This document discusses sinusitis, beginning with a definition and causes. It then covers the clinical presentation, investigations, differential diagnosis, treatment, and complications of both acute and chronic sinusitis. Key points include that acute sinusitis is usually preceded by a viral upper respiratory infection and is commonly caused by Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Facial pain, nasal discharge, and swelling over the affected sinus are common symptoms. Treatment involves antibiotics, analgesics, nasal decongestants, and irrigation. Complications can include orbital or intracranial infections if not properly treated.

1. Sinusitis

4. What is sinusitis?
An acute inflammatory process involving
one or more of the paranasal sinuses.
A complication of 5%-10% of URIs in children.
Maxillary and ethmoid sinuses are most
frequently involved

5. Causes:
1. Acute infective rhinitis.
2. Swimming & diving .
3. Dental extraction & infection.
4. Fractures involving sinuses.
5. Barotrauma.
Note : Rashid do skin flab
Acute sinusitis
R = Rhinitis
S = Swimming
D = Dental extraction
& infection
F = Fractures
B = Barotrauma

6. Predisposing factors:
A. Local:
Nasal obstruction.
Sinus meatus obstruction.
Neighboring infection.
Previous infection.
B. General:
Debilitation & immune deficiency
Mucociliary disorders (cystic fibrosis)
Irritating atmospheric conditions.
Note : PN infection , NS obstruction = Local
P = Previous infection
N = Neighboring infection
N = Nasal obstruction
S = Sinus meatus Ob.

7. Bacteriology:
Usually mixed & preceded by viral infection
* Strep. pneumonia,
* Staph. Aureus ,
* Moraxella catarrhalis
* Kleb. , E.coli .
* Anaerobic infection ( dental origin).

8. Pathophysiology
 The mucosal lining of the sinuses produce mucoid
secretion transmitted toward the sinus ostium, this
process will be stopped during inflammation of the
nasal mucosa because of edema of the sinuses ostia
leading to accumulation of the secretion inside these
sinuses. Bacteria invade and pus accumulates inside
the sinus cavities.
 Postnasal drainage causes obstruction of nasal
passages and an inflamed throat.

9.  Acute Sinusitis – respiratory symptoms
last longer than 10 days but less than 30
days.
 Subacute sinusitis – respiratory
symptoms persist longer than 30 days
without improvement.
 Chronic sinusitis – respiratory symptoms
last longer than 120 days.

10. Clinical presentation:
1. Preceding URTI.
2. Constitutional symptoms (headache, fatigue, fever)
3. Nasal obstruction.
4. Nasal discharge ,postnasal drip & halitosis
5. Sever facial pain over sinus , increases by bending
or coughing.
6. Swelling &tenderness over affected sinus.
Note : NO ipad I had, So I Sad
NO = Nasal discharge &
Obstruction
i = infection
pad = postnasal drip
H = halitosis
S = Severe facial pain
S = Swelling

11. Investigations:
1. Endoscopical examinations.
2. Radiological examinations:
(X-ray sinuses, CT scan, MRI).

12. Differential diagnosis:
1. Dental pain.
2. Migraine.
3. Trigeminal neuralgia.
4. Neoplasms of sinuses.
5. Infections e.g. erysipelas & H. Zoster.
6. Temporal arteritis, Angioneurotic oedema &
Insect bite.
Note : DM in ENT
D = Dental pain
M = Migraine
i = infections
E = Edema (angioneurotic edema)
N = Neoplasms of sinuses
T = Trigeminal neuralgia & Temporal
arteritis

13. Treatment:
1. Treatment of infections.
2. Treatment of pain.
3. Decongestant
4. Irrigation.

14.  Antimicrobials: treat for 10-14 days, depending upon
severity, with one of the following:
 Amoxicillin:20-40mg/kg/d in 3 divided doses(>20kg,
250mg tid)
 Augmentin:25-45mg/kg/d in 2 divided doses(>20kg,
400mg q12) Use chewable or suspension if child is less
than 40kg.
 Analgesia
 Acetaminophen , or ibuprofen
 Codeine – for severe pain
 Nasal douche with saline
 Rhinocort nasal spray – 2 sprays in each nostril every 12
hours for children over 6 years of age.

