, edema, portal hypertension, and hypoalbuminemia. EN is
the preferred route of nutrition therapy in ICU patients with acute
and/or chronic liver disease. Nutrition regimens should avoid
restricting protein in patients with liver failure.
Standard enteral formulations should be used in ICU patients with
acute and chronic liver disease. Branched chain amino acid
formulations (BCAA) should be reserved for the rare encephalopathic
patient who is refractory to standard treatment with luminal acting
antibiotics and lactulose.
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Acute Pancreatitis
On admission, patients with acute pancreatitis should be evaluated for
disease severity. Patients with severe acute pancreatitis should have a
nasoenteric tube placed and EN initiated as soon as fluid volume
resuscitation is complete.
Patients with mild to moderate acute pancreatitis do not require
nutrition support therapy (unless an unexpected complication develops
or there is failure to advance to oral diet within 7 days). The gastric or
jejunal route may be used to feed patients with severe acute
pancreatitis enterally.
Tolerance to EN in patients with severe acute pancreatitis may be
enhanced by the following measures:

Minimizing the period of ileus after admission by early initiation
of EN.

Displacing the level of infusion of EN more distally in the GI
tract.

Changing the content of the EN delivered from intact protein to
small peptides, and long-chain fatty acids to medium-chain
triglycerides or a nearly fat-free elemental formulation.

Switching from bolus to continuous infusion.
For the patient with severe acute pancreatitis, when EN is not feasible,
use of PN should be considered. PN should not be initiated until after
the first 5 days of hospitalization.
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Nutrition Therapy in End-of-Life
Specialized nutrition therapy is not obligatory in cases of futile care or
end-of-life situations. The decision to provide nutrition therapy should
be based on effective patient/family communication, realistic goals,
and respect for patient autonomy.
Total Parenteral Nutrition
Total parenteral nutrition (TPN) or Total Enteral Nutrition (TEN) may
be needed for patients with some stages of ulcerative colitis, short
bowel syndrome, bowel obstruction and in certain pediatric disorders
such as congenital anomalies or prolonged diarrhea. The major
indication for TPN is some failure of the GI tract to perform normally.
Children may need more energy and amino acids and may have
different fluid requirements. Use of TPN requires adequate water,
calories, amino acids, essential fatty acids, vitamins and minerals.12
A recent systematic review indicated that between 38-78% of ICU
show signs of malnutrition — this increases re-admission, infections
and mortality.13 A NUTRIC scoring system can be used to determine
nutritional status and disease severity. A more comprehensive
nutritional assessment can include:

Medical/surgical History
 History of weight loss
 Any conditions that may be associated with an acute
inflammatory response such as a major infection, major
abdominal surgery, closed head injuries, sepsis, adult
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respiratory distress syndrome, severe burns and systemic
inflammatory response syndrome
 Chronic conditions that may predispose to nutritional risk.
Examples include GI surgery and hemorrhage, fistulas, GI
obstruction, ischemia, pancreatitis, inflammatory bowel
disease, malignancy, post-transplantation, major organ
failure and HIV-AIDs.

Clinical diagnosis of conditions associated with inflammation and
malnutrition

Physical exam including both specific or non-specific signs of
inflammation

Anthropometric data
 Sudden or unexplained weight loss and underweight status

Laboratory indicators such as albumin and prealbumin

Dietary evaluation

Functional outcomes (strength and physical performance related
to muscle mass)
Energy Estimation
Energy expenditure (EE) is often used to determine the caloric needs
of a patient in the ICU. During the early phases of a critical illness,
however, it is believed that the caloric needs are likely to be lower
than the EE while during later phases the caloric needs are likely to be
higher than the EE. In addition, patients with liver dysfunction may
have energy requirements significantly different than the EE. In
general, a fixed amount of calories (per kg of body weight) are
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recommended. Many equations have been derived that may be
predictive for energy needs, but may be difficult to implement
clinically.
Total parenteral nutrition can be life saving in a number of clinical
conditions, but there are a number of serious adverse effects that
must be monitored and addressed. Nutritional support teams can often
provide specific advice for specific situations, but TPN can result in:14,15

