Approach to Sepsis and Septic Shock. Emergency Medicine.

1. APPROACH TO SEPSIS
AND SEPTIC SHOCK
BY DR. ANGEL GOVEKAR
MBBS

2. WHAT IS SEPSIS AND SEPTIC SHOCK?
SEPSIS
Life threatening organ dysfunction secondary to a dysregulated host
response to infection consistent with the Sepsis-3 consensus definition.
SEPTIC SHOCK
Septic shock is subset of sepsis in which underlined circulatory and
cellular metabolism abnormalities are profound enough to increase
mortality

3. CRITERIA
Sepsis
Suspected or proven infection and increase in sequential organ failure
assessment (SOFA) score of 2 or more baseline.
Septic shock
Sepsis and vasopressor required to maintain a mean arterial pressure of
>65mm Hg and lactate more than 2mmol/litre despite adequate fluid
therapy.

4. QUICK SEQUENTIAL ORGAN
FAILURE ASSESSMENT (qSOFA)
screening tool derived to identify patients at higher risk of death.
criteria includes:
• altered mental status
• respiratory rate ≥22 breaths/min
• systolic blood pressure ≤100 mm Hg
with a score ≥2 indicating a high risk for poor outcome.

5. Pathophysiology

6. CLINICAL FEATURES
can be subtle or present in occult manner.
• Vital sign abnormalities—notably fever, hypotension, and/or
tachycardia—are a hint to sepsis.
• ED patients with sepsis are often volume depleted from decreased intake
and increased fluid losses (from emesis, diarrhea, or insensible losses)
• Further complicating matters is septic cardiomyopathy, a reversible
process with impaired systolic function and diastolic relaxation.
• The combination of intravascular volume depletion and septic
cardiomyopathy may manifest as “cold shock” impaired peripheral
perfusion and cool extremities.

7. SYSTEMIC MANIFESTATIONS
PULMONARY INJURY
 Acute Lung Injury is common and may result in the acute respiratory
distress syndrome (ARDS), it’s classification uses the degree of
hypoxemia and radiographic findings

8. When do we say ARDS?
Acute onset bilateral pulmonary infiltrate on chest radiogram that
cannot be explained by effusions, heart failure or volume overload.
Clinically, hypoxia and respiratory distress is evident.
Categorization of ARDS:
PaO2/FiO2 200-300 – mild
100-200 – moderate
<100 – severe

9. RENAL INJURY
 Acute kidney injury can present with azotemia, oliguria, or anuria.
 Risk Factors:
• preexisting kidney dysfunction
• depth and duration of hypotension, hypoperfusiom
• dehydration
• use of nephrotoxic substances (e.g., aminoglycoside antibiotics, furosemide)
• toxic products resulting from neutrophil–endothelial interactions,
endothelial damage by various mediators
• reperfusion injury
• microvascular thrombosis.

10. HEPATIC INJURY
• Increased concentrations of transaminase, alkaline phosphatase (one to
three times the normal level), and bilirubin (usually not >10 milligrams/
dL) are evidence of this injury
• Lessor elevations in liver function tests can result from intermittent or
prolonged macro- or microvascular hypoperfusion and ischemia or be
secondary to direct endotoxin, cytokines, or immune complex damage.
• Red blood cell hemolysis from microvascular coagulation can cause
jaundice

11. GI CHANGES
• The most common GI manifestation of sepsis is ileus, which may persist
for days after shock resolves.
• Major blood loss secondary to upper GI bleeding is rare in septic
patients.
• Minor GI blood loss within 24 hours of developing severe sepsis can
result from painless erosions in the mucosal layer of the stomach or
duodenum.

12. HEMATOLOGICAL CHANGES
All kind of multiple abnormalities are possible like neutrophilia,
neutropenia, thrombocytopenia and DIC is possible.

13. METABOLIC CHANGES
• Hypoperfusion with anaerobic metabolism as well as increase
production of lactate.
• Hyperglycemia is seen in non diabetic patient.
• Adrenaline insufficiency

14. SKIN
• Bacterial Infections (cellulitis, erysipelas, and fasciitis)
• Hematogenous Lesions (petechiae, pustules, cellulitis, ecthyma
gangrenosum)
• Hypotensive/DIC lesions (acrocyanosis and necrosis of peripheral tissues)
• Intravascular Infections (microemboli / immune complex vasculitis)
• Toxic lesions (toxic shock syndrome)
Look for any necrotizing or surgical source of sepsis

15. Infectious Triggers for Sepsis
1. Acute Bacterial Pneumonia
• The most common trigger implicated in sepsis
• The most frequent causative organisms are Streptococcus pneumoniae,
S. aureus, gram-negative bacilli and Legionella pneumophila.
2. Acute Pyelonephritis
• Caused by gram negative bacteria and enterococci
3. Acute Cholecystitis and cholangitis
4. Acute Pancreatitis
5. Cellulitis due to S. aureus or Streptococcus pyogenes

16. In reproductive age group females,
6. Septic abortion
7. Postpartum endometritis
8. Myometritis
9. Primary Bacteremia & Endocarditis
Caused by S. aureus, S. pneumoniae, and Neisseria meningitidis.
Pseudomonas aeruginosa and other gram-negative bacteria
10. Acute Bacterial Meningitis
caused by S. pneumoniae or N. meningitidis

17. Diagnosis
• Sepsis is a clinical diagnosis predicated on suspicion or confirmation
of infection, systemic inflammation, and evidence of new organ
dysfunction and/or tissue hypoperfusion.
• The differential diagnosis of shock includes cardiogenic,
hypovolemic, anaphylactic, neurogenic, or obstructive shock
(pulmonary embolism, cardiac tamponade) or endocrine disorders
(adrenal insufficiency, thyroid storm) that mimic sepsis.
• Once sepsis is diagnosed, seek the source, but do not withhold
interventions such as resuscitative measures and antimicrobials.