15. Non-pharmacological treatment
 Humidifier to relieve the drying of mucous
membrane associated with mouth breathing
 Increase oral fluid intake
 Saline irrigation of the nostrils
 Moist heat over affected sinus
 Prolonged shower to help promote drainage

16. Chronic Sinusitis

17. Predisposing Factors:
1. Vasomotor rhinitis (VMR), allergic rhinitis (AR).
2. Smoking & other pollutions.
3. Nasal polyposis.
4. Endocrine disorders, e.g. Myxedema.
5. Congenital mucociliary disorders.

18. Bacteriology:
Usually mixed
*Strep.
*Pneumococci.
*Proteus, Pseudomonus & E.coli
*Anaerobic.

19. Clinical features:
Same as acute but lesser degree:
*Nasal &post nasal discharge of mucoid or
purulent.
*Headache; heavy or dull ache.
*Anosmia or cacosmia.
*Less sever constitutional symptoms.

20. Principles of Treatment:
*Decongestants;
- topical decongestants for a short time,
- systemic may be of value.
*Steroid may of benefit (systemic or local).
*Systemic antibiotics.
*Surgical drainage .

21. Complications of sinusitis:
The orbital is the most common complication
of acute sinusitis in children

22. Mode of spread:
1. Direct: through bony wall.
2. Venous.
3. Lymphatics.
4. Via perineural space of Olfactory nerve to
subarachnoid space.

23. Types:
1. Extracranial complicatons:
a. Osteomayelitis:
Rare ,usually of frontal sinus, increases in
young adults. Forehead oedema (Pott’s puffy
tumor).
b. Orbital complications:
Rare but more in children due to ethmoiditis

26. c. Others:
1. Infection of nasopharynx.
2. Lateral pharyngitis & Tonsillitis.
3. Otitis media.
4. Laryngo-tracheitis.
5. Bronchitis.
6. Association with bronchiectasis.
7. Association with asthma.

27. 2.Intracranial complications:
a. Meningitis +/- extradural or subdural
abscesses.
b. Cavernous sinus thrombosis.
c. Brain lesion: According to affected sinus:-
1. Frontal lobe abscess (frontal).
2. Diffuse supp. Meningitis near cribriform
plate (ethmoid).
3. Diffuse meningitis (sphenoid).
4. Maxillary sinusitis rarely causes
Intracranial complications

28. Review MCQs
1. Which microorganism is not commonly implicated in
acute rhinosinusitis?
A. P. aeruginosa
B. H. influenza
C. M. catarrhalis
D. Pneumoniae
2. Local precipitating factor for maxillary sinusitis:
A. Poor diet
B. Fatigue
C. Nasal obstruction
D. Chilling
E. Irritating atmospheric conditions

29. 3. The most common three causative bacterial
agents of acute sinusitis are:
A. Streptococcus pneumoniae, Haemophilus
influenzae, and Moraxella catarrhalis.
B. Streptococcus pneumoniae, Staphylococcus aureus,
and Moraxella catarrhalis.
C. Streptococcus pneumoniae, Haemophilus
influenzae, and Staphylococcus aureus.
D. Staphylococcus aureus, Haemophilus influenzae,
and Moraxella catarrhalis.
E. Streptococcus pneumoniae, Haemophilus
influenzae, and anaerobic bacteria.

30. 4. A ten year old girl presented with pain between the
eyes, frontal headache, discharge from the nose, post
nasal drip and high fever; what is the provisional
diagnosis?
A. Acute maxillary sinusitis.
B. Acute ethmoidal sinusitis.
C. Acute sphenoidal sinusitis.
D. Chronic ethmoidal sinusitis.
5. All of the following are complications of sinusitis,
except:
A. Cavernous sinus septic thrombosis
B. Meningitis
C. Pott's puffy tumor
D. Glomerulonephritis
E. Toxic shock syndrome

31. 6. Pott's puffy tumor is related to:
A. Cavernous sinus infection
B. Infected middle turbinate
C. Pyogenic frontal sinusitis
D. Tuberculosis of sinuses
7. Complication of sinusitis:
A. Usually fatal
B. Cavernous sinus thrombosis may be fatal
C. Pott puffy tumor is a complication of sphenoid sinusitis.
D. Orbital cellulitis is most serious one

