Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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PHILOSOPHY & PRINCIPLES OF CRITICAL CARE

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Attention to Psychosocial

& Other Needs of the Patient

Psychosocial needs of the patient must be a major considera-

tion in the ICU. The psychological consequences of critical

illness and its treatment have a profound impact on patient

outcome. Leading factors include the patient’s lack of control

over the local environment, severe disruption of the sleep-

wake cycle, inability to communicate easily and quickly with

critical care providers, and pain and other types of physical

discomfort. Inability to communicate with family members,

as well as concern about employment status, activities of daily

living, finances, and other matters, further inflates the emo-

tional costs of being seriously ill. The intensivist and other

staff members must pay close attention to these problems

and issues and consider psychological problems in the differ-

ential diagnosis of any patient’s altered mental status.

Adequate yet appropriate sedation and analgesia are manda-

tory to preserve the balance of comfort with patient assess-

ment and interaction needs.

There is increased awareness of the potential harm to

patients and caregivers from the ICU environment. The

noise level is high (reported to exceed 60–84 dB, where a

busy office might have 70 dB and a pneumatic drill at 50 feet

might be as loud as 80 dB), notably from mechanical venti-

lators, conversations, and telephones but especially from

audio alarms on ICU equipment. One study found that care-

givers were unable to discern and identify alarms accurately,

including alarms that indicated critical patient or equipment

conditions.

Sleep disruption deserves much more attention. Very dis-

ruptive sleep architecture has been identified in patients in

the ICU. Frequent checking of vital signs and phlebotomy

were most disruptive to patients, and environmental factors

were less of a problem to patients surveyed. Most recently, in

addition, the impact of duty hours, sleep, and time off on the

cognitive and patient care ability of house officers is being

studied and reported.

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Understand the Limits of Critical Care

All physicians involved with critical care must be familiar

with the limitations of such care. Interestingly, physicians

and other care providers may have to be reminded that

Things To Think About Reminders

Fever, Recurrent or Persistent

1. New, unidentified source of infection.

2. Lack of response of identified or presumed source of infection.

3. Opportunistic organism (drug-resistant, fungus, virus, parasite,

acid-fast bacillus).

4. Drug fever.

5. Systemic noninfectious disease.

6. Incorrect empiric antibiotics.

7. Slow resolution of fever (deep-seated infection: endocarditis,

osteomyelitis).

8. Infected catheter site or foreign body (medical appliance).

9. Consider infections of sinuses, CNS, decubitus ulcers; septic arthritis.

1. Examine catheter sites (old and new), surgical wounds, sinuses, back

and buttocks, large joints, pelvic organs, catheters and tubes, skin

rashes, hands and feet.

2. Consider pleural, pericardial, subphrenic spaces; perinephric infection;

spleen, prostate, intra-abdominal abscess; bowel infarction or necrosis.

3. Abscess in area of previous known infection.

4. Review prior culture results and antibiotic use.

5. Consider change in empiric antibiotics.

6. Culture usual locations plus any specific areas.

7. Discontinue or change catheters.

8. Consider candidemia or disseminated candidiasis.

9. Discontinue antibiotics?

10. Abdominal ultrasound, CT scan, gallium, leukocyte scans.

Pancytopenia (After Chemotherapy)

1. Fever, presumed infection, response to antimicrobials.

2. Thrombocytopenia and spontaneous bleeding.

3. Drug fever.

4. Transfusion reactions.

5. Staphylococcus, candida, other opportunistic infections.

6. Infection sites in patient without granulocytes may have induration,

erythema, without fluctuance.

7. Pulmonary infiltrates and opportunistic infection.

1. Fever workup; see above.

2. Special sites: soft tissues, perirectal abscess, urine fungal cultures,

lungs.

3. Bronchoscopy with bronchoalveolar lavage.

4. Empiric antibiotics, continue until afebrile, doing well, granulocytes

>1000/μL.

5. Empiric or directed vancomycin, antifungal drugs, antiviral drugs, antitu-

berculous drugs.

6. Check intravascular catheters, bladder, catheter.

7. Platelet transfusions, prophylaxis for spontaneous bleeding (or if

already bleeding).

Table 1–3. Things to think about and reminders for ICU patient care. (continued)

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CHAPTER 1

critical illness is and always will be associated with high

morbidity and mortality rates. The outcome of some dis-

ease processes simply cannot be altered despite the avail-

ability of modern comprehensive treatment. On the basis

of medical evidence and after consultation with the

patient and family, some patients will continue to receive

aggressive treatment; for others, withdrawal or withhold-

ing of ICU care may be the most appropriate and correct

decision.

