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. shown to offer a survival advantage to patients. b. known to reduce production of erythropoietin. c. shown to depress new blood cells. d. associated with the risk of infection.
3. 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. with adequate blood flow (hemodynamic stability). b. with acute hemorrhage but only in single units. c. with evidence of hemorrhagic shock. d. as an absolute method to improve tissue oxygen consumption.
5. The Nyquist-Shannon Theorem posits that there is an appropriate relationship between the number of samplings and the likelihood that
a. a test will identify the presence of a disease. b. the risk of clinically inappropriate treatments c. there will be a medically appropriate solution. d. 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 5 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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
6 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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 Provides a Requires a buy-in Formulary particularly uniform policy, from all involved those with similar to a recognized pharmacy (evidence- formulary. based) utility Exceptions can be determined as needed.
Combining Any test Combining Can be logistically Intervention interventions difficult and increase the complex, effectiveness by particularly allowing one because it requires intervention to the involvement 7 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
complement (buy-in) from all another parties.
Banning Daily testing Powerful way to Providers are often Repetitive reduce automatic concerned about Orders testing. Often missing important providers are not data. Indeed, aware of there is some risk automatic — i.e., not testing. ordering coagulation studies for patients
Limit Ordering Complex tests, Increases cost Adds a layer of Privileges to expensive tests effectiveness and bureaucracy and Specific or those tests diagnostic yield. possibly Providers that may provide competitiveness. questionable benefits. Require Pre- Complex tests, Specialists may Time consuming, approval for expensive tests have a better adds a layer of Tests or those tests understanding of bureaucracy that may provide necessary and questionable effective testing benefits. Change Order Primarily Difficult to Requires Options computerized subvert or “get involvement of the ordering around” IT department and universal cooperation and use of computer ordering Encourage Any test where a Allows for the Only useful for Reflexive less expensive use of ordering analytes with a Testing screening test algorithms. less expensive can be used Increases the screening test before a more efficacy of more available (eg. TSH expensive test expensive testing 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
9 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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. In addition, the significance of RBC storage duration and transfusion-associated end- organ 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 14 nursece4less.com nursece4less.com nursece4less.com nursece4less.com amplitude of T-wave, increased amplitude of U-wave (mostly in V4- V6)) 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 < 1.3mEq/L. In general, every 2 g 1.2-1.4mg/dL:4g 0.8-1.1mg/dL: 6g 2+ of MgSO4 will raise the serum Mg <.8mg/dL: 8g Torsades des Pointes: 2g IV push by 0.5 mEq/L. Magnesium can be Low K+/Ca2+ with tetany or arrhythmia given by mouth (usually as MgO) 50meq (~6g) of IV Mg2+ given slowly over 8-24 hrs 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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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 Corrected Ca2+ = [(4 – albumin) x 0.8] + measured calcium. serum calcium < 8.4 mg/dL or an Symptomatic or acute serum Ca2+ ionized calcium < 4.2 mg/dL. <7.5 mg/dL: - IV Calcium gluconate 1-2 g (amp) over Calcium should only be given IV for 10-20min. severe or symptomatic - Temporary rise for 2-3 hrs, must be followed by slower infusion hypocalcemia. Pseudohypcalcemia - 50 mL/hr if Ca2+ remains low) should be ruled out by determining Asymptomatic and serum Ca >7.5 the corrected calcium levels. As a mg/dL or chronic: Oral therapy: calcium carbonate or citrate general rule, every 1 g of calcium 1-2 g/day (500 mg bid-qid) gluconate given will raise the serum Consider Vitamin D in following cases: Hypoparathyroidism: Vitamin D calcium by 0.5 mg/dL. Signs and - Calcitriol: 0.25-0.5 mcg bid - Vitamin D deficiency: 50,000 IU/week symptoms of acute hypocalcemia 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 time- critical 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 18 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
• 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 ü 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). ü 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 92- 100% saturation. The American Thoracic Society recommends a 6-step approach to the interpretation of arterial blood gasses.10 21 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
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
Step 2:
• Determine if there is acidemia or alkalemia present based 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. 22 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
• 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 Increase in [HCO3-] = ∆ PaCO2/10 +/- 3 acidosis
- Chronic respiratory Increase in [HCO3 ] = 3.5(∆ acidosis PaCO2/10)
- Metabolic alkalosis Increase in PaCO2 = 40 + 0.6(∆HCO3 )
- Acute respiratory Decrease in [HCO3 ] = 2(∆ PaCO2/10) alkalosis
- Chronic respiratory Decrease in [HCO3 ] =5(∆ PaCO2/10) alkalosis 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 24 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
• 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 30 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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 31 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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 35 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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
36 nursece4less.com nursece4less.com nursece4less.com nursece4less.com with severe sepsis. ICU patients not meeting criteria for immune- modulating 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
38 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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
43 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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 80- 145mg/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, 45 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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)
46 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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(2- ethylhexyl) 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
48 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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
49 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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 fish- oil based essential fatty acids (EFAs) on the reversal of TPN-associated liver disease in both pediatric patients and in adults. Parenteral 50 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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 fibrinogenà 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 52 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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
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 180- 199 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 non- diabetic 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
56 nursece4less.com nursece4less.com nursece4less.com nursece4less.com 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. shown to offer a survival advantage to patients. b. known to reduce production of erythropoietin. c. shown to depress new blood cells. d. associated with the risk of infection.
3. Red blood cell transfusion is indicated for a patient
a. with adequate blood flow (hemodynamic stability). b. with acute hemorrhage but only in single units. c. with evidence of hemorrhagic shock. d. based on caloric needs.
4. The Nyquist-Shannon Theorem posits that there is an appropriate relationship between the number of samplings and the likelihood that
a. a test will identify the presence of a disease. b. the risk of clinically inappropriate treatments. c. there will be a medically appropriate solution. d. the sample signal will be properly determined.
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
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a. 13g/dL. b. 7g/dL. c. 8.7g/dL. d. 11g/dL.
6. 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. hyponatremia. b. the Gibbs-Donnan effect. c. hypernatremia. d. hypokalemia.
8. Active de-resuscitation can involve the use of ______or, if necessary, hemodialysis to maintain fluid and electrolyte balance.
a. diuretics b. saline solutions c. phosphates d. liberal transfusions
9. Hypokalemia can be defined as a serum ______level of <3.5 mEq/L.
a. magnesium b. chloride c. potassium d. 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. 58 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
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. Parenteral b. Intravenous c. Subcutaneous d. 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. parenteral nutrition b. probiotic agents c. liberal transfusions d. 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 59 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
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.” 60 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
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.” 62 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
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, 63 nursece4less.com nursece4less.com nursece4less.com nursece4less.com
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/ajrccm- conference.2013.187.1_MeetingAbstracts.A5322 (Accessed 10/2016) 8. http://www.choosingwisely.org/societies/critical-care-societies-collaborative- critical-care/ (Accessed 10/2016) 9. http://mghlabtest.partners.org/criticalvalues.htm (Accessed 10/2016) 10. https://www.thoracic.org/professionals/clinical-resources/critical-care/clinical- education/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/nutritional- support/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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