NEONATAL SEPSIS BY NICOLE STEVENS NEONATAL SEPSIS Definition

NEONATAL SEPSIS BY: NICOLE STEVENS

NEONATAL SEPSIS Definition Causes, incidence & risk factors Signs & Symptoms Investigations Nursing Management With prompt treatment, many babies will recover completely from episodes of sepsis. But neonatal sepsis is a leading cause of infant death. The more quickly an infant receives treatment, the better the outcome. If concerned seek advice.

SEPSIS: DEFINITION A clinical syndrome due to the presence of microorganisms or their toxic products in the bloodstream, which results in systemic signs and symptoms of bacteraemia (during the neonatal period). Neonatal period: 1 st 28 days of life Early onset sepsis is seen in the first week of life (more specifically the first 48 hrs) Late onset after the first week Late, late onset: beyond 30 days Micro-organisms are classified as bacteria (either Gram-positive or Gram-negative), viruses, fungi, protozoa and spirochaetes

SEPSIS: RISK FACTORS Risk factors for early onset: Prolonged rupture of membranes Prolonged labour Fetal distress Maternal pyrexia (> 38 • C) or overt infection (eg UTI, gastoenteritis) Multiple obstetric procedures Presence of cervical suture Preterm delivery & very low birth weight (VLBW) History of GBS infection in previous infant, GBS bacteriuria in this pregnancy (Neonatal Handbook 2010)

SEPSIS: RISK FACTORS Risk factors for late onset: Prolonged hospitalisation Presence of foreign bodies (ETT’s, IVC’s) Cross infection from staff, visitors Malformations such as urinary tract anomalies (eg. vesico-ureteric reflux) or neural tube defects (Neonatal Handbook 2010) Late, late onset Defined as sepsis in infants over 30 days old, occuring in the VLBW or low gestation infants who have prolonged stays in NICU; usually have compromised immune systems and underlying illnesses.

SEPSIS: INCIDENCE Advances in perinatal care have increased survival of premature and critically ill infants This has increased the rate of sepsis Incidence is highly dependent on gestational age and birth weight > 2500 g: approx 1 in 1000 (3% mortality) 1000 – 2500 g: 4 – 9 in 1000 (30% mortality) < 1000 g: 26 in 1000 (90% mortality) The morbidity due to sepsis is often great as survivors may be left with long-term residual deficits.

SEPSIS: SYMPTOMS Temperature instability Respiratory problems: apnoea, tachypnoea Loose stools Hypoglycaemia or hyperglycaemia Reduced activity & muscle tone Poor feeding Irritability, seizures Distended abdomen Feed intolerance

SEPSIS: INVESTIGATIONS If there is a suspicion of sepsis initial tests performed may be: C-reactive protein, Full blood count, Blood culture If there is suspicion of meningitis a lumbar puncture should be added. Other investigations may include urine micro and culture (obtained by supra pubic aspirate or catheter insertion) Radiology investigations: chest xray, abdo xray

IMMUNE SYSTEM Essential to a neonates survival is an ability to respond effectively to hostile environmental factors. The developing immune system has functional (but limited) defensive, homeostatic and surveillance capabilities. 3 primary funtions of the immune system: DEFENSE (protect from invading microorganisms), HOMEOSTASIS (eliminate worn out host cells), SURVEILLANCE (recognise and remove mutant cells). Fetus is protected inutero, and doesn’t have to develop its own defensive immune responses. With exposure to a variety of organisms during & after birth the neonate must develop a balance between its host defences and the hostile environment to survive

IMMUNE SYSTEM Development starts early in gestation (6 – 8 wks) The newborn, particularly a premature one, is a susceptible host, they have low levels of immunoglobulin, complement system and natural killers. Babies are exposed to a large no. of organisms in the hospital setting They are bacteriologically sterile before birth The immune system components required to maintain defense mechanisms and recognise pathogens are immature, compromised and slow to respond. Neutrophil storage pools are rapidly depleted and slow to rebuild When the pace of bacterial replication exceeds clearance by innate defences, systemic infection supervenes.