It is not surprising that critical care physicians, together

with medical ethicists, have played a major role in devel-

oping a body of ethical constructs concerned with such

issues as forgoing of care, determination of brain death,

and withholding feeding and hydration. The critical care

physician must be familiar with ethical and legal concepts

of patient autonomy, informed consent and refusal, appli-

cation of advanced directives for health care, surrogate

decision makers, and the legal consequences of decisions

made in this context. The cost of care in the ICU will be

scrutinized increasingly because of economic constraints

on health care.

There is evidence that care in the ICU improves outcome

in only a small subgroup of patients admitted. Some patients

may be so critically ill with a combination of chronic and

acute disorders that no intervention will reverse or even ame-

liorate the course of disease. Others may be admitted with

very mild illness, and admission to the ICU rather than a

non-ICU area does not improve the outcome. On the other

hand, two other subgroups emerge from this analysis of ICU

patients. First, a small subgroup with a predictably poor out-

come may have an unexpectedly successful result from ICU

care. A patient with cardiogenic shock with a predicted mor-

tality rate of over 90% who survives because of aggressive

management and reversal of myocardial dysfunction would

fall into this group. The other small group consists of

patients admitted for monitoring purposes only or for minor

therapeutic interventions who develop severe complications

of treatment. In these patients with predicted favorable out-

comes, unanticipated adverse effects of care may result in

severe morbidity or death.

Areas of critical care outcome research have, for example,

focused on the elderly, those with hematologic and other

malignancies, patients with complications of AIDS, and

those with very poor lung function from chronic obstructive

pulmonary disease, interstitial lung disease, acute respiratory

distress syndrome, multiorgan failure, or pancreatitis. Much

more needs to be learned about prognosis and factors that

determine outcome, but it is essential that data be used

appropriately and not applied indiscriminately for individual

patient decisions.

Alternatives to current care should be reviewed periodi-

cally and considered in every patient in the ICU. Some

patients may no longer require the type of care available in

the ICU; transfer to a lower level of care may benefit the

patient medically and emotionally and may decrease the

risk of complications and the costs of treatment. Admission

criteria should be reviewed regularly by the medical staff.

Similarly, ongoing resource utilization efforts should be

directed at determining which types of patients are best

served by continued ICU care.

ROLE OF THE MEDICAL DIRECTOR

OF THE INTENSIVE CARE UNIT

The medical director of the ICU has administrative and

regulatory responsibilities for this patient care area. As

medical director, leadership is vital in establishing policies

and procedures for patient care, maintaining communica-

tion across health care disciplines, developing and ensuring

quality care, and helping to provide education in a rapidly

and constantly changing medical field. The medical direc-

tor and the ICU staff may choose to coordinate care in a

number of areas.

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Protocols, Practice Guidelines,

& Order Sets

A survey of outcomes from ICUs concluded that established

protocols for management of specific critical illnesses con-

tribute to improved results. The medical director and medical

staff, nursing staff, and other health care practitioners may

choose to develop protocols that define uniformity of care or

ensure that complete orders are written. Some protocols may

be highly detailed, complete, and focused on a single clinical

condition. An example might be a protocol for treatment of

patients with suspected acute myocardial infarction—the

protocol could specify the frequency, timing, and types of car-

diac enzyme or troponin determination and the timing for

ECGs and other diagnostic tests. Certain standardized med-

ications, such as aspirin, heparin, angiotensin-converting

enzyme inhibitors, and beta-adrenergic blockers, might be

included in such a protocol, and the physician could choose

to give these or not depending on the particular clinical situ-

ation. Protocols are used by many ICUs for community-

acquired pneumonia, ventilator-associated pneumonia,

sepsis, ventilator weaning, and other clinical situations.

Another type of protocol can be “driven” by critical care

nurses or respiratory therapists. In these protocols, nurses or

therapists are given orders to assess the effectiveness and side

effects of therapy and are given freedom to adjust therapy

based on these results. A protocol for aerosolized bronchodila-

tor treatment might specify administration of albuterol by

metered-dose inhaler, but the respiratory therapist would

determine the optimal frequency and dose on the basis of how

much improvement in peak flow or FEV

was obtained and

how much excessive tachycardia was encountered.

The ICU medical director may consider limiting the use

of certain medications based on established protocols. For

example, some antibiotics may be restricted because of cost,

toxicity, or potential for development of microbial resistance.

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PHILOSOPHY & PRINCIPLES OF CRITICAL CARE

Neuromuscular blocking agents may be restricted to use only

by certain qualified personnel because of need for special

expertise in dosing or patient support. Protocols can take

several different forms, and patient care in the ICU may ben-

efit from their development.

