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Dr. Mahadevan Sugunadevan,

MBBS: MD (anaes): FRCA,

Consultant anaesthetist.

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Contents: Introduction.

Patho-physiology.

Initial resuscitation.

investigations.

Management.

Anaesthesia and labour analgesia.

Conclusion.

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Pregnant women are vulnerable to infection and

risk of developing serious complications from an

infection.

In UK, sepsis is leading cause for maternal deaths

from CMACHE reports 2006-2008.

Increased risk of community acquired haemolytic

Streptococci group A infections.

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What is sepsis? Sepsis is defined as infection together with systemic

manifestation of infection.

A suspected or documented infection in the presence of

two or more of the following is defined as sepsis. Temperature more than 38 or less than 36.

Heart rate more than 90/min in adult.

WBC more than 12,000 or less than 4000 or more than 10%of immature blast cells.

Respiratory rate more than 20/min or PaCO2 less than32mmHg.

Blood sugar more than 140mg% in non-diabetic.

Altered mental status.

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What is severe sepsis? Severe sepsis is defined as sepsis with sepsis

induced organ dysfunction or tissue hypo-perfusion.

Sepsis induced hypotension is defined as SBP lessthan 90mmHg or MAP less than 65 mmHg in adult or

reduction in BP less than 40% of the expected value

for the age and sex after excluding the other causes

of hypotension.

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What is septic shock? Septic shock is defined as a life threatening clinical

syndrome where there is sepsis induced hypotension

with decreased tissue perfusion and impaired

oxygen delivery despite of adequate fluid

resuscitation.

Need for inotrope support to maintain adequate

mean arterial pressure in-order to maintain tissueperfusion.

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What is multi-organ dysfunction

syndrome? Multi organ dysfunction means impaired organ

function and patient depend on two or more organ

support.

Organ support could be:

Inotrope for to maintain cardiac output.

Ventilation to improve lung oxygenation.

Renal replacement therapy for renal impairment. Blood and blood products for haematology.

Hepatic support for liver impairment.

Neurological support for cerebral impairment.

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Indicators for severe sepsis? Sepsis induced hypotension.

Lactate levels more than 2mmol/l.

Urine output less than 0.5ml/kg/hour.

Acute lung injury PaO2:FiO2 less than 300.

Altered mental status.

Serum creatinine more than 2mg%.

Serum bilirubin more than 2mg%.

Platelet count less than 100,000 or INR more than

1.5.

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Reasons for infection during

pregnancy: Physiological changes in lower genital tract.

Decrease pH.

Increased glycogen deposition.

Increases intra-amniotic infections.

Enlargement of uterus. Can cause stricture or obstruction to ureter.

Increase risk for pyelonephritis.

Hyper-coagulable state. Increase risk for venous thrombo-embolic events.

Masking of signs. Elevated leucocytes and C reactive protein.

Increase in heart rate and respiratory rate.

Can mask the signs of SIRS.

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Common pathogens: Aerobic bacteria:

haemolytic Streptococci.

Entero-coccus.

Haemophilus influenza. Staphylococcus.

Klebsiella.

Anaerobic bacteria: Clostridium.

Bacteroids. Others:

Mycobacteria.

Clamydia.

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Conditions predispose: Obstetric causes:

Intra-amniotic infections.

Chorio-amnionitis.

Septic abortions.

Post partum endometritis.

Non-obstetric causes: Pyelonephritis.

Pelvic thrombophlebitis.

Appendicular abscess.

Pneumonia. Peritonitis.

Wound infection. Necrotising fasciitis.

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As a result:

Vasodilatation.

Increased vascular permeability. Impaired cellular integrity.

Increased in gap between endothelium and cells.

Therefore, high chances for intra-cellular hypoxia.

Increased anaerobic metabolism. Intra-cellular lactic acidosis.

Activation of coagulation cascade.

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Systemic effects: CVS:

Cardiac dysfunction.

