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Subpart IVF
Chapter
43
Clinical – Hematologic
Transfusions
Rokhsanna Sadeghi, MD
Jonathan Glauser, MD, FACEP
Introduction
There is a wealth of clinical situations in which
patients presenting to an Emergency Department
(ED) require a blood product transfusion in order
to treat their condition. Many of these patients are
optimal candidates for transfusion in an observation unit (OU), with correction of their presenting condition within 24 hours. The objective of
this chapter is to provide an overview and guide
to blood product transfusions in an OU. The
products that will be covered include packed
RBC, fresh frozen plasma, common plasma
derivatives, and platelets. Finally, identifying and
managing transfusion reactions will be discussed.
Exchange transfusions, as for acute chest syndrome in sickle cell disease, and transfusions for
trauma are best managed in a setting other than
the OU.
Red Blood Cell Transfusion
RBC transfusion is the most common blood product transfused in clinical practice. There are
approximately 85 million units of RBC transfused
annually, worldwide.
1
There is a wide variation in
transfusion practices among clinicians, thus multiple guidelines have been developed in order to
standardize which patients would benefit from
RBC transfusion in order to prevent over- and
under-transfusion.
Despite multiple studies and expert panels,
there is no single hemoglobin concentration
threshold or “transfusion” trigger that can be
applied universally. Each patient’s medical condition must be taken into consideration and a clinician must fully weigh the risk of the transfusion
to the benefit of having the anemia corrected.
For many decades, a transfusion trigger of
hemoglobin 10 g/dL was used in clinical practice.
Multiple organizations, including the AABB (formerly, American Association of Blood Banks),
Australian and New Zealand Society of Blood
Transfusion, and British Committee for Standards
in Hematology, have adopted the restrictive transfusion strategy as opposed to a liberal transfusion
strategy.
1,2,3
Restrictive blood transfusion strategy
has been found to decrease hospital length of stay
and all-cause mortality.
2
Through extensive review
of existing studies, these organizations have found
that there is no clinical benefit to transfusing
patients to maintain a hemoglobin concentration
above 10 g/dL. Furthermore, a hemoglobin concentration of 5 g/dL in healthy individuals does not
demonstrate inadequate oxygenation.
2
A reason for the lack of a commonly used
transfusion trigger is the absence of a reliable way
to measure oxygen delivery to critical organs.
Given that the objective of a blood transfusion is
to increase the oxygen carrying capacity of blood, it
is essential to identify patients in whom there is
end-organ hypoxia, and therefore those patients
who would benefit from a RBC transfusion.
Making the determination of whom the benefit of
transfusion outweighs the risk is a complex decision in which multiple factors need to be taken into
consideration, such as age, patient’s ability to compensate, coexisting cardiovascular, cerebrovascular,
respiratory disease, cause of anemia, severity, and
chronicity.
2
There is no consensus as to which
subjective or objective findings are reliable indicators of symptomatic anemia, but fatigue, shortness
of breath, increased respiratory rate and pulse
are common parameters.
3
Furthermore, the cause
of anemia should be identified and treated before
transfusion is initiated, such as iron deficiency
anemia or megaloblastic anemia. It is expected that
long-term management of chronic asymptomatic
anemia may involve therapy with iron, B12, folate
or recombinant erythropoietin as indicated. One
study involving Jehovah’s Witnesses indicated that
no one died with a hemoglobin in the 5–8g/dL
range because of their anemia.
4
Once the decision has been made to transfuse
RBC, a treatment end point must be defined, such
047
21:12:22
as a goal hemoglobin concentration or change in
symptoms. For a 50 kg individual, one unit of
RBC should increase the hemoglobin concentration by 1 g/dL or hematocrit by 3%. Likewise, if
an individual is 100 kg, the hemoglobin concentration may only be raised 0.5 g/dL or the hematocrit increased 1.5% for each unit of packed
RBCs transfused.
5
For the most accurate posttransfusion evaluation of hemoglobin level of
increase, a blood sample should be drawn within
10–60 minutes. During this window of time, the
transfusion is less affected by concurrent physiologic processes such as splenic sequestration,
sepsis, and consumption.
6
Some comments specifically related to sickle
cell (SS) disease are in order. It should be noted
that leukocyte-poor antigen-matched blood
should be used to reduce the development of
antibodies and frequency of future transfusion
reactions. Exchange transfusion may prevent iron
accumulation and reverse iron overload in chronically transfused patients, but is not suitable for
observation care. Transfusion indications in SS
disease, after discussion with the patient’s hematologist, may include severe anemia, transient red
cell aplasia, or acute splenic sequestration.
7
Acute
chest syndrome, stroke, and stroke prevention for
those at risk by transcranial doppler are best
managed in a setting other than the OU.
For OU transfusions, a set protocol for monitoring patients during and post-transfusion must
be developed by each institution. Minimum level
of monitoring includes frequent visual observation throughout transfusion, complete vital signs
within 60 minutes prior to transfusion, complete
set of vital signs 15 minutes after each transfusion
initiation, and a complete set of vital signs within
60 minutes of the end of the transfusion. If there
is evidence for a possi ble transfusion reaction,
vital signs should be recorded and appropriate
steps taken to address the reaction.
3
When the
patient is discharged from the OU, signs of
delayed transfusion reactions should be reviewed
with the patient and provided in the discharge
instructions. In addition, patients should be provided with a 24-hour clinical advice line.
Plasma Products and Warfarin Reversal
Fresh Frozen Plasma
Fresh frozen plasma (FFP) transfusions are used to
replace plasma proteins that are deficient or defective. These may be secondary to congenital or
acquired processes.
1
As with red blood cell trans-
fusions, there are specific indications in which a
patient’s emergent condition can be treated with
FFP transfusion in an OU. Some indications for
FFP are unsuitable for management in the OU:
multi-factor deficiencies or disseminated intravascular coagulation (DIC) plus bleeding, or the preoperative bleeding patient who requires multiple
plasma coagulation factors. Patients with thrombotic thrombocytopenic purpura (TTP) may
require plasma exchange over 2 days, and are
therefore unsuitable for OU care. Massively transfused patients with clinically significant coagulation deficiencies, as with multiple trauma, will be
managed elsewhere. FFP should be ABO compatible. The risk for infection transmission is not
negligible, as FFP is not considered viral attenuated. This section will outline indications and
guidelines on when and how to transfuse FFP.
In the OU, inherited coagulation factor deficiencies can be treated with FFP if there are no
other virus safe fractionated products available,
such as Factor V Leiden or Factor XI deficiencies.
2,8,9
If a patient with these deficiencies has
moderate to severe bleeding or requires an
Table 43.1 Summary of Recommendations of Transfusion
for Packed Red Blood Cells
Hemoglobin
Concentration
Transfusion
Recommendations
> 10 g/dL Transfusion likely not necessary
unless there are specific
indications.*
7–10 g/dL Transfusion may be beneficial if
patient is symptomatic** or has
cardiovascular or respiratory
disease limiting ability to
compensate.
< 7 g/dL Transfusion appropriate,
especially if known coronary
artery disease and/or
symptomatic. If patient is
asymptomatic or other specific
treatment is available, lower
Hgb threshold may be used.
* Severely ill, advanced coronary artery disease,
cerebrovascular, or pulmonary disease
** Symptoms include chest pain, orthostatic hypotension or
tachycardia unresponsive to fluid resuscitation, or
congestive heart failure
Rokhsanna Sadeghi and Jonathan Glauser
047
21:12:22
invasive procedure, transfusion of FFP must be
considered. If a congenital bleeding disorder is
suspected but unknown, it may be reasonable to
administer FFP 15 ml/kg pending results, as the
deficiencies will most likely be in factors VIII, IX,
and XI. Rarely, patients with C1 inhibitor deficiencies presenting with angioedema may require
FFP if no recombinant product is available.
For patients with liver disease, FFP may also be
beneficial if they are bleeding or must undergo a
high-risk procedure, such as a liver biopsy. There
are some recommendations that prior to liver
biopsy the PT should be within 4 seconds of the
normal range.
8
The severity of patients’ disease
and the characteristics of the planned procedure
(i.e., esophagogastroduodenoscopy) or amount
and location of active bleeding must be taken
into consideration on an individual basis in order
to prevent unnecessary transfusions and to
ensure that patients are managed in the appropriate setting.
Warfarin is a vitamin K antagonist that results
in coagulopathy, which can lead to bleeding, especially if levels are supratherapeutic or if trauma
occurs. This coagulopathy can lead to excessive
bleeding with invasive procedures. FFP transfusion is indicated if the patient needs to undergo
an emergent invasive procedure in which vitamin
K could not reverse coagulopathy rapidly enough.
The effect of vitamin K can be expected within
6 to 12 hours of administration, but its full effect
typically only occurs after 24 hours.
10
One must
keep in mind that Prothrombin Complex Concentrates (PCC) given 25–50 U/kg work more
quickly than does FFP, and that for warfarin
reversal 15 ml/kg of FFP must be administered –
a significant volume load in many patients.
2
Generally, FFP should not be given for warfarin
reversal unless there is severe bleeding.
1, 2, 8, 10
For patients on warfarin, if the International
Normalized Ratio (INR) is supratherapeutic, but
less than 5 and there is no bleeding, the dose
of warfarin can be decreased or next dose should
be held. The risk of bleeding increases exponentially between an INR of 5–9 (Australian Consensus for Warfarin Reversal, ACWR)
11
. Patients
considered to have high risk for bleeding include
active peptic ulcer disease (PUD) or inflammatory
bowel disease (IBD), current antiplatelet use,
major surgical procedure in the past 2 weeks,
and thrombocytopenia. If there is no bleeding
with an INR between 5 to 9 the warfarin dose
should be held, and in the presence of a high
bleeding risk, vitamin K should be given. The
INR should be rechecked in 24 hours, and if the
level has decreased, the patient should resume
warfarin at a lower dose. With an INR > 9 and
no active bleeding, warfarin should be held and
vitamin K administered. If the patient is at high
risk for bleeding, an FFP transfusion should be
considered. Once the INR is below 5, warfarin
may be resumed at a lower dose. If there is clinically significant bleeding in the setting of an elevated INR, warfarin should be withheld, and
vitamin K given intravenously, with FFP administered. The patient should be monitored until
bleeding has stopped. Do not restart warfarin
until the INR is < 5.
10
In general, FFP will be effective when prothrom-
bin time (PT) and activated partial thromboplastin
Table 43.2 Management Guidelines for Supratherapeutic
INR Secondary to Warfarin
10
INR Recommended
Management
INR higher than
therapeutic range but
< 5 and bleeding
absent
Omit the next dose,
consider lowering
subsequent doses
INR 5–9, bleeding
absent
Hold warfarin; If
bleeding risk is high*,
give vitamin K 1–2mg
PO, recheck INR in
24 hours and resume
therapy at lower dose
INR > 9, bleeding
absent
If low bleeding risk, hold
warfarin, give vitamin
K 2.5–5mgPOor1mg
IV, and resume warfarin
at lower dose once
INR < 5
If high bleeding risk*,
hold warfarin, give
vitamin K, consider FFP,
resume warfarin at lower
dose when INR < 5
Clinically significant
bleeding where
warfarin-induced
coagulopathy is a
contributing factor
Hold warfarin, give
vitamin K IV up to 10 mg
and FFP; assess patient
until INR < 5 and
bleeding stops
* High risk for bleeding: active GI conditions (PUD or IBD),
concomitant antiplatelet therapy, major surgical procedure
within the preceding 2 weeks, and low platelet count
Transfusions
047
21:12:22
time (aPTT) are both 1.5 times greater than the
upper limit of normal.
9
FFP will not be beneficial
for patient with only minimal elevated INR. The
INR of FFP has been noted to be as high as 1.3,
1
and therefore FFP cannot completely normalize
the INR. The goal of an FFP transfusion is to
increase plasma factor concentration to at least
30%. Typical doses for FFP are between 10–30
ml/kg. Since each unit is approximately 250 ml,
volume overload may be a consideration.
9
Repeat
PT and aPTT levels should be drawn after transfusion to guide treatment. FFP transfusion may
need to be repeated within 6 hours if rapid reversal
of coagulopathy is needed.
12
FFP should not be
used for volume replacement, and its use has often
been supplanted by specific recombinant viralattenuated products.
Other Plasma Products
Cryoprecipitate
Cryoprecipitate is the cold-insoluble precipitate
protein fraction derived from FFP. Cryoprecipitate
contains factor VIII 60–100 units/bag, fibrinogen
(factor I), von Willebrand factor (vWF), and factor
XIII. Cryoprecipitate transfusions are indicated in
the setting of fibrinogen deficiency with bleeding,
prior to invasive procedures, trauma, or DIC.
2
When the fibrinogen level is less than 100–120
mg/dL, cryoprecipitate transfusion will elevate
fibrinogen levels by approximately 50 mg/dL for
every unit/10 kg body weight transfused.
8,9
There
is no set guideline regarding a level at which cryoprecipitate should be transfused in presence of
clinically significant hypofibrinogenemia.
