Pneumonia (PNA)
Balance between the organisms residing in the lower respiratory tract and the local and systemic defense mechanisms (both innate and acquired) become disturbed
Bacterial, viral, or fungal organisms that reach the alveoli, cause an immune response giving rise to inflammation of the lungs
Multi-Organ System Failure
Macrophages engulf pathogens triggering cytokine molecules and recruitment of neutrophils to site of infection
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Inflammation of lung parenchyma
Lining capillaries become "leaky", which leads to exudative congestion
Consolidation of lung(s)
Infection from the lungs enters the blood stream
Bacteremia
bacterial infection present in the body(streptococcus pneumoniae)
secretion of coagulase protein that activates host hemostatic factor prothrombin
bacterial display of surface proteins that bind polymerized fibrin called agglutinins
culmination of abscess lesions
recruitment and destruction of immune cells via secreted factors associated with the pathogen controlled process
transformation of abscess lesions into purulent exudate w/ which bacteria (streptococcus pneumoniae) disseminate to produce new infectious lesions or infect new hosts
can often progress to
Sepsis
body has a localized infection, normal response: process that localizes and controls phagocytic cells to fight the bacterial invasion while also repairing injured tissue with pro-inflammatory and anti-inflammatory mediators
Impaired systemic defense mechanisms (e.g. autoimmune)
sepsis occurs when release of pro-inflammatory mediators becomes generalized instead of staying within local boundaries
The development of potentially reversible physiologic derangement involving two or more organ systems not involved in the disorder that resulted in ICU admission, and arising in the wake of potentially life-threatening physiologic insult.
Inability to produce productive cough to clear secretions
Altered organ function that causes the body to fail to maintain homeostasis
Other than the organ systems failing, this process can also affect the hematologic system, immune system, and the endocrine system.
patients at higher risk
chronic medical conditions (diabetes, lung disease, cancer, kidney disease)
signs and symptoms
clammy/sweaty skin
Development of atelectasis
blood then spreads the pro-inflammatory mediators (cytokines and tumor necrosis factor) throughout the interstitial space throughout the body producing a generalized response
Contributes to development/worsening of PNA
This process is often caused by uncontrolled infection in the body, which then leads to multiple organ system dysfunction.
Compromised mucociliary clearance due to smoking hx predisposes risk for PNA
fever, shivering, or feeling very cold
Several descriptive scales use the same six organ systems to characterize MOSF - respiratory, cardiovascular, renal, hepatic, neurologic, and hematologic systems.
extreme pain/discomfort
SOB
high heart rate
Predisposes individuals to infection by intracellular organisms such as bacteria, viruses and fungi
Bronchial breath sounds due to alteration of low pass filtering function of alveoli from consolidation
Histologic features of the organ systems that fail are less understood, but often include edema, inflammation, tissue ischemia/necrosis, fibrosis and repair.
confusion/disorientation
d/t increase in cytokines in bloodstream
d/t proinflammatory mediators being carried throughout the bloodstream to produce a more generalized response instead of local, pain becomes more widespread
Gastrointestinal/Hepatic
Neurologic
Heart/Cardiovascular System
Hematologic
Kidney
Immunologic
Lung
Endocrine/Metabolic
Presence of patchy white opacities on radiography
d/t breakdown of the blood brain barrier allowing inflammatory mediators through to interact with the brain causing a change in metabolism and cell signaling, allows other neurotoxic factors through
d/t a systemic response by the body to attack the infection, increased cardiac output and oxygen required by tissues is increased. eventually RR increases to compensate for metabolic acidosis
d/t increased parasympathetic activity which affects ability to thermoregulate
weakened immune systems
children <1 yo
Due to impaired gas exchange
Could be from atelectasis, intravascular thrombosis, trauma to the lungs, or altered regional flow that contributes to issues with ventilation/perfusion
This leads to increased capillary permeabillity, that causes alveolar flooding and then increased diffusion distance for O2
Systemic signs and symptoms such as fever with chills, malaise, myalgias
Results in decreased gas exchange and the need for increased respiratory effort
if not treated quickly enough the cellular injury and release of pro-inflammatory and anti-inflammatory mediators spreads throughout the bloodstream to reach other organs and leads to organ dysfunction and potentially death
Due to the trauma to the lung tissue, the process of tissue repair starts and that is when there is an increase in inflammatory cells rushed to the injured areas, and this could result in fibrosis and therefore, decreased lung function.
Due to impairment of normal selective excretory function
adults 65+ yo
Starts are oliguria (production of abnormally small amounts of urine), then rising creatinine levels, then drastic fluid/electrolyte changes, eventually leading to a need for dialysis
d/t increased workload of the heart as it tries to pump blood throughout body to help defeat the infection
Generalized reduction in peripheral vascular tone
Due to interacting effects of reduced regional blood flow, impaired motility, and alterations in the normal microbial flora.
Leads to an increase in capillary permeability producing diffuse capillary leak, and contributing to further dysfunction in other organ systems
Multiple causes such as the iatrogenic effects of sedatives and analgesics, metabolic alterations, subclinical cerebral edema and reduced cerebral perfusion pressure, and, perhaps, micro-abscesses in the brain
Alterations in regional blood flow to specific organ beds
Microvascular plugging/stasis, resulting from occlusion of the microvasculature, which results in arteriovenous shunting
Due to multiple abnormalities of specific and non-specific immune function
Myocardial depression, affecting the R side of the heart in particular
Leukocytosis (an increase in the number of white cells in the blood, especially during an infection), and thrombocytopenia (low blood platelet count that help to repair and form plugs in blood vessel injuries) are common in MOSF
Most clinically relevant is nosocomial ICU-acquired infection, caused by relatively avirulent organisms.
Hyperglycemia and relative insulin resistance are both common in MOSF. Failure of a gland to stimulate another gland to release hormones.
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