32. 8. Following structures open into middle meatus:
A. Sphenoid sinus.
B. Frontal sinus.
C. Posterior ethmoid cells.
D. Nasolacrimal duct
9. Which of the following paranasal sinuses is
commonly involved by osteoma?
A. Maxillary
B. Ethmoid
C. Frontal
D. Sphenoid

33. 10. Best radiological test for maxillary sinus is:
A. Occipito-frontal view
B. Occipito-mental view
C. Lateral
D. CT scan
11. The best radiological study of the sinus diseases is:
A. Water's view plane X-ray
B. MRI
C. Ultrasound of the sinuses
D. CT scan
E. All of the above

34. 12. Which of the following arteries belongs to internal
carotid system?
A. Sphenopalatine
B. Greater palatine
C. Anterior ethmoidal
D. Nasopalatine
13. All of the following are correct regarding frontal
sinus, except:
A. Acute infection causes diurnal headache
B. Most common site for osteoma formation
C. Involved in Pott’s puffy tumour
D. Involved in multiple polypi

35. 14. A 25-year-old boy received 10-day treatment with
amoxicillin for acute sinusitis. The symptoms and
signs of disease still persist. Which of the following
antibiotics should now be used?
A. Cephalexin
B. Erythromycin
C. Both amoxicillin and erythromycin
D. Amoxicillin with clavulanic acid
15.Opening of nasolacrimal duct is situated in:
A. Superior meatus
B. Middle meatus
C. Ethmoid infundibulum
D. Inferior meatus

36. 16. The lymphatic drainage of the nose:
A. Go directly to the inferior deep cervical lymph nodes.
B. Never pass to the submental lymph nodes.
C. The tip of the nose is devoid of lymphatic drainage.
D. The posterior part of the nose is drained to the
retropharyngeal and upper deep cervical lymph nodes.
17. Blood supply of the nose:
A. Supplied by external carotid artery only.
B. Supplied by internal carotid artery only.
C. There is no connection with the sagittal sinus.
D. The maxillary artery is the main arterial supply to the
nasal cavity.
E. The facial artery is a terminal branch of the external
carotid artery.

37. 18. The external nose shape is maintained by skeletal
framework which is composed of:
A. Bone only.
B. Cartilage only.
C. Bone in upper 1/3 and cartilage in lower 2/3.
D. Bone in upper 2/3 and cartilage in lower 1/3.
E. Bone in upper 1/2 and cartilage in lower 1/2.
19. Pain due to acute sinusitis:
A. It is not related to the sinus involved.
B. It has a diurnal variation.
C. It is agonizing in open type of sinusitis.
D. Not associated with otalgia.
E. Pain killers alone relieve it.

38. 20. The little’s area is supplied by :
A. Superior labial, anterior ethmoidal, greater palatine and
spheno-ethmoidal arteries.
B. Superior labial, posterior ethmoidal, greater palatine and
spheno-ethmoidal arteries.
C. Superior labial, anterior ethmoidal, lesser palatine and
spheno-ethmoidal arteries.
D. Inferior labial, anterior ethmoidal, greater palatine and
spheno-ethmoidal arteries.
E. None of the above.

39. 21. Which of the following is not a symptom of acute
maxillary sinusitis?
A. Pain in the cheek.
B. Tenderness over the cheek.
C. Edema over the cheek.
D. Discharge from the middle meatus.
E. Dullness on trans-illumination.
22. The commonest paranasal sinus to cause an
intracranial complication in a 2 years old child is:
A. Frontal
B. Maxillary
C. Ethmoid
D. Sphenoid

40. 23. What is most true about the function of the
paranasal sinuses?
A. They protect the eye.
B. Help in olfaction.
C. They reduce the weight of the skull.
D. Do not appear to have a function.
E. They produce resonance of sound

41. Respiratory Tract Disorders

42.  Respiratory disorders are the most frequent cause of
admission for neonatal intensive care in both term and
preterm infants.
 Signs and symptoms of respiratory distress include:
 Cyanosis
 Grunting
 Nasal flaring
 Retraction
 Tachypnea
 Decreased breath sounds with or without rales
 Pallor

