CHILD WITH COUGH

ODUSANYA BILIKISU MED/12/13/0032

SADIQ ABIMBOLA MED/13/14/0063
ODUBELA YEMISI MED/12/13/0057
SHONEYE JOHNSON 01036915
 OUTLINE
• INTRODUCTION
• EPIDEMIOLOGY
• PHYSIOLOGY OF COUGH
• AETIOLOGY
• MANAGEMENT
• COMPLICATIONS
• PREVENTION
• PROGNOSIS
 INTRODUCTION
• Cough is the most important symptom of the respiratory disease. It is
a physiological reflex action induced by the presence of irritant
substances (e.g exudate, dust, fumes, foreign body etc) in the airway.
• It has 2 functions;
• 1. to expel secretions and other materials in the airway
• 2. to protect against aspiration.
• Cough is not a disease in itself rather it is a symptom of many
underlying conditions. It may be the presenting symptom of a serious
underlying pulmonary or extra-pulmonary disease.
 INTRODUCTION
Cough is classified based on its duration, character and timing.
• Based on duration,
-Acute: cough occurring for less than 3weeks
-Chronic: cough occurring for more than 3weeks
-Sudden: occurring while feeding
• Based on character,
-Productive: when sputum is coughed up.
• -Non Productive (dry cough) Barking cough
• Brassy cough
• Whooping cough
• Dry / Hacking cough
Based on timing,
-Night
-Both night and day
-Just during the day
EPIDEMIOLOGY
 AETIOLOGY
1. Acute cough
• Classical recognizable cough:
• Laryngotracheobronchitis – barking cough
• Paroxymal – pertussis and para-pertussis

• Acute upper / lower respiratory tract infection (ARI)- Common cold,

Sinusitis, Pharyngo- tonsillitis, Acute bronchitis, Acute bronchiolitis,
Pneumonia, foreign body aspiration, Asthma,
• Inhalation injury (acute exposure to smoke or volatile substances).
• Congenital causes, such as Tracheomalacia, bronchomalasia, tracheo-
oesophageal fistula, congenital diaphragmatic hernia.
 AETIOLOGY
2. Chronic cough
• Asthma
• Gastro esophageal reflux disease.
• Post nasal drip syndrome (upper airway cough syndrome)
• INFECTIONS;
-Tuberculosis
-Pertussis
• Non asthmatic eosinophilic bronchitis.
• Bronchiectasis
• Foreign body aspiration
• Cystic fibrosis
• MEDICATIONS; (side effect)
-angiotensin converting enzyme inhibitor (enalapril, captopril, lisinopril etc).
• Congestive cardiac failure
 PHYSIOLOGY OF COUGH
PHYSIOLOGY OF COUGH
NEURAL PATHWAY OF COUGH REFLEX
• Cough reflex has 3 components
1.An afferent sensory component
2.Central processing centre
3.Efferent component
• There are 3 types of receptor in the airway
-Rapidly acting receptor located mainly on posterior wall of the trachea,carina,pharynx.
This receptor responds to mechanical and chemical stimulus causing transient/rapid
discharge in their afferent nerve
-Slow adapting receptor which causes a prolonged discharge of afferent fibre
-Nociceptor of C-fibres which are located close to pulmonary vessels,they are stimulated
by hyperinflation of the lungs and by a chemical called capsaicin and others like
histamine,bradykinin,prostaglandin.
When these receptor are stimulated either chemically or mechanically, a
cough reflex takes place.
• The need to cough is usually increased when there is damage to the
ciliary mechanism (from acute infection) or increased mucus
secretion(asthma). Irritant stimulate sensory receptors in respiratory
tract mucosa. Afferent impulses are sent along vagus nerve to the
respiratory control(cough centre in medulla). Efferent impulses pass
down in 9th and 10th cranial nerve to muscles of inspiration.
• First there is a rapid inspiration, then a forced expiratory effort against a
closed glottis. This increases the intra thoracic pressure and when it
increases to > 100cm water, the glottis opens, a rapid expulsion of air
takes place and the irritant material is expelled.