Re-feeding Syndrome
 Vitamin B1 deficiency and acute beriberi
 Volume overload, edema, cardiac insufficiency, pulmonary
edema
 Electrolyte disorders
 Arrhythmias
 Hyperglycemia

Hyperglycemia, especially in pre-diabetic or diabetic patients
 Glucose should be monitored and maintained between 80145mg/dL

Hypertriglyceridemia
 Triglycerides should be monitored and maintained below
400mg/dL

Dyslipoproteinemia and EFA deficiencies
 A triene to tetraene ratio of > 0.1 is diagnostic of an EFA
deficiency
 Lipid emulsions with low amounts of polyunsaturated fatty
acids (PUFA) and low amounts of medium chain
triglycerides should be used with total calories of lipids
≤30%.
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
Acid-base imbalances
 Serum electrolytes, blood gases must be consistently
monitored

Liver dysfunction
 Using minimal enteral feeding may reduce the risk of
biliary complications (a trial of enteral feeding should be
used as soon as clinically possible)
 In liver dysfunction, the reduction of the use of lipids
should be considered
 Consider choline, glutamine and/or lecithin
supplementation
 Patients with liver dysfunction may require carnitine
supplementation to maintain levels between 30-60μmol/L
with free carnitine at 20μmol/L

Bone demineralization/Osteoporosis
 Serum Ca2+ levels, parathyroid hormone levels, levels of
25-OH-vitamin D, urinary Ca2+ and Mg2+ should be
regularly monitored, particularly patients on long-term TPN

Infections
 Infections should be monitored and treated aggressively

Intestinal effects can include mucosal atrophy and leaky gut
syndrome
 Small intestinal bacterial overgrowth (SIBO) should be
aggressively treated
Strict sterile techniques must be consistently used and the central
venous catheter must be monitored for signs of infection. TPN is
generally begun starting at 50% of the expected requirements with
5% dextrose used to complete the fluid component. Insulin, if needed,
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can be added to the TPN solution. Patient progress is generally also
constantly monitored; this usually entails weight measurements, CBCs,
electrolyte levels, BUN and blood glucose levels. Blood glucose
abnormalities are common and are an independent predictor or
mortality in patients treated with TPN.
Other common complications are catheter-related sepsis, liver
dysfunction, increased ammonia levels (particularly in infants), volume
overload, bone disease or demineralization, cholelithiasis, cholecystitis
and accumulation of ‘sludge’ in the gallbladder. More rarely, there are
adverse reactions to the use of lipid emulsions — these can include
dyspnea, nausea, headaches, allergic reaction, back pain, dizziness
and sweating.
Omega-3 and omega-6 essential fatty acids can be used to help
decrease inflammatory markers in all patients, including septic
patients. It should be mentioned that a recent meta-analysis indicated
that supplementation with omega-3 (ω-3) essential fatty acids do not
improve mortality, complications due to infections, and ICU length of
stay, though they do appear to reduce the total length of stay in
hospital. It should also be mentioned, however, that other larger,
meta-analyses have concluded that inclusion of omega-3 essential
fatty acids in TPN are safe, effective and reduce the rates of infection
in both surgical and in ICU patients and reduce the duration of stay in
both groups of patients.
The use of omega-3 supplementation with TPN in neonates had been
reviewed relative to parenteral nutrition-associated cholestasis (PNAC)
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and reversal or prevention of PNAC in this patient population. It was
found that the while omega-3 containing emulsions were not effective
in preventing PNAC, the omega-3 containing emulsions were more
effective at reversing PNAC than were similar emulsions containing
either soybean or olive oil.
Liver Function Tests
Liver function tests are usually recommended at least weekly,
particularly in patients receiving total parenteral nutrition. Significant
percentages of patients on long-term TPN suffer deleterious liver
effects, primarily diagnosed by elevated bilirubin and liver enzymes.
Up to 40% of adult patients experience liver dysfunction and 22% of
deaths in long term TPN are related to liver disease. Other
complications include hypertriglyceridemia, hyperglycemia and fatty
liver disease. Adult patients on TPN are at higher risk of:16

