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2014 bedside critical care guide

OMICS Group eBooks

Bedside Critical Care Guide


Edited by
Ramzy H Rimawi


Bedside Critical Care Guide
Edited by: Ramzy H. Rimawi
Published by OMICS Group eBooks
731 Gull Ave, Foster City. CA 94404, USA

Copyright © 2014 OMICS Group
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First published January, 2014
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Critical care medicine is an intriguing, rapidly evolving medical field aimed
to support and restore productive lives in seriously ill patients. Critical care
specialists often seek up-to-date, evidence-based literature applicable at the
patient bedside for common and uncommon disorders encountered in the
intensive care unit (ICU). In this review of adult critical care medicine, we provide
a comprehensive guide of bedside ICU principles and best practice standards.
East Carolina University has a 24-bed medical ICU (MICU), a 24-bed
cardiac ICU (CICU), and a 24-bed surgical ICU (SICU). The MICU commonly
admits critically ill patients with infectious disease, central nervous system,
respiratory, metabolic and endocrine, hematologic, oncologic, gastrointestinal,
environmental, obstetric, pharmacologic disorders and renal disorders. Our
CICU typically admits patients suffering from myocardial infarctions, congestive
heart failure, arrhythmias, cardiogenic shock and post-cardiovascular surgical
complications. The SICU cares for patients with surgical and trauma related
Currently, critical care is a multidisciplinary specialty that includes many
subspecialties of medicine, surgery and anesthesiology. I have personally
asked the contributing authors of multidisciplinary departments at East Carolina
University, including critical care medicine, pulmonology, infectious diseases,
nephrology, cardiology, and trauma. The contributing authors and I thank OMICS
for their assistance is publishing this text.

Thank you,
Ramzy H Rimawi

About Editor

Dr. Ramzy Rimawi earned his BA in English and Biology at the State
University at Stony Brook. He then earned his medical doctorate degree
from Ross University School of Medicine. After completing his Internal
Medicine residency training, he pursued a fellowship in Infectious Diseases
followed by Critical Care Medicine at East Carolina University for the Brody
School of Medicine. His passion for critical care lies in its’ rapid physiologic
and complex reasoning often in the face of uncertainty. His clinical interests
are nosocomial infections in the ICU, antibiotic stewardship, infection
control and HIV.

Dr. Ramzy Rimawi has established himself as not only a competent clinician,
but also quickly becoming a leader in the field of infectious disease and critical
care medicine. At a young age he has been very successful in publishing several
articles in his field of practice and continues to contribute to the progression of
science and medicine. He has presented and been recognized for his work
at a national and local level. He has board certifications in Internal Medicine,
Infectious disease medicine and currently completing his training in critical care
Bowling Mark
I had the pleasure to work with Dr. Ramzy over the past 3 years. He is a great
example of ambition, dedication, hard working and a great team player. His
shinning mind has brought our department to a whole new level. I have no doubt
that he will be an exceptional physician. Bringing the critical care to bedside and
presenting it in such simplified way to assist other medical providers is a true
example of his thrives to provide a better care for patients.
Saadah Khalid
This is my first year working with Dr. Rimawi. During my time with him, I
have found him to be very smart and hardworking. He is an ardent supporter
of antibiotic stewardship, has worked a great deal in the use of procalcitonin
assay, and his work in the field of Penicillin allergy skin testing to help choose
appropriate antibiotics is remarkable.
Dr. Rimawi has taken a lot of initiatives to help improve the healthcare at our
hospital. He is very active academically and has worked on multiple research
projects and publications. The initiative he took to get this eBook published is a
testament to his academic inclinations.
The idea of a bedside ICU eBook was excellent, especially with the limited
availability of content at the graduate medical education level for residents. The
book had to be something that was evidence based, concise and practical, and
easy to understand. I am sure this book meets the above requirements and will
be of great benefit to all.
Nazia Sultana

Ramzy Rimawi and I both did our training in Infectious Diseases together at
East Carolina University for the Brody School of Medicine. While there, Ramzy
has been great mentor that helped oversee my fellowship training as a chief
fellow and research career. We presented several oral and poster presentations
at national and international conferences together. We have successfully
published several articles in well-recognized, peer-reviewed journals on topics
such as MRSA screening in an ICU setting, tularemia, and infectious disease/
critical care practitioner collaboration. But other than being great academic
partner, Ramzy and I have been great friends. It was an honor to be able to work
with him on this e-Book and I look forward to future joint collaborations with him
and OMICS.
Kaushal B Shah
I am pleased to write about Dr Ramzy Rimawi. I have known Dr. Rimawi since
July 2013 as a colleague at ECU Brody School of Medicine (BSOM). He has
extensive fund of knowledge and practices evidence based medicine. He is
very well respected as a finest clinician, avid clinical researcher and mentor for
fellows/house staff at Vidant Medical Centre.
Dr Rimawi has done a great effort in compiling “Bedside Critical Care Guide”
as excellent evidence based guide for house staff and busy clinicians.
Manjit Singh Dhillon
Dr Rimawi is an outstanding clinician with excellent bedside manners. He has
demonstrated an ongoing commitment to research as well as teaching, and this
book will go a long way in furthering the understanding of critical illness and its
Abid Butt
It was a great experience for me to write the chapter on scoring systems in
critically ill patients. I thank Dr Ramzy Rimawi for the opportunity of writing the
chapter. He is a great physician and person.
Ogugua N Obi

I am pleased to say that the contributors have provided information
that was accurate, up-to-date, evidence-based and unbiased. I would like
to express my sincere appreciation to them for their generous, voluntary
Ramzy H Rimawi

The chapters in this eBook include topics from cardiology, nephrology,
pulmonary, infectious disease (including sepsis), neuro-critical care,
burns, and gastroenterology. Highly specialized topics have been left to
qualified authors of other specialty texts. Each chapter is meant to provide
pertinent clinical, diagnostic, and management strategies when caring for
critically ill patients. The chapters are relatively brief, clinically relevant
and evidence-based according to currently accepted literature. References
are provided for readers wanting to explore subjects in greater detail. I
have edited and revised the content and style of each chapter so as to
unify the voice of the entire text.

Chapter 1: Principles of Mechanical Ventilation
Chapter 2: Management of Common Respiratory Disorders in the ICU: Asthma,
Chapter 3: Bedside approach to Gastrointestinal Bleeding in the Intensive Care Unit

Page #

Chapter 4: Renal Disorders in the ICU


Chapter 5: Nutritional Support in an ICU Setting


Chapter 6: An ICU Bedside Review of Burns


Chapter 7: Management of Common Neurocritical Care Disorders


Chapter 8: ICU Delirium - Attention to Inattention


Chapter 9: Approach to Fever In the Intensive Care Unit


Chapter 10: Bedside Fundamentals of Pneumonia in the ICU


Chapter 11: Antibiotic Therapy in Sepsis


Chapter 12: ICU Infection Control and Preventive Measures


Chapter 13: Bedside Management of Shock


Chapter 14: Acute Myocardial Infarction in an ICU


Chapter 15: Heart failure in an ICU


Chapter 16: Critical Care Scoring Systems and Checklists


Principles of Mechanical Ventilation
Robert A Shaw*
Critical Care & Sleep Medicine, Section of Pulmonary, Department of
Internal Medicine, Brody School of Medicine, East Carolina University,
*Corresponding author: Robert A. Shaw, Critical Care & Sleep
Medicine, Section of Pulmonary, Department of Internal Medicine,
Brody School of Medicine, East Carolina University, Brody 3E-149,
Greenville, NC 27834, USA, Tel: 252-744-4650

In this chapter, you will learn basic pulmonary physiology necessary to understand the modes of mechanical ventilation. You will
then learn how these ventilator modes can be applied in the different types of respiratory failure. Using ventilator monitoring to trouble
shoot patient/ventilator asynchrony problems will be discussed. Finally clinical cases to illustrate teaching points will be presented.

Basic Respiratory System Mechanics and Pathophysiology
In the spontaneously breathing patient, downward movement of the diaphragm during inspiration generates negative pressure
in the chest relative to atmospheric pressure, and air moves from the atmosphere into the lungs. In spontaneously breathing patients
on mechanical ventilators, positive pressure from the ventilator assists this effort by the patient and reduces the work the patient
must do to inhale a given tidal volume. In patients who have respiratory failure, the ventilator reduces the work of breathing and
aids in inflating the lungs. The work of breathing is related to a pressure-time product, which is the pressure needed to inflate the lungs
multiplied by the time of inspiration. For our purpose, we will assume that expiration does not involve significant work by the patient. The
pressure which is needed to drive air into the lungs is related to the resistance and compliance of the system. Resistance is increased by
narrowing of the airways or narrowing of the endotracheal tube, which can occur if a patient bites on the tube or secretions collect on
the inside. Calculation of resistance, which modern ventilators can estimate, is related to Δ pressure/Δ flow (R= ΔP/ΔFlow). Compliance
is simplistically understood as the work needed to inflate a balloon. Stiff balloons like stiff alveoli require more pressure to inflate.
Compliance = Δvolume/Δpressure [1]. Compliance is the opposite of elastance, thus alveoli with high elastance have low compliance.
There are 2 components of compliance: compliance related to the alveoli and compliance related to the chest wall. Diseases which cause
low compliance of the lungs include fibrosis, interstitial edema, and pneumonia. Conditions in which there is low chest wall compliance
include abdominal distention, pleural effusion, or obesity. The following image demonstrates how at low lung volumes compliance is
low, but as the lungs are inflated compliance increases.

It is also important to know that diseased lungs are heterogeneous, and there are areas with low compliance (severely injured
areas) and high compliance (emphysema), and also areas with high resistance (bronchospasm) and less resistance. If the physician
orders a high tidal volume to be delivered by the ventilator, that volume may go mostly to the more compliant (normal) part of the
lung and cause over distention and injury to that part of the lung. This is called volutrauma and is why lower tidal volumes (6-8 mL/
kg/IBW) are recommended in patients with ARDS. Lower tidal volumes (i.e. 4 mL/kg/IBW) have also been described). Positive end
expiratory pressure (PEEP) is used to inflate the lungs and usually improves the compliance by putting the lung in a more favorable
place on the pressure volume curve seen in Figure 1 [2]. A sudden drop in compliance would be manifested by the ventilator graphics
showing a higher pressure at the end of both inspiration and expiration and sudden drop in tidal volumes. This could be seen with a

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Figure 1: Compliance in Relation to Pressure and Volume.


