Professional Documents
Culture Documents
• HEMORRHAGE
• ANAPHYLAXIS
• SEPSIS
• AFE
• UTERINE INVERSION
• CARDIAC ARRHYTHMIA
• ACUTE HEART FAILURE
• CEREBRAL POST ICTAL (EPILEPSY)
• ECLAMPSIA CEREBROVASCULAR ACCIDENT
AMNIOTIC FLUID EMBOLISM (AFE)
BACTERIAL ANTIGENS MAY PLAY A ROLE INSTEAD OF, OR IN ADDITION TO, FETAL
ANTIGENIC MATERIAL. ABNORMAL ACTIVATION OF HUMORAL AND IMMUNOLOGICAL
PROCESSES AND RELEASE OF VASOACTIVE AND PROCOAGULANT SUBSTANCES, SIMILAR TO
THE SYSTEMIC INFLAMMATORY RESPONSE SYND. BACTERIAL ANTIGENS MAY PLAY A ROLE
INSTEAD OF, O IN ADDITION TO, FETAL ANTIGENIC MATERIAL
PATHOGENESIS
• AS A RESULT, PULMONARY PRESSURES USUALLY BECOME ACUTELY
ELEVATED, THE RIGHT VENTRICLE (RV) PRESSURE INCREASES, AND THE RV
BEGINS TO FAIL.
• MECHANICAL OBSTRUCTION OF PULMONARY ARTERIES FROM CELLULAR
COMPONENTS OF AND DEBRIS IN AMNIOTIC FLUID PLAYS NO ROLE IN THIS
RV FAILURE .
• RV FAILURE MAY SUBSEQUENTLY LEAD TO LEFT VENTRICLE (LV) FAILURE
AND SYSTEMIC HYPOTENSION.
• LV FAILURE MAY ALSO BE A DIRECT EFFECT OF HYPOXIC INJURY TO THE
LEFT VENTRICLE, RELEASE OF MATERNAL INFLAMMATORY MEDIATORS, OR
A DIRECT DEPRESSANT EFFECT OF AMNIOTIC FLUID ON THE MYOCARDIUM
PATHOGENESIS
• ACUTE PULMONARY HYPERTENSION ALSO RESULTS IN SEVERE
VENTILATION/PERFUSION MISMATCHING, CARDIOGENIC PULMONARY
EDEMA, AND HYPOXEMIC RESPIRATORY FAILURE LATER,
NONCARDIOGENIC PULMONARY EDEMA CAN OCCUR IN SOME
PATIENTS.
• ACTIVATION OF FACTOR VII AND PLATELETS AND RELEASE OF
INFLAMMATORY MEDIATORS LIKELY ACTIVATES THE COAGULATION
CASCADE, RESULTING IN (DIC) AND, IN TURN, ISCHEMIC DISTAL
ORGAN DYSFUNCTION AND MULTI-ORGAN FAILURE.
• HEMORRHAGE FROM DIC FURTHER CONTRIBUTES TO HEMODYNAMIC
INSTABILITY FLUID AND AMNIOTIC FLUID DEBRIS IN THE SPUTUM AND
ALVEOLAR SPACES OF THESE PATIENTS
RISK FACTORS
THE WHO ESTIMATED THAT THE GLOBAL PREVALENCE OF MATERNAL SEPSIS IS 4.4%
AMONG LIVE BIRTHS, WITH AN INCIDENCE OF 9–49 PER 100 000 DELIVERIES IN HIGH
INCOME COUNTRIES DEPENDING ON THE DEFINITION USED AND POPULATION STUDIED.
SEVERAL STUDIES FROM DEVELOPED COUNTRIES HAVE SHOWN THAT THE RATE OF
MATERNAL SEPSIS HAS BEEN INCREASING IN THE LAST DECADE, WITH HIGH
MORTALITY RATES.
THE DEFINITION OF SEPSIS
FURTHER SUBSETS OF PATIENTS WHO HAVE “SEPTIC SHOCK” INCLUDE THOSE WHO
REQUIRE VASOPRESSORS TO MAINTAIN A MEAN ARTERIAL PRESSURE OF AT LEAST 65 MM
HG AND WHO HAVE A SERUM LACTATE LEVEL OF AT LEAST 2 MMOL/L.
PATIENTS WHO MET THESE CRITERIA AND HAD ORGAN DYSFUNCTION WERE CLASSED
AS HAVING “SEVERE SEPSIS”, AND PATIENTS WHO HAD HYPOTENSION WHICH DID NOT
RESPOND TO FLUID RESUSCITATION WERE CLASSED AS HAVING “SEPTIC SHOCK”.
