2. EPIDEMILOGY
• The incidence of sepsis and the number of sepsis-related
deaths are increasing because of an increased use of
immunosuppressive medications. The incidence varies by
race and sex. The highest incidence is among Black males.
The incidence also shows seasonal variation, with the
highest number of cases in winter, probably because of the
increased prevalence of respiratory infections during this
season. Older patients (≥65 years) account for most (60-
85%) sepsis cases, attributable to multiple comorbidities and
frequent hospitalizations.
3. • A recent scientific publication estimated that in 2017 there were 48.9 million
cases and 11 million sepsis-related deaths worldwide, which accounted for
almost 20% of all global deaths .
• In 2017, almost half of all global sepsis cases occurred among children, with
an estimated 20 million cases and 2.9 million global deaths in children under
5 years of age .
• Regional disparities in sepsis incidence and mortality exist; approximately
85% of sepsis cases and sepsis-related deaths worldwide occurred in low-
and middle-income countries .
• Health care-associated infections are one of the most frequent types of
adverse event to occur during care delivery and affect hundreds of millions
of patients worldwide every year.
4. PATHOGEN
•The predominant infectious organisms that
cause sepsis have changed over the years.
Gram-positive bacteria are the most common
etiologic pathogens, although the incidence of
gram-negative sepsis remains substantial. The
incidence of fungal sepsis has been rising with
more patients on immunosuppressive
therapies and more cases of HIV infection. In
approximately half of sepsis cases, the
organism is not identified (culture-negative
sepsis)
7. •Septic shock
“a subset of sepsis in which particularly profound
circulatory, cellular, and metabolic abnormalities are
associated with a greater risk of mortality than with
sepsis alone”, identified clinically by a vasopressor
requirement to maintain a MAP ≥ 65 and serum lactate
≥ 2 mmol/L in the absence of hypovolemia.
9. • Multiple organ dysfunction
syndrome (MODS)
is characterized by progressive
organ dysfunction in a severely
ill patient, with failure to maintain
homeostasis without
intervention such as pressors or
IV fluids
10. • Pseudo sepsis
is defined as fever, leukocytosis, and hypotension due to
causes other than sepsis. Examples might include the clinical
picture seen with salicylate intoxication, methamphetamine
overdose, or bilateral adrenal hemorrhage.
11. clinical tool to aid in the recognition of sepsis and septic
shock
SIRS
SOFAqSOFA
NEWS 2
1- Systemic inflammatory response
syndrome
2- Sequential organ failure
assessment
3- quick sofa
4- National early warning score
12.
13.
14.
15.
16.
17.
18.
19. Sources of sepsis
• Skin/soft tissue: Necrotizing fasciitis, cellulitis, myonecrosis, or gas
gangrene
• Wound infection: Inflammation, edema, erythema, discharge of
pus, with positive Gram stain and culture results from incision and
drainage or deep cultures
• Upper respiratory tract: Pharyngitis, tonsillitis, or sinusitis
• Lower respiratory tract: Pneumonia, empyema, or lung abscess
23. Risk Factors
ICU admission with subsequent nosocomial infection
Bacteremia
Advanced age (≥65 years)
Immunosuppression
Community-acquired pneumonia
Previous hospitalization and antibiotic therapy in the preceding 90 days
Genetic factors - Defects of cellular and humoral immunity (low or absent antibody
production,T cells, phagocytes, natural killer cells, complement)
Urosepsis due to benign prostatic hypertrophy (BPH) in older males or complicated UTI
Major trauma and burn injuries
24. Clinical picture
General
signs and
symptom
s of
sepsis
may
include
the
following
Fever, with
or without
shaking
chills
(temperatu
re >38.3ºC
or < 36ºC)
Impaired mental
status (in the
setting of fever
or
hypoperfusion)
Increased
breathing
rate (>20
breaths/min)
resulting in
respiratory
alkalosis
Warm or
cold skin,
depending
on the
adequacy of
organ
perfusion
and dilation
of the
superficial
skin vessels
Hypotension
requiring
pressor
agents to
maintain
systolic
blood
pressure
above 65
mm Hg
25.
26.
27. Special considerations
• Elderly patients may present with peritonitis and may not experience
rebound tenderness of the abdomen.
• Elderly individuals, persons with diabetes, and patients on beta-blockers
may not exhibit an appropriate tachycardia as blood pressure falls.
• Younger patients develop a severe and prolonged tachycardia without
hypotension until acute decompensation occurs.
• Patients with chronic hypertension may develop critical hypoperfusion at a
blood pressure that is higher than in healthy patients (ie, relative
hypotension).
• An acute surgical abdomen in a pregnant patient may be difficult to
diagnose. The most common cause of sepsis in pregnancy is urosepsis.
29. GeneralWork up for sepsis
CBC
CHEMEISTRY AND ELECTROLYTES
CO AGULATION PROFILE
LACTATE
PROCALCITONINE
BLOOD GASES
CRP
URINE ANALYSIS &CULTURE
BLOOD CULTURE
CHEST X RAY
ABDOMINAL US IF NEEDED
CRP
30. Unique laboratory findings
• Leukocytosis (WBC count >12,000/µL) or leukopenia (WBC count <
4000/µL)
• Normal WBC count with greater than 10% immature forms (left shift
with bandemia)
• Hyperglycemia (plasma glucose level >140 mg/dL or 7.7 mmol/L) in
the absence of diabetes
• Plasma C-reactive protein level of more than 2 standard deviations
above the reference value
• Arterial hypoxemia (PaO 2/FiO 2 ratio < 300 mm Hg)
• Acute oliguria (urine output < 0.5 mL/kg/hour for at least 2 hours
despite adequate fluid resuscitation)
• Creatinine increase >0.5 mg/dL or 44.2 mmol/L
• Coagulation abnormalities (INR >1.5 or PTT >60 seconds)
31. • Thrombocytopenia (platelet count < 100,000/µL)
• Hyperbilirubinemia (plasma total bilirubin >4 mg/dL or 70
mmol/L)
• Adrenal insufficiency (eg, hyponatremia, hyperkalemia) and
euthyroid sick syndrome can also be found in sepsis.