Impaired vaso-motor control.

Renal: Renal hypo-perfusion.

Acute renal impairment.

Pulmonary: Alveolar collapse.

Pulmonary shunting. Decreased compliance.

Increased work of breathing.

Hypoxia.

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Haematology: DIC.

Low platelet count.

Low fibrinogen levels.

Activation of coagulation cascade.

Liver: Liver dysfunction.

Elevated liver enzymes.

Impaired hepatic blood flow.

Metabolic: Glucose- high blood glucose.

Protein- high protein break down.

Lipids- high lipid break down.

Lactate- anaerobic metabolism and lactic acidosis.

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Response depends on: Virulence of organism.

Size of inoculum.

Co-morbid conditions. Age.

Nutritional status.

Genetic polymorphism.

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Key recommendations: Modified Early Obstetric Warning Scores MEOWS:

Mental function.

Heart rate. Blood pressure- systolic and diastolic pressure.

Respiratory rate.

Temperature.

Urine output.

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Initial resuscitation ( first 6

hours): Start resuscitation patients with hypotension and

elevated serum lactate more than 4 mmol/l.

Do not delay pending ICU admission.

Need to give fluid either crystalloid or colloid.

Need to aim to improve response.

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Resuscitation goals: Central venous pressure more than 8mmHg.

higher CVP values are recommended for patients on

mechanical ventilators and those with pre-existing

decreased ventricular compliance.

Mean arterial pressure more than 65mmHg.

Urine output more than 0.5ml/Kg/hour.

Central venous oxygen saturation more than 70% ormixed venous oxygen saturation more than 65%.

Haematocrit value more than 30%.

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Diagnosis: Obtain cultures before starting antibiotics.

Obtain two more blood cultures.

Culture form other sites as clinically indicated. One blood culture from each vascular access sites.

Perform imaging studies promptly in order to

confirm

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Antibiotic therapy: Start antibiotics as early as possible.

Always within first hour of recognising as severe sepsisand septic shock.

Start with broad spectrum antibiotics more than oneagent to cover the likely pathogen with goodpenetration into presumed source.

Reassess antibiotic regime to optimise efficacy, preventresistance, avoid toxicity and minimise cost.

Duration of therapy usually limited to 7-10 days. Ifresponse is slow should consider for un-drained focus orimmune deficiency.

Stop antibiotics if the cause if found non-infectious.

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Source identification and

control: A specific anatomic site of infection should be

established as early as possible ( within 6 hours of

recognition of sepsis ).

Early surgical intervention is needed like abscess

drainage or wound debridement.

Implement source control following successful fluid

resuscitation. Choose source control measures with minimal

physiological disturbances to patient.

Remove IV lines if potentially infected.

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Fluid therapy: Fluid resuscitation with colloid or crystalloid.

Target CVP more than 8 ( more than 12 if mechanicallyventilated).

Use a fluid challenge to check the haemodynamicresponse.

Usual fluid challenge: Colloids 250-500ml of either starch or gelatine

preparations.

Crystalloids- 10-20ml/Kg over 30-60 minutes. More rapid and larger volume of resuscitation is

necessary for sepsis induced tissue hypo perfusion.

Rate of infusion may be reduced in a patient withcardiac problems.

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Vaso-pressor support: Main aim is to maintain mean arterial pressure more than65mmHg.

After initial fluid therapy if the response is poor can try withvasopressor support.

Can try with ephedrine or phenylepherine initially. The inotrope of choice for sepsis is noradrenalin in-order to

improve the after load of the myocardium.

If the response is poor need to add Dobutamine in-addition tonoradrenalin.

Dobutamine will: Improve myocardial dysfunction.

Improve the cardiac output.

When the vasopressor support is established arterial catheterwill be very essential.

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Steroids: Consider IV hydrocortisone.

Usual dose is 50mg 6 hourly.

Or 200mg given as infusion over 24 hours.