Mechanical Ventilation Principles
As mentioned above, a mechanical ventilator assists breathing and inflates lungs by delivering oxygen enriched air into the lungs.
The ventilator will target either pressure or volume in doing this. In spontaneously breathing patients, each breath will be triggered by
a change in pressure or flow in the circuit. Each inspiration will be cycled off by either a time limit or decrease in flow. Let us make this
terminology understandable so that you will know what different modes of ventilation mean.
A. Volume targeted ventilation: When patients are intubated, usually a volume targeted mode is initiated. This is because you
would like to assure that the patient is receiving an adequate tidal volume with each breath. In volume targeted ventilation, the therapist
“tells” the ventilator to deliver a given volume, say 500 ml. The therapist sets a flow rate and the machine delivers the gas at that flow rate
until the desired volume is given. The machine times how long it takes to give that volume. This is commonly called assist control mode
(AC). In more modern ventilators, a microprocessor looks at previous breaths, and if they have been below the target, it will increase the
pressure and inspiratory time to reach the targeted tidal volume. An example of this mode is: pressure regulated volume control (PRVC)
or sometimes called APV-CMV. With this mode of ventilation, the patient can trigger the breath or if the patient has no drive to breath
a back- up rate is set to insure that a minimum number of breaths occur each minute.
B. Pressure targeted ventilation: In this mode, the therapist “tells” the ventilator to deliver the gas at a given inspiratory pressure
above the PEEP. Breaths are generated by the patient or the machine and the machine then delivers the gas with a high flow rate until
the targeted pressure is achieved. Note that there is no guarantee of a set tidal volume. If compliance drops or resistance increases,
the patient will receive a lower tidal volume. Examples of pressure targeted modes are: pressure support ventilation (PSV), pressure
control (PC), and airway pressure release ventilation (APRV). In reality, when a therapist is doing PSV, the inspiratory pressure is set so
the patient receives tidal volumes that are comfortable for the patient. The work of breathing is reduced and the patient breaths with a
lower respiratory rate. For example, if a patient is tachypneic with low tidal volumes on PSV, the therapist would usually increase the
pressure support so the patient receives higher tidal volumes and becomes less tachypneic. It is important to realize that with PSV, the
patient must trigger each breath, and this mode is not appropriate for patients who have no drive to breath or cannot generate a breath
due to paralysis. Pressure control mode is a mode in which the therapist sets the time for inspiration and expiration. Patients are heavily
sedated or paralyzed.
C. Airway pressure release ventilation: Another pressure targeted mode, which is often used in patients with ARDS, is airway
pressure release ventilation (APRV). This mode is similar to having a patient on continuous airway pressure (CPAP) with intermittent
drops in the pressure. APRV holds the alveoli inflated (during P HIGH), except for the brief releases (P LOW) and recruits (opens)
alveoli similar to higher PEEP, as illustrated in Figure 2 [3]. It is used to reduce shunt and improve oxygenation in patients with ARDS.
The following graphic illustrates the physiology of APRV:

Figure 2: Airway pressure release ventilation vs Conventional Volume-Targeted Ventilation.

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D. Combined pressure and volume targeted ventilation: Some ventilators can target either pressure or volume with delivered
breaths. An example of this is synchronized intermittent mandatory ventilation (SIMV). In this mode, some breaths are triggered by
the patient initiating a breath and some are time cycled by the ventilator. The therapist “tells” the ventilator to give a minimum number
of breaths/minute. These are the intermittent mandatory breaths, and they are volume targeted. The ventilator also allows the patient to
trigger breaths spontaneously and these breaths are pressure supported. Graphically this is shown in Figure 3:

Figure 3: Synchronized Intermittent Mandatory Ventilation.


If the ventilator is set on SIMV mode and the therapist “tells” the machine to do 6 intermittent mandatory breaths/minute with tidal
volume 400 cc and pressure support of 15 cm H2O, then the patient will receive a 400 cc tidal volume every 10 seconds synchronized with
the patient’s effort. Other patient initiated breaths will be pressure support breaths with 15 cm pressure.

Positive End Expiratory Pressure (PEEP)
PEEP is the pressure that the ventilator maintains at the end of exhalation. When you see a patient with COPD doing pursed lip
breathing, he/she is exhaling against “pursed lips”, which is creating a small amount of PEEP. PEEP helps to prevent atelectasis and
also opens previously closed alveoli. It “recruits” alveoli and can improve oxygen entering into the capillaries supplying those alveoli.
Increasing PEEP will usually improve compliance (unless the lung is over distended) and improve oxygenation. It also helps to reduce
“atelectrauma”, which is lung injury caused by repeated closure and opening of alveoli. There are tables which help in setting the amount
of PEEP to use but in reality, most physicians gradually increase PEEP so that the inspired FiO2 is <0.6 with a pO2 >60. In patients with
very low compliance, such as severe obesity, higher PEEP is really effective in opening the lungs and improving oxygenation. In ARDS
patients PEEP is often as high as 20 cm H2O and in obese patients PEEP is sometimes as high as 30-35 cm H2O. Some centers insert an
esophageal balloon in patients in order to measure transpulmonary pressure (TPP) and set the PEEP high enough so that TPP is positive.

Weaning from Mechanical Ventilation or “Liberation from Mechanical
Assuming that the underlying cause of the respiratory failure has been improved, one then considers transition to having the patient
assume more of the work of breathing and ultimately being “liberated from mechanical ventilation.” Spontaneous breathing trials (SBT)
are conducted to evaluate the readiness of the patient to be extubated. Before starting an SBT, the patient should be alert and able to follow
simple commands. The patient should be adequately oxygenated with FiO2 of 0.4 or less and PEEP should be <10. The exception to this
is in obese patients, who often are on higher PEEP amounts to maintain inflation of the lungs. Usually patients are on pressure support
mode and respiratory rate is <24 before considering an SBT. Most physicians and therapists will calculate the rapid shallow breathing
index (respiratory rate/tidal volume) and if <105 it is reasonable to do an SBT. An SBT means the patient is on minimal PS (5 cm H2O)
or just on T Bar (oxygen but no positive pressure). A successful SBT means the patient breaths spontaneously for >30 minutes with
respiratory rate <35 breaths/minute, O2 sat> 90%, heart rate increase of <20%, no significant change in blood pressure, and no severe
anxiety. Before removing the tube, the patient should be able to protect the airway and clear secretions effectively. If the patient fails the
SBT, then he/she is placed back on mechanical ventilation (usually PS mode) for 24 hours and the underlying problems are addressed
further. This often requires diuresis and/or antibiotics to treat an infection. Patients with COPD sometimes fail the SBT because of
weakness of the respiratory muscles, and they should be rested on adequate PS so that they are not tachypneic.

Noninvasive Positive Pressure Ventilation NIPPV
This refers to positive pressure ventilation via a mask rather than insertion of an endotracheal tube. Endotracheal intubation can have
the following complications: trauma to airway, infection due to bypassing the airway defenses, discomfort, need for sedation and pain
control. While NIPPV can be uncomfortable, it reduces the risks of intubation. NIPPV, sometimes simply called noninvasive ventilation
(NIV), can deliver a fixed pressure CPAP or a higher pressure during inspiration than during expiration (BIPAP bilevel pressure). CPAP
is used to treat diseases where the problem is simply oxygenation, such as pulmonary edema. BIPAP is used when there is a problem of
both ventilation and oxygenation, such as COPD, neuromuscular disease like amyotrophic lateral sclerosis, or obesity hypoventilation
NIPPV has improved outcomes in patients with obstructive disease such as COPD. It has also been beneficial in restrictive chronic
diseases such as kyphoscoliosis, obesity hypoventilation syndrome, and neuromuscular disease (amyotrophic lateral sclerosis). It
also has helped in patients with extubation failure. There are many contraindications to NIPPV including hemodynamic instability,
respiratory arrest, excessive secretions, agitated, unable to fit mask, or recent airway surgery. It can be time consuming for respiratory
care practitioners to work with the patient to help him/her get used to the device and find the right mask. Frequent assessment of the
patient is important, and if the patient is not breathing with a slower rate and improved oxygenation and ventilation after 2 hours, then
intubation will probably be necessary.
An Ideal patient, who would benefit from short term CPAP, would be one who comes to the emergency department with acute
pulmonary edema and needs help with oxygenation until diuresis occurs. Typically a pressure of 10-12 cm H2O is used. An ideal patient,
who would benefit from BIPAP would be one with COPD exacerbation and labored breathing that is hypercapnic. BIPAP at 14/8 cm
H2O would help reduce the work of breathing while bronchodilators and steroids start working. A COPD patient who is extubated and
is working hard to breath might also benefit by avoiding re-intubation. There are complications from NIPPV including: mask discomfort,
air leaking, aspiration, failure to ventilate, and pneumothorax. Patients should always have head of bed elevated and be monitored with
oximitry and EKG.

Case 1: A patient with COPD has been converted from a volume targeted mode to a pressure targeted mode, pressure support. The
therapist places the patient on PS 12/5 cm pressure with FiO2 of 0.4. The patient has a RR of 35 breaths/minute, O2 sat is 93%, and tidal
volumes are 200 cc-260 cc. Arterial Blood Gas: pCO2 45, pO2 75, pH 7.38. What would you recommend?
Case 2: A patient with diffuse infiltrates caused by sepsis and fluid resuscitation is on a volume targeted mode, PRVC. The ventilator
has the following settings: target tidal volume 400 cc (6 cc/kg IBW), FiO2 0.8, set rate 8/minute, PEEP 20cm H2O. ABG: pCO2 38, pO2
50, sat 82%, pH 7.36. What options do you have?
Case 3: A patient with COPD is on a volume targeted mode, PRVC. Target tidal volume is 500cc, FiO2 0.4, PEEP 5. He has become
very tachypneic and is fighting the ventilator. You notice that he is trying to breathe with his abdomen protruding 40 times per minute but
the ventilator is only delivering 20 breaths/minute. The following graphic is noted (the patient in blue, normal in red). Why is the patient
not getting a breath with every effort? What is the problem?

