UNIVERSITY OF MAKATI COLLEGE OF ALLIED HEALTH STUDIES J.P. RIZAL EXTENSION, WEST REMBO, MAKATI CITY ‘’Neonatal Sepsis’’ A Case Study in Partial Fulfilment of the Requirements in NEWBORN SERVICES UNIT (NSU) DUTY (James L. Gordon Memorial Hospital) Submitted by: Amparo, Roxanne Azul, Deneice Patricia Balbarono, Mary Ann Castro, Roger Dayao, Irish Grace de Guerto, Camille Anne Dionisio, Errica Joice Formaran, Kevin Manila, Ciara Alyssa Nichole Simangan, Precious Anne Serad, Donna Usman, Amal Villar, Michael Vincent Yu, Arnilyn
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UNIVERSITY OF MAKATI COLLEGE OF ALLIED HEALTH STUDIES
J.P. RIZAL EXTENSION, WEST REMBO, MAKATI CITY
‘’Neonatal Sepsis’’A Case Study in Partial Fulfilment of the Requirements in
NEWBORN SERVICES UNIT (NSU) DUTY(James L. Gordon Memorial Hospital)
Submitted by:
Amparo, RoxanneAzul, Deneice PatriciaBalbarono, Mary Ann
Castro, RogerDayao, Irish Grace
de Guerto, Camille AnneDionisio, Errica Joice
Formaran, KevinManila, Ciara Alyssa Nichole
Simangan, Precious AnneSerad, DonnaUsman, Amal
Villar, Michael VincentYu, Arnilyn
October 24-26, 2011
I. INTRODUCTION
Septic shock is a syndrome in which a potentially lethal drop in blood pressure occurs as
a result of an overwhelming bacterial infection. Septic shock is a possible consequence of
bacteremia, which is also called sepsis. Bacterial toxins, and the immune system's response to
them, can cause a dramatic drop in blood pressure and may result in under-perfusion to various
organs. Septic shock can lead to multiple organ failure, including respiratory failure, and may
cause rapid death.
In 1914, Schottmueller wrote, “Septicemia is a state of microbial invasion from a portal
of entry into the blood stream which causes sign of illness.” The definition did not change much
over the years, because the terms sepsis and septicemia referred to several ill-defined clinical
conditions present in a patient with bacteremia. In practice, the terms often were used
interchangeably; however, fewer than half the patients with signs and symptoms of sepsis have
positive results on blood culture.
Furthermore, not all patients with bacteremia have signs of sepsis; therefore, sepsis and
septicemia are not identical. In the past few decades, the discovery of endogenous mediators of
the host response has led to the recognition that the clinical syndrome of sepsis is the result of
excessive activation of host defense mechanisms rather than the direct effect of microorganisms.
Sepsis and its sequelae represent a continuum of clinical and pathophysiologic severity.
Serious bacterial infections at any site, with or without bacteremia, are usually associated
with important changes in the function of every organ system in the body. These changes are
mediated mostly by elements of the host immune system against infection. Shock is deemed
present when volume replacement fails to increase blood pressure to acceptable levels and
associated clinical evidence indicates inadequate perfusion of major organ systems, with
progressive failure of organ system functions.
Multiple organ dysfunctions, the extreme end of the continuum, are incremental degrees
of physiologic derangements in individual organs (ie, processes rather than events). Alteration in
organ function can vary widely from a mild degree of organ dysfunction to frank organ failure.
During an infection, certain bacteria can release complex molecules, called endotoxins,
which may provoke a dramatic response by the body's immune system. Endotoxins are
particularly dangerous; as they become widely dispersed, they cause arteries and the smaller
arterioles to dilate. At the same time, the walls of the blood vessels become leaky, allowing fluid
to seep into the tissues, lowering intravascular volume (the amount of fluid left in circulation).
This combination, of arterial dilation and decreased intravascular volume, causes a dramatic
decrease in blood pressure and impaired blood flow to multiple organs. Other changes seen in
septic shock are disseminated intravascular coagulation (DIC), which can further impair organ
perfusion (blood flow).
Septic shock is seen most often in patients with impaired host defenses (patients who are
immunosuppressed), and is often due to nosocomial (hospitalacquired) infections. The immune
system is suppressed by drugs used to treat cancer, autoimmune disorders, organ transplants, and
diseases of immune deficiency such as AIDS. Malnutrition, chronic drug abuse, and long-term
illness also increase the likelihood of succumbing to bacterial infection. Bacteremia is more
likely with preexisting infections such as urinary or gastrointestinal tract infections, or skin
ulcers. Bacteria may be introduced to the blood stream by surgical procedures, catheters, or
intravenous equipment.