Maximum recommended dose is 300mg for 24 hours.

ACTH stimulation test is not recommended.

Hydrocortisone is preferred to dexamethazone.

Fludrocortisone could be added if the patient showssignificant lack of mineralocorticoid activity.

Corticosteroids are not recommended in theabsence of septic shock.

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Blood product administration Consider blood transfusion if Hb% less than 8g%. Try to

keep Hb% above 10g% if adult to improve the tissueoxygenation.

Higher Hb% is required in: Myocardial ischemia.

Severe hypoxia.

Lactic acidosis.

Cyanotic heart disease.

No place for erythropoietin. Use FFP if bleeding or prior to any invasive procedures.

Use platelets if platelet count less than 5000 orbleeding or surgical or invasive procedures.

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Mechanical ventilation: Can develop sepsis induced acute lung injury.

So need measures for lung protection strategies:

Target tidal volume 6ml/kg. Upper limit of plateau pressure of 30cmH2O.

Allow permissive hypercapnoea.

PEEP should be set to avoid extensive lung collapse

at the time of expiration. Try to avoid injurious levels of FiO2.

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Head end elevation.

Non-invasive ventilation could be considered for:

Mild to moderate hypoxic respiratory failure. Haemodynamically stable patients.

Comfortable.

Able to protect airway or clear airway.

Expected to recover rapidly. Need to consider the weaning from the time of

ventilation.

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Sedation and analgesia:

Use sedation protocols with a sedation goal for

critically ill mechanically ventilated patients.

Preferred as infusion with daily sedation holidays to

produce awakening. Re-titrate if necessary.

Avoid Neuro-muscular blockers where possible.

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Glucose control: Use IV insulin to control high blood sugars in patients

with severe sepsis following stabilisation in ICU.

Keep the blood sugar below 140mg%using a validated

protocol for insulin dose adjustment. Need to monitor the blood sugar levels every 1-2 hours.

Once stable 4-6 hourly.

Earlier tight glycaemic control was recommended.

Keep sugar levels below 110 mg%.

Associated with hypoglycaemia.

But NICE sugar guidelines recommends to keep bloodsugar around 140 gives better outcome.

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Renal replacement: Intermittent haemodialysis or continuous veno-

venous haemo-filtration should be considered.

CVVH is better in haemo-dynamically unstable

patients.

Early renal replacement therapy had shown

improved outcome.

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Bicarbonate therapy: Considered only when pH value less than 7.0 or

acidaemia induced myocardial dysfunction.

Bicarbonate can cause:

Shift of ODC to left.

Intra-cellular acidosis.

Sodium overload.

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DVT prophylaxis: Use either unfractionated heparin or low molecular

weight heparin unless contra-indicated.

Can use mechanical prophylactic device like

stockings, intermittent compression device.

Can use combination of mechanical and

pharmacological therapy for patients with high risk

for DVT. LMWH is preferred to unfractionated heparin.

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Stress ulcer prophylaxis: Can use either histamine 2 receptor blocker or

proton pump inhibitor.

Improvement in cardiac output is very important to

prevent stress ulcer.

But potential risk of ventilator associated

pneumonia with use of ulcer prophylaxis

medications. Potential risk for gastro-intestinal bleeding should

be weighed against the development of VAP.

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New ideas: Statins in sepsis.

Anti-oxidants.

Vitamin C and vitamin E. Extra-corporeal membrane oxygenation.

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Options: Opiods-

Morphine IV or sc.

Pethidine IV or IM.

Entonox.

Regional- epidural.

Other techniques.

Accupunture.

Massage.

Hypnotherapy.

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GA.

Need RSI.

Opiod based analgesia.

Antibiotics.

Post op ICU or HDU care.

Regional.

If epidural in-situ epidural top-up. Not advice to keep epidural for a long time.

Single shot spinal if haemo-dynamically stable.

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Thank you for listening