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Cases to Illustrate Common Ventilator Related Problems


Figure 4: Graphic for Case 3.

Case 4: A patient was on volume mode, PRVC, and was improving so you decide to put him on pressure support mode (PSV) to see
if he could do a spontaneous breathing trial and be weaned. On the PRVC mode, the set rate was 14/breaths/minute and the patient was
breathing 14 breaths/minute. ABG: pCO2 34 pO2 70 pH 7.48. After being placed on PSV, the nurse calls and reports the patient has long
apnea periods. What is the problem and what would you do?
Case 5: A patient is on PRVC mode and suddenly becomes tachypneic and airway pressures increase. The ventilator graphic
shows that the difference between the peak airway pressure and the plateau pressure (pressure when expiratory hold is prolonged) has
decreased significantly. This is shown below:

Figure 5: Graphic for Case 5.

Discussion of Cases 1-5
Case 1: This COPD patient is very tachypneic with low tidal volumes on PSV 12/5. Many events could cause tachypnea, including
pulmonary embolism, sepsis, pneumothorax, or metabolic acidosis. The most often cause of this, however, would be that the patient is
not getting enough help from the ventilator. Patient needs more pressure support. After examining the patient, it would be appropriate
to increase the PS to 16 and see if that corrected the tachypnea and labored breathing. Remember that with mechanical ventilation, we
are trying to partially unload the breathing muscles but do not want to excessively work them. It is not known exactly how much work
to impose on the patient, but tachypnea (RR>30) often is a sign of fatigue of respiratory muscles. Exhausting the muscles will prolong
weaning in a COPD patient.

Case 3: You should note on the graphic that even at the end of exhalation, the patient has flow continuing. In a normal patient, all
of the air is exhaled and flow goes to 0 at end exhalation. When there is continuing flow at the end of exhalation, which means there is
air trapping and auto-PEEP. Auto Peep means there is pressure in the alveoli at the end of expiration because not all of the inspired gas
was exhaled. Remember that in order to trigger the ventilator the patient must generate about 2 cm of negative pressure below the set
PEEP. If, for example, there is 6 cm of auto-PEEP the patient will have to generate negative 8cm pressure to trigger the next breath. In a
hyper-inflated COPD patient that may be impossible. This patient is not triggering the ventilator due to auto-peep. The solution to this
includes bronchodilators, reducing the tidal volume, sedation of patient to slow the respiratory rate and allow more time for exhalation,
or increasing the inspiratory flow rate so as to give longer exhalation time [4]. When auto-peep is severe, it is best to disconnect the
patient from the ventilator to let trapped air to escape and bag the patient for a few minutes.
Case 4: On the PRVC mode this patient is on a rate of 14. This is really a back-up rate meaning the patient will receive a minimum
of 14 breaths/minute, even if the patient is apneic. This patient is “riding the rate” and is not breathing over the rate. The ABG indicates
respiratory alkalosis, which will reduce the drive to breath. When the patient is changed to PSV, there is no back up rate, and since the
drive to breath has been reduced by the respiratory alkalosis, the patient has apneas. You could just let the apneas continue and the
patient’s pCO2 will rise, and then the patient will have increased ventilatory drive. Another option would be to put the patient back on
the PRVC mode but decrease the rate to a more appropriate rate, say 6. The patient will eventually start breathing over the rate and then

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Case 2: This patient has severe ARDS with a pO2/FiO2 ratio of 62. Patient has hypoxemia with low oxygen saturation, and that will
reduce oxygen delivery to the tissues. You would like to increase saturation to >90%. Option 1 would be to increase the FiO2, but that
is not the best option because of potential oxygen toxicity. You would like to “recruit lung” in order to better oxygenate the patient and
reduce FiO2. Since the patient is already on 20cm PEEP, which is about as high as is generally done (except in patients with obesity or
low chest wall compliance), raising the PEEP further is not a good option. This is a situation where changing the mode to airway pressure
release ventilation (APRV) would be appropriate. On this mode, the mean airway pressure would increase and areas of collapsed alveoli
would open up. Changing to this mode will often reduce the shunt fraction and oxygenation of blood will improve. This often takes 6-12
hours to work, so do not expect immediate improvement in ABG. You may want to also increase the FiO2 temporarily to insure adequate
oxygenation of the patient. The respiratory care practitioner will help in deciding the best P high and P low.


can be put back on PSV. In patients like this narcotics/sedatives should be reduced because that can cause apneas. In a few patients,
too much oxygen can reduce drive to breath, and FiO2 should be reduced. This is often the case in obesity hypoventilation syndrome
Case 5: It is important to know that airway resistance is related to the difference between the peak airway pressure and the plateau
pressure. In this graphic that difference is higher in the graphic on the left (patient in trouble) than the graphic on the right (patient doing
well). Thus the patient in trouble on the left has higher airway resistance than the patient on the right, possibly due to bronchospasm or
mucous in the endotracheal tube. In this case, you would be sure the tube is clear and it is easy to pass suction catheter. Bronchodilators
would help if there is wheezing and bronchospasm. If both the peak pressure and plateau pressure suddenly increase by the same
amount, then there has been a drop in compliance (pneumothorax could cause that).

Respiratory failure usually occurs because there is high airway resistance or low compliance. Less common is decreased drive to
breath, such as with benzodiazepine or narcotic ingestion. The high work of breathing can be relieved by either non-invasive positive
pressure ventilation, NIPPV (COPD exacerbation or pulmonary edema), intubation with volume targeted mode (assist control or
PRVC), or intubation with pressure targeted mode (pressure support or airway pressure release ventilation). Positive end expiratory
pressure (PEEP) is used to recruit alveoli and improve oxygenation. When the underlying problem has been corrected, the patient should
be evaluated for liberation from mechanical ventilation with a spontaneous breathing trial.

1. MacIntyre NR, Branson RD (2009) In: Mechanical Ventilation. (2ndedn), Saunders Elsevier, St. Louis, USA.
2. Berne RM, Levy MN (1999) In: Berne & Levy Principles of Physiology. (3rdedn), Mosby, USA.
3. Habashi NM (2005) Other approaches to open-lung ventilation: airway pressure release ventilation. Crit Care Med 33: S228-240.

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4. Dhand R (2005) Ventilator graphics and respiratory mechanics in the patient with obstructive lung disease. Respir Care 50: 246-261.


Management of Common
Respiratory Disorders in the ICU:
Asthma, COPD, and ARDS
Mark A Bowling1* and Hunter A Coore2
Assistant Professor of Medicine, Brody School of Medicine, East
Carolina University, Greenville, USA

Chief Resident/Clinical Instructor, Brody School of Medicine, East
Carolina University, Greenville, USA

*Corresponding author: Mark R Bowling, Assistant Professor
of Medicine, Brody School of Medicine - East Carolina University,
Department of Internal Medicine, Division of Pulmonary, Critical Care
and Sleep Medicine, 3 E-149 Brody Medical Sciences Building, 600
Moye Blvd., Mail Stop 328, Greenville, NC, USA, Tel: 278834-4354;
Off: 252-744-4650; Fax: 252-744-1115; E-mail: bowlingm@ecu.edu

Source of Funding/Conflicts of Interest: Author Mark A Bowling has a potential conflict of interest

with Covidien Surgical Solutions (consultant). Covidien Surgical Solutions was not involved in the production of this manuscript.
Dr. Hunter Coore does not have financial disclosures to report. None of the authors have received any source(s) of funding for this
manuscript. The corresponding author, Mark A. Bowling, had full access to all the data in the study and had final responsibility for the
decision to submit for publication.

Pulmonary disorders are frequently encountered in the intensive care unit (ICU). Complications of asthma, chronic obstructive
pulmonary disease (COPD) and acute respiratory distress syndrome (ARDS) are three of the most common respiratory disorders faced
by the ICU physician. This chapter will focus on the basic ICU management for these pulmonary disorders.

Keywords: ARDS; Asthmaticus; COPD exacerbation; Hypercapnia; Status respiratory failure
Respiratory disorders are a common problem faced in the intensive care unit. In this section we will discuss three of the most
common pulmonary disorders seen in critical care medicine; this includes chronic obstructive pulmonary disease (COPD) exacerbation,
acute asthma, and acute respiratory distress syndrome (ARDS).

Chronic Obstructive Pulmonary Disease Exacerbation
Chronic obstructive pulmonary disease (COPD) is characterized by persistent non-reversible airflow obstruction due to destruction
of the distal airways from local inflammation as a result of exposure to noxious particles and gases (mostly from tobacco abuse). This
permanent change in lung structure coupled with chronic inflammation leads to a progressive decline in lung function, abnormal
gas exchange, pulmonary hypertension, air trapping (inability to deflate the lung), increased sputum production, skeletal muscle
wasting and cachexia [1]. The Global Initiative for Chronic Obstructive Lung Disease (GOLD guidelines)defines COPD as a ratio of
forced expiratory volume in 1second (FEV1) over forced vital capacity<0.70 (FEV1/FVC<0.70) [1]. The severity of airflow obstruction
measured by spirometry is based on the measurement of the FEV1:

The Center for Disease Control and Prevention (CDC) in 2011 reported that COPD was the third leading cause of death in the
United Statesand approximately fifteen million people have been diagnosed with the disease [2]. It is has been predicted that in 2020
it will be the 3rd leading cause of mortality worldwide and the 5th leading cause of burden of disease [3,4]. Many of the patients that
are diagnosed with COPD will have acute symptoms of the disease termed exacerbations. In the United States, acute exacerbations of
COPD (AECOPD) are responsible for about 500,000 admissions to the hospital yearly, with half of these admissions requiring ICU
level care [4]. The mainstays of therapy for AECOPD include the maintenance of adequate oxygenation and ventilation, bronchodilator
therapy, corticosteroids and antibiotics [5]. Below we will describe the definition, risk factors and therapy in the care of patients with
these exacerbations.

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Stage 1 = mild (FEV1>70 ml)
Stage 2 = moderate (FEV1 50-70 ml)
Stage 3 = severe (FEV1 30-50 ml)
Stage 4 = very severe (FEV1 <30)


Definition and risk factorst
COPD exacerbations are defined by the GOLD criteria as an increase in the frequency or severity of a cough, worsening dyspnea and
a change in character or volume of sputum production [1]. There are several identifiable predictors for patients at risk for COPD, which
include: the duration of COPD diagnosis, number of hospitalizations, sputum production, steroid use, antibiotic use, and co-morbidities
(cardiovascular disease) [6]. Additionally, those with GOLD Stage 3-4 are at an increased risk for exacerbations [1].

Clinical presentation and initial evaluation
Patients experiencing an AECOPD may present with several complaints and symptoms, including increased dyspnea and cough,
worsened hypoxemia, hypercapnia (resulting in an acute metabolic acidosis), mental status changes, and symptoms related to a primary
issue such as pneumonia, cardiovascular events, arrthymias, and organ failure [7]. Many of these patients will require ICU admission
[7]. The initial approach in the care of these patients starts with a history and physical examination focusing on potential causes of the
exacerbation (infections, cardiac events) and evidence of impending respiratory failure. It is important to remember that many of these
patients will have significant co-morbidities, which may add to the complexity of the situation. For example, it is rare that a patient with
COPD and heart failure will present with just heart failure or COPD symptoms alone, it is usually a combination of both. Therefore, both
problems need to be addressed. A quick evaluation of the patient’s ability to maintain adequate oxygenation and ventilation is necessary
and pertinent. The following may help in this assessment:

Oxygen saturation <88% on room air
Use of accessory muscles
Increase respiratory rate
Inability to talk clearly due to difficulty breathing
Mental status changes and evidence of inability to adequately protect the airway (i.e. decrease gag reflex).
Arterial blood gas demonstrating hypoxia and hypercapnia with an acute respiratory acidosis

If there is concern that the patient cannot adequately protect the airway or experiencing significant hypercapnic respiratory failure,
either endotracheal intubation or non-invasive mechanical ventilation should be considered immediately. If airway protection is of a
concern, non-invasive mechanical ventilation should not be utilized. Other studies to consider include a chest roentogram (to evaluate
for lung parenchymal abnormalities such as pneumonia, pneumothorax, or pulmonary edema, etc.), measurement of arterial blood gas,
and appropriate studies focusing on the underlying cause of the exacerbation.

Mechanical ventilation and Oxygen therapy
Non-invasive mechanical ventilation: Most patients with acute respiratory failure from a COPD exacerbation can be managed with
non-invasive positive pressure ventilation (NIPPV). NIPPV is considered first-line therapy for patients with COPD exacerbations that
have acute hypercapnic respiratory failure and no contraindications to NIPPV [1]. Several studies have reported improvement in clinical
outcomes such as a decrease in mortality, need for intubation, treatment failure, improvement in respiratory failure, and decreased
respiratory rate [8]. It is unclear as to what initial settings one should consider when treating these patients. An approach can be to place
these patients on a bi-levelventilator mode, triggered by spontaneous breathing. The inspiratory pressure is initially started at 10-12 cm
H2O and expiratory pressures at 5 cm H2O. The inspiratory pressure is adjusted to ensure comfort and ventilator synchrony. The goal of
therapy is to relieve the work of breathing and increase ventilation. Attempt to correct the hypercapnia by following the change in pH to
near normal levels and not to a normal pCO2, since a majority of these patients have a baseline chronic hypercapnia.
Invasive mechanical ventilation: Some AECOPD patients, based on clinical judgment, require endotracheal intubation and
mechanical ventilation to maintain adequate oxygenation and ventilation. There are several different strategies for managing patients on
a mechanical ventilator with COPD and it is unclear if which particular strategy is best. However, it has beenwell describedthat liberation
from the ventilatorshould begin early to prevent muscle atrophy.
Oxygen therapy: Oxygen therapy and smoking cessation remainsa corner stone of COPD treatment. Best practices with oxygen
therapy are to observer the arterial hemoglobin saturation with pulse oximetry and maintain the level of approximately 90%, commonly
between 88-92%, but not higher [4].

Pharmacologic therapy

Ipratropium bromide

1) MDI: 18 mcg 2 puffs with spacer every 4 hours
2) Nebulizer: 500 mcg every 4 hours


1) MDI: 90mcg four puffs every 4 hours with a spacer
2) Nebulizer: 2.5 mg (dilute to 3 ml) every 4 hours

Ipratropium bromide & albuterol combination

1) MDI: (90 mcg albuterol/18 mcg Ipratropium) 2 puffs with a spacer every 4 hours
2) Nebulizer: (2.5 mg albuterol/0.5 mg ipratropium) in 3 ml vial every 4 hours
Table 1: Common dosing regimens in AECOPD

Glucocorticoids: Systemic corticosteroids have been shown to improve symptoms, lung function, and decrease hospital length of
stay [1,12]. The optimal dose and duration of glucocorticoids is unknown and may depend on the patient’s response to therapy. While
the consensus in the literature favors a moderate dose of steroids (30 to 40 mg daily), this may not pertain to critically ill patients [1].
Evidence suggests oral administration is just as efficacious as an intravenous route [13]. A commonly prescribed agent is 125 mg of
methylprednisolone every 6 hours for 72 hours followed by a 2-week oral taper starting at 60 mg [8]. Prolonged treatment leads to
increased adverse reactions from corticosteroids without improving efficacy, morbidity or mortality [12-15]. Hence, shorter tapering
regimens have been suggested starting witha standard 3-day intravenous regimen noted above followed by a 30 mg dose for 5-10 days.

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Bronchodilators: Short acting inhaled anticholinergic agents (i.e. ipratropium) and beta-agonist (i.e. albuterol) are the main
stay of therapy for AECOPD. Although they can be given separately or in combination solutions, several studies have demonstrated
thesignificant bronchodilatation when these agents are givenconcomitantlyversuseither agent being given alone [9-11]. These agents have
a rapid onset and can be administered in a nebulizer fashion or a metered dose inhaler (MDI) (Table 1). Evidence suggests that there is
no difference in the efficacy between nebulizer versus MDI with a spacer in the delivery of inhaled medication [1]. In the acute setting,
the nebulizer method may be easier for the patient to administer [1].


Antibiotics: There is a large and consistent beneficial effect of antibiotics in AECOPD patients admitted to an ICU [16]. Typical
bacteria isolates recovered in AECOPD patients include Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis
[17]. While mild-moderate AECOPD is usually treated with a conventional broad-spectrum agent (i.e. doxycycline, trimethoprimsulfamethoxazole and amoxicillin-clavulonate potassium), severe AECOPD usually includes a 3rd generation cephalosporin (i.e.
ceftriaxone) in combination with a macrolide (i.e. azithromycin) or a fluoroquinolone (i.e. moxifloxacin). Agents may be changed based
on community or institutional antibiogram and resistance patterns. While it may not provide efficacy in the ICU setting, influenza and
pneumococcal vaccines should be considered prior to hospital discharge.

Asthma is a chronic inflammatory disease of the airways similar to COPD in that patients typically have recurrent respiratory
symptoms such as cough, chest tightness, dyspnea and wheezing. The pathophysiology of asthma includes airway inflammation,
hyper-responsiveness, and remodeling resultingin completely reversible airflow obstruction either spontaneously or with therapy.The
severe airflow obstruction can result from bronchial constriction, edema, and/or secretions from inflammation. In turn, this can lead
to air trapping (increasing intrathoracic pressure), hypercapnia, hypoxemia, and an increase in the work of breathing. If not treated
appropriately, the airflow obstruction can be permanent as a result of this alteration of the bronchial mucosa.
The CDC reports that 1 in every 12 adults have asthma in the US [18]. In the 2009, there were 1.9 million adult and child emergency
department (ED) visits as a result of asthma, of which 479,000 required hospital admission and 3,388 died (an age-adjusted death rate
of 1.1 per 100,000 population) [19]. Like COPD, asthma can have acute worsening of symptoms (exacerbations) and require ICU
admission. The major risk factors for a patient suffering from severe asthma include a slow onset of symptoms [20] and prior history of
poorly controlled or near fatal asthma [21-23].

Clinical presentation and initial evaluation
On physical exam you may find the patient in significant respiratory distress with inability to talk in full sentences or lie flat. An
increase in the respiratory rate is often observed with use of accessory muscles. Pulsus paradoxicus (a significant decrease in systolic
blood pressure upon inspiration) is often present in severe cases as a result of an increase in the intrathoracic pressure from air trapping.
A chest roentogram may demonstrate hyperinflation and peak flow measurements may be significantly decreased from the patient’s
baseline values.

