OBSTETRIC SEPSIS

CAUSES AND PATHOPHYSIOLOGY

DR.MOMINA ZULFEEN

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.

• 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

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

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.creatRaised serum biomarkers

Difficulty in standardization of tests

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.

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

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

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

Endothelial permeability. The normal interendothelialinterface is shown in the left inset. Cytokines and otherinflammatory mediators disassemble the cellular junctions, resultingin microvascular leaks (right).Courtesy- Williams 24E

• 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

• DEATHHemodynamic 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

Physiological response and clincialmanifestations

•CONFUSION, SOMNOLENCE, COMA, COMBATIVENESS, FEVER, HYPOXEMIACNS

•TACHYCARDIA, REDUCED C.O, ISCHEMIA, RAISED LVEDP

•HYPOTENSION AND SHOCKCVS

• PAO2 < 65MMHG , TACHYPNEA, AV SHUNTING, HYPOXEMIA

• ARDS AND PULMONARY HYPERTENSIONPULMONARY

G.I

RENAL

HEMATOLOGICAL

HYPOXIC MUCOSAL INJURY AND GLYCOGENOLYSISNAUSEA,VOMINTING,DIARRHEA, JAUNDICE, HYPERGLYCEMIA

DECREASED GFR , PATCHY AND MASSIVE CORTICAL NECROSISPRERENAL OLIGURIA , ACUTE KIDNEY INJURY

ALTERED COAGULOPATHYLEUKOPENIA, THROMBOCYTOPENIA, DIC

OTHERS- CUTANEOUS- ACROCYNOSIS, ERTYTHRODERMA, BULLAE AND DIGITAL GANGRENE

• 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)

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.

THANK YOU FOR CARING

THANK YOU FOR CARING