Emergency Medicine Sepsis

Severe Sepsis and Septic Shock
Cardiovascular Emergencies and Shock
With Julianna Jung, MD, FACEP
Brovada Hunter, bavoca7081@djpich.com

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Learning Objectives
By the end of this lecture, the learner will be able to:
• Define sepsis and septic shock.
• Describe the pathophysiology of septic shock.
• List common etiologies of septic shock.
• Describe the essential elements of management of

patients with septic shock.

In Practical Terms Sepsis Definition
Circulatory system
Liver (transaminitis,
(myocardial depression,
synthetic dysfunction)
vasodilation)
Clinical pearl
Kidneys (oliguria,
Lungs (ARDS)
anuria, AKI)
Central nervous system

GI tract (dysmotility)
(altered mental status)

In Practical Terms Septic Shock Definition
Clinical pearl
Septic shock occurs when sepsis impairs circulation,
leading to cellular hypoxia and anaerobic metabolism.

Pathophysiology of Sepsis Pathology
• Infection stimulates normal release of

inflammatory mediators.
• In sepsis, this process becomes self-stimulating:

• Further release of inflammatory mediators.
• Recruitment of lymphocytes, macrophages,
and PMNs.
• Destruction of healthy tissue by immune
system.
• Loss of normal homeostasis is a major

contributor to organ failure.
• Organ failure is not simply due to circulatory

insufficiency!
Clinical Definition of Sepsis Definition
SIRS
Clinical Definition of Sepsis Definition
• SOFA: Sequential Organ Failure Assessment
• Reliable and valid
• Designed for use over time in ICU setting
• qSOFA (q = quick!)
• Altered mental status (GCS < 15)
• RR > 22
• SBP < 100

Clinical Definition of Sepsis
Clinical pearl
Presence of any 2 of 3 qSOFA criteria in setting of infection reliably predicts
increased risk of death or prolonged hospitalization!

Clinical Definition of Septic Shock Definition
Despite adequate fluid resuscitation:
Hypotension requiring vasopressors
Elevated lactate level (> 2 mmol/L)
Mortality > 40%

Clinical Definition of Septic Shock Definition
There is no adequate fluid need for

vasopressor these will vary based on patient presentation
and comorbidities.

Diagnostic Algorithm for Sepsis Diagnosis
Patient with suspected infection

Monitor clinical condition,
No Sepsis still No
qSOFA and reevaluate for possible
suspected?
Yes sepsis if indicated
Assess for evidence of Yes
organ dysfunction
Monitor clinical condition,
No
SOFA and reevaluate for possible
Yes sepsis if indicated
Sepsis
Despite adequate fluid resuscitation,

1. Vasopressors required to maintain Yes
Septic shock
MAP
2. Serum lactate level > 2 mmol/L
Etiologies of Sepsis Etiology
Infections Common sources Bacteria

• Any infection can lead • Lung • Vast majority are
to sepsis bacterial
• Urinary tract
• GI tract
• Skin/soft tissue

Diagnostic Evaluation for Suspected Sepsis Diagnosis
Thorough history and

Lactate level
physical exam
CXR Blood cultures
Urinalysis/culture

Diagnostic Evaluation for Suspected Sepsis Diagnosis
Consider additional tests when workup is nondiagnostic:

• Chest/abdomen CT
• Lumbar puncture
• Other body fluid sampling (peritoneal, pleural, joint)

Commonly Missed Sepsis Sources Etiology
Skin decubitus ulcers,

Meningitis/encephalitis
perineal lesions
ENT sinusitis, Intra-abdominal

epiglottitis, abscesses processes
Endocarditis

Commonly Missed Sepsis Sources Etiology
Patients who are unable to give a history are at highest

risk of having their sepsis sources overlooked.
Search exhaustively for a source in every patient!

Why is Sepsis Source Important? Etiology
It identifies the need for Some infections are These require invasive procedures
source control. not responsive to to reduce microbial burden: intra-
antibiotics alone. abdominal processes, septic joints,
abscesses, necrotizing fasciitis,
empyema.

Why is Sepsis Source Important? Etiology
Prompt identification and control of the infection source is a top

priority in sepsis management!

Why Check Lactate?
• Cellular hypoxia forces anaerobic

metabolism.
• Lactate is a by-product of this

metabolic pathway.
• It is a surrogate marker for the

adequacy of tissue-level perfusion.
• It may be the earliest clue in well-

compensated patients.
• It has good sensitivity, but only

moderate specificity.

Sepsis Management Management
Monitoring response to
Source control
treatment
Antibiotics Vasopressors
Fluid resuscitation

Antibiotics Management
Broad-spectrum coverage
Tailored to most likely pathogens
Based on local microbial resistance patterns
Administered as soon as sepsis is suspected
Within 1 hour of ED arrival

Fluid Resuscitation Management
Give a minimum of 30 cc/kg within 3 hours of ED

arrival.
You can give more based on clinical volume status

and patient response.
Start with isotonic crystalloid (NS or LR).
Consider albumin for patients in need of large

volume resuscitation.
Consider blood for patients with severe anemia

(Hgb < 7).

Vasopressors Management
Indicated for MAP < 65 despite adequate fluid

resuscitation.
Norepinephrine is the first-line agent.
Epinephrine or vasopressin may be added if

needed.
Place arterial line and titrate infusion to MAP > 65.

Monitoring Response to Treatment Examination
There is no single best approach to monitoring response to

treatment; instead use multiple methods.

Monitoring Response to Treatment Examination
Clinical exam (VS, Central venous Central venous Passive leg raise
heart, lung, skin, pressure (goal 8 12) oxygen saturation (10% increase in
capillary refill) (goal > 70%) pulse pressure
indicates fluid
responsiveness)

Ultrasound In Shock Examination
• Cardiac ultrasound for

contractility
• IVC ultrasound to assess

volume status:
• IVC < 1.5 cm or collapsible
suggests hypovolemia
• IVC > 2.5 cm suggests
volume overload
Patrick J. Lynch and C. Hunter,

Brovada Carl Jaffe, Apical four chamber view of heart, cropped,
bavoca7081@djpich.com
https://commons.wikimedia.org/wiki/File:Apical_4_chamber_view.png, CC BY 2.5
Sepsis Treatment Overview Management
One hour Three hours Six hours or if no response to fluid
Blood cultures 30 cc/kg IV fluid Vasopressors

Lactate
Broad-spectrum antibiotics

Take-Home Points
In patients with sepsis, always:
Provide broad-spectrum antibiotics.
Provide adequate fluid resuscitation.
Administer vasopressors for MAP < 65

despite fluids.

Learning Outcomes
 You can describe the pathophysiology of

sepsis.
 You can identify patients with sepsis and

septic shock.
 You are able to provide treatment in

accordance with international guidelines.

This document is a property of: Brovada Hunter
Note: This document is copyright protected. It may not be copied, reproduced, used, or
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Severe Sepsis and Septic Shock

Cardiovascular Emergencies and Shock

With Julianna Jung, MD, FACEP

Brovada Hunter, bavoca7081@djpich.com

By the end of this lecture, the learner will be able to:

• Define sepsis and septic shock.

• Describe the pathophysiology of septic shock.

• List common etiologies of septic shock.

• Describe the essential elements of management of

Brovada Hunter, bavoca7081@djpich.com

Central nervous system

Brovada Hunter, bavoca7081@djpich.com

Brovada Hunter, bavoca7081@djpich.com

• Infection stimulates normal release of

• In sepsis, this process becomes self-stimulating:

• Loss of normal homeostasis is a major

• Organ failure is not simply due to circulatory

• SOFA: Sequential Organ Failure Assessment

• Reliable and valid

• Designed for use over time in ICU setting

• Altered mental status (GCS < 15)

• SBP < 100

Brovada Hunter, bavoca7081@djpich.com

Brovada Hunter, bavoca7081@djpich.com

Despite adequate fluid resuscitation:

Hypotension requiring vasopressors

Elevated lactate level (> 2 mmol/L)

Mortality > 40%

Brovada Hunter, bavoca7081@djpich.com

There is no adequate fluid need for

Brovada Hunter, bavoca7081@djpich.com

Patient with suspected infection

Despite adequate fluid resuscitation,

Infections Common sources Bacteria

Brovada Hunter, bavoca7081@djpich.com

Thorough history and

CXR Blood cultures

Brovada Hunter, bavoca7081@djpich.com

Consider additional tests when workup is nondiagnostic:

Brovada Hunter, bavoca7081@djpich.com

Skin decubitus ulcers,

ENT sinusitis, Intra-abdominal

Brovada Hunter, bavoca7081@djpich.com

Patients who are unable to give a history are at highest

Brovada Hunter, bavoca7081@djpich.com

Brovada Hunter, bavoca7081@djpich.com

Prompt identification and control of the infection source is a top

Brovada Hunter, bavoca7081@djpich.com

• Cellular hypoxia forces anaerobic

• Lactate is a by-product of this

• It is a surrogate marker for the

• It may be the earliest clue in well-

• It has good sensitivity, but only

Brovada Hunter, bavoca7081@djpich.com

Brovada Hunter, bavoca7081@djpich.com

Tailored to most likely pathogens

Based on local microbial resistance patterns

Administered as soon as sepsis is suspected

Within 1 hour of ED arrival

Brovada Hunter, bavoca7081@djpich.com

Give a minimum of 30 cc/kg within 3 hours of ED

You can give more based on clinical volume status

Start with isotonic crystalloid (NS or LR).

Consider albumin for patients in need of large