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NS7920 > Module 2: Mai > Flashcards

Module 2: Mai Flashcards

1
Q

What is the purpose of diagnostic reasoning?

A

The purpose of diagnostic reasoning is to determine what could possibly be wrong.

abnormal assessment finding –> hypotheses generation –> further assessment –> ruling in/ruling out hypotheses

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2
Q

What are 5 signs&symptoms respiratory distress infants with TTN will show?

A
  • cyanosis,
  • chest retraction
  • expiratory grunting,
  • nasal flaring,
  • tachypnea
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3
Q

For TTN infant, what does their chest X-ray look like?

A

On a chest x-ray, the lungs appear wet because of increased interstitial and alveolar fluids and decreased thoracic gas volume.

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4
Q

While TTN and pneumonia have similar clinical presentations, what is one difference between them?

A
  • Whereas TTN resolves with time,
  • pneumonia can severely compromise an infant’s respiratory status and may progress to sepsis if not treated.
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5
Q

What is this blood gas showing?
pH 7.25
pCO2 55
pO2 38
HCO3 15
Base excess −6.3

A

mixed respiratory and metabolic acidosis

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6
Q

How does the predominant transfer of maternal antibodies occurs?

A

The predominant transfer of maternal antibodies, an important source of a fetus’ and newborn’s immunity,
- occurs by way of passage of immunoglobulin G (IgG) from maternal to fetal circulation during the last trimester of pregnancy.

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7
Q

What important sources of immunity are found in plasma and tissues fluids?

A

Immunoglobulins, or antibodies

**The immunity that results from the passage of IgG is transient
- it may provide protection from microorganisms during fetal growth and development and in the immediate newborn period

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8
Q

Where can microorganisms colonize in infants (4)?

A

The microorganisms can colonize in a variety of place:
- skin,
- mucous membranes,
- gut,
- lungs,
- venipuncture sites, and so on
***produce either a localized infection and/or sepsis.

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9
Q

Why is it that localized infections can quickly become systemic and result in sepsis in infants?

A
  • Because infants have immature and inexperienced immune systems,
  • localized infections can quickly become systemic and result in sepsis.
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10
Q

What is Chorioamnionitus?

A

Chorioamnionitus is a maternal infection that affects the placenta and the membranes that surround the growing baby.

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11
Q

How can a pregnant woman get Chorioamnionitus?

A

A pregnant woman can get Chorioamnionitus
- when bacteria move upward through her vagina and into her uterus.

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12
Q

What can mismanaged Chorioamnionitus cause (3)?

A

Mismanaged Chorioamnionitus can cause
- neonatal infection,
- preterm labour,
- HIE,
- cerebral palsy,
- periventricular leukomalacia (PVL), and
- other injuries and complaications.

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13
Q

What are the presentation of infection? NOT RIGHT

A

Neurological symptoms: lethargy, seizures, hypotonia, hypertonia
Other symptoms: glucose instability, metabolic acidosis,
Tachycardia

Respiratory distress, cyanosis, apnea
Increasing feeding intolerance
GI poor feeding
Hypotension, hypertension
Thermal instability

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14
Q

What are the manifestation and infections of congenital infections?

A

manifestations
- growth retardation
- congenital malformation
- fetal loss

infections
- rubella
- CMV
- HIV
- toxoplasma
- parvovirus
- VZV

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15
Q

What are the manifestation and infections of perinatal infections?

A

manifestations
- meningitis
- septicemia
- pneumonia
-preterm labor

infections
- genococcus
- chlamydia
- HSV
- VZV
- Group B strep
- e. coli
- usteria

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16
Q

What are the manifestation and infections of postnatal infections?

A

manifestations
- meningitis
- septicemia
- conjunctivitis
- pneumonitis

infections
- breastmilk: HIV, CMV
- umbilicus: staphylococci, tetanus
- person to person: group b strep, listeria, e. coli
- N. gonorrhea
- chlamydia

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17
Q

How does infection occur in neonate?

A
  • infections occur when a susceptible host, or newborn, comes in contact with a potentially pathogenic organism.
  • When an encountered organism proliferates and
  • overcomes a newborn’s host defenses —> infection results.

***The most serious of postnatal infections are caused by organisms that result in bacterial sepsis, or bacteremia (the presence of bacteria in the blood).

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18
Q

What are the two categories that neonatal sepsis is categorized into?

A
  • early-onset sepsis
  • late-onset sepsis
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19
Q

How is early-onset sepsis acquired and the most common microorganisms?