Toxic shock syndrome (TSS) is a potentially fatal disorder resulting from infection with
Staphylococcus aureus, a toxin-producing strain of bacteria. When it was first reported about 25
years ago, toxic shock syndrome was associated with menstruation and linked to super-absorbent
tampon use. Today, it is recognized that use of super-absorbent tampons does increase the risk of
TSS, as the use of a contraceptive sponge or diaphragm. Postpartum patients (women who have
just given birth) and patients with wound infections, or recovering from nasal surgery also are at
risk for TSS. The illness appears suddenly, with fever, rash, low blood pressure, and episodes of
fainting. Survival has improved since the 1980s, approximately 2–5% of patients die from this
dis-order. Patients recovering from TSS face increased risk of recurrence. To prevent TSS,
menstruating women are advised to avoid use of super-absorbent tampons.
Septic shock is most likely to develop in the hospital, since it frequently results from
hospital-acquired infection. Close monitoring and early, aggressive therapy can minimize the
likelihood of progression. Nonetheless, death occurs in at least 25% of all cases.
The likelihood of recovery from septic shock depends on many factors, including the
degree of immunosuppression of the patient, underlying disease, timeliness of treatment, and
type of bacteria responsible. Mortality is highest in the very young and the elderly, those with
persistent or recurrent infection, and those with compromised immune systems.
Generally, care for the septic patient is delivered by hospital-based health care
professionals in the hospital ICU (intensive care unit). Physicians, intensive care nurses, and
other nursing personnel closely monitor patients' vital signs and administer antibiotics and fluids.
Laboratory technologists perform necessary blood tests, and respiratory therapists may provide
oxygen to patients in respiratory distress.
II. ETIOLOGY
Most patients who develop sepsis and septic shock have underlying circumstances that
interfere with the local or systemic host defense mechanisms. Sepsis is seen most frequently in
elderly persons and in those with comorbid conditions that predispose to infection, such as
diabetes or any immunocompromising disease.
The most common disease states predisposing to sepsis are malignancies, diabetes
mellitus, chronic liver disease, chronic renal failure, and the use of immunosuppressive agents.
In addition, sepsis also is a common complication after major surgery, trauma, and extensive
burns. Patients with indwelling catheters or devices are also at high risk.
In most patients with sepsis, a source of infection can be identified, with the exception of
patients who are immunocompromised with neutropenia, where an obvious source often is not
found. Multiple sites of infection may occur in 6-15% of patients.
Before the introduction of antibiotics in clinical practice, gram-positive bacteria were the
principal organisms causing sepsis. More recently, gram-negative bacteria have become the key
pathogens causing severe sepsis and septic shock.
Anaerobic pathogens are becoming less important as a cause of sepsis. In one institution,
the incidence of anaerobic bacteremia declined by 45% over a 15-year period. Fungal infections
are the cause of sepsis in 0.8-10.2% of patients with sepsis, and their incidence appears to be
increasing.
Respiratory tract infection and urinary tract infection are the most frequent causes of
sepsis, followed by abdominal and soft tissue infections. Each organ system tends to be infected
by a particular set of pathogens (see below).
Lower respiratory tract infections are the cause of septic shock in 25% of patients, and the
following are the common pathogens:
Streptococcus pneumoniae
Klebsiella pneumoniae
Staphylococcus aureus
Escherichia coli
Legionella species
Haemophilus species
Anaerobes
Gram-negative bacteria
Fungi
Urinary tract infections are the cause of septic shock in 25% of patients, and the following are
the common pathogens:
E coli
Proteus species
Klebsiella species
Pseudomonas species
Enterobacter species
Serratia species
Soft tissue infections are the cause of septic shock in 15% of patients, and the following are the
common pathogens:
S aureus
Staphylococcus epidermidis
Streptococci
Clostridia
Gram-negative bacteria
Anaerobes
GI tract infections are the cause of septic shock in 15% all patients, and the following are the
common pathogens:
E coli
Streptococcus faecalis
Bacteroides fragilis
Acinetobacter species
Pseudomonas species
Enterobacter species
Salmonella species
Infections of the male and female reproductive systems are the cause of septic shock in 10% of
patients, and the following are the common pathogens:
Neisseria gonorrhoeae
Gram-negative bacteria
Streptococci
Anaerobes
Foreign bodies leading to infections are the cause of septic shock in 5% of patients, and S aureus,
S epidermidis, and fungi/yeasts (eg, Candidaspecies) are the common pathogens.
Risk factors
Risk factors for severe sepsis and septic shock include the following: