Peer Reviewed SYSTEMIC INFLAMMATORY RESPONSE SYNDROME & SEPSIS

PART 1: RECOGNITION & DIAGNOSIS

Systemic Inflammatory Response

Syndrome & Sepsis
Deborah Silverstein, DVM, Diplomate ACVECC
University of Pennsylvania

Small animals frequently present to veterinarians

TABLE 1.
with vague signs of illness. The decision whether to
Examples of Inciting Factors of SIRS
treat dogs or cats symptomatically as outpatients or
STERILE INFLAMMATORY INFECTIOUS
immediately perform diagnostics and recommend
DISEASES INSULTS
hospitalization requires an astute clinician and Nonseptic SIRS Septic SIRS
logical approach to:
• Burns • Anaerobic bacteria
• Patient history
• Chemical aspiration • Fungi
• Physical examination • Heatstroke • Products of gram-
• Preliminary diagnostic findings. • Immune-mediated disease negative bacteria
Animals with evidence of a widespread • Ischemic organ necrosis • Products of gram-
(eg, splenic torsion) positive bacteria
systemic inflammatory condition should never be
• Neoplasia • Protozoa
ignored; the deleterious consequences of excessive • Pancreatitis • Viruses
inflammation may include organ injury and death. • Trauma
Recognition and diagnosis of these emergent
patients is the focus of Part 1 of this article series; TABLE 2.
Part 2 will review stabilization and treatment. Distinctions Between SIRS & Sepsis
SIRS Clinical manifestation of systemic
PROFILE inflammation, which results from
Definition either:
Systemic inflammatory response syndrome • Infectious insult (septic SIRS)
• Noninfectious insult (nonseptic
(SIRS) describes a clinical condition characterized
SIRS)
by widespread activation of the inflammatory
SEPSIS Clinical manifestation of SIRS, sec-
system, secondary to a sterile inflammatory disease
ondary to an underlying pathogenic
or infectious insult (Table 1). organism
The term SIRS was first introduced by the
SEVERE Sepsis—with associated SIRS—with
Learn More American College of Chest Physicians and SEPSIS 1 or more of the following:
Society of Critical Care Medicine (ACCP/SCCM) • Arterial hypotension
Read the ACCP/SCCM
Consensus Conference Consensus Conference in 1991, in an attempt to • Organ dysfunction
Committee’s emphasize the importance of the inflammatory • Hypoperfusion; abnormalities
Definitions for Sepsis suggestive of hypoperfusion
process as a systemic contributor to organ failure in
and Organ Failure may include hyperlactatemia and
patients with sepsis.1 oliguria
and Guidelines
for the Use of SEPTIC Despite adequate intravascular fluid
Innovative Therapies Inflammatory Response SHOCK resuscitation, sepsis-associated:
in Sepsis at journal In sites of localized tissue damage or infection, it is • Acute circulatory failure
.publications.chestnet • Persistent arterial hypotension
well known that the localized inflammatory response
.org/data/journals/
chest/21647/1644.pdf. is characterized by 5 cardinal signs—heat, pain, MODS Physiologic derangements of at least
redness, swelling, and loss of function—which 2 major organ systems associated
are caused by local capillary dilation and an increase with SIRS (see Table 4)
in permeability, and occur in order to protect the MODS = multiple organ dysfunction syndrome

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 SYSTEMIC INFLAMMATORY RESPONSE SYNDROME & SEPSIS Peer Reviewed

TABLE 3.
Clinical Manifestations of SIRS & Sepsis
PHYSICAL FINDINGS: • Bounding pulses*
Hyperdynamic Phase • Brick red mucous membranes (Figure 1)*
• Fever
• Tachycardia*
• Tachypnea
PHYSICAL FINDINGS: • Hypotension
Advanced Disease • Hypothermia
Progression • Pale mucous membranes
• Weak pulses
HISTORICAL FINDINGS • Diarrhea
• Lethargy
• Loss of appetite
• Mental depression
• Vomiting FIGURE 1. Brick red mucous membranes of a dog in the
* Cats frequently do not develop these clinical signs.
hyperdynamic phase of SIRS.