NURSING MANAGEMENT Early recognition of at risk neonates and clinical signs Knowledge of maternal and neonatal history Awareness of normal behaviour Initial frequent examination of neonate, and at least once each shift as ongoing Observations taken and recorded Report abnormal behaviour, observations or findings promptly Listen to the mothers

NURSING MANAGEMENT Minimise environmental stress Minimal handling Cluster cares Quiet environment (cot covers, reduce light and noise) Monitor and restrict excess visitors

NURSING MANAGEMENT Maintain neutral thermal environment Nurse in an incubator if required, set appropriate termperature (per NTE guidelines), check ½ to hrly initially with any environment change until temperature stable Minimise heat loss Decrease risk of cold stress (which can cause hypoglycaemia & respiratory distress); decrease the metabolic rate, conserve energy

NURSING MANAGEMENT Provide respiratory support if required Monitor and assess oxygenation Provide oxygen as required and be aware of target saturations appropriate for gestation Minimal handling, nurse prone CPAP or ventilation if required IV therapy or enteral feeds (consider gastric tube feeding if oral feeds not appropriate)

NURSING MANAGEMENT Maintain nutrition, hydration and normal metabolic status Maintain normal blood glucose levels Calculate fluid/caloric requirement Consider: small frequent feeds, gastric tube feeding, IV therapy as ordered If enteral feeding contraindicated (eg with suspected or known NEC) parenteral nutrition will be required – dextrose with electrolytes & amino acids and a fat/vitamin solution

NURSING MANAGEMENT Administer drug therapy Check appropriate drug, dose and interval Monitor IV insertion site Management of localised infections (eg. Conjunctivitis – attend to eye toilet with saline and cotton balls and then administer drops) Be aware of side effects of drugs (eg. Gentamycin is ototoxic so be mindful of appropriate rate of administration; is excreted in the kidneys so monitor urine output, consider need to withhold if output is low; requires levels – usually prior to 3 rd dose)

NURSING MANAGEMENT Provide skin care Observe skin for integrity, hydration – an intact skin barrier is a major factor in resistance against infection Provide analgesia PRN May be required in cases of severe infection eg. Meningitis, septicaemia, osteomyelitis, NEC Signs of a baby ‘not coping’ may not always be obvious – stop sign, A’s & B’s, tachycardia, shrill cry in the older baby (term as opposed to preterm)

NURSING MANAGEMENT Prevention of spread of infection Universal precautions at all times Strict hand hygiene with neonates at all times (hand wash or hand rub before and after every contact) Isolate neonate if indicated (involve infection control team for advice) Parent support and education Explain procedures and treatments (and isolation if required) Offer emotional support

ROTAVIRUS Rotavirus The most common cause of severe gastroenteritis in early childhood. Almost all children have been infected by the time they reach five years of age. In developing countries rotavirus is responsible for approximately half a million deaths per year. In developed countries death is rare, but hospitalisations are common, especially in children under 2 years of age. Immunisation is recommended and is part of the vaccination schedule.

PERTUSSIS Pertussis (whooping cough) is an acute illness caused by the Bordetella pertussis bacterium. It is spread by air -borne respiratory droplets or by direct contact with secretions. Begins with an irritating cough that gradually becomes paroxysmal and lasts for 1 – 2 months or longer. In Australia, epidemics occur every 3 – 4 yrs. Infants aged less than 6 months are at greatest risk of severe disease due to partial immunisation. Level of immunity, whether from immunisation or infection, wanes after approx. 6 – 10 yrs, resulting in renewed susceptibility to infection. Hence the need for booster immunisations.

Cerebrum, acute bacterial meningitis, gross Here is another example of an acute meningitis from bacterial infection. The cerebrospinal fluid (CSF) obtained via lumbar puncture in such cases typically has a low glucose, high protein, and a cell count with many PMN's. A gram stain should be done to identify organisms.

Cerebrum, external view, vertex, acute bacterial meningitis, gross The yellow-tan exudate of acute bacterial meningitis seen here obscures the sulci.

Cerebrum, external view, base, acute bacterial meningitis, gross In this case of acute meningitis, the thick tan-green exudate is located at the base of the brain in a term infant. Ibn Sina (981 -1037), known in the West by the name of Avicenna, was a famous physician who was the first to describe meningitis. His major contribution to medical science was the al-Qanun fi al-Tibb, known as the Canon in the West where it was translated into Latin in the twelfth century. The Qanun covers general medicine, drugs, diseases affecting all parts of the body, anatomy, and pathology. Avicenna's work grew from a well-established body of Islamic medical knowledge, which built upon Greek, Persian, and Indian sources. Its influence extended throughout Islamic lands and into Europe and the Far East. Out of this tradition arose concepts of preventive medicine, hospitals, and pharmacies. The hospital was one of the great achievements of medieval Islamic society, driven by a moral imperative to treat all the ill regardless of financial or social status, religion, sex, or age.

CASE STUDY: BABY HARRY Maternal hx: G 1 P 0 Serology NAD AN scans NAD Maternal flu-like illness 2/52 prior Labour & birth Spontaneous labour @ 41. 3 wks ARM during labour (clear liquor) NVB, Apgars 9/10, Nil resus required BW: 3600 g

HARRY Postnatal Poor feeding, reviewed by Paed prior to discharge, FBE (NAD) and CRP (6. 2) collected Discharged home day 3 with feeding plan & review with LC the next day Referred to paeds day 7 from LC with poor feeding and sleepiness On examination: irritable and weak cry, hypotonic lower and upper limbs when awake, flat anterior fontanelle

HARRY Day 7: Admitted to SCN IVC inserted & bloods collected Tachycardic, febrile, low Sa. O 2 (60’s) Placed in incubator, cot oxygen commenced IV fluids commenced, Na. Cl bolus (10 m. L/kg) Renal ultrasound performed 4 limb BP’s NAD Echo attended Urine specimen attended Swabs (eye/throat/umbi/rectal) sent Commenced cefotaxime and acyclovir, IM konakion given

HARRY FBE (platelets low 110), CRP (elevated 35) Blood cultures (no growth after 7 days) Abnormal liver function results Discussion with NETS (not for transfer at this stage) Next day Other studies sent Result back for Urine specimen: Detected HSV 1 CRP (22) Further discussion with NETS, transferred to RCH for ongoing care under infectious diseases team

HARRY At RCH/diagnosis: HSV 1 infection (disseminated) Acute liver failure Coagulopathy Thrombocytopenia Frontal lobe changes Hydrocele Issues: RDS (required several days of CPAP and O 2 therapy) Received transfusion of platelets, plasma, was on TPN and AB’s Noted to be encephalopathic (hypertonia, posturing, irratable) Hepatomegaly Seen by haemotology, metabolics, gastroenterology and neuro. teams

HARRY Transferred back to SCN at 3 weeks of age (2 weeks later) to complete course of IV acyclovir and to establish suck feeds NGT removed 3 days later and remained fully suck feeding (breast/bottle), all breast milk Liver function tests remained abnormal Pale/jaundice in appearance “sickly looking” in colour but very alert interactive and full of personality! Discharged home for ongoing care in the community at 5 weeks of age

HARRY Now over 2 months down the track and Harry is still having paediatric follow up and blood tests Liver function tests are improving, but still abnormal Has an elevated cholesterol level Platelet levels normalised Slightly anaemic Seen in paediatric clinic (early October)and weighed in at 4835 g. Continuing on prophylactic oral acyclovir. Having monthly bloods. Under care of infectious diseases clinic at RCH. Being seen monthly in paediatric clinic