8
It is
cell-free, so the patient should not need Rh typing,
but it is not viral-attenuated, so there is risk of
infection transmission. Cryoprecipitate is secondline therapy for factor VIII deficiency (Hemophilia
A disease) and for von Willebrand Disease.
Cryoprecipitate transfusions are also indicated
for clinically significant bleeding or pre-procedure
for patients with single factor deficiencies in which
no other factor concentrates are available. Factor
XIII deficiency is an example, although factor XIII
concentrate is preferred, since cryoprecipitate has
not undergone viral attenuation steps.
1,9
Cryoprecipitate is only recommended for patients with
hemophilia A or von Willebrand disease (vWD)
if isolated factor VIII concentrates or factor VIII:
vWF concentrates are not available.
9
In addition,
cryoprecipitate may be used for patients who are
uremic and bleeding, if other treatment options
have been unsuccessful.
9
The following calculation from the American
Red Cross (ARC) can be used to estimate how
many cryoprecipitate units to transfuse in a
patient with fibrinogen deficiency:
Weight ðKgÞ ×70mL=Kg ¼ blood volume ðmLÞ
Blood volume ðmLÞ × ð1:0 hematocritÞ
¼ plasma volume ðmLÞ
f ibrinogen required ðmg Þ¼ðdesired
f ibrinogen levelðmg=dLÞinitial
f ibrinogen level ðmg=dLÞÞ ×
plasma volume ðmLÞ100
Bags of cryoprecipitate required
¼ mg fibrinogen required 250 mg
fibrinogen per bag of cryoprecipitate
For clinical bleeding, the number of bags should
approximate 0.2 times the patient’s body weight
in kilograms. Without ongoing factor consumption or large volume blood loss, one unit of cryoprecipitate per 10 kg (of body weight) will
increase fibrinogen levels by 50 mg/dL unless
there is bleeding or product consumption.
9
Quantitative and Qualitative Factor Deficiencies
The three most common inherited factor disorders
are hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency), and von Willebrand
disease. In specific clinical situations, these conditions may be treated with single factor transfusions. For patients with hemophilia A and B,
bleeding episodes should be urgently treated by
factor replacement, within 2 hours of onset of
symptoms, if possible. Ideally, treatment should
commence prior to the onset of physical symptoms.
Furthermore, communication with a hematologist,
ideally the patient’sphysician,isrecommendedin
order to achieve the highest quality of care.
13
Hemophilia A (Factor VIII Deficiency) Recombi-
nant factor VIII is the first line treatment for
hemophilia A. It is recommended over plasmaderived factor VIII, since plasma derived transfusions carry the risk of transmission of a viral
illness, while there has been no documented viral
transmission with recombinant transfusion.
Cryoprecipitate can be used, but overall is not
Rokhsanna Sadeghi and Jonathan Glauser
047
21:12:22
recommended if factor VIII is available.
13,14
Desmopressin (DDAVP) 0.3 mcg/kg IV over
30 minutes in 50–100 ml saline or as 300 mcg
nasal spray) administration should be considered
for every patient, especially if they phenotypically
have a mild form of hemophilia A ( 5% factor
VIII activity), since it can raise factor VIII levels
to 3–6 times baseline.
14
One unit of factor VIII
per kilogram of body weight will increase the
plasma factor VIII level by approximately 2%.
13
Therefore, the dose of factor VIII equals weight in
kg times percentage required of factor VIII times
0.5; with severe factor VIII deficiency, one should
assume that the patient is starting at a factor VIII
level of zero.
15
Hemophilia B (Christmas Disease)(Factor IX
Deficiency) Recombinant factor IX is the first line
treatment for hemophili a B. As for factor VIII,
plasma derived factor IX poses risk of transmission of viral illness.
14
One unit of factor IX per
kilogram of body weight will increase the plasma
factor IX level by approximately 1%. FFP use is
only recommended if factor IX derivatives are
not available.
13
von Willebrand Disease von Willebrand disease
(vWD) has multiple phenotypes which are associated with various clinical courses and treatment.
15
Type 1 is the mildest form and can be treated with
desmopressin (DDAVP). Types 2A, 2B, 2M, and
2N can be treated with factor VIII–von Willebrand
factor concentrate. Type 3 can also be treated with
factor VIII–von Willebrand factor concentrate, but
if there are alloantibodies present, then it is recommended to use recombinant factor VIII for treatment. Approximately 10–15% of patients with type
3 vWD develop alloantibodies that bind and inactivate vWF.
16
Platelet transfusions should also be
considered as an adjunct to treatment, specifically
in type 3, platelet low, or platelet-type vWD, since
human platelets contain 10–15% of total blood
vWF.
17
Guidelines for prophylaxis against bleeding
from minor surgery recommend vWF:RCo (von
Willebrand Factor: Ristocetin factor activity) and
factor VIII activity levels > 30 IU/dL, and ideally >
50 IU/dL.
18
Platelets
Platelet transfusions are essential in order to
achieve hemostasis during active bleeding in a
patient with thrombocytopenia. As with all blood
product transfusions, a restrictive strategy is
used in order to decrease the amount of unnecessary transfusions and adverse reactions, including alloimmunization with mayresultinplatelet
refractoriness.
9
This strategy also applies to
platelet transfusions. By using current guidelines
in conjunction with thorough evaluation of
the pati ent’s medical condition, a safe and appropriate decision for transfusion of platelets can be
made.
2
Prophylactic platelet transfusion is recom-
mended at platelet levels of ≤10,000/mm
3
in the
absence of risk factors such as sepsis, active antibiotic use, or other abnormalities of coagulopathy.
1,2,9,19,20
If the thrombocytopenia is chronic as
in bone marrow failure / myelodysplasia, the
patient is asymptomatic, and has no risk factors,
an even lower platelet threshold is thought to be
appropriate, possibly as low as 5,000/mm
3.9,19
It is
recommended to consider platelet transfusion
when platelets are ≤ 20,000/mm
3
and patients
are medi cally unstable, but not bleeding.
9
Platelet
transfusions are appropriate in massive hemorrhage if the platelet count is ≤ 50,000/mm
3
, and
in the presence of diffuse microvascular bleeding
≤ 100,000/mm
3.2
Additional platelet thresholds
are noted in Table 43.3.
In order to decrease the frequency of adverse
reactions such as fever, non-hemolytic transfusion
reactions, HLA alloimmunization, and transmitted
CMV infections, platelet leukocytes reduced or
apheresis platelets leukocytes reduced may be used.
One unit of platelets typically increases the platelet
count by 5,000–10,000/mm
3
for a 70 kg adult.
1
Platelet counts should be collected approximately
Table 43.3 Recommended Platelet Threshold Achieved
Prior to Various Interventions
9
Procedure Platelet Count
(×10
3
/mm3)
Spinal epidural anesthesia 80
Major invasive procedures* 40–50
Fiberoptic bronchoscopy
without biopsy
20
GI endoscopy without biopsy 20
* Major invasive procedures includes central venous catheter
placement, paracentesis, thoracentesis, respiratory tract
biopsy, GI tract biopsies, closed liver biopsy, lumbar
puncture, sinus aspiration, epidural anesthesia, and dental
extraction
Transfusions
047
21:12:22
10–180 minutes after the platelet transfusion has
been completed. During this time period, the
transfused platelets are most vulnerable to immune
platelet destruction. Additional platelet counts
should be drawn at 24-hour post-transfusion,
which would help identify how many of the transfused platelets are being destroyed by non-immune
processes.
1
For the majority of patients with thrombocytopenia secondary to platelet destruction, such
as idiopathic thrombocytopenia purpura (ITP),
thrombotic thrombocytopenia purpura (TTP),
and hemolytic uremic syndrome (HUS), platelet
transfusions are not indicated and are unlikely to
be beneficial. If a patient is actively bleeding with
thrombocytopenia in these conditions, transfusion of platelets may be required to aid in hemostasis while adjunct medications begin to work.
When the platelet count is < 30,000/mm
3
in ITP,
consider a long course of steroids and IVIG/antiD immunoglobulin for treatment.
20,22
Transfusion Reactions
There is a wide spe ctrum of transfusion reactions
from mild pruritus to respiratory failure and
shock. Blood product transfusions are associated
with a risk of transmission of infections. The
AABB, formerly American Association of Blood
Banks, noted that the risks of human immunodeficiency virus (HIV) and hepatitis C virus (HCV)
transmission from PRBCs from 2007–2008 were
approximately 1 in 1,467,000 and 1 in 1,149,000,
respectively. The risk of hepatitis B virus (HBV)
transmission from 2006 to 2008 for PRBCs was
approximately 1 in 300,000.
1
Bacterial (Yersinia,
syphilis), parasitic (malaria, Chagas), and prion
(Jakob-Creutzfeldt) transmission have also been
reported. For these reasons, risks of transfusions
must be weighed against the benefits, and ultimately health care providers should strive to
decrease the frequency of unnecessary blood
product transfusions.
Acute adverse reactions can occur within
minutes to hours from onset of transfusion. The
reactions include acute hemolytic transfusion
reaction (AHTR), febrile non-hemolytic transfusion reaction s (FNHTR), allergic transfusion
reactions, transfusion-related acute lung injury
(TRALI), transfusion-associated circulatory overload (TACO) , and transfusion related sepsis.
23
FFP is most commonly implicated in TRALI.
24
When an acute transfusion reaction is suspected,
the transfusion should be immediately held. The
patient should be closely monitored and evaluated
for indications of the type of reactions. Symptoms
may include fevers, chills, pruritus, urticaria,
tachycardia, hypotension (rarely hypertension),
tachypnea, shortness of breath, bronchospasm,
stridor, angioedema, chest tightness, pain in chest,
back, and abdomen, congestive heart failure, pulmonary edema, generalized edema, and shock.
23
These reactions must be immediately medically
managed and laboratory studies sent to further
identify the cause.
Delayed reactions to blood product transfusions typically occur from 24 hours posttransfusion up to several weeks. Delayed reactions
include delayed hemolytic transfusion reactions
(DHTRs), post-transfusion purpura (PTP), iron
overload, transfusion-associated graft-versushost-disease (TA-GVHD), and transfusionassociated thrombosis and immunomodulation/
inflammation.
23
It is imperative that patients be
given information regarding warning signs of
these reactions and ins tructions for follow-up
once discharged from the OU.
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text]. 2011. Available at:
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Guidelines/6584.aspx. Accessed
February 20, 2016.
22. Cines DB, Blanchette VS.
Immune Thrombocytopenic
Purpura. N Engl J Med 2002;
346:995–1008.
23. McCullough J, Refaai MA,
Cohn CS. Blood Procurement
and Red Cell Transfusion. In:
Kaushansky K, Lichtman MA,
Prchal JT, et al. eds. Williams
Hematology. 9th ed. New York:
McGraw-Hill; 2016, chapter
138. www.accessmedicine.
com.library.ccf.org/content
.aspx?aID=6236286. Accessed
February 20, 2016.
24. Vigue B. Bench-to-bedside
review: Optimizing emergency
reversal of Vitamin
K antagonists in severe
haemorrhage – from theory to
practice. Crit Care 2009; 13: 209.
Transfusions
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Subpart IVG
Chapter
44
Clinical – Infections
Skin and Soft Tissue Infections (SSTI)
Robert S. Bennett, MD
Introduction
A growing number of patients present to emergency departments (EDs) with skin and soft tissue
infections (SSTIs). Between 1993 and 2005, the
number of visits to US EDs for SSTIs nearly
tripled increasing from 1.2 to 3.4 million.
1
Hospital
admissions for SSTIs increased by 29% from
2000 to 2004.
2
Many of these patients are ideal
candidates for initial management in an observation unit (OU). Patients with SSTIs make up about
2% of all patients cared for in OUs in the United
States.
3
(It is the fourth most common diagnosis, if
cardiovascular conditions are grouped together.)
3
Within the broad spectrum of illness severity for
SSTIs, there is a group of patients who could be
appropriately cared for in an OU.
The overwhelming majority of SSTIs are
caused by Staphylococcal and Streptococcal species
of bacteria. More severe SSTIs, including necrotizing fasciitis or extensive cellulitis with septicemia,
will require inpatient management. Patients who
appear to have only mild disease can be discharged home directly from the ED with close
follow-up. OU care can be an effective management choice for patients who require only a day
or two of intravenous antibiotics to assure sufficient response while monitoring for clinical progression to more serious conditions.
This chapter will review the basic pathophysiology and etiology of commo n SSTIs, and discuss how to identify patients who can be ideally
managed in an OU. Management of SSTIs will be
reviewed with reference to the 2011 IDSA (Infectious Diseases Society of America) guidelines.
4
Potential challenges and pitfalls of caring for SSTI
patients will be identified.
Discussion
Patients with cellulitis are the most common
SSTI that should be considered as a candidate
for OU care. Most uncomplicated SSTIs are
caused by Streptococcal or Staphylococcal organisms. The dramatic rise in the incidence of community acquired methicillin resistant Staphylococcal
(MRSA) infections has led to changes in the
approach to antibiotic choice and management of
abscesses. Prior to the rise in MRSA, uncomplicated
cellulitis patients could be discharged home on a
single antibiotic such as cephalexin.