Physician practice guidelines are being developed for

many aspects of medical practice. Although some critics of

guidelines argue that these are unnecessarily restrictive and

that elements of medical practice cannot be rigidly defined,

practice guidelines may be useful for diagnosing and treating

patients in the ICU. Guidelines may vary from recommenda-

tions for dose and adjustment of heparin infusion for antico-

agulation to specific minimum standards of care for status

asthmaticus, unstable angina, heart failure, or malignant

hypertension. Practice guidelines will be found commonly in

the ICU of the near future, and ICU directors will be called

on to develop, review, accept, or modify guidelines for indi-

vidual ICUs.

The next step beyond practice guidelines is ICU order

sets. Order sets, either paper or paperless, can streamline

practice guidelines accepted by the ICU staff. Highly recom-

mended orders can be preselected, whereas guidance may be

given for other choices. A major feature of order sets will be

reduction of errors because the order sets include preprinted

medication names, recommended dosages, and potential

drug interactions. Computerized order entry goes beyond

the ICU order set, permitting immediate dosage calculations,

for example, or other real-time recommendations. Although

some have questioned the “one size fits all” nature of order

sets, evidence suggests that there is an increase in the correct

application of evidence-based treatment with implementa-

tion of ICU order sets.

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Quality Assurance

The ICU medical director participates in quality-of-care

evaluation. Quality of care may be assessed by measure-

ment of patient satisfaction, analyzing frequency of deliv-

ery of care, monitoring of complications, duration of

hospitalization, analysis of mortality data, and other ways.

Patient outcome eventually may emerge as the most effec-

tive global determination of the quality of care, but such

measures suffer from the difficulty in stratifying severity in

very complex patients with multiple medical problems. The

development of protocols and programs to measure and

enhance the quality of care is beyond the scope of this pres-

entation. However, the medical and nursing leadership of the

ICU must play key roles in any such projects.

The medical director also plays an important role in

granting privileges to practice in the ICU. Competence in

and experience with medical procedures must be investi-

gated, documented, and maintained for all physicians who

use the service. While this is especially important for invasive

procedures such as placement of pulmonary artery catheters

and endotracheal intubation, consideration also should be

given to developing and granting privileges for mechanical

ventilator management, management of shock, and other

nonprocedural care. Similarly, the skills and knowledge of

nurses, respiratory therapists, and other professionals in the

ICU should be determined, documented, and matched to

their duties. The ICU medical director has the responsibility

to develop standards for those who care for the patients in

that unit.

Effective quality improvement activities go far beyond

simple data collection and reporting. A dedicated group of

health care providers should meet regularly to review the

data, establish trends, and suggest methods for improve-

ment. The importance of “closing the loop” in the quality

improvement process cannot be overstated. Monitoring of

outcomes after instituting change is an important part of this

activity and is mandatory if patient care is to be effectively

and expeditiously improved.

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Infection Control

Nosocomial infections are important problems in the ICU,

and their prevention and management can provide insight

into the effectiveness of protocols and quality assurance

functions. Infection control is particularly important

because of increased antimicrobial resistance of organisms

such as methicillin-resistance Staphylococcus aureus (MRSA),

multidrug-resistant Acinetobacter, vancomycin-resistant

enterococci (VRE), and Clostridium difficile. As described

elsewhere, nosocomial infections are often preventable by

adherence to procedures and policies designed to limit

spread of infection between patients and between ICU staff

and patients. The ICU medical director must take the lead in

establishing infection control protocols, including proce-

dures for aseptic technique for invasive procedures, stan-

dards for universal precautions, duration of invasive catheter

placement, suctioning of endotracheal tubes, appropriate use

of antibiotics, procedures in the event of finding antibiotic-

resistant microorganisms, and the need for isolation of

patients with communicable diseases. Consequently, an

important measure of the quality of care being provided is

the nosocomial infection rate in the ICU, especially intravas-

cular infections secondary to indwelling catheters. The ICU

medical director should work closely with the nursing staff

and hospital epidemiologist in the event of excessive nosoco-

mial infections. Often a breach in procedures can be identi-

fied and corrected. Importantly, it has been demonstrated

that simple measures to prevent infection at the time of

placement of intravenous catheters is highly effective.

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Education & Errors

The ICU medical director is required to provide educational

resources for the staff of the ICU, including critical care

nurses, respiratory therapists, occupational therapists, and

other physicians. This may be in the form of lectures, small

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CHAPTER 1

group discussions, audiovisual presentations, or prepared

handouts or directed readings. An effective strategy is to

focus presentations on problems recently or commonly

encountered; recent experience may help to clarify and

amplify the more didactic portion. Very often in critical care

areas there is a need for personnel to develop skills for using

new equipment such as monitors, catheters, and ventilators.

Appropriate time and feedback should be planned with the

introduction of such equipment before it can be assumed

that it can be used for patient care.