“SEPSIS ONSET IN PREGNANCY CAN BE INSIDIOUS, AND PATIENTS MAY APPEAR
DECEPTIVELY WELL BEFORE RAPIDLY DETERIORATING WITH THE
DEVELOPMENT OF SEPTIC SHOCK, MULTIPLE ORGAN DYSFUNCTION SYNDROME,
OR DEATH .THE OUTCOME AND SURVIVABILITY IN SEVERE SEPSIS AND SEPTIC
SHOCK IN PREGNANCY ARE IMPROVED WITH EARLY DETECTION, PROMPT
RECOGNITION OF THE SOURCE OF INFECTION, AND TARGETED THERAPY.”
- BARTON & SIBAI, 2012
MATERNAL SEPSIS
MATERNAL SEPSIS IS THE MAIN CAUSE OF MATERNAL DEATH AND A MAJOR CONTRIBUTOR
TO SEVERE MATERNAL MORBIDITY WORLDWIDE, ACCOUNTING FOR 11% OF MATERNAL
DEATHS
WORLDWIDE AND IS THE THIRD MOST COMMON DIRECT CAUSE OF MATERNAL DEATH.
MATERNAL SEPSIS IS CURRENTLY THE THIRD OR FOURTH LEADING CAUSE OF MATERNAL
MORTALITY IN THE USA,
ACCOUNTING FOR 13% OF ALL MATERNAL DEATHS WITH A CAUSE SPECIFIC MATERNAL
MORTALITY RATIO OF 2.2 DEATHS PER 100 000LIVE BIRTHS
MATERNAL SEPSIS
Infection
was the third leading cause of pregnancy-
related death between 2011-2016.
Source: CDC, 2019
PATHOPHYSIOLOGY
THE PATHOPHYSIOLOGY CORE ISSUE IS A MULTIFACETED HOST RESPONSE TO AN
INFECTING PATHOGEN THAT MAY BE SIGNIFICANTLY AMPLIFIED BY
ENDOGENOUS FACTORS.
THE “SEPSIS 1” AND “SEPSIS 2” FOCUSED SOLELY ON INFLAMMATORY EXCESS.
SEPSIS IS NOW RECOGNIZED TO INVOLVE EARLY ACTIVATION OF BOTH PRO/AND
ANTI-INFLAMMATORY RESPONSES, ALONG WITH MAJOR MODIFICATIONS IN
NONIMMUNOLOGIC PATHWAYS SUCH AS CARDIOVASCULAR, NEURONAL,
AUTONOMIC, HORMONAL, BIOENERGETIC, METABOLIC, AND COAGULATION, ALL
OF WHICH HAVE PROGNOSTIC SIGNIFICANCE.
PATIENTS WITH SEPSIS CAN HAVE CLINICAL PRESENTATIONS IN VARIOUS
SYSTEMS, INCLUDING RESPIRATORY, CARDIOVASCULAR, HEPATIC AND
GASTROINTESTINAL, RENAL, HEMATOLOGICAL, ENDOCRINOLOGICAL, AND
CENTRAL NERVOUSSYSTEMS.25 MATERNAL SEPSIS MAY CAUSE INTRA-
AMNIOTIC INFECTION, WHICH RESULTS IN
(1) PREMATURE RUPTURE OF MEMBRANES OR PRETERM LABOR OR BIRTH;
(2) CEREBRAL WHITE MATTER DAMAGE OR CEREBRAL PALSY OR
NEURODEVELOPMENT ALDELAY
(3) STILLBIRTH
(4) EARLY- OR LATE-ONSET SEPSIS
(5) PERINATAL DEATH.
CAUSES, RISK FACTORS, AND MICROORGANISMS
CAUSES AND RISK FACTORS
CHANGES IN MATERNAL IMMUNE RESPONSES OCCUR DURING PREGNANCY TO
PROTECT THE UNBORN FETUS FROM REJECTION.
THESE CHANGES MAY PREDISPOSE PREGNANT PATIENTS TO THE DEVELOPMENT
OF INFECTIONS. SEPSIS MAY BE DUE TO OBSTETRIC OR NON-OBSTETRIC CAUSES.
THE OBSTETRIC CAUSES INCLUDE UTERINE INFECTION, SUCH AS
CHORIOAMNIONITIS AND ENDOMYOMETRITIS, SEPTIC ABORTION, AND WOUND
INFECTION. SEPSIS MAY FOLLOW INVASIVE PROCEDURES SUCH AS
AMNIOCENTESIS, CHORIONICVILLUS SAMPLING, CERVICAL CERCLAGE, OR
PERCUTANEOUS UMBILICAL BLOOD SAMPLING.