Pharmacologic therapy
The goal of therapy is to quickly reverse the significant airflow obstruction and inflammation with bronchodilators and glucocorticoids,
Inhaled beta-agonist: Short-acting β-receptor agonists (i.e. albuterol) are the drugs of choice in acute asthma exacerbations and
quickly cause bronchial smooth muscle relaxation [24]. Long-acting beta-agonist is not typically used in these acute cases. Inhaled
MDI or aerosol delivery is preferred over oral or intravenousroute due to improved efficacy [25-27]. There does not appear to be any
difference in efficacy between the nebulized versus MDI with a spacer administration [28]. When giving these therapies one needs to be
mindful of the side effects of the β-receptor agonists in high doses, these include tachycardia, tremor, and hyperglycemia and decreased
serum potassium. Dosing can either be recurring/cyclic or continuous: repetitive nebulizer treatments (2.5-5 mg dose) or in the case of
ventilated patient’s repetitive use of MDI (4-8 puffs of 90 μg of albuterol per puff); continuously given as 1-hour nebulizer treatments
using 10-15 mg of albuterol.
Anticholinergic therapy: Inhaled anticholinergic agents (i.e., ipratropium) are recommended for acute asthma inED, but not
hospitalized, patients [29]. However, many studies have suggested that the combination of inhaled anticholinergics and beta-agonists be
utilized in ED patients with severe airflow obstruction since this combination results in a greater bronchodilation than either drug alone
[10,30,31]. When using ipratropium in combination with albuterol, the dosing is 0.5 mg every 20 minutes x 3 doses then every 2 to 4
hours as needed (nebulized). If using an MDI, the dose is 4-8 puffs (18 μg per puff) in the same regimen.
Systemic steroids: The goal of using corticosteroids is to help reduce inflammation. It may take a few hours before it is effective and
therefore, the quick relief of bronchoconstriction by a short-acting beta-agonist and anticholinergic is important. Systemic steroids may
help improve long-term recovery by decreasing airways inflammation. Steroids are recommended in patients with severe acute asthma
and should be administered intravenously [29]. Based on expert opinion [32], the dosing should include intravenous methylprednisolone
(60-80 mg every 12 hours) followed by a transition to10-14 day course of oral steroids when the patient can tolerate oral medications.
Magnesium sulfate: Magnesium sulfate (2 grams administered IV over 20 minutes) may be helpful in acute asthma due to its ability
to relax bronchial smooth muscle [33]. Its use is recommended to patients with severe symptoms that have not resolved after one hour
of aggressive conventional therapy [29].

Approximately 4% of hospitalized asthmatics develop significant respiratory failure that requires endotracheal intubation and
mechanical ventilation [34]. This can be a very challenging problem to manage as they can develop various complications from securing
the airway to barotrauma from the mechanical ventilation. In this section, we will highlight some of the basic ICU principals in the airway
management and ventilation strategies for the patient with respiratory failure due to acute asthma.
Airway management: The decision to intubate is based on clinical judgment based on the patients’ ability to protect their airway
and maintain adequate oxygenation with supplemental oxygen and NIPPV. It is important to remember that the patient’s respiratory
issues can continue post-intubated and adding a mechanical ventilator may further complicate the problem. It is highly recommended
that experienced physicians and respiratory therapists treat patients with acute asthma. Additionally, it is also recommended that the
healthcare provider performing the intubation be experienced and trained in the management of patients with potentially difficult

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Respiratory failure


Non-invasive mechanical ventilation: NIPPV is an excellent option for patients that do not require immediate endotracheal
intubation or have a contraindication to NIPPV therapy [35-39]. Typically, a bi-level mode with inspiratory pressure starting at 10-12
cm H2O and expiratory pressures of 5-8 cm H2O is used and adjustments are made to increase ventilation and work of breathing. Of
importance is that if NIPPV is utilized, frequent monitoring is necessary for response to therapy and a declining respiratory status.
NIPPV should not be a substitute for the patient that requires endotracheal intubation and mechanical ventilation.
Invasive mechanical ventilation: Due to the physiologic consequences of significant airway constriction (airflow obstruction,
hypoxia, hypercapnia, air trapping) in asthmatic patients, the ventilator management can be very challenging and may result in
complications. General principles to consider in the ventilator management of these patients include dynamic hyperinflation as a result
of a prolonged expiration from constricted airways. This can be made worse by mechanical ventilation if the respiratory rate is not
spaced far enough apart allowing the inhaled gas time to escape before a second breathe is administered. This can cause a tremendous
amount of pressure in the chest, resulting in hypotension from a decrease in blood return to the right heart, worsening hypercapnia, and
barotrauma (pneumothorax, pneumomediastinium, etc.).
Strategies to decrease hyperdynamic inflation include [40]:
• Increase the ventilator flow rate in order to decrease the inspiratory time and increase the expiratory time.
• Decrease the respiratory rate, allowing the inhaled gas time to be exhaled.
• Decrease the tidal volume, allowing less inhaled gas to be exhaled.
Adjunctive therapies: In some severe cases when oxygenation and ventilation cannot be achieved by conventional methods, other
therapies have been utilized in the management of acute asthma. Listed below is a brief description of these therapies. We recommend
that only those physicians that are familiar with the utility of these agents should administer these treatments
i. Heliox Therapy
Heliox is the blend of helium and oxygen that can be helpful by enhancing the delivery of oxygen and inhaled medication to the
distal airway in acute asthmatics [41]. It has a density less than air and can overcome the significant airway resistance in these patients
ii. General Anesthesia
Several different agents such as ketamine and isoflurane have been used in the management of these patients mostly due to their
bronchodilatation properties [45-47].

Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) is a common condition encountered in the ICU with an estimated 190,000 cases per
year in the United States [48]. Respiratory failure results from an acute inflammation resulting in diffuse alveolar damage, non-cardiac
pulmonary edema, poor lung compliance and significant hypoxemia. In general, there is an indirect (transfusion reactions, sepsis,
pancreatitis,) or direct (trauma, aspiration, pneumonia) insult to the lungs that results in diffuse alveolar damage from disruption
of the alveolar lining and capillary endothelium. In turn, this leads to alveolar edema and protein exudation coupled with a marked
inflammatory response consequentially resulting in fibrosis. The physiological effect of this damage manifests as abnormal gas exchange
due to ventilation perfusion disparities [49] and poor lung compliance [50] and pulmonary hypertension [51].

Clinical presentation and initial evaluation
The initial signs of ARDS are tachypnea and progressive hypoxemia. Physical exam may reveal manifestations of the initial insult
such as pneumonia, sepsis or trauma. Typically, the patient will have an increased respiratory rate, use of accessory muscles and diffuse
crackles upon auscultation of the lungs. There may be signs of peripheral cyanosis and poor perfusion if shock is present. The chest
roentogram is often unrevealing in the first few hours, but will eventually show dense bilateral infiltrates. As the disease progresses, the
patients’ hypoxemia often progresses to require mechanical ventilation.
Appropriate laboratory and radiologic studies should be directed to the underlying disease. For example, if pneumonia is suspected,
blood and sputum cultures may be appropriate. If the patient had significant trauma, radiologic studies should be directed to evaluate
the extent of the injury. It is imperative to evaluate the arterial oxygen and carbon dioxide tension with arterial blood gas monitoring
in all these patients.


• Respiratory symptoms must occur or become worse within one week of the initial insult
• Bilateral pulmonary opacities consistent with pulmonary edema on radiographic imaging (not be due to pleural effusions, lobar
or lung collapse, or pulmonary nodules)
• The respiratory failure must not be due to cardiac failure or volume overload. This must be verified by an objective measure
such as (echocardiogram, pulmonary occlusion pressure, etc.) to exclude hydrostatic pulmonary edema if there is no risk factors
explain the ARDS.
• Impaired oxygen exchange must be present as defined by the ratio of arterial oxygen tension to fraction of inspired oxygen
The severity of hypoxemia defines the severity of ARDS and associated mortality risk:

Mild (27% mortality risk): PaO2/FiO2>200mmHgbut ≤ 300 mmHg, [positive end-expiratory pressure (PEEP) ≥ 5 cm H2O]

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In 2011, an expert panel from an initiative of the European Society of Intensive Care Medicine endorsed by the American Thoracic
Society and the Society of Critical Care Medicine developed the Berlin definition of ARDS [52]. According to the Berlin ARDS definition,
all of the following criteria must be met:



Moderate (32% mortality risk): PaO2/FiO2 >100 mmHg but < 200 mmHg. [PEEP ≥ 5 cm H2O]
Severe (45% mortality risk): PaO2/FiO2 <100 mmHg [PEEP ≥5 cm H2O]

Initial therapy should focus on treating the underlying cause of ARDS (i.e. antibiotics for infections, reversing antidote for overdoses,
etc) and maintaining adequate gas exchange while minimizing complications that are common in patients with ARDS.
The following treatment modalities may be used:
Mechanical ventilation lung protective strategy:
¾¾ Low tidal volume ventilation: In patients with ARDS, positive pressure ventilation may generate extreme pressure in the distal
airways due to the decrease in lung compliance from pulmonary edema, proteinaceous material, and fibrosis. This can lead to
further lung damage, resulting in worsened hypoxemia, pneumothorax, and pneumomediastinium (coined ventilator induced
lung injury and barotrauma). Therefore, the lung protective strategy approach to mechanical ventilation in ARDS patients is to
minimize the elevated distal airway pressure (displayed by the mechanical ventilator as the plateau pressure) by utilizing low
tidal volumes defined as 6-8 mL/kg of ideal body weight [53]. Mortality is also reduced with low distal airway pressures (plateau
pressure <30cm H2O) [54,55]. Our experience has been to utilize lung protective strategies by targeting tidal volumes to 6-8 mL/
kg of ideal body weight.
¾¾ PEEP: One of the factors that may contribute to ventilator induced lung injury is inflammation from cyclic atelectasis (termed
alectotrauma). PEEP improves oxygenation and prevents alectotrauma, although it is unclear at what level of PEEP prevents
this complication [55-57]. Several studies have evaluated various approaches to utilizing PEEP with conflicting results [58-62].
While some studies report no difference in mortality between higher versus lower levels of PEEP [58], other studies illustrate an
improved mortality with higher levels of peep in patients with severe hypoxemia (PaO2/FiO2<200mmHg) [61,62]. Furthermore,
studies have shown a decrease in hypoxemia, ventilator free days, and days free of organ failure when combined with a low tidal
volume strategy [59,60]. While nearly all patients should have a minimum PEEP of 5 cm H2O, PEEP is increased to a plateau
pressure of 30-32 cm H2O in patients with severe hypoxemia (PaO2/FiO2<200mmHg).
¾¾ Fluid management strategies: Patients with ARDS have non-cardiogenic pulmonary edema due to vascular permeability from
inflammation and changes in oncotic forces due to damage to the alveolar-capillary interface. Conservative fluid management
approaches have shown to have a significant clinical benefit by decreasing ventilator free days, ICU days, improved oxygenation
and lung injury scores [63]. A conservative fluid management strategy should therefore be pursued as long as the patient is not
in shock or experiencing hypo perfusion. Effective fluid strategies can be achieved with daily diuretics, avoiding unnecessary
intravenous fluids, and meticulously monitoring fluid intake/output and electrolytes if diuretics are utilized.
¾¾ Novel therapies: Several other therapies and management strategies have been utilized in the management of ARDS such as
systemic steroids [64], antioxidants [65] and prone positioning [66] to improve oxygenation. The benefits of these treatment
modalities remain controversial and should be approached with caution under the direction of a physician that is an expert in
the management of patients with ARDS.
¾¾ Supportive care: Appropriate supportive measures should be given to all patients in the ICU. Maintaining adequate nutrition,
sedation and pain control is paramount but often overseen. The prevention of secondary infections by maintaining aggressive
hand hygiene, ventilator-associated infection preventative measures, and diligent central venous and urinary catheter care is vital.
Gastric ulcers and deep venous thrombosis prophylaxis should be addressed on a case-by-case basis.