In the teaching hospital, the faculty and attending staff not

only must convey the principles of critical care practice but

also must foster an attitude of rigorous critical review of data,

cooperation between medical and other personnel, and atten-

tion to detail. The new focus on reduction of medical errors

has greatly changed the way critical care medicine is prac-

ticed. The potential for errors is enormous in the ICU. Data

show that changing error reporting from a potentially puni-

tive system to one in which future errors are prevented is key.

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Communication

The ICU medical director serves as a communication link

between physician staff, including primary care and consult-

ing physicians, and the nursing and other health care profes-

sional staff in the ICU. Most of this communication will

occur naturally as a result of interaction during patient care,

quality assurance activities, and other administrative meet-

ings. On occasion, further communication is needed to

address specific complaints, procedures, or policies.

Depending on the organization of the hospital, the ICU also

may be served by a multidisciplinary committee that can

participate in development of protocols and policies. This

committee may function with respect to a single ICU in a

hospital or may have responsibility for standardization of

activities in several ICUs in the area.

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Burnout

A different topic is burnout among ICU physicians, nurses,

and other health care workers. Valuable data are now avail-

able about the risks of burnout and its effects on patient

care, productivity, and career planning. Burnout is one

effect of psychosocial stress and is related to duration of

work hours, the impact of taking care of patients with criti-

cal illness, the effects of poor patient outcome despite max-

imal effort, and organizational issues. Intensivists, ICU

nurses, and respiratory therapists may experience occupa-

tional burnout.

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Outcomes & Alternatives

In many facilities, ICU beds are limited in number, and

incoming patients with varying degrees of morbidity

often must be evaluated and compared to determine who

might best be treated in the ICU. A number of published

studies have confirmed that a good proportion of patients

admitted to ICUs receive diagnostic studies and monitor-

ing of physiologic variables only—ie, no therapy that could

not be given outside the ICU. On the other hand, other

patients admitted to the ICU do receive such “intensive”

therapy, and some of these have better outcomes. Because

ICU beds are a limited resource in all hospitals, ICU med-

ical directors must develop familiarity with the overall out-

comes and results of patients admitted to their ICU beds.

They will be called on not infrequently to make decisions

about admissions, discharge, and transfer from the ICU,

and these decisions at times may be arrived at painfully. As

with all decisions affecting patient care, the medical direc-

tor must weigh the body of medical knowledge available;

the wishes of patients, families, and physicians; and the

likelihood or not that intensive care will benefit the patient.

At times, these decisions will involve only “medical judg-

ment”; at other times, the choice will reflect an ethical,

legal, or philosophical perspective.

Specific practice guidelines for individual diseases have

been developed for the purpose of identifying particular

patients. Recognition that many patients previously admitted

to ICUs did not require or receive major diagnostic or thera-

peutic interventions led to the design of progressive care,

“step-down,” or noninvasive monitoring units in some hos-

pitals. Equipped and staffed generally for electrocardiogra-

phy, pulse oximetry, and sometimes for noninvasive

respiratory impedance plethysmography—but not for

intravascular instrumentation—these units have potential as

highly effective, less costly alternatives to ICUs. A number of

studies have provided justification for intermediate care

units either as an area for patients leaving the ICU or as an

area devoted to care of certain kinds of medical problems—

primarily mild respiratory failure, cardiac arrhythmias, or

moderately severe electrolyte disorders.

CRITICAL CARE SCORING

The combination of an increasing patient population and

diminished funding for hospital services is creating a need

for optimized distribution of medical resources. This chal-

lenge is being met in a number of ways, including regional-

ization of care, specialization of critical care facilities (both

between and within hospitals), and better allocation of avail-

able personnel and equipment. To this end, the intensivist

must be prepared to make both administrative and medical

decisions about which patients will benefit most from admis-

sion to a critical care unit. Data in 1987 indicated that up to

40% of patients in ICUs were inappropriately admitted

either because they probably would have died regardless of

the care provided or because their illnesses were not life-

threatening enough to require ICU care. Indeed, a substantial

number of patients treated in critical care units at teaching

hospitals are admitted for “observation and monitoring”

only.

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PHILOSOPHY & PRINCIPLES OF CRITICAL CARE

Illness scoring has become a popular method for triage

within and between hospitals. Many such scores have been

introduced over the past two decades in an attempt to prior-

itize illness and injury for ICU admission purposes. Such

scores must be used with full appreciation of their limita-

tions. While they are useful for comparing institutional per-

formances and outcomes in studies of certain groups of

patients, great caution must be exercised when applying

these protocols to individual patients.

The most commonly used trauma and critical care scores

are discussed below and are illustrated in the accompanying

tables.