A

Acquisition:
- microorganisms from the mother
- neonate acquires the microorganism as it passes through the colonized birth canal at delivery
- sepsis within the first 7 days of life

Most Common Microorganisms:
- group B streptococcus (GBS)
- escherichia coli
- streptococcus viridans
- streptococcus pneumoniae
- enterococcus
- entrobacter
- staphylococcus aureus
- haemophilus influenzae

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20
Q

How is late-onset sepsis acquired and the most common microorganisms?

A

Acquisition:
- acquired from the caregiving environment
- sepsis occurs > 7 days of life

Most Common Microorganisms:
- coagulase-negative staphylococcus
- escherichia coli
- klebsiella
- enterobacter
- candida
- group B streptococcus

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21
Q

What is Early-Onset Sepsis EOS?

A
  • EOS is sepsis that occurs in the first 7 days of life, with most infants becoming symptomatic in the first 24 hours.
  • EOS sepsis usually results from vertical transmission and is consequently associated with organisms that colonize the birth canal.
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22
Q

What are risk factors for Early-Onset Sepsis EOS (3)?

A
  • maternal GBS colonization in current pregnancy
  • GBS bacteriuria anytime in the current pregnancy
  • a previous infant with invasive GBS disease
  • prolonged ROM ≥18 hours
  • maternal fever ≥38° C
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23
Q

What is Group B streptococcal (GBS) disease most common cause of?

A

Group B streptococcal (GBS) disease is the most common cause of
- neonatal infectious morbidity and mortality and a
- significant cause of maternal illness during the perinatal period.

**GBS remains one of the most prevalent and devastating pathogens for childbearing women and their unborn and newborn infants.

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24
Q

How does Group B streptococci (GBS) ascend during pregnancy?

A
  • During pregnancy, Group B streptococci can ascend a woman’s genitourinary tract and enter the bloodstream.
  • An infant may acquire GBS by aspirating infected amniotic fluid in utero or may become colonized during delivery through the birth canal.
  • In addition, GBS may be transmitted transplacentally.

***The majority of early-onset GBS infection takes the form of pneumonia.

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25
Q

What happens when severe sepsis develops?

A
  • Neonatal sepsis, a neonate’s systemic response to infection, manifests itself in a number of body systems and organs.
  • In neonates, when severe sepsis develops, multisystem and multi-organ involvement often ensue and can rapidly progress towards a life-threatening health challenge known as septic shock.
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26
Q

What is shock best understood as?

A
  • an inability of the circulatory system to adequately perfuse the body cells.
27
Q

What 3 factors are responsible for maintaining cellular perfusion?

A
  • blood volume—the amount of circulating blood
  • rate and force of the heart beat—pumping action
  • vascular tone—resistance, tension within the blood vessels
28
Q

What are the three essential components of circulation?

A
  • blood volume
  • cardiac pump
  • vascular tone

**Shock results from the loss of integrity of one of three essential components of circulation

29
Q

What is the final common pathway of shock?

A

Regardless of the etiology, the final common pathway of shock is cell destruction caused by inadequate perfusion.

30
Q

What are the three broad classification of shock?

A
  • hypovolemic shock—occurs due to an inadequate blood volume
  • cardiogenic shock—occurs due to an inadequate pump (heart) function
  • distributive or maldistributive shock—occurs due to a malfunction in vascular tone

**Shock is a progressive disorder.

31
Q

How is shock a progressive disorder?

A

Shock is a progressive disorder.
- Despite the varying causes of shock and their associated etiologies—hypovolemic, septic or distributive, and cardiogenic—all result in inadequate tissue perfusion.
- As shock progresses, the body attempts to adapt to the inadequate perfusion and preserves vital organ function.
—> If not treated, inadequate tissue perfusion eventually causes hypoxia, acidosis, and cell death

32
Q

What is hypovolemic shock caused by?

A
  • caused by acute blood loss or fluid and electrolyte losses
33
Q

What can cause hypovolemic shock during antepartum/intrapartum periods (4)?

A
  • acute blood loss arising from placenta previa
  • spotting during the last trimester
  • abruptio placenta
  • twin-to-twin transfusion
  • birth asphyxia
  • birth injuries such as rupture of umbilical vessels, spleen or liver
34
Q

What cause hypovolemic shock during the neonatal periods (4)?

A
  • intraventricular hemorrhage
  • pulmonary hemorrhage
  • disseminated intravascular coagulation
  • vitamin K deficiency
  • other iatrogenic causes of reduction in blood volume include accidental disconnection of or a loose connection in the tubing of an umbilical arterial catheter
35
Q

What can cause hypovolemic shock from diminished intravascular volume (3)?

A
  • Loss of volume may also be in the form of plasma, extracellular fluid, or a combination of all three.
  • Loss of blood and/or fluid from intravascular spaces does not necessarily entail losses from the body.
  • Volume may be lost from vascular spaces into interstitial spaces (edema) or into cerebral ventricles (IVH).
  • Any decreases in blood volume disrupt the delicate balance necessary for normal circulation.
36
Q

What are some conditions can cause cardiogenic shock (4)?

A

Cardiogenic shock results from any condition that causes the heart to fail as a pump, such as:

congestive heart failure CHF
PPHN
perinatal asphyxia
hypoxic/ischemic episodes
hypothermia
hypoglycemia and acidosis
congenital heart defects CHD
anemia
pneumothorax
pneumopericardium
diaphragmatic hernia CDH
airway obstruction
acute hypovolemia
severe pulmonary interstitial emphysema PIE

37
Q

What is distributive shock?

A
  • Distributive shock is characterized by excessive vasodilation and abnormal distribution of blood in the circulatory system.
  • This kind of shock is an abnormal distribution that occurs due to altered elasticity of blood vessels, causing the vessels to dilate.
    **Remember that blood vessels are elastic, not rigid, and have the ability to dilate or constrict.
38
Q

What are the 3 sub-classifications of distributive shock?

A
  • septic shock
  • anaphylactic shock
  • neurogenic shock
39
Q

What is the common precursor of distributive shock?

A

neonatal sepsis

40
Q

How does sepsis lead to maldistribution of blood?

A
  • Once activated, the immune system releases neutrophils, immune globulins, and other components of the immune defense system into the blood.
  • In order to rapidly deliver these components to sites of infection, the circulatory system dilates.
  • The toxins released by certain microorganisms also causes vasodilation.
    **When massive vasodilation occurs, blood tends to pool in the peripheral circulation.
    As a result, less blood is available for central circulation. In this way, the blood volume is maldistributed.
41
Q

What is the term when distributive shock is precipitated by sepsis?

A
  • septic shock
42
Q

What are 2 microorganisms are common cause of gram-negative and gram-positive sepsis and shock in newborns?

A

Escherichia coli and Group B streptococcus

43
Q

What happens when massive vasodilation occurs?

A
  • When massive vasodilation occurs, blood tends to pool in the peripheral circulation.
  • As a result, less blood is available for central circulation.
  • In this way, the blood volume is maldistributed.
44
Q

What does it mean by septic shock is conceptualized as a clinical response?

A
  • beginning with sepsis —> progressing to septic shock, —> then to multisystem organ dysfunction
45
Q

How many stages of septic shock?

A
  • early stage
  • middle stage
  • late stages
46
Q

What is the early stage of septic shock?

A
  • Infant responses during the early stage are usually subtle, nonspecific, and insidious.
  • An infant may be described as “not doing well,” “not right,” or “not handling well.”
  • Some infants in the early phase may be lethargic and not feeding well, with unstable temperatures.
    ***Knowing an infant and his/her usual behaviours is very helpful in terms of recognizing responses during the early stage of septic shock.
47
Q

What is the middle stage of septic shock?

A
  • During the middle stage of shock, some infants will look quite well perfused.
  • This is because of peripheral vasodilation.
  • Although pink with normal capillary refill times, infants are also often lethargic and hypotonic during this phase.
  • Temperature instability, apnea, and bradycardia may also be present.
48
Q

What is the late stage of septic shock (8)?

A

The late stage of septic shock is often referred to as end-stage shock:
- changes in capillary dynamics result in increased capillary permeability,
- which, in turn, causes leakage of intracellular fluid into interstitial spaces.
- which produces a decrease in circulating blood volume,
- which results in decreased cardiac output.
- which causes vasoconstriction,
- which reduces tissue perfusion,
- which, in turn, results in more hypoxia and tissue damage,
- and eventually cell death.

49
Q

What are some signs/symptoms of end-stage shock (4)?

A
  • cold, clammy skin
  • pale, mottled gray color, cyanosis
  • sluggish capillary refill (> 3 seconds); infant looks poorly perfused
  • weak, thready, rapid peripheral pulses
  • hypotension
  • tachycardia
  • decreased urine output
  • lethargy
50
Q

What are some treatment for restoring ventilation and perfusion to minimize irreversible tissue and organ damage (4)?