COPD, asthma and ARDS are common pulmonary disorders encountered in the ICU. COPD and asthma are initially managed
initially with rapid bronchodilators, anti-inflammatory steroids, and oxygenation via invasive and non-invasive ventilation. In patients
with ARDS, management focuses primarily on treating the underlying cause, lung protective strategies for those receiving mechanical
ventilation, and adequate supportive care. Management of all these conditions can be challenging and a consultation by experts in critical
care medicine is often warranted. Providers caring for critically ill patients should be familiar with the identification and management of
patients with COPD, asthma and ARDS.

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46.Johnston RG, Noseworthy TW, Friesen EG, Yule HA, Shustack A (1990) Isoflurane therapy for status asthmaticus in children and adults. Chest 97:
47.Hemming A, MacKenzie I, Finfer S (1994) Response to ketamine in status asthmaticus resistant to maximal medical treatment. Thorax 49: 90-91.
48.Rubenfeld GD, Caldwell E, Peabody E, Weaver J, Martin DP, et al. (2005) Incidence and outcomes of acute lung injury. N Engl J Med 353: 1685-1693.
49.Dantzker DR, Brook CJ, Dehart P, Lynch JP, Weg JG (1979) Ventilation-perfusion distributions in the adult respiratory distress syndrome. Am Rev
Respir Dis 120: 1039-1052.

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44.Schaeffer EM, Pohlman A, Morgan S, Hall JB (1999) Oxygenation in status asthmaticus improves during ventilation with helium-oxygen. Crit Care
Med 27: 2666-2670.


50.Roupie E, Dambrosio M, Servillo G, Mentec H, el Atrous S, et al. (1995) Titration of tidal volume and induced hypercapnia in acute respiratory distress
syndrome. Am J Respir Crit Care Med 152: 121-128.
51.Villar J, Blazquez MA, Lubillo S, Quintana J, Manzano JL (1989) Pulmonary hypertension in acute respiratory failure. Crit Care Med 17: 523-526.
52.Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, et al. (2012) Acute respiratory distress syndrome: the Berlin Definition. JAMA 307: 25262533.
53.Sud S, Sud M, Friedrich JO, Wunsch H, Meade MO, et al. (2013) High-frequency ventilation versus conventional ventilation for treatment of acute lung
injury and acute respiratory distress syndrome. Cochrane Database Syst Rev 2:CD004085.
54.[No authors listed] (2000) Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory
distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 342: 1301-1308.
55.Needham DM, Colantuoni E, Mendez-Tellez PA, Dinglas VD, Sevransky JE, et al. (2012) Lung protective mechanical ventilation and two year survival
in patients with acute lung injury: prospective cohort study. BMJ 344: e2124.
56.Webb HH, Tierney DF (1974) Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflation pressures. Protection
by positive end-expiratory pressure. Am Rev Respir Dis 110: 556-565.
57.Muscedere JG, Mullen JB, Gan K, Slutsky AS (1994) Tidal ventilation at low airway pressures can augment lung injury. Am J Respir Crit Care Med
149: 1327-1334.
58.Brower RG, Lanken PN, MacIntyre N, Matthay MA, Morris A, et al. (2004) Higher versus lower positive end-expiratory pressures in patients with the
acute respiratory distress syndrome. N Engl J Med 351: 327-336.
59.Meade MO, Cook DJ, Guyatt GH, Slutsky AS, Arabi YM, et al. (2008) Ventilation strategy using low tidal volumes, recruitment maneuvers, and high
positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 299: 637-645.
60.Mercat A, Richard JC, Vielle B, Jaber S, Osman D, et al. (2008) Positive end-expiratory pressure setting in adults with acute lung injury and acute
respiratory distress syndrome: a randomized controlled trial. JAMA 299: 646-655.
61.Briel M, Meade M, Mercat A, Brower RG, Talmor D, et al. (2010) Higher vs lower positive end-expiratory pressure in patients with acute lung injury and
acute respiratory distress syndrome: systematic review and meta-analysis. JAMA 303: 865-873.
62.Gattinoni L, Caironi P (2008) Refining ventilatory treatment for acute lung injury and acute respiratory distress syndrome. JAMA 299: 691-693.
63.National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Wiedemann HP, Wheeler AP, et al.
(2006) Comparison of two fluid-management strategies in acute lung injury. N Engl J Med 354: 2564-2575.
64.Steinberg KP, Hudson LD, Goodman RB, Hough CL, Lanken PN, et al. (2006) Efficacy and safety of corticosteroids for persistent acute respiratory
distress syndrome. N Engl J Med 354: 1671-1684.
65.Gadek JE, DeMichele SJ, Karlstad MD, Pacht ER, Donahoe M, et al. (1999) Effect of enteral feeding with eicosapentaenoic acid, gamma-linolenic
acid, and antioxidants in patients with acute respiratory distress syndrome. Enteral Nutrition in ARDS Study Group. Crit Care Med 27: 1409-1420.

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66.Sud S, Friedrich JO, Taccone P, Polli F, Adhikari NK, et al. (2010) Prone ventilation reduces mortality in patients with acute respiratory failure and
severe hypoxemia: systematic review and meta-analysis. Intensive Care Med 36: 585-599.


Bedside approach to Gastrointestinal
Bleeding in the Intensive Care Unit
Diana A Gliga, Ramzy H Rimawi, Zahid Vahora and Mark
A Mazer
Brody School of Medicine at East Carolina University, Jacksonville, NC
28546, USA
*Corresponding author: Diana A. Gliga, MS, Brody School of
Medicine at East Carolina University, 134 Empire BLVD, Jacksonville,
NC 28546, USA, E-mail: gligad05@students.ecu.edu

Disclosure/Funding: Dr. Ramzy Rimawi is on the speakers’ bureau for ALK-Abello. None of the other authors have
conflicts of interest. None of the authors have received funding for this manuscript.

Keywords: Bleeding; Critical care; Gastrointestinal system; Intensive care; Resuscitation
Acute gastrointestinal bleeding is a common problem in the intensive care unit (ICU). Depending on comorbidities and other critical
factors, it can be potentially life threatening and thus, requires prompt assessment and often multidisciplinary medical management
[1]. Admission to ICU takes into account various “high-risk” profiles, which are often associated with a poor outcome and prolonged
ICU stay [2,3]. These features include hemodynamic instability, incessant bleeding, coagulopathy, aspirin use, comorbid conditions and
age above 65 years, anemia, elevated blood urea nitrogen and leukocytosis [3]. This chapter will integrate current research findings and
recommendations for managing ICU adult patients with GI bleeding.
Although the BLEED classification tool developed in 1997 suggested a great percentage of low-risk patients were hospitalized in
the ICU, it helped to identify high-risk patients that required immediate intervention, developed bleed recurrence, required surgery for
source control, and had increased mortality [4]. High-risk patients had additional multi-organ failure, required more transfusions of
blood products, and were hospitalized for longer periods of time. The BLEED criteria should be used as a triage prediction tool for of
ICU admission, as well as probable length of stay in the hospital. Other prognostic indicators include the Rockall bleeding score and
the Glasgow Blachford prognostic scales.

Upper vs. Lower GIB
Gastrointestinal (GI) bleeding can be overt (i.e., hematemesis, coffee-ground emesis, hematochezia, melena) or occult. Occult blood
can be detected by guaiac examination of the stool. Acute upper GI bleed (AUGIB) has a yearly incidence of 40-150 per 100,000 persons,
with a 6-10% mortality rate [5]. Acute lower GI bleed (ALGIB) is defined as bleeding distal to the ligament of Treitz and has incidence
estimated at 20-30 per 100,000 adults. ALGIB is primarily caused by non-life threatening anal pathology, with hemorrhoids or fissures
being the most common cause of rectal bleeding in individuals up to 30 years of age. In older individuals, the main source is colonic
diverticula (80%).
Overall, 80% of GI bleeds cease without intervention. However, the overall risk of recurrence is about 25%. Moreover, the mortality
rate increases in patients with advanced age and comorbid conditions, specifically renal and/or hepatic dysfunction, heart disease, and
malignancy. Intermittent or spontaneous cessation of bleeding, along with anatomical barriers such as the intra-peritoneal location of
the intestines, the robust intestinal contractility, and the superimposed bowel loops lead to an overall difficulty of diagnosing a precise
source for ALGIB in 10% of the cases [6] (Table 1). The Rockall Scoring System is a parameter used for stratifying the risks of rebleeding
and death after admission to the hospital for an acute GI bleed.
Causes of AUGIB

Causes of ALGIB

Ulcers (esophageal, gastric, duodenal)


Dieulafoy’s lesions

Ischemic colitis

Arterial-venous malformations

Vascular ectasias

Varices (esophageal, gastric)


Aortoesophageal fistula

Rectal varices
NSAID induced
Inflammatory Bowel Disease

Risk Factors
There are various reversible and irreversible pharmacologic agents associated with GI bleeding. For example, numerous studies have
illustrated the risk of GI bleed and GI perforation with non-steroidal anti-inflammatory drugs (NSAID) use [7]. As the incidence of GI
bleeding in elderly patients using NSAIDS is up to 1 in 7 persons, NSAID use is responsible for about 30% of GI bleed hospitalizations
and mortality [8]. Multiple locations, including gastric, duodenal and pre-pyloric areas may be affected by NSAID use. Aspirin is

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Table 1: Causes of AUGIB and ALGIB.


associated with about a 4-time increase risk of GI bleed. Coating the ASA enterically does not reduce its’ risk. There is also a positive
correlation between higher doses of ASA and GI bleed. The concomitant use of clopidogrel and warfarin versus monotherapy is related
to higher incidence of bleeding.