Glasgow Coma Scale

The Glasgow Coma Scale assesses the extent of coma in patients

with head injuries (Table 1–4). The scale is based on eye open-

ing, verbal response, and motor response. The total is the sum

of each of the individual responses and varies between 3 points

and 15 points. Mortality risk is correlated with the total score

and with a similar Glasgow Outcome Scale. Examination of the

patient and calculation of the score can be accomplished in less

than 1 minute. The scale is easy to use and highly reproducible

between observers. It has been incorporated into several other

scoring systems. The Glasgow Coma Scale is useful for prehos-

pital trauma triage as well as for assessment of patient progress

after arrival and during critical care admission.

Trauma Score and Revised Trauma Score

Because of the increasing number of trauma patients admitted

to critical care facilities, familiarity with trauma scales is impor-

tant. The Trauma Score is based on the Glasgow Coma Scale

and on the status of the cardiovascular and respiratory systems.

Weighted values are assigned to each parameter and summed

to obtain the total Trauma Score, which ranges from 1 to 16

(Table 1–5). Mortality risk varies inversely with this score.

After extensive use and evaluation of the Trauma Score, it

was found to underestimate the importance of head injuries.

In response to this, the Revised Trauma Score (RTS) was intro-

duced and is now the most widely used physiologic trauma

scoring tool. It is based on the Glasgow Coma Scale, systolic

blood pressure, and respiratory rate. For evaluation of in-

hospital outcome, coded values of the Glasgow Coma Scale,

blood pressure, and respiratory rate are weighted and summed

(Table 1–6). Better prognosis is associated with higher values.

CRAMS Scale

The Circulation, Respiration, Abdomen, Motor, Speech

(CRAMS) Scale is another trauma triage scale that has found

A. Systolic blood pressure B. Respiratory rate C. Respiratory effort D. Capillary refill

>90 4

70–90 3

59–69 2

<50 1

10–24 4

25–35 3

>35 2

10 1

Normal 1

Shallow or retractions 0

Normal 2

Delay 1

None 0

E. 4 GCS points

1. Eye opening

Spontaneous 4

To voice 3

To pain 2

None 1

2. Motor response

Obedient 6

Purposeful 5

Withdrawal 4

Flexion 3

Extension 2

None 1

3. Verbal response

Oriented 5

Confused 4

Inappropriate 3

Incomprehensible 2

None 1

(1 + 2 + 3)

14–15 5

11–13 4

8–10 3

5–7 2

3–4 1

TRAUMA SCORE (A + B + C + D + E) ______

Table 1–5. Trauma Score.

Eye Motor Verbal

4 = Spontaneous 6 = Obedient 5 = Oriented

3 = To Voice 5 = Purposeful 4 = Confused

2 = To pain 4 = Withdrawal 3 = Inappropriate

1 = None 3 = Flexion 2 = Incomprehensible

2 = Extension 1 = None

1 = None

Table 1–4. The Glasgow Coma Scale.

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CHAPTER 1

regional acceptance (Table 1–7). It is frequently used to

decide which patients require triage to a trauma center.

Patients with lower CRAMS Scale scores would be expected

to require critical care unit admission.

Injury Severity Score (ISS)

The ISS attempts to quantitate the extent of multiple injuries

by assignment of numerical scores to different body regions

(head and neck, face, thorax, abdomen, pelvic contents,

extremities, and external). A book of codes is available that

provides information on the scoring of each injury. The worst

injury in each region is assigned a numerical value, which is

then squared and added to those from each of the other areas.

The total score ranges from 1 to 75 and correlates with mor-

tality risk. The major limitation of the ISS is that it considers

only the highest score from any body region and considers

injuries with equal scores to be of equal importance irrespec-

tive of body region. Similarly, since the ISS is an anatomic

score, a small injury with a significant potential for deleterious

outcome (closed head injury) may lead to the false impression

of a minimally injured patient. ISS is the most commonly used

measure of the severity of anatomic injury and provides a

rough survival estimate for the severely injured patient.

Acute Physiology, Age, Chronic Health

Evaluation (APACHE)

The APACHE scoring system (APACHE III) is probably the

most widely used critical care scale. It permits comparisons

between groups of patients and between facilities. It was not

designed to evaluate individual patient outcomes. To this

end, APACHE III was introduced to objectively estimate

patient risk for mortality and other important outcomes

related to patient stratification. While some centers have

adopted the APACHE III score, it is not used widely except

for study of trends in patient groups.

CURRENT CONTROVERSIES

& UNRESOLVED ISSUES

The usefulness of scales such as the APACHE III scoring sys-

tem remains to be determined long after their introduction.

Furthermore, the ability of experienced physicians to make

such management decisions may be as good as such scales

and perhaps often better. Some authors have concluded that

ICU scoring systems can be used to compare outcomes

within and between ICUs and can provide adequate adjust-

ment of mortality rates based on preadmission severity for

the purpose of assessing quality of care.

