RESPIRATORY SYSTEM

ANATOMY
❖ Comprised of the upper airway and lower airway structures.

❖ Upper respiratory system

❖ Filters, moistens and warms air during inspiration.

● Nose

✔ Serves as a passageway for air to pass to and from the lungs. It filters impurities and humidifies and
warms the air as it is inhaled
● Paranasal Sinuses

✔ Prominent function of the sinuses is to serve as a resonating chamber in speech

● Pharynx

● Throat, is a tube-like structure that connects the nasal and oral cavities to the larynx

● Larynx

✔ Voice organ, is a cartilaginous epithelium lined structure that connects the pharynx and the trachea.

✔ The major function is for vocalization

● Trachea (Windpipe)

✔ Serves as the passage between the larynx and the bronchi

❖ Lower respiratory system

❖ Enables the exchange of gases to regulate serum PaO2, PaCO2 and pH.

❖ Lungs

✔ Paired elastic structures enclosed in the thoracic cage, which is an airtight chamber with distensible walls

● Pleura

✔ Serous membrane that lined the lungs and wall of the thorax

● Bronchi and Bronchioles

● Alveoli

✔ Basic gas-exchange unit of the respiratory system is the alveoli.

✔ Alveolar stretch receptors respond to inspiration by sending signals to inhibit inspiratory neurons in the brain stem
to prevent lung over distention.
✔ During expiration stretch receptors stop sending signals to inspiratory neurons and inspiratory is ready to start
again.
✔ Oxygen and carbon dioxide are exchanged across the alveolar capillary membrane by process of diffusion.

✔ Neural control of respiration is located in the medulla. The respiratory center in the medulla is stimulated by the
concentration of carbon dioxide in the blood.
✔ Chemoreceptors, a secondary feedback system, located in the carotid arteries and aortic arch respond to
hypoxemia. These chemoreceptors also stimulate the medulla.
DISORDERS OF THE UPPER RESPIRATORY SYSTEM

RHINITIS

❖ A group of disorders characterized by inflammation and irritation of the mucous membranes of the nose
❖ Allergic rhinitis
 ● Further classified as seasonal rhinitis (occurs during pollen seasons) or perennial rhinitis (occurs
throughout the year)
● Commonly associated with exposure to airborne particles such as dust, dander, or plant pollens in people who
are allergic to these substances
● Clinical Manifestations
✔ Rhinorrhea (excessive nasal drainage, runny nose)

✔ Nasal congestion

✔ Sneezing

✔ Pruritus of the nose, roof of the mouth, throat, eyes, and ears

● Management

✔ Antihistamines

✔ Corticosteroid nasal sprays

✔ Desensitizing immunizations

● Nursing Intervention

✔ Instruct the patient with allergic rhinitis to avoid or reduce exposure to allergens and irritants

✔ Instructs the patient in correct administration of nasal medications

 ✔ To achieve maximal relief, the patient is instructed to blow the nose before applying any medication into the
nasal cavity

VIRAL RHINITIS (COMMON COLD)

● Most frequent viral infection in the general population caused by coronavirus

● Highly contagious because virus is shed for about 2 days before the symptoms appear and during the first part of the
symptomatic phase
● Clinical Manifestation

✔ Low-grade fever

✔ Nasal congestion

✔ Rhinorrhea and nasal discharge

✔ Halitosis, sneezing

✔ Tearing watery eyes

✔ “Scratchy” or sore throat

✔ General malaise, chills

✔ Headache and muscle aches

● Management

✔ Symptomatic therapy

✔ Adequate fluid intake and rest

✔ Prevention of chilling

✔ Warm salt-water gargles to soothe the sore throat

✔ NSAIDs to relieve aches and pains

✔ Antihistamines are used to relieve sneezing, rhinorrhea, and nasal congestion

✔ Inhalation of steam or heated, humidified air

ACUTE PHARYNGITIS
❖ A sudden painful inflammation of the pharynx, the back portion of the throat that includes the posterior third of the
tongue, soft palate, and tonsils
❖ Commonly referred to as a sore throat

❖ Clinical Manifestations

● Fiery-red pharyngeal membrane and tonsils

● Swollen lymphoid follicles

● Enlarged and tender cervical lymph nodes

● Fever

● Malaise

● Sore throat

❖ Pharmacologic Therapy

● Penicillin is the treatment of choice

● Cephalosporins
 ● Macrolides

● Gargles with benzocaine may relieve symptoms

❖ Nursing Interventions

● Liquid or soft diet is provided during the acute stage

● Cool beverages, warm liquids, and flavored frozen desserts such as Popsicles are often soothing

● Warm saline gargles or throat irrigations

● Increase oral fluid intake

● Ice collar can relieve severe sore throats

● CBR during febrile stage

● Instruct the patient about preventive measures

CHRONIC PHARYNGITS
❖ Chronic pharyngitis is a persistent inflammation of the pharynx. It is common in adults, who work in dusty
surroundings, use their voice to excess, suffer from chronic cough, or habitually use alcohol and tobacco.
❖ Three types of chronic pharyngitis
● Hypertrophic – characterized by general thickening and congestion of the pharyngeal mucous membrane

● Atrophic – late stage of the first type (the membrane is thin, whitish, glistening, and at times winkled)
 ● Chronic Granular (“clergyman’s sore throat”) – characterized by numerous swollen lymph follicles on the
pharyngeal wall
❖ Clinical Manifestations
● Constant sense of irritation or fullness in the throat

● Mucus that collects in the throat

● Difficulty swallowing

❖ Management

● Nasal sprays or medications containing ephedrine sulfate or phenylephrine hydrochloride

● Antihistamine decongestant medications

● Acetaminophen

❖ Nursing Management

● Instruct the patient to avoid contact with others until the fever subsides to prevent the spread of infection

● Avoidance of alcohol, tobacco, secondhand smoke, and exposure to cold or to environmental or occupational
pollutants

TONSILITIS AND ADENOIDITIS

● The tonsils are composed of lymphatic tissue and are situated on each side of the oropharynx

● The adenoids or pharyngeal tonsils consist of lymphatic tissue near the center of the posterior wall of the
nasopharynx
● Acute inflammation/infection that is usually caused by GABHS (group A beta-hemolytic streptococcus)
Clinical Manifestations
● Sore throat, fever, snoring and difficulty swallowing

● Enlarged adenoids may cause mouth-breathing, earache, draining ears, frequent head colds, bronchitis, foul-
smelling breath, voice impairment, and noisy respiration
❖ Management
● Penicillin (first-line therapy) or cephalosporins

● Tonsillectomy or adenoidectomy is indicated if the patient has had repeated episodes of tonsillitis despite
antibiotic therapy
❖ Nursing interventions (post-op)

● In the immediate postoperative period, the most comfortable position is prone, with the patient’s head turned to
the side to allow drainage from the mouth and pharynx
● Apply ice collar to the neck

● Assess for post op bleeding such as frequent swallowing

● Instruct the patient to refrain from coughing and too much talking

● Ice chips may be given to the patient

● Alkaline mouthwashes and warm saline solutions are useful in coping with the thick mucus and halitosis that may
be present after surgery
● Milk and milk products (ice cream and yogurt) may be restricted

● Provide soft, adequate diet

● Instruct the patient to avoid vigorous tooth brushing or gargling

 ● Encourage the use of a cool-mist vaporizer or humidifier in the home

● Instruct patient to avoid smoking and heavy lifting or exertion for 10 days

PERITONSILLAR ABSCESS (QUINSY)

❖ Most common major suppurative complication of sore throat/tonsillitis. This collection of purulent exudate between the
tonsillar capsule and the surrounding tissues, including the soft palate, may develop after an acute tonsillar infection
that progress to a local cellulitis and abscess
❖ Clinical Manifestations

● Severe sore throat, fever trismus (inability to open the mouth), and drooling.

● Severe pain, raspy voice

● Odynophagia (a severe sensation of burning, squeezing pain while swallowing)

● Dysphagia (difficulty swallowing)

● Otalgia (pain in the ear), tender and enlarged cervical lymph nodes

● Airway obstruction may occur

Management
● Antimicrobial agents (Penicillin)

● Corticosteroid therapy
 ● Needle aspirations are performed to decompress the abscess

❖ Nursing Interventions

● Assist in performing intubation, cricothyroidotomy, or tracheotomy to treat airway obstruction

● Assist in needle aspiration when indicated

● Gentle gargling after the procedure with a cool normal saline gargle may relieve discomfort

● Provide cool liquids

● Instruct the patient to refrain from or cease smoking

● It is also important to reinforce the need for good oral hygiene

LARYNGITIS
❖ An inflammation of the larynx, often occurs as a result of voice abuse or exposure to dust, chemicals, smoke and
other pollutans
❖ Most common cause is virus, bacterial invasion may be secondary

❖ Clinical manifestations

● Hoarseness of voice – initial sign

● Aphonia (complete loss of voice)

● Severe cough

● Throat feels worse in the morning and improves when the patient is in a warmer climate

❖ Management

● Instruct the patient to rest the voice and avoid irritants (including smoking)

● Inhaling cool steam or an aerosol is provided

● Administer antibacterial therapy as ordered

● Topical corticosteroids may be given by inhalation

● Increased oral fluid intake

CANCER OF THE LARYNX

❖ Etiology

● Most tumors of the larynx are squamous cell carcinoma

● Men > women, age 60-70

● Cigarette smoking and alcohol consumption are associated with laryngeal cancer

❖ Clinical Manifestations

● Hoarseness of voice for more than 2 weeks

● Persistent cough and sore throat

● Dyspnea

● Dysphagia

● Pain radiating to ear and burning sensation in the throat

● Weight loss

● Enlarged cervical lymph nodes

 ● Unilateral nasal obstruction

❖ Diagnostic Procedures

● Virtual endoscopy

● Optical imaging

● CT scan MRI

● Direct laryngoscopic examination

❖ Management

● Radiation therapy

● Chemotherapy

● Surgery:

✔ Partial Laryngectomy – A portion of the larynx is removed, along with one vocal cord and the tumor
Complication: change in voice quality or hoarseness of voice
✔ Total Laryngectomy – Laryngeal structures are removed, including the hyoid bone, epiglottis, cricoid
cartilage, and two or three rings of the trachea
Complication: permanent loss of voice, salivary leak, wound infection, stomal stenosis and dysphagia
❖ Nursing interventions

● Arrange for clients with larnygectomies to meet with members of support groups

● Establish a method for communication before surgery

● Maintain airway; have suction equipment at bedside

 ● Observe for signs of hemorrhage or infection

● Teach about tracheostomy and stoma care

● Assist with period of grieving

DISORDERS OF THE LOWER RESPIRATORY SYSTEM

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

❖ Refers to a disease characterized by airflow limitation that is not fully reversible. The airflow limitations is generally
progressive and is normally associated with an inflammatory response of the lungs due to irritants, COPD includes
chronic bronchitis and pulmonary emphysema
❖ Diagnostic Criteria: Cough of 3 months for 2 consecutive years

❖ Chronic Bronchitis

● Chronic inflammation of the lower respiratory tract characterized by excessive mucous secretion, cough, and
dyspnea associated with recurring infections of the lower respiratory tract characterized by three primary
symptoms: chronic cough, sputum production, and dyspnea on exertion
● Clinical Manifestations
✔ Blue bloater

✔ Usually insidious, developing over a period of years

✔ Presence of a productive cough lasting at least 3 months a year for 2 successive years

✔ Production of thick, gelatinous sputum; greater amounts produced during superimposed infections

✔ Wheezing and dyspnea as disease progresses

❖ Emphysema

● Complex lung disease characterized by destruction of the alveoli, enlargement of distal airspaces, and a
breakdown of alveolar walls. There is a slowly progressive deterioration of lung function for many years
before the development of illness
● 2 types:

✔ Panlobular Emphysema – destruction of respiratory bronchiole, alveolar duct and alveolus

⮚ All air spaces within the lobule are essentially enlarged, but there is little inflammatory disease

⮚ Hyperinflated (hyperexpanded) chest, marked dyspnea on exertion, and weight loss typically occur

⮚ Negative pressure is required during inspiration to move air into and out of the lungs

⮚ Expiration becomes active and requires muscular effort

✔ Centrilobular (Centroacinar) Emphysema – pathologic changes take place mainly in the center of the
secondary lobule, preserving the peripheral portions of the acinus
⮚ There is a derangement of ventilation-perfusion rations, producing chronic hypoxemia, hypercapnia,
polycythemia, and episodes of right-sided heart failure
⮚ Leads to central cyanosis and respiratory failure, and patient also develops peripheral edma

● Clinical Manifestations

✔ Pink puffer

✔ Dyspnea, decreased exercise tolerance

✔ Cough may be minimal, except with respiratory infection

✔ Sputum expectoration
 ✔ Barrel chest – Increased anteroposterior diameter of chest due to air trapping with diaphragmatic
flattening
❖ Diagnostic Procedure for COPD

● Spirometry - used to evaluate airflow obstruction

● ABG levels – decreased Pao2, pH, and increased CO2

● Chest X-ray – in late stages, hyperinflation, flattened diaphragm, increased retrosternal space, decreased
vascular markings, possible bullae
● Alpha-1-antitrypsin assay useful in identifying genetically determined deficiency in emphysema

❖ Medical Management for COPD

● Smoking cessation

● Bronchodilators to relieve bronchospasm

● Inhaled and systemic corticosteroids

● Alpha 1-antitrypsin augmentation therapy

● Antibiotic agents, Mucolytic agents Antitussive agents, vasodilators and narcotics

❖ Surgical Management

● Bullectomy – surgical removal of enlarged airspaces that do not contribute to ventilation but occupy space in the
thorax
● Lung Volume Reduction Surgery – removal of a portion of the diseased lung parenchyma
❖ Nursing Interventions For COPD

● Pulmonary rehabilitation to reduce symptoms, improve quality of life and increased physical and emotional
participation in everyday activities
● Pursed-lip breathing helps slow expiration, prevents collapse of small airways, and helps the patient control the
rate and depth of respiration
● Instruct the patient to coordinate diaphragmatic breathing with activities such as walking, bathing, bending, or
climbing stairs
● Provide small frequent meals and offer liquid nutritional supplements to improve caloric intake and counteract
weight loss
● Administer low flow of oxygen (1-2L/min)
● Administer bronchodilator as prescribed

● Adequately hydrate the patient

● Instruct the patient to avoid bronchial irritants

● If indicated, perform CPT int the morning and at night as prescribed

● Encourage alternating activity with rest periods

● Teach relaxation technique or provide a relaxation tape for patient

● Enroll patient in pulmonary rehabilitation program where available

● Monitor respiratory status, including rate and pattern of respirations, breath sounds, and signs and symptoms of
acute respiratory distress

BRONCHIAL ASTHMA
❖ Chronic inflammatory disease of the airways that causes airway hyperresponsiveness, mucosal edema, and mucus
production is reversible and diffuse airway inflammation that leads to airway narrowing
❖ Clinical Manifestations

● Three most common symptoms of asthma:

✔ Cough

✔ Dyspnea

✔ Wheezing

● Chest tightness, diaphoresis, tachycardia, and a widened pulse pressure, hypoxemia and central cyanosis

❖ Pharmacologic Therapy

● There are two general classes of asthma medications:

✔ Quick relief medications for immediate treatment of asthma symptoms and exacerbations

⮚ Short-acting beta2-adrenergic agonists (albuterol [Proventil Ventolin], levalbuterol [Xopenex], and

pirbuterol [Maxair])
✔ Long acting medications to achieve and maintain control of persistent asthma
⮚ Corticosteroids
 ⮚ Long-acting beta2-adrenegic agonists

⮚ Leukotriene modifiers (inhibitors)

⮚ Antileukotrienes, Montelukast (Singulair), zafirlukast (Accolate), and zileuton (Zyflo)

❖ Nursing Interventions

● Assesses the patient’s respiratory status by monitoring the severity of symptoms, breath sounds peak flow, pulse
oximetry, and vital signs
● Administer medications as prescribed and monitor the patient’s responses to those medications

● Administer fluids if the patient is dehydrated emphasize adherence to prescribed therapy, preventive measures, and
the need to keep follow-up appointments with health care providers

BRONCHIECTASIS
❖ A chronic, irreversible dilation of the bronchi and bronchioles

❖ Etiology

● Airway obstruction

● Diffuse airway injury

● Pulmonary infections and obstruction of the bronchus or complications of long-term pulmonary infections

● Generic disorders such as cystic fibrosis

 ● Abnormal host defense (eg, ciliary dyskinesia or humoral immunodeficiency)

● Idiopathic causes

❖ Diagnostic Procedure

● CT scan – reveals bronchial dilation

❖ Clinical Manifestations

● Chronic cough with copious amount of purulent sputum

● Hemoptysis

● Clubbing of the fingers

● Repeated episodes of pulmonary infection

❖ Management

● Smoking cessation

● Chest physiotherapy

● Bronchoscopy to remove mucopurulent sputum

● Antimicrobial therapy based on result of culture and sensitivity of the sputum

● Influenza and pneumococcal vaccines

● Bronchodilators

● Surgical interventions for patients who continue to expectorate large amount of sputum and hemoptysis
despite adherence to treatment regimen
❖ Nursing intervention

● Assess the patient in alleviating the symptoms and in clearing pulmonary secretions

● Encourage the patient in smoking cessation

● Educate the patient and his family in performing postural drainage

● Instruct the patient to avoid exposure to people with upper respiratory or other infection

● Assess nutritional status and ensure adequate diet

OCCUPATIONAL LUNG DISEASES

❖ Asbestosis is diffuse interstitial fibrosis of the lung caused by inhalation of asbestos dust and particles.

● Found in workers involved in manufacture, cutting and demolition of asbestos-containing materials

❖ Silicosis is a chronic pulmonary fibrosis caused by inhalation of silica dust

● Exposure to silica dust is encountered in almost any form of mining because the earth’s crust is composed of
silica and silicates (gold, coal, tin, copper mining); also stone cutting, quarrying, manufacture of abrasives,
ceramics, pottery, and foundry work
❖ Sarcoidosis
● Granulomatous disease in which clumps of inflammatory epithelial cells occur in many organs, primarily in lungs.

● Lymph node enlargement seen on chest X-ray

❖ Clinical Manifestations

● Chronic cough; productive in silicosis

● Dyspnea on exertion; progressive and irreversible in asbestosis

 ● Susceptibility to lower respiratory tract infections

● Bibasal crackles in asbestosis

❖ Management

● There is no specific treatment; exposure is eliminated, and the patient is treated symptomatically

● Give prophylactic isoniazid (INH) to patient with positive tuberculin test, because silicosis is associated with high risk
of TB
● Persuade people who have been exposed to asbestos fiber to stop smoking to decrease risk of lung cancer
● Keep asbestos worker under cancer surveillance; watch for changing cough, hemoptysis, weight loss, melena

● Bronchodilators may be of some benefit if any degree of airway obstruction is present

❖ Nursing Interventions

● Administer oxygen therapy as required

● Administer or teach self-administration of bronchodilators as ordered

● Encourage smoking cessation

● Advise patient on pacing activities to prevent fatigue

● Provide information to healthy workers on prevention of occupational lung disease

 PENETRATING TRAUMA
❖ Pneumothorax

● Pneumothorax occurs when the parietal or visceral pleura is breached, and the pleural space is exposed to
positive atmospheric pressure
❖ Simple/Spontaneous Pneumothorax

● Occurs when air enters the pleural space through a breach of either the parietal or visceral pleura. Most
commonly, this occurs as air enters the pleural space through the rupture of a bleb or a bronchopleural fistula
❖ Traumatic Pneumothorax

● A traumatic pneumothorax occurs when air escapes from a laceration in the lung itself and enters the pleural space or
from a wound in the chest wall, it may result from blunt trauma (eg, rib fractures), penetrating chest or abdominal
trauma (eg, stab wounds or gunshot wounds), or diaphragmatic fear
❖ Open Pneumothorax
● One form of traumatic pneumothorax. It occurs when a wound in the chest wall is large enough to allow air to pass
freely in and out of the thoracic cavity with each attempted respiration
❖ Tension Pneumothorax
● Occurs when air is drawn into the pleural space from a lacerated lung or through a small opening or wound in the
chest wall. It may be a complication of other types of pneumothorax. The air that enters the chest cavity with each
inspiration is trapped. this causes the lung to collapse and the heart, the great vessels, and the trachea to shift toward
the unaffected side of the chest (mediastinal shift)
❖ Clinical Manifestations
● Hyperresonance; diminisher breath sounds
o Reduced mobility of affected half of thorax
● Tracheal deviation away from affected side in tension pneumothorax
o Clinical picture of open or tension pneumothorax is one of air hunger, agitation, hypotension, cyanosis and
profuse diaphoresis
● Mild to moderate dyspnea and chest discomfort may be present with spontaneous pneumothorax

❖ Management
Spontaneous Pneumothorax
● Treatment is generally nonoperative if pneumothorax is not too extensive.
✔ Observe and allow for spontaneous resolution for less than 50% pneumothorax in otherwise healthy person.

✔ Needle aspiration or chest tube drainage may be necessary to achieve re-expansion of collapsed lung if
greater than 50% pneumothorax
● Surgical intervention by pleurodesis or thoracotomy with resection of apical blebs is advised for patients with
recurrent spontaneous pneumothorax
Tension Pneumothorax
● Immediate decompression to prevent cardiovascular collapse by thoracentesis or chest tube insertion to let air
escape
● Chest tube drainage with underwater-seal suction to allow for full lung expansion and healing
Open Pneumothorax
● Close the chest wound immediately to restore adequate ventilation and respiration

✔ Patient is instructed to inhale and exhale gently against a closed glottis (Valsalva maneuver) as a pressure
dressing (petroleum gauze secured with elastic adhesive) is applied. This maneuver helps to expand collapsed
lung
● Chest tube is inserted and water-seal drainage set up to permit evacuation of fluid/air and produce re-expansion of
the lung
 ● Surgical intervention may be necessary to repair trauma
❖ Nursing Intervention

● Apply petroleum gauze to sucking chest wound

● Assist with emergency thoracentesis or thoracostomy

● Position patient upright if condition permits to allow greater chest tubes

● Maintain patency of chest tubes

● Assist patient to splint chest while turning or coughing and administer pain medications as needed

● Monitor oximetry and ABG levels to determine oxygenation

● Provide oxygen as needed

 PLEURAL
CONDITIONS PLEURAL
EFFUSION
❖ Collection of fluid (transudate or exudate) in the pleural space
❖ Maybe a complication of heart failure, pulmonary infection or nephrotic syndrome

❖ Usually caused by underlying disease

❖ Clinical Manifestations

● Dyspnea

● Difficulty lying on flat

● Coughing/fever

● Chills

● Pleuritic chest pain

❖ Diagnostic Procedure

● CT scan

● Lateral Decubitus X-ray

❖ Management

● Treatment of underlying disease

● Thoracentesis or chest tube drainage is performed

● Surgical pleurectomy for pleural effusion caused by malignancy

● Pleuroperitoneal shunt – fluids from the pleural space is drain into the peritoneum

❖ Nursing Intervention

● Assist in thoracentesis

● Record the amount of fluid aspirated and send it to the laboratory

● Administer medications as ordered such as analgesics and antibiotics

● Assist the patient in a comfortable position

HEMOTHORAX
❖ Blood in pleural space as a result of penetrating or blunt chest trauma

❖ Accompanies a high percentage of chest injuries

❖ Can result in hidden blood loss

❖ Patient may be asymptomatic, dyspneic, apprehensive, or in shock

❖ Management

● Assist with thoracentesis to aspirate blood from pleural space

● Assist with chest tube insertion and set up drainage system for complete and continuous removal of blood and air

✔ Auscultate lungs and monitor for relief of dyspnea

✔ Monitor amount of blood loss in drainage

❖ Replace volume with I.V. fluids or blood products

PLEURISY (PLEURITIS)
❖ Inflammation of both layers of the pleurae (parietal and visceral)

❖ May develop in conjunction with pneumonia or an upper respiratory tract infection, TB or collagen disease

❖ When the inflamed pleural membranes rub together during respiration (intensified on inspiration), the result is
severe, sharp, knifelike pain
❖ Clinical Manifestations
● Pleuritic pain during deep breath, coughing or sneezing

● Pain is limited in distribution rather than diffuse

● Pleural friction rub can be heard with stethoscope

❖ Diagnostic Procedures

● Chest X-ray

● Sputum Analysis

● Thoracentesis

● Pleural Biopsy

❖ Management

● Treatment of underlying condition causing pleurisy

● Topical applications of heat or cold

● Indomethacin for pain relief

● Intercostal Nerve Block if pain is severe

 ❖ Nursing Interventions

● Instruct the patient in heat/cold application for pain relief

● Instruct the patient to turn onto the affected side to splint the chest wall and reduce the stretching of the
pleauare
● Teach the patient to use hands or pillow to splint the ribcage while coughing

EMPYEMA THORACIS
❖ Accumulation of purulent fluid in the pleural space

❖ Occur as complication of bacterial pneumonia, lung abscess or chest trauma

❖ Patient is acutely ill and has signs and symptoms similar to acute respiratory infection

❖ Diagnosis is established by chest CT

❖ Main objective is to drain the fluid in the pleural cavity

❖ Thoracentesis is done if fluid is not too thick

❖ Tube Thoracostomy is done to patients with loculated or complicated pleural effusions

❖ Open chest drainage via thoracotomy is done to remove thickened pleura, pus and debris

❖ Nursing intervention: provide care specific to the method of drainage of the pleural fluid
INFECTIOUS DISEASES OF THE LOWER RESPIRATORY TRACT
PNEUMONIA
❖ Inflammation of the lung parenchyma caused by various microorganisms, including bacteria, mycobacteria, fungi and
viruses
❖ Community-Acquired Pneumonia

● Occurs either in the community setting or within the first 48 hours after hospitalization or institutionalization

❖ Hospital-Acquired Pneumonia

● Also known as nosocomial pneumonia, is defined as the onset of pneumonia symptoms more than 48 hours after
admission in patients with no evidence of infection at the time of admission
❖ Aspiration Pneumonia
● Refers to the entry pulmonary consequences resulting from entry of endogenous or exogenous substances into the
lower airway
❖ Clinical Manifestation
● Sudden onset, rapidly rising fever of 38.3°C to 40.5°C

● Cough productive of purulent sputum

● Pleuritic chest pain aggravated by deep respiration/coughing

● Dyspnea, tachypnea accompanied by respiratory grunting, nasal flaring use of accessory muscles of respiration
fatigue
● Rapid, bounding pulse
● Orthopnea

● Rusty, blood-tinged sputum

● Poor appetite, diaphoresis

❖ Diagnostic Procedure

● Chest X-ray shows presence/extent of pulmonary disease typically consolidation.

 ● Gram stain and culture and sensitivity test of sputum may indicate offending organism

● Blood culture detects bacteremia (bloodstream invasion) occurring with bacterial pneumonia

❖ Management

● Administration of the appropriate antibiotic as determined by the results of a Gram stain

✔ S. pneumonia – macrolide antibiotic (azithromycin, clarithromycin, or erythromycin)

✔ Pseudomonas infection – anti pneumococcal, antipseudomonal beta-lactam

● Treatment of viral pneumonia is primarily supportive

● Oxygen therapy if patient has inadequate gas exchange

❖ Complications

● Shock and respiratory failure

● Pleural Effusion
NURSING INTERVENTIONS
● Encourage coughing and deep breathing after chest physiotherapy, splinting the chest if necessary

● Maintain semi-Fowler’s position

● Promote hydration (2-3 L/day) to liquefy secretions

● Teach effective coughing techniques to minimize energy expenditure; plan rest periods

● Suction if necessary

● Instruct client to cover nose and mouth when coughing

● Teach the need to continue entire course of antimicrobial therapy which is usually seven to ten days

● Teach the patient about proper administration of antibiotics and potential side effects

● Teach that findings are expected to be less within 48 to 72 hours of initial therapy

● Nutritionally enriched drinks or shakes maybe helpful in maintaining nutrition

PULMONARY TUBERCULOSIS
❖ Tuberculosis (TB) is an infectious disease that primarily affects the lung parenchyma. It also may be transmitted to
other parts of the body, including the meninges, kidneys, bones and lymph nodes
❖ The primary infectious agent, M, tuberculosis, is an acid-fast aerobic rod that grows slowly and is sensitive to heat and
ultraviolet light spreads from person to person by airborne transmission
❖ Clinical Manifestations

● Fatigue, anorexia, weight loss, low-grade fever, night sweats

● Some patients have acute febrile illness, chills, and flu-like symptoms

● Cough (insidious onset) progressing in frequency and producing mucoid or mucopurulent sputum

● Hemoptysis, chest pain, dyspnea (indicates extensive involvement)

❖ Diagnostic Evaluation

● Sputum smear/Sputum culture confirms a diagnosis of TB

● Chest X-ray to determine presence and extent of disease

● Tuberculin skin test (purified protein derivative [PPD] or Mantoux test)

❖ Classification

● Data from the history, physical examination, TB test, chest x-ray, and microbiologic studies are used to classify TB
into one of five classes. A classification scheme provides public health officials with a systematic way to monitor
epidemiology and treatment of the disease
✔ Class 0: no exposure; no infection
✔ Class 1: exposure; no evidence of infection

✔ Class 2: latent infection; no disease (eg, positive PPD reaction but no clinical evidence of active TB)

✔ Class 3: disease; clinically active

✔ Class 4: disease; not clinically active

✔ Class 5: suspected disease; diagnosis pending

❖ Management

● Pulmonary TB is treated primarily with antituberculosis agents for 6 to 12 months

● The initial phase consists of a multiple-medication regime of INH, rifampin, pyrazinamide, and ethambutol and is
administered daily for 8 weeks
● Continuation phase of treatment include INH and rifampicin and lasts for an additional 4 or 7 months
● Vitamin B (pyridoxine) is usually administered with INH to prevent IHN-associated peripheral neuropathy

FIRST-LINE ANTITUBERCULOSIS MEDICATIONS

Commonly Adult Daily Dosage Most Common Side Effects
Used Agents
Isoniazid (INH) 5 mg/kg (300 mg maximum Peripheral neuritis, hepatic enzyme elevation, hepatitis,
daily) hypersensitivity

Rifampicin 10 mg/kg (600 mg maximum Hepatitis, febrile reaction, purpura (rare), nausea, vomiting
daily)

Pyrazinamide 15-30 mg/kg (2.0 g maximum Hyperuricemia, hepatotoxicity, skin rash, arthralgias, GI
daily) distress

Ethambutol 15-25 mg/kg (no Optic neuritis (may lead to blindness; very rare at 15
(Myambutol maximum daily dose, but mg/kg), skin rash
) base on lean body)

❖ Nursing Intervention

● Instructs the patient to increase fluid intake and about correct positioning to facilitate airway drainage

● Discuss the medications schedule and side effects of the drugs

● Instructs the patient to take the medication either on an empty stomach or at least 1 hour before meals
because food interferes with medication absorption
● Patients taking INH should avoid foods that contain tyramine and histamine because it may result in
headache, flushing, hypotension, lightheadedness, palpitations, and diaphoresis
● Monitors for side effects of anti-TB drugs

● Encourage rest and avoidance of exertion

● Provide nutritional plan that allows for small, frequent meals

● Instruct the patient about important hygiene measures, including mouth care, covering the mouth and nose
when coughing and sneezing, proper disposal of tissues, and hand washing

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

❖ Severe form of acute lung injury. This clinical syndrome is characterized by a sudden and progressive pulmonary
edema, increasing bilateral infiltrates on chest x-ray, hypoxemia unresponsive to oxygen supplementation regardless of
the amount of Positive End-Expiratory Pressure (PEE) and the absence of an elevated left atrial pressure
❖ Patients often demonstrate reduced lung compliance
❖ Clinical Manifestations

● Typically develops over 4 to 48 hours

● Severe dyspnea, severe hypoxemia

● Arterial hypoxemia that does not respond to supplemental oxygen

● Chest x-ray are similar to those seen with cardiogenic pulmonary edema

● Increased alveolar dead space

● Severe crackles and rhonchi heard on auscultation

 ● Labored breathing and tachypnea

❖ DIAGNOSTICS

● Clinical presentation and history of findings

● Hypoxemia on ABG despite increasing inspired oxygen level

● Chest x-ray shows bilateral infiltrates

● Plasma Brain Natriuretic Peptide (BNP)

● Echocardiography

● Pulmonary Artery Catheterization

❖ Management

● Treatment of the underlying condition

● Optimize oxygenation

● Intubation and mechanical ventilation

● Sedation may be required

● Paralytic agents may be necessary

● Antibiotics, as indicated

● PEEP usually improves oxygenation

● Supportive drugs includes surfactant replacement therapy, pulmonary antihypertensive agents and antisepsis
agent
❖ Nursing Intervention
● Requires close monitoring in the intensive care unit

● Assess the patient’s status frequently to evaluate the effectiveness of the treatment

● Turn the patient frequently to improve ventilation and perfusion in the lungs and enhance drainage secretions

● Res is essential for patient to limit oxygen consumption and reduce oxygen needs

● Adequate nutritional support is vital, 35 to 45 kcal/kg/day is required to meet caloric requirements

● Identify problems with ventilation that may cause anxiety reaction to the patient
 PULMONARY EMBOLISM
❖ Refers to the obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originates
somewhere in the venous system in the right side of the heart
❖ Often associated with trauma, surgery (orthopedic, major abdominal, pelvic, gynecologic, pregnancy, heart failure, age
older than 50 years, hypercoagulable states, and prolonged immobility
❖ Clinical Manifestations

● Dyspnea is the most frequent symptom

● Chest pain (sudden and pleuritic), may be substernal and any mimic angina pectoris or a myocardial
infarction.
● Petechiae over the chest
● Anxiety, fever, tachycardia and apprehension

● Cough, diaphoresis, hemoptysis, and syncope. The most frequent sign is tachypnea

❖ Diagnostic Procedures

● Chest x-ray – shows infiltrates, atelectasis, elevation of the diaphragm on the affected side

● ECG – shows sinus tachycardia, PR-interval depression and nonspecific T-wave changes

● Arterial blood gas analysis – shows hypoxemia and hypocapnia

● Ventilation-perfusion (V/Q.) scan

● Pulmonary angiography is considered the best method to diagnose PE

● Spiral computed CT scan of the lung

❖ Management

● Treatment goal is to dissolve the existing emboli

● Improve respiratory and vascular status, anticoagulation therapy, thrombolytic therapy, and surgical
intervention
● Stabilize the cardiopulmonary system

● Nasal oxygen is administered immediately to relieve hypoxemia, respiratory distress, and central cyanosis

● Intravenous infusion lines are inserted to establish routes for medications or fluids that will be needed

● Hypotension is treated by a slow infusion of dobutamine (Dobutrex), which has a dilating effect on the
pulmonary vessels and bronchi, or dopamine (Intropin)
● Small doses of IV morphine or sedatives are administered to relieve patient anxiety, to alleviate chest
discomfort, to improve tolerance of the endotracheal tube, and to ease adaptation to the mechanical
ventilator
● Anticoagulant therapy (heparin, warfarin sodium
● Coumadin has traditionally been the primary method for managing PE

● Thrombolytic therapy (urokinase, streptokinase, alteplase) is used in treating PE, particularly in patients who are
severely compromised
● Surgical embolectomy is performed if the patient has massive PE.

❖ Nursing Intervention

● Monitor oxygen therapy and assess the patient for hypoxia

● Watch patient for signs of discomfort and pain

● Assess patient for bleeding related to anticoagulant or thrombolytic therapy

● Advise patient of the possible need to continue taking anticoagulant therapy

● Monitor for potential complication of cardiogenic shock or right ventricular failure

● Encourage ambulation and active/passive leg exercises to prevent venous stasis

● Advise the patient not to sit or lie in bed for prolonged periods, not to cross the legs, and not to wear
constrictive clothing
 CARDIOVASCULAR NURSING
THE HEART
❖ Hollow, muscular organ

❖ Weight approximately 300 g

❖ It occupies the space between the lungs (mediastinum) and rests on the diaphragm

❖ The heart pumps blood to the tissues supplying them with oxygen and other nutrients.

THREE LAYERS OF THE HEART

● Endocardium-lines the inside of the heart and valves

● Myocardium-made up of muscle fibers and is responsible for the contraction

● Epicardium- Exterior layer of the heart in which pericardium can be found

✔ Outermost

✔ Essential coronary arteries are located

Pericardium- thin layer of fibrous tissue that contains pericardial fluid that lubricates the lining of the heart, it consists of two
layers:
● Adhering to the epicardium is the visceral pericardium.

● Enveloping the visceral pericardium is the parietal pericardium, which supports the heart in the mediastinum. "The

pumping action of the heart is accomplished by the rhythmic relaxation and contraction"

Systole- refers to the events in the heart during, contraction of the two top chambers (atria) and two lower chambers (ventricles)

Diastolic- is characterized by relaxation of the lower chambers which allows the ventricles to fill in preparation for contraction

2 CHAMBERS

UPPER
❖ ATRIUM

❖ Collecting/ Receiving chamber

LOWER
❖ VENTRICLES

❖ Pumping/ Contracting chamber

Apical impulse (also called the point of maximal impulse [PMI]) located at the 15th intercostal space (ICS), left mid-
clavicular line.

MECHANICAL PROPERTIES OF THE HEART

CARDIAC OUTPUT

❖ Volume of blood (liters) ejected by the heart each minute 5 L/min

❖ During exercise the total cardiac output may increase fourfold, to 2 L/min.

❖ Cardiac Output = Heart Rate x Stroke Volume

● CO = HR x SV

PULSE RATE/ HEART RATE

❖ Number of times the ventricles contract each minute

❖ 60-100 beats/min

❖ Controlled by the ANS

STROKE VOLUME
❖ Volume of blood ejected by the left ventricle during each systole

❖ Affected by 3 factors:
o Preload
o Contractility
o Afterload
 PRELOAD
❖ Degree of myocardial stretch at the end of diastole & just before contraction

❖ Determined by the amount of blood returning to the heart from venous & pulmonary system

STARLING'S LAW
❖ The more the heart is filled during diastole, the more forcefully it contracts

❖ The higher the preload, the higher the stroke volume.

CONTRACTILITY
❖ Force generated by the contracting enhanced by myocardium

❖ Catecholamines, sympathetic activity and with medications such as the 3 D's

● Digoxin, Dopamine, Dobutamine

❖ The higher the contractility, the higher the stroke volume.

AFTERLOAD
❖ Pressure or resistance that the ventricles must overcome to eject blood through the semi-lunar valves

❖ Directly proportional to the BP & Diameter of blood vessels

❖ The higher the afterload, the lower the stroke volume.

HEART SOUNDS
1. The first heart sound (S1) is heard as the atrioventricular valves close and is heard loudest at the apex of the heart.
2. The second heart sound (S2) is heard when the semilunar valves close and is heard loudest at the base of the heart.
3. A third heart sound (S3) may be heard if ventricular wall compliance is decreased and structures in the ventricular wall
vibrate heart; this can occur in conditions such as congestive heart failure or valvular regurgitation. However, a third heart
sound may be normal in individuals younger than 30 years.
4. A fourth heart sound (S4) may be heard on atrial systole if resistance to ventricular filling the is present; this is an
abnormal finding, and causes include cardiac hypertrophy, disease, or injury to the ventricular wall.

CARDIAC ELECTROPHYSIOLOGY
Automaticity: ability to initiate an electrical impulse by itself
Excitability: ability to respond to an electrical impulse
Conductivity: ability to transmit an electrical impulse from one cell to another

SINOATRIAL (SA) NODE

❖ Location: Junction of Superior vena cava & Right Atrium

❖ Function: Pacemaker of heart

❖ Initiates 60-100 bpm

ATRIOVENTRICULAR (AV) NODE

❖ Location: Interatrial septum

❖ Delays the electric impulse to allow ventricular filling of 0.8 milliseconds

❖ 40-60 beats/min

BUNDLE OF HIS
❖ Location: Interventricular septum

❖ Branches out into:

● Right main Bundle Branch

 ● Left main Bundle Branch

PURKINJE FIBERS
❖ Location: Walls of ventricles

❖ Ventricular contractions

❖ Fastest conduction is: 20 - 40 beats/min

❖ It can function as a backup pacemaker if all other pacemakers fail

FACTS:
❖ “The parasympathetic impulses, which travel to the heart through the Vagus nerve, can slow the cardiac rate,
whereas sympathetic impulses increase it.”
❖ Baroreceptors are specialized nerve cells located in the aortic arch and in both right and left internal carotid arteries. The
baroreceptors are sensitive to changes in blood pressure.

❖ Hypotension can result in less baroreceptor stimulation, which prompts a decrease in parasympathetic inhibitory activity in
the SA node, allowing for enhanced sympathetic activity. The resultant vasoconstriction and increased heart rate elevate
the blood pressure.

ELECTRICAL CONDUCTION THROUGH THE HEART

P WAVE
❖ The P wave represents atrial muscle depolarization. It is normally small, smoothly rounded, and no wider than 0.12
second

QRS COMPLEX
❖ The QRS complex represents ventricular muscle depolarization

❖ Normal QRS width is 0.04 to 0.10 second.

❖ Atrial repolarization happens simultaneously.

T WAVE
❖ The T wave represents ventricular repolarization

❖ T waves are not normal more than 5 mm

PR INTERVAL
❖ The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex and
represents the time required for the impulse to travel through atria, AV junction, and Purkinje system. The
normal PR interval is 0.12 to 0.20 seconds.

QT INTERVAL
❖ It represents the total time for ventricular depolarization and repolarization.

❖ QT interval is usually 0.32 to 0.40

❖ If QT interval becomes prolonged, the patient may be at risk for a lethal ventricular dysrhythmia called torsades de
pointes.

PP INTERVAL
❖ The duration between the beginning of one P wave and the beginning of the next P wave

❖ Used to calculate atrial rate and rhythm

RR INTERVAL
❖ The duration between the beginning of one QRS complex and the beginning of the next QRS complex; used to
calculate ventricular rate and rhythm

U WAVE
❖ The part of an ECG that may reflect Purkinje fiber repolarization: usually it is not seen unless a patient's serum
potassium level is low (Hypokalemia)

CORONARY ARTERY DISEASE

❖ Coronary artery disease (CAD) is the most prevalent type of cardiovascular disease in adults.
❖ Most common cause of cardiovascular disease is atherosclerosis- (abnormal accumulation of fats)

CLINICAL MANIFESTATIONS

● Symptoms and complications according to the location and degree of narrowing of the arterial lumen, if impediment to
the blood flow has occurred, inadequate supply to cardiac cells will lead to a condition known as ischemia.

MODIFIABLE RISK FACTORS

• Hyperlipidemia
• Cigarette smoking, tobacco use
• Hypertension
• Diabetes mellitus
• Metabolic syndrome
• Obesity
• Physical inactivity

NON-MODIFIABLE RISK FACTORS

● Family history' of CAD (first-degree relative with cardiovascular disease at 55 years of age or younger for men and at 65
years of age or younger for women)
✔ Increasing age '4 More than 45 years for men

✔ More than 55 years for women

● Gender (men develop CAD at an earlier age than women)

● Race (higher incidence of heart disease in African Americans than in Caucasians)

CLINICAL MANIFESTATION
● Possibly normal asymptomatic periods

● Chest pain

● Palpitations

● Dyspnea

● Syncope

● Excessive fatigue

SURGICAL PROCEDURES
❖ PTCA to compress the plaque against the walls of the artery and dilate the vessel

❖ Laser angioplasty to vaporize the plaque

❖ Atherectomy to remove the plaque from the artery

❖ Vascular stent to prevent the artery from closing and to prevent restenosis

❖ Coronary Artery Bypass Grafting (CABG) to improve blood flow to the myocardial tissue at risk for ischemia or
infarction because of the occluded artery

MEDICATIONS
❖ Nitrates to dilate the coronary arteries and decrease preload and afterload

❖ Calcium channel blockers to dilate coronary arteries and reduce vasospasm

❖ Cholesterol-lowering medications to reduce the development of atherosclerotic plaques

❖ Beta-Blockers to reduce the BP in individuals who are hypertensive

*All adults 20 years of age or older should have a fasting lipid profile (total cholesterol, LDL, HDL, and triglyceride I performed
at least once every 5 years and more often if the profile is abnormal"

*HDL, (high density lipoprotein) is known as good cholesterol because it transports other lipoproteins such as LDL to theliver, where
they can be degraded and excreted. Because of this, a high HDL level is a strong protective factor for heart disease.

*Mediterranean diet another diet that promotes the ingestion of vegetables and fish and restricts red meat, is also
reported to reduce mortality from cardiovascular disease"

*Cholesterol is present in all body tissues and is a major component of low-density lipoproteins, brain and nerve cells, cell
membranes, and some gallbladder stones

*Increased cholesterol levels, LDL (Low density lipoprotein) levels, and triglyceride levels place the client at risk for coronary
artery disease

INSTRUCT THE CLIENT REGARDING DIET COMPOSED OF:

❖ Low-calorie

❖ Low-sodium

❖ Low-cholesterol

❖ Low-fat diet

❖ Increase in dietary fiber

 VALUES
❖ Cholesterol: 140 to 199 mg/dL

❖ Low-density lipoproteins: Lower than 130 mg/dL

❖ High-density lipoproteins: 30 to 70 mg/dL

❖ Triglycerides: Lower than 200 mg/dL

HEART FAILURE (HF)

❖ HF is the inability of the heart to pump enough blood to meet the needs of tissues for oxygen and nutrients.

❖ Decreased heart contractility/ Pump failure

❖ Inadequacy of the heart to pump blood throughout the body

❖ Insufficient perfusion of body tissues (decreased cardiac output)

COMMON CAUSES OF HEART FAILURE

● Hypertension

● CAD

● Cardiomyopathy

● Substance abuse (Alcohol, Cocaine, Amphetamines)

● Valvular disease

● History of myocardial infarction

● Congenital defects

● Cardiac infections & inflammations

● Hyperkinetic conditions

ACC/AHA CLASSIFICATION OF HEART FAILURE

STAGE A Patients at high risk for Developing left ventricular

Dysfunction but without structural heart disease or symptoms of heart failure
STAGE B Patients with left ventricular dysfunction or structural heart disease who have not developed symptoms of
heart failure
STAGE C Patients with left ventricular dysfunction or structural heart disease with current or prior symptoms of heart
failure
STAGE D Patients with refractory end-stage heart failure requiring specialized interventions

TWO MAJOR TYPES OF HEART FAILURE

❖ Systolic heart failure- alteration in ventricular contraction which is characterized by weakened heart muscle

❖ Diastolic heart failure- characterized by a stiff and non- compliant heart muscle making it difficult for the ventricle to fill.
The signs and symptoms of HF can be related to which ventricle is affected.

LEFT-SIDED HEART FAILURE

❖ Pulmonary venous blood volume and pressure increase, forcing fluid from the pulmonary capillaries into the
pulmonary, tissues and alveoli, causing pulmonary„' interstitial edema and impaired Bas exchange.
❖ Pulmonary congestion occurs

❖ Signs and symptoms: Pulmonary/Lung (Left=Lung)

o Dyspnea, cough, pulmonary crackles/rales, and low oxygen saturation levels.
o Orthopnea, difficulty breathing when lying flat.
 o Frothy, pink (blood-tinged) sputum: pulmonary congestion (pulmonary edema)
❖ An extra heart sound, the S3, or "ventricular gallop," may he detected on auscultation.
❖ The dominant feature in HF is inadequate tissue perfusion

Compensatory Mechanisms
❖ Compensatory mechanisms act to restore cardiac output to near-normal levels.

● Sympathetic nervous system stimulation

✔ Arterial vasoconstriction

✔ Increases afterload

✔ Increased left cardiac workload

✔ Increased heart rate

✔ Improved stroke volume

✔ Arterial vasoconstriction
● Renin-angiotensin system activation

❖ A decrease in renal perfusion due to low cardiac output causes the release of renin by the kidneys.

❖ Renin promotes the formation of Angiotensin I, a benign, inactive substance.

❖ Angiotensin- converting enzyme (ACE) in the lumen of pulmonary blood vessels converts angiotensin I to angiotensin II a
potent vasoconstrictor, which then increase blood pressure and afterload.

❖ Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, resulting in sodium and fluid retention
by the renal tubules and stimulation of antidiuretic hormone. These mechanisms lead to the fluid volume overload
commonly seen in HF.

COMMON NURSING DIAGNOSES

● Impaired gas exchange related to ventilation perfusion imbalance

● Decreased CO related to altered contractility, preload & afterload

● Activity intolerance related to an imbalance between 02 supply and demand

● Potential for pulmonary edema, pneumonia, dysrhythmias

MANAGEMENT
● Patients with orthopnea usually prefer not to lie flat. They may need pillows to prop themselves up in bed, or they may
sit in a chair and even sleep sitting up.
● Monitor vital signs and look for changes.
● Record fluid intake and output—weigh daily to assess for fluid overload.

● Position patient in semi-Fowler's position to oxygen as ordered because it ease breathing

● Administer oxygen as ordered because it helps to decrease workload of heart.

● Administer diuretic as prescribed.

● Tell the patient:

✓ Eat foods low in sodium to avoid fluid retention.

RIGHT-SIDED HEART FAILURE

❖ Right side of the heart cannot eject blood and cannot accommodate all the blood that normally returns to it from the
venous circulation
❖ Increased venous pressure leads to Jugular vein distention and increased capillary hydrostatic pressure throughout the
venous system
❖ Edema of the lower extremities (dependent system edema)

❖ Hepatomegaly (enlargement of the liver)

❖ Ascites (accumulation of fluid in the peritoneal al cavity)

❖ Weight gain due to retention of fluid.

"Inability of the right heart to empty its blood volume results in blood backing up into the systemic circulation. LV failure is the
most common cause of right ventricular (RV) failure. Sustained pulmonary hypertension also causes RV failure".

NURSING INTERVENTIONS
● Monitor heart rate and for dysrhythmias by using a cardiac monitor.

● Assess for edema in dependent areas and in the sacral, lumbar, and posterior thigh regions in the client on the bed rest.

● Avoid the unnecessary IV administration of fluids.

● Monitor weight to determine a response to treatment.

● Assess for hepatomegaly and ascites, and measure and record abdominal girth.
 PHARMACOLOGIC MANAGEMENT FOR HF

Administer diuretics for symptom control Furosemide, bumetanide, metolazone,

resulting in patient comfort by reducing hydrochlorothiazide, spironolactone-be aware of
blood volume electrolyte imbalance-these medications may alter the
K+ level

Administer ACE inhibitors to decrease Captopril, enalapril, lisinopril

afterload
Administer beta blocker, which help to raise Metoprolol (Lopressor, Toprol)
ejection fraction, and decrease ventricular Atenolol (Tenormin) Carvedilol
size (Coreg)
Administer inotrope to strengthen myocardial Digoxin
contractility
Administer vasodilator to reduce preload, Nitroprusside,
relieve dyspnea Nitroglycerin ointment

ARTERIOSCLEROSIS
❖ Thickening or hardening of the arterial wall

ATHEROSCLEROSIS
❖ Type of arteriosclerosis where a fatty plaque as formed within the arterial wall

❖ Leading contributor of CAD (coronary artery disease) and CVA (cerebrovascular accident)

VALVULAR HEART DISEASE

❖ Valvular heart disease occurs when the heart valves cannot fully open (stenosis) or closes inwards causing a leak
(insufficiency or regurgitation).

TYPES:
❖ Mitral Stenosis: Valvular tissue thickens and narrows the valve opening, preventing blood from flowing from the left
atrium to the left ventricle.
❖ Mitral Insufficiency, regurgitation: Valve is incompetent, preventing complete valve closure during systole.

❖ Mitral Valve Prolapse: Valve leaflets protrude into the left atrium during systole.

❖ Aortic Stenosis: Valvular tissue thickens and narrows the valve opening, preventing blood from flowing from the left
ventricle into the aorta.
❖ Aortic Insufficiency: Valve is incompetent, preventing complete valve closure during diastole.

MITRAL STENOSIS
❖ Usually due to rheumatic endocarditis

❖ Causing valve thickening by fibrosis and calcification

❖ Mitral valve opening narrows

❖ Left atrial pressure rises and dilates

❖ Pulmonary artery pressure increases

❖ Can cause right ventricular failure

CLINICAL MANIFESTATIONS
● A Iow-pitched, rumbling, diastolic murmur is heard at the apex

● Dyspnea on exertion

● Orthopnea

✔ Difficulty Breathing When Lying Flat

● Paroxysmal nocturnal dyspnea

✔ Shortness of Breath that occurs suddenly during sleep

● Dyspnea and dry cough

● Hemoptysis and pulmonary edema

● Right sided heart failure may occur late

● Atrial dysrhythmias

MEDICAL MANAGEMENT
● Patients with mitral stenosis may benefit from anticoagulants to decrease the risk for developing atrial thrombus

● Surgical intervention consist of valvuloplasty

● Percutaneous transluminal valvuloplasty

● Mitral valve replacement

NURSING MANAGEMENT
● Place patient in a nigh Fowler's position to ease breathing

● Monitor for:

✔ Pulmonary edema because it may be a complication of surgery

✔ Thrombus because of a valve.

✔ Arrhythmias because of an imitated heart- patient may feel palpitations, anxiety.

✔ Arterial Blood Gas (ABG) to monitor for oxygenation, acidosis, alkalosis.

✔ Weigh the patient daily to determine fluid balance

● Explain to the patient:

✔ Signs and symptoms to look for and to report changes in condition.

✔ Restrict diet to low-sodium and low-fat foods

MITRAL REGURGITATION (INSUFFICIENCY)

❖ Mitral regurgitation involves blood flowing back from the left ventricle into the left atrium during systole. Often the
edges of the mitral valve leaflets do not close during systole
❖ Most common cause is mitral valve prolapse and rheumatic heart disease

CLINICAL MANIFESTATIONS
● Dyspnea, fatigue, and weakness are the most common symptoms.

● Palpitations, shortness of breath on exertion, and cough from pulmonary congestion also occur.

● Systolic murmur is heard as a high- pitched, blowing sound at the apex

MANAGEMENT
● Patients with mitral regurgitation and heart failure benefit from afterload reduction (arterial dilation)

● Angiotensin-converting enzyme (ACE) inhibitor

● Surgical intervention consists of mitral valvuloplasty (ie, surgical repair of the valve) or valve replacement

AORTIC REGURGITATION
❖ Aortic regurgitation is the flow of blood back into the left ventricle from the aorta during diastole"

❖ Blood from the aorta returns to the left ventricle during diastole"
 ETIOLOGY
● Inflammatory lesions that deform the leaflets

● Rheumatic endocarditis,

● Congenital abnormalities

● Syphilis

● Dissecting aneurysm

“In many cases, the cause is unknown and is classified as idiopathic"

CLINICAL MANIFESTATIONS
● Patients experience forceful heart beats especially in the head and neck

● Marked arterial pulsations that are visible or palpable at the carotid or temporal arteries

● Palpable at the carotid or temporal arteries

● Exertional dyspnea and fatigue

● A diastolic murmur is heard as a high-pitched, blowing sound at the third or fourth intercostal space at the left sterna
border.
● Widening of pulse pressure
● One characteristic sign of the disease is the water-hammer (Corrigan's) pulse

SURGICAL MANAGEMENT
● The treatment of choice is aortic valvuloplasty or valve replacement, preferably performed before left ventricular
failure occurs.
● Surgery is recommended for any patient with left ventricular hypertrophy regardless of the presence or absence of
symptoms

NURSING MANAGEMENT
● Patient is advised to avoid physical exertion

● Vasodilators such as calcium channel blockers (eg. nifedipine [Adalat, Procardia))

● Ace inhibitors (eg. Captopril, enalapril, lisinopril, ramipril). or hydralazine

AORTIC STENOSIS
● Narrowing of the orifice between the left ventricle and the aorta,

CAUSE
● Degenerative calcifications caused by inflammatory changes that occur in response to years of normal mechanical
stress.

PATHOPHYSIOLOGY
● Progressive narrowing of the valve orifice occurs, the left ventricle contracts more forcefully and consumes more
energy. It compensates by thickening its walls or hypertrophies.

CLINICAL MANIFESTATIONS
● Exertional dyspnea caused by increased pulmonary venous pressure

● Pulmonary edema may also occur

● Syncope and dizziness because decreased circulation to the brain

● Angina pectoris from increased demands of the left ventricle

● Loud rough systolic murmur heard over the aortic area

● Blood pressure is normal

TREATMENT
● Surgical replacement of the aortic valve or Percutaneous valvuloplasty procedures

INFECTIVE ENDOCARDITIS
● Microbial infection of the endothelial surface of the heart, it usually develops in people with prosthetic heart valves or
structural heart defects

● Hospital acquired infective endocarditis occurs in patients with indwelling catheters

PATHOPHYSIOLOGY
● A deformity or injury of the endocardium brought about by infectious organisms leads to accumulation on the
 endocardium of fibrin and platelets. The infection may erode through the endocardium into underlying structures
(valves /leaflets) causing deformity.

ASSESSMENTS
● Cluster of petechiae may be found on the body

● Small painful nodules (Osiers nodes) may be present in pads of fingers or toes

● Irregular red, purple, painless, flat macules (Janeway Lesions) may be present on the palms fingers and toes.

● Hemorrhages with pale centers in the eyes caused by emboli (Roth spots) caused by emboli may be observed in the fundi
of the eyes
● Splinter hemorrhages (ie, reddish-brown lines and streaks) may be seen under the fingernails and toenails,
 PREVENTION
❖ Antibiotic prophylaxis is recommended for high-risk patients immediately before and sometimes after the following
procedures
● Dental procedures

● Tonsillectomy or adenoidectomy

● Bronchoscopy

● Cystoscopy

● Surgery involving infected skin musculoskeletal tissue

MEDICAL MANAGEMENT
● Antibiotic therapy is usually administered parenterally in a continuous IV infusion for 2 to 6 weeks. penicillin is usually the
medication of choice
● In fungal endocarditis, an antifungal agent, such as amphotericin B (eg, Abelcet, Amphocin, Fungizone), is the usual
treatment

Nurse Home Care Instructions for the Client with Infective Endocarditis
● Teach the client to maintain aseptic technique during setup and administration of intravenous antibiotics.

● Instruct the client to monitor intravenous catheter sites for signs of infection and report this immediately to the
physician.
● Instruct the client to record the temperature daily for up to 6 weeks and report fever.
● Encourage oral hygiene at least twice a day with a soft toothbrush and rinse well with water after brushing

● Client should avoid use of oral irrigation devices and flossing to avoid bacteremia.

MYOCARDITIS
❖ Myocarditis is an inflammation of the myocardium. It is usually diagnosed when it leads to significant cardiac
dysfunction. Myocarditis can cause considerable morbidity and mortality
❖ Infection could be bacterial, protozoal, fungal parasitic

❖ Viral myocarditis is the most common type

❖ Characterized by necrosis and cell injury associated with inflammation of the heart muscle

ASSESSMENT FINDINGS
● Non-specific symptoms: fatigue, dyspnea and palpitation

● If the disease has progressed, symptoms of heart failure present, such as tachycardia, pulmonary edema,
diaphoresis, neck vein distention, and cardiomegaly.
● In myocarditis, the ECG can show low-voltage QRS complexes, ST segment elevation, or heart block
● An S4 and systolic ejection murmurs may be heard on auscultation

● Patients may also sustain sudden cardiac death or quickly develop severe congestive heart failure

MEDICAL MANAGEMENT
● Patient are given specific treatment for the underlying cause if it is known (eg, penicillin for hemolytic streptococci)

● lnotropic support of cardiac function with dopamine, or dobutamine may be used Netroprusside and nitroglycerine may
be used to decrease afterload
● Beta Blocker are avoided because they decrease the strength of ventricular contraction (have a negative inotropic
effect)
● Sedation may be necessary to decrease cardiac workload
● Intra-aortic balloon pulsation and left ventricular assists devices have been used to improve cardiac output
myocarditis

NURSING ALERT
Patients with myocarditis are sensitive to digitalis. Nurses must closely monitor these patients for digitalis toxicity, which evidenced
by dysrhythmia, anorexia, nausea, vomiting, headache, and malaise,

Pericarditis
❖ Pericarditis refers to an inflammation of the pericardium, the membranous sac enveloping the heart. It may be a
primary illness or it may develop during various medical and surgical disorders.
PATHOPHYSIOLOGY
● The inflammation process of pericarditis may lead to an accumulation of fluid in the pericardial (pericardial effusion) and
increased pressure on the heart leading to cardiac tamponade
● Prolonged episodes of pericarditis may lead to thickening and decreased elasticity of pericardium. These conditions
restrict the heart's ability to fill with blood (constrictive pericarditis)
● Restricted filling may result in increased systemic venous pressure

ASSESSMENTS
● Chest pain- located beneath the clavicle, in the neck or in the left scapular region, may worsen with deep inspiration and
may be relieved with a forward leaning or sitting position. (Tripod Position)
● Most characteristic sign of pericarditis is a creaky or scratchy friction rub heard most clearly at the left lower sternal
border (pericardial friction rub)

MEDICAL MANAGEMENT
● Administer therapy for treatment and symptom relief, and detect signs and symptoms of cardiac tamponade.

● Analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs

● Indomethacin (Indocin) is contraindicated because it may decrease coronary blood flow

● A pericardial window, a small opening made in the pericardium

● May be performed to allow continuous drainage into the chest cavity.

● Surgical removal of the tough encasing pericardium (pericardiectomy) may be necessary to release both ventricles from
the constrictive and restrictive inflammation scarring.

PERICARDIOCENTESIS
❖ Procedure in which some of the pericardial fluid is removed

● Emergency resuscitation should be readily available

● The head of the bed is elevated to 45 to 60 degrees, placing the heart In proximity to the chest wall so that the
needle can be directly inserted into the pericardial sac
● Slow iv infusion is started in case it becomes necessary to administer emergency medications or blood products

● Ultrasound imaging is used to guide placement of the needle into the pericardial space

❖ Desired effect

● Decrease in central venous pressure

● Increase in blood pressure

● Withdrawal of pulsus paradoxus

✔ >10 mm Hg drop in blood pressure during inspiration

● Disappearance of prominent neck veins due to increased venous pressure

COMPLICATIONS OF PERICARDIOCENTESIS
● Coronary artery puncture

● Myocardial trauma

● Dysrhythmias

● Pleural laceration

● Gastric puncture

NURSING MANAGEMENT
● Patients with acute pericarditis require pain management with analgesics, positioning, and psychological support
caring for patients with pericarditis must be alert to cardiac tamponade
● After pericardiocentesis, the patient's heart rhythm, blood pressure, venous pressure, and heart sounds are
monitored to detect possible recurrence of cardiac tamponade

NURSING ALERT
● A pericardial friction rub is diagnostic feature of pericarditis. It has a creaky or Scratchy sound and is louder at the end
of exhalation.
● Nurses should monitor for the pericardial friction rub by placing the diaphragm of the stethoscope tightly against the
thorax and auscultating the left sternal edge in the fourth intercostal space, the site where the pericardium comes into
contact with the left chest wall.
● The rub may be heard best when a patient is sifting and leaning forward.
CARDIAC TAMPONADE
❖ A condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial
effusion)
❖ This condition restricts ventricular filling resulting to decreased cardiac output

❖ Acute tamponade happens when there sudden accumulation of more than 50 ml fluid in the pericardial sac

CAUSES
● Cardiac trauma

● Complication of Myocardial infarction

● Pericarditis

ASSESSMENT FINDING
● BECK's Triad

✔ Jugular vein distention

✔ Hypotension

✔ Distant/muffled heart sound

● Pulsus paradoxus
o >10 mm Hg drop in blood pressure during inspiration
● Increased Central Venous Pressure
● Decreased cardiac output

● Anxiety

● Dyspnea

LABORATORY FINDINGS
● Echocardiogram= shows accumulation of fluid in the pericardial sac

● Chest X-ray

NURSING MANAGEMENT
● The client needs to be placed in a critical care unit for hemodynamic monitoring.

● Administer fluids intravenously as prescribed to manage decreased cardiac output.

● Prepare the client for pericardiocentesis to withdraw pericardial fluid if prescribed.

● Monitor for recurrence of tamponade following pericardiocentesis.

● If the client experiences recurrent tamponade or recurrent effusions or develops adhesions from chronic pericarditis, a
portion (pericardial window) or all of the pericardium (pericardiectomy) may be removed to allow adequate ventricular
filling and contraction.

ANGINA PECTORIS
❖ Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the
anterior chest
❖ The cause is insufficient coronary blood flow, resulting in a decreased oxygen supply when there is increased
myocardial demand for oxygen

PATHOPHYSIOLOGY
● Angina is usually caused by atherosclerotic disease and associated with a significant obstruction of at least one major
 coronary artery

TYPES OF ANGINA
❖ Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin

❖ Unstable angina (also called pre-infarction angina or crescendo angina): symptoms increase in frequency and
severity; may not be relieved with rest or nitroglycerin
❖ Intractable or refractory angina: severe incapacitating chest pain

❖ Variant angina (also called Prinzmetal’s angina): pain at rest with reversible ST-segment elevation; thought to be
caused by coronary artery vasospasm
❖ Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress test), but patient
reports no pain
TRIGGERING FACTORS
● Exertion

● Exposure to cold

● Eating a heavy meal, which increases the blood flow to the mesenteric area for digestion, thereby reducing the blood
supply available to the heart muscle;
✔ In a severely compromised heart, shunting of blood for digestion can be sufficient to induce anginal pain

● Stress or any emotion-provoking situation, causing the release of catecholamine's, which increases blood pressure,
heart rate, and myocardial workload

MANIFESTATIONS
● Heavy sensation in the upper chest that ranges from discomfort to agonizing pain

● Severe apprehension and a feeling of impending death.

● Retrosternal pain

● Pain radiates to the neck, jaw, shoulders, and inner aspects of the upper am-is, usually the left arm

“An important characteristic of angina is that it subsides with rest or administering nitroglycerin. In many patients, anginal
symptoms follow a stable, predictable pattern."

ASSESSMENT AND DIAGNOSTIC FINDINGS

● ECG may show changes indicative of ischemia such as T-wave inversion

● Nuclear scan or invasive procedure (eg, cardiac catherization, coronary angiography).

● ST depression

MEDICAL MANAGEMENT
● The objectives of the medical management of angina are decrease the oxygen demand of the myocardium and to
increase the oxygen supply
● Percutaneous transluminal coronary angioplasty (PTCA)
✔ Balloon-tipped catheter is used to open blocked coronary vessels and resolve ischemia. The purpose of PTCA is to
improve blood flow within the coronary artery by compressing and “cracking” the atheroma
● Intracoronary stents
✔ A Stent is a metal mesh that provides structural support to vessel at risk of acute closure.

● Atherectomy

✔ Atherectomy removes plaque from a coronary artery by the use of a cutting chamber on the inserted catheter of a
rotating blade that pulverizes the plaque.
● CABG (Coronary Artery Bypass Graft)
✔ Surgical procedure in which a blood vessel is grafted to an occluded artery so that blood can flow beyond the
occlusion

PHARMACOLOGIC MANAGEMENT
● Nitroglycerine causes dilation of the veins the result is venous pooling of blood throughout the body. As a result, less
blood returns to the heart, decreasing the cardiac workload
● Facts about nitroglycerine
✔ Can be given:
o Sublingual tablet
o Spray
 o Topical agent,
o Intravenous I.V. administration

MEDICATIONS USED TO TREAT ANGINA

NITRATES
● Nitroglycerin (Nitrostat, Nitro-Bid): Short-term and long-term reduction of myocardial oxygen consumption through
selective vasodilation

Beta-Adrenergic Blocking Agents (beta- blockers)

● Metoprolol (Lopressor, Toprol) Reduction of myocardial oxygen consumption by blocking beta-adrenergic

● Atenolol (Tenormin) stimulation of the heart

 Calcium Ion Antagonists (calcium channel blockers)
● Amlodipine (Norvasc) Negative inotropic effects; indicated in patients not responsive to beta-blockers;

● Diltiazem (Cardizem, Tiazac) used primary treatment for vasospasm

● Felodipine (Plendil)

Antiplatelet Medications
● Aspirin Prevention of platelet aggregation

● Clopidogrel (Plavix)

● Glycoprotein agents:

● Abciximab (ReoPro)

● Tirofiban (Aggrastat)

● Eptifibatide (Integrilin)

Anticoagulants
● Heparin (unfractionated): Prevention of thrombus formation

● Low-molecular-weight heparins (LMWHs): Enoxaparin (Lovenox)

● Dalteparin (Fragmin)

MYOCARDIAL INFARCTION
❖ In an MI, an area of the myocardium is permanently destroyed, typically because plaque rupture and subsequent
thrombus formation result in complete occlusion of the artery.
❖ The ECG usually identifies the type and location of the MI, and other ECG indicators such as a Q wave and patient
history identify the timing. Regardless of the location, the goals of medical therapy are to prevent or minimize
myocardial tissue death and prevent complications

RISK FACTORS
Non-modifiable Risk Factor
● Age

✔ Average age of a person having a first heart attack is 65.8 yrs (male) and 70. 4 yrs (female) - AHA 2003

● Family history

● Ethnic background

✔ African-Americans has a higher risk for developing M.I.

Modifiable Risk Factor

● Hypertension

● Smoking

● Hyperlipidemia

● Obesity

● Impaired glucose tolerance (DM)

● Physical inactivity

● Stress
ASSESSMENT
SUBSTANTIAL CHEST PAIN
● The pain associated with an MI usually lasts longer than 30 minutes

● Radiating to the left arm, back or jaw

● Occurring w/o a cause usually in the morning

● Relieved only by opioids associated with nausea, diaphoresis, dyspnea, fear & anxiety, palpitations, fatigue, shortness of
breath.
● Decreased left ventricular function
● Decreased cardiac output

● Cardiovascular system compensates by increasing heart rate (Frank-Starling law)

CG AND CARDIAC ENZYMES ASSESSMENTS

● T-wave in

● ST-segment elevation

● Abnormal Q wave
● Elevated CKMB assessed by mass assay is an indicator of acute MI

● An increase in the level of troponin in the serum can be detected within a few hours during acute MI.

● Enzymes that indicate Myocardial Infarction

ENZYMES TIME DESCRIPTION

OF
ELEVATI
ON
MYOGLOBIN First 1-3 hours First enzyme to elevate due to decreased oxygenation
TROPONIN I 2-4 hours Released at the mentioned time frame
AST (aspartate amino transferase) 8 hours Is also used for liver damage
CK-MB 24 hours Cardiac- specific isoenzyme; it is found mainly in cardiac
cells and therefore increases only when there has been
damage to these cells
LDH (Lactic Dehydrogenase) 72 hours Reflects tissue breakdown and hemolysis

MEDICAL MANAGEMENT
❖ The goals of medical management are to minimize myocardial damage, preserve myocardial function, and prevent
complications this can be achieved by:
● Reperfusing the area with the emergency use of thrombolytic medications

● Reducing myocardial oxygen demand and increasing oxygen supply with medications, oxygen administration, and bed
rest

PHARMACOLOGIC THERAPY
❖ Drug of choice: Morphine I.V.
o Potent vasodilator: Increases oxygen supply to myocardial tissues
o Decreases oxygen demand
❖ (ACE) inhibitors decreases blood pressure thus decreasing the workload of the heart
❖ Thrombolytics dissolve (ie, lyse) the thrombus in a coronary artery (thrombolysis), allowing blood to flow through the
coronary artery again

❖ THROMBINS2 – “the new MONA (Morphine, Oxygen, Nitroglycerin, Aspirin)”

o Thienopyridines: Antiplatelet drugs (Clopidogrel, Prasurgel)
o Heparin: Anticoagulant
o RAAS Inhibitors: ACE-Inhibitors (-pril) or ARBs (-sartan)
o Oxygen
o Morphine
o Beta-blockers: -olol
o Invasive interventions
o Nitroglycerin: vasodilator
o Statin: reduces cholesterol levels (Atorvastatin, Rosuvastatin)
o Salicylate: aspirin/acetylsalicylic acid (ASA)

Common Physical Presentation of the Patient with Acute Myocardial Infarction

General Alert anxious, Restless often fatigued
Skin Cool, clammy; diaphoretic
Heart Cardiovascular S3 or S4 gallop may or may not be present; dysrhythmias or murmurs.
Jugular venous distention May be seen in the presence of pump failure
Lungs Dyspnea, tachypnea, rales (crackles) suggest pulmonary congestion and heart failure
Circulatory Peripheral pulses may be pounding or thready, regular or irregular
Gastrointestinal Nausea and vomiting

CARDIOMYOPATHY
❖ A heart muscle disease associated with cardiac dysfunction.
TYPES
● Dilated

● Hypertrophic

● Restrictive
 DILATED CARDIOMYOPATHY
❖ Extensive damage to the myofibrils & interference with myocardial metabolism

❖ Normal ventricular wall thickness but dilation of both ventricles & impairment of systolic function

❖ Decreased CO- inadequate heart pumping

❖ Dyspnea on exertion fatigue and palpitation

CAUSES
● Alcohol abuse

● Chemotherapy

ASSESSMENT
● Fatigue, weakness

● HF (left side)

● Dysrhythmias

● Moderate to severe cardiomegaly

HYPERTROPHIC CARDIOMYOPATHY

❖ Asymmetric ventricular hypertrophy and disarray of myocardial fibers

❖ LVH leads to a stiff LV that result in diastolic filling abnormalities

❖ Obstruction in LV outflow

❖ 50 % genetically inherited

ASSESSMENT
● Dyspnea

● Angina

● Fatigue, syncope, palpitations

● Mild cardiomegaly

● Ventricular dysrhythmias

● Sudden death common

● Heart failure

RESTRICTIVE CARDIOMYOPATHY
❖ Restriction or filling of the rigid ventricular walls

❖ The cause is unknown (ie, idiopathic) in most cases.

❖ Can be caused by endocrinal or myocardial disease and produce a clinical picture similar to constrictive pericarditis

❖ Fibrosed walls cannot expand or contract

❖ Chamber is also narrowed

ASSESSMENT
● Dyspnea & fatigue

● HF (Right side)
● Mild to moderate cardiomegaly

● Heart block

SHOCK
❖ Inadequate organ perfusion to meet the tissue's oxygenation demand.

❖ Hypoperfusion can be present in the absence of significant hypotension

❖ 3 Types of Shock
o Hypovolemic
o Cardiogenic
o Distributive – systemic vasodilation leading to decreased blood pressure and insufficient tissue perfusion
▪ Neurogenic
▪ Anaphylactic

▪ Septic
 TYPES OF SHOCK
HYPOVOLEMIC
❖ Occurs when there is a loss of fluid (blood, plasma) resulting in inadequate tissue perfusion; caused by:

✔ Hemorrhage/Excessive bleeding

✔ Excessive diarrhea or vomiting

✔ Dehydration

✔ Fluid loss from fistulas or burns

✔ Massive third spacing/edema

TREATMENT
● Primary problem/underlying cause must be treated

● Whole blood, plasma (fluid and blood) Replacement and electrolytes

MANAGEMENT:
Major goals in the treatment of hypovolemic shock are to restore intravascular volume to reverse the sequence of events leading to
inadequate tissue perfusion, to redistribute fluid volume, and to correct the underlying cause of the fluid loss as quickly as possible

CARDIOGENIC
❖ Occurs when pump failure causes inadequate tissue perfusion; caused by

✔ Congestive heart failure

✔ Myocardial infarction

✔ Cardiac tamponade

MANAGEMENT
● The goals of medical management in cardiogenic shock are to limit further myocardial damage and preserve the
healthy myocardium and to improve the cardiac function by increasing cardiac contractility, decreasing ventricular
afterload, or both.

NEUROGENIC
❖ Neurogenic shock develops as a result of the loss of autonomic nervous system function below the level of the
lesion in the spinal cord which caused rapid vasodilation and subsequent pooling of blood within the peripheral vessels

MANAGEMENT
● Treatment of neurogenic shock involves restoring sympathetic tone, either through the stabilization of a spinal cord
injury or, by positioning the patient properly.
● It is important to elevate and maintain the head of the bed at least 30 degrees to prevent neurogenic shock when a
patient receives spinal or epidural anesthesia. Elevation of the head helps prevent the spread of the anesthetic agent up
the spinal cord.

ANAPHYLACTIC
❖ Caused by an allergic/anaphylactic reaction that causes a release of histamine and subsequent systemic vasodilation

MANAGEMENT:
● Treatment of anaphylactic shock requires removing the causative antigen (eg, discontinuing an antibiotic
agent), administering medications that restore vascular tone, and providing emergency support of basic life
functions.
● Epinephrine is given for its vasoconstrictive action (emergency drug).
● Diphenhydramine (Benadryl) is administered to reverse the effects of histamine, thereby reducing capillary
 permeability.

SEPTIC
❖ Similar to anaphylaxis; the body's reaction to bacterial toxins (generally gram-negative infections) results in the
leakage of plasma into tissues

MANAGEMENT
● Current treatment of sepsis and septic shock involves identification and elimination of the cause of infection.
 TYPE MECHANISM
Hypovolemic Loss of blood or plasma
Cardiogenic Decreased pumping capability/contractility of heart
Distributive Systemic vasodilation
- Anaphylactic due to severe allergic reaction
- Septic due to severe infection
- Neurogenic due to loss of SNS and vasomotor tone

HYPERTENSION
❖ Hypertension is defined as a systolic blood pressure greater than 140 mm Hg and a diastolic pressure greater than 90
mmHg

TYPES OF HYPERTENSION
ESSENTIAL HYPERTENSION
● No known direct cause

● Risk factor

✔ Age > 60 yrs

✔ Family history of hypertension

✔ Excessive caloric consumption

✔ Physical inactivity

✔ Excessive alcohol intake

✔ Hyperlipidemia

✔ High salt intake or caffeine; reduced intake of potassium, calcium, or magnesium

✔ Smoking
SECONDARY HYPERTENSION
● Disease

✔ Renal vascular & parenchymal disease

✔ Primary aldosterone

✔ Pheochromocytoma

✔ Cushing's disease

✔ Coarctation of aorta

✔ Brain tumors

✔ Encephalitis

PHARMACOLOGIC THERAPY
● For patients with uncomplicated hypertension and no specific indications for another medication, the recommended
initial medications include diuretics, beta blockers and angiotensin-converting enzyme (ACE)

BETA-BLOCKERS
● First line drug therapy

● Reduce BP by decreasing CO

● Decrease sympathetic stimulation

● Inhibit release of renin from the kidneys

ANGIOTENSIN -CONVERTING ENZYME (ACE) INHIBITORS

● Lower BP by reducing peripheral vascular resistance w/o reflex increase in CO, HR or contractility.

✔ Captopril (Capoten)

✔ Enalapril (Vasotec)

✔ Lisinopril (Zestril)

● Decrease secretion of aldosterone

CENTRAL ALPHA ANTAGONIST

● Acts on CNS preventing reuptake of norepinephrine resulting in lower peripheral Vascular resistance & BP

✔ Clonidine (Catapres)

✔ Does not decrease renal blood flow

CALCIUM-CHANNEL BLOCKER
● Verapamil (Isoptin

● Amlodipine

● Diltiazem

● Nicardipine

DIURETICS (WATER PILL)

● Thiazide

✔ Chlorothiazide (Diuril)

✔ Hydrochlorothiazide (Hydrodiuril)

● Loop

✔ Furosemide (Lasix)

✔ Bumetanide (Bumex)

● Potassium - sparing

✔ Spironolactone (Aldactone)

NURSING INTERVENTIONS
● The objective of nursing care for patients with hypertension focuses on lowering and controlling the blood pressure
without adverse effects and without undue cost through:
✔ Adhere to the treatment regimen

✔ Implementing necessary lifestyle changes

✔ Taking medications as prescribed

✔ Scheduling regular follow-up appointments

THROMBOANGIITIS OBLITERANS/ BUERGER'S DISEASE

❖ Buerger's disease is characterized by recurring inflammation of the intermediate and small arteries and veins of the
lower and upper extremities
● Factors

✔ Men between 20-35 years of age

✔ Heavy smoking and chewing tobacco

CLINICAL MANIFESTATIONS
● Foot cramps, especially of the arch (instep claudication), after exercise

● Pain is relieved by rest

● Intense rubor (reddish-blue discoloration) of the foot and absence of the pedal pulse

MEDICAL MANAGEMENT
● The main objectives are to improve circulation to the extremities, prevent the progression of the disease

● Vasodilators are rarely prescribed

RAYNAUD'S PHENOMENON
❖ Raynaud's phenomenon is a form of intermittent arteriolar vasoconstriction that results in coldness, pain, and pallor of
 the fingertips or toes.
Factors:
● Raynaud's phenomenon is most common in women between 16 and 40 years of age, and it occurs more frequently in cold
climate

CLINICAL MANIFESTATION
● The characteristic sequence of color change of Raynaud's phenomenon is described as white, blue, and red.

● Numbness, tingling, and burning pain occur as the color changes.

● The manifestations tend to be bilateral and symmetric and may involve toes and fingers.

MEDICAL MANAGEMENT
● Avoiding the particular stimuli (E.g. cold, tobacco) that provoke vasoconstriction is a primary factor in controlling
Raynaud's phenomenon.
● Calcium channel blockers (Nifedipine [Procardia], amlodipine [Norvasc])
● Sympathectomy (interrupting the sympathetic nerves by removing the sympathetic ganglia or dividing their branches) may
help some patients.
NURSING MANAGEMENT
● Exposure to cold must be minimize

● Sweater should be available when entering air-conditioned rooms

✔ Avoid smoking and all sources of nicotine like nicotine gum or patches.

VENOUS THROMBOEMBOLISM
❖ Deep vein thrombosis (DVT)

● Virchow's triad

✔ Vessel wall injury

✔ Venous stasis (stasis of blood)

✔ Altered blood coagulation

● Risk Factors for Venous stasis

✔ Bed rest or immobilization

✔ Obesity

✔ History of varicosities

✔ Spinal cord injury

✔ Age (greater than 65 years)

ASSESSMENT
● Obstruction of the deep veins comes edema and swelling of the extremity because the outflow of venous blood is
inhibited
● Limb pain, a feeling of heaviness, functional impairment, ankle engorgement, and edema

PREVENTION
● Preventive measures include the application of graduated compression stockings

● In surgical patients is administration of subcutaneous unfractionated or low molecular- weight heparin (LMWH).

● Lifestyle changes as appropriate, which may include weight loss, smoking cessation, and regular exercise

MEDICAL MANAGEMENT
Anticoagulant therapy
● (Administration of a medication to delay the clotting time of blood, prevent the formation of a thrombus in
postoperative patients, and forestall the extension of a thrombus after it has formed)
● Oral Anticoagulant Warfarin (Coumadin)

Thrombolytic
● Alteplase (Activase, t-PA)

● Urokinase (Abbokinase)

● Streptokinase (Streptase)

NURSING MANAGEMENT
● If the patient is receiving anticoagulant therapy, the nurse must frequently monitor the aPTT, prothrombin time (PT) and
INR
● Elevation of the affected extremity, graduated compression stockings, and analgesic agents for pain relief are
adjuncts the therapy. They help improve circulation and increase comfort.
● Warm, moist- packs applied to the affected extremity reduce the discomfort associated with DVT
● The patient is encouraged to walk once anticoagulation therapy has been initiated. The nurse should instruct the
patient that walking is better than standing or sitting for long periods

NURSING ALERT
● For ambulatory patients, graduated compression stockings are removed at night and reapplied before the legs are
lowered from the bed to the floor in the morning.

ANEURYSMS
❖ An aneurysm is a localized sac or dilation formed at a weak point in the wall of the artery.
CAUSES
● Congenital: Primary connective disorders (Marfan's syndrome)

● Mechanical (hemodynamic): Poststenotic and arteriovenous fistula and amputation related

● Traumatic (pseudoaneurysms): Penetrating arterial injuries, blunt arterial (pseudoaneurysms)

● Infectious (mycotic): Bacterial, fungal, spirochetal infections

● Pregnancy-related degenerative:

● Nonspecific, inflammatory variant

● Anastomotic (postarteriotomy) and graft aneurysms: Infection, arterial wall failure, suture failure, graft failure

TYPES
❖ Normal artery.

❖ False aneurysm—actually a pulsating hematoma. The clot and connective tissue are outside the arterial wall,

❖ True aneurysm. One, two, or all three layers of the artery may be involved.

❖ Fusiform aneurysm—symmetric, spindle shaped expansion of entire circumference of involved vessel.

❖ Saccular aneurysm—a bulbous protrusion of one side of the arterial wall.

❖ Dissecting aneurysm—this usually is a hematoma that splits the layers of the arterial wall.

MEDICAL MANAGEMENT
● Antihypertensive agents, including:

✔ Diuretics,

✔ Beta blockers,

✔ Ace inhibitors,

✔ Angiotensin II receptor antagonists, calcium channel blockers

These drugs are frequently prescribed to maintain the patient's blood pressure within acceptable limits to prevent rupture of the
aneurysms

SURGICAL MANAGEMENT
● Resection of the vessel and sewing a bypass graft in place

● Endovascular grafting, which involves the transluminal placement and attachment of a sutureless aortic graft
prosthesis across an aneurysm
HEMATOLOGIC SYSTEM
❖ The hematologic system consists of the blood and the sites where blood is produced, including the bone marrow and the
reticuloendothelial system (RES).
❖ Blood is a specialized organ that differs from other organs in that it exists in a fluid state. Blood is composed of plasma and various types
of cells.
❖ Plasma is the fluid portion of blood; it contains various proteins, such as albumin, globulin, fibrinogen, and other factors
necessary for clotting, as well as electrolytes, waste products, and nutrients. About 55% of blood volume is plasma.
❖ Serum is plasma minus the clotting factors.

BLOOD CELLS

Cell Type Major Function

WBC Fights infection
(Leukocyte)
Normal: 4500-
11,000/mm3
Granulocytes
Neutrophil Essential in Preventing or limiting bacterial infection via phagocytosis

Eosinophil Involved in allergic reactions (neutralizes histamine), digests foreign proteins

Agranulocytes Enters tissue as macrophage; highly phagocytic, especially against fungus; immune surveillance
Monocyte
Responsible for cell- mediated immunity
T lymphocyte
Secretes immunoglobulin (Ig/ antibody)
Plasma Cell Most mature form of B lymphocytes
RBC (Erythrocyte) Carries hemoglobin to provide oxygen to tissues; average lifespan is 120 days
Hemoglobin
Male: 13-18
g/dL
Female: 12-16 g/dL

Hematocrit
Male: 42-
52%
Female: 35-47%
Platelet Fragment of megakaryocyte; provides basis for coagulation to occur; maintains hemostasis; average
(Thrombocyte) lifespan is 10 days.
Normal: 150,000
450,000/ mm3

IRON DEFICIENCY ANEMIA (IDA)

❖ Results when the intake of dietary iron is inadequate for hemoglobin synthesis

❖ Predisposing Factors

● Chronic blood loss due to trauma, menorrhagia, GI bleeding (hematemesis, melena, hematochezia)

● Inadequate Fe+2 in the diet

● Impaired Fe+2 absorption due to

✔ Chronic diarrhea

✔ Malabsorption syndrome

✔ Gastrectomy

✔ Celiac disease

❖ Clinical Manifestations

● Fatigue/Easy fatigability – hallmark sign

● Brittle hair, spoon-shaped nails (koilonychia) due to atrophy of epidermal cells

● Palpitations, cold sensitivity

● Pallor, fatigue

● Smooth, sore tongue

● Plummer Vinson's Syndrome - atrophic glossitis, stomatitis, dysphagia due to atrophy of papilla of the tongue, mouth and
pharyngeal cells
● Pica- due to neuronal degeneration that affects cognitive functions

● Angular cheilosis- ulceration of the corner of the mouth

● Cerebral hypoxia- dizziness, dyspnea

❖ Diagnostic Procedures

● RBC, Hemoglobin, Hematocrit, Reticulocyte count, Serum Fe+2, Ferritin

❖ Management

● Correction of chronic blood loss.

● Oral or parenteral iron therapy

❖ Nursing Management

● Monitor all signs of bleeding

● CBR

● Increase intake of Fe+2 rich foods such as:

✔ Green, leafy, vegetables,

✔ Organ liver meat

✔ Egg yolk

✔ Legumes

✔ California raisins

✔ Red Meats

✔ Molasses

● Administer Iron preparation as ordered.

✔ FeSO4, Fe+2 gluconate, Fe+2 Fumarate

✔ Taken with Vit C to increase absorption

✔ Instruct the patient to avoid taking antacids and dairy products (it decreases iron absorption)

✔ Best absorbed on an empty stomach, in between meals to prevent GI upset

✔ Monitor S/E: anorexia, N/V, abdominal pain, diarrhea/constipation, black stools

MEGALOBLASTIC ANEMIA: PERNICIOUS ANEMIA

❖ Most dangerous of all chronic anemia due to deficiency of intrinsic factor leading to Vit. B12 malabsorption

❖ Predisposing factors

● Unknown cause

● Subtotal gastrectomy

● Hereditary

● Inflammation disorders of the ileum

✔ Crohn's Disease

● Absence of intrinsic factor

● Strict vegetarian diet

❖ Clinical Manifestations

● Headache, dizziness, dyspnea, palpitations, cold sensitivity, general body malaise, extreme pallor

✔ Sore mouth, anorexia, nausea, vomiting, loss of weight, indigestion, epigastric discomfort, recurring diarrhea or
constipation.
✔ Red-beefy tongue/ Glossitis - pathognomonic sign

✔ Paresthesia in the extremities, difficulty maintaining their balance, lose position sense (proprioception)

❖ Diagnostic procedures
 ✔ CBC and blood smear decreased hemoglobin and hematocrit

✔ Schilling's test for absorption of vitamin B12 —patient receives small amount of radioactive B12 orally and 24-hour urine
collection is obtained
o Positive: Vitamin B12 absent in urine
o Negative: Vitamin B12 present in urine
❖ Nursing Management
● Enforce CBR and ensure safety

● Administer Vit. B12 injections at monthly intervals for lifetime as ordered.

● Diet

✔ Small frequent bland soft food

✔ Increase CHO, CHON, iron & Vit C

● Avoid irritating mouthwashes. Use of soft bristled toothbrush is encouraged

● Avoid excessive heat and cold temperature

● Administer parenteral Iron preparation as ordered

✔ Administer using Z-tract method to prevent discoloration and leakage to tissues

✔ Do not massage the injection site, encourage ambulation instead

✔ Monitor S/E such as:

⮚ Pain at injection site

⮚ Localized abscess

⮚ Lymphadenopathy

⮚ Fever and chills

⮚ Skin rashes

✔ Watch out for anaphylaxis due to parenteral Iron supplement

 MEGALOBLASTIC ANEMIA: FOLIC ACID DEFICIENCY
❖ Occurs if there is folic acid deficiency within 4 months

❖ Risk Factors

● People who rarely eat uncooked vegetables

● Alcoholism

● Chronic hemolytic anemia

● Pregnancy

● Malabsorptive diseases of the small bowel such as sprue

❖ Clinical Manifestations

● Fatigue, weakness

● Pallor, dizziness, headache

● Tachycardia.

● Sore tongue, cracked lips

❖ Diagnostic Procedure

● CBC will show decreased RBC, hemoglobin, and hematocrit with increased mean corpuscular volume and mean corpuscular
hemoglobin concentration
❖ Management

● Administer 1mg of folic acid daily

● Folic acid intramuscular for patients with malabsorption problem

● Small frequent meals of bland, soft food if

sore mouth and tongue are present
● Diet: food rich in folic acid such as beef liver, peanut butter, red beans, oatmeal, broccoli, asparagus

APLASTIC ANEMIA
✔ A rare disease caused by a decrease in or damage to marrow stem cells, damage to the microenvironment within the marrow, and
replacement of the marrow with fat resulting in pancytopenia (decreased RBCs, WBCs' and platelets)
Predisposing Factors
● Chemicals (Benzene & its derivatives, pesticides)

● Radiation

● Immunologic injury

● Drugs causing bone marrow depression

● Broad spectrum antibiotic

✔ Chloramphenicol

✔ Sulfonamides — Bactrim

● Chemo therapeutic agents

✔ Methotrexate

✔ Nitrogen mustard

✔ Vincristine

● Attack of T-cells against bone marrow

● Infections and pregnancy

Clinical Manifestations
● Signs of such as pallor, weakness, fatigue, exertional dyspnea, palpitations, fatigue
● Infections associated with Leukopenia: fever, headache, malaise, abdominal pain, diarrhea, erythema, pain, exudate at wounds or sites
of invasive procedures, Lymphadenopathies and Splenomegaly
● Thrombocytopenia: bleeding from gums, nose, GI or GU tracts; purpura, petechiae, ecchymoses, retinal hemorrhage, oozing of blood
from venipuncture site
Diagnostic Procedures
● Bone Marrow Aspiration shows an extremely hypoplastic or even aplastic (very few to no cells) marrow replaced with fat.

● CBC and peripheral blood smear shows decreased RBC, WBC and platelets (pancytopenia)

Management
● Removal of causative agent or toxin.

● Bone Marrow Transplantation (BMT) or Peripheral Blood Stem Cell Transplant (PBSCT)

● Immunosuppressive therapy

● Supportive treatment includes platelet and RBC transfusions, antibiotics, and antifungal administration

Nursing Management
● Administration of immunosuppressants as ordered

● Blood transfusion as ordered

● Complete bed rest

● O2dministration

● Teach patient how to minimize risk of infection

 ● Reverse isolation due leukopenia

● Monitor signs of infection

● Avoid SQ, IM injections Use only soft toothbrush for mouth care and electric razor for shaving

SICKLE CELL ANEMIA

❖ Is a severe hemolytic anemia that results from inheritance of the sickle hemoglobin gene. This gene causes the hemoglobin molecule
to be defective. The abnormal sickle hemoglobin (HbS) acquires a crystal-like formation when exposed to low oxygen tension.

❖ Clinical Manifestations

● Severe pain in various parts of the body

● Tachycardia, murmurs & cardiomegaly

● Chest pain, dyspnea

● Jaundice

● Enlarged skull & facial bones due to bone marrow expansion

❖ Complications

● Hypoxia, ischemia, infection, poor wood healing

● Impotence

● Cerebrovascular accident

● Renal failure

● Heart failure

● Pulmonary hypertension

❖ Sickle Cell Crisis

● Sickle crisis - most common and very painful

✔ Results from tissue hypoxia and necrosis due to inadequate blood flow to a specific region of tissue or organ

● Aplastic crisis - results from infection with the human parvovirus

● Sequestration crisis - results when other organs pool the sickled cells

❖ Treatment

● Bone marrow transplant

● Hydroxyurea = Increases production

● Long term RBC transfusion

● Splenectomy

● Peripheral Blood Stem Cell Transplant

❖ Nursing Management

● MANAGING PAIN

✔ Treat the triggering factors.

o Hypoxia: Provide oxygen support.
o Dehydration: Infuse intravenous fluids. Encourage increased oral fluid intake.
o Infection: Administer antibiotic medications as prescribed.
✔ Support & elevate acutely inflamed joint
✔ Relaxation techniques
 ● PREVENT AND MANAGE INFECTION

✔ Monitor patient for signs and symptoms of infection

✔ Initiate prompt antibiotic therapy

● MONITOR AND PREVENT POTENTIAL COMPLICATIONS

✔ Always provide adequate hydration

✔ Avoid cold temperature that may cause vasoconstriction

✔ Protect leg from trauma and contamination to prevent leg ulcer

✔ Aseptic technique

THALASSEMIA
❖ Group of hereditary anemias characterized by hypochromia (an abnormal decrease in the hemoglobin content of erythrocytes),
extreme microcytosis (smaller-than-normal erythrocytes), destruction of blood elements (hemolysis), and variables degrees of
anemia
❖ Associated with defective synthesis of hemoglobin; the production of one or more globulin chains within the hemoglobin molecule is
reduced
❖ 2 classifications:

● Alpha-thalassemia occur mainly in people from Asia and the Middle East

✔ Milder than the beta forms and often occurs without symptoms; the erythrocytes are extremely microcytic, but the
anemia, if present, is mild
● Beta-thalassemia are most prevalent in people from Mediterranean regions
✔ Patients with mild forms have microcytosis and mild anemia

✔ Severe beta-thalassemia (i.e., thalassemia major or Cooley’s anemia) can be fatal within the first few years of life if
untreated
❖ Management

● Bone Marrow Transplant

● Blood transfusion of Packed RBSs

❖ Thalassemia Major (Cooley’s Anemia)

● Characterized by severe anemia, marked hemolysis, and ineffective erythropoiesis

● With early regular transfusion therapy, growth and development through childhood are facilitated

● Management: PBSCT before liver damage occurs

● Watch out for iron overload which results from excessive iron in multiple packed RBC

✔ Management: regular chelation therapy

POLYCYTHEMIA VERA (PRIMARY POLYCYTHEMIA)

❖ Proliferative disorder of the myeloid stem cells

❖ The bone marrow is hypercellular.

❖ Elevated levels of blood cells (erythrocyte, leukocyte, platelets)

❖ Clinical Manifestations

● Ruddy complexion

● Splenomegaly

● Headache and dizziness

● Tinnitus, fatigue and paresthesia

● Blurred vison

● Increased blood viscosity: angina, claudication, dyspnea and thrombophlebitis

● Elevated blood pressure

● Uric acid maybe elevated resulting in gout and renal stone formation

● Generalized pruritus

● Erythromyalgia (burning sensation in fingers and toes)

❖ Diagnostic Procedures

● CBC

● Bone Marrow Aspiration

❖ Complications

● Cerebrovascular Accident

● Myocardial Infarction

● Bleeding due to dysfunctional large amount of platelet

❖ Management

● Phlebotomy – removing enough blood (initially 500 mL once or twice weekly) to reduce blood viscosity and to deplete the
patient’s iron stores
● Chemotherapeutic agents (eg, hydroxyurea) can be used to suppress marrow function
● Anagrelide (Agrylin) – inhibits platelet aggregation

● Interferon alfa-2b (Intron-A) – for management of pruritus (WOF: flulike syndrome and depression)

● Antihistamine

● Allopurinol

❖ Nursing Management

● Instruct the patient to avoid sedentary behaviours, crossing of legs, wearing tight or restrictive clothing

● Avoid aspirin and aspirin-containing medications

● Minimize alcohol intake

● Instruct the patient to avoid iron supplements

● For pruritus:

● Bathing in tepid or cool water

● Avoiding vigorous toweling off after bathing

● Use of cocoa butter or oat meal-based lotions and bath products

● Dissolved baking soda in bath water

HEMOPHILIA
❖ Inherited bleeding disorder

❖ Hemophilia A – caused by genetic disease that results in deficient or defective factor VIII

❖ Hemophilia B (Christmas Disease) – genetic defect that causes deficient or defective factor IX

❖ Both types of hemophilia are inherited as X-linked traits, so almost all affected people are males; females can be carriers

❖ Recognized in early childhood, usually in the toddler age group

❖ Clinical Manifestations

● Hemorrhages into various parts of the body

● Hemarthroses and hematomas

● 75% of all bleeding occurs into joints

● Chronic pain or ankylosis (fixation) of the joint occurs

● Spontaneous hematuria and GI bleeding

● Intracranial or extracranial bleeding – most dangerous

❖ Management

● Administration of factor VIII and factor IX concentrates

● Infusion of fresh frozen plasma

● Plasmapheresis or concurrent immunosuppressive therapy

● Aminocaproic acid inhibits fibrinolysis and therefore stabilizes the clot

● Desmopressin (DDAVP) – induces a significant but transient rise in factor VII levels

❖ Nursing Management

● Assist the child in coping with the condition

● Encouraged to be self-sufficient and to maintain independence by preventing unnecessary trauma that can
cause acute bleeding episodes
● Instruct the patient to avoid OTC medications such as aspirin, NSAIDs, herbs, nutritional supplements and
alcohol
● Nasal packing should be avoided, because bleeding frequently resumes when the packing is removed
● All injections should be avoided

● Splints and other orthopedic devices may be useful in patients with joint or muscle hemorrhages

● Warm baths promote relaxation, improve mobility, episodes

● Provide genetic testing and counselling to female carriers

 COMMUNICABLE DISEASE NURSING
TERMINOLOGIES
❖ Infection

● Implantation and success replication of an organism in the tissue of the host resulting to signs and
symptoms as well as immunologic response.
❖ Carrier

● An individual who harbors the organism and is capable of transmitting it to a susceptible host without
showing manifestations of the disease.
❖ Communicable Disease
● It is an illness caused by an infectious agent or its toxic products that are transmitted directly or indirectly to a
well person through an agency, and a vector or an inanimate object.
❖ Contact

● It is any person or animal who is in close association with an infected person, animal or freshly soiled
materials.
❖ Contagious Disease

● It is a term given to a disease that is easily transmitted from one person to another through direct or
indirect means.
❖ Disinfection

● It is the destruction of pathogenic microorganism on inanimate objects by directly applying physical or

chemical means.
❖ Concurrent

● it is a method of disinfection done immediately after the infected individual discharges infectious
material/secretions.
● Method of disinfection when the patient is still the source of infection.

❖ Terminal

● It is applied when the patient is no longer the source of infection

● This is done after patient is discharged from the hospital to prepare the room for the next patient.

❖ Habitat

● It is a place where an organism lives or where an organism is usually found.

❖ Host

● It is a person, animal or plant on which a parasite depends for its survival.

❖ Infectious Disease

● It is transmitted not only by ordinary contact but requires direct inoculation of the organism through a
break on the skin or mucous membrane.
❖ Isolation

● it is the separation from other persons of an individual suffering from a communicable disease during the
period of communicability.
❖ Quarantine

● It is the limitation of freedom of movement of persons or animals which have been exposed to
communicable disease/s for a period of time equivalent to the longest incubation period of that disease.
 ❖ Reservoir

● It is composed of one of more species of animal or plant in which an infectious agent lives and multiplies for
survival and reproduces itself in such a manner that it can be transmitted to man.

EPIDEMIOLOGY

● It is study of occurrences and disturbance of diseases as well as the distribution and determinants of health
states of events in specified population and application of this study to the control of health problems.
● Foundation of preventing disease

Uses
● Study the history of the health population and the rise and fall of disease and changes in their character.

● Diagnose the health of the community

● Study the work of health services with a view of improving them

● Estimate the risk of disease, accident, defects and the chances of avoiding them.

● Complete the clinical picture of chronic disease and describe their history
 Epidemiologic Triangle
● Consists of three components – host, environment and agent.
Host
● Any organism that harbors and provides nourishment for another organism
Agent
● Intrinsic property of microorganism to survive and multiply in the environment to produce disease.
Environment
● It is the sum total of all external conditions and influences that affect the development of an organism
which can be:
✔ Biological
✔ Social

✔ Physical
Patterns of Occurrence and Distribution
❖ Sporadic

● Intermittent occurrence of a few isolated and unrelated cases in a given locality.

● Cases are few and scattered

● E.G. Rabies

❖ Endemic

● Continuous occurrence throughout a period of time, of the usual number of case in a given locality.

● The disease is therefore always occurring in the locality and the level of occurrence is more or less constant
through a period of time.
● Examples:
▪ Schistosomiasis (Leyte & Samar)

▪ Filariasis (Sorsogon)

▪ Malaria (Palawan)

❖ Epidemic (Outbreak)

● Unusually large number of cases in a relatively short period of time.

❖ Pandemic

● The simultaneous occurrence of epidemic of the same disease in several countries.

● E.G. HIV/AIDS and SARS

CHAIN OF INFECTION
1. Causative Agent
❖ Any microbe capable of producing a disease

❖ Bacteria, spirochete, virus, ricketssia, chlamydiae, fungi, protozoa and parasites

2. Reservoir of Infection
❖ Refers to the environment and objects on which an organism survives and multiples
3. Portal of Exit
❖ It is the path or way in which the organism leaves the reservoir.

❖ Common portals of exit:

 ●Respiratory System

●Genitourinary Tract

●Gastrointestinal Tract

●Skin and Mucous Membrane

●Placenta
4. Mode of Transmission
❖ It is the means by which the infectious agent passes through from the portal of exit of the reservoir to the
susceptible host.
❖ Easiest link to break the chain of infection

Contact Transmission
● Most common mode of transmission.
Direct Contact
✔ Refers to a person to person transfer of organism.
Indirect Contact
✔ Occurs when the susceptible person comes in contact with a contaminated object.
 Droplet Spread
✔ It is the transmission through contact with respiratory secretions when the infected person coughs, sneezes or
talks.
✔ Transmission is limited within 3 feet.

Airborne Transmission
● Occurs when fine microbial particles or dust particles containing microbes remain suspended in the air for a
prolonged period.
● Transmission can be more than 3 feet.

Vehicle Transmission
● It is the transmission of infectious disease through articles or substance that harbor the organism until it is
ingested or inoculated into the host.

Vector-borne Transmission
● Occurs when intermediate carriers, such as fleas, flies and mosquitoes transfer the microbes to another living
organism.
5. Portal of Entry
❖ It is the venue the organism gains entrance into the susceptible host.

❖ The infective microbes use the same avenues when they exit from the reservoir.
6. Susceptible Host
❖ When the defenses are good, no infection will take place.

❖ However, in weakened host, microbes will launch an infectious disease.

IMMUNITY

❖ Natural

● Active

✔ Acquired through recovery from a certain disease

● Passive

✔ Acquired through placental transfer

❖ Artificial

● Active

✔ Acquired through the administration of vaccine and toxoid

● Passive

✔ Acquired through the administration of antitoxin, antiserum, convalescent serum, and

immunoglobulins

Type of Antigen
❖ Inactivated (killed organism)

● Not long lasting

● Multiple doses needed

● Booster dose needed

❖ Attenuated (live, weakened organism)

 ● Single dose needed

● Long lasting immunity

ISOLATION

❖ Separation of patients with communicable disease from other so as to prevent or reduce transmission or infectious
agent directly or indirectly.
Categories Recommended in Isolation
❖ Strict Isolation

● Prevents highly contagious or virulent infections

❖ Contact Isolation

● Prevents the spread of infection primarily by close or direct contact

❖ Respiratory Isolation

● Prevents the transmission of infectious diseases over short distance through the air
❖ TB Isolation

● For TB patients with positive smear or with chest X-ray which strongly suggests active tuberculosis.

❖ Enteric Isolation

● For infection with direct contact with feces

❖ Reverse/Neutropenic Isolation

● An immunocompromised client is separated to prevent contracting infection from environment.

❖ Standard Precaution

● To prevent infections that are transmitted by direct or indirect contact with secretions or drainage (except
sweat) from another person.
● Universal Precaution + Body Substance Isolation (BSI)

● Universal Precaution

▪ Intended to prevent parenteral mucous membrane and non-intact skin exposure of health care
workers to blood borne pathogens
❖ Transmission Based Precaution

● Second Tier of precaution

● Applicable to patient who are highly contagious

● Three types: Contact, Airborne, Droplet

INTEGUMENTARY DISEASE

CHICKEN POX
Other Term: Varicella zoster

Description: Acute infectious disease of sudden onset with slight fever, mild constitutional symptoms and eruptions which
are maculopapular for a few hours, vesicular for 3-4 days and leaves granular scabs.

Etiologic Agent: Human (alpha) herpes virus 3 (Varicella-zoster virus)

Sources of Infection:
❖ Secretions of respiratory tract of infected persons

❖ Lesions (little consequence)

❖ Scabs are not infective

Mode of Transmission
❖ Direct contact

❖ Contact with contaminated linen and fomites

❖ Airborne

Incubation Period
❖ 2 to 3 weeks

Period of Communicability
❖ Cases are infectious for up to 2 days before the onset of the rash until 5 days after the first crop of vesicles.
 Diagnostic Test
❖ Isolation of the virus from the vesicular fluid within the first 3 to 4 days of the rash

❖ Serum antibodies is present in 7 days after onset

Congenital Varicella results in:

❖ Hypoplastic, deformities and scarring of limb

❖ Retarded growth

❖ CNS and ophthalmic manifestation

Nursing Considerations
❖ Strict Isolation

❖ Exclusion from school for 1 week after eruption first appears and avoid contact with susceptible

❖ Concurrent disinfection if throat and nose discharge

❖ Tell the patient not to scratch the lesions

❖ Teach the child and the family how to apply topical antipruritic medication correctly

Susceptibility, Resistance & Occurrence

❖ Universal among those not previously attacked

❖ Severe in adults

❖ An attack confers long immunity

❖ Second attacks are rare

Prevention
❖ Vaccine

● Varicella – zoster Immune Globulin (VZIG)

✔ It should be given within 10 days of exposure

MEASLES
Other Terms: Rubeola / Morbili / 7 – day Measles

Description: it is an acute contagious and exanthematous disease that usually affects children who are susceptible to Upper
Respiratory Tract Infection (URTI)

Etiologic Agent
❖ Filterable virus of Measles (Paramyxoviridae)

Source of infection
❖ Secretions of nose and throat of infected persons

Mode of Transmission
❖ Droplet Spread / Direct Contact with Infected person

❖ Indirect Contact (articles with secretions)

❖ Airborne

Incubation Period
❖ 1-2 weeks

Period of Communicability
❖ Starts just before the prodrome and lasts until 4 days after the rash appears.

Clinical Manifestations
Koplik spots – pathognomonic sign

1. Pre-eruptive Stage
● Fever

● Catarrhal Symptoms (cough, conjunctivitis, coryza)

● Photophobia

● Stimson’s line (red line on the lower conjunctiva)

2. Eruptive Stage
 ● Maculo-papular rash

● High grade fever

● Anorexia and irritability

● Throat is red and extremely sore

3. Convalescence Stage
● Rashes fade away

● Fever subsides

● Desquamation begins

● Symptoms subside and appetite is restored

Diagnostic Procedures
❖ Nose and Throat Swab

❖ Urinalysis

❖ Blood exams (Single raised IgM or rise on IgG)

Treatment Modalities
❖ Anti-viral drug (Isoprenosine)

❖ Antibiotics

❖ Oxygen Inhalation

❖ IV fluids

Complications
❖ Bronchopneumonia

❖ Otitis Media

❖ Pneumonia

❖ Nephritis

❖ Encephalitis

Nursing Management
❖ Isolation

❖ Maintain standard and airborne precautions.

❖ Place the patient on a negative pressure room

❖ Tepid Sponge Bath (TSB)

❖ Skin care

❖ Oral and nasal hygiene

❖ Eye care (photosensitivity)

❖ Ear care

❖ Daily elimination (Mild laxative)

❖ During febrile stage, limit the diet to fruit juices, milk, and water.

❖ Give medication as ordered by the physician (Penicillin)

Preventive Measures
❖ Immunization with:

● Anti-measles at the age of 9 months as a single dose

● MMR vaccine (15 mos.); 2nd dose (11 to 12 years old)

❖ Measles vaccine should not be given to pregnant women, or to persons with active tuberculosis, leukemia, lymphoma or
depressed immune system.

LEPROSY
Other Terms: Hansen’s Disease / Hansenosis

Description: It is a chronic systematic infection characterized by progressive cutaneous lesions

 Three distinct forms
❖ Lepromatous (Multibacillary) leprosy

● Most serious type

● Not infectious

● Causes damage to the respiratory tract, eyes and testes and well as the nerves and the skin.

● Lepromin test is negative, but the skin lesion contains large amount of Hansen’s bacillus

● Slow involvement of the peripheral nerves, with some degree of anesthesia and loss of sensation and gradual
destruction of the nerves.
❖ Tuberculoid (Paucibacillary) Leprosy

● Affects the peripheral nerves and sometimes the surrounding skin, especially on the face, eyes and testes as well
as the nerves and the skin.
● Lepromin Test is positive, but the organism is rarely isolated from the lesions

● Macules are elevated with clearing at the center and more clearly defined than the lepromatous form

❖ Borderline (dimorphous)
 ● Has the characteristics of both lepromatous and tuberculoid leprosy.

Etiological Agent: Mycobacterium leprae

Incubation Period:
❖ The incubation period varies from a few months to many years. Lepromatous patients may be infectious for several
years.

Mode of Transmission
❖ Airborne

❖ Prolonged skin-to-skin contact

Clinical Manifestation
❖ Early

● Changes in skin color (reddish/white)

● Loss of sensation on the skin/Anesthesia

● Decrease/loss of sweating and hair growth over the lesion

● Thickened/painful nerves

● Muscle weakness

● Redness of the eye

● Nasal Obstruction

● Ulcers that do not heal

❖ Late

● Madarosis (Loss of eyebrow and eyelashes)

● Lagopthalmos (inability to close eyelids)

● Clawing of fingers and toes

● Contractures

● Sinking of the nose bridge

● Gynecomastia

Diagnostic Tests
❖ Slit skin Smear

❖ Blood Test (Inc. RBC & ESR; Dec, Ca, albumin & Cholesterol level)

Treatment Modalities
❖ Sulfone Therapy

❖ Rehabilitation, Recreational and Occupational Therapy

❖ Multiple Drug Therapy

● Multibacillary (Rifampicin, Clofazimine, Dapsone)

✔ Infectious Type

✔ Duration of treatment (12 months)

 ● Paucibacillary (Rifampicin and Dapsone)

✔ Tuberculoid & indeterminate

✔ Non-infectious types

✔ Duration of treatment (6-9 months)

Nursing Management
❖ Isolation and Medical Asepsis should be carried out

❖ Diet: Full, nutritious diet

❖ Give antipyretic, analgesics and sedative as needed.

❖ Provide emotional support throughout treatment and rehabilitation of affected extremities

❖ Patients with eye dryness need to use a tear substitute daily and protect their eyes to prevent corneal irritation and
ulceration.
❖ Tell the patient with an anesthetized leg to avoid injury by not putting to much weight on the leg, testing water
before entering to prevent scalding, and wearing appropriate footwear.

Prevention
❖ Report all cases and suspect of leprosy
❖ BCG vaccine

❖ Health education

SCABIES
Description: It is a highly transmissible skin, infection that is characterized by burrows, pruritus, and excoriations with secondary
bacterial infection.
Etiologic Agent: Sarcoptes scabei var. homonis
Source of Infection
❖ Human skin

Mode of Transmission
❖ Skin to skin contact

❖ Direct contact with fomites

Incubation Period
❖ The itch mite may burrow under the skin and lay ova within 24 hours of an original contact

Period of Communicability
❖ This disease is communicable for the entire period that the host is infected.

Clinical Manifestations
❖ Intense itching that becomes more severe at night

❖ Burrows (lesions) seen in webs of the fingers, wrists and elbows

❖ Burrows in immunocompromised, infants, young children and elderly appears in face, neck, scalp and ears

Complications
❖ Persistent pruritus

❖ Intense scratching can lead to excoriation, tissue trauma and secondary bacterial infection

Diagnostic Procedure
❖ Superficial scraping and examination under a low-power microscope of material from a burrow

Treatment
❖ Aqueous Malathion lotion

❖ Permethrin derma cream left on the skin for 8-12 hours

❖ Benzyl Benzoate

❖ Sulfur in petrolatum

❖ Ivermectin – Anti-helminthic drug is effective in resistant cases

❖ Antipruritic emollient or topical steroid for itching

Nursing Intervention
❖ Have the patient’s fingernails cut short to minimize skin breaks from scratching

❖ Instruct patient on proper application of the drugs

❖ Contaminated clothing or beddings should be dry-cleaned or boiled

❖ Advise patient to report any skin irritation

❖ Advise family member and other people who had close contact with the patient be checked for possible symptoms and
be treated if necessary
❖ Practice contact precaution

❖ Terminal disinfection should be carried out

❖ Encourage the patient to verbalize his/her feelings

Prevention and Control

❖ Good personal hygiene

❖ Avoid contact with infected persons

❖ All members of the household, including close contact should be treated

GERMAN MEASLES
Other Terms: Rubella / Three-day Measles
Description
❖ It is a mild viral illness caused by rubella virus

❖ It causes mild feverish illness associated with rashes and aches in joints.

❖ It has a teratogenic effect on the fetus.

Etiologic Agent: Rubella virus

Mode of Transmission
❖ Droplet transmission

❖ Transplacental transmission in congenital rubella

Incubation Period
❖ 2 to 3 weeks

Clinical Manifestations
❖ Prodromal Period

● Low grade fever

● Headache

● Malaise

● Mild coryza

● Conjunctivitis

● Post-auricular, sub-occipital and posterior cervical lymphadenopathy which occurs on the 3 rd to the 5th day after
onset

❖ Eruptive Period

● Forchheimer’s spot (pinkish rash on the soft palate)

● Eruption appears after the onset of adenopathy

● Children usually present less or no constitutional symptoms

● The rash may last for one to five days and leaves no pigmentation nor desquamation

● Testicular pain in young adults

● Transients polyarthralgia and polyarthritis may occur in adults and occasionally in children.

❖ Congenital Rubella

● Classic Congenital Rubella Syndrome

✔ Intrauterine growth retardation

✔ Infant has low birth weight

✔ Thrombocytopenic purpura known as “blueberry muffin” skin

● Intrauterine Infection

✔ May result in spontaneous abortion

✔ Birth result in spontaneous abortion one or multiple birth anomalies such as:

▪ Cleft palate, talipes and eruption of teeth

 ▪ Cardiac defects (patent ductus arteriosus, atrial septal defect)

▪ Eye defects (glaucoma, retinopathy, micropthalmia)

▪ Neurologic (Microcephaly, mental retardation, psychomotor retardation, vasomotor

instability)

Diagnostic Tests
❖ Clinical observation

❖ Cell cultures of the throat, blood, urine and cerebrospinal fluid confirm the presence of the virus

❖ Convalescent serum that shows a fourfold rise antibody titer supports that the diagnosis

Treatment Modalities
❖ Acetaminophen for fever and joint pain.

❖ Isolation

Complications
❖ Encephalitis

❖ Neuritis
❖ Arthritis

❖ Arthralgias

❖ Rubella syndrome manifested by:

● Microcephaly

● Mental retardation

● Cataract

● Deaf-mutism

● Heart Disease

Nursing Consideration
❖ Provide comfort

❖ Make sure female patients understand how important it is to avoid exposure to this disease when pregnant.

❖ Report confirmed cases of rubella to local public health officials

❖ Warn the patient about possible mild fever, slight rash, transient arthralgia, and arthritis.

❖ If lymphadenopathy persists after the initial 24 hours, suggest a cold compress to promote vasoconstriction and
prevent antigenic cyst formation.
❖ Patient’s room must be darkened to avoid photophobia

❖ Patient’s eyes should be irrigated with warm saline to relieve irritation

❖ Good ventilation is necessary.

Prevention
❖ Administration of live attenuated vaccine (MMR)

❖ Pregnant women should avoid exposure to patients infected with rubella virus

❖ Administration of Immune Serum Globulin one week after exposure to rubella

PEDICULOSIS
Description
❖ Any human infestation of lice

❖ May occur anywhere on the body

Types:
❖ Pediculosis capitis

● Lice feed on the scalp and rarely, on the skin under the eyebrows, eyelashes and beard

❖ Pediculosis Corporis

● Lice live next to the skin in clothing seams.

❖ Pediculosis pubis

● Lice are found primarily in pubic hairs but may extend to the eyebrows, eyelashes and axillary or body hair.

Mode of Transmission
❖ Head-to-head contact
❖ Fomites

❖ Sexual activity

Incubation Period
❖ 3 to 7 days

Clinical Manifestation
❖ Pruritis (most common symptom of infestation)

❖ Tickling sensation of something moving in the hair may be noticed

❖ Head lice and their nits are most commonly found behind the ears and on the hairs of the neck and occiput.

❖ Body lice are found on clothing seams

❖ Pubic lice will be found attached to the base of the pubic hair and the infestation generally results in severe itching.

Diagnostic Tests
❖ Wood’s light examination (fluorescence of the adult lice)

❖ Microscopic examination (presence of nits on the hair shaft)

 Treatment Modalities
❖ Permethrin (Eliminate) / Pyrethin (Rid Mousse)

● Initial treatment of choice

● Topical insecticide

● For Pediculosis capitis & Pediculosis pubis

❖ Fine-tooth comb dipped in vinegar

❖ Washing hair with ordinary shampoo

❖ Oral Anthelminthics (Ivermectin, Levamisole, Albendazole) are effective against head lice infestation

❖ Prevention of head reinfestation

● Clothes and bed linens must be washed in hot water, ironed or dry cleaned.

● Storing clothes or linens for more than 30 days or placing them in dry heat of 140 F (60 C) kislls lice

Complications
❖ Excoriation

❖ Secondary bacterial infections

❖ If left untreated, pediculosis may result in dry, hyperpigmented, thickly encrusted, scaly skin, with residual scarring

Nursing Considerations
❖ Contact precautions should be maintained until treatment is complete to prevent spreading the infection

❖ Have the patient’s fingernails cut short to prevent skin breaks and secondary bacterial infections caused by
scratching.
❖ Be alert for possible adverse reactions to treatment with an antiparasitic, including sensitivity reactions and in some
cases, central nervous system (CNS) toxicity.
❖ To prevent self-infestation, avoid direct contact with the patient’s hair, clothing and bedsheets.
❖ Use gloves, a gown, and a protective head covering when administering delousing treatment.

❖ After each treatment, inspect the patient for remaining lice and eggs.

❖ Teach the patient and family how to inspect and identify lice, eggs and related lesions

❖ Instruct the patient and family about the use of the creams, lotions, powders and shampoos that eliminate lice.

❖ Instruct the patient in the proper application of lindane, which can be absorbed by the skin and cause CNS
complications.

HERPES ZOSTER
Other Term: Shingles

Description
❖ It is acute unilateral and segmented inflammation of the dorsal root ganglia caused by reactivation of the herpes
varicella-zoster virus, which also causes chickenpox
❖ Usually occur in adults

Causative Agent
❖ Varicella virus

Incubation Period
❖ Unknown, but it is believed to be 13-17 days

Period of Communicability
❖ Communicable a day before the appearance of the first rash until 5-6 days after the last crust

Mode of Transmission
❖ Airborne

❖ Droplet

❖ Direct contact

Clinical Manifestations
❖ Begins with fever and malaise

❖ Severe deep pain, pruritus, and paresthesia and hyperesthesia, usually on the trunk and occasionally on the arms and legs

❖ Small, red, nodular skin lesions (Unilateral) erupt on the painful areas up to 2 weeks after first symptoms
❖ Vesicles filled with fluid or pus

❖ Cranial nerve involvement

Complications
❖ Generalized central nervous system infection

❖ Acute transverse and ascending myelitis

❖ Intractable neurologic pain

Diagnostic Procedure
❖ Differentiation of herpes zoster from herpes simplex virus through fluorescent light

❖ Tissue culture technique

❖ Smear of vesicle fluid

❖ Microscopy

Management
❖ Antiviral therapy – Acyclovir

❖ Analgesics to control pain

❖ Anti-inflammatory

Nursing Interventions
❖ Airborne and contact precautions

❖ If vesicles rupture, apply a cold compress as ordered

❖ To minimize neuralgic pain, administer analgesics as ordered and evaluate their effects

❖ Instruct the patients to avoid scratching the lesions

❖ Keep the patient comfortable and maintain meticulous hygiene

❖ Encourage sufficient bed rest and give supportive care

Prevention
❖ Vaccination against varicella

❖ Avoid exposure to patients with varicella infection

RESPIRATORY DISEASES

DIPHTHERIA

Description: Acute febrile infection of the tonsil, throat, nose, larynx or wound marked by patches of grayish membrane from
which the diphtheria bacillus is readily cultured.

Etiologic Agents: Corynebacterium, diphtheria (Klebs-Loeffier bacillus)

Sources of Infection
❖ Discharges and secretion from mucus surface of nose and nasopharynx and from skin and other lesions

❖ Reservoir = Man
 Mode of Transmission
❖ Contact with a patient or carrier or with articles soiled with discharges of infected persons.
❖ Milk (vehicle)

Incubation Period
❖ 2 to 5 days

Period of Communicability
❖ 2 weeks to more than 4 weeks

❖ Variable until virulent bacilli has disappeared from secretions and lesions

Types
❖ Nasal
 ● With foul – smelling serosanguinous secretions from the nose

❖ Tonsillar

● Low fatality rate

● Lesions are confined to the tonsils only but tend to spread over the pillars, into the soft palate and uvula.

❖ Nasopharyngeal

● Cervical lymph nodes are swollen

● Neck tissues are edematous

❖ Laryngeal

● Most commonly found in children ages 2 to 5 years old

● It is considered as most severe and more fatal type due to anatomical reason

● There is moderate hoarseness; voice is diminished until it is finally absent.

● Most fatal

❖ Wound / Cutaneous

● Affects to mucous membrane and any break in the skin.

Clinical Manifestation
❖ Bull neck formation (swelling of the soft tissues of the neck)

❖ Exudates forming the membrane are grayish in appearance (Pseudomembrane)

❖ Fatigue / malaise

❖ Slight sore throat

❖ Breathing difficulty

❖ Husky voice

❖ Swelling of the palate

❖ Low-grade fever

Methods of Prevention and Control

❖ Active immunization of all infants and children with 3 doses of DPT

❖ Pasteurization of milk

❖ Education of parents

❖ Reporting of case to the Health Officer of proper medical care

Diagnostic Tests
❖ Swab from the nose and throat

❖ Schick Test

● Involves giving an injection of 0.1 mL of dilute diphtheria toxin intradermally.

● Area is checked in 3-4 days and the reaction is documented

● Positive Test is indicated by inflammation or induration at the point of injection. This indicates that the client
lacks antibodies to diphtheria.
❖ Virulence Test
❖ Moloney Test

● A test to detect a high degree of sensitivity to diphtheria toxoid is given intradermally.

Treatment Modalities
❖ Penicillin

❖ Anti-toxin

❖ Erythromycin
Nursing Care
❖ Follow prescribed dosage and correct technique in administering anti toxin

❖ Provide comfort

❖ Absolute bed rest for at least two weeks

❖ Soft-food diet; small frequent feedings

❖ Ice collar applied to the neck

● Visiting bag should be set up outside the room of the patient of should be far from the bedside of the patient

❖ Watch for signs of shock, which can develop suddenly as a result of systematic vascular collapse, airway obstruction, or
anaphylaxis.
❖ If neuritis develops, tell the patient it’s usually transient. Be aware that peripheral neuritis may not develop until 2 to 3
months after the onset of illness.
❖ Explain how to properly dispose of nasopharyngeal secretion and teach proper infection precautions

PERTUSSIS
Other Term: Whooping Cough
Description: Acute infection of the respiratory tract characterized by repeated attacks of spasmodic coughing which consists of
a series of explosive expirations, producing a crowing sound, “the whoop”, and usually followed by vomiting.

Etiologic Agents
❖ Haemophilus pertussis

❖ Bordet Gengou bacillus

❖ Bordetella pertussis

Source of Infection
❖ Discharges from laryngeal and bronchial mucous membrane of infected persons.

Incubation Period: 7-10 days but may occasionally be up to 3 weeks

Period of Communicability
❖ Seven days after exposure to three weeks after typical paroxysms

Mode of Transmission
❖ Direct spread through respiratory and salivary contacts

Clinical Manifestations
❖ Violent coughing

❖ Nose bleeding

❖ Distended neck veins

❖ Periorbital edema

❖ Conjunctival hemorrhage

Complications
Most dangerous: bronchopneumonia
❖ Convulsion

❖ Umbilical hernia

❖ Otitis media

❖ Severe malnutrition and starvation

Diagnostic Tests
❖ Nasopharyngeal swabs (Positive for B. pertussis)

❖ Sputum culture

❖ CBC (leukocytosis)

❖ Chest Radiography may reveal infiltrates or pulmonary edema with atelectasis

Treatment Modalities
❖ Supportive Therapy
 ● Fluid & electrolyte replacement

● Adequate nutrition

● Oxygen therapy

❖ Antibiotics

● Erythromycin

● Ampicillin

❖ Post Exposure Treatment: Hyperimmune convalescent serum / gamma-globulin

Nursing Management
❖ Isolation and medical asepsis

❖ Suction Equipment should be present at bedside

❖ Provide warm baths

❖ Keep the bed dry and free from soiled linens

❖ I & O should be closely monitored

❖ General care of nose and throat discharges

❖ Instruct patients to cover their mouths when they cough or sneeze and to wash their hands immediately afterwards.

Prevention
❖ Any case of pertussis should be reported

❖ Patient should be isolated for 4 to 6 weeks

❖ Previously immunized children should be given reinforcing injection

INFLUENZA
Other Term: La Grippe
Description: It is an acute infectious disease affecting the respiratory system

Etiologic Agents
❖ Influenza virus A, B, C

Source of Infection: Discharges from the mouth and nose of infected persons

Mode of Transmission
❖ Droplet

❖ Direct contact through droplet infection

❖ Indirect contact (fomites)

Incubation Period
❖ 1 to 3 days, occasionally up to 5 days

Period of Communicability
❖ Infectious period lasts from 1 day before until 3-5 days after onset of symptoms in adults.

Clinical Manifestations
❖ Chilly sensation

❖ Hyperpyrexia

❖ Severe aches and pain usually at the back associated with severe sweating

❖ Vomiting

❖ Sore throat

❖ Coryza and cough

Complications
❖ Hemorrhagic pneumonia

❖ Encephalitis

❖ Myocarditis
❖ Sudden Infant Death Syndrome

❖ Myoglobinuria

Diagnostic Procedures
❖ Blood examinations

● Usually normal but leukopenia has been noted

❖ Viral Culture (oropharyngeal washing or swabbing during the first few days of illness)

❖ Viral Serology

● Complement Fixation Test

✔ It is an immunological medical test that can be used to detect the presence of either specific antibody or
specific antigen in a patient’s serum
❖ Chest Radiography may reveal bilateral symmetrical interstitial infiltrates indicative of pneumonia

❖ Arterial Blood Gas Testing may reveal hypoxemia in severe cases

❖ Laboratory Tests may reveal leukopenia, lymphopenia, and/or thrombocytopenia.

Management
❖ Stay at home

❖ Teach the patient about proper disposal of tissues and good handwashing technique

❖ Drink plenty of fluids

❖ Fever Management

● Paracetamol

● Ibuprofen

❖ Maintain contact and droplet precautions

❖ Limit strenuous activities

❖ Watch for signs and symptoms of developing pneumonia such as crackles, another temperature increase , or
coughing accompanied by purulent or bloody sputum
❖ Instruct patients who are sick with flu-like symptoms to avoid contact with others for at least 24 hours.

Preventive Measures
❖ Active immunization with influenza vaccine

❖ Education of the public as to sanitary hazard from spitting, sneezing and coughing

❖ Avoid crowded places

❖ Avoid use of common towels, glasses and eating utensils.

ANTHRAX
Other Terms: Wool-sorter’s Disease / Ragpicker’s Disease

Description: An acute bacterial disease usually affecting the skin but which may very rarely involve the oropharynx, lower
respiratory tract, mediastinum or intestinal tract.

Etiologic Agent: Bacillus anthracis

Mode of Transmission
❖ Cutaneous infection is by contact with:

● Tissues of animals (cattle, sheep, goats, horses, pigs and others) dying of the disease

● Contaminated hair, wool, or products made from them such as drums or brushes

● Soil associated with infected animals or contaminated bone meal used in gardening.

Incubation Period
❖ Inhalation Anthrax (1 to 7 days) usually within 48 hours

❖ Cutaneous anthrax (1 to 7 days rarely up to 7 weeks

❖ Ingestion (1 to 7 days)
 Clinical Manifestation
❖ Cutaneous Anthrax

● Most common (over 90% of cases)

● Infection is through the skin

● Over a few days a sore, which begins as a pimple, grows, ulcerates and forms a black scab, around which are
purplish vesicles
● Systemic symptoms may include rigors’ headache and vomiting
● The sore is usually diagnostic: 20% cases are fatal.

❖ Inhalational Anthrax

● Spores are inhaled with subsequent invasion of mediastinal lymph nodes.

● Abrupt onset of flu-like illness, rigors, dyspnea and cyanosis followed by shock and usually death over the next
2-6 days.
● Most Fatal
 ❖ Intestinal Anthrax

● Occurs following ingestion of meat from infected animals and is manifested as violent gastroenteritis with
fever, vomiting, bloody stools and then septicemia
● Poor prognosis

Diagnostic Tests
❖ Polymerase Chain Reaction (PCR)

● Definitive test for B. anthracis

❖ Swabs from cutaneous lesions

❖ Blood cultures

❖ Lymph node or spleen aspirates

❖ CSF shows characteristic bacilli on staining with polychrome methylene blue.

❖ Chest radiology may show fluid surrounding the lungs or widening of the mediastinum

Treatment Modalities
❖ Antibiotics

● Penicillin

● Ciprofloxacin (DOC)

● Doxycycline

❖ Treatment of cutaneous anthrax is oral antibiotic for 7 to 10 days

❖ Length of treatment for GI anthrax is 60 days, but safety has not been evaluated beyond14 days

Complications
❖ Cutaneous Anthrax

● Septicemia

❖ Inhalational Anthrax

● Hemorrhagic meningitis

● Pleural Effusions

● Mediastinitis

● Shock

● Acute Respiratory Distress Syndrome

❖ GI Anthrax

● Hemorrhage

● Shock

Nursing Considerations
❖ Obtain culture specimens before starting antibiotic therapy
❖ Supportive measures are geared toward the type of anthrax exposure

❖ Teach the patient and family that anyone who has been exposed to anthrax must see a doctor immediately.

❖ Instruct the patient to take antibiotics as prescribed and until completed.

❖ Instruct the patient with cutaneous anthrax not to scratch at the lesions.

❖ Alcohol-based hand sanitizers do not kill anthrax spores; wash hands with soap and water.

Prevention
❖ Pretreatment of animal product and good occupational health cover are the mainstays of control

❖ Animals believed to have died of anthrax should be disposed of under supervision.

❖ Mass vaccination of animals may reduce disease spread

❖ Non-cellular vaccines for human use are available for individuals at risk from occupational exposure

❖ Workers handling potentially infectious raw materials should be aware of the risks.
 PNEUMONIA

Description: An acute infectious disease of the lungs usually caused by the pneumococcus resulting in the consolidation of one
or more lobes of either one or both lungs.

Etiologic Agents
❖ Streptococcus pneumonia
❖ Staphylococcus aureus
❖ Haemophilus influenzae

❖ Pneumococcus of Friedlander

Incubation Period
❖ 2 to 3 days

Mode of Transmission
❖ Droplet infection

❖ Indirect contact (fomites)

Clinical Manifestations
❖ Rhinitis

❖ Chest indrawing

❖ Rusty sputum

❖ Productive cough

❖ High fever

❖ Vomiting

❖ Convulsions

❖ Flushed face

❖ Dilated pupils

❖ Pain over the affected lung

❖ Highly colored urine with reduced chlorides and increased urates

Complications
❖ Emphysema

❖ Endocarditis

❖ Pneumococcal meningitis

❖ Otitis Media

❖ Jaundice

Diagnostic Test
❖ Chest X-ray

❖ Sputum Analysis

❖ Blood/Serologic Exam
❖ Dull percussion note on affected side

Management
❖ Bed Rest

❖ Adequate salt, fluid, calorie, and vitamin intake

❖ TSB

❖ Frequent turning from side to side

Prevention and Control
❖ Prevent common colds, influenza and other upper respiratory infections

❖ Immunization with pneumonia vaccine

❖ Eliminate contributory factors such as exposure to cod, pollution, and physical conditions of fatigue and alcoholism.

TUBERCULOSIS
Other Terms: Koch’s Disease / Phthisis / Galloping Consumption Disease
❖ TOP 8 highest cases of TB in the world (Philippines)
 Description
❖ It is a chronic sub –acute or acute respiratory disease commonly affecting the lungs

❖ Characterized by the formation of tubercles in the tissue which tend to undergo ceseation necrosis and calcification

Etiologic Agents
❖ Mycobacterium tuberculosis
❖ M. africanum
❖ M. bovis

Source of Infection
❖ Sputum

❖ Blood from Hemoptysis

❖ Nasal discharge

❖ Saliva

Mode of Transmission
❖ Airborne

❖ Direct / Indirect contact with infected persons

Incubation Period
❖ 3 to 8 weeks (occasionally up to 12 weeks)

Period of communicability
❖ As long as the tubercle bacilli are being discharged in the sputum

Clinical Manifestations
❖ Cough of two weeks or more

❖ Afternoon rise of temperature

❖ Chest or back pains

❖ Hemoptysis

❖ Significant weight loss

❖ Fatigue

❖ Body malaise

❖ Shortness of breath

❖ Night sweating

❖ Sputum positive for AFB

Diagnostic Tests
❖ Sputum Analysis for AFB

● Confirmatory

❖ Chest X-ray
❖ Tuberculin Testing (for TB exposure)

✔ Mantoux Test (PPD)

✔ Tine Test

✔ Heaf Test

Treatment Modalities
❖ Short – course chemotherapy

● Six-month treatment (Isoniazid, Rifampicin, Pyrazinamide and Ethambutol)

Rifampicin
● Empty stomach

● Body fluid discoloration (red-orange)

● Hepatotoxic (metabolism)

● Nephrotoxic (elimination)
 ● Permanent discoloration of contact lenses

Isoniazid
● Empty stomach

● Peripheral Neuropathy

● Avoid alcohol

● Hepatotoxic

● Nephrotoxic

● Increase intake of Vitamin B6

Pyrazinamide
● Before meals

● Monitor s/sx of liver impairment

✔ Anorexia

✔ Fatigue

✔ Dark urine

✔ Photosensitivity

● Liver Function Studies

● Causes hyperuricemia

Ethambutol
● Not affected by food

● Report visual disturbances

● Hepatotoxic

● Not recommended for children (below 6 years old); can cause optic neuritis

Streptomycin
● After meals

● Report Oliguria – nephrotoxic

● Ototoxic

● Neurotoxic

Direct Observation Treatment Short Course

● Strategy to prevent non-compliance

Nursing Management
❖ Maintain respiratory isolation

❖ Administer medicines as ordered

❖ Educate patient all about PTB

❖ Stop smoking

❖ Cough or sneeze into tissue paper and dispose secretion properly

❖ Provide the patient with a well-balanced, high-calorie diet, preferably in small, frequent meals to conserve energy.

❖ Allow ret periods

❖ Caution the patient who is taking an oral contraceptive that the contraceptive may be less effective while she’s taking
rifampin.

Prevention and Control

❖ Submit all babies for BCG (Bacille Calmette-Guerin) immunization

❖ Avoid overcrowding

❖ Improve nutritional and health status

❖ Persons who have been exposed (Receive Tuberculin Test)

BIRD FLU
Other Term: Avian Influenza

Description: It is an infectious disease of birds ranging from mild to severe form of illness.

Source of Infection
❖ Viruses that normally infect only birds and less commonly pigs

Incubation Period
❖ 3 to 5 days

Clinical Manifestations
❖ Fever

❖ Body weakness / muscle pain

❖ Cough

❖ Sore throat

❖ May have difficulty of breathing in severe cases

❖ Sore eyes

Susceptibility, Resistance & Occurrence

❖ All birds are susceptible to infection but domestic poultry flocks are especially vulnerable to infection that can rapidly
reach epidemic proportion.

Control Measures
❖ Rapid destruction, proper disposal of carcasses and quarantining and rigorous disinfection of farms

❖ Restrictions on the movement of live poultry

Nursing Care
❖ Isolation precaution

❖ Infected Control

❖ Early recognition of cases of highly pathogenic Avian Influenza during outbreak among poultry

SEVERE ACUTE RESPIRATORY SYNDROME (SARS)

❖ Earliest known case (Guangdong Province, China, November, 2002)

❖ Outbreak and Worldwide Surveillance (March 12, 2003)

❖ First case in the Philippines (April 11, 2003)

Etiologic Agent
❖ Human coronavirus

Mode of Transmission:
❖ Droplet Contact

Incubation Period
❖ Mean incubation period is 5 days (range 2-10 days) and may reach up to 14 days

Clinical Manifestations
❖ Prodromal Phase

● Fever > 38oC (Initial Sign)

● Chills
 ● Malaise

● Myalgia

● Headache

❖ Respiratory Phase

● Dry, non-productive cough with or without respiratory distress

● Hypoxia

● Crackles

● Dullness on percussion

● Decreased breath sounds on physical examination

Preventive Measures and Control

❖ Screen patents for travel hx, symptoms and/or close contact ith cases

❖ Isolation of suspected probable case

❖ Barrier nursing technique for suspected and probable cases

 Nursing Care
❖ Maintain Isolation Measures

❖ Utilize Personal Protective Equipment (PPE)

❖ Apply principle of hand washing

GASTROINTESTINAL DISEASES

CHOLERA
Other Term: El Tor
Description: It is an acute bacterial enteric disease characterized by profuse diarrhea, vomiting, massive loss of fluid and
electrolytes that can result to hypovolemic shock, acidosis and death.
Etiologic Agent: Vibrio El Tor

Source of Infection
❖ Vomitus and feces of infected persons

Mode of Transmission
❖ Food and water contaminated with vomitus and stools of patients and carriers

Incubation Period
❖ 6 to 48 hours

Period of Communicability
❖ Cases are infectious during the period of diarrhea and up to 7 days after

Clinical Manifestations
❖ Rice-watery stool

❖ Washer-woman’s hands

❖ Vomiting

❖ Diarrhea

❖ Deep, rapid breathing

❖ Oliguria

Diagnostic Tests
❖ Rectal swab

❖ Darkfield or phase microscopy

❖ Stool exam

❖ Blood test

● Elevated BUN & Creatinine Levels

● Increase in serum lactate, protein and phosphate levels

Treatment Modalities
❖ IV treatment

❖ Oral Therapy Rehydration

❖ Coconut water

❖ Give ORESOL

❖ Antibiotics

● Tetracycline

● Furazolidone

● Chloramphenicol

● Cotrimoxazole

Nursing Management
❖ Medical Aseptic protective Care (Hand washing)

❖ Enteric Isolation

❖ VS

❖ I & O monitored accurately

❖ Personal hygiene

❖ Proper excreta disposal

❖ Environmental sanitation

Prevention
❖ Food and water supply must be protected from fecal contamination

❖ Water should be boiled and chlorinated

❖ Milk should be pasteurized

❖ Sanitary disposal of human excreta is a must

TYPHOID FEVER
Description: It is a systemic infection characterized by continued fever, anorexia, involvement of lymphoid tissue, especially
ulceration of Peyer’s patches.

Etiologic Agents
❖ Salmonella typhi or Typhoid bacillus

Sources of Infection
❖ Feces and urine of infected persons
Mode of Transmission
❖ Fecal-oral Transmission

❖ Contaminated Urine

❖ Direct/indirect contact with infected person

❖ Ingestion of contaminated food, water and milk

Incubation Period
❖ 1 to 3 weeks; average (2 weeks)

Period of Communicability
❖ As long as typhoid bacilli appears in excreta

Clinical Manifestations
❖ Onset

● Headache

● N/V

● Ladder-like fever

● Rose spots on the abdomen

❖ Typhoid State

● Coma vigil

● Subsultus tendinum

● Carphologia

● Delirium

Complications
❖ Hemorrhage/Perforation (most dreaded complications)

❖ Peritonitis

❖ Bronchitis and Pneumonia

❖ Typhoid spine

❖ Septicemia

❖ Reiter’s syndrome – joint pain, eye irritation

Diagnostic Tests
❖ Typhidot – confirmatory

❖ ELISA

❖ Widal

❖ Rectal swab

❖ Bone Marrow Aspiration (identifies S. typhi)

 Treatment Modalities
❖ Chloramphenicol – drug of choice

❖ Ampicillin

❖ Co-trimoxazole

❖ Ciprofloxacin

❖ Cefixime / Azithromycin

❖ Ceftriaxone (recommended for complicated cases)

Nursing Management
❖ Isolation

❖ Maintain standard precautions unless the patient is incontinent or in diapers or if an outbreak develops in an
institution.
❖ Give nourishment fluids in small quantities at frequent intervals

❖ Monitor VS

❖ Prevent further injury

❖ WOF: intestinal bleeding / bowel perforation, including sudden pain in the lower right side of the abdomen and
abdominal rigidity.
❖ Provide good skin and mouth care

❖ Turn the patient frequently and perform mild passive exercises, as indicated.

❖ Apply mild heat to the abdomen to relieve cramps.

Prevention and Control
❖ Sanitary and proper disposal of excreta

❖ Proper supervision of food handlers

❖ Enteric isolation

❖ Provision of safe drinking water supply

❖ Detection and supervision of typhoid carriers

BACILLARY DYSENTERY
Other Terms: Shigellosis / Bloody Flux

Description: It is an acute bacterial infection of the intestine characterized by diarrhea, fever, tenesmus and in severe cases,
bloody and mucoid stools.

Etiologic Agents
❖ Shigella sonnei (most common species in Western Europe)
❖ Shigella flexneri
❖ Shigella boydii
❖ Shigella dysenteriae

Incubation Period
❖ 12 to 96 hours, but may be up to 1 week

Period of Communicability
❖ The patient can transmit the microorganism during the acute infection until the feces are negative of the organism.

Mode of Transmission
❖ Ingestion of contaminated food

❖ Drinking contaminated water / milk

❖ Feco-oral transmission

Clinical Manifestations
❖ Fever

❖ Tenesmus

❖ N/V

❖ Headache

❖ Colicky or cramping abdominal pain associated with anorexia and body weakness

❖ Bloody-mucoid stool

❖ Rapid dehydration
 Diagnostic Tests
❖ Microscopic examination of a fresh stool specimen may reveal mucus, red blood cells, and polymorphonuclear
leukocytes.
❖ Direct immunofluorescence with specific antisera will demonstrate Shigella.

❖ Sigmoidoscopy or proctoscopy may reveal typical superficial ulcerations

❖ Stool culture must rule out other causes of diarrhea, such as enteropathogenic Escherichia coli infection,
malabsorption disease, and amebic or viral diseases.

Treatment Modalities
❖ Antibiotics

● Ampicillin

● Ceftriaxone

● Trimethoprim-sulfamethoxazole

● Ciprofloxacin

❖ IV Therapy

❖ Low Residue Diet

❖ Contraindicated: Anti-diarrheal drugs (they delay fecal excretion that can lead to prolong fever)

Prevention and Control

❖ Sanitary disposal of human feces

❖ Adequate personal hygiene, particularly handwashing after defecation.

❖ Sanitary supervision of processing, preparation and serving of food (raw)

❖ Fly control and protection against fly contamination

❖ Isolation (Acute Stage)

❖ Protection and purification of public water supply

❖ Routine cooking kills shigella

PARAGONIMIASIS
Etiologic Agents:
❖ Lung Fluke
❖ Paragonimus westermani

❖ Paragonimus siamenses

Mode of Transmission
❖ Ingestion of raw / uncooked crabs/crayfish

❖ Contamination of Food

❖ Using meat / juice of infected animals

Reservoir of Hosts
❖ Cats

❖ Dogs
❖ Rats

❖ Pigs

Clinical Manifestations
❖ Cough of long duration

❖ Recurrent blood-streaked sputum

❖ Chest/back pain

❖ PTB – like signs/symptoms not responding to anti-TB medication

Diagnostic Test
❖ Sputum Microscopy

❖ Immunology

❖ Cerebral Paragonimiasis

Treatment
❖ Praziquantel (Billtrizide)

Prevention and Control

❖ Treatment of infected person

❖ Anti-mollusk campaigns

❖ Educated of the population

❖ Avoid eating infected foods

MUMPS
Other Terms: Infectious Parotitis / Epidemic Parotitis
Description: It is a acute viral disease manifested by swelling of one or both parotid glands, with occasional involvement of
other glandular structures, particularly the testes in male.
Etiologic Agent: Paramyxoviridae

Source of infection: Secretion of the mouth and nose

Mode of Transmission
❖ Direct contact

❖ Indirect contact with the articles freshly soiled with secretion from the nasopharynx.

Period of Communicability
❖ Cases are infectious for up to a week (normally 2 days) before parotid swelling until 9 days after.

❖ 48 – hours period immediately preceding onset of swelling is considered the time of highest communicability.

Clinical Manifestation
❖ Sudden headache

❖ Earache

❖ Loss of appetite

❖ Fever

❖ Swelling of the parotid gland (between the earlobe and angle of the mandible)

Complications
❖ Orchitis

❖ Oophoritis

❖ Mastitis

❖ Nuchal rigidity

❖ Deafness

❖ Meningoencephalitis

❖ Pancreatitis

❖ Myocarditis

❖ Nephritis

Diagnostic Tests
❖ Serum amylase Determination (most useful test in making early presumptive diagnosis of mumps); elevated amylase level
❖ Complement Fixation Test

❖ Hemo-agglutination Inhibition Test

● Used to determine the immune status

❖ Neutralization Test

● Determines immunity to mumps

❖ Viral Culture

Treatment Modalities
❖ Analgesics for pain

❖ Antipyretics for fever

❖ IV Fluid Replacement

❖ Hot and Cold Application

 Nursing Management
❖ Medical Aseptic Protective Care

● Single-occupancy room

● Oral Care and Personal Hygiene (warm salt-water gargles)

❖ General Management of the disease

● Bed rest

● Diversional Activities

● Eye care

● Provide extra fluids

❖ Diet

● No restriction of food

● Soft bland and semi-solid is easily managed

● Acid foods (fruit juices) increases discomfort

Prevention and Control

❖ Active Immunization (MMR)

❖ Reporting of cases to health authorities

❖ Isolation of patient
BOTULISM
Description
❖ Rare but severe form of poisoning caused by a gram-positive, anaerobic bacteria.

❖ It is an illness of descending paralysis and autonomic dysfunction due to a neurotoxin

Causative Agent: Clostridium Botulinum

❖ Foodborne Botulism

❖ Wound Botulism

❖ Infant Botulism

Source of Infection
❖ Untreated water

❖ Undercooked and improperly preserved canned foods, especially those with a low acid content

❖ Home-canned vegetables

❖ Cured pork and ham

❖ Smoked or raw fish

❖ Honey and corn syrup

Mode of Transmission
❖ Ingestion (or injection) of preformed toxin

❖ Spores may resist 100 degree Celsius for many hours

❖ Inhalation of toxin may also cause disease

❖ Introduction of spores into the wound

Incubation Period: 12 to 72 hours but extremes of 2 hours to 10 days are reported.

Clinical Manifestations:
❖ Double or blurred vision

❖ Droopy eyelids

❖ Dry mouth

❖ Difficulty swallowing and talking

❖ Difficulty breathing

❖ Flaccid paralysis (descending)

❖ Deep tendon reflexes are decreased or absent

❖ Initial vomiting or diarrhea followed by constipation

Diagnostic Tests:
❖ A toxicity screen may identify C. botulinum.
❖ Stool culture may identify C. botulinum.

❖ The suspected food may also be cultured to isolate C. botulinum.

❖ Electromyography will show little response to nerve stimulation in the presence of botulism.

❖ Diagnostic tests should be conducted as needed to rule out diseases that may be confused with botulism, such as
myasthenia gravis and Guillain-Barre syndrome.
❖ A mouse-inoculation test will be positive and is the most direct way to confirm a diagnosis of botulism.

Complications
❖ Aspiration

❖ Weakness and nervous system problems can be permanent

❖ Death

Treatment Modalities
❖ Botulinus antitoxin- IV, IM

❖ Infants – inducing vomiting or giving an enema

❖ IV fluid can be administered

❖ Nasogastric tube

❖ Endotracheal intubation – respiratory distress

Nursing Consideration
❖ Obtain a careful history of foods eaten in the past several days.

❖ Monitor respiratory and cardiac function carefully

❖ Perform frequent neurologic checks

❖ Purge the GI tract as ordered

❖ If giving the botulinus antitoxin, check the patient’s allergies, perform a skin test first.

❖ Educate the patient and family about the importance of proper hand hygiene

❖ Teach the patient and family to cook food thoroughly before ingesting.

❖ Instruct the patient who eats home canned food to boil the food for 10 minutes before eating to ensure that it is safe to
consume.
❖ Teach patient and families to see their doctors promptly for infected wounds and to avoid injectable street drugs.

Suggested on-call action

❖ Ensure that the case is admitted to hospital

❖ Obtain food history as a matter of urgency

❖ Obtain suspect foods

❖ Identify others at risk

❖ Inform appropriate local and national authorities

AMOEBIASIS

Description: Protozoal infection that initially involves the colon but may spread into the liver and lungs by lymphatic dissemination
 Etiologic Agent
❖ Entamoeba Histolytica

● 2 stages

✔ Cyst – considered to be the infective stage and the resistance to environmental conditions and can
survive for few days outside the body
✔ Trophozoites / vegetative form – Facultative parasites that invades the tissue

Source of Infection
❖ Contaminated food and water

❖ Flies

Mode of Transmission
❖ Fecal-oral

❖ Oral-anal
 Incubation Period
❖ Severe infections: 3days

❖ Average 2-4 weeks

Period of Communicability
❖ Communicable for the entire duration of the illness or until cysts are present in the stool

Clinical Manifestation
❖ Acute Amoebic Dysentery

● Slight attack of diarrhea altered with PD of constipation

● Watery foul-smelling stools containing blood streaked mucus

● Gaseous distension of the lower abdomen

● Nausea, flatulence

● Tenderness in the right iliac region

❖ Chronic Amoebic Dysentery

● Diarrhea for several days, succeeded by constipation

● Anorexia, weight loss, weakness, fatigue

● Watery, bloody mucoid stool

● Flatulence and irregular bowel movement

● Abdomen loses its elasticity

● Severe cases – scattered ulceration is seen through sigmoidoscopy

Diagnostic Procedures
❖ Stool exams – cyst (plenty of amoeba on the stool)

❖ Blood exams – leukocytosis

❖ Sigmoidoscopy

Management
❖ Metronidazole (Flagyl) 800mg TID x 5 days

❖ Tetracycline, Ampicillin, Streptomycin, Chloramphenicol

Nursing Interventions
❖ Observe isolation and enteric precautions

❖ Proper collection of stool specimen

● No oil prep for 48 hours

● Large portion of stools containing blood mucus

● Label specimen properly

● Send specimen immediately to the laboratory

❖ Provide skin care and hygiene

❖ Provide optimum comfort dysenteric patient should never be allowed to feel cold

❖ Diet fluid should be forced

● Cereals and strained meat broths without fats

● Bland diet without cellulose or bulk producing foods

● Chicken and fish may be added when convalescence is established

Prevention
❖ Health education and Fly control

❖ Sanitary disposal of feces

❖ Safe drinking water

❖ Proper food preparation and food handling

❖ Detection and treatment of carriers

SCHISTOSOMIASIS
Other Terms: Bilharziasis / Snail Fever
Description: Slowly progressive disease caused by blood flukes
 Causative Agent
❖ Schistosoma japonicum – endemic in the Philippines and China
❖ Schistosoma mansoni – South America, the Caribbean, Africa and countries of the Arab Middle East
❖ Schistosoma haematobium – Africa and the Middle East

Source of Infection
❖ Stool and urine of infected persons or animals

Mode of Transmission
❖ Ingestion of contaminated water

❖ Penetration through the skin pores

❖ *Oncomelania hupensis quadrasi is the intermediary host

Incubation Period
❖ At least 2 months

Clinical Manifestations
st
❖ 1 stage

● Pruritic rash known as “swimmers itch” occurs 24 hours after penetration of cercariae in the skin

❖ 2nd Stage

● Bloody mucoid stools (on and off for weeks)

● Katayama Fever – clinical constellation of the following:

✔ Fever, headache

✔ Cough, chills and sweating

✔ Lymphadenopathy and hepatosplenomegaly

❖ 3rd (Chronic) Stage

● Granulomatous reactions to egg deposition in the intestine, liver, bladder

● Inflammation of the liver

Icteric and jaundice
● Bulging of the Abdomen
● Enlargement of the Spleen

● Sometimes the brain is affected that caused epilepsy

● Eggs are deposited in the bladder wall, leading to hematuria, bladder obstruction

● Hydronephrosis and recurrent urinary tract infection

● Pale and marked muscle wasting

Complications
❖ Liver cirrhosis and portal hypertension

❖ Bleeding esophageal varices

❖ Bladder cancer
❖ Pulmonary hypertension

❖ Heart failure

❖ Ascites

❖ Renal failure

❖ Cerebral schistosomiasis

Diagnostic Procedure
❖ Fecalysis

❖ Liver and rectal biopsy

❖ ELISA

❖ Circumoval precipitation test (COPT) – confirmatory test

Management
❖ Drug of choice: PRAZIQUANTEL for 6 months

● 1 tab 2x a day for 1st 3 mos

● 1 tab a day for next 3 mos

● Alternative: Ovamniquine
 Nursing Interventions
❖ TSB

❖ Skin care

❖ Provide comfort

❖ Proper nutrition

Prevention and Control

❖ Reduce snail density

● Molluscicides

● Stream Cleaning Vegetation (expose the snails to sunlight)

❖ Proper waste disposal

❖ Control of stray animals

❖ Safe and adequate water supply for bathing, laundering and drinking

❖ Foot bridges over snail-infested streams

❖ Health education about mode of transmission and prevention

SEXUALLY TRANSMITTED INFECTIONS

SYPHILIS
Other Terms: Sy, Bad blood, The Pox, Lues Venereal, Morbus Gallicus

Description: it is an acute, chronic infectious disease caused by spirochete and is acquired through sexual contact

Etiologic Agent: Treponema pallidum

Source of Infection
❖ Discharges from obvious or concealed lesions of the skin or mucous membrane

❖ Semen

❖ Blood

❖ Tears

❖ Urine

❖ Mucous discharge from the nose, eyes, genital tract

❖ Surface lesions

Incubation Period
❖ Varies, but typically lasts about 3 weeks

Period of Communicability
❖ Variable and indefinite

Mode of Transmission
❖ Sexual Contact

❖ Indirect contact with the articles freshly soiled with discharges or blood

❖ Transmission via placenta

Clinical Manifestation
❖ Primary

● Painless chancre (sore) at site of entry of germs, swollen glands

● Chancres disappears after three to six weeks even without treatment

❖ Secondary

● Rash can be macular, papular, pustular or nodular

● Macules often erupt between rolls of fat on the trunk and on the arms, palm, sole face and scalp

● Alopecia (temporary)
 ● Nails become brittle and pitted

❖ Latent

● Patient is asymptomatic for a few months

● Dormancy stage of bacteria

❖ Late

● Varies from no symptoms to indication of damage to body organs such as brain and heart and liver

Diagnostic Tests
❖ Dark Field Illumination Test identifies T. pallidum from lesion exudates and provides an immediate diagnosis

❖ Fluorescent treponemal antibody absorption test

❖ Venereal Disease Research Laboratory (VDRL) test detects nonspecific antibodies that become reactive within 1 to 2
weeks after the primary syphilis lesion appears or 4 to 5 weeks after the infection begins
❖ CSF analysis, identifies neurosyphilis when the total protein level is higher than 40 mg/dL

Treatment Modalities
❖ IM Penicillin G benzathine

❖ Tetracycline

❖ Doxycycline

Nursing Considerations
❖ Stress the importance of completing the treatment even after the symptoms subside

❖ Practice universal precaution

❖ In secondary syphilis, keep the lesions dry as much as possible

Prevention and Control
❖ Report cases to the Department of Health

❖ Control prostitution

❖ Require sex worker to have check up

❖ Proper sex education

TRICHOMONIASIS
Other Term: Trich

Etiologic Agent: Trichomonas vaginalis

Mode of Transmission
❖ Direct sexual contact

❖ Indirect contact (towels, wash clothes, douching equipment)

Incubation Period
❖ 5 to 21 days

Clinical Manifestations
Females: White or greenish – yellow odorous discharge; vaginal itching and soreness, painful urination.
Males: Slight itching of penis, painful urination, clear discharge from penis
 Diagnosis:
❖ Microscopic slide of discharge

❖ Culture of urethral tissue, urine or semen

❖ Physical Examination

❖ The OSOM Trichomonas Rapid Test identifies infection within 10 to 45 minutes, but it is less sensitive and specific than
culture.

Treatment
❖ Metronidazole (Flagyl) – treatment of choice

❖ Tinidazole (Tindamax)

Complication
❖ Cervical cancer
 Nursing Considerations
❖ Follow standard precautions

❖ Assist with obtaining appropriate specimen for culture or testing

❖ Tell the patient to avoid ingesting alcohol while taking metronidazole (and for 48 hours after completing the
prescription), as the combination may cause severe nausea and vomiting, abdominal pain, headaches, and flushing.

CHLAMYDIA

Etiologic Agent
❖ Chlamydia trachomatis

Mode of Transmission
❖ Vaginal / Rectal intercourse

❖ Oral-genital contact

Incubation Period
❖ 7 to 14 days

❖ Case will remain infectious until treated

Clinical Manifestations
❖ Cervical erosion

❖ Mucopurulent discharges

❖ Dyspareunia

❖ Pain and tenderness of the abdomen

❖ Chills

❖ Fever

❖ Dysuria

❖ Urinary frequency

❖ Painful scrotal swelling

❖ Diarrhea

❖ Tenesmus

Diagnostic Test
❖ Culture of the site of infection will reveal C. trachomatis
❖ Nucleic acid probe will be positive for C. trachomatis

Treatment
❖ Tetracycline

❖ Erythromycin

❖ Azithromycin

Complications
❖ Sterility
❖ Prematurity

❖ Stillbirths

❖ Infant pneumonia

❖ Eye Infections (infants)

Nursing Management
❖ Observe standard precautions

❖ HIV testing for both partners

❖ Assess newborn for signs of chlamydial infection

❖ Urge the patient to inform sexual contacts of his or her infection so they can receive appropriate treatment.

❖ Stress the importance of completing the course of antibiotics even after symptoms subside.

❖ Teach the patient to follow meticulous personal hygiene measures

❖ Instruct the patient to avoid touching any discharge and to wash and dry the hands thoroughly before touching the eyes
to prevent eye contamination.
 GONORRHEA
Other Terms: Clap / Flores Blancas / Gleet / Drip

Description: It is a sexually transmitted bacterial disease involving the mucosal lining of the genitor-urinary tract, the rectum,
and pharynx

Etiologic Agent
❖ Neisseria gonorrhoeae

Incubation Period
❖ 2 to 5 days

Mode of Transmission
❖ Direct contact through sexual intercourse

❖ Direct contact with contaminated secretions of the mother during vaginal delivery

❖ Indirect contact (fomites)

Clinical Manifestations
❖ Females

● 80% are aysmptomatic

● Burning sensation and frequent urination

● Yellowish purulent vaginal discharge

● Redness and swelling of the genitals

❖ Males

● Dysuria with purulent discharge

● Rectal infection

● Inflammation of the urethra

● Prostatitis

● Pelvic Pain

Complications
❖ Sterility

❖ Pelvic Infection

❖ Epididymitis

❖ Arthritis

❖ Endocarditis

❖ Conjunctivitis

❖ Meningitis

Diagnostic Tests
❖ Gram staining

❖ Culture of cervical & urethral smear

 Treatment
❖ Ceftriaxone (IM)

❖ Azithromycin or Doxycycline (po)

Nursing Considerations
❖ Standard precautions

❖ Sexual abstinence until he/she recovers from the disease

❖ For gonococcal arthritis (apply moist heat to relieve pain)

Prevention and Control

❖ Sex education

❖ Case finding

❖ Report cases of gonorrhea

 CANDIDIASIS
Other Term: Candidosis / Moniliasis

Description: Superficial fungal infection that usually infects the skin, nails, mucous membrane, vagina, esophagus and GI
tract

Etiologic Agent: Candida albicans

Sources of infection
❖ Candida are part of the normal flora of the GI tract, mouth vagina and skin, They cause infection when some changes in
the body (such as increased blood glucose or immunocompromised) occurs

Clinical Manifestations
❖ Skin

● Scaly, erythematous, popular rash, sometimes covered with exudates, appearing below the breast, between the
fingers, and the axillae, groin, and umbilicus
❖ Nails

● Red, swollen, darkened nail bed

● Occasionally, purulent discharge and the separation of a pruritic nail from the nail bed

❖ Oropharyngeal mucosa (thrush)

● Cream-colored or bluish white curd-like patches of exudates on the tongue, mouth, or pharynx that reveal
bloody engorgement when scraped
❖ Esophageal mucosa

● Dysphagia

● Retrosternal pain, regurgitation

● Occasionally, scales in the mouth and throat

❖ Vaginal mucosa

● White or yellow discharge, with pruritus and local excoriation

● White or gray raised patches on vaginal walls, with local inflammation

● Dyspareunia

❖ Lungs – hemoptysis, cough, fever

❖ Kidney – fever, flank pain, dysuria, hematuria, pyuria, cloudy urine

❖ Brain – headache, nuchal rigidity, seizures, focal neurologic deficits

❖ Endocardium – systolic or diastolic murmur, fever, chest pain, embolic phenomena

❖ Eye – Endophthalmitis, blurred vision, orbital or periorbital pain, scotoma, exudates

Diagnostic Procedures
❖ Blood Culture

❖ Culture of vaginal scraping

❖ Echocardiography if here is cardiac involvement

❖ Fundoscopy for patients with endophthalmitis

Management
❖ Antifungal: Nystatin, Clotrimazole, Miconazole

✔ Mutism

✔ Coma

Diagnostic Tests
❖ Enzyme linked Immuno-Sorbent Assay (ELISA) – presumptive test

❖ Western Blot – confirmatory test

❖ Particle agglutination (PA)

❖ Immunofluorescent Test

Treatment Modalities
❖ Reverse transcriptase inhibitors (Zidovudine)

❖ Protease inhibitors (Ritonavir)

 Nursing Management
❖ Avoid accidental wounds from infectious materials used in HIV patients

❖ Avoid contact of open skin lesions

❖ Gloves should be worn when handling blood specimens

❖ Handwashing

❖ Blood and other specimens should be labelled prominently

❖ Instruments with lenses should be sterilized after use on AIDS patient

❖ Needles should not be bent after use, placed it under puncture – resistant

❖ Patients with active Aids should be isolated

❖ Care of thermometer – wash with warm soapy water, Soak in 70% alcohol for 10 minutes, dry and store.

VECTOR-BORNE DISEASES

DENGUE FEVER
Other Terms: Breakbone Fever / Hemorrhagic Fever / Dandy Fever / Infectious Thrombocytopenic Purpura

Description: It is an acute febrile disease caused by infection with one of the serotypes of dengue virus.

Etiologic Agents
❖ Dengue Virus Types 1, 2, 3, & 4

❖ Chikungunya Virus

Mode of Transmission
❖ Bite of female infected mosquito (Aedes aegypti)
Incubation Period
❖ 3 to 15 days

Period of Communicability
❖ Unknown
❖ Presumed to be on the 1st week of illness (when the virus is still present in the blood)

❖ Human-to0human spread of dengue has not been recorded, but people are infectious to mosquitoes during the
febrile period

Clinical Manifestations
Herman’s sign (maculopapular rash with patches of normal skin) – pathognomonic sign

❖ Febrile / Invasive Stage

● First 4 days

● High fever (39 – 40 C)

● Abnormal pain

● Headache

● Later flushing

❖ Toxic / Hemorrhagic Stage

 ● Lowering of temperature

● Severe abdominal pain

● Vomiting

● Melena

● Hematemesis

❖ Convalescent / Recovery Stage

● Generalized flushing with areas of blanching appetite

● BP stable

Diagnostic Tests
❖ Tourniquet test (Rumpel – Leede Test)

❖ Platelet count (decreased)

❖ Hemoconcentration (increased of at least 20%)

❖ Occult blood
❖ Hemoglobin determination

❖ Dengue NS1 Test (confirmatory)

Treatment Modalities
❖ Give analgesic (Don’t give Aspirin)

❖ Rapid replacement of body fluids

❖ Oxygen Therapy

❖ Oral Rehydration Solution

❖ Blood Transfusion (for severe bleeding)

❖ Sedatives

Nursing Management
❖ Patient should be kept in mosquito-free environment

❖ Monitor VS

❖ Provide periods

❖ Nose bleeding (apply ice bag on the forehead and at the bridge of the nose)

❖ Watch out for: signs of shock

❖ Diet: Low fat, low fiber, non-irritating, non-carbonated

Prevention & Control

❖ Health education

❖ Early detection and treatment of cases

❖ Treat mosquito nets with insecticides

❖ House spraying

❖ Avoid too many hanging clothes

❖ Case finding
MALARIA
Other Term: Ague and Marsh Fever

Description: It is an acute and chronic parasitic disease transmitted by bite of infected mosquitoes and it is confined mainly to
tropical and subtropical areas.

Etiologic Agents
❖ Plasmodium falciparum (most common)
❖ Plasmodium vivax
❖ Plasmodium malariae

❖ Plasmodium ovale

Incubation Period
❖ P. falciparum (5 to 7 days)
❖ P. vivax (6 to 8 days)
❖ P. ovale (8 to 9 days)
❖ P. malariae (12 to 16 days)

Mode of Transmission
❖ Transmitted mechanically through bite of an infected female Anopheles mosquito

❖ Blood transfusion

❖ Transplacental transmission

Clinical Manifestation:
❖ Paxoysms with shaking chills

❖ Rapid rising fever with severe headache

❖ Profuse sweating

❖ Myalgia

❖ Splenomegaly

❖ Hepatomegaly

Chemoprophylaxis
❖ Chloroquine

● This must be taken at weekly intervals, starting from 1-2 weeks before entering endemic areas.

Preventive and Vector Control Measures

❖ Insecticide – treatment of mosquito nets

❖ House Spraying

❖ On-stream seeding

❖ On-stream clearing

❖ Wearing of clothes that covers arms and legs in the evening

❖ Avoiding outdoor night activities (9PM to 3AM)

❖ Planting of Neem tree

❖ Zooprophylaxis

FILIRIASIS
Other Term: Elephantiasis

Description
❖ It is a parasitic disease caused by an African eye worm, microscopic thread-like worm

❖ Extremely debilitating and stigmatizing disease

Etiologic Agents
❖ Wuchereria bancrofti
❖ Brugia malayi
❖ Brugia timori
❖ Loa loa

Mode of Transmission
❖ Mosquito bite (Aedes poecilius)

Incubation Period
❖ 8 to 16 months

Clinical Manifestations
❖ Asymptomatic Stage

● No clinical signs and symptoms of the disease

❖ Acute Stage

● Lymphadenitis

● Lymphangitis

● Epididymitis

● Orchitis

❖ Chronic Stage

● Develop 10 to 15 years from the onset of the first attack

 Chronic Signs and Symptoms
● Hydrocele

● Lymphedema

● Elephantiasis

Diagnosis
❖ Physical examination

❖ History taking

Laboratory Examinations
❖ Nocturnal Blood Examination (NBE)

● Blood are taken from the patient’s residence (8pm)

❖ Immunochromatographic Test (ICT)

● Rapid Assessment Method

● Antigen test can be done at daytime

 Treatment
❖ Diethylcarbamazine citrate (Hetrazan)

Nursing Management
❖ Health Education

❖ Environmental Sanitation

❖ Psychological and emotional support

❖ Personal hygiene

Prevention and Control

❖ Mosquito net

❖ Mosquito repellent

❖ Yearly dose of medicine

LEPTOSPIROSIS
Other Terms: Canicola Fever / Hemorrhagic Jaundice / Mud Fever / Swine Herd Disease / Flood Fever / Trench Fever / Spirochetal
Jaundice / Japanese Seven Days Fever

Description: It is a zoonotic infectious bacterial disease carried by animals, both domestic and wild, whose urine contaminates
water or food which is ingested or inoculated through the skin.

Etiologic Agent: Leptospira interrogans

Incubation Period
❖ 7 to 13 days (range 4 to 19 days)

Mode of Transmission
❖ Direct contact on the skin through open wounds

Clinical Manifestations
❖ Leptospiremic Phase (4 to 7 days)

● Nausea

● Vomiting

● Fever

● Headache

● Myalgia

● Chest pain

❖ Immune Phase (4 to 30 days)

● Meningeal irritation

● Oliguria

● Anuria

● Severe cases (shock, coma, congestive, heart failure)

❖ Convalescence Phase

● Relapse may occur during the 4th to 5th week

 Laboratory Tests
❖ ELISA

❖ Liver Function Tests

❖ Leptospira Antigen-antibody test

❖ Leptospira Antibody Test

Complications
❖ Meningitis

❖ Respiratory distress

❖ Renal interstitial tubular necrosis

❖ Cardiovascular problems
 Treatment
❖ Doxycycline (Prophylactic)

❖ Penicillin

❖ Tetracycline

❖ Erythromycin

❖ Administration of Fluid and Electrolyte and Blood

Nursing Management
❖ Isolate patient

❖ Darken patient’s room

❖ Observe meticulous skin care

❖ Wide Rat Eradication Program

❖ Encourage Oral fluid intake

Prevention & Control

❖ Environment Sanitation

❖ Proper Drainage System and Control of Rodents

❖ Information - dissemination campaign

CNS DISEASES
RABIES
Other Terms: Hydrophobia / Lyssa

Description: It is a specific, acute, viral infection communicated to man by saliva of an infected animal.

Etiologic Agent
❖ Rhabdovirus (Bullet Shape Virus)

Incubation Period
❖ 3 to 8 weeks, but may be as short as 9 days or as long as 7 years, depending on the amount of virus introduced, the
severity of the wound and its proximity to the brain

Susceptibility and Resistance

❖ All warm-blooded mammals are susceptible

Clinical Manifestations
❖ Prodromal / Invasion Phase

● Fever

● Malaise

● Irritability

● Restlessness

● Apprehensiveness

● Melancholia
 ● Sensitive to light and sound

❖ Excitement / Neurological Phase

● Marked excitation and apprehension

● Nuchal rigidity

● Involuntary twitching

● Severe and painful spasm of the muscles of the mouth, pharynx and larynx

● Hydrophobia

● Aerophobia

● Profuse drooling of saliva

❖ Terminal / Paralytic Phase

● Quiet and unconscious

● Loss of bowel and urinary control

● Cessation of spasms and progressive paralysis

 ● Tachycardia; respiratory paralysis, heart failure

Diagnostic Tests
❖ Virus isolation from the patient’s saliva / throat

❖ Fluorescent rabies antibody (RFA) – most definitive diagnosis

❖ Presence of negri bodies in the dog’s brain

Treatment Modalities
❖ Wash with soap and water

❖ Application of antiseptics such as povidone iodine may be done

❖ Patients should not be bathed and there should not be any running water in the room

❖ Concurrent and terminal disinfection should be carried

Prevention and Control

❖ Vaccination of all dogs (immunized 3 months of age and every year thereafter)

❖ Confinement of any dog that has bitten a person for 10 to 14 days

❖ Provide public education

TETANUS
Other Term: Lock Jaw

Description: It is an acute illness caused by toxin of the tetanus bacillus. This infection is usually systemic; less
commonly, it is localized.

Etiologic Agent: Clostridium tetani

Source of Infection:
❖ Soil

❖ Feces

Mode of Transmission
❖ Transmission occurs when spores are introduced in the body through

● Dirty wound

● Injecting drug use and occasionally during abdominal surgery

Incubation Period
❖ 3 to 21 days depending on the site of the wound and the extent of contamination

Clinical Manifestation
❖ Localized

● Spasm

● Increased muscle tone in the wound

❖ Generalized

● Marked muscles hypertonicity

● Hyperactive deep tendon reflexes

● Tachycardia

● Profuse sweating

● Low-grade fever

● Painful, involuntary muscle contractions:

✔ Neck and facial muscles

⮚ Lockjaw (trismus)

⮚ Painful spasms of masticatory muscles

⮚ Difficulty opening the mouth

⮚ Risus sardonicus

✔ Somatic Muscles

⮚ Arched-back rigidity and board-like abdominal rigidity

 ✔ Intermittent tonic seizures lasting several minutes, which may result in cyanosis and sudden death by
asphyxiation

Diagnostic Tests
❖ Clinical features

❖ Blood cultures and tetanus antibody tests are often negative, only a third patients have a positive wound culture

❖ Cerebrospinal fluid pressure may rise above normal

Treatment Modalities
❖ Drainage of ski abscesses

❖ Administration of antibodies

● Metronidazole (first-line agent)

● Pen G

❖ Administration of tetanus immunoglobulin (TIG)

❖ Sedatives

❖ Patients with severe, generalized or rapidly progressing muscle spasm should be intubated sedated and paralyzed if
necessary
❖ Manage autonomic instability

● Labetalol

Complications
❖ Atelectasis

❖ Pneumonia

❖ Pulmonary emboli

❖ Acute gastric ulcers

❖ Seizures

❖ Flexion contractures

❖ Cardiac Arrhythmias

Nursing Management
❖ Maintain an adequate airway and ventilation to prevent pneumonia and atelectasis

❖ Suction often and watch for signs of respiratory distress

❖ Maintain an IV line for medications and emergency care, if necessary

❖ Monitor for arrhythmias

❖ Record intake and output accurately and check vital signs often

❖ Keep the patient’s room quiet and dimply & Warn visitors not to upset or overly stimulate the patient

❖ Give muscle relaxants

❖ Perform passive-range-of-motion

❖ Provide adequate nutrition to meet the patient’s increased metabolic needs.

❖ Stress the importance of maintaining active immunization with a booster dose of tetanus toxoid every 10 years
❖ Teach the patient or family about proper wound care.

POLIOMYELITIS
Other Terms: Polio / Infantile Paralysis

Description: It is an acute communication disease caused by the poliovirus

Etiologic Agent: Poliovirus Types 1, 2 and 3

Mode of Transmission
❖ Direct contact with infected oropharynges secretions or feces

Incubation Period
❖ 7 to 14 days

Clinical Manifestations
❖ Fever

❖ Headache
❖ Vomiting

❖ Lethargy

❖ Irritability

❖ Pains in the neck, back, arms, legs and abdomen

❖ Muscle tenderness, weakness an spasms in the extensors of the neck, back, hamstring and other muscles during
range-of-motion exercises
❖ Loss of superficial and deep reflexes
❖ Positive Kernig’s and Brudzinski’s signs

❖ Hypersensitivity to touch

❖ Urinary retention

❖ Tripod (arms extended behind for support when sitting up)

❖ Hoyne sign (head falls back when surprise and shoulders are elevated)

❖ Inability to raise the legs a full 90 degrees from a supine position.

❖ Diplopia

❖ Dysphasia

❖ Difficulty chewing

❖ Inability to swallow or expel saliva

Diagnostic Tests
❖ Viral culture = Stool sample

❖ Convalescent serum antibody titers four times greater than acute titers support the diagnosis

❖ CSF pressure and protein levels may be slightly increased, and the white blood cell count elevated initially, thereafter
mononuclear cells constitute most of the diminished number of cells.
❖ Electromyographic findings in early poliomyelitis show a reduction in the recruitment pattern and a diminished
interference pattern due to acute motor axon fiber involvement.
❖ Fibrillations develops in 2 to 4 weeks, and fasciculations also may be observed

Treatment Modalities
❖ Analgesics (No Morphine)

❖ Moist heat application

❖ Bed rest is necessary only until extreme discomfort subsides

❖ Physical therapy

❖ Braces

❖ Corrective shoes

Complications
❖ Respiratory failure

❖ Pulmonary edema

❖ Pulmonary embolism

❖ Urinary Tract Infection

❖ Urolithiasis

❖ Atelectasis

❖ Pneumonia

❖ Cor Pulmonale

❖ Paralytic shock

Nursing Considerations
❖ Observe the patient for paralysis and other neurologic damage

❖ Maintain patent airway

❖ Check blood pressure frequently

❖ Provide an adequate, well-balanced diet

❖ Good skin care and frequent repositioning

❖ Inform ambulatory patients about the needs for careful handwashing.

❖ Instruct the patient or caregivers about measures need to manage symptoms and prevent complications.

Prevention
❖ Administration of Oral Polio Vaccine
❖ Boosters are required at 10-years intervals for travel to endemic areas.
 GASTROINTESTINAL SYSTEM
DEFINITION
❖ 23-26 foot long pathway that the:

● Mouth

● Esophagus

● Stomach

● Small intestines

● Large intestines

● Rectum

● Anus
ESOPHAGUS
❖ Located in the mediastinum, anterior to the spine and posterior to the trachea

❖ Approximately 25cm in length

❖ Tube connecting the mouth to the stomach

STOMACH
❖ Distensible pouch into which the food bolus passes to be ingested by gastric enzymes

❖ Hollow muscular organ with a capacity of approximately 1500mL

❖ Stores food during eating

SMALL INTESTINE
❖ Longest segment of the GI tract where the process of absorption of nutrients takes place

❖ Consisting of three parts:

● Duodenum

● Jejunum

● Ileum
LARGE INTESTINE
❖ The portion of the GI tract into which waste material from the small intestine passes as absorption continues and
elimination begins
❖ Consists of several parts:

● Ascending colon

● Transverse colon

● Descending colon

● Sigmoid colon

● Rectum
FUNCTIONS OF THE DIGESTIVE SYSTEM
Digestion
❖ Occurs when digestive enzymes and secretions mix with ingested food and when proteins, fats and sugars are
broken down into their component smaller molecules.
Absorption
❖ Occurs when small molecules, vitamins, and minerals pass through the walls of the small and large intestine and into
the bloodstream
 Elimination
❖ Occurs after digestion and absorption, when waste products are evacuated from the body

❖ Chewing and swallowing

● 1st process of digestion

● Approximately 1.5 L of saliva is secreted daily from the parotid, the submaxillary, and the sublingual glands

● Salivary amylase

✔ Is an enzyme that begins the digestion of starches

● Swallowing begins as a voluntary act that is regulated by the swallowing center in the medulla oblongata of the
central nervous system.
❖ Gastric Function
● Secretes highly acidic fluid in response to the presence of anticipated ingestion of food (hydrochloric acid)

● Intrinsic Factor

✔ Secreted by the gastric mucosa, combines w/ dietary vitamin B12

● Pepsin

✔ An important enzyme for protein digestion.

 ✔ End-product of the conversion of pepsinogen from the chief cells.

● Food remains in the stomach for variable length of time, from 30 minutes to several hours, depending on the:

✔ Volume

✔ Osmotic pressure

✔ Chemical composition of the gastric contents.

❖ Small Intestine Function

● Secretions contain digestive enzymes:

✔ Amylase

⮚ Aids in digesting starch

✔ Lipase

⮚ Aids in digesting fats

✔ Trypsin

⮚ Aids in digestion of protein

✔ Bile

⮚ Secreted by the liver and stored in the gallbladder

⮚ Aids in emulsifying ingested fats

⮚ Making them easier to digest and absorb.

● Intestinal secretions total approximately 1L/day of pancreatic juice, 0.5 L/day of bile, and 3 L/day of secretions from
the glands of small intestine.
● Two types of contractions occur regularly in the small intestines:

✔ Segmentation contractions

⮚ Produce mixing waves that move the intestinal contents back and forth in a churning motion.

✔ Intestinal peristalsis

⮚ Propels the contents of the small intestine toward the colon

❖ Colonic Function

● Bacteria assist in completing the breakdown of waste material, especially of undigested or unabsorbed pro and
bile salts.
● The slow, weak peristaltic activity along the tract allows for efficient reabsorption of water and electrolytes,
which is the primary purpose of the colon.
● Intermittent, strong peristaltic waves propel the contents and eventually reach the rectum, usually in about 12
hours
❖ Physical examination:
● Inspection

● Auscultation

● Percussion

● Palpation

❖ Order of Palpation

● Right Lower Quadrant

 ● Right Upper Quadrant

● Left Upper Quadrant

● Left Lower Quadrant

❖ Right Hypochondriac

● Right lobe of the liver

● Gallbladder

● Part of the duodenum

● Hepatic flexure of colon

● Upper half of the right kidney

● Suprarenal gland

❖ Epigastric

● Aorta

● Pyloric end of stomach

● Pancreas

● Part of live

❖ Left hypochondriac

● Stomach

● Spleen
 ● Tail of pancreas

● Splenic flexure of the colon

● Upper half of the left kidney

● Suprarenal gland

❖ Right Lumbar

● Ascending colon

● Lower half of right kidney

● Part of duodenum and jejunum

❖ Umbilical

● Omentum

● Mesentery

● Lower part of duodenum

● Part of jejunum and ileum

❖ Right Inguinal

● Cecum

● Appendix

● Lower end of the ileum

● Right ureter

● Right spermatic cord

● Right ovary

❖ Hypogastric

● Ileum

● Bladder (if enlarged)

● Uterus (if enlarged)

❖ Left Inguinal

● Sigmoid colon

● Left ureter

● Left spermatic cord

● Left ovary

Diagnostic Studies
UPPER GI SERIES
❖ Delineates the entire GI tract after the introduction of a contrast agent (Barium swallow)

❖ Enables the examiner to detect or exclude anatomic or functional derangement of the upper GI organs or sphincters.

❖ Also aids in the diagnosis of ulcers, varices, tumors, regional enteritis, and malabsorption syndromes
Nursing Interventions:
● Clear liquid diet with NPO from midnight the night before the study.

● Smoking, chewing gum, and mints can stimulate gastric motility, so the nurse advises against these practices
● Increase fluid intake to facilitate evacuation of stool and the radiopaque liquid

● Typically, oral medications are withheld on the morning of the study and resumed that evening, but each
patient's medication regimen is evaluated on an individual basis

LOWER GI SERIES
❖ Visualization of the lower GI tract

❖ With introduction of barium enema

❖ The procedure usually takes about 15 to 30 minutes, during which time x-ray images are obtained

❖ The patient must be assessed for allergy to iodine or contrast agent.

Nursing Interventions:
● Emptying and cleansing the lower bowel prior to the procedure

● Low residue diet 1 to 2 days before the test

● Clear liquid diet, NPO after midnight; and cleansing enemas until returns are clear the following morning.

● Laxative is given before and after the procedure.

● Increased fluid intake after the procedure.

● Evaluation of bowel movement for evacuation of barium

 ESOPHAGO-GASTRO-DUODENOSCOPY (EGD)
❖ Direct visualization

● Esophageal

● Gastric

● Duodenal mucosa through a lighted endoscope

❖ After the patient is sedated, the endoscope is lubricated with a water-soluble lubricant and passed smoothly and
slowly along the back of the mouth and down into the esophagus
❖ The procedure usually takes about 30 minutes.

❖ The patient may experience:

● Nausea

● Gagging

● Choking

❖ Use of topical anesthetic agents and moderate sedation makes it important to monitor and maintain the patient's oral
airway during and after the procedure.
❖ Precautions must be taken to protect the scope, because the fiberoptic bundles can be broken if the scope is bent at
an acute angle.
❖ The patient wears a mouth guard to keep from biting the scope.

❖ Nursing Interventions:

● The patient should be NPO for 8 hours prior to the examination.

● Before the introduction of the endoscope, the patient is given a local anesthetic gargle or spray.

● Midazolam (Versed), a sedative that provides moderate sedation and relieves anxiety during the
procedure
● Atropine may be administered to reduce secretions, and glucagon may be administered to relax smooth
muscle.
● The patient is positioned in the left lateral position to facilitate clearance of pulmonary secretions and
provide smooth entry of the scope.
● After gastroscopy, assessment includes
✔ Level of consciousness
✔ Vital signs

✔ Oxygen saturation

✔ Pain level

● Monitor for signs of perforation

✔ Pain

✔ Bleeding

✔ Unusual difficulty swallowing

✔ Rapidly elevated temperature

● After the patient's gag reflex has returned, lozenges, saline gargle, and oral analgesic agents may be
offered to relieve minor throat discomfort
● Patients who were sedated for the procedure must remain in bed until fully alert
Endoscopic Retrograde Cholangio-pancreatography (ERCP)
❖ Visualization of the common bile duct, the Pancreatic, hepatic ducts through the Ampulla of Vater in the
duodenum
❖ Uses the endoscope in combination with X-ray techniques to view the ductal structures of the biliary tracts.

COLONOSCOPY
❖ Direct visual inspection of the large intestine (anus, rectum, sigmoid, transverse, descending and ascending
colon)
❖ Therapeutically, the procedure can be used to remove all visible polyps with a special snare and cautery through the
colonoscope.

LAPAROSCOPY
❖ Direct visualization of the organs and structures within the abdomen, permitting visualization and identification of any
growths, anomalies, and inflammatory processes.
❖ A pneumoperitoneum (injecting carbon dioxide into the peritoneal cavity to separate the intestines from the pelvic
organs) is created
 ❖ Biopsy samples can be taken from the structures and organs as necessary

❖ Laparoscopy usually requires general anesthesia and sometimes requires that the stomach and bowel be
decompressed
ESOPHAGEAL DISORDERS

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

❖ Excessive back-flow of gastric and duodenal contents into the esophagus due to incompetent lower esophageal
sphincter
❖ Clinical Manifestation:

● Burning sensation in the esophagus (Pyrosis)

● Dyspepsia (Indigestion)

● Dysphagia

● Hypersalivation

● Esophagitis

Note: The symptoms may mimic those of a heart attack. The patient's history aids in obtaining an accurate diagnosis.
❖ Diagnostic Procedures:

✔ Endoscopy or barium swallow Ambulatory 12 to 36 hour esophageal pH monitoring

✔ Bilirubin Monitoring (Bilitec)

❖ Pharmacologic Management:

✔ Antacids- neutralize acid

❖ H2 receptor antagonist

✔ Decreases amount of HCI produced by stomach by blocking action of histamine on histamine receptors of
parietal cells in the stomach
● Proton Pump Inhibitors

✔ Decreases gastric acid secretion by slowing the ATPase pump on the surface of the parietal cells

✔ More potent than H2 receptor antagonists

● Prokinetic agents

✔ Enhancing colonic transit by increasing propulsive motor activity

❖ Nursing Management:

✔ Teaching the patient to avoid actions that decrease lower esophageal sphincter pressure or cause esophageal
irritation
✔ Low fat diet

✔ Maintain normal body weight

✔ Avoid caffeine, tobacco, beer, milk, and carbonated drinks, spicy foods

✔ Avoid eating/drinking 2hours before bedtime.

✔ Avoid tight fitting clothes

✔ Elevate head of bed on 6 to 8 inches.

✔ Avoid lying after meals

❖ Surgical Management:

✔ Nissen Fundoplication

✔ Wrapping of a portion of the gastric fundus around the sphincter area of the esophagus.

BARRETT'S ESOPHAGUS
✔ A condition in which the lining of the esophageal mucosa is altered.

✔ Associated with GERD

✔ Reflux causes changes in the lining of the lower esophagus.

✔ The cells that are laid to cover the exposed area are no longer squamous in origin

✔ Precursor to esophageal cancer

❖ Clinical Manifestation:

✔ Burning sensation in the esophagus (Pyrosis)

✔ Dyspepsia (Indigestion)

✔ Dysphagia

✔ Hypersalivation

✔ Esophagitis
 ❖ Diagnostic Procedure:

✔ Esophagogastroduodenoscopy (EGD)

✔ Biopsy

❖ Management:

● Photodynamic therapy

✔ Laser thermal ablation; destroy the metaplastic cells

● Esophagectomy
Total resection of the esophagus with removal of the tumor plus a wide tumor-free margin of the esophagus
and the lymph nodes the area.

HIATAL HERNIA
❖ The opening in the diaphragm through which the esophagus passes becomes enlarged and part of the
upper stomach tends to Move up into the lower portion of the thorax.
❖ Types:

● Sliding

✔ Upper stomach and the gastroesophageal junction are slide displaced upward and out of the thorax.

● Paraesophageal

✔ All or part of the stomach pushes through the diaphragm beside the esophagus

❖ Clinical Manifestation

● Heartburn

● Regurgitation

● Dysphagia

● Sense of fullness after eating or chest pain

❖ Diagnostic Procedure:

● Xray studies

● Barium swallow

● Fluoroscopy

❖ Management:

● Same pharmacological management with GERD

● Small frequent feedings

● Patient is advised not to recline for 1 hour after eating

● Elevate head of bed

● Surgery is indicated in about 15% of patients.

❖ Surgical management:

● Nissen Fundoplication

GASTRITIS
 ❖ Inflammation of the gastric mucosa
Causes:
● Repeated exposure to irritating agents (e.g. highly seasoned foods)

● Overuse of aspirin and other non-steroidal anti-inflammatory drugs Excessive alcohol intake

● Bile reflux

● Radiation therapy

● Ingestion of strong acid or alkali

● Bacteria (helicobacter pylori)

DUODENAL ULCER GASTRIC ULCER

INCIDENCE -usually 50 and over
-Age 30-60 -15% of peptic ulcers
-80% of peptic ulcers
SIGNS, SYMPTOMS, AND CLINICAL FINDINGS
Hypersecretion of HCI Normal to hyposecretion of HCI
May have weight gain Weight loss may occur
Pain occurs 2-3 hrs after meal Pain occurs ½ -1 hr after meals
Vomiting uncommon Vomiting common
Hemorrhage less likely than gastric ulcer Hemorrhage more likely to occur

Melena more common than hematemesis Hematemesis more common than melena
Relieved by eating Aggravated by eating
MALIGNANCY POSSIBILITY -occasionally
-rare
RISK FACTORS -H. pylori
-alcohol -gastritis
-smoking -alcohol
-stress -use of NSAID’s
-H. pylori -stress

❖ Clinical Manifestation:

● Abdominal discomfort

● Headache

● Lassitude

● N/V and hiccupping

● Heartburn after eating

● Intolerance to spicy or fatty foods

● Vitamin deficiency (Vit. B12)

● Belching

❖ Assessment and Diagnostic:

● Achlorhydria or hypochlorhydria (Absence or low levels of HCI)

● Can be determined by an upper GI series or endoscopy

● Tissue specimen (Biopsy)

❖ Medical Management:
 ● H2 blockers

● Antibiotics (Amoxicillin, Clarithromycin)

● Proton Pump Inhibitors

❖ Surgical Management:

● Gastrojejunostomy

✔ Anastomosis of jejunum to stomach to detour around the pylorus.

❖ Nursing Management:

● Avoidance to gastric irritating agents

✔ Alcohol

✔ Spicy

✔ Fatty foods

✔ Aspirin

✔ NSAID's until symptoms subside.

● Discourage caffeinated beverages.

● Be alert for indicator of hemorrhagic gastritis (hematemesis, tachycardia, hypotension.)

● Notify the physician if signs of hemorrhagic gastritis are present.

PEPTIC ULCER DISEASE

❖ Excavation that forms in the mucosa wall of

❖ The stomach, in the pylorus, or in the duodenum.

❖ Causes:

● Gram-negative bacteria (H. Pylori)

● Excessive secretion of HCL in the

● Stomach due to ingestion of caffeinated beverages, spicy foods, smoking, and alcohol
Zollinger-Ellison Syndrome
● Consists of severe peptic ulcers, extreme gastric hyperacidity, and gastrin-secreting benign or malignant tumors.
Medical Management:
❖ Pharmacologic Therapy

● H2 Blockers (Ranitidine, Cimetidine)

● Antibiotics

● Proton Pump Inhibitors (Omeprazole)

● Antacid

● Cytoprotectants
 ✔ Creates a viscous substance in the presence of gastric acid that forms a protective barrier, binding to the
surface of the ulcer, and prevents digestion by pepsin
✔ Misoprostol, Sucralfate
❖ Surgical Management

● Vagotomy and Pyloroplasty

✔ Transecting nerves that stimulate acid secretion and opening the Pylorus

● Billroth I (Gastroduodenostomy)

✔ Removal of the lower portion of the antrum of the stomach (which contains the cells that secrete gastrin) as
well as a small portion of the duodenum segment.
✔ Upper portion of stomach anastomosed to duodenum.

● Billroth II (Gastrojejunostomy)

✔ Removal of lower portion (antrum) of stomach with anastomosis to jejunum. A duodenal stump remains and
is oversewn.
❖ Nursing Management

● Stress reduction and rest

● Smoking cessation

● Dietary modification

✔ Avoidance to the food and beverages that irritate the gastric mucosa (alcohol, coffee, milk spicy foods, soft
drinks, tea, NSAID's, Aspirin)

DUMPING SYNDROME
❖ It is partially the result of rapid gastric emptying, which prevents adequate mixing with pancreatic and biliary
secretions.
❖ It is an unpleasant set of and GI symptoms that sometimes occur in patients who have had gastric surgery or a form
of vagotomy.
❖ Clinical Manifestations:

● Symptoms occurring 30 minutes after eating

● Nausea and vomiting

● Feelings of abdominal fullness and

● Abdominal cramping

● Diarrhea

● Palpitations and tachycardia

● Perspiration

● Weakness and dizziness

● Borborygmi Sound

● Steatorrhea- "fats in the stool"

❖ Management:

● Lie down after meals

● Avoid sugar, salt, and milk

 ● Take anti-spasmodic medications as prescribed to delay gastric emptying

● Fluid intake with meals is discouraged, instead fluids may be consumed up to 1 hour before or 1 hour after
mealtime.
● Meals should contain more dry items than liquid items.

● The patient can eat fat as tolerated but should keep carbohydrate intake low and avoid concentrated sources of
carbohydrate

INTESTINAL AND RECTAL DISORDERS

DIVERTICULAR DISEASE
● A sac-like herniation of the lining that of the bowel that extends through a defect in the muscle layer

● Most commonly occur in the sigmoid colon.

❖ Diverticulosis
o Multiple diverticula are present w/o inflammation or symptoms
❖ Diverticulitis
o Diverticulosis with inflammation
o Results when food and bacteria retained in a diverticulum produce infection.
❖ Clinical Manifestations:
● Bowel irregularity with intervals of diarrhea
 ● Nausea and anorexia

● Bloating or abdominal distention

● Narrow stools

● Increased constipation or at times intestinal obstruction

● Signs and symptoms of infection

❖ Diagnostic Procedure:

● Colonoscopy

● Barium enema

● CT Scan (test of choice for diverticulitis, and can also reveal fiber abscesses)

● Abdominal x-rays

❖ Management:

● Antibiotics, analgesics and anticholinergics to reduce bowel spasms as prescribed

● An opioid (eg, Meperidine [Demerol]) is prescribed for pain relief.

● Morphine is contraindicated because it can increase intraluminal pressure in the colon, exacerbating symptoms.

● Instruct the client to refrain from lifting, straining, coughing, or bending to avoid increased intra-abdominal
pressure
● Diet:

✔ For diverticulosis, soft, high fiber foods are indicated for diverticulosis.

✔ For diverticulitis, a low fiber diet may be necessary until signs of infection decrease.

✔ Monitor for perforation, hemorrhage, fistulas, and abscesses

✔ Avoid gas forming foods

❖ Surgical Interventions:

● Colon resection with primary anastomosis

● Temporary or permanent colostomy may be required for increased bowel inflammation

INFLAMMATORY BOWEL DISEASES

CROHN'S DISEASE (REGIONAL ENTERITIS)
❖ Description:

● Subacute and chronic inflammation of the GI tract wall that extends through all layers, (transmural lesion)

● Most common in ileum and colon but can occur anywhere along the GI tract.

● Leads to thickening and scarring, a narrowed lumen, fistulas, ulcerations, and abscesses

● (Classic cobblestone appearance)

❖ Clinical Manifestation:

● Fever and leukocytosis

● Cramp-like and colicky pain after meals

● Diarrhea (Semi solid), which may contain mucus or pus

● Abdominal Distention

● Anorexia, nausea, and vomiting

● Weight loss

● Anemia

● Dehydration

● Electrolyte imbalances

ULCERATIVE COLITIS
❖ Recurrent ulcerative and inflammatory disease of the mucosal and submucosal layers of the colon and rectum
Risk Factors:
● Prevalence is highest in Caucasians and Jewish

● NSAIDs exacerbate IBD

Clinical Manifestations:
● Anorexia

● Weight loss

● Diarrhea (10 to 20 liquid stools per day)

● Malaise

● Left lower quadrant abdominal

● Tenderness and cramping

● Rectal Bleeding

● Dehydration and electrolyte imbalances

● Anemia and hypocalcemia

● Vitamin K deficiency
Diagnostic Procedures:
● Colonoscopy

● Sigmoidoscopy

● Barium Enema

● CBC

● Abdominal X-ray

● Stool Examination
Management for Inflammatory Bowel Diseases:
● Pharmacologic Therapy (Priority:
Relieve inflammation.)
✔ Salicylate Compounds

⮚ Effective for mild or moderate inflammation and are used to prevent or reduce recurrences in long-term
maintenance regimens
✔ Corticosteroids

⮚ Are used to treat severe and fulminant disease and can be administered orally in outpatient treatment or
parenterally in hospitalized patients
✔ Immunosuppressants

⮚ Have been used to alter the immune response. The exact mechanism of action of these medications in
treating IBD is unknown
✔ Anti—diarrheal drugs

⮚ Are used to minimize peristalsis to rest the inflamed bowel. They are continued until the patient's stools
approach normal frequency and consistency.
❖ Nursing Interventions:

● NPO status and administer fluids and electrolytes for acute episodes

● Diet

✔ Low residue

✔ High protein

✔ High calorie diet

✔ Supplemental vitamin therapy

✔ Iron replacement.

● IV or via parenteral nutrition as prescribed

● Monitor for bowel perforation, peritonitis, and hemorrhage

● Avoid gas-forming food

❖ Surgical Interventions:

● Proctocolectomy with permanent ileostomy

✔ An ileostomy, the surgical creation of an opening into the ileum or small intestine (usually by means of an
ileal stoma on the abdominal wall), is commonly performed after a total colectomy (ie, excision of the
entire colon).
 ● Continent Ileostomy (Kock ileostomy)
✔ Creation of a continent ileal reservoir (ie, Kock pouch) by diverting a portion of the distal ileum to the
abdominal wall and creating a stoma
● Restorative Proctocolectomy
✔ Surgical procedure of choice in cases where the rectum can be preserved in that it eliminates the need
for a permanent ileostomy. It establishes an ileal reservoir that functions as a "new" rectum, and anal
sphincter control of elimination is retained
● Ileoanal Anastomosis (Ileorectostomy)

✔ Involves connecting the ileum to the anal pouch (made from a small intestine segment), and the
surgeon connects the pouch to the anus in conjunction with removing the colon and the rectal
mucosa

APPENDICITIS
❖ Inflammation of the appendix

❖ Appendix

● Small, fingerlike appendage about 10 cm (4 in) long that is attached to the cecum just below the ileocecal
valve.
❖ Risk factors:

● Between the ages of 10 and 30 years

❖ Causes:

● Kinked or occluded by a fecalith

● Tumor

● Foreign body

❖ Clinical Manifestations:

● Vague epigastric or periumbilical pain

● Right lower quadrant pain (ie, parietal pain that is sharp, discrete, and well localized)

● Low-grade fever

● Nausea and Vomiting

● Loss of appetite

● Rebound tenderness (ie, production or intensification of pain when pressure is released)

● Rovsing's sign may be elicited by palpating the left lower quadrant; this paradoxically causes pain to be felt in
the right lower quadrant
❖ Diagnostic Procedures:
● Complete blood cell count- Increase WBC

● Abdominal x-ray films

● Ultrasound studies

● CT scans- right lower quadrant density

● Pregnancy test- to rule out ectopic pregnancy

❖ Complications:

● Perforation of the appendix

● Peritonitis

● Abscess formation (collection of purulent material)

● Portal pylephlebitis- septic thrombosis of the portal vein caused by vegetative emboli that arise from septic
intestines
❖ Pharmacologic Management
● IV fluids are administered

● Antibiotic therapy to prevent infection

● Morphine sulfate: prescribed to relieve pain.

❖ Surgical Management

● Appendectomy (ie, surgical removal of the appendix) is performed as soon as possible to decrease the risk of
perforation
✔ Low abdominal incision (laparotomy)
✔ Laparoscopy

● Perforation- place a drain in the abscess

❖ Nursing Management:
 ● Post-operatively, the nurse places patient in a high- Fowler's position.

✔ Reduces the tension on the incision and abdominal organs, helping to reduce pain.

● Discharge teachings:

✔ Have the surgeon remove the sutures between the 5th and 7th days after surgery.

✔ Incision care

✔ Heavy lifting is to be avoided postoperatively

✔ Normal activity can usually be resumed within 2 to 4 weeks.

HEMORRHOIDS
❖ Dilated portions of veins in the anal canal.

❖ Causes:

● 50 years of age

● Shearing of the mucosa during defecation

● Increased pressure in the hemorrhoidal tissue due to pregnancy

❖ Types:

● Internal hemorrhoids

✔ Above the internal sphincter

● External hemorrhoids

✔ Appearing outside the external sphincter

 ❖ Clinical manifestations:

● Itching

● Pain

● Bright red bleeding

● External hemorrhoids severe pain from the inflammation and edema caused by thrombosis

● Internal hemorrhoids are not usually painful until they bleed or prolapse when they become enlarged.

❖ Pharmacologic Management:

● Hydrophilic bulk-forming agents (Psyllium)

● Analgesic ointments and suppositories

● Astringents (eg, witch hazel)

❖ Non-Surgical & Surgical Management:

● Infrared photocoagulation

● Bipolar diathermy

● Laser therapy

● Injection of sclerosing agents

● Rubber-band ligation procedure

● Cryosurgical hemorrhoidectomy

● Hemorrhoidectomy

❖ Nursing Management:

● Good personal hygiene

● Avoiding excessive straining during defecation

● High-residue diet that contains fruit and bran

● Increase fluid intake

● Warm compresses/Sitz baths

● Bed rest

HEPATOBILIARY SYSTEM
❖ Liver

● Largest gland of the body

● Divided into four lobes

✔ Left

✔ Right

✔ Caudate

✔ Quadrate

● Contains several cell types, including hepatocytes and Kupffer's cells

● Regulating blood glucose level by

● Making glycogen, which is stored in hepatocytes

 ● Converting ammonia produced from gluconeogeneticby-products and bacteria to urea

❖ Gall Bladder

● Pear-shaped organ attached to the liver under the right lobe.

● Normally holds 30-50m1 of bile and can hold up to 70 ml when fully distended

❖ Pancreas

● A slender, fish-shaped organ, that lies horizontally in the abdomen behind the stomach and extends roughly
from the duodenum to the spleen
● Endocrine and exocrine functions Has pancreatic juice:
✔ Amylase

✔ Lipase

✔ Trypsin

DISORDERS OF THE LIVER, GALLBLADDER, AND PANCREAS

HEPATITIS
● Inflammatory disorder of the liver parenchyma
● Occurring in Hepatitis A, B, C, D, E, and toxic or drug-induced hepatitis

● Hepatocellular damage results from the body's immune response to the virus or toxin and is characterized by
diffuse inflammatory infiltration with local necrosis
❖ Clinical Manifestation:
● Pre-Icteric Stage
 ✔ Earliest symptoms are not specific

✔ Flu-like symptoms

✔ Malaise

✔ Fatigue

✔ Headache

✔ Myalgias

✔ Anorexia

✔ Nausea & vomiting

✔ Diarrhea

● Icteric Stage

✔ Few days to weeks after pre-icteric stage

✔ Jaundice

✔ Dark-colored urine

✔ Light-colored stool

✔ Steatorrhea

✔ Enlarged liver
Viral hepatitis Mode of transmission Incubation Outcome
Hepatitis A Fecal-oral route In: 15-50 days Usually mild with recovery

Hepatitis B Parenterally; perinatal: In: 28-160 days May be severe

sexual
Hepatitis C Blood transfusion: sexual In: 15-160 days Frequent occurrence of chronic hepatic cancer carrier
transmission state and chronic liver disease.
Hepatitis D Same as HBV In: 21-140 days Similar to HBV but greater likelihood of carrier state
Hepatitis E Fecal-oral route In: 15 to 65 days Similar to HAV except very severe in pregnant women
● Post- Icteric Stage

✔ Convalescent stage lasting a few weeks

✔ Fatigue decreases

✔ Appetite returns

❖ Diagnostic Procedures:

● Liver function test results are elevated

● Serum bilirubin level is increased

● Urinalysis reveals increased bilirubin levels

❖ Management:

● Administer prescribed medications, which may include:

✔ Immunoglobulins

✔ Immunizations

✔ Antiviral

● Prevent transmission of infection

 ● Promote adequate rest without complications

● Encourage proper nutrition

LIVER CIRRHOSIS
❖ Chronic liver disease marked by diffuse destruction and fibrotic regeneration of hepatic cells

❖ Classifications:

● Laennec’s Cirrhosis

✔ Commonly caused by alcoholism and

✔ Chronic nutritional deficiencies

● Biliary cirrhosis

✔ Caused by bile duct disorders that suppress bile flow

● Post- hepatic cirrhosis

✔ Caused by various types of hepatitis

❖ Clinical Manifestation:

● Enlarged, firm liver

● Chronic dyspepsia

● Constipation or diarrhea
 ● Gradual weight loss

● Ascites

● Splenomegaly

● Spider telangiectasis

● Caput Medusae

✔ Dilated abdominal blood vessels

● Portal Hypertension

● Mental deterioration

❖ Laboratory and Diagnostic Findings:

● Liver biopsy

● Liver Scan

● Liver function test (ALT, AST)

● Serum protein levels

● Prothrombin time

❖ Management:

● Administer diuretics to decrease ascites.

● Promote adequate nutrition (Vitamins and nutritional supplements promote healing of damaged liver cells.)

● Prevent threats to skin integrity

● Minimize risk of bleeding

✔ Antacid/ H2 antagonist to minimize possibility of GI bleeding

● Limit visitors, and orient the client to date, time, and place

● Avoid drinking alcoholic beverages Institute safety measures, such as raising side rails and assisting with
ambulation
● Diet:

✔ Early Phase: High protein diet- to promote healing of the liver

✔ Late Phase: Low protein diet- to decrease ammonia levels in the

PORTAL HYPERTENSION
❖ Elevated pressure in the portal vein associated with increased resistance to blood flow through the portal venous
system
❖ Obstruction of portal venous flow through the liver lead to:
● Formation of esophageal, and hemorrhoidal varicosities due to

✔ Increased venous pressure

✔ Accumulation of fluid in the abdominal cavity

❖ Clinical Manifestation:

● Ascites

● Rapid weight gain

● Shortness of breathing
 ● Fluid wave on abdominal percussion

● Liver dullness

● Dilated abdominal vessels radiating from umbilicus (caput medusa)

● Enlarged, palpable spleen

● Fluid and electrolyte imbalance

❖ Management:

● Bed rest

● Administering medications which may include diuretics

● Measure & record abdominal girth & body weight daily

● Promote measures to prevent or reduce edema

● Assist the health care provider with paracentesis

● Monitor serum ammonia and electrolyte levels.

ESOPHAGEAL VARICES
❖ Hemorrhagic process involving dilated, tortuous veins in the submucosa of the lower esophagus

❖ Caused by portal hypertension

❖ Clinical Manifestations:

● Hematemesis and melena

● Massive hemorrhage occurs

 ● Signs of hepatic encephalopathy

● Dilated abdominal veins

● Ascites

● History of Alcohol Abuse

❖ Diagnostics:

● Endoscopy

● Lab. Tests: ALT, AST,Bilirubin (increased)

● Portal Hypertension Measurements

❖ Management:

● Assess for ecchymosis, epistaxis, petechiae, and bleeding gums

● Monitor level of consciousness, vital signs, and urinary output to evaluate fluid balance

● Monitor the client during blood transfusion

● Provide nursing care for the client undergoing prescribed tamponade to control bleeding balloon

✔ Sengstaken-Blakemore Tube

✔ Four openings:

⮚ Gastric aspirations

⮚ Esophageal aspiration

⮚ Gastric balloon inflation

⮚ Esophageal balloon inflation

✔ Instrument at the bedside- Scissors (Cut the tube in case of respiratory distress.)

✔ The patient being treated with balloon tamponade must remain under close observation in the ICU because of
the risk of serious take complications. Precautions must be taken to ensure that the patient not pull on or
inadvertently displace the tube.
● Vasopressin- initial mode of therapy
● Sclerotherapy

✔ After treatment for acute hemorrhage, the patient must be observed for bleeding, perforation of the
esophagus, aspiration pneumonia, and esophageal stricture
● Variceal Band Ligation

✔ A modified endoscope loaded with an elastic rubber band is passed through a band directly onto the varix (or
varices) to be banded.
✔ Complications:
⮚ Superficial ulceration

⮚ Dysphagia

⮚ Transient chest discomfort

⮚ Esophageal strictures

HEPATIC ENCEPHALOPATHY
❖ Neurologic syndrome that develops as a complication of liver disease

❖ It may be acute and self –limiting and progressing or chronic

❖ Incidence is similar to cirrhosis
Due to:
● Severe liver damage

● Hepatocellular failure

❖ Increased serum ammonia levels from:

● GI bleeding

● High-protein diet

● Bacterial growth in the intestine Uremia

❖ Pathophysiology:

Hepatic Insufficiency
↓
Inability to detoxify toxic by-products of metabolism (ammonia)
↓
Ammonia enters the brain
↓
 Excites peripheral
benzodiazepine-type receptors on
↓
Stimulates GABA

Depression of Central Nervous System

↓
↓
Encephalopathy

❖ Clinical Manifestations:

● Neurological dysfunction progressing from minor mental aberrations and motor disturbances to coma

● Flapping tremors/Liver flap (Asterixis)

✔ The patient is asked to hold the arm out with the hand held upward (dorsiflexed). Within a few seconds, the
hand falls forward involuntarily and then quickly returns to the dorsiflexed position.
● Fetor hepaticus

✔ A sweet, slightly fecal odor to the breath that is presumed to be of intestinal origin,

● Constructional Apraxia

✔ Deterioration of handwriting and inability to draw a simple star figure occurs with progressive hepatic
encephalopathy.
● Serum ammonia level is elevated

● Serum bilirubin level is elevated

● Prothrombin time is prolonged

❖ Management:

● Administer prescribed medications which may include laxatives (Lactulose)

✔ Ammonia is kept in the ionized state, resulting in a decrease in colon pH

✔ Evacuation of the bowel takes place, which decreases the ammonia absorbed from the colon

✔ The fecal flora are changed to organisms that do not produce ammonia from urea

● Administer antibiotics (Neomycin)

✔ Reduce levels of ammonia-forming bacteria in the colon

● Closely monitor neurologic status for any changes

● Evaluate serum ammonia values daily

● Monitor for signs of impending coma.

● Reduce or eliminate the client's dietary protein intake if you detect evidence of impending coma.

● Monitor the client closely, and administer a conservative dose of prescribed sedative or analgesic medication,
because liver damage alters drug metabolism.

GALL BLADDER DISORDERS

❖ Risk Factors:

● Obesity

● Women especially who have had

 ● Multiple pregnancies or who are of Native American or U.S. Southwestern Hispanic Ethnicity

● Frequent changes on weight

● Rapid weight loss

● High dose estrogen

● Ileal resection or disease

● Cystic Fibrosis

● Diabetes mellitus

❖ Cholelithiasis

● Formation of calculi in the gallbladder

● Causes:

✔ Result from changes in bile components or bile stasis, which may be associated with such factors as
infection, cirrhosis, and pancreatitis
❖ Cholecystitis

● Acute or chronic inflammation of the gallbladder

● Causes
 ✔ Obstruction of the cystic duct by impacted gallstone

✔ Tissue damage due to trauma, massive burns, or surgery

✔ Gram-negative septicemia

✔ Overuse of opioid analgesics

❖ Clinical manifestations:

● Cholelithiasis

✔ Episodic, cramping pain in the RUQ of the abdomen or the epigastrium, possibly radiating to the back
near the right scapular tip
✔ Nausea and vomiting

✔ Fat intolerance

✔ Fever and leukocytosis

✔ Jaundice

✔ Epigastric distress

❖ Cholecystitis

✔ Biliary colic

✔ Tenderness and rigidity in the RUQ elicited on palpation

✔ Murphy's sign- Pain on taking a deep breath when the examiner's fingers are on the approximate location of
the gallbladder.
✔ Fever

✔ Nausea and vomiting

✔ Fat intolerance

✔ Heart burn

✔ Flatulence

✔ Vitamin deficiency

❖ Diagnostic Tests:

● Abdominal X-ray

● Ultrasonography- diagnostic procedure

● of choice

● Cholescintigraphy- radioactive agent is administered intravenously

● Cholecystography- iodide containing contrast agent is administered before xray

● Endoscopic Retrograde

● Cholangiopancreatography (ERCP)

✔ Permits direct visualization of structures that previously could be seen only during laparotomy

✔ A fiberoptic duodenoscope, with side-viewing apparatus is inserted into the duodenum. The ampulla of
Vater is catheterized, and the biliary tree is injected with contrast agent
❖ Management:

● Pharmacologic Management
✔ Ursodeoxycholic acid (UDCA [URSO, Actigall]) - dissolve small radiolucent gall stone

✔ Administer prescribed medication, which may include analgesic {morphine sulfate} and antacids

● Nutritional therapy

✔ Low-fat liquids

✔ High in protein and carbohydrates

● Non-surgical Approach

✔ Intra-corporeal Lithotripsy

⮚ Stones in the gallbladder or common bile duct may be fragmented by means of laser pulse technology

✔ Extracorporeal Shockwave Lithotripsy

⮚ Non-invasive procedure; uses repeated shock waves directed at the gallstones in the gallbladder or common bile
duct to fragment the stones.
● Surgical Approach

✔ Laparoscopic Cholecystectomy

⮚ Performed through a small incision or puncture made through the abdominal wall at the umbilicus

✔ Cholecystectomy

⮚ Gall bladder is removed through an abdominal incision after the cystic duct and artery are ligated.

⮚ A drain is placed close to the gall bladder if there is a bile leak, removed after 24 hours

⮚ Bile duct injury-serious complication

✔ Choledochostomy

⮚ Making an incision in the common bile duct for removal of stones.

 ● Maintaining skin integrity and Promoting Biliary Drainage

✔ If bile is not draining properly, an obstruction is probably causing the bile to be forced back into the liver or
bloodstream
✔ To prevent loss of bile, the physician may want the drainage tube or collection receptacle elevated above the level
of the abdomen
✔ Every 24 hours, the nurse measures the bile collected and records the amount, color and character of
drainage.
✔ After several days of drainage, the tube may be clamped for 1 hour before and after each meal to deliver bile to
the duodenum to aid in digestion
✔ Within 7 to 14 days, the drainage tube is removed.

ACUTE PANCREATITIS
❖ Self- digestion of the pancreas by its own proteolytic enzymes, principally trypsin

❖ Inflammation of the pancreas ranging from a relative mild, self-limiting disorder to rapidly fatal, acute
hemorrhagic pancreatitis
❖ Cause
✔ Alcoholism

✔ Cholecystitis

✔ Surgery involving or near the pancreas

❖ Clinical Manifestation:

● Abdominal Tenderness with back pain

● GI problems, such as nausea, vomiting, diarrhea, and steatorrhea

● Fever

● Jaundice

● Mental confusion

● Flank or umbilical bruising

● Hypotension

● Signs of hypovolemia

● Internal bleeding:

✔ Cullen's sign- bluish discoloration around the umbilicus

✔ Turner's sign- discoloration lateral of the trunk or posteriorly

❖ Diagnostic Tests:

● Elevated amylase

● Lipase

● Increase WBC Levels

● Hypocalcemia

❖ Management:

● Administer prescribed medications, which include opioid or non-opioid analgesics histamine receptor antagonist
proton pump inhibitors
 ● Drug of Choice for pain: Morphine sulfate

● The client should avoid oral intake to inhibit pancreatic stimulation and secretion of pancreatic enzymes

● Maintain fluid and electrolyte balance

● Promote adequate nutrition

CHRONIC PANCREATITIS
❖ Progressive pancreatic inflammation resulting in permanent structural damage to pancreatic tissue

❖ Results from repeated episodes of acute pancreatitis

❖ More than half of chronic pancreatitis cases are associated with alcoholism

❖ Long term alcohol consumption causes hypersecretion of protein in pancreatic secretions, resulting in protein
plugs and calculi within the pancreatic ducts.
❖ Clinical Manifestations:

● Recurring attacks of severe upper abdominal and back pain

● Weight loss

● Steatorrhea

✔ Stools become frequent, frothy, and foul-smelling because of impaired fat digestion, which results in stools with
a high fat content
● Anorexia
 ❖ Assessment and Diagnostics:

● Serum lipase and amylase elevated

● WBC elevated

● Endoscopic retrograde

● Cholangiopancreatography

✔ Detects pancreatic calcification

● Glucose tolerance test values are abnormal

❖ Management:
• Administer prescribed medications, which include pancreatic enzymes,
• Non-opioid pain medications, antacids, histamine receptor antagonist, and proton-pump inhibitors
• Provide symptomatic treatment focusing on relieving pain, promoting comfort, and treating new attacks
• Emphasize the importance of avoiding alcohol, caffeine, and foods that tend to cause abdominal
discomfort
• Manage any endocrine insufficiency such as Diabetes Mellitus, by initiating dietary and insulin or oral
hypoglycemic therapy.
❖ Surgical Management:
• Pancreatic jejunostomy (Roux-en-Y)
✔ Joining of the pancreatic duct to the jejunum.

✔ Allows drainage of the pancreatic duct to the jejunum.

• A Whipple resection (pancreaticoduodenectomy)
✔ Can be carried out to relieve the pain of chronic pancreatitis

PERITONITIS
❖ Inflammation of the peritoneum, the serous membrane lining the abdominal cavity and covering the viscera.

❖ Cause:
• Bacterial infection
• Injury or trauma
• Inflammation that extends from an organ outside the peritoneal area
• Appendicitis
• Perforated ulcer
• Diverticulitis
• Bowel perforation
• Abdominal surgical procedures
• Peritoneal dialysis
❖ Clinical manifestations:
• Diffuse pain, becomes constant localized and more intense on the site of maximal peritoneal irritation
• Muscles become rigid and tender
• Rebound tenderness
• Paralytic ileus
• Anorexia
• Nausea and vomiting
• Pyrexia
• Increased pulse rate
❖ Diagnostic Findings:
• Increase WBC
• Altered levels of Potassium, Sodium and Chloride
• Abdominal Xray- distended bowel loops

❖ Management:
 ● Fluid, colloid, replacement

● Analgesics are prescribed for pain

● Antiemetics

● Intestinal intubation and suction

✔ Relieves abdominal distention and promotes intestinal function

● Oxygen therapy by nasal cannula or mask

● Antibiotic therapy

❖ Surgical Management
 • Removing the infected area
- Excision (ie, appendix)
- Resection (ie, intestine)
• Correcting the cause
- Repair (ie, perforation)
- Drainage (ie, abscess).
❖ Nursing Management
• Positioning the patient for comfort are helpful in decreasing pain
• Patient is placed on the side with knees flexed- decreases tension on the abdominal organs
• Drains are frequently inserted during the surgical procedure.
• Prevent dislodging of the drain