Sepsis syndrome is a life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs. It ranges from sepsis to severe sepsis to septic shock. The pathophysiology involves a complex interaction between pathogens and the host's inflammatory response that results in widespread endothelial damage and microvascular thrombosis leading to multiple organ dysfunction. Management involves early recognition, source control, antibiotics, fluid resuscitation and monitoring for organ dysfunction. Despite treatment, sepsis syndrome remains associated with high morbidity and mortality rates.

1. SEPSIS SYNDROME
AIMIEN, Efosa E (MBBS Zaria)
DEPARTMENT OF SURGERY
FMC LOKOJA

2. OUTLINE
• INTRODUCTION
• EPIDEMIOLOGY
• RISK FACTORS
• AETIOLOGY
• PATHOPHYSIOLOGY
• CLINICAL FEATURES
• DIFFERENTIAL DIAGNOSIS
• MANAGEMENT
• COMPLICATIONS
• PROGNOSIS
• CONCLUSION

3. INTRODUCTION
• It is a continuum of a spectrum
• SIRS → Sepsis → Severe sepsis → septic shock → MODS → MOF
• Sepsis is a life threatening organ dysfunction due to dys-regulated immune
response to severe infection
• SIRS is a syndrome characterized by two or more of the following clinical
criteria:
• l. Temperature >38°Cor <36°C
• 2. Heart rate > 90 beats per min. –
• 3. Respiratory rate > 20 breaths/min. or PaCO, < 32mmHg
• 4. WBC>12,000/mm3 or <4,000/mm3or > 10% immature band forms.

4. • Severe sepsis is sepsis accompanied by evidence of organ damage.
• Organ dysfunction – an acute change in total SOFA ( sequential organ
failure assessment)
• Septic shock is defined by persisting hypotension requiring
vasopressors to maintain a mean arterial pressure of 65mmHg or a
serum lactate level > 2mmol/L despite adequate volume resuscitation

5. • MODS: Clinical syndrome characterized by the development of
progressive and potentially reversible physiologic dysfunction in two
or more organs or organ systems that is induced by a variety of acute
insults, including sepsis.

6. SEPSIS RELATED SOFA SCORE
System 0 points 1 point 2 points 3 points 4 points
Respiration
PaO2/FiO2
≥400mmH
g
<400mmHg <300mmHg <200mmHg
With
respiratory
support
<100mmHg
With
respiratory
support
Liver
Bilirubin
level
<1.2mg/dL 1.2-
1.9mg/dL
2-5.9mg/dL 6-
11.9mg/dL
>12mg/dL
Cardiovascu
lar
MAP
≥70mmHg
MAP
<70mmHg
Dopamine
<15
Dopamine
5.1-15
Dopamine
<5
CNS
GCS score
15 13-14 10-12 6-9 <6
Renal
Creatinine
Urine
output
<1.2mg/dL 1.2-
1.9mg/dL
2-3.4mg/dL 3.5-
4.9mg/dL
>5mg/dL

7. EPIDEMIOLOGY
• Severe sepsis and septic shock are contributing factors in >200 000
deaths/year in the US
• The incidence of sepsis has increased over the past 30yrs
• Approximately 2/3 of the cases occur in patients with significant
underlying illness
• Sepsis and septic shock occur at all ages

8. • A sharp increase in the number of cases in patients >50yrs
• Occurs in both sexes
• A study showed Increased risk of septic shock in the black population
due to increased rate of infection
• In sub Saharan Africa, sepsis accounts for ¼ of deaths in children > 1yr

9. RISK FACTORS
• Extremes of age ( <10yrs and > 70yrs)
• Primary diseases
• Immunosuppression
• Major surgery, trauma, burns
• Invasive procedures
• Prolonged hospitalization

10. • Gut: Obstruction, Gangrene, Inflammation, Perforation, Operation
• Peritoneum: Peritonitis, Abscess
• Biliary tract: Cholecystitis, Cholangiris.Operation
• Urinary tract: Infection, Obstruction Instrumentation, Operation
• Female genital: Abortion, Pose partum sepsis,PID tract Operation
• Respiratory: Pneumonia, Mediaslinitis Tract Tracheostomy with JPPV
Vascular system: Venous cuts, Indwelling catheters
• Others: Haemorrhagic or hypvolaemic shock, Burns, Severe injuries
Skin or soft tissue infection, Acute pancreatitis, Gangrene,
lmmunosuppression Agranulocytosis, Leukemia Carcinoma

11. AETIOLOGY
• Most patients with sepsis, a source of infection can be identified
except in immunocompromised patients with neutropenia
• Gram positives commonly implicated include; S. aureaus,
Streptoccocus spp
• Gram negative; E.coli, pseudomonas aeruginosa
• Fungal infections; candida spp
• Endogenous and exogenous sources