host and eliminate noxious agents and injured cells.
However, in patients with SIRS, severe local or
regional inflammation leads to an “overflow” of
inflammatory mediators into the systemic circulation
that results in a variety of global derangements
that are characterized by vasodilation and increased
vascular permeability.
SIRS versus Sepsis
The distinction between SIRS and sepsis is based
upon the presence or absence of underlying infection
(Table 2).
DIAGNOSIS
Clinical Manifestations
Clinical manifestations of SIRS and sepsis are often
nonspecific and vary depending on the underlying
disease process; historical findings also differ and may
be nonspecific (Table 3).
It is important to note that clinical signs of
SIRS differ in dogs and cats. Cats frequently
do not develop a hyperdynamic response (ie, no
red mucous membranes nor bounding pulses) and
are more likely to have relative bradycardia and
hypothermia.2,3 In 1 study, bradycardia was identified
in 66% of cats, highlighting the difference between
dogs and cats with regard to their physiologic
responses to sepsis.2
Diagnostic Criteria
Criteria proposed for the diagnosis of SIRS have
been extrapolated from the human medical literature
for use in dogs and cats.
Table 4 outlines the clinical criteria that provide
the best sensitivity and specificity in diagnosing SIRS
in septic and nonseptic dogs and cats.2,4
• In cats, proposed criteria for SIRS were derived
from a retrospective study of clinical findings in
cats with severe sepsis confirmed at necropsy.2
• In order for a diagnosis of SIRS to be made, dogs
must have at least 2 of the 5 criteria present and
cats, 3 of the 5 criteria. Sensitivity is increased
with the use of stricter inclusion criteria; therefore,
the presence of more SIRS criteria in a given
patient increases the likelihood of a true systemic
inflammatory process.
• However, depending on the criteria and reference
values used, sensitivity and specificity range from
77% to 97% in dogs and 64% to 77% in cats.
• The clinician should use the SIRS criteria in the
context of the clinical picture and the underlying
inflammatory disease process to enhance the
specificity of the diagnosis.
Diagnostic Approach
Patients with SIRS and/or sepsis should have a
complete blood count, serum biochemical profile,
urinalysis, and coagulation testing performed.
Animals with SIRS frequently have concomitant
organ injury or dysfunction that must be detected
TABLE 4.
Proposed Criteria for Diagnosis of SIRS in Dogs & Cats
CRITERIA DOGS CATS
2 criteria required4 3 criteria required2
Temperature (F) < 100.6o or > 102.6o < 100o or > 103.5o
Heart rate (beats/min) > 120 < 140 or > 225
Respiratory rate (breaths/min) > 20 > 40
White blood cells (× 103) < 6 or > 16 < 5 or > 19.5
Band cells (%) >3 >5

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Peer Reviewed SYSTEMIC INFLAMMATORY RESPONSE SYNDROME & SEPSIS
A
FIGURE 2. Lateral (A) and ventrodorsal (B) abdominal
radiographs from a dog with partial mesenteric torsion
and ileocolic intussusception. This dog presented with
vomiting and clinical signs consistent with septic shock.
early in order to determine appropriate therapy,
monitor for changes, and assist with prognosis.
Hematologic and biochemical changes in small
animals with sepsis typically reflect the underlying
disease process and secondary indices of organ
dysfunction, as outlined in Table 5.
Specifically, hypoalbuminemia is likely due to 1 or
more of the following:5
1. Loss of albumin from the body via the
gastrointestinal tract or wounds, effusion into a
third body space, or vascular permeability into
interstitial space
2. Hepatic dysfunction
3. Preferential synthesis of acute phase proteins by the
liver.
Hyperbilirubinemia may be secondary to cholestasis
in dogs and, possibly, hemolysis in cats. Ionized
hypocalcemia is associated with a longer length of
hospitalization in both dogs and cats.6,7
Coagulation testing may reveal abnormalities
associated with disseminated intravascular
coagulation (DIC) due to:8
• Cytokine-mediated endothelial cell activation
• Platelet stimulation
• Increased tissue factor expression
• Circulating microparticles
• Fibrin deposition in the microvasculature
• Decreased endogenous anticoagulants
• Perturbations in fibrinolysis.
Animals with SIRS or sepsis are initially
hypercoagulable (this can be difficult to
diagnose), but often develop hypocoagulability
due to consumption of clotting factors. Changes
consistent with later stages of DIC are outlined in
Table 5.9
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B
In patients with suspected SIRS/sepsis, additional
diagnostic tests should include mixed venous
or arterial blood gas measurements and
measurement of serum lactate. Many patients have
a metabolic acidosis that reflects poor tissue perfusion
and hyperlactatemia.
Thyroid function tests are frequently deranged in
dogs with sepsis or SIRS, but these tests are usually
not part of the initial evaluation of these patients.10
Urinalysis abnormalities may include isosthenuria
due to loss of concentrating ability, proteinuria due to
glomerular and/or tubular damage, glucosuria due to
tubular damage and/or hyperglycemia, bacteria (if a
urinary tract infection is present), pyuria, hematuria,
and casts secondary to acute kidney injury.
Thoracic and abdominal imaging (radiographs
and ultrasonography) should be performed in all
patients with suspected SIRS or sepsis. Diagnostic
imaging should focus on detecting the underlying
infectious or sterile inflammatory disease process
(eg, pancreatitis), as well as any coexisting secondary
organ damage (eg, acute respiratory distress
syndrome) (Figure 2).
Identifying Source of Infection
A diagnosis of sepsis can be made once infection
is documented and the patient fulfills the species
specific criteria for SIRS (Table 4). Patient history
and physical examination may initially help guide the
search for the source of infection.
Appropriate samples (Table 6, page 42) should
be collected for culture and susceptibility testing
to identify the cause of sepsis and best direct
antimicrobial therapy. Aerobic and anaerobic
gram-negative and gram-positive bacteria are both
 SYSTEMIC INFLAMMATORY RESPONSE SYNDROME & SEPSIS Peer Reviewed