Age over 65 years is the strongest risk factor GI bleeding and is associated with increased morbidity and mortality compared with the
general population [7,9]. Male gender, extensive comorbidities, prior history of complicated peptic ulcer disease or alcoholic cirrhosis,
and presence of neoplasm are other common risk factors associated with poor prognosis. Rebleeding is primarily encountered in
hemodynamically unstable patients or those with elevated blood urea nitrogen, creatinine, or liver enzymes (particularly aminotransferases).
Other risks for rebleeding include GI hemorrhage (>20 g/L reduction in hemoglobin), septic shock, prior abdominal aortic aneurysm
repair, and malnutrition [10]. As expected, length of stay in the ICU is prolonged in these patients. The incidence of stress associated GI
bleed is about 0.17% due to the use of routine prophylaxis in the ICU.

Helicobacter pylori
Bacterial infection with Helicobacter pylori is a well-described risk factor in the development of ICU upper GI bleed. A multicenter
cohort study conducted in medical and surgical ICUs suggested that an increase in anti-H. pylori immunoglobulin A concentration was
predictive of an active infection and risk of developing GI bleeding [11]. Additionally, the mortality rate was substantially increased by
34% in those who developed this infection.

Portal hypertension
Esophageal or gastric variceal bleeding is associated with portal hypertension, the most common cause of morbidity and mortality
in liver cirrhosis [12]. When the hepatic venous pressure exceeds 12 mmHg, acute esophageal variceal bleeding can occur. With an
associated mortality rate of 20-25%, clinical scoring predicting the risk of bleeding in this patient population is of tremendous importance.
Cholinesterase level <2.25 kU/L, INR >1.2, variceal presence and viral or alcoholic etiology were four parameters effective in identifying
high-risk patients [13]. These factors were used to supplement EGD diagnostic power. Treating the underlying cause is an essential part
of variceal bleeding prevention. This includes hepatitis C antiviral therapy, alcohol abstinence, and iron chelation. Other modalities that
may prevent rebleeding secondary to portal hypertension include nitrates, non-selective beta-blockers, and diuretics [12]. The efficacy of
the somatostatin analogue, octreotide, in stopping variceal bleeding is controversial [14].

Dysenteric diarrhea
Infectious diarrhea involving dysentery can be caused by enteric pathogens such as Salmonella, Shigella, enterohemorrhagic E. coli
(O157:H7), enteroinvasive E. coli, Yersinia, Entamoeba histolytica, and Clostridium difficile. Campylobacter jejuni is the most common
identified organism, associated with grossly blood diarrhea in up to 91% of patients [15]. Stool cultures are usually requested but their yield
is low (0.9% in Salmonella, 0.6% in Shigella, 1.4% in Campylobacter, and 0.3% in E. coli O157 infections). Presence of stool leukocytes and
fecal lactoferrin are also used in guiding infectious etiology of bloody stools. The “three day rule” is enforced to diminish extraneous stool
cultures in patients with non-Clostridium difficile diarrhea related to hospitalization >3 days. Exceptions to this include HIV, neutropenia,
age over 65 years, or those with questionable C. difficile infection.

Diverticular disease
Diverticular bleeding accounts for approximately 40% of ALGIB [16]. As diverticulosis incidence increases with age, diverticular
bleeding is an important consideration in the differential diagnosis of GI bleeding. They can often present without pain, potentially
making the presentation of such a patient misleading. Such bleeds can be arterial in origin, frequently from the neck or dome of the
diverticulum [17]. While diverticular bleeds often cease without intervention, they have high rates of rebleeding, often prompting further
radiologic studies as there is a wide range in diagnostic yield of colonoscopy in all ALGIB, ranging from 48-90% [18].

Aggressive hemodynamic resuscitation is imperative in patients with rapid bleeding, defined as a hemorrhage >100 mL/hr with
signs of hypovolemic shock (i.e., tachycardia, hypotension, tachypnea). The estimated blood volume depletion in such cases is 15%.
Hemodynamic stability is a provider’s top priority and should supersede diagnostic interventions [19].

Setup and consult requisitions
Aggressive and early resuscitation in the ICU care is warranted in patients who meet high-risk criteria with hemodynamic instability,
active hemorrhage, and/or comorbid risk factors. Immediate intravenous access should be obtained with large bore peripheral catheters
or a central venous line. Large bore venous access, ideally through peripheral catheters, is essential for volume resuscitation, serial blood
count monitoring, medication infusion(s), and transfusion of blood products when appropriate. Consultation with gastroenterology,
general surgery, and/or interventional radiology should be requested early to avoid delays in diagnostic and therapeutic interventions.

Most AUGIB secondary to peptic ulcers and other non-variceal bleeds cease spontaneously [15]. However, the majority of patients
with bleeding, and rebleeding complications require hemostasis with the use of endoscopic therapy to obtain source control. Despite rapid
endoscopic repair, subsequent rebleeding occurs in 20% of patients. Histamine-2-receptor antagonists are efficient in preventing these
rebleeding episodes; however, their use is limited in reducing the need for transfusions or surgical interventions. While intravenous proton
pump inhibitors (PPI) are effective in reducing bleeding recurrences, they have little-to-no impact on mortality or need for surgery [20-22].

Transfusion of red-blood-cell products may be warranted in patients with active bleeding, hypovolemia, and hemodynamic instability
regardless of laboratory values. Due to the paucity of coagulation factors in packed red cells, one unit of fresh frozen plasma should
be administered for every four units of packed red blood cells transfused [3]. At concentration hemoglobin levels lower than 5-6 g/dL,

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Hemostasis control


cognitive impairment may become clinically apparent. In cases of acute GI bleeding at hemoglobin levels below 7-8 g/dL, the risk of
postoperative death increases. Based on randomized trials, hemoglobin goals in the ICU are a concentration of 7 g/dL in hemodynamically
stable young patients without comorbidities and 8 g/dL for other medical or surgical patients who are hemodynamically stable [23]. A
liberal transfusion trigger of hemoglobin level of 10 g/dL was associated with higher mortality than a restrictive trigger of 7 g/dl, except
in older patients and those with active coronary artery disease [24]. If the patient is hemodynamic stable, esophagogastroduodenoscopy
(EGD) can be performed during the blood product transfusion [25]. If coagulopathy is present, fresh frozen plasma (FFP), prothrombin
complex concentrate, or cryoprecipitate should be transfused depending on the circumstances. As FFP (typically dosed 10-15 mL/kg)
contains about 70% of the original coagulant factor VIII, normal stable clotting factor levels, albumin and immunoglobulins, is not
recommended when INR is below <1.5 [26]. Platelet infusions are recommended when platelet counts fall below 50,000/microL [3].

The incidence of acute GI bleeding from oral anticoagulants (OA) is higher than the incidence related to acetaminophen, NSAIDs, and
aspirin (ASA) [4]. Dabigatran is particularly problematic in patients with superimposed renal failure [27]. Concomitant anticoagulants
and/or antiplatelet therapies yield a greater risk of GI bleeding: 8.0 incidence ratio (IR) versus OA use with Tylenol (4.4 IR) and OA use
with ASA (3.8 IR) [4]. If the risks of anticoagulants and platelet inhibitor agents outweigh their benefits, these agents, including aspirin,
should be held in patients with GI bleeding [4]. While there are no set criteria for these scenarios, consulting the prescribing provider in
a timely fashion is highly recommended [3]. Reversal of these agents is often necessary to help achieve timely source control. In patients
with INR is >3, EGD may need to be postponed until the anticoagulation is reversed. If the INR is still >1.5 prior to the procedure, fresh
frozen plasma can also be administered during the endoscopy.
Additional pharmacologic modalities for GI hemorrhage management are under investigation. In animal models, nitric oxide-based
therapy (i.e., nitroglycerin) helps reduce the NSAID induced damage to the gastric mucosa. However, this effect may be limited by an
inhibitory effect on platelet aggregation [8]. Statistical analysis of agents that predispose to a bleeding event showed an odds-ratio (OR) of
7.4 with NSAIDS, 2.4 with aspirin, and 0.6 with nitro-vasodilators and anti-secretory therapies [28].

The diagnostic tool of choice in patients who have been resuscitated is colonoscopy and esophagogastroduodenoscopy (EGD) for
ALGIB and AUGIB, respectively.

AUGIB pre-endoscopic management
An appropriate history and physical can help direct one’s clinical suspicion as to the cause of a patient’s bleeding. The suspicion of
peptic ulcer disease will prompt a clinician to infuse a PPI (80mg bolus, followed by 8mg/hr) versus a history of liver cirrhosis, which
would prompt octreotide infusion [14,29]. Unfortunately in the ICU setting, appropriate history acquisition can be difficult and clinical
judgment must often be used.
Active bleeding, a visible vessel at the ulcer base with an adherent clot, and an ulcer larger than 2 cm are factors associated with a
greater risk of re-bleeding [9]. In these patients, endoscopic interventions such as cautery, injection, or hemoclipping therapies are effective
in achieving hemostasis during acute bleeding and may help decrease the risk of future bleeding. Early EGD can improve outcome while
reducing ICU length of stay and rate of re-bleed [30]. Conversely, inaccurate diagnosis due to delayed endoscopy increases risks of
re-bleed, surgery, hospitalization, ICU stay, and ICU re-admission. In patients without frank signs of AUGIB, a lavage via nasogastric
tube may be done to help identify whether the bleeding is distal to ligament of Treitz. EGD should follow a bloody lavage [5]. However,
nasogastric lavage remains controversial as approximately 15% of gastric aspirates in patients with AUGIB will not yield blood return
[31]. Radionuclide imaging and computed tomographic (CT) angiography are two other useful diagnostic interventions. However, their
sensitivity depends on the presence of active bleeding during the examination. Post-procedure high-dose PPI infusion is recommended
for 72 hours to reduce the risk of rebleeding in patients with ulcers and high risk stigmata [14].

