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pneumonia in children

Pneumonia in Children

Pneumonia 

Pneumonia is an inflammation of the lung parenchyma characterized by cough, tachypnea and dyspnea.

The causative agent usually various microorganisms, including bacteria, mycobacteria, fungi, and viruses are introduced into the lungs through  inhalation or from  the blood stream.

pneumonia parenchyma

Causes of Pneumonia

  • Bacterial ; streptococcus pneumoniae, haemophilus influenzae ,mycoplasma pneumoniae, staphylococcus aureus, pseudomonas aeruginosa, klebsiella pneumoniae, Moraxella catarrhalis and legionella spp.
  • Viral; respiratory syncytial viruses, Influenza A and B, adeno viruses, parainfluenza virus etc.
  • Fungal; Histoplasma capsulatum, coccidioides immitis, pneumocystis jirovecii or cryptococcus neoformans.

Classifications of Pneumonia.

Classification is according to;

  1. Etiology
  2. Anatomical
  3. Duration
  4. Clinical grounds
1. Etiologic classification
  1. Infective pneumonia:

    –Viral pneumonia e.g Influenza A virus   –Bacterial pneumonia e.g S. Pneumonia   –Fungal pneumonia -Tuberculous pneumonia e.g M.TB

  2. Non Infective pneumonia: causes;  –Toxins  –Chemicals e.g. paraffin and vomitus   –Radiotherapy  –Allergic mechanisms
2.  Anatomical   
  1. Lobar pneumonia – Inflammation is localized on one or more lung lobes
  2. Bronchopneumonia – Pneumonia with inflammation of bronchi and bronchioles –Inflammation is diffuse and primarily affects lobules of the lung.
  3. Interstitial pneumonia – Pneumonia with inflammation of the lung interstitial tissue.
3.  Duration
  1. Acute pneumonia: Type of pneumonia that lasts only for a few days to and not more than two weeks.
  2. Chronic Pneumonia: –Lasts for more than two weeks.  –Common in Immune Suppressed  patients – TB is most common.
4. Clinical Grounds

Pneumonia is classified as:

1.  Community-acquired pneumonia (CAP):

  • CAP occurs either in the community setting or within the first 48 hours after hospitalization. The causative agents include streptococcus pneumoniae, H. influenza, Legionella, and Pseudomonas aeruginosa.
  • Pneumonia is the most common cause of CAP in people younger than 60 years of age.
  • Viruses are the most common cause of pneumonia in infants and children.

2.  Hospital acquired (Nosocomial pneumonia): 

  • Hospital Acquired Pneumonia is also called nosocomial pneumonia and 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.
  • HAP is the most harmful nosocomial infection and the leading cause of death in patients with such infections.
  • Common microorganisms that are responsible for HAP include Enterobacter species,  Escherichia coli, influenza, Klebsiella species, Proteus, Serratia marcescens,  S. aureus, and S. pneumonia.

3. Aspiration pneumonia:

  • Aspiration pneumonia refers to the pulmonary consequences resulting from entry of endogenous or exogenous substances into the lower airway.
  • The most common form of aspiration pneumonia is a bacterial infection from aspiration of bacteria that normally reside in the upper airways.
  • Aspiration pneumonia may occur in the community or hospital setting.
  • Common pathogens are S. pneumonia, H.influenza, andS. aureus.

4. Pneumonia in immunocompromised patients

  • Pneumonia in immunocompromised patients includes Pneumocystis pneumonia, fungal pneumonias and Mycobacterium tuberculosis.
  • Patients who are immunocompromised commonly develop pneumonia from organisms of low virulence.
  • Pneumonia in immunocompromised patients may be caused by the organisms also observed in HAP and CAP.

5. Primary or secondary pneumonia

  1. Primary pneumonia: Type that occurs in a previously healthy persons living in community. Its usually lobar pneumonia due to strep pneumoniae.
  2. Secondary pneumonia 
  • Develops in after;
  • History of prior respiratory disease
  • Immunocompromised e.g. AIDs patients
  • Surgical operation thus in post-operative patientts

Pathophysiology of Pneumonia

  • When the infective agents reach the alveoli , they adhere to the walls of bronchi and bronchioles
  • They multiply extracellularly , trigger inflammation and pouring of exudates into the air spaces.
  • WBCs migrates to alveoli, the alveoli become more thick due to filling with exudates (consolidation).
  • Due to inflammation, involved areas are not adequately ventilated, due to increased secretions and edema.
  • This will lead to partial occlusion of alveoli and bronchi causing a decrease in alveolar oxygen content.
  • Venous blood from the affected areas thus returns to the heart without being oxygenated.
  • This will lead to arterial hypoxemia and even death due to interference with gas exchange.

Clinical Features of Pneumonia

  • Fever with chills (Temperature 38-39◦c)
  • Cough (may be absent in neonates and infants) with sputum production in older children
  • Fast breathing (Tachypnea)
  • Nasal flaring (with inspiration, the side of the nostrils flares outwards)
  • Chest indrawing ( it is inward movement of the lower chest wall when the child is breathes in)
  • Altered consciousness
  • Irritability
  • Shortness of breath
  • Grunting respirations
  • Chest in-drawing
  • Stridor
  • Wheezing
  • Crackles
  • Decreased breath sounds

Diagnosis and Investigations

  • History taking. The diagnosis of pneumonia is made through history taking, particularly a recent respiratory tract infection.
  • Physical examination. Mainly, the number of breaths per minute and breath sounds is assessed during physical examination.
  • Chest x-ray. Identifies structural distribution (e.g., lobar, bronchial); may also reveal multiple abscesses/infiltrates, empyema (staphylococcus); scattered or localized infiltration (bacterial); or diffuse/extensive nodular infiltrates (more often viral). In mycoplasma pneumonia, chest x-ray may be clear. 
  • Arterial Blood Gas/pulse oximetry. Abnormalities may be present, depending on extent of lung involvement and underlying lung disease.
  • Gram stain/cultures. Sputum collection; needle aspiration of empyema, pleural, and transtracheal or transthoracic fluids; lung biopsies and blood cultures may be done to recover causative organism. More than one type of organism may be present; common bacteria include Diplococcus pneumoniae, Staphylococcus aureus, a-hemolytic streptococcus, Haemophilus influenzae; cytomegalovirus (CMV). Note: Sputum cultures may not identify all offending organisms. Blood cultures may show transient bacteremia.
  • CBC. Leukocytosis usually present, although a low white blood cell (WBC) count may be present in viral infection, immunosuppressed conditions such as AIDS, and overwhelming bacterial pneumonia. Erythrocyte sedimentation rate (ESR) is elevated.
  • Serologic studies, e.g., viral or Legionella titers, cold agglutinins. Assist in differential diagnosis of specific organism.
  • Pulmonary function studies. Volumes may be decreased (congestion and alveolar collapse); airway pressure may be increased and compliance decreased. Shunting is present (hypoxemia).
  • Electrolytes. Sodium and chloride levels may be low.
  • Bilirubin. May be increased.

Management of Pneumonia

  • Although viruses are major causes of pneumonia in infants and young children, pneumonia should always be considered potentially bacterial and patient treated with antibiotics.
  • Prompt treatment with appropriate antibiotics e.g.
  • Amoxicillin is the antibiotic of first choice in children with no serious pneumonia. In infants under 2 months with severe pneumonia, the first line treatment is a combination of ampicillin (150-200mg/kg/day in divided doses) plus gentamycin (5-6 mg/kg/day) intravenously for 10 days. If penicillin is not available, alternative may be cefotaxime. If child condition does not improve, add cloxacillin.
  • For older children 2 months to 5 years, ceftriaxone is first line treatment or ampicillin plus gentamycin.
  • Fever is treated with paracetamol. Tepid sponging when necessary.
  • Nurse patient in semi-sitting up position of head elevated to aid breathing.
  • In neonates, clear the airway or nasal irrigation with sodium chloride 0.9%
  • Monitoring for increased respiratory distress
  • Assist the patient to cough if unable clear the airway by suction
  • Administer broncho-dilators
  • Oxygen therapy where cyanosis has occurred.
  • Fluid- Promote adequate rehydration. In children with severe respiratory difficulty, place and i.v. line and give 70% of normal maintenance fluids. Resume oral fluids as soon as possible.
  • Well balanced nutrition, may be via NGT. In the absence of severe respiratory difficulty breastfeed on demand.
  • Observations of respiratory rate, temperature, and pulse rate.
  • Hygiene: This should be maintained.
  • Keep the patient warm and dry. Change position of the patient where indicated.
  • Physiotherapy: Chest exercises may be done.

Complications of Pneumonia

  • Bacteria in blood stream( bacteremia)/ sepsis
  • Lung abscesses
  • Empyema
  • Pleural effusion
  • Obstructive airway secretion
  • Shock and respiratory failure
  • Necrotizing pneumonia
  • Chronic lung disease
Nursing Diagnosis
  1. Impaired tissue oxygenation related to inflammatory process in airway passages evidenced by cyanosis
  2. Extreme anxiety related to the frequent life threatening asthmatic attacks evidenced by patient asking many questions
  3. Impaired breathing patterns related to inflammatory process in the lungs evidenced by use of accessory muscles/wheezing.
  4. Altered body temperature related to inflammatory process in the lungs evidenced by a high thermometer reading.
  5. Ineffective airway clearance related to copious tracheobronchial secretions.
  6. Risk for deficient fluid volume related to fever and a rapid respiratory rate.

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Asthma in children

Asthma in Children

ASTHMA

Asthma is a  chronic reversible inflammatory disease of the airways characterized by an obstruction of airflow.

  • Inflammation causes recurrent typical characteristics of recurrent episodes of wheezing(occurs during expiration), breathlessness, chest tightness, and coughing, which respond to treatment with bronchodilators.
  • Many inflammatory mediators play a role; mast cells, eosinophils, T-lymphocytes, macrophages, neutrophils, and epithelial cells.
  • No precise cause but genetic and triggers are associations

Classification of Asthma

Asthma can be divided into;

(a)Intrinsic asthma– when no causative agent can be identified.

(b)Extrinsic or cryptogenic asthma– implying a definite external cause. 

Levels of Asthma

These guidelines were established by the National Institutes of Health so that physicians and pediatricians can determine the extent of your child’s asthma.

1. Intermittent asthma

Asthma is considered intermittent if without treatment any of the following are true:

  • Symptoms (difficulty breathing, wheezing, chest tightness, and coughing):
  • Occur on fewer than 2 days a week.
  • Do not interfere with normal activities.
  • Nighttime symptoms occur on fewer than 2 days a month.

2. Mild persistent asthma

Asthma is considered mild persistent if without treatment any of the following are true:

  • Symptoms occur on more than 2 days a week but do not occur every day.
  • Attacks interfere with daily activities.
  • Nighttime symptoms occur more than twice a month.

3. Moderate persistent asthma

Asthma is considered moderate persistent if without treatment any of the following are true:

  • Symptoms occur daily. Inhaled short-acting asthma medication is used every day.
  • Symptoms interfere with daily activities.
  • Nighttime symptoms occur more than 1 time a week, but do not happen every day

4. Severe persistent asthma

Asthma is considered severe persistent if without treatment any of the following are true:

Symptoms:

  • Occur throughout each day.
  • Severely limit daily physical activities.
  • Nighttime symptoms occur often, sometimes every night
asthma triggers

Etiology/Risk Factors.

Multiple environmental factors and genetic determinants are implicated in the development of asthma.

 These include;

  1. Endogenous factors 

(a) Genetic predisposition; There is familial association of asthma and a high degree of occurrence of asthma in identical twins

(b) Atopy: A form of allergy in which there is a hereditary tendency to develop hypersensitivity reactions like; Hay fever/allergic rhinitis & atopic eczema /dermatitis & asthma. Atopy is due to the genetically determined production of specific IgE antibody, with many patients showing a family history of allergic diseases

        2. Infection and Diseases 

(a) Upper Respiratory Tract viral infections

  • Rhinitis  and Sinusitis
  • Postnasal drip
  • Respiratory syncytial virus infection in infancy
  1.   Drugs like;
  • Beta 2 blockers cause bronchoconstriction
  • ACEI like Captopril

        4.  Environmental Factors.

(a) Air Pollution

  • Air pollutants, such as sulfur dioxide, nitrogen dioxide, diesel particulates
  • Indoor air pollution; Leads to exposure to nitrogen oxides from cooking stoves and exposure to passive cigarette smoke

(b) Allergens;

  • Indoor allergens like cats ,cockroaches house, dust mites often found in pillows, mattresses, furniture, carpets and drapes
  • Outdoor allergens like pollen grains , animal fur
  • All these inhaled allergens are common triggers of asthma

  • Food: e.g. Nuts, chocolate, milk.

(c) Occupational Exposure;

  • Occupational asthma is relatively common
  • Over 200 sensitizing agents have been identified
  • Some chemicals, fungal amylase in wheat flour bakers

(d) Changes in the weather

(e) Irritants like household sprays, paint fumes

(i) Others may include;

  • Strong emotions: e.g. fear, laughing.
  • Exercise or hyperventilation,
  • Temperature and weather changes.
asthma pathophysiology

Pathophysiology of Asthma

Summary

The  pathophysiology in asthma is reversible and airway inflammation leads to airway narrowing.

  • Trigger Factor. When a person is exposed to a trigger, it causes airway inflammation and mast cells are activated.
  • Activation. When the mast cells are activated, it releases several chemicals called mediators.  These chemicals perpetuate the inflammatory response, causing increased blood flow, vasoconstriction, hypersecretion of mucus, the attraction of white blood cells to the area, airway muscle constriction and bronchoconstriction.
  • Narrow Breathing Passages. Acute bronchoconstriction due to allergens results from a release of mediators from mast cells that directly contract the airway.
  • Asthma features: As asthma becomes more persistent, the inflammation progresses and other factors may be involved in the airflow limitation, Signs include wheezing, cough, dyspnea, chest tightness. etc.
Full Pathophysiology Context
  • Exposure to a stimulus –Release of substances from immune cells: mast cells, eosinophils, basophils, neutrophils, and macrophages.
  • The initial step: T-cell activation. Lymphokines are produced which amplify the immune response, notably by the production of IgE antibodies and their induction of allergic reactions.
  • Early-phase reaction: Release of IgE and the activation of cells bearing allergen specific IgE receptors, particularly airway mast cells.
  • The activated cells produce proinflammatory mediators such as histamine, eicosanoids, and reactive oxygen species (ROS). 
  • Some of these substances, such as histamine, adenosine, bradykinin, and major basic protein, are stored in cells as granules.
  • Other substances are formed and immediately released in response to asthmatic stimuli, including lipid mediators derived from arachidonic acid, such as leukotrienes and prostaglandins.
  • Proinflammatory mediators induce contraction of airway smooth muscle, mucus secretion, and vasodilation.
  • Airflow obstruction is caused by inflammatory mediators that induce microvascular leakage and exudation of plasma into the airways.
  • Plasma protein leakage induces a thickened, engorged, and edematous airway wall and a narrowing of the airway lumen.
  • The late-phase reaction occurs 6 to 9 hours after the early-phase reaction and is characterized by recruitment and activation of eosinophils, CD4+ cells, basophils, neutrophils, and macrophages. Adhesive interactions occur among the various cell types.
  • T cells are recruited 24 hours after the early-phase reaction and are thought to play a role in the chronic phase of the response and the enhancement of non-specific bronchial hyper-responsiveness.
  • All of these substances contribute to inflammation of the airway,
    edema and desquamation of the bronchial epithelium, and
    hypertrophy of smooth muscles in the respiratory tract.
    • These chemical mediators also increase the responsiveness of
    smooth muscles and the permeability of bronchioles to
    allergens, infectious agents, mediators of inflammation, and
    other irritants.
    • As a result of these effects, mucus production increases and leads to mucus plugging of the airways, thereby decreasing the ability of the airways to remove noxious substances.
    • As a result, patients develop airway obstruction and must use
    accessory muscles to breathe.
  • Airway obstruction in asthma results from a combination of
    bronchial inflammation, smooth muscle constriction, and obstruction of the lumen with mucus, inflammatory cells, and epithelial debris.
  • Symptoms of obstruction include dyspnea (difficult breathing), coughing, wheezing, headache, tachycardia, syncope, diaphoresis, pallor, and cyanosis

Clinical Manifestations

  Principal symptoms

  • Wheezing attacks
  • Episodic shortness of breath

 Typical symptoms

  •  Wheezing
  • Chest tightness
  • Breathlessness
  • Non-productive cough 

Signs

  • Diaphoresis
  • Tachycardia
  • Widened pulse pressure
  • Hypoxemia
  • Central cyanosis
  • Tachypnoea (RR> 25BPM)
  • Cyanosis
  • Feeble respiratory effort
  • Bradycardia or arrhythmias
  • Hypotension
  • Exhaustion
  • Confusion
  • Coma

Acute severe asthma

  • Respiratory rate ≥ 25/min
  • Heart rate ≥ 110/min
  • Inability to complete sentences in 1 breath

Diagnosis and Investigations

To determine the diagnosis of asthma, the clinician must determine that episodic symptoms of airway obstruction are present.

  • Positive family history. Asthma is a hereditary disease, and can be possibly acquired by any member of the family who has asthma within their clan.

  • Physical Examination:  Auscultation, Wheezing allover the lung, Breathlessness, Cyanosis

  • Diagnostic techniques Chest x-ray ,Blood and sputum tests, Skin tests, CBC

management of asthma

Management of Asthma

Aims

  • Achieve and maintain control of symptoms
  • Prevent asthma exacerbations
  • Maintain pulmonary function as close to the normal as possible (Homeostasis)
  • Avoid adverse effects from asthma medications
  • Prevent development of irreversible airflow limitation
  • Prevent asthma mortality
  • Restore normal or best possible lung function
  • Reduce the risk of severe attacks
  • Enable normal growth to occur in children
  • Minimize absence from school

Step Ladder Management.

  • Step 1: Occasional use of inhaled short-acting β2-adrenoreceptor agonist bronchodilators
  • Step 2: Introduction of regular preventer therapy preferably inhaled corticosteroids-ICS
  • Step 3: Add-on therapy Long-acting β2-agonists (LABAs), such as salmeterol and formoterol.
  • Step 4: Poor control with step 3: addition of a fourth drug eg leukotriene receptor antagonists, theophyllines
  • Step 5: Continuous or frequent use of oral steroids
  • Reassure the patient
  • Keep patient in upright position
  • Oxygen 50-60%

  • Peak Flow Monitoring

    Peak Flow Meter
    • Peak flow meters. Peak flow meters measure the highest airflow during a forced expiration.
    • Daily peak flow monitoring. This is recommended for patients who meet one or more of the following criteria: have moderate or severe persistent asthma, have poor perception of changes in airflow or worsening symptoms, have unexplained response to environmental or occupational exposures, or at the discretion of the clinician or patient.
    • Function. If peak flow monitoring is used, it helps measure asthma severity and, when added to symptom monitoring, indicates the current degree of asthma control.

Pharmacological management

Quick response medicines

  • Bronchodilators
  • Short acting inhaled beta 2 agonists
  • Salbutamol (albuterol), Terbutaline, Levalbuterol, Pirbuterol
  • Anticholinergics (Ipratropium 500mcg)
  • Corticosteroids (Hydrocortisone)

Long term medicines

  • Anti-inflammatory drugs
  • Montelclust/levocetirizine
  • Corticosteroids
  • Bronchodilators
  • Long acting beta 2 agonists
  • Salmeterol, Formoterol
  • Theophylline 5-7mg/kg
Nursing Care after an Acute Attack
  1. Give high flow oxygen to patient to relieve hypoxemia.
  2. Prepare and give the patient a bed in a propped up position to help improve breathing patterns
  3. Start up an IV access for IV drugs
  4. Give IV fluids if the patient is dehydrated and encourage oral fluid intake by patient.
  5. Prepare a fluid balance chart if patient is on IV fluids
  6. Take all patient vitals to monitor response to treatment
  7. Give emergency treatment like nebulized salbutamol or IV aminophylline /hydrocortisone to relieve Difficult in Breathing
  8. Administer all prescribed drugs for the patient and monitor for any Side and effects of drugs

NURSING DIAGNOSIS

  • Impaired breathing patterns related to severe inflammatory process in the lungs evidenced by wheezing
  • Impaired tissue oxygenation related to inflammatory process in airway passages evidenced by cyanosis
  • Extreme anxiety related to the frequent life threatening asthmatic attacks evidenced by patient asking many questions
  • Ineffective airway clearance related to increased production of mucus and bronchospasm evidenced by wheezing and dyspnea
  • Impaired gas exchange related to altered delivery of inspired Oxygen.

Complications of Asthma.

  • Airway infection like bronchiolitis
  • Cor pulmonale; Rheumatic Heart Failure secondary to chronic chest disease
  • Pneumonia
  • Hypoxic respiratory failure in severe disease
  • Atelectasis
  • Pneumonia
  • Status asthmaticus
  • Pneumothorax /Air-leak syndromes (rare)
  • Death

Asthma in Children Read More »

Pericarditis

Pericarditis

Nursing Notes - Inflammatory Diseases of the Heart

PERICARDITIS

Introduction

Pericarditis is the inflammation of the pericardium,
a double-layered sac that encloses the heart and the roots of the great vessels (aorta, pulmonary artery, vena cavae). This sac provides protection, lubrication, and helps to anchor the heart within the chest cavity. When inflamed, the layers of the pericardium can rub against each other, causing characteristic pain and other symptoms.

The Pericardium

The pericardium is a thin, two-layered, fluid-filled sac that covers the outer surface of the heart.(normal volume of the fluid is around 50ml)

  • It also prevents the heart from over-expanding when blood volume increases, which keeps the heart functioning efficiently.
  • It shields the heart from infection or malignancy and contains the heart in the chest wall.
Etiology (Causes) of Pericarditis

Pericarditis can be caused by various factors, with idiopathic (unknown cause) being the most common, often suspected to be viral in origin.

  • Infections:
    • Viral: Most common cause of acute pericarditis (e.g., coxsackievirus, echovirus, influenza, HIV).
    • Bacterial: Less common but more severe (e.g., tuberculosis, staphylococcal, streptococcal).
    • Fungal and Parasitic: Rare, typically in immunocompromised individuals.
  • Autoimmune Diseases: Systemic inflammatory conditions like Systemic Lupus Erythematosus (SLE), rheumatoid arthritis, scleroderma, and inflammatory bowel disease.
  • Myocardial Infarction (Heart Attack):
    • Early Post-MI Pericarditis: Occurs within a few days of a heart attack due to inflammation from myocardial necrosis.
    • Dressler's Syndrome (Post-cardiac Injury Syndrome): An autoimmune reaction occurring weeks to months after a heart attack, cardiac surgery, or trauma.
  • Uremia: Occurs in patients with kidney failure due to the buildup of toxins (uremic pericarditis).
  • Malignancy: Cancer spreading to the pericardium (e.g., lung cancer, breast cancer, lymphoma).
  • Trauma: Injury to the chest or heart, including iatrogenic (due to medical procedures).
  • Radiation Therapy: Can lead to acute or chronic pericarditis.
  • Drugs: Certain medications (e.g., procainamide, hydralazine, isoniazid) can induce drug-induced lupus-like syndromes with pericardial involvement.
  • Metabolic Disorders: Hypothyroidism (myxedema).

    • According to Culprit

    Infectious Pericarditis

    Infections are a common cause, particularly viral, leading to acute pericarditis. Other pathogens are less frequent but can cause more severe disease.

  • Viral: This is the most common cause of acute pericarditis. Viruses directly infect and inflame the pericardium.
    • Common culprits: Coxsackievirus B (most frequent), Adenovirus, Echovirus, Influenza virus (A and B), Parvovirus B19, Herpesviruses (CMV, EBV, VZV), HIV.
    • Mechanism: Direct viral invasion and replication within pericardial cells, triggering an inflammatory response.
  • Bacterial: Less common in developed countries due to widespread antibiotic use, but can be severe, often leading to purulent (pus-filled) pericarditis.
    • Pyogenic (Pus-forming) Bacteria: Staphylococcus aureus, Streptococcus pneumoniae (Pneumococci), other Streptococci.
    • Routes of Infection: Hematogenous spread (from bloodstream, e.g., septicemia), direct extension from adjacent infections (e.g., pneumonia, empyema), or direct inoculation (e.g., cardiac surgery, trauma).
    • Tuberculosis (TB): A significant cause in endemic areas. Tuberculous pericarditis can lead to chronic, constrictive pericarditis.
  • Fungal: Rare, typically seen in immunocompromised individuals.
    • Examples: Histoplasma capsulatum, Candida species, Aspergillus.
  • Parasitic: Extremely rare in most regions, but important in specific geographic areas.
    • Example: Toxoplasma gondii, Entamoeba histolytica (amoebic pericarditis), Echinococcus (hydatid cyst).
    • Non-Infectious Pericarditis

    A significant proportion of pericarditis cases are not caused by direct infection but rather by systemic conditions, injury, or other inflammatory processes.

  • Autoimmune/Inflammatory Diseases: Conditions where the immune system mistakenly attacks the body's own tissues.
    • Systemic Lupus Erythematosus (SLE): Pericarditis is a common manifestation of lupus.
    • Rheumatoid Arthritis (RA): Less common, but can cause pericardial involvement.
    • Scleroderma (Systemic Sclerosis): Can lead to pericardial effusion and thickening.
    • Ankylosing Spondylitis: A chronic inflammatory disease primarily affecting the spine, but can have cardiac manifestations.
    • Inflammatory Bowel Disease (IBD): (Crohn's disease, Ulcerative colitis) can have extra-intestinal manifestations, including pericarditis.
    • Rheumatic Fever: An inflammatory disease that can develop as a complication of untreated streptococcal infection, affecting the heart (rheumatic carditis), joints, brain, and skin. Pericarditis is one component of carditis.
  • Post-Cardiac Injury Syndromes: Inflammatory reactions following damage to the heart or pericardium.
    • Dressler's Syndrome (Post-Myocardial Infarction Syndrome): An immune-mediated inflammation of the pericardium that occurs weeks to months after a myocardial infarction (heart attack).
    • Post-Pericardiotomy Syndrome (PPS): Occurs after cardiac surgery (e.g., bypass surgery, valve replacement, pacemaker insertion) due to inflammation from surgical trauma.
    • Trauma: Direct chest trauma (e.g., blunt force, penetrating injuries) can cause pericardial injury and inflammation.
  • Metabolic Disorders:
    • Uremia: Occurs in patients with severe kidney failure (end-stage renal disease) due to the accumulation of metabolic toxins that irritate the pericardium. It typically does not respond to anti-inflammatory drugs and requires dialysis.
    • Myxedema (Severe Hypothyroidism): Can lead to pericardial effusion due to increased capillary permeability and fluid retention.
  • Malignancy (Cancer):
    • Metastatic Cancer: Cancer cells can spread to the pericardium from primary tumors (e.g., lung cancer, breast cancer, lymphoma, leukemia, melanoma). This often leads to malignant pericardial effusion.
    • Primary Pericardial Tumors: Very rare (e.g., mesothelioma).
  • Radiation-Induced Pericarditis: Can occur as a complication of radiation therapy to the chest for cancer treatment (e.g., breast cancer, Hodgkin's lymphoma). Can manifest acutely or years after treatment.
  • Acute Myocardial Infarction (MI): Early pericarditis can occur in the first few days after a transmural (ST-elevation) MI due to inflammation over the necrotic myocardial tissue.
  • Aortic Dissection: If an aortic dissection extends into the pericardial sac, it can cause hemopericardium (blood in the pericardial sac) and acute pericarditis-like pain. This is a medical emergency.
  • Drug-Induced Pericarditis: Certain medications can trigger a lupus-like syndrome or direct pericardial inflammation.
    • Examples: Isoniazid, Procainamide, Hydralazine, Phenytoin, Minoxidil, Cyclosporine, Anthracyclines (some chemotherapy drugs).
  • Idiopathic Pericarditis: When no specific cause can be identified despite thorough investigation, it is termed idiopathic. This is the most common diagnosis for acute pericarditis, often presumed to be viral.

    • Pathophysiology of Pericarditis

    • The acute inflammatory response in pericardium can produce either serous or purulent fluid, or a dense fibrinous material. In viral pericarditis, the pericardial fluid is most commonly serous, is of low volume, and resolves spontaneously.
    • Neoplastic, tuberculous, and purulent pericarditis may be associated with large effusions that are exudative, hemorrhagic, and leukocyte filled.
    • Gradual accumulation of large fluid volumes in the pericardium, even up to 250 mL, may not result in significant clinical signs.
    Clinical Manifestations of Pericarditis
  • Beck's triad is a collection of three medical signs associated with acute cardiac tamponade.

    • The signs are:-

    • Low arterial blood pressure
    • Distended neck veins
    • Distant, muffled heart sounds.

    Chest pain symptoms associated with pericarditis can be described as:

    • Sharp and stabbing chest pain (caused by the heart rubbing against the pericardium). May increase with coughing, deep breathing or lying flat.
    • Can be relieved by sitting up and leaning forward .
    • You may also feel the need to bend over or hold your chest to breathe more comfortably.

    Other clinical features include;

    The symptoms of pericarditis can range from mild to severe and may mimic other cardiac conditions. The classic symptoms include:

    1. Chest Pain:
      • Character: Typically sharp, stabbing, or pleuritic (worsens with deep breath, cough, or swallowing). Can also be dull, aching, or pressure-like.
      • Location: Usually substernal (behind the breastbone) or precordial (over the heart), often radiating to the left shoulder, neck, trapezius ridge (shoulder blade area), or back.
      • Aggravating Factors: Worsens with lying flat (supine position), deep inspiration, coughing, swallowing, and sometimes with movement.
      • Relieving Factors: Often eased by sitting up and leaning forward. This position reduces pressure on the inflamed pericardium.
    2. Pericardial Friction Rub: A characteristic scratching, grating, or squeaking sound heard during auscultation of the heart, caused by the inflamed pericardial layers rubbing against each other. It is best heard with the diaphragm of the stethoscope over the left sternal border, with the patient leaning forward and exhaling. This is a highly specific sign.
    3. Dyspnoea (Shortness of Breath): May be due to pleuritic chest pain limiting deep breaths, or in severe cases, due to pericardial effusion leading to cardiac tamponade.
    4. Low-Grade Fever: Common, especially in infectious causes.
    5. Fatigue and Malaise: Generalized symptoms due to the inflammatory process.
    6. Palpitations: Can occur if the inflammation irritates the heart muscle or conductive system.
    7. Cough: May be present due to irritation of the airways or associated pleural inflammation.
    8. Anxiety: Often results from the frightening nature of chest pain and other symptoms.
    Cardinal Signs and Symptoms of Pericarditis (Mnemonics)

    Remember “Friction” (as previously noted) and also consider the more comprehensive "PERICARDITIS" mnemonic for key features:

    • Friction rub pericardial (sounds like a grating, scratching sound), Fever
    • Radiating substernal pain to left shoulder, neck or back
    • Increased pain when in supine position (leaning forward relieves pain)
    • Chest pain that is stabbing (will feel like a heart attack)
    • Trouble breathing when lying down (supine position)
    • Inspiration or coughing makes pain worse
    • Overall feels very sick and weak
    • Noticeable ST segment elevation on ECG (often widespread concave up)

    P.E.R.I.C.A.R.D.I.T.I.S. Mnemonic:

    • Pleuritic chest pain (worsens with breathing)
    • ECG changes (widespread ST elevation, PR depression)
    • Rub (pericardial friction rub)
    • Increased pain with supine position
    • Cough, fever, malaise (flu-like symptoms)
    • Autoimmune disease history
    • Radiation to trapezius ridge (classic finding)
    • Difficulty breathing (dyspnoea)
    • Increased pain with inspiration
    • Treatment with NSAIDs (often effective)
    • Idiopathic or Infectious cause (viral most common)
    • Sitting up and leaning forward relieves pain
    Types of Pericarditis

    Pericarditis is classified based on its temporal course and characteristics:

    1. Acute Pericarditis:
      • Onset: Sudden and rapid.
      • Duration: Typically resolves within 3 weeks.
      • Characteristics: Often associated with severe chest pain and a pericardial friction rub. Usually self-limiting, but can recur.
      • Common Causes: Viral infections, idiopathic.
    2. Incessant Pericarditis:
      • Duration: Lasts for more than 4-6 weeks but less than 3 months, with continuous presence of symptoms and signs without remission.
      • Characteristics: Symptoms persist despite initial treatment, indicating ongoing inflammation.
    3. Recurrent Pericarditis:
      • Onset: Occurs after a symptom-free interval of at least 4-6 weeks following an acute episode.
      • Characteristics: Can be very distressing for patients, with repeated episodes of chest pain and inflammation. Often requires long-term management.
      • Causes: Often idiopathic, but can be associated with autoimmune conditions.
    4. Chronic Pericarditis:
      • Duration: Develops slowly and lasts for more than 3 months.
      • Characteristics: Can lead to pericardial thickening and fibrosis, potentially progressing to more serious conditions like constrictive pericarditis. Symptoms may be less acute but persistent.
    5. Constrictive Pericarditis:
      • Nature: A serious complication of chronic pericarditis where the pericardium becomes thick, rigid, and fibrotic.
      • Mechanism: This hardened sac restricts the heart's ability to expand and fill with blood properly during diastole.
      • Consequences: Leads to impaired cardiac filling, elevated venous pressures, and symptoms of right-sided heart failure (e.g., severe edema, ascites, jugular venous distension).
    Investigations for Pericarditis

    Diagnosing pericarditis involves a combination of clinical assessment, specific tests to confirm inflammation, identify the cause, and assess for complications.

    Medical History and Physical Exam:
    • History: Detailed inquiry about chest pain characteristics (onset, location, radiation, aggravating/relieving factors), fever, recent infections, autoimmune conditions, trauma, medications, and travel history.
    • Physical Exam:
      • Pericardial Friction Rub: The hallmark sign, a scratching or squeaking sound best heard with the diaphragm of the stethoscope over the left sternal border, with the patient leaning forward and holding their breath in expiration.
      • Signs of Pericardial Effusion/Tamponade: Muffled heart sounds, pulsus paradoxus, jugular venous distension, hypotension (late signs).
      • Signs of Systemic Disease: Rash, joint swelling (suggesting autoimmune disease).
    Electrocardiography (ECG):
    • Classic Findings: Widespread ST-segment elevation (concave upwards) in most leads (unlike MI, which is localized and convex), and PR-segment depression (especially in leads II, aVF, V5, V6). These changes reflect inflammation of the epicardium.
    • Evolution: ECG changes typically evolve over days to weeks, from ST elevation to T-wave inversion, then normalization.
    Echocardiography (Echo):
    • Purpose: The most important imaging test. It is essential for assessing for pericardial effusion (fluid around the heart) and its hemodynamic significance (e.g., signs of cardiac tamponade).
    • Information Provided: Can visualize the pericardium, quantify effusion size, assess cardiac chamber size and function, and identify signs of cardiac tamponade (e.g., right ventricular diastolic collapse, paradoxical septal motion).
    Cardiac CT scan/MRI:
    • Cardiac Computed Tomography (CT): Useful for visualizing pericardial thickening, calcification (in constrictive pericarditis), and large effusions. Can help differentiate pericardial disease from myocardial disease.
    • Cardiovascular Magnetic Resonance Imaging (MRI): Provides excellent soft tissue characterization. It is the gold standard for detecting pericardial inflammation, edema, and fibrosis. Can also differentiate constrictive pericarditis from restrictive cardiomyopathy.
    Blood Tests:
    • Inflammatory Markers:
      • C-reactive protein (CRP): Usually elevated and helps confirm inflammation. Serial CRP levels can monitor disease activity and response to treatment.
      • Erythrocyte Sedimentation Rate (ESR): Also typically elevated, another general marker of inflammation.
    • Cardiac Biomarkers:
      • Troponin (I or T): May be mildly elevated in pericarditis if there is associated myocardial inflammation (myopericarditis), indicating some degree of myocardial cell injury. Higher levels raise suspicion for myocarditis or myocardial infarction.
      • CK-MB and Myoglobin: Less specific than troponin for cardiac injury, but may be checked.
    • Infectious Workup: Depending on clinical suspicion, tests for specific pathogens:
      • Viral Serology: (e.g., Coxsackievirus antibodies) may be done but often not helpful for acute management.
      • Bacterial Cultures: Blood cultures if sepsis is suspected. Pericardial fluid culture if pericardiocentesis is performed.
      • TB Tests: Tuberculin skin test (PPD), interferon-gamma release assays (IGRAs), and acid-fast bacilli (AFB) stains/cultures on pericardial fluid.
    • Autoimmune Markers:
      • Antinuclear Antibodies (ANA), Rheumatoid Factor (RF), Anti-dsDNA: If autoimmune disease is suspected.
    • Renal Function Tests:
      • Blood Urea Nitrogen (BUN) and Creatinine: To assess for uremia in patients with kidney disease.
    Radionuclide Scanning (e.g., PET scan): May be used in complex cases to detect areas of active inflammation or malignancy, particularly if other tests are inconclusive.
  • Pericardiocentesis and Pericardial Biopsy:
    • Pericardiocentesis: A procedure to drain fluid from the pericardial sac. Indicated for large effusions, signs of cardiac tamponade, or for diagnostic purposes (e.g., to analyze fluid for infection, malignancy, or specific inflammatory markers).
    • Pericardial Biopsy: Rarely performed, but may be considered in cases of chronic or recurrent pericarditis with an unknown etiology, or suspicion of specific infiltrative diseases.

    • Nursing Interventions and Management of Pericarditis

    Nursing care for patients with pericarditis focuses on pain management, monitoring for complications, providing emotional support, and patient education.

    General Principles of Management
    • Goal: Relieve pain, reduce inflammation, prevent complications (e.g., cardiac tamponade, constrictive pericarditis), and treat the underlying cause.
    • Setting: Mild cases may be managed outpatient, while moderate to severe cases, or those with complications, require hospitalization.
    Management for Mild Pericarditis

    Patients with mild, uncomplicated pericarditis often respond well to conservative measures and oral medications.

    Pain Assessment and Management:
    • Assess Patient’s Pain: Characterize the pain (sharp, stabbing, dull), location, radiation, and aggravating/relieving factors. Use a pain scale (e.g., 0-10) to quantify severity. Pericarditis pain can be excruciatingly painful.
    • Positioning for Pain Relief: Keep patient in a high Fowler’s position (sitting upright) or encourage leaning forward. Avoid a supine (lying flat) position, as it exacerbates pericardial pain by increasing pressure on the inflamed pericardium.
    Monitoring for Complications (e.g., Cardiac Tamponade):
    • Constant Vigilance: Cardiac tamponade is a life-threatening complication that requires immediate recognition and intervention.
    • Key Signs to Monitor (Beck's Triad):
      • Muffled or Distant Heart Sounds: Due to fluid buildup around the heart.
      • Jugular Venous Distension (JVD) with Clear Lungs: Increased pressure in the right atrium due to restricted filling, but without pulmonary congestion typical of heart failure.
      • Hypotension: Decreased cardiac output due to compression of the heart.
    • Pulsus Paradoxus: A significant (typically >10 mmHg) drop in systolic blood pressure during inspiration. This is a classic sign of cardiac tamponade and severe restrictive filling.
    • Tachycardia: The heart attempts to compensate for reduced cardiac output by increasing its rate.
    • Other Signs: Narrowed pulse pressure, decreased urine output, cool extremities, altered mental status (signs of decreased perfusion).
    Administer Medications as Prescribed by Physician:
    • First-line Therapy:
      • High-dose Aspirin: Often used, especially for post-MI pericarditis. It has both anti-inflammatory and anti-platelet effects.
      • NSAIDs (Nonsteroidal Anti-Inflammatory Drugs): Such as Ibuprofen, Indomethacin. These are the cornerstone of treatment for acute pericarditis.
        • Nursing Considerations: Administer with food or milk to minimize gastrointestinal (GI) upset. Monitor for GI bleeding (e.g., black, tarry stools; coffee-ground emesis). Advise patients to take with a full glass of water.
    • Colchicine: An anti-inflammatory agent that works by inhibiting microtubule assembly, reducing inflammation. It is increasingly used as first-line therapy or in combination with NSAIDs, and is particularly effective in preventing recurrence.
      • Nursing Considerations: Do not take with grapefruit juice as it increases colchicine toxicity (nausea, vomiting, abdominal pain, diarrhea). Can be taken with or without food. Monitor for GI side effects.
    • Corticosteroids: Such as Prednisone. Reserved for patients who do not respond to NSAIDs/Colchicine, have contraindications to them, or have specific etiologies (e.g., autoimmune).
      • Nursing Considerations: Administer with food. Monitor for side effects (e.g., hyperglycemia, increased infection risk, fluid retention, mood changes). Taper slowly to prevent rebound inflammation.
    • IV Antibiotics: Administered if bacterial pericarditis is diagnosed or strongly suspected. Based on culture and sensitivity results.
    Management for Moderate to Severe Pericarditis / Hospitalized Patients

    These patients require more intensive monitoring and often invasive procedures.

    Comprehensive Assessment:
    • Establish Good Rapport: Essential for building trust and reducing patient anxiety.
    • Detailed History Taking: Include smoking history, anginal pain characteristics (differentiate from pericardial pain), and other presenting symptoms.
    • Continuous Observations: Monitor vital signs (temperature, pulse, respiration, blood pressure) frequently. Perform a thorough general examination, including cardiovascular, respiratory, and peripheral assessments.
    Pain Management Intensified:
    • Positioning: Continue to keep the patient in high Fowler’s position or encourage leaning forward to relieve pain.
    • Pain Level Monitoring: Continuously monitor patient pain level using a standardized scale and evaluate the effectiveness of analgesics within 30 minutes of administration.
    • Administer Prescribed Pain Medication: May include stronger analgesics such as morphine or other opioids if NSAIDs are insufficient.
    Intensive Cardiac Monitoring:
    • Monitor for Cardiac Tamponade: Hourly or more frequent assessment for signs of cardiac tamponade (pulsus paradoxus, JVD, muffled heart sounds, hypotension, tachycardia). Notify physician immediately if signs develop.
    • Continuous ECG Monitoring: To detect arrhythmias or worsening ST-T changes.
    Fluid Balance and Hemodynamic Support:
    • Careful Maintenance of Fluid Intake and Output (I&O): Essential, especially if there's a risk of fluid overload or if diuretics are used.
    • Daily Weight Check: To monitor for fluid retention.
    • Administer O2: Maintain SpO2 >90% to optimize oxygen delivery to tissues.
    • IV Antihypertensive Medication: If persistent blood pressure elevation is a concern (though hypotension is more common with tamponade).
  • Medication Administration and Monitoring:
    • Administer NSAIDs and Steroids with Food: To reduce GI side effects.
    • Ensure Timely Administration of Antibiotics: If bacterial infection is the cause.
    Patient Education and Psychological Support:
    • Disease Process Discussion: Explain pericarditis, its causes, and signs/symptoms. Reassure the patient that the chest pain is not a myocardial infarction (unless it is a co-existing condition).
    • Anxiety Reduction: Build a strong rapport with the patient to reduce anxiety associated with chest pain and hospitalization.
    • Preparation for Procedures: If surgical intervention (e.g., pericardiocentesis, pericardiectomy) is needed, provide psychological support and prepare the patient for the procedure.
    • Post-Surgical Education: For post-surgical patients, discuss warning signs of postoperative complications such as fever, inflammation at the surgical site, bleeding, and excessive swelling.
    • Activity Progression: Advise the patient to resume daily activities slowly and gradually to prevent symptom recurrence. Ensure bed rest until fever, chest pain, and friction rub disappear.
    • Warning Signs for Home: Educate on when to seek medical attention after discharge (e.g., recurrent chest pain, fever, increasing shortness of breath, swelling).
    Bowel and Bladder Care:
    • Provide a Bedside Commode: To reduce stress on the heart during defecation, especially if patient is on strict bed rest.
    • Assist with Bathing if Necessary: To conserve patient energy.
  • Monitoring for Specific Complications (less common but severe):
    • Persistent Cough, Vomiting, or Systolic BP >180 mmHg: Closely monitor and notify physician immediately, as these may increase risk for specific complications (e.g., hemorrhage in aortic dissection if not carefully managed).

    • Nursing Interventions for Pericarditis

    Nursing care for patients with pericarditis is crucial for symptom management, monitoring for complications, providing emotional support, and educating the patient and family. The following is a comprehensive list of nursing interventions:

    1. Pain Management and Comfort:
      • Assess the patient’s pain level regularly using a standardized pain scale (e.g., 0-10) and document findings.
      • Evaluate the effectiveness of administered analgesics (e.g., NSAIDs, aspirin, colchicine, opioids) within 30 minutes to 1 hour of administration.
      • Administer prescribed pain medication promptly and on schedule to maintain comfort.
      • Position the patient comfortably, typically in a high Fowler’s position (sitting upright) or leaning forward, as this position significantly alleviates pericardial chest pain. Avoid supine (lying flat) positioning.
      • Provide non-pharmacological pain relief measures, such as guided imagery, distraction, or quiet environment, as appropriate.
    2. Vital Signs and Hemodynamic Monitoring:
      • Monitor vital signs (temperature, pulse, respiration, blood pressure) frequently and continuously, especially during the acute phase or if complications are suspected.
      • Continuously monitor the patient's electrocardiogram (ECG) for rhythm disturbances, ST-T wave changes, or PR segment depression characteristic of pericarditis.
      • Assess for signs and symptoms of cardiac tamponade (e.g., muffled heart sounds, jugular venous distension [JVD] with clear lung sounds, hypotension, pulsus paradoxus [a significant drop in systolic BP during inspiration], tachycardia, narrowed pulse pressure) at least every 4-8 hours and as needed (PRN). Report any changes immediately to the physician.
      • Monitor for signs of decreased cardiac output and perfusion (e.g., cool extremities, decreased urine output, altered mental status).
      • Administer supplemental oxygen as prescribed to maintain oxygen saturation (SpO2) above 90% or as per target.
    3. Medication Administration and Monitoring:
      • Administer all prescribed medications (e.g., NSAIDs, colchicine, corticosteroids, antibiotics) as ordered, ensuring correct dosage, route, and timing.
      • Administer NSAIDs and corticosteroids with food or milk to minimize gastrointestinal irritation and reduce the risk of peptic ulcers.
      • Educate the patient about each medication, its purpose, potential side effects, and the importance of adherence.
      • Monitor for adverse effects of medications (e.g., GI bleeding with NSAIDs, hyperglycemia with corticosteroids, diarrhea with colchicine).
      • If antibiotics are prescribed, ensure timely administration and monitor for signs of infection resolution.
    4. Fluid Balance and Nutritional Support:
      • Maintain accurate intake and output (I&O) records, especially if the patient has a pericardial effusion or is receiving diuretics.
      • Monitor daily weights to assess for fluid retention or dehydration.
      • Encourage adequate oral fluid intake unless contraindicated.
      • Provide a diet that is easily digestible and well-tolerated. Assist with feeding if the patient is too weak or fatigued.
    5. Activity and Rest:
      • Ensure the patient has adequate bed rest during the acute inflammatory phase, usually until fever, chest pain, and pericardial friction rub have resolved.
      • Assist the patient with activities of daily living (ADLs) as needed to conserve energy and reduce cardiac workload.
      • Provide a bedside commode to reduce straining during bowel movements, which can increase intrathoracic pressure.
      • Educate the patient on the importance of gradual resumption of physical activity after the acute phase, advising avoidance of strenuous activities for several weeks to months to prevent recurrence.
    6. Patient Education and Psychological Support:
      • Explain the disease process of pericarditis, its causes, symptoms, and the rationale behind the treatment plan to the patient and family.
      • Reassure the patient that the chest pain, although severe, is typically not indicative of a myocardial infarction (heart attack), which can alleviate significant anxiety.
      • Build a trusting and empathetic rapport with the patient to reduce anxiety and promote open communication.
      • Provide psychological support, acknowledging the patient's fears and concerns related to chest pain and their condition.
      • If pericardiocentesis or other procedures are anticipated, explain the procedure clearly, address patient questions, and provide emotional support before, during, and after.
      • For post-surgical patients (e.g., after pericardiectomy or creation of a pericardial window), educate on warning signs of postoperative complications such as fever, signs of infection at the surgical site, unusual bleeding, or excessive swelling.
      • Educate the patient on warning signs of recurrence (e.g., return of chest pain, fever) and when to seek medical attention after discharge.
      • Discuss the importance of medication adherence, follow-up appointments, and lifestyle modifications.
    7. Monitoring for Other Complications:
      • Closely monitor for and report persistent cough, vomiting, or significant changes in blood pressure (e.g., systolic BP >180 mmHg), as these may indicate other underlying issues or increase the risk for certain complications.
      • Assess for signs of chronic or constrictive pericarditis in patients with recurrent or persistent symptoms (e.g., persistent JVD, ascites, peripheral edema, Kussmaul's sign).

    Nursing Diagnoses for Pericarditis

    Nursing diagnoses provide a framework for nursing care, identifying patient problems that nurses can independently address. For pericarditis, these diagnoses often revolve around pain, inflammation, potential cardiac complications, and the psychological impact of the illness. Here are several common and relevant nursing diagnoses, with supporting evidence:

    1. Acute Pain related to inflammatory process of the pericardium as evidenced by:
      • Verbalization of severe chest pain (e.g., "10 out of 10," sharp, stabbing, precordial pain radiating to neck/shoulder).
      • Facial grimacing, guarding behavior (e.g., clutching chest), restlessness.
      • Increased heart rate and blood pressure (unless in tamponade, where BP may drop).
      • Pain exacerbated by deep breathing, coughing, lying supine, or movement.
      • Pain relieved by leaning forward.
      • Shortness of breath (due to pain and/or effusion).

      Rationale: The hallmark of acute pericarditis is severe, often pleuritic, chest pain caused by the inflammation and irritation of the pericardial layers. This pain significantly impacts comfort and can trigger sympathetic responses.

    2. Hyperthermia related to inflammatory process (e.g., infection, autoimmune response) as evidenced by:
      • Body temperature above normal range (e.g., 38.0°C or higher).
      • Flushed skin, warm to touch.
      • Increased heart rate and respiratory rate.
      • Profuse sweating and/or chills.
      • Malaise and generalized weakness.

      Rationale: Inflammation, particularly if infectious (e.g., bacterial, viral), often leads to a systemic febrile response as the body attempts to combat the underlying cause and inflammatory mediators are released.

    3. Decreased Cardiac Output related to impaired ventricular filling due to pericardial inflammation and/or effusion as evidenced by:
      • Fatigue, weakness, and generalized malaise.
      • Inability to perform usual Activities of Daily Living (ADLs) or requiring increased rest.
      • Shortness of breath, dyspnea on exertion, or orthopnea.
      • Tachycardia (compensatory mechanism).
      • Hypotension (especially with significant effusion/tamponade).
      • Weak or thready peripheral pulses.
      • Cool, clammy skin.
      • Delayed capillary refill.
      • Decreased urine output.
      • Altered mental status (in severe cases).
      • Abnormal hemodynamic readings (e.g., low cardiac index, elevated central venous pressure).

      Rationale: Inflammation of the pericardium can lead to fluid accumulation (effusion) or thickening/constriction, both of which can impede the heart's ability to fill adequately, thereby reducing the amount of blood pumped out to the body.

    4. Activity Intolerance related to acute chest pain, decreased cardiac output, and systemic inflammation as evidenced by:
      • Verbalization of fatigue, tiredness, or weakness after minimal exertion.
      • Dyspnea on exertion.
      • Disinterest or inability to participate in activities of daily living (ADLs) due to pain or fatigue.
      • Reported need for increased rest periods.
      • Changes in vital signs (e.g., increased heart rate, respiratory rate, or blood pressure) with activity.

      Rationale: The pain associated with pericarditis makes movement difficult, and the systemic inflammatory response, coupled with potentially decreased cardiac output, reduces the patient's physiological reserve for physical activity.

    5. Excessive anxiety related to chest pain of unknown etiology (initially), fear of serious cardiac event (e.g., heart attack), or threat to health status as evidenced by:
      • Verbalization of feeling nervous, fearful, worried, or helpless.
      • Increased heart rate and respiratory rate (beyond that caused by pain/fever).
      • Restlessness, agitation, or irritability.
      • Crying or tearfulness.
      • Sleep disturbances.
      • Questioning about the prognosis or cause of illness.
      • Preoccupation with symptoms.

      Rationale: Chest pain is often associated with myocardial infarction, leading to significant anxiety for patients. The uncertainty of the diagnosis, the severity of symptoms, and the potential for complications can further exacerbate anxiety.

    6. Risk for Ineffective Health Management related to insufficient knowledge of the disease process, treatment regimen, and potential for recurrence as evidenced by:
      • (No subjective/objective data yet, as it's a risk diagnosis, but factors include:)
        • Lack of previous experience with pericarditis.
        • Complex medication regimen (e.g., multiple anti-inflammatory drugs).
        • Need for activity restrictions.
        • Potential for recurrent episodes.

      Rationale: Patients need comprehensive education on their condition, medications, symptom recognition, and activity modifications to prevent recurrence and manage the disease effectively post-discharge.

    7. Risk for Fluid Volume Deficit (in specific cases, e.g., if experiencing excessive sweating due to fever and inadequate fluid intake, or with aggressive diuretic therapy) related to:
      • Fever-induced diaphoresis.
      • Nausea/vomiting impacting oral intake.
      • Aggressive diuretic therapy for effusion management.

      Rationale: While fluid overload is a concern with effusions, certain interventions or symptoms can lead to dehydration, necessitating careful fluid balance monitoring.

    8. Risk for Impaired Gas Exchange (in cases of significant pericardial effusion leading to lung compression or severe cardiac compromise) related to:
      • Decreased lung expansion due to large pericardial effusion.
      • Reduced cardiac output impacting pulmonary perfusion.

      Rationale: While not a primary diagnosis for all pericarditis, a very large effusion can restrict lung expansion, and severe cardiac compromise can lead to ventilation-perfusion mismatch.

    9. Risk for Infection (post-procedural) related to invasive procedures (e.g., pericardiocentesis, pericardiectomy) as evidenced by:
      • Presence of surgical incision or puncture site.
      • Disruption of skin integrity.
      • Invasive lines (e.g., IV, drain).

      Rationale: Any break in skin integrity or invasive procedure introduces a risk of localized or systemic infection.

    Complications of Pericarditis

    While most cases of acute pericarditis are benign and self-limiting, complications can occur, ranging from mild to life-threatening.

    1. Pericardial Effusion:
      • Description: Accumulation of excess fluid within the pericardial sac. It is a common complication.
      • Severity: Can range from small and asymptomatic to large and rapidly accumulating, which can lead to cardiac tamponade.
    2. Cardiac Tamponade:
      • Description: A medical emergency where a large or rapidly accumulating pericardial effusion compresses the heart, severely restricting its ability to fill with blood during diastole.
      • Consequences: Leads to a significant decrease in cardiac output, hypotension, and shock if not treated promptly.
      • Treatment: Requires urgent pericardiocentesis (fluid drainage) or surgical drainage.
    3. Recurrent Pericarditis:
      • Description: Episodes of pericarditis that recur after a symptom-free interval following an initial acute episode. This can be very distressing for patients.
      • Management: Often requires long-term anti-inflammatory therapy, sometimes with colchicine.
    4. Chronic Pericarditis:
      • Description: Pericarditis that persists for more than 3 months. Can lead to thickening and fibrosis of the pericardium.
    5. Constrictive Pericarditis:
      • Description: A severe, long-term complication where the pericardium becomes thick, rigid, and fibrotic, preventing the heart from filling properly.
      • Consequences: Leads to symptoms of right-sided heart failure (e.g., severe peripheral edema, ascites, elevated JVD) and can be progressive.
      • Treatment: Often requires surgical pericardiectomy (removal of the pericardium).
    6. Myocarditis (Myopericarditis):
      • Description: Inflammation of the heart muscle occurring concurrently with pericarditis.
      • Consequences: Can lead to myocardial dysfunction, arrhythmias, and elevated cardiac biomarkers (e.g., troponin).
    7. Fatal Hemorrhage:
      • Context: This is a very rare but catastrophic complication, typically associated with traumatic pericardial injury, iatrogenic injury during procedures (e.g., central line insertion, pericardiocentesis), or rupture of a large vessel (e.g., aortic dissection) into the pericardial sac.
    8. Stroke and Paraplegia due to Interruption of the Anterior Spinal Artery, Abdominal Ischemia:
      • Context: These are not direct complications of typical pericarditis. They are severe complications specifically associated with Aortic Dissection, especially if it involves the great vessels originating from the aorta or compromises blood supply to the spinal cord or abdominal organs. If an aortic dissection leads to hemopericardium, it can mimic pericarditis. It's crucial to differentiate these conditions due to the vastly different prognoses and emergency management required for aortic dissection.

    Pericarditis Read More »

    Rheumatic Heart Disease

    Rheumatic Heart Disease

    Rheumatic Heart Disease

    Rheumatic heart disease is  a condition in which the heart valves have been permanently damaged by rheumatic fever.

    Rheumatic Heart Disease can also be defined as a chronic stage of Rheumatic Fever involving all the layers of the heart causing major cardiac sequelae

    So what is Rheumatic Fever?

    Rheumatic Fever is an autoimmune, systemic, post-streptococcal, inflammatory disease, principally affecting the heart, joints, central nervous system, skin and subcutaneous tissues.

    ‘rheumatism licks the joint, 
but bites the whole heart’.

    Causes/Etiology of Rheumatic Heart Disease

    • Infection: The heart damage may start shortly after untreated streptococcal throat infection referred to as strep throat or scarlet fever. The disease is caused by rheumatic fever and the bacteria responsible is group A beta-hemolytic streptococci. (Streptococcus pyogenes).

    >  The heart valve can be inflamed  and become scarred  over time.
    >  This can result in narrowing  or leaking (regurgitation) of the heart valve making it harder for the heart to function normally. 
     > The commonest valves affected are the mitral valve and the aortic valve however all 4 valves may be affected.  This may take years to develop and can result to heart failure.

    rheumatic heart disease

    Heart Valves

    Pathophysiology of Rheumatic Heart Disease.

    Causative agent (Group A Beta hemolytic streptococci) causing Strep throat, untreated strep throat infection leads to rheumatic fever several weeks after a sore throat has resolved (only infections of the pharynx have been shown to initiate or reactivate rheumatic fever.

    Severe scarring of the valves develops during a period of months to years after an episode of  rheumatic fever, and recurrent episodes may cause progressive damage to the heart valves. The mitral valve is affected most commonly and severely (65-70% of patients) followed by aortic valve. This eventually can lead to heart failure.

    Clinical features of Rheumatic Fever.

    • Fever (39 degrees Celcius)
    • Swollen, tender, red and extremely painful joint –particularly the knees and ankles. (Migrating Poly arthritis)
    • Nodules (lumps under the skin)
    • Shortness of breath and chest discomfort. Uncontrolled movement of arms, legs or facial muscle
    • General weakness
    • Carditis presenting with chest pain, dyspnea, palpitations, 

    Clinical features of Rheumatic Heart Disease.

    • Carditis: Carditis can involve the pericardium (pericarditis), myocardium (myocarditis), and endocardium (endocarditis) /
    • Polyarthritis: Acute pain and swelling in the joints, starting with one joint and onto the other(migratory polyarthritis),less often in kids.
    • Chorea: involuntary, irregular, unpredictable muscle movement
    • Erythema marginatum:  A long-lasting reddish rash that begins on the trunk or arms as macules, which spread outward and clear in the middle to form rings, which continue to spread and coalesce with other rings, ultimately taking on a snake-like appearance
    • Subcutaneous nodules:  Painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees

    Diagnosis of Rheumatic Heart Disease

    • People with rheumatic heart disease will have or recently had strep throat infection ( throat culture / blood test may be used to check for streptococcus)
    • The patient may have the murmurs or rub that may  be heard during auscultation this may be due to blood leaking around the damaged valves
    • Along with complete medical history and physical examination, test to diagnosed rheumatic  heart disease may include:

    • Echocardiogram (cardiac echo).

      >  Electrocardiogram (ECG): valve insufficiency and ventricular dysfunction. are observed in patients with rheumatic heard disease.

      >  Cardiac MRI and Chest Radiography: Cardiomegaly, pulmonary congestion, and other findings consistent with heart failure may be observed on chest radiograph in individuals with rheumatic fever.

      >  Blood test:  C-reactive protein and erythrocyte sedimentation rate are elevated in individuals with rheumatic fever due to the inflammatory nature of the disease

    RHEUMATIC

    Modified JONES criteria guideline for the diagnosis of Rheumatic Heart Disease.

    (A)  Major  criteria

     Major criteria is a Jones criteria 

    • J – Joint involvement which is usually migratory and inflammatory joint involvement that starts in the lower joints and ascends to upper joints
    • O – (“O” Looks like heart shape) – indicating that patients can develop myocarditis or inflammation of the heart
    • N – Nodules that are subcutaneous
    • E – Erythema marginatum which is a rash of ring-like lesions that can start in the trunk or arms. When joined with other rings, it can create a snake-like appearance
    • S – Sydenham chorea is a late feature which is characterized by jerky, uncontrollable, and purposeless movements resembling twitches
    (B)  Minor Criteria

    Minor criteria include

    • C – CRP Increased (C-reactive Protein) High in cases of inflammation. (above 3mg/dl)
    • A – Arthralgia ( Joint pain)
    • F – Fever (> 38.5 degrees Celicius)
    • E – Elevated ESR (inflammation indicative) (>60mm/hr)
    • P – Prolonged PR Interval
    • A – Anamnesis (suggestive of rheumatism)
    • L – Leukocytosis

    Diagnostic

    • Evidence of Group A Streptococcal Infection + 2 major criteria
      or
    • 1 major + 2 minor criteria
    A prolonged PR interval 
    represents a delay in the time it takes for the 
    signal to move across the atria at the top of the heart,
    which receive blood flowing in from the veins, 
    into the ventricles at the bottom of the heart, 
    which pump blood out into the arteries
    (C) Supportive evidence of preceding group A streptococcal infection including;

    Positive throat culture for group A streptococci, raised titers of streptococcal antibodies (ant streptolysin O and S, ant streptokinase), and recent scarlet fever.

    Investigations for rheumatic heart disease

    • Throat swab/ culture.
    • Rapid antigen detection test
    • Anti-streptococcal antibody titers.
    • CBC
    • Physical examination; murmurs? Abnormal rhythms?
    • Chest x-ray may show cardiomegaly, congestion.
    • Echocardiogram/ Doppler echocardiography may show effusion, vulvular dysfunction

    Management of Rheumatic Heart Disease.

    The treatment depends on how much damage has been done to the heart valves. In severe cases, treatment may include surgery to replace or repair the badly damaged valves. The  medical treatment is divided into three parts i.e.

    1.  Prevent and eradicate infection
    2. Maximize cardiac output
    3. Promote comfort

     1.   To prevent and eradicate infection

    ´The best treatment  is to prevent rheumatic fever by giving antibiotic for throat infection and keep rheumatic fever from developing hence prevent damage to the  valves.

    >   i.m benzathine penicillin 0.6-1.2 mu every 4 weeks, the same dose is given every 3 weeks in areas where rheumatic fever is endemic.
    > Note. patients with rheumatic fever and have developed carditis and valve damage should receive antibiotic for at least 10 years or until age of 40 years. Patients who had rheumatic fever without valve damage do not need this prophylaxis.

    2.  To maximize cardiac output

    • Anti-inflammatory. Treatment of the acute inflammatory manifestations of acute rheumatic fever consists of salicylates and steroids; aspirin in anti-inflammatory doses effectively reduces all manifestations of the disease except chorea.
    • Analgesics for pain relief such as Paracetamol are preferred to opioids.
    • Corticosteroids. If moderate to severe carditis is present as indicated by cardiomegaly, third-degree heart block, or Congestive Heart Failure, add orally prednisone to salicylate therapy.
    • Anticonvulsant medications. For severe involuntary movements caused by Sydenham chorea, prescribe an anticonvulsant, such as valproic acid or carbamazepine (Carbatrol, Tegretol, others).
    • Antibiotics. Such as penicillin or erythromycin or another antibiotic to eliminate remaining strep bacteria.
    • Surgical care. When heart failure persists or worsens after aggressive medical therapy for acute Rheumatic Heart Disease, surgery to decrease valve insufficiency may be lifesaving; approximately 40% of patients with acute rheumatic fever subsequently develop mitral stenosis as adults.
    • Diet. Advise nutritious diet without restrictions except in patients with Congestive heart failure, who should follow a fluid-restricted and sodium-restricted diet; potassium supplementation may be necessary because of the mineralocorticoid effect of corticosteroid and the diuretics if used.
    • Activity. Initially, place patients on bed rest, followed by a period of indoor activity before they are permitted to return to school or work; do not allow full activity until the PRs have returned to normal; patients with chorea may require a wheelchair and should be on homebound instruction until the abnormal movements resolve.
    • ACE Inhibitors e.g captopril, enapril, beta blockers e.g. bisoprolol, metoprolol, diuretics and digitalis e.g digoxin.
    • Therapy for congestive heart failure. Heart failure in Rheumatic heart disease probably is related in part to the severe insufficiency of the mitral and aortic valves and in part to pancarditis; therapy traditionally has consisted of an inotropic agent (digitalis) in combination with diuretics (furosemide, spironolactone) and afterload reduction (captopril).

    3.   To promote comfort

    • Patients with arthritic complication are given salicylate e.g. aspirin
    • Encouraged to have bed rest
    • Warm compress on the joints
    • And use of bed cradle to lift the weight of bed linen from the affected joints
    Complications of rheumatic heart disease
    • Heart failure: This occur from either narrowed or leaking heart valve.
    • Bacterial endocarditis .infection of the inner lining of the heart this occur when the rheumatic fever has damaged the heart valves.
    • Raptured heart valves. this is a medical emergency that require urgent surgery to replace or repair the damaged heart valve.
    • Cerebral stroke: this occur when  a piece of vegetation dislodges itself and join circulation to the cerebral vessels.
    • Pulmonary hypertension due to systemic congestion with blood.
    • Atrial fibrillation. happens when abnormal electrical impulses suddenly start firing in the atria. These impulses override the heart’s natural pacemaker, which can no longer control the rhythm of the heart. This causes you to have a highly irregular pulse rate.
    • Infective Endocarditis, pericarditis and myocarditis.
    Nursing Diagnosis
    1. Decreased cardiac output related to valve stenosis as evidenced by shortness of breath, fatigue, dizziness.
    2. Acute pain related to inflammation of synovial membranes as evidenced by patient verbalizing about painful joints.
    3. Hyperthermia related to inflammation of synovial membranes and heart valves as evidenced by a thermometer reading of 38 degrees Celsius.
    4. Activity intolerance related to muscle weakness as evidenced by prolonged bed rest.
    5. Self care deficit related to polyarthritis, therapy, bed rest.
    6. Impaired skin integrity related to skin inflammation as evidenced by subcutaneous nodules and skin rash.
    7. Risk for impaired Gas exchange related to blood accumulation in the lungs due to atrial filling.
    8. Risk for injury related to chorea.
    9. Risk for non-compliance with prophylactic drug therapy related to financial or emotional burden of lifelong therapy.

    Rheumatic Heart Disease Read More »

    Sickle Cell Disease

    Sickle Cell Disease

    Sickle Cell Disease/Sickle Cell Anaemia

    Sickle cell disease is an inherited red-blood cell disorder which causes the body to produce abnormally shaped red blood cells.

    Sickle cell disease is inherited as an autosomal recessive trait. Normal Hb A gets replaced with Abnormal Hb S.

    Children with this disorder have atypical haemoglobin  molecules called haemoglobin S which can distort red blood cells into a sickle or crescent shape.

    sickle cell normal and abnormal

    Red blood cells with normal hemoglobin are smooth, disk-shaped, and flexible, like doughnuts without holes. They can move through the blood vessels easily.

    Cells with sickle cell hemoglobin are stiff and sticky. When they lose their oxygen, they form into the shape of a sickle or crescent, like the letter C.

    These cells stick together and can’t easily move through the blood vessels. This can block small blood vessels and the movement of healthy, normal oxygen-carrying blood. The blockage can cause pain

    Classification of sickle cell disease

    Disease is broadly classified into;

    1.  Sickle Cell Anaemia (Homozygous): Are patients whose Red blood cells only contain abnormal beta chains leading to HbSS (SS). These patients are said to have sickle-cell anaemia and they have S+S of Sickle cell disease. Individuals with sickle cell anaemia inherit two copies of the faulty haemoglobin gene, one from each parent. This is denoted as HbSS or SS. Other names: HbSS, SS disease, Haemoglobin S.

    2. Sickle Cell Trait (Heterozygous): Patients whose Red blood cells contain a mixture of normal beta chains of HbA and abnormal beta chains of HbS. Thus patients have both HbA and HbS (HbAS). Individuals with sickle cell trait inherit one copy of the normal haemoglobin gene and one copy of the faulty haemoglobin gene. This is denoted as HbAS. People with sickle cell trait are usually asymptomatic, meaning they don’t experience the typical symptoms of SCD. They are carriers of the faulty gene and can pass it on to their children.

    To understand Homozygous and Heterozygous,

    SCD (Sickle Cell Disease): Think of this as a house built with a faulty instruction manual. The manual has instructions for building strong, healthy red blood cells (the “bricks” of your blood), but the instructions are messed up. This leads to problems with the shape and function of red blood cells, causing sickle cell disease.

    Autosomal: This refers to the chromosomes that determine most of your traits, except for sex (male or female). Imagine these chromosomes like the foundation of your house.

    Heterozygous: You have two copies of each autosomal chromosome, one from each parent. Imagine you received an instruction manual with good instructions from your mom and a manual with a faulty set from your dad. This means you have a good copy and a faulty copy of the gene that causes sickle cell disease. You are a “carrier” of the faulty gene, but you don’t have SCD.

    Homozygous: You received the same instruction manual from both parents. There are two possibilities:

    • Homozygous dominant: You received two good instruction manuals (from both parents). Your house is built strong and healthy, you don’t have SCD.
    • Homozygous recessive: You received two faulty instruction manuals (from both parents). Your house has serious problems, you have SCD.

    Recessive: A recessive gene only causes a disease when you have two faulty copies (like in the homozygous recessive case). Think of it as needing two faulty instruction manuals to build a house with problems.

    Dominant: A dominant gene always causes a disease, even if you only have one faulty copy (like in the heterozygous case). Imagine the faulty instruction manual overrides the good one.

    Summary:

    • SCD: A faulty instruction manual leads to problems with red blood cells.
    • Autosomal: The chromosomes that determine most traits (the house’s foundation).
    • Heterozygous: You have one good and one faulty copy of a gene (one good and one faulty instruction manual).
    • Homozygous: You have two identical copies of a gene (two good or two faulty instruction manuals).
    • Recessive: You need two faulty copies to express the disease (two faulty instruction manuals to build a bad house).
    • Dominant: You only need one faulty copy to express the disease (one faulty instruction manual is enough to build a bad house).
    • Red Blood Cells: These cells carry oxygen throughout the body.
    • Haemoglobin: A protein within red blood cells that binds to oxygen.
    • Haemoglobin Gene: A gene located on chromosome 11 that provides instructions for making haemoglobin.

    Possibility of Sickle cell Disease

    Problems in sickle cell disease begin around 5 to 6 months of age. Sickle-cell disease occurs when a person inherits two abnormal copies of the haemoglobin gene, one from each parent. This gene occurs in chromosome 11.

    Type of GeneNormalTraitDisease
    One Parent with Trait50%50%0%
    Both Parents with Trait25%50%25%
    One Parent with Disease50%50%50%
    Both Parents have Disease0%0%100%

    Cause of Sickle Cell Disease

    • It is caused by a defect in beta chains where a given amino acid is replaced by another (Substitution of valine for glutamic acid) at position 6 of the chain.
    • This change creates abnormal hemoglobin called HbS.

    Sickle cell disease is caused by a genetic mutation in the gene that produces haemoglobin, a protein in red blood cells that carries oxygen.

    • Normal Haemoglobin: Normal haemoglobin is made up of two alpha chains and two beta chains, denoted as HbA.
    • Sickle Cell Haemoglobin: In sickle cell disease, there’s a single point mutation in the beta chain of haemoglobin, replacing a glutamic acid with valine, at position 6 of the chain.This mutated haemoglobin is called HbS.

    Pathophysiology of Sickle Cell Disease.

    Normally each haemoglobin molecule consists of four molecules of haem folate into one molecule of globin.

    But in sickle cell disease this is altered and cells become sickle shaped, glutamine is replaced by valine. The sickle cells elongate under conditions of lower oxygen concentration, Acidosis takes place and dehydration.

    When red blood cells (RBCs) containing homozygous HbS are exposed to deoxygenated conditions, the sickling process begins. This distorts the membranes of red blood cells. The cell becomes easily entangled leading to blood viscosity, vessel occlusion and tissue necrosis.

    These cells fail to return to normal shape when normal oxygen tension is restored. As a result, these rigid blood cells are unable to deform as they pass through narrow capillaries, leading to vessel occlusion and ischemia. The actual anaemia of the illness is caused by haemolysis, the destruction of the red cells, because of their shape.

    Although the bone marrow attempts to compensate by creating new red cells, it does not match the rate of destruction. Healthy red blood cells usually function for 90–120 days, but sickled cells only last 10–20 days. Increased sequestration of Red blood cells in the spleen also cause anaemia

    Clinical Presentation of SCD 

    Children are rarely symptomatic until late in the first years of life related to increased amounts of fetal haemoglobin being cleared from blood. The severity of symptoms can vary from person to person. Sickle-cell disease may lead to various acute and chronic complications, several of which have a high mortality rate.

    • Painful swelling of hands and feet (Hand-foot syndrome): This is a common presentation in children, caused by vaso-occlusive crisis in the small blood vessels of the hands and feet.
    • Pain crisis (sickle crisis): This is a major complication characterized by intense pain due to blocked blood flow to a specific area of the body and can last for days or weeks. Pain in the chest, abdomen, limbs, and joints.
    • Anaemia: A consistent feature, as the lifespan of sickle red blood cells is shortened. This leads to fatigue, weakness, and paleness.
    • Jaundice: Caused by the breakdown of red blood cells, leading to a yellowish discoloration of the skin and eyes.
    • Haemoglobin levels: Usually low, ranging from 6 g/dL to 9 g/dL, indicating the severity of anaemia.
    • Shortness of breath: Caused by complications like pneumonia, acute chest syndrome, and pulmonary hypertension.
    • Fatigue and weakness: A common symptom due to the low oxygen levels caused by anaemia.
    • Priapism: A painful erection lasting for hours or days, caused by blocked blood flow in the penis. If not promptly treated, it can lead to impotence.
    • Abdominal swelling and pain: Often associated with spleen enlargement (splenomegaly) or blockages in the blood vessels supplying the intestines.
    • Unusual headache: May be a sign of stroke, as sickled cells can block blood flow to the brain.
    • Loss of appetite: A common symptom associated with anaemia and pain.
    • Irritability: Can be a response to pain, fatigue, or other symptoms.
    • Bossing of the bones of the skull: Indicates active erythropoiesis (red blood cell production) to compensate for the loss of sickle cells.
    • Intercurrent infections: Patients with sickle cell disease are more susceptible to infections like pneumonia, acute respiratory infections, and malaria, often complicated by severe anaemia.
    • Splenomegaly: Enlarged spleen, common in younger children, but often shrinks in older children due to splenic infarction.
    • Growth retardation: Can occur due to chronic illness, pain, and infections.
    • Stroke: A serious complication resulting from blocked blood flow to the brain, leading to brain damage.

    Newborns: May present with jaundice, delayed cord clamping, and possible failure to thrive.

    Children:

    • Dactylitis (Hand-foot Syndrome): Painful swelling of hands and feet due to vaso-occlusive crisis.
    • Splenomegaly: Often present in young children, but can be absent in older children due to splenic infarction (damage).
    • Delayed growth and development are common due to recurrent infections and pain crises.
    • Delayed puberty: Can be a feature, especially in males.

    Adults:

    • Chronic pain is a defining feature, often with unpredictable patterns.
    • Pulmonary complications: Pulmonary hypertension, acute chest syndrome, and pneumonia are frequent issues.
    • Osteonecrosis: Damage to bone due to lack of blood flow.
    • Avascular necrosis: Can affect bones, especially hips and shoulders.
    • Chronic kidney disease: Can develop over time due to repeated damage to the kidneys.
    Chronic Symptoms:
    • Jaundice: Yellowing of the skin and whites of the eyes due to the breakdown of red blood cells.
    • Gallstones: Formation of stones in the gallbladder, often caused by a build-up of bilirubin from red blood cell breakdown.
    • Progressive kidney impairment: Damaged blood vessels in the kidneys can lead to reduced kidney function over time.
    • Growth retardation: Slower growth of long bones and skeletal deformities, particularly in the spine, can occur.
    • Delayed puberty: The chronic illness can delay the onset of puberty.
    • Chronic painful leg ulcers: Related to chronic anaemia and poor blood flow to the extremities.
    • Decreased lifespan: While advancements in medical care have improved life expectancy, individuals with sickle cell disease still have a shortened lifespan compared to the general population.
    • Altered body structures: These include “bossing” of the skull (abnormal thickening of the skull bones), as well as septic necrosis (bone death due to infection) in the femur (thigh bone) and head of the humerus (upper arm bone).

    Sickle-cell crisis

    Sickle cell crisis is pain that can begin suddenly and lasts several hours to several days.

    The terms “sickle-cell crisis” or “sickling crisis” may be used to describe several independent acute conditions occurring in patients with Sickle Cell Disease. It happens when sickled red blood cells block small blood vessels that carry blood to bones. Children may present with pain in the back, knees, legs, arms, chest or stomach. The pain can be throbbing, sharp, dull or stabbing.

    Types of Sickle Cell Crisis.

    (i)  Vaso-occlusive Crisis: This is the most common form of crisis. Small blood vessels are occluded by the sickle cells causing distal ischemia and infarction, leading to pain, swelling, and inflammation.

    • Symptoms: Intense pain in the bones, joints, abdomen, chest, or head. Other symptoms may include fever, fatigue, and shortness of breath.
    • Extremities.  Bone destruction leading to osteoporosis or ischaemic necrosis.
    • Foot and hand syndrome due to aseptic infarction of metacarpals and metatarsals causing swelling and pains often this is seen in infants and toddlers.
    • Triggers: Dehydration, infection, cold weather, high altitude, and strenuous physical activity.
    • Treatment: Pain management with analgesics, intravenous fluids, and blood transfusions in severe cases.

    (ii)  Splenic sequestration Crisis:  Large amounts of blood become pooled to the spleen, leading to a decrease in blood volume and blood pressure. The spleen becomes massively enlarged.

    • Symptoms: Abdominal pain, swelling, fever, and shock. Great decrease in Red blood cells mass occurs within hours. Signs of circulatory collapse develop rapidly.
    • This is the most frequent cause of death in infants with sickle cell disease.
    • Treatment: Immediate medical attention with intravenous fluids, blood transfusions, and sometimes splenectomy.

    (iii) Aplastic Crisis:  The bone marrow ceases to produce RBCs. A sudden drop in red blood cell production, leading to severe anaemia and worsening of symptoms. There will be low blood cell circulation in blood hence anaemia.

    • Cause: Usually triggered by viral infections like parvovirus B19. Folic acid deficiency and Ingestion of bone marrow toxins (eg, phenylbutazone).
    • Symptoms: Fatigue, weakness, pallor, and shortness of breath.
    • Treatment: Blood transfusions to increase red blood cell count.

    (iv) Haemolytic Crisis:  Hemolytic crisis occurs when large numbers of red blood cells are destroyed over a short time. The loss of red blood cells occurs much faster than the body can produce new red blood cells.

    • Cause: Often triggered by infections.
    • Symptoms: Fatigue, pallor, jaundice, and dark urine.
    • Treatment: Blood transfusions and treatment of underlying infections.

    Causes of hemolysis include:

    • A lack of certain proteins inside red blood cells
    • Autoimmune diseases
    • Certain infections
    • Defects in the haemoglobin molecules inside red blood cells
    • Defects of the proteins that make up the internal framework of red blood cells
    • Side effects of certain medicines
    • Reactions to blood transfusions.

    (v)  Acute chest syndrome. This occurs in the chest, when sickled red blood cells block blood flow to the lungs, leading to inflammation and damage. This can be life-threatening. It often occurs suddenly, when the body is under stress from infection, fever, or dehydration. 

    • Symptoms: Chest pain, fever, shortness of breath, cough, and rapid breathing.
    • Treatment: Oxygen therapy, antibiotics, pain management, and sometimes mechanical ventilation.

    Precipitating Factors of Sickle Cell Crisis

    Sickle cell crises are painful episodes that occur when sickle red blood cells block blood flow in the body. These crises can be triggered by various factors, including:

    Environmental and Physiological Factors:

    • Dehydration: Lack of fluids can thicken the blood, making it harder for sickle cells to flow through small blood vessels.
    • Infection: Infections can increase the body’s demand for oxygen, putting stress on already compromised red blood cells.
    • Trauma: Injury, including even minor cuts or bruises, can lead to localized blood clotting and trigger a crisis.
    • Extreme Temperature Fluctuations: Both extreme heat and cold can constrict blood vessels and lead to blockage.
    • High Altitude: The thinner air at high altitudes can lead to oxygen deprivation, increasing the likelihood of sickling.
    • Hypoxia: Low oxygen levels in the blood, from any cause, can trigger sickling.
    • Acidosis: Increased acidity in the blood can also contribute to sickling.

    Lifestyle and Emotional Factors:

    • Strenuous Physical Exercise: Intense physical activity can increase the body’s demand for oxygen and contribute to sickling.
    • Extreme Fatigue: Prolonged exhaustion weakens the body’s ability to fight off crises.
    • Extreme Exertion: Similar to intense exercise, any extreme physical effort can trigger a crisis.
    • Emotional Stress: Stress hormones can constrict blood vessels and increase the likelihood of sickling.

    Other Contributing Factors:

    • Pregnancy: The increased blood volume and hormonal changes during pregnancy can make women more susceptible to crises.
    • Asthma: The inflammatory response in asthma can trigger sickle cell crises.
    • Anxiety: Similar to stress, anxiety can constrict blood vessels and increase the risk of a crisis.
    • Dehydration.
    • Infection.
    • Trauma.
    • Strainous Physical exercises.
    • Extreme fatigue.
    • Extreme exertion
    • Severe cold that constricts peripheral vessels
    • Fever Excessive exercise
    • Hypoxia.
    • Acidosis.
    • Extreme temperature
    • High attitude
    • Emotional stress
    • Pregnancy
    • Asthma
    • Anxiety
    • Abrupt changes in temperature
    Diagnosis and Investigations sickle (2) (1)

    Diagnosis and Investigations:

    • Family history: A strong family history of sickle cell disease is a big indicator.
    • Full blood count and peripheral film: The blood test may show leukocytosis (increased white blood cell count) due to bacterial infection and reveal the presence of sickle cells.
    • Haemoglobin estimation: Will reveals a low haemoglobin level (6-8 g/dL) with a high reticulocyte count (10-20%), indicating the body’s attempt to compensate for the loss of red blood cells.
    • Sickling test: This simple test, done by finger or heel prick, observes a drop of blood under a microscope after removing oxygen. Sickle-shaped cells are indicative of the disease. However, it doesn’t distinguish between the trait and the disease or other sickle haemoglobin opathies.
    • Haemoglobin electrophoresis: This more definitive test involves separating different types of haemoglobin through an electric current. It identifies the presence and amount of HbS (sickle haemoglobin), providing a definitive diagnosis for both the trait and the disease.
    • Sickledex test: A rapid screening test for detecting the presence of HbS in the blood.
    • Peripheral blood smear: Examines a blood sample under a microscope to identify sickle cells and reticulocytes.
    • Urinalysis: Analyzes urine for signs of kidney damage.
    • Liver and renal function tests: Assess the function of the liver and kidneys.
    • Chest radiography: Used to diagnose Acute Chest Syndrome.
    • Abdominal ultrasound: Can help detect problems in the abdomen, such as a mesenteric crisis (blockage of blood vessels in the intestines).
    • Sickling test (emergency screening): Can be performed before surgery to identify individuals with sickle cell disease.
    Differential Diagnosis
    • Acute anaemia
    • Carotid-Cavernous Fistula (CCF)
    • haemoglobin  C Disease
    • Hemolytic Anaemia
    • Osteomyelitis in Emergency Medicine
    • Pulmonary Embolism (PE)
    • Rheumatoid Arthritis Hand Imaging
    • Septic Arthritis

    Management of Sickle Cell Disease.

    Management is according to the type of crisis .

    Aims of Management

    • Avoiding pain episodes.
    • Relieving symptoms.
    • Preventing complications.
    1. Acute painful attacks require supportive therapy with intravenous fluids, oxygen, antibiotics and adequate analgesia.
    2. Crises can be extremely painful and usually require narcotic analgesia. Morphine is the drug of choice. Milder pain can sometimes be relieved by codeine, paracetamol and NSAIDs.
    3. Oxygen Therapy: Supplementary oxygen is provided to address hypoxia and alleviate symptoms.
    4. Prophylaxis is with penicillin twice daily, up to 5 years of age due to the immature immune system that makes them more prone to early childhood illnesses is recommended and vaccination with polyvalent pneumococcal and Haemophilus influenzae type B vaccine .
    5. Hydration: Drinking plenty of fluids is essential to prevent dehydration and improve blood flow.
    6. Blood Transfusions: Regular transfusions are used to increase haemoglobin levels and reduce the frequency of crises. Transfusions should be given for heart failure, strokes, acute chest syndrome, acute splenic sequestration and aplastic crises.
    7. Anaemia Transfusions should only be given for clear indications.
    8. Patients with steady state anaemia, those having minor surgery or having painful episodes without complications should not be transfused.
    9. Transfusion and splenectomy may be life-saving for young children with splenic sequestration. A full compatibility screen should always be performed.
    10. Folic acid 5 mg daily for life is recommended.
    11. Hydroxycarbamide (hydroxyurea)starting dose 20 mg/kg is the first drug which has been widely used as therapy for sickle cell anaemia. It acts by increasing Hb F concentrations but the reduction in neutrophils may also help. Hydroxycarbamide has been shown in trials to reduce the episodes of pain, the acute chest syndrome and the need for blood transfusions.
    12. Malaria prevention: Since they are more vulnerable to malaria, because the most common cause of painful crises in malaria countries is infection with malaria. It has therefore been recommended that people with sickle-cell disease living in malarial countries should receive anti-malarial chemoprophylaxis monthly for life i.e sulfadoxine pyrimethamine.
    13. Pain management. 
    14. Home management
    • Paracetamol 1 g every 8 hours
    • Child: 10-15 mg/kg 6-8 hourly
    • And/or ibuprofen Child: 5-10 mg/kg 8 hourly.
    • Adults 400-600 mg 6-8 hourly.
    • And/or diclofenac 50 mg 8 hourly
    • Children only >9 years and >35 kg: 2 mg/kg in 3 divided doses.
    • If pain not controlled, add:
    • Codeine 30-60 mg every 6 hours (only in patients >12 years).
    • Or tramadol 50-100 mg every 6-8 hours (only in  patients >12 years)
    • Or Oral morphine at 0.2-0.4 mg/kg every 4 hours and re-assess pain level.

    • If pain still not controlled, refer to hospital

    • At the hospital; 

    • Morphine oral: Child and Adult: 0.3-0.6 mg/kg per dose and re-assess

    • Morphine Intravenously.

    • Child: 0.1-0.2 mg/kg per dose

    • Adult: 5-10 mg dose and re-assess

    • Use of laxative: bisacodyl 2.5 mg to 5 mg orally to prevent constipation due to morphine intake.

    Cure: 

    • The only therapy approved by the FDA that may be able to cure SCD is a bone marrow or stem cell transplant.
    • Bone marrow or stem cell transplants are very risky and can have serious side effects, including death. For the transplant to work, the bone marrow must be a close match. Usually, the best donor is a brother or sister.

     Lifestyle Modifications:

    • Regular Exercise: Moderate exercise, when tolerated, can improve cardiovascular health and reduce the risk of complications.
    • Stress Management: Techniques like relaxation, meditation, and yoga can help manage stress levels and reduce the risk of crises.
    • Healthy Diet: A nutritious diet rich in fruits, vegetables, and whole grains can support overall health.
    • Avoidance of Extreme Temperatures: Extreme heat and cold can trigger crises.
    • Altitude Management: Individuals should avoid high altitudes to minimize the risk of hypoxia.

    Surgery:

    • Bone Marrow Transplant: This is a potential cure, but it is a high-risk procedure with limited availability.
    • Other Surgical Interventions: Surgical procedures may be necessary to correct bone deformities or treat complications like leg ulcers.

    Support and Counseling:

    • Genetic Counselling: Provides information about the inheritance of sickle cell disease and family planning options.
    • Psychosocial Support: Provides emotional and practical support to help individuals cope with the challenges of living with sickle cell disease.
    • Patient Education: Empowers individuals to manage their condition effectively by providing information on symptoms, triggers, and treatment options.

    Prevention of Sickle cell crisis.

    1. Hydration:

    • Drink plenty of water: Staying well-hydrated is crucial for maintaining adequate blood flow and preventing sickling.
    • Carry a water bottle and sip water regularly throughout the day.
    • Avoid dehydration, especially during exercise, hot weather, or travel.

    2. Temperature Management:

    • Avoid extreme temperatures: Both excessive heat and cold can trigger sickle cell crises.
    • Stay in air-conditioned environments during hot weather.
    • Dress in layers to adjust to temperature changes.
    • Be aware of the risk of hypothermia during cold weather.

    3. Altitude Management:

    • Avoid high altitudes: Low oxygen levels at high altitudes can worsen sickle cell symptoms.

    4. Oxygen Management:

    • Avoid situations with low oxygen levels: Avoid intense physical exertion, especially in hot, humid, or high-altitude environments.
    • Use proper breathing techniques during exercise.

    5. Infection Prevention:

    • Vaccination: Receive all recommended vaccinations, including the pneumococcal vaccine, to protect against infections.
    • Wash your hands frequently with soap and water.
    • Use hand sanitizer when soap and water are unavailable.
    • Avoid close contact with sick individuals.
    • Practice safe food handling and preparation to prevent foodborne illness.

    6. Routine Medical Care:

    • Yearly visits to an eye doctor: Regular eye exams are crucial to monitor for signs of retinopathy, a serious complication of sickle cell disease.
    • Regular checkups with a haematologist: Follow your doctor’s recommendations for regular blood tests and monitoring.
    • Early intervention: Seek medical attention promptly for any unusual symptoms or signs of a sickle cell crisis.

    7. Stress Management:

    • Practice stress-reducing techniques: Stress can trigger sickle cell crises.
    • Engage in activities you enjoy, like meditation, yoga, or spending time in nature.
    • Seek counselling or therapy if you’re struggling to manage stress.

    8. Lifestyle Modifications:

    • Maintain a healthy weight: Obesity can worsen sickle cell symptoms.
    • Eat a balanced diet rich in fruits, vegetables, and whole grains.
    • Avoid smoking and excessive alcohol consumption.
    • Get regular exercise, but consult your doctor about safe levels.

    9. Advocacy and Support:

    • Join a sickle cell support group: Connect with other individuals living with sickle cell disease and share experiences and resources.
    Nursing Diagnosis
    1. Acute pain related to tissue hypoxia due to agglutination of sickled cells within blood vessels evidenced by patient verbalization.
    2. Risk for infection related to lowered immunity.
    3. Impaired Gas Exchange related to decreased oxygen-carrying capacity of the blood, reduced RBC life span/premature destruction, abnormal RBC structure; sensitivity to low oxygen tension (strenuous exercise, increase in altitude) as evidenced by difficulty in breathing.
    4. Ineffective Tissue Perfusion related to vaso-occlusive nature of sickling as evidenced by changes in vital signs: diminished peripheral pulses/capillary refill, general pallor or decreased mentation, restlessness.
    5. Risk for Deficient Fluid Volume related to increased fluid needs, e.g., hypermetabolic state/fever, inflammatory processes.
    6. Acute Pain related to Intravascular sickling with localized stasis, occlusion, and infarction/necrosis as evidenced by  generalized pain, described as throbbing,  or severe ; affecting peripheral extremities, bones, joints, back, abdomen, or head (headaches)
    7. Risk for Impaired Skin Integrity related to impaired circulation (venous stasis and vaso-occlusion)

    Prevention Of Sickle Cell Disease

    • Genetic counselling is important to prevent passing on the trait or disease to children for those wanting to have them.
    • Premarital counselling is encouraged. Early recognition/screening of children with low Hb.

    Complications of Sickle Cell anaemia

    1. Stroke. Issues in circulation will result to blockages, therefore predisposing the patient to develop thrombolytic strokes
    2. Acute chest syndrome. This is characterized by chest pain, fever and difficulty breathing requiring emergency medical treatment
    3. Pulmonary hypertension. This type of anaemia can cause build-up of unnecessary lung pressure due to problems with circulation as a result of erythrocyte clumping
    4. Organ damage. Due to the chronic inability of the red blood cells to provide essential oxygen for normal organ function, patients with sickle cell anaemia may develop organ failure, which can be fatal.
    5. Blindness. One of the potential complications of having abnormal red blood cells circulating in the body is damage to smaller blood vessels, particularly the eye. This in turn will cause eye damage and eventually blindness.
    6. Leg ulcers. Poor wound healing and rampant skin breakdown can be observed for patients suffering from sickle cell anaemia.
    7. Gallstones. The build of bilirubin caused by the metabolism of the abnormal erythrocytes will result to gall stones that will block the flow of bile.
    8. Priapism. This is a condition wherein men with Sickle cell anaemia will present with painful and long-lasting erections due to the blockages of the tiny blood vessels of the penis.
    9. Pregnancy complications. Sickle cell anaemia increases the risk of high blood pressure and the presence of clots that will interfere with the normal development of the fetus.

    NURSING CARE PLAN FOR A PATIENT WITH SICKLE CELL CRISIS

    Assessment

    Diagnosis

    Goals/Expected Outcomes

    Intervention

    Rationale

    Evaluation

    Cyanosis, breathlessness at a rate of 28 breaths/min, restlessness, and SpO2 of 80%.

    Impaired gaseous exchange related to increased viscosity of blood evidenced by cyanosis, breathlessness, restlessness, and SpO2 of 80%.

    – Establish adequate gaseous exchange within 2 hours.

    – Improve SpO2 by 10% within the first 30 minutes.

    – Establish a normal breathing pattern without assisted respiration within 1 hour.

    – Restore normal skin color in 30 minutes.

    – Establish an intravenous line and administer fluids (normal saline 500 mL every 6 hours for 24 hours).

    – Encourage fluid intake by mouth.

    – Start a fluid input and output chart.

    – Assess the need for more fluids after 24 hours.

    – Take vital signs every 30 minutes for 2 hours, paying attention to breathing and SpO2, then adjust according to findings.

    – Administer oxygen 3 L/min for 1 hour using a face mask.

    – Establishing IV access and administering fluids help to reduce blood viscosity and improve circulation.

    – Encouraging oral fluid intake promotes hydration.

    – Fluid balance chart helps to monitor fluid status.

    – Regular assessment ensures timely adjustments in fluid therapy.

    – Oxygen therapy increases oxygen saturation in the blood.

    – Patient is resting.

    – Normal breathing pattern restored, rate 20 breaths/min.

    – SpO2 improved to 98% on room air.

    – Normal skin colour restored, lips look pink.

    Patient verbalizing throbbing pain in the legs and joints, rating score of 8 on the pain scale.

    Acute pain related to intravascular sickling with localized stasis evidenced by patient verbalizing throbbing pain in the legs and joints.

    – Relieve pain within 4 hours.

    – Improve venous patency

    –  Improve circulatory flow.

    – Administer analgesia (pethidine 50 mg single dose, then tramadol 50 mg every 8 hours for 3 days as prescribed and document).

    – Continue intravenous fluids as above and monitor pain hourly.

    – Analgesics provide comfort and relieve restlessness.

    – IV fluids maintain normal circulatory flow.

    – Patient reports pain relief after 4 hours, score 2 on the pain scale.

    Reduced haemoglobin  levels of 5 g/L according to laboratory results, swelling of the lower limbs and joints.

    Altered tissue perfusion related to decreased red blood cells as evidenced by reduced haemoglobin levels of 5 g/L, swelling of the lower limbs and joints.

    – Restore normal tissue perfusion within 24 hours.

    – Establish normal tissue perfusion.

    – Transfuse with units of packed cells 5 mL/kg/h as prescribed.

    – Continue with fluid balance chart.

    – Apply a warm compress to the affected areas.

    – Elevate the affected limbs.

    – Blood transfusion increases haemoglobin levels.

    – Fluid balance chart monitors fluid status.

    – Warm compresses promote vasodilation and circulation to hypoxic areas.

    – Elevation reduces swelling and promotes venous return.

    – Increased haemoglobin  levels of 7 g/dL as seen in post-transfusion lab report.

    – Swelling has subsided, and the patient is able to move the limb.

    Fever, hypermetabolic state, dehydration symptoms (dry mucous membranes, poor skin turgor).

    Risk for fluid volume deficit related to increased fluid needs due to hypermetabolic state or fever.

    – Maintain adequate hydration.

    – Prevent fluid volume deficit.

    – Monitor vital signs and fluid status regularly.

    – Encourage oral fluid intake and administer IV fluids as needed.

    – Educate the patient on the importance of fluid intake.

    – Regular monitoring detects early signs of fluid deficit.

    – Ensuring adequate hydration prevents complications.

    – Fluid balance is maintained, and signs of dehydration are absent.

    Presence of venous stasis, vaso-occlusion, decreased mobility, and risk of skin breakdown.

    Risk for impaired skin integrity related to impaired circulation due to venous stasis and vaso-occlusion, and decreased mobility.

    – Prevent skin breakdown.

    – Maintain skin integrity.

    – Assess skin regularly for signs of breakdown.

    – Reposition the patient every 2 hours.

    – Provide skin care and keep the skin clean and dry.

    – Use pressure-relieving devices as needed.

    – Regular assessment and repositioning prevent pressure ulcers.

    – Good skin care promotes skin integrity.

    – Skin remains intact without signs of breakdown.

     

    Sickle Cell Disease Read More »

    Eating Disorders in Children and Adolescents

    Eating Disorders in Children and Adolescents

    EATING DISORDERS

    Eating disorders are conditions characterized by an extreme disturbance in eating related behaviour.

    OR

    Eating disorders are moderate to severe illnesses that are characterized by disturbances in thinking and behaviour around food, eating and body weight or shape.

    The DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, American Psychiatric Association,
    2013) outlines six types of disordered eating patterns but four types are commonly diagnosed:

    1.  Anorexia Nervosa (AN)
    2. Bulimia Nervosa (BN)
    3. Binge Eating Disorder (BED)
    4. Avoidant Restrictive Food Intake Disorder (ARFID)

    The rest of the two types are;

    5. Other Specified Feeding or Eating Disorders (OSFED)
    OSFED is also a moderate to severe illness and may include eating disorders of clinical significance that do not meet the criteria for AN or BN. OSFED and USFED may be as severe as AN or BN.
    6. Unspecified Feeding or Eating Disorders (USFED)
    USFED applies to where behaviours cause significant distress or impairment of functioning, but do
    not meet the full criteria of any of the other feeding or eating disorder criteria.

    ANOREXIA NERVOSA

    Anorexia nervosa (AN) is a severe eating disorder characterized by a distorted body image that leads to restricted eating, over exercise and other behaviors that prevents a person from gaining weight or
    maintaining a healthy weight.

    OR

    Anorexia Nervosa is defined as self-induced starvation resulting from fear of gaining weight rather than from true loss of appetite.

    Person with anorexia nervosa continues to feel hunger but persists in denying himself or her self food. 

    eating disorders anorexia nervosa

    Children and teens with anorexia have a distorted body image. People with anorexia view themselves as heavy, even when they are dangerously skinny. They are obsessed with being thin and refuse to maintain even a minimally normal weight.

    Signs and Symptoms of Anorexia Nervosa
    • Refusal to maintain a minimum normal body weight.
    • Is intensely afraid of gaining weight.
    • Significant disturbance in the perception of the shape or size of his or her body.(distorted image)
    • Dieting even when one is thin or emaciated
    • The individual maintains a body weight that is below a minimally normal level for age and weight.
    • They exclude from their diet what they perceive to be highly caloric foods. ie they restrict diet.
    • Purging i.e. self-induced vomiting or misuse of laxatives, diuretics.
    • There is excessive exercise to reduce weight.
    • Reduced total food intake
    • Intense fear of becoming fat or obese.
    • Strange eating habits, very picky.
    • Infrequent menstruation or Amenorrhea due to reduced estrogen and loss of weight
    • Oligomenorrhoea or failure to reach menarche.
    • Loss of sexual interest
    • Anxiety, depression, perfectionism(hold themselves to impossibly high standards)
    Possible complications of Anorexia Nervosa

    Anorexia nervosa is fatal in about 10% of cases. Most common death from anorexia nervosa is due to, cardiac arrest, electrolyte imbalance and suicide.

    • Heart muscle damage that can occur as a result of malnutrition or repeated vomiting may be life threatening. 
    • Arrhythmias (a fast, slow, or irregular heartbeat)
    • Hypotension (low blood pressure)
    • Electrolyte imbalance.
    • Anaemia (low RBC’s) and Leukopenia(low WBC’s)
    • GIT disturbances.
    • Dehydration
    • Refeeding Syndrome,
      Refeeding Syndrome “is potentially a fatal condition defined by severe electrolyte and fluid shifts as a result of a rapid reintroduction of nutrition after a period of inadequate nutritional intake
    Management or Treating Anorexia Nervosa

    Refer to General Management,

    • The major aim of treatment is to bring the young person back to normal weight and eating habits.
    • Hospitalization, sometimes for weeks, may be necessary. In cases of extreme or life-threatening malnutrition, tube or intravenous feeding may be required.

    Nursing care

    • Short term management is focused on ensuring weight gain and correcting nutritional deficiencies. maintaining normal weight and preventing relapses
    • provide a balanced diet of at least 3000 calories in 24 hours
    • a nurse should always supervise the patient during meals
    • patient should be under complete bed rest initially under nurses observation so as to achieve a weight gain goal of 0.5 to 1kg per week
    • control vomiting by making the bathroom inaccessible 2 hours after food
    • in extreme cases when the patient refuses to comply with treatment and eating, gavage feeding may need to be instituted
    • weight should be checked regularly and plotted on a weight chart
    • maintain a strict intake and output chart
    • monitor skin status and oral mucous membrane for signs of dehydration
    • encourage patient to verbalise feelings of fear and anxiety related to the achievement
    • encourage family to participate in education regarding patients disorder
    • avoid discussions that focus on food and weight

    Long-term treatment addressing psychological issues include:

    • antidepressant medication
    • Neuroleptics
    • appetite stimulants
    • behavioral therapy
    • individual therapy
    • cognitive behavioural therapy
    • family therapy
    • psychotherapy
    • support groups

    BULIMIA NERVOSA

    Bulimia nervosa, or bulimia, is a type of eating disorder in which a person engages in episodes of bingeing—during which he or she eats a large amount of food—and then purges, or tries to get rid of the extra calories.

    OR

    Bulimia nervosa is a syndrome of episodes of binge eating followed by self-induced vomiting or purge behaviour accompanied by an excessive pre occupation with weight and body shape.

    Young people with bulimia try to prevent weight gain by inducing vomiting or using laxatives, diet pills, diuretics, or enemas. After purging the food, they feel relieved. Binge eating is often done in private. Because most people with bulimia are of average weight or even slightly overweight, it may not be readily apparent to others that something is wrong.

    The condition often begins in the late teens or early adulthood and is diagnosed mostly in women. People with bulimia may have other mental health issues, including depression, anxiety, drug or alcohol abuse, and self-injurious behaviors.

    Doctors make a diagnosis of bulimia after a person has two or more episodes per week for at least three months. People with bulimia usually fluctuate within a normal weight range, although they may be overweight, too. As many as one out of every 25 females will have bulimia in their lifetime.

    Binge is eating in a discrete period of time an amount of food that is definitely larger than most individuals would eat under similar circumstances.

    eating disorder bulimia nervosa
    Signs and Symptoms of Bulimia Nervosa
    • The individual is typically ashamed of his or her eating problem.
    • Persistent heart burn and sore throat.
    • Abdominal and epigastric pain.
    • They tend to conceal their symptoms, It occurs in secrecy
    • Food is consumed rapidly
    • Binge eating continues until the individual is uncomfortable or even painfully full.
    • The binge eating is usually triggered by low mood, interpersonal stressors, intense hunger
      following dietary restraint.
    • Loss of self control, Difficult in resisting binge eating or difficult in stopping it.
    • Employs compensatory technique for example induce vomiting after binge eating.
    • They place emphasis on body shape and weight in their self evaluation.
    • Have fear in losing weight.
    • May be overweight or underweight
    • Low self esteem
    • Increased frequency of anxiety for example fear of social situation
    • Fluid and electrolyte imbalance due to purging
    • Menstrual irregularity or amenorrhea may occur
    • Rectal prolapse
    • Increased dental caries
    • Scarring of knuckles from using fingers to induce vomiting.

    Management or Treating Bulimia Nervosa

    Refer to General Management,

    Treatment aims to break the binge-and-purge cycle. Treatments may include the following:

    Nursing care

    • engage patient in therapeutic alliance to obtain commitment to treatment
    • establish contract with the patient that specifies amount and type of food she must eat at each meal
    • set a time limit for each meal
    • identify patients elimination patterns
    • encourage the patient to recognize and verbalize her feelings about her eating behavior
    • explain the risks of laxative, emetic and diuretic abuse
    • assess and monitor patients suicide potential

    Other treatment modalities

    • antidepressants medication
    • behavior modification
    • individual, family, or group therapy
    • nutritional counseling
    • self help groups
    Complications of Bulimia Nervosa
    • Stomach acids from chronic vomiting can cause,
    • damage to tooth enamel,
    • inflammation of the esophagus,
    • swelling of the salivary glands in the cheeks,
    • low potassium which can lead to abnormal heart rhythms.

    BINGE EATING DISORDER

    Binge eating is similar to bulimia.

    Binge eating refers to  chronic, out-of-control eating of large amounts of food in a short time, even to the point of discomfort without  purging the food through vomiting or other means.

    People with binge eating disorder eat unusually large amounts of food often and in secret but do not attempt to get rid of calories once the food is consumed. People with the condition may be embarrassed or feel guilty about binge eating, but they feel such a compulsion that they cannot stop.

    These people can be of average weight, overweight, or obese. They may also have other mental health disorders, such as depression. Many binge eaters have trouble coping with anger, sadness, boredom, worry, and stress.

    Binge eating disorder often has no physical symptoms, but it has psychological symptoms that may or may not be apparent to others, such as depression, anxiety, or shame or guilt over the amount of food eaten. Frequent dieting without weight loss is another symptom.

    The excess weight caused by binge eating puts the child at risk of these health problems:

    Treatments include the following: Refer to General Management,

    • behavioral therapy
    • medications, including antidepressants
    • psychotherapy

    AVOIDANT/RESTRICTIVE FOOD INTAKE DISORDER

    Avoidant/restrictive food intake disorder, is an eating disorder where a person is unable to or refuses to eat certain foods based on texture, color, taste, temperature, or aroma.

    The condition can lead to weight loss, inadequate growth, nutritional deficiencies, and impaired psychosocial functioning, such as an inability to eat with others. Unlike anorexia nervosa, there are not weight or shape concerns or intentional efforts to lose weight.

    For instance, a child may consume only a very narrow range of foods and refuse even those foods if they appear new or different. This type of eating disorder commonly develops in childhood and can affect adults as well.

    Assessment/Screening for an Eating Disorder

    1. The SCOFF Test: 

    Early detection in patients with unexplained weight loss improves prognosis and may be aided by use of the SCOFF questionnaire, developed by John Morgan at Leeds Partnerships NHS Foundation
    Trust.

    This questionnaire uses five simple screening questions and has been validated in specialist and primary care settings. It has a sensitivity of 100% and specificity of 90% for anorexia nervosa. A score of 2 or more positive answers should raise your index of suspicion of a case, highlighting the need for a comprehensive assessment for an eating disorder and
    consultation with an eating disorder expert or mental health clinician. 

    scoff test eating disorder

    2.  SUSS (Sit up – Squat – Stand Test) for muscle strength

    1. Sit-up: patient lies down flat on the floor and sits up without, if possible, using their hands

    2. Squat–Stand: patient squats down and rises without, if possible, using their hands.

    Scoring (for Sit-up and Squat-Stand tests separately)

    ParameterScore
    Unable0
    Able only when using hands to help1
    Able with noticeable difficulty2
    Able with no difficulty3

    A Sit up – Squat – Stand(SUSS) score ≤ 2 indicates a RED FLAG.

    Anorexia Nervosa (AN) has the HIGHEST MORTALITY rate of ALL mental health illnesses
    Patients with AN are at risk of sudden death if the have the RED FLAGS below.

    RED FLAGS

    • SUSS score less or equal to 2
    • Postural drop
    • Bradycardia
    • Hypothermia
    • Electrolyte abnormalities
    Nurses Role during assessment
    • Nurses in the hospital or primary care setting are in a crucial position to screen for and detect eating disorders, hence the importance for nurses to have an awareness of the indicators for eating disorder assessment.
    • supporting psychological based therapies, psycho-education regarding
      effects of the eating disorder,
    • assessment of risk,
    • promoting recovery and hope,
    • involving famil and caretakers,
    • observing for co-morbidities.

    GENERAL MANAGEMENT OF EATING DISORDERS

    Aims

    •  To restore the patient’s nutritional status.
    • To prevent complications.


    General management

    1.  Develop a trusting relationship with the patient.
    2. Convey positive regard to the patient
    3. Stay with the patient especially at the time of meals and 1 hour after meals.
    4. Avoid arguing or bargaining with the patient who is resistant to treatment.
    5. State matters of facts which behaviours are unacceptable.
    6. Encourage the patient to verbalize feelings regarding role within the family and issues related to dependence.
    7. Help the patient to recognize ways to gain control over these problems in life.
    8. Help the patient to develop a realistic perception of body image and relationship with food.
    9. Promote feelings of control within the environment through participation and dependent
      decision making.
    10. Weigh patient daily. Always use the same weighing scale to avoid errors.
    11. Keep strict record of observations especially fluid input and output.
    12. Assess skin; motility and tugor regularly.
    13. Assess moistness and color of the skin and oral mucus membranes.


    Behaviour modification

    •  Develop care plan together with the client
    • Encourage the client to sign a contract is necessary
    • Staff and client can agree on a system of reward.
    • Individual therapy such as psychotherapy may be important. This is particularly helpful when there is underlying psychological problems contributing to the maladaptive behaviour.
    • Family therapy:
      > Counsel the family members. This includes educating the family about the disorder, assessing the family perception or attitudes.
      > Support given to the family
    • Refer if necessary
    • Chemotherapy: there are no specific drugs indicated for the treatment of the condition. Drugs
      such as flouxetine, chlorpromazine, and lithium carbonate have been used.

    Nursing Diagnoses

    •  Imbalanced nutrition less than body requirement related to refusal to eat or self induced vomiting as evidenced by loss of weight.
    • Ineffective denial related to fear of losing or retarded ego development as evidenced by inability to admit the impact of maladaptive eating behaviours on life pattern.
    • Disturbed body image related to false perception of increased body weight evidenced by patient’s verbalization of that she has global over weight.

    Eating Disorders in Children and Adolescents Read More »

    disaster management and occupational health

    Disaster Preparedness and Management

    DISASTER

    Disaster is an occurrence disrupting the normal conditions of existence and causing a level of suffering that exceeds the capacity of adjustment of the affected community, WHO

    Disaster is also defined as a sudden/unexpected catastrophic event causing serious disruption of the functioning of a community or society that exceed the ability of the affected community or society to cope using its own resources.

    Key words used in Disaster

    1. Vulnerability: Is lack of capacity to deal with potential threat. Lack of information, resources and technology. There are many
      aspects of vulnerability, arising from various physical, social, economic, and environmental factors. Examples may include: poor design and construction of buildings, inadequate protection of assets, lack of public information and awareness, limited official
      recognition of risks and preparedness measures, and disregard for wise environmental management
      There are four (4) main types of vulnerability:
      (a). Physical Vulnerability may be determined by aspects such as population density levels, remoteness of a settlement, the site, design and materials used for critical infrastructure and for housing. Example: Wooden homes are less likely to collapse in an earthquake, but are more vulnerable to fire.
      (b). Social Vulnerability refers to the inability of people, organizations and societies to withstand adverse impacts to hazards due to characteristics inherent in social
      interactions, institutions and systems of cultural values. It includes aspects related to levels of literacy and education, the existence of peace and security, access to basic human rights, systems of good governance, social equity, positive traditional values, customs and ideological beliefs and overall collective organizational systems  Example: When flooding occurs some citizens, such as children, elderly and differently-able, may be unable to protect themselves or evacuate if necessary.
      (c). Economic Vulnerability. The level of vulnerability is highly dependent upon the economic status of individuals, communities and nations i.e. the poor are usually more vulnerable to disasters because they lack the resources to build sturdy structures and put other engineering measures in place to protect themselves
      from being negatively impacted by disasters. Example: Poorer families may live in squatter settlements because they cannot afford to live in safer (more expensive) areas.
      (d). Environmental Vulnerability. Natural resource depletion and resource degradation are key aspects of environmental vulnerability. Example: Wetlands, such as the Caroni Swamp, are sensitive to increasing salinity from sea water, and pollution from storm water runoff containing agricultural chemicals, eroded soils, etc.
    2. Disaster risk:  Is the likelihood of specific hazard occupancy and its probable consequence for people, property and environment.
       (a). Acceptable risk: The extent to which a disaster risk is deemed acceptable or tolerable depends on existing social, economic, political, cultural, technical and environmental conditions.
      (b). Residual risk: is the disaster risk that remains even when effective disaster risk
      reduction measures are in place, and for which emergency response and recovery
      capacities must be maintained. T
    3. Intensity: Refers to a disaster agent’s ability to inflict damage and injury.
    4. Scope: Refers to the geographic area and social space dimension impacted by the disaster agent.
    5. Frequency:  Refers to the number of times certain disasters occur in certain geographical locations that may give time to the community to take measures in preparation.
    6. Controllability: Refers to some control measures that can reduce the impact of the disaster. It helps the emergency planners.
    7. Triage: Refers to sorting out victims according to the extent of severity.
    8. Time:  Refers to the period when certain disasters can last that can allow the affected people to vacate when there is a period of warning the community to vacate for protection.
    9. Capacity: The ability of a community to use all the available resources that can reduce risk level and disaster effects. 
    10. Capacity building: It is the efforts to develop human skills within a community to reduce
      risk levels.
    11.  Emergency: a state in which normal procedures are suspended and extra-ordinary measures are taken in order to avert a disaster, WHO.
    12. Catastrophe: It is a large scope of impact event that affects multiple communities, produces very high levels of damage and social disruption, and sharply and concurrently interrupts community and lifeline services. A broad scope of impact impairs each community’s emergency response system and greatly limits extra community support.”
    13.  Hazard: A natural or human-made event that threatens to adversely affects human life, property or activity to the extent of causing a disaster.

    Epidemiology of a disaster

    Epidemiology is the study of patterns of a disease occurrence in human population and the factors that influence these patterns.

    Epidemiology is divided into 3 parts namely i.e. Agent, host
    and environment

    1.  DISASTER AGENT: The agent is the physical agent that actually causes the injury or destruction.
      (a). Primary agents include; falling, building, heat, winds or using water.
      (b). Secondary agents include; bacteria and viruses that produce contamination or infection after primary agents.
    2.  HOST: These are the characteristics of humans that influence several of the disaster effects e.g. ages, immune status, pre-existing health status, degree of morbidity and emotional stability. The individuals who are mostly affected are the pregnant mothers, the elderly and the children because they are vulnerable.
    3.  ENVIRONMENT: Environmental factors that affect outcome of disaster include; physical, chemical, biological and social factors.
      (a). Physical factors include; the time when disaster occurs, weather conditions, availability of good water supply and functionality facilities and others for example communication system.
      (b). Chemical factors. Influencing disasters include leakage of stored ground water or food supply that may directly affect human life when consumed.
      (c). Biological factors are those that occur as a result of contaminated water, waste disposal, and improper food storage.
      (d). Social factors are those factors that contribute to the individuals’ social support systems, loss of family members and changes in responsible roles.

    Causes of Disasters

    1. Geological and Climatic Changes: This causes disasters if they become extreme e.g. lack or insufficiency of rain for an extended period that severely disturbs the hydrologic cycle in an area.
    2. Poverty: It generally makes people vulnerable to the impact of hazards because they settle on hills that are prone to landslide, along the riverside invaluably flood their banks
    3. Population Growth: More people will be forced to live and work in unsafe areas which cause increasing numbers of people will be competing for limited amount of resources such as employment opportunities, and land which can lead to conflict; this conflict may result in crisis—induced migration thereby resulting in disasters.
    4. Rapid Urbanization: It is characterized by rural poor moving to metropolitan areas in search of economic opportunities and security which may cause them not find safe and desirable places to build their houses that can lead to human-made disasters.
    5. Transitions in Cultural Practices: This involves cultural Introduction of new construction material to build houses or materials used incorrectly may lead to house that cannot withstand earthquake.
    6. Environmental Degradation: Drought conditions exacerbated by poor cropping patterns, overgrazing, the stripping of topsoil, poor conservation techniques, depletion of both surface and subsurface water supply.
    7. Lack of Awareness and Information: Lack of knowledge about protective measures, safe locations, safe evacuation routes and procedures that can be accessed during a disaster can lead to community to experience impacts of the disaster since they don’t know how to reduce the effects.
    8. War and Civil Strife: Includes competition for scarce resources, religious or ethnic intolerance and ideological differences e.g. the Rwandan massacre.

    Phases of Disaster, victim’ response and roles of a Nurse

    DISASTER

    Disaster Action Phase

    These are the steps in which a disaster will occur
    There are three phases to any disaster. The actions on emergency personnel and others professional depend on which of the disaster is at hand.

    1. Pre-impact Phase
    2. Impact Phase
    3. Post Impact Phase

    PRE-IMPACT PHASE: This is an initial phase of disaster prior to the actual occurrence of warning is given at a sign of the first possible danger to the community.  The earliest possible warning is crucial in preventing loss of life and minimizing damage. It is a period when emergency preparedness plan is made, first Aids Centre is opened and communication is very important, time for educating the community. The nurse’s role is to sensitize the community assist in making emergency shelters and prepare medical equipment.

    IMPACT PHASE: Occurs when disaster has actually happened; it is time for enduring hardship or injury and trying to survive. It is an emergency period when the individual helps neighbours and families at a “scene”, a time of holding “on” until outside helps arrive. The phase may last longer depending on the type of disaster. This phase provides preliminary assessment of the nature extent and geographical area of the disaster. A period when needs of the victim in the community is assessed. The type and number of needed disaster health services is assessed, reports are given to centre for disease control and action taken. The role of a nurse is to assess health needs, provide physical and psycho-social support to mothers and children, given special shelters, injured persons are treated, coordinate search is made and re-union activities are made

    POST IMPACT PHASE:  This is a period of recovery from emergency phase and ends with return of normal community order and functioning. The phase may live longer and care must be given. The role of a nurse is to counsel, start rehabilitation, and sensitize the community for empowerment to start income generating activities

    types-of-disasters

    Classification of Disasters

    1.  Natural Disasters.
    2.  Human made Disasters
    Natural Disasters

    A natural disaster is a major adverse event or disaster resulting from natural processes of the Earth.

    1. SUDDEN OCCURRENCE (MONOCAUSAL)
    2. PROGRESSIVE OCCURRENCE (MULTICAUSAL)
    SUDDEN OCCURANCE (MONOCAUSAL)PROGRESSIVE OCCURRENCE (MULTICAUSAL)
    STORMLANDSLIDE
    HEAT WAVEDROUGHT
    FREEZEFLOODS
    EARTHQUAKEEPIDEMIC
    VOLCANIC ERUPTIONPESTS
    HUMAN MADE DISASTER

    Human-made disasters are Emergency situations which are the results of deliberate human actions. They involve situations in which people suffers casualties, losses of basic services and means of livelihood

    SUDDEN OCCURANCE (MONOCAUSAL)PROGRESSIVE OCCURRENCE (MULTICAUSAL)
    FIREWAR
    EXPLOSIONECONOMIC CRISIS
    COLLISION
    SHIPWRECK
    STRUCTURAL COLLAPSE
    ENVIRONMENTAL POLLUTION

    Stages of emotional response

    Victims of disaster usually go through 4 stages of emotional response.

    1.  Denial stage: Period when victims deny the magnitude of the problem or more likely may understand the problems but seems unaffected emotionally.
    2.  Strong Emotional Response: It is a stage when the person is aware but regards it as overwhelming and unbearable. Common reaction during this stage is fighting of feel, weeping, speaking with difficulty, trembling, and sadness. It is a period of counselling and reassurance.
    3.  Acceptance stage: It is the time when victims begin to accept either being handicapped with one leg.” I accept disaster, I try to make a decision for what to do next and develop hope.” The role of a Health worker is to help victim develop decision making, and take specific action.
    4.  Recovery stage: It is a stage of recovery from crisis reaction. Victims feel that they are back to normal and routines become important again and sense of wellbeing is restored.
      Ability to make decision and carry out plans, returns victims, develops realistic memory.
      The role of a nurse is to resettle the victims and discuss issues of empowerment if facilities are accessed.

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    Introduction To Palliative Care

    Introduction To Palliative Care

    Palliative Care

    Palliative care is an approach  that improves  the quality  of life  of patients   and families   facing  the problem  associated  with  life threating  illness  through  the prevention and relief  of suffering   by means  of  early identification and assessment  and treatment of pain  and  other problems  which are physical , psychological and spiritual. WHO definition

     Palliative care is the Active Total Care of patients with life limiting disease and their families, when the disease is no longer responsive to curative medicine.

    Palliative care aims at achieving physical symptom relief but also extends far beyond it. It seeks to integrate physical, psychological, social and spiritual aspects of care so that patients may come to terms with their impending death as fully and constructively as they can.

    History of Palliative Care

    In 1960`s  British Psychiatric  John  Hinton  marked  societal  neglect  and deficiency  in the end  of the  life care.  Hospices were sanctuaries provided by religious orders for the dying poor, providing food, clothes and shelter.

    Dame Cicely Saunders  an oxford  trained  nurse  noted  the trouble of dying  and  the need  for  improved  pain control. She was a doctor, nurse social worker and a writer. She  was the founder of the “Hospice Movement” in 1918. In 1967, Dame Cicely Saunders oversaw the building of the world’s first purpose built modern Hospice: St Christopher’s Hospice in London, England.

    Saunders gave special care for the dying by providing expert pain and symptoms relief, with holistic care to meet the physical, social, psychological and spiritual needs of the patients and their families and friends.

    Initially Hospice was reserved for those with incurable cancer. Now it has moved to include all “life limiting diseases” cancer, HIV/AIDS, Neurological disorders, Heart failure

    At first, Hospices provided only inpatient care, isolated from mainstream care. Now there is inpatient Hospice care, home based care, hospital based teams and community outreach services.

    Hospice is no longer a building it is a philosophy of care (Active Total Care of patients)

    So now, What is Hospice Care, and  is it the same
    or 
    different from Palliative care.

    Hospice Care

    Hospice is  an umbrella  term  for the carrying  out of palliative care services  and is  usually a Centre  where  the team of professional and volunteers offer palliative services  to people mainly with  life limiting illness 

     There is an interface between hospice and palliative care. People often wonder the difference between hospice and palliative care 

     Therefore hospice is not the building

     The word hospice origins from   the hospes (Greek) and Hospitum (Latin) meaning hospitality

    The major aim of hospice is to put life in the remaining days of a patient. It gives the possible quality of care for patient and their families from diagnosis of illness through critical episodes, end of life and bereavement support. Patients and their families are guests as they have choices and are encouraged to participate in discussions and make  treatments and management choices.

     Palliative care is the art and science of providing relief from illness – related suffering. Alleviation of suffering is needed   for all patients who have curable and incurable illness. Hospice or end of life care can be used synonymous from palliative.

    Hospice in Africa

    Hospice has been established in the following countries: Zimbabwe, South Africa, Kenya, Uganda

    In Uganda, Hospice services,  were started in Nsambya Hospital in 1993 by Dr. Anne Merriman and since then organizations as well as hospitals have come up to offer palliative care services in Uganda such as Hospice Africa Uganda (HAU) and Mild may Uganda.
    These service has further been extended to other parts of the Country by training specialist nurses and clinical officers who then deliver this care.  

     Seven (7) strategic objectives/Goals of Hospice
    1.  To provide High Quality African Palliative Care for cancer / HIV AIDS patients in Uganda;
    2.  To strengthen and maintain capacity of HAU(Hospice Africa Uganda) to produce oral liquid morphine;
    3. To provide high quality palliative care training in Africa;
    4. To build and strengthen capacity of other African countries to deliver palliative care;
    5.  To strengthen research, innovations, advocacy and networking for palliative care in Uganda and Africa;
    6.  To ensure effective and efficient governance at HAU(Hospice Africa Uganda)  
    7.  To enhance financial efficiency and sustainability.

     Need for palliative care

    • WHO estimates 9 million new cases of cancer each year (50% in developing countries).
    • More than 80% disease presents late and is often incurable.
    • Pain occurs in more than 66% of patients with advanced cancer
    • 5 million HIV+ people live in sub–Saharan Africa
    • 20-50% HIV patients can expect to suffer from severe

     

    Philosophy/Roles of Palliative care

    • Affirms life.
    • Regards dying as a normal process.
    • Neither hastens nor postpones death.
    • Relieves pain and other distressing symptoms.
    • Integrates the psychological and spiritual aspects of care.
    • Offers support systems for patients to live as actively as possible until death
    • Offers support systems to help patients’ families cope during the patient’s illness and in their own bereavement.
    • Appropriate ethical considerations: Do good; do no harm, patient’s right to decide; and fairness.

    Attributes of Palliative Care

    Palliative care has a range of distinctive characteristics or attributes. 

    In palliative care, “attributes” refers to the characteristics, features, or qualities that are  associated with or define palliative care. These attributes are the essential elements that make up the nature and scope of palliative care as a specialized form of medical care.

    Here are the key attributes of palliative care:

    1. Holistic approach: Palliative care takes a comprehensive approach to address the physical, emotional, psychological, social, and spiritual needs of the patient. It considers the person as a whole and not just the disease.

    2. Pain and symptom management: Palliative care aims to alleviate pain, manage symptoms, and improve the patient’s comfort level. This involves using a combination of medications, therapies, and other interventions to control distressing symptoms.

    3. Communication and coordination: Effective communication is crucial in palliative care. The care team works closely with the patient and their family to understand their preferences, goals, and values. They also facilitate coordination between different healthcare professionals to ensure seamless care delivery.

    4. Patient-centered care: Palliative care respects the patient’s autonomy and individual preferences. It involves shared decision-making, where patients are actively involved in making choices about their care and treatment options.

    5. Family support: Palliative care recognizes the impact of serious illness on the patient’s family members and caregivers. It offers emotional support, education, and guidance to help them cope with the challenges they may face.

    6. Continuity of care: Palliative care is not limited to a specific location or time frame. It can be provided alongside curative treatments and is often delivered at different stages of the illness.

    7. Advance care planning: Palliative care encourages patients to discuss and document their preferences for medical treatment and end-of-life care in advance. This helps ensure that their wishes are respected and followed.

    8. Bereavement support: Palliative care extends its support to the family even after the patient’s death. Bereavement services help family members cope with grief and loss.

    9. Interdisciplinary care team: Palliative care involves a team of healthcare professionals with various specialties, including doctors, nurses, social workers, chaplains, and other specialists as needed. This interdisciplinary approach ensures a comprehensive and well-coordinated care plan.

    10. Dignity and respect: Palliative care emphasizes the importance of treating patients with respect, preserving their dignity, and providing compassionate care throughout their journey.

    Essential components of palliative care

    Palliative care has two components:

    • Pain and symptom control: Modern methods are used for pain relief, including oral morphine for severe pain, and symptom treatment and management.
    • Supportive care: The psychological, social, spiritual and cultural needs of the patient and the family, including bereavement care, are attended to.
     Key aspects to palliative care
    • Focus on quality of life
    • Holistic approach
    • Multi disciplinary team (MDT)- doctor, nurse, physiotherapist, occupation therapist, social worker
    • Patient and family at center of care
    • Attention to details
    • Availability of essential drugs e.g. morphine
    • Peace, comfort and dignity of the patient and family.

    Principles of Palliative Care

    1. Patient centered: Palliative care revolves around the patient and their family. The focus is on maintaining hope with realistic goals, supporting the patient and their loved ones throughout different stages of the illness. Sustain hope with realistic goals in order to help patient and families cope in appropriate way through the different phase of the illness.
    2.  Appropriate ethical consideration: There are many ethical issues that arise in care of all patients. Seek to do good or do no harm, patients’ rights must be considered to decide fairly. Palliative care involves navigating various ethical issues. Remember to balance doing what’s best for the patient while respecting their rights and autonomy. 
    3. Continuum of treatment. This involves management of pain and other symptoms i.e. Palliative care begins from the time of diagnosis and extends beyond the patient’s passing. It includes pain and symptom management as well as providing bereavement care for the family after death. (bereavement
      care).
    4. Teamwork and partnership: Palliative care requires an interdisciplinary team to address the diverse needs of patients effectively. It is not easy to address all patients’ needs alone. An interdisciplinary team should be established to deal with all the problems. i.e. no single profession can address all issues that cause total pain. Team members share challenges facing the patient and plan effective management of the patient using their skill mix. A palliative care team includes:
      1. Nurses
      2. Doctor
      3. Social workers
      4. Religious leaders
      5. Teachers
      6. Community health providers > Others as appropriate.

    5. Holistic care approach: Holistic care treats the patients as a whole person, not just as a medical case. This approach focuses not only on physical care, but also psychological (emotional), social and spiritual care. This psychological and emotional support and care should be available for the caregivers as well as the patient, family members, community volunteers, professional care and support workers (health workers, counselors, social workers), before, during and after periods of care giving.

      Holistic care: this is care of whole person and is more than only drug and physical care

    Components of holistic care

    1.  Physical care: This involves the assessment and management of pain and other physical symptoms. Its important because if physical symptoms are with them if they controlled other aspects will be different to carry.
    2.  Psychological care: Effective communication skills are crucial in caring for patients holistically. Providing emotional support, active listening, and compassionate understanding help patients cope with the emotional challenges they face.
    3.  Spiritual care: This is important to terminally ill and it includes allowing patients to express their spirituality, praying with them if they request for arranging for an appropriate leader to visit them.
    4.  Family support: The terminal phase of illness is often very difficult for patients’ family. Support therefore needs to be offered to the family. It includes spending time, listening and giving support to them.
    5.  Social care: This incorporates discussion of social and family issue e.g. This could include considering the well-being of young children who may become orphans and discussing financial matters that can impact the patient and their family.

    Models of Palliative Care

    1.  Health facilities based: Palliative care is provided either in hospital at the outpatient department or in other clinics as designated by the in-charge. Health Centers IV and Ill with palliative care trained
      health workers provide palliative care services using a facility palliative care team.
    2.  Health facility Out-reach programs: specialist palliative care health workers travel to other center to provide palliative care. Palliative care in this modal is provided by palliative care trained health workers. The team moves to the community to provide palliative care services closer to the community. Facility outreach programs are important in that they bring the services nearer to the
      people. Hence patients do not have to walk long distances and a mass of people can be seen within their villages.
    3.  Roadside clinics/stopovers: This is a model of care that enables patients who live far away from health facilities to access palliative care. Health care providers plan with patients and their caregivers to
      meet- in identified place along the route or on their way to an outreach. They make a stopover in an agreed place. The place location can be a trading Centre, under a tree, at a particular signpost or at a school.
    4.  Facility day care: This is when a day is set aside for the patient and their caretaker to spend time with other patients in at the facility. This facility could be a hospital, health Centre a hospice. This activity
      enables recreation as well as socialization. Patients get to share their challenges encounter during the disease trajectory arid even counsel themselves. They interact as they enjoy lunch or tea, they also get an opportunity to see their nurses or doctors at the site and have they needs attended to.
    5. Community day care: It is similar to facility day care except it is done within the community. Health care workers move to the community and spend the day with patients at a designated area in the community, it could be at the church, health Centre community hall or someone’s home.
    6.  Home based palliative care model: This means a delivery of a comprehensive package of care to the patient and the family at home. The package includes spiritual, psychological, pain and symptom management as well as support in activities of daily living. This model of care is best provided by a specialist palliative care team working in partnership with trained community health volunteers.

    Services offered during home based palliative care:

    • Basic physical care such as recognition of symptoms; basic treatment and symptom management
    • Basic nursing care, such as positioning and mobility, bathing, wound cleaning, skin care, maintaining basic hygiene, oral care, taking medication.
    • Psychosocial support and counseling: being with the patient and family during a difficult time, providing listening and understanding, sharing a quiet moment, helping the family to access legal support.
    • Preventing transmission of infections such as HIV testing, disclosure, condoms, safe water
    • Provide spiritual support: listening to patients and families’ spiritual troubles and anxieties, praying with the patient, and preparation for death.
    • Household assistance- support patients with practical support such as washing clothes, cleaning, shopping
    • Providing health promotion: disease prevention such as HIV, TB
    • Training care takers in basic nursing skills and care.

    Advantages and disadvantages of each model

    Palliative Care ModelAdvantagesDisadvantages
    Health Facilities Based– Accessible within health facilities– May not reach patients in remote areas
     – Utilizes facility-based palliative care team– Limited to patients who visit health centers
     – Expert care provided by trained health workers 
    Health Facility Outreach– Brings care closer to the community– Limited to specific outreach locations
    Programs– Allows for mass outreach and care provision– Requires additional resources for travel
     – Utilizes trained palliative care specialists 
    Roadside Clinics/Stopovers– Enables care for patients in remote areas– Requires planning and coordination for stopovers
     – Convenient for patients and caregivers on the go– May have limited medical resources during stopovers
    Facility Day Care– Provides recreation and socialization for patients– Limited to designated facility and day
     – Allows patients to interact and share experiences– Patients may require transportation to the facility
    Community Day Care– Brings care directly to the community– Limited to specific designated areas
     – Enhances community involvement and support– May lack necessary medical equipment and supplies
    Home-Based Palliative Care– Provides comprehensive care at home– Requires a specialized palliative care team
    Model– Allows for spiritual, psychological, and symptom– May be challenging in remote or underserved areas
     management in the comfort of the patient’s home– Depends on the availability of trained volunteers
     – Supports the patient and family in daily activities 
    Challenges for implementing palliative care
    1. Perception and recognition: many people still fear palliative care because they link it to death and many do not want to admit that they are dying. It is also common with health worker, policy makers
      and others.
    2.  Policy development; sustainable, affordable and effective palliative care must be an integral of a country’s health system. To achieve this there must be coordination with all health sectors. Some
      policies prohibit use of oral opioids, so advocacy for change is important
    3.  Education: health providers and community members need to be educated on diagnosis, classification and application of holistic approach. Training should be in medical/nursing schools
    4.  Drug availability: there are limited recourses including limited drug budget a palliative drugs are given priority because they are for symptoms relief. It is important for these drugs to be included in the
      essential drug list.

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    Nephritic and Nephrotic syndromes

    Nephrotic and Nephritic syndromes

    NEPHROTIC SYNDROME.

    Nephrotic syndrome, or nephrosis, is a constellation of symptoms characterized by nephrotic range, massive proteinuria, edema, and hypoalbuminemia with or without hyperlipidemia.

    MASSIVE Proteinuria >3.5g/24 hours Or spot urine protein: creatinine ratio >300 – 350 mg/mmol Hypoalbuminemia <25g/L,

    Edema,(Generalized edema is called Anasarca)

    And often: Hyperlipidemia/dyslipidemia (total cholesterol >10 mmol/L) 

     

    Additionally, the loss of immunoglobulins increases the risk of infection, while the loss of proteins that prevent clot formation puts patients at risk for blood clots.

     

    NEPHROTIC syndrome PATHOPHYSIOLOGY

    Pathophysiology of Nephrotic Syndrome.

    Nephrotic syndrome results from damage to the kidney’s glomeruli, the tiny blood vessels that filter waste and excess water from the blood and send them to the bladder as urine. 

    Damage to the glomeruli from diabetes or even prolonged hypertension causes the membrane to become porous, so that small proteins such as albumin pass through the kidneys into urine.

    • Glomerular Filtration Barrier Disruption: The renal glomerulus, responsible for filtering blood entering the kidney, consists of capillaries with small pores. In nephrotic syndrome, inflammation or hyalinization affects the glomeruli, allowing proteins, including albumin, antithrombin, and immunoglobulins, to pass through the normally restrictive cell membrane.
    • Proteinuria: Increased permeability results in the leakage of proteins into the urine. Albumin, a key protein for maintaining oncotic pressure in the blood, is lost in significant amounts.
    • Hypoalbuminemia: Loss of albumin in the urine reduces the oncotic pressure in the blood. Reduced oncotic pressure leads to the accumulation of fluid in the interstitial tissues, causing edema.
    • Hyperlipidemia: Hypoalbuminemia triggers compensatory mechanisms in the liver. The liver increases the synthesis of proteins such as alpha-2 macroglobulin and lipoproteins. Elevated lipoprotein levels contribute to hyperlipidemia associated with nephrotic syndrome.
    Nephrotic Syndrome signs and symptoms

    Signs and symptoms

    Manifestation of glomerular disease, characterized by nephrotic range proteinuria and a triad of clinical findings associated with large urinary losses of protein : hypoalbuminaemia , edema and hyperlipidemia 

    Weight Gain: Patients experience noticeable weight gain due to fluid retention. The retention of fluids, primarily as a result of massive proteinuria and reduced oncotic pressure, leads to increased body weight.

    Facial Edema (Puffiness Around the Eyes):  Swelling, particularly around the eyes, with a distinctive pattern. Generalized edema is called Anarsaca.

    • Morning Onset: The puffiness is most apparent in the morning and tends to subside throughout the day.
    • Location: Predominantly observed around the eyes.

    Abdominal Swelling:  Enlargement of the abdominal region. Associated with; 

    • Pleural Effusion: Accumulation of fluid in the pleural cavity.
    • Labial or Scrotal Swelling: Swelling in the genital areas.

    Edema of Intestinal Mucosa:  Swelling of the intestinal mucosa leading to various gastrointestinal symptoms. Such as 

    • Diarrhea: Resulting from edema affecting the intestinal lining.
    • Anorexia: Loss of appetite due to abdominal discomfort.
    • Poor Intestinal Absorption: Impaired absorption of nutrients, contributing to malnutrition.

    Ankle/Leg Swelling: Edema affecting the lower extremities. Fluid accumulation in the ankles and legs due to altered fluid balance.

    Behavioral Changes: Altered mood and behavior. Manifested as;

    • Irritability: Restlessness or frustration.
    • Easily Fatigued: Fatigue occurs more quickly than expected.
    • Lethargy: Persistent tiredness, indicating overall weakness.

    Susceptibility to Infection: Increased vulnerability to infections. Loss of immunoglobulins in the urine, combined with potential immune system suppression from treatments like corticosteroids, increases the risk of infections.

    Urine Alterations: Changes in urine characteristics. Such as;

    • Decreased Volume: Reduced urine output.
    • Frothy Urine: Presence of foam or bubbles in the urine, indicating significant proteinuria.
    • Lipiduria (lipids in urine) can also occur, but is not essential for the diagnosis of nephrotic syndrome. Hyponatremia also occurs with a low fractional sodium excretion. 

    Hyperlipidaemia: Hypoproteinemia stimulates protein synthesis in the liver, resulting in the overproduction of lipoproteins.

    Anaemia (iron resistant microcytic hypochromic type) may be present due to transferrin loss.

    Dyspnea may be present due to pleural effusion or due to diaphragmatic compression with ascites.

    Other features: May have features of the underlying cause, such as the rash associated with systemic lupus erythematosus, or the neuropathy associated with diabetes.

     
    Nephrotic Syndrome causes

    Causes of Nephrotic Syndrome

    Nephrotic syndrome has many causes and may either be the result of a glomerular disease that can be either limited to the kidney, called primary nephrotic syndrome (primary glomerulonephrosis), or a condition that affects the kidney and other parts of the body, called secondary nephrotic syndrome and other genetic causes.

    Primary causes

    • Minimal change disease (MCD): is the most common cause of nephrotic syndrome in children. It owes its name to the fact that the nephrons appear normal when viewed with an optical microscope as the lesions are only visible using an electron microscope. Another symptom is a pronounced proteinuria.
    • Focal segmental glomerulosclerosis (FSGS): is the most common cause of nephrotic syndrome in adults.  It is characterized by the appearance of tissue scarring in the glomeruli. The term focal is used as some of the glomeruli have scars, while others appear intact; the term segmental refers to the fact that only part of the glomerulus suffers the damage.
    • Membranous glomerulonephritis (MGN): The inflammation of the glomerular membrane causes increased leaking in the kidney. It is not clear why this condition develops in most people, although an auto-immune mechanism is suspected.
    • Membranoproliferative glomerulonephritis (MPGN): is the inflammation of the glomeruli along with the deposit of antibodies in their membranes, which makes filtration difficult.
    • Rapidly progressive glomerulonephritis (RPGN): (Usually presents as a nephritic syndrome) A patient’s glomeruli are present in a crescent moon shape. It is characterized clinically by a rapid decrease in the glomerular filtration rate (GFR) by at least 50% over a short period, usually from a few days to 3 months.

    Secondary causes

    • Diabetic nephropathy: is a complication that occurs in some diabetics. Excess blood sugar accumulates in the kidney causing them to become inflamed and unable to carry out their normal function. This leads to the leakage of proteins into the urine.
    • Systemic lupus erythematosus: this autoimmune disease can affect a number of organs, among them the kidney, due to the deposit of immune complexes that are typical to this disease. The disease can also cause lupus nephritis.
    • Infections like; Syphilis: Kidney damage can occur during the secondary stage of this disease (between 2 and 8 weeks from onset). Hepatitis B: certain antigens present during hepatitis can accumulate in the kidneys and damage them. HIV: the virus’s antigens provoke an obstruction in the glomerular capillary’s lumen that alters normal kidney function.
    • Vasculitis: inflammation of the blood vessels at a glomerular level impedes the normal blood flow and damages the kidney.
    • Cancer: as happens in myeloma, the invasion of the glomeruli by cancerous cells disturbs their normal functioning.
    • Genetic disorders: congenital nephrotic syndrome is a rare genetic disorder in which the protein nephrin, a component of the glomerular filtration barrier, is altered.
    • Drugs ( e.g. gold salts, penicillin, captopril): gold salts can cause a more or less important loss of proteins in urine as a consequence of metal accumulation. Penicillin is nephrotoxic in patients with kidney failure and captopril can aggravate proteinuria.
    diagnosis of nephrotic

    Diagnosis and Investigations

    Initial Assessment:

    • Obtain a thorough medical history, including any acute or  chronic conditions, family history of kidney disease, and a review of systems to identify symptoms such as edema, fatigue, and foamy urine.
    • Perform a physical examination focusing on signs of fluid overload, such as edema and ascites, as well as other systemic findings.

    Laboratory Investigations:

    • Conduct urinalysis to detect the features of nephrotic syndrome: high levels of proteinuria.
    • Microscopic hematuria that may occasionally be present.
    • Biochemical tests to evaluate kidney function, including serum creatinine, blood urea nitrogen (BUN), electrolytes, albumin levels, and a lipid profile, as hyperlipidemia is often associated with nephrotic syndrome.
    • Perform a urine protein-to-creatinine ratio to quantify the degree of proteinuria.

    Imaging Studies:

    • Ultrasound imaging: the kidneys may appear hyperechoic with a loss of corticomedullary differentiation.
    • If indicated, conduct an ultrasound of the entire abdomen to evaluate for complications such as venous thrombosis or to rule out other causes of proteinuria.

    Immunological and Serological Testing:

    • Analyze auto-immune markers, including antinuclear antibodies (ANA), anti-streptolysin O titers (ASOT), complement components (such as C3), cryoglobulins, and perform serum electrophoresis to detect monoclonal gammopathy.

    Kidney Biopsy:

    • If the initial tests are inconclusive or if it is important to determine the specific cause of nephrotic syndrome, Carry out a kidney biopsy. Histological examination can identify the type of glomerulonephritis or other glomerular pathology.

    Additional Investigations:

    • Consider genetic testing if there is a suspicion of hereditary causes of nephrotic syndrome, especially in pediatric cases or when there is a family history of kidney disease.
    • Assess for secondary causes of nephrotic syndrome, which may include tests for infectious diseases (like hepatitis B and C, HIV), diabetes mellitus control (HbA1c), and evaluation for malignancies if clinically indicated.

    Treatment of Nephrotic Syndrome

    Aims of Management.

    • To reduce edema
    • To correct hypoalbuminemia
    • To lower blood pressure
    • To reduce proteinuria
    • To prevent complications such as infection, thrombosis, and malnutrition

    Medical Management:

    1. Diuretics: Loop diuretics, such as furosemide, are the mainstay of treatment for edema. Thiazide diuretics, such as hydrochlorothiazide, can be added if needed.
    2. Albumin: Albumin infusions may be necessary to correct hypoalbuminemia and reduce edema. Not used because they are expensive.
    3. ACE inhibitors or ARBs: ACE inhibitors, such as lisinopril, or ARBs, such as losartan, are used to lower blood pressure and reduce proteinuria.
    4. Corticosteroids: Prednisone is the most commonly used corticosteroid for the treatment of nephrotic syndrome. Prednisone is started at a dose of 1-2 mg/kg/day and then tapered over several weeks.  Lack of response to prednisolone therapy for 4 weeks is an Indication for renal biopsy.
    5. Immunosuppressive drugs: Immunosuppressive drugs, such as cyclophosphamide, are used to treat patients who do not respond to corticosteroids.
    6. Statins: Statins, such as atorvastatin, are used to lower cholesterol levels.
    7. Antiplatelet agents: Antiplatelet agents, such as aspirin, are used to prevent thrombosis.
    8. Nutritional support: Nutritional support, including a high-protein diet, is important to prevent malnutrition.
    9. Vitamin D and calcium supplements: Vitamin D and calcium supplements may be necessary to prevent hypocalcemia.
    10. Antibiotics: Antibiotics are used to treat infections.
    11. Vaccinations: Vaccinations against pneumococcal pneumonia and influenza are recommended for patients with nephrotic syndrome.

    Nursing Interventions for Nephrotic Syndrome:

    Fluid Volume Excess:

    • Elevate the child’s legs and feet to promote fluid drainage.
    • Monitor for signs of fluid overload, such as edema, ascites, and pleural effusions.
    • Restrict fluid intake as prescribed by the physician.
    • Administer diuretics, such as furosemide (Lasix), as prescribed to promote fluid excretion.
    • Monitor intake and output strictly and maintain accurate fluid balance charts.
    • Weigh the child daily to monitor fluid status.

    Ineffective Breathing Pattern:

    • Assess respiratory status regularly, including oxygen saturation, respiratory rate, and effort.
    • Position the child in a semi-Fowler’s position or over a table supported by pillows to improve lung expansion.
    • Provide oxygen therapy, if prescribed, to maintain adequate oxygenation.
    • Encourage the child to take slow, deep breaths and use relaxation techniques to reduce anxiety and improve breathing patterns.
    • Administer bronchodilators, if prescribed, to improve airflow and reduce wheezing.

    Risk for Infection:

    • Monitor the child for signs of infection, such as fever, chills, and increased white blood cell count.
    • Administer antibiotics, as prescribed, to treat or prevent infections.
    • Practice strict hand hygiene and maintain aseptic technique when handling the child and performing procedures.
    • Keep the child’s skin clean and dry to prevent skin infections.
    • Monitor the child’s nutritional status and provide a diet rich in protein and vitamins to support the immune system.

    Altered Nutrition: Less Than Body Requirements:

    • Provide small, frequent meals that are high in protein and calories to meet the child’s increased nutritional needs.
    • Offer a variety of foods to encourage the child to eat and prevent monotony.
    • Consult with a registered dietitian to develop a personalized nutrition plan that meets the child’s individual needs and preferences.
    • Supplement the child’s diet with nutritional supplements, as prescribed, to ensure adequate intake of essential nutrients.

    Dietary Management of Nephrotic Syndrome:

    • Provide a balanced diet with adequate protein (1.5-2 g/kg) and calories.
    • Limit fat intake to less than 30% of total calories and avoid saturated fats.
    • Encourage the child to follow a “no added salt” diet to reduce fluid retention.
    • Discourage the consumption of high-sugar drinks and snacks to prevent weight gain and fluid overload.
    • Monitor the child’s weight regularly and adjust the diet as needed to maintain a healthy weight.

    Complications:

    • Monitor for complications of nephrotic syndrome, such as ascites, pleural effusion, generalized edema, coagulation disorders, thrombosis, recurrent infections, renal failure, growth retardation, and calcium and vitamin D deficiency.
    • Provide appropriate interventions and treatments for any complications that arise.
    • Educate the child and family about the potential complications of nephrotic syndrome and the importance of regular follow-up care.
    Complications of Nephrotic Syndrome:

    Complications of Nephrotic Syndrome:

    • Thromboembolic Disorders:  Caused by decreased levels of antithrombin III, a protein that inhibits blood clotting. Antithrombin III is lost in the urine due to the increased permeability of the glomerular basement membrane. This can lead to the formation of blood clots in the veins (deep vein thrombosis) or arteries (pulmonary embolism).
    • Infections:  Increased susceptibility to infections due to:
    1. Loss of immunoglobulins and other protective proteins in the urine.
    2. Decreased production of white blood cells.
    3. Impaired immune cell function.
    4. Common infections include pneumonia, cellulitis, and peritonitis.
    • Acute Kidney Failure: Caused by a decrease in blood volume (hypovolemia) due to fluid loss into the tissues (edema). Hypovolemia leads to decreased blood flow to the kidneys, which can damage the kidneys and cause acute kidney failure.
    • Pulmonary Edema: Caused by the loss of proteins from the blood plasma, which leads to a decrease in oncotic pressure. Decreased oncotic pressure allows fluid to leak out of the blood vessels into the lungs, causing pulmonary edema.
    • Hypothyroidism: Caused by the loss of thyroxine-binding globulin (TBG), a protein that binds to thyroid hormone and transports it in the blood. Decreased TBG levels lead to decreased levels of free thyroid hormone, which can cause hypothyroidism.
    • Vitamin D Deficiency: Caused by the loss of vitamin D-binding protein, a protein that binds to vitamin D and transports it in the blood. Decreased vitamin D-binding protein levels lead to decreased levels of free vitamin D, which can cause vitamin D deficiency.
    • Hypocalcemia: Caused by the loss of 25-hydroxycholecalciferol, the storage form of vitamin D. Vitamin D is necessary for the absorption of calcium from the intestines. Decreased vitamin D levels lead to decreased calcium absorption, which can cause hypocalcemia.
    • Microcytic Hypochromic Anemia:  Caused by the loss of ferritin, a protein that stores iron in the body. Decreased ferritin levels lead to decreased iron stores, which can cause iron-deficiency anemia.
    • Protein Malnutrition: Caused by the loss of protein in the urine, which exceeds the amount of protein that is ingested.  Protein malnutrition can lead to a number of health problems, including weakness, fatigue, and impaired immune function.
    • Growth Retardation: Can occur in children with nephrotic syndrome due to a number of factors, including:
    1. Protein malnutrition.
    2. Anorexia (reduced appetite).
    3. Steroid therapy (which can suppress growth).
    • Cushing’s Syndrome:  Can occur in patients with nephrotic syndrome who are treated with high doses of corticosteroids. Cushing’s syndrome is caused by the overproduction of the hormone cortisol, which can lead to a number of health problems, including weight gain, high blood pressure, and diabetes.

    Related Question of Nephrotic Syndrome 

    1. An adult male patient has been brought to medical ward with features of nephrotic syndrome 

    (a) List five cardinal signs and symptoms of nephrotic syndrome 

    (b) Describe his management from admission up to discharge. 

    (c) Mention five likely complications of this condition. 

    SOLUTIONS 

    (a) NEPHROTIC SYNDROME. 

    Is a syndrome caused by many diseases that affect the kidney characterized by severe and prolonged loss of protein in urine especially albumen, retention of excessive salts and water, increased levels of fats. 

    FIVE CARDINAL SIGNS AND SYMPTOMS. 

    • Massive proteinuria.
    • Generalized edema.
    • Hyperlipidemia.
    • Hypoalbuminemia.
    • Hypertension.

    (b) MANAGEMENT. 

    Aims of management 

    • To prevent protein loss in urine. 
    • To prevent and control edema.
    • To prevent complications. 

    ACTUAL MANAGEMENT. 

    1. Admit the patient in the medical ward male side in a warm clean bed in a well ventilated room and take the patient’s particulars such as name, age, sex, religion, status. 
    2. General physical examination is done to rule out the degree of oedema and other medical conditions that may need immediate attention. 
    3. Vital observations are taken such as pulse, temperature, blood pressure recorded and any abnormality detected and reported for action to be taken. 
    4. Inform the ward doctor about the patient’s conditions and in the meantime, the following should be done. 
    5. Position the patient in half sitting to ease and maintain breathing as the patient may present with dyspnoea due to presence of fluids in the pleural cavity. 
    6. Weigh the patient to obtain the baseline weight and daily weighing of the patient should be done to ascertain whether edema is increasing or reducing which is evidenced by weight gain or loss. 
    7. Monitor the fluid intake and output using a fluid balance chart to ascertain the state of the kidney. 
    8. Encourage the patient to do deep breathing exercises to prevent lung complications such as atelectasis. 
    9. Provide skin care particularly over edematous areas to prevent skin breakdown. 
    10. On doctor’s arrival, he may order for the following investigations. 
    11. Urine for culture and sensitivity to identify the causative agent. 
    12. Urinalysis for proteinuria and specific gravity, blood for; 
    13. Renal function test, it will show us the state of the kidney function. 
    14. Cholesterol levels; this will show us the level of cholesterol in blood. 
    15. Serum albumen; this will show us the level of protein or albumin in blood. 
    16. The doctor may prescribe the following drugs to be administered; 
    17. Diuretics, such as spironolactone 100-200mg o.d to reduce edema by increasing the fluid output by the kidney. 
    18. Antihypertensives such as captopril to control the blood pressure. 
    19. Infusion albumin 1g/kg in case of massive edema ascites and this will help to shift fluid from interstitial spaces back to the vascular system. 
    20. Plasma blood transfusion to treat hypoalbuminemia. 
    21. Cholesterol reducing medication to have the cholesterol levels in blood such as lovastatin. 
    22. Anticoagulants to reduce the blood ability to clot and reduce the risk of blood clot formation e.g. Heparin.
    23. Immune suppressing medications are given to control the immune system such as prednisolone if the cause is autoimmune. 
    24. Antibiotics such as ceftriaxone to treat secondary bacterial infections. 
    25. The doctor may order for renal transplant if the chemotherapy fails. 

    Routine nursing care. 

    • Continuous urine testing is done to see whether proteinuria is reducing or increasing. 
    • Encourage the patient to take a deity rich in carbohydrates and vitamins but low in protein and salts. 
    • Ensure enough rest for the patient as this will reduce body demand for oxygen and hence prevent fatigue. 
    • Promote physical comfort by ensuring daily bed bath, change of position, oral care and change of bed linen. 
    • Reassure the patient to alleviate anxiety and hence promote healing. 
    • Ensure bladder and bowel care for the patient. 

    ADVICE ON DISCHARGE 

    The patient is advised on the following: 

    • To take a deity low in salt and protein. 
    • Drug compliance. 
    • Personal hygiene. 
    • Stop using drugs like heroin, NSAIDs. 
    • Screening and treating of diseases predisposing or causing the disease. 
    • To come back for review on the appointment given. 

    COMPLICATIONS. 

    • Acute kidney failure. 
    • Kidney necrosis. 
    • Ascites. 
    • Pyelonephritis. 
    • Cardiac failure
    • Pulmonary embolism. 
    • Atherosclerosis. 
    • Deep venous thrombosis. 

    NEPHRITIC SYNDROME

    Differences between Nephrotic syndrome and Nephritic syndrome

    differences between nephrotic and nephritic syndrome.
    Differences between Nephrotic syndrome and Nephritic syndrome

    Nephrotic and Nephritic syndromes Read More »

    Glomerulonephritis

    Glomerulonephritis

    Glomerulonephritis (GN)

    Glomerulonephritis (GN) refers to a group of kidney diseases characterized primarily by inflammation and damage to the glomeruli, the tiny filtering units within the kidneys.

    Glomerulonephritis is an inflammatory condition of the kidneys characterized by increased permeability of the glomerular filtration barrier causing filtration of RBCs and proteins.

    While the primary site of injury is the glomerulus, inflammation can sometimes extend to the small blood vessels (capillaries, arterioles) within the kidney.

    • Bilateral Involvement: GN usually affects both kidneys simultaneously due to the systemic nature of many underlying causes (e.g., immune responses, infections).
    Nephrotic Syndrome causes

    Review of Relevant Anatomy and Physiology: The Nephron and Glomerulus

    Functional Unit: The nephron is the fundamental structural and functional unit of the kidney, responsible for filtering blood and producing urine. Each kidney contains approximately 1 million nephrons.

    Nephron Structure:

    • Glomerular Capsule (Bowman’s Capsule): A cup-shaped structure at the closed end of the nephron tubule. It surrounds the glomerulus.
    • Glomerulus: A network (tuft) of tiny arterial capillaries enclosed within Bowman’s capsule. This is where blood filtration begins. Blood enters via the afferent arteriole and exits via the efferent arteriole.
    • Renal Tubule: Extending from Bowman’s capsule, this tubule is about 3 cm long and consists of three main parts:
    1. Proximal Convoluted Tubule (PCT): Responsible for reabsorbing the majority of filtered water, electrolytes (Na+, K+, Cl-), glucose, amino acids, and bicarbonate.
    2. Loop of Henle: A hairpin-shaped loop (with descending and ascending limbs) extending into the medulla. Crucial for establishing the concentration gradient in the kidney, allowing for urine concentration. Further water and electrolyte reabsorption occurs here.
    3. Distal Convoluted Tubule (DCT): Involved in fine-tuning electrolyte and acid-base balance (e.g., reabsorbing Na+, Ca++; secreting K+, H+). Influenced by hormones like aldosterone and ADH (indirectly).
    • Collecting Duct: Several DCTs empty into a collecting duct. These ducts pass through the medulla, further adjusting water reabsorption (under ADH influence) and electrolyte balance before delivering urine to the renal pelvis.

    Glomerular Filtration Membrane (GFM): The crucial barrier separating blood in the glomerular capillaries from the filtrate in Bowman’s space. It consists of three layers:

    • Endothelium: The inner lining of the capillaries, featuring fenestrations (pores) that allow passage of water and small solutes but block blood cells.
    • Glomerular Basement Membrane (GBM): A middle layer, acting as a key size-selective and charge-selective barrier, preventing larger proteins (like albumin) from passing through.
    • Epithelial Cells (Podocytes): The outer layer facing Bowman’s space. These cells have foot processes (pedicels) separated by filtration slits, covered by a slit diaphragm, providing a final barrier, particularly to medium-sized proteins.

    Glomerular Filtration Rate (GFR): The volume of fluid filtered from the glomerular capillaries into Bowman’s capsule per unit of time.

    • Normal GFR: Approximately 125 mL/minute or 180 Liters/day.
    • Filtration Process: Water and small molecules (electrolytes, glucose, urea, amino acids) pass freely through the GFM. Blood cells and large proteins (like albumin) are normally retained in the blood.
    • Reabsorption: Most of the filtrate (over 99%) is reabsorbed back into the bloodstream by the renal tubules. Only about 1-1.5 mL of fluid per minute is typically excreted as urine.

    Renal Blood Flow Regulation: The kidneys have intrinsic mechanisms (autoregulation) and are influenced by the autonomic nervous system (sympathetic and parasympathetic nerves) and hormones (like angiotensin II, prostaglandins) to maintain relatively stable blood flow and GFR despite fluctuations in systemic blood pressure.

    Classification of Glomerulonephritis

    GN can be classified in several ways, which often overlap:

    Onset and Duration:

    • Acute Glomerulonephritis (AGN): Develops suddenly, often following an infection (like streptococcus). Onset can be days to weeks after the trigger. Typically presents with nephritic features (see below).
    • Chronic Glomerulonephritis (CGN): Develops gradually over several years, often silently in the early stages. It may follow an episode of acute GN or arise insidiously. It represents progressive scarring and loss of kidney function, eventually leading to Chronic Kidney Disease (CKD).
    • Rapidly Progressive Glomerulonephritis (RPGN): Characterized by rapid loss of kidney function (often a 50% decline in GFR within weeks to months). Histologically associated with crescent formation in Bowman’s space. This is a medical emergency.

    Histological Pattern (Based on Kidney Biopsy):

    • Proliferative GN: Characterized by an increase in the number of cells within the glomerulus (e.g., endothelial, mesangial, epithelial cells, infiltrating inflammatory cells). Examples include:
    1. IgA Nephropathy (most common primary GN worldwide)
    2. Post-Infectious GN (e.g., post-streptococcal)
    3. Membranoproliferative GN (MPGN)
    4. Lupus Nephritis (certain classes)
    5. RPGN (Crescentic GN)
    • Non-Proliferative GN: Characterized primarily by structural changes without significant hypercellularity. Examples include:
    1. Minimal Change Disease (common cause of nephrotic syndrome in children)
    2. Focal Segmental Glomerulosclerosis (FSGS)
    3. Membranous Nephropathy (common cause of nephrotic syndrome in adults)

    Clinical Manifestations (Signs and Symptoms)

    Symptoms vary widely depending on the type, severity, and acuity of GN. Some patients may be asymptomatic initially.

    Common Features (especially Nephritic pattern):

    • Hematuria: Blood in the urine. May be microscopic (detected only by test) or macroscopic (visible, often described as cola-colored, tea-colored, or smoky). RBC casts in urine sediment are highly suggestive of glomerular origin.
    • Proteinuria: Excess protein in the urine. Can range from mild to nephrotic range (>3.5g/day). May cause foamy urine.
    • Edema: Swelling, often starting around the eyes (periorbital edema, especially in the morning) and progressing to the legs (pedal edema), ankles, and potentially generalized (anasarca), including ascites (fluid in abdomen) and pleural effusions (fluid around lungs). Due to sodium/water retention and sometimes low albumin (in nephrotic syndrome).
    • Hypertension: New onset or worsening high blood pressure. Often related to fluid retention. Can be severe.
    • Oliguria/Anuria: Decreased urine output (<400-500 mL/day) or very low/no urine output. Indicates significant decline in GFR.
    • Dysuria: Painful urination (less common, but can occur).

    Systemic Symptoms:

    • Fatigue/Malaise/Weakness: Due to anemia (from reduced erythropoietin production by failing kidneys or chronic inflammation), uremia, or the underlying disease.
    • Flank Pain: Aching pain in the back/sides over the kidney area (less common than in kidney stones or pyelonephritis, but can occur due to capsular stretching).
    • Fever & Chills: More common in acute, infection-related GN or systemic inflammatory conditions.
    • Headache: Often related to hypertension.
    • Gastrointestinal Disturbances: Nausea, vomiting, anorexia, abdominal pain (can be due to uremia or ascites).

    Symptoms Related to Complications or Underlying Disease:

    • Shortness of Breath: Due to pulmonary edema (fluid in lungs) from fluid overload or heart failure.
    • Visual Disturbances: Blurred vision due to hypertensive retinopathy or retinal edema.
    • Symptoms of SLE, Vasculitis, etc.: Rash, joint pain, etc.
    • Chronic GN Symptoms: May be subtle initially, presenting later with signs of CKD like nocturia (frequent urination at night), bone pain/deformity (renal osteodystrophy), anemia, failure to thrive (in children).

    Clinical Presentation of Glomerulonephritis

    Nephritic Syndrome: Characterized by inflammation. 

    • Key features include Hematuria (blood in urine, often cola-colored), 
    • Hypertension, 
    • Oliguria (reduced urine output), 
    • Azotemia (increased BUN/Creatinine), and 
    • mild to moderate Proteinuria. 
    • Edema is common. 
    • Post-streptococcal GN is a classic example.

    Nephrotic Syndrome: Characterized by 

    • heavy proteinuria (>3.5 g/day ), 
    • Hypoalbuminemia (low blood albumin), 
    • severe Edema, and 
    • Hyperlipidemia (high cholesterol/triglycerides). 
    • Minimal Change Disease and Membranous Nephropathy are classic examples.
    • (Note: Some GN types can present with mixed nephritic/nephrotic features or evolve from one pattern to another).

    Etiology of Glomerulonephritis

    • Primary GN: The disease originates within the kidney itself, without evidence of a systemic disease trigger (though often immune-mediated). Examples: IgA Nephropathy, Minimal Change Disease, FSGS, Membranous Nephropathy.
    • Secondary GN: Occurs as a consequence of another underlying systemic disease or condition. Examples: Lupus Nephritis (from SLE), Diabetic Nephropathy, Vasculitis-associated GN (e.g., Wegener’s/GPA, Microscopic Polyangiitis), Anti-GBM Disease (Goodpasture’s Syndrome), GN related to infections (Hepatitis B/C, HIV, Endocarditis), certain cancers, or drug reactions.

    Factors that can cause or increase the risk of developing GN include:

    Infections:

    • Streptococcal Infections: Group A beta-hemolytic streptococci (causing strep throat or skin infections like impetigo) are a classic trigger for Post-Streptococcal Glomerulonephritis (PSGN), especially in children. Typically occurs 1-3 weeks after infection.
    • Other Bacterial Infections: Bacterial endocarditis, infected shunts.
    • Viral Infections: Hepatitis B, Hepatitis C, HIV.
    • Fungal/Parasitic Infections: Less common causes.

    Immune Diseases (Autoimmune Conditions):

    • Systemic Lupus Erythematosus (SLE): Lupus nephritis is a common and serious complication.
    • Goodpasture’s Syndrome: Autoantibodies attack the GBM in kidneys and lungs.
    • IgA Nephropathy (Berger’s Disease): IgA antibody deposits in the glomeruli.
    • Vasculitis: Inflammation of blood vessels (e.g., Granulomatosis with Polyangiitis [Wegener’s], Microscopic Polyangiitis, Henoch-Schönlein Purpura [IgA Vasculitis]).

    Systemic Diseases:

    • Diabetes Mellitus: Diabetic nephropathy is a leading cause of CKD, involving glomerular damage.
    • Hypertension: Can both cause kidney damage (nephrosclerosis) and be a consequence of GN. High BP exacerbates glomerular injury.

    Hereditary Factors: Some forms of GN, like Alport syndrome or certain types of FSGS, have a genetic basis.

    Other Factors:

    • Certain Cancers (e.g., lymphomas, solid tumors via paraneoplastic syndromes).
    • Exposure to certain drugs or toxins (e.g., NSAIDs, lithium, some antibiotics).
    • Idiopathic: In many cases, the specific cause remains unknown.
    glomerulonephritis pathophysiology

    Pathophysiology of Glomerulonephritis 

    • Acute glomerulonephritis following an infection and is thought to be as a result of immunological response.
    • The body responds to streptococci by producing antibodies which combine with bacterial antigens to form immune complexes.
    • As these antigen-antibody complexes travel through circulation, they get trapped in the glomeruli and activate an inflammatory response that results in injury to capillary walls.
    • As a result of the inflammation, the capillary lumen becomes smaller leading to renal insufficiency .
    • Injury to the capillaries increases permeability to large molecules-proteins hence can leak into urine.

    Structural Damage:

    • Thickening of GFM: Basement membrane can thicken due to deposits or increased matrix production.
    • Cell Proliferation: Increased cell numbers within the glomerulus.
    • Podocyte Injury: Damage or effacement (flattening) of podocyte foot processes leads to increased protein leakage (proteinuria).
    • Breaks in GFM: Allows passage of red blood cells (hematuria) and larger amounts of protein.
    • Crescent Formation (in RPGN): Proliferation of cells (parietal epithelial cells, infiltrating macrophages) in Bowman’s space, compressing the glomerular tuft.

    Functional Consequences:

    • Decreased GFR: Inflammation, scarring, and reduced filtration surface area impair the kidney’s ability to filter waste products.
    • Increased Permeability: Damage to the GFM leads to proteinuria and hematuria.

    Progression:

    • Scarring (Glomerulosclerosis): Persistent injury leads to replacement of functional glomerular tissue with scar tissue.
    • Tubulointerstitial Fibrosis: Damage often extends to the surrounding tubules and interstitial tissue.
    • Loss of Nephrons: Progressive scarring leads to irreversible loss of nephrons and decline in kidney function (CKD).

    Consequences of Reduced GFR and Damage:

    • Retention of Sodium and Water: Impaired filtration leads to fluid overload.
    • Hypertension: Caused by fluid overload and activation of the Renin-Angiotensin-Aldosterone System (RAAS).
    • Edema: Accumulation of excess fluid in interstitial spaces.
    • Azotemia/Uremia: Accumulation of nitrogenous waste products (urea, creatinine) in the blood.

    Types of Glomerulonephritis 

    1. Diffuse proliferative glomerulonephritis

    This is inflammation of the glomerulus affecting all glomeruli (diffuse) with an increased number of cells in them (proliferative). It usually follows transient infection especially beta hemolytic streptococci but other organisms can cause it. 

    It presents as acute nephritis with haematuria and proteinuria. Recovery is good in children and in adults 40% cases may develop hypertension and renal failure.

    2. Focal/segmental proliferative glomerulonephritis:

    This is inflammation of the glomerulus affecting some glomeruli (focal) with increased number of cells in them (proliferative). It is associated with systemic lupus erythematosus(SLE) or infective endocarditis. It presents also as an acute nephritis with haematuria and proteinuria and recovery is variable. 

    3. Membranous/mesangial proliferative/ membranoproliferative glomerulonephritis. 

    This is inflammation of the glomerulus with thickening of the glomerular basement membrane. It is due to infections like syphilis, malaria, hepatitis B, drugs like penicillamine, gold, diamorphine and tumors. 

    It presents as nephrotic syndrome with haematuria and proteinuria and recovery is variable but most case progress to chronic renal failure 

    4. Minimal change glomerulonephritis

    This is inflammation of the glomerulus with no exact known cause. It presents as nephrotic syndrome with haematuria and proteinuria and recovery is good in children but recurrences are common in adults. 

    • Glomerulonephritis can be acute if it occurs in days or weeks ie 1 – 3 weeks following a streptococcal infection or glomerular damage 
    • Chronic glomerulonephritis occur over months or years and is characterized by progressive destruction (sclerosis) or glomeruli and gradual loss of renal function 

    Diagnostic Evaluation of Glomerulonephritis

    A combination of history, physical exam, and laboratory/imaging tests are used. Kidney biopsy is often the definitive test.

    History:

    • Recent infections (sore throat, skin infection).
    • Symptoms: onset, duration, nature (edema, urine color changes, fatigue, HTN).
    • Past medical history (diabetes, SLE, hypertension, prior kidney disease).
    • Family history of kidney disease.
    • Medication history (including NSAIDs, nephrotoxic drugs).

    Physical Examination:

    • Blood pressure measurement.
    • Assessment for edema (periorbital, peripheral, ascites).
    • Signs of fluid overload (jugular venous distension, lung crackles/rales indicating pulmonary edema).
    • Skin examination (rashes, signs of infection like impetigo, signs of vasculitis).
    • Observation for pallor (anemia), signs of uremia (e.g., uremic frost – rare now).
    • Assessment of visual acuity and fundoscopy (for hypertensive changes).

    Urinalysis (Crucial first step):

    • Dipstick: Detects protein, blood, leukocytes, nitrites.
    • Microscopy: Quantifies RBCs, WBCs. Crucially looks for casts (cylindrical structures formed in tubules):
    1. RBC Casts: Strongly suggest glomerular bleeding (hallmark of nephritic syndrome).
    2. WBC Casts: Indicate inflammation (can be seen in GN, pyelonephritis, interstitial nephritis).
    3. Granular Casts/Waxy Casts: Indicate tubular damage/stasis, often seen in more chronic disease.
    • Urine Protein Quantification: 24-hour urine collection or spot urine protein-to-creatinine ratio (UPCR) or albumin-to-creatinine ratio (UACR) to measure protein loss accurately.
    • Urine pH, specific gravity.

    Blood Tests:

    • Renal Function Tests: Blood Urea Nitrogen (BUN) and Serum Creatinine (elevated levels indicate reduced GFR). Estimated GFR (eGFR) calculation.
    • Electrolytes: Sodium, Potassium (can be elevated, especially with oliguria), Chloride, Bicarbonate (may be low – metabolic acidosis). Calcium, Phosphorus (abnormalities common in CKD).
    • Complete Blood Count (CBC): Assess for anemia (normocytic, normochromic often seen in CKD), signs of infection.
    • Serum Albumin: Low levels (hypoalbuminemia) are characteristic of nephrotic syndrome.
    • Lipid Profile: Cholesterol and triglycerides are often elevated in nephrotic syndrome.
    • Inflammatory Markers: Erythrocyte Sedimentation Rate (ESR) or C-Reactive Protein (CRP) may be elevated.
    • Serological Tests (to identify cause):
    1. Complement Levels (C3, C4): Low C3 is typical in post-streptococcal GN and some forms of MPGN/lupus nephritis. C4 may also be low in lupus.
    2. Anti-Streptolysin O (ASO) Titre: Elevated titres suggest recent streptococcal infection (useful for PSGN diagnosis). Anti-DNase B is another marker for strep.
    3. Antinuclear Antibody (ANA): Screening test for SLE.
    4. Anti-dsDNA Antibody: Specific for SLE.
    5. Anti-Glomerular Basement Membrane (Anti-GBM) Antibody: For Goodpasture’s syndrome.
    6. Antineutrophil Cytoplasmic Antibodies (ANCA – c-ANCA, p-ANCA): For ANCA-associated vasculitis (GPA, MPA).
    7. Hepatitis B/C Serology, HIV Test: To rule out infection-associated GN.

    Imaging Studies:

    • Renal Ultrasound (USG): Assesses kidney size (often normal/enlarged in acute GN, small/scarred in chronic GN), echogenicity, rules out obstruction, and guides biopsy.
    • Chest X-ray: May show signs of fluid overload (pulmonary edema, pleural effusions, cardiomegaly).
    • Intravenous Pyelogram (IVP): Less commonly used now due to contrast risks and availability of other imaging; previously used to visualize urinary tract structures. CT or MRI may sometimes be used.

    Kidney Biopsy:

    • Gold Standard: Provides a definitive diagnosis by allowing histological examination of kidney tissue (glomeruli, tubules, interstitium, vessels).
    • Information Gained: Identifies the specific type of GN, assesses the severity of inflammation/scarring (activity and chronicity), guides treatment decisions, and helps determine prognosis. Performed using light microscopy, immunofluorescence (to detect immune deposits like IgG, IgA, IgM, C3, C1q), and electron microscopy (for ultrastructural details like deposit location, podocyte changes).
    Dietary restrictions on salt, fluids, protein, and other substances may be recommended to help control of high blood pressure or kidney failure.

    Management of Glomerulonephritis

    Aims of Management

    Treatment goals depend on the type, severity, and underlying cause of GN. 

    General goals include: 

    • preserving kidney function, 
    • managing symptoms, 
    • treating the underlying cause if possible, and 
    • preventing complications.

    General Supportive Measures:

    Blood Pressure Control: Crucial for slowing progression. Often requires multiple medications. ACE inhibitors (ACEi) or Angiotensin II Receptor Blockers (ARBs) are often preferred as they can also reduce proteinuria. Target BP is usually <130/80 mmHg, potentially lower if proteinuria is significant.

    Maintain Healthy Weight: Through appropriate diet and exercise (as tolerated).

    Fluid Management:

    • Sodium and Water Restriction: To control edema and hypertension. Fluid intake may be limited based on urine output and fluid status.
    • Diuretics: Loop diuretics (e.g., furosemide) are commonly used to manage fluid overload and edema. Thiazides may be added if needed.

    Dietary Modifications:

    • Protein Restriction: May be recommended in CKD to reduce workload on kidneys, but needs careful balancing to avoid malnutrition. Limit usually guided by GFR level. Less restriction or even normal intake may be needed in nephrotic syndrome to compensate for losses, requires careful monitoring.
    • Potassium, Phosphorus, Magnesium Restriction: Necessary if levels are elevated, common in advanced CKD. Requires avoiding certain foods and potentially using phosphate binders.
    • Calcium Supplements: May be needed if dietary intake is low or due to CKD mineral bone disease, often alongside Vitamin D analogues.

    Specific Treatments (Based on GN type/cause):

    Treating Underlying Infections: Antibiotics for bacterial infections (e.g., penicillin for post-streptococcal GN prevention in outbreaks or treating active infection; treatment for endocarditis). Antivirals for Hepatitis B/C or HIV.

    Plasma Exchange (Plasmapheresis): Removes harmful antibodies from the blood. Used in conditions like Anti-GBM disease and severe ANCA-associated vasculitis.

    Immunosuppression: Used for many primary immune-mediated GN and secondary forms like lupus nephritis or vasculitis. Aims to reduce inflammation and harmful immune responses.

    • Corticosteroids (e.g., Prednisone): Mainstay for many types.
    • Cytotoxic Agents (e.g., Cyclophosphamide, Mycophenolate Mofetil [MMF], Azathioprine): Used for more severe or resistant cases.
    • Calcineurin Inhibitors (e.g., Tacrolimus, Cyclosporine): Used for some types like Minimal Change, FSGS, Membranous.
    • Biologic Agents (e.g., Rituximab – targets B cells): Increasingly used for ANCA vasculitis, lupus nephritis, some other types.
      (Immunosuppression carries risks of infection, malignancy, and other side effects, requiring careful monitoring).

    Management of Complications:

    • Dialysis (Hemodialysis or Peritoneal Dialysis): Required for acute kidney injury with severe complications (fluid overload, hyperkalemia, acidosis, uremia) or for End-Stage Renal Disease (ESRD) when GFR is very low (<15 mL/min).
    • Anemia Management: Erythropoiesis-stimulating agents (ESAs) and iron supplementation.
    • Mineral and Bone Disorder Management: Phosphate binders, Vitamin D analogues, calcimimetics.
    • Hyperlipidemia Management: Statins may be used, especially in nephrotic syndrome.

    Lifestyle Changes & Patient Education:

    • Adherence to medications, diet, and fluid restrictions.
    • Regular monitoring of BP, weight, and symptoms.
    • Smoking cessation.
    • Avoidance of nephrotoxic substances (e.g., NSAIDs, certain contrast dyes).
    • Understanding the disease, treatment plan, and potential complications.

    Physiotherapy and Supportive Care:

    • Endurance Exercise: As tolerated (walking, swimming, cycling) can improve cardiovascular health, circulation, and well-being. Helps kidneys discharge waste and toxins by improving overall circulation.
    • Breathing Exercises: Pursed-lip breathing and diaphragmatic breathing can help manage shortness of breath associated with fluid overload or anxiety.
    • Edema Management: Elevation of edematous limbs, gentle range-of-motion exercises. Lymphatic massage may be considered for persistent edema, but primary treatment is addressing the underlying fluid overload medically.
    • Energy Conservation Techniques: Pacing activities, rest periods, especially if fatigued due to anemia or uremia.

    Nursing Management

    Goals of Nursing Care:

    • Maintain fluid and electrolyte balance.
    • Achieve and maintain target blood pressure.
    • Alleviate pain and discomfort.
    • Maintain effective breathing pattern and gas exchange.
    • Prevent skin breakdown.
    • Prevent infection.
    • Maintain adequate nutritional status.
    • Patient verbalizes understanding of disease and treatment plan.
    • Patient copes effectively with diagnosis and lifestyle changes.

    Assessment:

    • Vital Signs: Frequent BP monitoring, heart rate, respiratory rate, temperature.
    • Fluid Balance: Strict intake and output monitoring, daily weights (most sensitive indicator of fluid status), assessment for edema (location, severity, pitting), jugular venous distension, lung sounds.
    • Symptoms: Assess for changes in urine (color, amount, foaminess), fatigue, shortness of breath, pain, nausea/vomiting.
    • Skin Integrity: Assess edematous areas for breakdown.
    • Neurological Status: Assess for headache, visual changes, confusion (signs of severe HTN or uremia).
    • Psychosocial Assessment: Coping mechanisms, anxiety, knowledge about the disease.
    • Monitor Lab Results: BUN, Creatinine, electrolytes, CBC, albumin, etc.

    Nursing Diagnoses :

    • Excess Fluid Volume related to compromised regulatory mechanisms (renal failure) and sodium/water retention as evidenced by edema, weight gain, hypertension, abnormal lung sounds, decreased urine output.
    • Acute Pain related to inflammation of the renal cortex/capsular distension as evidenced by patient report of flank pain, facial grimacing.
    • Ineffective Breathing Pattern or Impaired Gas Exchange related to fluid overload (pulmonary edema) as evidenced by dyspnea, tachypnea, abnormal breath sounds, low oxygen saturation.
    • Risk for Impaired Skin Integrity related to edema.
    • Decreased Activity tolerance related to fatigue (anemia, uremia) and fluid overload.
    • Inadequate nutritional intake related to anorexia, nausea, dietary restrictions.
    • Risk for Infection related to altered immune status or immunosuppressive therapy.
    • Disrupted Body Image related to edema, presence of dialysis access, or chronic illness.
    • Excessive anxiety related to diagnosis, prognosis, and treatment complexity.
    • Deficient Knowledge related to disease process, dietary restrictions, medications, and self-care management.

    Interventions:

    • Fluid Management: Administer diuretics as ordered, enforce fluid/sodium restrictions accurately, monitor I&O and daily weights meticulously, elevate edematous extremities, assist with frequent position changes to mobilize fluid and prevent skin breakdown.
    • Blood Pressure Management: Administer antihypertensives as ordered, monitor BP closely (before/after meds, postural checks if indicated).
    • Pain Management: Assess pain thoroughly (onset, location, quality, severity), provide comfort measures (positioning, quiet environment), administer analgesics as ordered (use caution with NSAIDs), explore relaxation techniques/diversion therapy.
    • Respiratory Support: Elevate head of bed (Semi-Fowler’s or High-Fowler’s position) to ease breathing, monitor respiratory status (rate, depth, effort, O2 saturation), administer oxygen as needed, encourage deep breathing/coughing exercises (if appropriate, not overly strenuous).
    • Nutritional Support: Collaborate with dietitian, provide prescribed diet, monitor intake, manage nausea/vomiting (antiemetics as ordered), provide oral care.
    • Skin Care: Gentle cleansing, moisturizing, use pressure-relieving surfaces if bed-bound, handle edematous skin carefully.
    • Activity Management: Encourage rest periods, assist with ADLs as needed, gradually increase activity as tolerated, plan activities to conserve energy.
    • Infection Prevention: Monitor for signs of infection (fever, increased WBC, site-specific signs), use aseptic technique, educate patient on hand hygiene and avoiding sick contacts (especially if immunosuppressed).
    • Medication Administration: Administer all medications accurately and on time (diuretics, antihypertensives, immunosuppressants, antibiotics, phosphate binders, etc.), monitor for therapeutic effects and side effects. Administer albumin infusions as ordered (helps shift fluid from interstitial space to intravascular space, often followed by diuretics).
    • Psychosocial Support: Provide emotional support, encourage verbalization of feelings, involve family, provide clear explanations, refer to support groups or counseling if needed.
    • Patient Education: Teach about the disease, medications (purpose, dose, side effects), dietary/fluid restrictions, monitoring (BP, weight, symptoms), when to seek medical attention, importance of follow-up.
    • Preparation for Procedures: Educate and prepare patient for kidney biopsy, dialysis initiation if necessary.

    Complications of Glomerulonephritis

    GN can lead to various acute and chronic complications:

    1. Acute Kidney Injury (AKI) / Acute Renal Failure: Rapid decline in kidney function.
    2. Chronic Kidney Disease (CKD): Progressive, irreversible loss of kidney function over time.
    3. End-Stage Renal Disease (ESRD): Kidney function fails completely, requiring dialysis or transplantation.
    4. Nephrotic Syndrome: (If not the primary presentation).
    5. Hypertension: Often difficult to control, increases cardiovascular risk.
    6. Electrolyte Imbalances: Hyperkalemia (high potassium – dangerous!), hyperphosphatemia, hypocalcemia, metabolic acidosis.
    7. Anemia: Due to decreased erythropoietin production.
    8. Increased Susceptibility to Infections: Due to the disease itself or immunosuppressive therapy.
    9. Cardiovascular Disease: Increased risk of heart attack, stroke.
    10. Renal Osteodystrophy: Bone disease related to CKD.
    11. Hypertensive Encephalopathy: Neurological symptoms due to severely elevated blood pressure (headache, confusion, seizures).
    12. Fluid Overload: Leading to:
    • Pulmonary Edema: Fluid accumulation in the lungs, causing severe shortness of breath.
    • Congestive Heart Failure (CHF): Heart struggles to cope with excess fluid volume.

    Glomerulonephritis Read More »

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