TABLE 5.
Clinical Pathology & Sequelae
Associated with SIRS & Sepsis
HEMATOLOGIC ABNORMALITIES
Sepsis or SIRS • Anemiaa
• Elevated hematocritb
• Increased band cells (Figure 3)
• Leukocytosis or leukopenia
• Monocytosis
• Thrombocytopeniac 3 4
• Toxic neutrophils (Figure 4)
FIGURE 3. Blood smear from a dog. The central band neutrophil is
SERUM BIOCHEMICAL PROFILE toxic, with foamy basophilic cytoplasm indicating premature release
Underlying • Blood glucose variabled from the bone marrow due to increased demand. (Wright’s stain;
disease process • Hyperbilirubinemia original magnification, x100)
Progressive • Hyperglycemiae FIGURE 4. A toxic band neutrophil containing several distinct Dohle
organ • Hyperlactatemia
dysfunction bodies, which indicate presence of systemic toxins (often bacterial)
• Hypoalbuminemia
that are interfering with development of neutrophils in the bone
• Ionized hypocalcemia
• Metabolic acidosis marrow or accelerated neutrophil production. (Wright’s stain; original
magnification, x100)
COAGULATION TESTING
Disseminated • Elevated D-dimer PATHOGENESIS OF SIRS
intravascular • Elevated fibrin or fibrinogen The pathophysiologic mechanisms responsible for
coagulation degradation products
generation of SIRS are complex and incompletely
• Prolonged activated partial
thromboplastin time understood. The initial insult that stimulates
• Prolonged prothrombin time SIRS can come from a variety of sterile sources or
• Reduced antithrombin infectious agents (Table 1).
• Reduced protein C activity
a. Cats are frequently anemic
b. Dogs often have elevated hematocrit, reflecting
Spread of Inflammation
hemoconcentration secondary to volume depletion, The inflammatory response may initially start locally
splenic contraction, or a combination of both
c. Platelet counts frequently decrease due to consumption
(eg, abscess on a limb, trauma) (Figure 5) but, if
in hypercoagulable animals or loss in animals that severe, can progress to cause systemic signs when
suffer from vascular leak syndromes or bleeding due to
mediators of inflammation enter the circulatory
hypocoagulable states
d. Hypoglycemia or hyperglycemia is commonly reported in dogs4 system and instigate global activation of the
e. Commonly seen in cats2,4
inflammatory system.

frequently cultured from septic dogs and cats,

depending on the source of the infection.3
In addition to culture and sensitivity testing,
fecal testing should be considered in animals with
hemorrhagic diarrhea (eg, parvovirus, salmonellosis).
Cats should be tested for retroviral diseases, and
dogs tested for rickettsial diseases, fungal diseases,
and other infectious agents based on regional
epidemiology or travel history.

Cardiopulmonary Function
Baseline cardiopulmonary function should be
established since the underlying disease, cytokine-
mediated effects, and secondary organ derangements
may lead to abnormalities in any or all of the
following:
• Arterial blood pressure
FIGURE 5. A dog with trauma resulting in global activation of
• Electrocardiography the inflammatory system.
• Pulse oximetry.

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Peer Reviewed SYSTEMIC INFLAMMATORY RESPONSE SYNDROME & SEPSIS

TABLE 6. TABLE 8.
Possible Sample Sources to Cytokines Generated During
Identify Cause of Sepsis Gram-Negative Sepsis
• Blood PROINFLAMMATORY ANTI-INFLAMMATORY
• Bronchoalveolar wash fluid CYTOKINES CYTOKINES
• Cerebrospinal fluid
• Endotracheal or transtracheal wash fluid • Bradykinin • IL-4
• Joint fluid • IL-1, IL-6, and IL-8 • IL-10
• Organ aspirates • Interferon-gamma • IL-13
• Peritoneal effusion • Nitric oxide • Transforming growth
• Pleural effusion • Platelet-activating factor factor-beta
• Urine • Tumor necrosis factor-
alpha

TABLE 7. • Initiation of intracellular signaling that begins

Potential Activators of Macrophages
• Acidosis
• Extracellular adenosine triphosphate
• Lipopolysaccharide
• Low oxygen tension
• Proinflammatory molecules, resulting from tissue
injury/stress (eg, thrombin)
Although certain cells, such as platelets,
polymorphonuclear leukocytes, and the endothelium,
also play a role, it appears that the stimulation
of macrophages (Table 7) and their release of
inflammatory cytokines are pivotal in the generation
of SIRS.
Production of Cytokines
During gram-negative sepsis, the lipid A portion of
lipopolysaccharide (LPS)—the glycolipid component
of the cell wall—binds to LPS binding protein (LBP).
This LPS–LBP complex binds to membrane-bound
CD14 on macrophages, and this binding leads to:
• Activation of macrophages
transcription of inflammatory cytokines (Table 8).
In addition to proinflammatory mediators, the
response also generates anti-inflammatory cytokines
(Table 8), soluble receptors, and receptor antagonists
for cytokines. This compensatory response is often
referred to as compensatory anti-inflammatory
response syndrome (CARS).
Although CARS beneficially balances out the
proinflammatory state often seen with SIRS,
excessive CARS stimulation may contribute to
immunodeficiency and increased susceptibility to
infection in the later stages of sepsis.11,12
Immune Response
When the immune system is fighting pathogens or
repairing damaged tissue, proinflammatory cytokines
signal immune cells, such as T-cells and macrophages,
to travel to the site of infection. In addition,
cytokines activate these recruited immune cells to
produce more cytokines.
While cytokines trigger a beneficial inflammatory

A B
FIGURE 6. A dog with acute respiratory distress syndrome secondary to SIRS; following
intubation for unsuccessful cardiopulmonary cerebral resuscitation, a large volume of bloody
fluid poured out of the endotracheal tube (A). Thoracic radiograph of a dog with acute
respiratory distress syndrome showing diffuse severe bilateral alveolar infiltrates (B).

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 SYSTEMIC INFLAMMATORY RESPONSE SYNDROME & SEPSIS Peer Reviewed

TABLE 9.
Organs at Risk for Dysfunction
Animals with septic or nonseptic SIRS frequently
develop microcirculatory dysfunction in which Changes in
Secondary to SIRS there is a decrease in density of capillary
vessels and decrease in flow of red blood cells
Microcirculatory
ORGAN MANIFESTATION OF
SYSTEM DYSFUNCTION
within the functional microcirculatory vessels
(arterioles, venules, and capillaries). In addition,
Blood Flow
Cardiac • Decreased contractility heterogeneous distribution of blood frequently
• Arrhythmias occurs and the normal mechanisms to increase or
decrease blood flow to a particular tissue bed are
Coagulation • Disseminated intravascular deranged secondary to the effects of cytokines.
coagulation The end result is cellular hypoxia and organ
Endocrine dysfunction.
• Critical illness related
corticosteroid insufficiency
Gastro- • Constipation Normal microcirculation. Note the large
intestinal • Diarrhea number of capillaries that allow movement of
• Ileus only one red blood cell at a time.
• Regurgitation
• Vomiting
Hepatic • Decreased albumin
• Decreased clotting factor
synthesis
• Icterus Microcirculation of a dog with septic
peritonitis. There are few capillaries visible,
Renal • Acute kidney injury indicating microvascular shunting and
Nervous • Encephalopathy decreased perfusion of the associated tissue.
• Seizures
Pulmonary • Acute lung injury
• Acute respiratory distress
syndrome (Figure 6)
• Myocardial dysfunction
Vascular • Microcirculatory dysregulation
• Mitochondrial dysfunction.
• Vascular leakage
• Vasoplegia Mitochondrial dysfunction, which leads to a
reduction in cellular adenosine triphosphate, is
response that promotes local coagulation to thought to play an important role in development of
confine tissue damage, excessive production of organ dysfunction and/or failure. This mitochondrial
proinflammatory cytokines can be more dangerous failure likely occurs secondary to tissue ischemia,
than the original stimulus because they: resulting from:
• Overcome the normal regulation of the immune • Circulatory collapse
response • Hypoxemia
• Produce the clinical signs classically seen in patients • Poor microcirculatory blood flow (see Videos 1
with SIRS. and 2, available at tvpjournal.com)
This production of a “cytokine storm” and • Mitochondria may also be damaged (or inhibited)
global activation of white blood cells (WBCs) by reactive nitrogen and oxygen species.
ultimately overwhelms the CARS, becoming In the lungs, however, acute respiratory distress
the key component in the pathogenesis of syndrome results directly from inflammation rather
SIRS. The diagnostic and prognostic utility than mitochondrial dysfunction.
of serum cytokine levels in animals with sepsis
and SIRS is the subject of recent and continued Multiple Organ Dysfunction
investigation.5,13-20 These deleterious sequelae of systemic inflammation
can lead to the syndrome of multiple organ
Development of Organ Dysfunction dysfunction (MODS) (Table 9). MODS—
In addition to systemic activation of WBCs, other characterized by abnormalities in organs that were
pathologic effects of inflammatory mediators include: not affected by the original insult—is associated
• Increased capillary permeability with a high morbidity and mortality rate; there
• Vasodilation is a 20% increase in mortality for each failing
• Activation of coagulation system.21 The resulting organ damage may resolve

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 Peer Reviewed SYSTEMIC INFLAMMATORY RESPONSE SYNDROME & SEPSIS

partially or completely once the underlying cause of
inflammation has been successfully treated.
IN SUMMARY
Once a patient has been identified as having clinical
evidence of SIRS—with or without sepsis—it is
paramount that rapid treatment is initiated to:
• Correct the underlying disease process(es)
• Restore oxygen delivery to the tissues, using
goal-directed therapy to maximize the chance for a
successful outcome.
These treatment modalities will be discussed in-
depth in Part 2 of this article series, which will be
published in an upcoming issue of Today’s Veterinary
Practice.
CARS = compensatory anti-inflammatory response
syndrome; DIC = disseminated intravascular
coagulation; LBP = lipopolysaccharide binding
protein; LPS = lipopolysaccharide; MODS =
multiple organ dysfunction syndrome; SIRS =
systemic inflammatory response syndrome; WBC =
white blood cell
References
1. Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and
organ failure and guidelines for the use of innovative therapies
in sepsis. The ACCP/SCCM Consensus Conference Committee.
American College of Chest Physicians/Society of Critical Care
Medicine. Chest 1992; 101(6):1644-1655.
2. Brady CA, Otto CM, Van Winkle TJ, King LG. Severe sepsis in
cats: 29 cases (1986–1998). JAVMA 2000; 217(4):531-535.
3. Hauptman JG, Walshaw R, Olivier NB. Evaluation of the
sensitivity and specificity of diagnostic criteria for sepsis in dogs.
Vet Surg 1997; 26(5):393-397.
4. Greiner M, Wolf G, Hartmann K. A retrospective study of the
clinical presentation of 140 dogs and 39 cats with bacteraemia. J
Small Anim Pract 2008; 49(8):378-383.
5. DeClue AE, Delgado C, Chang C-H, Sharp CR. Clinical and
immunologic assessment of sepsis and the systemic inflammatory
response syndrome in cats. JAVMA 2011; 238(7):890-897.
6. Luschini MA, Fletcher DJ, Schoeffler GL. Incidence of ionized
hypocalcemia in septic dogs and its association with morbidity
and mortality: 58 cases (2006–2007). J Vet Emerg Crit Care
2010; 20(4):406-412.
7. Kellett-Gregory LM, Mittleman BE, Brown DC, Silverstein DC.
Ionized calcium concentrations in cats with septic peritonitis: 55
cases (1990–2008). J Vet Emerg Crit Care 2010; 20(4):398-405.
8. Ralph AG, Brainard BM. Hypercoagulable states. In Silverstein
DC, Hopper K (eds): Small Animal Critical Care Medicine, 2nd
ed. St. Louis: Elsevier Saunders, 2015, pp 541-554.
9. Bauer N, Moritz A. Coagulation response in dogs with and
without systemic inflammatory response syndrome–Preliminary
results. Res Vet Sci 2013; 94:122-131.
10. Pashmakova MB, Bishop MA, Steiner JM, et al. Evaluation of
serum thyroid hormones in dogs with systemic inflammatory
response syndrome or sepsis. J Vet Emerg Crit Care 2014;
24(3):264-271.
11. van der Poll T, van Deventer SJH. Cytokines and anticytokines
in the pathogenesis of sepsis. Infect Dis Clin North Am 1999;
13(2):413-426.
12. Frazier WJ, Hall MW. Immunoparalysis and adverse outcomes
from critical illness. Pediatr Clin North Am 2008; 55(3):647-
668.
13. Osterbur K, Whitehead Z, Sharp CR, DeClue AE. Plasma
nitrate/nitrite concentrations in dogs with naturally developing
sepsis and non-infectious forms of the systemic inflammatory
response syndrome. Vet Rec 2011; 169(21):554.
14. Yu DH, Nho DH, Song RH, et al. High-mobility group box
1 as a surrogate prognostic marker in dogs with systemic
inflammatory response syndrome. J Vet Emerg Crit Care 2010;
20(3):298-302.
15. Gebhardt C, Hirschberger J, Rau S, et al. Use of C-reactive
protein to predict outcome in dogs with systemic inflammatory
response syndrome or sepsis. J Vet Emerg Crit Care 2009;
19(5):450-458.
16. Fransson BA, Bergstrom A, Hagman R, et al. C-reactive protein,
tumor necrosis factor alpha, and interleukin-6 in dogs with
pyometra and SIRS. J Vet Emerg Crit Care 2007; 17(4):373-
381.
17. Rau S, Kohn B, Richter C, et al. Plasma interleukin-6 response
is predictive for severity and mortality in canine systemic
inflammatory response syndrome and sepsis. Vet Clin Pathol
2007; 36(3):253-260.
18. DeClue AE, Sharp CR, Harmon M. Plasma inflammatory
mediator concentrations at ICU admission in dogs with naturally
developing sepsis. J Vet Intern Med 2012; 26(3):624-630.
19. DeClue AE, Williams KJ, Sharp C, et al. Systemic response to
low-dose endotoxin infusion in cats. Vet Immunol Immunopathol
2009; 132(2–4):167-174.
20. Karlsson I, Hagman R, Johannisson A, et al. Cytokines as
immunological markers for systemic inflammation in dogs with
pyometra. Reprod Domest Anim 2012; 47(S6):337-341.
21. Kenney EM, Rozanski EA, Rush JE, et al. Association between
outcome and organ system dysfunction in dogs with sepsis: 114
cases (2003–2007). JAVMA 2010; 236(1):83-87.

DEBORAH SILVERSTEIN
Deborah Silverstein, DVM, Diplomate ACVECC, is an associate
professor of critical care at University of Pennsylvania Ryan Veterinary
Hospital. Her primary research interests include diagnosis and
treatment of circulatory shock, microcirculatory imaging in small
animals, vasopressor therapy, and fluid therapy. Dr. Silverstein is the
co-editor of the Small Animal Critical Care Textbook, speaks both
nationally and internationally about numerous topics relating to
critical care medicine in small animals, and has published numerous
articles based on her research interests. For questions or comments,
she can be reached by email at dcsilver@vet.upenn.edu.

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