A presentation on Sepsis recognition & management

1. Sepsis
Alan Batt,
Clinical Educator, CCP

2. Sepsis…so what?
• 8,000,000 people per year worldwide die from
sepsis
• Someone dies from sepsis every 2 minutes
• The overall mortality rate for patients severe sepsis
is 35% - approximately 5 times higher than for
STEMI and stroke
• We could save 10-15% with early recognition &
treatment

3. Sepsis…so what?

4. Sepsis…so what?
• For every hour that appropriate antibiotic
administration is delayed, there is an 8% increase in
mortality
• Around 40-50% of patients diagnosed with sepsis in
the ED are admitted via ambulance

5. What is Sepsis?
• It is a profound systemic inflammatory response to
an infection.
• An infection triggers the inflammatory response to
the presence of microorganisms in normally sterile
host tissue

6. SIRS
• Systemic Inflammatory Response Syndrome is a
systemic inflammatory response resulting from
activation of the immune system in response to any
physiologic insult (regardless of the cause).
• Two or more of the following must be present:
• Temp >38 or <36 degrees Celsius
• Heart rate >90
• Resp rate>20 or PaCO2 <32mmhg
• WBC >12,000 or <4,000 or >10% immature
forms

7. Defining Sepsis
• Sepsis is SIRS plus a confirmed or suspected
infection (bacterial, viral, fungal or parasitic).
• It can be a complication following burns,
trauma, surgery, or illness.
• Widespread inflammation, coagulation and
suppression of fibrinolysis occurs.

8. Defining Sepsis
Is the patient history suggestive of new infection?
• Pneumonia
• UTI
• Acute abdomen infection
• Meningitis
• Skin/soft tissue infection
• Bone joint infection
• Wound infection
• Catheter related Blood stream infection
• Endocarditis
• Implantable device infection

9. Adapted from Bone, R. C.,
Sibbald, W. J., & Sprung, C.
L. (1992). The ACCP-SCCM
consensus conference on sepsis
and organ failure. Chest,
101(6), 1481–3.

10. Severe Sepsis
• Severe sepsis is sepsis associated with the
dysfunction of one or more organs.
• Hypotension and hypoperfusion with lactic acidosis
occurs.
• Low blood pressure, high lactate levels and signs of
organ dysfunction are seen.
• The patient may also exhibit chills, tachypnea,
tachycardia, poor capillary refill and petechiae

11. Transitioning to Severe Sepsis
• The Signs of Severe Sepsis
• Arterial hypoxemia (PaO2/FIO2 <300)
• Spo2 <90% on Room air or supplemental O2
• Acute oliguria (UO<.5ml/kg/hr)
• Acutely altered mental status
• Creatinine >2.0
• Bilirubin >2.0
• Thrombocytopenia plt <100,000
• Lactate > 4 mmol/L
• SBP <90 MAP<65 * *These are the classic
indicators to trigger EGDT
• Coagulopathy INR>1.5 PTT>60

12. Septic Shock
• Is acute circulatory failure unexplained by other
causes
• Patient has persistent arterial hypotension SBP<90
[MAP <60] despite adequate volume resuscitation
• Patients don’t always look “sick” until this point

13. SIRS…a progression
Infection → sepsis → severe sepsis → septic shock → MODS
→ death
• Mortality is 50-60% in septic shock
• Early intervention is key
• We need to identify patients quickly and initiate treatment
Bundles
• Bundles are a group of interventions based on scientific
evidence

14. Understanding Sepsis
• Gram neg organisms cause most of adult cases
• E. Coli, Klebsiella, Enterobacter and Psuedomonias
• Gram positive organisms such as staphylococcus,
streptococcus, pneumococcus and enterococcus cause
others (these are associated with invasive devices)
• Viruses, Protozoa, parasites, fungi (Candida) and anaerobic
organisms like Clostridium can also cause sepsis
• Most common sites of origin are
• Skin and wounds, GI, Respiratory, Urinary tract

