Sepsis is a life-threatening condition that can affect millions each year. It accounts for 15-19% of maternal deaths globally. Physiological changes in pregnancy can both mask and increase susceptibility to sepsis. The pathophysiology of sepsis involves a complex cytokine storm response to infection that leads to widespread endothelial damage, capillary leakage, and multi-organ dysfunction across the cardiovascular, pulmonary, renal and other systems. Prompt recognition and treatment of sepsis is critical to preventing maternal mortality, as early intervention can prevent many sepsis-related deaths.

1. OBSTETRIC SEPSIS
CAUSES AND
PATHOPHYSIOLOGY
DR.MOMINA ZULFEEN

2. Incidence and
significance
• Sepsis is a life threatening condition with millions of people
being effected every year.
• Africa and Asia together account for 80% of maternal
mortality and sepsis accounts for 15-19% of all maternal
deaths
• Incidence of sepsis in pregnancy is 0.3% compared to 0.6%
in general population , although the mortality is much higher
in pregnancy ranging from 15% in severe sepsis to 30% in
septic shock.

3. • Third leading cause of
maternal mortality and the
leading cause of preventable
maternal deaths.
• Its importance can be further
signified by the fact that
early recognition and
treatment can prevent these
deaths and also reduce
perinatal mortality. And
physiological changes in
pregnancy further challenge
early recognition.
The following topic shall discuss causes and
pathophysiology of sepsis to help us recognize
and treat better

4. Definition
• Sepsis = ancient greek word ‘sepein’ = ‘to rot’
• 2016 SCCM definition –
life threatening organ dysfunction caused by a
regulated host response to infection.
• Sepsis exists on a continuum of severity ranging
from infection and bacteremia to sepsis and
septic shock, which can lead to MODS and death

5. Sepsis or no sepsis?
Physiological changes in pregnancy
• Physiological changes in pregnancy pose a
challenge to diagnose sepsis in pregnancy
CHANGES IMPLICATION
↑ C.O, P.R Masks hypovolemia
ECG changes Mimic myocardial ischemia
Leucocytosis Masking leucocytosis of
sepsis
↑ functional residual
capacity, metb. alkalosis
Rapid onset hypoxemia
Immunemodulation Increased susceptibility
Lowered blood urea,
se.creat
Raised serum biomarkers
Difficulty in
standardization of tests

6. Etiology- CAUSES AND RISK
FACTORS
• Genital tract causes: chorioamnionitis, endometritis, septic
abortion, wound infection after vaginal tear, episiotomy, or
Caesarean section
• Renal causes: lower urinary tract infection, pyelonephritis
• Respiratory causes: pneumonia—bacterial, viral; tuberculosis
• Intraperitoneal causes: ruptured appendix, acute appendicitis,
acute cholecystitis, bowel infarction
• Other causes: breast infection, septic pelvic thrombophlebitis,
necrotizing fasciitis, malaria, miliary tuberculosis.

7. Obstetric factors
During pregnancy Amniocentesis
Cervical suture
During vaginal delivery Prolonged rupture of membranes
Prolonged labour
Vaginal trauma
Surgical procedures Episiotomy
Caesarean section
Retained products
Non-obstetric factors Obesity
Diabetes
Immunosuppression
Anaemia
Socioeconomic deprivation
History of pelvic inflammatory disease
Black or other ethnic minority group
RISK FACTORS

8. PATHOGENESIS
• Most of what is known concerning sepsis comes from study
of endotoxin -lipopolysaccharide-LPS
• The lipid A moiety is bound by mononuclear blood
cells,becomes internalized and stimulates release of
mediators and a series of complex downstream events.
Clinical effects manifested by cytokine effects.
• Most of the pathogens produce endotoxins e.g klebsiella ,
some produce exotoxin eg. Clostridium,Staph