Steatosis

Steatohepatitis

Biliary sludge

Fatty liver

Cholelithiasis

Cholestasis

Fibrosis

Micronodular cirrhosis

Phospholipidosis
Infants and neonates are at higher risk of:

Cholestasis
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
Distended gallbladder (abdominal pseudotumor)

Fibrosis

Cirrhosis

Biliary sludge

Cholelithiasis
While the causes of liver dysfunction during TPN are not well
understood, they appear to be related to excess caloric intake,
impaired triglyceride secretion, increased hepatic fat deposition,
increased insulin secretion and deficiencies in essential fatty acids. Up
to 40% of adult patients experience liver dysfunction and 22% of
deaths in long term TPN are related to liver dysfunction. The
dysfunctions include hepatic steatosis, cholecystitis, biliary sludge and
cholestasis.
In very low birth-weight infants, cyclic/continuous TPN is also
associated with cholestasis. In these infants, the use of Di(2ethylhexyl) phthalate (DEHP)-containing polyvinylchloride infusion
systems may increase the risk. The risk in very low-birth-weight
infants may be decreased with the use of ursodiol (10-30 mg/kg/day)
within 14 days after cholestasis onset.
Liver function tests (LFT), including tests on hepatic enzymes such as
alanine transaminase (ALT or SGPT), aspartate transaminase (AST or
SGOT), alkaline phosphatase (ALP) and gamma-glutamyl
transpeptidase (GGT) should be routinely done as should liver protein
tests for albumin, globulin, prothrombin. Bilirubin, serum ammonia,
creatinine and other levels specific to the individual patient can also be
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monitored. The timing of these tests may depend on clinical judgment
but should likely be done at least twice a week in the ICU. It should be
remembered that LFTs are not truly functional tests, but can allow the
health clinician to derive conclusions regarding the overall state of liver
functions and aid in differential diagnoses.
Prothrombin, prothrombin time (PT) and the International Normalized
Ratio (INR) can determine the presence and the severity of
coagulopathies and are sensitive markers for liver failure. Non-liver
causes such as Vitamin K deficiency, the presence of disseminated
intravascular coagulation (DIC) may complicate and worsen the
results.
Aminotransferase levels can be used to detect liver injury and to
monitor therapeutic progress. There are some ethnic differences; both
AST and ALT tend to be higher in non-Hispanic blacks and Mexican
Americans than in non-Hispanic whites. Elevations of both AST and
ALT are more common in persons over the age of 30 but tend to
decline after the age of 60. In all patients, elevations are associated
with hepatocellular injury due to ethanol, medications, hepatitis B or C
viruses, and, more rarely, underlying liver diseases. (i.e.,
hemochromatosis). Significant elevations of aminotransferase levels
can also occur in viral infections, ischemic injury and in drug-induced
liver disorders.
Moderate elevations of both AST and ALT can be seen in liver
dysfunction associated with TPN as well as non-alcoholic fatty liver
disease (NAFLD), chronic viral hepatitis, chronic cirrhosis and in
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cholestatic disease. Liver dysfunction as sequelae of TPN is associated
with significant elevations of transaminases, alkaline phosphatases and
conjugated bilirubin levels. GGT may be particularly useful in patients
undergoing TPN and associated cholestasis. Elevated GGT may be seen
in those patients undergoing TPN and with acute biliary tract stones.
In these cases, the aminotransferase levels may be elevated > 500U/l
and associated with either normal or mildly elevated ALP levels.
Bilirubinemia can occur in both chronic and in acute liver disease as
well as in congenital disorders. Unconjugated bilirubinemia may be
Gilbert’s syndrome, where hepatocytes have an impaired bilirubin
uptake, with a glucuronyl transferase deficiency (Crigler-Najjar’s
syndrome), in various forms of hemolysis or erythropoietic
dysfunction. Conjugated bilirubinemia occurs in impaired secretion.
Direct bilirubin levels ≥ 0.4mg/dL must be evaluated further; 5’
nucleotidase levels can be used to determine the likelihood of
cholestasis.
Low serum albumin is associated with a poor prognosis. Adding
albumin to the parenteral solution may allow for a slow and steady
increase in serum albumin. In general, however, adding albumin to the
parenteral solution is not recommended due to concerns surrounding
increased risk of infectious complications, flow rate and filter
questions.
A number of recent studies have examined the positive effects of fishoil based essential fatty acids (EFAs) on the reversal of TPN-associated
liver disease in both pediatric patients and in adults. Parenteral
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nutrition-associated liver disease (PNALD) may occur in both adult and
in pediatric populations after recurrent septic events, delayed enteral
feeding, specific hepatotoxic medications, high caloric intake, high
levels of lipid infusions, various deficiencies such as cysteine, taurine
and choline deficiency as well as anatomic factors such as a short
bowel or, specifically in pediatric patients, gastroschisis and jejuna
atresia. In addition, underlying disease and the duration of parenteral
nutrition are important factors in the development of PNALD.
Finally, in pediatric populations, the situation is complicated by
prematurity and low birth weights. EFAs are essential because they are
needed for a wide array of cellular and organ functions including
platelet function, clotting, inflammation, immunocompetence, wound
healing, skin integrity and maintaining the barrier function and
prostaglandin synthesis. Intravenous fat emulsions (IVFE) can provide
the necessary fatty acids to maintain function and reduce the risk of
PNALD. IVFE can also allow for the reduction of the volume of the
parenteral fluids, potentially avoiding volume overload.
Coagulation Studies
Mechanical complications such as catheter dislodgement or occlusions
can result in a thrombosis. Complications in central lines most
commonly are pneumothorax and hemothorax while complications in
PICC lines commonly include thrombophlebitis. Prophylactic heparin
has not been shown to significantly reduce the incidence of
thromboembolic events.
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Coagulation factors that should be monitored, usually weekly, include:

Prothrombin time (PT):
The PT measures the time needed to generate fibrin after the
activation of Factor VII, measuring the extrinsic and common
coagulation factors VII, V, X, prothrombin and fibrinogen.
Acquired deficiencies are commonly due to liver disease, use of
anticoagulants, depletion of factors secondary to consumptive
coagulopathy, severe bleeding, or massive transfusion.

Partial thromboplastin time (aPTT):
aPTT is used to determine inherited or acquired factor
deficiencies. In the ICU, a prolonged aPTT may indicate Vitamin
K deficiency, liver dysfunction, or the use of an anticoagulant. A
shortened aPTT may be indicative of a hypercoagulable stite and
possibly, the early stages of DIC, but is not diagnostic.

Thrombin time (TT):
Thrombin time measures the integrity of fibrinogen fibrin in the
presence of thrombin. An acquired deficiency is most commonly
due to consumptive coagulopathy or severe liver disease.
Glucose Monitoring
Glucose level is one of the most critical metabolic parameters to
monitor. A dextrose infusion of 4-5mg/kg/minute is most commonly
recommended. 50-60% of total calories should be derived from
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dextrose. Those patients with Types 1 or 2 diabetes, sepsis, acute
pancreatitis, liver dysfunction and on corticosteroids are at greatest
risk of hyperglycemia. However, reactive hypoglycemia can also occur
within 60 minutes after cessation of parenteral feeding. Those patients
at greatest risk include patients with renal or liver disease, those who
are severely malnourished, septic patients and those patients with
hyperthyroidism.
Other Tests

Fluid balance:
Fluids “in” versus fluids “out” should be strictly monitored to
prevent fluid overload and edema.

