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Miss: Kamlah Olaimat 1

Neonatal Sepsis

Presented by

Kamlah olaimat


Welcome !!

Causes

Symptoms

Diagnosis

Treatments

Summary

What is Neonatal Sepsis?

Objectives


Tutorial Objectives

Completing this tutorial will provide the learner with a better

understanding of Neonatal Sepsis:

* Pathology

* Causes

* Symptoms

* Diagnosis

* Treatments

What will I learn?


What is Neonatal Sepsis?

Neonatal Sepsis is a term

used for a severe infection

in newly born infants.

Clinical syndrome of systemic illness accompanied by bacteremia occurring in the first month of life

Image used with permission and provided by www.steliz.org/newborn_center.htm


More facts about Neonatal Sepsis

Neonatal Sepsis affects approximately 2 infants per 1000 births with a higher incidence in premature & low birth weight infants [2].

Mortality rate is 13-25% Higher rates in premature infants and those with early disease

There are two types of Neonatal Sepsis: Early OnsetLate Onset


Causes of Neonatal Sepsis

The primary causes of Neonatal Sepsis are bacteria, such

as Staphylococcus and Group Beta Strep (GBS).

Bacteria may be the cause of neonatal sepsis, but neonates are more susceptible to these bacteria for two reasons [3&6]:

Immature immune response

Genetic predisposition


What makes a neonates immune system immature?

Normally an immune system

responds to a pathogen in a specific manner, but if there are problems with any

element the immune system is unable to function properly

Pathogen enters body

Neutrophils move in

Chemotaxis occurs

Opsonization causes

phagocytosis

Monocytes kill pathogen


pathogens can enter a neonates body in many ways !

Pathogens can enter through the prenatal, perinatal, and postnatalperiods [6].

Prenatal Maternal Substance Abuse

Premature Rupture of Membranes (>18 Hours)

Maternal Infection

Perinatal Microbial Colonization at Birth

Maternal Infection

Vaginal Exam of Mother

Postnatal Invasive Catheters

Endotracheal Intubation

Exposure to Nosocomial Microorganisms


Neutrophils: An important cell in immunity against pathogens

Neonatal neutrophils are deficient in

their ability to adhere to vessel walls at site of infection [2&6].

Further release of neutrophils

depletes a neonatal storage

pool because the bone marrow

storage of a neonate is only 20-30%

of the pool in an adult [2&6].

Neonatal neutrophils have a

decreased ability to deform &

migrate into tissues [2&6].Neutrophils

Red Blood Cells

Image provided with permission from

http://en.wikipedia.org/wiki/Image:Segmented_neutrophils.jpg


Chemotaxis

Imagine: Being in a dark tunnel without any direction or a way out. Finally you see light. You move towards the light and get out of the tunnel. Well this is like chemotaxis. The sun is the chemoattractant attracting you out to the world!!

Neonatal neutrophils have

decreased chemotaxis due to

decreased chemoattractant

Production [2&6].

Chemoattractants attract

neutrophils to the site of infection

[2&6].

Neonatal neutrophils therefore

cannot reach the site of infection

because of the chemotaxis

deficiency caused by decreased

chemoattractant production.


Opsonization

Opsonization is the coating of a pathogen with antibodies that makes it susceptible to phagocytosis [2&6].

Phagocytosis is the process of cells (phagocytes) engulfing, ingesting, &

destroying pathogens [2&6].

Neonates have a decreased amount of opsonins (antibodies that promote

opsonization) [2&6].

Opsonization

Pathogen


Monocytes: Another important cell in the fight against pathogens

Monocytes are a type of White Blood Cell that ingests

pathogens.

Neonates have a sufficient amount of

monocytes and full capability to kill organisms [2], but because of a neonates deficiencies previously

discussed very few monocytes get to

the site of infection.

Image provided with permission and copyrighted by amaxa GmbH at

www.amaxa.com/mission3.html


What makes a neonates immune system susceptible to sepsis?

OR

Maturity

Immaturity


Youre Right!!!!

The immaturity of a neonates immune system makes them MORE SUSCEPTIBLE to sepsis.


Not Quite! Try Again


Genetic Predisposition to Sepsis

Multiple factors play into a neonates response to infection and the

possible development of sepsis. One of these factors is genetics. As

science has moved into recognizing the human genome there have

also been advances with finding genetic contributions to sepsis.

The bodys first response to infection requires recognition of the presence of a pathogen. After recognition has occurred the body responds appropriately to resolve the problem [3&14]. Many polymorphisms have been recognized within both of these phases and they have been implicated in

influencing the susceptibility to and/or outcome from sepsis [3&14].

Lets look further into these two phases to see the effect

polymorphisms have on neonatal sepsis:

Recognition Phase Response Phase


Recognition Phase

The bodys initial response to infection requires recognition of the

presence of a pathogen [3].

Polymorphisms in genes coding for proteins involved in the recognition

of pathogens can influence the susceptibility to and/or outcome of

neonatal sepsis [3].

Lets look into two of these:

Mannose-Binding Lectine (MBL)

Lipopolysaccharide (LPS)


Response PhaseAfter the initial recognition of a pathogen occurs the body responds by releasing elevated levels of proinflammatory cytokines followed by a release of anti-inflammatory cytokines [3]. This dual release of opposite cytokines helps the cytokines return to a baseline level and that enables the start of tissue repair to start [3].

It is generally accepted that an imbalance between proinflammatory and anti-inflammatory cytokines result in clinical manifestations of sepsis [3]. This Imbalance is due to polymorphisms in various proteins involved in the response to pathogens.


Not quite! Try again.


Great answer! Youre correct!

Polymorphisms cause either an over expression or under expression of

proteins and/or genes that have significant roles in the immune

response to infection. This alters their ability to properly function

which makes a neonate more susceptible to sepsis.


Early Onset

First 5-7 days of life Usually multisystem fulminant illness with

prominent respiratory symptoms (probably due to aspiration of infected amniotic fluid)

High mortality rate 5-20%

Typically acquired during intrapartum period from maternal genital tract Associated with maternal chorioamnionitis


Late Onset

May occur as early as 5 days but is most common after the first week of life

Less association with obstetric complications

Usually have an identifiable focus Most often meningitis or sepsis

Acquired from maternal genital tract or human contact


Nosocomial sepsis

Occurs in high-risk newborns

Pathogenesis is related to the underlying illness of the infant

the flora in the NICU environment

invasive monitoring

Breaks in the barrier function of the skin and intestine allow for opportunistic infection


Risk factors

Prematurity and low birth weight Premature and prolonged rupture of

membranes Maternal peripartum fever Amniotic fluid problems (i.e. mec, chorio) Resuscitation at birth, fetal distress Multiple gestation Invasive procedures Galactosemia Other factors: sex, race, variations in immune

function, hand washing in the NICU


Symptoms of Neonatal Sepsis

The symptoms of neonatal sepsis are not concrete and vary widely [9].

TachpneaHeart Rate Changes

Feeding difficulties

Difficulty Breathing Temperature Instability

Jaundice Irritability

Why are symptoms so broad?


Clinical presentation Temperature irregularity (high or low) Change in behavior

Lethargy, irritability, changes in tone

Skin changes Poor perfusion, mottling, cyanosis, pallor, petechiae,

rashes, jaundice

Feeding problems Intolerance, vomiting, diarrhea, abdominal distension

Cardiopulmonary Tachypnea, grunting, flaring, retractions, apnea,

tachycardia, hypotension

Metabolic Hypo or hyperglycemia, metabolic acidosis


Inflammation in Neonatal Sepsis

It is widely known that sepsis occurs

because of an exaggerated

systemic inflammatory response (SIR) [12].

Lets find out how this is true Inflammatory Process


Inflammatory Process

[12]

Pathogen enters body

Inflammatory mediators released (cytokines)

Injury to endothelium

Tissue factors released

Production of thrombin

Coagulation promotes clot formation

Increased activity of fibrinolysis inhibitors

Decreased fibrinolysis


Inflammation

Overall, the imbalance among inflammation, over coagulation, and decreased fibrinolysis are the cause for the majority of deaths

in sepsis [12].


How is Neonatal Sepsis Diagnosed?

There is no definite marker in neonatal sepsis, but there are determinants of infection.

When a neonate presents with sepsis symptoms a septic work-up

is completed [2]. What is included in a septic work up?

* Complete Blood Count (CBC)

* Blood & Urine cultures

* Lumbar Puncture (LP)

* Chest X-Ray

* Line cultures


Is there a diagnostic marker for neonatal sepsis?

True

False


Yeah!!! You are correct!

There is NOT a specific diagnostic marker, only determinants of infection (labs, x-rays).


Are you sure? Try again!


Treatments for Neonatal Sepsis

It is of vital importance that treatment is initiated as soon as sepsis is suspected, especially for those

infants at risk.

Broad Spectrum Antibiotics (Ampicillin & Gentamycin) are the first line of defense against neonatal sepsis

[2].

Why????

What are other recommendations/options?


Why is it so important to start antibiotic treatment?

If not treated as soon as sepsis is suspected a neonate is more likely to die from sepsis and its complications.

For this reason it is of vital importance that healthcare workers (nurses and physicians) notice and act upon even the most subtle changes in a neonates assessment, particularly those infants at

risk (GBS+).


Treatment Recommendations

Antibiotics should be initiated after all cultures and lab work is completed to ensure proper diagnosis.

All neonates will remain on IV antibiotics until blood/urine culture results

come back in approximately 2-3 days. Further therapy will depend on

lab work results and the neonates response to treatment.* Every hospital/organization has an antibiotic protocol specific to their site.

Although antibiotic therapy is vital, it is just as important to continue the overall support of the neonate (i.e. respiratory &

cardiac).


Infection control in NICU

Its an important part of every copmonant of care of a neonate baby .

The most important factors contributing to nasocomial infection are :-

o Noncompliance to infection control policy (hand washing )

o Invasive procedure which interrupt normal body barriers as intubations

o Overcrowding and understanding in NICU

o Immaturity of immune system

o Antibiotic abuse


General principle of infection control in NICU

1) Appropriate physical setup of NICU environment ( isolated , no windows open to outside , avoid overcrowding , adequately ventilated)

2) Provide routine care for the newborn baby

3) Consider every person as potentially infectious ( including member of staff )

4) Wash hand or use alcohol based hand scrub


General principle of infection control in NICU

1) Wear protective clothing and gloves

2) Sterilize or disinfect instrument and equipment

3) Routinely clean the NICU and dispose of waste

4) Isolated the infectious baby

5) Surveillance for nasocomial infection


Neonate

Neonate should be bath 3 time/week using baby soap

Electrodes should be changed every third day

Umbilical stump should be treated with alcohol / shift

Prophylactic eye drop at first day

Neonate admitted from out side of hospital isolated or 72 hours


Staff health

Health care should be immune to rubella, measles, chicken pox

Health care yearly receive influinza vaccination

Any person with any disease (common cold) not have direct contact with neonate

Limited the number of person handle the baby


Had washing

Mother should wash hand after and before handle baby

Remove accessory before inter NICU

Finger nails trimmed short , no false nail use

Antiseptic preparation

At least 10 second washing

Hand wash even when use gloves

Hand washing is the single most important procedure for infection control


Protective clothes and gloves

Sterile gowns must be worn by all person in direct contact with baby

Use gloves when handle the baby


General housekeeping and waste disposable

Clean NICU as order :-

Patient area , accessory , adjacent halls

From top to bottom

Counter , work surface , horizontal area cleaned once daily

Clean up spill of blood or bodily fluid immediately by using disinfectant solution

Separate contaminated waste from non contaminated

Use a puncture proof container for sharps

Destroy container when it is two third full


General housekeeping and waste disposable

Change breathing material and CPAP / 3 day

Change suction apparatus daily

Change suction tube after use by each infant

Incubator changed for cleaning with 10% hypochlorite

Every 5 day for infant 1000gm

Linen changed every day in incubator


Feeding and nutrition equipment

Sterilization of feeding bottles

Sterile water for formula preparation

Feeding tube changed \ 2-3 days

Hand washing before and after feeding


Isolated infectious baby

Isolated room or area should be available

Keep door closed

When entering the room

wear a clean gown

wear gloves

Before leaving room:-

remove gown and gloves

wash hand with alcohol

The nurse work with infectious baby should give few assignment


Surveillance for nasocomial infection

Routine surveillance of the incidence of acquired infections in nursery should be mandatory

Perform culture by swabbing for bacteria on likely surface area

Perform blood culture of infected neonate

Identify bacterial isolated

Bacterial culture from person and equipment are necessary


I hope you have enjoyed your experience and have learned some new information

about neonatal sepsis.

mailto:[email protected]


References1. Amaxa Biosystems. (n.d.). Mission #3: Transfect human monocytes. [Online image]. Retrieved March 22,

2006 from www.amaxa.com/mission3.html

2. Bellig, L.L. & Ohning, B.L. (2004). Neonatal Sepsis. Retrieved February 8, 2006, from emedicine:http://wwwemedicine.com/ped/topic2630.htm

3. Dahmer, M.K., Randolph, A., Vitali, S., & Quasney, M.W. (2005). Genetic polymorphisms in sepsis. Pediatric Critical Care Medicine, 6(3), 61-73. Retrieved February 23, 2006 from PubMed database.

4. Farlex Inc. (n.d.). The Free Dictionary. Retrieved March 30, 2006, from www.thefreedictionary.com

5. LaRosa, S.P. (2002). Sepsis. Retrieved February 14,2006, from The Cleveland ClinicWebsite: http://www.clevelandclinicmeded.com/diseasemanagement/infectiousdisease/sepsis.htm

6. McKenney, W.M. (2001). Neonatal nursing: Understanding the neonatal immune system: High risk for infection. Crtitical Care Nurse, 21(6), 35-58. Retrieved February 14, 2006, from ProQuest database.

7. Microsoft Corp. (2006). Microsoft Clip Art. Retrieved March 30, 2006, from www.microsoftclipart.com

8. Mrozek, J.D., Georgieff, M.K., Blazer, B.R., Mammel, M.C., & Schwarzenburg, S.J. (2000). Effect of sepsis syndrome on neonatal protein and energy metabolism. [Electronic version] Journal of Perinatology, 2, 96-100.


References9. Neonatal Handbook:Sepsis. (n.d.). Retrieved February 14, 2006, from

http://www.netsvic.org.au/nets/handbook/index.cfm?doc_id=898

10. Oostdyk, R. (2005). Neutrophil. [Online image]. Retrieved April 20, 2006, fromhttp://en.wikipedia.org/wiki/Image:Segmented_neutrophils.jpg

11. Orr, P.A., Case, K.O., & Stevenson, J.J. (2002). Metabolic response and parenteral nutrition in trauma sepsis and burns. Journal of Infusion Nursing, 25(1), 45-53. Retrieved March 7, 2006 from Ovid database.

12. Sharma, S. & Mink, S. (2004). Septic shock. Retrieved February 14, 2006, from emedicine: http://www.emedicine.com/MED/topic2101.htm

13. St. Elizabeth Hospital. (n.d.). The newborn center at St. Elizabeths. [Online image]. Retrieved March 22, 2006 from www.steliz.org/newborn_center.htm

14. Villar, J., Maca-Meyer, N., Perez-Mendez, L., & Flores, C. (2204). Bench to bedside review: Understanding genetic predisposition to sepsis. Critical Care, 8(3), 180-189. Retrieved February 23, 2006, from PubMed

database.

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