9. invasion
• Begins with inflammatory response against microbial endo and
exotoxins
• CD4 T cells and leukocytes stimulated
reaction
• Proinflammatory compounds-TNF-α, Interleukins, cytokines, proteases,
oxidants, bradykinin – result in:
• CYTOKINE STORM - procoagulant activity, gene activation,
receptor regulation and immune suppression
response
• Pathophysiological response to this cascade is selective vasodilation
with maldistribution of blood flow
• Leukocyte and platelete aggregation cause capillary plugging
• Worsening endothelial injury with profound capillary permeability
capillary leakage and interstitial fluid accumulation

12. Endothelial
permeability. The
normal interendothelial
interface is shown in
the left inset.
Cytokines and other
inflammatory
mediators disassemble
the cellular junctions,
resulting
in microvascular leaks
(right).
Courtesy- Williams
24E

13. • CAPILLARY LEAKAGE INITALLY CAUSES
HYPOVOLEMIA, IF CRYSTALLOID GIVEN
• HIGH CARDIAC OUTPUT, LOW SYSTEMIC
VASCULAR RESISTANCE CONDITION
• MYOCARDIAL DEPRESSION
• IF NOT CORRECTED AND NOT RESPONSIVE TO
IONOTROPES, WITH OLIGURIA AND PERIPHERAL
VASOCONSTRICTION
• COLD PHASE
• POOR PROGNOSIS
• CEREBRAL, RENAL AND PULMONARY
DYSFUNCTION
• DEATH
Hemodynamic effects of sepsis syndrome. Values
for normal women at term are shown by dots. With early sepsis,
there is high cardiac output and low vascular resistance. With fluid
resuscitation, cardiac output increases even more, but so does
capillary hydraulic pressure. With continued sepsis, there may be
myocardial depression to further increase capillary hydraulic pressure.
Decreased plasma oncotic pressure (serum albumin [g] ×
6 mm Hg) contributes to interstitial lung fluid and endo/epithelial
leak causes alveolar flooding
LVSWI = left ventricular stroke work
index; PCWP = pulmonary capillary wedge pressure
HEMODYNAMIC CHANGES IN SEPSIS

14. Physiological response and clincial
manifestations
•CONFUSION, SOMNOLENCE, COMA, COMBATIVENESS, FEVER,
HYPOXEMIA
CNS
•TACHYCARDIA, REDUCED C.O, ISCHEMIA, RAISED LVEDP
•HYPOTENSION AND SHOCK
CVS
• PAO2 < 65MMHG , TACHYPNEA, AV SHUNTING, HYPOXEMIA
• ARDS AND PULMONARY HYPERTENSION
PULMONARY
G.I
RENAL
HEMATOLOGICAL
HYPOXIC MUCOSAL INJURY AND GLYCOGENOLYSIS
NAUSEA,VOMINTING,DIARRHEA, JAUNDICE, HYPERGLYCEMIA
DECREASED GFR , PATCHY AND MASSIVE CORTICAL NECROSIS
PRERENAL OLIGURIA , ACUTE KIDNEY INJURY
ALTERED COAGULOPATHY
LEUKOPENIA, THROMBOCYTOPENIA, DIC
OTHERS- CUTANEOUS- ACROCYNOSIS, ERTYTHRODERMA, BULLAE
AND DIGITAL GANGRENE

15. • Depending on degree of injury and inflammatory
response there is a pathophysiological and clinical
continuum- ranging from subtle signs to septic
shock(hypotension unresponsive to IV hydration)

16. Summary
• Sepsis is a continuum from infection to septic
shock.
• Physiological changes in pregnancy mask and also
predispose these women to sepsis.
• Prophylaxis and knowing the risk factors can
prevent most of the sepsis.
• Sepsis involves complex pathophysiology involving
multiple systems, and a background knowledge of
these changes is required to make a diagnosis
• Early recognition and early treatment is the
main stay.

17. THANK YOU FOR
CARING
THANK YOU FOR CARING