Although most “non-suppurative” SSTIs are
caused by Streptococcal species, studies have demonstrated the inability of clinicians to accurately
judge the likelihood of MRSA infection.
5
Therefore, there is increased risk of failure with treatment using traditional antibiotics for cellulitis. It
often makes sense, therefore, to initiate antibiotic
treatment in an observation setting to assure sufficient response to the chosen regimen. The previously established practice of incision and drainage
(I and D) of abscesses followed by discharge home
without antibiotic coverage is being reexamined.
New guidelines from the IDSA recommend antibiotic coverage after I and D under numerous conditions.
4
Some of these patients may require
intravenous antibiotics and inpatient or OU care.
Clinical Prese ntation
The clinical manifestations of SSTIs are widely
variable, but generally include presentations of
skin erythema, warmth, swelling, and pain in the
affected area. Patients may complain of a “spider
bite,” which more likely represents infection
rather than any kind of bite.
6
Abscesses are sometimes obvious, but can also present more insidiously with edema and no apparent collection. An
underlying abscess should be suspected in
patients with presumed cellulitis who have failed
to respond to initial antibiotic therapy.
7
In the era prior to the rise in community-
acquired MRSA infections, most abscesses
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presenting to the ED could be reliably managed
by I and D without antibiotic coverage. If antibiotics were used, most patients would be treated as
outpatients with oral medications. The dramatically increased prevalence of MRSA has resulted in
the recognition that many patients with abscesses
may now require oral or intravenous antibiotics.
Thus, a number of patients who previously would
be discharged home after I and D have become
candidates for referral to the OU. Studies of this
situation have produced conflicting results and
there is general disagreement about the appropriate course of action. A 2008 New England Journal
article
8,9
polled over 10,000 physicians regarding
three different mana gement choices for a patient
presenting with a simple 5 cm abscess. Three
different experts discussed rationale for selecting
either I and D alone (31% of votes), I and D with
anti-MRSA coverage (41% of votes) or I and
D with anti-methicillin sensitive Staphylococcal
aureus coverage (28% of votes).
The 2011 IDSA guidelines
4
recommend antibiotic coverage following I and D of abscesses associated with the following conditions: multiple sites of
infection, rapid progression, signs and symptoms
of systemic illness, associated comorbidities (such
as diabetes) or immunosuppression, extremes of
age, areas difficult to drain (face, hand, genitals)
or lack of response to I and D. Other studies have
recommended antibiotic coverage for abscesses
greater than 5 cm in diameter.
10
Laboratory Evaluation and Imaging
Patients with simple cellulitis, normal vital signs,
and no underlying conditions should not require
extensive laboratory evaluation. A white blood
cell count (WBC) may be useful in identifying
patients at risk for extended hospitalization.
11
However, most patients with SSTIs in the ED will
not be triaged based upon laboratory data. Prior
to the rise in prevalence of MRSA, pus from
uncomplicated abscesses generally did not require
culture. However, due to the change in the epidemiology of SSTIs, purulent material from an
abscess or wound should be cultured if the patient
is to be started on antibiotics (2011 IDSA recommendation).
4
It is widely recognized that blood
cultures are not useful for the majority of patients
with SSTIs.
7,12
This is especially true in patients
with purulent material readily available. However,
patients with extensive disease or signs of sepsis
should have blood cultures performed. This
would usually preclude OU placement. It is
also widely accepted that needle aspiration or
biopsy of inflamed skin (or “leading edge” )is
not useful.
12
Other ancillary laboratory tests for patients
with SSTIs have been proposed as useful in
detecting patients at risk for necrotizing infections. The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score has been studied
to identify patients with SSTIs who are evolving
into a life-threatening infection.
13
The score is
based upon laboratory values including C-reactive
protein (CRP), tot al WBC count, serum sodium,
creatinine, glucose, and hemoglobin. However,
most patients with an elevated score have other
signs indicating serious disease. The utility of
the score in identifying early cases of necrotizing
infections has not been validated. Therefore,
ordering tests such as CRP in patients with SSTIs
need not be routine. It has also been proposed
that an elevated creatine phosphokinase level
should increase suspicion of a necrotizing infection, but this has not been well studied.
7
Under certain conditions, radiologic s tudies
such as plain radiographs, computed tomography, or magnetic resonance imaging can provide useful information. Circumstances include
concerns about o steomyelitis or foreign body
retention. Duplex venograms should be considered in patients with extremity swelling more
consistent with deep venous thrombosis. Bedside
ultrasound has become more prevalent in many
EDs and can provide assistance with diagnosing
occult cutaneous abscesses. Ultrasound has been
found to provide greater sensitivity and specificity in detecting deep abscesses than clinical
examination alone.
14,15
Detection of abscesses
with ultrasound can be readily learned by novice
sonographers.
16
Patient Selection Criteria
The selection process of app ropriate patients with
SSTIs for an OU has several dimensions. One
dimension is the identification of patients who
appear likely to fail outpatient treatment with oral
antibiotics and prevent subsequent return visits to
the hospital. Another is the selection of patients
who clearly need intravenous antibiotics, but are
likely to improv e sufficiently for discharge home
in less than 24 hours. Finally, patients who are
Skin and Soft Tissue Infections (SSTI)
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21:12:33
at risk for deterioration or who are likely to
require an extended stay should be directed to
an inpatient unit.
There have been no prospectively validated
selection criteria or guidelines to assist in the
selection of appropriate patients with SSTIs for
an OU. A retrospective cohort study identified the
presence of fever in patients presenting to an ED
with SSTIs to be a predictor of need for greater
than 24 hours of care in the hospital.
17
However,
many patients with fever could, at least initially,
be managed in an OU. Conversely, there are
many patients without fever presenting with complex SSTIs who are clearly not appropriate for
observation care. Another retrospective cohort
study attempted to predict treatment failures in
OU patients treated with SSTIs. Among the variables evaluated (intravenous drug use, positive
MRSA culture, abscess drainage), only female
gender and white blood cell count > 15,000 were
significantly associated with failure to discharge.
11
Guidelines submitted by the Infectious Diseases Society of America (IDSA) propose hospital
admission for patients presenting with SSTIs who
are hypotensive or have elevated creatinine, creatine phosphokinase, or C-reactive protein levels,
low serum bicarbonate level or left shift of the
white blood cell differential.
12
These guidelines
are not useful for identifying appropriate OU
patients and would likely indicate patients at risk
for more serious conditions such as septicemia or
necrotizing fasciitis. Most candidates for OU care
should not require the extensive laboratory evaluation proposed by the IDSA.
A classification system of illness severity has
been proposed to assist in the triage of patients
with SSTIs.
18
(Table 44.1). Most patients with Class
1 criteria (afebrile and healthy) could be considered for discharge home on oral antibiotics.
Some of these patients should be considered as
observation candidates based upon circumstances
such as lack of follow-up care or predicted noncompliance. Many Class 2 patients (febrile or illappearing with stable comorbidity) should be considered for OU management. It would be expected
that a certain proportion of these patients may
require transfer to an inpatient unit for failure to
improve. About 30% of patients with SSTIs
required inpatient conversion in a national survey.
3
Few Class 3 patients (toxic appearance or unstable
comorbidity) should be routinely considered for
referral to an OU.
Certain features of patients with SSTIs presenting to the ED can be used to identify who
would likely benefit from a stay in an OU
(Table 44.2). These include failure of outpatient
treatment, inability to tolerate oral antibiotic or
risk of noncompliance due to social circumstances. Conversely, there are features of patients
with SSTIs that would identify those who are at
greater risk of complications or a prolonged stay
and would be better served by disposition to an
inpatient unit (Table 44.3). These include patients
Table 44.1 Disposition According to Classification System
for Patients with SSTIs*
Class Patient Criteria Disposition/
Suitability for
Observation
Unit Care
1 Afebrile, healthy
(aside from SSTI)
Home or
observation if risk
features present
(see text)
2 Febrile, appear ill, or
stable comorbidity
Observation unit
management
appropriate
3 Toxic appearance, or
unstable
comorbidity,
threatened limb
Unlikely to be
safely managed in
observation unit
4 Septicemia,
life-threatening
infection
(necrotizing fasciitis)
Inpatient or
intensive care unit
most appropriate
SSTIs = skin and soft tissue infections
*One proposed classification system for SSTIs adapted and
modified from
18
Table 44.2 Features of Patients with SSTIs Suggesting
Benefit from Observation Unit Placement
Failure of outpatient treatment
Inability to tolerate oral antibiotic
Multiple antibiotic allergies
Pain management issues but not chronic pain
Risk of noncompliance due to social circumstances
Abscess with indications for antibiotic coverage
Multiple sites of involvement
Fever (without Systemic Inflammatory Response
Syndrome [SIRS])
Diabetes mellitus
SSTIs = skin and soft tissue infections
Robert S. Bennett
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