Pathophysiology- Sarina Asuncion, Janhine Nicole Baclig

Pathophysiology of Neonatal Sepsis secondary to Neonatal Pneumonia

Non-modifiable Modifiable
Age: 0-5 yrs old – their Diet: Poor (poor
immune system is still breastfeeding by mother)
immature
Infections: Streptococcus
Pneumoniae

Virulent Microorganism
Streptococcus Pneumoniae
Microorganism enters the
nose (nasal passages)

Passes through the larynx,

pharynx, trachea
Microorganism enters lung
parenchyma

Hypertrophy of mucous membrane

(mucus production)
Cough
• inflamation
• vasodilation
• leukocyte and macrophage
• wheezing upon auscultation

Bacteria multiplies in the alveoli

Fever Release of endotoxins and exotoxins from the bacteria
(toxins are directly causing the damage to the tissues)

Antibiotics
Continuous mucus production
Narrowing of air passage

1
 Lung consolidation (region of lung tissue
filled with liquid) due to cellular exudates Difficulty of breathing
(fluid, pus, and blood) from inflammation of (Intercostal retractions,
the pleura causes chest pain subcostal retractions.)

Impaired 02 and C02 exchange

due to lung consolidation
Increased respiratory
rate
Increase oxygen demand

O2 administration Increased pulse rate

Hypoxia
(earlysx: irritable,jitteriness)

Necrosis of pulmonary tissue

Failure of immune response in

the pulmonary tissues

The bacterium goes with the blood and

release toxins

Whole-body inflammatory state

Inflammatory response Systemic Reaction

• Neutrophils –
marks the
pathogen as
foreign then
Pro-Inflammatory Response Anti-Inflammatory Response
signals
(Cytokines) Interleukin 10 (IL-10) – and
phagocytes for
anti-inflammatory cytokine
ingestion of
bacteria

Antibiotic Therapy
Failure of
Whole-body inflammatory state

2
 Systemic Infection
(Septicemia)

Initial Phase (1-3 days)

Body compensates from systemic inflammatory response by slowing

things down in order for body to recover.

Decrease systemic Hypometabolism

vascular resistance

Decreased energy
Warm, bounding
expenditure
pulses, with brisk
capillary refill, edema

Decrease o2
Antibiotic therapy consumption
broad spectrum
cephalosporin
Vasoconstriction

Cool extremities, poor

peripheral pulses, and Late Phase
hypotension Compensatory
mechanism:
• Increase BP
Hyperdrive (Compensatory mechanism)
• Increase PR
(If the body doesn’t recover it goes into hyperdrive)
This is partly due to the • Increase RR
Exaggerated inflammatory response • Increase TEMP

End of compensatory mechanism Negative Feedback:

(negative feedback mechanism) • sudden decrease BP
• deminished PR
• decrease body TEMP
Poor perfusion

Lactic acidosis
Inadequate 02 delivery
and nutrients to tissues
3
 Metabolic acidosis
Fluid Replacement
therapy

Shock or septic shock

MODS
Multiple Organ Dysfunction
Syndrome due to inability to
maintain homeostasis

Hepatic Acute renal Impaired Disseminated intravascular coagulation

dysfunction failure pulmonary (DIC) -also known as consumptive
function coagulopathy a pathological
activation of coagulation
(blood clotting) mechanisms

Hyperbilirubinemia
DEATH