15. Understanding Sepsis
• Regardless of what caused it, the inflammatory response is
the same and is designed to help the body fight infection
and repair itself.
• SIRS is local inflammatory response that gets out of control.
• An avalanche of chemical mediators is set off that leads to
tissue/organ damage
• Endotoxins from bacteria signal release of cytokines and
other mediators that circulate throughout the body and
cause a number of responses:

16. Understanding Sepsis
• Systemic vasodilation which causes hypotension and
decreased afterload (SVR)
• Increased capillary permeability which causes edema and
decreased preload (CVP)
• Platelet aggregation, fibrin deposits and activation of
clotting cascade cause microcirulatory coagulation & further
tissue hypoxia and other chemicals prevent the breakdown
of these clots

17. Understanding Sepsis
• Multiple organ dysfunction results due to hypoperfusion
caused by the hypotension, hypovolemia and thrombus
formation.
• Hypermetabolic state where the body breaks down fat and
muscle for energy
• As tissue damage progresses, more organs begin to fail
ultimately leading to death
• Early intervention is the key

18. Treating Sepsis
• Goal is to identify patients with Severe Sepsis And
Septic Shock early
&
• Initiate treatment using the Early Goal-Directed
Therapy Protocols and following the Surviving
Sepsis Guidelines

19. Who is at risk?
• Very young and very old
• Those who have a compromised immune system e.g..
Patients on steroids, chemo, pneumonia
• Have wounds or injuries (burns/ trauma)
• Have alcohol or drug addiction
• Any one with intravenous catheters, wound drainage,
urinary catheters etc.
• Those with malnutrition (TPN)
• Pts with no spleen
• Recent surgery
• Diabetics

20. Identifying Risk for Sepsis
• Patients who are admitted to the hospital with serious
diseases are at the highest risk of developing sepsis because
of:
• Their underlying disease
• Their previous use of antibiotics
• The presence of drug-resistant bacteria in the hospital
• The fact that they often require invasive tubes or lines.
Especially if intubated/mechanically ventilated
>48hours

21. Identifying Sepsis
What do these patients look like?
• Fatigued, anorexic
• Fever (or hypothermic)
• Edema
• Tachycardic
• Tachypnoea and or dyspnoea
• Altered mental status (especially >65)
• Hypotensive
• Skin may be flushed, warm and dry or cool and mottled

22. Identifying Sepsis
• Look for:
• Low SpO2, abnormal blood gases
• CO2 may decrease as an early attempt to
compensate for lactic acidosis
• Low urine output, creatinine >2
• Abnormal WBC (high or low)
• Hyperglycemia (serum glucose elevates as part of the
stress response)
• Abnormal coagulation studies
• High bilirubin
• Key signs are SBP <90 or lactate >4
• Cultures can help identify infection and source

23. Case 1
• 78 year old male
presents awake,
confused, and in
moderate distress
• Emesis in basin at
bedside
• When asked, patient
states “I’m weak, and
don’t feel well”
• Skin is pale, dry

24. Case 1
• General Impression:
Patient responds to your
questions. GCS = E-4, V-4,
M-6
• Airway: Patent, no stridor
• Breathing: tachypneic,
tidal volume slightly
shallow
• Circulation: tachycardic
and weak radial pulse,
capillary refill 4 seconds
• Skin dry, pale, warm

25. Case 1
• S: Son states that patient is
“slightly more confused”
than normal over the past
24 hours. Patient states he
“feels sick and weak”, has
abdominal pain, and is
vomiting.
• A: Aspirin
• M: Insulin
• P: Dementia, IDDM
• L: light breakfast 2 hrs ago
• E: Progressively worse
nausea and vomiting over
past day.
• Vital signs: HR = 88, RR = 26
normal TV, BP = 96/52,
SpO2 = 98% room air up to
100% with cannula
• Lung sounds: slight
expiratory wheezing and
crackles in middle right lobe
• Skin dry and warm to touch
• Mucus membranes dry, skin
turgor poor
• Oral temperature = 100.3°F
• Good tidal volume