43. The first breath
Initiation of the first breath is caused by:
1. Decline in PaO2 and PH and a rise in Paco2 as a result of
interruption of the placental circulation
2. A redistribution of cardiac output
3. A decrease in body temperature and
4. Various tactile and sensory inputs

44. Hyaline membrane disease
(Respiratory distress syndrome of newborn)
 Is a respiratory disorder that primarily affects preterm
infants who are born before the biochemical maturation of
their lungs.
 Biochemical development: The most important prenatal
event is the production of surfactant by type II alveolar cells
The major function of surfactant is to decrease alveolar
surface tension and increasing lung compliance.
 Surfactant prevent alveolar collapse at the end of expiration
and allows for opening of the alveoli at a low intra-thoracic
pressure. The ratio of lecithin to sphingomyelin in the
aminiotic fluid is areflection of the amount of intrapulmonary
surfactant and lung maturity .an L/S ratio of 2:1 or greater
usually indicates biochemical lung maturity .

45.  Surfactant is increased by:
A. Steroid administration
B. Prolonged membrane rupture
C. Preeclampsia
D. Placental insufficiency
E. Thyroid hormone
F. Theophyline
 Surfactant is decreased by:
A. Maternal diabetes
B. acute asphyxia (but not Chronic)

46. Pathophysiology
 The lungs are poorly compliant owing to deficiency of
surfactant resulting in classic complex of progressive
atelectasis, intrapulmonary shunting, hypoxemia, and
cyanosis.
 The hyaline membrane that forms and lines the alveoli is
composed of protein and sloughed epithelium – the result
of oxygen exposure , alveolar capillary leakage and the
forces generated by the mechanical ventilation of these
infants.

47.  Affected infants characteristically present with tachypnea ,
grunting, nasal flaring, chest retraction, and cyanosis in
first three hours of life.
 There is a decrease in air entry on auscultation.
 Apnea and irregular respiration are ominous sign requiring
immediate action.
 Respiratory failure may occur in severe course
Clinical features

48. Clinical course
 The natural course is a progressive worsening over the
first 48- 72 hrs of life.
 After the initial insult to the airway lining , the epithelium is
repopulated with type II alveolar cells. Subsequently , there
is increase production and release of surfactant, so that
there are sufficient quantities in the air spaces by 72 hours
of life. This result in improvement in lung compliance and
resolution of the respiratory distress .

51. Diagnosis
 The diagnosis is confirmed by a chest radiograph that
reveals a uniform ground-glass pattern and an air
bronchogram that is consistent with a defuse atelectasis ,
clinical manifestation and gas analysis.
 RDS should be differentiated from ( early onset sepsis,
pneumonia, cyanotic heart diseases, aspiration syndromes,
spontaneous pneumothorax, transient tachypnea of
newborn).

52. Therapy and prognosis:
a- Conventional therapy
 The conventional therapy for the affected premature
infant include supportive care as well as the
administration of oxygen. It also necessary to increase
the main airway pressure by use of continuous positive
airway pressure, intermittent assisted ventilation, or a
high frequency oscillation.
 Outcome with conventional therapy is good
b- Exogenous surfactant replacement therapy with
artificial or bovine surfactant
 It has become an important intervention for those
infants with severe surfactant deficiency.
 Alveolar opening and improvement in oxygenation and
ventilation occur almost immediately.

53. Prevention:
When amniotic fluid assessment reveals fetal lung immaturity
and preterm delivery can not be prevented, administration of
corticosteroid to the mother 48 hours before delivery can
induce or accelerate the production of fetal lung surfactant.
Complications:
Common complications and associated findings include:
1. Pneumothorax
2. Patent ductus arteriosus
3. Intraventricular hemorrhage
4. Necrotizing enterocolitis
5. Bronchopulmonary dysplasia
6. Retinopathy of prematurity

54. Transient tachypnea of newborn:
 Is thought to result from decreased lymphatic absorption
of fetal lung fluid
 It most commonly occurs in the infant born near term by
cesarean section, without preceding labor (the
catecholamine surge associated with labor and delivery
which is thought to enhance pulmonary lymphatic drainage
does not occur in this setting)
Clinical features:
 The tachypnea is quiet or mild and usually not associated
with retraction.
 The infant appears comfortable and rarely cyanotic.