• The characteristic noise of coughing is due to the vibration of the vocal
cord.
• The intensity of cough depends on how adherent the irritant substance is to the
respiratory tract. e.g in whooping cough, the exudate produced is very sticky and a
very forceful expiratory effort is required to dislodge or expell it. This is usually
achieved by a series of coughs(usually >5 in 1 expiratory phase) which ensures a
much higher pressure build up behind the glottis. This series are called paroxysm
• The cough reflex has been shown to have neuroplasticity such that a
hypersensitive response is elicited over time due to the cough itself inducing
chronic irritation, inflammation and tissue remodeling.
• Both peripheral (increase in sensitivity of cough receptors) and central(changes in
the central processing in the brain stem) sensitization can account for an
exaggerated cough response that is common in these patients and further
contributes to the maintenance of chronic cough.
• Summary of the cough reflex…
This is discussed in four phases;
1. PHASE1:Deep Inspiratory - which accounts for about 50% of vital capacity
2. PHASE2:Compression- the glottis closes for about 0.2secs and respiratory muscles
are also contracted.
3. PHASE3:Expiratory - there is forced expiration against a closed glottis which
increases the intrapleural pressure to about 100mmhg or more. This causes a
sudden opening of the glottis resulting in a violent release of air from the lungs. This
phase is associated with a distinctive sound that is due to the vibration of vocal
cords.
4. PHASE4:Relaxation- this completes the act as respiratory muscles relax with a
reversal of the intrapleural pressure.
ACUTE COUGH
 COMMON COLD
• Acute viral inflammation of nasal mucous membranes and pharynx.
• Most common childhood infection.
• Etiology includes mainly rhinovirus, other viruses e.g. corona and RSV
may also cause it.
• Role of bacteria is 2O most of the time
• Clinical features include: cough, nasal discharge, nasal obstruction,+/-
low grade fever, sneezing
 PATHOGENESIS
• Most commonly, rhinoviruses are transmitted to susceptible individuals through
direct contact or via aerosol particles. The primary site of inoculation is the nasal
mucosa, though the conjunctiva may be involved to a lesser extent. Rhinovirus
attaches to respiratory epithelium and spreads locally.
• Viral particles are usually transmitted via inoculation into the eye or the nose from
contact with the fingers that harbor the rhinovirus, especially since rhinoviruses are
capable of surviving on hands for hours.
• Highly contagious behavior includes nose blowing, sneezing, and physically
transferring infected secretions onto environmental surfaces or paper tissue
• . Symptoms develop 1-2 days after viral infection, peaking 2-4 days after inoculation.
• A local inflammatory response to rhinovirus in the respiratory tract can lead to nasal
discharge, nasal congestion, sneezing, and throat irritation
 ACUTE BRONCHITIS
• It refers to non specific bronchial inflammation and is associated with a number of childhood
conditions e.g. viral URTIs, measles, pertussis, and Hemophilus influenzaB infection.
• Aetiology; Mainly viral but could also result from from exposure to dust, toxic chemical gases
e.g. tear gas, smoke.
Pathogenesis; viral and bacterial toxins inhibit the motility of the ciliated epithelium. As a result
of infiltration, mucosal edema, ad increased secretion of viscous mucus the ciliary action gets
slowed down further, which turns off the mechanism of bronchus self purification. This leads to
a sharp decrease in the drainage of function of bronchi and obstruction of the outflow if mucus
from the lower respiratory tract. Consequently, this creates the conditions for further
propagation and spread of the infection and obstruction with the mucus of the smaller bronchi.
Clinical features; cough is the prominent feature. Initially frequent , dry, hacking, unproductive.
The cough may be paroxysmal or associated with gagging or post tussive vomiting. Other
features; Wheezing, dyspnea
Signs ; low grade fever, coarse breath sounds, crepitation s (due to secretions) and scattered
high pitched rhonchi on chest
ACUTE BRONCHIOLITIS
This is an acute inflammation of the bronchioles, resulting in lower airway obstruction
• Etiology ; caused by Respiratory Syncytial virus
• Pathogenesis of Acute Bronchiolitis
• Viral invasion, which results in destruction of the cilia on bronchioles epithelium
• Oedema of the bronchiolar muscle and submucosa
• Excessive mucus secretion and accumulation of mucus and cellular debris.
• Constriction of the muscle in bronchiolar wall, which all leads to reduction in size of lumen
of the bronchioles, and finally obstruction of the lumen.
• Resistance to outflow of air both at inspiration or expiration, but more marked at
expiration because normally the diameter of the airways is reduced during expiration.
• With incomplete obstruction, air is trapped and there is hyperinflation, while with
complete obstruction, trapped air is absorbed and there is Atelectasis(alveolar collapse).
• Impairment of normal gaseous exchange at alveolar level results in hypoxaemia and
hypercabia.
RADIOLOGICAL FINDING IN
BROCHOLITIS
-An history of an upper respiratory tract infection, days or week earlier.
• -Fever, malaise, Noisy breathing, Wheezing, difficulty in breathing,
Poor feeding.
• On Examination; Patient usually irritable, obviously dyspneic,
with or without features of respiratory distress, low Grade
pyrexia and has some dehydration as a result of irreversible
water loss, Increase respiratory rate, barrel shaped chest.
 PNEUMONIA

• This is an inflammation of the lung parenchyma ,i.e. the alveolar walls ,spaces and interstitial tissue, due
to infection by micro-organisms.
• Causes; Neonate- Staphylococus aureus, Klebsella spp, Escherichia coli, Pseudomonas spp, Proteus spp.
• Infancy and young children- Streptococus pneumonia, Hemophilus influenza, Stapylococus aureus.
• Older children-Streptococus pneumonia, Mycoplasma pneumonia, Clamydia.
PATHOGENESIS
Lung consolidation, from accumulation of fluid in the lung parenchyma, resulting in obliteration of air
spaces
↓
Impaired gaseous exchange, resulting in hypoxemia, hypercarbia, respiratory acidosis.
↓
Hypoxemia results in stress, resulting in stimulation of the sympathetic nervous system leading to
tachycardia.
↓
Hypoxemia also result in stimulation of the respiratory Centre in CNS resulting in tachypnea,
• Clinical features; An history of catarrh, dry cough with or without
production of sputum, fever, grunting, difficulty in breathing, dyspnea,
tachypnea, tachycardia.
• On Examination-signs of respiratory distress, increased tactile
fremitus, chest may be dull on percussion due to consolidation, on
auscultation, reduced air entry on affected side, bronchial breath
sound, increased vocal resonance, fine or coarse crepitation may be
heard in one or more lung zone
RADIOLOGICAL FINDING IN
PNEUMONIA
CHRONIC COUGH
Emphasis shall be laid on the commonest causes of chronic cough in
this environment:
-Bronchial Asthma
-Pulmonary Tuberculosis
-Pertussis (whooping cough).
 ASTHMA
• Asthma is a Chronic Inflammatory disorder characterized by hyperactive airways leading
to episodic, reversible bronchoconstriction, owing to increased responsiveness of the
tracheobronchial tree to various stimuli e.g. environmental allergies and irritants.
• Some of these stimuli would have little or no effect on non-asthmatics with normal
airways
SYMPTOMS:-
• Cough- Character – Paroxysm,
-Productiveness – Phlegm/Sputum, color (mucoid, clear, or sticky)
-worse at night.
• other associated symptom
(1) Wheeze (whistling, musical sound produced in the chest usually during expiration).
(2) Shortness of breath
(3) Chest tightness
(4) Fever when infection sets in
 PATHOGENESIS
• Cough in asthma is triggered by exercise, cold air and allergens to
which the patient has been previously sensitized to. Continuous
exposure to the triggers leads to inflammation of the airway and
subsequent hyper responsiveness (bronchospasm).
Exercise, cold air and allergens (to which patient has been previously
sensitized to)
↓
Inflammation
↓
Increase in airway responsiveness (bronchospasm
↓
Coughing, sneezing and severe dyspnea
 PULMONARY TUBERCULOSIS
• It is an infectious disease caused by the bacterium-Mycobacterium
tuberculosis.
• It was first identified by Koch in 1882.
Other species that can cause TB are;
• Mycobacterium bovis(unpasteurized milk)
• Mycobacterium carnetti
• Mycobacterium africanum
• Mycobacterium tuberculosis,acid & alcohol fast bacilli (waxy outer capsule),non motile, non -
sporulating, aerobic ,produces no exotoxin or endotoxin, and causes disease by invoking
immune reactions.
• MODE OF SPREAD FOR TUBERCULOSIS.
• Inhalation of infected droplets through sneezing, coughing and talking.
• Drinking milk infected with M.bovis(cattle TB)
• Abrasion of skin and mucous membrane
• Placenta TB can spread to the fetus
• Endocervical TB can spread by aspiration
SYMPTOMS AND SIGNS
chronic cough, Heamoptysis (though not common in children),Fever (low grade),Dyspnea,
Localized wheezing, Night sweat, Anorexia, and Weight loss.
 PATHOGENESIS
• Cough in pulmonary tuberculosis is due to immune reaction. The
bacilli elicit a prompt and marked tissue response that tends to wall
off the focus of infection. Cavitation is almost inevitable in secondary
tuberculosis and erosion of the cavities in to the airways is an
important source of infection because the person now coughs sputum
that contains bacteria.
• Pulmonary tuberculosis is also associated with hemoptysis due to
massive tissue damage that leads to destruction of pulmonary
capillary endothelium which causes hemorrhage.
• Infact during chronic inflammation, blood vessels surrounding the
infected sites are engorged and are highly susceptible to destruction.
The leakage of blood vessels leads the patient to cough out not only
pus containing sputum but also blood.
RADIOLOGICAL FINDING IN PULMONARY
TUBERCULOSIS
 PERTUSSIS
• Also known as Whooping cough
• Pertusis is defined as an infection of the respiratory system
• Occurs worldwide (pertussis –intensive cough)
• Pertussis is one of the major causes of childhood mortality in the developing world.
• It is an infectious disease caused by the bacterium Bordetella pertussis. This organism is the sole cause
of endemic pertussis.
• Bordetella parapertusis is also an occasional cause of pertussis.
• B. pertussis is a small aerobic gram-negative coccobacillus.
• It produces multiple antigenic and biologically active products, including pertussis toxin, filamentous
hemagglutinin, agglutinogens, adenylate cyclase, pertactin, and tracheal cytotoxin.
• These products are responsible for the adherence of the organism to the epithelial linings and the
clinical features of pertussis disease.
• IP of pertussis is usually 7–10 days, with a range of 4–21 days, and rarely may be as long as 42 days
Catarrhal stage-1st stage (1-2/52)
• insidious onset of coryza (runny nose), sneezing, low-grade fever, and
a mild, occasional cough, similar to the common cold.
• Cough gradually becomes more severe
Paroxysmal stage- 2nd stage; begins after the catarrhal stage.
• Paroxysms of numerous, rapid coughs. At the end of the paroxysm, a
long inspiratory effort is accompanied by a characteristic high-pitched
whoop as air is inhaled forcefully through narrow bronchial tree.
 PATHOGENESIS
• Pertussis is primarily a toxin-mediated disease.
• The bacteria colonizes the brush border of the bronchial epithelium.
• The bacteria attach to the respiratory cilia, produce toxins that causes
epithelia damage and paralysis of the cilia, this leads to inflammation of
the respiratory tract, which interferes with the clearing of pulmonary
secretions.
• Pertussis antigens appear to allow the organism to evade host
defenses. Despite remarkable lymphocytosis, chemotaxis is impaired.
• This initiates a cough reflex but it becomes persistent because clearing
of pulmonary secretions become impaired.
• Infants younger than 3 months do not whoop.
• Cyanosis & apnea may occur in very young children.
• Paroxysmal attacks occur more frequently at night and increase in
frequency during the first 1 or 2 weeks of this stage.
• It remains at the same level for 2 to 3 weeks, and then gradually
decrease. The paroxysmal stage usually lasts for about 6 weeks but
may persist for up to 10 weeks
• Convalescent stage-3rd stage; recovery is gradual.
• The cough becomes less paroxysmal and disappears in 2 to 3 weeks.
• However, paroxysms often recur with subsequent viral respiratory
infections for many months after the onset of pertussis .
MANAGEMENT
 DIAGNOSIS
Evaluation of the coughing child
• History
- In evaluating a child with cough; the following should be asked about;
The character of the cough;
- Brassy? – tracheal involvement
- Barking? (like sea lion) – LTB
- Paroxysmal? – pertussis, foreign body aspiration, asthma, endo-bronchial TB, diphtheria
- Terminal whoop? - pertussis
- Productive of sputum? If yes; Quantity? Color? Quality?
- mucoid, clear, tough, sticky? – asthma
- purulent, thick, yellow? – LRTI – pneumonia, lung abscess, bronchiectasis
- Frothy? Blood stained? – Pulmonary oedema.
- Bloody (haemoptysis) – Klebsiella pneumoniae, PTB bronchiectasis, Paragonimiasis (lung
fluke) disease)
• The timing;
Acute? - onset < 3/52.
Chronic? - onset > 3/52
Sudden? occurred while feeding? – aspiration
• Provoking factors?;
Hx of choking while feeding
Hx of force - feeding
Hx of being worse at night → sinusitis, asthma, hyper reactive airway dz, Sudden onset
after
Hx of exposure to allergens; wool, dust, pets,cold, damp, exercise
Aspiration Asthma
• Associated symptoms;
Fever? → infection
Preceeding catarrh? → downward extension of URTI
Post tussive vomiting →→ pertussis
Drooling, refusal of solids → tonsillitis
Night sweats, Weight loss → PTB
Fast breathing/difficulty in breathing,Grunting → pneumonia
Chest tightness? → Asthma
Chest pain? → lobar pneumonia/ pleuritis /bronchitis
• Cough is a natural response to an insult and treatment should be
directed at the insult/underlying pathology
• N:B Because the respiratory system interacts with many other
systems, questions related to those others system may be relevant.
For e.g.; questions about gastro esophageal reflux or immune status
may be important in a child with recurrent pneumonia.
 Physical examination

GENERAL EXAMINATION
•Pallor
•cyanosis
•Check for signs of respiratory distress(nasal flaring, grunting, audible wheezes,)
•Finger clubbing (bronchiectasis)
•Growth parameters (height, length, weight)
Temperature
SYSTEMIC EXAMINATION
Central nervous system:
•examine the ear, nose and throat.
•Cervical lymph node.
•Supraclavicular lymph node
Respiratory system:
•tachypnea
•trachea
•Air entry
•Wheeze/rhonchi
•Crackles (bronchiectasis, acute/subacute exacerbation of asthma)
Cardiovascular system:
• tachycardia
• Pulse rate
• Blood pressure
Abdominal examination:
• tender abdomen
• Distended abdomen
• hepatomegaly
 INVESTIGATION
• Full blood count- to check for eosinophilia
• Sputum culture or throat culture
• A chest x-ray to look for infection of any evidence of a tumor
• A CT Scan of your chest or CT Scan of your sinuses to look for signs of infection or a
tumor
• Allergy testing
• Pulmonary function tests to screen for lung conditions such as in asthma and
emphysema
• Spirometry (the measuring of breath). It is the most common of the pulmonary
function test measuring lung function. For assessing asthma.
• Esophageal pH testing to test for the presence of acid reflux as a possible cause of a
persistent cough
• Bronchoscopy to check for foreign bodies or evaluate your airways for a tumor
• Laryngoscopy to examine your throat and voice box
TREATMENT
•The treatment of cough will depend upon the underlying cause, as well as the degree in which the cough is
interfering with day to day activities.
Cough can be managed by:
•Proper treatment and appropriate medications
•Acute cough is usually self-limiting but requires medical intervention if it is severe
•Avoid exposure to smoke
•Avoiding irritants and other pollutants which cause cough
However patient may get relieve from doing the following;
•Expectorant
•Drinking lots of water, Inhaling steams
•Pharyngeal demulcents e.g. lozenges, cough drops, linctus's (soothes the throat).
•Antitussives (cough suppressant): in severe cases e.g. codeine, dextromethorphan ,chlorpheniramine,
promethazine
•They reduce tussal impulses
•
 COMMON COLD COUGH
• No specific treatment required
• Condition is self-limited
Symptomatic treatment:
• For complete nasal obstruction; Keep warm, steam inhalation Short term topical or oral
nasal decongestants abound e.g. xylometazoline, oxymetazoline or phenylephrine
N.B Must not be used for >48 – 72hrs, prolonged use – Rhinitis medicamentosa, rebound
sensation of nasal obstruction when drug is discontinued. Nasal drops may even run down to
LRT – extension of infection – LRTI. Not approved for use in kids < 2 yrs old. For rhinorrhea
• Intermittent suctioning with soft bulb syringe
• Clearing of nostrils with twist of cotton wool/cloth wick
• Give first generation antihistamines; e.g chlorpheniramine - reduces rhinorrhea by 25 to 30
%. Major side effect – sedation, thickening of nasal secretions; more difficult to extrude/
expel in infants; increased risk of bact. colonizion.
• For fever & irritability (if significant); give PCM 10-15 mg/kg/ dose 6
hrly or Ibuprofen 5-10mgkg/dose 6-8hrly
• Don’t give aspirin: because it may cause Reye’s syndrome in children
with influenza virus infection Parental counseling
• N.B. No need for antibiotics unless there’s evidence of bacterial super-
infection. Antibiotics do not alter course of illness, do not reduce
incidence of bacterial super-infection, may mask serious disease e.g
meningitis
• See patient a week later.
 ACUTE BRONCHITIS
; No specific treatment
Antipyretics and good fluid intake
Frequent shifts in position may facilitate pulmonary drainage in
infants
Steam inhalation may provide some relief
Recovery is usually spontaneous
Antibiotics can be given if there is evidenced of underlying
bacterial infections.
 ACUTE BRONCHIOLITIS
Admit
-Give cool humidified oxygen, through headbox or nasal prongs to maintain oxygen
saturation>92%
-Give intravenous fluids
-Avoid steroids and sedatives.
-Give nebulized Ribavirin
-Give antibiotics if patient is critically I'll
-NPO initially, later feed with NG tube.
• -If respiratory distress increases in spite of treatment, intubate and start mechanical
ventilation.
PNEUMONIA
• Eradication of infection, using antibiotics whose choice is dependent on common
causative organism in that environment.
• Give antipyretics
• Advice increase fluid intake
• In case of complication such as;
• Heart failure, digitalize and give diuretics.
• Pneumothorax, small size may resolve spontaneously, however thoracentesis is done
2nd intercostal space at mid-clavicular line if large.
• In Anemia, transfuse patient with partially packed cell with furosemide.

•
 ASTHMA
• Admit the individual
• Put the individual in cardiac position.
• Oxygen delivered by nasal catheter or mask Give nebulized salbutamol.
• Give Ipratropium bromide (anticholinergic)
• Inhaled bronchodilator; rapid acting inhaled B2 agonist e.g salbutamol (8-
10 pops/ 1hr),
• Other drugs like terbutaline, amniophylline are also indicated.
• Inhaled steroids (corticosteroids) for resolution of the inflammation.
 PERTUSSIS
• The medical management is mainly supportive
• Maintenance of adequate fluid and caloric balance. (small frequent feeds are
preferred).
• Steam inhalation may improve breathing by making the respiratory secretions
less viscid.
• Antibiotics do not usually alter the course of the disease but if given earlier
may shorten the duration of paroxysmal stage.
• This therapy eradicates the organism from respiratory secretions, thereby
decreasing communicability.
• Erythromycin is the drug of choice. 40mg/kg in divided doses given orally for
14days.
• Other drugs like azithromycin. 10-12mg/kg/day orally for a total of 5days.
• Clarithromycin . 15-20mg/kg/day in 2 divided doses given orally (are useful).
 TB RELATED COUGH
1ST line anti tuberculosis drugs are given as Directly Observed Therapy. They are;
• Rifampicin(R)
• Isoniazid (H)
• Pyrazinamide(Z)
• Ethambutol (E)
• Streptomycin (S)
• Other drugs are,
• paraaminosalicylic acid
• Ethionamide
• Amikacin
• Other antibiotics e.g clarithromycin,azithromycin
• There are 2 phases of treatment;
• Initial phase: usually 2 months. To kill the largest proportion of the
bacilli
• Continuation phase: between 4 and 10 months. This is to ensure cure
and prevent relapse.
• Short course chemotherapy; usually done for 8 months Initial phase;
RHZS daily for 2months.
• Continuation phase; RH daily for 4months.
 Home remedies for managing cough
• Eat fruits; research suggest that diets high in fruit fibers and flavonoids
may prevent chronic productive cough.
• Honey can be an effective treatment for a persistent cough. Can be taken
with hot tea. It soothe the throat.
• Ginger prepared as a tea is often used to help reduce symptom of chronic
cough and clear the nasal passages.
• Gargling with hot water can help clean the throat and rid it off mucus.
• A vaporizer or steamy shower may help a dry cough by increasing the
humidity in the air
• Elevate your head with extra pillows at night to ease a chronic dry cough
• Cough drops may soothe an irritated throat
 COMPLICATIONS
The following are the acute complications
• Headache
• Dizziness
• Insomnia
• Cough induced vomiting
• Excessive sweating
Chronic complications are;
• hernia
• Urinary incontinence
• Fractures of lower ribs
• Costochondritis
COMPLICATION FROM COMMON COLD
• Most common complication is Otitis Media.
Others include: Sinusitis, exacerbation of asthma, extension to the lower respiratory tract.
COMPLICATION FROM ASTHMA
• Respiratory depression
• Coma
• Death
Complications from TB,
• Anemia
• Wasting
• Malnutrition
Complications from pertussis,
• Secondary bacterial pneumonia.
• Dehydration.
• Otitis media.
• Severe malnutrition.
• Pnemothorax and subcutaneous emphysema.
• Epistaxis.
• Umbilical and inguinal hernias.
• Rectal prolapse.
• Subconjuctival haemorrhage.
• Seizures and encephalopathy.
 PREVENTION
Do’s and Dont’s for cough
• Drink extra fluids to help thin the secretions in your throat and make
them easier to cough up.
• Avoiding of mucous-producing foods can be effective in healing a
cough condition. These mucous-producing foods can vary, based on
individual intolerance, but dairy products are a major mucous-
producing food for most people.
• Avoid exposure to smoke and tobacco
• Avoid inhaled irritants such as smoke, dust or other pollutants.
Prevention of pertussis
• Active immunization is quite effective
• The use of the triple vaccine DPT is recommended at 6,10 and 14
weeks of life in Nigeria. (killed B.pert
• Booster doses of pertussis vaccine may also be given at school entry.
• Un-immunized contacts of pertussis cases should be given
prophylactic erythromycin for 10 days.
Prevention of TB
• BCG Vaccination Bacillus Calmette- Guerin (BCG) is, a vaccine
against tuberculosis that is prepared from a strain of the attenuated
(weakened) live bovine tuberculosis bacillus, Mycobaterium bovis that
has lost its virulence in humans by being specially subcultured in an
artificial medium for 13years, and also prepared from Mycobacterium
tuberculosis. The vaccine is 70-80% effective against the most severe
forms of TB such as Tb meningitis in children
• BCG is given anytime from birth to 15days of life along with the zero
dose of oral polio vaccine
• It is given over the left arm at a dose of 0.05mls.
 REFERENCES
• Nelson textbook of pedriatrics 18th edition.
• Jolly textbook of Tropical pedriatrics.
• Paedriatric society of New Zealand(2005).
• American Academy of pedriatrics subcommittee on Diagnosis and
management of Bronchiolitis.
• Class note on Respiratory system.