12. PATHOPHYSIOLOGY
• The pathophysiology of septic shock is not precisely understood
• A complex interaction between pathogen and host’s immune
response
• The inflammatory cascade is triggered by the presence of
Severe infection
Large damaged tissues (trauma)
Prolonged episodes of hypoperfusion
• Systemic activation of leucocytes and release of potentially damaging
mediators

13. • The normal physiologic response to localized infection;
 activation of host defense mechanism
 Influx of neutrophils and monocytes
 Release of inflammatory mediators, local vasodilation
 Activation of coagulation pathways
• These occur during septic shock but on a systemic scale, leading to
diffuse endothelial disruption, vascular permeability, vasodilation
• Thrombosis of end organ capillaries and consequently damage

14. • TNF-𝛼 and IL-1𝛽; potent pro-inflammatory effect
• IL-6 acts as a pyrogen, stimulates B and T cell proliferation
• IL-8 acts as a neutrophil chemotactic factor, activation and
degranulation of neutrophils
• IL-10 anti-inflammatory effect, inhibits cytokines
• Complement factors promote neutrophil, macrophage and platelet
activation

15. • NO involved in hemodynamic alterations of septic shock
• Arachidonic acid and metabolites augment vascular permeability
• Adhesion molecules enhance neutrophil-endothelial cell interaction
• Inflammatory mediators instigate direct injury to the vascular
endothelium
• Endothelial cells release tissue factor

16. • Activation of extrinsic pathway accelerating thrombin formation
• Fibrinogen to fibrin leads to intravascular clots
• Endotoxins increase the activity of inhibitors of fibrinolysis
• The imbalance among inflammation, coagulation and fibrinolysis
results in DIC and microvascular thrombosis ultimately leading to
MODS

17. MODS
• Respiratory
• Cardiovascular
• Hematological
• Neurological
• Renal
• Hepatic
• Gut

18. CLINICAL FEATURES
• In the early stages of septic shock that is not associated with
hypovolaemia, the patient starts with shivering and malaise and has
warm, dry, flushed skin, moderate hypotension, hyperventilation,
rapid but bounding pulse and fever ranging from 38.3° to 41° C.
Sudden circulatory collapse or restlessness, apprehension and
confusion may be the initial manifestation. As the condition
progresses, the patient may become semicomatose with cold clammy
skin, collapsed superficial veins, pale mucosa with a tinge of cyanosis,
rapid and feeble pulse, severe hypotension and oliguria. J

19. DIFFERENTIAL DIAGNOSIS
• Distributive shock
• Hypovolemic shock
• Obstructive shock
• Acute kidney injury
• ARDS
• DKA
• Toxic shock syndrome

20. MANAGEMENT
• Resuscitation
• Detailed history
• Physical examination
• Investigations
• Treatment

21. • The term Early Goal Directed Therapy has been coined to set targets
for management
• The aims are to improve the haemodynamic state, restore tissue
perfusion (thereby increasing oxygen delivery), administer oxygen,
combat the bacteria and cytokines and eliminate the septic focus

22. • Volume replacement
• Oxygen
• Antibiotics
• Corticosteroids
• Ibuprofen
• Insulin therapy
• Inotropic agents
• Organ involvement treatment
• Surgery
• Monitoring

23. COMPLICATIONS
• ALI/ARDS
• AKI
• DIC
• Ileus
• Septic encephalopathy
• Septic polyneuropathy
• Immunosuppression

24. PROGNOSIS
• Approximately 20-30% of patients with severe sepsis and 40-60% of
patients with septic shock die within 30days
• Age
• Underlying conditions
• Timing and type of antimicrobial therapy
• Offending organism
• Location of patient at time of septic shock onset
• MODS
• It is a strong predictor of both short and long term morbidity and mortality

25. CONCLUSION
• Sepsis syndrome is a continuum which requires early recognition,
early resuscitation, immediate empirical antimicrobial therapy. It is
associated with high morbidity and mortality, thus prevention of
septic shock and/or its complications is better than cure.

26. REFERENCES
• Archampong E, et al. BAJA’s Principle and practice of surgery, 5th Edition.
2015.
• Robbins and Cotran Pathological basis of diseases.
• Williams N et al. Bailey and Love’s Short Practice of Surgery. 25th Ed. 2008
• Parvin K, Micheal C. Kumar and Clark’s Clinical Medicine, 7th Edition. 2009
• Kasper, Fauci, Hauser….et al. Harrison’s principles of internal medicine. 19th
Edition. 2015
• Lecture Notes
• www.emedicine.medscape.com/article/169640