26. Case 1

27. Case 1

28. Case 1
• Differential diagnoses?
• Treatment plan?
• Treatment priorities?

34. Resuscitation Bundle:
Tasks in the First 3 - 6 Hours
1. Measure serum lactate
2. Obtain Blood cultures prior to antibiotic administration
3. Administer broad spectrum antibiotic within 3 hrs if in ED (1 hr
if inpatient)
4. In event of hypotension and/or lactate >4
a. Deliver initial fluid bolus of 20cc/kg crystalloid or
equivalent
b. Vasopressors for hypotension not responsive to initial
fluid to maintain MAP > 65
5. For persistent hypotension despite fluid resuscitation (septic
shock) and/or lactate >4mmol/L
a. Achieve CVP >8
b. Achieve ScvO2 > 70% or SvO2 > 65%

35. NNT
• PCI in STEMI = 45-90
• TXA in trauma = 67
• Aspirin in AMI = 42
• CPAP for pulmonary oedema = 13
• Sepsis Six = 4.6!
• Defibrillation in cardiac arrest = 2.5

36. Management Bundle
First 24 hours
Consider low dose steroids for septic shock according to a
standard policy
• Or document why it is not appropriate
Consider human activated protein C (XIGRIS) according to a
standard policy
• Or document why it is not appropriate
Maintain glucose control >120 but <180
Maintain median inspiratory plateau pressures <30 for
mechanically ventilated patients

37. Treating Sepsis
• Rapid placement of a central venous line is priority
• IJ or SC
• To measure CVP and ScVO2
• Fluid challenges are given to
• CVP 8-12 (15-18 if mech vent)
• SBP >90 or MAP >65
• UO > 0.5ml/kg/hr
• Levophed is started if hypotension is unresponsive to fluid
• For ScVo2 <70
• If Hgb <7 consider transfusing blood to goal of Hgb 7-9g/dl
• Dobutamine is started if ScVo2 still <70
• O2 therapy or intubation/ventilation if needed

38. Treating Sepsis
• Transfer to ICU ASAP
• Central line is priority if not already in
• Arterial line may be needed to monitor blood
pressure
• Continue sepsis protocols
• Fluid for CVP <8 MAP <65
• Vasopressor if not fluid responsive
• Inotrope and transfusion for ScVO2 <70 and Hg <7
• Monitor CVP, ScVO2, lactate every 30 min
• Until goals met

39. Treating Sepsis
• Continuing Treatment
• Airway Ventilator management
• HOB is at 30 degrees & mouth care to prevent VAP
• DVT prophylaxis
• Plateau pressures < 30
• Weaning assessed daily
• Consideration of hydrocortisone 50mg IV Q 6 hrs for 7
days
• Strict glucose control >120 to <180 with protocol or
sliding scale (median glucose of 140)
• Consider Xigris (Activated protein C)

40. Treating Sepsis
• Other Considerations
• Nutrition is important due to the hyper-metabolic state
• Skin care and assessment to prevent breakdown
• Sedation, analgesia, paralytics, must be used cautiously
to optimize ventilation yet prevent prolonged intubation
• RAAS / Pain scales are used to measure patients
progress
• Strict I/O Use foley catheters only if truly necessary

41. Case 2
• 44 y/o female
• Lying in bed
• Opens eyes when you
say “hello”
• Seems confused
• Skin pale, slightly moist

42. Case 2
• Conscious, alert to verbal
stimuli, confused to
person, place, time
• Airway: open
• Breathing: normal rate
and tidal volume
• Circulation: weak,
tachycardic radial pulse,
cap refill 4 seconds
• Skin warm, slightly moist

43. Case 2
• S: Patient complains of
weakness. Husband
reports a 3 day historyof
worsening AMS, patient
normally conscious, alert,
and oriented.
• A: NKDA
• M: Glyburide, propranolol,
nifedipine
• P: AMI 3 years prior, HTN,
Type II DM, recent UTI
• L: Breakfast this morning
• E: No known events that
precipitated AMS
• Vital signs: HR = 92, BP =
88/42, RR = 20 and regular
tidal volume, SpO2 = 96%
RA up to 100% with oxygen
4 lpm via cannula
• Mucus membranes dry,
poor skin turgor
• Skin warm to touch, slightly
moist
• Temperature = 98.8°F via
oral thermometer

44. Case 2

45. Case 2

46. Case 2
• Differential diagnoses?
• Treatment plan?
• Treatment priorities?

47. Highlights from the Guidelines
• Supplemental oxygen
• Sepsis causes an imbalance between tissue oxygen
supply and demand. Adequate tissue oxygenation is
essential to the treatment of a patient with sepsis.
• Continuous pulse oximetry is performed. Supplemental
oxygen is utilized to maintain the oxygen saturation ≥
94%.

