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Pathophysiology Plueral Effusion Secondary To Pneumonia: Green

This document describes the pathophysiology of a pleural effusion secondary to pneumonia. Key points: 1) Pneumonia leads to inflammation and damage to the lungs which causes fluid to accumulate in the pleural space between the lungs and chest wall. 2) Symptoms include shortness of breath, chest pain, fever, and cough as the buildup of fluid impairs breathing. 3) Treatment involves draining the fluid via thoracentesis or chest tube and administering antibiotics to treat the underlying pneumonia.

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0% found this document useful (0 votes)
138 views7 pages

Pathophysiology Plueral Effusion Secondary To Pneumonia: Green

This document describes the pathophysiology of a pleural effusion secondary to pneumonia. Key points: 1) Pneumonia leads to inflammation and damage to the lungs which causes fluid to accumulate in the pleural space between the lungs and chest wall. 2) Symptoms include shortness of breath, chest pain, fever, and cough as the buildup of fluid impairs breathing. 3) Treatment involves draining the fluid via thoracentesis or chest tube and administering antibiotics to treat the underlying pneumonia.

Uploaded by

kuro hanabusa
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Legend:

PATHOPHYSIOLOGY - - - Symptoms/Manifestations
 Disease Process
PLUERAL EFFUSION SECONDARY TO PNEUMONIA
In red- manifested by client
In green- treatments received/
undertaken by client

PRECIPITATING FACTORS
PREDISPOSING FACTORS
 Existing comorbidities: (Heart FailurePulmonary
 Genetics: infections: Pneumonia (viral/bacterial), tuberculosis,
 Familial/Idiopathic pulmonary Nephrotic syndrome, Liver cirrhosis, Neoplastic
hypertension tumors, Connective tissue disease: SL)
 Age  Trauma: Chest Injuries
 Sex: Male  Surgery: heart, lungs, abdomen and organ transplant
 Radiation therapy
 Lifestyle:
 Smoking
 Alcohol intake
 Environmental:
 Chemicals: Asbestos
 Drugs: nitrofurantoin, dantrolene, methysergide,
amiodarone, interleukin-2, procarbazine,
methotrexate, clozapine, phenytoin, and beta-blockers

Exposure of the infectious pathogen.

Pathogen invasion and proliferation in the lower respiratory tract Produce of endotoxin
Tissue damage within the endothelial cells
Activation of immune responses

Disruption of the blood vessels

Stimulation of goblet cells


Accumulation of blood into the
Productive Cough pleural spaces
Increase mucus production into
Wheezing during the airways
expiration

Decrease exchange of oxygen Pro-inflammatory mediators: Leukotrines, Histamines,


and carbon dioxide prostaglandin, TNF-a, IL-1, PAF

Decreased O2: (90%) Inadequate supply of oxygen Vasodilation and increase capillary
Dyspnea into the body. permeability
Use of accessory
muscles
Pallor
Fatigue 0xygen @ Protein and large Increased numbers of WBC
Peripheral cyanosis Hypoxemia 3L/min molecules diffuses into and chemical mediators at
Restlessness the interstitial spaces site of infection
Confusion
Triggers peripheral and
Decreased Increase Hydrostatic
Tachypnea: 28 cpm
central chemoreceptors to
Oncotic pressure pressure
Tacyhcardia increase respiratory drive

Leakage of fluid into the Shortness of


Breath
lower pleural space (via
Dull upon
gravity) and into alveoli percussion in the
lower part
Diminished vocal
Decrease lung fremitus
expansion Coarse Crackles
Dry Cough
Irritation of pleural
spaces
Pleuritic Thoracentesis
Chest pain (2L of
during serosanguinous
inspiration Stimulation of the fluid)
Dyspnea nerves in the pleura
Macrophage Travels and
engulfs the across the
bacteria blood stream
produces TNF-a,
IL-8
Release of Prostaglandins
(PGE-2)

Disruption of hypothalamic
thermoregulation

Fever (37.9 degrees


Celsius)

WITHOUT INTERVENTION WITH INTERVENTION

Continuous build-up of fluids into


the pleural space
Diagnostic Tests:

 Physical examination
 Chest x-rays (lateral decubitus)
 Chest CT scan
 Empyema - Infected Pleural  Ultrasound of the chest
Effusion/pus formation  Thoracentesis
 Lobar Lung Collapse or Atelectasis  Pleural fluid analysis (culture, chemistry, cytology)
 Lung Scarring Severe Chest pain  Pleural biopsy
 Permanent decrease in lung function
 Pleural fibrosis Re-expansion Medical Management:
 Pulmonary edema Pseudochylothorax  Thoracentesis
 Chest tube and water-seal drainage
 Chemical pleurodesis
 Surgical pleurectomy
BAD PROGNOSIS  Supplemental oxygen (oxygen therapy)
 Diet modifications: high protein and low salt, low fat diet

Pharmacologic Management:
DEATH
 Antidepressants
 Antimetabolites
 Antibiotics
 Antiepileptic
 Antiarrhythmic
 Beta blockers
 Ergot Alkaloids

Nursing Management:

 Administer supplemental oxygen therapy to help meet body’s needs.


 Monitor for changes in vital signs.
 Have the patient perform turning, coughing, deep-breathing exercises to enhance
lung expansion.
 Monitor chest tube drainage for color, amount, and changes in drainage.
 Assure patency of chest tube to make sure the tube is draining properly
 Assist patient in pain relief.
 Assist patient to assume positions that are least painful.
 Administer pain medication as prescribed and needed to continue frequent turning
and ambulation.
 If the patient is to be managed as an outpatient with a pleural catheter for drainage,
educate the patient and family about management and care of the catheter and
drainage system.
GOOD PROGNOSIS

Reference:
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http://calgaryguide.ucalgary.ca/adult-pneumonia-pathogenesis-and-clinical-findings/
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Wei Yang1, Bo Zhang1, Ze-Ming Zhang. Infectious pleural effusion status and treatment progress. Retrieved From
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