A
  • providing ventilatory support
  • oxygen therapy
  • correction of mixed acidosis
  • antimicrobial therapy, if indicated
  • volume expansion
  • inotropic support
51
Q

Which interventions would you expect to be ordered based on Mai’s deterioration and diagnosis of distributive shock? Select all that apply.

a. Volume replacement

b. Diuretics

c. Inotropes

d. Antibiotics

e. Packed red blood cells (PRBCs)

A

Volume replacement
Inotropes
Antibiotics

52
Q

What is Disseminated Intravascular Coagulation (DIC)?

A
  • DIC is a pattern of simultaneous, uncontrolled bleeding and clotting within the vascular system.
  • In addition, DIC is usually a symptom of an underlying pathologic event, such as sepsis.
53
Q

When is neonatal Disseminated Intravascular Coagulation (DIC) thought to result from?

A

Neonatal DIC is thought to
- result when a severe insult, such as sepsis or hypoxia,
- leads to endothelial tissue damage.
- This damage activates the clotting cascade,
- which promotes consumption of platelets and coagulation factors,
- which results in bleeding.

***In addition, microthrombi can obstruct blood flow, leading to ischemic tissue damage and organ failure.

54
Q

What can confirm Disseminated Intravascular Coagulation (DIC)?

A

Laboratory tests and an infant’s clinical status confirm a diagnosis of DIC
- platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen levels, and D-dimers, Factor V, VIII, X, XIII

55
Q

What are some important supportive measures for Disseminated Intravascular Coagulation DIC (4)?

A
  • ventilatory support,
  • volume support, and
  • pressor support if the patient is hypotensive,
  • as well as close monitoring of neurologic and renal function
  • providing fresh frozen plasma (FFP), platelets, cryoprecipitate
56
Q

What is Multi-Organ Dysfunction Syndrome (MODS)?

A
  • Multi-organ dysfunction (previously known as multisystem organ failure [MSOF]) is the presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention.
  • It usually involves two or more organ systems.
  • Alteration in organ function can vary widely from a mild degree of organ dysfunction to completely irreversible organ failure.
57
Q

What is one problems with identifying organ failure?

A
  • One of the problems with identifying organ failure is that it is not always easy to distinguish between organ dysfunction and organ failure.
  • This is particularly the case in neonatal nursing as the physiological condition rendered by MODS/MSOF may be indistinguishable from that which occurs as a result of prematurity and perinatal asphyxia.
58
Q

What is Systemic Inflammatory Response Syndrome SIRS?

A
  • SIRS is the process that occurs when sepsis overstimulates the inflammatory response,
  • triggering a cascade of harmful physiological responses that could lead to MODS and death.
59
Q

Why is it believed that infants who develop sepsis, the host develops a systemic reaction to the bacteria?

A
  • This reaction induces the release of substances known as inflammatory mediators,
  • which contribute to the signs and symptoms and to the pathophysiological sequelae of sepsis.
60
Q

What is the physiological regulatory response to sepsis? Pathophysiological changes initiate what?

A
  • The physiological regulatory response to sepsis is “turned on” and remains activated.
  • Instead of remaining a local reaction, the infant’s response to the invader becomes diffuse, widespread, and inflammatory.
  • This initiates the pathophysiologic changes, tissue destruction and ultimate organ dysfunction and failure that can be seen in sepsis.
61
Q

What are 3 clinical responses to Systemic Inflammatory Response Syndrome SIRS include?

A
  • Uncontrolled systemic vasodilation results in hypotension and decreased systemic vascular resistance.
  • Increased capillary permeability leads to third spacing, peripheral edema, and pulmonary edema.
  • Overstimulation of the clotting cascade may lead to disseminated intravascular coagulopathy (DIC).
62
Q

What is sepsis pathway

A

SIRS (suspected infection) –> SEPSIS (SIRS and proven infection) –> SEVERE SEPSIS (sepsis and organ damage) –> SEPTIC SHOCK (severe sepsis and hypotension)

63
Q

What is the primary goal of treatment of neonatal MODS?

A
  • The primary goal of treatment of neonatal MODS is to recognize, prevent, and limit tissue injury due to hypoxia and acidosis prior to the occurrence of permanent organ damage and death.
  • Delays in appropriate therapy that will improve ventilation and perfusion may exacerbate cellular injury in all organ systems and death may rapidly ensue.

NS7920 (5 decks)

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