18. LABS
• CBC with platelet count
• Serum electrolytes (including calcium and glucose)
• Renal function panel (BUN and creatinine levels)
• Lactic acid level
• Liver function panel (bilirubin, alkaline phosphate, and aspartate and
alanine aminotransferase levels)
• Urinalysis
• An ABG aids the metabolic, ventilatory, and oxygenation assessment in
select patients.
• In the setting of active bleeding or suspected DIC, obtain prothrombin
time, activated PTT, fibrinogen, and d-dimer

19. IMAGING
• Chest radiograph
• Abdominal plain radiographs
• CT scan (soft tissue) to assess for the presence of free air in the tissue
or deep space abscesses may assist in making the diagnosis of
necrotizing skin and soft tissue infections.
• CT scan (head) & lumbar puncture to rule out meningitis.
• MRI to check for epidural abscess if present.
• Blood Cultures for gram staining and culture of secretions from any
potential site of infection when possible.

20. INVESTIGATIONS In Summary,
• CBC with platelet count
• Serum electrolytes (including calcium and glucose)
• Renal function panel (BUN and creatinine levels)
• Lactic acid level
• liver function panel (bilirubin, alkaline phosphate, and aspartate and alanine
aminotransferase levels); and urinalysis.
• ABG
• prothrombin time, activated PTT, fibrinogen, and d-dimer.
• chest radiograph.
• abdominal plain radiographs
• US can identify
• CT and lumbar puncture but do not delay antibiotics pending these tests.
• In adults with sepsis, obtain at least two separate sets of blood cultures from different
venipuncture sites when possible. Order Gram staining and culture of secretions from any
potential site of infection when possible.
• Other tests of interest in the assessment of sepsis include C-reactive protein and procalcitonin,
both of which reflect systemic inflammation; neither of these tests excludes sepsis, and they
are not routinely needed.

21. Prognostic markers
• Serum lactate is used as a prognostic marker in those with sepsis, but it
cannot be used to diagnose or exclude sepsis. As lactate increases, the risk
of mortality rises.
• The 28-day mortality rate associated with modest elevation of serum
lactate to 2 to 4 mmol/L approaches 15% even in those patients without
hypotension.
• Hypotension
• In general, venous or arterial lactate levels are good indicators but even
better are serial levels using the same method of sampling (arterial or
venous)
• Neutropenia occurs rarely and is associated with increased mortality
• Hyperglycemia
• Thrombocytopenia
• Disseminated Intravascular Coagulation

23. However, SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME (SIRS) is not a diagnosis or a good indicator of outcome;
it is a crude means of stratification of patients with systemic
inflammation

24. Treatment
Cornerstones of initial treatment & stabilization of severe sepsis
include early recognition, early reversal (or prevention) of
hemodynamic compromise, and early infection control.
Goals of the treatment is to improve preload, tissue perfusion, and
oxygen delivery.

25. sepsis checklist
• In those with signs or symptoms of infection, look for occult shock: check
vital signs and consider lactate early and repeat if in doubt.
• Give appropriate antimicrobials to patients with suspected sepsis as soon
as possible.
• Look hard for the infection source, including getting blood cultures and
seeking a surgical, gynecologic, or indwelling medical device infection.

26. • Give at least 1 to 2 L bolus of IV crystalloid (RL) to hypotensive
patients or patients with elevated lactate and monitor the response.
• Recheck resuscitation responses using more than one measure—better
vital signs/shock index, improved clinical appearance, improved
mentation and urine output, decreasing lactate, and/or improved central
venous pressure or oxygen saturation.
• Give more fluids if not clinically better and there is no evidence of
volume overload.
• Administer norepinephrine as the first-line vasopressor to patients
with refractory hypotension despite adequate fluid resuscitation.

27. • EARLY QUANTITATIVE RESUSCITATION
Lactate clearance–guided therapy (titrating fluids and vasopressors)
became an alternative to invasive SCVO2 monitoring and early goal-
directed therapy.
early recognition of sepsis, administration of antimicrobials,
adequate volume resuscitation, and assessment of the adequacy of
circulation are the important elements that improve outcomes, not any
specific path of resuscitation.

28. • VOLUME RESUSCITATION
an initial 20 to 30 milligrams/kg crystalloid bolus, preferably through
large-bore IVs
• VASOPRESSORS
an approximate 1- to 2-L bolus of lactated Ringer’s or normal saline
solution in a 70-kg adult, although some patients require more or less.
• CENTRAL VENOUS OXYGENATION
measuring continuous SCVO2 with a catheter can aid additional therapy
as outlined in the early goal-directed therapy approach.

29. • LACTATE CLEARANCE
Improvement of 10% or more is associated with improved clinical
outcomes.
• TREAT INFECTION
Give broad-spectrum antibiotics as early as possible for severe sepsis.
42 Combination antibiotic therapy as opposed to monotherapy leads to
improved outcomes, potentially due to higher rates of bactericidal
activity

30. • OTHER THERAPIES: VENTILATION, GLYCEMIC
CONTROL, ACTIVATED PROTEIN C, STEROIDS, AND
OTHER ADJUNCTIVE TREATMENTS
• Hyperglycemia is associated with worsened outcomes in the setting of
sepsis therefore, Glucose control is most important after initial care.
• Hydrocortisone shortens the time to shock reversal in refractory
hemodynamic shock (i.e., requiring more than one vasopressor after
adequate volume restoration) as well as those receiving mechanical
ventilation.