Crossover of infection (via Bacteria, most commonly

medical care worker, visitor, Escherichia coli, but also

medical instrument) other pathogens, enter the
urinary tract.

Bacterial Bacteria adhere to the

Inhalation Aspiration epithelial cells lining the
Translocation
urinary tract

Colonization in Colonization in
gastrointestinal Bacterial adherence is
nasopharynx facilitated by specific
track
virulence factors such as
fimbriae or pili.

Bacterial invasion triggers an

inflammatory response in the lungs.
Bacterial invasion triggers an
inflammatory response, leading to the
release of cytokines, chemokines, and
other inflammatory mediators.
Inflammation leads to the recruitment
of immune cells, release of
inflammatory mediators, and increased
vascular permeability.

Inflammation can cause damage to the

alveoli, leading to consolidation
(solidification) of lung tissue.

Impair gas exchange

Predisposing Factors Precipitating Factors

Bacteria enters the
Age bloodstream vausing systemic Hemodynamic Instability
Vascular Conditions spread Bacterial Infection
Comorbidities Microbial Toxins

Presence of an infection triggers a

systemic inflammatory response.

Infection activates immune cells

leading to the release of Body Malaise
pro-inflammatory mediators.

Pro-inflammatory cytokine causes

endothelial cell avctivation and
dysfunction.

Increased vascular permeability

leading to leakage of fluid and proteins Edema
into tissues.

Systemic inflammatory response

affects microvascular function.

Uneven blood distribution and tissue

perfusion.

Inflammatory mediators and

microvascular dysfunction can
compromise the integrity of
blood-brain-barrier (BBB).

Entry of immune cells and

pro-inflammatory mediators into the Alteration of Sleep-Wake Cycle
brain trigers a localized inflmmatory
response within the CNS.

If Treated
Microglial cells activated.

Laboratory and Diagnostic Medications:

citicholine Activated microglial release additional
telmisartan + amlodipine cytokines and inflammatory mediators
cilostazol within the brain.
Sputum GS CT Scan Urinalysis Arterial Blood Gas Complete Blood Serum Electrolytes atorvastatin
Count Lumbar Tap KCl
Epithelial Cells: >10/LPF Consider acute infarct right Yellow PCO2: 31 mmHg (L) K: 2.40 mmol/L (L) febuxostat
Gram (+) cocci: -1+ lobe and Slightly Cloudy PO2: 109 mmHg (H) RBC: 4.48 (L) Mg: 1.10 mmol/L (H) CSF Glucose: 5.07 colchine
Gram (-) rods: -1+ thalamocapsuloganglionic Specific Gravity: 1.036 HCO3: 21.1 mmol/L (L) WBC: 16.4 (H) Crea: 111.8 umol/L (H) piperacillin + Sepsis-induced inflammation and
Fungus: Few area. (H) tCO2: 22.1 (L) Segmenters: 0.85 (H) (H) CSF Protein: 42.8 (H) tazobactam oxidative stress
Periventricular hypodensity Protein (+) BEecf: -3.1 (L) Lymphocytes: 0.11 (L) RBC: 19.3 (H) mannitol
changes can be due to WBC: 104.8 (H) Eosinophils: 0.00 (L) ceftazidime
microangiopathy. RBC: 23.8 (H) RESPIRATORY Platelet Count: 431 (H) vancomycin
Cerebral atrophy can be Epithelial Cells: 21.9 (H) ALKALOSIS
age related with ex vacuo Bacteria: 3968.5 (H) Mitochondrial dysfunction in various
dilation of the anterior horn tissues.
of the right lateral ventricle.
Arteriosclerotic internal
Urine GS
carotid and vertebral
arteries. Mitochondrial impairment disrupts Generation of reactive oxygen
cellular energy production and species.
contributes to cellular injury.

Increased ROS production, coupled

with reduced antioxidant defenses, Cognitive Impairment
results in oxidative stress.

Altered Mental Status

Disrupt neurotransmitter balance

in the brain.
Anorexia

Cellular injury and dysfunction can

lead to the accumulation of fluid Increased intracranial
within brain cells, known as pressure.
cytotoxic edema.

Microglia becomes activated in

response to inflammmation

Dysregulation of cerebral blood

flow autoregulation occurs.

Cumulative effects of the

inflammatory response and
cellular dysfunction

If untreated

Shock Coma

Poor Prognosis