• Hyperlactatemia (serum lactate >2 mmol/L) can result from
organ hypoperfusion in the presence or absence of
hypotension and indicates a poor prognosis. A serum lactate
level of 4 mmol/L or more (especially arterial lactate)
indicates septic shock.
• Plasma procalcitonin and presepsin elevation is associated
with bacterial infection and sepsis
32. • Imaging modalities should be focused on areas of clinical concern,
based on the history and physical examination, and may include the
following:
• Chest radiography (to rule out pneumonia and diagnose other
causes of pulmonary infiltrates)
• Chest CT scanning (to further evaluate for pneumonia or other lung
pathology)
• Abdominal ultrasonography (for suspected biliary tract obstruction)
• Abdominal CT scanning or MRI (for assessing a suspected non-
biliary intra-abdominal source of infection or delineating intrarenal and
extrarenal pathology)
• Site-specific soft tissue imaging, including ultrasonography, CT
scanning, or MRI (to assess for possible abscess, fluid collection, or
necrotizing skin infection)
• Contrast-enhanced CT scanning or MRI of the brain/neck (to assess
for possible masses, abscess, fluid collection, or necrotizing infection)
35. BASICS OF SEPSIS MANGEMENT
AIRWAY FLUID
ANTIBIOTIC
VASOPRES
SORS
36. Management
• Early aggressive medical therapy is indicated in patients
with suspected sepsis
• AIRWAY
High-flow nasal cannula (HFNC): in sepsis-induced hypoxemic respiratory
failure, HFNC is recommended over non-invasive positive pressure ventilation
Intubation: low tidal volume strategy and upper plateau pressure of 30 cm H2O;
in ARDS, consider using higher PEEP
V-V ECMO can be considered if conventional mechanical ventilation fails
37. Fluid resuscitation
•Patients with sepsis should receive an
intravenous balanced crystalloid at 30
mL per kg within the first three
hours.21 Infusing an initial 1-L bolus
over the first 30 minutes is an accepted
approach.The remainder of fluid
resuscitation should be given by repeat
bolus infusions
38. ANTIBIOTIC
• Multiple studies indicate that early initiation of appropriate antibiotic
therapy is associated with improved clinical outcomes.The precise timing
is controversial. SSC guidelines recommend administration of antibiotics
within the first hour.
• In patients with possible sepsis without shock, consider investigating for
other causes for up to 3 hours before starting antimicrobial therapy
(adjusted from 1 hour from previous guidelines)
39.
40.
41.
42.
43. vasopressor
In most patients, norepinephrine is the first-line vasopressor, followed by
vasopressin, then epinephrine
• In patients with cardiac dysfunction, use norepinephrine as first line then
dobutamine or epinephrine alone
• Vasopressor therapy clearly improves survival in these patients and
should be started within the first hour following initial fluid
resuscitation. Failure to initiate early vasopressor therapy in patients with
septic shock increases mortality rates by 5% per hour of delay
44. Goal of initial resuscitation first 6 hours
Central venous pressure 8-12
mmhg
Venous oxygen saturation 65 %
ScvO 2 >70 %
Map more than 65 mmhg
Urine out put > 0.5mlkgh
50. Post-sepsis syndrome (PSS) is a condition that
affects up to 50% of sepsis survivors.
Physical Psychological
51. Physical –
Difficulty sleeping, either difficulty getting to sleep or staying
asleep
• Fatigue, lethargy
• Shortness of breath, difficulty breathing
• Disabling muscle or joint pain
• Swelling in the limbs
• Repeat infections, particularly in the first few weeks and months
following the initial bout of sepsis
• Poor appetite
• Reduced organ function, eg kidney, liver, heart
• Hair loss
• Skin rash
52. • Psychological or emotional
• Hallucinations
• Panic attacks
• Flashbacks
• Nightmares
• Decreased cognitive (mental) functioning
• Loss of self-esteem
• Depression
• Mood swings
• Difficulty concentrating
• Memory loss
• Post-traumatic stress disorder (PTSD)
53. TAKE HOME MESSAGE
Calculate NEWS to detect subtle cases of occult septic shock.
Less saline, more Ringer’s, even if acute heart failure, especially in renal failure and severe acidosis.
Norepinephrine whenever MAP <65 – earlier rather than later.
Early antibiotics (within 1hr of the diagnosis rather than 1 hour of arrival at ED), given over 5 minutes (except
vancomycin over 30 minutes), chosen wisely according to local antibiograms.
Use a combination of MAP, GCS, urine output, initial lactate, capillary refill time, POCUS IVC to guide initial fluid
resuscitation, individualized to each patient.
If the lactate is rising despite resuscitative efforts call your intensivist. Early to ICU is preferable, but remember that
capillary refill time may be as good, or even better than lactate at guiding resuscitation.
Consider vasopressin and hydrocortisone if a MAP of 65 cannot be maintained with 35mcg/min norepinephrine and
ongoing fluid resuscitation.