55. Diagnosis: is based on:
 The delivery.
 Chest radiograph, which is characterized by:
1. Fluid in the major fissure
2. Prominent vascular marking
3. Increased interstitial markings and hyperinflation
 Auscultation may reveal rales.
Therapy:
 Is supportive, the tachypnea resolves in a few days.
 Low doses of supplemental oxygen may be required.

56. Persistent of the fetal circulation
(Persistent pulmonary hypertension)
 Usually a disease of term infants who are experience acute or chronic
in utero hypoxia.
 It is seen frequently in infant with meconium aspiration syndrome.
Pathophysiology:
the primary abnormality is a failure of the pulmonary vascular resistance to
fall with postnatal lung expansion and oxygenation.
(a) Normally at birth the systemic vascular resistance rises as a result of
cessation of blood flow through the placenta, and pulmonary vascular
resistance falls with the first breath.
(b) With persistence of the fetal circulation, the pulmonary vascular
resistant continues to be high and may in fact be higher than the
systemic resistance. This result in shunting of the deoxygenated blood
which is returning to the right side of the heart away from the lungs.
The right to left shunt can occur at both the atrial level (foramen of
ovale) and through the ductus arteriosus. Because the lung are
bypassed the blood is not oxygenated and hypoxemia ensues

57. Clinical features:
 These infants have rapidly progressive cyanosis associated
with mild to severe respiratory distress.
 There is a varied response to oxygen administration depending
on the size of the shunt.
Diagnosis:
(a) The diagnosis is suggested by a history of perinatal asphyxia
and clinical cyanosis at birth combined with a negative
cardiovascular examination and negative chest radiograph,
although parenchymal disease may coexist (MAS, RDS).
(b) Echocardiography should be used to establish the diagnosis
and should demonstrate:
 The absence of cyanotic heart disease .
 An increased pulmonary vascular resistance
 The presence of right to left shunt at the foramen of ovale,
ductus arteriosus, or both

58. Therapy:
It Includes:
1. Supplemental oxygen
2. Mechanical ventilation
3. Hyperventilation
4. Support of systemic blood pressure
5. Administration of sodium bicarbonate and pulmonary
vasodilators
Prognosis:
 The overall mortality rate associated with this disease is
high.
 Extra-corporeal membrane oxygenation (ECMO) may
improve the outcome.

59. Apnea
 Apnea is cessation of breathing for longer than 20 seconds
 Apnea often occurs in preterm infants (apnea of
prematurity) and reflect immaturity of the respiratory control
mechanism in the brain stem.
Clinical features:
 Bradycardia (HR less than 80 beats/min) often
associated with apnea.
 Apnea of prematurity is characterized by periodic
breathing and intermittent hypoxia, which further
diminish respiratory derive.

60. Diagnosis:
Apnea of prematurity is made after excluding other reason
for the apnea like:
 Respiratory (pneumonia, airway obstruction, hypoxia,
pneumothorax).
 CNS (intracranial hemorrhage, seizure, drugs, hypoxic
injury).
 Infections (sepsis, meningitis).
 Metabolic (hypoglycemia, hypocalcemia, decrease or
increase sodium, hypothermia).
 Cardiovascular (heart failure, hypotension).
 Gasrtointestinal (necrotizing enterocolitis).

61. Therapy:
Therapy of apnea of prematurity include one of the following:
A. Tactile stimulation
B. Maintain body temperature
C. Supplemental oxygen
D. Administration of respiratory stimulant (theophylline,
caffeine)
E. Use continuous positive air way or intermittent assisted
ventilation
F. Treatment of underling cause
Prognosis:
Apnea of prematurity does not alter prognosis unless it severe
recurrent and refractory to therapy

62. Choanal atresia
 Is a unilateral or bilateral obstruction of the posterior nasal
airway by a membrane or bony septum.
 This life threatening anomaly result from failure of the
bucconasal mucosa to rupture.
Clinical features:
 Because most newborn are obligate nose breathers,
bilateral atresia usually presents in the delivery room as
airway obstruction, apnea and cyanosis.
 Distressed neonate then cry, which relieves the cyanosis.
 Unilateral atresia may be asymptomatic.