ALGIB pre-endoscopic management
Colonoscopy can diagnose the source of up to 89% of ALGIB, as compared to angiography, which has a diagnostic sensitivity of about
41% [5]. Colonoscopy can provide for direct visualization of the entire colon, biopsy, and therapy (laser, pharmaceutical, or physical
ligation). Colonoscopy is associated with low mortality and morbidity risks (0.1% and 0.3% respectively) and shortened length of stay
[14]. Urgent colonoscopy can result in successful permanent hemostasis in 67% of the cases [32].

Push enteroscopy or endoscopy is a procedure reserved for identifying small bowel bleeding past the ligament of Treitz (2-10% of all
GI bleeding cases) [5]. This procedure is essentially an upper endoscopy with an additional 15-160 cm of small intestine visualization. The
evaluator can take biopsy samples and apply treatment, but the diagnostic yield reaches a mere 54%. While capsule endoscopy is painless,
non-invasive and has a diagnostic yield of 66-69%, biopsies cannot be taken. As a last resort, exploratory laparotomy may be employed,
with a sensitivity of 70% in locating GI bleeding sources [5].
While sclerotherapy and variceal band ligation with rubber rings via endoscopy can help control or prevent rebleeding in patients
who cannot tolerate beta blockade, it does not reduce the portal pressure. In cirrhotic patients, variceal bleeding related to portal
hypertension can be managed via transjugular intrahepatic portosystemic shunting (TIPS). If placed within three days, TIPS improved
two-year survival, reduced rebleeding rates, and reduced the risk of hepatic encephalopathy. Given the risk of esophageal rupture, balloon
tamponade is only reserved for 24-hour hemostasis in patients with massive bleeding. In cirrhotic patients, the only definitive therapy for
variceal rebleeding is liver transplantation [12].

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Specialized procedures are employed in cases where the source of bleeding is more enigmatic. These include Meckel’s scan, barium
contrast upper GI series with small bowel follow-through, technetium-99m–tagged red blood cell scan, and push enteroscopy [5]. Nuclear
studies (i.e., technetium-99m–tagged red blood cell scan) are indicated in cases with a low rate of bleeding (0.1 to 0.4 mL per minute).
The accuracy is increased when used concomitantly with arteriography. Angiography is the desired diagnostic tool if the rate of bleeding
is approximately 0.5 mL/min, and if the patient experiences active bleeding. However, this intervention is invasive and nephrotoxic.
Sensitivity is also poorer than that of colonoscopies, with an estimated upper range of 65% [19]. The advantages include embolization and
infusion of vasoactive treatment.


Stress Ulcers Prophylaxis
Ulceration and stress-related mucosal disease (SRMD) are some of the more common GI complications in patients hospitalized in
the ICU, with an associated increase mortality rate [33]. The majority of critically ill patients who develop SRMD are affected within 24
hours of admission to ICU, likely related to acid production and ischemia. Suppressing hydrogen ion production with antacids, sucralfate,
histamine2-receptor antagonists or PPI is critical in SRMD prophylaxis [13]. Ranitidine and enteral feeding were shown to be superior
to sucralfate in ensuring lower bleeding rates in mechanically ventilated patients [34]. While a gastric pH >4 is adequate to prevent stress
ulcers, a pH >6 is necessary to prevent rebleeding from a peptic ulcer. Also, while both IV histamine-2-receptor antagonists and PPIs
increase the gastric pH, maintenance at pH >6 are primarily achieved with PPIs [22]. As critically ill patients rarely develop clinically
significant GI bleeding, stress ulcer prophylaxis should be withheld unless they have a coagulopathy or require mechanical ventilation [34].

Laboratory Markers
Early hemodynamic resuscitation, correction of coagulopathy and judicious blood transfusions are imperative for patients with an
acute GIB in the ICU [35]. Complete blood counts should be frequently and serially monitored every 4-6 hours. Critically ill patients with
GI bleeding can progress to disseminated intravascular coagulation as a result of the hypovolemic shock. Activated partial thromboplastin,
prothrombin time, and D-dimer should be monitored to assess for this complication. D-dimer elevation at the time of ICU admission
suggests a 5.6 times increased risk of developing a venous thromboembolic event and a 3.94 greater relative mortality risk [36]. GI
bleeding may be associated with inflammatory bowel disease exacerbations. In such instances, mean platelet volume, mean platelet count,
white blood cell count, and inflammatory markers (i.e., C-reactive protein, erythrocyte sedimentation rate) should be monitored [37].

Other Considerations
Restarting aspirin for primary cardiovascular prophylaxis is not recommended, except in secondary prophylaxis for patients with a
history of CAD where it is recommended to restart soon (1-7 days) in addition to a PPI. In terms of restarting NSAIDs in patients with
bleeding ulcers, it is recommended not to resume NSAIDs and, if necessary, cyclo-oxygenase (Cox)-2 selective NSAIDS be started with
PPI [38].

The ICU provider plays an important role in coordinating and managing the care of high-risk patients with acute GI bleeding. These
patients require intensive clinical and hemodynamic monitoring, correction of coagulopathy, appropriate pharmacologic intervention,
and rapid diagnostic and therapeutic intervention. As GI bleeds are frequently encountered in the ICU setting, ICU providers should
obtain adequate education and training in the timely and effective management of acute GI bleeds.

1. Beejay U, Wolfe MM (2000) Acute gastrointestinal bleeding in the intensive care unit. The gastroenterologist’s perspective. Gastroenterol Clin North
Am 29: 309-336.
2. Cook DJ, Griffith LE, Walter SD, Guyatt GH, Meade MO, et al. (2001) The attributable mortality and length of intensive care unit stay of clinically
important gastrointestinal bleeding in critically ill patients. Crit Care 5: 368-375.
3. Strate L (2013) Approach to resuscitation and diagnosis of acute lower gastrointestinal bleeding in the adult patient. UpToDate.
4. Kollef MH, O’Brien JD, Zuckerman GR, Shannon W (1997) BLEED: a classification tool to predict outcomes in patients with acute upper and lower
gastrointestinal hemorrhage. Crit Care Med 25: 1125-1132.
5. Manning-Dimmitt LL, Dimmitt SG, Wilson GR (2005) Diagnosis of gastrointestinal bleeding in adults. Am Fam Physician 71: 1339-1346.
6. Imdahl A (2001) Genesis and pathophysiology of lower gastrointestinal bleeding. Langenbecks Arch Surg 386: 1-7.
7. Gutthann SP, García Rodríguez LA, Raiford DS (1997) Individual nonsteroidal antiinflammatory drugs and other risk factors for upper gastrointestinal
bleeding and perforation. Epidemiology 8: 18-24.
8. Bhatt DL, Scheiman J, Abraham NS, Antman EM, Chan FK, et al. (2008) ACCF/ACG/AHA 2008 expert consensus document on reducing the
gastrointestinal risks of antiplatelet therapy and NSAID use: a report of the American College of Cardiology Foundation Task Force on Clinical Expert
Consensus Documents. J Am Coll Cardiol 52: 1502-1517.
9. Pitchumoni CS, Brun A (2012) Geriatric Gastroenterology. Springer, New York.
10.Pimentel M, Roberts DE, Bernstein CN, Hoppensack M, Duerksen DR (2000) Clinically significant gastrointestinal bleeding in critically ill patients in an
era of prophylaxis. Am J Gastroenterol 95: 2801-2806.
11.Ellison RT, Perez-Perez G, Welsh CH, Blaser MJ, Riester KA, et al. (1996) Risk factors for upper gastrointestinal bleeding in intensive care unit
patients: role of helicobacter pylori. Federal Hyperimmune Immunoglobulin Therapy Study Group. Crit Care Med 24: 1974-1981.
12.Ashkenazi E, Kovalev Y, Zuckerman E (2013) Evaluation and treatment of esophageal varices in the cirrhotic patient. Isr Med Assoc J 15: 109-115.
13.Tacke F, Fiedler K, Trautwein C (2007) A simple clinical score predicts high risk for upper gastrointestinal hemorrhages from varices in patients with
chronic liver disease. Scand J Gastroenterol 42: 374-382.

15.Guerrant RL, Van Gilder T, Steiner TS, Thielman NM, Slutsker L, et al. (2001) Practice guidelines for the management of infectious diarrhea. Clin
Infect Dis 32: 331-351.
16.Schuetz A, Jauch KW (2001) Lower gastrointestinal bleeding: therapeutic strategies, surgical techniques and results. Langenbecks Arch Surg 386:
17.Davila RE, Rajan E, Adler DG, Egan J, Hirota WK, et al. (2005) ASGE Guideline: the role of endoscopy in the patient with lower-GI bleeding.
Gastrointest Endosc 62: 656-660.
18.Zuckerman GR, Prakash C (1998) Acute lower intestinal bleeding: part I: clinical presentation and diagnosis. Gastrointest Endosc 48: 606-617.
19.Edelman DA, Sugawa C (2007) Lower gastrointestinal bleeding: a review. Surg Endosc 21: 514-520.
20.Conrad SA (2002) Acute upper gastrointestinal bleeding in critically ill patients: causes and treatment modalities. Crit Care Med 30: S365-368.

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14.Hwang JH, Fisher DA, Ben-Menachem T, Chandrasekhara V, Chathadi K, et al. (2012) The role of endoscopy in the management of acute nonvariceal upper GI bleeding. Gastrointest Endosc 75: 1132-1138.


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