48. Antibiotic Therapy
• Intravenous antibiotic therapy should be started within the
first hour of recognition of severe sepsis, after appropriate
cultures have been obtained.
• Broad-spectrum agents are ordered initially.
• This treatment should be reevaluated after culture results
are available.

49. Fluid Therapy
• Two large bore peripheral catheters should be inserted
initially and a central venous catheter should be placed
ASAP.
• Fluid resuscitation (the number one priority) is
accomplished with either crystalloids or colloids. Neither
has been proven to be better than the other.
• The target is to maintain a CVP between 8-12 mmHg, with a
higher CVP recommended for a mechanically ventilated
patient. (due to positive pressure ventilation)
• RASP trial ongoing comparing Ringers v Albumin

50. Vasopressor Therapy
• Once fluid resuscitation has been accomplished, if adequate
blood pressure and organ perfusion has not been restored,
vasopressor therapy should be started.
• Norepinephrine is the initial vasopressor of choice.
• Phenylephrine may be considered.
• An arterial catheter should be placed as soon as possible for
monitoring of arterial pressures and blood gases.
• Vasopressin may be added in patients with refractory shock
despite adequate fluid resuscitation and high dose
vasopressor agents.

51. Inotropic Therapy
• In patients with low cardiac output despite adequate fluid
resuscitation, dobutamine may be used to increase cardiac
output.
• If the blood pressure is low, it is used in combination
with a vasopressor.
• ScVO2 of >70% is the goal.
• Blood transfusion should be considered if Hgb is less than 7
to optimize the oxygen carrying capacity of the blood.

52. Steroids
• IV corticosteroids (hydrocortisone 200-300 mg/day for 7
days in 3 or 4 divided doses or by continuous infusion) are
recommended in patients in septic shock who, despite
adequate fluid replacement, require vasopressor therapy to
maintain an adequate blood pressure.
• Corticosteroids must be started when the patients BP is
refractory to vasopressor therapy.
• Once vasopressor therapy is no longer required, steroid
therapy can be weaned.

53. Blood Product Administration
• The recommendation is to transfuse packed red blood cells
when the hemoglobin decreases to < 7 g/dl.
• This optimizes the oxygen carrying capacity of the
patients blood.
• Platelets may be needed for those patients with a platelet
count <50,000 mm3.

54. Glucose Control
• Hyperglycemia and insulin resistance occur in severe sepsis.
• Tight glucose control with insulin is used to maintain blood
glucose 6.5-10 mmol/L [120-180 mg/dl]
• Hypoglycemia has shown to cause higher mortality in critical
patients.
• Insulin protocols should be followed.

55. Mechanically Ventilated Patients
• Maintain Inspiratory Plateau Pressure < 30 cm H2O)
• Patients with sepsis are at increased risk for developing
acute respiratory failure. Most patients with severe sepsis
and septic shock will require mechanical ventilation.
• Nearly 50% of patients with severe sepsis will develop acute
lung injury (ALI (acute respiratory distress syndrome).
• High tidal volumes along with high plateau pressures should
be avoided.
• The goal is to maintain a tidal volume of 6mL/kg lean
body weight in addition to end-inspiratory plateau
pressure < 30 cm H2O.

56. Bottom line?
• Everyone with suspected sepsis needs to get to
hospital…quickly!
• Everyone should get high flow oxygen – regardless
of SpO2 reading!
• Everyone should get fluids if they’re in shock
• Pre-alert the ED and mention the word “sepsis”
• Sepsis kills – let’s stop it – the simple stuff saves
lives

57. More information
• http://www.survivingsepsis.org
• http://www.uksepsis.org/
• http://sepsistrust.org/
• http://www.cdc.gov/sepsis/