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Angus DC et al: Critical care delivery in the United States:

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Glasgow

Coma

Scale (GCS)

Systolic

Blood Pressure

(SPB) (mm Hg)

Respiratory

Rate (RR)

(Breaths/min)

Coded Value

13–15

>89 10–29 4

9–12

76–89 >29 3

6–8

50–75 6–9 2

4–5

1–49 6–9 1

0 1–5 0

RTS = 0.9368 GCSc + 0.7326 SBPc + 0.2908 RRc, where the sub-

script c refers to coded value.

Table 1–6. Revised Trauma Score.

Table 1–7. The CRAMS Scale.

Circulation

Normal capillary refilll and BP >100 mm Hg

Delayed capillary refill or 85 <BP <100

No capillary refill or BP <85 mm Hg

Respiration

Normal

Abnormal

Absent

Abdomen

Abdomen and thorax nontender

Abdomen or thorax tender

Abdomen rigid or flail chest

Motor

Normal

Responds only to pain (other than decerebrate)

No response (or decerebrate)

Speech

Normal

Confused

No intelligible words

Score ≤ 8 indicates major trauma; score ≥ 9 indicates minor

trauma.

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PHILOSOPHY & PRINCIPLES OF CRITICAL CARE

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DISORDERS OF FLUID VOLUME

In normal persons, water, distributed between the intracellu-

lar and extracelluar spaces, makes up 50–60% of total body

weight. Critical illness not only can result from abnormalities

in the amount and distribution of water but also can cause

strikingly abnormal disorders of water and solutes.

Distribution of Body Water

Total body water is distributed freely throughout the body

except for a very few areas in which movement of water is lim-

ited (eg, parts of the renal tubules and collecting ducts). Water

diffuses freely between the intracellular space and the extra-

cellular space in response to solute concentration gradients.

Therefore, the amount of water in different compartments

depends entirely on the quantity of solute present in that

compartment.

The two major fluid compartments of the body are the

intracellular space, in which the major solutes are potassium

and various anions, and the extracellular space, for which

sodium and other anions are the major solutes. Sodium moves

into and potassium out of cells passively along concentration

gradients. Thus active transport of sodium and potassium by

-ATP-dependent pumps on the cell membrane deter-

mines the relative quantities of these cations on the inside and

outside of each cell. The distribution of Na

and K

determines

the relative volumes. In normal individuals, about two-thirds of

total body water is intracellular and one-third is extracellular.

Addition of solute to either compartment will increase the

volume of that compartment by redistribution of water from

the compartment of lower solute (higher water) concentration

into the compartment to which the solute was added. Thus

the solute concentration in both compartments will increase

(see “Water Balance”). To restore normal volumes, the body

will seek to eliminate or redistribute the added solute and cor-

rect the increased solute concentration (eg, stimulation of thirst

or conservation of water). Similarly, the loss of solute from a

compartment results in a shrinkage of that compartment. The

body then tries to restore the lost solute to reestablish the

original volume and distribution of solute and water.

Distribution of Extracellular Volume

Extracellular volume is divided into the interstitial and the

intravascular space. The distribution of water between these

two compartments is complex in normal subjects and more

so during disease states in which edema (increase in intersti-

tial volume) or accumulation of fluid in normally nearly dry

spaces (eg, peritoneal cavity or pleural space) is present.

Normally, intravascular volume is maintained by the oncotic

pressure of large molecules that are confined to the intravas-

cular space, by movement of lymph from the interstitial to

the intravascular space, and by forces that maintain extracel-

lular volume. Countering these are the hydrostatic pressure

developed by the heart and circulation and interstitial fluid

oncotic pressure, which tend to push fluid out of the

intravascular space. The volume of the intravascular com-

partment determines the adequacy of the circulation; this, in

turn, determines the adequacy of delivery of oxygen, nutri-

ents, and other substances needed for organ function.

Hypovolemia and Hypervolemia

Because sodium is the predominant extracellular solute, extra-

cellular volume is determined primarily by the sodium content

of the body and the mechanisms responsible for maintaining

sodium content (Table 2–1). However, the term hypovolemia

generally refers only to decreased intravascular volume and not

decreased extracellular volume, and this disorder results from

inadequate intravascular volume maintenance. On the other

hand, the term hypervolemia generally denotes increased extra-

cellular volume with or without increased intravascular vol-

ume. Thus patients with edema or ascites have hypervolemia

(frequently with decreased intravascular volume), but so do

Fluids, Electrolytes,

& Acid-Base

Darryl Y. Sue, MD

Frederic S. Bongard, MD



FLUIDS, ELECTROLYTES, & ACID-BASE

patients with congestive heart failure (who have increase in

both intravascular and extracellular volumes).

Normally, daily sodium excretion equals intake, so sodium

excretion varies with dietary or other intake. The average diet

contains 4–8 g of sodium daily, and this quantity must be

excreted. With severe limitation of dietary sodium, normal kid-

neys can vigorously reabsorb sodium, so as little as 1–5 meq

/L of urine appears, and only 1–2 meq of Na

is excreted

daily. A daily sodium intake and excretion of approximately

40–65 meq (about 1–1.5 g) is sufficient in normal individuals.



Hypovolemia

ESSENTIALS OF DIAGNOSIS



Evidence of decreased intravascular volume: hypoten-

sion, low central venous or pulmonary artery wedge

pressures



Indirect evidence of decreased effective intravascular vol-

ume: tachycardia, oliguria, avid renal sodium reabsorption



Circumstantial evidence of depleted effective intravas-

cular volume: end-organ dysfunction, peripheral

vasoconstriction



Potential source of loss of extracellular volume or

evidence of inadequate repletion

General Considerations

A. Definition—Hypovolemia is decreased volume of the

intravascular space. Although extracellular volume, of which

the intravascular space is a part, is often diminished, hypov-

olemia can occur even in the presence of normal or increased

extracellular volume (Table 2–2). The assessment of ade-

quacy of intravascular volume in the presence of normal or

increased extracellular volume is often difficult, especially in

critically ill patients. It is central to the concept of hypov-

olemia that total intravascular volume need not be dimin-

ished but that effective intravascular volume is low, such that

there is insufficient volume in the circulation to provide cir-

culatory adequacy. The term effective arterial volume is some-

times used to characterize the physiologically effective part of

the intravascular volume.

Some clinicians use the term dehydration as a substitute

for hypovolemia. This is incorrect, and this term should be

reserved to mean insufficient water relative to total body

solute (see below).

B. Pathophysiology—Decreased effective intravascular vol-

ume can occur with decreased, normal, or increased extracel-

lular volume. Decreased extracellular volume leading to

depletion of intravascular volume is most common and can

arise from increased loss of extracellular fluid, failure to

replete normal losses, or a combination of both. Bleeding,

diarrhea, vomiting, and excessive skin loss of fluid (sweating,

burns) can quickly deplete extracellular volume. Abnormally

large urinary losses of sodium and water from renal disease,

adrenal insufficiency, diuretics, or hyperglycemia (osmotic

diuresis) also should be considered as sources of volume

depletion. Decreased extracellular volume also can arise

Table 2–1. Factors affecting body sodium balance.

Increased body sodium content (increased extracellular volume)

• Increased sodium intake (in absence of increased sodium excretion)

• Decreased sodium excretion by kidneys

Decreased glomerular filtration

Increased renal tubular sodium reabsorption

Increased renin, angiotensin, aldosterone

Excessive mineralocorticoid activity

Decreased body sodium content (decreased extracellular volume)

• Decreased sodium intake (in presence of normal sodium excretion)

• Increased sodium excretion

Renal:

Renal failure

Salt-losing nephropathy

Osmotic diuresis

Diuretic drugs

Atrial natriuretic peptide

Decreased renin, angiotensin, aldosterone, or cortisol

Extrarenal:

Diarrhea

Vomiting

Sweating

Surgical drainage

Table 2–2. Hypovolemia (decreased effective intravascular

volume).

With decreased extracellular volume

• Increased fluid losses

Gastrointestinal tract (diarrhea, vomiting, fistulas, nasogastric suction)

Renal (polyuria with renal sodium wasting, osmotic diuresis)

Skin or wound losses (sweating, burns)

Hemorrhage (trauma, other bleeding site)

• Decreased intake of sodium and water

• Impaired normal capacity to retain sodium and water

Renal sodium wasting (polycystic kidneys, diuretics)

Adrenal insufficiency

Osmotic diuresis (hyperglycemia)

With increased or normal extracellular volume

• Cirrhosis with ascites

• Protein-losing enteropathy

• Congestive heart failure

• Increased vascular permeability (sepsis, shock, trauma, burns)



CHAPTER 2

from inadequate replacement; this is particularly likely to

occur in ill patients who do not eat or drink appropriately or

who do not have access to adequate amounts of water and

solutes.

Hypovolemia with normal extracellular volume results

from any disorder that alters the balance between intravascu-

lar and extravascular fluid compartments. Intravascular

oncotic pressure and intact vascular integrity largely main-

tain intravascular volume, whereas hydrostatic pressure

tends to push fluid out of the circulation. Sepsis, acute respi-

ratory distress syndrome (ARDS), shock, and other critical

illnesses alter this balance by increasing the permeability of

the vasculature, thereby raising nonintravascular fluid vol-

ume (ie, interstitial compartment, pleural effusions, or

ascites) at the expense of the intravascular volume. Although

decreased vascular oncotic pressure and increased hydro-

static pressure also should shift fluid balance in this direc-

tion, these rarely develop rapidly enough to be seen with

unchanged total extracellular fluid volume.

Disorders that increase hydrostatic pressure in certain

vascular beds or reduce intravascular oncotic pressure also

can deplete intravascular volume. Reduced intravascular vol-

ume stimulates increased renal sodium reabsorption, which

causes an increase in total extracellular volume. Thus cirrho-

sis with hypoalbuminemia results in ascites from a combina-

tion of portal hypertension and decreased oncotic pressure,

heart failure leads to edema as a result of increased hydro-

static pressure, and edema in nephrotic syndrome results

from severely reduced oncotic pressure. The paradox in these

clinical situations is that effective intravascular volume may

be severely reduced even though the extracellular volume is

greatly increased.

Clinical Features

The diagnosis of volume depletion in the critically ill patient

is often difficult largely because of the confounding effects of

organ system dysfunction and the frequency with which

drugs, edematous states, altered cardiovascular and renal

function, and other factors interfere with assessment of vol-

ume status.

A. Symptoms and Signs—Symptoms and signs suggesting

hypovolemia in the critically ill patient may or may not be

helpful. Volume depletion causing inadequate systemic per-

fusion leads to altered mental status, confusion, lethargy, and

coma; cold skin and extremities from vasoconstriction; car-

diac ischemia and dysfunction; and liver and kidney failure.

None of these are specific for hypovolemia, but all are com-

mon to hypotension and shock from any cause. A potentially

important symptom is thirst in a patient with hyponatremia;

lack of an osmotic stimulus leaves volume depletion as the

only physiologic reason for thirst. In the patient with hypov-

olemia with increased extracellular fluid volume, edema, and

ascites make determination of effective intravascular volume

even more difficult.

Symptoms and signs do not have sufficiently high sensi-

tivity and high specificity to be of strong clinical value.

Postural lightheadedness increases the likelihood of volume

depletion, but an increase in heart rate from supine to stand-

ing must be greater than 30 beats/min to be specific for

hypovolemia. Orthostatic blood pressure changes lack sensi-

tivity and specificity, but these should be part of the evalua-

tion of potential hypovolemia. Dry axillae, longitudinal

furrows on the tongue, and sunken eyes have some slight pre-

dictive value for hypovolemia.

A source of volume loss or an explanation for inadequate

volume repletion strongly supports the diagnosis of hypov-

olemia. In the ICU patient, blood loss, diarrhea, and polyuria

are usually obvious; less easily identified are heavy sweating

during fever, fluid losses from extensive burns, volume

changes during hemodialysis or ultrafiltration, and drainage

from surgical incisions or wounds. Review of intravenous

and enteral fluid intake is often helpful, along with compari-

son of patient weights on a daily basis or more often.

Indirect evidence of hypovolemia can come from the

response of the cardiovascular and renal systems. Depleted

intravascular volume leads to decreased venous return to the

heart; the normal response is a lower stroke volume and

sinus tachycardia to maintain cardiac output.

B. Laboratory Findings—Intravascular volume depletion

may lead to avid retention of water because of increased

antidiuretic hormone (ADH) release and, if there is sufficient

water intake, hyponatremia. Decreased intravascular volume

causes prerenal azotemia with elevation of plasma creatinine

and urea nitrogen concentrations.

Except in the case of a primary renal cause of hypov-

olemia, decreased renal blood flow, even if glomerular filtra-

tion is maintained, increases renal tubular sodium

reabsorption. Urine volume diminishes, and urine becomes

highly concentrated under the influence of ADH and other

factors. Urine sodium and chloride concentrations may

become very low (<5–10 meq/L) with correspondingly low

fractional excretion of sodium (FE

<1%), chloride, and urea

(<35%). Because of decreased renal tubular flow, urea is reab-

sorbed more readily, and the plasma urea nitrogen:plasma cre-

atinine ratio increases, often greater than 30:1. In some

patients, avid sodium reabsorption comes at the expense of

increased potassium losses in the urine and hypokalemia.

Potassium depletion and increased sodium reabsorption in

the distal tubule enhance hydrogen ion excretion, leading to

metabolic alkalosis (contraction alkalosis); this is especially

common in volume depletion owing to vomiting.

On the other hand, if there is a primary renal-mediated

mechanism of hypovolemia, urine sodium concentration

and FE

may not decrease in the face of decreased intravas-

cular volume. Urinary indices of volume depletion may be

misleading, and paradoxical polyuria and high urine sodium

may be found. For patients taking diuretics, the fractional

excretion of urea may be low (<35%) in the face of hypov-

olemia even though the fractional excretion of sodium is