IN A FRENCH STUDY, THE MOST COMMON SOURCE OF BACTEREMIA WAS
CHORIOAMNIONITIS(47%). THE NON-OBSTETRIC CAUSES OF SEPSIS INCLUDE
PYELONEPHRITIS AND PNEUMONIA
RISK FACTORS ASSOCIATED WITH MATERNAL
SEPSIS
• Definition: Set of specific vital sign and physical exam findings that prompt a bedside
evaluation and/or work-up
• Goal: Prompt and timely identification and treatment of women developing critical illness
“An effective early-warning system should facilitate timely diagnosis and treatment, and thereby limit
the severity of any morbidity.”
– Mhyre et al., 2014
EXAMPLE
1. Simplicity
2. Balance between sensitivity and specificity
EXAMPLE
MATERNAL SEPSIS
STANDARDIZED SEPSIS WORK-UP CRITERIA
EXAMPLE
The ongoing assessment recommendations are based on ‘Time Zero.’ Once the patient triggers a positive Initial Sepsis Screen, ‘Time Zero’ will start. A review of
nursing technique for collecting a urine sample from a Foley catheter is provided in Appendix E of the Toolkit.
Source: Adapted from Gibbs et al., 2020, CMQCC Maternal Sepsis Toolkit
EXAMPLE
Any 2 abnormalities:
• Maternal temperature > 38.9o C or < 34o C
• Bands ≥10%
56
Maternal Septic Shock Diagnosis
Sources: Barton & Sibai, 2012; Rhodes et al., 2017; Sepsis Alliance, 2019
Maternal Sepsis: Standardized Sepsis
Management Algorithm
Maternal Sepsis Management
Antibiotics:
Sources: Bauer et al., 2018; Padilla & Palanisamy, 2017; Rhodes et al., 2017
Antibiotic Regimens by Source of Infection
(excerpted from CMQCC Maternal Sepsis Toolkit)
Hospital-acquired pneumonia High mortality risk patients: double coverage for pseudomonas (beta lactam
plus an aminoglycoside or a quinolone) and MRSA coverage with vancomycin
or linezolid
Fluid Management:
For sepsis-induced hypoperfusion:
• Administer initial 30cc/kg bolus of IV crystalloids (1-2L minimum) within 3 hours of
diagnosis
• Fluid approach requires clinical judgement & may require adjustment based on clinical situation
• Highest risk for fluid overload in patients with preeclampsia, cardiovascular disease
• Close monitoring of the patient with obesity
• Reevaluate patient’s status after IV bolus
• Failure to respond higher level care/ICU
Sources: Plante, 2016; Rhodes et al., 2017; SMFM, 2019; Adams et al., 2017; Taylor et al., 2018
Maternal Septic Shock Management
Source Control:
• After cultures obtained and antibiotics started
• Drainage, evacuation, removal, or other clinically appropriate
procedure
Source: SMFM, 2019; Gibbs et al., 2020, CMQCC Maternal Sepsis Toolkit
Maternal Sepsis Management
Fetal Considerations:
• Antenatal steroids are considered safe in sepsis
• Consider per usual guidelines for fetal lung maturity
• “…in the context of maternal critical care, antenatal
corticosteroids are not contraindicated, even in the
setting of sepsis.”
VTE Prophylaxis:
• Provision of pharmacologic prophylaxis may be with
unfractionated heparin (UFH) or low-molecular weight
heparin (LMWH)
Continued Management
(for patients not requiring ICU admission):
• Antibiotics – narrow spectrum once sensitivities available
• Fluids – after correction of hypoperfusion, give maintenance fluids only:
≈100-150 cc/hr (include PO fluids)
• Check labs every 6-8 hrs for first 24 hrs after diagnosis
• Continuous pulse oximeter for first 24 hrs after diagnosis
• Strict I/Os – hourly for first 12 hrs, and then q 2 hrs if normal
• Monitor vital signs per unit protocol
• Delivery timing based on routine obstetric indications
Maternal Sepsis Management
• Conduct a multidisciplinary
review of all cases of
septic shock and/or
admission to higher level
of care
• Monitor process metrics
and outcomes in a
standardized fashion
• Debrief all cases of
maternal sepsis for systems
issues and compliance
with protocols
Conclusions & Clinical Pearls
• All team members should feel empowered to speak up, and maintain a
high index of suspicion for maternal sepsis
• Timing is critical cultures should be taken and antibiotics started
within 1 hour of suspicion of sepsis
• Antenatal steroids are NOT contraindicated
• Follow-up on interventions is critical escalate care if there is no
response
Move fast during the golden hour to save lives: fluid resuscitation should be
initiated rapidly for patients with a blood lactate level greater than 4
mmol/L or mean arterial pressure less than 65 mm Hg.