Blood glucose levels:
Blood glucose levels should be closely monitored, particularly in
those patients receiving TPN or partial enteral nutrition.
Increased mortality is directly associated with hyperglycemia: in
patient with a mean blood glucose of 80-99 mg/dL, mortality
was 9.6%; in those patients with a mean blood glucose of 180199 mg/dL, mortality was 29.4%; in those with a mean blood
glucose greater than 300 mg/dL, mortality was 42.5%. Equally,
hypoglycemia is also associated with increased mortality,
prompting a mover away from intensive insulin therapy.
Diabetic and non-diabetic patients evidence different responses
to glucose variability, with high levels of variability associated
with greater mortality, particularly in non-diabetic patients.
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While the benefits of continuous glucose monitoring have not
been rigorously established, the current guidelines recommend
initiating insulin infusions to maintain blood glucose <
180mg/dL.

Blood lipid levels:
Blood lipid levels can rise, particularly when receiving lipid
infusion. In cases of hypertriglyceridemia, the dextrose load can
be reduced. If this does not correct the hyperlipidemia, cycling
lipid infusions as 250 mL of 20% IV fat emulsion twice weekly if
serum triglyceride > 400 mg/dL (4.5 mmol/L) can be
considered. If the patient is receiving propofol, the additional
kcal should be accounted for and included in the total kcal
provided. (propofol provides 1.1 kcal/mL of infusion). The goal
for serum triglycerides should be < 400 mg/dL (4.5 mmol/L) in
adult patients on continuous total parenteral nutrition.