63. Diagnosis:
The diagnosis is confirmed either by inability to pass a suction
catheter through the nostril into the oropharynx or by
radiography using radioopaque dye to show the area of nasal
obstruction.
Therapy:
 Emergency management consists of establishing an
airway either with an oral airway or by endotracheal
intubation.
 Definitive therapy is surgical reconstruction performing
in neonatal period.

64. Diaphragmatic hernia is a displacement of the abdominal
content into the thoracic cavity through a defect in the
diaphragm.
Types :
A. Hernias through the foramen of bochdalek are by far the
most commonly seen diaphragmatic hernia. The defect ,
which almost always is on the left occurs in the posterio-
lateral portion of the diaphragm. It results from failure of
the pleuroperitoneal canal to close, which normally occurs
between 6-8 wks gestation.
B. Hernias through the foramen of morgagni are somewhat
rare, the hernia usually on the right. Frequently, the hernia
contain only omentum and the affected newborn is
asymptomatic.
Diaphragmatic hernia

65. Pathophysiology:
 Ipsilateral pulmonary hypoplasia results from compression of
the affected lung by the displaced gastrointestinal organs.
 A shift of the mediastinal structures resulting in compression
of the contralateral lung may cause hypoplasia of the lung to
a lesser degree.
Diagnosis:
Is confirmed by a chest radiograph demonstrating air-filled
bowel in the hemithorax.

67. Therapy :
Includes intubation, vigorous oxygenation and mechanical
ventilation, decompression of the intestinal tract with a
nasogastric tube, correction of metabolic acidosis, and
surgical removal of the abdominal contents from the thorax
with repair of the hernia.
A. Mask and bag ventilation should be avoided or minimized
because it results in distension of the bowel and further
compromises the pulmonary function of the affected
newborn.
B. Pulmonary hypertension frequently complicates the
preoperative and postoperative course.
C. Extracorporeal membrane oxygenation may be helpful in
selected infants.

68. Prognosis :
Survival rates depend on:
1. The degree of the lung hypoplasia
2. The presence of other anomalies
3. Symptoms before 24 hours of age
4. Herniation to the contralateral lung
5. Need for ECMO
*With conventional therapy, survival rates are approximately
67%, however the use of extracorporeal membrane
oxygenation may improve survival.

69. Meconium aspiration syndrome (MAS)
MAS is a multiorgan disorder with perinatal asphyxia as the
underlying cause . it is most commonly occurs in post term
infants and
in infants who are small for gestational age due to intrauterine
growth
retardation . both have placental insufficiency as a common
for fetal
hypoxia .
(1) Pathophysiology . the fetal hypoxia triggers via a vagal
reflex ,
the passage of thick meconium into the amniotic fluid .the
contaminated amniotic fluid is swallowed into the oropharynx
and
aspirated at birth with the initiation of breathing . with severe

70.  Is a respiratory disorder that primarily affects preterm
infants who are born before the biochemical maturation of
their lungs.
 Biochemical development: The most important prenatal
event is the production of surfactant by type II alveolar cells
The major function of surfactant is to decrease alveolar
surface tension and increasing lung compliance.
 Surfactant prevent alveolar collapse at the end of expiration
and allows for opening of the alveoli at a low intra-thoracic
pressure. The ratio of lecithin to sphingomyelin in the
aminiotic fluid is areflection of the amount of intrapulmonary
surfactant and lung maturity .an L/S ratio of 2:1 or greater
usually indicates biochemical lung maturity .

71.  Is a respiratory disorder that primarily affects preterm
infants who are born before the biochemical maturation of
their lungs.
 Biochemical development: The most important prenatal
event is the production of surfactant by type II alveolar cells
The major function of surfactant is to decrease alveolar
surface tension and increasing lung compliance.
 Surfactant prevent alveolar collapse at the end of expiration
and allows for opening of the alveoli at a low intra-thoracic
pressure. The ratio of lecithin to sphingomyelin in the
aminiotic fluid is areflection of the amount of intrapulmonary
surfactant and lung maturity .an L/S ratio of 2:1 or greater
usually indicates biochemical lung maturity .

72. Thank You