HERPES SIMPLEX VIRUS HSV 1 & HSV 2 are uncommon, but important, causes of neonatal illness Neonatal infection is usually the result of HSV 2 as this is the main virus associated with genital infection Women can be asymptomatic, have no history of lesions, but still shed the virus HSV can remain latent for long periods, with shedding or reactivation occuring at any time There is a 1% chance of a woman with a past history of genital infection shedding virus at the time of delivery

HERPES SIMPLEX VIRUS In cases of neonatal infection, most women do not give a history of active genital herpes at the time of delivery Babies born to mothers with a primary genital infection at the time of delivery have a 50% risk of developing infection, compared with <5% in cases of recurrent infection present at the time of delivery SO PREGNANT WOMEN BEWARE – YOU DON’T WANT A NEWLY ACQUIRED HSV INFECTION WHILE YOU ARE PREGNANT, HIGH LEVEL OF RISK FOR THE NEONATE

HSV: CLINICAL FEATURES Neonatal HSV usually presents within 2 weeks of birth Infection occurs in less than 5 per 100, 000 births (up to 10 times more in the USA) 90% are acquired during passage through the birth canal or through ascending infection 5% have congenital HSV infection 5% have post-natally acquired infection (from family, visitors or health care providers)

HSV: CLINICAL FEATURES Usual clinical presentations are: skin/eye/mouth (SEM) localised disease untreated, 70% will progress to disseminated disease 25% will have the virus in CSF at initial presentation isolated vesicles other skin reactions, including zoster-like eruptions conjuctivitis and lesions around eyes choriod retinits single or multiple oral vesicles

HSV: CLINICAL FEATURES Desseminated disease (HARRY) poor prognosis, with over 70% mortality if untreated non-specific presentation with: lethargy, poor feeding, fever, convulsions, apnoea, resp. distress, hepatomegaly, jaundice, DIC Pneumonitis (inflammation of lung tissue) tends to occur day 4 - 7 respiratory distress, +/- pulmonary haemorrhage CXR showing diffuse pneumonic change Can go onto dissemination if untreated Meningo-encephalitis isolated or part of disseminated disease, presents with encephalopathy, seizures, absent gag

Cerebrum, temporal lobe, Herpes simplex virus infection with hemorrhages, gross An uncommon but distinctive form of viral infection of the brain is herpes simplex virus encephalitis. The cases are sporadic and can occur in nonimmunocompromised persons. HSV infection often produces hemorrhages in the temporal lobe. Like other viral infections, HSV can produce mononuclear cell infiltrates microscopically. [Image contributed by Jeannette J. Townsend, MD, University of Utah]

MANAGEMENT Acyclovir 10 mg/kg IV 8/24 for 14 – 21 days Supportive care, ie. Maintenance fluids, pain relief, respiratory support, GNC, cluster cares, minimise handling Investigations: Examine for vesicles, including oral Swab any lesions and throat and eyes LP with CSF sent for PCR and culture EEG and brain imaging can be helpful Recurrent skin and eye eruptions can occur, oral acyclovir has a role in this setting

PREVENTION LUSCS if there active lesions, and preferably within 6 hrs of ruptured membranes Send swabs from babies eyes and throat Nosocomial infection can occur and vigorous infection control measures should be instituted Relatives or staff with ‘cold-sores’ should be discouraged from handling newborns Mothers with cold sores present low risk to the infant because passive antibody protection of the baby should be present, but in this situation the wearing of masks and doing vigorous hand washing should be advocated, as well as topical treatment of the lesion on the mother

REFERENCES Verani JR, Mc. Gee L, Schrag S. Prevention of Perinatal Group B Streptococcal Disease, Revised Guidelines from CDC, 2010. Morbidity and Mortality Weekly Report. 59(RR-10): 1 -36, 2010. Stoll et al. Early onset neonatal sepsis: the burden of group B streptococcal and E. coli disease continues. Pediatrics 2011: 127: 817 -826. www. netsvic. org. au/nets/handbook