Blood Cultures/Fever Work-up:
Severe sepsis can be defined as sepsis-induced tissue
hypoperfusion or organ dysfunction. The diagnostic criteria
include a number of physical signs and symptoms, including
general variables such as body temperature, heart rate,
respiratory rates and mental status, but also include some
variables related to lab tests. In severe sepsis, the central
venous pressure (CVP) is of 8-12 mm Hg, a mean arterial
pressure (MAP) of ≥65mm Hg. These include:
 Significant edema/positive fluid balance
>20 mL/kg over 24 hr
 Hyperglycemia
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Plasma glucose > 140 mg/dL or 7.7 mmol/L in nondiabetic patients
 Leukocytosis
WBC count > 12,000/μL
 Leukopenia
WBC count < 4000/μL
 Normal WBC count with more than 10% immature forms
 Plasma C-reactive protein greater than two SD above
normal
 Plasma procalcitonin greater than two SD above normal
 Arterial hypoxemia
Pao2/Fio2 < 300
or
< 250 with no signs of pneumonia as the source of
infection
or
<200 with positive signs of pneumonia as the source
of infection
 Acute oliguria
Urine output < 0.5mL/kg/hr for a minimum of 2 hrs
in the face of appropriate fluids
 Creatinine increase
Greater than 0.5mg/dL (44.2μmol/L)
or
Greater than 2 mg/dL (176.8 μmol/L) in severe
sepsis
 Coagulation abnormalities
INR > 1.5
or
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aPTT > 60 s
 Ileus (absent bowel sounds)
 Thrombocytopenia
Platelet count < 100,000/μL
 Hyperbilirubinemia
Plasma total bilirubin > 4 mg/dL (70 μmol/L)
 Hyperlactatemia
>1 mmol/L
Summary
There are a number of unresolved issues in patient care regarding the
interpretation of the various lab values that may be produced during
the patient’s time in the ICU. While individual clinical decisions must
be based on individual patients, reducing the number of laboratory
tests can be important to reduce patient discomfort as well as the risk
of additional injury. Several benefit to risk analyses have indicated
that laboratory blood draws may be reduced without reducing the
clinical benefit.
Please take time to help NurseCe4Less.com course planners
evaluate the nursing knowledge needs met by completing the
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self-assessment of Knowledge Questions after reading the
article, and providing feedback in the online course evaluation.
Completing the study questions is optional and is NOT a course
requirement.
1.
Laboratory test sensitivity refers to the ability of a
a. patient to tolerate a test.
b. test to identify the presence of a disease or condition
correctly.
c. test to identify true negative.
d. test to identify the absence of a disease or condition correctly.
2.
Transfusion of whole blood, packed cells or blood
components has been
a.
b.
c.
d.
3.
Red blood cell transfusion is indicated for a patient
a.
b.
c.
d.
4.
with adequate blood flow (hemodynamic stability).
with acute hemorrhage but only in single units.
with evidence of hemorrhagic shock.
based on caloric needs.
The Nyquist-Shannon Theorem posits that there is an
appropriate relationship between the number of samplings
and the likelihood that
a.
b.
c.
d.
5.
shown to offer a survival advantage to patients.
known to reduce production of erythropoietin.
shown to depress new blood cells.
associated with the risk of infection.
a test will identify the presence of a disease.
the risk of clinically inappropriate treatments.
there will be a medically appropriate solution.
the sample signal will be properly determined.
There is no absolute hematocrit or hemoglobin level that
universally should prompt a transfusion, though patients at
risk for myocardial ischemia are generally transfused when
Hgb levels fall below
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a.
b.
c.
d.
6.
13g/dL.
7g/dL.
8.7g/dL.
11g/dL.
True or False: Wellness testing is not an aspect of lab
testing in the ICU setting.
a. True
b. False
7.
Additional sodium levels in an ICU patient may result from
saline used to dilute medication and to keep catheters
open, which can result in
a.
b.
c.
d.
8.
Active de-resuscitation can involve the use of
________________ or, if necessary, hemodialysis to
maintain fluid and electrolyte balance.
a.
b.
c.
d.
9.
hyponatremia.
the Gibbs-Donnan effect.
hypernatremia.
hypokalemia.
diuretics
saline solutions
phosphates
liberal transfusions
Hypokalemia can be defined as a serum ____________
level of <3.5 mEq/L.
a.
b.
c.
d.
magnesium
chloride
potassium
phosphorus
10. Diagnostic tests, i.e., complete blood counts (CBCs), blood
chemistries, arterial blood gases and ECGs, should
a. be ordered liberally as a safety precaution.
b. be ordered routinely in-hospital.
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c. be restricted based on cost.
d. be ordered only in response to specific clinical questions.
11. True or False: Initial chloride levels in patients are
generally lower than initial sodium concentrations.
a. True
b. False
12. __________ nutrition is the preferred route of feeding for
the critically ill patient who requires nutrition support
therapy.
a.
b.
c.
d.
Parenteral
Intravenous
Subcutaneous
Enteral
13. Administration of _______________ has been shown to
improve outcome (most consistently by decreasing
infection) in specific critically ill patient populations
involving transplantation, major abdominal surgery, and
severe trauma.
a.
b.
c.
d.
parenteral nutrition
probiotic agents
liberal transfusions
saline solutions
14. True or False: If early enteral nutrition is not feasible or
available the first 7 days following admission to the ICU,
no nutrition support therapy should be provided.
a. True
b. False
15. Energy expenditure (EE) is often used to determine the
___________________ of a patient in the ICU.
a. phosphorus levels
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b. red blood count
c. caloric needs
d. the potassium levels
CORRECT ANSWERS:
1.
Laboratory test sensitivity refers to the ability of a
b. test to identify the presence of a disease or condition
correctly.
p. 6: “Test sensitivity is the ability of any test to correctly
identify the presence of a disease or condition (true positives)
while specificity is the ability of any test to correctly identify
the absence of a disease or condition (true negatives).
Clinicians should only order those tests that have a
reasonable probability of providing useful information, either
for ruling in or for ruling out a particular diagnosis. Ruling out
a diagnosis with laboratory testing has the highest power for
diagnoses with a low probability.”
2.
Transfusion of whole blood, packed cells or blood
components has been
d. associated with the risk of infection.
p. 9: “Transfusion of whole blood, packed cells or blood
components has not been shown to offer a survival advantage
and has been associated with a number of risks including
infection; febrile, allergic and hemolytic transfusion reactions;
transfusion-related circulatory overload and acute lung
injury.”
3.
Red blood cell transfusion is indicated for a patient
c. with evidence of hemorrhagic shock.
p. 10: “Recommendations for Indications related to RBC
Transfusion in the General Critically Ill Patient: RBC
transfusion is indicated for patients with evidence of
hemorrhagic shock.”
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4.
The Nyquist-Shannon Theorem posits that there is an
appropriate relationship between the number of samplings
and the likelihood that
d. the sample signal will be properly determined.
pp. 6-7: “The Nyquist-Shannon Theorem posits that there is
an appropriate relationship between the number of samplings
and the likelihood that the sample values will be properly
determined; in other words, there is a relationship between
how often one should sample a varying laboratory test. For
example, blood glucose values will vary based on meal
frequency or if the patient is receiving total parenteral
nutrition. Oversampling (for example) every 30 minutes will
not reveal any more information as compared to sampling 2
hours after a meal. With oversampling, while sensitivity may
be increased, specificity will necessarily be decreased, which
will reduce the accuracy of the test. Undersampling, on the
other hand, can be just as problematic.”
5.
There is no absolute hematocrit or hemoglobin level that
universally should prompt a transfusion, though patients at
risk for myocardial ischemia are generally transfused when
Hgb levels fall below
b. 7 g/dL.
p. 19: “There is no absolute hematocrit or hemoglobin level
that universally should prompt a transfusion, though patients
at risk for myocardial ischemia are generally transfused when
Hgb levels fall below 7 g/dL.”
6.
True or False: Wellness testing is not an aspect of lab
testing in the ICU setting.
a. True
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p. 6: “Wellness testing is obviously not an aspect of lab
testing in the ICU setting.”
7.
Additional sodium levels in an ICU patient may result from
saline used to dilute medication and to keep catheters
open, which can result in
c. hypernatremia.
p. 11: “Sources of additional sodium include saline used to
dilute medication and to keep catheters open. This can result
in hypernatremia in many patients ….”
8.
Active de-resuscitation can involve the use of
________________ or, if necessary, hemodialysis to
maintain fluid and electrolyte balance.
a. diuretics
p. 13: “Active de-resuscitation can involve the use of diuretics
or, if necessary, hemodialysis to maintain fluid and electrolyte
balance.”
9.
Hypokalemia can be defined as a serum ____________
level of <3.5 mEq/L.
c. potassium
p. 27: “Hypokalemia can be defined as a serum potassium
level of <3.5 mEq/L.”
10. Diagnostic tests, i.e., complete blood counts (CBCs), blood
chemistries, arterial blood gases and ECGs, should
d. be ordered only in response to specific clinical questions.
p. 17: “Diagnostic tests — including complete blood counts
(CBCs), blood chemistries, arterial blood gases and ECGs —
should only be ordered as a response to specific clinical
questions and not as a matter of routine.”
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11. True or False: Initial chloride levels in patients are
generally lower than initial sodium concentrations.
a. True
p. 12: “Initial chloride levels in patients are generally lower
than initial sodium concentrations; this can lead to uneven
increases is chloride levels as compared to sodium levels after
infusions containing the same amounts (in mEq/L) of each
ion.”
12. __________ nutrition is the preferred route of feeding for
the critically ill patient who requires nutrition support
therapy.
d. Enteral
p. 32: “Enteral nutrition is the preferred route of feeding over
parenteral nutrition for the critically ill patient who requires
nutrition support therapy.”
13. Administration of _______________ has been shown to
improve outcome (most consistently by decreasing
infection) in specific critically ill patient populations
involving transplantation, major abdominal surgery, and
severe trauma.
b. probiotic agents
p. 38: “Administration of probiotic agents has been shown to
improve outcome (most consistently by decreasing infection)
in specific critically ill patient populations involving
transplantation, major abdominal surgery, and severe
trauma.”
14. True or False: If early enteral nutrition is not feasible or
available the first 7 days following admission to the ICU,
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no nutrition support therapy should be provided.
a. True
p. 32: “If early EN is not feasible or available the first 7 days
following admission to the ICU, no nutrition support therapy
should be provided.”
15. Energy expenditure (EE) is often used to determine the
___________________ of a patient in the ICU.
c. caloric needs
p. 43: “Energy expenditure (EE) is often used to determine
the caloric needs of a patient in the ICU. During the early
phases of a critical illness, however, it is believed that the
caloric needs are likely to be lower than the EE while during
later phases, the caloric needs are likely to be higher than the
EE.”
References Section
The References below include published works and in-text citations of
published works that are intended as helpful material for your further
reading.
1. Corwin HL, Parsonnet KC, Gettinger A. RBC transfusion in the ICU is there a
reason? Chest. 1995; 108:767–71.
2. Dolman, HS., et al, Impact of minimizing diagnostic blood loss in the critically ill.,
Surgery, 158(4), 1083-1088, 2015.
3. Srivastava, R., Bartlett, WA., Kennedy, IM., Hiney, A., Fletcher, C., Murphy, MJ.
Reflex and reflective testing: efficiency and effectiveness of adding on laboratory
tests. Ann Clin Biochem. 47 (3) 223-227, 2010.
4. Baird, G., The laboratory test utilization management toolbox. Biochemia Medica
2014;24(2):223-34.
5. Flegel, WA., Natanson, C., Klein, HG. Does prolonged storage of red blood cells
cause harm? Accessed at http://rdcr.org/wp-content/uploads/2012/08/BJH-2014.pdf
(9/2016)
6. Napolitano, LM., et al, Clinical practice guideline: Red blood cell transfusion in
adult trauma and critical care. Accessed at:
http://www.learnicu.org/docs/guidelines/redbloodcell.pdf (9/2016)
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7. Iosfina, I. et al, Implementation Of An On-Demand Strategy For Routine Blood
Testing In ICU Patients, D23. QUALITY IMPROVEMENT IN CRITICAL CARE. May 1,
2013, A5322-A5322. Accessed at
http://www.atsjournals.org/doi/abs/10.1164/ajrccmconference.2013.187.1_MeetingAbstracts.A5322 (Accessed 10/2016)
8. http://www.choosingwisely.org/societies/critical-care-societies-collaborativecritical-care/ (Accessed 10/2016)
9. http://mghlabtest.partners.org/criticalvalues.htm (Accessed 10/2016)
10. https://www.thoracic.org/professionals/clinical-resources/critical-care/clinicaleducation/abgs.php (Accessed 9/2016)
11. http://www.lumen.luc.edu/Lumen/MedEd/nutrition/JPEN%2033%202009.pdf
(Accessed 10/2016)
12. https://www.merckmanuals.com/professional/nutritional-disorders/nutritionalsupport/total-parenteral-nutrition-tpn (Accessed 10/2016)
13. Lew, CC., et al, Association Between Malnutrition and Clinical Outcomes in the
Intensive Care Unit: A Systematic Review. J Parenteral Nutrition, Feb, 2016.
14. Hartl, WH., et al, Complications and Monitoring – Guidelines on Parenteral
Nutrition, Chapter 11, Ger Med Sci, 7, Doc 17, 2009.
15. Rees Parrish, C.,(ed) Liver Dysfunction Associated with Parenteral Nutrition:
What are the Options? Nutrition issues in Gastroeneterology, Series #4, Accessed at
(10-2016) http://www.practicalgastro.com/pdf/December06/LeeArticle.pdf
16. Venecourt-Jackson, Esra, Simon J. Hill, and Russell S. Walmsley. "Successful
treatment of parenteral nutrition–associated liver disease in an adult by use of a fish
oil–based lipid source." Nutrition 29.1 (2013): 356-358.
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